$EPA
United States
Environmental Protection
Agency
Great Lakes
National Program Office
77 West Jackson Boulevard
Chicago, Illinois 60604
EPA 905-R94-025
October 1994
Assessment and
Remediation of
Contaminated Sediments
(ARCS) Program
BASELINE HUMAN HEALTH RISK
ASSESSMENT: GRAND CALUMENT
RIVER/INDIANA HARBOR CANAL,
INDIANA, AREA OF CONCERN
United States Areas of Concern
ARCS Priority Areas of Concern
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BASELINE HUMAN HEALTH RISK ASSESSMENT:
GRAND CALUMET RIVER/INDIANA HARBOR CANAL,
INDIANA, AREA OF CONCERN
BY
JUDY L. CRANE
AScI CORPORATION
ATHENS, GEORGIA 30605
PROJECT OFFICER
ROBERT B. AMBROSE, JR.
ENVHIONMENTAL RESEARCH LABORATORY
ATHENS, GEORGIA 30613
ENVIRONMENTAL RESEARCH LABORATORY
OFFICE OF RESEARCH AND DEVELOPMENT
U.S. ENVIRONMENTAL PROTECTION AGENCY
ATHENS, GEORGIA 30613
U.S Environmental Protection Agency
7R^'on f5-Library (PL.12J) ^
II West Jackson Bou/evard is>fh n
Chicago, II 60604 3590 h Fl00f
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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-Cl-
0012. 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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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 L. 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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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 (AOQ
Buffalo River, NY, Grand Calumet River/Indiana Harbor Canal, 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 Grand
Calumet River/Indiana Harbor Canal 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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ABSTRACT
The Assessment and Remediation of Contaminated Sediments (ARCS)
program, a 5-year study and demonstration project relating to the control and
removal of contaminanted 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 Grand Calumet River/Indiana Harbor
Canal (GCR/IHC), located in northwestern Indiana, 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 severely degraded GCR/IHC 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.
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TABLE OF CONTENTS
DISCLAIMER ii
PREFACE iii
FOREWORD iv
ABSTRACT v
LIST OF FIGURES ix
LIST OF TABLES x
ACKNOWLEDGMENTS xii
1. EXECUTIVE SUMMARY 1-1
1.1 OVERVIEW 1-1
1.2 EXPOSURE ASSESSMENT 1-1
1.3 RISK ASSESSMENT 1-2
1.3.1 Determination of Risk 1-2
1.3.2 Dermal Exposure Risk Estimates 1-4
1.3.3 Fish Consumption Risk Estimates 1-4
1.3.4 Uncertainties 1-6
2. INTRODUCTION 2-1
3. GRAND CALUMET RIVER/INDIANA HARBOR CANAL AREA OF
CONCERN 3-1
3.1 INTRODUCTION 3-1
3.2 GRAND CALUMET RIVER BASIN 3-1
3.2.1 Environmental Setting 3-1
3.2.2 Grand Calumet River 3-3
3.2.3 Indiana Harbor Canal 3-3
3.2.4 Indiana Harbor 3-5
3.3 WATER QUALITY STANDARDS 3-5
3.4 OVERVIEW OF CONTAMINATION PROBLEMS 3-6
3.5 LAND USE PATTERNS 3-8
3.6 DRINKING WATER INTAKES 3-10
3.7 CONTAMINATION OF FISH 3-10
3.7.1 Routes of Contamination 3-10
3.7.2 Fish Advisories 3-12
4. RISK ASSESSMENT FRAMEWORK 4-1
4.1 CONCEPT OF RISK 4-1
4.2 RISK FRAMEWORK 4-2
VI
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TABLE OF CONTENTS
5. EXPOSURE ASSESSMENT 5-1
5.1 OVERVIEW 5-1
5.2 EXPOSURE PATHWAYS 5-1
5.2.1 Incomplete Exposure Pathways 5-1
5.2.2 Complete Exposure Pathways 5-2
5.2.2.1 Complete Exposure Pathways in the
Grand Calumet River 5-3
5.2.2.2 Complete Exposure Pathways in the
Indiana Harbor 5-6
5.3 DATA USED IN THE EXPOSURE ASSESSMENT 5-6
5.3.1 Sources of Data Reports 5-6
5.3.2 Data Review 5-7
5.3.3 Data Used 5-7
5.3.3.1 Porewater Data 5-7
5.3.3.2 Water Column Data 5-9
5.3.3.3 Fish Data 5-9
5.4 EXPOSURE ASSESSMENT 5-11
5.4.1 General Determination of Chemical Intakes 5-11
5.4.2 Intakes: Ingestion of Contaminated Fish 5-11
5.4.3 Intakes: Dermal Contact with Surface Water 5-14
5.4.4 Intakes: Dermal Contact with Sediments 5-15
6. TOXICITY ASSESSMENT 6-1
6.1 TOXICITY VALUES 6-1
6.2 LIMITATIONS 6-1
7. BASELINE RISK CHARACTERIZATION FOR THE GRAND CALUMET
RIVER/INDIANA HARBOR CANAL AREA OF CONCERN 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 GRAND CALUMET RR^ER . 7-2
7.3.1 Dermal Exposure to Surface Water 7-2
7.3.2 Dermal Exposure to Sediments 7-3
7.3.3 Ingestion of Contaminated Fish 7-4
7.3.3.1 Noncarcinogenic Effects 7-4
7.3.3.2 Carcinogenic Effects 7-4
7.4 HUMAN HEALTH RISKS IN INDIANA HARBOR 7-5
7.4.1 Noncarcinogenic Effects from Consuming Fish 7-5
7.4.2 Carcinogenic Effects from Consuming Fish 7-5
vn
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TABLE OF CONTENTS
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 8-3
8.2.4 Risk Characterization 8-4
8.3 SUMMARY 8-5
REFERENCES 9-1
APPENDIX A: Fish Data for the Grand Calumet River and Indiana
Harbor Canal A-l
APPENDK B: Human Toxicity Estimates for Contaminants Present
in the Grand Calumet River/Indiana Harbor Canal
Area of Concern B-l
APPENDDI C: Dermal Exposure Estimates at Other Sites Along
the Grand Calumet River C-l
vin
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LIST OF FIGURES
Figure " Page
2.1 Map of ARCS priority Areas of Concern (USEPA, 199Ib) 2-3
3.1 Grand Calumet River/Indiana Harbor Canal Area of
Concern (IDEM, 1991) 3-2
3.2 Location of point source discharges (HydroQual,
1986) 3-4
3.3 Composite of all sampling in the GCR/IHC AOC from
1972 to 1989 3-7
3.4 Major land uses in the Area of Concern 3-9
4.1 Components of the baseline human health risk
assessments 4-3
5.1 Location of potential exposure areas along the Grand
Calumet River 5-4
5.2 Location of Roxana Marsh 5-5
IX
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LIST OF TABLES
Table Page
1.1 Amount of Fish Assumed to be Consumed per Person per Day
from the Grand Calumet River for each Exposure
Scenario 1-3
1.2 Results of the Dermal Exposure Assessment to the 7 to 17
Years Old Age Group at Roxana Pond 1-4
1.3 Summary of Noncarcinogenic and Carcinogenic Risks
Resulting from Fish Consumption in the GCR/IHC AOC . . 1-5
5.1 Potential Pathways in the GCR/IHC AOC 5-2
5.2 Complete Exposure Pathways in the GCR/IHC AOC 5-3
5.3 Sediment Pore water and Surface Water Chemical
Concentrations used in the Dermal Exposure Assessment . 5-8
5.4 Sampling Information for GCR/IHC Fish Species 5-10
5.5 Generic Equation for Calculating Chemical Intakes (USEPA,
1989a) 5-12
5.6 Equation Used to Estimate Contaminant Intakes Due to the
Ingestion of Fish 5-13
5.7 Parameters Used to Estimate Contaminant Intakes Resulting
from the Consumption of Contaminated Fish from the
GCR/IHC AOC 5-16
5.8 Equation for Estimating Absorbed Doses of Contaminants due
to Dermal Contact with Chemicals in the Sediment
Porewater or Surface Water 5-17
5.9 Parameter Values Used in Estimating the Absorbed Dose due
to Dermal Contact with Chemicals in the Surface Water
while Wading in Roxana Pond 5-18
5.10 Estimated Permeability Constants (Rp) for Chemicals Used in
the Dermal Exposure Assessment 5-19
5.11 Parameter Values Used in Estimating the Absorbed Dose due
to Dermal Contact with Chemicals in the Sediment
Porewater while Wading in Roxana Pond 5-21
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 GCR/IHC Area of Concern 6-3
7.1 Risk Associated with Dermal Exposure to Contaminated Surface
Water, Typical Exposure, 7 to 17 Years Old Age Group ... 7-6
7.2 Risk Associated with Dermal Exposure to Surface Water,
Reasonable Maximum Exposure, 7 to 17 Years Old Age
Group 7-7
7.3 Risk Associated with Dermal Exposure to Contaminated
Sediments, Typical Exposure, 7 to 17 Years Old Age Group 7-8
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LIST OF TABLES
Risk Associated with Dermal Exposure to Contaminated
Sediments, Reasonable Maximum Exposure, 7 to 17
Years Old Age Group 7-10
7.5 Noncarcinogenic Risks Associated with Consuming Whole
Pumpkinseed Collected from the Grand Calumet River
(7/8/87) 7-12
7.6 Noncarcinogenic Risks Associated with Consuming Whole
Golden Shiners Collected from the Grand Calumet
River (7/8/87) 7-13
7.7 Noncarcinogenic Risks Associated with Consuming Whole Carp
Collected from the Grand Calumet River (11/18/87) 7-14
7.8 Noncarcinogenic Risks Associated with Consuming Skin-on-
Fillet Carp Collected from the Indiana Harbor Canal
(11/1/88) 7-15
7.9 Noncarcinogenic Risks Associated with Consuming Whole Carp
Collected from the Indiana Harbor Canal (11/18/87) 7-16
7.10 Carcinogenic Risks Associated with Consuming Whole
Pumpkinseed Collected from the Grand Calumet River
(7/8/87) 7-17
7.11 Carcinogenic Risks Associated with Consuming Whole Golden
Shiners Collected from the Grand Calumet River
(7/8/87) 7-18
7.12 Carcinogenic Risks Associated with Consuming Whole Carp
Collected from the Grand Calumet River (11/18/87) 7-19
7.13 Carcinogenic Risks Associated with Consuming Skin-on-Fillet
Carp Collected from the Indiana Harbor Canal (11/1/88) . 7-20
7.14 Carcinogenic Risks Associated with Consuming Whole Carp
Collected from the Indiana Harbor Canal (11/18/87) 7-21
7.15 Noncarcinogenic Risks Associated with Consuming a Mixture
of Indiana Harbor Fish Excluding Carp 7-22
7.16 Noncarcinogenic Risks Associated with Consuming Indiana
Harbor Carp 7-23
7.17 Noncarcinogenic Risks Associated with Consuming Nearshore
Lake Michigan Fish 7-24
7.18 Carcinogenic Risks Associated with Consuming a Mixture
of Indiana Harbor Fish Excluding Carp 7-25
7.19 Carcinogenic Risks Associated with Consuming Indiana
Harbor Carp 7-26
7.20 Carcinogenic Risks Associated with Consuming Nearshore Lake
Michigan Fish 7-27
7.21 Summary of Noncarcinogenic and Carcinogenic Risks Resulting
from Fish Consumption in the GCR/IHC AOC 7-28
XI
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ACKNOWLEDGMENTS
Several people provided helpful information about the Grand Calumet
River/Indiana Harbor Canal Area of Concern including: Bob Tolpa (U.S. EPA
Region V), Michael Mikulka (U.S. EPA Region V), Dave Dabertin (IDEM), Lee
Bridges (IDEM), Anne Spacie (Purdue University), and Doreen Carey (Grand
Calumet Task Force). Members of the ARCS Risk Assessment and Modeling Work
Group have provided useful feedback for the preparation of this risk assessment,
especially Marc Tuchman (U.S. EPA/GLNPO), Carole Braverman (U.S. EPA
Region V), James Martin (AScI Corp.), and Bill Sutton (ERL-Athens).
Appendix C was added to the original report to address the concerns of
dermal exposure. This section was compiled and written by Amy Pelka (U.S. EPA
Region V), and Diane Dennis-Flagler (U.S. EPA/GLNPO).
XII
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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 Grand Calumet River/Indiana Harbor
Canal (GCR/IHC), located in northwestern Indiana, is one of these AOCs.
In this report, exposure and risk assessment guidance, developed for the
EPA Superfund program, has been applied to determine the baseline human
health risks associated with direct and indirect exposures to sediment-derived
contaminants in the severely degraded GCR/IHC 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 EXPOSURE ASSESSMENT
Due to the extensive contamination of the GCR/IHC AOC, a number of
contaminants have been detected in the water, sediment, and biota of this area.
These contaminants include heavy metals, phenols, PCBs, pesticides, and several
other organic chemicals.
This assessment focused on three pathways by which residents of the
GCR/IHC AOC could be exposed to sediment-derived contaminants: 1)
consumption of contaminated fish from the Grand Calumet River and Indiana
Harbor, 2) dermal exposure to contaminated water at Roxana Pond, an extension
of the Grand Calumet River, and 3) dermal exposure to contaminated sediment at
Roxana Pond. Other exposure pathways were determined to be either incomplete
(e.g., ingestion of sediments) or insignificant in terms of risk (e.g., limited dermal
exposure to surface water in the Indiana Harbor while fishing).
Exposure sites were selected in the AOC based on where people would have
access to the site and on reports of people using certain sections of the Grand
Calumet River for fishing and playing (e.g., wading). Access to the Grand
Calumet River is restricted in several areas, and wading by children is most likely
to occur at Roxana Pond. Fishing may occur at several different locations within
the Grand Calumet River. As for the Indiana Harbor Canal, this area did not
1-1
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appear to be a place that people fished or played in, mainly because the canal is
flanked on both sides by industrial development. Thus, the Indiana Harbor Canal
was not chosen as an exposure site. People have been observed fishing in the
Indiana Harbor, thus the entire harbor area was selected as a site where people
might fish and come in dermal contact with surface water. Fishing and other
recreational activities also occur in the nearshore Lake Michigan area; however, it
was beyond the scope of this risk assessment to estimate potential risks resulting
from exposure to the nearshore Lake Michigan area. An exposure and risk
assessment using fish collected in the nearshore Lake Michigan area was
conducted for the purpose of comparing the results to the Indiana Harbor risk
estimates.
The list of chemicals included in the exposure assessment were selected
based on their prevalence in the sediment porewater, surface water, and fish
tissue, and also on the availability of toxicity information. Noncarcinogenic and
carcinogenic risks were estimated for both typical and reasonable maximum
exposures. Typical (i.e., average) exposures were assumed to occur over a period
of 9 years; reasonable maximum (i.e., the maximum exposure that is reasonably
expected to occur at a site) exposures were assumed to occur over a period of 30
years (USEPA, 1989a). These exposure durations were extrapolated over a period
of 70 years for estimating carcinogenic risks. For both exposure scenarios,
exposures were determined for each chemical and added for each pathway. In
addition, exposures were added across pathways for typical and reasonable
maximum exposures.
The dermal exposure pathway was limited to the 7 to 17 years old age
group, whereas the fish consumption pathway was not age specific. Different fish
consumption patterns were assumed to take place (Table 1.1). These
consumptions patterns were based, in part, on recommended values given in EPA
Superfund guidance (USEPA, 1989a,b; 1991a) or else on study assumptions.
1.3 RISK ASSESSMENT
1.3.1 Determination of Risk
Noncarcinogenic effects were evaluated by comparing an exposure level over
a specified time period with a reference dose (RfD)1 derived from a similar
exposure period [otherwise known as a hazard quotient (HQ)]. Thus, HQ =
exposure level/RfD. The sum of more than one HQ value for multiple substances
and/or multiple exposure pathways is represented by the Hazard Index (HI). An
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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TABLE 1.1. AMOUNT OF FISH ASSUMED TO BE CONSUMED PER
PERSON PER DAY FROM THE GRAND CALUMET RIVER
FOR EACH EXPOSURE SCENARIO
Exposure Scenario
Typical
Ingestion
Rate* x
(g/day)
6.5
Reasonable Maximum 54
Amount of
GCR
Fish
FI** = Consumed
(g/day)
0.05 0.3
0.1 5.4
* Source: USEPA (1991a)
** FI = Fraction of fish estimated to be ingested from the Grand Calumet
River (study assumption). For the Indiana Harbor and nearshore
Lake Michigan fish:
FI = 0.1 for typical exposures
FI = 0.25 for reasonable maximum exposures
HI value of less than 1 indicates that exposures are not likely to be associated
with adverse noncarcinogenic effects. HI 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, 1989a). This assumption of
additivity does not account for any synergistic or antagonistic effects that may
occur among chemicals.
Carcinogenic risks were estimated as the incremental probability of an
individual developing cancer over a lifetime as a result of exposure 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 represented an upper-bound estimate,
because slope factors were usually based on upper 95th percentile confidence
limits. Carcinogenic effects were summed for all chemicals in an exposure
pathway as well as for multiple pathways. This summation of carcinogenic risks
assumed that intakes of individual substances were small, that there were no
2 Slope factors are estimated through the use of mathematical extrapolation
models 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. RESULTS OF THE DERMAL EXPOSURE ASSESSMENT TO
THE 7 TO 17 YEARS OLD AGE GROUP AT ROXANA POND
Exposure Pathway HI Cancer Risk
Surface Water Exposure
Typical 0.0003 4 x 10'8
RME* 0.001 6 x 10'7
Sediment Porewater Exposure
Typical 0.03 4 x 10'7
RME 0.1 4 x IP'6
* RME = Reasonable Maximum Exposure
synergistic or antagonistic chemical interactions, and that all the chemicals
included could cause cancer. The EPA believes it is prudent public health policy
to consider actions to mitigate or minimize exposures to contaminants when
estimated, upper-bound excess lifetime cancer risks exceed the 10"5 to 10"6 range,
and when noncarcinogenic health risks are estimated to be significant (USEPA
1988a).
1.3.2 Dermal Exposure Risk Estimates
The only risk estimate that approached a level of concern was the
carcinogenic risk resulting from dermal exposure to sediment porewater under the
reasonable maximum exposure (Table 1.2). These risk estimates were only
calculated for children and teenagers in the 7 to 17 years old age group. It was
assumed that contaminants in the sediment porewater would come in contact with
the skin when someone stepped into the sediments barefoot or dipped their hand
into the sediments.
1.3.3 Fish Consumption Risk Estimates
Separate risk estimates were made for several species of fish collected from
the Grand Calumet River, Indiana Harbor Canal (IHC), Indiana Harbor, and
nearshore Lake Michigan area (Table 1.3). The IHC fish data were included
because fish will travel throughout the GCR/IHC system. The nearshore Lake
Michigan data were included for comparison purposes.
The only noncarcinogenic risk estimate that reached a level of concern (i.e.,
HI>1) was for the consumption of whole carp collected from the Indiana Harbor
Canal under a reasonable maximum exposure scenario. The noncarcinogenic risk
was due primarily to 2,3,7,8-TCDD. However, this risk estimate was based on the
1-4
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TABLE 1.3. SUMMARY OF NONCARCINOGENIC AND CARCINOGENIC
RISKS RESULTING FROM FISH CONSUMPTION IN THE
GCR/IHC AOC
Fish/Location/Sampling Date
Whole PumDkinseed/GCR/(7/8/87)*
Typical
RME**
Whole Golden Shiners/GCR/(7/8/87)
Typical
RME
Whole Carp/GCR/(ll/18/87)
Typical
RME
Skin-on-Fillet Can>/IHC/( 11/1/88)
Typical
RME
Whole CarD/IHC/(ll/18/87)
Typical
RME
Whole Fish/Indiana Harbor/no date given
Typical
RME
Whole Carp/Indiana Harbor/no date given
Typical
RME
Whole Fish/Nearshore L. Michigan/no date given
Typical
RME
HI
0.0008
0.01
0.01
0.2
0.02
0.4
0.03
0.5
0.08
1
0.03
0.7
0.04
0.8
0.02
0.5
Carcinogenic
Risk
IE- 10
6E-09
IE-OS
7E-04
2E-05
1E-03
1E-05
5E-04
3E-05
2E-03
4E-06
3E-04
2E-05
2E-03
2E-06
2E-04
* Fish were not analyzed for PCBs
** RME = Reasonable Maximum Exposure
1-5
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body burden of contaminants in raw, whole fish. Different cooking and
preparation methods would probably reduce the levels of hydrophobic organic
contaminants, like 2,3,7,8-TCDD, in the edible fish tissue. Because some of the
chemicals (e.g., PCBs) detected in these fish do not presently have RfD values, it
would be premature to state that no noncarcinogenic risk exists for the other fish
species. The noncarcinogenic risk reported here is an estimated risk based on
currently available data and toxicity information and should not be construed as
an absolute risk.
The carcinogenic risk resulting from the consumption offish was at or above
levels of concern (i.e., 106) for all fish species and sites except for pumpkinseed
collected from the Grand Calumet River. However, the pumpkinseed were not
analyzed for PCBs, the major contributor to carcinogenic risk in the other fish
species. The carcinogenic risks from consuming whole carp from either the Grand
Calumet River, Indiana Harbor Canal, or Indiana Harbor were almost identical.
This may be the result of fish travelling throughout the GCR/IHC system. In
addition, the carcinogenic risk for a pooled data set of Indiana Harbor fish (i.e.,
gizzard shad, alewife, and sunfish) was about the same as a pooled data set of
alewife and yellow perch from the nearshore Lake Michigan area.
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.
1.3.4 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. These uncertainties were
addressed in a qualitative way. A complete description of the level of uncertainty
associated with all of the assumptions and data used in this risk assessment
cannot be made. As additional data on contaminant levels in fish are collected in
the GCR/IHC AOC, 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.
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 20 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,
1991b), 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
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)
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estimate the magnitude and frequency of human exposures to sediment-derived
contaminants in the AOC, and 2) determine 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. Conservative risk
estimates are determined for both noncarcinogenic (i.e., chronic or subchronic
effects) and carcinogenic (i.e., upper-bound probability of an individual developing
cancer over a lifetime) effects resulting from direct and indirect exposures to
sediment-derived contaminants. Examples of possible exposure pathways include
the consumption of contaminated fish and waterfowl, ingestion of surface water
while swimming, and dermal contact with contaminated sediments and water.
This document presents a baseline human health risk assessment for the
Grand Calumet River and Indiana Harbor. Although the Indiana Harbor Canal
and nearshore Lake Michigan areas are also included in the AOC, people were not
determined to be exposed to contaminants in the Indiana Harbor Canal. In
addition, the nearshore Lake Michigan area encompassed too large of an area to
include under the time frame of this risk assessment. The next chapter describes
the GCR/IHC 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
' Assessment and Remediation of Contaminated Sediments
»
I . I
1» 3M
II
Figure 2.1.
Map of ARCS priority Areas of Concern (USEPA, 1991b).
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CHAPTER 3
GRAND CALUMET RIVER/INDIANA HARBOR CANAL AREA OF CONCERN
3.1 INTRODUCTION
The Grand Calumet River/Indiana Harbor Canal (GCR/IHC) AOC is located
in a heavily industrialized region of northwestern Indiana, approximately 32 km
southeast of Chicago, IL (Figure 3.1). This area underwent rapid industrialization
during the late 1800s to early 1900s and currently supports one of the most
concentrated steel and petrochemical industrial complexes in the United States
(Crawford and Wangsness, 1987; USEPA, 1990a). Contamination problems within
the AOC are extensive. Five Superfund sites, 56 Comprehensive Environmental
Response, Compensation, and Liability Act (CERCLA) sites, 425 Resource
Conservation and Recovery Act (RCRA) sites, 23 facilities which treat, store, or
dispose (TSD) of hazardous waste, 9 hazardous waste landfills or surface
impoundments, and approximately 150 leaking underground storage tanks lie
within the AOC (Bunner, 1991). It is beyond the scope of this baseline risk
assessment to address the health risks resulting from each of these sources of
contamination. This baseline risk assessment will only evaluate potential human
health risks resulting from exposure to sediment-derived contaminants in the
AOC.
The purpose of this chapter is to give a brief overview of the exposure
setting of the GCR/IHC AOC. A detailed historical description of this area,
including information on land use patterns, water resource issues, and sources of
pollution in the GCR/IHC AOC, has been given in the draft Stage One Remedial
Action Plan (RAP) (IDEM, 1991).
3.2 GRAND CALUMET RIVER BASIN
3.2.1 Environmental Setting
The GCR/IHC AOC includes the East and West Branches of the Grand
Calumet River, Indiana Harbor Canal, Indiana Harbor, and nearshore Lake
Michigan; the AOC is bounded on the west by the Illinois-Indiana state line. As
shown in Figure 3.1, these waterways are connected. From its headwaters (near
Marquette Park Lagoon), the Grand Calumet River flows westward
(approximately 21 km) before joining the Indiana Harbor Canal and the West
Branch of the Grand Calumet River (Brannon et al., 1986). Waters entering the
Indiana Harbor Canal flow about 8 km to the north and then northeast, exiting
into Indiana Harbor and southern Lake Michigan (USEPA, 1982).
A number of industries are located in this area, and the hydrology of the
GCR/IHC river system has been altered due to channelling and dredging
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Chicago
West Branch East Branch
(irttes. tcate approximate)
2 i o i 2
Little
Calumet
River
Figure 3.1. Grand Calumet River/Indiana Harbor Canal Area of Concern (IDEM, 1991).
3-2
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activities. This river system is used primarily for ship transportation in the canal
and as a conduit for effluent discharges from adjacent industries and sewage
treatment plants (STPs) in Gary, Hammond, East Chicago, and Whiting, IN
(Figure 3.2). USX Gary Works (formerly U.S. Steel), Inland Steel, and LTV Steel
(formerly Jones & Laughlin Steel) account for 28 of the 39 permitted outfalls on
the GCR/IHC and provide greater than 95% of the industrial effluent volume
(Figure 3.2) (HydroQual, 1984).
3.2.2 Grand Calumet River
The Grand Calumet River is formed by a combination of upstream flow,
surface runoff, ground water inflow, combined sewer overflows, and many point
source outfalls (HydroQual, 1986). The contribution of surface runoff is small
because of the small drainage area (approximately 65 km2) and sandy texture of
the soils (Crawford and Wangsness, 1987). More important is the contribution
from point source outfalls, which can contribute as much as 100% of the river flow
during dry weather periods (HydroQual, 1984). The volume of flow in the Grand
Calumet River is subject to wide variations depending on wind, wastewater
discharges, and storm water runoff (LMF, 1984 cited in Brannon et al., 1986). In
turn, this flow variation affects the resuspension, transport, and deposition of
contaminants associated with the soft sediments in this river.
The East Branch of the Grand Calumet River (Figure 3.1) is essentially
formed, and greatly affected, by discharge from U.S. Steel (HydroQual, 1984).
Approximately 67% of the industrial effluent entering the East Branch is
noncontact cooling water from Lake Michigan; the remainder is process water
from U.S. Steel (Gary Works Mill Operations) (Crawford and Wangsness, 1987).
The settling of particulate material from these effluent discharges has decreased
the depth of the East Branch. The depth of the upstream reaches ranges from
approximately 0.9 to 1.2 m, and the river increases in depth to about 2.4 to 3 m
near its confluence with the Indiana Harbor Canal; the average stream velocity is
approximately 0.3 m/see (Crawford and Wangsness, 1987).
Treated wastewaters from the Hammond Sewage Treatment Plant (STP)
and East Chicago Sanitary District contribute most of the flow to the West Branch
(HydroQual, 1984). This branch has a depth of about 0.6 m with a variable
stream velocity ranging from 0.06 to 0.3 m/sec (Crawford and Wangsness, 1987).
The West Branch reverses flow near the Hammond municipal STP because of a
natural divide that bisects the river (Figure 3.2) (Brannon et al., 1986). West of
the divide, water usually flows toward the Mississippi drainage basin via the Cal-
Sag Channel, and east of the divide, it flows to the Indiana Harbor Canal (Lake
Michigan Federation, 1984). However, the flow can reverse itself.
3.2.3 Indiana Harbor Canal
The Indiana Harbor Canal (Figure 3.1) is an important pathway for the
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Leaf MO
NUMBERS AE'EM TO TA«LE I I
Q j«u ITEEL
^7 ""LAND »T££L
u s.
OIM£» OUTFALLS
» CSO LOCATIONS
O SLUDGE LAGOONS
OHI TING
G< CAMT
H» HAMMOND
EC > EAST CHICAGO
Figure 3.2. Location of point source discharges (HydroQual, 1986).
3-4
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transportation of goods and materials to and from the various industries located in
this area. However, it has become difficult for commercial traffic to pass through
the canal because it has not been dredged since 1972. Prior to 1968, dredged
material from the Indiana Harbor deep-draft navigation project, as authorized by
the River and Harbor Act of 1910, was placed in the open waters of Lake
Michigan. After 1968, the federal government prohibited the unconfined disposal
of contaminated dredged material.
The U.S. Army Corps Engineer Waterways Experiment Station (WES)
(1987) has evaluated three disposal alternatives for removing PCB contaminated
sediments from the Indiana Harbor: contained aquatic disposal, confined disposal
in an in-lake confined disposal facility (CDF), and confined disposal in an upland
CDF. The final location and type of CDF must be approved by the Indiana
Department of Environmental Management (IDEM), as specified in Section 401 of
the Clean Water Act. If a CDF is built, the navigation channel will be dredged.
Based on historical dredging of the Indiana Harbor Canal, future dredging will
allow it to act as a sediment trap, retaining contaminated sediment that would
otherwise be transported into Lake Michigan (Brannon et al, 1986).
Under present conditions, sediment deposition has reduced the shipping
clearance in the Indiana Harbor Canal (USCOE, 1986). The shipping capacity in
the harbor and canal has been reduced by 15% and has resulted in a substantial
increase in shipping costs (IDEM, 1991). Although it is more difficult for boat
traffic to get through the canal, some boats are able to power their way through
the soft sediments. This frequent churning up of sediments from both ship traffic
and storm events results in the resuspension, transport, and deposition of
contaminated sediments. Data from bathymetric surveys for the years 1972, 1976,
1980, and 1984 indicates that incoming sediment is equal to outgoing sediment in
the Canal (Brannon et al., 1986). Since the incoming sediments are probably
contaminated sediments from the Grand Calumet River, this area may be
receiving a continuous load of contaminants throughout the year.
3.2.4 Indiana Harbor
The contamination problems within the Grand Calumet River and Indiana
Harbor Canal have resulted in the Indiana Harbor (Figure 3.1) becoming one of
the most highly contaminated harbors in the Great Lakes (Bremer, 1979). Even
though harbor water is diluted by the intrusion of lake water (HydroQual, 1984),
the sediments are a source of contaminants to the water column. The major
contaminant transport mechanism is probably the resuspension of contaminated
sediments followed by partitioning to the water column.
3.3 WATER QUALITY STANDARDS
Water quality standards have been established in the GCR/IHC river
system to designate the proper uses and water quality criteria these waterways
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should maintain. Until recently, the Indiana Stream Pollution Control Board has
designated the waters of the GCR/IHC river system for recreation on or near the
body, for limited aquatic life, and for industrial-water supply. Lake Michigan has
been classified for whole body contact, support of a well balanced fish community,
potable water supply, and industrial water supply (HydroQual, 1984). In addition,
specific numerical standards have been established by the State of Indiana for
Lake Michigan, Indiana Harbor, and the Grand Calumet River.
New standards were put into effect March 3, 1990 to upgrade the use of the
river and harbor as whole body contact "recreation" waters (IDEM, 1991). In
addition, the Indiana portion of Lake Michigan was recently designated as a state
resource water (i.e., existing water quality shall be maintained or improved with
no degradation) (IDEM, 1991). Although these new standards are probably not
immediately feasible for the GCR/IHC river system, they set a legal framework for
pursuing enforcement actions and to further protect the quality of Lake Michigan
waters.
3.4 OVERVIEW OF CONTAMINATION PROBLEMS
Progress has been made in alleviating some of the contamination problems
made in the last century of industrial activity in the GCR/IHC AOC. Since 1974,
treatment improvements have been completed at several municipalities and
industries, industrial recycle programs have been initiated, state water quality
standards have been upgraded, and U.S. Steel has reduced industrial production
resulting in decreased flow to the East Branch. Yet, major contamination
problems remain.
The GCR/IHC river system has been sampled frequently over the past 20
years to monitor contaminant concentrations in the water, sediment, and fish
(Figure 3.3). Water quality data have shown problems in these waters with
several parameters including ammonia, dissolved oxygen, total phosphorus,
chloride, sulfates, oil and grease, bacteria, cyanide, lead, copper, mercury, and
PCBs. More recent monitoring data from 1988-89 indicate that many of these
same parameters are still at levels that exceed applicable water quality standards,
although most are found at lower levels than in the past (IDEM, 1991).
According to the U.S. Army Engineer's WES (1987), PCBs are the
contaminant of most concern in Indiana Harbor sediments. Approximately 190 kg
of PCBs, 1000 kg of cadmium, and 50,000 kg of lead are transported to Lake
Michigan every year along with about 8 x 107 kg of sediment from the harbor and
canal. (IDEM, 1991). Other potentially toxic compounds (e.g., polyaromatic
hydrocarbons, dioxins, and heavy metals) were detected in Indiana Harbor
sediment samples collected in 1989 as part of the ARCS program. Oil
contamination of the sediments remains a problem, and the banks of the harbor
appear to be saturated with petroleum. The river and the harbor often have an
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Calumet
ftoer
UtOe
Calumet
River
2 SAMPLES IN LAKE
BEYOND MAP BOUNDARY
Lake Michigan
Grand Calumet River
Figure 3.3. Composite of all sampling in the GCR/IHC AOC from 1972 to 1989.
3-7
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oily sheen, and the nearshore Lake Michigan waters frequently appear murky
(IDEM, 1991).
Sediments in the harbor area are much more contaminated than in Lake
Michigan. Concentrations of cadmium, lead, and zinc in Indiana Harbor
sediments were nearly 200, 80, and 80 times, respectively, that in Lake Michigan
sediments. The concentration of organic chemicals ranged from more than 30
times for Aroclor 1248 to several orders of magnitude higher for aldrin in Indiana
Harbor sediments (U.S. Army Engineer WES, 1987). The continued transport of
these contaminants to nearshore Lake Michigan may threaten its water quality.
Groundwater contamination is another environmental problem in the AOC.
The GCR/IHC AOC is located on a thin sand aquifer that is hydraulically
connected to the river, canal, and Lake Michigan (Banaszak and Fenelon, 1988).
Groundwater flow has been affected over large areas by a system of shallow wells
used to prevent oil-contaminated water from leaving oil refinery property
(Banaszak and Fenelon, 1988). In addition, most of the groundwater samples
collected from wells in or near heavy industry contained concentrations of organic
chemicals (e.g., phenols and benzene) above their recommended levels (Banaszak
and Fenelon, 1988). Groundwater probably contributes >10% of the total load to
the Grand Calumet River of ammonia, chromium, and cyanide; 5 to 10% of
dissolved solids, sulfate, copper, iron, and lead; 1 to 5% of chloride, fluorine, and
hardness; and <1% of nitrate plus nitrite, phosphorus plus orthophosphate,
mercury, and zinc (IDEM, 1991). Groundwater is not used for any municipal
drinking water supplies in the AOC.
3.5 LAND USE PATTERNS
The GCR/IHC AOC supports several types of land uses. These include
residential land (40%), commercial areas and light industry (25%), steel (15%) and
petrochemical (10%) industries, and parks, natural areas, and agriculture (10%)
(Figure 3.4) (Banaszak and Fenelon, 1988). Some of the industrial areas have
already been discussed in preceding sections. The residential area contains a
combined population of about 290,000 people in Gary, Hammond, East Chicago,
and Whiting, IN. There is a proportionately large concentration of people south of
the Grand Calumet River, stretching though Roxana in East Chicago, Hessville in
Hammond and Brunswick-West Side in Gary (Lake Michigan Federation, 1984).
Five different neighborhoods in Gary lie partially within the river corridor: Miller,
Downtown east, Downtown west, Ambridge-Mann, and Brunswick (Lake Michigan
Federation, 1984).
Several natural areas exist within the GCR/IHC AOC. The Lake Michigan
Federation (1984) and IDEM (1991) have described these areas in detail. One of
the most popular recreation sites is Roxana Marsh, located east of the Hammond
STP. Dune and swale areas are found along the Grand Calumet River; five
quality wetlands have been rated in this area by the Indiana DNR. These areas
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EXPLANATION
«r«j-jr fI mat
L-J Residential Area wA Steel Industry
Petrochemical Industry
It Commercial or Light Industrial Area
ri;-
- UTC-
Figure 3.4. Major land uses in the Area of Concern.
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are important for supplying wildlife habitat and recreational opportunities for
people (e.g., bird watching). No natural areas are located along the Indiana
Harbor Canal or Indiana Harbor. Large numbers of waterfowl use the nearshore
waters of Lake Michigan, adjacent to Jeorse Park, during migration. In addition,
people use the nearshore waters of Lake Michigan for fishing, boating,
windsurfing, and swimming by the designated swimming beaches (e.g., Jeorse
Park) (IDEM, 1991).
3.6 DRINKING WATER INTAKES
As discussed in the RAP, there are three public water intakes in the
nearshore Lake Michigan area that serve AOC communities. The Whiting intake
is about 2.4 km west of the harbor entrance (USCOE, 1986); the East Chicago, IN,
intake is about 0.8 km southeast of the Inland Steel Company fill area and 3 km
east/northeast of the East Chicago water filtration plant (IDEM, 1991). The
Hammond water supply intake is located about 1.6 km north of the Hammond
Filtration Plant (IDEM, 1991) The water intake pipes for these areas are within
0.8 km of sediments that have been transported into Lake Michigan from the
Indiana Harbor (Bunner, 1991); the continued movement of these sediments into
the lake may pose a potential risk to drinking water supplies in the future.
Public water supplies in Lake County, IN, that use Lake Michigan water
(i.e., Gary-Hobart, Whiting, Hammond, Dune Acres, and East Chicago) were
tested periodically for inorganics, volatile organic compounds (VOCs), and bacteria
during 1989-1990 (GLNPO, personal communication, 1990). In general, most
VOCs and other organic compounds were either not detected or were detected at
levels far below the maximum contaminant levels (MCLs) for drinking water. The
MCL for lead was exceeded by 10 ug/L for one water sample collected from the
East Chicago Water Works. No bacteriological counts were present in any of the
samples. Thus, at the present time, drinking water supplies in the GCR/IHC AOC
appear to be safe.
3.7 CONTAMINATION OF FISH
3.7.1 Routes of Contamination
One of the primary ways in which people in the Great Lakes region,
including the GCR/IHC area, 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 may
accumulate contaminants, assuming that the major source of pollutants comes
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from in-place contaminated sediments. The next section will discuss specific fish
advisories for the GCR/IHC AOC.
The group of contaminants that have been of major concern in the Great
Lakes region 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 Hites, 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: 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 consumers (i.e., pumpkinseed) 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
a degree of uncertainty associated with this linkage. One of the difficulties with
3-11
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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 (Bierman,
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 to 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
(Spigarelli et al., 1983).
Other contaminants, such as mercury, are also of concern in the Great
Lakes. Unlike HOCs, mercury appears to accumulate in fish tissue 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.
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.
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3.7.2 Fish 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 the 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.
Stringent fish advisories have been issued for the GCR/IHC AOC. The 1990
fish advisory states that no fish should be eaten from the waters of the Grand
Calumet River and Indiana Harbor Canal (Bunner, 1991). The 1990 Lake
Michigan advisory suggests that the following species should not be eaten from
Indiana waters: brown trout and lake trout over 58 cm, Chinook salmon over 81
cm, catfish, and carp. In addition, Chinook salmon over 53 cm, lake trout between
51 and 58 cm, Coho salmon over 66 cm, and brown trout up to 58 cm should not
be eaten by children age 15 or under, pregnant women, women who may become
pregnant, or nursing mothers. All others should limit their consumption to one
meal (0.23 kg) per week (IDEM, 1991). Despite these warnings, some anglers may
not be aware of specific advisories or may choose to ignore them (West et al.,
1989). People have been observed fishing in the Grand Calumet River near the
Gary STP, by DuPont, and on the breakwaters of the Indiana Harbor (D. Carey,
Lake Michigan Federation, personal communication, 1990).
The environmental conditions in the GCR/IHC AOC are too poor to support
an adequate sport fishery. The fish communities in the river and harbor are
depressed from a combined lack of food resources, low dissolved oxygen, and toxic
stress (Bunner, 1991). However, biological monitoring by the Indiana State Board
of Health since 1979 has shown an increasingly diverse aquatic community in the
Indiana Harbor Canal and lower Grand Calumet River. Some fish species
(especially goldfish and golden shiners) appeared to be reproducing successfully in
these waters during 1986 and 1987 (IDEM, 1991). However, these fish species
may contain potentially harmful levels of contaminants in their tissues.
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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 that 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 United States
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 for 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 (i.e., 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 and early infancy health status (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, that are not yet 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 detail (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 Grand Calumet
River/Indiana Harbor Canal itself 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 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 GCR/IHC AOC.
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 AOC from
documents such as the draft Stage One Remedial Action Plan (IDEM, 1991) and
ARCS "Information Summary" (Simmers et al., 1991). 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-derived contaminants from the river and harbor. The most
complete and current data sets were then evaluated to judge whether adequate
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 mg 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 lower Saginaw River.
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 Characterization
Rev i ew & Eva Iuati on
of Existing
ChemIcaI Data
i
ToxIc i ty Prof i Ies
Evaluation of
Base line R1sks
Determination of
Pr obabIe Expos ur e
Pathways
i
Determination of
Exposure Point
ConcentratI one
Determination of
Contamlnant
Intakes/Exposure
Risk/Hazard
Character IzatI on
Character Izatlon
of Uncertainty
Figure 4.1.
Components of baseline human health risk assessments.
4-3
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CHAPTER 5
EXPOSURE ASSESSMENT
5.1 OVERVIEW
In this exposure assessment, the magnitude, frequency, duration, and route
of direct and indirect exposures of people to sediment-derived contaminants from
the GCR/IHC 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 GCR/IHC AOC was toured on 20 August 1991 with Bob Tolpa (Region
V) so that researchers could become familiar with the AOC and to determine
relevant exposure pathways. Additional information about the AOC was obtained
from Michael Mikulka (Region V), Dave Dabertin (IDEM), Lee Bridges (IDEM),
Robert Bunner (RAP Coordinator), Anne Spacie (Purdue University), Doreen
Carey (Lake Michigan Federation), and other state and federal personnel. A
number of agencies, consultants, industries, and university personnel are involved
with studying and regulating the many contamination problems in the GCR/IHC
AOC. Consequently, some studies may have been missed for inclusion in this risk
assessment, although an effort was made to include the most up-to-date data.
5.2 EXPOSURE PATHWAYS
5.2.1 Incomplete Exposure Pathways
The potential pathways by which people may be exposed to contaminants
from the GCR/IHC 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. Six pathways appear to be incomplete:
1) Ingestion of contaminated drinking water: the Grand
Calumet River and Indiana Harbor are not used as a source of
drinking water in the AOC.
2) Ingestion of sediments: the ingestion of bottom sediments by
children does not appear to be occurring.
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TABLE 5.1. POTENTIAL EXPOSURE PATHWAYS IN THE GCR/IHC AOC
INGESTION OF CONTAMINATED:
- Surface Water
- Fish and Wildlife
- Drinking Water
- Sediments
- Contaminated Soils
DERMAL CONTACT WITH CONTAMINATED:
- Surface Water
- Sediments
- Soils
INHALATION OF AIRBORNE CONTAMINANTS
3) Ingestion of contaminated soils: the ingestion of
contaminated soils from the river banks does not appear to be
occurring. Some parts of the Grand Calumet River are not
easily accessible, and the river is bordered by cattails in several
stretches, 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 urban
areas that border the AOC.
6) Ingestion of surface water: no swimming areas are located
along the river or in the harbor area. In addition, the river is
often covered with an oily sheen, and is unappealing for
swimming.
5.2.2 Complete Exposure Pathways
Four exposure pathways were considered complete in the GCR/IHC AOC
(Table 5.2). 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 pathways that will be considered for this risk
5-2
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TABLE 5.2. COMPLETE EXPOSURE PATHWAYS IN THE GCR/IHC AOC
Consumption of Contaminated Fish
Dermal Contact with Water while playing in the Roxana Pond
area or while fishing
Dermal Contact with Sediments while playing in the Roxana
Pond area
Inhalation of Airborne Contaminants
assessment are the consumption of fish from the GCR/IHC system, and the dermal
exposure to contaminated water and sediment in the Grand Calumet River area.
An exposure assessment was not conducted for the Indiana Harbor Canal because
it was not documented as a site that people in the community used or visited.
5.2.2.1 Complete Exposure Pathways in the Grand Calumet River
The Grand Calumet River is used for limited recreational purposes by
people who gain access to the river from bridges, railroad tracks, public land (e.g.,
Roxana Pond), and in some cases, illegal entry onto private land (e.g., the DuPont
Tract). Most of the land along the northern stretch of this river is industrial while
several neighborhoods lie south of the river. Access to the river is restricted in
many areas by fences, an interstate toll road, and by marshland (Lake Michigan
Federation, 1984). The most accessible areas along the river include the following
sites (Figure 5.1):
from the Bridge Street bridge to the Industrial Highway bridge
(roughly adjacent to the Gary STP),
from the Cline Avenue bridge to the Kennedy Avenue bridge
(along the DuPont Tract), and
from the Indianapolis Boulevard bridge to the Columbia
Avenue bridge (including the Hammond STP and Roxana Pond
areas).
The most likely places for people to fish the Grand Calumet River include
the sites described above. Children may be dermally exposed to contaminated
water and sediments at Roxana Pond. Roxana Pond is a slow moving part of the
Grand Calumet River which has a marshy section along the shoreline (Figure 5.2).
It is located between Calumet Avenue and Indianapolis Boulevard in East
5-3
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Calumet
River
LJtOe
Calumet
River
Grand Galumet River
Lake Michigan
West Branch
East Branch
Figure 5.1.
Location of potential exposure areas along the Grand Calumet River.
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en
to
o
S3
S,
o
X
I
en
en
-------
Chicago. Children have been observed wading in the pond and running along the
edge of the bank (A. Spacie, Purdue University, personal communication, 1991).
5.2.2.2 Complete Exposure Pathways in the Indiana Harbor
The Indiana Harbor is used primarily as a shipping area for industries.
Most of the property around the harbor is owned by either LTV Steel or Inland
Steel. Despite the amount of private land around the harbor, people can gain
access to the breakwater along Indiana Harbor to fish (D. Carey, Lake Michigan
Federation, personal communication, 1990). The Stage One RAP (IDEM, 1991)
also indicates that some sport fishing may occur in the harbor although it is not
generally pursued because of pollution, ship traffic, and heavy industrial
congestion along the banks. Based on this information, the major exposure
pathways for Indiana Harbor are: 1) dermal contact with surface water (most
likely to occur while fishing) and 2) ingestion of contaminated fish. Dermal
contact with sediments was not chosen as an exposure pathway because people
fishing from the breakwater and by boat would not be exposed to the sediments.
Contaminant transport in this area is not well quantified; some studies
have suggested that contaminant loads leaving Indiana Harbor may be
transported northward towards Chicago (Harrison et al., 1977, personal
communication cited in Risatti and Broeren, 1988). However, it is impossible to
assess, at this time, whether sediment-derived contaminants leaving Indiana
Harbor are contributing to contaminant loads along nearshore areas where people
may gather for recreation (e.g., fishing, swimming). In addition, it would be as
difficult to determine how much of the contaminant burden in fish caught in the
nearshore Lake Michigan area would be due to contaminants leaving Indiana
Harbor.
5.3 DATA USED IN THE EXPOSURE ASSESSMENT
5.3.1 Sources of Data Reports
The Grand Calumet River, Indiana Harbor Canal, and Indiana Harbor have
been monitored by local, state, and federal agencies over the past 10 to 20 years to
determine contaminant levels in the water, sediments, and biota. This monitoring
will continue in the future to verify that water quality standards are being met, to
evaluate fish consumption advisories, to pursue litigation against polluters, and to
evaluate results of remediation efforts.
For this baseline risk assessment, references to technical reports containing
contaminants data were obtained primarily from two sources: 1) "Information
Summary, Area of Concern: Grand Calumet River" (Simmers et al., 1991) and 2)
draft Stage One Remedial Action Plan (IDEM, 1991). Additional data reports
were obtained from the Indiana Department of Environmental Management
(IDEM) and the EPA's Great Lakes National Program Office (GLNPO). An effort
5-6
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was made to obtain data from the original data reports or lab sheets so that a
better assessment of the analytical quality assurance/quality control (QA/QC)
could be determined. For the Roxana Pond area, no data were available on
contaminant levels in the water column and porewater. Thus, a major assumption
was made to use data collected from nearby areas to be representative of the
contaminant levels in Roxana Pond.
5.3.2 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.
Lockheed-ESC could not conduct a complete review of the data because
insufficient QA/QC information was available. Thus, an assessment of the
accuracy of the data could not be made. Although inadequate QA/QC information
was available to fully assess the quality of the data, the data were assumed to be
of adequate quality for use in this risk assessment.
No assumptions about the temporal and spatial variability of contaminants
data in the GCR/IHC AOC will be made. The Indiana Department of
Environmental Management (1991) has discussed some of the spatial variability of
contaminants in the Grand Calumet River and compared them with statewide
background values. In general, all sampling sites had one or more metals present
in the sediment at greater than ten times statewide background levels (IDEM,
1991).
5.3.3 Data Used
5.3.3.1 Porewater Data
The porewater data used in this risk assessment represents preliminary
draft data on organic chemical analyses of sediment and porewater samples
collected by linger and others in 1989 from several locations in the Grand
Calumet River. These data were presented to the EPA Great Lakes National
Program Office on 23 March, 1990, by M. Zabik. The QA/QC data have not been
released with these data yet. However, the researchers did use EPA methods for
sample preparation and extract cleanup. The qualitation and quantitation of
samples were confirmed by gas chromatography/mass spectrometry.
No porewater data were available for the Roxana Pond area. However, a
sample collected nearby, approximately 1 km west of Indianapolis Boulevard, was
used in the exposure assessment. These data are given in Table 5.3.
5.3.3.2 Water Column Data
The IDEM has collected water samples from the Grand Calumet River
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TABLE 5.3.
SEDIMENT POREWATER AND SURFACE WATER
CHEMICAL CONCENTRATIONS USED IN THE DERMAL
EXPOSURE ASSESSMENT
Chemical
Concentration
(mg/L)
METALS
Antimony
Arsenic
Barium
Chromium VI
Copper
Manganese
Mercury
Nickel
Zinc
PAHs
Benzo(a)anthracene
Benzo(a)pyrene
Benzo(b)fluoranthene
Benzo(k)fluoranthene
Chrysene
Fluoranthene
Phenanthrene
Pyrene
PHENOLS
2,4-Dichlorophenol
2,4-Dinitrophenol
Hydroquinone
Pentachlorophenol
Phenol
o-Cresol
AROMATIC HYDROCARBONS
1,1-Biphenyl
Hexachlorobenzene
Naphthalene
PCBs
ORGANOCHLORINE INSECTICIDES
Chlordane
Dieldrin
Heptachlor
7.6E-02*
2.1E-03*
4.9E-02*
7.7E-03*
2.1E-02*
2.1E-01*
1.7E-04*
3.8E-03*
6.8E-02*
1.6E-02
3.3E-03
1.2E-02
5.7E-03
9.0E-03
3.2E-02
2.5E-01
2.0E-02
2.4E-02
3.5E-02
1.3E-02
1.9E-02
3.3E-01
2.4E-02
2.6E-02
2.1E-03
3.8E-01
1.1E-02
6.0E-04
l.OE-03
5.0E-04
Denotes surface water samples, all other values represent sediment porewater samples
5-8
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TABLE 5.3. CONTINUED
Water
Cone.
Chemical (mg/L)
ORGANOCHLORINE INSECTICIDES
p,p' DDE 6.9E-03
p,p' DDT 2.4E-03
Toxaphene 5.6E-03
PURGEABLES
Acrylonitrile 1.8E-03
Chlorobenzene 2.9E-03
1,2-Dichlorobenzene 5.0E-04
Ethylbenzene 1.6E-02
Styrene 1.6E-02
Tetrachloroethylene 2.8E-03
OTHER
1,2 Dichloroethane 2.6E-011'
* Denotes surface water samples, all other values represent sediment porewater samples
regularly as part of its monitoring efforts. The most recent data available were
collected in 1988. No data were available specifically for Roxana Pond, although
surface water samples were collected monthly from the river at Calumet Avenue
(Mile Point 11.46). Sample results were averaged to produce one mean value
(Table 5.3). In cases where chemicals were not detected part of the year, a value
of one-half the detection limit was used when deriving a mean value.
5.3.3.3 Fish Data
Biological monitoring by the Indiana State Board of Health (ISBH),
beginning in 1979, has shown an increasingly diverse aquatic community in the
Indiana Harbor Canal and lower Grand Calumet River. Extremely pollutant
tolerant forms such as carp are losing dominance to more sensitive species such as
golden shiners [IDEM, 1987 cited in the RAP (IDEM, 1991)]. Some fish species,
especially goldfish and golden shiners, appeared to be reproducing successfully in
these waters in 1986 and 1987. However, the aquatic community still appears to
be adversely impacted by moderate organic pollution and toxic stress.
The latest available fish data for the Grand Calumet River and Indiana
Harbor Canal date back to samples collected by IDEM in 1987 and 1988. More
recent fish samples have been collected, but are being stored pending the
allocation of funds for chemical analysis (L. Bridges, IDEM, personal
communication, 1992). Information about the types of fish used in this risk
5-9
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assessment are given in Table 5.4; the contamination levels in the fish are given
in Appendix A. Separate exposure and risk assessments were conducted for each
species of fish Since these fish tend to travel up and down the Indiana Harbor
Canal and the Grand Calumet River as conditions allow, they should be
considered as integrators of the contamination problems in the entire system.
TABLE 5.4. SAMPLING INFORMATION FOR GCR/IHC FISH SPECIES
Fish Species Sampling Location Sampling Date
Pumpkinseed (whole) Grand Calumet River 07/08/87
Golden Shiners (whole) Grand Calumet River 07/08/87
Carp (whole) Grand Calumet River 11/18/87
Carp (whole) Indiana Harbor Canal 11/18/87
Carp (skin-on-fillet) Indiana Harbor Canal 11/01/88
Additional fish data obtained from a study by Risatti and Broeren (1988)
were used to assess the risk from consuming fish from the Indiana Harbor and
nearshore Lake Michigan area. Risatti and Broeren (1988) collected 31 whole fish
samples (eight of which were composites) from four sites in the Indiana Harbor
Canal, Indiana Harbor, and nearshore Lake Michigan. The samples were
analyzed for contaminants known to be present in Indiana Harbor sediments. The
researchers ran duplicates on 10 percent of their samples, ran blanks, and added
spikes to some samples to evaluate recoveries and to verify their methods.
Although there was not enough information supplied with the report to adequately
judge the QA/QC procedures used, the data were assumed to be of adequate
quality for use in this risk assessment. The following fish species were collected
from the Indiana Harbor: 3 carp, 10 gizzard shad (including 3 composite samples
of 2 fish each), 5 alewife (including one composite of 2 fish), and 3 sunfish
(composite). One alewife and a composite sample of 10 yellow perch, collected
from the nearshore Lake Michigan area, were also analyzed. The nearshore Lake
Michigan fish data were included since fish are likely to travel between the harbor
and nearshore area.
5.4 EXPOSURE ASSESSMENT
5.4.1 General Determination of Chemical Intakes
Once the complete exposure pathways were identified and contaminant
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concentrations for relevant media were obtained, an exposure assessment could be
conducted for each pathway. 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. For dermal contact, exposure is
calculated as an absorbed dose and not the amount of chemical that comes in
contact with the skin. The general equation for calculating chemical intakes is
given in Table 5.5. Several variables were used to determine intakes, including
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 a conservative estimate of either the
typical or reasonable maximum intakes.
5.4.2 Intakes: Ingestion of Contaminated Fish
Some local residents appear to fish the Grand Calumet River and Indiana
Harbor. At the present time, specific information on fish consumption rates and
trends in the GCR/IHC AOC is not available. The equation used to estimate
intakes of contaminants due to the ingestion of contaminated fish is provided in
Table 5.6. Because the consumption of fish was not assumed to be age dependent,
only lifetime intake rates were calculated. These intake rates varied with the
consumption rate as well as with the fraction of fish consumed that had been
taken from the contaminated site. Because there was not any quantitative
information available on the fraction of fish ingested from the Grand Calumet
River, Indiana Harbor, and nearshore Lake Michigan area, conservative estimates
were made.
Separate exposure assessments were conducted for each species of fish
collected from the Grand Calumet River and Indiana Harbor Canal by the IDEM.
However, the exposure assessment was done differently for the Indiana Harbor
and nearshore Lake Michigan samples. For the Indiana Harbor, one exposure
assessment was conducted for the carp data. A second exposure assessment was
conducted for a pooled sample of the gizzard shad, alewife, and sunfish data; an
overall mean value for each contaminant was used. The alewife and yellow perch
data were also pooled for the Lake Michigan samples. These pooled data were
used to be more representative of the contaminant levels an angler and his family
might be exposed to in the fish.
The parameter values used to calculate chemical intakes are given in Table
5.7. Parameter values were obtained mostly from recommended EPA sources.
The exposure parameters used in the typical scenario were assumed to be
applicable to the general population of anglers and their families in the Grand
Calumet River AOC, whereas the reasonable maximum exposure scenario applied
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TABLE 5.5.
GENERIC EQUATION FOR CALCULATING CHEMICAL
INTAKES (USEPA, 1989a)
J =
C X CR X EFD
BW X AT
where:
I
CR
EFD
BW
AT
Intake = the amount of chemical at the exchange boundary (tag/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 (kg) over the exposure
period
Assessment-Determined Variables
Averaging Time = period over which exposure is averaged (days)
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TABLE 5.6.
EQUATION USED TO ESTIMATE CONTAMINANT
INTAKES DUE TO THE INGESTION OF FISH
Intake =
C X IR X FI X EF X ED
BW X AT
where:
Intake
C
IR
FI
EF
ED
BW
AT
Intake Rate (mg/kg-day)
Contaminant Concentration in Fish (mg/kg)
Ingestion Rate (kg/day)
Fraction of Fish Ingested from Contaminated Sources (unitless)
Exposure Frequency (days/yr)
Exposure Duration (yr)
Body Weight (kg)
Averaging Time (days)
to more recreational anglers and their families. The fish population in the Grand
Calumet River is not strong enough to support a sports fishery; consequently the
number of recreational anglers that would be fishing from this area would
probably be small. People would be more likely to fish from the Indiana Harbor
than the Grand Calumet River.
The contaminant intake levels were based on the consumption of raw fish
fillets. At the present time, contaminant concentrations in raw fish cannot be
extrapolated to concentrations in cooked products. 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 fish (Smith et
al., 1973; Stachiw et al., 1988; Zabik et al., 1979, 1982). However, their 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 DDT 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 alter the level of
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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 be
done for 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, anglers can use the
following cooking techniques to reduce their risk to contaminants: 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.
5.4.3 Intakes: Dermal Contact with Surface Water
Dermal contact with surface water may occur in the Roxana Pond area and
in the Indiana Harbor as a result of wading and fishing activities, respectively.
The equation used to estimate the absorbed dose of contaminants is provided in
Table 5.8 followed by a listing of the parameter values used in this risk
assessment (Tables 5.9). Some values were obtained from EPA guidance
documents (USEPA, 1989a,b), whereas other values were based on professional
judgment.
The intake rate varies with the surface area available for sorption as well
as the permeability of the skin to a particular contaminant. The movement of
chemical across the skin to the stratum corneum and into the bloodstream is
described by a permeability constant (PC) (USEPA, 1989a). Permeability
constants are specific to each chemical. Although permeability constants were not
available for all chemicals, a value was estimated for chemicals of similar
structure (Table 5.10).
Since the surface area of exposure, contact rate, frequency and duration of
exposure vary with age, specific parameters were estimated for the affected age
classes. Only children and teenagers in the 7 to 17 years old age group were
assumed to play in the water and sediments of Roxana Pond. Under a typical
scenario, this age group was assumed to have dermal contact with the water 3
days/week during the summer for a total exposure frequency of 40 days/year.
Under a reasonable maximum exposure scenario, this age group was assumed to
have dermal contact with the water 4 days/week during June through August and
1 day/week during May and September (i.e., 60 days). For the Indiana Harbor, it
was assumed that all age groups could be exposed to some surface water while
fishing. However, since the dermal exposure assessment to surface water in the
Roxana Pond area did not result in a significant noncarcinogenic or carcinogenic
risk (see Chapter 7), and since the contaminant concentrations were less in the
Indiana Harbor, it was assumed that limited dermal exposure to the hands and
forearms while fishing would be insignificant. Thus, chemical intakes were not
calculated for the limited exposure to surface water in the Indiana Harbor.
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The typical exposure duration of 9 years and reasonable maximum exposure
duration of 30 years during a 70 year lifetime were subdivided among the 7 to 17
years old age group. Thus, the proportion of the age group exposure duration (X)
divided by the entire exposure duration (i.e., 9 years for typical and 30 years for
reasonable maximum exposures) was equivalent to the ratio of the age group
range divided by 70 years. For example, the proportion of a typical 9 year
exposure (i.e., X) that the 7 to 17 years old age group would experience would be
calculated as follows:
X years = 11 years
9 years 70 years
X = 1.4 years
5.4.4 Intakes: Dermal Contact with Sediments
The EPA has not developed any generic guidance for exposure to chemicals
in sediment. The approach taken here was to assume that a chemical in the
sediment would become available for dermal absorption by partitioning to the
porewater with subsequent absorption through the skin. Porewater data were
available for organic contaminants from samples collected at Calumet Avenue
downstream of Roxana Pond (Table 5.3). Because the samples were not analyzed
for metals, surface water data were used. This assumed that the chemical
concentrations in the sediment porewater and surface water were in equilibrium
for heavy metals. The flux of the chemical through the skin was then estimated
by using the skin permeability coefficient for the chemical in water. Once the flux
was obtained, the absorbed dose could be calculated by multiplying the flux by the
estimated time of exposure and by the surface area of skin exposed.
The equation used to estimate absorbed doses is provided in Table 5.8. The
permeability constants and other parameter values used for this risk assessment
are given in Tables 5.10 and 5.11, respectively. This exposure pathway assumed
that the exposed skin surface area was limited to the feet under typical exposures.
Under the reasonable maximum exposure scenario, the feet and hands would be
exposed. The surface area of the exposed skin was estimated by values given in
the EPA's "Exposure Factors Handbook" (USEPA, 1989b) for the 7 to 17 years old
age class. The exposure frequency values given in Table 5.11 are less than those
given in Table 5.9 because it was assumed that kids would not ail ways be wading
barefoot in Roxana Pond. Thus, it was assumed that sediments would not come in
contact with the feet when shoes were worn.
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TABLE 5.7.
PARAMETERS USED TO ESTIMATE CONTAMINANT
INTAKES RESULTING FROM THE CONSUMPTION OF
CONTAMINATED FISH FROM THE GCR/IHC AOC
Var.
CV
IR
FI**
EF
ED
BW
AT:
Units
kg/g
kg/day
-
day/yr
yrs
kg
days
Value
Used
0.001
0.0065
0.054
0.05
0.1
350
9
30
70
3285
10950
25550
Comment
Typical: USEPA (1991a)
RME*: USEPA (199 la)
Typical: study assumption
RME: study assumption
USEPA (1991a)
Typical: USEPA (1989a)
RME: 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 noncarcinogenic risk)
70 yrs x 365 days/yr (carcinogenic risk)
RME = Reasonable Maximum Exposure
For the Indiana Harbor and nearshore Lake Michigan fish:
FI = 0.1 for typical exposures
FI = 0.25 for reasonable maximum exposures
5-16
-------
TABLE 5.8.
EQUATION FOR ESTIMATING ABSORBED DOSES OF
CONTAMINANTS DUE TO DERMAL CONTACT WITH
CHEMICALS IN THE SEDIMENT POREWATER OR
SURFACE WATER
AD =
ED
TOyrs
X SA± X PC X ET± X EFi X ED± X CF
BWi X AT±
where:
AD
i
j
CW
SA,
PC
ET,
EF,
ED,
CF
AT,
Absorbed Dose (mg/kg/day)
Age Group
Chemical
Chemical Concentration in Water (mg/L)
Age Group Specific Skin Surface Area Available for Contact (cm2)
Chemical Specific Dermal Permeability (cm/hr)
Age Group Specific Exposure Time (hours/day)
Age Group Specific Exposure Frequency (days/year)
Age Group Specific Exposure Duration (years)
Conversion Factor (1 L/1000 cm3)
Age Group Specific Body Weight (kg)
Age Group and Pathway Specific Period of Exposure, Averaging Time (days)
5-17
-------
TABLE 5.9.
PARAMETER VALUES USED IN ESTIMATING THE
ABSORBED DOSE DUE TO DERMAL CONTACT WITH
CHEMICALS IN THE SURFACE WATER WHILE WADING
IN ROXANA POND
Var.
CF
SA,
EF
ED
BW
AT:
Noncarc.
AT: Care.
ETi
Units
L/cm3
cm2/event
day/yr
yrs
kg
days
days
hr/day
Value
Used
lO'3
1740
4820
40
60
1.4
4.7
44
511
1716
25550
1
1
Reference
Typical: SA of hands and feet (USEPA,
1989b)
RME*: SA of hands, forearms, lower legs
and feet (USEPA, 1989b)
Typical: Study Assumption
RME: Study Assumption
Typical: Proportion of 9 yr exposure
(USEPA, 1989a)
RME: Proportion of 30 yr exposure
(USEPA, 1989a)
50th percentile average weight calculated
from 1 yr incremental age groups (7 to < 18
yrs) for males and females (USEPA, 1989b)
Typical: 1.4 yr x 365 days/yr
RME: 4.7 yr x 365 days/yr
70 yr x 365 days/yr (USEPA, 1989a)
Typical: Study Assumption
RME: Study Assumption
* RME = Reasonable Maximum Exposure
5-18
-------
TABLE 5.10.
ESTIMATED PERMEABILITY CONSTANTS (Kp) FOR
CHEMICALS USED IN THE DERMAL EXPOSURE
ASSESSMENT
Chemical
METALS
Antimony
Arsenic
Barium
Chromium
Copper
Manganese
Mercury
Nickel
Zinc
PAHs
Benzo(a)anthracene
Benzo(a)pyrene
Benzo(b)fluoranthene
Benzo(k)fluoranthene
Chrysene
Fluoranthene
Phenanthrene
Pyrene
PHENOLS
2,4-Dichlorophenol
2,4-Dinitrophenol
Hydroquinone
Pentachlorophenol
Phenol
o-Cresol
AROMATIC HYDROCARBONS
1,1-Biphenyl
Hexachlorobenzene
Naphthalene
PCBs
ORGANOCHLORINE INSECTICIDES
Chlordane
Dieldrin
Sources: A) Flynn (1990), estimated by
Kp
cm/hr
3.16E-04
3.16E-04
3.16E-04
3.16E-04
3.16E-04
3.16E-04
5.13E-05
3.16E-04
3.16E-04
2.34E-02
3.16E-02
3.16E-02
3.16E-02
3.16E-02
3.16E-02
3.16E-02
3.16E-02
2.29E-02
5.37E-02
l.OOE-02
3.16E-02
9.12E-03
2.82E-02
3.16E1-02
3.16E-02
3.16E-01
3.16E-02
3.16E-02
3.16E-02
equations
Source
Study Assumption
A
Study Assumption
A
A
Study Assumption
C
A
A
A
B
B
Study Assumption
B
B
B
Study Assumption
A
A
Study Assumption
B
A
A
Study Assumption
Study Assumption
B
B
B
A
B) Flynn (1990), adjusted values
C) Kasting et al. (1987)
5-19
-------
TABLE 5.10. CONTINUED
Kp
Chemical cm/hr Source
ORGANOCHLORINE INSECTICIDES
Heptachlor 3.16E-02 B
p,p' DDE 3.16E-02 B
p,p' DDT 3.16E-02 B
Toxaphene 3.16E-02 B
PURGEABLES
Acrylonitrile l.OOE-03 B
Chlorobenzene 2.19E-01 A
1,2-Dichlorobenzene 3.16E-02 B
Ethylbenzene 3.16E-01 B
Styrene 2.82E-01 A
Tetrachloroethylene 7.94E-03 A
1,2 Dichloroethane 1.95E-02 A
Sources: A) Flynn (1990), estimated by equations
B) Flynn (1990), adjusted values
C) Kasting et al. (1987)
5-20
-------
TABLE 5.11.
PARAMETER VALUES USED IN ESTIMATING THE
ABSORBED DOSE DUE TO DERMAL CONTACT WITH
CHEMICALS IN THE SEDIMENT POREWATER WHILE
WADING IN ROXANA POND
Var.
CF
SA,
EF
ED
BW
AT:
Noncarc.
AT: Care.
ET,
Units
L/cm3
cm2/event
day/yr
yrs
kg
days
days
hr/day
Value
Used
io-3
1010
1740
15
30
1.4
4.7
44
511
1716
25550
1
1
Reference
Typical: SA of feet (USEPA, 1989b)
RME*: SA of hands and feet (USEPA,
1989b)
Typical: Study Assumption
RME: Study Assumption
Typical: Proportion of 9 yr exposure
(USEPA, 1989a)
RME: Proportion of 30 yr exposure (USEPA
1989a)
50th percentile average weight calculated
from 1 yr incremental age groups (7 to <18
yrs) for males and females (USEPA, 1989b)
Typical: 1.4 yr x 365 days/yr (USEPA,
1989a)
RME: 4.7 yr x 365 days/yr (USEPA, 1989a)
70 yr x 365 days/yr (USEPA, 1989a)
Typical: Study Assumption
RME: Study Assumption
RME = Reasonable Maximum Exposure
5-21
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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 calculate noncarcinogenic and
carcinogenic health risks. 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 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 complete
exposure pathways 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 detected in the Grand Calumet River and Indiana Harbor (e.g., RfD
value for PCBs). In other cases, toxicity values were available for a particular
metal species rather than for the total metal. Consequently, a conservative
assumption was made about metal speciation in the AOC. In particular, methyl
mercury and vanadium pentoxide were assumed to be the major forms of mercury
and vanadium present in this system. In addition, chromium VI was assumed to
be the major valence state of chromium in the water column and in fish tissue.
6-1
-------
TABLE 6.1. EPA WEIGHT-OF-EVIDENCE CLASSIFICATION SYSTEM
FOR CARCINOGENICITY (USEPA, 1989a)
Group Description
A Human carcinogen
Bl or Probable human carcinogen
B2
Bl indicates that limited human data are available
B2 indicates sufficient evidence in animals and
inadequate or no evidence in humans
C Possible human carcinogen
D Not classifiable as to human carcinogenicity
E Evidence of noncarcinogenicity for humans
The uncertainties involved in these assumptions will be listed in a subsequent
chapter.
6-2
-------
TABLE 6.2.
HUMAN HEALTH RISK TOXICITY DATA FOR CHEMICALS
OF INTEREST IN THE GCR/IHC AREA OF CONCERN
Oral RfD
Chemical (mg/kg/day)
METALS
Antimony
Arsenic
Barium
Beryllium
Cadmium
Chromium VI
Copper
Manganese
Mercury, methyl
Nickel
Vanadium pentoxide
Zinc
PAHs
Acenaphthene
Benzo (a) anthracene
Benzo (a)pyrene
Benzo (b) f luoranthene
Benzo (k) f luoranthene
Chrysene
Fluoranthene
Phenanthrene
Pyrene
PHENOLS
2, 4-Dichlorophenol
2, 4-Dinitrophenol
Hydroquinone
Pentachlorophenol
Phenol
o-Cresol
AROMATIC HYDROCARBONS
Benzene
1, 1-Biphenyl
Hexachlorobenzene
Naphthalene
PCBs
Toluene
ORGANOCHLORINZ INSECTICIDES
Aldrin
alpha-HCH
Chlordane
Dieldrin
Heptachlor
Heptachlor epoxide
Mirex
p,p' ODD
p,p' DDE
p,p' DDT
Toxaphene
PURGEABLES
Acrylonitrile
Chlorobenzene
1, 2-Dichlorobenzene
1, 2-Dichloroethane
Ethylbenzene
Pentachlorobenzene
Styrene
Tetrachloroethylene
MISCELLANEOUS
2378-TCDD
Carbon disulfide
Dibenzof uran
4.0E-04
l.OE-03
7.0E-02
5.0E-03
5.0E-04
5.0E-03
1.3E-03
l.OE-01
3.0E-04
2.0E-02
9.0E-03
2.0E-01
6.0E-02
4.0E-02
3.0E-02
3.0E-03
2.0E-03
4.0E-02
3.0E-02
6.0E-01
5.0E-02
5.0E-02
8.0E-04
4.0E-03
2.0E-01
3.0E-05
6.0E-05
5.0E-05
5.0E-04
1.3E-05
2.0E-06
5.0E-04
l.OE-01
l.OE-04
2.0E-02
9.0E-02
l.OE-01
8.0E-04
2.0E-01
l.OE-02
l.OE-09
l.OE-01
Carcinogenic
Weight of
Evidence
Form Source Class
water
water
water
water
water
diet
poisonings
diet
diet
gavage
gavage
gavage
water
medication
diet
gavage
gavage
diet
diet
gavage
diet
diet
diet
diet
diet
diet
diet
diet
gavage
gavage
gavage
gavage
a
b
a
a
a
a
b
a
a
a
a
b
a
a
a
a
a
b
a
a
a
a
a
b
a
a
a
a
a
a
a
a
e
e
a
a
a
a
a
a
f
A
B2
Bl
A
D
D
D
B2
B2
B2
B2
B2
D
D
D
D
C
A
B2
D
B2
D
B2
B2
B2
B2
B2
B2
B2
B2
B2
B2
B2
Bl
D
D
B2
D
B2
D
Source
a
a
a
a
a
a
a
a
a
a
a
a
a
a
c
a
a
a
b
a
a
a
a
a
a
a
a
a
b
a
a
a
a
a
a
a
a
a
f
a
Oral Slope
Factor
11 (mg/kg/day) Source
4.30E+00
1.15E+01
1.15E+01
1.15E+01
1.15E+01
1.15E+01
2.90E-02
1.70E+00
7.70E+00
1.70E+01
6.30E+00
1.30E+00
1.60E+01
4.50E+00
9.10E+00
1.80E-1-00
2.40E-01
3.40E-01
3.40E-01
1.10E+00
5.40E-01
9.10E-02
1.60E-13
a
d
d
d
d
d
a
b
a
a
a
a
a
a
a
b
a
a
a
a
a
a
f
Sources
a: IRIS (current as of yi/91) b: USEPA (1989c) c: CRAVE Work Group Meeting Notes
d: Interim guidance, relative to Benzo(a)Pyrene, suggested by OERR (USEPA, 1989d)
e: USEPA (1990b) f: USEPA (1988a)
6-3
-------
CHAPTER?
BASELINE RISK CHARACTERIZATION FOR THE GRAND CALUMET
RIVER/INDIANA HARBOR CANAL AREA OF CONCERN
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
exposure to sediment-derived contaminants from the GCR/IHC AOC under present
conditions. 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 following
chapter.
Three means of expressing the carcinogenic and noncarcinogenic risks of
adverse health effects are presented in this chapter. First, chemical specific risks
were estimated for each exposure pathway. Secondly, chemical specific risks were
added to estimate a cumulative pathway specific risk. Finally, risks were added
across all chemicals and relevant pathways to estimate the total human health
risks to people residing in the GCR/IHC AOC.
7.2 QUANTIFYING RISKS
7.2.1 Determination of Noncarcinogenic Risks
Noncarcinogenic effects are evaluated by comparing an exposure level over a
specified time period with a RfD derived from a similar exposure period (otherwise
known as the hazard quotient (HQ)). Thus, HQ = exposure level (or intake)/RfD.
Hazard quotients are expressed to 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
7-1
-------
increase linearly as the RfD is approached or exceeded 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. For this risk assessment, 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
perhaps 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
Carcinogenic risks are estimated as the incremental probability of an
individual developing cancer over a lifetime as a result of exposure to the potential
carcinogen. This risk is computed using average lifetime exposure values that are
multiplied by the oral slope factor for a particular chemical. 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 106 range, and when noncarcinogenic health risks are estimated
to be significant (USEPA, 1988a).
Carcinogenic effects are summed for all chemicals in an exposure pathway
as well as for multiple pathways. 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 GRAND CALUMET RIVER
7.3.1 Dermal Exposure to Surface Water
For children and teenagers in the 7 to 17 years old age group,
noncarcinogenic risks were far below levels of concern (i.e., HI<1) for dermal
exposure to surface water in the vicinity of Roxana Pond (Tables 7.1 and 7.2).
Cumulative carcinogenic effects were also below a level of concern (i.e., <10"6) for
7-2
-------
typical and reasonable maximum exposure scenarios. Bacteriological data were
not available for Roxana Pond; thus, it was not known whether children would
become ill if they got their hands wet in the water and then licked their fingers or
wiped their hand across their mouth.
Based on these very low risk estimates, it was also assumed that the
noncarcinogenic and carcinogenic risks to anglers exposed to less polluted surface
water in the Indiana Harbor would be insignificant. The anglers would most
likely only get their hands wet while fishing.
7.3.2 Dermal Exposure to Sediments
Dermal exposure to sediments in the vicinity of Roxana Pond was estimated
by assuming that contaminants in the sediment porewater would come in contact
with the skin. The noncarcinogenic risks were very low (i.e., HI<1) for typical and
reasonable maximum exposures (Tables 7.3 and 7.4). The typical carcinogenic risk
for the 7 to 17 years old age group was also below a level of concern (i.e., <10"6).
However, the carcinogenic risk under a reasonable maximum exposure reached a
level of concern of 4 x 10~6. Since the porewater data used in this risk assessment
came from a site in the Grand Calumet River approximately 1 km west of
Indianapolis Boulevard, there is probably a medium level of uncertainty associated
with this risk estimate. Additional porewater data should be collected from
Roxana Pond to verify the possible carcinogenic risk to children and teenagers
wading in the pond. The potential risk resulting from limited dermal exposure to
contaminated sediments from the river area encompassing the Bridge Street
bridge to the Industrial Highway bridge will be discussed in Appendix C.
Another source of uncertainty with these cancer risk estimates is that EPA
guidance (USEPA, 1989a) states that it is inappropriate to use the oral slope
factor (such as done here) to evaluate the risks associated with dermal exposure to
carcinogens, such as benzo(a)pyrene, which cause skin cancer through a direct
action at the point of application. However, a clear consensus among EPA work
groups does not exist on a proper slope factor to use for these types of carcinogens
for dermal absorption pathways. Therefore, the lifetime cancer risk values listed
for these PAHs in the Grand Calumet River represent conservative estimates of
risk.
The additive risk resulting from exposure to the surface water and
sediments was controlled by the risk estimates for dermal contact with the
sediment porewater. These risk estimates were not added to the fish consumption
risk estimates because the dermal estimates were limited to a specific age group.
The risk estimates for fish consumption apply to all people in the AOC.
7-3
-------
7.3.3 Ingestion of Contaminated Fish
7.3.3.1 Noncarcinogenic Effects
Separate risk estimates were made for several species of fish collected from
the Grand Calumet River and Indiana Harbor Canal. The IHC fish data were
included because fish will travel throughout the GCR/IHC system.
Noncarcinogenic risk estimates were insignificant for the consumption of
whole pumpkinseed (Table 7.5), whole golden shiners (Table 7.6), whole carp
collected from the river (Table 7.7), and skin-on-fillet carp collected from the canal
(Table 7.8) under typical and reasonable maximum exposure scenarios. The
consumption of whole carp collected from the canal only reached a borderline level
of concern under the reasonable maximum exposure scenario (Table 7.9); the
noncarcinogenic risk was due primarily to 2,3,7,8-TCDD. However, this risk
estimate was based on the body burden of contaminants in raw, whole fish.
Different cooking and preparation methods would probably reduce the levels of
hydrophobic organic contaminants, like 2,3,7,8-TCDD, in the edible fish tissue.
7.3.3.2 Carcinogenic Effects
The carcinogenic risk estimates exceeded levels of concern for people that
consumed golden shiners and carp. The consumption of whole pumpkinseed did
not result in a significant carcinogenic risk estimate (Table 7.10); this risk
estimate may be incomplete because the fish were not analyzed for PCBs. The
carcinogenic risk was due mostly to PCB contamination in the carp and shiners
(Tables 7.11-7.14). The risk from consuming fish under the reasonable maximum
exposure scenario increased by almost two orders of magnitude over the typical
scenario. Whole carp collected from the river and the canal had similar risk
estimates, and the risk was reduced by an order of magnitude when the carp were
filleted. Although carp are generally regarded as an undesirable "trash" fish by
many anglers, some people do consume them.
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
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 that may readily accumulate contaminants through the ingestion and
7-4
-------
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.
7.4 HUMAN HEALTH RISKS IN INDIANA HARBOR
7.4.1 Noncarcinogenic Effects from Consuming Fish
The risk estimates for fish collected from the Indiana Harbor were based on
a pooled data set of gizzard shad, alewife, and sunfish. In addition, separate risk
estimates were made for the more contaminated carp species. In both cases, the
noncarcinogenic risk indices were less than one for the typical and reasonable
maximum exposure scenarios (Tables 7.15 and 7.16). Since heavy metals are
known to accumulate in the bones of fish and since these fish concentrations were
based on whole fish (rather than fillets), these risk estimates may be overly
conservative. These risk estimates should be updated as new data and toxicity
values (especially for PCBs) become available.
By comparison, the noncarcinogenic risk from consuming yellow perch and
alewife from the nearshore Lake Michigan area was similar (Table 7.17) for both
exposure scenarios. Additional fish surveys should be conducted to verify whether
the fish collected in the Indiana Harbor and nearshore Lake Michigan areas
accumulate similar levels of heavy metals.
7.4.2 Carcinogenic Effects from Consuming Fish
Carcinogenic effects were of concern for fish consumed from the Indiana
Harbor under both typical and reasonable maximum exposures. The risk from
consuming carp was an order of magnitude greater than that of the combined
consumption of gizzard shad, alewife, and sunfish (Tables 7.18 and 7.19). By
comparison, the carcinogenic risk for the pooled Indiana Harbor fish was about the
same as a pooled data set of alewife and yellow perch from the nearshore Lake
Michigan area (Table 7.20). The total lifetime cancer risk was based on only two
chemicals: beryllium and total PCBs. As with the other carcinogenic risk
estimates for fish, PCBs contributed most of the risk.
The carcinogenic risk from consuming whole carp from either the Grand
Calumet River, Indiana Harbor Canal, or Indiana Harbor was almost identical
(Table 7.21). This may be the result of fish travelling throughout the GCR/IHC
system.
7-5
-------
TABLE 7.1.
RISK ASSOCIATED WITH DERMAL EXPOSURE TO CONTAMINATED SURFACE
WATER, TYPICAL EXPOSURE, 7 TO 17 YEARS OLD AGE GROUP
Chemical
Antimony
Arsenic
Barium
Chromium
Copper
Manganese
Mercury
Nickel
Zinc
1,2 dichloroethane
Cumulative Risk
Noncarc.
Intake
(mg/kg-day)
l.OE-07
2.8E-09
6.7E-08
1.1E-08
2.9E-08
2.9E-07
3.8E-11
5.2E-09
9.4E-08
2.2E-05
HI
2.6E-04
9.4E-06
9.6E-07
2.1E-06
2.2E-05
2.9E-06
1.3E-07
2.6E-07
4.7E-07
0.0003
Carcin.
Intake
(mg/kg-day)
2.1E-09
5.7E-11
1.3E-09
2.1E-10
5.8E-10
5.8E-09
7.6E-13
l.OE-10
1.9E-09
4.3E-07
Cancer Risk
3.9E-08
3.9E-08
7-6
-------
TABLE 7.2.
RISK ASSOCIATED WITH DERMAL EXPOSURE TO SURFACE WATER, REASONABLE
MAXIMUM EXPOSURE, 7 TO 17 YEARS OLD AGE GROUP
Chemical
Antimony
Arsenic
Barium
Chromium
Copper
Manganese
Mercury
Nickel
Zinc
1,2 dichloroethane
Cumulative Risk
Noncarc.
Intake
(mg/kg-day)
4.3E-07
1.2E-08
2.8E-07
4.4E-08
1.2E-07
1.2E-06
1.6E-10
2.2E-08
3.9E-07
9.0E-05
HI
1.1E-03
3.9E-05
4.0E-06
8.8E-06
9.3E-05
1.2E-05
5.2E-07
1.1E-06
1.9E-06
0.0012
Care.
Intake
(mg/kg-day)
2.9E-08
7.9E-10
1.9E-08
2.9E-09
8.1E-09
8.1E-08
1.1E-11
1.5E-09
2.6E-08
6.0E-06
Cancer Risk
5.5E-07
5.5E-07
7-7
-------
TABLE 7.3.
RISK ASSOCIATED WITH DERMAL EXPOSURE TO CONTAMINATED SEDIMENTS,
TYPICAL EXPOSURE, 7 TO 17 YEARS OLD AGE GROUP
Chemical
METALS
Antimony
Arsenic
Barium
Chromium VI
Copper
Manganese
Mercury
Nickel
Zinc
PAHs
Benzo(a)anthracene
Benzo(a)pyrene
Benzo(b)fluoranthene
Benzo(k)fluoranthene
Chrysene
Fluoranthene
Phenanthrene
Pyrene
PHENOLS
2,4-Dichlorophenol
2,4-Dinitrophenol
Hydroquinone
Pentachlorophenol
Phenol
o-Cresol
Noncarc.
Intake
(mg/kg-day)
2.3E-08
6.2E-10
1.5E-08
2.3E-09
6.3E-09
6.3E-08
8.2E-12
1.1E-09
2.0E-08
3.6E-07
9.8E-08
3.6E-07
1.7E-07
2.7E-07
9.6E-07
7.3E-06
5.9E-07
5.1E-07
1.8E-06
1.2E-07
5.6E-07
2.8E-06
6.3E-07
HI
5.7E-05
6.2E-07
2.1E-07
4.6E-07
4.9E-06
6.3E-07
2.7E-08
5.7E-08
l.OE-07
2.4E-05
2.0E-05
1.7E-04
8.7E-04
3.0E-06
1.9E-05
4.7E-06
1.3E-05
Care.
Intake
(mg/kg-day)
4.5E-10
1.2E-11
2.9E-10
4.6E-11
1.3E-10
1.3E-09
1.6E-13
2.3E-11
4. IE- 10
7.2E-09
2.0E-09
7.3E-09
3.4E-09
5.4E-09
1.9E-08
1.5E-07
1.2E-08
l.OE-08
3.5E-08
2.4E-09
1.1E-08
5.6E-08
1.3E-08
Care.
Risk
8.2E-08
2.3E-08
8.4E-08
3.9E-08
6.2E-08
7-8
-------
TABLE 7.3.
CONTINUED
Chemical
AROMATIC HYDROCARBONS
1,1-Biphenyl
Hexachlorobenzene
Naphthalene
PCBs
ORGANOCHLORINE INSECTICIDES
Chlordane
Dieldrin
Heptachlor
p,p' DDE
p,P' DDT
Toxaphene
PURGEABLES
Acrylonitrile
Chlorobenzene
1,2-Dichlorobenzene
Ethylbenzene
Styrene
Tetrachloroethylene
Cumulative Risk
Noncarc.
Intake
(mg/kg-day)
7.6E-07
6.3E-08
1.1E-04
3.2E-07
1.8E-08
3.0E-08
1.5E-08
2.1E-07
7.2E-08
1.7E-07
1.7E-09
6.0E-07
1.5E-08
4.7E-06
4.2E-06
2.1E-08
HI
1.5E-05
7.8E-05
2.8E-02
3.0E-04
6.0E-04
3.0E-05
1.4E-04
1.7E-06
1.7E-05
3.0E-05
1.7E-07
4.7E-05
2.1E-05
2.1E-06
0.03
Care.
Intake
(mg/kg-day)
1.5E-08
1.2E-09
2.2E-06
6.4E-09
3.6E-10
6.0E-10
3.0E-10
4.11E-09
1.43E-09
3.34E-09
3.40E-11
1.20E-08
2.98E-10
9.42E-08
8.30E-08
4.19E-10
Care.
Risk
2.1E-09
4.9E-08
4.6E-10
9.5E-09
1.3E-09
1.4E-09
4.9E-10
3.7E-09
1.8E-11
3.6E-07
7-9
-------
TABLE 7.4.
RISK ASSOCIATED WITH DERMAL EXPOSURE TO CONTAMINATED SEDIMENTS,
REASONABLE MAXIMUM EXPOSURE, 7 TO 17 YEARS OLD AGE GROUP
Chemical
METALS
Antimony
Arsenic
Barium
Chromium VI
Copper
Manganese
Mercury
Nickel
Zinc
PAHs
Benzo(a)anthracene
Benzo(a)pyrene
Benzo(b)fluoranthene
Benzo(k)fluoranthene
Chrysene
Fluoranthene
Phenanthrene
Pyrene
PHENOLS
2,4-Dichlorophenol
2,4-Dinitrophenol
Hydroquinone
Pentachlorophenol
Phenol
o-Cresol
Noncarc.
Intake
(mg/kg-day)
7.8E-08
2.1E-09
5.0E-08
7.9E-09
2.2E-08
2.2E-07
2.8E-11
3.9E-09
7.0E-08
1.2E-06
3.4E-07
1.3E-06
5.9E-07
9.2E-07
3.3E-06
2.5E-05
2.0E-06
1.7E-06
6.0E-06
4.1E-07
1.9E-06
9.7E-06
2.2E-06
HI
2.0E-04
2.1E-06
7.2E-07
1.6E-06
1.7E-05
2.2E-06
9.4E-08
2.0E-07
3.5E-07
8.2E-05
6.8E-05
5.8E-04
3.0E-03
l.OE-05
6.4E-05
1.6E-05
4.3E-05
Care.
Intake
(mg/kg-day)
5.3E-09
1.4E-10
3.4E-09
5.3E-10
1.5E-09
1.5E-08
1.9E-12
2.6E-10
4.7E-09
8.3E-08
2.3E-08
8.4E-08
3.9E-08
6.2E-08
2.2E-07
1.7E-06
1.4E-07
1.2E-07
4.0E-07
2.8E-08
1.3E-07
6.5E-07
1.5E-07
Care.
Risk
9.5E-07
2.6E-07
9.7E-07
4.5E-07
7.1E-07
7-10
-------
TABLE 7.4.
CONTINUED
Chemical
AROMATIC HYDROCARBONS
1,1-Biphenyl
Hexachlorobenzene
Naphthalene
PCBs
ORGANOCHLORINE INSECTICIDES
Chlordane
Dieldrin
Heptachlor
p,p' DDE
p,p' DDT
Toxaphene
PURGEABLES
Acrylonitrile
Chlorobenzene
1,2-Dichlorobenzene
1,2 Dichloroethane
Ethylbenzene
Styrene
Tetrachloroethylene
Cumulative Risk
Noncarc.
Intake
(mg/kg-day)
2.6E-06
2.2E-07
3.9E-04
1.1E-06
6.2E-08
l.OE-07
5.1E-08
7.1E-07
2.5E-07
5.8E-07
5.9E-09
2.1E-06
5.1E-08
1.6E-05
1.6E-05
1.4E-05
7.2E-08
HI
5.3E-05
2.7E-04
9.6E-02
l.OE-03
2.1E-03
l.OE-04
4.9E-04
5.8E-06
5.9E-05
l.OE-04
5.7E-07
1.6E-04
7.1E-05
7.2E-06
0.1
Care.
Intake
(mg/kg-day)
1.8E-07
1.4E-08
2.6E-05
7.4E-08
4.1E-09
6.9E-09
3.4E-09
4.8E-08
1.7E-08
3.9E-08
3.9E-10
1.4E-07
3.4E-09
1.1E-06
1.1E-06
9.6E-07
4.9E-09
Care.
Risk
2.5E-08
5.7E-07
5.4E-09
1.1E-07
1.6E-08
1.6E-08
5.6E-09
4.2E-08
2.1E-10
9.9E-08
4.2E-06
7-11
-------
TABLE 7.5.
NONCARCINOGENIC RISKS ASSOCIATED WITH CONSUMING WHOLE PUMPKINSEED
COLLECTED FROM THE GRAND CALUMET RIVER (7/8/87)
Chemical
METALS
Manganese
Zinc
ORGANICS*
Benzene
Toluene
HAZARD INDEX
* Note:
Noncarcinogenic Intake Hazard Quotient
Fish Cone. (mg/kg/day) (Intake/RfD)
(mg/kg) Typical RME Typical RME
3.6E+00 1.6E-05 2.7E-04 1.6E-04 2.7E-03
2.9E+01 1.3E-04 2.1E-03 6.4E-04 1.1E-02
7.0E-03 3.1E-08 5.2E-07
3.7E-02 1.6E-07 2.7E-06 8.2E-07 1.4E-05
0.00080 0.013
Fish were not analyzed for PCBs.
7-12
-------
TABLE 7.6.
NONCARCINOGENIC RISKS ASSOCIATED WITH CONSUMING WHOLE GOLDEN
SHINERS COLLECTED FROM THE GRAND CALUMET RIVER (7/8/87)
Noncarcinogenic Intake
Chemical
METALS
Chromium VI
Copper
Manganese
Mercury, methyl
Zinc
ORGANICS
Acenaphthene
Benzene
Dibenzofuran
PCBs
HAZARD INDEX
Fish Cone.
(mg/kg)
1.7E+00
3.1E+00
1.2E+01
3.0E-02
4.7E+01
8.6E-01
2.0E-02
5.4E-01
2.9E+00
(mg/kg/day)
Typical RME
7.6E-06
1.4E-05
5.3E-05
1.3E-07
2.1E-04
3.8E-06
8.9E-08
2.4E-06
1.3E-05
1.3E-04
2.3E-04
8.9E-04
2.2E-06
3.5E-03
6.3E-05
1.5E-06
4.0E-05
2.1E-04
Hazard Quotient
(Intake/RfD)
Typical RME
1.5E-03
1.1E-02
5.3E-04
4.5E-04
1.1E-03
6.3E-05
0.014
2.5E-02
1.8E-01
8.9E-03
7.4E-03
1.8E-02
1.1E-03
0.24
7-13
-------
TABLE 7.7.
NONCARCINOGENIC RISKS ASSOCIATED WITH CONSUMING WHOLE CARP
COLLECTED FROM THE GRAND CALUMET RIVER (11/18/87)
Noncarcinogenic Intake
Chemical
METALS
Chromium VI
Copper
Manganese
Mercury, methyl
Zinc
ORGANICS
Aldrin
Benzene
Carbon Disulfide
Chlordane
p,p' ODD
PCBs
Toluene
HAZARD INDEX
Fish Cone.
(mg/kg)
7.5E-01
3.3E+00
2.1E+00
4.8E-02
l.OE+02
5.0E-02
1.3E-02
4.2E-03
7.5E-03
2.1E-02
3.8E+00
1.6E-02
(mg/kg/day)
Typical
3.3E-06
1.4E-05
9.4E-06
2.1E-07
4.6E-04
2.2E-07
5.8E-08
1.9E-08
3.3E-08
9.1E-08
1.7E-05
6.9E-08
RME
5.5E-05
2.4E-04
1.6E-04
3.6E-06
7.7E-03
3.7E-06
9.6E-07
3.1E-07
5.5E-07
1.5E-06
2.8E-04
1.1E-06
Hazard Quotient
(Intake/RfD)
Typical
6.7E-04
1.1E-02
9.4E-05
7.1E-04
2.3E-03
7.4E-03
1.9E-07
5.6E-04
3.5E-07
0.023
RME
1.1E-02
1.8E-01
1.6E-03
1.2E-02
3.8E-02
1.2E-01
3.1E-06
9.2E-03
5.7E-06
0.38
7-14
-------
TABLE 7.8.
NONCARCINOGENIC RISKS ASSOCIATED WITH CONSUMING SKIN-ON-FILLET CARP
COLLECTED FROM THE INDIANA HARBOR CANAL (11/1/88)
Noncarcinoeenic Intake
Chemical
METALS
Cadmium
Mercury, methyl
ORGANICS
Carbon Bisulfide
Chlordane
p,p' DDD
p,p' DDE
Dieldrin
Heptachlor Epoxide
PCBs
Tetrachloroethylene
HAZARD INDEX
Fish Cone.
(mg/kg)
1.4E-02
l.OE-01
5.5E-02
4.2E-02
5.2E-02
2.1E-01
1.2E-01
5.3E-02
1.9E+00
1.7E-02
(mg/kg/day)
Typical
6.2E-08
4.6E-07
2.4E-07
1.9E-07
2.3E-07
9.1E-07
5.1E-07
2.3E-07
8.2E-06
7.6E-08
RME
l.OE-06
7.7E-06
4.1E-06
3.1E-06
3.8E-06
1.5E-05
8.5E-06
3.9E-06
1.4E-04
1.3E-06
Hazard Quotient
(Intake/RfD)
Typical
1.2E-04
1.5E-03
2.4E-06
3.1E-03
l.OE-02
1.8E-02
7.6E-06
0.033
RME
2.1E-03
2.6E-02
4.1E-05
5.2E-02
1.7E-01
3.0E-01
1.3E-04
0.55
7-15
-------
TABLE 7.9.
NONCARCINOGENIC RISKS ASSOCIATED WITH CONSUMING WHOLE CARP
COLLECTED FROM THE INDIANA HARBOR CANAL (11/18/87)
Noncarcinoeenic Intake
Chemical
ORGANICS
1,1-Biphenyl
Chlordane
p,p' DDE
Dieldrin
alpha-HCH
Mirex
PCBs
Pentachlorobenzene
Styrene
2378-TCDD
HAZARD INDEX
Fish Cone.
(mg/kg)
2.6E-02
7.0E-02
3.8E-01
2.6E-02
6.3E-03
1.5E-03
6.8E+00
8.3E-04
2.3E-03
1.5E-05
(mg/kg/day)
Typical
1.2E-07
3.1E-07
1.7E-06
1.1E-07
2.8E-08
6.5E-09
3.0E-05
3.7E-09
l.OE-08
6.7E-11
RME
2.0E-06
5.1E-06
2.8E-05
1.9E-06
4.7E-07
1.1E-07
5.0E-04
6.1E-08
1.7E-07
1.1E-09
Hazard Quotient
(Intake/RfD)
Typical
2.4E-06
5.2E-03
2.3E-03
3.2E-03
4.6E-06
5.1E-08
6.7E-02
0.078
RME
3.9E-05
8.6E-02
3.8E-02
5.4E-02
7.7E-05
8.5E-07
1.1E+00
1.3
7-16
-------
TABLE 7.10.
CARCINOGENIC RISKS ASSOCIATED WITH CONSUMING WHOLE PUMPKINSEED
COLLECTED FROM THE GRAND CALUMET RIVER (7/8/87)
Chemical
Fish Cone.
(mg/kg)
Carcinogenic Intake
(mg/kg/day)
Typical RME
Lifetime Cancer Risk
(Intake*Slope Factor)
Typical RME
METALS
Manganese
Zinc
ORGANICS*
Benzene
Toluene
3.6E+00
2.9E+01
7.0E-03
3.7E-02
2.1E-06
1.6E-05
4.0E-09
2.1E-08
1.1E-04
9.1E-04
2.2E-07
1.2E-06
1.2E-10
6.4E-09
CUMULATIVE CARCINOGENIC RISK
* Note: Fish were not analyzed for PCBs.
1.2E-10
6.4E-09
7-17
-------
TABLE 7.11.
CARCINOGENIC RISKS ASSOCIATED WITH CONSUMING WHOLE GOLDEN SHINERS
COLLECTED FROM THE GRAND CALUMET RIVER (7/8/87)
Chemical
Fish Cone.
(rag/kg)
Carcinogenic Intake
(mg/kg/day)
Typical RME
Lifetime Cancer Risk
(Intake*Slope Factor)
Typical RME
METALS
Chromium VI
Copper
Manganese
Mercury, methyl
Zinc
ORGANICS
1.7E+00
3.1E+00
1.2E+01
3.0E-02
4.7E+01
9.7E-07
1.8E-06
6.9E-06
1.7E-08
2.7E-05
5.4E-05
9.8E-05
3.8E-04
9.5E-07
1.5E-03
Acenaphthene 8.6E-01
Benzene 2.0E-02
Dibenzofuran 5.4E-01
PCBs 2.9E+00
CUMULATIVE CARCINOGENIC RISK
4.9E-07
1.1E-08
3.1E-07
1.7E-06
2.7E-05
6.3E-07
1.7E-05
9.2E-05
3.3E-10
1.3E-05
1.3E-05
1.8E-08
7.1E-04
7.1E-04
7-18
-------
TABLE 7.12.
CARCINOGENIC RISKS ASSOCIATED WITH CONSUMING WHOLE CARP COLLECTED
FROM THE GRAND CALUMET RIVER (11/18/87)
Chemical
METALS
Chromium VI
Copper
Manganese
Mercury, methyl
Zinc
ORGANICS
Aldrin
Benzene
Carbon Bisulfide
Chlordane
p,p' DDD
PCBs
Toluene
CUMULATIVE CARCINOGENIC
Fish Cone.
(mg/kg)
7.5E-01
3.3E+00
2.1E+00
4.8E-02
l.OE+02
5.0E-02
1.3E-02
4.2E-03
7.5E-03
2.1E-02
3.8E+00
1.6E-02
RISK
Carcinogenic Intake
(mg/kg/day)
Typical RME
4.3E-07 2.4E-05
1.9E-06 l.OE-04
1.2E-06 6.7E-05
2.7E-08 1.5E-06
6.0E-05 3.3E-03
2.9E-08 1.6E-06
7.4E-09 4.1E-07
2.4E-09 1.3E-07
4.3E-09 2.4E-07
1.2E-08 6.5E-07
2.2E-06 1.2E-04
8.9E-09 4.9E-07
Lifetime Cancer Risk
(Intake*Slope Factor)
Typical RME
4.9E-07 2.7E-05
2.2E-10 1.2E-08
5.6E-09 3.1E-07
2.8E-09 1.6E-07
1.7E-05 9.3E-04
1.7E-05 9.6E-04
7-19
-------
TABLE 7.13.
CARCINOGENIC RISKS ASSOCIATED WITH CONSUMING SKIN-ON-FILLET CARP
COLLECTED FROM THE INDIANA HARBOR CANAL (11/1/88)
Carcinogenic Intake
Chemical
METALS
Cadmium
Mercury, methyl
ORGANICS
Carbon Bisulfide
Chlordane
p,p' DDD
p,p' DDE
Dieldrin
Heptachlor Epoxide
PCBs
Tetrachloroethylene
CUMULATIVE CARCINOGENIC
Fish Cone.
(mg/kg)
1.4E-02
l.OE-01
5.5E-02
4.2E-02
5.2E-02
2.1E-01
1.2E-01
5.3E-02
1.9E+00
1.7E-02
RISK
(mg/kg/day)
Typical
8.0E-09
6.0E-08
3.1E-08
2.4E-08
3.0E-08
1.2E-07
6.6E-08
3.0E-08
1.1E-06
9.7E-09
RME
4.4E-07
3.3E-06
1.7E-06
1.3E-06
1.6E-06
6.5E-06
3.6E-06
1.7E-06
5.9E-05
5.4E-07
Lifetime Cancer Risk
(Intake*Slope Factor)
Typical
3.1E-08
7.1E-09
4.0E-08
1.1E-06
2.7E-07
8.2E-06
9.6E-06
RME
1.7E-06
4.0E-07
2.2E-06
5.8E-05
1.5E-05
4.5E-04
5.3E-04
7-20
-------
TABLE 7.14.
CARCINOGENIC RISKS ASSOCIATED WITH CONSUMING WHOLE CARP COLLECTED
FROM THE INDIANA HARBOR CANAL (11/18/87)
Carcinogenic Intake
Chemical
ORGANICS
1,1-Biphenyl
Chlordane
p,p' DDE
Dieldrin
alpha-HCH
Mirex
PCBs
Pentachlorobenzene
Styrene
2,3,7,8-TCDD
CUMULATIVE CARCINOGENIC
Fish Cone.
(mg/kg)
2.6E-02
7.0E-02
3.8E-01
2.6E-02
6.3E-03
1.5E-03
6.8E+00
8.3E-04
2.3E-03
1.5E-05
RISK
(mg/kg/day)
Typical
1.5E-08
4.0E-08
2.2E-07
1.5E-08
3.6E-09
8.3E-10
3.9E-06
4.8E-10
1.3E-09
8,
RME
8.4E-07
2.2E-06
1.2E-05
8.1E-07
2.0E-07
4.6E-08
2.2E-04
2.6E-08
7.3E-08
.7E-12 4.8E-10
Lifetime Cancer Risk
(Intake*Slope Factor)
Typical
5.2E-08
7.4E-08
2.3E-07
2.3E-08
1.5E-09
3.0E-05
1
3.2E-05
RME
2.9E-06
4.1E-06
1.3E-05
1.3E-06
8.3E-08
1.7E-03
.4E-06 7.7E-05
1.8E-03
7-21
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TABLE 7.15.
NONCARCINOGENIC RISKS ASSOCIATED WITH CONSUMING A MIXTURE OF INDIANA
HARBOR FISH EXCLUDING CARP
Noncarcinogenic Intake
Chemical
METALS
Antimony
Arsenic
Barium
Beryllium
Cadmium
Chromium VI
Copper
Manganese
Mercury, methyl
Nickel
Vanadium pentoxide
Zinc
ORGANICS
PCBs
HAZARD INDEX
Fish Cone.
(mg/kg)
4.0E-01
7.4E-01
4.4E-01
1.5E-02
5.5E-02
1.2E+00
1.8E+00
4.0E+00
3.6E-02
3.4E-01
5.3E-01
2.3E+01
5.0E-01
(mg/kg/day)
Typical
3.6E-06
6.6E-06
3.9E-06
1.3E-07
4.9E-07
l.OE-05
1.6E-05
3.5E-05
3.2E-07
3.0E-06
4.7E-06
2.1E-04
4.4E-06
RME
7.4E-05
1.4E-04
8.1E-05
2.8E-06
l.OE-05
2.1E-04
3.4E-04
7.3E-04
6.6E-06
6.3E-05
9.8E-05
4.3E-03
9.2E-05
Hazard Quotient
(Intake/RfD)
Typical
8.9E-03
6.6E-03
5.6E-05
2.7E-05
9.8E-04
2.1E-03
1.3E-02
3.5E-04
1.1E-03
1.5E-04
5.2E-04
l.OE-03
0.034
RME
1.8E-01
1.4E-01
1.2E-03
5.5E-04
2.0E-02
4.3E-02
2.6E-01
7.3E-03
2.2E-02
3.2E-03
1.1E-02
2.2E-02
0.72
7-22
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TABLE 7.16.
NONCARCINOGENIC RISKS ASSOCIATED WITH CONSUMING INDIANA HARBOR CARP
Noncarcinogenic Intake
Chemical
METALS
Antimony
Arsenic
Barium
Beryllium
Cadmium
Chromium VI
Copper
Manganese
Mercury, methyl
Nickel
Vanadium pentoxide
Zinc
ORGANICS
PCBs
HAZARD INDEX
Fish Cone.
(mg/kg)
5.4E-01
6.5E-01
8.7E-01
1.5E-02
1.3E-01
9.0E-01
1.6E+00
2.6E+00
9.1E-02
6.5E-01
4.9E-01
9.9E+01
2.6E+00
(mg/kg/day)
Typical
4.8E-06
5.8E-06
7.8E-06
1.3E-07
1.1E-06
8.0E-06
1.4E-05
2.3E-05
8.1E-07
5.8E-06
4.4E-06
8.8E-04
2.3E-05
RME
9.9E-05
1.2E-04
1.6E-04
2.8E-06
2.3E-05
1.7E-04
3.0E-04
4.8E-04
1.7E-05
1.2E-04
9.1E-05
1.8E-02
4.8E-04
Hazard Quotient
(Intake/RfD)
Typical
1.2E-02
5.8E-03
1.1E-04
2.7E-05
2.2E-03
1.6E-03
1.1E-02
2.3E-04
2.7E-03
2.9E-04
4.8E-04
4.4E-03
0.041
RME
2.5E-01
1.2E-01
2.3E-03
5.5E-04
4.6E-02
3.3E-02
2.3E-01
4.8E-03
5.6E-02
6.0E-03
l.OE-02
9.2E-02
0.85
7-23
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TABLE 7.17.
NONCARCINOGENIC RISKS ASSOCIATED WITH CONSUMING NEARSHORE LAKE
MICHIGAN FISH
Noncarcinoeenic Intake
Chemical
METALS
Antimony
Arsenic
Barium
Beryllium
Cadmium
Chromium VI
Copper
Manganese
Mercury, methyl
Nickel
Vanadium pentoxide
Zinc
ORGANICS
PCBs
HAZARD INDEX
Fish Cone.
(mg/kg)
4.0E-01
6.5E-01
6.2E-01
1.5E-02
5.5E-02
6.0E-01
4.4E-01
2.9E+00
3.1E-02
2.2E-01
4.9E-01
2.1E+01
2.4E-01
(mg/kg/day)
Typical
3.6E-06
5.8E-06
5.6E-06
1.3E-07
4.9E-07
5.3E-06
3.9E-06
2.5E-05
2.7E-07
1.9E-06
4.4E-06
1.9E-04
2.2E-06
RME
7.4E-05
1.2E-04
1.2E-04
2.8E-06
l.OE-05
1.1E-04
8.1E-05
5.3E-04
5.7E-06
4.0E-05
9.1E-05
3.9E-03
4.5E-05
Hazard Quotient
(Intake/RfD)
Typical
8.9E-03
5.8E-03
8.0E-05
2.7E-05
9.8E-04
1.1E-03
3.0E-03
2.5E-04
9.1E-04
9.7E-05
4.8E-04
9.4E-04
0.022
RME
1.8E-01
1.2E-01
1.7E-03
5.5E-04
2.0E-02
2.2E-02
6.3E-02
5.3E-03
1.9E-02
2.0E-03
l.OE-02
1.9E-02
0.47
7-24
-------
TABLE 7.18.
CARCINOGENIC RISKS ASSOCIATED WITH CONSUMING A MIXTURE OF INDIANA
HARBOR FISH EXCLUDING CARP
Chemical
METALS
Antimony
Arsenic
Barium
Beryllium
Cadmium
Chromium VI
Copper
Manganese
Mercury, methyl
Nickel
Vanadium pentoxide
Zinc
ORGANICS
PCBs
CUMULATIVE CARCINOGENIC
Fish Cone.
(mg/kg)
4.0E-01
7.4E-01
4.4E-01
1.5E-02
5.5E-02
1.2E+00
1.8E+00
4.0E+00
3.6E-02
3.4E-01
5.3E-01
2.3E+01
5.0E-01
RISK
Carcinogenic Intake
(mg/kg/day)
Typical RME
4.6E-07 3.2E-05
8.5E-07 5.9E-05
5.0E-07 3.5E-05
1.7E-08 1.2E-06
6.3E-08 4.4E-06
1.3E-06 9.2E-05
2.1E-06 1.5E-04
4.5E-06 3.1E-04
4.1E-08 2.8E-06
3.9E-07 2.7E-05
6.1E-07 4.2E-05
2.7E-05 1.9E-03
5.7E-07 4.0E-05
Lifetime Cancer Risk
(Intake*Slope Factor)
Typical RME
7.4E-08 5.1E-06
4.4E-06 3.0E-04
4.5E-06 3.1E-04
7-25
-------
TABLE 7.19.
CARCINOGENIC RISKS ASSOCIATED WITH CONSUMING INDIANA HARBOR CARP
Carcinogenic Intake
Chemical
METALS
Antimony
Arsenic
Barium
Beryllium
Cadmium
Chromium VI
Copper
Manganese
Mercury, methyl
Nickel
Vanadium pentoxide
Zinc
ORGANICS
PCBs
CUMULATIVE CARCINOGENIC
Fish Cone.
(mg/kg)
5.4E-01
6.5E-01
8.7E-01
1.5E-02
1.3E-01
9.0E-01
1.6E+00
2.6E+00
9.1E-02
6.5E-01
4.9E-01
9.9E+01
2.6E+00
RISK
(mg/kg/day)
Typical
6.1E-07
7.4E-07
l.OE-06
1.7E-08
1.4E-07
l.OE-06
1.8E-06
3.0E-06
l.OE-07
7.4E-07
5.6E-07
1.1E-04
2.9E-06
RME
4.3E-05
5.2E-05
6.9E-05
1.2E-06
9.9E-06
7.1E-05
1.3E-04
2.1E-04
7.2E-06
5.2E-05
3.9E-05
7.8E-03
2.0E-04
Lifetime Cancer Risk
(Intake*Slope Factor)
Typical RME
7.4E-08 5.1E-06
2.3E-05 1.6E-03
2.3E-05 1.6E-03
7-26
-------
TABLE 7.20.
CARCINOGENIC RISKS ASSOCIATED WITH CONSUMING NEARSHORE LAKE
MICHIGAN FISH
Chemical
METALS
Antimony
Arsenic
Barium
Beryllium
Cadmium
Chromium VI
Copper
Manganese
Mercury, methyl
Nickel
Vanadium pentoxide
Zinc
ORGANICS
PCBs
CUMULATIVE CARCINOGENIC
Fish Cone.
(mg/kg)
4.0E-01
6.5E-01
6.3E-01
1.5E-02
5.5E-02
6.0E-01
4.4E-01
2.9E+00
3.1E-02
2.2E-01
4.9E-01
2.1E+01
2.4E-01
RISK
Carcinogenic Intake
(mg/kg/day)
Typical RME
4.6E-07 3.2E-05
7.4E-07 5.2E-05
7.2E-07 5.0E-05
1.7E-08 1.2E-06
6.3E-08 4.4E-06
6.9E-07 4.8E-05
5.0E-07 3.5E-05
3.3E-06 2.3E-04
3.5E-08 2.4E-06
2.5E-07 1.7E-05
5.6E-07 3.9E-05
2.4E-05 1.7E-03
2.8E-07 1.9E-05
Lifetime Cancer Risk
(Intake*Slope Factor)
Typical RME
7.4E-08 5.1E-06
2.1E-06 1.5E-04
2.2E-06 1.5E-04
7-27
-------
TABLE 7.21. SUMMARY OF NONCARCINOGENIC AND CARCINOGENIC
RISKS RESULTING FROM FISH CONSUMPTION IN THE
GCR/IHC AOC
Fish/Location/Sampling Date
Whole PumDkinseed/GCR/(7/8/87)*
Typical
RME
Whole Golden Shiners/GCR/(7/8/87)
Typical
RME
Whole Carp/GCR/( 11/18/87)
Typical
RME
Skin-on-Fillet Caro/IHCA 11/1/88)
Typical
RME
Whole Carp/IHC/( 11/18/87)
Typical
RME
Whole Fish/Indiana Harbor/no date given
Typical
RME
Whole Carp/Indiana Harbor/no date given
Typical
RME
Whole Fish/Nearshore L. Michigan/no date given
Typical
RME
HI
0.0008
0.01
0.01
0.2
0.02
0.4
0.03
0.5
0.08
1
0.03
0.7
0.04
0.8
0.02
0.5
Carcinogenic
Risk
1E-10
6E-09
1E-05
7E-04
2E-05
1E-03
1E-05
5E-04
3E-05
2E-03
4E-06
3E-04
2E-05
2E-03
2E-06
2E-04
* Fish were not analyzed for PCBs
7-28
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CHAPTER 8
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.
Some data studies may have been missed in the data
compilation step. There are many agencies involved with studying
contaminants in the GCR/IHC AOC (in some cases for litigation
purposes), and there is no central agency responsible for keeping
track of historical and ongoing studies in the AOC. Consequently,
there is a low to moderate level of uncertainty that some studies were
missed for inclusion in this risk assessment.
The available data for contaminant levels in surface water,
sediment porewater, and fish tissue were representative of the
true distribution of contaminants in the GCR/IHC AOC. A
moderate level of uncertainty is probably associated with this
assumption. Because porewater and water column data were not
available for Roxana Pond, data from nearby sites were used to be
representative of contaminant concentrations in this exposure site.
The uncertainty with this assumption would have been reduced if
actual data had been available for Roxana Pond. Additional
sampling, over at least a few seasons, 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
medium of interest.
A complete QA/QC review of the data reports obtained for this
8-1
-------
risk assessment could not be made because of a lack of
information supplied with the reports. Thus, for several studies,
the quality of the data was unknown. This risk assessment used
more recent data, when possible, because data quality issues have
become more prevalent at analytical laboratories in recent years. The
uncertainty associated with using this data is not well established,
but may have been minimized by using more up-to-date monitoring
studies.
Preliminary data used in this risk assessment may be subject
to change when it is formerly released by the researcher or
analytical laboratory (e.g., data from Zabik, 1990). This
statement points out one of the problems with using recently collected
data that has not gone through all of the QA/QC procedures at a lab
yet, or else has not been written up in a report. These raw,
preliminary data are subject to change, but are being used here to
give an indication of risk. Thus, the uncertainty associated with
these data is not well established.
Contaminant burdens in most of the fish data were based on
total body concentrations rather than on fillets. This would
result in an overestimation of risk since some contaminants (e.g.,
metals) accumulate in the bones of fish which people are unlikely to
consume. In addition, hydrophobic organic contaminants (e.g., PCBs)
accumulate in the lipids of fish. The uncertainty associated with this
overestimation of risk is not well established.
Contaminant burdens in fish may decrease depending on how
the fish is prepared and cooked. Contaminant levels may be
reduced 10 to 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.
Metal speciation was not reported for most of the metals data
and were assumed to represent total metal concentrations.
This assumption is important in terms of the toxicity values used in
this risk assessment. The uncertainty associated with this
assumption is probably low since many analytical laboratories report
metal concentrations as total metals.
8.2.2 Exposure Assessment
A number of assumptions were made in the exposure assessment step of
this baseline human health risk assessment.
8-2
-------
An adequate assessment of complete and incomplete exposure
pathways was made. The complete pathways chosen were based
primarily on documented activities in the AOC. There is always the
possibility that another pathway (e.g., children ingesting sediment)
may occur but was not documented. The uncertainty associated with
this assumption is probably low.
The exclusion of some complete exposure pathways (e.g.,
dermal exposure to surface water in the Indiana Harbor by
anglers) 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 resulting from
dermal exposure to surface water in the Grand Calumet River was
not significant. Consequently, it was assumed that dermal exposure
to less contaminated water would be insignificant as well.
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, surface area of exposed body parts,
life expectancy) were based on EPA guidance (USEPA, 1989a,b;
199 la) 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.
The selection of the 7 to 17 years old age group for the dermal
exposure assessment was appropriate. This age group was
selected based on observations by researchers collecting samples at
Roxana Pond. A low to moderate level of uncertainty is probably
associated with this assumption.
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 a
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
prepared. Listed below are the uncertainties associated with using these toxicity
values.
RfD values and slope factors have a certain amount of
uncertainty associated with them. Uncertainty and modifying
8-3
-------
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.
The use of oral slope factor values was appropriate for the
dermal exposure pathway. Since a dermal slope factor was not
available, the oral slope factor represented a "best estimate." A
moderate amount of uncertainty is probably associated with this
assumption.
Toxicity values were not available for all of the chemicals
detected in the GCR/IHC AOC. For some chemicals, such as lead,
a risk characterization could not be performed because of a lack of
toxicity values. The uncertainty of not being able to include some
chemicals in this risk assessment is not well established.
A conservative assumption for metal speciation in the AOC
was made for chromium, mercury, and vanadium since
toxicity values for the total metal forms of these chemicals
were not available. Thus, toxicity values for chromium VI, methyl
mercury, and vanadium pentoxide were used to represent the major
forms of these metals. The use of these more toxic chemical species
results in a conservative estimate of risk. A moderate level of
uncertainty is probably associated with this assumption.
Based on interim guidance, oral slope factors for some PAHs
were made relative to benzo(a)pyrene. Thus, these toxicity
values may be subject to change as additional information becomes
available. A medium level of uncertainty is proba.bly associated with
these estimated values.
8.2.4 Risk Characterization
The uncertainties associated with the risk characterization step are listed
below.
Current levels of exposure will remain constant over the
duration time of the exposure (i.e., 9 or 30 years). 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
8-4
-------
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. The level of uncertainty
will probably increase with longer exposure durations.
No distinction was made for the weight of evidence
classifications corresponding to oral slope factors (i.e., all
slope factors are assumed to reflect a similar level of risk).
This assumption was made even though contaminants known to
cause cancer in humans would result in a higher level of expressed
risk than those contaminants for which carcinogenicity has been
shown in animals and only suspected to occur in humans. A
moderate level of uncertainty is probably associated with this
assumption.
Health risks are additive for both noncarcinogenic and
carcinogenic effects. The uncertainty associated with this
assumption is not well established. 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 Grand Calumet
River/Indiana Harbor, 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.
8-5
-------
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October 1984. U.S. Geological Survey Water-Resources Investigations
Report 86-4208.
Flynn, G.L. 1990. Physiochemical determinants of skin absorption, pp. 93-127 in
T.R. Gerity and C.J. Henry, Eds. Principles of Route-to-Route Extrapolation
for Risk Assessment. Elsevier Science Publishing Co., Inc.
Foran, J.A. 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.
HydroQual. 1984. Grand Calumet River wasteload allocation study. Prepared
for Indiana State Board of Health, Indianapolis, IN. Project Number:
ISBH0010.
HydroQual. 1986. Priority Pollutants in the Grand Calumet River, Indiana.
Prepared for U.S. EPA - Chicago, Project Number: HAZE0233.
IDEM. 1991. The remedial action plan for the Indiana Harbor Canal, the Grand
Calumet River and the nearshore Lake Michigan. Stage One. (Draft).
Indiana Department of Environmental Management
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.
Kasting, G.B., R.L. Smith, and E.R. Cooper. 1987. Effect of Lipid Solubility and
Molecular Size on Percutaneous Absorption. Pharmacol. Skin. 1:138-153.
Kononen, D.W. 1989. PCBs and DDT in Saginaw Bay White Suckers.
Chemosphere. 18:2065-2068.
9-2
-------
Kuehl, D.W., P.M. Cook, A.R. Batter-man, 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.
Lake Michigan Federation. 1984 The Grand Calumet: Exploring the river's
potential.
Malins, B.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.
Oliver, E.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. II. Accumulation from Dietary Sources. Aquatic Toxicol. 3:313-327.
Risatti, J.B. and S. Broeren. 1988. Chemical analyses of sediments and biological
samples from Indiana Harbor Canal, Indiana Harbor and adjacent Lake
Michigan. Illinois State Geological Survey, Champaign, IL.
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.
Simmers, J.W., C.R. Lee, D.L. Brandon, H.E. Tatem, and J.G. Skogerboe. 1991.
Information Summary, Area of Concern: Grand Calumet River.
Miscellaneous Paper EL-91-10, U.S. Army Engineer Waterways Experiment
Station, Vicksburg, MS.
Smith, W.E., K. Funk, and M.E. Zabik. 1973. Effects of Cooking on
Concentrations of PCB and DDT Compounds in Chinook (Oncorhynchus
tshawytscha) and Coho (0_. 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.
Stachiw, N., M.E. Zabik, A.M. Booren, and M.J. Zabik. 1988. Tetrachlorodibenzo-
p-dioxin Residue Reduction through Cooking/Processing of Restructured
9-3
-------
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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.
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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 Engineer Waterways Experiment Station. 1987. Disposal
alternatives for PCB-contaminated sediments from Indiana Harbor, Indiana.
Volume 1. Final report for U.S. Army Engineer District, Chicago, IL.
USCOE. 1986. Indiana Harbor confined disposal facility and maintenance
dredging, Lake County, Indiana. Draft Environmental Impact Statement.
U.S. Army Corps of Engineers, Chicago District.
U.S. EPA. 1982. Environmental - regulatory review: Grand Calumet River and
Indiana Harbor Canal. U.S. Environmental Protection Agency, Great Lakes
National Program Office, Chicago, IL.
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IL. EPA-905/4-88-005.
U.S. EPA. 1988b. Superfund Exposure Assessment Manual. U.S. Environmental
Protection Agency, Washington, DC. EPA/540/1-88/001.
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Health Evaluation Manual Part A. Interim Final. OSWER Directive
9285.7-Ola.
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Agency, Washington, DC. EPA/600/8-89/043.
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FY 1989. OERR 9200.6-303-(89-4).
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with Exposures to Polycyclic Aromatic Hydrocarbons (PAHs). OSWER
Directive #9285.4-02. (Contained in Memorandum from H. L. Longest and
B. Diamond to Region Directors).
9-4
-------
U.S. EPA. 1990a. Polynuclear aromatic hydrocarbon sediment investigation.
Draft document.
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Drinking Water. April, 1990.
U.S. EPA. 1991a. Risk assessment guidance for Superfund. Volume I: Human
Health Evaluation Manual. Supplemental Guidance: "Standard Default
Exposure Factors." Interim Final (March 25, 1991). OSWER Directive
9285.6-03.
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1991 Work Plan. Great Lakes National Program Office, Chicago, IL.
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Ph.D. thesis. University of Wisconsin-Madison, Madison, WI.
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Fish Consumption Survey. University of Michigan School of Natural
Resources, Natural Resource Sociology Research Lab Technical Report #1.
Zabik, M. 1990. Preliminary draft data on organic chemical analyses of samples
collected by Unger et al. in 1989. Presentation at USEPA Great Lakes
National Program Office on March 23, 1990.
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.
Zabik, M.E., C. Merrill, and M.J. Zabik. 1982. PCBs and Other Xenobiotics in
Raw and Cooked Carp. Bull. Environm. Contain. Toxicol. 28:710-715.
9-5
-------
APPENDK A
FISH DATA FOR THE GRAND CALUMET RIVER
AND INDIANA HARBOR CANAL
-------
UNITED STATES ENVIRONMENTAL PROTECTION AGENCY
REGION 5
230 SOUTH DEARBORN ST.
CHICAGO, ILLINOIS 60604
REPLY TO ATTENTION OF:
July 18, 1991 5WQP-TUB-8
Ms. Judy Grain
ASCI Corporation
987 Gains School Road
Athens, Georgia 30605
Dear Ms. Grain:
Enclosed is a copy of the tissue residue data for two carp
samples collected from the Indiana Harbor Ship Canal. Episode
2059 was collected 10/9/84 and consisted of a composite of four
whole carp. Episodes 3356 was collected in 11/18/87 and also was
a composite of four whole carp. Both of these samples were
analyzed in Duluth as part of the National Bioaccumulation Study.
The third item is a confirmation re-analysis of 3356 for PCDD &
PCDF.
As usual, these are whole fish samples. In addition, you should
be aware that these fish, along with most others in this system,
probably move up and down the canal and the Grand Calumet River
as conditions allow, so they are good integrators, but only of
the whole system.
If I can be of further assistance, please call.
Sincerely yours,
Pete Redmon, Biologist
Unit #1, Permits Section
Enclosure
-------
NDS PHASE II: SICACCJMUL/iTIVr PCLLUTANT STUDY:
Ssmole Trgckin, System ERL-D Lee
EPlSCDc
3356
SCC *: DEG3C201
695
Sampling Information:
Samoling Office: INDIANA DEM
State u City: IN INDIANAPOLIS
Sampling Contact: GREG 3RIGHT
Date Sampled: 11/18/87
Slt« Location: IN INDIANA HARBOR
Latitude: N 41 37*10"
Analysis Lab: C
Matrix Tyae: = * £ CARP
Sample Composite: 4
CANAL 5! EAST CHICAGO
Longitude: W 87 29'15"
Date Received: 12/22/87
Speci? s Code:
Analytical:
Extraction Date
GC/MS - ID
LAB ID
weight
SLipio
3?E Incicstion
PCD3/PC2P D95ticide I Incustri?! Chemicals
6/3:/5r 10/22/53
MflTeei367 3RSS1061
I063086DF A102288LL
20.C5 19.66
10.4 10.1
Msss lioio on 3PC: O.SOO
Comments:
Xenooiotic Definitions:
QA CLAGS:
j - axceeos richest c=liDr=tion
D - belou/ liir.it of quan titEt ion
Limits of quantitation:
Pesticides - 2.5 ppb
?CSs: 1-3 chloro - 1.25 ppb
4-6 chloro - 2.50 ppb
7-3 chloro - 3.75 ppb
9-10 chloro - 6.25 ppb
st?
-------
f,uS pnise ::: iiCACC'j»'JLiT:v = =>:LLUTANT STUDY
IS^E *: 3556
SCC a: 3=030201
5RL-D Loc.: 695
DATA for 513 S ISNI rIC ANT POLYCHL35INAT ED DI5EN2DDI OXI NS AND FURANS:
Anslyte CAS No.: Ion Ratio S/N %REC Det. Liw. AmountCos/3
2,3,7,is- TCDF
2,3,5,7- TCDF
3,*,6,7- TCDF
51207-31-9
0.79 79.11 63 0.0000
0.95 1.00 62 0.9100 ND
0.00 1.00 63 0.4900 ND
5.33
2,2,7,5- TCuJ
1746-01-6 0.76
67.63 70
0.0000
6.55
1,2,3,7,8- ^eCCF
2,3,4,7,3- PsCIF
2,3,4,6,7- 5sCCF
57117-41-&
37117-31-6
1.57
35.65
3£0.94
1.00
66
66
66
0.0000
0.0000
0.8200
3.35
24.81
ND
1,2,3,7,8- PeCCD
40321-76-4
0.60
111.19
75
0.0000
9.35
1,2,3,4,6,7- uxCD=
1,2»3»H»7»5- nxCDF
1,2,3,6,7,5- ^xCDF
2,3,^,6,7,8- HxCDF
1,2,3,7,3,3- nxCDF
1,2,3,4,7,8- ixCDD
1 ,2 ,i,6,7 , E- -ixCDD
1,2,3,7,6,^- ixCDD
1,2,3,4,6,7,8- HoCDF
1,2,3,4,7,5,9- HpCDF
1*408-74-?
70648-26-9
57117-^4-9
60351-34-5
72915-21-9
3259B-13-3
57753-2r-7
1940 £-74-3
67562-39-4
55673-89-7
1.32
1.37
1.25
0.00
1.29
1.25
1.33
0.99
0.00
49.35
39.05
24. SO
1.00
24.24
82.45
20.73
33.78
1.00
67
67
67
67
73
72
73
59
59
0.0000
0.0000
0.0000
2.770-0
0.0000
0.0000
0.0000
0.0000
2.6100
2.37
3.30
1.29
ND
3.00
7.77
1.73
2.43
ND
1,2,3,4,6,7,8- *oCDD 37871-00-4 1.03
*: Coslutes uiith 123473 rlxCDF on DBS 30 M,
212.04
66
0.0000
12.44
Toxicity Equivalency Concentration: 15.16
Percent contribution of 2378 TCDF,
2378 TCDD anc 12378 PeCDD to total
TEFvalue: 73
-------
NDS PHASE II: BIOACCUMULATIVE POLLUTANT STUDY:
Sample Tracking System ERL-D Loc.:
695
EPISODE *: 3356
SCC : DE030201
Sampling Information:
Sampling Office: INDIANA DEM
State & City: IN INDIANAPOLIS
Sampling Contact: GREG BRIGHT
Date Sampled: 11/18/87
Site Location: IN INDIANA HARBOR CANAL @ EAST CHICAGO
Latitude: N 41 37'10" Longitude: V 87 29'15"
Analysis Lab: D Date Received: 12/22/87
Matrix Type: F VB CARP Species Code:
Sample Composite: 4
Analytical:
Extraction Date:
GC/HS ID:
LAB ID:
Veight:
ZLipid:
DPE Indication:
PCDD/PCDF Pesticide & Industrial Chemicals
6/30/88 10/22/88
MAT881367 DR881061
I063088DF A102288LL
20.05 19.66
10.4 10.1
Mass lipid on GPC: 0.800
Comments:
Xenobiotic Definitions:
QAFLAGS:
E - exceeds highest calibration standard
D - belov detection limit
Limits of Detection:
Pesticides - 2.5 ppb
PCBs: 1-3 chloro - 1.25 ppb
4-6 chloro - 2.50 ppb
7-8 chloro - 3.75 ppb
9-10 chloro - 6.25 ppb
-------
Target Analyte
1,3,5- Trichlorobenzene
1,2,4- Trichlorobenzene
1,2,3- Trichlorobenzene
Hexachlorobutadiene
1,2,4,5- Tetrachlorobenzene
1,2,3,5- Tetrachlorobenzene
Biphenyl
1,2,3,4- Tetrachlorobenzene
Pentachlorobenzene
Trifluralin
Alpha-BHC
Hexachlorobenzene
Pentachloroanisole
Gamma-BBC (Lindane)
Pentachloronitrobenzene
Diphenyl Disulfide
Beptachlor
Chlorpyrifos
Isopropalin
Octachlorostyrene
Heptachlor epoxide
Oxychlordane
Chlordane, trans
Chlordane, cis
Nonachlor, trans
p,p'- DDE
Dieldrin
Nltrofen
Endrin
Perthane
Chlorbenzilate
Nonachlor, cis
Methoxychlor
Dicofol (Relthane)
Mi rex
Total Monochlorobiphenyl
Total Dichlorobiphenyl
Total Trichlorobiphenyl
Total Tetrachlorobiphenyl
Total Pentachlorobiphenyl
Total Hexachlorobiphenyl
Total Beptachlorobiphenyl
Total Octachlorobiphenyl
Total Nonachlorobiphenyl
Total Decachlorobiphenyl
Total Polychlorinated Biphenyls
Mercury ( AA analysis)
CASRN QA Flag
108-70-3
120-82-1 D
87-61-6
87-68-3
95-94-3
634-90-2
92-52-4
634-66-2
608-93-5 D
1582-09-8
319-84-6
118-74-1
1825-21-4 D
58-89-9
82-68-8
882-33-7
76-44-8
2921-88-2
33820-53-0
29082-74-4 D
1024-57-3
26880-48-8
5103-74-2
5103-71-9
39765-80-5
72-55-9 E
60-57-1
1836-75-5
72-20-8
72-56-0
510-15-6
3734-49-4
72-43-5
115-32-2
2385-85-5 D
27323-18-8
25512-42-9
25323-68-6 E
26914-33-0 E
25429-29-2 E
26601-64-4 E
28655-71-2 E
31472-83-0
53742-07-7
2051-24-3
7439-97-6 NA
CONCN
ND
ND
ND
ND
ND
ND
ND
ND
ND
ND
ND
ND
ND
ND
ND
ND
-------
INDIANA DEPARTMENT OF ENVIRONMENTAL MANAGEMENT
105 South Meridian Street
P.O. Box 6015
Indianapolis 46206-6015
Telephone 317/232-8603
November 18, 1991
Ms. Judy Crane
ASCI Corporation
987 Gaines School Road
Acton, GA 30605
Dear Ms. Crane:
Enclosed you will find the July 1987 and November 1988 Indiana Harbor
Canal fish tissue contaminant results you requested November 15, 1991. I
hope they will assist you with your risk assessment that you are
performing for USEPA's ARCS program.
Your request amounts to 8 pages which at 15^/page comes to a total of
$1.20 (U.S. dollars). Since you represent a consulting firm without a
reported history of nonpayment, I am allowed to send these data to you
and to assume you will have a check promptly mailed for this amount to:
Indiana Department of Environmental Management
Attn: Cashier, Room 140
105 South Meridian Street
Indianapolis, IN 46225
Requestors that are slow to pay, never pay or require follow-up will
be placed on at "Cash Only" list pursuant to IDEM Policy #17-90.
Cordially,
C. Lee Bridges, Chief
Biological Studies Section
Office of Water Management
Enclosure
cc: Cashier's Office
Syed GhiasUddin
An Equal Opportunity Employer
-------
FISH TISSUE CONTAMINATION RESULTS
INDIANA DEPARTMENT OF ENVIRONMENTAL MANAGEMENT
OUM-B10LOG1CAL STUDIES
LAB NUMBER:90602983 SITE:INDIANA HARBOR CANAL
COLLECTION DATE:11/01/88 LOCAT10N:DICKEY RD.
MEAN LENGTH(CH):61.5 RANGE(CM):60.5-63.0
|SPECIES:3 CARP
LAB:H |PREPARATION:SK-ON FILLETS.SCALELESS
COUNTY;LAKE
LA
MEAN WEIGHT(CM):3440 RANGE(GM):3119-3686
XL1PID:6.08
METALS ( HG/KG )
ALUMINUM NA
ANTIMONY NA
ARSENIC NA
BARIUM NA
BERYLLIUM NA
CADMIUM 0.017
CALCIUM NA
CHROMIUM NA
COBALT NA
COPPER NA
IRON NA
LEAD 0.850
MAGNESIUM NA
MANGANESE NA
MERCURY 0.084
NICKEL NA
POTASSIUM NA
SELENIUM NA
SILVER NA
SODIUM NA
THALLIUM NA
VANADIUM NA
ZINC NA
ACID EXTRACTABLE COMPOUNDS
BENZOIC ACID
PHENOL <
2-CHLOROPHENOL <
2,4-DICHLOROPHENOL <
2,4.5-TRlCHLOROPHENOL <
2,4.6-TRICHLOROPHENOL <
PENTACHLOROPHENOL <
2-METHYLPHENOL <
4-METHYLPHENOL J
2,4-DIMETHYLPHENOL <
4-CHLORO-3-METHYLPHENOL <
4.6-DINITRO-2-METHYLPHENOL
2-NITROPHENOL <
4-NITROPHENOL <
2,4-DlNITROPHENOL
ACETONE BE
BENZENE <
CHLOROBENZENE <
ETHYLBENZENE J
2-BUTANONE <
CARBON DISULFIDE
CHLOROETHANE <
1,1-DICHLOROETHANE <
1,2-01 CHLOROETHANE <
1,1,1-TR I CHLOROETHANE <
1,1,2-TRlCHLOROETHANE <
1,1,2,2-TETRACHLORETHANE <
PESTICIDES (HG/KG)
ALDRIN < 0.016
alpha-BHC < 0.008
beta-BHC < 0.008
delta-BHC < 0.008
gamma-BHC < 0.008
alpha-CHLORDANE < 0.008
gamma-CHLORDANE < 0.008
cis-NONACHLOR 0.013
trans-NONACHLOR < 0.008
OXYCHLORDANE < 0.008
p.p'-DDD 0.043
O.p'-DDD < 0.010
p.p'-DDE 0.130
o,p'-DDE < 0.010
p,p'-DDT < 0.010
o,p'-DDT < 0.010
DIELDRIN 0.020
ENDOSULFAN I < 0.020
ENOOSULFAN II < 0.020
ENDOSULFAN SULFATE < 0.020
ENDRIN < 0.010
ENDRIN ALDEHYDE < 0.010
ENDRIN KETONE < 0.010
HEPTACHLOR < 0.016
HEPTACHLOR EPOXIDE < 0.008
HEXACHLOROBENZENE < 0.010
METHOXYCHLOR < 0.020
PENTACHLOROANISOLE < 0.008
TOXAPHENE < 0.010
TOTAL PCS 1.500 MG/KG
(MG/KG)
NA
0.660
0.660
0.660
3.200
0.660
3.200
0.660
0.510
0.660
0.660
NA
0.660
3.200
NA
0
/ VOLATILE ORGANIC COMPOUNDS
0.210 « 1,1-DICHLOROETHYLENE <
0.005 1,2-DICHLOROETHYLENE <
0.005 TRICHLOROETHYLENE(TOTAL) <
0.002 TETRACHLOROETHYLENE
0.010 2-HEXANONE <
0.055 BROMOMETHANE <
0.010 TRIBROMOMETHANE <
0.005 (BROMOFORM)
0.005 BROMOD I CHLOROMETHANE <
0.005 DIBROMOCHLOROMETHANE <
0.005 CHLOROMETHANE <
0.005 DICHLOROMETHANE <
(METHYLENE CHLORIDE)
BASE/NEUTRAL EXTRACTABLE COMPOUNDS(MG/KG:
(MG/KG)
0.005
0.005
0.005
0.017
0.010
0.010
0.005
0.005
0.005
Q.010
0.005
ACENAPHTHYLENE <
ACENAPHTHENE <
4-CHLOROANILINE <
2-N1TROANILINE <
3-NITROANILINE <
4-NITROAN1LINE <
ANTHRACENE <
BENZO(B) ANTHRACENE <
DIBENZO(a,h)ANTHRACENE <
3,3'-DICHLOROBENZIDINE <
1,2-D I CHLOROBENZENE <
1,3-DICHLOROBENZENE <
1,4-DICHLOROBENZENE <
1,2,4-TRICHLORBENZENE <
HEXACHLOROBENZENE <
NITROBENZENE <
BENZYL ALCOHOL « <
CHRYSENE ^ <
n-NITROSODlPHENYLAMINE <
n-NITROSO-di-n-PROPYLAMINE <
HEXACHLOROETHANE <
BIS(2-CHLOROETHYL)ETHER <
BIS(2-CHLOROISOPROPYL)ETHER <
4-BROMOPHENYL-PHENYLETHER <
4-CHLOROPHENYL-PHENYLETHER <
FLUORANTHENE <
FLUORENE <
BENZO(beta)FLUORANTHENE <
BENZO(kappa)FLUORANTHENE <
DIBENZOFURAN <
BIS(2-CHLOROETHOXY)METHANE <
1SOPHORONE <
NAPHTHALENE <
2-CHLORONAPHTHALENE <
2-METHYLNAPHTHALENE <
HEXACHLOROCYCLOPENTADIENE
BENZO(ghi)PERYLENE <
PHENANTHRENE <
di-n-BUTYLPHTHALATE <
DIETHYLPHTKALATE <
DIMETHYLPHTHALATE <
di-n-OCTYLPHTHALATE <
BIS(2-ETHYLHEXYL)PHTHALATE <
BUTYLBENZYLPHTHALATE <
PYRENE
B£NZO(alpha)PYRENE
INDENOO.2,3-c,d)PYRENE
2,4-DINITROTOLUENE
2,6-0 IN 1TROTOLUENE
HEXACHLOROBUT AD 1 ENE
TR I CHLOROMETHANE J
(CHLOROFORM)
TETRACHLOROMETHANE <
(CARBON TETRACHLORIDE)
4-METHYL-2-PENTANONE <
1,2-DICHLOROPROPANE <
C-1.3-D1CHLOROPROPYLENE <
t-1,3-DICHLOROPROPYLENE <
STYRENE <
TOLUENE J
VINYL ACETATE <
VINYL CHLORIDE - <
TOTAL XYLENE X
0.66C
0.66C
0.66C
3.20C
3.20C
3.20C
0.66C
0.66C
0.66C
1.30C
0.66C
0.66C
0.66C
0.660
0.660
0.660
0.660
0.660
0.660
0.660
0.660
0.660
0.660
0.660
0.660
0.660
0.660
0.660
0.660
0.660
0.660
0.660
0.660
0.660
0.660
NA
0.660
0.660
0.660
0.660
0.660
0.660
0.660
0.660
0.660
0.660
0.660
0.660
0.660
0.660
0.002
0.005
0.010
0.005
0.005
0.005
0.005
0.003
0.010
0.010
0.018
RESULTS REPORTED ON A WHOLE SAMPLE BASIS. D=DUPLICATE
H=HAZLETON LABORATORIES OF AMERICA 1=1SBH FOOD AND DRUG LAB
NA=NOT ANALYZED ND=NONE DETECTED
OTHER FLAGS ARE EXPLAINED ON A SEPARATE SHEET
PRINT DATE: 06/19/90
-------
FISH TISSUE CONTAMINATION RESULTS
INDIANA DEPARTMENT OF ENVIRONMENTAL MANAGEMENT
OWM-BIOLOGICAL STUDIES
LAB NUMBER:90602984 D
COLLECTION DATE:11/01/88
S1TE:1ND1ANA HARBOR CANAL COUNTY:LAKE
LOCATION:DICKEY RD. DUP OF 90602983
LAB:K
SPECIES:3 CARP
| PREPARATION DUPLICATE OF 90602983
MEAN LENGTH(CM):61.5 RANGE(CM):60.5-63.0 MEAN WEIGHT(CM):3440 RANGECCM):3119-3686 XLIPID:6.4
HETALS (HG/KG)
ALUMINUM NA
ANTIMONY NA
ARSENIC NA
BARIUM NA
BERYLLIUM NA
CADMIUM NA
CALCIUM NA
CHROMIUM NA
COBALT NA
COPPER NA
IRON NA
LEAD NA
MAGNESIUM NA
MANGANESE NA
MERCURY NA
NICKEL NA
POTASSIUM NA
SELENIUM NA
SILVER NA
SODIUM NA
THALLIUM NA
VANADIUM NA
ZINC NA
ACID EXTRACTABLE COMPOUNDS
BENZOIC ACID
PHENOL
2-CHLOROPHENOL
2,4-DICHLOROPHENOL
2,4,5-TRICHLOROPHENOL
2,4.6-TRICHLOROPHENOL
PENTACHLOROPHENOL
2-HETHYLPHENOL
4-METHYLPHENOL
2,4-DIMETHYLPHENOL
4-CHLORO-3-METHYLPHENOL
4.6-DINITRO-2-METHYLPHENOL
2-NITROPHENOL
4-NITROPHENOL
2,4-DINITROPHENOL
PESTICIDES
ALDRIN <
alpha-BHC <
beta-BHC <
delta-BHC <
gamma-BHC <
alpha-CHLORDANE <
gamma-CHLORDANE <
cis-NONACHLOR
trans-NONACHLOR <
OXYCHLORDANE <
p,p'-DDD
o,p'-DDD <
p.p'-DDE
o,p'-DDE <
p.p'-DDT <
o.p'-DDT <
DIELDRIN
ENDOSULFAN I <
ENDOSULFAN II <
ENDOSULFAN SULFATE <
ENDRIN <
ENDRIN ALDEHYDE <
ENDRIN KETONE <
HEPTACHLOR <
HEPTACHLOR EPOXIDE <
HEXACHLOROBENZENE <
METHOXYCHLOR <
PENTACHLOROANISOLE <
TOXAPHENE <
TOTAL PCB 1.700
(MG/KG)
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
(HG/KG)
0.016
0.008
0.008
0.008
0.008
0.008
0.008
0.012
0.008
0.008
0.037
0.010
0.160
0.010
0.010
0.010
0.021
0.020
0.020
0.020
0.010
0.010
0.010
0.016
0.008
0.010
0.020
0.008
0.010
MG/KG
BASE/NEUTRAL EXTRACTABLE COHPOUNDSCHG/K
ACENAPHTHYLENE NA
ACENAPHTHENE
4-CHLOROANIL1NE
2-NITROANILINE
3-NITROANILINE
4-NITROANILINE
ANTHRACENE
BENZO(a)ANTHRACENE
DIBENZO(a,h)ANTHRACENE
3,3'-DICHLOR08ENZIDINE
1,2-DICHLOROBENZENE
1,3-DICHLOROBENZENE
1,4-DICHLOROBENZENE
1,2,4-TRICHLORBENZENE
HEXACHLOROBENZENE
NITROBENZENE
BENZYL ALCOHOL
CHRYSENE %:--
n-NITROSOOIPHENYLAHINE
n-NITROSO-di-n-PROPYLAMINE
HEXACHLOROETHANE
BIS(2-CHLOROETHYL)ETHER
B1S(2-CHLOROISOPROPYL)ETHER
4-BROMOPHENYL-PHENYLETHER
4-CHLOROPHENYL-PHENYLETHER
FLUORANTHENE
FLUORENE
BENZO(beta)FLUORANTHENE
BENZO(kappa)FLUORANTHENE
D1BENZOFURAN
BIS(2-CHLOROETHOXY)METHANE
ISOPHORONE
NAPHTHALENE
2-CHLORONAPHTHALENE
2-HETHYLNAPHTHALENE
HEXACHLOROCYCLOPENTAD I ENE
BENZO(ghi)PERYLENE
PHENANTHRENE
di-n-BUTYLPHTHALATE
DIETHYLPHTHALATE
DIMETHYLPHTHALATE
di-n-OCTYLPHTHALATE
BIS(2-ETHYLHEXYL)PHTHALATE
BUTYLBENZYLPHTHALATE
PYRENE
BENZO(alpha)PYRENE
INDENO(1,2,3-c,d)PYRENE
2,4-DINITROTOLUENE
2,6-DINITROTOLUENE
HEXACHLOROBUTADIENE
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA'
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
ACETONE
BENZENE
CHLOROBENZENE
ETHYLBENZENE
2-BUTANONE
CARBON DISULFIDE
CHLOROETHANE
1,1-DICHLOROETHANE
1,2-DICHLOROETHANE
1.1,1-TRICHLOROETHANE
1,1,2-TRICHLOROETHANE
1,1,2,2-TETRACHLORETHANE
VOLATILE ORGANIC COMPOUNDS
NA 1,1-DICHLOROETHYLENE
NA 1,2-DICHLOROETHYLENE
NA TRICHLOROETHYLENE(TOTAL)
NA TETRACHLOROETHYLENE
NA 2-HEXANONE
NA BROMOMETHANE
NA TRIBROMOMETHANE
NA (BROMOFORM)
NA BROMODICHLOROMETHANE
NA DIBROMOCHLOROMETHANE
NA CHLOROMETHANE
NA DICHLOROMETHANE
(METHYLENE CHLORIDE)
TRICHLOROMETHANE
(CHLOROFORM)
TETRACHLOROMETHANE
(CARBON TETRACHLOR1DE)
4-METHYL-2-PENTANONE
1,2-DICHLOROPROPANE
C-1.3-D1CHLOROPROPYLENE
t-1.3-DICHLOROPROPYLENE
STYRENE
TOLUENE
VINYL ACETATE
VINYL CHLORIDE ,
TOTAL XYLENE
RESULTS REPORTED ON A WHOLE SAMPLE BASIS. D=DUPLICATE
H=HAZLETON LABORATORIES OF AMERICA I=1SBH FOOD AND DRUG LAB
NA=NOT ANALYZED ND=NONE DETECTED
OTHER FLAGS ARE EXPLAINED ON A SEPARATE SHEET
PRINT DATE: 06/19/1
-------
FISH TISSUE CONTAMINATION RESULTS
INDIANA DEPARTMENT OF ENVIRONMENTAL MANAGEMENT
OUM-BIOLOGICAL STUDIES
LAB NUMBER:90602985
COLLECTION DATE:11/01/88
SITE;INDIANA HARBOR CANAL
LOCATION-.OICKEY RD.
COUNTY.-LAKE |SPECIES:3 CARP
LAB:H I PREPARATIONS-ON FILLETS. SCALELESS
MEAN LENGTH(CM>:74.0 RANGE(CM):74.0-74.0
MEAN UEIGHT(GM):6691 RANGE(GM):6691-6691
XL1PID:21.6J
METALS
ALUMINUM
ANTIMONY
ARSENIC
BARIUM
BERYLLIUM
CADMIUM
CALCIUM
CHROMIUM
COBALT
COPPER
IRON
LEAD
MAGNESIUM
MANGANESE
MERCURY
NICKEL
POTASSIUM
SELENIUM
SILVER
SODIUM
THALLIUM
VANADIUM
ZINC
(MG/KG)
NA
NA
NA
NA
NA
0.010
NA
NA
NA
NA
NA
0.560
NA
NA
0.124
NA
NA
NA
NA
NA
NA
NA
NA
ACID EXTRACTABLE COMPOUNDS
BENZ01C ACID
PHENOL
2-CHLOROPHENOL
2,4-DlCHLOROPHENOL
2,4,5-TRICHLOROPHENOL
2,4,6-TRICHLOROPHENOL
PENTACHLOROPHENOL
2-HETHYLPHENOL
4-METHYLPHENOL
2.4-DIMETHYLPHENOL
4-CHLORO-3-METHYLPHENOL
4.6-DINITRO-2-METHYLPHENOL
2-HITROPKENOL
4-NITROPHENOL
2,4-DINITROPHENOL
ACETONE
BENZENE
CHLOROBENZENE
ETHYLBENZENE
2-BUTANONE
CARBON D1SULFIDE
CHLOROETHANE
1.1-DICHLOROETHANE
1,2-DICHLOROETHANE
1.1,1-TRICHLOROETHANE
1,1,2-TRICHLOROETHANE
1.1,2,2-TETRACHLORETHANE
PESTICIDES
ALDR1N
alpha-BHC
beta-BHC
delta-BHC
gamna-BHC
alpha-CHLORDANE
gamma-CHLORDANE
cts-NONACHLOR
trans-NONACHLOR
OXYCHLORDANE
p.p'-DDD
o.p'-DDD
p,p'-DDE
o.p'-DDE
p.p'-DDT
O,p'-DDT
DIELDRIN
ENDOSULFAN I
ENDOSULFAN II
ENDOSULFAN SULFATE <
ENDRIN <
ENORIN ALDEHYDE <
ENDRIN KETONE <
HEPTACHLOR <
HEPTACHLOR EPOXIDE
HEXACHLOROBENZENE <
METHOXYCHLOR <
PENTACHLOROANISOLE <
TOXAPHENE <
(MG/KG)
0.040
0.040
0.040
0.040
0.040
0.080
0.040
0.040
0.040
0.040
0.061
0.050
0.280
0.050
0.050
0.050
0.210
0.100
0.100
0.100
0.050
0.050
0.050
0.040
0.101
0.050
0.100
0.040
0.050
TOTAL PCS
2.200 MG/KG
(MG/KG)
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
VOLATILE ORGANIC COMPOUNDS
1,1-DICHLOROETHYLENE
1,2-DlCHLOROETHYLENE
TRICHLOROEThYLENE(TOTAL)
TETRACHLOROETHYLENE
2-HEXANONE
BROMOMETHANE
TRIBROMOMETHANE
(BROHOFORM)
BROMODICHLOROMETHANE
DIBROMOCHLOROMET HANE
CHLOROMETHANE
DICHLOROMETHANE
(HETHYLENE CHLORIDE)
BASE/NEUTRAL EXTRACTABLE COMPOUNDS(HG/KG3
ACENAPHTHYLENE NA
ACENAPHTHENE NA
4-CHLOROAN1LINE NA
2-NITROANILINE NA
3-N1TROANIL1NE NA
4-NITROANILINE NA
ANTHRACENE NA
BENZO(a)ANTHRACENE NA
DIBENZO(a,h)ANTHRACENE NA
3,3'-DICHLOROBENZlDlNE NA
1,2-DlCHLOROBENZENE NA
1,3-DICHLOROBENZENE NA
1,4-DICHLOROBENZENE NA
1,2,4-TRICHLORBENZENE NA
^HEXACHLOBOBENZENE NA
NITROBENZENE NA
BENZYL ALCOHOL NA
CHRYSENE *"~ NA
n-NITROSODIPHENYLAMINE NA
n-NITROSO-di-n-PROPYLAMINE NA
HEXACHLOROETHANE NA
B1S(2-CHLOROETHYL)ETHER NA
BIS(2-CHLOROISOPROPYL)ETKER NA
4-BROMOPHENYL-PHENYLETHER NA
4-CHLOROPHENYL-PHENYLETHER NA
FLUORANTHENE NA
FLUORENE NA
BENZO(beta)FLUORANTHENE NA
BENZOCkappa)FLUORANTHENE NA
DIBENZOFURAN NA
BIS(2-CHLOROETHOXY)METHANE NA
ISOPHORONE NA
NAPHTHALENE NA
2-CHLORONAPHTHALENE NA
2-METHYLNAPHTHALENE NA
HEXACHLOROCYCLOPENTADIENE NA
BENZO(ghi)PERYLENE NA
PHENANTHRENE NA
di-n-BUTYLPHTHALATE NA
DIETHYLPHTHALATE NA
DIMETHYLPHTHALATE NA
di-n-OCTYLPHTHALATE NA
BIS(2-ETHYLHEXYL)PHTHALATE NA
BUTYLBENZYLPHTHALATE NA
PYRENE NA
BENZO(alpha)PYRENE HA
INDENO(1,2,3-c,d)PYRENE NA
2,4-DlNlTROTOLUENE NA
2,6-DINITROTOLUENE NA
HEXACHLOROBUTADIENE NA
TRICHLOROMETHANE NA
(CHLOROFORM)
TETRACHLOROMETHANE NA
(CARBON TETRACHLORIDE)
4-HETHYL-2-PENTANONE NA
1,2-DlCHLOROPROPANE NA
C-1.3-DICHLOROPROPYLENE NA
t-1,3-DICHLOROPROPYLEME NA
STYRENE NA
TOLUENE NA
VINYL ACETATE NA
VINYL CHLORIDE NA
TOTAL XYLENE NA
RESULTS REPORTED ON A WHOLE SAMPLE BASIS. DUPLICATE
H=HAZLETON LABORATORIES OF AMERICA I=ISBH FOOD AND DRUG LAB
NA=NOT ANALYZED ND=NONE DETECTED
OTHER FLAGS ARE EXPLAINED ON A SEPARATE SHEET
PRINT DATE: 06/19/90
-------
FISH TISSUE CONTAMINATION RESULTS
INDIANA DEPARTMENT OF ENVIRONMENTAL MANAGEMENT
OWM-BIOLOGICAL STUDIES
LAB NUMBER:80502410
COLLECTION DATE:07/08/87
S1TE:GRAND CALUMET RIVER
LOCATION:BRIDGE ST.
COUNTY:LAKE
LAB:H
SPECIES:! CARP
PREPARATION:WHOLE
MEAN LENGTH(CM):38.5 RANGE(CM):38.5-38.5
MEAN WEIGHT(GM):888 RANGE(GM):888-888
XLIP1D:4.7I
METALS (MG/KG)
ALUMINUM < 20.000
ANTIMONY < 2.000
ARSENIC < 1.000
BARIUM < 5.000
BERYLLIUM < 0.500
CADMIUM < 0.500
CALCIUM 5950.00
CHROMIUM < 1.000
COBALT < 5.000
COPPER 4.000
IRON 45.700
LEAD < 0.500
MAGNESIUM 270.000
MANGANESE < 1.500
MERCURY 0.045
NICKEL < 4.000
POTASSIUM 2450.000
SELENIUM < 1.000
SILVER < 0.500
SODIUM 830.000
THALLIUM < 2.000
VANADIUM < 5.000
ZINC 122.000
PESTICIDES
ALDRIN
alpha-BHC
beta-BHC
delta-BHC
gamna-BHC
alpha-CHLORDANE
gamma-CHLORDANE
cis-NONACHLOR
trans-NONACHLOR
OXYCHLORDANE
p,p'-DDD
o,p'-DDD
p.p'-DDE
o.p'-DDE
p,p'-DDT
o.p'-DDT
DIELDRIN
ENDOSULFAN I
ENDOSULFAN II
ENDOSULFAN SULFATE
ENDRIN
ENDRIN ALDEHYDE
ENDRIN KETONE
HEPTACHLOR
HEPTACHLOR EPOXIDE
HEXACHLOROBENZENE
METHOXYCHLOR
PENTACHLOROANISOLE
TOXAPHENE
<
<
<
<
<
<
<
<
<
<
<
<
<
<
<
<
<
<
<
<
<
<
<
<
<
<
<
<
TOTAL PCS 3.300
ACID EXTRACTABLE COMPOUNDS
BENZOIC ACID
PHENOL <
2-CHLOROPHENOL <
2,4-DICHLOROPHENOL <
2.4,5-TRICHLOROPHENOL <
2.4.6-TRICHLOROPHENOL <
PENTACHLOROPHENOL <
2-METHYLPHENOL <
4-METHYLPHENOL <
2,4-DIMETHYLPHENOL <
4-CHLORO-3-METHYLPHENOL <
4.6-DINITRO-2-METHYLPHENOL
2-NITROPHENOL <
4-NITROPHENOL <
2,4-DINITROPHENOL
(MG/KG)
NA
0.660
0.660
0.660
3.200
0.660
3.200
0.660
0.660
0.660
0.660
NA
0.660
3.200
NA
(MG/KG)
0.168
0.008
0.008
0.008
0.008
0.008
0.008
0.008
0.008
0.008
0.010
0.010
0.210
0.010
0.010
0.010
0.010
0.020
0.020
0.020
0.010
0.010
0.010
0.168
0.008
0.010
0.020
0.008
NA
MG/KG
BASE/NEUTRAL EXTRACTABLE COMPOUNDS(MG/KI
ACENAPHTHYLENE < Q.6(
ACENAPHTHENE J
4-CHLOROAN1LINE <
2-NITROANILINE <
3-NITROANILINE <
4-NITROANILINE <
ANTHRACENE <
BENZO(a)ANTHRACENE <
OIBENZO(a,h)ANTHRACENE <
3,3'-DICHLOROBENZIDINE <
1,2-DlCHLOROBENZENE <
1,3-DICHLOROBENZENE <
1,4-DIGHLOROBENZENE <
1,2,4-TRICHLORBENZENE <
-HEXACHLOROBENZENE <
NITROBENZENE <
BENZYL ALCOHOL <
CHRYSENE ' <
n-NITROSODIPHENYLAMINE <
n-NITROSO-di-n-PROPYLAMINE <
IHEXACHLOROETHANE <
BIS(2-CHLOROETHYL)ETHER <
BIS(2-CHLOROISOPROPYL)ETHER <
4-BROMOPHENYL-PHENYLETHER <
4-CHLOROPHENYL-PHENYLETHER <
FLUORANTHENE <
FLUORENE J
BENZO(beta)FLUORANTHENE <
BENZO( kappa) FLUORANTHENE <
DIBENZOFURAN J
BIS(2-CHLOROETHOXY)METHANE <
ISOPHORONE <
NAPHTHALENE J
,2-CHLORONAPHTHALENE <
2-METHYLNAPHTHALENE J
HEXACHLOROCYCLOPENTADIENE
BENZO(ghi)PERYLENE <
PHENANTHRENE <
di-n-BUTYLPHTHALATE BJ
DIETHYLPHTHALATE <
DIMETHYLPHTHALATE <
di-n-OCTYLPHTHALATE
BIS(2-ETHYLHEXYL)PHTHALATE
BUTYLBENZYLPHTHALATE
PYRENE
BENZO(alpha)PYRENE
INDENO(1,2,3-C,d)PYRENE <
2,4-DINITROTOLUENE <
2,6-DINITROTOLUENE <
HEXACHLOROBUTAD1ENE <
0.6
0.6(
3.2I
3.2I
3.2I
0.6<
0.6i
0.6i
1.31
0.6<
0.6i
0.6i
0.6i
0.6i
0.6
0.6i
0.6i
0.6(
0.6<
0.6(
0.6<
OM
0.6l
0.6t
O.(x
0.11
0.6<
0.6<
0.2!
0.6<
0.6)
0.0!
0.61
0.2i
NA
0.6i
0.6.
0.2:
0.6<
0.6,
0.6,
0.6<
0.&
0.6i
O.(x
O.(x
0.6t
0.6t
0.6(
ACETONE BE 1.600
BENZENE 0.017
CHLOROBENZENE < 0.005
ETHYLBENZENE < 0.005
2-BUTANONE B 0.099
CARBON DISULFIDE < 0.005
CHLOROETHANE < 0.010
1,1-DICHLOROETHANE < 0.005
1,2-DICHLOROETHANE < 0.005
1,1,1-TRICHLOROETHANE BJ 0.002
1,1,2-TRICHLOROETHANE < 0.005
1,1,2,2-TETRACHLORETHANE < 0.005
VOLATILE ORGANIC COMPOUNDS
1,1-DICHLOROETHYLENE <
1,2-DICHLOROETHYLENE <
TRICHLOROETHYLENE(TOTAL) <
TETRACHLOROETHYLENE <
2-HEXANONE <
BROMOMETHANE <
TRIBROMOMETHANE <
(BROMOFORM)
BROMODICHLOROMETHANE <
DIBROMOCHLOROMETHANE <
CHLOROMETHANE <
DICHLOROMETHANE B
(METHYLENE CHLORIDE)
;MG/KG)
0.005 TRICHLOROMETHANE
0.005 (CHLOROFORM)
0.005 TETRACHLOROMETHANE
0.005 (CARBON TETRACHLORIDE)
0.010 4-METHYL-2-PENTANONE
0.050 1,2-DICHLOROPROPANE
0.025 C-1.3-DICHLOROPROPYLENE
t-1,3-DICHLOROPROPYLENE
0.025 STYRENE
0.025 TOLUENE
0.010 VINYL ACETATE
0.065 VINYL CHLORIDE
TOTAL XYLENE
BJ
RESULTS REPORTED ON A WHOLE SAMPLE BASIS. D=DUPLICATE
H=HAZLETON LABORATORIES OF AMERICA I=ISBH FOOD AND DRUG LAB
NA=NOT ANALYZED ND=NONE DETECTED
OTHER FLAGS ARE EXPLAINED ON A SEPARATE SHEET
PRINT DATE: 06/19/<
-------
FISH TISSUE CONTAMINATION RESULTS
INDIANA DEPARTMENT OF ENVIRONMENTAL MANAGEMENT
OUM-BIOLOGICAL STUDIES
LAB NUMBER-.80502411
COLLECTION DATE:07/08/87
S1TE;GRAND CALUMET RIVER
LOCATION:BRIDGE ST.
MEAN LENGTH(CM):9.7 RANGE(CM):7.0-14.0
COUNTY:LAKE
MEAN WEIGHT(GM):12
LAB:H
[SPECIES:H GOLDEN SHINER
PREPARATION .-WHOLE
RANGE(GM):2-36
XLIP10-.1.60
METALS (MG/KG)
ALUMINUM 75.700
ANTIMONY < 2.000
ARSENIC < 1.000
BARIUM < 5.000
BERYLLIUM < 0.500
CADMIUM < 0.500
CALCIUM 11000.00
CHROMIUM 1 .700
COBALT < 5.000
COPPER 4.900
IRON 1080.000
LEAD 8.900
MAGNESIUM 440.000
MANGANESE 17.300
MERCURY 0.031
NICKEL < 4.000
POTASSIUM 2490.000
SELENIUM < 1.000
SILVER < 0.500
SODIUM 760.000
THALLIUM < 2.000
VANADIUM < 5.000
ZINC 49. BOO
ACID EXTRACTABLE COMPOUNDS
BENZOIC ACID
PHENOL <
2-CHLOROPHENOL <
2.4-DICHLOROPHENOL <
2,4,5-TRICHLOROPHENOL <
2,4,6-TRICHLOROPHENOL <
PENTACHLOROPHENOL <
2-METHYLPHENOL <
4-METHYLPHENOL <
2,4-DIMETHYLPHENOL <
4-CHLORO-3-METHYLPHENOL <
4,6-OINITRO-Z-METHYLPHENOL
2-NITROPHENOL <
4-NITROPHENOL <
2,4-DINITROPHENOL
ACETONE BE
BENZENE
CHLOROBENZENE <
ETHYLBENZENE <
2-BUTANONE B
CARBON DISULFIDE <
CHLOROETHANE <
1,1-DlCHLOROETHANE <
1,2-Dl CHLOROETHANE <
1.1,1-TR I CHLOROETHANE <
1,1. 2- TR I CHLOROETHANE <
1,1,2.2-TETRACHLORETHANE <
PESTICIDES (HG/KG)
ALDRIN NA
alpha-BHC NA
beta-BHC NA
detta-BHC NA
gamma- BHC NA
alpha-CHLORDANE NA
gamma- CHLORDANE NA
cis-NONACHLOR NA
trans-NONACHLOR NA
OXYCHLORDANE NA
p,p'-DDD NA
o.p'-DDD NA
p,p'-DDE NA
o,p'-DDE NA
p.p'-DOT NA
o,p'-DDT NA
D1ELDRIN NA
ENDOSULFAN I NA
ENDOSULFAN 11 NA
ENDOSULFAN SULFATE NA
ENDRIN NA
ENDRIN ALDEHYDE NA
ENDRIN KETONE NA
HEPTACHLOR NA
HEPTACHLOR EPOX1DE NA
HEXACHLOROBENZENE NA
METHOXYCHLOR NA
PENTACHLOROAN1SOLE NA
TOXAPHENE NA
TOTAL PCS NA HG/KG
(HG/KG)
NA
0.660
0.660
0.660
3.200
0.660
3.200
0.660
0.660
0.660
0.660
NA
0.660
3.200
NA
VOLATILE ORGANIC COMPOUNDS
1.900 1,1-DICHLOROETHYLENE <
0.022 1,2-DICHLOROETHYLENE <
0.005 TRICHLOROETHYLENE(TOTAL) <
0.005 TETRACHLOROETHYLENE <
0.069 2 -HEX ANON E <
0.005 BROMOMETHANE <
0.010 TRIBROMOMETHANE <
0.005 (BROMOFORM)
0.005 BROMOD I CHLOROMETHANE <
0.005 D1BROMOCHLOROMETHANE <
0.005 CHLOROMETHANE <
0.005 DICHLOROMETHANE B
(METHYLENE CHLORIDE)
BASE/NEUTRAL EXTRACTABLE COMPQUNDS(MG/KG)
(HG/KG)
0.005
0.005
0.005
0.005
0.010
0.050
0.025
0.025
0.025
0.010
0.0&4
ACENAPHTHYLENE <
ACENAPHTHENE
4-CHLOROANILINE <
2-NITROANILINE <
3-N1TROANILINE <
4-NITROANILINE <
ANTHRACENE <
BENZO(a)ANTHRACENE <
DIBENZO(a,h)ANTHRACENE <
3,3'-DlCHLOROBENZIDINE <
1,2-D I CHLOROBENZENE <
1. 3-D I CHLOROBENZENE <
1,4-DICHLOROBENZENE <
1,2,4-TRICHLORBENZENE <
HEXACHLOROBENZENE <
NITROBENZENE <
BENZYL ALCOHOL <
CHRYSENE <
n-NITROSODIPHENYLAMINE <
n-NITROSO-di-n-PROPYLAMINE <
HEXACHLOROETHANE <
BIS(2-CHLOROETHYL)ETHER <
B1S(2-CHLOROISOPROPYL)ETHER <
4-BROMOPHENYL-PHENYLETHER <
4-CHLOROPHENYL-PHENYLETHER <
FLUORANTHENE J
FLUORENE J
BENZO(beta) FLUORANTHENE <
BEN20(kappa)FLUORANTHENE J
DIBENZOFURAN
B1S(2-CHLOROETHOXY)METHANE <
ISOPHORONE <
NAPHTHALENE J
2-CHLORONAPHTHALENE <
2-METHYLNAPHTHALENE J
HEXACHLOROCYCLOPENTAD I ENE
BENZO(ghi)PERYLENE <
PHENANTHRENE J
di-n-BUTYLPHTHALATE <
DIETHYLPHTHALATE <
DIMETHYLPHTHALATE <
di-n-OCTYLPHTHALATE <
BIS(2-ETHYLHEXYL)PHTHALATE <
BUTYLBENZYLPHTHALATE <
PYRENE <
BENZO(atpha)PYRENE <
INDENO(1,2,3-c,d)PYRENE <
2,4-DlNlTROTOLUENE <
2,6-DINITROTOLUENE <
HEXACHLOR08UTADIENE <
TR I CHLOROMETHANE B
(CHLOROFORM)
fETRACHLOROMETHANE <
(CARBON TETRACHLORIDE)
4-METHYL-2-PENTANONE <
1,2-DICHLOROPROPANE <
C-1.3-D1CHLOROPROPYLENE <
t-1,3-DICHLOROPROPYLENE <
STYRENE <
TOLUENE B
VINYL ACETATE
VINYL CHLORIDE <
TOTAL XYLENE X
0.660
1.200
0.660
3.200
3.200
3.200
0.660
0.660
0.660
1.300
0.660
0.660
0.660
0.660
0.660
0.660
0.660
0.660
0.660
0.660
0.660
0.660
0.660
0.660
0.660
0.490
0.470
0.660
0.240
0.770
0.660
0.660
0.290
0.660
0.460
NA
0.660
0.470
0.660
0.660
0.660
0.660
0.660
0.660
0.660
0.660
0.660
0.660
0.660
0.660
0.009
0.025
0.010
0.005
0.025
0.025
0.005
0.033
NA
0.010
0.027
RESULTS REPORTED ON A WHOLE SAMPLE BASIS. DUPLICATE
H=HAZLETON LABORATORIES OF AMERICA I=ISBH FOOD AND DRUG LAB
NA=NOT ANALYZED ND=NONE DETECTED
OTHER FLAGS ARE EXPLAINED ON A SEPARATE SHEET
PRINT DATE: 06/19/90
-------
FISH TISSUE CONTAMINATION RESULTS
INDIANA DEPARTMENT OF ENVIRONMENTAL MANAGEMENT
OWM-BIOLOGICAL STUDIES
LAB NUMBER:80502406
COLLECTION DATE:07/08/87
SITE:GRAND CALUMET RIVER
LOCATIONiCLINE AVE.
COUNTY:LAKE
LAB:H
I SPECIES:2 CARP
PREPARATION:UHOLE
MEAN LENGTH(CM):29.3 RANGE(CM):22.0-36.5
MEAN UEIGHT(GM):490 RANGE(GM):190-790
%LIPID:5.BO
METALS (MG/KG)
ALUMINUM 122.000
ANTIMONY < 2.000
ARSENIC < 1.000
BARIUM < 5.000
BERYLLIUM < 0.500
CADMIUM < 0.500
CALCIUM 5200.00
CHROMIUM 1.000
COBALT < 5.000
COPPER 2.500
IRON 285.000
LEAD 2.600
MAGNESIUM 290.000
MANGANESE 3.500
MERCURY 0.052
NICKEL < 4.000
POTASSIUM 2450.000
SELENIUM < 1.000
SILVER < 0.500
SODIUM 800.000
THALLIUM < 2.000
VANADIUM < 5.000
ZINC 86.000
ACID EXTRACTABLE COMPOUNDS
BENZ01C ACID
PHENOL <
2-CHLOROPHENOL <
2,4-DICHLOROPHENOL <
2.4.5-TRICHLOROPHENOL <
2,4,6-TRICHLOROPHENOL <
PENTACHLOROPHENOL <
2-HETHYLPHENOL <
4-METHYLPHENOL <
2,4-DIMETHYLPHENOL <
4-CHLORO-3-METHYLPHENOL <
4.6-DINITRO-2-METHYLPHENOL
2-NITROPHENOL <
4-NITROPHENOL <
2,4-DINITROPHENOL
PESTICIDES
ALDR1N
alpha-BHC <
beta-BHC <
detta-BHC <
gamma-BHC <
alpha-CHLORDANE 1
gamma- CHLORDANE
cis-NONACHLOR <
trans-NONACHLOR <
OXYCHLORDANE <
p,p'-DDD
o,p'-DDD <
p,p'-DDE <
O.p'-DDE 1
p,p'-DDT <
0,p'-DDT <
DIELDR1N <
ENDOSULFAN I <
ENDOSULFAN II <
ENDOSULFAN SULFATE <
ENDRIN <
ENDRIN ALDEHYDE <
ENDRIN KETONE <
HEPTACHLOR <
HEPTACHLOR EPOXIDE <
HEXACHLOROBENZENE <
METHOXYCHLOR <
PENTACHLOROAN1SOLE <
TOXAPHENE
TOTAL PCB 4.300
(MG/KG)
NA
0.660
0.660
0.660
3.200
0.660
3.200
0.660
0.660
0.660
0.660
NA
0.660
3.200
NA
(MG/KG)
0.016
0.008
0.008
0.008
0.008
0.011
0.011
0.008
0.008
0.008
0.036
0.010
0.210
0.017
0.010
0.010
0.010
0.020
0.020
0.020
0.010
0.010
0.010
0.168
0.008
0.010
0.020
0.008
NA
MG/KG
BASE/NEUTRAL EXTRACTABLE COMPOUNDSCMG/KG
ACENAPHTHYLENE J
ACENAPHTHENE . J
4-CHLOROANILINE <
2-NITROANILINE <
3-NITROANlLlNE <
4-NITROANILINE <
ANTHRACENE <
BENZO(a)ANTHRACENE <
DIBENZO(a,h)ANTHRACENE <
3.3'-DICHLOROBENZIDINE <
1,2-DICHLOROBENZENE <
1,3-DICHLOROBENZENE <
1,4-DICHLOROBENZENE <
1,2,4-TRICHLORBENZENE <
TOACHLOgOBENZENE <
NITROBENZENE <
BENZYL ALCOHOL <
CHRYSENE <
n-NITROSOOIPHENYLAMINE <
n-NITROSO-di-n-PROPYLAMlNE <
HEXACHLOROETHANE <
BIS(2-CHLOROETHYL)ETHER <
BIS(2-CHLOROISOPROPYL)ETHER <
4-BROMOPHENYL-PHENYLETHER <
4-CHLOROPHENYL-PHENYLETHER <
FLUORANTHENE J
FLUORENE J
BENZO(beta)FLUORANTHENE <
BENZO(kappa)FLUORANTHENE <
DIBENZOFURAN J
BIS(2-CHLOROETHOXY)METHANE <
ISOPHORONE <
NAPHTHALENE J
2-CHLORONAPHTHALENE <
2-METHYLNAPHTHALENE J
HEXACHLOROCYCLOPENTADIENE
BENZO(ghi)PERYLENE <
PHENANTHRENE <
di-n-BUTYLPHTHALATE BJ
DIETHYLPHTHALATE <
DIMETHYLPHTHALATE <
di-n-OCTYLPHTHALATE <
BIS(2-ETHYLHEXYL)PHTHALATE BJ
BUTYLBENZYLPHTHALATE <
PYRENE <
BENZO(alpha)PYRENE <
INDENO(1,2,3-c,d)PYRENE <
2.4-DINITROTOLUENE <
2,6-DINITROTOLUENE <
HEXACHLOROBUTADIENE <
0.03
0.641
0.661
3.201
3.201
3.201
0.661
0.661
0.661
1.301
0.661
0.66
0.66
0.66i
0.66
0.66
0.66
0.66
0.66i
0.66!
0.661
0.661
0.661
0.661
0.661
0.201
0.201
0.661
0.661
0.201
0.66<
0.661
o.or
0.66
0.14
NA
0.66
0.66
0.14
0.66
0.66
0.66
0.20
0.66
0.66
0.66
0.66
0.66
0.66
0.66
ACETONE BE 1.500
BENZENE 0.009
CHLOROBENZENE < 0.005
ETHYLBENZENE < 0.005
2-BUTANONE 0.170
CARBON DISULFIDE 0.006
CHLOROETHANE < 0.010
1,1-DICHLOROETHANE < 0.005
1,2-DICHLOROETHANE < 0.005
1,1,1-TRICHLOROETHANE < 0.005
1,1,2-TRICHLOROETHANE < 0.005
1,1,2,2-TETRACHLORETHANE < 0.005
VOLATILE ORGANIC COMPOUNDS (MG/KG)
1.1-DICHLOROETHYLENE < 0.005
1,2-DICHLOROETHYLENE < 0.005
TRICHLOROETHYLENE(TOTAL) < 0.005
TETRACHLOROETHYLENE < 0.005
2-HEXANONE < 0.010
BROMOMETHANE < 0.050
TRIBROMOMETHANE < 0.025
(BROMOFORM)
BROMODICHLOROMETHANE BJ 0.008
DIBROMOCHLOROHETHANE < 0.025
CHLOROMETHANE < 0.010
DICHLOROMETHANE B 0.038
(METHYLENE CHLORIDE)
TRICHLOROMETHANE
(CHLOROFORM)
TETRACHLOROHETHANE
(CARBON TETRACHLORIDE)
4-METHYL-2-PENTANONE
1,2-DICHLOROPROPANE
C-1,3-DICHLOROPROPYLENE
t-1,3-DICHLOROPROPYLENE
STYRENE
TOLUENE
VINYL ACETATE
VINYL CHLORIDE
TOTAL XYLENE
RESULTS REPORTED ON A WHOLE SAMPLE BASIS. D=DUPLICATE
H=HAZLETON LABORATORIES OF AMERICA I=ISBH FOOD AND DRUG LAB
NA=NOT ANALYZED ND=NONE DETECTED
OTHER FLAGS ARE EXPLAINED ON A SEPARATE SHEET
PRINT DATE: 06/19/9
-------
FISH TISSUE CONTAMINATION RESULTS
INDIANA DEPARTMENT OF ENVIRONMENTAL MANAGEMENT
OWM-BIOLOGICAL STUDIES
LAB NUMBER:80502407
COLLECTION DATE:07/08/87
SITE-.GRAND CALUMET RIVER
LOCATIONzCLINE AVE.
MEAN LENGTH(CM):10.7 RANGE(CM):8.1-14.0
COUNTY;LAKE
MEAN WE1GHT(GM):20
(SPECIES:16 GOLDEN SHINERS
LAB:H |PREPARATION:WHOLE
RANGE(GM):10-30 XLIPID-.3.7C
METALS (HG/KC)
ALUMINUM 49.900
ANTIMONY < 2.000
ARSENIC < 1.000
BARIUM < 5.000
BERYLLIUM < 0.500
CADMIUM < 0.500
CALCIUM 12900.00
CHROMIUM 1.700
COBALT < 5.000
COPPER < 2.500
IRON 487.000
LEAD 1.800
MAGNESIUM 470.000
MANGANESE 6.700
MERCURY 0.029
NICKEL < 4.000
POTASSIUM 2880.000
SELENIUM < 1.000
SILVER < 0.500
SODIUM 880.000
THALLIUM < 2.000
VANADIUM < 5.000
ZINC 45.000
ACID EXTRACTABLE COMPOUNDS
BENZOIC ACID
PHENOL <
2-CHLOROPHENOL <
2,4-DICHLOROPHENOL <
2.4,5-TRICHLOROPHENOL <
2,4,6-TRICHLOROPHENOL <
PENTACHLOROPHENOL <
2-METHYLPHENOL <
4-HETHYLPHENOL <
2,4-DIMETHYLPHENOL <
4-CHLORO-3-METHYLPHENOL <
4.6-OINITRO-2-METHYLPHENOL
2-NITROPHENOL <
4-NITROPHENOL <
2,4-DINlTROPHENOL
ACETONE BEX
BENZENE
CHLOROBENZENE <
ETHYLBENZENE <
2-BUTANONE
CARBON DISULFIDE <
CHLOROETHANE <
1 1-D I CHLOROETHANE <
1 2-DICHLOROETHANE <
1 1,1-TR I CHLOROETHANE <
1 1,2-TRICHLOROETHANE <
1 1.2,2-TETRACHLORETHANE <
PESTICIDES (MG/KG)
ALORIN < 0.101
atpha-BHC < 0.017
beta-BHC < 0.017
delta-BHC < 0.017
gamna-BHC < 0.017
alpha-CHLORDANE < 0.017
gamma- CHLORDANE < 0.017
cis-NONACHLOR < 0.017
trans-NONACHLOR < 0.017
OXYCHLORDANE < 0.017
p.p'-DDD < 0.021
o,p'-DDD < 0.021
p.p'-DDE < 0.126
o,p'-DDE < 0.021
p.p'-DDT < 0.021
o.p'-DDT < 0.021
DIELDRIN < 0.021
ENDOSULFAN I < 0.042
ENDOSULFAN 11 < 0.042
ENDOSULFAN SULFATE < 0.042
ENDRIN < 0.021
ENDRIN ALDEHYDE < 0.021
ENDRIN KETONE < 0.021
HEPTACHLOR < 0.101
HEPTACHLOR EPOX1DE < 0.017
HEXACHLOROBENZENE < 0.021
METHOXYCHLOR < 0.042
PENTACHLOROANISOLE < 0.017
TOXAPHENE NA
TOTAL PCB 2.900 MG/KG
(MG/KG)
NA
0.660
0.660
0.660
3.200
0.660
3.200
0.660
0.660
0.660
0.660
NA
0.660
3.200
NA
VOLATILE ORGANIC COMPOUNDS
1.800 1,1-DICHLOROETHYLENE <
0.019 1,2-DlCHLOROETHYLENE <
0.005 TRICHLOROETHYLENE(TOTAL) <
0.005 TETRACHLOROETHYLENE <
0.074 2-HEXANONE <
0.005 BROMOMETHANE <
0.010 TRIBROMOMETHANE <
0.005 (BROMOFORH)
0.005 BROMOD1CHLOROMETHANE BJ
0.005 DIBROMOCHLOROMETHANE <
0.005 CHLOROMETHANE <
0.005 DICHLOROMETHANE B
(METHYLENE CHLORIDE)
BASE/NEUTRAL EXTRACTABLE COMPOUNDS (HG/KC
ACENAPHTHYLENE <
ACENAPHTRENE J/
4-CHLOROANILINE <
2-NITROANILINE <
3-NITROANILINE <
4-NITROANILINE <
ANTHRACENE <
BENZO( a) ANTHRACENE <
D1BENZO(a,h)ANTHRACENE <
3,3'-DICHLOROBENZIDINE <
1,2-DICHLOROBENZENE <
1,3-DICHLOROBENZENE <
1,4-DlCHLOROBENZENE <
1,2,4-TRICHLORBENZENE <
HEXACHL040BENZENE <
NITROBENZENE <
BENZYL ALCOHOL ' <
CHRYSENE " <
n-NITROSXIPHENYLAMINE <
n-NITROSO-di-n-PROPYLAMINE <
HEXACHLOROETHANE <
BIS(2-CHLOROETHYL)ETHER <
BIS(2-CHLOROISOPROPYL)ETHER <
4-BROMOPHENYL-PHENYLETHER <
4-CHLOROPHENYL-PHENYLETHER <
FLUORANTHENE J
FLUORENE J
BENZO(beta)FLUORANTHENE <
BENZO(kappa)FLUORANTHENE <
DIBENZOFURAN J
BIS(2-CHLOROETHOXY)METHANE < c
ISOPHORONE <
NAPHTHALENE J
2-CHLORONAPHTHALENE <
2-METHYLNAPHTHALENE J
HEXACHLOROCYCLOPENTAD I ENE
BENZO(ghi)PERYLENE <
PHENANTHRENE J
di-n-BUTYLPHTHALATE BJ
DIETHYLPHTHALATE <
D1METHYLPHTHALATE <
di-n-OCTYLPHTHALATE <
BIS(2-ETHYLHEXYL)PHTHALATE <
BUTYLBENZYLPHTHALATE <
PYRENE . J
BENZO(alphe)PYRENE <
INDENO(1,2,3-c,d)PYRENE <
2,4-DINITROTOLUENE <
2,6-DINITROTOLUENE <
HEXACHLOROBUTADIENE <
(MG/KG)
0.005 TR I CHLOROMETHANE B
0.005 (CHLOROFORM)
0.005 TETRACHLOROMETHANE <
0.005 (CARBON TETRACHLOR1DE)
0.010 4-METHYL-2-PENTANONE <
0.050 1,2-DICHLOROPROPANE <
0.025 C-1.3-DICHLOROPROPYLENE <
t-1,3-DICHLOROPROPYLENE <
0.008 STYRENE <
0.025 TOLUENE
0.010 VINYL ACETATE
0.130 VINYL CHLORIDE <
TOTAL XYLENE X
0.6Z
0.51
^=B3>6
3.20
3.20
3.20
0.66
0.66
0.66
1.30
0.66
0.66
0.66
0.66'
0.66I
0.66I
0.661
0.661
0.66C
0.66C
0.66C
0.66C
0.66C
0.660
0.660
0.220
0.210
0.660
0.660
0.300
-"'0.660'
0.660
0.081
0.660
0.130
NA
0.660
0.210
0.120
0.660
0.660
0.660
0.660
0.660
0.180
0.660
0.660
0.660
0.660
0.660
0.046
0.025
0.010
0.005
0.025
0.025
0.005
0.058
NA
0.010
0.041
RESULTS REPORTED ON A WHOLE SAMPLE BASIS. 0=DUPL1CATE
H=HAZLETON LABORATORIES OF AMERICA I=ISBH FOOD AND DRUG LAB
NA=NOT ANALYZED ND=NONE DETECTED
OTHER FLAGS ARE EXPLAINED ON A SEPARATE SHEET
PRINT DATE: 06/19/90
-------
FISH TISSUE CONTAMINATION RESULTS
INDIANA DEPARTMENT OF ENVIRONMENTAL MANAGEMENT
OWM-BIOLOGICAL STUDIES
LAB NUMBER:80502408
COLLECTION DATE:07/08/87
SITE:GRAND CALUMET RIVER
LOCATION:CLINE AVE.
MEAN LENGTH(CM):8.2 RANGE(CM):7.5-10.3
COUNTY;LAKE
MEAN WEIGHT(GM):12
LAB:H
SPECIES:10 PUMPKINSEED
PREPARAT10N:UHOLE
RANGE(GM):10-28
%LIP1D:1.50
METALS (HG/KG)
ALUMINUM < 20.000
ANTIMONY < 2.000
ARSENIC < 1.000
BARIUM < 5.000
BERYLLIUM < 0.500
CADMIUM < 0.500
CALCIUM 14600.00
CHROMIUM < 1.000
COBALT < 5.000
COPPER < 2.500
IRON 151.000
LEAD < 0.500
MAGNESIUM 450.000
MANGANESE 3.600
MERCURY < 0.025
NICKEL < 4.000
POTASSIUM 2830.000
SELENIUM < 1.000
SILVER < 0.500
SOOtUM 1120.000
THALLIUM < 2.000
VANADIUM < 5.000
ZINC 28.800
ACID EXTRACT ABLE COMPOUNDS
BENZOIC ACID
PHENOL <
2-CHLOROPHENOL <
2.4-DICHLOROPHENOL <
2.4,5-TRICHLOROPHENOL <
2,4,6-TRICHLOROPHENOL <
PENTACHLOROPHENOL <
2-METHYLPHENOL <
4-METHYLPHENOL <
2.4-DIMETHYLPHENOL <
4-CHLORO-3-METHYLPHENOL <
4.6-DINITRO-2-METHYLPHENOL
2-NITROPHENOL <
4-NITROPHENOL <
2,4-DINITROPHENOL
ACETONE BE
BENZENE
CHLOROBENZENE <
ETHYLBENZENE <
2-BUTANONE
CARBON DISULFIDE <
CHLOROETHANE <
1,1-DICHLOROETHANE <
1,2-0 1 CHLOROETHANE <
1.1,1-TRl CHLOROETHANE <
1,1,2-TRICHLOROETHANE <
1,1,2.2-TETRACHLORETHANE <
PESTICIDES (MG/KG)
ALDR1N NA
alpha-BHC NA
beta-BHC NA
delta-BHC NA
ganroa-BHC NA
alpha-CHLORDANE NA
ganma-CHLORDANE NA
cis-NONACHLOR NA
trans-NONACHLOR NA
OXYCHLORDANE NA
p,p'-DDD NA
o.p'-DDD NA
p.p'-DDE NA
0,p'-DDE NA
p,p'-DDT NA
O.p'-ODT NA
DIELDRIN NA
ENDOSULFAN I NA
ENDOSULFAN II NA
ENDOSULFAN SULFATE NA
ENDRIN NA
ENDRIN ALDEHYDE NA
ENDRIN KETONE NA
HEPTACHLOR NA
HEPTACHLOR EPOX1DE NA
HEXACHLOROBENZENE NA
METHOXYCHLOR NA
PENTACHLOROANISOLE - NA
TOXAPHENE NA
TOTAL PCB NA MG/KG
(HG/KG)
NA
0.660
0.660
0.660
3.200
0.660
3.200
0.660
0.660
0.660
0.660
NA
0.660
3.200
NA
VOLATILE ORGANIC COMPOUNDS
1.300 1,1-DICHLOROETHYLENE <
0.007 1,2-DlCHLOROETHYLENE <
0.005 TRICHLOROETHYLENE(TOTAL) <
0.005 TETRACHLOROETHYLENE <
0.096 2-HEXANONE <
0.005 BROMOMETHANE <
0.010 TR I BROMOMETHANE <
0.005 (BROMOFORM)
0.005 BROMODICHLOROMETHANE BJ
0.005 DIBROMOCHLOROMETHANE <
0.005 CHLOROMETHANE <
0.005 Dl CHLOROMETHANE BE
(METHYLENE CHLORIDE)
BASE/NEUTRAL EXTRACTABLE COMPOUNOS(MG/KG)
(HG/KG)
0.005
0.005
0.005
0.005
0.010
0.050
0.025
0.006
0.025
0.010
1.300
ACENAPHTHYLENE <
ACENAPHTHENE J
4-CHLOROANILINE < ,
2-NITROANILINE <
3-NITROANILINE <
4-NITROANILINE <
ANTHRACENE <
BENZO(a)ANTHRACENE <
DIBENZO(a,h)ANTHRACENE <
3,3'-DlCHLOROBENZIDINE <
1.2-DICHLOROBENZENE <
1.3-DICHLOROBENZENE <
1,4-DICHLOROBENZENE <
1,2.4-TRICHLORBENZENE <
HEXACHLOROBENZENE <
NITROBENZENE <
BENZYL ALCOHOL f
CHRYSENE '~~ <
n-NITROSODIPHENYLAMINE <
n-NlTROSO-di-n-PROPYLAMINE <
HEXACHLOROETHANE <
BIS(2-CHLOROETHYL)ETHER <
BIS(2-CHLOROISOPROPYL)ETHER <
4-BROMOPHENYL-PHENYLETHER <
4-CHLOROPHENYL-PHENYLETHER <
FLUORANTHENE J
FLUORENE J
BENZO(beta)FLUORANTHENE <
BENZO(kappa)FLUORANTHENE <
DIBENZOFURAN J
BIS(2-CHLOROETHOXY)METHANE <
ISOPHORONE <
NAPHTHALENE J
2-CHLORONAPHTHALENE <
2-METHYLNAPHTHALENE J
HEXACHLOROCYCLOPENTADIENE
BENZO(ghi)PERYLENE <
PHENANTHRENE J
di-n-BUTYLPHTHALATE BJ
OIETHYLPHTHALATE <
DIMETHYLPHTHALATE <
di-n-OCTYLPHTHALATE <
B1S(2-ETHYLHEXYL)PHTHALATE <
BUTYLBENZYLPHTHALATE <
PYRENE J
B!£NZO(alpha)PYRENE <
INDENO(1,2.3-c,d)PYRENE <
2,4-DlNITROTOLUENE <
2,6-DINITROTOLUENE <
HEXACHLOROBUTADIENE <
TR I CHLOROMETHANE B
(CHLOROFORM)
TETRACHLOROMETHANE <
(CARBON TETRACHLORIDE)
4-METHYL-2-PENTANONE <
1,2-DICHLOROPROPANE <
C-1.3-DICHLOROPROPYLENE <
t-1,3-DICHLOROPROPYLENE <
STYRENE <
TOLUENE
VINYL ACETATE
VINYL CHLORIDE <
TOTAL XYLENE X
0.66G
0.140
0.660
3.200
3.200
3.200
0.660
0.66G
0.66C
1.30C
0.66C
0.66C
0.66C
0.66C
0.66C
0.66C
0.66C
0.66G
0.660
0.660
0.660
'0.660
0.660
0.660
0.660
0.130
0.069
0.660
0.660
0.090
0.660
0.660
0.020
0.660
0.033
NA
0.660
0.089
0.240
0.660
0.660
0.660
0.660
0.660
0.051
0.660
0.660
0.660
0.660
0.660
0.049
0.025
0.010
0.005
0.025
0.025
0.005
0.037
NA
0.010
0.012
RESULTS REPORTED ON A WHOLE SAMPLE BASIS. D=DUPLICATE
H=HAZLETON LABORATORIES OF AMERICA I=ISBH FOOD AND DRUG LAB
NA=NOT ANALYZED ND=NONE DETECTED
OTHER FLAGS ARE EXPLAINED ON A SEPARATE SHEET
PRINT DATE: 06/19/90
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,_1«V»XF*M.U : l?<35-0.O& |3. P5"~s- MODE ^^.O% -C»»t.. -nt. H *Jv*"~^WIS.0'v)
C.c~*'~7 ' tJj'aS^ LAMP CURRENT fK<>*jH:
' jo.o'i-7 v '°°*> « / yy. 6 1, FLAME, fit- STANDARI
''7 INTEGRATION TIMEJ?.*» CURVE «
P08 SAMP »/OCC SAMPLE DESCRIPTION CLIENT CLAIM HIGH LIMIT
PRI ABBR/UNITS V-DATA 'DO' VALUE AVE VALUE 1
1 80S02396 UHOLE FISH: 4-68; CRAND CALUMET RIVER .000 . .000
6 01 STIN INDPLS. BLVD ; 3 CARP; 6/25/86 '
PPM PPM 0 . 000
e 80502397 UHOLE FISH. 6-88; UPPER (OR 1ST) MARO .000 000
. t .01 STIN UETTE PARK LACOON; 5 CARP; 7/15/86
PPM PPM 0 .000
3 80502398 UHOLE FISH: 3-68; CRAND CALUHET RIVER .000 .000
6 01 STIN KENNEDY AVENUE; 4 CARP; 6/25/86
PPM PPM 0 . ... _.. 000 _
_ _4 80502399 UHOLE FISH. 1-88; CRAND CALUMET RIVER 000 ,JOO
01 STIN CLINE AVENUE; 4 CARP; 6/26/86
PPH PPH 0 .000
S 60502400 UHOLE FISH 7-88; UPPER (OR 1ST) MARO 000 .000
* 01 STIN UETTE PARK LACOON; 1 LARCEMOUTH BASS;
PPM PPM 7/15/86 0 .000
' 1
6 60502401 UMOLC FISH 8-88; MIDDLE (OR END) MAR 000 .000
C 01 STIN OUETTE PARK LACOON; 4 CARP; 8/14/86
PPM PPM 0 ..000
7 80502402 UHOLE FISH. 9-88; LOWER tOR WEST OR 3 .000 .000
6 01 STIN RD) MARQUETTE PARK LACOON; 4 CARP;
PPM PPH 8/14/86 0 .000
6 60502403 UHOLE FISH: 5-88; IND. HARBOR CANAL; .000 .000
- ft 01 STIN S CARP; 6/2S/86
PPM PPM 0 000
*««,«,*,
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UKSTi 000196-00 FOR ANAL8
878 SAT, JUN 35, 1988, 9:57 AM REPTD BY MIX iii/JL'-fuf APPROVED.
BALANCE . .?$£? ... . WEIGHED BY. . . . 4-fcl0«,» DATE
-^"INSTRUMENT . . . . TRANSFERRED BY .. .X-Jki0«.-* DATE . J
1 UAVELENGTH DILUTED BY JET.**. . DATE.''
J SLIT OPERATOR ?W?",T*rv1 DATE
\ ENERGY CALCULATED BY ?*T DATE
i\ MODE __ .
LAMP CURRENT
I FLAME STANDARD CODE «. ...
PACE I
PCS SAMP.i/OCC
1 80503404
6 01 STIN
PPM PPM
3 80503405
t 01 STIN .
PPH PPH
3 80508406
6 01 STIN
. PPM PPH
4 80503107
6 Ol STIN
PPM PPM
5 80503408
6 0| STIN
PPM PPM
6 8GS03403
6 Ol STIN
ppn ppn
7 805034)0
6 Ol STIN
PPM PPH
8 8050341 I
6 01 STIN
PPM PPH
SAMPLE DESCRIPTION
Y-BATft
UHOLE FISH: 3-88;
BRIDGE STREET; 3
UHOLE FISH: 10-88;
4 CARP; 7/7/87 .
.UHOLE FISH: 11-88;
R CLINE AVENUE; 3
UHOLE FISH: 12-68,
R CLINE AVENUE; It
7/8/87
UHOLE FISH. 13-88;
R CLINE AVENUE; 10
7/8/87
UHOLE FiSK: I4-S8;
R KENNEDY AVENUE;
UHOLE FISH: 15-88;
R BRIDCE STREET; 1
UHOLE FISH: 16-88;
R BRIDCE STREET; 1
7/8/87
,_..
CRAND CALUMET- RIVER
CARP; 6/36/86
IND. HARBOR CANAL;
GRAND CALUMET RIVE
CARP; 7/8/87
CRANO CALUMET RIVE
COLDEN SHINER*
CRAND CALUHET RIVE
PUHPKINSEEDi.
CRAND CALUHET RIVE
4 CARP; 7/8/87
CRANO CALUMET RIVE
CARP; 7/8/87
CRAND CALUHET RIVE
4 COLDEN SHINER;
CLIENT CLAIM
DD' VALUE
. . .. .000
0
.000
0
.000
.040
0
000
0
000
9
.000
0
.000
0
HIGH LIMIT
AVE V*LUE
. _ .000 .
.000
.000
000
.000
000..
.000
.000
. 000
.000
. 000
. .000
.000
.000
. 000
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UT V
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' «»BE PPM UKSTt 000203-60 FOR ANALi 878 SAT, JUN 25, 1988, 9 57 AM REPTD BY flW^ j°_/J(
' Jylc-Au, : I-00-} % __ _ BALANCE » 0001200009 / 000120001^
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". . . INTEGRATION TIME .':>*«-
" POS SAMP t/OCC SAMPLE DESCRIPTION CLIENT CLAIM HIGH LIMIT
" PR1 ABBR/UNITS V-DATA 'DO' VALUE AVE VAL.UE UT
'... 1 60502396 UHOLE FISH: 4-68; GRAND CALUMET RIVER .000 .000. ,
'* 6 01 STIN INDPLS. BLVD.; 3 CARP; 6/25/86
" PPM PPM 0 .000
*° a 80502397 UHOLE FISH: 6-88; UPPER (OR 1ST) MARQ .000 .000
1 ft_ 01 STIN UETTE PARK LACOON; 5 CARP; 7/15/86
" PPH PPM 0 .000
" 3 80508398 UHOLE FISH: 3-88; GRAND CALUMET RIVER .000 .000
'* 6 01 STIN KENNEDY AVENUE; 4 CARP; 6/85/86
?!__ PPM PPM . 0. ^.000
M
*
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" ft 01 STIN CLINE AVENUE; 4 CARP; 6/86/86
" PPM PPM 0 .000
«
34 . - - . . . _
n 5 80502400 UHOLE FISH: 7-88; UPPER (OR 1ST) MARQ .000 .000
!* $ PJ.ST1N UETTE PARK LAGOON; 1 LARCEMOUTH BASS;
" PPM PPM 7/15/86 0 .000
40 6 80508401 UHOLE FISH: 8-88; MIDDLE (OR 8ND) MAR 000 .000
" 6 01 STIN OUETTE PARK LACOON; 4 CARP; 8/14/86
" PPM PPM 0 .000
0
44
" 7 80502402 UHOLE FISH: 9-86; LOUER (OR UEST OR 3 000 000
" 6 01 STIN RD) MARQUETTE PARK LACOON; 4 CARP;
" PPM PPM 8/14/86 0 .000
«
M 8 60502403 UHOLE FISH: 5-86; IND. HARBOR CANAL; .000 .000
^ 6 0.1 STIN 5 CARP; 6/E5/86 .
" PPM PPM 0 000
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PBE PPM WKST* 006204-00 FOR ANAL* 878 SAT, JUN 25, 1988, 9:57 AM REPTD BY.
BALANCE OOOI20G009 / 000120001
("INSTRUMENT 0001200010 / 000120
WAVELENGTH
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DP' VALUE AVE VALUE WT
APPROVED
J£//IL/A£' PAGE 1
MEASURED BY .*-*«»f. . DATE
TRANSFERRED BY . . .*&« *>*. . DATE.
DILUTED/ALIQUOT
OPERATOR.
CALCULATED
ILIQUOT BY..*** DATE/»-.*.-/f.
7 D*TE. J....
:o BY -r. DATE. 4-....
PCS SAHP.tt/OCC SAMPLE DESCRIPTION
PR1 ABBR/UN1TS V-DATA
STANDARD CODE *.
CURVE I DATA ON WORKSHEET I/??.-.*?
ALIQUOT jtt AJS PO
VOL OIL
PTD UC/ML RESULT REPT DE
80502404 WHOLE FISH: a-Mj. GRAND CALUMET RIVER
01 STIN BRIDGE STREET; 3 CARP; 6/26/86
000.
000
Kf
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PPM PPM
2 80502405
. 6 01 STIN
PPM PPM
3 80502406
6 01 STIN
PPM PPM
4 80502407
6 01 STIN
PPM PPM
5 80502408
6 01 STIN
PPM PPM
6 80502409
6 01 STIN
PPH PPM.
7 80502410
6 01 STIN
PPM PPH
8 80502411
6 01 STIN
PPM PPH
wn A wwb 0 nbc* i j§ w
WHOLE FISH: 10-88;
4 CARP; 7/7/87. .-
INO. HARBOR CANAL;
WHOLE FISH: 11-88; GRAND CALUMET RIVE
R CLINE AVENUE; 2 CARP; 7/8/87
WHOLE FISH te-ee;
R CLINE AVENUE; 16
7/8/87
WHOLE FISH. 13-88;
R CLINE AVENUE; 10
7/8/87
WHOLE FISH: 14-88:
R KENNEDY AVENUE; 4
WHOLE FISH: 15-88;
R BRIDGE STREET, 1
WHOLE FISH. 16-88;
R BRIOCE STREET; 14
7/8/87
GRAND CALUMET RIVE
GOLDEN SHINER;,
GRAND CALUMET RIVE
PUMPKINSEED;
GRAND CALUMET RIVE
CARP; 7/8/87
GRAND CALUMET RIVE
CARP, 7/8/87
GRAND CALUMET RIVE
GOLDEN SHINER;
0
.000
0
.000
0 ..
,000
0
.000
0
.000
.. . . 0. . .
.000
0
.000
0
. 000
.000
. 000
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000
.000
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| MCE PPH UKSTH 000199-00/FpR ANALt 878 SAT, JUN 25. 1988. 9^57 AM REPTD BY ~1U
BALANCE OOOI^rtTOOOjj) / OOOIgJtJJLM
INSTRUMENT o oBT?oo o 1 3 t&GSfraaSKr^
. WAVELENGTH^ .^VJt")«W\
' SLIT . tVP-7 . . .
" EXPANSION. . .IO<
*-- .-- - MODE. .Co*c.s . .
'" LAMP CURRENT. . V tOatts ...
" P0« SAMP.»/OCC SAMPLE DESCRIPTION CLIENT CLAIM MICH LIMIT
" PHI ABBR/UNITS V-DATA -00' VALUE AVE VALUE
" 1 80502396 WHOLE FISH: 4-88; CRAND CALUMET RIVER . .000 .0002'
' 6 01 STIN INDPLS. BLVD.; 3 CARP; 6/35/86
" PPH PPM *«t 0 .000
;t **CB , 0.1 .^Mj *f*t - - - -
" 2 80502397 WHOLE FISH: 6-88; UPPER »OR 1ST) MARQ 000 .000
*:_._«. Ot STIN UETTE PARK LACOON; 5 CARP; 7/15/86
" PPM PPM 0 .000
t«
*' 3 80503398 UHOLE FISH: 3-88; CRAND CALUMET RIVER .000 .000
' 6 Ot STIN KENNEDY AVENUE; 4 CARP; 6/25/86
" PPM PPM 0 000
> -
n
!° 4_ 80502399 UHOLE FISH 1-88; CRAND CALUMET RIVER .000 .000
« 01 STIN CLINE AVENUE; 4 CARP; 6/26/86
" PPH PPH 0 .000
S9
" 5 60502400 UHOLE FISH: 7-88; UPPER (OR 1ST) MARQ .000 .000
!! »_OJ.STIN UETTE PARK LACOON; 1 LARCEMQUTH BASS;
" PPM PPM 7/15/86 0 - - - g0-
t*
" 6 80502401 UHOLE FISH 8-88; MIDDLE < OR 2ND) MAR .000 .000
" 6 01 STIN OUETTE PARK LACOON; 4 CARP; 8/14/86
? PPM PPM 0 ..000
44
" 7 80502402 UHOLE FISH: 9-88; LOWER (OR WEST OR 3 000 000
* 6 01 STIN RD) MAROUETTE PARK LACOON; 4 CARP;
" PPM PPM 8/14/86 0 .000
"" '
"° 8 80502403 UHOLE FISH. 5-88; IND. HARBOR CANAL; .000 .000
V ft 01 STIN 5 CARP; 6/E5/86
" PPH PPM 0 000
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MCE PPM UKST« 000200-00 FOR ANAL! 878 SAT. JUN 25, 1988. 9:57 AH REPTD BY.
BALANCE
INSTRUMENT
WAVELENGTH.
SLIT H\P.~l
EXPANSION *X.
MODE.Co'VA-.'SfV .
LAMP CURRENT..
PACE I
MEASURED Br *'.f DATE.<"°'/? J5?
TRANSFERRED BY/&C.* DATE .P'^'Vfc
DILUTED BY.SV.t DATE ....
OPERATOR. PC-ri DATE.JO-I7-8S
CALCULATED BY .9"^ DATE .tt>r
POS SAMP.t/OCC SAMPLE DESCRIPTION
CLIENT CLAIM HIGH LIMIT
'DO' VALUE AVE VALUE
STANDARD CODE * . >lG,f>'Vl HC.KS 1W]
CURVE i DATA ON WORKSHEET i . i\ff£.Oee.ic>?. *
WT VOL OIL RX PH, UC HG RSLT REPT PO
zax PE.
1 80502404 WHOLE FISH: 2-83; GRAND CALUMET RIVER .000 . 000 j
6 01 STIN BRIDGE STREET; 3 CARP; 6/26/86
PPM PPM 0 .000
2 80503405 WHOLE FISH: 10-88; 1NO. HARBOR CANAL; .000 .000
6 01 STIN 4 CARP; 7/7/87
PPM PPM 0 .000
3 80502406 WHOLE FISH: 11-88; GRAND CALUMET RIVE / .000 .000
& 01 STIN R CLINE AVENUE; 2 CARP; 7/8/87 /
PPM PPM [/ 0 .000
4 8QSOc407 WHOLE FISH: 12-88; GRAND CALUMET RIVE .000 .000 .
6 01 STIN R CLINE AVENUE; 16 GOLDEN SHINER; /
PPM PPM 7/8/87 (/ 0 .000 '
5 80502403 WHOLE FISH- 13-88; GRAND CALUMET RIVE / .000 .000
i 01 STIN R TLINE AVENUE; 10 PUMPKINSEED; /
PPM PPM 7/8/87 V 0 .000***
M to
,
OJL S
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SEE PPH UKSTt 0001(1-00 FOR ANALO
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SAMPLE DESCRIPTION
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6 01 STIN BRIDGE STREET; 3 CARP; 6/86/86 '
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6 01 STIN 4 CARP; T/7/B7
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3 80508406 UHOLE FISH: 11-88; CRANO CALUMET RIVE .000 .000
6 01 STIN R CLINE AVENUE; E CARP; 7/8/87
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4 80508407 UHOLE FISH: 18-88; CRAND CALUMET RIVE .000 .. .000
6 01 STIN R CLINE AVENUE; 16 GOLDEN SHINER;
PPM PPM 7/8/87 0 .000
5 80502408 UHOLE FISH: 13-88; GRAND CALUMET RIVE .000 .000
6 01 STIN R CLINE AVENUE; 10 PUMPKINSEED;
PPM PPM 7/8/87 0 .000
6 80508409 UHOLE FISH: 14-88; CRAND CALUMET RIVE .000 .000
6 01 STIN R KENNEDY AVENUE; 4 CARP; 7/8/87
PPM PPf1 . P..._ .000
7 80502410 UHOLE FISH: 15-88;. CRAND CALUMET RIVE .000 000
6 01 STIN R BRIDGE STREET; 1 CARP; 7/8/87
PPM PPM 0 -000
8 80508411 UHOLE FISH: 16-88; CRAND CALUMET RIVE .000 .000
6 01 STIN R BRIDGE STREET; 14 GOLDEN SHINER; .
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J 4._.OI BTIN . UET.TE PARK LACOON; S CARP;. 7/15/84
PPH PPH 0 .000
3 80508398 UHOLE FISH: 3-88; GRAND CALUMET RIVER .000 .000
4 01 BTIN KENNEDY AVENUE; 4 CARP; 4/85/84
PPH . PPH . . _ 0 .*0fl._.
4_00.5PS3U. UHOLE FISH: 1-88; CRAND CALUHET RIVER .000 .000
4 01 BTIN CLINE AVENUE; 4 CARP; 4/84/84
PPH PPH 0 .000
5 80508400 UHOLE FISH: 7-88; UPPER (OR 1ST) MARO .000 .000
4 01 STIN UETTE PARK LAGOON; 1 LARCEHOUTH BASS;
PPN PPH 7/15/8* 0 .000
4 80502401 UHOLE FISH: 8-88; MIDDLE (OR 2ND) MAR .000 .000
4 01 STIN OUETTE PARK LACOON; 4 CARP; 8/14/84
PPH. PPH __ . . . Q ,000
7 B0508408 UHOLE FISH: S-8B; LOUER .tOR UEST. OR. 3 _. . .000 _ 800
4 01 STIN RD) HARQUETTE PARK LACOON; 4 CARP;
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PR I ABBR/l/NITS V-0ATA 'DO' VALUE AVE VALUE WT
1 80502396 WHOLE FISH: 4-88; GRAND CALUMET RIVER .000 .000
6 01 STIN INDPLS. BLVD.; 3 CARP; 6/25/86
PPM PPM 0 .000
E 80508397 WHOLE FISH: 6-88; UPPER (OR 1ST) MARQ .000 .000
6 01 STIN UETTE PARK LdtfOON; 5 CARP; 7/15/86
PPM PPM 0 .000
3 80502398 WHOLE FISH: 3-88; GRAND CALUMET RIVER .000 .000
t 01 STIN KENNEDY AVENUE; 4 CARP; 6/25/86
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ft 01 STIN CLINE AVENUE; 4 CARP; 6/86/86
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5 80502400 UHOLE FISH: 7-88; UPPER (OR 1ST) MARQ .000 .000
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PPM PPM 7/15/86 0 .000
6 80502401 WHOLE FISH. 8-88; MIDDLE t OR 2ND) MAR 000 .000
6 01 STIN QUETTE PARK LAGOON; 4 CARP; 8/14/86
PPH PPH .8 . . .000
7 80508408 WHOLE FISH: 9-88; LOWER (OR WEST OR 3 .000 . ^000 .
t 01 STIN RD> MAROUETTE PARK LAGOON; 4 CARP;
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3 80503405 WHOLE FISH: 10-88; INO. HARBOR CANAL; .000 .000
6 01 STIN.. . . 4 CARP: 7/7/87 .
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3 80503406 WHOLE FISH: 11-88; GRAND CALUMET RIVE .000 .000
t 01 STIN R CLINE AVENUE; t CARP; 7/8/87
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4 805Q3407 WHOLE FISH: 18-89; GRAND CALUMET RIVE 099. .000
6 01 STIN R CLINE AVENUE; It GOLDEN SHINERj
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S 80503408 WHOLE FISH: 13-88; GRAND CALUMET RIVE .000 .000
6 Ot STIN R CLINE AVENUE; 19 PUflPKlNSEED,
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6 80503409 WHOLE FISH: 14-88; GRAND CALUHE7 RIVE .000 000
6 01 STIN R KEHNEDY AVENUE; « CARP; 7/8/87
PPM PPH 0 .000
7 80503410 WHOLE FISH; 15-88; GRAND CALUMET .RIVE . . .000.. . .000
6 01 STIN R BRIDGE STREET; 1 CARP; 7/8/87
PPH PPH 0 .000
8 80503411 WHOLE FISH: 16-88; GRAND CALUHE7 RIVE .000 .000
6 01 STIN R BRIDGE STREET; 14 COLDEN SHINER; ...
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APPENDIX B
HUMAN TOXICITY ESTIMATES FOR CONTAMINANTS PRESENT IN THE
GRAND CALUMET RIVER/INDIANA HARBOR CANAL 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 Grand Calumet River and Indiana
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 Toxicity
The RfD is the toxicity value used most often in evaluating noncarcinogenic
effects. RfDs are based on the 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 "RfDB") or
during the lifetime (i.e., chronic RfD or "RfD"). This toxicity value has an
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:
ofr, _ NOAEL or LOAEL
RfD UFXMF
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 Carcinogenicity
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
B-2
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limits), at low extrapolated doses, that is consistent with the data. The slope
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
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-3
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TABLE B.I.
ORAL RfD SUMMARY FOR CHEMICALS LISTED IN IRIS AS
OF 01/01/92
Chemical
METALS
Antimony
Barium
Beryllium
Cadmium
Chromium VI
Manganese
Mercury, methyl
Nickel
Vanadium pentoxide
PAHs
Acenaphthene
Fluoranthene
UF
1000
3
100
10
500
1
10
100
100
3000
3000
Confidence
In Oral
MF RfD
1 Low
1 Medium
1 Low
1 High
1 Low
1 Medium
1 Medium
3 Medium
1 Low
1 Low
1 Low
Critical Effects
Longevity, blood glucose, and cholesterol in rats
Increased blood pressure in human males
No adverse effects in rats
Significant proteinuria in humans
No effects reports in rats
Central nervous system effects in humans
Central nervous system effects in humans
Decreased body and organ weights in rats
Decreased hair cystine in rats
Hepatotoxicity in mice
Nephropathy, increased liver weights.
Pyrene
PHENOLS
3000
Low
hematological alterations, and clinical
effects in mice
Kidney effects (remal tubular pathology, decreased
kidney weights) in mice
2, 4-Dichlorophenol
2, 4-Dinitrophenol
Pentachlorophenol
Phenol
o-Cresol
AROMATIC HYDROCARBONS
1, 1-Biphenyl
Hexachlorobenzene
Toluene
ORGANOCHLORINE INSECTICIDES
Aldrin
Chlordane
Dieldrin
Heptachlor
Heptachlor epoxide
Mirex
p,p' DDT
P0RGEABLES
Chlorobenzene
1, 2-Dichlorobenzene
Ethylbenzene
Styrene
Tetrachloroethylene
100
1000
100
100
1000
100
100
1000
1000
1000
100
300
1000
10000
100
1000
1000
1000
1000
1000
1
1
1
1
1
10
1
1
1
1
1
1
1
1
1
1
1
1
1
I
Low
Low
Medium
Low
Medium
Medium
Medium
Medium
Medium
Low
Medium
Low
Low
Low
Medium
Medium
Low
Low
Medium
Medium
Decreased delayed hypersensitivity response
rats
Cataract formation in humans
Liver and kidney pathology in rats
Reduced fetal body weight in rats
Decreased body weights and neurotoxicity in
Kidney damage in rats
Liver effects in rats
Changes in liver and kidney weights in rats
Liver toxicity in rats
Regional liver hypertrophy in female rats
Liver lesions in rats
Liver weight increases in male rats
Increased iiver-to-body weight ratio in both
and female dogs
Decreased pup survival in prairie voles
Liver lesions in rats
Hlstopathologic change's in dog livers
No adverse effects observed in rats
Liver and kidney toxic Lty in rats
Red blood cell and liver effects in dogs
Heptatotoxicity in mice, weight gain in rats
in
rats
male
B-4
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APPENDIX C
DERMAL EXPOSURE ESTIMATES AT OTHER SITES ALONG THE
GRAND CALUMET RIVER
C.I INTRODUCTION
Along the Grand Calumet River, including the East Branch, there are areas on the
banks where people have access to the river and its sediments. For example,
several homes have backyards abutting the river, and large areas of floodplains
lining the river are easily accessible and potentially attractive to children and
adults. This addendum focuses on the possibility of exposure to sediments in the
East Branch area near Bridge Street. Of the three areas described in the
document, area one describes this area the best (refer to Figure 5.1).
Based on the geographical setting and the distribution of contamination (discussed
further in the document), the only route of exposure considered here is dermal
contact with contaminated sediments that might occur during infrequent wading
or incidentally during recreational or residential activities.
The sediments in this area are heavily contaminated with PCBs, PAHs, and
metals. Because of the significant concentrations of carcinogenic contaminants,
this assessment assumed that certain compounds would drive or make up the
majority of the potential risk. Therefore, compounds of interest via the dermal
exposure pathway are carcinogenic compounds that can potentially pass through
the skin and may have potential adverse impact. For this study, carcinogenic
PAHs and PCBs were considered the relevant compounds.
In this document, two methods have been utilized for estimating contaminant
intake concentration resulting from dermal exposure to the sediments. One way,
referred to here as Method 1, and used in the parent document, assumed that
contaminants in the sediment first partitioned to pore water, and then entered the
skin surface (sediment->water->skin). Another method, which we have termed
Method 2, assumed there is a more direct interface between the skin and the
sediments themselves, such that contaminants move from the sediment to skin.
Because these two methods consider two different pathways for the transport of
contaminants to the skin surface, there are differences in the exposure equations
used. The tables and narration below discusses the details and the differences of
the two methods.
C.2 EXPOSURE
There are several potentially carcinogenic compounds in this area, however this
study will be limited to PCBs and carcinogenic PAHs, because these two categories
of compounds are considered to pose the most significant risk to human health.
Non-cancer endpoints, such as reproductive effects were considered to be less of a
risk, therefore, the probability of cancer was assessed.
C-l
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Note that exposure events here would probably be at a much lower frequency than
in a harbor or a similarly high use area. Discussion of event frequency and other
variables in the exposure equation, from the Risk Assessment Guidance for
Superfund (RAGS), is given below. (USEPA, 1989a)
The risk analysis considered different wading behaviors for children and adults to
estimate carcinogenic risks to an individual over an entire lifetime. This
addendum divides an average lifetime into two potential exposure behavior
groups: children and teenagers (under 18 years of age) in one group and adults in
the other. The lifetime exposure for children and teens is estimated at 10 yrs,
(exposure estimated by best professional judgment), adults lifetime exposure
estimated at 30 years, (RAGS). Assessing each group separately is reflected in the
choices of the appropriate parameter values, as discussed below in the exposure
equations in Tables C.I and C.2
TABLE C-l:
EQUATION FOR EXPOSURE TO CONTAMINANTS
DUE TO DERMAL CONTACT WITH SEDIMENT POREWATER - Method 1
abs = ED,
dose 70yrs
fcWj
'A, x ET xPCx EFt x ED,x
BW.XAT,
where:
i age group specific
j chemical specific
CW chemical concentration in water (mg/L)
SA surface area (cm2)
ET exposure time (hr/day)
PC permeability constant (cm/hr)
EF exposure frequency (days/yr)
ED exposure duration (yrs)
CF conversion factor (L/cm3)
BW body weight (kg)
AT averaging time (days)
C-2
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TABLE C-2:
EQUATION FOR ESTIMATING EXPOSURE INTAKE TO CONTAMINANTS DUE TO
DERMAL CONTACT WITH CHEMICALS IN THE SEDIMENTS - Method 2
EXPOSURE = ED,
70yrs
fa
XSA:XAFX ABS: X EF: X ED: X CF]
where:
i age group specific
j chemical specific
CS concentration in sediment (mg/kg)
SA surface area (cm2)
AF soil to skin adherence factor (mg/cm2)
ABS absorption (percent)
EF exposure frequency (event/yr)
ED exposure duration (yrs)
CF conversion factor (10~6)
BW body weight (kg)
AT averaging time (days)
C.2.1 Wading/Exposure Frequency (EF)
The frequency of coming into contact with the sediment will depend on age. Most likely
children, or individuals under 18, will have a greater number of events of coming into contact
with sediment than adults. Reasonable ranges of event frequency were estimated to be one to
two per year for adults and five to ten each year for children, based on best professional
judgement.
C.2.2 Exposure Duration/Averaging Time (ED and AT)
Assumptions for exposure duration and averaging time reflect the time period in question.
Table C-3 (and Table 5-11 ) give the values used in the exposure assessment. For example,
carcinogenic effects are extrapolated over a 70 year period, and in this case the exposure
duration in 30 years. The averaging time is 365 days times thirty or 10950 days.
C-3
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C.2.3 Surface Area (SA)
For this exposure pathway, age specific surface areas for hands and feet were obtained from
standard default exposure factors (USEPA 1991a). Surface area for skin was limited to hands
and feet. A typical exposure involved individuals with shoes on, a reasonable maximum
exposure scenario would involve an individual barefooted.
C.2.4 Absorption (ABS) / Permeability Constant (PC)/ Adherence Factor (AF)
The sediments in this area are very oily, which could act to either increase or decrease
absorption. To account for this, a range that spanned low end possible to higher conservative
values was used. Method One only uses PC to estimate partitioning of sediment contaminants
to water and then the absorbed doses to skin. Method Two utilizes both ABS and AF.
Absorption percent estimates the concentration of chemical absorbed directly from sediment.
The Adherence Factor estimates the amount of sediment that may adhere to the skin, for this
study AF was assumed to be two, (according to the US EPA Risk Assessment Guidance for
Superfund and best professional judgment, this is the average of 2 AF's given for soil in the
before mentioned guidance document).
C.2.5 Body Weight (BW)
Body weight values are age dependent; default EPA values were considered acceptable. For
children and teenagers, 36 kilograms is the default value and for adults the value used was 69
kilograms.
C-4
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TABLE C-3:
PARAMETERS USED IN ESTIMATING DERMAL EXPOSURE
TO CONTAMINATED SEDIMENTS IN THE EAST BRANCH THE
GCR/IHC AOC
Variable
K^
ED
SA
EF
BW
TOC
ABS
PC
CF
CS
CW
AT
AF
Units
---
years
cm2
event/yr
kg
%
""-
cm/hr
L/cm3
kg/mg
mg/kg
mg/L
days
mg/cm2
Value Used
524807 PCBs
891251 BaP*
10
30
817
1220
5- 10
1 -2
36
69
2.6
1
.0316
.001
.000001
681
29
5.00E-02 cPAH
2.13E-03 PCBs
3650
10950
1
Comment
Partitioning constant
for children and teenagers
for adults
children & teenagers
adults
range for children/teenagers
range for adults
children & teenagers
Adults
percent total organic C
absorption (study
assumption)
permeability constant (Flynn 1990,
see references)
Method 1 conversion factor
Method 2 conversion factor
total PAHs
total PCBs
(Floyd Brown, Jan. 1993)
CS =CW
K^* TOC
for children & teenagers
for adults
adherence factor for soil to skin
(study assumption)
*Benzo[a]pyrene was assumed to be representative for all carcinogenic PAHs
C-5
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C.3 RISK
Risk can be characterized by combining the exposure and toxicity estimates into an integrated
expression of human health risk. This section presents the calculated potential human health
risk associated with dermal absorption of contaminants from sediments in the East Branch of
the Grand Calumet River.
Carcinogenic risks are estimated as the incremental probability of an individual developing
cancer over a lifetime as a result of exposure to the potential carcinogen. Increased risk from
all of the above chemicals (PCBs and PAHs), was calculated by multiplying exposure by the
oral slope factor, [for cPAHs the slope factor is 7.3 and 7.7 for PCBs] representing toxicity,
for the carcinogenic endpoint. Refer to Section 7.2 for an additional discussion of how risk is
calculated. The risk estimates for Method One and Two are given in Table C-4.
TABLE C-4:
SUMMARY OF CARCINOGENIC RISK RANGE RESULTING FROM
DERMAL EXPOSURES TO SEDIMENTS IN EAST BRANCH OF GCR/IHC
AOC
METHOD &
COMPOUND
CARCINOGENIC RISK
Compounds
Method 1 cPAHs1:
PCBs:
TOTAL:
Method 2 cPAHs:
PCBs:
TOTAL:
CHILDREN &
TEENS
2.97E-7 to 5.94E-7
2.30E-8 to 4.60E-8
3.1E-7 to6.4E-7
4.42E-4 to 8.83E-4
1.98E-5 to 3.97E-5
4.6E-4 to 9.21-4
ADULTS
1.39E-7 to 2.78E-7
1.08E-8 to 2.15E-8
1.6E-7 to2.9E-7
2.06E-4 to 4.13E-4
9.27E-6 to 1.85E-5
2.1E-4 to43E-4
1 = cPAHs = carcinogenic PAHs
These ranges are based on exposure events of 5 (low) and 10 (high). As one would expect,
method 2 estimates a higher risk than method 1 by three orders of magnitude because method
2 assumes the total concentration of contaminants in the sediments is available for dermal
absorption. Conversely, the porewater method assumes a partitioning between the
contaminants bound to the sediments and the porewater and that the exposure will be from
porewater, not sediment. Actual carcinogenic risk may lie somewhere in between these two
methods' predictions. Method 2 clearly generates risk estimates of concern (1E-4), and
method 1, while not in the E-4 to E-6 range, are just outside levels of possible concern.
Taken together, the two methods might represent the bounds in which actual risk may lie and
indicates that dermal exposure to sediments may result in a health risk, even at relatively low
levels of exposure.
C-6
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C.4 UNCERTAINTY
In addition to the previously mentioned applicable uncertainties, this exposure pathway and
accompanying risk assessment has specific uncertainties associated with it. They include: (1)
the assumption that the exposure,has a fairly regular pattern, even though infrequent, (2) that
contaminants will be absorbed through the skin, and (3) that there may be great variability
between individuals and groups. This last uncertainty could not be considered given that age
specific (or any other factors) absorption data is not available.
C-7
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