PA-905/4-88-005 C. 1 United States Regions EPA-905/4-88-005
Environmental Protection 230 South Dearborn Street April 1988
Agency Chicago, Illinois 60604
G
Risk Assessment for
Dioxin Contamination
Midland, Michigan
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FINAL
RISK ASSESSMENT FOR DIOXIN CONTAMINATION
AT MIDLAND, MICHIGAN
Second Edition
April 1988
REGION V
U.S. ENVIRONMENTAL PROTECTION AGENCY
CHICAGO, ILLINOIS
U.S. Environmental Protection Agency
Region 5, Lihrary (5PL-16)
230 S. Dearborn Street, Room 1670
Chicago, IL 60604
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ACKNOWLEDGEMENTS
This document was prepared by Ian C.T. Nisbet, Ph.D., of I.C.T. Nisbet &
Company, Inc. (Nisbet), and William M. Mendez, Jr., Ph.D., and William Phillips,
M.S., of ICF-Clement Associates, Inc. (ICF), incorporating substantial portions,
and generally following the design, of an extensive initial draft written by
Donald G. Barnes, Ph.D., Science Advisor to the USEPA Assistant Administrator
for Pesticides and Toxic Substances. After the lead responsibility for
production of the document was assumed by Nisbet and ICF, Dr. Barnes retained a
major role in the project, providing important input to each of the succeeding
drafts. The participation of ICF and Nisbet was made possible through the
CERCLA (Superfund) REM III Program, Contract Number 68-01-7250, Work Assignment
Number 172-52G1.
The primary authors drew on certain preliminary USEPA assessments of the Midland
contamination and benefited from numerous thoughtful reviews and comments by
technical experts in several Agency offices (unless otherwise noted, all persons
mentioned are USEPA staff members). The initial Midland risk evaluation work by
Milton Clark, Region V Pesticides and Toxic Substances Branch, and the
assessment of Midland air exposure risks performed for Region V by David
Cleverly, Office of Air Quality Planning and Standards, were important
resources. Along with several suggestions from Larry Fink, Great Lakes National
Program Office, this material facilitated the early stages of the process.
Clark continued to provide helpful toxicological insights from a Regional
perspective through the remaining phases of the project.
Howard Zar, Chairman of the Region V Dioxin Task Force, provided Regional policy
guidance and overall project direction. Gary Amendola, Region V Eastern District
Office, in addition to directing the Michigan Dioxin Studies, contributed to
many aspects of the risk assessment, helping to maintain correct technical
progress.
Valuable comments on the early drafts were provided by the Agency's Chlorinated
Dioxins Work Group. Other USEPA reviewers who made important contributions, in
addition to those named above, included Renate Kimbrough, Headquarters Office of
Regional Operations; Michael Callahan, John Schaum, and other staff of the
Office of Health and Environmental Assessment in Headquarters and Cincinnati;
and a number of Region V staff including Nagib Ali, David Barna, Daniel
Bicknell, Donald Bruce, Rebecca Calby, Harriet Croke, Cynthia Fuller, Carlton
Nash, Walter Redmon, Martin Trembly, and Carol Witt.
The Agency for Toxic Substances and Disease Registry and the Centers for Disease
Control reviewed the final draft and provided many useful comments.
Jonathan Barney, Region V Water Division, served as project officer
and managing editor throughout the risk assessment, assisting the authors
through coordination and integration of reviewers' comments and detailed review
and revision of critical data and text.
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Table of Contents
List of Tables v
List of Figures vii
Preface ix
I. Introduction 1-1
A. History of CDD/CDF Contamination at Midland . 1-2
B. Risk Assessment Structure and Methods 1-8
II. Hazard Identification and Dose-Response Assessments II-l
A. Cancer 11-4
1. Hazard identification for 2378-TCDD II-4
2. Dose-response assessment for 2378-TCDD II-5
B. Reproductive and Teratogenic Effects II-8
1. Hazard identification for 2378-TCDD II-8
2. Dose-response assessment for 2378-TCDD . II-9
3. Other Toxic Effects 11-11
C. Hazard Identification and Dose-Response
Assessments for Mixtures of CDDs/CDFs,
Including 2378-TCDD 11-14
1. Carcinogenicity 11-14
2. Reproductive/Teratogenic Effects 11-15
3. Other Toxic Effects 11-16
4. Toxicity Equivalence Factors 11-16
D. Risk Assessment of CDD/CDF Mixtures 11-20
III. Exposure Assessment III-l
A. Introduction III-l
B. Exposures to CDDs/CDFs In Air III-3
1. Background III-3
2. Ambient monitoring data III-4
3. Stack emissions data 111-16
4. Comparison of stack emissions and ambient
air sampling results 111-21
5. Populations at risk of ambient air exposure 111-31
6. Exposure estimation 111-32
a. Exposure Scenario 1:
Fence Line Case 111-33
b. Exposure Scenario 2:
Residential Area Case 111-37
c. Intake Assumptions 111-40
7. Exposure Estimate from Incinerator Emissions Data. .111-44
8. Limitations of the air exposure assessment 111-46
a. Data limitations 111-47
b. Limitations of models and methods used
to estimate exposures 111-49
C. Soil 111-53
1. CDD/CDF concentrations in soils 111-53
2. Populations at risk and exposure assumptions . . . .111-67
3. Data limitations 111-76
D. Water 111-79
1. CDD/CDF concentrations in water 111-79
a. Surface water supplies 111-79
b. Potable ground water supplies. 111-81
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c. Dow Midland Brine Operations 111-85
2. Populations at risk 111-88
E. Fish 111-91
1. CDD/CDF residue levels 111-92
2. Populations at risk and exposure assumptions ... III-104
3. Other contaminants III-108
4. Data limitations III-112
a. Fish III-112
b. Analysis for CDDs/CDFs III-115
c. Populations at risk III-115
F. Other Routes of Exposure III-117
1. Exposure to indoor dust III-117
2. Ingestion of vegetables grown in
contaminated soils III-118
3. Ingestion of meat and dairy products III-119
4. Exposure of infants via breast milk III-119
IV. Risk Characterization IV-1
A. Introduction IV-1
B. Summary of Hazard Identification and Dose-Response
Assessment for CDDs/CDFs IV-1
1. Cancer risk assessment IV-2
2. Non-cancer risk assessment IV-3
C. Risks Associated with Exposure to
CDD/CDF Contaminated Air IV-6
D. Risks Associated with Exposure to
CDD/CDF Contaminated Soil IV-9
E. Risks Associated with Exposure to
Water and Brine Sediments IV-13
F. Risks Associated with Consumption of Fish IV-13
G. Estimates of Risks from Other Routes of Exposure IV-18
H. Integrated Risk Characterization IV-19
V. References • . V-l
Appendix A. Population At Risk A-l
Appendix B. Other Toxic Pollutants Present in Fish B-l
Appendix C. Glossary C-l
Appendix D. Brominated Compounds D-l
Appendix E. Possible Hazards to Wildlife E-l
IV
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LIST OF TABLES
Table 1-1 A Compilation of the Commercially Significant
Chlorophenolic Compounds Reported to Have Been
Manufactured at the Dow Midland Facility 1-5
Table II-1 Toxicity Equivalence Factors (TEFs) for CDDs/CDFs . . . .11-18
Table III-l Wind Data--Ambient Air Sampling Program
Midland, Michigan--September 7-27, 1984 III-7
Table III-2 Concentrations (pg/m ) of CDDs/CDFs Detected
in Midland Ambient Air, September 8, 12, and
22, 1984--Site 1. . , IH-9
Table III-3 Concentrations (pg/m ) of CDDs/CDFs Detected
in Midland Ambient Air, September 8, 12, and
22, 1984--Site 2. 111-10
Table III-4 Concentrations (pg/m ) of CDDs/CFs Detected
in Midland Ambient Air, September 8, 12, and
22, 1984--Site 3. III-ll
Table III-5 Concentrations (pg/m ) of CDDs/CFs Detected
in Midland Ambient Air, September 8, 12, and
22, 1984--Site 4. . 111-12
Table III-6 Concentrations (ng/m ) of CDDs/CDFs In Chemical
Waste Incinerator Emissions--August/September 1984. . . .111-19
Table III-7 Concentrations (ng/m ) of CDDs/CDFs In Chemical
Waste Incinerator Emissions--June 25, 1987 111-20
Table III-8 Ratio of Selected Homologues to Total CDD and
CDF Levels in Midland Ambient Air, Incinerator Stack
Emissions, and Soil Data from Midland Public
Areas and Minnesota National Areas Ill-28
Table III-9 Average CDD/CDF Levels in Air, and Toxicity
Equivalents for Monitoring Sites 2 and 4 III-34
Table III-10 Average CDD/CDF Levels in Air, and Toxicity
Equivalents for Monitoring--Site 3 111-38
Table III-ll Physiologic Parameters for Inhalation Intake
Estimation 111-42
Table III-12 Exposure Levels and Doses of CDD/CDF Toxicologic
Equivalents (TEQs) Calculated for Ambient Air Exposure
Scenarios Ill-43
Table III-13 PCDDs and PCDFs in Midland, Michigan Area
Surface Soil Samples--Upwind and Dow Chemical In-plant. .111-54
Table III-14 PCDDs and PCDFs in Midland, Michigan Area
Surface Soil Samples--Public Use Areas 111-55
Table III-15 2378-TCDD in Dow Chemical Midland Plant Surface
Soil Samples 111-56
Table 111-16 2378-TCDD in Midland, Michigan Area Surface
Soil Samples 111-57
Table 111-17 2378-TCDD in Midland, Michigan Area Surface
Soil Samples 111-58
Table III-18 2378-TCDD Toxicity Equivalents (TEQs) in Surface
Soil Samples 111-68
Table 111-19 Assumptions Used When Calculating Intakes of
CDDs/CDFs by Residents Exposed to Soils 111-74
Table 111-20 Intakes of CDDs/CDFs Associated with Exposure of
v
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Table
Table
Table
Table
Table
Table
Table
Table
Table
III-21
111-22
111-23
111-24
111-25
111-26
111-27
111-28
111-29
Table III-30
Table III-31
Table 111-32
Table 111-33
Table IV-1
Table IV-2
Table IV-3
Table IV-4
Table IV-5
Table IV-6
.111-86
.111-89
Residents to Soils Downwind of the Dow Midland Facility .111-75
Midland Area Ground Water Samples-2378-TCDD--
December 3-5, 1984 111-83
Midland Area Ground Water Samples-2378-TCDD--
June 12, 1985 111-84
Midland Area Ground Water Samples-2378-TCDD--
September 3, 1985
CDDs/CDFs Detected in Brine Pond Sediments
Tittabawassee River Native Fish Collections--2378-
TCDD--1978-1985 111-93
Tittabawassee River Native Fish Collections--Trends
in 2378-TCDD Concentrations 111-97
Tittabawassee River Native Fish Collection--PCDDs
and PCDFS--1985 111-99
Tittabawassee River Fish--2378-TCDD Toxicity
Equivalents (Partial TEQs)--1985 III-101
Tittawassee River Fish Downstream of Dow Chemical
Plant. 1983-1987 Data. 2378-TCDD and Partial
TEQs III-103
Tittabawassee River Fish. Comparison of Partial
TEQs over Different Years Ill-105
Scenarios for Exposure to CDDs/CDFs from Consumption
of Tittabawassee Fish Ill-109
Single-Meal (Bolus) Intakes of CDDs/CDFs from
Consumption of Tittabawassee River Fish Ill-110
Relative Intakes of Fish by Children and Adults .... Ill-111
Risk Characterization for Inhalation of CDDs/CDFs
in Ambient Air in Midland
Risk Characterization for Ingestion of CDDs/CDFs in
Soil in Midland
Risk Characterization for Ingestion of CDDs/CDFS
in Fish from the Tittabawassee River
Risk Characterizatin for Ingestion of CDDs/CDFs in Fish
from the Tittabawassee River. Short-Term Exposures . .
Summary of Upper-Bound Estimates of Cancer Risk
Estimates from exposure to CDD/CDF Contamination in
Midland, Michigan IV-20
Summary of Hazard Indices for Non-Cancer Effects from
Exposure to CDD/CDF Contamination in Midland, Michigan. . IV-21
. IV-8
. IV-11
. IV-14
. IV-17
VI
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LIST OF FIGURES
Figure 1-1 Midland, Michigan, Area and Dow Midland Facility 1-3
Figure III-l Dow Midland Facility Boundaries,
Chlorophenol Production Areas, Incinerator
Building and Ambient Air Monitoring Locations Ill-5
Figure III-2 Profile of CDDS/CDFs Detected in Midland, MI
Ambient Air--Site 1 111-22
Figure III-3 Profile of CDDS/CDFs Detected in Midland, MI
Ambient Air--Site 2 111-23
Figure III-4 Profile of CDDS/CDFs Detected in Midland, MI
Ambient Air--Site 3 111-24
Figure III-5 Profile of CDDS/CDFs Detected in Midland, MI
Ambient Air--Site 4 111-25
Figure III-6 Profile of CDDs/CDFs in Chemical Waste Incinerator
Emissions 111-26
Figure III-7 Surface Soil Sampling Locations: Midland, Michigan . . .111-60
Figure III-8 Patterns of CDDs/CDFs Detected in Soils Upwind of
the Dow Midland Facility 111-62
Figure III-9 Patterns of CDDs/CDFs Detected in Soils of the
Dow Midland Facility 111-63
Figure III-10 Patterns of CDDs/CDFs Detected in Midland
Public Use Area Soils Downwind of the Dow Midland
Facility 111-65
Figure III-11 Public Water Supply Intakes for Saginaw Bay Ill-80
Figure 111-12 Potable Groundwater Sampling Locations 111-82
Figure III-13 Dow Midland Facility Brine System Ill-87
Figure III-14 Fish Sampling Locations: Midland, Michigan Area Ill-95
Figure III-15 Tittabawassee River Native Fish Collection--
2378-TCDD--1983 and 1985 111-98
Figure IV-1 Upper-Bound Cancer Risks Associated with Consumption
of CDD/CDF Contaminated Fish from the Tittawabassee
River IV-15
vii
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PREFACE
The second edition is identical to the first, which was dated March 1988,
except for the following corrections:
Explanatory footnotes have been added on pages III-106 and III-107,
and footnotes d and f to Table 111-31 on page III-109, have been
amended accordingly.
ix
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PART I
INTRODUCTION
Chlorinated dibenzo-p-dioxins and dibenzofurans (CDDs and CDFs,
respectively; see Appendix C for discussion of nomenclature used in this
report) are families of toxic and persistent organic chemicals which are formed
as side products in certain commercially significant chemical reactions, and
during high temperature decomposition and combustion of certain chlorinated
organic chemicals. Over the past decade, the United States Environmental
Protection Agency (USEPA) has become increasingly concerned about the presence
and significance of environmental levels of CDDs/CDFs. USEPA's initial
concern, in the 1970's, was focused on 2,3,7,8-tetrachlorodibenzo-p-dioxin
(2378-TCDD) (known to be an impurity in certain chlorinated phenolic chemicals,
including the herbicide, 2,4,5-T) which had demonstrated reproductive toxicity
and carcinogenic activity in animal systems at very low doses. Many later
studies (see Part II) have shown that other compounds sharing the same general
structure (dibenzo-p-dioxin or dibenzofuran substituted with two or more
chlorine atoms) also share the same general toxic properties of 2378-TCDD,
although their degree of toxicity is lower.
In the late 1970's, evidence of environmental contamination with CDDs/CDFs
in the Midland area came to light, prompting a series of investigations of the
sources and levels of contamination and analyses of the potential risks to the
health of individuals living in and around Midland. The investigations were
undertaken by the USEPA and the Michigan Departments of Natural Resources
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(MDNR) and Public Health (MDPH). The Dow Chemical Company, which operates a
large chemical production facility in Midland (the Michigan Division of Dow
Chemical U.S.A., hereafter referred to as the Dow Midland facility), was
suspected of being the major source of the contamination. Dow Chemical also
conducted investigations of dioxins in and around the Dow Midland facility.
This report presents the results of analyses conducted by the USEPA of the
potential risks associated with exposure to CDDs/CDFs in the environment in and
around Midland. In conducting this analysis, the authors have drawn on studies
performed by USEPA and its contractors, the State of Michigan, and Dow, in an
attempt to synthesize all the available data regarding risks and exposures and
to present the most comprehensive assessment possible.
A. History of CDD/CDF Contamination at Midland
The Dow Midland facility is a large chemical manufacturing complex
encompassing about 1,500 acres along both banks of the Tittabawassee River at
Midland, Michigan (Figure 1-1). Throughout its history, Dow Chemical has
manufactured over 1,000 different inorganic and organic chemicals at the
Midland facility, including cyclic intermediates, industrial organic and
inorganic chemicals, plastic materials, synthetic resins, nonvulcanized
elastomers, medicinal chemicals, surface active agents, finishing agents,
sulfonated oils, insecticides, herbicides, and formulated pesticides. The
manufacture of chlorinated phenols and herbicides, and the formulation of
pesticides and other products derived from them have been major operations at
the Dow Midland facility for many years. Commercial production of chlorinated
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x^4x£'' ptvr : r"'l\
M-i U
Facility Boundary
. _
Figure 1-1
Midland, Michigan Area and
Dow Midland Facility
Sources: USGS (1973),
Dow (1984)
Scale in feet
0 WOO 2000 3000
1-3
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phenols began in the 1930's and continued at substantial levels into the
1970's. Dow Chemical reports that only two chlorinated phenolic products are
currently manufactured (Dow 1984):
• 2,4-dichlorophenol, and
• 2,4-dichlorophenoxyacetic acid (2,4-D).
Production of all other chlorinated phenolic intermediates and products
was terminated in the late 1970's. A list of chlorinated phenolic compounds
that have been produced at the Dow Midland facility is presented in Table 1-1.
The Dow-Corning plant (not known to have been involved in the production of
chlorinated phenols or their derivatives) is adjacent to the Dow Midland
facility to the east. The main residential and commercial areas of the city
are located to the north and the northeast of the Dow Midland facility.
In June 1978, the Dow Midland facility informed the MDNR that rainbow
trout exposed to a mixture of Dow Chemical's treated effluent prior to
discharge from outfall 031 to the Tittabawassee River accumulated significant
levels of 2378-TCDD, the most toxic of the CDD/CDF compounds. Supplemental
analyses of edible portions of Tittabawassee River native catfish, previously
collected in 1976 downstream of the discharge from the Dow Chemical facility,
showed concentrations of 2378-TCDD ranging from 70 to 230 parts per trillion
(ppt). Fish collected upstream of the facility, above Dow Dam, did not contain
detectable levels of 2378-TCDD. The results of these studies prompted the
Michigan Department of Public Health to issue a formal advisory in June 1978
warning against consumption of any fish collected from the Tittabawassee River
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TABLE 1-1
A COMPILATION OF THE COMMERCIALLY SIGNIFICANT CHLOROPHENOLIC
COMPOUNDS REPORTED TO HAVE BEEN MANUFACTURED AT
THE DOW MIDLAND FACILITY
Chlorophenols
2-chloropheno1
4-chlorophenol
2,4-dichlorophenol
2,4,5-trichlorophenol
sodium 2,4,5-trichlorophenate
zinc 2,4,5-trichlorophenate
2,4,6-trichlorophenol
sodium tetrachlorophenate
2,3,4,6-tetrachlorophenol
pentachloropheno1
sodium pentachlorophenate
Chlorophenoxy Derivatives
2,4-dichlorophenoxyacetic acid (2,4-D)
2-(2,4-dichlorophenoxy)-propanoic acid
2-methyl-4-chlorophenoxyacetic acid
2,4,5-trichlorophenoxyacetic acid (2,4,5-T)
2-(2,4,5-trichlorophenoxy)-propanoic acid
Other Chlorophenol Derivatives
2-(2,4,5-trichlorophenoxy) ethanol
2-(2,4,5 -trichlorophenoxy)-ethyl-2,2-dichloropropanoate
0,0-dimethyl-0-(2,3,5-trichlorophenyl) phosphorothioate
2 -cyclopenty1-4 -chlorophenol
4-1-butyl- 2 -chlorophenol
4-1-butyl- 2 -chlorophenyl-methyl-N-methy1-phosphoramidate
chlorinated phenylphenols
chlorinated diphenyl oxide derivatives
Source: Dow 1984.
a2,4-dichlorophenol and 2,4-D are the only compounds from this list that
are currently being manufactured on the Midland plant site.
These chlorophenoxy acid derivatives have also been converted into
various water soluble salts.
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downstream of Dow Dam. (The advisory remained in effect until March 1986, when
the Department of Health modified it to apply only to catfish and carp.)
In response to the Dow Chemical findings, the MDNR and USEPA, Region V
undertook a number of investigations during the period 1978-1981 to determine
whether, or to what extent, the Dow Chemical operations at Midland contributed
to 2378-TCDD contamination in Tittabawassee River fish. These investigations
included a caged fish bioaccumulation study and an experimental large volume
wastewater effluent sampling program conducted in September 1981. The results
of those studies conclusively demonstrated that the Dow Chemical wastewater
effluent was a significant source of 2378-TCDD to the Tittabawassee River. The
preliminary results from those studies were released in March 1983 with a
series of recommendations for more comprehensive dioxin studies in Midland and
elsewhere. Most of those recommendations were subsequently incorporated into
USEPA's Dioxin Strategy and National Dioxin Study (USEPA 1983b, 1987a)
Also, in March 1983, the State of Michigan made a formal request to the
then acting administrator of USEPA for assistance in conducting a comprehensive
multi-media investigation of dioxin emissions and discharges from Dow Chemical
and dioxin contamination in the Midland area. In the spring and summer of
1983, Region V collaborated with the Michigan Departments of Agriculture,
Natural Resources, and Public Health, and the Michigan Attorney General's
Office in planning for the requested studies. At about the same time local
environmental groups petitioned USEPA pursuant to Section 8(e) of the Toxic
Substances Control Act for broad scale toxic pollutant investigations of an
eight-county area in mid-Michigan including Midland County. Although USEPA
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subsequently denied that petition, some of the requested investigations were
within the scope of those being planned by Region V and the state agencies.
The studies conducted by USEPA and the State were formally called the
Michigan Dioxin Studies and included the following major programs:
1. Supplemental native fish and sediment sampling in the Tittabawassee
River.
2. Surface soil sampling at the Dow Chemical facility, in the City of
Midland, and in comparison sites.
3. Evaluation of public and private potable water supplies and Dow
Chemical brine operations.
4. Supplemental Dow Chemical wastewater and sewer system sampling.
5. Incinerator emissions and limited ambient air monitoring.
These investigations included analyses of dioxins and other toxic
pollutants that might be present, and were consistent with the then-evolving
USEPA Dioxin Strategy. Since the Dow Chemical Plant was considered to have
operations within Tiers 1, 2, 3, 4, and 6 of the Dioxin Strategy, funding for
the studies was provided principally through the CERCLA (or Superfund) program.
All Tier 1 and 2 facilities in the Dioxin Strategy were studied through
Superfund.
In 1983, Dow Chemical initiated its own independent point source
investigation of dioxins at the Midland Plant. That work included
comprehensive surface soil sampling at the plant, untreated and treated process
wastewater sampling, incinerator emissions testing and limited ambient air
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monitoring. Dow Chemical has also conducted supplemental incinerator emissions
testing in 1987, supplemental monitoring of Tittabawassee River fish in
response to a consent order with USEPA, and twice monthly monitoring for
2378-TCDD in the process wastewater discharge to the Tittabawassee River.
Studies by Dow and USEPA revealed widespread contamination of the surface
soil at the Midland facility (average of 0.5 ppb 2378-TCDD). Several small
areas within the facility were found to be highly contaminated (2-50 ppb).
USEPA studies indicated lower level contamination of the soils throughout the
community, with CDDs/CDFs (average <0.1 ppb 2378-TCDD). Since these studies
were undertaken, Dow has been ordered to remediate areas of high onsite
contamination to prevent the spread of contaminated soil. The source of the
on-site soil contamination appears to have been a combination of leaks or
fugitive emissions from one or more of the production processes discussed above
and fallout from the .waste incinerator. The off-site soil contamination has
been attributed to airborne emissions of CDDs/CDFs from the waste incinerator,
wind-borne transport of contaminated soil from the facility, and possibly past
fugitive emissions from production operations.
B. Risk Assessment Structure and Methods
The USEPA has compiled the data from its testing program (USEPA 1985a,
Barna and Amendola 1985, Amendola and Barna 1986, Trembly and Amendola 1987)
and, in this document, presents its assessment of these data as they reflect on
I-f
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the risks posed by the CDDs/CDFs in the areas sampled. This report builds on
preliminary studies prepared by other offices (Clark 1985, Cleverly 1986).
This document follows the conceptual fiamework for risk assessment
articulated by the USEPA Guidelines for Carcinogen Risk Assessment (USEPA
1986a) and Guidelines for Estimating Exposures (USEPA 1986b). It is also
consistent with the 1983 report of the National Academy of Sciences (NAS),
"Risk Assessment in the Federal Government: Managing the Process" (NRG 1983).
As envisioned by the NAS and USEPA Guidelines, risk assessment contains four
parts: hazard identification, dose-response assessment, exposure assessment,
and risk characterization. In keeping with this scheme, Part II of this report
contains a brief summary of the Hazard Identification and Dose-Response
Assessment of CDDs/CDFs, referring to other agency documents for elaboration.
Part III describes the site-specific Exposure Assessment for each of the
contaminated media, based on the data derived from the USEPA field
investigations in Midland, and Part IV, Risk Characterization, integrates the
information from Parts II and III to develop quantitative estimates of risks
faced by the exposed populations. Part III also includes a discussion of the
uncertainties associated with the estimates of exposure, and Part IV includes a
discussion of the uncertainties associated with the estimates of risk.
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PART II
HAZARD IDENTIFICATION AND DOSE-RESPONSE ASSESSMENT
The USEPA and other organizations have compiled and evaluated the existing
toxicological data on CDDs and CDFs (e.g., USEPA 1984a, 1985b, Ontario Ministry
of the Environment (Ontario) 1984). Although there is extensive literature on
some of these compounds, the toxicological information on these families of
more than 200 compounds is far from complete. Nevertheless, a growing body of
information on mechanisms of action and structure-activity relationships within
these families of compounds makes it possible, with reasonable confidence, to
infer information where data are missing.
Among the 210 congeners of CDDs and CDFs, the compound that appears to be
the most toxic and has generally raised the greatest health concerns is
2,3,7,8-tetrachlorodibenzo-p-dioxin, abbreviated as 2378-TCDD. Experimental
studies with 2378-TCDD in animal systems have demonstrated a variety of toxic
effects resulting from exposure to this compound (USEPA 1985b). These effects
include carcinogenesis, cancer promotion, reproductive and teratogenic effects,
immunotoxic effects, thymus atrophy, liver damage, and effects on the skin and
thyroid. Acute exposures of sensitive species of animals to 2378-TCDD result
in a characteristic "wasting syndrome," followed by death. Extensive
experimental studies have revealed marked variations among species in both the
array of effects caused by 2378-TCDD and the dose levels at which these effects
are elicited (USEPA 1985b, Pitot et al. 1986). Limited toxicological testing
of other CDDs/CDFs has demonstrated that several of these compounds cause
similar toxicological effects, but that higher doses of these compounds are
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generally required to cause effects of comparable magnitude to those induced by
2378-TCDD.
The nature and extent of effects in humans exposed to 2378-TCDD are not
nearly so well defined (USEPA 1985b, Ontario 1984, Pitot et al. 1986). There
is a consensus that exposure of humans to 2378-TCDD can result in a skin
condition known as chloracne, an acne-like lesion which, while not
life-threatening, can be disfiguring, persistent, and refractory to treatment.
Several studies of human populations exposed to chemical mixtures containing
2378-TCDD have suggested increased frequencies of certain cancers (e.g.,
Hardell and Sandstrom 1979, Hardell et al. 1981, Thiess et al. 1982, MDPH
1983a, Hoar et al. 1986), but inconsistencies among the studies and incomplete
characterization of exposure make the evidence, taken as a whole, inconclusive
(USEPA 1985b, Blair 1986). Evidence for reproductive impairment in humans
exposed to 2378-TCDD (including one study conducted in Midland County: MDPH
1983b) is inconclusive for similar reasons (USEPA 1985b, Kimbrough 1986).
Other effects in humans that have been more clearly associated with exposure to
mixtures containing 2378-TCDD include disturbances in lipid metabolism (Moses
et al. 1984, Suskind and Hertzberg 1984) and increased frequency of gastric
ulcers (Bond et al. 1983, Suskind and Hertzberg 1984).
More specific and quantitative information is available on toxic effects
of CDFs in humans, as a result of two large-scale poisoning incidents in Japan
and Taiwan (Kuratsune and Shapiro 1984). The affected persons ingested, over
periods of weeks to months, food contaminated with a mixture of CDFs,
polychlorinated biphenyls (PCBs) and polychlorinated quaterphenyls (PCQs).
II-2
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Comparative toxicological studies have indicated that CDFs were the primary
toxic agents in these poisoning incidents and that 23478-PeCDF was probably the
most important single compound (Masuda and Yoshimura 1984, Kunita et al. 1984,
1985, Bandiera et al. 1982, Masuda et al. 1985, Chen et al. 1985, Miyata et al.
1985). The most prominent toxic signs were skin eruptions similar to those of
chloracne, along with skin pigmentation and eye abnormalities (Lu and Wong
1984, Urabe and Asahi 1985). Other effects reported include impairments in
lipid metabolism and immune function (Okumura et al. 1974, Chang et al. 1980,
1982) and persistent respiratory symptoms (Nakanishi et al. 1985). A
preliminary report by Kuratsune et al. (1987) indicates a significant excess
frequency of liver cancer and possibly lung cancer among male victims within 15
years after exposure. Reported effects on reproduction include menstrual
disturbances (Kusuda 1971), skin hyperpigmentation in infants (Yamashita and
Hayashi 1985, Hsu et al. 1985), and perinatal mortality (Hsu et al. 1985).
These effects observed in humans are qualitatively similar to those reported in
animals exposed to CDFs and CDDs (McNulty 1985); this provides support for the
use of animal data as the basis for hazard assessment for other members of
these families of compounds.
USEPA has determined that the critical end points of concern for purposes
of assessing risk associated with exposure to CDDs/CDFs from the Midland
facility are cancer and reproductive and teratogenic effects. This portion of
the Risk Assessment briefly summarizes the evidence for these effects for
2378-TCDD (and, in a few cases, other CDDs or CDFs) and discusses how these
data have been used to generate quantitative measures of toxic potency for use
in Dose-Response Assessment. The concluding section discusses how these
II-3
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results have been extended to include other CDDs/CDFs which have not been as
extensively tested.
A. Cancer
1. Hazard Identification for 2378-TCDD
The USEPA Health Assessment Document on CDDs (USEPA 1985b) summarized the
results of several long-term animal studies in which 2378-TCDD has been
investigated as a possible carcinogen. The principal studies provide clear
evidence for the conclusion that 2378-TCDD is an animal carcinogen (Kociba et
al. 1978, NTP 1982a, NTP 1982b). These data show that exposure of rats and
mice to 2378-TCDD at very low doses is related to the development of tumors at
a variety of sites, principally and most consistently in the liver.
On the basis of these animal studies and associated factors, such as
short-term tests and structure/activity considerations, USEPA has concluded
that 2378-TCDD should be regarded as a potential human carcinogen (USEPA
1985b). This substance has been assigned a designation of "B2" in USEPA's
scheme of categories for qualitative weight-of-evidence of carcinogenic
potential. This designation is given to agents for which there is "sufficient"
evidence of carcinogenicity based on animal studies and "inadequate" data
regarding carcinogenicity from human epidemiologic studies (USEPA 1986a).
II-4
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2. Dose-Response Assessment for 2378-TCDD
USEPA (1985b) has developed a Dose-Response Assessment for 2378-TCDD based
upon data from the study by Kociba et al. (1978). The procedures used by USEPA
are in keeping with its recently published Cancer Risk Assessment Guidelines
(USEPA 1986a) which are consistent with the Cancer Principles laid out by the
Office of Science and Technology Policy in 1985 (OSTP 1985). Briefly, USEPA
employed the linearized multi-stage (LMS) model to estimate an upper bound on
the excess lifetime cancer risk at doses below those used in the animal
experiment. In order to extrapolate from dose-response data in animals to
predict human risk, USEPA used its standard procedure of adjusting relative
doses on a body surface area basis, reflective of relative metabolic rate
(USEPA 1985b).
Applying these procedures, USEPA (1985b) used the experimental animal data
to estimate an upper bound on the cancer potency factor for 2378-TCDD. The
cancer potency factor is equivalent to the slope of the projected linear
dose-response curve in the low-dose region, adjusted to apply to humans. The
upper bound on the cancer potency factor estimated for 2378-TCDD (designated
and referred to as q^*) is 1.6 x 10-> (mg/kg-d)" . The actual potency is not
likely to exceed this upper bound estimate, formally referred to as the upper
95% confidence limit (UCL).
In recent years, several alternative approaches to carcinogenic risk
assessment for 2378-TCDD have been presented by scientists or regulatory
agencies, both in the U.S. (e.g., Miller 1983, Kimbrough et al. 1984, Portier
II-5
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et al. 1984, MDH 1985, MDPH 1986, Hoel 1986, Sielken 1987, Shu et al. 1987,
Thorslund et al. 1987) and in other countries (e.g., Ontario 1984, FRG 1984).
Most of these assessments remain unpublished and have not been peer-reviewed.
In general, they differ from the USEPA dose-response assessment in one or both
of two respects:
• Several assessments that utilized the linearized multi-stage model
incorporated different data or made different assumptions about the
way in which the data should be used. Examples include the use of
different sets of tumor data as the basis for extrapolation
(Kimbrough et al. 1984, Portier et al. 1984), the use of tissue
concentrations as measures of dose (Portier et al. 1984), the use of
mg/kg body-weight scaling (Miller 1983, Kimbrough et al. 1984, MDH
1985, MDPH 1986), or the use of different ways of averaging lifetime
dose (Kimbrough et al. 1984). The most important of these
differences is the use of mg/kg body-weight scaling, which results in
a human cancer potency factor about 6 times lower than that derived
from body-surface-area scaling. Primarily for this reason, estimates
of cancer potency developed by other U.S. agencies (including the
Centers for Disease Control, the Food and Drug Administration, and
the States of Michigan and Minnesota) have ranged from a value near
to the USEPA value to a value about one order of magnitude less
potent (Kimbrough et al. 1984, FDA 1983, MDH 1985, MDPH 1986).
Although the selection of an interspecies scaling factor is a matter
for scientific judgment, the greater retention time of 2378-TCDD in
humans than in rats provides a rationale for the selection of the
more "conservative" body-surface-area scaling factor used by USEPA.
• Several assessments have been based on the assumption that 2378-TCDD
acts primarily as a cancer promoter, and on the further assumption
that cancer promotion is a reversible phenomenon with a threshold-
type dose-response relationship. On the basis of these assumptions,
"acceptable" daily intakes for 2378-TCDD have been proposed by
applying "Uncertainty Factors" to dose-levels thought to be "Lowest-
Observed-Adverse-Effect-Levels" (Ontario 1984, FRG 1984, Shu et al.
1986). Although there is evidence that 2378-TCDD is a potent
promoter and has little propensity to interact with DNA in the manner
of a classical cancer initiator (Pitot et al. 1986), currently
available evidence on mechanisms of cancer promotion does not support
the assumption that promoting activity would be reversible and have a
threshold-type dose-response relationship (Upton et al. 1985,
Weinstein 1984, 1987, Yamasaki and Weinstein 1985, Gallagher 1986).
Goodrow et al. (1986) have reported that cancer promotion by 2378-
TCDD is associated with its binding to receptors associated with the
Ah gene locus and receptors for epidermal growth factor. Other
studies have suggested that binding to one or both of these receptors
results in activation of certain genes (Israel and Whitlock 1984,
Whitlock et al. 1984, Jones et al. 1985, 1986a,b). There is no
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evidence that these molecular mechanisms would necessarily be
reversible and would display threshold-type dose-response
relationships. Even if receptor binding is assumed to be reversible,
the fact that 2378-TCDD is more strongly retained in human tissues
than in those of other animals would have to be taken into account
(Hoel 1986). Finally, the promoting effects of 2378-TCDD might
augment risks resulting from prior human exposure to initiating
carcinogens. At present, there are no accepted models that can be
used to predict low-dose risks resulting from these effects of 2378-
TCDD. Thorslund et al. (1987) have presented preliminary results of
a model in which 2378-TCDD is assumed to act by causing proliferation
of initiated cells, but it has not been demonstrated that this
approach accurately reflects the biochemical mode of action of 2378-
TCDD in cancer causation.
For the above reasons, it remains appropriate to use the dose-response
assessment for 2378-TCDD derived by USEPA (1985b) , based on the linearized
multistage model (LMS) with body-surface-area scaling. Portier et al. (1984)
have reported that available dose-response data fit a linear model if tissue
concentration is used as a measure of dose. USEPA recognizes, however, that
use of the LMS model is controversial at the present time; dose-response
assessment for carcinogenic effects of 2378-TCDD is currently under review by
the Agency, and this review may lead to revision of the cancer potency factor.
Ongoing work on mechanisms of action (Jones et al. 1986a,b, Goodrow et al.
1986), pharmacokinetics (Leung et al. 1987, Van den Berg and Poiger 1987), and
mathematical modeling (Thorslund et al. 1987) will eventually help to resolve
the controversies surrounding cancer risk estimates for 2378-TCDD. Pending
this resolution, it should be recognized that these features of the biological
activity of 2378-TCDD add substantial uncertainty to risk estimates derived
from the LMS model. These estimates are intended to represent upper bounds on
risk and will be reported as such. Even as upper bounds, however, they could
be too high (e.g., if the dose-response relationship is strongly non-linear) or
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too low (e.g., if CDDs/CDFs act to promote cancers initiated by other
widespread environmental carcinogens).
B. Reproductive and Teratogenic effects
1. Hazard Identification for 2378-TCDD
2378-TCDD has been shown to be teratogenic in all strains of mice which
have been tested. Further, this compound has produced teratogenic and
fetotoxic effects in all strains of rats tested. Reproductive effects have
been demonstrated in other species as well, including subhuman primates (USEPA
1985b).
For reproductive effects, USEPA has focused on a three-generation rat
feeding study (Murray et al. 1979) as the critical study for estimating the
non-cancer risk posed by 2378-TCDD. The Centers for Disease Control (CDC) have
cited a reproductive study in monkeys (Allen et al. 1979) as the critical study
(Kimbrough et al. 1984). USEPA (1985b) also cited this study, as well as
another report on the same research (Schantz et al. 1979) in support of their
findings. For teratogenic effects, the critical study is a study in rats
treated with 2378-TCDD, administered daily by gavage on days 6-15 of gestation
(Sparschu et al. 1971).
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2. Dose-Response Assessment for 2378-TCDD
In assessing toxic effects produced by non-carcinogens (i.e., "systemic
toxicants"), USEPA has adopted the concept of the Reference Dose (RfD) (USEPA
1987b). The RfD is operationally defined as the "no observed adverse effect
level (NOAEL)" (i.e., the highest dose level at which no adverse effects were
observed in an experiment using an adequate number of test animals) determined
in the critical toxicological study, divided by an "Uncertainty Factor (UF)"
which is selected on the basis of specific attributes of the data base. (In
some cases, an additional modifying factor (MF) is introduced to account for
peculiarities in the data base.) The RfD can be defined as an estimate (with
uncertainty spanning perhaps an order of magnitude) of the daily exposure to
the human population (including sensitive subpopulations) that is likely to be
without an appreciable risk of deleterious effect during a lifetime. The RfD
supersedes, and is generally equivalent to, the Acceptable Daily Intake (ADI)
values previously used by USEPA and other agencies to define dose levels for
non-cancer endpoints.
There has been some debate as to whether or not a dose of as little as 1
ng/kg-d (1000 pg/kg-d) of 2378-TCDD was a NOAEL in the three-generation
reproductive study in the rat (Murray et al. 1979, Nisbet 'and Paxton 1982,
Kimbrough et al. 1984, USEPA 1985b). USEPA has examined this study in detail
and selected a combined UF of 1000, (including subfactors of 10 because the
lowest administered dose was not a NOAEL, 10 to account for possible
interspecies differences in sensitivity, and 10 to account for possible
intraspecies differences in sensitivity) such that an RfD of 1 pg/kg-d is
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derived (USEPA 1987c). USEPA (1985b, 1987c) also placed weight on the study by
Schantz et al. (1979), which reported adverse reproductive effects in rhesus
monkeys exposed to 2378-TCDD at about 1.5 ng/kg-d, leading to a similar value
for the RfD. As noted above, the CDC selected a different critical study in
deriving their functional equivalent of the RfD, but the CDC scientists
obtained essentially the same value as USEPA, i.e., 1-2 pg/kg-d (Kimbrough et
al. 1984).
In addition to effects associated with low level, long-term exposures to
CDDs and CDFs, USEPA is also concerned about relatively large doses which
pregnant women might ingest at a critical time of organogenesis in the
development of the fetus. A rat gavage study (Sparschu et al. 1971) yielded a
NOAEL of 30 ng/kg-d for these teratogenic effects. USEPA has adopted
procedures to issue "health advisories" (HAs) for exposures associated with
such less-than-lifetime situations. These standard procedures lead to
selection of an UF of 100 (Kimmel 1987) , and hence to a "health advisory" dose-
level of 300 pg/kg-d for protection against teratogenic effects. This HA dose-
level is appropriate for comparison with single-dose or single-day intakes,
whereas the RfD of 1 pg/kg-d is more appropriate for comparison with long-term
or lifetime exposures (see below for further discussion).
Dose-response data for reproductive/teratogenic effects of 2378-TCDD
are well established, and there is a reasonably sound basis for the
establishment of the RfD and the HA. The reports of reproductive impairment in
humans exposed to CDFs add qualitative support for the use of these data in
risk assessment. However, one additional factor may need to be considered.
11-10
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Bowman et al. (1987a,b) have reported apparently adverse reproductive effects
in rhesus monkeys exposed to 2378-TCDD at a dose rate of about 0.125 ng/kg-day,
a factor of 8-10 lower than the previous LOAELs. These reports are presently
available only in abstract form; if confirmed, they may require downward
revision of the RfD.
3. Other Toxic Effects
Although USEPA has determined that reproductive/teratogenic effects are
the critical, noncarcinogenic toxic effects for dose-response assessment of
2378-TCDD, some uncertainty may arise if dose-response data for such effects
are used in risk assessment for persons of non-reproductive age (e.g., for
children or post-menopausal women) or persons who are not reproducing for other
reasons. The RfD is probably applicable to children, both because 2378-TCDD is
retained for periods of years in the body and hence may exert effects long
after exposure occurs, and because germ cells in females are subject to
exposure at any time after they are formed during embryonic development.
However, it is not clear that the HA based on teratogenic effects can be
applied directly to any population group except pregnant women. To reduce such
uncertainty, it is desirable to consider data on other toxic end points of
2378-TCDD. This section briefly considers dose-response data for other toxic
effects of 2378-TCDD, based on the literature review by USEPA (1985b).
Chronic toxicity studies have been conducted in non-human primates, and in
rats and mice. In studies in rhesus monkeys, exposure to a dietary
concentration of 50 ppt 2378-TCDD (about 1.5 ng/kg-day) resulted in hair loss,
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edema and pancytopenia (Schantz et al. 1979). In one study in mice, exposure
by gavage to doses of 10 ng/kg-week 2378-TCDD resulted in a significant
increase in the incidence of toxic hepatitis (NTP 1982a); in another study in
mice, exposure by gavage to doses of 7 ng/kg-week 2378-TCDD resulted in skin
lesions and amyloidosis of the kidney, liver, and spleen (Toth et al. 1978,
1979). All three of these dose-levels were Lowest-Observed-Adverse-Effect
Levels (LOAELs); No-Observed-Adverse-Effect Levels (NOAELs) have not been
reported for chronic exposure to 2378-TCDD in these species (USEPA 1985b). In
rats, USEPA (1985b) reported that 1 ng/kg-day was a NOAEL, but the study on
which this conclusion was based (Kociba et al. 1978) actually reported a
statistically significant increase in foci or larger areas of slight
hepatocellular alterations in female rats at this dose level. On the basis of
the studies cited in this paragraph, doses in the range 1-1.5 ng/kg-day should
be regarded as LOAELs for these effects of 2378-TCDD in animals. This is the
same range of doses as that cited above as LOAELs for reproductive effects in
animals. Hence, it is appropriate to apply the RfD of 1 pg/kg-day to all
individuals in the human population, regardless of their reproductive status.
For acute or subchronic effects of 2378-TCDD, USEPA (1987c) has cited a
study by Turner and Collins (1983) as the critical study for dose-response
assessment. In this study, a single dose of 100 ng/kg administered to female
guinea pigs was a LOAEL, causing histopathologic changes in the liver. USEPA
(1987c) used this LOAEL to derive One-day and Ten-day Health Advisories, by
applying Uncertainty Factors of 100 and 1,000, respectively. These SAB-
reviewed HAs are equivalent to intakes of 280 pg/kg (single dose) and 28 pg/kg-
day (for 10 days), respectively. The former HA is very close to that derived
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above on the basis of teratogenic effects, justifying the application of this
HA to population segments other than pregnant women. The latter HA provides a
basis for risk assessment for subchronic exposures (ranging in duration from a
few days to a few weeks).
In general, RfDs are based on studies involving lifetime exposure of
animals and are formally defined for comparison with lifetime average dose
rates in humans (USEPA 1987b). In the case of 2378-TCDD, the RfD is based on a
three-generation reproductive study in which rats were exposed for two
reproductive cycles, and another study in which rhesus monkeys were exposed for
only 7 months yielded a similar LOAEL (see above). Hence, it is appropriate to
compare this RfD with dose-rates for less-than-lifetime exposure in humans. In
Chapter IV of this report, the RfD for 2378~-TCDD will be compared with average
dose rates for human exposure lasting for several months or longer; the 10-day
HA will be compared with average dose-rates for human exposure lasting for a
few days to a few weeks; the 1-day HA will be compared with single-dose or
single-day intakes.
Although dose-response data for liver effects yield HAs very similar to
those for reproductive/teratogenic effects, one additional factor should be
considered. Immunotoxic effects of 2378-TCDD have been reported at very low
doses (1 ng/kg-week) by Clark et al. (1983). Reports of immune system
impairment in humans exposed to CDFs (Chang et al. 1982a,b) and perhaps in
humans exposed to 2378-TCDD (Hoffman et al. 1986, but see Evans et al. 1987)
suggest that the findings of Clark et al. (1983) are relevant to assessment of
potential human risks. However, there is no precedent or accepted procedure
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for the use of immunotoxicity data in establishing RfDs or HAs. Along with the
preliminary data reported by Bowman et al. (1987a,b), the results of Clark et
al. (1983) suggest that there may be some risk resulting from dose rates at or
even below the RfD or HAs for other toxic effects.
C. Hazard Identification and Dose-Response Assessments for Mixtures
of CDDs/CDFs, Including 2378-TCDD
While the toxicological properties of 2378-TCDD have been reasonably well
characterized, the toxicological data base for the other CDDs and CDFs is
limited. This section summarizes the limited testing of other CDDs and CDFs
for carcinogenicity, cancer promotion and/or teratogenicity.
1. Carcinogenicity
Only six CDD/CDF congeners other than 2378-TCDD have been tested for
carcinogenic activity. In a study reported by NCI (1980), a mixture of the two
2378-substituted-HxCDDs induced liver tumors in rats and mice. Based on this
study, USEPA (1985b) assigned this mixture to the category "B2" in USEPA's
qualitative weight-of-evidence scheme (see definition above) and calculated a
cancer potency factor of 3.9 x 10 (mg/kg-d)~ . In another study conducted by
NCI (1979), suggestive evidence was found for the carcinogenicity of 27-DCDD
when administered at high doses to male mice. In a two-stage bioassay for
cancer promotion on the skin of hairless mice, 2378-TCDF was found to be a
potent cancer promoter, but was about 20 times less potent than 2378-TCDD which
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was tested in the same study (Poland and Knutson 1982, Poland et al. 1983). In
a two-stage bioassay for cancer promotion in rat liver, 23478-PeCDF and
123478-HxCDF were found to be potent cancer promoters, the former being more
potent (Nishizumi and Masuda 1986) .
2. Reproductive/Teratogenic Effects
Only limited testing for teratogenic effects and no testing for other
reproductive effects has been conducted with other CDDs and CDFs. Several
studies have shown that 2378-TCDF induces cleft palates and hydronephrosis in
fetal mice when administered on days 10-13 of gestation (Weber et al. 1984,
Hassoun et al. 1984, Krowke 1986). Krowke (1986) reported that 12378-PeCDD and
123478-HxCDD also caused cleft palates in mice exposed in utero. Birnbaum et
al. (1987a,b) reported that 12378-PeCDF, 23478-PeCDF, and 123478-HxCDF also
caused cleft palates and hydronephrosis in mice exposed in utero. All these
effects were similar to those induced by 2378-TCDD in the same or in parallel
experiments, but 2378-TCDD was the most potent of the compounds tested in all
these respects.
3. Other Toxic Effects
A somewhat larger number of CDDs and CDFs has been tested for acute and
subacute toxic effects, primarily on the liver and thymus (McKinney and
McConnell 1982, Mason et al. 1985, 1986a,b, Safe 1986). These studies have
generally shown that most CDDs and CDFs cause similar effects to those caused
by 2378-TCDD in the same bioassay systems, but that 2378-TCDD is the most
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potent congener among those tested to date in all systems. Further, these
studies have shown structure-activity relationships within both families of
compounds, with a general parallelism between relative potencies in in vivo and
in vitro bioassays (Safe 1986). The results of these studies have suggested a
general approach to risk assessment for these compounds, which can be applied
to complex mixtures of the type commonly found in the environment.
4. Toxicity Equivalence Factors
Given the lack of information on most of the CDDs and CDFs at a time when
reports of these compounds in the environment increasingly call for some type
of interpretation, USEPA has adopted an interim science policy position for
assessing risks of CDDs/CDFs other than 2378-TCDD (USEPA 1987d, Thomas 1987).
The procedure is called the "toxicity equivalence factor (TEF)" approach and,
in the process of gaining USEPA acceptance, underwent internal and external
USEPA review, including examination by the USEPA's Science Advisory Board (SAB
1986). It has been adopted by USEPA as an interim procedure to be used until
sufficient additional data are available to derive a more accurate procedure
that can be scientifically validated. The TEF approach is based on the
similarity of structure and activity seen in the behavior of members of the
CDD/CDF family. This similarity is used as the basis for estimating the
toxicity, with regard to both carcinogenic and non-carcinogenic endpoints, of
any CDD/CDF mixture in terms of an equivalent amount of 2378-TCDD. Within each
homologue group, distinction is made between those CDD/CDF congeners which are
"2378-substituted" (i.e., substituted with chlorine at the lateral 2, 3, 7, and
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8 positions; see Appendix C) and those which are not, and a common TEF is
applied to all congeners in each category as shown in Table II-l. Structure-
activity studies have shown that 2378-substituted congeners are more potent in
a number of assays than non-2378-substituted congeners (Poland et al. 1979,
Mason et al. 1985, 1986a,b, Safe 1986, USEPA 1985b) and the former are assigned
much higher TEFs (USEPA 1987d). In cases where analytical procedures identify
CDDs/CDFs only to the homologue level and do not distinguish between 2378-
substituted and non-2378-substituted congeners, the USEPA's interim procedure
(USEPA 1987d) proposes two alternative procedures:
A. Assume that all CDDs/CDFs are 2378-substituted and apply the TEF for
2378-substituted congeners to the total quantity of each homologue
reported; or
B. Assume that all CDD/CDF congeners are equally likely to occur and
allocate congeners to 2378-substituted and non-2378-substituted
categories in proportion to the numbers of each type of congener
within each homologue group.
The "A-method" yields an "upper bound" estimate of risk. The "B-method"
typically leads to an estimate of risk about an order of magnitude lower,
depending upon the exact mixture of congeners and the quality of the data
regarding the amounts of specific congeners present (USEPA 1987d); it is
appropriate as an alternative method of risk estimation, but does not
necessarily yield a reliable point estimate or "most likely" case because
conditions of formation, persistence, or bioaccumulation may favor unequal
distributions of congeners.
The TEF approach is used in Part III of this report to convert reported
quantities of CDDs/CDFs in environmental samples to equivalent quantities of
2378-TCDD. The resulting concentrations of "2378-TCDD toxicity equivalents"
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TABLE II-1
TOXICITY EQUIVALENCE FACTORS (TEFs) FOR CDDs/CDFs
Congener Group2
TEF
Proportion of
Homologue'3
Total TCDDs
2378-TCDDs
other TCDDs
Total PeCDDs
2378-PeCDDs
other PeCDDs
Total HxCDDs
2378-HxCDDs
other HxCDDs
Total HpCDDs
2378-HpCDDs
other HpCDDs
Total TCDFs
2378-TCDFs
other TCDFs
Total PeCDFs
2378-PeCDFs
other PeCDFs
Total HxCDFs
2378-HxCDFs
other HxCDFs
Total HpCDFs
2378-HpCDFs
other HpCDFs
1
1
0.01
0.5
0.5
0.005
0.04
0.04
0 . 0004
0.001
0.001
0.00001
0.1
0.1
0.001
0.1
0.1
0.001
0.01
0.01
0.0001
0.001
0.001
0.00001
1
0.05
0.95
1
0.07
0.93
1
0.3
0.7
1
0.5
0.5
1
0.03
0.97
1
0.07
0.93
1
0.25
0.75
1
0.50
0.50
aTEFs for all congener groups not listed here are zero.
"Proportion of congeners within the homologue group that falls into this
subgroup; this proportion is used in calculating TEQs by the "B-method" (see
text).
SOURCE: USEPA 1987d.
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(TEQs) are summed over all congeners present in the mixture, and are then
treated as if they were concentrations of 2378-TCDD itself. The "A-method" is
used to yield maximum estimates of TEQs; the "B-method" is also applied (except
for exposure via fish) for comparative purposes.
The TEF procedure incorporates a number of assumptions with varying
scientific basis and degree of validation; these assumptions are listed below
with comments on their basis and limitations.
1. All CDD/CDF congeners have the same mechanism of action and cause the
same spectrum of toxic effects; there is an extensive empirical basis
for this assumption, at least for mechanisms of action and acute
toxic effects (Safe 1986, USEPA 1987d).
2. The relative potencies of the CDD/CDF congeners are similar for
different toxic effects, so that measures of relative potency derived
from in vitro or short-term in vivo tests can be used to predict
relative potencies for the critical toxic effects used in risk
assessment; there is a fairly extensive empirical basis for
similarity in relative potencies between in vitro and short-term in
vivo measures of activity (Safe 1986); only a few CDD/CDF congeners
have been tested for carcinogenicity and teratogenicity, but the
results of these tests are consistent with the assumption (see
references cited above).
3. The effects of different CDD/CDF congeners are additive; two in vitro
studies (Sawyer et al. 1983, Safe et al. 1986) and one teratogenicity
study (Krowke 1986) provide very limited support for this assumption,
although two other teratogenicity studies (Weber et al. 1985,
Birnbaum et al. 1987b) suggested synergistic action.
4. Within each congener group, all 2378-substituted congeners have
similar relative potencies; however, available studies actually
suggest moderate variability, sometimes by an order of magnitude
(Poland et al. 1979, Knutson and Poland 1981, Mason et al. 1985,
1986a,b, Safe 1986).
5. All CDD/CDF congeners with 1-3 chlorine atoms substituted at any
position have negligible biological activity; available studies
suggest a low level of activity, at least for 237-substituted
congeners (NCI 1979, Knutson and Poland 1981, Mason et al. 1985).
11-19
-------
6. In cases where congener-specific analyses are not available, the "A-
method" provides a reasonable upper bound estimate on TEQ, and the
"B-method" provides an informative alternative; this assumption has
been discussed above.
Because of the limited validation available for these assumptions, the TEF
procedure is recognized to yield risk estimates with a substantial degree of
uncertainty; however, it is believed that the estimates of TEQ are generally
reliable to within at least to order of magnitude (USEPA 1987d). Uncertainties
arising from specific features of the data for the Midland site will be
discussed in Part IV.
D. Risk Assessments of CDD/CDF Mixtures
When applied to analytical data on a CDD/CDF mixture, the TEF procedure
yields an estimate of TEQ, i.e., the Toxicity Equivalent Quantity of 2378-TCDD.
This is then combined with dose-response data on 2378-TCDD (specifically, the
cancer potency factor and the RfD and HAs) and exposure estimates to yield
estimates of health risks faced by individuals exposed to the mixture. In
interpreting the results of this procedure, several additional factors should
be taken into account:
The dose-response assessment for 2378-TCDD incorporates certain
assumptions about scaling of doses between species; specifically, it
uses body-surface-area scaling for carcinogenic effects and a scaling
factor (incorporated into the uncertainty factors) of 10 for
reproductive, teratogenic, and other toxic effects. There are no
dose-response data for 2378-TCDD with which these factors can be
validated. However, for oculodermatological effects of CDFs,
effective doses reported for humans (Hayabuchi et al. 1979, Hsu et
al. 1985) are similar to those reported for rhesus monkeys (McNulty
et al. 1981, Yoshimura et al. 1981).
11-20
-------
2. The dose scaling factors and uncertainty factors used in the dose-
response assessments for 2378-TCDD take no account of differential
pharmacokinetics. In fact, preliminary data suggest that biological
half-lives for 2378-TCDD and other CDDs/CDFs are much longer (on the
order of years) in humans than in laboratory animals (on the order of
weeks) (Poiger and Schlatter 1986, Kunita et al. 1984, Neal et
al. 1982). This suggests that humans may be subject to
proportionately larger internal exposure, so that risks may be
greater than those predicted using the current dose-response
assessments for 2378-TCDD.
3. Recent data suggest that the U.S. population has substantial body
burdens of CDDs/CDFs, including 2378-TCDD (Rappe et al. 1986, USEPA .
1986c, Ryan 1986, Graham et al. 1986). Additional site-related
exposures would be expected to add to these pre-existing internal
exposures, and this should be taken into account in interpreting the
risk assessments. For carcinogenic effects, site-related risks will
be additive to those resulting from other sources of exposure. For
noncarcinogenic effects, the RfD approach incorporates the concept of
a threshold exposure level; in the presence of pre-existing body
burdens, smaller incremental exposures will be required to exceed the
threshold, so that doses below the RfD may give rise to adverse
effects. In other words, the RfD should be compared with total
exposure (background exposure and site-specific exposure) for
purposes of risk assessment.
Taken together, these factors suggest that USEPA's procedures for risk
assessments of CDDs/CDFs may not be particularly "conservative." These
procedures incorporate upper bounds on carcinogenic risk, body-surface-area
scaling factors, and relatively high Uncertainty Factors, which are generally
designed to avoid underestimation of risks in areas of uncertainty (USEPA
1986b, 1987b). In the case of CDDs/CDFs, however, the factors discussed above
may offset to some degree the "conservatism" of USEPA's standard risk
assessment procedures.
11-21
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PART III
EXPOSURE ASSESSMENT
A. Introduction
This part presents a qualitative and quantitative assessment of human
exposure to CDDs/CDFs in the Midland area. Successive sections evaluate the
potential for exposure via each of the media whose contamination has been
investigated: air (Section B), soil (Section C), water (Section D), and fish
(Section E). Section F briefly considers other routes of exposure which may be
significant but which have not been investigated directly. Appendix A
characterizes the populations at risk of exposure by the various routes.
Each section in-this chapter summarizes the information available on
levels of contamination of the medium under consideration with CDDs/CDFs (and,
in a few cases, other contaminants) and derives estimates of average
concentrations in the medium at points of exposure. These are combined with
estimates of rates at which humans contact the medium (breathing rates, fish
consumption rates, etc.) and with data on bioavailability, to yield estimates
of rates of intake of CDDs/CDFs into the body. To the extent possible,
estimates of exposure are expressed as TEQs, to take account of likely exposure
to complex mixtures of CDDs/CDFs. Each section also characterizes the
populations at risk of exposure via the medium under consideration.
In keeping with USEPA's guidelines on exposure assessment (USEPA 1986b),
this chapter generates two or more sets of exposure assessments for each route
III-l
-------
of exposure, using different assumptions, as appropriate, about environmental
levels of CDDs/CDFs present, congener distributions, durations of exposure, and
other factors affecting the intake of CDDs/CDFs. These estimates are intended
to span the range of exposure which could plausibly occur under the given
circumstances of exposure and to provide an assessment of the magnitude of
uncertainty introduced into the exposure assessment by specific analytical
assumptions.
The exposure estimates derived in this chapter are most directly
applicable to the period at which the data were collected (in most cases, 1984-
85, although data on CDD/CDF levels in fish obtained in 1987 are also
included). Information on changes in manufacturing processes and waste
treatment practices at the plant, combined with limited data on emission rates,
suggests that emissions of CDDs/CDFs had been much higher prior to 1984.
Limited data available suggest that a reduction in emissions to the air from
the waste incinerator has occurred since 1983 (see Section III.B, below) and
several areas of soil contamination in the facility have been remediated.
However, because some CDDs/CDFs are still being released from the plant and
because the existing environmental contamination with CDDs/CDFs is likely to
persist, exposure is likely to continue into the indefinite future. Although
it is expected that ambient concentrations of CDDs/CDFs will eventually
decline, no information is yet available from which the rate of such decline
could be predicted. For this reason, this exposure assessment takes no account
of any declines in exposure during the period for which risks are calculated;
more data would be required before any such changes could be assessed.
III-2
-------
B. Exposures to CDDs/CDFs in Air
1. Background
In September of 1984, USEPA conducted air sampling for CDDs/CDFs at four
locations near the Dow Midland facility. Significant amounts of CDDs/CDFs were
detected in air at all four locations (one upwind-"- of the facility, three
downwind^-) on all 3 days during which 8-hour, high-volume samples were
collected. These observations provide direct evidence that CDD/CDF exposure to
the general population outside the facility boundary could be occurring through
exposure to ambient air. Two of the downwind sampling locations were in light
industrial areas near the facility boundary; the third was in a residential
area about 1 mile from the facility boundary, and about 1.8 miles from the
waste incinerator. The observed ambient air contamination with CDDs/CDFs was
thought to be related to operations at the Dow Midland facility, for several
reasons:
• Historical data indicate that the Dow Midland facility engaged in the
production of chlorinated benzenes, chlorinated phenols, and
chlorinated diphenyl ethers and their derivatives in various
combinations since the 1930s (Dow 1984). Many of the processes used to
produce these materials are known to result in the generation of CDDs
or CDFs in varying amounts. Fugitive and stack emissions from these
operations may have resulted in releases of CDDs/CDFs.
• Wastes at the facility, including those generated by the operations
just discussed, have been burned at a waste incinerator that has been
operating on the site since 1971. Studies of the emissions from the
incinerator stack (Bumb et al. 1980; Dow 1984, 1987a; Trembly and
Amendola 1987) have repeatedly shown that CDDs/CDFs are being released
by the incinerator into the air.
In accordance with the prevailing wind directions derived from recorded
meteorological data for the area and, except as noted, during the sampling.
III-3
-------
• Several areas of near-surface and surface soil contamination have been
detected at locations in the Dow Midland facility. Two have been
remediated (capped with limestone and paved over), and another is
currently being remediated. It is possible that CDD/CDF-contaminated
dust from these and possibly other areas at the facility has been
transported as wind-borne particulate to contribute to observed ambient
air contamination off-site.
In the section that follows, the available data regarding air
contamination in the vicinity of the Dow Midland facility will be reviewed,
along with data concerning the nature and amounts of CDDs/CDFs released in the
»
incinerator stack emissions, which represent a possible primary source of
airborne CDD/CDF contamination. Quantitative assessments of CDD/CDF exposures
in air for populations near the Dow Midland facility are developed, based on
the ambient monitoring data, and the uncertainties and limitations associated
with the exposure estimates are discussed. The reasons for using the ambient
data rather than the incinerator stack emissions as the basis for exposure
estimates are also discussed.
2. Ambient Monitoring Data
As detailed by Trembly and Amendola (1987), specially equipped ambient air
samplers were installed at four different locations in and around Midland to
permit collection of simultaneous samples on three separate days (September 8,
12, and 22, 1984). Figure III-l shows the locations of the sampling sites in
relation to the incinerator building, plant boundaries, and chlorophenol
production areas. Site 1 was located across the Tittabawassee River from the
facility, about 1.2 miles to the west of the waste incinerator. Site 2 was
located at the fence line of the facility at the (then) intersection of Ball
Street and Bay City Road in a light industrial area about 0.9 mile northeast of
III-4
-------
MIDLAND \
' ' JiJJ
'53t -^'
T Site 4 ft
•••:•:.; i .I
Chlorophenol Production Areas \^
(Approximate Boundaries)
Site 1
Bring Pond No 6
JrL- H» \
Incinerator (703 Building)
lr-
I: Bullock Creek
Facility Boundary
M " i D
Figure III-1
Dow Midland Facility Boundaries,
Chlorophenol Production Areas
Incinerator Building, and Ambient
Air Monitoring Locations.
Sources: USGS (1973),
Dow (1984)
Scale in Feet
1000 2000 3000
-------
the incinerator. Site 3 was atop the Midland Community Center in a residential
area about 1.9 miles north of the facility. Site 4 was also at the fenceline,
about 1.2 miles northeast of the incinerator. Total airborne particulate
levels were not measured at any of the ambient monitoring sites.
The Dow Midland facility waste incinerator located in the 703 Building was
in operation on all 3 days on which ambient air samples were collected. The
mean wind direction and observed variability in wind direction on these 3 days
are summarized in Table III-l. On all 3 days, sampling location No. 1 was
upwind from the incinerator. ("Upwind" is defined as being more than two
standard deviations away from the mean downwind direction during the sampling
periods). It was also in a generally upwind direction from the major
production areas at the Dow facility during the three sampling events.
Sampling locations 2, 3, and 4 were all located within two standard deviations
of the mean downwind direction from the incinerator on all three sampling days,
with the exception of location 3, which would have been slightly to the west of
a narrowly dispersed plume emanating from the incinerator on September 22.
Locations 2, 3, and 4 were also generally downwind of the major production
areas at the facility, with the exception of location 3, which was slightly to
the west of some of them (see Figure III-l) . It should be pointed out that
local meteorologic conditions and normal diffusion and advection processes may
have substantially broadened plumes of CDD/CDF-laden particulate from the
incinerator stack or from other sources that may have existed on site on any or
all days during which ambient monitoring took place. Thus, it is unlikely that
either monitoring station 2 or 4 actually experienced the CDD/CDF levels equal
to those that would be calculated for the centerline of a theoretically modeled
III-6
-------
TABLE III-l
WIND DATA - AMBIENT AIR SAMPLING PROGRAM
MIDLAND, MICHIGAN - SEPTEMBER 7-27, 1984
4ata«
9/7-«
»/•-»
9/U- 12
9/12-13
9/13-14
9/14-13
9/13-14
9/14-17
9/17-U
9/1*- I*
9/W-20
9/20-21
9/21-22
9/22-23
9/23-24
9/14-25
9/23-2*
9/24-2T
CCA
3
4
5
4
7
1
9
10
11
12
13
14
13
14
17
U
19
20
IP4
Mo.
84CTOt
MCT09
44ET10
•4CTU
I4ITV2
UCT13
UIT14
MCT13
MtTU
MIT 17
S4CTU
S4KT19
umo
umi
•4CT22
•4ER3
•4CT24
•4CR3
Win4 Direction
Moan,
4«|r«*a
1S4
199
329
191
309
331
J94
257
212
235
230
334
12
212
197
193
2M
293
4."«i*.
12
14
91
40
32
23
42
3f
9
30
44
41
134
13
42
23
23
31
Vi.4
••«
3.9
4.2
3.1
5.4
3.1
4.4
4.9
3.3
4.1
4.0
4.1
3.7
4.1
4.9
2.4
4.9
4.1
2.7
Jt«.
1.3
2.1
0.9
1.3
1.3
1.4
2.«
2.4
1.5
2.0
1.3
2.0
1.7
2.1
1.1
1.4
1.9
1.4
Source: Trembly and Amendola 1987
III-7
-------
plume for the entire monitoring period. It is also probable that, on
September 22, a small amount of CDDs/CDFs could have been expected to reach
monitoring station 3 under reasonable assumptions about atmospheric conditions
and plume dispersion, despite the fact that it was not directly "downwind" from
some or all of the likely sources. As will be discussed further below, it also
appears likely that directly transported emissions from the incinerator stack
are not the only source of CDDs/CDFs detected in air at the ambient monitoring
locations.
Modified high-volume samplers were used to collect the CDD/CDF samples
(Trembly and Amendola 1987), with analysis of both the first-stage particulate
filters and polyurethane foam (PUF) backing for CDDs/CDFs. Samples were
extracted, "cleaned up" by solvent partitioning and liquid chromatography, and
analyzed using standard gas chromatographic/mass spectrometry (GC/MS) methods.
The analyses were conducted by Midwest Research Institute, with QA/QC oversight
by the USEPA Sample Management Office and USEPA Region V Central Regional
Laboratory. Two samples were reanalyzed by the USEPA Environmental Monitoring
and Support Laboratory (EMSL) at Research Triangle Park, North Carolina.
The results of the analysis are summarized for sampling locations 1-4 in
Tables III-2 through III-5, respectively. While less evident in these data
than in other cases in this investigation where samples sizes were larger
(e.g., soil and fish samples), the statistical distribution of CDD/CDF levels
tended to be positively skewed, with a few values much higher than the
arithmetic mean or median. In such circumstances, the arithmetic mean is
dominated by these high values, and is higher than the geometric mean or
III-8
-------
TABLE III-2
CONCENTRATIONS (pg/m3) OF CDDs/CDFs DETECTED
IN MIDLAND AMBIENT AIR
SEPTEMBER 8, 12, AND 22, 1984a
SITE 1
Compound
9/8
9/12
9/22
Mean
2378-TCDD
Total TCDDs
PeCDDs
HxCDDs
HpCDDs
OCDD
2378-TCDF
Total TCDFs
PeCDFs
HxCDFs
HpCDFs
OCDF
(--)
0.99
(--)
0.95
0.81
1.2
(--)
0.86
(--)
(--)
(--)
(--)
(0.19)
0.13
(0.38)
(1.0)
0.69
1.7
(0.18)
14.5
(2.9)
(0.62)
(2.2)
0.99
(0.06)
(--)
(0.24)
(0.18)
(0.69)
0.30
(0.11)
(--)
0.13
(0.26)
(0.83)
0.13
0.0
0.33
0.0
0.32
0.50
1.1
0.0
5.1
0.04
0.0
0.0
0.37
NOTES:
Source: Trembly and Amendola, 1987 and Appendices
values in parentheses indicate the substance in question was not detected
(ND), and denote detection limits; where no value is given, no detection limit
was available.
Means are calculated counting "NDs" as zero. Arithmetic means are calculated
for the reasons stated in the text (pp. III-8 and 111-13).
III-9
-------
TABLE III-3
CONCENTRATIONS (pg/m3) OF CDDs/CDFs DETECTED
IN MIDLAND AMBIENT AIR
SEPTEMBER 8, 12, AND 22, 1984a
SITE 2
Compound
2378-TCDD
Total TCDDs
PeCDDs
HxCDDs
HpCDDs
OCDDs
2378-TCDF
Total TCDFs
PeCDFs
HxCDFs
HpCDFs
OCDFs
9/8
(0.85)
44.8
9.3
(0.84)
2.1
7.7
(0.84)
250
30
4.2
5.0
3.4
9/12
(0.24)
(--)
(0.43)
(2.6)
(3.5)
(6.7)
(0.24)
14.5
(1.1)
(1.0)
(1.9)
(3.3)
9/22
(0.05)
22.4
(0.32)
0.55
2.7
14.3
(0.99)
156
7.5
4.5
2.9
1.6
Mean
0.0
22.4
3.1
0.2
1.6
7.3
0.0
140
12.5
2.9
2.6
1.7
NOTES:
Source: Trembly and Amendola, 1987 and Appendices
values in parentheses indicate the substance in question was not detected
(ND), and denote detection limits; where no value is given, no detection limit
was available.
Means are calculated counting "NDs" as zero. Arithmetic means are calculated
for the reasons stated in the text (pp. III-8 and 111-13).
111-10
-------
TABLE III-4
CONCENTRATIONS (pg/m3) OF CDDs/CDFs DETECTED
IN MIDLAND AMBIENT AIR
SEPTEMBER 8, 12, AND 22, 1984
SITE 3
Compound
2378-TCDD
Total TCDDs
PeCDDs
HxCDDs
HpCDDs
OCDDs
2378-TCDF
Total TCDFs
PeCDFs
HxCDFs
HpCDFs
OCDFs
9/8
(0.22)
2.4
(0.46)
(0.32)
2.1
7.9
(0.34)
15
4.4
(0.37)
(0.79)
(1.4)
9/12
(1.1)
3.3
(0.80)
(1.2)
0.65
5.1
(0.24)
45
2.2
(1.3)
(1.2)
0.81
9/22
(0.08)
0.59
(0.48)
(0.39)
0.55
2.7
(0.12)
2.1
(0.23)
(0.15)
(0.80)
0.70
Mean
0.0
2.10
0.0
0.0
1.10
5.2
0.0
20.7
2.2
0.0
0.0
0.50
NOTES:
Source: Trembly and Amendola, 1987 and Appendices
Values in parentheses indicate the substance in question was not detected
(ND), and denote detection limits; where no value is given, no detection limit
was available.
Means are calculated counting "NDs" as zero. Arithmetic means are calculated
for the reasons stated in the text (pp. III-8 and 111-13).
III-ll
-------
TABLE III-5
CONCENTRATIONS (pg/m3) OF CDDs/CDFs DETECTED
IN MIDLAND AMBIENT AIR
SEPTEMBER 8, 12, AND 22, 1984a
SITE 4
Compound
2378-TCDD
Total TCDDs
PeCDDs
HxCDDs
HpCDDs
OCDDs
2378-TCDF
Total TCDFs
PeCDFs
HxCDFs
HpCDFs
OCDFs
9/8
(0.09)
0.86
(0.09)
0.86
1.0
2.7
(0.12)
1.5
1.2
(0.65)
(0.52)
1.7
9/12
(0.15)
0.38
(0.15)
2.9
1.5
6.8
(0.20)
14
1.1
(1.3)
(0.90)
2.7
9/22
(1.6)
74
1.4
0.28
1.1
4.0
(1.6)
375
37
3.0
3.0
4.6
Mean
0.0
25.1
0.47
1.4
1.2
4.5
0.0
130
13.1
1.0
.1.0
3.0
NOTES:
Source: Trembly and Amendola, 1987 and Appendices
values in parentheses indicate the substance in question was not detected
(ND), and denote detection limits; where no value is given, no detection limit
was available.
Means are calculated counting "NDs" as zero. Arithmetic means are calculated
for the reasons stated in the text (pp. III-8 and 111-13).
111-12
-------
median. For purposes of statistical characterization or statistical testing
with skewed distributions, the geometric mean or median are more appropriate
measures of central tendency than is the arithmetic mean. For exposure
assessment, however, the arithmetic mean is the appropriate measure of average
population exposure, because population exposure is determined by the total
quality of the contaminant that is contacted. In the linearized risk model
used in this study, carcinogenic risks are proportional to exposure, and hence
most of the population risk results from contact with locally high residue
levels. In the threshold risk model used in this report, non-carcinogenic
risks result from exposure above the individual's threshold level, and hence
may result exclusively from contact with locally high residue levels. For
these reasons, arithmetic means are calculated throughout Chapter III and are
used as the basis for risk assessment in Chapter IV.
Several features of these data are of interest. Given the scarcity of
analytical standards for the dozens of congeners which could be present in the
samples, USEPA analysts followed current scientific practice in using a limited
number of standards and reporting, primarily, homologue-specific data. The
first three columns of figures in Tables III-2 through III-5 contain the
estimated concentrations for two specific congeners (2378-TCDD and 2378-TCDF)
and for the homologues tetra-, penta-, hexa-, hepta- and octa-CDDs/CDFs for
each day of monitoring. The fourth column of figures is the arithmetic average
of the concentrations over the three days of sampling, where non-detectable
(ND) levels are treated as zero values. As was the case for the ambient data,
these results are reported on a homologue-specific basis. In addition, no
2378-TCDD or 2378-TCDF were found above detection limits at any sampling
111-13
-------
location on any day. There is, however, some evidence that low levels of these
congeners were, in fact, present in some of the samples. The two samples that
were reanalyzed by EMSL (extracts of filters and PUF plugs from locations 2
and 3 on September 8) did show levels of these congeners (0.49 pg/m 2378-TCDD
at location 2, 0.49 pg/m 2378-TCDF at location 3) below the detection limits
achieved by MRI (Trembly and Amendola 1987) . For purposes of comparison,
however, CDD/CDF values tabulated in Tables III-2 through III-5 count "non-
detects" for 2378-TCDD/TCDF and other homologues as zero values. Detection
limits will, however, be factored into the development, of exposure estimates,
as described below.
The second interesting feature of the ambient air data is the generally
consistent pattern of lower levels of total CDD/CDFs at the upwind sampling
location 1 than at the three "downwind" locations. The 3-day average total
CDD/CDF level at location 1 (8.37 pg/m ) was substantially lower than the 3-
day average total levels at the other locations (196.68, 32.3, 180.86,
respectively, for the downwind locations 2, 3, and 4), and the daily total
CDD/CDF levels at location 1 were lower than the total daily levels of CDD/CDFs
at all of the other three locations on all three sampling days. As will be
discussed below, these relationships also hold true when the specific congener
patterns detailed at each site are converted to TEQs. This finding is
consistent with the hypothesis that the Dow Midland facility is a primary
source of the CDD/CDF air contamination in the Midland area. The pattern of
total CDD/CDF levels found at location 3 is also consistent with this
hypothesis, in that the observed CDD/CDF levels were substantially lower on
111-14
-------
September 22, a day on which this location was not directly downwind from the
waste incinerator and not downwind from the majority of the production areas.
It is also important to note, however, that significant levels of
CDDs/CDFs were detected at the upwind location on two of the three sampling
days (see Table III-2). On the third day, only very low levels of CDDs/CDFs
o
were detected, and the predominant homologues were HpCDDs (0.81 pg/mj) and OCDD
(1.2 pg/iP). These findings suggest that there may be other sources of
CDD/CDFs in the Midland area outside the Dow facility boundaries, such as
deposits of contaminated dust or soil, which are contributing to the observed
air contamination. Whether these sources were originally related to operations
at the plant cannot be proven conclusively with the available data.
Another finding of importance with regard to the ambient air data is the
•
observed congener/homologue pattern. At most sampling locations on most days,
the octa-substituted homologues (OCDD, OCDF) accounted for a substantial
portion of the total CDD/CDF contamination observed. As is discussed in more
detail below, OCDD and OCDF were detected only at very low levels in the
incinerator stack emissions compared with the other homologues, providing
additional evidence that the waste incinerator may not be the only source of
the observed air contamination.
The quality and limitations of the ambient air sampling data will be
discussed in more detail below.
Ill-15
-------
3. Stack Emissions Data
Characterization of the CDD/CDF emissions from the waste incinerator is
important because the incinerator may be a major point source of GDD/CDF
emissions. Recently, an assessment has been performed using data from USEPA's
1984 sampling efforts as inputs to an atmospheric transport model (Cleverly
1986), which generated quantitative estimates of exposures of Midland residents
to airborne CDDs/CDFs. The results of this assessment are discussed in more
detail in this section.
Several efforts have been undertaken to measure the levels of CDDs/CDFs in
the stack emissions from the chemical waste incinerator at the Dow Midland
facility. Prior to 1987, the only set of data available which measured a
nearly comprehensive range of congeners/homologues was that gathered by USEPA
on 3 days in the fall of 1984 (Trembly and Amendola 1987). Prior to this
effort, other studies (Bumb et al. 1980, Dow 1984) had measured only selected
subsets of CDD/CDF compounds or used analytical methods that have been
superseded by more modern approaches.
Recently Dow has submitted additional data, on a preliminary basis,
describing the CDD/CDF emissions from the incinerator during operations on
June 25, 1987 (Dow 1987a). In addition, Dow (1984) reported stack emissions
data gathered in 1983, when water pollution control sludges known to contain
significant amounts of CDDs/CDFs and their parent compounds were still being
burned in the incinerator, a practice that was ended in early 1984. The 1983
111-16
-------
data also did not include analytical results for any CDF congeners or
homologues.
Since the USEPA data represent the most complete, thoroughly documented,
and validated set of information regarding the nature and amount of CDD/CDF
emissions from the waste incinerator when wastewater treatment sludges were not
being burned, and since these data were gathered at roughly the same time as
the ambient monitoring samples discussed previously, they are now briefly
reviewed to help provide insight into the development of the quantitative
exposure assessment. Both these and the 1987 Dow data will be used later to
develop rough exposure estimates for purposes of comparison with the exposure
estimates derived from the ambient monitoring results.
Stack emission samples were gathered on August 28 and 30 and on
September 5, 1984. Samples were collected using a USEPA Modified Method 5
sampling train, XAD resin absorbent and polyurethane foam (PUF) plug supports,
each of which was analyzed for CDDs/CDFs. Chemical analyses for CDDs/CDFs were
conducted by Brehm Laboratory of Wright State University with QA oversight by
USEPA Sample Management Office and USEPA Region V Central Regional Laboratory.
Waste feeds to the incinerator were also analyzed on the same days as the
stack emissions were monitored. The wastes contained very high levels of
volatile chlorinated organics (up to 450,000 mg/kg carbon tetrachloride, up to
18,000 mg/kg chlorobenzene) and appreciable amounts of semi-volatile organics,
including 1,2-dichlorobenzene (up to 1,570 mg/kg), 2,4,5-trichlorophenol (up to
111-17
-------
4,690 mg/kg), and 2,4,6-trichlorophenol (up to 8,320 mg/kg). Also present were
CDDs/CDFs at total levels up to 147 Mg/kg (Trembly and Amendola 1986).
The results of the USEPA stack emissions analyses from 1984 are summarized
in Table III-6. Estimates are given of the concentrations of CDDs/CDFs which
were in the stack emissions during each of the three separate days on which
sampling was conducted.
The results of the USEPA study revealed no detectable emissions of
2378-TCDD. However, Dow conducted similar tests on the same facility, but on
different days, and detected the presence of 2378-TCDD in the emissions on all
3 days at levels up to 0.71 ng/m (Dow 1984). Possible reasons for the
qualitative differences between the USEPA and Dow results on the question of
the presence of 2378-TCDD include the following:
• The sampling was performed on different days; therefore, differences in
incinerator feed, operation conditions, etc., could have resulted in
different rates of 2378-TCDD emission.
• The detection limits of the Dow investigators were lower than those of
the USEPA investigators. (Only on Day 3 of USEPA's study were the
detection limits sufficiently low that any of the 2378-TCDD levels
reported by Dow would have been detected.)
• The experiments were performed by different researchers, using somewhat
different techniques.
The more recent Dow data (Table III-7) also indicate the presence of 2378-
TCDD in stack emissions (Dow 1987a). These data, while they have not been
fully validated, can, along with the data from the 1984 USEPA sampling, be used
to help elucidate and compare patterns of incinerator stack emissions with the
ambient data discussed above. The basic pattern of homologue/congener
emissions is similar in the 1984 and 1987 sampling results, with relatively
111-18
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TABLE III-6
CONCENTRATIONS (ng/m3) OF CDDs/CDFs IN CHEMICAL WASTE INCINERATOR EMISSIONS3
AUGUST/SEPTEMBER 1984
Compound
2378-TCDD
Total TCDDs
PeCDDs
HxCDDs
HpCDDs
OCDDs
2378-TCDF
Total TCDFs
PeCDFs
HxCDFs
HpCDFs
OCDFs
August 28
(0.72)
46
5.5
0.88
0.21
0.93
1.5
81
13
' 2.5
0.26
0.06
August 30
(3.08)
44
1.9
0.37
0.84
2.5
1.7
77
4.3
2.0
0.55
0.17
September 5
(0.17)
4.9
(0.85)
(0.72)
(0.19)
(0.82)
(.21)
125
0.07
(0.48)
(0.87)
(4.6)
Mean
0
31.5
2.81
0.42
0.35
1.15
1.06
94
5.8
1.5
0.27
0.08
NOTES:
Source: Trembly and Amendola, 1987 and Appendices
Value in parentheses are non-detect levels.
In calculating means, "non-detects" are counted as zero values. Arithmetic
means are calculated for the reasons stated in the text (pp. Ill-8 and
111-13).
111-19
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TABLE III-7
SUMMARY OF HAZARD INDICES FOR NON-CANCER EFFECTS
FROM EXPOSURE TO CDD/CDF CONTAMINATION IN MIDLAND, MICHIGAN
Hazard Index (HI)a
Exposure
Route Exposure Scenario Long-Term Short-Term Single Meal
Fishb Plausible maximum consumer 50 5 8
High sports fisherman 20 2 0.5
Median sports fisherman 9 0.7 0.2
General consumer 0.7 0.4 0.2
Soil Upper estimate young child
— with pica 6 0.2
— normal 0.6 <0.1
Lower estimate young child <0.1 <0.1
Upper estimate adult <0.1 <0.1
Air Infant at fence!inec 3 0.1
Child at fenceline 1 <0.1
Child in residential area 0.3 <0.1
Adult in residential area <0.1 <0.1
aHazard Index is the ratio of intake dose to:
— RfD (1 pg/kg/day) for long-term exposures (several months or more)
-- 10-day HA (28 pg/kg/day) for short-term exposures (few days to few weeks)
-- Single-dose HA (300 pg/kg/day) for single-meal or single-day exposures
bSmall child could be at 2-3 times higher risk than adult. Breast-fed infant
could be at 10-times higher risk than mother. Other contaminants such as
PCBs, found in the fish, add to the toxicity (see Appendix B of the Risk
Assessment).
clncludes exposures from breast-feeding.
Ill-20
-------
high levels of tetra- and penta-substituted CDDs/CDFs predominating, and only
low levels of OCDD and OCDF present. As will be discussed later, however, the
1987 Dow results show a considerably higher ratio of TCDFs to TCDDs than the
1984 USEPA results, and the total TEQ values calculated for the 1987 Dow data
are somewhat lower than the TEQs calculated for the 1984 EPA data. The more
recent data also show a higher ratio of TCDFs to total CDDs/CDFs and a
correspondingly lower ratio of TCDD to total CDDs/CDFs than the earlier data.
It is not clear that either of these differences indicate a permanent or
systematic difference in incinerator emissions between 1984 and 1987; the
patterns may merely reflect sample-to-sample variability. The pattern of
CDD/CDF homologue in the incinerator emissions in both the 1984 and 1987
samples, particularly the low levels of OCDD/OCDF, is strikingly different from
the pattern observed in the ambient air samples (Tables III-2 through III-5).
These issues are discussed in more detail below.
4. Comparison of Stack Emissions and Ambient Air Sampling Results.
Figures III-2 through III-6 display profiles of the congener/homologue
distributions of the CDDs/CDFs found in the ambient air at locations 1 through
4 and during 1984 USEPA and 1987 Dow sampling of the stack emissions,
respectively. It can be seen that there are some striking differences between
the congener patterns observed in the ambient air and those found in the stack
emissions. These differences may be interpreted as combinations of two basic
patterns, represented, respectively, by that observed at the "upwind" ambient
monitoring site 1 on all three days, and the pattern observed in the stack
emissions. The former pattern ("pattern 1") is characterized by the
111-21
-------
FIGURE ni-2 : Profile of CDD's/CDF's Detected In Midland, Ml Ambient Air-Site I
60 -
40-
20
0
Ck
8
* ^
H <
a
M
6 ? I
g
OTAL Hx
Q 9/8-1
D 9/i:--
n 9/2:--
-------
FIGURE in 3 : Profile of CDD's/CDK's Detected In Midland, Ml Ambient Air- Site 2
ro
OJ
i
80
bO -
40-
20
n
Ck
o
o
6
w
0
o
_
_
fi
M
n
il
HI
r'l r~i n r-i
D 9/8-2
D 9/12-2
D 9/22-2
-------
FIGURE III-A : Profile of CDD's/CDPs Delected in Midland, Ml Ambient Air- Site 3
H
ou -
60 -
§
h- 40 -
•
4
i
L
20-
/•>
- -
01
u u
H H
09 _l
-
. .
all
-
•-- -
g g g g £ £
o t-) o o u ^
flu I I « K
i n.
§?1
8
D 9/8-3
D 9/12-3
D 9/22-3
*^
-------
FIGURE in-5 : Profile of CDD's/CDI's Detected in Midland, Ml Ambient Air Site A
4
e
&
80
60
40
20-
1
£
o
8
2
i
8 § 8 §
K H * K
eg;;
D 9/8-4
D 9/12-4
D 9/22-4
-------
FIGURE 111-6: Profile of CDD's/CDPs In Chemical Waste Incinerator Emissions
100
80
60
Ki
40
20
0
D
DAY 1
DAY2
DAY3
DOW 1987
§
-------
predominance of highly substituted congeners, particularly HpCDDs, OCDD and
OCDF. The latter pattern ("pattern 2"), from the incinerator emissions, is
characterized by comparatively high levels of TCDDs and particularly TCDFs, and
the almost total absence of OCDD or OCDF. The patterns are illustrated
numerically in Table III-8, where the ratios of TCDDs, TCDFs, and OCDD to total
CDDs + CDFs are tabulated for each ambient sampling location, for the 1984 (and
1987) stack emissions data, and for soil samples from Midland and non-
industrialized areas of Minnesota.
The "downwind" ambient sampling stations (sites 2 and 3), exhibit various
patterns of congener distribution on different days, with variations among
sites as well as between OCDD and TCDD levels observed on different days.
Sites 2 and 4, near the facility fenceline, relatively close to the incinerator
and more or less directly downwind from it on all three sampling days, in
general display a pattern that is a mixture of the two basic patterns described
above, with high levels of TCDDs and TCDFs observed on all three days, but
significant levels of OCDD also being observed in most of the samples. The
OCDD to total CDD/CDF ratios in the ambient samples exceed those in the stack
emissions by at least one order of magnitude. At site 3, the pattern was also
"mixed" on September 8 and 22 when the site was downwind from the incinerator,
but on September 28, when the sampling station may have been outside of a
narrow incinerator stack plume, the pattern of congeners observed at site 3 was
much more similar to the "upwind" pattern 1.
There are a number of possible explanations for the observed differences
in the patterns of congener distribution between the stack and ambient air.
111-27
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TABLE III-8
RATIOS OF SELECTED MONOLOGUES TO TOTAL CDD + CDF LEVELS IN MIDLAND
AMBIENT AIR, INCINERATOR STACK EMISSIONS, AND SOIL DATA
FROM MIDLAND PUBLIC AREAS AND MINNESOTA NATURAL AREAS
Proportion of Total CDDs + CDFs Accounted for By:
Sample
TCDDs
TCDFs
OCDD
Incinerator Emissions
1984 USEPA Study
1987 Dow Study
Ambient Air
1984 USEPA Study
Site 1 Day 1
Day 2
Day 3
Mass-Weighted Average-*-
Site 2 Day 1
Day 2
Day 3
Mass-Weighted Average
Site 3 Day 1
Day 2
Day 3
Mass-Weighted Average
Site 4 Day 1
Day 2
Day 3
Mass-Weighted Average
Midland Public Areas
(soil, ave.)
Minnesota Natural Areas
(soil, ave,)
0.22
0.04
0.21
0.007
0.0
0.04
0.13
0.00
0.11
0.12
0.08
0.06
0.09
0.07
0.09
0.01
0.15
0.14
0.02
0.02
0.54
0.95
0.18
0.81
0.0
0.66
0.70
1.00
0.71
0.72
0.45
0.79
0.32
0.64
0.15
0.48
0.75
0.72
NA
NA
0.006
0.003
0.25
0.09
0.70
0.014
0.021
0.0
0.07
0.03
0.25
0.09
0.41
0.16
0.27
0.23
0.008
0.02
0.70
0.72
Sources:
Calculated from Trembly and Amendola 1987 and Appendices, Amendola
1987, and preliminary data submitted by Dow Chemical Company (Dow
1987a) .
-weighted average values do not equal the means of the daily average
values because the levels and ratios of CDD/CDF congeners varied widely from
day to day at some sampling sites and observations from one or two days may
dominate the mass -weighted average.
NA = not analyzed.
111-28
-------
One possibility is that the incinerator is sole source of the observed airborne
CDD/CDFs, but that feed wastes were different on the days during which stack
emissions were sampled than on days during which the ambient air was sampled.
This appears unlikely, given the consistent pattern of appearance of one group
of congeners (OCDD/OCDF) in the air on all three ambient sampling days.
Another possibility is that there is an additional source or sources of
CDD/CDF air contamination in the Midland area. Sources could include fugitive
CDD/CDF emissions from activities in the facility, resuspended soil or
particulate contaminated with CDDs/CDFs from the facility area, or additional
sources of CDDs/CDFs outside the facility.
In addition, the results could be interpreted to show that the collection
efficiencies were different for different congeners for the stack and ambient
sampling methods. There is, however, no reported evidence to suggest that
either the stack or ambient sampling methods employed are selectively more
efficient for specific congeners or homologues.
A final possibility is that emissions from the stack were, in fact, the
major source of the observed ambient air contamination, but that the
differences in congener/homologue distribution between the stack and ambient
samples are the results of environmental processes which changed congener
distribution between the time the emission entered the stack and the time they
arrived at the sampling stations. Postulated mechanisms could include either a
selective decomposition of the less-substituted congeners or the addition of
chlorine to the less-substituted congeners to give the observed higher
111-29
-------
OCDD/CDD+CDF ratios. Neither of these mechanisms seems very plausible on
kinetic or mechanistic grounds and neither would explain the observed upwind
CDD/CDF air contamination.
It is significant to note that "pattern 1" is very similar to the
homologue distribution observed in soil samples taken from natural (non-
industrialized) areas of Minnesota (USEPA 1985a, see Table III-8) . The results
at the upwind ambient station could thus be interpreted to be evidence of some
kind of "background" contamination, although the ultimate source of this
"background" cannot be identified, and could be facility-related. For example,
contaminated soil to the south-west of the facility and sampling location 1
(see section III.C), could be the source of the observed CDD/CDF contamination
in the "upwind" ambient air samples. Additional evidence for the facility-
relatedness of the observed contamination, however, is the consistent pattern
of much higher CDD/CDF levels in the downwind air samples. This holds true
even for the OCDD/OCDF homologues.
There are thus several plausible hypotheses that could explain the
observed pattern of ambient air contamination. They could, for example, be the
result of direct airborne transport of incinerator emissions and fugitive
emissions or resuspended soils from the facility (the soil presumably being
selectively contaminated with OCDD/OCDF from past releases or depleted of
TCDFs/TCDDs by selective volatilization or degradation of these congeners).
Alternatively, the downwind air contamination could be the result of a
combination of directly transported incinerator emissions and resuspended soil
or dust from the downwind sampling areas outside the facility (again, these
111-30
-------
soils would have been selectively contaminated with the more highly substituted
or depleted of the less-substituted homologues, as discussed above).
Whatever the specific source or sources of ambient air contamination, the
available data do strongly suggest that the waste incinerator is not the sole
source of this contamination. For this reason, it appears advisable not to
rely on the incinerator emission data, coupled to air transport models, as the
basis for exposure estimation for ambient air exposures. Rather, the ambient
air data provide the more reliable guide as to exposures likely to be
experienced by populations residing near the facility, and therefore they are
used as the basis of the central exposure estimation effort in this analysis.
5. Populations at Risk of Ambient Air Exposure.
The population at risk of exposure to CDD/CDF air contamination is taken
to include all individuals residing and/or working near the Dow Midland
facility. On-site and occupational exposure to the facility itself is not
considered in the analysis. Exposure of populations outside the city and
county of Midland is not considered, because levels of CDDs/CDFs are expected
to decline rapidly with distance due to mixing with ambient air. However, it
should be recognized that residents just outside the city and county lines are
also exposed to airborne contaminants, at levels lower than those occurring
within the city.
As discussed in Appendix A, there are approximately 32,000 people living
in the Midland area, of which approximately 26,000 live in areas within 3 miles
111-31
-------
of the facility boundary in a generally downwind direction. The closest
residences to the facility to the north-east of the facility are about 0.25
miles from the fenceline, the intervening distance being devoted largely to
light industrial uses. To the northwest and east of the facility, there are a
number of residences directly adjacent to the facility boundary, but not
adjacent to currently used production areas. Most of the population of the
Midland area resides in residential areas to the north of the facility at
distances between 0.5 and 3.5 miles from the facility boundary.
6. Exposure Estimation.
In this section, quantitative estimates are developed for inhalation
exposure to CDDs/CDFs for persons residing in the Midland area in the vicinity
of the Dow Midland facility. Because of the limited amount of data available,
in order to provide some quantitative measure of the range of exposures that
may actually occur, and to provide an illustration of the impact of different
assumptions on the exposure estimates, two exposure scenarios are developed.
The first "fenceline case" incorporates assumptions consistent with long-term
exposures at the Dow facility fence line near the two "downwind" monitoring
locations. The other "residential area case" employs assumptions corresponding
more closely to exposures occurring in residential areas of Midland, further
from the facility. As noted previously, data on CDD/CDF levels in ambient air
near the facility are used to provide the quantitative basis for the exposure
estimates. Data from the four sampling locations are used to construct the two
exposure scenarios as described below.
111-32
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a. Exposure Scenario 1: Fenceline Case
The fenceline case scenario attempts to simulate the long-term exposures
received by a hypothetical individual living near the northern facility
boundary. Pooled data from ambient monitoring sites 2 and 4 are used to
provide an estimate of the average lifetime inhalation exposures for this
scenario. Observations on CDD/CDF levels from the two sites are averaged (see
Table III-9) using values equal to the detection limits for homologues and
congeners that were not detected at these locations. The rationale for doing
so is that it is likely that at least some of the congeners not detected were,
in fact, present at levels lower than the detection limits during the sampling,
and that using the detection limit to fill the data gaps gives an upper-bound
on the levels of the non-detected congeners that were actually present. Also,
as discussed previously, reanalysis of two of the ambient air samples by
USEPA's EMSL laboratory did, in fact, detect 2378-TCDD and 2378-TCDF (the most
toxicologically significant of the "non-detect" congeners) at levels comparable
to the MRI detection limits at site 2 on one day.
In the last column of Table III-9, the averaged air concentrations of the
CDDs/CDFs detected at sites 2 and 4 are summed using the Toxicity Equivalence
Factor (TEF) approach described in Chapter II. Both the "A-method" (assuming
all congeners among the penta- through hepta-substituted homologues are 2378-
substituted) and "B-method" (assuming a uniform statistical distribution of
congeners within each of these homologues) are used to develop total Toxicity
Equivalents (TEQs) for the averaged site 2 and 4 data. This approach, again,
helps to ensure that the exposure estimates span the range of likely values,
111-33
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TABLE III-9
AVERAGE CDD/CDF LEVELS IN AIR AND TOXICm EQUIVALENTS FOR MONITORING SITES 2 AND 4
Compound
Total TCDD
2378
Other
Total PeCDD
2378
Other
Total HxCDD
2378
Other
Total HpCDD
2378
Other
Total OCDD
Total TCDF
2378
Other
Total PeCDF
2378
Other
Total HxCDF
2378
Other
Total HpCDF
2378
Other
Total OCDF
Total TEQs
Total TEQs from
"Non-Detects"
Proportionality
TEF Factor
1.00
1.00
0.01
0.50
0.50
0.005
0.04
0.04
0.0004
0.001
O.OQ1
0.00001
0
0.100
0.100
0.001
0.100
0.100
0.001
0.01
0.01
0.0001
0.001
0.001
0.00001
0
—
"
1.00
0.05
0.95
1.00
0.07
0.93
1.00
0.30
0.70
1.00
0.50
0.50
1.00
1.00
0.03
0.97
1.00
0.07
0.93
1.00
0.50
0.50
1.00
0.50
0.50
1.00
—
Average Air
Level
(ps/m3)
23.74
3t0.50)
23.24
(1.95)
NA
NA
(1.34)
NA
NA
(1.99)
NA
NA
7.03
135.13
a(0.67)
134.46
(12.95)
NA
NA
(2.44)
NA
NA
(2.38)
NA
NA
(2.88)
—
TEQ (pg/m3)
Method Method
A B
..
0.500
0.232
0.975
—
—
0.054
--
--
0.002
—
—
0
--
0.067
0.134
1.295
—
--
0.024
—
—
0.002
—
--
0
3.285
0.703
..
0.500
0.232
—
0.068
0.009
—
0.016
0
—
0.001
0
0
--
0.067
0.134
--
0.091
0.012
—
0.006
0
—
0.001
0
0
1.137
0.584
Source: Calculated from Trembly and Amendola (1987) and appendices.
NOTE: Figures in parentheses represent average observed levels where one or more "non-detects" were included
in the averaging process. Non-detect values were counted as observations at the calculated detection
limits.
3A11 the data for the indicated congener/homologues were derived from non-detect values.
Arithmetic means are calculated for the reasons stated in Section III.C (footnote to p. 111-59).
111-34
-------
and provides information concerning the magnitude of the impacts of specific
assumptions on the exposure estimates.
As can be seen in Table III-9, use of the "A-method" results in a higher
total average TEQ (3.29 pg/m3 TEQ) than use of "B-method" (1.14 pg/m3 TEQ).
The proportion of the calculated total TEQ for the site 2 and 4 data that is
derived from the use of the detection limits in place of "non-detects" is 21
percent for the "A-method" and 51 percent for the "B-method". Thus, using one-
half the detection limits for "non-detect" values (a possible alternative
approach) would reduce the calculated total exposure during downwind exposures
by only 11% using "A-method", and 25% using the "B-method" to calculate TEQs.
Neither of these reductions would be significant, given the level of
uncertainty inherent in other aspects of the exposure assessment.
In order to take into account, at least in a crude fashion, the presumed
facility-relatedness of the observed CDD/CDF concentrations in the fenceline
case scenario, an adjustment needs to be made for the proportion of the time
that the hypothetical exposure point (at the northern facility boundary,
between sampling locations 2 and 4) would be downwind from the incinerator and
from other potential CDD/CDF sources at the facility. For the purpose of this
assessment, it is assumed that this would be the case any time the exposure
point is downwind from an appreciable proportion of the Dow Midland (but not
Dow Corning) facility, that is, when the wind blows from any direction between
south-southeast (157°) and west-northwest (293°). Using meteorologic data for
the Consumer's Power Nuclear Plant (USEPA 1985a), it is estimated that the wind
will blow from these directions about 58% of the time, on average. During the
111-35
-------
time that the exposure point is not downwind of the major production areas and
the incinerator, it is assumed that the ambient air levels are the same as
those measured at the "upwind" site 1. From the data in Table III-2, it can be
calculated that the average total TEQs measured at site 1 for the three
sampling days were 0.34 and 0.12 pg TEQ/m , using the "A" and "B" methods,
respectively. These calculations were again made using detection limit values
for non-detects (where detection limits were available) and zero when no
detection limits were available. For the "background" (site 1) monitoring
results, TEQs derived from nondetect results for particular congeners account
for 91% and 77% of the total TEQs calculated using the "A" and "B" methods,
respectively.
The total exposure levels calculated for the fenceline scenario using the
time-averaged "downwind" and "background" exposure levels are 2.1 pg/m TEQs
3
("A" method) and 0.71 pg/m TEQs ("B" method). As expected, the contribution
of the "background" CDD/CDF levels represent only a small proportion (<8%) of
the total TEQ levels calculated using either method. For the overall exposure
estimates, "NDs" account for 26% and 52% of the total TEQs, using the "A" and
"B" methods, respectively.
As discussed previously, this approach only approximates actual
meteorologic conditions; natural atmospheric instability and normal plume
dispersion would actually result in less than theoretical peak exposures during
periods when the exposure point was "downwind" of the facility, and also could
result in some appreciable levels of CDD/CDF air contamination from the
facility reaching the exposure point even when it was not nominally downwind of
111-36
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likely contaminant sources. Also, given the large area of the facility, it is
not possible to make a precise, conclusive judgment as to when the exposure
points might actually be in a downwind direction from sources other than the
waste incinerator. Again, the effect of utilizing this assumption is small
relative to the other sources of uncertainty in the exposure assessment.
b. Exposure Scenario 2: Residential Area Case
The "residential area case" exposure scenario is defined as occurring near
ambient monitoring site 3, in an area of higher population density than the
"fenceline case" scenario, further away from the Dow Midland facility, and less
directly downwind of the incinerator and major production areas. The average
CDD/CDF levels measured in ambient air at site 3 are used to calculate ground-
level inhalation exposures for a population residing in this area (Table III-
10). Again, both methods of calculating TEQs are employed, although in this
scenario, "non-detect" values were replaced by values equal to one-half the
detection limit for the congeners/homologues in question. The rationale for
doing so is similar to that employed in adjusting the "non-detect" values for
the fenceline case scenario, except that one-half the detection limit is in the
middle of the possible range of values for the non-detected congeners and is
less likely to represent upper-bound estimates for the non-detected compounds.
As shown in the last column of Table III-10, the estimated ground-level
exposures for the residential area scenario during periods when the exposure
•3 -3
point is downwind from the facility are 0.67 pg/mj TEQs and 0.32 pg/m0 TEQs,
when using the "A" or "B" methods, respectively. Unlike the scenario
previously described, the "non-detect" values make a major contribution to the
111-37
-------
TABLE 111-10
AVERAGE CDD/CDF LEVELS IN AIR AHD TOXICITY EQUIVALENTS FOR MONITORING SITE 3
Total TCDD
2378
Other
Total PeCDD
2378
Other
Total HxCDD
2378
Other
Total HpCDD
2378
Other
Total OCDD
Total TCDF
2378
Other
Total PeCDF
2378
Other
Total HxCDF
2378
Other
Total HpCDF
2378
Other
Total OCDF
Total TEQs
Total TEQs from
"Non-Detects"
TEF
1.00
1.00
0.01
0.50
0.50
0.005
0.04
0.04
0.0004
0.001
0.001
0.00001
0
0.100
0.10
0.001
0.100
0.100
0.001
0.01
0.01
0.00001
0.001
0.001
0.00001
0
—
"
Proportionality
Factor
1.00
0.05
0.95
1.00
0.07
0.93
1.00
0.30
0.70
1.00
0.50
0.50
1.00
1.00
0.03
0.97
1.00
0.07
0.93
1.00
0.50
0.50
1.00
0.50
0.50
1.00
—
"
Average Air
Level
(pg/m3)
2.10
a(0.23)
1.870
a(0.290)
NA
NA
(0.32)
NA
NA
1.10
NA
NA
5.23
20.70
3(0.12)
20.58
(2.24)
NA
NA
a(0.30)
NA
NA
0.47
--
--
0.97
--
~~
TEQ
Method
A
0.230
0.019
0.145
--
—
0.013
. --
--
0.001
--
--
0
__
0.012
0.020
0.224
--
--
0.003
--
--
0
--
--
0
0.667
0.420
(pg/m3)
Method
B
0.230
0.019
0.010
0.001
0.004
0
—
0.001
0
0
0.012
0.020
—
0.016
0.002
—
0.001
0
—
0
0
0
0.316
0.277
Source: Calculated from Trembly and Amendola (1987) and appendices.
NOTE: Figures in parentheses represent average observed levels whera one or more "non-detects" were included
in the averaging process. Non-detect values were counted as observations at one-half of the calculated
detection limits.
All the data for the indicated congener/homologues were derived from non-detect values.
Arithmetic means are calculated for the reasons stated in Section III.C (footnote to p. 111-59).
111-38
-------
total exposure at this exposure point. Substitution of one-half detection
limit values for "non-detects" accounts for 63% of the total TEQ calculated
using the "A-method" and 88% of the TEQ calculated using the "B-method". This
occurs primarily because all of the information at monitoring site 3 regarding
the GDD congeners with the highest toxicity (2378-TCDD and PeCDDs) is derived
from "non-detects". This suggests that the exposure estimates for this
scenario are substantially more uncertain, and more dependent on the quality of
the analytical results, than those for the fenceline case scenario.
A long-term exposure level for the residential area scenario is calculated
using a factor to convert for the proportion of the time the exposure point
would be downwind of possible on-site CDD/CDF sources, with "background" level
again assumed to be occurring at times when the exposure point was not
"downwind," just as was done for the fenceline case scenario. For this
scenario, it is estimated that the exposure point will be downwind of potential
facility-related sources whenever the wind blows from any direction between
southwest (235°) and southeast (135°), or about 33% of the time (USEPA 1985a).
"Background" exposure levels, calculated using the "A" and "B" methods and the
data from monitoring site 1 (counting nondetects as being equal to one-half the
detection limit for this scenario) are 0.16 and 0.070 pg/rn^ TEQs, respectively.
TEQ estimates derived from nondetect values account for 80% and 84% of the
total "A" method and "B" method background TEQs, respectively.
The time-weighted average long-term exposure levels for the residential
3 3
area case are calculated to be 0.34 pg/m TEQ ("A" method) and 0.15 pg/m TEQ
("B" method). Overall, TEQs derived from "NDs" account for 72% and 87% of the
111-39
-------
total exposure for this scenario calculated using the "A" and "B" methods,
respectively. In this scenario, "background" exposures account for a
significant proportion of the total exposures, 42% for the "A" method and 39%
for the "B" method. This is not unexpected, in that the residential area
exposure point is assumed to be "downwind" from the Dow facility less than one-
third of the time and because measured CDD/CDF levels at monitoring site 3 are
lower than at the fenceline exposure point and only moderately higher than
those measured at the "upwind" site 1.
c. Intake Assumptions
The last step in the development of quantitative exposure estimates for
the two exposure scenarios is to define a set of assumptions which characterize
the relationships between the long-term average air levels and the doses of
CDDs/CDFs to exposed populations that would be associated with these levels.
For the purpose of this analysis, a number of assumptions are made, the most
important of which are the following.
For both exposure scenarios, it is assumed that the exposed individuals
live their entire lifespan at the hypothetical exposure points. Exposures are
assumed to occur 24 hours per day to the long-term average ambient air levels
calculated above. It is assumed that indoor exposure will be neither higher
nor lower than outdoor exposure, thus discounting either a protective effect of
being indoors, or an increase in indoor exposure levels due to exposure to
contaminated household dust. Dose levels are calculated for infants (age less
than 1 year), children aged 1-6 and 6-12, and adults (age 12-70). Values for
111-40
-------
the physiological parameters used to calculate inhalation intake of CDD/CDFs
for each age group are summarized in Table III-11. Following the approach of
Schaum (USEPA 1984b), it is assumed that 27% of the inhaled CDD/CDF is retained
in the body.
Applying the assumptions just described to the long-term air levels of
CDDs/CDFs calculated for the two exposure scenarios results in the calculated
doses for the two exposure scenarios which are summarized in Table III-12. As
«
expected, the average daily intakes are greatest on a mg/kg-day basis for small
children who have relatively low body weights and high metabolic rates and
respiratory volumes.
As will be discussed in Part IV, the intake values developed here
represent estimates of the absolute amounts of CDDs/CDFs taken into the body of
the exposed individuals. When these intake estimates are compared in Part IV
with dose-response data for 2378-TCDD, it will be necessary to taken into
account the fact that the RfD and HAs are derived from the results of
experiments in which 2378-TCDD was administered to animals in feed and are
expressed in terms of administered dose. Because the bioavailability of 2378-
TCDD from feed is less than 100%, the administered dose in these experiments
was greater than the absorbed dose. In Chapter IV, an additional adjustment
will be applied to the intake estimates derived above to make them
commensurable with the administered doses that form the basis of the RfD and
HAs.
111-41
-------
TABLE III-11
PHYSIOLOGIC PARAMETERS FOR INHALATION INTAKE ESTIMATION
24-Hour Respiratory
Age Group Body Weight (kg)1 Volume (m3)
Infants (age 0-1 years) 9 3.6
Young children (ages 1-6) 15 16
Older children (ages 6-12) 31 23
Adults (ages 12+) 70 20
•* _____
Source: Anderson, et al. (1984) USEPA (1984b, 1985c,d).
^Body weights for children and infants are calculated using 50th-percentile
age-group data from the NHANES survey, as cited in Anderson, et al. (1984)
f\
^Respiratory volumes for children were calculated using age-group-specific
rates from Anderson, et al. (1984), adjusting for mean body surface area when
data for a specific age group were not available, assuming 40% rest, 30% light
activity, 20% moderate activity, 10% heavy activity.
111-42
-------
TABLE 111-12
EXPOSURE LEVELS AHD DOSES OF CDD/CDF TOXICOLOGIC EQUIVALENTS (TEQs)
CALCULATED FOR AMBIEHT AIR EXPOSURE SCENARIOS
Scenario 1—Fenceline
Case
Infants (0-1 year)
Children:
1-6 years
6-12 years
Adults (12-70 years)
Lifetime (0-70 years)
Scenario 2--Residential
Area Case
Infants (0-1 year)
Children:
1-6 years
6-12 years
Adults (12-70 years)
Lifetime (0-70 years)
Long-Term Average
Exposure
Scenarios
Air Concentrations
(ps/m3 TEQs)
Method A Method B
Dose to Receptors
(pg/kg/day TEQs)
Method A Method B
2.1 0.71
0.34 0.15
0.22
0.59
0.41
0.16
0.21
0.037
0.098
0.068
0.026
0.035
0.077
0.20
0.1*
0.055
0.073
0.017
044
031
012
0.016
Source: Calculated from ambient monitoring results as described in the text.
aln Scenario 1, the receptor is assumed to be downwind of source(s) 58Z of the
time, and receive "background" exposure when not downwind. In Scenario 2, the
receptor is assumed to be downwind 33Z of the time. The long-term average air
concentration is calculated as the time-weighted average of the "upwind" (site
1) air concentration and either the averaged sites 2 and 4 air concentration
(fenceline case) or site 3 air concentration (residential case).
Assumes lifetime 24 hr/day exposures, respiratory volumes and body weights as
described in Table III-ll, 27Z absorption of inhaled CDDs/CDFs by all age
groups. The long-term average dose (D, pg/kg/day) due to air exposure is
calculated as:
CCRVXFj)
where
C
m
BW
BW
the long-term average air concentration (pg/m TEQs),
the average-specific respiratory volume (m /day), and
the age-specific body weight (kg) for the exposed population.
111-43
-------
7. Exposure Estimates from Incinerator Emissions Data
As discussed previously, there are several reasons why the available
incinerator emissions data are less than ideal for use in developing exposure
estimates. Aside from the small number of observations, and the variations in
the quality and completeness of data gathered at various times by Dow and
USEPA, it is clear that the patterns of CDD/CDF congeners found in the stack
emissions during all of the sampling events are significantly different from
the patterns observed in the ambient monitoring results (see Table III-8 and
Figures III-2 through III-6. In addition, while the ambient data provide
direct estimates of CDD/CDF levels at specific locations of interest for the
exposure assessment, developing exposure estimates using the emissions data
requires the use of air transport models, which add significantly to the level
of uncertainty in the exposure estimates.
Despite these uncertainties, it is possible to develop exposure estimates
for pollutants emitted by the incinerator in the manner just described. In the
discussion that follows, the results of a recent study which employed the 1984
USEPA stack emissions data and the USEPA Human Exposure Modeling System (HEMS)
to generate exposure estimates for CDDs/CDFs in Midland will be briefly
reviewed for purposes of comparison with the exposure estimates generated using
the ambient data, as described above. In addition, the 1987 Dow data will be
used in a similar manner to develop exposure estimates that will help to
illustrate how changes in emissions since 1984 may have affected incinerator-
related exposure levels.
111-44
-------
Cleverly (1986) used the 1984 USEPA stack emissions data to provide inputs
to HEMS and developed estimates of the maximum total TEQ exposures associated
with incinerator emissions. Where data for a specific congener was not
available, e.g., 2378-TCDD, the corresponding average value for the 1984 Dow
results was used. Using meteorologic data from 5 years of observations at
Midland and an average concentration of 3.80 ng/m TEQ in the incinerator stack
gases ("A" method), it was estimated that the maximum annual ground-level
CDD/CDF concentrations of 0.101 pg/m TEQ would be achieved at points 0.6 miles
north and northeast of the incinerator. These points lie in the same general
direction from the incinerator as the fenceline scenario exposure point but are
3
slightly closer to it. The modeled TEQ level (0.101 pg/m ) is lower than the
3
estimated exposures at the fenceline site (2.1 or 0.71 pg/m TEQ, "A" or "B"
method, respectively), and CDD/CDF intakes estimated at the site using the
modeling results would also be correspondingly lower.
If, however, it is assumed that there is a "background" CDD/CDF level in
the Midland area, which contributes to the total CDD/CDF levels observed
downwind from the incinerator, then the model predictions are essentially the
same as the observed levels for the residential sampling site. When the site 1
"background" is added to the model predictions, the total annual maximum
predicted CDD/CDF level for the highest-concentration downwind location becomes
0.45 or 0.22 pg/m3 ("A" or "B" method, respectively). These levels, while
nearly the same as those measured at the residential site, are still somewhat
lower than those measured at the fenceline sites. However, the difference
between the two values is probably well within the expected range of variation
for the model predictions and the measured CDD/CDF levels.
111-45
-------
Substituting the 1987 Dow data into the HEMS model also gives lower
exposure levels than estimated using ambient data. From the data in
Table III-7, it can be calculated that the total TEQ levels measured by Dow in
3 3
1987 (0.606 pg/m and 0.371 pg/m , "A" and "B" methods, respectively) would
yield estimates of the maximum annual downwind concentration of 0.016 pg/m TEQ
and 0.010 pg/m TEQ, respectively. These estimates assume conditions identical
to those used by Cleverly to estimate downwind exposures; most importantly,
perhaps, it assumes the same flow rate in the stack of the incinerator. In
fact, data regarding stack flow rates for 1987 are not available at this time,
thus adding to the uncertainty in this estimate. These levels would not add
significantly to a "background" CDD/CDF level equivalent to that found at
monitoring site 1.
The maximum ground-level concentration modeled using the HEMS system and
either the 1984 USEPA or 1987 Dow data are thus lower than both the measured
ambient concentrations at the closest corresponding monitoring locations (2 and
4) and the estimated long-term exposures derived from these data. Implications
of these results will be discussed below.
8. Limitations of Air Exposure Assessment
Many factors contribute to the uncertainty surrounding the exposure
estimates just discussed. The two major sources are the uncertainties and
limitations associated with the ambient air data for CDDs/CDFs and the
111-46
-------
uncertainties associated with the methods and models used to derive the
exposure estimates from these data.
a. Data Limitations
A number of practical difficulties are inherent in the collection and
analysis of samples for the detection and quantification of the wide range of
CDDs/CDFs at the low levels encountered in this study. The collection
efficiency of the high volume samplers used to gather these data has not, for
example, been measured on an absolute basis for all the specific compounds
being analyzed (Trembly and Amendola 1987). Analysis of similar compounds
(specifically DDT) suggests that some of the lower molecular weight CDDs/CDFs
may pass through the XAD resin cartridge to the backup PUF filter. Most of the
ambient air samples were within satisfactory analytical recovery and precision
targets on all three sampling days. Nine of the 45 samples had percent
recoveries exceeding the 150% upper-bound target for Cl4-HpCDD, indicating
that sampling results for the hexa- and hepta-CDDs and CDFs, although deemed
acceptable for this risk analysis, may actually be overestimated. The
consistent patterns of monitoring results at the various monitoring sites
suggest that the loss of lower-substituted CDDs/CDFs could not explain the
differences in observed congener/homologue profiles at the different sites.
There is, however, some ambiguity in the definition of detection limits
for the various homologues in the ambient air sampling data. Detection limits
were set for each sample, following standard USEPA procedures, using the
highest detection limit of all of the elements in the sampling train that were
111-47
-------
analyzed (filter, XAD, PUF plug, etc.). This approach may add to the
uncertainty in the exposure estimates, in that the detection limit for the
sampling train as a whole could, in theory, be different from that calculated
using the least sensitive element of the train.
The number of analytical chemistry standards available for use in this
study was also limited. Therefore, estimates of the concentrations of some of
the homologues have been made without benefit of homologue-specific, let alone
congener-specific, standards. Only one isomer was used for a calibration
standard for all isomers within a homologue series. This practice is based on
the assumption that the response factors for all isomers in a homologous series
are equal to that of the calibration isomer. On the whole, the available data
do not appear to support the existence of any systematic error or bias in the
analytical results for the ambient air sampling, although it is clear that
these results are subject to a large degree of uncertainty.
The extent to which these data are representative of the actual CDD/CDF
levels in ambient air at the location monitored depends upon many factors,
including the meteorologic conditions during the sampling, variations in
incinerator feed materials and operating parameters, conditions governing
releases from other possible sources, and any other local conditions affecting
CDD/CDF transport, persistence, and transformation in the air. With the
exception of the prevailing wind direction, it is not possible, due to a lack
of data, to incorporate quantitative considerations of any of these factors
into the exposure assessment.
111-48
-------
b. Limitations of Models and Methods Used to Estimate Exposures
The scenarios and assessment methods used to develop quantitative exposure
estimates are designed, to the extent possible, to combine the available data
with plausible, realistic assumptions, and to elucidate the impacts of various
key assumptions by providing ranges of estimates where more than one assumption
appeared reasonable. The exposure scenarios themselves are designed to reflect
the exposure experience of two different potentially exposed populations, one
living near the facility fenceline, in a direction directly downwind from the
facility, the other further away and less directly downwind, based on the
prevailing wind direction. The first represents an attempt to combine
prudently but realistically conservative assumptions to derive an exposure
estimate unlikely to be lower than that received by anyone near the facility.
In fact, there are only a small number of residences as near to the incinerator
and production areas and downwind from them as the two sampling locations which
provided data for the assessment.
The second scenario is designed to more closely reflect conditions at a
location closer to the center of population density in Midland, although still
relatively near the facility. The monitoring station which provided the data
for this assessment is, in fact, in a residential area, not far from the center
of population density in the Midland area.
For both scenarios, the conservative assumption is made of full lifetime
exposure. In addition, full 24-hour per day inhalation exposure is assumed.
This assumption could be "conservative" or not, depending upon the proportion
111-49
-------
of time spent by exposed individuals in other less (or more) heavily
contaminated areas, and the extent to which exposures to potentially
contaminated household dust were also occurring (Section III.F).
The exposure estimates were also developed using a model which assumed
direct windborne transport of pollutants from sources at the Dow Midland
facility to receptors near the various exposure points. Corrections were made,
using site-specific meteorologic data, for seasonal variations in wind
direction, based on the assumption that the observed air contamination was, in
fact, either due to releases directly from the facility or due to "background"
contamination represented by the monitoring results from site 1. If this
assumption is not correct (if some of the CDD/CDF contamination observed at the
monitoring locations comes from sources other than the facility, or from
resuspension of contaminated soils near the specific monitoring sites), then
the method used to correct for wind direction may underestimate exposures. If,
as is possible, resuspended soil is contaminated primarily with the less toxic
hepta-and octa-substituted congeners, then this factor may not introduce any
significant bias into the analysis. Short-term variations in meteorologic
patterns and local meteorologic conditions could also affect ambient air levels
in ways not taken into account in this analysis.
Another important factor in developing exposure assessments for the two
scenarios is the treatment of "non-detect" values in quantifying exposures. As
noted previously, "non-detect" values were counted as being observations equal
to the detection limits for the fenceline scenario and equal to one-half the
detection limits for the residential area scenario. These approaches are often
111-50
-------
employed in risk analysis when, as is the case here, the measured analytes are
at or near analytical detection limits and there is additional reason for
suspecting the presence of the non-detected pollutants. The basis for
suspecting the presence of the non-detected congeners is well established in
this case. The most toxicologically significant non-detected
congeners/homologues (2378-TCDD and 2378-TCDF and, in one case, PeCDDs) are
known to be constituents of the stack emissions, a major suspected source of
the observed contamination. Also, 2378-TCDD and 2378-TCDF were detected in the
samples from monitoring site 2 on September 8, 1984, which were reanalyzed by
EMSL, at levels (0.49 pg/m^) comparable to the detection limit obtained at that
and other sites during the ambient sampling. The use of the two scenarios
helps to illustrate the degree of uncertainty associated with the lack of
knowledge about the actual levels of CDDs/CDFs present in the "non-detect"
samples.
As discussed previously, "non-detects" account for less than 53% of the
total TEQ exposures predicted for the fence-line scenario. They do account,
however, for up to 87% of the TEQ exposure for the residential area exposure
scenario calculated using the "B" method. This suggests that as a significant
source of potential bias in the exposure estimates, the use of detection limit
values for the scenario is not likely to be important, while for the
residential scenario, the use of one-half the detection limit for "non-detects"
could add appreciably to the uncertainty of the estimated exposures.
Taken together, the factors just discussed may exert a combined influence
which would cause exposure estimates to err slightly on the side of
III-51
-------
conservatism. That is, they could cause the estimated exposure to be slightly
higher than values derived using other, less conservative methods. On the
whole, however, it is not expected that there would be any major systematic
bias in the estimates, since factors which contribute to conservatism (use of
detection limits, one-half detection limits, assumption of full lifetime
exposure) are at least partially counterbalanced by those factors (lack of
congener- and some homologue-specific standards for the analytical data,
assumptions of no indoor or non-site related exposures) which could result in
underestimation of exposures.
The differences between the exposure levels estimated using the ambient
data and those derived using the HEMS model and the incinerator stack emissions
are not great enough to call either approach seriously into question. The
difference between the predicted and measured levels is probably within the
range of uncertainty associated with the modeling process, and in the chemical
analyses, especially if any reasonable "background" level of CDD/CDF
contamination in the Midland air is taken into account. These data should
certainly not be interpreted to indicate that the incinerator accounts for only
a small proportion of the total ambient exposures. While there is good reason
to believe that there are sources of airborne CDDs/CDFs in the Midland area
other than the Dow incinerator stack, the modeling results themselves do not
provide conclusive evidence as to the identity or relative importance of these
sources.
111-52
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C. Soil
Surface soil sampling was conducted in the City of Midland during the
period October 10-20, 1983, and at the Dow Midland facility on December 1, 1983
(USEPA 1985a). Samples obtained from the grounds of the Dow Midland facility
were composites obtained from grids established at each sampling location.
Both composite and grab samples were taken from around the inside perimeter of
the Dow Midland facility. All samples were composites of soil obtained within
1 inch (25 mm) of the surface.
Sampling in the City of Midland was focused on the outside perimeter of
the Dow Midland facility, and in public use and residential areas throughout
the city. The residential sampling program included both open yard composite
samples and composite samples taken at roof gutter downspouts or roof
driplines. The downspout and dripline samples were obtained to help define the
degree to which atmospheric deposition contributes to surface soil
contamination in the Midland area.
1. CDD/CDF Concentrations in Soils
Two separate analytical programs were conducted by USEPA. Selected
samples were analyzed for CDD and CDF homologues, and the results are presented
in Tables III-13 and III-14. The majority of the samples were analyzed for
2378-TCDD only. These results are presented in Tables 111-15, 111-16, and
III-17. Figure III-7 shows the locations that are referred to in the tables.
111-53
-------
TABLE III-13
PCDDs and PCDFs
SITE II - Midland. Michigan Area
Surface Soil Samples
PCDDs (PL)
2378-TCDO
Total Iso TCODs
Total penta COOs
Total hexa CDOs
Total hepta CDOs
OCDD
PCDFs (PL)
2378-TCDF
Total TCPFs
Total penta COFs
Total hexa COFs
Total hepta CDFs
OCDF
Upwind
Dow Chemical
In-Plant
Sample No.:
Field ID.:
Location:
13401
UPH-2-L
Pleasant
View School
13395
UPH-4-L
4853 W. Kent
13406
Station 5
Incinerator
13412
Station 14
West of 934 Bui
NO
NO
HP
NO
0.15
0.34
(0.004)
(0.004)
(0.024)
(0.024)
(0.024)
(0.026)
HP (0.004)
NO (0.008)
NO (0.022)
NO (0.031)
NO (0.051)
NO (0.004)
NP (0.023)
NO (0.023)
0.17 (0.034)
0.33 (0.034)
NO (0.004)
NO (0.008)
NO (0.023)
NO (0.028)
NO (0.045)
Notes: (1)
3.5 (0.039)
0.45 (0.06)
Concentrations of PCDDs, PCDFs. and detection
levels (PL) reported In parts per billion (ppb)
0.27
0.32
0.24
4.0
75.0
375.0
0.027
0.90
3.1
15.4
8.6
(0.007)
(0.067)
(0.067)
(0.9)
(1.3)
(0.007)
(0.14)
(0.13)
(0.38)
(0.48)
Source: Soil Survey (U.S. EPA 1985a)
-------
TABLE III-14
PCDDs and PCDFs
SITE II - Midland. Michigan Area
Surface Soil Samples
Public Use Areas
Saaple No.:
Field 10.:
13374
P-5-L
13392
P-6-L
13393
P-7-L
i
On
Oi
PCDDs (DL)
2378-TCDO
Total Iso TCDOs
Total penta CDOs
Total hexa COOs
Total hepta CDOs
OCDD
PCDFs (DL)
2378-TCDF
Total TCOFs
Total penta COFs
Total hexa COFs
Total hepta CDFs
OCDF
0.003 (0.001)
NO (0.001)
NO (0.014)
0.067 (0.007)
0.35 (0.013)
3.1 (0.096)
NO (0.002)
NO (0.002)
NO (0.01)
NO (0.01)
0.065 (0.02)
0.044 (0.023)
0.015 (0.003)
0.040
NO (0.035)
0.063 (0.035)
0.38 (0.028)
0.86 (0.027)
0.078 (0.003)
0.17
Interference
0.34 (0.02)
2.3 (0.055)
7.0 (0.068)
Notes: (1)
Source: Soil Survey (U.S. EPA 1985a)
Concentrations of PCDOs. PCOFs. and detection
levels (DL) reported In parts per billion (ppb).
13375
P-9-L
Location: County Line Rd. Mapleton School longvlew School Virginia Park
NO (0.002)
NO (0.002)
NO (0.01)
NO (0.01)
0.065 (0.02)
0.044 (0.023)
NO (0.005)
NO (0.008)
NO (0.024)
0.14 (0.043)
0.10 (0.071)
0.013 (0.007)
NO (0.025)
0.26 (0.036)
0.72 (0.021)
0.64 (0.037)
0.013 (0.002)
0.040 (0.01)
0.064 (0.01)
0.50 (0.034)
0.37 (0.049)
13391
P-10-L
Central School
(ball dlanond)
13394
P-ll-L
Bullock School
0.076
0.29
0.10
0.24
0.41
12.0
(0.003)
(0.018)
(0.018)
(0.093)
(1.5)
0.012
0.040
NO
0.086
0.35
0.68
(0.034)
(0.034)
(0.031)
(0.031)
NO (0.005) 0.015 (0.003)
0.11
0.22
0.12
0.41
2.4
7.0
(0.002)
(0.022)
(0.022)
(0.042)
(0.052)
NO (0.007)
NO (0.029)
0.16 (0.062)
0.11 (0.070)
0.11 (0.017)
0.17 (0.037)
0.82 (0.045)
0.66 (0.045)
-------
TABLE III-15
2378-TCOO
Dow Chemical - Midland Plant
In-plant Surface Soil Samples
Staple
Number
13404
14176
14190
14192
13406
14180
14178
14193
14194
1340S
14187
14182
13407
13412
13413
Field
Identification
Station 1
Station 2
Station 3
Station 4
Station 5
Station 6
Station 7
Station 8
Station 9
Station 10
Station 11
Station 12
Station 13
Station 14
Station IS
location
South of 492 Building
South of 1005 Building; Southwest of 703 Building
South of 703 Building
West of 703 Building
Southwest of 956 Building; East of 703 Building
Northwest of 1159 Building; North of Shot Pond
llth and J Streets - Northwest Corner
8th and G Streets - Northwest Corner at Steam Pipeline
Northwest of 1050 Building at F Street
South of 543 Building; West of 14th Street
16th and G Streets - Southwest Corner
16th and G Streets - Northwest Corner
17th and G Streets - Northwest Corner
West of 934 Building
South and East of 674 Building North of RR Tracks
2378-TCOO (DL)
(ppb)
0.018
0.074
0.42
0.020
3.50
0.13
4.60
0.15
0.010
0.045
0.44
0.46
0.22
0.27
25.0
[36.0]R
(0.003)
(0.005)
(0.013)
(0.003)
(0.039)
(0.013)
(0.083)
(0.010)
(0.003)
(0.005)
(0.016)
(0.012)
(0.007)
(0.007)
(0.50)
(0.28)
I Recovery I Solids
71
52
90
63
100
103
101
65
61
80
119
94
51
100
66
92
96
96
95
96
98
96
99
90
99
99
96
99
100.0
85.5
Notes: (1) 2378-TCDO concentrations and detection levels (DL) reported In parts per
billion (ppb).
(2) I Recovery - Recovery of Internal standard (C1*7 2378-TCDO or 13C 2378-TCDO)
expressed as percent.
(3) I Solids - Solids content of staple determined after sample homogenlzatlon.
expressed as percent. Analytical results not adjusted for moisture content.
(4) [ JR • Repeat analysis of same sample.
Source: Soil Survey (U.S. EPA 1985a)
-------
TABLE III-16
2378-TCOD
SITE #1 - Midland, Michigan Area
Surface Soil Samples
Sanple
Nunber
Upwind
13354
13343
13401
13395
13342
Field
Identification
Areas
UPH-l-L
UPW-1-1
UPW-2-L
UPW-4-L
UPW-4-0
Track Out and Perlmetei
13353
13360
13367
14188
14177
14191
13402
13389
14181
Public
13362
13364
13374
13392
13393
13340
13375
13391
13394
TO-4-G
TO-6-S
TO-9-G
PER-2-L
PER-2-1
PER-5-L
PER-8-L
PER-9-6
PER-10-L
Use Areas
P-l-L
P-2-L
P-5-L
P-6-L
P-7-L
P-8-L
P-9-L
P-10-L
P-ll-L
2378-TCDD (DL)
(ppb)
NO (0.002)
0.006 (0.002)
NO (0.004)
NO (0.004)
0.009 (0.001)
% Recovery % Sol Ids
821
76%
90%
84%
84%
94.9%
98.6%
94.0%
98.1%
84.2%
0.011 (0.003)
0.25 (0.018)*
0.014 (0.002)
0.31 (0.014)
0.069 (0.003)
0.21 (0.008)
0.010 (0.005)
2.03 (0.042)
0.040 (0.002)
0.019
0.028
0.003
0.015
0.078
0.17
0.076
0.012
(0.002)
(0.002)
(0.001)
(0.003)
(0.003)
(0.006)
(0.003)
(0.003)
52%
21%
68%
84%
55%
62%
104%
72%
73%
0.108 (0.002)
64%
64%
104%
86%
88%
94%
58%
92%
81%
99.3%
99.0%
99.0%
82.8%
99.0%
99.2%
99.0%
95.6%
97.1%
99.5%
89.7%
99.7%
80.2%
98.8%
96.5%
89.2%
96.6%
100.0%
Source: Soil Survey (U.S. EPA 1985a)
111-57
-------
TABLE III-17
2378-TCDO
SITE #1 - Midland. Michigan Area
Surface Soil Samples
Sample Field
Number Identification
Residential Areas
13007
13008
13101
13102
13328
13305
13306
13325
13103
13104
13317
13303
13314
13307
13105
13106
13318
13331
13319
13316
13329
13312
13330
13301
13304
13302
13313
A-l-l
A-l-1
A-3-L
A-3-1
B-l-L
B-l-1
B-3-L
B-3-1
B-4-L
8-4-1
C-l-L
C-l-1
C-3-L
C-3-1
C-4-L
C-4-1
D-l-l
0-1-0
0-2-6
D-3-L
0-3-1
E-l-L
E-l-1
E-3-L
E-3-1
F-l-L
F-l-1
2378-TCDO (DL)
(ppb)
0.075 (0.006)
0.090 (0.008)
0.009 (0.002)
0.112 (0.008)
0.076 (0.007)
0.16 (0.006)
0.020 (0.001)
0.27 (0.013)
0.019 (0.002)
0.028 (0.004)
0.026 (0.001)
0.054 (0.003)
0.012 (0.001)
0.24 (0.015)
0.024 (0.002)
0.032 (0.005)
NO (0.001)
0.024 (0.001)
0.028 (0.001)
0.018 (0.001)
0.031 (0.004)
0.026 (0.003)
0.049 (0.001)
O.X9 (0.001)
0.020 (0.001)
0.013 (0.001)
0.013 (0.001)
I Recovery I Sol Ids
1021
521
1021
321
1001
631
711
741
881
541
861
641
1001
711
861
881
941
1001
921
1001
861
961
801
751
701
731
921
83.01
89.71
88.51
76.51
93.21
97.01
97.81
87*11
84.71
88.11
78.71
84.41
98.61
98.11
91.01
88.91
84.01
99.51
94.91
90.91
99.81
97.51
97.01
97.61
99.11
99.01
96.81
Miscellaneous
14175
Sludge
0.021 (0.008)'
491
88.71
111-58
-------
TABLE III-17 (Continued)
2378-TCDO
SITE II - Midland, Michigan Area
Surface Soil Samples
Notes: (1) 2378-TCDO concentrations and detection levels (DL) reported 1n parts pe
billion (ppb).
(2) % Recovery - Recovery of Internal standard (Cl37 2378-TCDO or ^C 2378-TCDO
expressed as percent.
(3) 1 Sol Ids - Solids content of sample determined after sample homogen1zat1on
expressed as percent. Analytical results not adjusted for moisture content
(4) Field Identification of samples:
Location Type
UPW - Upwind L - Yard, lawn, or open area composite
TO - Track Out 1 or 0 - Downspout or drlpHne composite
PER - Perimeter G - Open area grab sample
P - Public Use
A-K - Residential
* Data not valid. Quality assurance objective not achieved.
Source: Soil Survey (U.S. EPA 1985a)
111-59
-------
ill-/
SURFACE SOIL SAMPLING LOCATIONS: MIDLAND, MICHIGAN
A3
UPW1
UPW2
UPVM4
f 1
[Oi
MIDLAND
P 1O
1O I
• 2
P«
• I
• 3
PI
C4
I I i • I I I I M
Pat 2
•ar-5 *
lfto.
S X V/ 1
Y
E 3
Hi-
,„..
E 1
E2
> w
Ipaf 4
DOW
CHEMK
COMPA
«•
1 D
P*S;
^
pit
H
OTO 10
* I I TO I
I 14
HnclM»l*i.
Dow Chemical
Lagoons
T ^•••^
Consumers \%
Power Company ^'
Lagoons
C2
P 7
DOW
CORNING
TO 2 O2
P»« 1
^
D3
(A F| Ratidanlial SampU
(Pai.TO) Panmatar •§ Trackoul
SampU
(116) Inplanl SampU
|P| Public AccaM SampU
|UPW| Upwind SampU
O SampU Obtained.
*••
Source: Soil Survey (U.S. EPA 1985a)
-------
The upwind residential samples were located west-southwest of the Dow
Midland facility. Five composite samples were analyzed for 2378-TCDD. The
three samples obtained from the lawns did not contain detectable levels
(detection limits ranged from 2-4 ppt). The two samples collected near
downspouts or roof driplines contained 6 and 9 ppt of 2378-TCDD. Two upwind
lawn samples were analyzed for CDD/CDF homologues. The soils contained HpCDDs
ranging from 150 to 170 ppt and OCDD ranging from 330 to 340 ppt. No other CDD
homologues and no CDF homologues were detected. The results are displayed
graphically in Figure III-8.
Results of analyses for 2378-TCDD of 15 surface soil samples obtained from
inside the Dow Midland facility revealed concentrations ranging from 10 ppt to
30,000 ppt (mean 2,700 ppt; for discussion of use of arithmetic means, see
p. III-8). All samples contained detectable concentrations of 2378-TCDD.
Eight samples were obtained from the perimeter of the facility, and 2378-TCDD
concentrations ranged from 10 ppt to 2,030 ppt (mean 340 ppt). All eight
samples were positive for the presence of 2378-TCDD. Concentrations of CDD/CDF
homologues were determined in one soil sample. All homologues were detected,
except TCDFs, for which an analysis was not performed. The results are
presented graphically in Figure III-9, and differ noticeably from the upwind
samples presented in Figure III-8 due to the presence of CDFs and less
chlorinated CDD congeners.
Public use areas of Midland downwind (north-northeast) of the Dow Midland
facility were sampled, and all samples contained detectable levels of 2378-
TCDD. Nine samples analyzed for 2378-TCDD contained concentrations ranging
111-61
-------
FIGURE III-8
PATTERN OF CDDs/CDFs DETECTED IN SOILS UPWIND OF THE DOW MIDLAND FACILITY
I
&
80
60 -
40
20
Q UPWIND 2-L
Q UPWIND 4-1
'-
i
-------
*
i
£
FIGURE III-9
PATTERN OF CDDs/CDFs DETECTED IN SOILS OF THE DOW MIDLAND FACILITY
20-
8
i
77K
E
a.
_i
o
o
El DOW IN PLAN!
-------
from 3 ppt to 170 ppt (mean 57 ppt). Of the above samples, six were analyzed
for CDD/CDF homologues, and the results are presented in Figure 111-10. The
pattern of CDD/CDF congeners detected in the public use areas is similar to
that in soil samples obtained from the Dow Midland facility.
In the residential areas of Midland downwind of the Dow Midland facility,
lawn and downspout/dripline samples were obtained. Twelve of thirteen lawn
composite samples analyzed were positive for the presence of 2378-TCDD, and
concentrations ranged from undetected to 76 ppt (mean of 25 ppt, assigning one-
half of the detection limit to the one "not detected" report). All of the 13
downspout/dripline samples contained detectable concentrations of 2378-TCDD,
ranging from 13 ppt to 270 ppt (mean of 86 ppt). With one exception
(sample F-l), all of the downspout/dripline samples contained higher
concentrations of 2378-TCDD than did the lawn samples. Analyses for CDD/CDF
homologues were not performed on the residential samples.
In general, the analytical results of the surface soil sampling program
are consistent with the hypothesis that the Dow Midland facility is the primary
source of CDD/CDF compounds detected in environmental media in the Midland
area. The following results contribute to this hypothesis.
• Upwind, residential lawn samples contained primarily HpCDDs and OCDD,
a pattern similar to that seen in natural areas and in cities that do
not contain extensive chemical manufacturing facilities (EPA 1985a).
Soil samples from upwind lawns did not contain detectable quantities
of 2378-TCDD. The 2378-TCDD isomer could be detected only at
locations that received the composite, concentrated products of
atmospheric deposition on roof surfaces, such as roof downspouts and
driplines.
• All samples obtained from the grounds of the Dow Midland facility
contained detectable concentrations of 2378-TCDD and also contained
detectable concentrations of all CDD/CDF homologues for which
111-64
-------
FIGURE III-10
PATTERN OF CDDs/CDFs DETECTED IN MIDLAND PUBLIC USE AREA
SOILS DOWNWIND OF THE DOW MIDLAND FACILITY
20 -
_ffTrti
Lin
n.
ill 1
[0 COUNTY LINE
0 MAPI ETON
Q BULLOCK
D LONG VIEW
D VIRGINIA PK
0 CENTRALSCH
-------
analysis was performed. The HpCDD and OCDD congeners that were
dominant in upwind samples were present at the Dow Midland facility
at concentrations that were 2-3 orders of magnitude higher than the
upwind samples.
All samples, except one, from the public use and residential areas of
Midland downwind from the Dow Midland facility contained detectable
concentrations of 2378-TCDD. The downspout/dripline samples
generally contained higher concentrations of 2378-TCDD than did the
lawn samples. The concentrations of the CDD/CDF homologues in the
public use areas were about 1-2 orders of magnitude less than the
concentrations in the Dow Midland facility soils. However, the
downwind public use-area samples contained concentrations of HpCDDs
and OCDD that were an order of magnitude higher than in samples that
were upwind of the Dow Midland facility. The downwind samples also
contained CDD/CDF homologues that were not detected in upwind
samples, but were detected in the Dow Midland facility soils.
Table 111-18 presents calculated TEQs (toxicity equivalents of 2378-TCDD;
see Section II) for the CDDs/CDFs measured at the locations discussed above.
These calculations use the "B-method" (USEPA 1987d), in which it is assumed
that all CDD/CDF congeners are equally likely to occur and congeners are
allocated to 2378-substituted and non-2378-substituted categories in proportion
to the number of each type of congener within each homologue group (except
TCDDs, for which these results are available). Based upon the limited number
of samples that received homologue-specific analyses, a significant
contribution to the TEQs comes from 2378-TCDD in the Dow Midland facility and
Midland public use area samples. The TEQs were greater than the 2378-TCDD
concentrations by a factor of 1.4 in the Dow Midland facility samples and 1.1
in the Midland public use area samples. Because 2378-TCDD contributes such a
large fraction of the TEQs, use of the "A-method" gives very similar estimates
and the results are not presented separately here.
111-66
-------
The second section of Table III-18 shows estimates of TEQs based on all of
the soil samples, including those which are analyzed only for 2378-TCDD. As in
Clark (1985), these estimates were derived by assuming that the ratio of
TEQ/2378-TCDD in these latter samples would have been approximately the same as
that derived for the soil samples in the first section of Table III-18. These
ratios are then multiplied by the mean concentration of 2378-TCDD in the soil
samples from the same general location to yield the estimates of TEQ listed in
the right-hand column. "Average" residential soil concentrations of 2378-TCDD
and TEQs are calculated by assuming that the downspout/dripline-contaminated
areas represent 10 percent of the area of the yard (Clark 1985). The TEQs
calculated in Table III-18 will be used in the subsequent exposure assessment.
2. Populations at Risk and Exposure Assumptions
Children may ingest soil by playing or crawling on their hands and then
placing their hands in their mouths. Some children even directly eat soil, a
behavior known as pica. Older children are less likely to exhibit this
behavior. Adults may be exposed to soil contaminants by inadvertent ingestion
of soils resulting from smoking or eating with contaminated hands. Exposure to
soil is difficult to quantify due to the uncertainties caused by individual
behavioral differences. As a result, the exposure assumptions will be defined
as ranges, incorporating an upper and lower estimate of exposure.
LaGoy (1987) discusses the assumptions used to estimate the quantities of
soil that could be inadvertently ingested by various age groups. The most
likely population at risk is younger children. For 1 to 6-year-old children,
III-67
-------
TABLE III-18
2378-TCDD TOXICITY EQUIVALENTS (TEQs)
SURFACE SOIL SAMPLES
(PPt)
A. Isomer/Homologue-Specific Analysis
Sample
Upwind lawn
Dow-Midland facility
Downwind public use
Number of
Samples
2
1
area 6
Mean
Concentration
of 2378-TCDD
ND (2)1
270
49
TEQ
ND (3)
390
53
Ratio of TEQ/
2378-TCDD
(1.5)
1.4
1.1
B. Estimates of TEQs From Analyses For 2378-TCDD
Sample
Number of
Samples
Mean
Concentration
of 2378-TCDD
Ratio of TEQ/
2378-TCDD2
Estimate
TEQ:
Upwind
Lawn
Downspout/drip1ine
Dow Facility
Plant
Perimeter
3
2
15,
ND (2)'
8
2,700
340
(1.5)
1.5
1.4
1.4
ND (3)
12
,800
480
Downwind
Public use area
Residential lawn
Residential downspout
Residential Average
96
136
13b
57
25
86
31
1.1
1.1
1.1
1.1
63
28
95
34
-One-half of the detection limit used to estimate concentrations.
-From Part A of the table.
.Product of third and fourth columns.
,-Includes samples from locations that have since been remediated.
gSample TO-6-G rejected for QA/QC reasons.
Sample D-2-6 could not be identified as to type of sample and was not included.
"Average" residential soil concentrations of 2378-TCDD are calculated by the
method of Clark (1985), assuming that the downspout/dripline-contaminated areas
represent 10% of the area of the yard.
111-68
-------
incidental ingestion of 500 and 100 mg/day of soil are the upper and lower
estimates, respectively. For 0 to 1 and 6 to 12-year-old children, ingestion
rates of 250 and 50 mg/day are assumed. For older children and adults,
ingestion rates of 100 and 25 mg/day are estimated.
Although children who exhibit pica may ingest significantly higher
quantities of soil, these children are assumed to comprise a small percentage
of the children in the age group of concern. Dermal absorption of CDDs/CDFs
from soil and dust is not considered since the absorption and therefore dose
received by this route are expected to be one or two orders of magnitude below
the exposure from soil ingestion (Poiger and Schlatter 1980).
The actual duration of exposure to outdoor soils varies, but a "severe
worst-case" for most situations has been developed by USEPA (1984b) as 247
days/year by assuming that, on the average, soil in the northern United States
remains frozen 118 days each year. For the purposes of this assessment, it
will be assumed that children (less than 12 years old) will be exposed 250
days/year as the upper estimate, and about half this number, or 125 days/year,
for the lower estimate. Adults are estimated to be exposed via yard work
approximately once each week during the months of May-October (25 days/yr), or,
for avid gardeners, 4 days per week (100 days/year) during the same period.
It is also assumed that the most probable location of periodic exposure of
younger children and adults is the individual's residence. Residential samples
collected downwind of the Dow Midland facility did not receive
isomer/homologue-specific analyses for CDDs/CDFs. The estimated TEQs from
111-69
-------
Table 111-18 for downwind "average" residential yards are used to estimate
chemical intakes resulting from exposure of younger children and adults to
soils. For older children (6-12 years), it is assumed that they are more
likely to play in parks, and be exposed to soils in locations other than their
residences. Chemical intakes resulting from exposure of older children to
soils will be calculated using the average of the "public use" TEQs and the
"average" residential TEQs.
McConnell et al. (1984) and Rumbaugh et al. (1984) investigated the
absorption of 2378-TCDD from soil after ingestion by administering contaminated
soil from Times Beach and Minker-Stout, Missouri, to guinea pigs and rats. The
soil was suspended in water and administered by gavage. The toxic responses
(death in guinea pigs, AHH induction in rats) and tissue residues were compared
with those observed when similar quantities of 2378-TCDD were administered in
corn oil. The relative responses suggested that about one-third as much 2378-
TCDD was absorbed from soil as from corn oil by guinea pigs, and 50-100 percent
(mean 84%) as much 2378-TCDD was absorbed from soil as from corn oil by rats.
Other studies have suggested that when 2378-TCDD is administered to rats in
feed (Fries and Marrow 1975) or in ethanol (Poiger and Schlatter 1980), between
50% and 70% is absorbed into the body. Hence these results suggest that
percentage absorption from ingested Times Beach soil is about 20% by guinea
pigs and about 50 percent by rats.
Umbreit et al. (1985) fed contaminated soil from an industrial site in New
Jersey to guinea pigs and found no deaths or toxic signs; their data suggest
that considerably less than half as much 2378-TCDD was absorbed from
111-70
-------
contaminated soils collected in the field as from soils to which 2378-TCDD was
added in the laboratory. Umbreit et al. (1986) fed 2378-TCDD-contaminated soil
from Newark, New Jersey and Times Beach, Missouri to guinea pigs. Missouri
soils were observed to be toxic (LE>50 <10 ug/kg) while Newark soils were not
toxic at comparable concentrations. USEPA (1984b) recommended a range of 20-26
percent for absorption of 2378-TCDD from ingested soils based on data of Poiger
and Schlatter (1980). However, all the studies cited above (McConnell et al.
1984, Rumbaugh et al. 1984, Umbreit et al. 1985, 1986, Poiger and Schlatter
1980) were of soils in which 2378-TCDD was present in mixtures with other
organic compounds or soils to which 2378-TCDD had been added in solution. It
is not clear that such studies will provide reliable measures of
bioavailability in circumstances such as those prevailing at Midland, where
most of the CDDs/CDFs would have been deposited onto the soil from the air,
probably mostly attached to fly ash particulates. It is not known to what
extent the CDDs/CDFs would subsequently have been desorbed from the fly ash
particulates and resorbed onto the soil, but it is likely that at least some of
the CDDs/CDFs would remain attached to fly ash.
Bonaccorsi et al. (1983) performed an experiment with contaminated soil
from Seveso, Italy, and found that 32% as much 2378-TCDD was absorbed from the
soil as from an alcohol-water solution after ingestion by rabbits. The soil at
Seveso was contaminated by deposition from the air, but this took place in a
"toxic cloud" released in an industrial accident, and is unlikely to be
representative of deposition on fly ash.
111-71
-------
The most relevant study of bioavailability of CDDs/CDFs from fly ash is
that of Van den Berg et al. (1983). These authors prepared diets containing
either fly ash from a municipal incinerator or toluene extracts of this fly
ash. These diets were fed to rats for 19 days, at which time the rats were
killed and their livers were analyzed for CDD/CDF homologues and for selected
congeners. Although Van den Berg et al. (1983) did not report estimates of
bioavailability, such estimates can be derived from their Table 6, which
reports percentages of 11 congeners (mostly 2378-substituted) retained in
livers of the rats. These data suggest that, relative to the rats fed food
containing toluene extracts of the fly ash, rats fed food containing whole fly
ash accumulated about 24% of the TCDDs and TCDFs, 10% of the PeCDDs and PeCDFs,
and 7% of the HxCDDs and HxCDFs. These percentages are estimates of relative
bioavailability; the data of Fries and Marrow (1975) indicated that rats fed
food contaminated with 2378-TCDD via a solvent absorbed between 50 and 70
percent (mean, 55 percent) of the quantity administered. Assuming the same
range of values would apply to other CDDs/CDFs, estimates of absolute
bioavailability from fly ash would be about 13% for TCDDs/TCDFs, 5% for
PeCDDs/PeCDFs, and 4% for HxCDDs/HxCDFs. Since TCDDs and TCDFs accounted for
most of the TEQs for soil samples at Midland (Tables IIIrl3 and 111-18), an
overall estimate of bioavailability for the TEQs found in soil would be about
12%. This is about half the range of values (20-26%) suggested for
bioavailability from soil by USEPA (1984b). Since it is not clear to what
extent the CDDs/CDFs would have been desorbed from fly ash particles and
resorbed onto soil paricles at Midland, this report uses an intermediate value
of 18% as an estimate of bioavailability for the "lower estimate" exposure
scenario. For the "upper estimate" exposure scenario, a value of 40% is used,
111-72
-------
based on the higher value derived for Times Beach soil (see above and USEPA
1984b). These assumptions are listed in Table 111-19.
Intake estimates for soil ingestion are calculated as follows:
PgAg/day - (C,)(D(E)(X)(A)
(BW)(D)
where
C - Chemical concentration in soil (pg/g or ppt)
I - Amount of soil ingested (mg/day)
E - Number of days of exposure (days/yr)
X - Conversion factor (g/10 mg)
A - Relative absorption rate (percent/100)
BW - Average body weight (kg)
D - 365 days/yr
Table 111-20 presents the amounts of 2378-TCDD and estimated TEQs ingested
under the assumptions discussed above for soil concentrations and ingestion
rates.
The estimates of intake tabulated in Table III-20 represent estimates of
the absolute amounts of CDDs/CDFs taken into the body of the exposed
individuals. As discussed earlier in Section III.a.6, these estimates require
further adjustment when they are compared with the RfD and HAs, because the
latter are expressed in terms of adminstered dose. In Chapter IV, an
additional factor will be applied to the estimates of absorbed dose tabulated
in Table III-20, to make them commensurable with the RfD and HAs.
111-73
-------
TABLE III-19
ASSUMPTIONS USED WHEN CALCULATING INTAKES OF CDDs/CDFs
BY RESIDENTS EXPOSED TO SOILS
Parameter
Lower
Estimate
Upper
Estimate
Exposure events
Children (0-12 years)
Adults (12-70 years)
Period of exposure:
Children aged 0 to 1 year
Children aged 1 to 6 years
Children aged 6 to 12 years
Ages 12 and greater
Average weight over period of exposure:
Children aged 0 to 1 year
Children aged 1 to 6 years
Children aged 6 to 12 years
Ages 12 and greater
Incidental ingestion of soil:
Children aged 0 to 1 year
Children aged 1 to 6 years
Children aged 6 to 12 years
Ages 12 and greater
Concentration of CDDs/CDFs in soil:
Younger Children (0-6) and Adults (12-70)
Older Children (6-12)
125 days/yr
25 days/yr
1 year
5 years
6 years
58 years
50 mg/day
100 mg/day
50 mg/day
25 mg/day
250 days/yr
100 days/yr
1 year
5 years
6 years
58 years
8 kg 8 kg
15 kg 15 kg
30 kg 30 kg
70 kg 70 kg
250 mg/day
500 mg/day
250 mg/day
100 mg/day
34 ppt
(Downwind
Residential
Average TEQs)
49 ppt
(50% Downwind
Residential
Average TEQs
and 50% Public
Use Area TEQs)
Fraction of CDDs/CDFs absorbed from ingested soils 0.18
34 ppt
(Downwind
Residential
Average TEQs)
49 ppt
(50% Downwind
Residential
Average TEQs
and 50% Public
Use Area TEQs)
0.40
111-74
-------
TABLE 111-20
INTAKES OF CDDs/CDFs ASSOCIATED WITH EXPOSURE OF RESIDENTS TO
SOILS DOWNWIND OF THE DOW MIDLAND FACILITY
Age Group
(Years)
Dose Rate (pg/kg-day)
Soil Ingested
(mg/day)
Assumed
Body Weight
(kg)
Frequency of Exposure Soil
(days/yr) Concentration 2378-TCDD
(pg/g)
TEQ
Lower Upper Lower Upper Lower Upper Lower Upper
Estimate Estimate Estimate Estimate 2378-TCDD TEQ Estimate Estimate Estimate Estimate
0 to 1 8
1 to 6 15
6 to 12 30
12 to 70 70
Child average
(0-12 yrs)
Lifetime Average
(0-70 yrs)
50
100
50
25
250
500
250
100
125
125
125
25
250
250
250
100
31 34 0.012 0.27
31 34 0.013 0.28
45 49 0.0045 0.10
31 34 0.00014 0.0049
0.013 0.29
0.014 0.31
0.0050 0.11
0.00015 0.0053
0.0087
0.0016
0 19
0.036
0.0094
0.21
0.0017 0.040
111-75
-------
3. Data Limitations
The soil samples obtained from residences downwind of the Dow Midland
facility were analyzed for the 2378-TCDD isomer only. The soil exposure
assessment was therefore performed using measured concentrations of 2378-TCDD
and estimated concentrations of TEQs. A review of the data shows that the
large majority of the estimated TEQ for lawn, downspout, and public use area
samples is contributed by the measured 2378-TCDD, however.
No information is available on time trends in soil contamination, i.e.,
whether the concentrations of CDDs/CDFs are increasing or decreasing with time.
The available data were collected October-December 1983. Limited data
summarized in section III.A (above) suggest that emissions of CDDs/CDFs from
the Dow Midland facility waste incinerator were much higher on days for which
sampling was conducted in 1983 than in 1984 or 1987. Hence, it is likely that
atmospheric inputs of CDDs/CDFs into Midland soils have decreased since 1983.
However, the rate of decrease of the soil concentrations of CDDs/CDFs, if any,
will be determined by the rate at which the CDDs/CDFs in the soil will be lost
by degradation or other processes.
The persistence of CDDs/CDFs in Midland soils is poorly characterized but
likely to be variable. Concentrations of CDDs/CDFs in the top few millimeters
of soil or on the surfaces of plants, buildings, etc. can be expected to be
depleted due to environmental degradation processes (i.e., photolysis,
resuspension, volatilization) (Thibodeaux and Lipsky 1985). The CDDs/CDFs that
are in deeper layers of soil are more resistant to degradation. In addition,
111-76
-------
activities such as landscaping, gardening, or tilling may mix soils at
different depths and, hence, reduce the surface concentrations.
A major source of uncertainty in exposure estimates is the lack of
information on the vertical distribution of CDDs/CDFs in soil. Available data
from Midland represent composites of the topmost inch (25 mm) of the soil
column. Most exposure of children is likely to be to soil in the topmost few
millimeters. If the soil has not been disturbed or well mixed, CDDs/CDFs may
be concentrated in this surface sublayer because atmospheric deposition is the
primary route of input. On the other hand, if the soil has been mixed
periodically, CDFs may be depleted in the surface sublayer through
volatilization, photodegradation, or other loss processes that occur when soil
is exposed at the surface (Thibodeaux and Lipsky 1985) . Adults may be exposed
to soil from the same surface sublayer if their exposure derives primarily from
casual contact, but may be exposed to soil from depths greater than 25 mm if
their exposure is primarily from gardening.
In the absence of data on trends in atmospheric deposition, persistence of
CDDs/CDFs in soil, or vertical distribution of residues, it is assumed in this
exposure assessment that the concentrations measured in residential soils in
1983 are representative of those to which people are currently exposed and will
remain essentially constant, at least for the 12-year period during which most
lifetime exposure takes place (Table 111-20). It should be recognized,
however, that the estimates of intakes presented in Table III-20 may be too'
high or too low, depending on the factors discussed above.
111-77
-------
Another source of uncertainty in exposure estimates is the limited body of
information on soil ingestion rates. The available information is discussed by
LaGoy (1987). Although the "upper" and "lower" rates of soil ingestion listed
in Table III-19 are reasonable, each could be either too high or too low for
conditions in the Midland area. In particular, children with pica may ingest
soil at a rate one order of magnitude higher than the maximum listed in
Table 111-19 (LaGoy 1987); such children could have intakes of CDDs/CDFs an
order of magnitude higher than those listed in Table III-20.
A final source of uncertainty in exposure estimates is the estimates used
for bioavailability. The values listed in Table 111-19 are derived from a
study of fly ash containing CDDs/CDFs, and from a study of Missouri soils,
which had been contaminated with 2378-TCDD by application of contaminated oil
12 years earlier. Most CDDs/CDFs in Midland soil will presumably have been
deposited on airborne particulates and have been retained in soil from varying
periods. It is not clear to what extent the CDDs/CDFs would have been desorbed
from fly ash particles and resorbed onto soil particles. Bioavailability of
CDDs/CDFs from these soils may be higher or lower than indicated by the values
used in this exposure assessment.
Overall, as indicated by the discussion in this section, the exposure
estimates derived in this section are subject to substantial uncertainty.
Although the assumptions and parameters used in this assessment are reasonable,
the estimates of intake listed in Table 111-20 could be either too high or too
low, possibly by a large factor in either direction. This range of uncertainty
will be taken into account in the risk assessment in Part IV of this report.
111-78
-------
D. Water
Samples of potable groundwater, potable surface water, and brine from the
Dow Midland facility's brine operations were obtained by USEPA between August
1984 and September 1985. The results of the sampling and analyses were
reported in December 1985 (Barna and Amendola 1985). This section of the
exposure assessment presents the results of that analysis.
1. CDD/CDF Concentrations in Water
a. Surface Water Supplies.
Three intakes in Saginaw Bay are used as raw water supplies for four
Michigan communities. The Saginaw/Midland intake extends about 2 miles into
Saginaw Bay east-northeast of Whitestone Point. The Bay City intake extends
about 3-1/2 miles into the bay from shore in a northerly direction. The
Pinconning intake extends about one mile into the bay in an east-northeast
direction. Figure III-ll is a location map for these intakes.
Raw water samples were collected from taps in the pump buildings for the
above cities on August 5, 1984, and December 3-5, 1984. A sample from the
Saginaw River, identified as a standby water intake for the City of Saginaw,
and a sample of finished tap water from the City of Midland were also taken,
for a total of five samples.
111-79
-------
FIGURE III-ll
PUBLIC WATER SUPPLY INTAKES FROM SAGINAW BAY
p;»»M~* SAG I NAVY
Approx. scale (miles)
20
Source: Barna and Amendola 1985
FLIUT
-------
2378-TCDD was not detected in any of these samples. Detection limits
ranged from 2-10 parts per quadrillion (ppq) or picograms/liter (pq/1). These
samples were not analyzed for other CDDs and CDFs. The detection of 2378-TCDD
in surface water intakes was not expected given the low documented discharge
levels of CDDs/CDFs from the Dow Midland facility, the low water solubility and
strong tendency of CDDs/CDFs to adsorb to particulate matter, and the
considerable dilution afforded by the distance from the point of discharge from
the Dow Midland facility to the respective water intakes (Barna and Amendola
1985).
b. Potable Groundwater Supplies.
One public groundwater supply, 14 private groundwater supplies generally
located near Dow Midland brine operations and landfills, and one artesian well
reportedly used as a source of drinking water were sampled. The locations of
the sampled wells are presented in Figure 111-12.
Groundwater samples were obtained on December 3-5, 1984. 2378-TCDD was
not detected in any of the samples, with limits of detection ranging from 4-50
ppq (Table 111-21). Five supplemental samples were obtained on June 12, 1985,
and apparent positive findings of 2378-TCDD were found in two samples
(Table 111-22). However, these findings were not confirmed by subsequent split
sample analyses (detection limit 6-10 ppq) or by analyses of additional samples
obtained on August 2, 1985, at those two locations (detection limit 1-10 ppq)
as shown in Table 111-22.
111-81
-------
FIGURE' III-12
POTABLE GROUNDWATER SAMPLING LOCATIONS
LEGEND:
" -PUBLIC WATER SUPPLY
M
O -PRIVATE WELL
A -ARTESIAN WELL
Brine System
Production Well
Reinfection Well
Approx. scale (miles)
Source: Barna and Amendola 1985
HIDlANO COUKTY
COUNTY
111-82
-------
TABLE 111-21
Midland Area Ground Water Samples
2378-TCOO — December 3-5, 1984
(parts per quadrillion)
Well Location 2378-TCDD (PL)
A
8
C
0
E
F
G
H
I
L
M
N
P
Notes: (1) Samples analyzed by Midwest Research Institute (MRI)
(2) NO - Not detected.
(3) Detection level - ( ).
Source: Barna and Amendola 1985
NO
NO
NO
NO
NO
NO
NO
NO
NO
NO
NO
NO
NO
( 4)
( 7)
( 4)
(50)
( 4)
( 5)
(12)
( 4)
( 2)
( 6)
(12)
( 4)
( 7)
111-83
-------
TABLE III-22
Midland Area Ground Water Samples
2378-TCDP -- June 12. 19d5
(Results in parts per quadrillion (ppq).)
Sample
Number Location NWQL Brehm Laboratory Pow Chemical
2378- 2378- 2378-
TCDD (PL) TCDD (PL) TCPP (PL)
Samples Collected on June 12. 1985
PE017601 Hapleton 20 (10) -- -- NO (6)
602 Hapleton (Pup) NP (10) Nl) (8)
603 Artesian NP* (10) -- -- NO (8)
604 Private NP (10) -- -- NO (7)
605 Private NP (10) NO (9)
606 Private 30-40 (10) NO (10)
607 • Field Blank NP (10) NP (9)
— NWQL Lab Blank NP (10)
-- Brehm Laboratory -- -- NP (6)
Reagent Blank
Do* Chemical -- -- -- -- NP (5)
Heayent Blank
*ND (10) at resolution 9000; 40 (10) at resolution 5000.
All other samples analyzed at resolution 5000.
Samples Collected on August 2, 1985
85EG09S02 Mapleton NO ( 7) -- -- NO (I)
SOI Artesian NO (10) . -- -- NO (1)
001 Artesian (Pup) NP (6)
Field Blank NP (3)
NWQL Lab Blank NO (3)
Notes: 1. PL - Petection level.
2. NP - Not detected at stated detection level.
3. Screening analyses for PCPPs and PCPFs by NWQL fur samples collected
on June 12. 19Mb. showed no detectable PCIMs or ITIH s .
-------
To ensure that 2378-TCDD was not present in groundwater from these wells,
USEPA initiated a follow-up survey which involved analyses of six potable water
samples. Split samples analyzed by three laboratories show that groundwater at
these locations did not contain detectable concentrations of 2378-TCDD
(detection limits of 0.2-3.6 ppq), as shown in Table 111-23.
One set of analyses for other CDDs/CDFs in potable well water samples was
invalidated due to in-lab contamination problems with TCDDs, OCDD, and OCDF.
Screening analyses for CDDs/CDFs in subsequent samples collected on June 12,
1985, showed no detectable CDDs or CDFs.
c. Dow Midland Brine Operations.
The Dow Midland facility was founded in 1897 as a producer of brine
chemicals. Naturally occurring brine was pumped from the Sylvania aquifer, a
sandstone formation about 5,000 feet below the surface. After removal of salts
and minerals, the spent brine was sent to Brine Pond No. 6 for holding prior to
filtration and pressure injection to the same formation through return wells.
The brine operations are being shut down as part of a consent order with the
Michigan Department of Natural Resources (Barna and Amendola 1985). The Dow
Midland facility brine operations are shown in Figure III-13.
The north, south-southwest, combined raw brine main lines, and production
well 29 were sampled for the presence of CDDs/CDFs in raw brine liquid. Brine
pond sediments were sampled at three locations in Brine Pond 6: near the inlet
111-85
-------
TABLE 111-23
NldUnd Are* bround Utter Staples
2318-ICUO -- S*pte^>«r 3. IMS
(PA
field
>les:
00
DC 017901
M 011*02
Of 011*03**
oe 011904
DC 011*08
Of 011*0*
OAStaples:
Field lltnk
(DC OU90S)
field Staple Spiked
(DC 011*0*)
field Hank Spiked
(Ot OIIMI)
USCr A - NUQL
Method
23II-ICOO efficiency
PfH (••/»•) «t IIS M/kg
NO
NO
NO
NO
NO
NO
1.0
O.t
0.)
1.0
1.3
)..
Ml
(SI
Ml
Ml
111*
391*
NO (0.3) 181
MO (11)
»
Notes
11. S
III*
I III
•lltnk utter - 3*1*. N0(0.2)
•Spiked utterl - 4S1.29|l.lj
• StapU DC 011*0* - positive
slgntls observed for
M/f 320 tnd 322; did not
•eet
lofl-rttlo-crlterlt.
•Method efficiency belo«
tccepttble level for
national
dleiln study.
'Spike level 24 pg/kg (pp<|).
Irehu Ltborttory
HrtflNt Sttte University
Nethod
2378-ICDO irriclcncy
ppq (pi/kg) it I2S pg/k]
NO 1 4 l/NO (1.2 S21/S9I
NO 1 S)/NO (|.a S91/SOI
NO | 4 /NO (2.0 44I/4S1*
NO 1 1 /NO I.I I31/S11
NO 1 4) /NO (I.I) 481/411
NO/11. 9) SSI
NO (I.2)/NO (2.0) Sal/481*
11.4/9.9 SSS/S91
13. 9/10. S 411/SII
Notes;
•Method efficiency below
tccepttble level for
national dloiln study.
Oo« Chcalcal
23/8-ICOO «JC 23/8-ICOO pg
(PPI) 1 Recovery*
NU (1) 461
NO (0.9) 811
NO (1) 821
NO (0.8) 4U
NO (1) 8)1
NO (0.8) 8S1
NO (0.8) 811
10 (0.8) 8)1
12 (0.8) 4/1
Notes:
Reagent Analyses 2318-ICUO
Blank f Set 1 (pa)
II Set II NO (3)
12 Set 12 NO (3)
f) Set |3 NO (!)
• fortification level • S.O ng 'JC
per staple.
• IHO staples »ere spiked with 40
2378-ICOO.
2318-ICM)
Observed0
—
...
—
—
~ * ""
...
3S P9
40 pg
•k 23/8-KUO
1 Recovery*
481
111
m
23/8-ICUO
pg native
••Field settle spiked Ot 01/904 corresponds to field staple Oi 01/903.
Source: Barna and Amendola 1985
-------
FIGURE 111-13
DOW MIDLAND FACILITY BRINE SYSTEM
Production Well
R«in|«ction Well
N
Approx. scale (miles)
k
Gfitiot County
Midland County
S«9in«w County
Source: Barna and Amendola 1985
111-87
-------
and outlet and at one intermediate location. Samples were collected on August
13-14, 1984, October 22, 1984, and December 3, 1984.
2378-TCDD was not detected in any of the liquid brine samples. Detection
limits ranged from 2-54 ppq. Analyses for other CDD/CDF homologues in the
liquid brine samples were invalidated due to the presence of CDDs/CDFs in
laboratory method blank samples (Barna and Amendola 1985).
In the brine pond sediments, 2'378-TCDD was not detected, with detection
limits ranging from 6.9 to 15.7 ppt. However, CDD/CDF homologues were
positively detected in the three brine.pond sediment samples, as shown in Table
111-24. A possible source of the CDDs/CDFs may be deposition from atmospheric
emissions from the Dow Midland facility (Barna and Amendola 1985).
2. Populations at Risk
Analyses of public and private water supplies from both surface water and
groundwater sources did not detect CDDs or CDFs at detection limits as low as
0.2 ppq. Analyses of the water samples indicate that there is little
likelihood of a public health concern associated with ingestion of water from
the sampled surface and groundwater sources. As a result, exposure to
CDDs/CDFs in potable water is not quantified.
The brine pond sediments contain ppt levels of CDDs and CDFs. There is no
reasonable likelihood of direct public exposure to these sediments, and the
111-88
-------
TABLE III-24
CDDs/CDFs DETECTED IN BRINE POND SEDIMENTS
CDDs
Ranee (ppb)
CDFs
Range (ppb)
Total TCDDs
Total PeCDDs
Total HxCDDs
Total HpCDDs
OCDD
ND-0.016
ND-0.15
ND-0.07
0.19-0.21
1.5-3.8
2378-TCDF
Total TCDFs
Total PeCDFs
Total HxCDFs
Total HpCDFs
OCDF
0.03-0.11
0.04-0.21
ND
ND-3.5
ND-2.8
0.5-5.8
111-89
-------
presence of CDDs and CDFs in the brine pond sediments is not likely to pose a
public health threat (Barna and Amehdola 1985) . Exposure to CDDs/CDFs in brine
pond sediments is also not quantified.
111-90
-------
E. Fish
In 1978, the Dow Chemical Company submitted a report to the USEPA which
indicated that detectable levels of 2378-TCDD had been found in Tittabawassee
River fish taken downstream, but not upstream, of the plant process outfalls
and that these results had been corroborated by fish bioaccumulation studies,
indicating that the outfall was a likely source of 2378-TCDD to the river (Dow
1978).
In subsequent years, a number of additional studies of 2378-TCDD
contamination of fish from the river have been conducted by the industry and by
State and Federal governments. In addition, there have been investigations of
a wide range of chemical contamination in river sediment and various process
streams within the manufacturing facility. In the summer of 1986, USEPA Region
V produced a report which summarizes this information (Amendola and Barna
1986).
The fish studies have used one of two approaches: 1) harvest native fish
upstream and downstream of the Dow Midland facility or 2) place caged fish
upstream and downstream of the plant for a period of 30 days. In either case,
the collected fish were subsequently subjected to extraction of CDDs/CDFs,
"clean-up" (to isolate the CDDs/CDFs from other compounds which could
potentially interfere with the final analysis), and analysis by gas
chromatography/mass spectrometry (GC/MS).
111-91
-------
The Tittabawassee River is not a commercial fishery. However, the river
is used by sports fishermen, from above Midland to its confluence with the
Saginaw River some 30 miles downstream. Stocking of walleye in the
Tittabawassee River has resulted in a popular sports fishery, with reports of
fishermen catching fish even within the plant's process outfall mixing zone.
1. CDD/CDF residue levels
Table III-25 (Table 38 from Amendola and Barna 1986) summarizes data on
concentrations of 2378-TCDD in fish collected between 1978 and 1985. Figure
111-14 (Figure 11 from Amendola and Barna 1986) shows the locations referred to
in the Table. Note that Dublin Road and Emerson Park are identified in
footnotes (4) and (5) to the Table as sites which are upstream from the Dow
Midland facility.
Three different types of samples have been analyzed: whole fish, fillets
with the skin on, and fillets with the skin off. Concentrations measured in
whole fish include contributions from contaminants in the viscera, generally
not eaten by humans and possibly containing contaminated ingested material,
e.g., sediment particulates. Fish skin is often fattier than the remainder of
the fillet and may for this reason contain higher concentrations of
contaminants, but is often eaten by humans. The only direct comparison
possible within the data tabulated in Table III-25 is for carp in 1983: the
average concentration in whole fish was about 4 times higher than that in
fillets with skin off, but fell within the observed range for these fillets.
111-92
-------
TABLE III-25
Study
Location/Species
Tittabawas&ee River Native Fish Collections
2378-TCOO
1978-1985
(parts per trillion)
Whole Fish Filet - Skin On
No. Range Average
No. RangeAverage
Filet - Skin Off
No. Range Average
1978 USE PA Dow Dam to
Center Road
Carp
Channel Catfish
Yellow Perch
Dublin Road
Carp
1980 MONR/ Dow Dam to
USEPA Center Road
Carp
White Sucker
Emerson Park
Carp
1983 HONR/ Smiths Crossing
USEPA Road
Carp
Catfish
Small mouth Bass
Walleye
5
3
3
1°
33-142
3-10
7-62
89.6
7.0
40.7
190
-
lb
5
2.8-5.1
5.1
3.9
6
3
3*
1
25
1°
NO-93
42-695
NO-20
12-530
41
337
10
ND
50
75
Notes: (1) a - includes two. 2-fish composites
(2) b - five-fish composite
(3) ND - not detected
(4) The Dublin Road sampling site is located upstream of
the Dow Chemical - Midland Plant.
(5) The Emerson Park sampling site Is located upstream of
the Dow Chemical - Midland Plant.
-------
TABLE III-25
Tittabaw
-------
FIGURE III-14
Fish Sampling Locations
Tittabawassee River
S«« detail b«>« Oow Ch«m«ca4 Company
Approx. scale (miles)
Source: Amendela and Barna 1986
111-95
-------
Table III-26 (Table 39 from Amendola and Barna 1986) and Figure III-15
(Figure 21 from Amendola and Barna 1986) present Che same data by species and
year of harvest. Carp and catfish, two fatty bottom-feeders, consistently show
the highest concentrations of 2378-TCDD. In fact, the levels of 2378-TCDD in
generally non-migratory, relatively fatty, bottom-feeding fish such as carp and
catfish caught in an area with contaminated sediment are higher than those in
sport fish caught in the same area by roughly an order of magnitude.
In general, Tittabawassee River game species (walleye, smallmouth bass,
crappie, northern pike, and yellow perch), when analyzed on a skin-on fillet
basis, are contaminated with 2378-TCDD at average levels ranging from ND-15
ppt, with an overall average that is close to 5 ppt (Amendola and Barna 1986).
Two studies have been conducted (by Dow Chemical under a consent agreement
with USEPA) to determine the presence of CDDs/CDFs other than 2378-TCDD in fish
from the Tittabawassee River. PeCDDs and" CDFs other than 2378-TCDF were not
analyzed for in these studies. The results from these investigations are found
in Table III-27. The bottom feeders had generally higher concentrations of
CDDs/CDFs than the game fish. These data indicate the possibility of a
downward trend in the fish tissue concentrations of CDDs/CDFs, but a firm
conclusion is not possible at this time, given the small number of fish tested
and the wide variation among fish observed in previous studies.
Recently, limited research by USEPA has indicated that, in a single
walleye specimen analyzed, concentrations of 2378-TCDD and 2378-TCDF in the
111-96
-------
TABLE III-26
Tfttabawassee River Native Fis* Collections
Trends In 2378-TCOO Concentrations
2378-TCOO (ppt)
Year Number
Carp - Whole Fish
1980 5
1983 5 (comp)
Carp - Skin-off Filet
1978 6
1983 25
1985 2
Catfish - SJc1n-off Filet
1978 3
1983 5 (comp)
1985 1
Walleye - Sk1n-on Filet
1983-summer 5
1985-sprlng 8
-s urine r 6
-fall 5
Small mouth Bass - Sk1n-on
1983 S (comp)
1985 3
Range
33-142
NO-93
12-530
3.8-54
42-695
• «»
2.8-5.1
2.5-7.6
2.6-14.0
NO-3.6
Filet
2.8-6.4
Average
89.6
190
41
50
28.9
337
75
39
3.9
4.4
6.5
2.3
5.1
5.0
Source: Amendola and Barna 1986
111-97
-------
FIGURE III-15
540 -i
620-
500-
Tittabawassee River Native Fish
1983 and 1985 Collections
2378-TCDD
100-
a
a
g BOH
u
00
Pi
(M
40-
2O-
MM
M.n
Singl*
1983
Clip
C*il
Sm
-------
TABLE 111-27
PCDDs and PCDFs
NATIVE FISH COLLECTION
TITTABAWASSEE RIVER, 1985 and 1987
(parts per trillion)
Species
Date Taken
Location Taken
2378-TCDD
2378-TCDF
Total TCDDs
Total HxCDDs Total HpCDDs OCDDs
Walleye
Walleye
Walleye
Walleye
Walleye (a)
8/22/85
8/22/85
8/22/85
8/22/85
8/22/85
Smith's Crossing
Smith's Crossing
Smith's Crossing
Smith's Crossing
Smith's Crossing
2.5
2.6
3.0
3 6
NDU.8)
34
24
28
40
11
2 8
1.9
17
NDU.4)
NDU.5)
36
19
5.6
ND(2.7)
ND(2.5)
34
26
6.2
ND(ll)
NDC2.8)
95
55
16
15
6.4
Composite of Walleye Viscera (b)
Carp (c)
Carp
Catfish (d)
Carp
Carp
Carp
Walleye
Walleye
Walleye(e)
8/22/85
8/22/85
8/30/85
10/21/85
10/21/85
10/21/85
9/25/87
9/25/87
9/25/87
Smith's Crossing
Smith's Crossing
Smith's Crossing
Dublin Road
Dublin Road
Dublin Road
Dow Dam
Dow Dam
Dow Dam
Walleye Viscera (f)
22
3.8
54
39
NDU.7)
1.9
24
1.4
1.1
1.5
16
300
8.7
94
28
ND(4.4)
3.3
83
40
13
33
520
36
7.8
59
92
ND(2.3)
ND(8.8)
ND(1.6)
ND(0.5)
ND(0.4)
ND(0.4)
1.7
ND(5.3)
6.8
ND(9.1)
23
ND(2.0)
ND(3.8)
15
ND(2)
ND(2)
ND(2)
13
ND(3.9)
9.3
26
27
ND(3.7)
5.1
15
6
8
5
10
29
15
26
43
3.8
8.5
14
8
9
8
10
Carp
Carp
Carp
Carp (J)
Carp
Carp
9/15/87
9/15/87
9/15/87
9/25/87
9/25/87
9/25/87
Dublin
Dublin
Dublin
Smith'
Smith'
Smith'
Road
Road
Road
s Crossing
s Crossing
s Crossing
Carp Viscera (h)
Notes :
CD Walleye --
1
a
23
9
4
4
19
.6
.1
.0
.7
.0
4.7
17
10
14
21
27
26
ND(0
ND(0.
ND(0.
ND(0.
ND(0
ND(0
0.6
7)
8)
7)
.7)
.6)
6)
ND(1)
11
35
5.7
4
5
17
3
10
23
5.9
8.3
4
14
5
6
11
5
12
5
13
skin-on fillet.
(2) Carp and catfish -- skin-off fillet.
(3) Total TCDDs do not Include 2378-TCDD.
(4) Samples collected and analyzed by Dow Chemical Company pursuant to settlement agreement in Civil Action No. 83-CV7011BC
(United States vs. The Dow Chemical Company).
(5) The Dublin Road sampling site is located upstream of the Dow Chemical Midland Plant.
(6) Percent lipid content for selected 1985 samples are as follows (average of 10 replicate 2 g samples):
(a) Walleye filet . -- 1.9% * 0 41
(b) Walleye viscera composite -- 14. 61 + 0.81
(c) Carp fillet -- 3.01 + 0.41
(d) Catfish fillet — 9.1Z ± 2.71
(7) Percent lipid content for selected 1987 samples are as folLowj (average of 3 replicate 2 g samples):
(e) Walleye fillet -- 2.48 + 0.05
(f) Walleye viscera -- 15.12 +0.52
(g) Carp fillet -- 7 54 + 0.31
(h) Carp viscera -- 13.54 + 0.86
Source: Amende la and Barna 1986. Dow 1987b
-------
visceral fat were at least 10 times higher than the concentrations found in the
fillet (Naumann 1986). Table 111-27 also suggests that viscera of walleye
contained concentrations of 2378-TCDD and 2378-TCDF about 10 times higher than
those in the fillet. However, this difference was not found for HxCDDs,
HpCDDs, or OCDD. More limited support derives from the data in Table III-26,
which show that the average concentration of 2378-TCDD in whole carp was
greater than that in skin-off fillets from the same species. Since CDDs/CDFs
tend to concentrate in the fatty tissues, and several fish species have a fatty
layer just below the skin, the skin-on fillets would be expected to reflect
higher concentrations of CDDs/CDFs than comparable skin-off fillet samples.
However, no direct comparisons are available within the data listed in
Table III-25. Since humans often eat fish skin, exposure assessments in this
section are based on contaminant concentrations measured in both skin-on and
skin-off fillets, pooling all available data.
Table 111-28 presents calculated TEQs (toxicity equivalents of 2378-TCDD:
see Section II) for the CDDs/CDFs measured in each fish listed in Table 111-27.
This calculation uses the "A-method" (see Section II), in which all the HxCDDs
and HpCDDs are assumed to be 2378-substituted and TEFs for 2378-substituted
congeners are applied. Use of the "A-method" is reasonable in this case, since
2378-CDDs/CDFs are selectively absorbed and/or retained in fish (Kuehl et al.
1985, 1987). Based upon the limited data in Table 111-28, the TEQs are greater
than the 2378-TCDD residue concentrations by an average factor of 2.6 in the
game fish and 1.3 in the bottom feeders. A significant contribution to the
TEQs comes from 2378-TCDF. Note that analyses were not available for PeCDDs or
any CDFs other than 2378-TCDF; for this reason, the TEQs are referred to in
III-100
-------
TABLE III-28
TITTABAWASSEE RIVER FISH, 1985 AND 1987
2378-TCDD TOXICITY EQUIVALENTS (PARTIAL TEQs)
(parts per trillion)
Sample
1. Game Fish
1985 Walleye
Walleye
Walleye
Walleye
Walleye
Mean (n-5)
1987 Walleye
Walleye
Walleye
Mean (n-3)
Both Years Mean (n-8)
2. Bottom Feeder
1985 Carp
Carp
Catfish
Mean (n-3)
1987 Carp
Carp
Carp
Mean (n-3)
Both Years Mean (n-6)
2378-TCDD
2.5
2.6
3.0
3.6
0.9
2.5
1.4
1.1
1.5
1.3
3.8
54
39
32
9.0
4.7
4.0
5.9
Partial
TEQ
7.4
5.8
6.2
7.7
2.1
5.8
5.4
2.4
4.8
4.2
5.0
64
44
38
10.6
7.0
6.9
8.2
Ratio
Partial TEQ:
2378-TCDD
3.0
2.2
2.1
2.1
2.3
2.3
3.9
2.2
3.2
3.1
2.6
1.3
1.2
1.1
1.2
1.2
1.5
1.7
1.5
1.3
NOTES: (1) Data from Amendola & Barna 1986, Table 38, and Dow 1987b.
Downstream, fillet data only. Assumes all hexa- and hepta-CDDs are
2378-substituted. ND values are treated as equal to 1/2 the level
of detection. Data for penta-CDDs and all CDFs other than 2378-TCDF
are not available.
III-101
-------
Table 111-28 as "partial TEQs." Given the historical inventory of chemicals
which were manufactured in the area and contaminated with CDFs (e.g.,
pentachlorophenol), the Dow incinerator as a source of PeCDDs and CDFs (see
Section III.A above), and the persistence of PeCDDs and CDFs in the
environment, the presence of residues of 12378-PeCDD and higher-chlorinated
2378-substituted-CDFs in the Tittabawassee fish would not be surprising.
Omission of these congeners from the analysis is likely to have led to
underestimation of the TEQs, since PeCDDs and PeCDFs contribute substantially „
to the TEQs for air emissions (see Section III.B).
Table 111-29 shows estimates of TEQs based on all the fish fillet samples
for 1983 through 1987, including those listed in Table III-25, which were
analyzed only for 2378-TCDD. (Data for fish collected in earlier years showed
higher concentrations of 2378-TCDD and may not have been representative of the
current situation; they are not used in the exposure assessment.) These
estimates are derived by assuming that the average ratio TEQ:2378-TCDD in these
latter samples would have been the same as that derived for the same class of
fish in Table 111-28. These average ratios are then multiplied by the mean
concentration of 2378-TCDD in the available fillet samples for the same class
of fish, to yield the estimates of TEQ listed in the right-hand column. (Note
that these estimates of TEQ, like those in Table III-28, are "partial TEQs,"
and are likely to be underestimates of total TEQ for the reasons discussed in
the previous paragraph.) The -overall averages -- 13 ppt for game fish and 58
ppt for bottom feeders -- are used in the subsequent exposure assessment.
Repetition of the calculation using the detection limits in cases where
III-102
-------
TABLE 111-29
TITTABAWASSEE RIVER FISH DOWNSTREAM OF DOW CHEMICAL PLANT
1983-1987 DATA3
2378-TCDD AND PARTIAL TEQs
(parts per trillion)
TCDD
Year
Species
Range
Mean
Partial TEQsc
(DE/E)
Range
Mean
Bottom- Feeders
1983 Carp
1985
1987
Catfish
Carp (Dow)d
Catfish (Dow)d
Carp (Dow)d
Totals
Weighted Means
25
1
2
1
3
32
12-530
3
4
3
.8-
.0-
.8-
54
9.0
530
50
75
29
39
5
45
.9
16-
-
5.0
-
6.9
5.0
690
-
-64
-
-11
-690
65
98
35
43
8.
58
,2
Gane Fish
1983
1985
1987
Smallmouth Bass
Walleye
Walleye (Spring)
Walleye (Summer)
Crappie
Northern Pike
White Bass
Smallmouth Bass
Walleye (Dow)d
Walleye (Dow)d
Totals
Weighted Means
1
5
8
6
3
3
4
3
5
3
41
2
2
2
2
6
5
2
ND(
1
ND(
_ _
.8-
.5-
.6-
.8-
.1-
.7-
.8-
5.1
7.6
14
4.5
15
15
6.4
1.8)-3.6
.1-
1.8
1.5
)-15
5.
3.
4.
6.
3.
9.
8.
5.
2.
1.
5.
1
9
4
5
9
5
2
0
5
3
0
.
7.3
6.5
6.8
7.3
16-
15-
7.3
ND(4.
2.4
ND(4.
.
-13
-20
-36
-12
39
39
-17
D-7.7
-5.4
l)-39
13
10
11
17
10
25
21
13
5,
4.
13
.8
,2
aFillet data only. From Amendola and Barna 1986, Dow 1987b.
Number of samples analyzed (some are composites of several fish).
clncludes 2378-TCDD, other TCDDs, HxCDDs, HpCDDs, and 2378-TCDF only. Units
are pg/g (parts per trillion). Except as indicated, partial TEQs estimated
from 2378-TCDD values by multiplying by 1.3 (Bottom) or 2.6 (Game), the average
ratios of mean partial TEQ to mean 2378-TCDD.
dActual data used for calculating partial TEQs (Table 111-28).
III-103
-------
congeners or homologues were not detected gave virtually identical estimates,
and the results are not presented separately here.
Table III-30 shows the results of averaging partial TEQs for Tittabawassee
River fish over different years of collection. As discussed earlier, the
average partial TEQs for the fish collected in 1987 was smaller than those for
earlier years, but the sample sizes (3 individual fish from each class) were so
small that it is not possible to conclude reliably that an overall decrease has
taken place. Pending better evidence for a decreasing trend, the average
concentrations for 1983-87 (58 ppt partial TEQs for bottom-feeding fish, 13 ppt
»
partial TEQs for game fish) will be used for subsequent exposure assessment.
The data in Table III-30 show that comparable averages are derived from all
other averaging schemes except that limited to the 6 fish analyzed in 1987.
2. Populations at Risk and Exposure Assumptions
Although the Tittabawassee River does not serve as a commercial fishery,
it has been a source of recreational fishing over the years. It has been
reported that catches resulting from these activities can make a significant
contribution to the diet of some people, particularly certain local residents
who fish the river regularly (Smith and Thompson 1984).
Given the wide variety of fishermen on the river,- it is likely that there
is a wide variety of consumption patterns for Tittabawassee fish. USEPA has
cited 6.5 g/day as an average level of fish and shellfish consumption in the
U.S. (USEPA 1980). In a more recent survey, USDA (1982) found that 14.5% of
III-104
-------
TABLE III-30
TITTABAWASSEE RIVER FISHa
COMPARISON OF PARTIAL TEQsb AVERAGED OVER DIFFERENT YEARS
(parts per trillion)
Bottom- Feeding Fish
Years
1978-87
1978
1985
1987
1985
1983
-85
only
only
-87
-87
Nc
41
38
3
3
6
32
Range
5
5
5
6
5
5
.0
-900
.0-900
.0
.9
.0
.0
-64
-11
-64
-690
Meand
86
92
38
8.2
23
58
Nc
44
41
32
3
35
41
Game Fish
Range
2
6
6
2
2
2
.4-
.5-
.5-
.4-
.4-
.4-
39
39
39
5.4
39
39
Meand
14
14
14
4.2
13
13
aFillet data only. From Amendola and Barna 1986, Dow 1987b.
blncludes 2378-TCDD, other TCDDS, HxCDDs, HpCDDs, and 2378-TCDF only. Units
are pg/g (parts per trillion). Except for 1987, partial TEQs are estimated
from 2378-TCDD values by multiplying by 1.3 (Bottom) or 2.6 (Game), the
average ratios of mean partial TEQ to mean 2378-TCDD (Table 111-28). NDs not
included in ranges.
GNumber of samples analyzed (some are composites of several fish).
dND values treated as equal to 1/2 the detection limit.
III-105
-------
37,874 individuals surveyed throughout the U.S. consumed "finfish other than
canned, dried, and raw" during a 3-day period, and that the average quantity
eaten by these consumers was 54 g/day; this indicates an overall average
consumption of 7.8 g/day for the population surveyed. However, these overall
averages include a large proportion of individuals who eat no fresh-water fish
at all, and thus may not be appropriate for assessing exposure of many local
consumers such as Tittabawassee River fishermen and their families.
The Food and Drug Administration (FDA) has estimated an upper 90th
percentile ingestion rate of 16 g/day of freshwater fish in the Great Lakes
area (USEPA 1984a). The FDA further assumed that the concentrations of 2378-
TCDD were higher in bottom-feeding fish and that these fish constitute about
10% of the freshwater fish in the diet. Jacobson et al. (1984) found roughly
the same in a sample of more than 8000 pregnant women surveyed about their
consumption of Lake Michigan fish. An Ontario study (Cox et al. 1985)
determined an 80th percentile ingestion rate of 40 g/day for sports fish.
Humphrey et al. (1976) studied active sports fishermen* around Lake Michigan
and found their median consumption rate to be about 44 g/day (35 Ib/yr), and
the 90th percentile consumption rate to be about 100 g/day (81 Ib/yr).
In a more recent survey of a larger population of sports fishermen*,
Humphrey (1983) reported a median consumption rate of 48 g/day (38.5 Ib/yr); he
did not report percentiles for this population. These data are the most
relevant to fishermen (and their families) in the Midland area who fish the
Tittabawassee River. There are indications that sports fishing, and hence the
size of the sports fish consuming public, is increasing along the Tittabawassee
*Cohorts comprised of sports fishermen living in the vicinity of Lake Michigan
who reported consuming at least 24 Ibs of fish per year.
III-106
-------
River, although river-specific data are not available. A study is currently
underway to obtain more specific data on fishing populations along the
Tittabawassee River.
Estimates of the size of single meal servings range from roughly 1/4 to
1/2 Ib (113-227 g). USDA (1982) found that the average quantity of finfish
consumed per eating occasion was 145 g, with a median of 113 g, a 90th
percentile of 255 g, and a 95th percentile of 340 g. Humphrey (1983) reported
a median meal size of 319 g (340 g for men and 227 g for women) among Michigan
sports fishermen*. Humphrey did not report percentiles in this study.
Four scenarios for long-term fish exposure have been developed based on
the data just discussed. The first is for a "general consumer" who eats an
average of 7.8 g/day of fish (about 1 quarter-pound meal every two weeks),
equivalent to the overall average for the U.S. (USDA 1982), of which half is
assumed to be game fish from the Tittabawassee and the other half fish from
other sources free of CDD/CDF contamination. In the remaining three scenarios,
all of the fish eaten are assumed to come from the Tittabawassee. In the
second scenario, a "median sports fisherman" is assumed to eat an average of
48 g/day of game fish (3.0 quarter-pound meals per week), equal to the median
fish consumption among Michigan sports fishermen* (Humphrey 1983). In the
third scenario, a "high sports fisherman" is assumed to eat an average of 100
g/day of game fish (about 3 half-pound meals per week), equal to the 90th
percentile for Michigan sports fishermen* (Humphrey et al. 1976). In the final
scenario, the "plausible maximum consumer" also is assumed to eat an average of
100 g/day, but 50 percent is assumed to be game fish and the other 50 percent
*See footnote on previous page.
III-107
-------
are assumed to be the more highly-contaminated bottom fish. Table III-31
presents the scenarios for consumption of fish from the Tittabawassee River.
Table III-31 shows the amounts of 2378-TCDD and estimated TEQs ingested
under the assumptions listed above for fish tissue concentrations and ingestion
rates on a long-term average daily basis. In order to provide an idea of the
potential for adverse health effects associated with short-term consumption of
Tittabawassee River fish, estimates of single-meal fish (and TEQ) ingestion
have also been developed, as shown in Table 111-32. These estimates were
based on the median and 90th percentile of single-meal fish consumption as
reported by USDA (1982), using the mean and maximum TEQ levels found in game
and bottom fish, as shown in Table III-29.
The final step in the exposure assessment is to explore how CDD/CDF intake
could vary among age groups, especially for children. Table III-33 presents
data on the fish consumption of children in three age-groups. Per unit of
body mass, children ingest more fish than adults and hence would ingest more
CDDs/CDFs. The largest mass-specific exposures would be to children under 5
years old, whose doses (on an average and single-meal basis) would be about 2.2
times higher than that of adults.
3. Other Contaminants
This exposure assessment focuses on 2378-TCDD -and on the estimated TEQs.
Other carcinogenic contaminants, such as PCBs, have been detected in
Tittabawassee River fish, and, while their potencies are several orders of
III-108
-------
TABLE 111-31
SCENARIOS FOR EXPOSURE TO CDDs/CDFs FROM
CONSUMPTION OF TITTABAWASSEE FISH
Exposure Scenario
Fish Consumption
Meal
Mean Size
' (g/day) (g)
Concentration3
2378- Partial
TCDD TEQsc
• (pg/g)
Dose Rateb
2378- Partial
TCDD TEQsc
(pg/kg/day)
Plausible Maximum Consumer
(50% game + 50% bottom fish;
90th percentile MI sports
fisherman)
High Sports Fisherman
(100% game fish; 90th
percentile MI sports
fisherman)
Median Sports Fisherman
(100% game fish; median
MI sports fisherman)
General Consumer
(50% game + 50% clean fish;
USDA average consumer)
100d
100d
48f
255e
255e
1138
7.8h 1138
25
2.5
36
5.0 13
5.0 13
36
51
7.1 19
3.4 8.9
6.5 0.28 0.72
aParts per trillion (ppt), from Table 111-29. All fish are assumed to be from
the Tittabawassee River, except "clean" fish which are assumed to be free of
CDD/CDF contamination.
bpor a 70 kg human.
clncludes 2378-TCDD, other TCDDs, HxCDDs, HpCDDs, and 2378-TCDF only.
"90th percentile consumption rate for a cohort of Lake Michigan sports
fishermen consuming at least 24 Ibs/yr of fish (Humphrey et al. 1976).
e90th percentile fish meal size (USDA 1982).
^Median for a cohort of Lake Michigan sports fishermen consuming at least
24 Ibs/yr of fish (Humphrey 1983).
gMedian fish meal size (USDA 1982).
nOverall average consumption of "finfish other than canned, dried, and raw" by
U.S. population (USDA 1982).
III-109
-------
TABLE III-32
SINGLE-MEAL (BOLUS) INTAKES OF CDDs/CDFs FROM
CONSUMPTION OF TITTABAWASSEE RIVER FISH
Fish Tissue
Concentration
(Pg/g) [1]
Amount
Fish Tissue
Consumed (g)
Median Meal
Sizes f41
Game Fish 113
Bottom Feeder 113
2378-TCDD
Mean Max.
5.0 15
45 530
Partial
TEQ[3]
Mean Max.
13 39
58 690
Bolus Dose
(pg/kg-d) [2]
2378-TCDD
Mean Max.
8.1 24
73 860
Partial
TEQ[3]
Mean
21
94
Max.
63
1,100
90th Percentile
Meal Sizes f41
Game Fish
Bottom-Feeder
255
255
5.0 15 13 39 18 55 47 140
45 530 58 690 160 1,900 210 2,500
NOTES:
1. Parts per trillion (ppt); based on all fish collected in 1983-87.
2. For 70 kg human.
3. Includes 2378-TCDD. Does not include penta-CDDs or any CDFs other than 2378-TCDF.
4. From USDA (1982); data of Humphrey (1983) suggest larger meal sizes for
sports fishermen and their families.
III-110
-------
TABLE III-33
RELATIVE INTAKES OF FISH BY CHILDREN AND ADULTSa
Age Group
1-5 6-14 >14b All
Mean body mass (kg)c
Average fish intake:
g/day
g/kg-day
Ratio
Average
g
gAg
Ratio
to adult
meal size:
to adult
95th percentile meal size:
g
gAg
Ratio
to adult
9
15
1
2
44
4
2
91d
10
2
.7
.0
.9
.3
.2
15
28
1.
2.
76
5.
2.
157
10
2.
8
3
0
3
2
35
37
1.
1.
107
3.
1.
240
6.
1.
1
3
1
4
9
5
71
58
0
1
153
2
1
328
4
1
.82
.0
.2
.0
.6
.0
62
54
0,
1
145
2
1,
340
5,
1.
.88
.1
.4
.1
.5
.2
aSource: USDA (1982), Table 7.20: "Finfish other than canned, dried, and
raw." All averages and percentiles refer to individuals who ate fish at least
once during the 3-day period of the survey.
bAdult.
cFrom USEPA (1985d).
^Maximum reported.
III-lll
-------
magnitude lower than that of 2378-TCDD, their concentrations in the fish are
higher (Amendola and Barna 1986). A summary of the concentrations of these
contaminants in Tittabawassee River fish and of the cancer potency factors for
those known to be carcinogenic is presented in Appendix C. Possible
contributions of these contaminants to the overall risks posed by consumption
of Tittabawassee River fish (e.g., through additive toxicity or initiation-
promotion interactions with CDDs/CDFs) are discussed in Appendix C.
4. Data Limitations
a. Fish
The number of samples and analytes in each of these studies is small
compared to the number desirable for reaching statistically precise conclusions
regarding fish contamination levels. The high cost of analysis for CDDs/CDFs,.
the scarcity of analytical standards, and competing priorities for the same
analytical services are contributing causes for the limited data set. It
should be noted, however, that the number of analyses of fish taken from the
Tittabawassee River is large compared to environmental investigations of
CDD/CDF contamination conducted in most other locations. The data available in
this case provide a reasonable basis for estimating exposure.
As part of its National Dioxin Study, USEPA collected and analyzed whole
fish composite samples (generally bottom-feeders) from approximately 400 sites
representing a wide variety of land use patterns across the country (USEPA
1987a). 2378-TCDD was detected in the samples from 28 percent of the sites.
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At sites where 2378-TCDD contamination was found in the whole bottom-feeders,
game fish also were analyzed. The measured whole fish concentrations at two-
thirds of those sites where 2378-TCDD was detected were below 5 ppt, and
concentrations for all fillet samples from the study were below the average
concentration for carp fillet samples from the Tittabawassee River.
It would be useful to establish time trends in these residue data; i.e.,
to determine whether the 2378-TCDD contamination in the fish is increasing or
decreasing with time. The data in hand and their inherent limitations do not
lend themselves to addressing this question easily. On the one hand, given
past production, wastewater treatment, and incineration operations at the Dow
Midland facility, it is likely that wastewater discharges and atmospheric
emissions of CDDs and CDFs were significantly higher in the past than at
present. With continuing efforts to control emissions and discharges, future
releases can be expected to decrease further. On the other hand, because of
the distribution of CDDs/CDFs in Midland area soils and the persistence of
these contaminants in the environment, and the continuing finite--albeit
reduced--levels of CDD/CDF emissions, Tittabawassee River fish may not exhibit
significantly lower levels of CDDs/CDFs in the near future.
On balance, it is likely that the levels of CDDs and CDFs in fish will
decrease at some slow, undetermined rate in the future. For conservatism
(i.e., to avoid understating risks), however, the risk assessment in Section IV
will make the assumption that the CDD/CDF levels in the fish will remain
constant at current levels. Should the possible downward trend suggested by
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the most recent data be confirmed, the estimated risks can be revised
accordingly.
The fish analyses reported to date reflect levels in uncooked fish. From
a human health point of view, one is most concerned about the levels of
contaminants in food "as eaten"; i.e., after fish have been broiled, baked,
fried, or otherwise cooked. There are no data currently available on the
effect of cooking procedures on the CDD/CDF levels in fish. Humphrey (1983)
found no marked differences between concentrations of PCBs and organochlorine
pesticides in raw and cooked fish in a study conducted in Michigan. Studies to
investigate the effects of preparation and cooking on CDD/CDF levels in fish
are currently under way in Michigan.
Pending results of the current study, the Great Lakes States have agreed
that the effects of cooking should not be considered in their derivation of
fish consumption advisories, although some of the advisories do inform
consumers that certain cooking procedures which allow fats to be drained away
may reduce the levels of fat-soluble contaminants (such as CDDs/CDFs) in the
portion eaten. For purposes of the risk assessment in Section IV, any effects
associated with cooking will not be considered, since (1) the potential
reduction from cooking procedures is not known, (2) there is no way to estimate
the extent to which any given procedure may actually be followed, and (3) other
factors associated with cooking could conceivably increase the level of
CDDs/CDFs in the portion eaten.
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b. Analyses for CDDs/CDFs.
The major limitation of the existing data on CDDs/CDFs in Tittabawassee
River fish is the limited body of data on CDDs/CDFs other than 2378-TCDD, and
the total lack of data on PeCDDs and CDFs other than 2378-TCDF. To overcome
the first limitation, this exposure assessment makes the assumption that the
ratio TEQ:2378-TCDD in all Tittabawassee River fish is similar to those in the
fish that have been more completely analyzed (Table 111-29). This procedure is
reasonable when average exposures are being calculated (Table III-31), but may
lead to underestimation of high single-dose exposures (Table 111-32). The
second limitation is more serious, because the air emissions data (Section II-
A) indicate that PeCDDs and PeCDFs may contribute substantially to total TEQs.
It should be recognized that the exposure estimates in Tables III-31 and III-32
represent partial TEQs only, and may underestimate total exposure to 2378-TCDD
toxicity equivalents.
c. Populations at Risk
While it is generally acknowledged that sport fishing can contribute
significantly po the diet of some people, estimates of the size of that
contribution and the size of the population vary, as noted above. Also
referred to above is a local subpopulation, of undetermined size, in the
Midland area, some members of which may regularly supplement their diet through
extensive fishing on the Tittabawassee. As a plausible maximum assumption, the
exposure assessment assumes that these local fishermen and their families
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consume at higher rates than most sports fishermen and eat a significant
percentage (50%) of bottom-feeders in addition to game fish.
In the absence of data specific to the Tittabawassee River, this risk
assessment employs data obtained from other studies, most of which relate to
the Great Lakes area. It is likely, but by no means certain, that these data
are reasonable approximations of the consumption patterns along the
Tittabawassee.
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F. Other routes of exposure
This section briefly considers other potential routes of exposure to
CDDs/CDFs derived from the Dow Midland facility. These routes of exposure are
considered because they have been identified as possibly significant in studies
conducted elsewhere. Lack of data precludes development of quantitative
estimates of exposure via these routes in the Midland area. The purpose of
this section is to discuss each of these routes in a qualitative manner and to
identify whether any is sufficiently likely to be important to justify further
investigation.
1. Exposure to Indoor Dust
Thibodeaux and Lipsky (1985) have identified indoor dust as a potentially
significant route of exposure to 2378-TCDD carried on airborne particulates.
In circumstances where CDDs/CDFs are emitted in association with airborne
particulates (e.g., from incinerators such as that at the Dow Midland
facility), mass concentrations of CDDs/CDFs on these particulates may be
relatively high. Thus, although only a fraction of the airborne particulates
is expected to penetrate into houses and to be deposited onto surfaces, the
resulting mass concentrations of CDDs/CDFs in house dust may be relatively
high. In specific cases modeled by Thibodeaux and Lipsky (1985), based on
empirical data for airborne lead, concentrations of 2378-TCDD in indoor dust
can be much higher than those in outdoor soil, because of the much greater mass
of soil into which deposited airborne particulates are mixed outdoors. Once
CDDs/CDFs are deposited in indoor dust, there is a potential for human exposure
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via inhalation and inadvertent ingestion (primarily by small children who crawl
on the floor). It is not possible to model such exposure for the Midland area,
because no data are available on the fraction of CDDs/CDFs attached to
particulates, on the size distribution or rate of deposition of these
particulates, or on the rates of ingestion and inhalation of indoor
particulates. Hawley (1985) proposed the same rates of ingestion for indoor
dust as for outdoor soil, but this seems implausible because the opportunity
for bulk ingestion is much greater outdoors. Even so, the calculations
presented by Thibodeaux and Lipsky (1985) show that ingestion of CDDs/CDFs by
children in indoor dust can, under some assumptions, substantially exceed that
in outdoor soil. Direct measurements of CDD/CDF concentrations in indoor dust
in Midland residences are needed to determine whether such exposures may be
significant.
2. Ingestion of Vegetables Grown in Contaminated Soils
Another potential route of exposure to CDDs/CDFs in the Midland area is
via ingestion of vegetables grown in domestic gardens. Limited data suggest
that highly lipophilic chemicals such as CDDs/CDFs are not translocated
significantly from contaminated soils into the edible parts of plants (Briggs
et al. 1982). However, there is a potential for human exposure to CDDs/CDFs
adsorbed to airborne particulates that are deposited on external plant sur-
faces, particularly if the CDDs/CDFs are absorbed into the waxy coatings found
on the surfaces of many plants (Hattemer-Frey and Travis 1987). Uptake of
CDDs/CDFs has also been observed into the edible portions of some root crops
(Cocucci et al. 1979). Insufficient data are available to model human exposure
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via this route in the Midland area, but a study of CDD/CDF concentrations in
vegetables is currently underway.
3. Ingestion of Meat and Dairy Products
Cattle and other domestic animals can ingest chemicals such as CDDs/CDFs
through ingestion of grass contaminated with airborne particulates, or through
inadvertent ingestion of soil while grazing (Kimbrough et al. 1984). Because
CDDs/CDFs are lipophilic and Strongly retained in the body, they concentrate in
fatty tissues and are excreted in milk. Several studies have identified meat
and milk as potential routes of exposure of humans to CDDs/CDFs (Kimbrough et
al. 1984, Rappe et al. 1985, USEPA 1984b, Hattemer-Frey and Travis 1987). In
the Midland area, the potential for significant exposure is limited because
there are few, if any, beef or dairy farms close to the Dow Midland facility.
However, evaluation of potential exposure would require information on the
fraction of CDDs/CDFs attached to airborne particulates, particle size
distributions or measurements of dustfall rates, and parameters required to
model uptake by cattle, retention in fat and excretion in milk. None of this
information is presently available.
4. Exposure of Infants via Breast Milk
Several studies have identified relatively high levels of CDDs/CDFs in
human breast milk (Rappe et al. 1986, Tarkowski and Yrjanheikki 1986). Breast-
feeding is a potentially significant route of exposure of infants to CDDs/CDFs
(and other lipophilic compounds) because these compounds are retained in the
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fatty tissues of the mother, are readily excreted in the lipid-rich milk, and
are ingested by infants who depend on the milk for most or all of their
nutrition. Exposure of breast-fed infants may be estimated using a simple
pharmacokinetic model presented by Smith (1987). Smith's model suggests that
exposure of infants of nursing mothers who have substantial long-term exposure
themselves, may be an order of magnitude higher. It should be noted, however,
that this model for exposure is a highly simplified representation of complex
physiological processes and its predictions, therefore, are accompanied by very
large uncertainties (as will be discussed in Chapter IV).
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PART IV
RISK CHARACTERIZATION
A. Introduction
In this section, information from the Hazard Identification, Dose-Response
Assessment and Exposure Assessment sections are combined in order to generate
qualitative and quantitative estimates of the risks associated with exposure to
the chemicals in question. In the case of the CDDs/CDFs around Midland, the
Agency focuses on the risks of cancer and reproductive/teratogenic effects,
with limited consideration of other toxic effects (see Part II). A discussion
of the qualitative features of the case and of the uncertainties associated
with quantitative risk estimates is also included as an integral part of the
overall assessment.
B. Summary of Hazard Identification and Dose-Response Assessment for
CDDs/CDFs
Hazard identification and dose-response assessment for CDDs/CDFs are
presented in Part II, based in part on findings of peer-reviewed USEPA
assessments. Despite some data limitations, the non-human in vivo and in vitro
toxicity data on CDDs/CDFs and particularly 2378-TCDD clearly indicate that
these substances are highly toxic materials. Comparative toxicity studies and
in vitro structure-activity studies have provided a framework for understanding
the relative potencies of the CDDs and CDFs and for identifying the more potent
congeners. Despite extensive studies of human populations exposed to phenoxy
IV-1
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herbicides and other mixtures putatively containing 2378-TCDD, data on effects
of 2378-TCDD itself in humans remain conflicting and inconclusive. However,
experience derived from the Yusho and Yucheng incidents provides strong
evidence that humans are sensitive to at least some of the toxic effects of
CDFs. This experience, with the other structure-activity data which are
embodied in the principles of the TEF approach, provides a reasonable basis for
the use of animal toxicology data on CDDs/CDFs, including 2378-TCDD, to predict
human risks resulting from exposure to CDD/CDF mixtures.
1. Cancer Risk Assessment
USEPA (1985b) has evaluated the data from long-term animal studies with
2378-TCDD and a mixture of 2378-substituted HxCDDs and has concluded that these
materials are carcinogenic in rats and mice. On this basis, USEPA (1985b,
1986d) has concluded that it is prudent to treat these substances (and, via the
TEF approach, the rest of the 2378-substituted CDDs/CDFs) as if they could
cause cancer in humans as well; hence, the weight-of-evidence designation of
"B2". See Section II.A above for a more complete discussion.
USEPA has conducted, following its Cancer Risk Assessment Guidelines
(USEPA 1986a), a quantitative dose-response assessment for the carcinogenic
effects of 2378-TCDD and the mixture of 2378-substituted HxCDDs. Using
"conservative" assumptions about the shape of the dose-response curve in the
low dose region (e.g., linear, non-threshold behavior) and a "conservative"
assumption for extrapolating from animal data to predict human risk (body-
surface-area scaling), USEPA (1985b) has generated upper-bound potency factors
IV-2
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(i.e., upper bounds on the estimates of excess lifetime risk of contracting
cancer per unit dose) of 1.6 x 105 (mg/kg-d)'1 [B2] and 6.3 x 103 (mg/kg-d)'1
[B2] for 2378-TCDD and the 2378-HxCDDs, respectively. According to the TEF
approach, the former cancer potency factor should be applied to the lifetime
average intake of 2378-TCDD equivalents (i.e., TEQs), expressed in mg/kg-d, to
provide an estimate of lifetime cancer risk for exposed individuals.
Substantial uncertainties result from the application of the linearized multi-
stage (IMS) model to data on 2378-TCDD and from use of the TEF approach, and a
review of the potency factor is currently under way by USEPA. These
uncertainties are discussed at length in Part II.
2. Non-Cancer Risk Assessment
In Part II of this report, Hazard Identification and Dose-Response
Assessments were also presented for the other toxic effects caused by low-dose
exposure to CDDs/CDFs, especially 2378-TCDD and 2378-TCDF. Among the effects
most thoroughly studied to date are the reproductive and teratogenic effects
(e.g., Courtney and Moore 1971, Allen et al. 1979, Murray et al. 1979, Weber et
al. 1985, Birnbaum et al. 1985, 1987a,b; see reviews by Nisbet and Paxton 1982
and USEPA 1985b). Data from the Yusho and Yucheng incidents provide limited
evidence that CDFs can cause reproductive impairment in humans (Kusuda 1971,
Yamashita and Hayashi 1985, Hsu et al. 1985), although there is little evidence
for teratogenic effects other than skin hyperpigmentation (Hsu et al. 1985).
This provides support for the inference that other CDDs/CDFs, including 2378-
TCDD, are likely to cause reproductive and/or teratogenic effects in humans.
Accordingly, USEPA has adopted the standard toxicological procedure of using
IV-3
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animal dose-response data on 2378-TCDD to evaluate risks posed to humans
exposed to that compound (and, via the TEF approach, to the other CDDs/CDFs as
well).
In general, reproductive and teratogenic effects are thought to follow
"threshold"-type dose-response relationships, in contrast to carcinogenesis,
which is assumed by USEPA to follow a "non-threshold"-type dose-response
relationship. That is, there is assumed to be a dose of the reproductive and
teratogenic toxicant which is so low (a "threshold" dose) that there is no risk
of the adverse effects appearing in an exposed individual. "Threshold" doses
are likely to vary among individuals; the "threshold" dose for a given
population is the lowest "threshold" dose for an individual in that population.
Operationally, "threshold" doses cannot be measured exactly within limited
groups of experimental animals; they are estimated from "No-Observed-Adverse-
Effect-Levels" (NOAELs).
NOAELs determined in experimental studies with animals are used to
generate Reference Doses (RfDs) or Health Advisories (HAs) by applying
appropriate Uncertainty Factors (UFs). UFs are intended to take account of
differences in sensitivity between animals and humans, variability in
susceptibility among members of the human population, and other factors. As
explained in Part II, RfDs are estimated daily exposures for the human
population (including sensitive subpopulations) that are likely to be without
appreciable risk of deleterious effect during a lifetime. HAs are
corresponding estimates of exposures that can occur daily for shorter periods
without the expectation that adverse health effects will occur.
IV-4
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Part II summarized the derivation of an RfD and HAs for the
reproductive/teratogenic effects of 2378-TCDD (and, via the TEF approach, the
rest of the CDDs/CDFs). Part II also discussed dose-response data for other
toxic effects of 2378-TCDD and showed that an RfD and HAs derived on the basis
of liver toxicity were similar to those derived on the basis of
reproductive/teratogenic effects. The RfD derived for 2378-TCDD is 1 pg/kg-d,
while HAs are in the range 280-300 pg/kg (single-dose) and 28 pg/kg-d (10-day
exposure). While an argument can be made that the RfD does not apply to
exposures lasting less than a lifetime, USEPA has chosen, for the purposes of
this risk assessment, to use the following conservative guidelines for
evaluating the potential for adverse health effects other than cancer (making
it unlikely that adverse health effects will actually occur in populations
exposed at the reference levels for the specified periods):
Period of Exposure
Single dose/Single day
Few days to few weeks
Several months or longer
Reference Level for Comparison
280 pg/kg/day
(HA for single dose)
28 pg/kg/day
(HA for 10-day exposure)
1 pg/kg/day
(RfD for lifetime)
To evaluate the likelihood that adverse effects may occur, estimates of daily
intake are compared with the RfD or HA, depending on the anticipated duration
of exposure. The ratio between the estimated daily intake and the RfD (for
chronic exposure) or the HA (for one-day or subchronic exposure) is referred to
as the "Hazard Index" (USEPA 1986e). These Hazard Indices are calculated and
presented in tables in the following sections. Hazard Indices greater than 1
IV-5
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indicate that the estimated dose rate exceeds the RfD or HA for the route of
exposure and population in question. Hazard Indices for populations receiving
exposure by more than one route can be calculated by summing the calculated
intake values for each route of exposure.
C. Risks Associated with Exposure to CDD/CDF-Contaminated Air.
Estimates of intakes of CDDs/CDFs by inhalation of ambient air for the two
exposure scenarios are summarized in Table III-12. As discussed at the end of
Section III.B.6, these estimates incorporate a correction for bioavailability
and thus represent absorbed doses of CDDs/CDFs. The cancer potency factor,
RfD, and HAs, however, are derived from studies in which rats were exposed to
2378-TCDD in the diet, and are expressed in terms of administered dose.
Studies by Fries and Marrow (1975) suggest that only 50-70% (mean, about 55%)
of 2378-TCDD administered to rats in the diet is absorbed into the body.
Accordingly, when estimates of absorbed dose are compared with the cancer
potency factor, RfD, or HAs, it is necessary to multiply the absorbed doses by
1.8 (1/0.55) to yield estimates of equivalent administered dose. This factor
(referred to as a "correction for oral bioavailability") is applied to all the
estimates in Table III-12.
These adjusted estimates are now multiplied by the cancer potency factor
to yield upper-bound estimates of lifetime cancer risk, and divided by the RfD
to yield estimates of the long-term Hazard Index. These comparisons are made
for both the exposure scenarios considered in Section III.B.6, and for both the
IV-6
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"A-Method" and the "B-Method" of calculating TEQs. The results of these
calculations are tabulated in Table IV-1. Estimated upper-bound cancer risks
are in the range 2x10 to 6x10 for the "fenceline case" and in the range
5x10"" to lxlO'5 for adults for the "residential area case." Cancer risks for
infants and children are not calculated because lifetime intakes for children
exposed at these levels are expected to approximate those of the adults when
averaged over a complete 70-year lifespan. Hazard indices for the non-cancer
effects are all less than or equal to 1 while shorter exposures (a few days to
a few weeks) would yield hazard indices no higher than 0.04.
In interpreting these estimates, the following should be borne in mind:
(1) The exposure estimates are subject to a number of limitations that
have been discussed in Section III.B.8. Specifically, the estimates
are based on measurements of ambient concentrations on only 3 days;
the residential area exposure scenario is based on data from only one
sampling station, which may have been outside the main contaminant
plume on one day; estimates of TEQs were based in part (21-50%) on
"non-detects" at the fenceline station and largely (72-77%) on "non-
detects" at the residential station; the intake calculation assumes
24-hour daily exposure to outdoor concentrations and 70-year
residence at the exposure points.
(2) The cancer risk estimates are "upper bound" estimates of lifetime
risk. That is, the actual risk is not likely to be greater than
these levels; the actual risks could be significantly lower. Because
of uncertainties about the mechanisms of action of- 2378-TCDD and the
implications of these mechanisms for dose-response modeling, these
estimates are subject to additional uncertainties, as discussed
above.
(3) The hazard indices calculated for children are based on an RfD
originally defined for reproductive effects, which are expressed only
during adulthood. This approach to defining the non-cancer risk
levels for children was adopted because, as discussed in Section II,
RfDs or other critical toxicity values which could be derived for
other non-cancer endpoints (e.g., liver and immunotoxicity) are also
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TABLE IV-1
RISK CHARACTERIZATION FOR INHALATION OF CDDs/CDFs
IN AMBIENT AIR IN MIDLAND
Exposure Scenarioa
Residential Area
Infants 0-1 year
Children:
1-6 years
6-12 years
Adults (12-70)
Lifetime
Upper-Bound Cancer Riskb Hazard Index0 (Long-Term)
A-Methodd B-Method4
A-Method B-Methodd
1.
Fenceline Case:
Infants 0-1 year
Children:
1-6 years
6-12 years
Adults (12-70)
Lifetime
0.4
1
0.7
0.3
6xlO'5 ["B2"l 2xlO"5 ["B2"]
0
0
0
0
.1
.4
.3
.1
—
IxlO'5 ["B2"] 5xlO'6 ["B2"
0.05
0.2
0.1
0.05
0.02
0.08
0.06
0.02
aFrom Section II.B.6. All exposure estimates assume 24 hr/day exposure to
outdoor concentrations, long-term residence (lifetime for cancer risks).
"Upper-bound estimate of lifetime cancer risk, obtained by multiplying
exposure estimate in Table 111-12 by cancer potency factor of 1.6x10"^
(pg/kg-day)"^ and multiplying by correction for oral bioavailability of 1.8
(see Section IV.C).
°Ratio of exposure estimate in Table III-12 to RfD of 1 pg/kg/day, multiplied
by correction for oral bioavailability of 1.8, for exposures lasting several
months or more. Shorter exposures (a few days to a few weeks) would yield
indices about 28-times lower.
dA-Method assumes all Pe-, Hx- and Hp-CDDs and CDFs are 2378-substituted.
B-Method assumes all congeners within these groups are equally prevalent (see
Part II).
IV-8
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on the order of 1 pg/kg-d. In addition, if the reproductive effects
of CDD/CDF exposure are the result of damage to germ cell lines
(precursors to sperm and ova), such damage could arise from exposure
during infancy and childhood, as well as during adulthood.
(4) 2378-TCDD and HxCDDs were detected only in trace quantities in
ambient air. Most of the risk calculated by means of the "A-
Method"and much of the risk calculated by means of the "B-Method" is
derived by applying TEFs to measurements or estimates of other
congeners. For this reason, the cancer risks estimated and tabulated
in Table IV-1 are dominated by risks ascribed, through use of the TEF
procedure, to exposure to compounds whose potential carcinogenicity
has never been investigated directly. Although the TEF procedure is
reasonable and has been widely accepted in the scientific community,
the indirect basis for inferring these cancer risks should be
recognized as contributing additional uncertainty to the risk
estimates. To emphasize this uncertainty, the weight-of-evidence
designation of B2 is placed in quotation marks.
(5) There is a question about the collection efficiency of the sampling
procedures used in these studies which could mean that the measured
amounts of CDDs/CDFs were underestimated. USEPA is currently
studying this question.
For the above reasons, the values tabulated in Table IV-1 are subject to
substantial uncertainties. They are best regarded as order-of magnitude
estimates of risk, and will be so treated in the integrated characterization at
the end of this Part.
D. Risks Associated with Exposure to CDD/CDF Contaminated Soil.
Estimates of intakes of CDDs/CDFs by ingestion of soil are presented in
Table III-20. These estimates are of absorbed dose and require adjustment for
oral bioavailability as discussed in the previous section. For this reason,
all these estimates are adjusted for oral bioavailability by multiplying by l.£
before comparison with the cancer potency factor or the RfD.
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The adjusted estimates of lifetime average intake are now multiplied by
the cancer potency factor to yield upper-bound estimates of lifetime cancer
risk. The adjusted estimates of intake for the various age groups being
considered are divided by the RfD to yield estimates of long-term Hazard Index.
These calculations are performed for both the exposure scenarios detailed in
Table III-20. The results of these calculations are presented in Table IV-2.
The estimates of upper-bound cancer risk are about 5x10"^ ["B2"] for the "lower
estimate" case, and 1x10"^ ["B2"] for the "upper estimate" case. Hazard
Indices are below 1 in both exposure scenarios for all age groups, but could
approach 1 in the "upper estimate" case when exposure of small children is
considered and could exceed 1 for children with pica.
In interpreting these estimates, the following should be borne in mind:
(1) The exposure estimates are subject to a number of limitations that
have been discussed in Section III.C.3. The most important of these
limitations is probably the lack of information on the vertical
distribution of the CDDs/CDFs in soil: the concentrations in soil
that is actually ingested could be either higher or lower than the
measured average in the top 25 mm of the soil column. Estimates of
soil ingestion rates are based on limited data, as discussed by LaGoy
(1987). The estimates of bioavailability are derived from studies of
soil and fly ash which yielded widely varying estimates of
bioavailability, and it is not clear which of these studies is most
predictive of the bioavailability of CDDs/CDFs from Midland soil.
(2) The cancer risk estimates are "upper bound" estimates of lifetime
risk. That is, the actual risk is not likely to be greater than
these levels; the actual risks could be significantly lower. Because
of uncertainties about the mechanisms of action of 2378-TCDD and the
implications of these mechanisms for dose-response modeling, these
estimates are subject to additional uncertainties, as discussed
above.
(3) As was the case for the air risk estimates, non-cancer Hazard Indices
are developed using RfDs originally derived for reproductive effects.
These values are relevant to risk assessments for infants and
children for the reasons discussed in Section IV.C.
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TABLE IV-2
RISK CHARACTERIZATION FOR INGESTION OF CDDs/CDFs
IN SOIL IN MIDLAND
Upper-Bound Lifetime Hazard Index0
Exposure Scenario3- Cancer Risk*3 (Long-Term)
Lifetime Average Exposure:
1. Lower Estimate:
Infants 0-1 year -- 0.02
Children:
1-6 years -- 0.03
6-12 years -- 0.009
Adults (12-70) -- 0.0003
Lifetime average 5x10" ["B2"]
2. Upper Estimate:
Infants 0-1 year -- 0.5
Children:
1-6 years -- 0.6
6-12 years -- 0.2
Adults (12-70) -- 0.01
Lifetime average 1x10 ["B2"]
Assumptions and parameters are listed in Table III-19. Note that the upper
estimate does not include individuals with pica. Individuals with this
disorder could incur risks 10-fold higher.
"Upper-bound estimate of lifetime cancer risk, obtained by multiplying lifetime
average TEQ dose rate from Table III-20 by cancer potency factor of 1.6xlO~
(pg/kg-day) and multiplying by adjustment for oral bioavailability of 1.8
(see Section IV.C).
°Ratio of adult TEQ dose rate from Table 111-20 to RfD of 1 pg/kg-day,
multiplied by adjustment for oral bioavailability of 1.8 for exposures lasting
several months or more. Shorter exposures (a few days to a few weeks) would
yield indices about 28-times lower.
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(4) See note (4) in Section C above.
An alternative approach to assessment of risks posed by 2378-TCDD in
residential soils has been developed by the Centers for Disease Control
(Kimbrough et al. 1984). This approach followed the same general methodology
as that used in this report for estimating cancer risks, except that the CDC
scientists used higher values for soil intake rates, lower values for the
cancer potency factor, and a different method of averaging lifetime dose rates.
These differences tended to offset each other, so that the overall result of
the CDC analysis is comparable to that presented in this report. Specifically,
the CDC report identified a concentration of 1 ppb 2378-TCDD in residential
soil as the level at which to begin consideration of action to limit human
exposure. According to the methodology developed in this report, a
concentration of 1 ppb TEQ would yield an upper-bound lifetime cancer risk of
about 1x10"-^ in the lower estimate scenario and about 3x10"^ in the upper
estimate scenario. The former estimate is consistent with the range estimated
by the CDC method (upper-bound about 10"^) for similar exposures.
In June, 1985, the Agency released its report on the levels of 2378-TCDD
in the soils in the Midland area (USEPA, 1985a). Based upon these data, the
Centers for Disease Control (CDC) concluded that the monitored levels did not
pose an unacceptable public health risk. The Agency's Chlorinated Dioxins Work
Group concurred in this assessment. The results of the present assessment are
generally consistent with these conclusions, with the upper estimate scenario
yielding an upper-bound cancer risk of about 10
IV-12
-------
E. Risks Associated with Exposure to Water and Brine Sediments
The information summarized in Section III.D provides no plausible evidence
of human exposure to CDDs/CDFs either in drinking water or through contact with
the brine pond sediments.
F. Risks Associated with Consumption of Fish
Estimates of adult intakes of CDDs/CDFs by ingestion of contaminated fish
are summarized in Tables III-31 and 111-32. These are estimates of quantities
ingested and hence do not need adjustment for oral bioavailability. The'
estimates of average rates of ingestion are multiplied by the cancer potency
factor to yield upper-bound estimates of lifetime cancer risks, and are divided
by the RfD to yield estimates of the Hazard Indices for long-term exposure. In
addition, the estimates of single-meal (bolus) intakes are compared with the
single-dose or 1-day HA to yield estimates of the Hazard Indices for single
exposures. All these calculations are performed for four sets of assumptions
about rates of consumption of fish, as specified in Tables 111-31 and 111-32.
The results of these calculations are presented in Table IV-3.
Estimates of upper-bound cancer risks resulting from ingestion of fish
range from 10"^ for the "general consumer" to about 10"^ (one percent) for the
"plausible maximum consumer." Figure IV-1 shows the relationship between
average consumption of Tittibawassee River fish and the resulting upper-bound
estimate of lifetime cancer risk, based on the calculations presented in
IV-13
-------
TABLE IV-3
RISK CHARACTERIZATION FOR INGESTION OF CDDs/CDFs*
IN FISH FROM THE TITTABAWASSEE RIVER
Exposure Scenario0
Upper-Bound
Cancer Riskd>e Long-Term6;
Hazard Index° (Ratio of Dose to
RfD or HA)
Single Meale>S
Mean Maximum
Plausible Maximum Consumer
(bottom + game fish)
High Sports Fisherman
(game fish only)
Median Sports Fisherman
(game fish only)
General Consumer
(game + clean fish)
1x10"2 ["B2"]
4x10"3 ["B2"]
2x10~3 ["B2"]
1x10'4 ["B2"
50
20
0.7
0.7n 8:
0.2 0.5
0.07 0.2
0.04J 0.2
aOther contaminants, such as PCBs, found in the fish could add to the risks
(see Appendix B).
bNote that Hazard Indices will be about 2-3 times higher for small children
(Table 111-33). Hazard Indices for breast-fed infants could be 10 times
higher than those of their mothers.
cFrom data in Section III.E.2 and Tables 111-31 and 111-32.
dUpper-bound estimate of lifetime cancer risk, obtained by multiplying dose
rate from Table III-31 by a cancer potency factor of 1.6x10"^ (pg/kg-d) "*• and
multiplying by a factor of 1.3 to incorporate contribution of higher intakes
in childhood to average lifetime intake in pg/kg-day (from data in Table
111-33).
eNote that all estimates of intake are "partial TEQs," including only 2378-
TCDD, other TCDDs, HxCDDs, HpCDDs, and 2378-TCDF.
fRatio of dose rate from Table III-31 to RfD of 1 pg/kg-day, for exposures
lasting several months or longer.
SRatio of bolus dose from Table 111-32 to single-dose HA of 280 pg/kg-day.
"Includes some meals of bottom feeders.
1Bottom feeders only.
JIncludes some clean fish.
IV-14
-------
Figure IV. I
Upper-Bound Cancer Risks
Associated With Consumption of CDD/CDF
Contaminated Fish From The Tittabawassee River
10
10
-O Bottom Fish
Game Fish
Fish Consumption (g/day)
-------
Table IV-3. Hazard Indices for long-term exposure (ratios of estimated intakes
to RfD) range from 0.7 for the "general consumer" to 50 for the "plausible
maximum consumer," with young children and breast-fed infants possibly 2 to 3
times and 10 times higher, respectively. Hazard Indices (ratios of estimated
intake to HA) for single exposures are less than 1 for the "general consumer,"
the "median sports fisherman," and the "high sports fisherman" but range up to
8 for adults in the "plausible maximum consumer" case (the higher values being
associated with consumption of bottom feeders). Again, young children and
breast-fed infants could have higher His, as discussed above (breast-fed
infants would be partially protected against the effects of high single intakes
by their mothers because of pharmacokinetic averaging in the mothers' tissues).
Finally, in order to evaluate the potential risks of non-carcinogenic
effects from short-term exposures, two consumption levels over a two-week
period for each of the four scenarios are compared to the 10-day HA (see
Table IV-4). The His for the higher level of consumption range from 0.4 for
the "general consumer" to 5 for the "plausible maximum consumer." Thus, the
His are in the same range as those resulting from the single-meal or one-day
exposures.
In interpreting these estimates, the following should be borne in mind:
9 The exposure estimates are subject to a number of limitations that
have been discussed in Section III.E.4. The most important of these
limitations is the lack of direct data on the consumption habits of
Tittabawassee River fishermen; the data of Humphrey (1983), although
relevant, refer to fishermen who fished in Lake Michigan.
IV-16
-------
TABLE IV-4
RISK CHARACTERIZATION FOR INGESTION OF CDDs/CDFs
IN FISH FROM THE TITTABAWASSEE RIVER
(Short-term exposuresa)
Short-Term
Exposure Scenario Hazard Index"
General Consumer (Each meal - 113 g of game fish or
"clean" fish)
Long-term average: 2 meals/month (1 of game fish)
-- 1 meal of game fish/2 weeks 0.05
Plausible maximum: 14 meals of game fish/2 weeks (7 of
game fish) 0.4
Median Sports Fisherman (Each meal - 113 g of game fish)
Long-term average: 6 meals/2 weeks 0.3
Plausible maximum: 14 meals/2 weeks 0.7
High Sports Fisherman (Each meal - 255 g of game fish)
Long-term average: 6 meals/2 weeks 0.7
Plausible maximum: 14 meals/2 weeks 2
Plausible Maximum Consumer (Each meal - 255 g of game fish or
bottom feeders)
Long-term average: 6 meals/2 weeks (3 of bottom feeders) 2
Plausible maximum: 14 meals/2 weeks (7 of bottom feeders) 5
aExposures resulting from consumption of fish over a period of a few days
to a few weeks.
"Average daily intake (pg/kg-day) divided by the 10-day HA of 28 pg/kg-day.
Hazard indices for young children may be 2-3 times higher than the hazard
indices for adults that are tabulated in this table.
IV-17
-------
The cancer risk estimates are "upper bound" estimates of lifetime
risk. That is, the actual risk is not likely to be greater than
these levels; the actual risks could be significantly lower. Because
of uncertainties about the mechanisms of action of 2378-TCDD and the
implications of these mechanisms for dose-response modeling, these
estimates are subject to additional uncertainties, as discussed
above.
G. Estimates of Risks from Other Routes of Exposure
Other potential routes of exposure are discussed briefly in Section III.F.
No quantitative estimates of exposure via ingestion or inhalation of indoor
dust, or via ingestion of vegetables, meat, or milk, are possible, although
each of these routes could be significant under appropriate circumstances.
Breast-fed infants are likely to ingest CDDs/CDFs at dose rates (expressed in
units of pg/kg-day) at least one order of magnitude greater than those of their
mothers. Although these relatively high rates of intake by infants at a
critical stage of development are of major concern, it is difficult to factor
them into formal risk assessments, for the following reasons. First, USEPA's
recommended procedure for assessing cancer risks resulting from time-varying
exposures is to calculate the time-weighted average dose rate in mg/kg-day
(USEPA 1986a). Infants are typically breast-fed for only about 1 percent of
their lifetimes; hence, even if their dose rates are elevated 10-fold, this
would lead only to a 1.1-fold increase in calculated lifetime risk. However,
the validity of the averaging procedure is subject to question when the time-
pattern of exposure is as extreme as this. Second, the HAs for CDDs/CDFs were
derived from studies of adult animals, and the RfD from multigeneration
feeding studies, none of which are good models for the short-term exposures
to infants which are being discussed here. In the next section, risks to
IV-18
-------
breast-fed infants are characterized by assuming that their intakes are one
order of magnitude higher than those of their mothers, and that the cancer
potency factor, RfD, and HAs are applicable to them. However, the uncertainty
of these assumptions should be recognized.
H. Integrated Risk Characterization
Because of the many limitations of the exposure and dose-response
estimates that have been discussed in the preceding paragraphs, the estimates
of upper-bound cancer risks and non-cancer hazard indices that are tabulated in
Tables IV-1, IV-2, IV-3, and IV-4 should be regarded as reliable only to order
of magnitude, i.e., to within about a factor of ten in either direction. To
facilitate comparison of risks posed by exposures via different routes, Table
IV-5 summarizes the order-of-magnitude upper-bound estimates of lifetime cancer
risks, while Table IV-6 summarizes the estimates of Hazard Indices for other
(non-cancer) toxic effects.
Tables IV-5 and IV-6 show that consumers of fish from the Tittabawassee
River are at much higher risks than other residents in the Midland area. Under
the assumptions listed in Part III (which include long-term consumption of fish
at current levels of contamination), additional lifetime cancer risks would be
in the range of 1 in 10,000 to 1 in 100; even consumers of game fish only could
experience cancer risks above 1 in 1,000 and could exceed the maximum
recommended long-term dose for non-cancer effects by 20-fold. Any consumer of
bottom fish at current (1983-87) levels of contamination would exceed the
IV-19
-------
TABLE IV-5
SUMMARY OF UPPER-BOUND ESTIMATES OF CANCER RISK FROM EXPOSURE
TO CDD/CDF CONTAMINATION IN MIDLAND, MICHIGAN
Exposure
Route
Upper-Bound Cancer Risk (Exposure Scenario)
Higher Estimate
Lower Estimate
-2
Fish 10 (plausible maximum consumer) 10 (median sports fishman)
10 (high sports fisherman)
Soil 10 (upper estimate)
-4
10 (child with pica)
-4
Air 10 (fenceline)
-4
10 (general consumer)
10 (lower estimate)
10-5 (residential area)
NOTES:
(1) 10"2, 10'3, 10"4, etc., indicate risks of roughly 1 in 100, 1 in
1,000, 1 in 10,000, etc.
(2) Other contaminants, such as PCBs, found in the fish add to the risk
from that exposure route (see Appendix B).
Sources: Tables IV-1, IV-2, and IV-3.
IV-20
-------
TABLE IV-6
SUMMARY OF HAZARD INDICES FOR NON-CANCER EFFECTS
FROM EXPOSURE TO CDD/CDF CONTAMINATION IN MIDLAND, MICHIGAN
Exposure
Route
Exposure Scenario
Hazard Index (HI)a
Long-Term Short-Term Single Meal
Fishb
Plausible maximum consumer
High sports fisherman
Median sports fisherman
General consumer
50
20
9
0.7
5
2
0.7
0.4
8
0.5
0.2
0.2
Soil
Upper estimate young child
— with pica
— normal
Lower estimate young child
Upper estimate adult
6
0.6
0.2
Airc
Infant at fenceline
Child at fenceline
Child in residential area
Adult in residential area
4
1
0.2
0.1
aHazard Index is the ratio of intake dose to:
— RfD (1 pg/kg/day) for long-term exposures (several months or more)
— 10-day HA (28 pg/kg/day) for short-term exposures (few days to few weeks)
— Single-dose HA (300 pg/kg/day) for single-meal or single-day exposures
^Small child could be at 2-3 times higher risk than adult. Breast-fed infant
could be at 10-times higher risk than mother. Other contaminants such as
PCBs, found in the fish, add to the toxicity (see Appendix B of the Risk
Assessment).
CA11 HI values calculated using the "A method."
exposure from breast-feeding.
Infant exposure includes
IV-21
-------
single-meal and short-term health advisory intakes by 5- to 8-fold. These
risks would be experienced by regular consumers of fish from the Tittabawassee
River (including fishermen and their families). This population has still not
been fully characterized, but an ongoing study is expected to provide more
information about its size and other characteristics. In all exposure
scenarios, small children of fishermen would be at greater risk than their
parents, and breast-fed infants would be at highest risk.
According to the findings summarized in Tables IV-5 and IV-6, exposure via
air and soil would not result in His greater than 10 for non-cancer effects
(even in the unlikely case of an infant breast-fed by a woman resident at the
fenceline, or in the case of a young child with pica). However, both air and
soil exposures could pose upper-bound cancer risks exceeding 1 in 100,000.
According to the exposure scenarios developed in Sections III.B and III.C, most
long-term residents in the area north and east of the Dow Midland facility
(i.e., about two-thirds of the population of the city--see Appendix A) would be
subject to risks on the order of those associated with the "residential area"
(air) and "lower exposure" (soil) scenarios. Residents nearer to the facility
would be subject to risks nearer to those of the "fenceline" (air) exposure
scenario.
According to the assumptions listed in the development of the exposure
scenarios, most residents would be exposed to CDDs/CDFs via both the air and
soil routes. Accordingly, exposures, and hence cancer risks, via these routes
would be additive. However, adding the risks tabulated in Tables IV-1 and
Table IV-2 would not change the general orders of magnitude indicated in
IV-22
-------
Table IV-5. Only an unusual combination of exposure circumstances (e.g., a
breast-fed infant who later developed pica and remained in the area for most of
the rest of his or her lifetime) would lead to an upper-bound estimate of
cancer risk on the order of 1 in 10,000. Such risks are experienced by regular
consumers of fish from the Tittabawassee River (Table IV-5).
In overall summary, this risk assessment indicates that the greatest
health risks posed by CDDs/CDFs to residents of the Midland area result from
the consumption of contaminated fish. Even individuals who limit their
consumption to game fish can experience additional cancer risks exceeding one
in a thousand and risks of reproductive effects and liver damage substantially
above recommended levels. Exposure of city residents via contaminated air and
soil poses smaller (but greater than one in a million) additional risks of
cancer. All these conclusions should be interpreted keeping in mind the
discussion of sources of uncertainty in earlier sections of this chapter.
IV-23
-------
PART V
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Office of Water Regulations and Standards. February.
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1984b. Risk Analysis of TCDD
contaminated soil. EPA 600/5-84-031. Office of Health and Environmental
Assessment. Washington, D.C.
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1985a. Soil screening survey at
four midwestern sites. EPA 905/4-85-005. Environmental Services
Division, Region 5. Westlake, Ohio.
V-13
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U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1985b. Health Assessment
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Office of Research and Development. Washington, D.C.
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1985c. Reference values for
risk assessment. ECAO-CIN-477. Environmental Criteria and Assessment
Office. Cincinatti, OH. Draft.
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1985d. Development of
statistical distributions of ranges of standard factors used in exposure
assessments. OHEA-E-161. Office of Health and Environmental Assessment,
Washington, D.C.
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1986a. Guidelines for
carcinogen risk assessment. Fed. Reg. 51:33992-34003.
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1986b. Guidelines for exposure
assessment. Fed. Reg. 51: 34042-34054.
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1986c. Broad scan analysis of
the FY82 National Human and Adipose Tissue Survey specimens. EPA-560/5-
86-038 Office of Toxic Substances. Washington, D.C.
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1986d. Superfund public health
evaluation manual. EPA-540/1-86/060 Office of Emergency and Remedial
Response. Washington, D.C.
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1986e. Guidelines for the
health risk assessment of chemical mixtures. Fed. Reg. 51:34014-34023.
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1987a. National dioxin study-
report to Congress. Office of Solid Waste and Emergency Response.
Washington, D.C. EPA/530-SW-87-025
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1987b. Reference Dose:
Description and use in health risk assessments. Integrated Risk
Information System. Appendix A. Washington, D.C.
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1987c. Health Advisory for
2,3,7,8-TCDD. Office of Drinking Water. Washington, D.C.
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1987d. Interim procedures for
estimating risks associated with exposures to mixtures of chlorinated
dibenzo-p-dioxins and dibenzofurans. EPA/625/3-87/012 Risk Assessment
Forum. March.
U.S. GEOLOGICAL SURVEY (USGS). 1973. Topographic quadrangle maps of Midland
North, MI, Averill, MI, Midland South, MI, and Gordonville, MI.
V-14
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UPTON, A.C., CLAYSON, D.B., JANSEN, J.D., ROSENKRANZ, H.S., and WILLIAMS, G.M.
1985. Task Group 5 Final Report: Report of the ICPEMC task group on the
differentiation between genotoxic and non-genotoxic carcinogens.
International Commission for Protection Against Environmental Mutagens and
Carcinogens (ICPEMC) BIol. Zbl. 104:417-453.
URABE, H., and ASAHI, M. 1985. Past and current dermatological status of
Yusho patients. Environ. Health Perspect. 59:11-15.
VAN DEN BERG, M. , OLIE, K., and HUTZINGER, 0. 1983. Uptake and selective
retention in rats of orally administered chlorinated dioxins and
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VAN DEN BERG, M. , and POIGER, H. 1987. Selective retention of PCDDs and PCDFs
in mammals: a multiple cause problem. Dioxin 87 Abstracts 2:144.
October 4-9, Las Vegas, Nevada.
WEBER, H., HARRIS, M. , HASEMAN, J., and BIRNBAUM, L.S. 1985. Teratogenic
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(TCDD) and 2,3,7,8-tetrachlorodibenzofuran (TCDF) in pregnant C57B1/6N
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V-15
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K., MURAI, K., OMAE, T., FUJITA, M., YAMAMOTO, T., KOHNO, T., OHNISHI, Y.,
HIRONAKA, H.L, FUKUYAMA, H., AKAMINE, A., andAONO, M. 1981. [Studies on
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V-16
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APPENDIX A
CHARACTERIZATION OF POTENTIALLY EXPOSED POPULATION
-------
APPENDIX A
CHARACTERIZATION OF POTENTIALLY EXPOSED POPULATION
The Dow Chemical Company operates a major chemical processing facility
wichin the cown of Midland, Michigan (population 37,016). A map of the Midland
area, divided into 1980 census tracts, is shown in Figure A-l. The population
within each tract is shown at the right of the figure. Some tracts, namely 5,
6, 8, 9, and 10, have areas inside and outside of the Midland city boundary.
The populations in these areas were tabulated separately. Areas inside the
city limits are denoted by the census tract number only, while those outside
are denoted by the census tract number with an asterisk. Also shown on the map
are concentric circles marking 1,2, and 3 miles from the Dow Midland facility
incinerator.
The Dow plant covers about 1,500 acres on the southwestern side of town
along the banks of the Tittabawassee River. To the north of the plant lies the
most densely populated area of Midland: the downtown area, the commercial
district, and residential areas with schools, parks, playfields, and shopping
malls. Moving east of the plant, the area remains residential but the
population density decreases slightly. To the south and west of the plant, the
population is the least dense and the area is predominantly rural/fanning. The
population is of normal age distribution and is very stable with 77% of the
population having lived in the county for at least 5 years.
Chemical processing and hazardous waste storage and incineration practices
at the plant have resulted in the release of CDDs/CDFs onto plant property and
A-l
-------
FIGURE A-l: Map and population* of census tracts in Midland County. Michigan
Census Tract Population
1
2
3
4
5
5*
6
6*
7
8
8*
9
9*
10
10*
4031
3871
4612
3108
145
1931
2521
117
2887
5816
19
5148
13
4469
91
0
-------
into the ambient air (Trembly and Amendola 1987, USEPA 1985a). Inhalation of
the ambient air around the plant is a potential route of exposure to CDDs/CDFs
for Midland residents, especially those living near the plant perimeter or
downwind of the incinerator. To the west and south of the incinerator, the
plant boundaries extend more than a mile but to the north and east, toward the
residential area, approximately 2,000 people can be found living within 1 mile
of the incinerator (Figure A-l). The closest residences are approximately 0.5
mile from the plant incinerator and 0.1 mile or less from the plant boundary.
In many areas, light industry and commerce begin at the plant boundary. An
additional 11,000 people live within a two mile radius of the incinerator and
13,000 more within three miles. The majority of these populations are also
concentrated in the residential/commercial areas to the north and east of the
plant. As the prevailing wind is from the southwest, the downwind area
includes the eastern edge of the most densely populated northern section and
most of the less densely populated northeastern areas of town. An arc drawn 45
degrees to either side of the most prevalent wind direction and three miles
from the incinerator encompasses approximately 12,000 people.
Inhalation of volatilized soil contaminants or suspended particulate
matter is another component of the ambient air exposure. Since the highest
concentrations of contamination have been found on plant property, the highest
levels of exposure may be expected for those persons living nearest the plant
perimeter or downwind of the plant property (USEPA 1985a). However, since soil
samples taken from several residential and public use areas within the town
also show contamination with CDDs/CDFs (USEPA 1985a), the actual number of
residents with exposures above background is probably larger. The majority of
A-3
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the city's residents may be exposed not only through inhalation pathways but
additionally through ingestion of vegetables grown in gardens containing
contaminated soil or of dust that has settled on eating vessels. There may be
direct ingestion of contaminated soil by children and pregnant women, and
regular use of contaminated public areas such as parks and playing fields may
result in additional exposure for such users.
There has been no CDD/CDF contamination of surface water or potable water
sources reported (Barna and Amendola 1985); therefore, this medium does not
currently pose a significant route of exposure. However, the Dow Midland
facility has several landfills and brine pond sediments contaminated with
CDDs/CDFs (Amendola and Barna 1986) , and the eventual contamination of ground
or surface water could potentially place some residents at risk. While the
majority of Midland residents receive their drinking water from Saginaw Bay,
and the inlets are far removed from the plant area, an unknown number of
residents draw their drinking water from at least one public and fourteen
private ground water supplies and one artesian well in the vicinity of the Dow
Midland brine operations and landfills (Amendola and Barna 1986).
Contaminated wastewater from the Dow Midland facility has been, and
continues to be, released into the Tittabawassee River. Fish tend to
accumulate CDDs/CDFs, and fish taken from the Tittabawassee have been found to
be contaminated (Amendola and Barna 1986). Although the river is not fished
commercially, it is fished recreationally, and the regular consumption of
contaminated fish may be a significant route of exposure for recreational
fishermen and their families. Specific data for the Tittabawassee fishermen
A-4
-------
are unavailable, and the number of spore fishermen is unknown. There is
evidence that the popularity of sport fishing is on the rise, and, with the
stocking of the Tittabawassee, sport fishermen may represent a significant and
increasing portion of the population.
Most of the residents of Midland are at risk of exposure to CDDs/CDFs
through at least one of the above routes. Certain subpopulations may be more
subject to exposure than others. Portions of the population at higher risk
include women of child bearing age. Fifty percent of the Midland population is
female and forty percent of the females are between the ages of 20 and 44 (1980
Census). Another sensitive subpopulation is disadvantaged residents. Many
disadvantaged residents are thought to rely heavily on fish in their diet and
may be consuming far more fish than the projected value for a typical sports
fisherman. An estimate of the number of individuals in this category in the
Midland area is unavailable; however, it may be significant since a recent
survey of 128 Tittabawassee fishermen indicated that 72% were unemployed (Smith
and Thompson 1984).
A-5
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APPENDIX B
OTHER TOXIC POLLUTANTS PRESENT IN FISH
-------
APPENDIX B
OTHER TOXIC POLLUTANTS PRESENT IN FISH
Limited sampling of fish from the Tittabawassee River has indicated that
these fish may be contaminated with a variety of toxic pollutants in addition
to CDDs/CDFs (Amendola and Barna 1986). Table B-l summarizes concentrations
of 9 pollutants (or groups of pollutants) detected in walleye specimens
collected in 1985; this is the most systematic set of data available for
comparison with concentrations of CDDs/CDFs. Seven of the 9 pollutants listed
in Table B-l are known to be carcinogenic, and their cancer potency factors
(qi*) as determined by USEPA (1986d) are also listed in Table B-l. To compare
the potential cancer risks posed by these pollutants with those posed by
CDDs/CDFs, the right-hand column of Table B-l presents a measure of the
Relative Hazard, i.e., the product of the average concentration c and the
cancer potency factor qi*. This Relative Hazard indicates the relative risks
posed by the various pollutants, for the following reason.
The upper bound on the lifetime cancer risk R posed to a person of body
weight W kg eating f grams of fish daily for a lifetime is given by the
formula:
(f)(c)(qi*)
(1,000)(W)
where 1,000 is a unit conversion factor (kg/g). Thus, for any individual
consumer of fish (with given values of W and f), R is proportional to the
Relative Hazard (c x q]_*).
B-l
-------
TABLE B-l
TOXIC ORGANIC POLLUTANTS
NATIVE FISH COLLECTION
TITTABAWASSEE RIVER 1985
Walleye
Concentration (rag/kg)
Compound
Number of
Analyses
Range
Average
Potency
Factor 1
(mg/kg-d)"
Relative
Hazard[5]
% Fat (hexane
(extractables)
PCTs (5432, 5442)
PCBs (1254)
Chlordane[l]
DDT[2]
Dieldrin
Hexachlorobenzene
Toxaphene
Octachlorostyrene
Heptachlor epoxide
CDDs/CDFs (TEQ) [3]
14
14
14
14
14
14
14
14
14
14
14
0.70-3.2
ND-0.500
0.197-1.653
ND-0.036
ND-0.212
ND-0.007
0.002-0.038
ND-0.222
ND-0.003
ND-0.005
2.5-15(4]
2.1
0.093
0.588
.009
.054
.001
.009
.097
.001
.002
13[4]
NA[6]
7.7
1.3
0.34
30.
1.69
1.1
NA[6]
2.6
1.6x10
-
4.5
0.01
0.02
0.03
0.02
0.11
-
0.05
2.1
1. Chlordane includes alpha-Chlordane, gamma-Chlordane, Oxychlordane, Cis-
nonachlor and trans-nonachlor.
2. DDT includes p,p'-DDD, p,p'-DDE and p,p'-DDT
3. From Table III-27
4. Concentrations in ng/kg
5. Product of two previous columns
6. No cancer potency factor derived
Source: Amendola and Barna (1986).
B-2
-------
Table B-l indicates that for 6 of the 7 carcinogenic pollutants found in
fish, upper-bound cancer risks posed by consumption of walleye from the
Tittabawassee River would be 1-2 orders of magnitude lower than those posed by
the CDDs/CDFs. For PCBs, however, upper-bound cancer risks posed by
consumption of walleye from the Tittabawassee River would be similar to those
posed by the CDDs/CDFs. Specifically, consumption of walleye by a 70-kg
person at the median rate for sports fishermen of 48 g/day (see Section III.E)
would lead to an upper-bound lifetime cancer risk of 3 x 10 . Since PCBs and
CDDs/CDFs are similar in their environmental behavior and tend to concentrate
in sediments and fish in the same way, it is likely that similar conclusions
would hold for bottom-feeding fish also.
A similar comparative analysis of potential noncarcinogenic effects of
the pollutants listed in Table B-l indicates that PCBs may also be of
comparable or greater concern than CDDs/CDFs at the relative levels found in
the walleye from the Tittabawassee River. In a series of experiments reported
by Allen et al. (1979), the LOAEL for adverse reproductive effects of PCBs
(Aroclor 1248) in rhesus monkeys was 7 ug/kg-day (0.5 ppm in the diet
administered 3 days/week); this was about 5,000 times higher than the LOAEL
for 2378-TCDD (50 ppt in the diet, or about 1.5 ng/kg-day) in parallel
experiments conducted in the same laboratory (Allen et al. 1979). In
Tittabawassee River walleye, PCBs were present at concentrations about 110,000
times higher than those of CDDs/CDFs (TEQs) (Table B-l). Thus, at the
comsumption rates discussed in Section III.E, PCBs would be judged to pose
reproductive hazards in addition to those posed by CDDs/CDFs. None of the
B-3
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other toxic pollutants listed in Table B-l would pose reproductive hazards at
the levels of contamination and rates of intake listed.
Although the source of PCBs in the Tittabawassee River is not known and
is not believed to be related to the Dow Midland facility, it is necessary,
for the reasons given in the two previous paragraphs, to consider whether the
presence of PCBs in the Tittabawassee River fish may augment the hazards
attributable to CDDs/CDFs. PCBs are complex mixtures, some of whose
components act by the same mechanisms as 2378-TCDD and cause similar toxic
effects, although with much lower potencies (Poland and Knutson 1982, Safe et
al. 1985a,b). Unfortunately, few studies of the joint effects of PCBs and
CDDs/CDFs have been reported. Birnbaum et al. (1985) reported that one PCB
component appeared to act synergistically with 2378-TCDD in inducing cleft
palates in mice. However, Haake et al. (1987) and Bannister et al. (1987)
have recently reported that co-administration of a PCB mixture (Aroclor 1254)
protected mice against the immunotoxic and teratogenic effects of 2378-TCDD.
All these studies involved acute administration of PCBs and 2378-TCDD, and
their relevance to chronic exposures is uncertain. Also, the protective
effect reported by Safe et al. (1987) was observed only for relative doses
(PCBs:2378-TCDD) in a range lower than that occurring in Tittabawassee River
fish. Much more study is needed before definitive conclusions can be drawn
about effects of joint exposure to PCBs and CDDs/CDFs.
Another hypothetical set of interactions between CDDs/CDFs and other
toxic pollutants that needs to be considered is initiation/promotion
interactions. 2378-TCDD is known to act as a potent late stage carcinogen, or
B-4
-------
promoter of earcinogenesis initiated by other carcinogens (Pitot 1986).
2378-TCDF has also been reported to act as a promoter (Poland et al. 1983,
Poland and Knutson 1982), and by inference, other CDDs/CDFs are likely to have
similar activity. Hypothetically, therefore, CDDs/CDFs ingested in fish might
act to promote cancers initiated by other carcinogens, thus augmenting the
risks posed by either group of chemicals considered in isolation. In fact,
however, none of the other carcinogens listed in Table B-l is known to act as
a cancer initiator, and several are known or suspected to act primarily as
late stage carcinogens. Thus, it is not clear that initiation/promotion
interactions would significantly augment the risks posed by CDDs/CDFs under
the circumstances of exposure prevailing in the Tittabawassee River.
B-5
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APPENDIX C
NOMENCLATURE FOR CHLORINATED
DIBENZO-p-DIOXINS AND DIBENZOFURANS
-------
APPENDIX C
NOMENCLATURE FOR CHLORINATED
DIBENZO-p-DIOXINS AND DIBENZOFURANS
The following terminology and abbreviations are used in this document
5.
The term "congener" refers to any one particular member of the same
chemical family: e.g., there are 75 congeners of chlorinated dibenzo-p-
dioxins.
The term "homologue" refers to a group of structurally related chemicals
which have the same degree of chlorination. For example, there are eight
homologues of CDDs, monochlorinated through octachlorinated.
The term "isomer" refers to substances which belong to the same
homologous class. For example, there are 22 isomers that constitute the
homologue of TCDDs.
A specific congener is denoted by unique chemical notation. Commas are
omitted for brevity. For example, 2,4,8,9-tetrachlorodibenzofuran is
referred to as 2489-TCDF.
Notation for homologous classes is as follows:
Dibenzo-p-dioxin
Dibenzofuran
No. of Halogens
2
3
4
5
6
7
8
1 through 8
D
F
Acronym
D
Tr
T
Pe
Hx
Hp
0
CDDs and CDFs
24-DCDD
2378-TCDD
12378-PeCDF
123478-HxCDD
C-l
-------
6. Dibenzo-p-dioxins and dibenzofurans chat are chlorinated at the 2,3,7,
and 8 positions are denoted as 2378-substituted congeners; e.g., 12378-
PeCDF and 23478-PeCDF are both referred to as "2378-substituted-PeCDFs"
C-2
-------
APPENDIX D
BROMINATED COMPOUNDS
-------
APPENDIX D
BROMINATED COMPOUNDS
Recent studies have indicated that combustion of wastes containing
brominated compounds can give rise to brominated dibenzo-p-dioxins and
dibenzofurans as well as mixed brominated/chlorinated dibenzo-p-dioxins and
dibenzofurans (Rappe et al. 1979, Buser 1987, Hutzinger and Thoma 1987). These
bromine-containing compounds (collectively referred to as BrDDs/BrDFs) have at
least some of the biochemical activity of CDDs/CDFs and some of them are
thought to have toxic potencies approaching those of CDDs/CDFs (Mason et al.
1986a, Mason et al. 1987). Dow Chemical has manufactured brominated organic
compounds at the Midland facility until 1987, and it is likely that some
bromine-containing wastes have been sent to the waste incinerator. Hence, it
is likely that some BrDDs/BrDFs have been emitted from the plant. However, no
investigations of their possible presence in the Midland environment have been
conducted.
D-l
-------
APPENDIX E
POSSIBLE HAZAPJ3S TO WILDLIFE
-------
APPENDIX E
POSSIBLE HAZARDS TO WILDLIFE
Little information is available to serve as the basis for assessment of
potential hazards to wildlife posed by residues of CDDs/CDFs in the Midland
area. As documented in Section III.E, residues of CDDs/CDFs (and other
contaminants, including PCBs) have been detected in fish in the Tittabawassee
River. It can therefore be presumed that other aquatic organisms in the river,
along with consumers of aquatic life, such as fish-eating mammals and fish-
eating birds, are exposed to these contaminants. It is also likely that
contaminated sediments have been transported downstream as far as Saginaw Bay,
raising the possibility that aquatic wildlife there may be exposed to
CDDs/CDFs. For example, Stalling et al. (1983) reported the presence of
CDD/CDF isomers in the tissues of fish and fish-eating birds collected from the
vicinity of Saginaw Bay.
Several studies have suggested that fish are adversely affected by 2378-
TCDD at water concentrations as low as 100 ppq (Yokim et al. 1978). These and
other studies (Miller et al. 1979, Branson et al. 1985) suggest that adverse
effects on fish are associated with whole-body concentrations of 2378-TCDD in
the range of 1-2 ppb or higher. Fish tissue concentrations of up to 700 ppt
2378-TCDD (equivalent to about 900 ppt TEQ) have been reported in fish in the
Tittabawassee River (Table 111-25). This approaches the lowest concentration
reported as associated with adverse effects. However, in view of the limited
range of species tested and the short duration of the experimental studies (up
E-l
-------
to 114 days), it is not possible to determine whether or not adverse effects
may be occurring.
Virtually no information is available on the toxicity of CDDs/CDFs to
fish-eating mammals or birds, except that the mink is extremely sensitive. In
a paper presently available only as an abstract, Hochstein et al. (1986)
reported that the 128-day dietary LC,Q for 2378-TCDD in mink was 0.85 ppb, only
slightly higher than the highest concentration reported in Tittabawassee River
fish. Field studies in Green Bay, Wisconsin, have shown reproductive
impairment in fish-eating birds associated with residues of CDDs/CDFs and PCBs
(Hoffman et al. 1987, Kubiak et al. 1987). An unpublished report by Kurita et
al. (1987) documents reproductive impairment in the same species (Forster's
tern) in Saginaw Bay in 1987. This raises the possibility that residues of
CDDs/CDFs (and/or other pollutants) may have accumulated in the Saginaw Bay
ecosystem to levels that pose chronic hazards to wildlife.
E-2
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