United States        Region 5         EPA-905/4-88-006
            Environmental Protection    230 South Dearborn     April 1988
            Agency          Chicago, Illinois 60604
x°/EPA      Proposed Risk
            Management Actions
            for Dioxin Contamination
            Midland, Michigan


                APRIL 14, 1988
                   REGION V
           CHICAGO, ILLINOIS 60604

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I.  Introduction

     Environmental Risk Assessment is a scientific process in which facts and
assumptions are integrated and used to estimate the potential for adverse
effects on human health or the environment that may result from exposures to
specific pollutants.  The risk assessment protocol followed by the United
States Environmental Protection Agency (USEPA) includes the following
components (USEPA 1986):

     o  Hazard Identification
     o  Dose-Response Assessment
     o  Human Exposure Assessment
     o  Risk Characterization

     The hazard identification is a qualitative risk assessment, establishing
the potential toxicity or hazard of a particular substance.  The dose-response
assessment defines the relationship between the dose of a substance and the
probability of induction of adverse health effects.  The human exposure
assessment is conducted to estimate,  in a specific situation or setting, what
are the probable and maximum human exposures to a substance (i.e., dose rates),
including evaluations of potential high risk groups.  In risk characterization,
outputs from the dose-response and human exposure evaluations are combined to
estimate potential  adverse health impacts, with a review of the uncertainties
in the overall analysis.  The risk assessment for dioxin contamination  in and
around Midland, Michigan, is fully described in a companion report to this
document, "Risk Assessment for Dioxin Contamination at Midland,  Michigan"
(USEPA 1988), referred to hereafter as the Risk Assessment.

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     Risk management, on the other hand, is a decision-making process which can

involve much more than consideration of the results of a risk assessment.

Often, such factors as technological feasibility, economic information about

costs and benefits, statutory requirements, and public concerns can heavily

influence risk management.  This report sets out USEPA's proposed risk

management actions for contamination with 2,3,7,8-tetrachlorodibenzo-p-dioxin

(2378-TCDD) and other polychlorinated dibenzo-p-dioxins (CDDs) and

polychlorinated dibenzo-furans (CDFs) in and around Midland, Michigan (see

Figure 1-1).  The principal purpose of this document is to present to the

people of the Midland area and to its institutions, both public and private, a

summary of the Risk Assessment and an outline of the proposed risk management

actions USEPA believes are appropriate.

     The reader should keep in mind that CDD/CDF contamination at Midland is

not a new issue.  Many of the remedial actions necessary to minimize human

exposures to CDDs and CDFs have already been taken, or are being taken,

by Dow Chemical in compliance with various statutory or regulatory

requirements.  Accordingly, factors such as economic costs and benefits  have

not been considered in great detail here since most of the costs to Dow

Chemical  have been, or are being, incurred.  There are, however, questions of

technical achievability, regarding additional  remedies, for which there  are

currently no answers.  In these circumstances  the proposed risk management

actions outline a process to develop the necessary information to answer

questions about technical achievability and related costs.

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            *•?•" •-TtJL*'"n

   - Facility Boundary
Midland, Michigan Area and
    Dow Midland Facility
                                                       Seal* in Fut

                                                     0 1000 2000 3000
 Sources: USCS (1973),
 Dow (1984)

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     USEPA developed the proposed risk management actions presented in this

report taking into account the Risk Assessment and the current  status  of

ongoing remedial actions.  We believe that these proposed actions are

reasonable and necessary measures which can be implemented without major

disruptions.  For the most part, USEPA believes that the measures relating to

the Dow Chemical plant can most effectively be implemented through existing

regulatory mechanisms including the air,  solid waste, and water pollution

control programs managed by MDNR and USEPA Region V.  Members  of the public,

and public and private institutions, in the Midland area are invited to comment

on the Risk Assessment and the proposed risk management actions.

     This document provides:  (1) a brief  summary of the results of a number of

studies undertaken by the USEPA, the State of Michigan, and Dow Chemical

Company; (2) a summary of possible health risks to Midland area residents

resulting from exposures to CDDs and CDFs; (3) proposed actions for minimizing

emissions and discharges to the environment from Dow Chemical;  (4)

recommendations for people living in the  Midland area on how to minimize their

exposures to CDDs and CDFs, and thus the  possible health risks

associated with those exposures; and (5)  proposed additional  monitoring

programs, some of a continuing nature, for the purposes of establishing long-

term trends in emissions and  discharges of CDDs/CDFs and to document changes  in

environmental contamination for the more  significant human exposure routes.

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11.  Summary of Past Environmental  and Point Source Investigations

     Polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans (CDDs

and CDFs, respectively) are closely-related families of highly toxic and

persistent organic chemicals which  have been formed as unwanted by-products in

some commercially significant chemical reactions, during high temperature

decomposition and combustion of certain chlorinated organic chemicals, and

through other reactions involving chlorine and organic materials.

     Dow Chemical has manufactured  over 1,000 different inorganic  and organic

chemicals at the Midland facility.   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 phenols began in the 1930's and continued

at substantial levels into the late 1970's.  Dow Chemical  reports  that only two

chlorinated phenolic products--2,4-dichlorophenol and 2,4-dichlorophenoxyacetic

acid (2,4-D)--are currently manufactured at Midland (Dow 1984).  Incineration

has been practiced since at least the 1930's with varying levels of emissions

controls.  Currently, Dow Chemical  operates a rotary kiln incinerator for

combustion of both hazardous and non-hazardous wastes.  Prior to 1980, a "tar

burner" was also operated at the site to dispose of still  bottoms  and other

hazardous chemical residuals.

     In June 1978, Dow Chemical informed the Michigan Department of Natural

Resources (MDNR) and USEPA 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 2,3,7,8-tetrachloro-

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dibenzo-p-dioxin (2378-TCDD), the most toxic of the COD/CDF compounds

(Dow 1978).  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).  The results of these studies prompted the

Michigan Department of Public Health (MDPH) to issue a formal advisory in June

1978 warning against consumption of any fish collected from the Tittabawassee

River downstream of Dow Dam (MDNR 1978).  The advisory remained in effect until

March 1986, when the MDPH modified it to apply only to catfish and carp, after

reviewing 1985 monitoring data showing that walleyes and other game fish were

contaminated at lower levels.

     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 CDD/CDF studies in Midland and

elsewhere (USEPA 1983a).  Most of those recommendations were subsequently

incorporated into USEPA's Dioxin Strategy and National  Dioxin Study

(USEPA 1983b, 1987a).

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     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 CDD/CDF emissions and discharges

from Dow Chemical  and CDD/CDF contamination in the Midland area (MDNR 1983).

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 (ECOMM and Foresight 1983).  Although USEPA subsequently denied

that petition, some of the requested investigations were within the scope of

those being planned by Region V and the State agencies for the Midland area

(USEPA 1983c).

     The studies conducted by USEPA and the State were formally called the

Michigan Dioxin Studies and included the following major elements:

     1.  Supplemental native fish and sediment sampling in the Tittabawassee

     2.  Surface soil sampling at Dow Chemical, in the City of Midland, and at
         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 CDDs and CDFs 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

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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

     In 1983, Dow Chemical initiated its own independent point source
investigation of CDDs and CDFs 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
monitoring (Dow 1984).  Dow Chemical has also conducted supplemental
incinerator emissions testing in  1987 (Dow 1987a), supplemental monitoring of
Tittabawassee River fish in response to  a  consent order with USEPA (U.S. v.
Dow 1984), and twice-monthly monitoring  for 2378-TCDD in the treated process
wastewater discharge to the Tittabawassee River (Dow 1984-1987).

     Studies by Dow and USEPA revealed widespread contamination of the surface
soil at the Midland facility (average of 0.5 ppb 2378-TCDD) (Dow 1984,
USEPA 1985a).  Several small  areas within the facility were found to be more
highly contaminated (2-50 ppb).    USEPA studies indicated lower-level contamina-
tion of the soils throughout the  community with CDDs/CDFs  (average <0.1 ppb
2378-TCDD) (USEPA 1985a).   Since these studies were undertaken, Dow has been
ordered to remediate areas of high on-site contamination to prevent the spread
of contaminated soil (USEPA 1985c).  The sources of the on-site soil  contamina-
tion appear to have been 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

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from the facility, and possibly past fugitive emissions from production

     Studies by Dow Chemical indicated the hazardous waste incinerator to be
the most significant current air emission source at the Midland Plant
(Dow 1984),  Emissions testing by USEPA in 1984 (Trembly and Amendola 1987)
and Dow Chemical in 1987 (Dow 1987a) indicated significantly reduced emission
levels from those measured in 1983 by Dow.

     Significant levels of CDDs/CDFs have also been detected in the effluent
from the Dow wastewater treatment system to the Tittabawassee River
(0.01-0.05 ppt 2378-TCDD in 1984; <0.005 ppt 2378-TCDD currently)
(Dow 1984-1987).  The current lower levels are the direct result of the 1984
Final Order of Abatement issued by the Michigan Water Resources Commission
(MWRC) and the MONR, requiring Dow Chemical to install a final  effluent
filtration system and implement a plant-wide program to reduce CDDs/CDFs
(MWRC 1984).  Studies conducted by USEPA, the U.S. Food and Drug Administration
(USFDA), the MDPH and MDNR, and Dow Chemical  between 1979 and 1985 revealed
that 2378-TCDD persisted at levels of concern in Tittabawassee River native
fish, despite shutdown of the Dow Midland production facilities for the
manufacture of 2,4,5-trichlorophenol, the derivative 2,4,5-T herbicide, and
pentachlorophenol, chemicals known to be contaminated with CDDs and CDFs
(Amendola and Barna 1986).

     However, the most recent data indicate 2378-TCDD levels in native fish  may
be declining.  Data collected in 1985 show that native Tittabawassee River fish
collected downstream of Dow Chemical are also contaminated with several  other
organic chemicals, the most significant being PCBs.   Dow Chemical  is not

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believed to be a significant source of PCBs.  Generally speaking, chemicals
other than CDOs/CDFs were not found in other media (air, soil, drinking water)
at levels that would warrant specific consideration in this report.

     The USEPA has compiled the data from its testing programs (USEPA 1985a,
Barna and Amendola 1985, Amendola and Barna 1986, Trembly and Amendola 1987)
and all available data from other investigations and has prepared a
comprehensive Risk Assessment (USEPA 1988) for individuals living in the
Midland area.  A summary of this document is presented in Section III.

III. Summary of USEPA's Risk Assessment

     In keeping with guidelines established by USEPA and by the National
Academy of Sciences and other scientific advisory bodies, USEPA's Risk
Assessment for Midland, Michigan, involved four distinct activities: hazard
identification, dose-response assessment, exposure assessment and risk
characterization.  As noted earlier, the first step, hazard identification,
defines the basic toxicologic properties of CDDs/CDFs and identifies the most
important toxic effects observed both in studies of animals exposed to these
compounds and in human epidemiological studies.  Dose-response assessment, the
second step, consists of further review and analysis of these studies in order
to develop an understanding of the relationships between the amount of
CDDs/CDFs to which humans may be exposed and the likelihood and severity of
adverse health effects.

     The exposure assessment consists of a review of the available data
regarding the levels of CDDs/CDFs found in and around Midland and the
development of quantitative estimates of the amount of CDDs/CDFs to which

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Midland area residents may be exposed.  Finally, risk characterization involves

the combination of the dose-response information and the exposure estimates to

derive an assessment of the levels of risks faced by the various exposed

populations in Midland.

     Also included in the Risk Assessment are discussions of the extent of

uncertainty associated with the exposure and risk estimates.  For each route of

exposure (inhalation of ambient air, contact with contaminated soils, etc.)

more than one exposure scenario was developed using ranges of assumptions about

environmental levels of CODs/CDFs and exposure-related behavior of the exposed


A.  Hazard Identification

     Chlorinated dibenzo-p-dioxins (CDOs) and dibenzofurans (CDFs) constitute

a family of over 200 related chemical compounds (congeners) with varying

chemical, physical, and toxicologic properties.  The congener 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.  Limited toxicological  testing of other

CDDs/CDFs has demonstrated that several  of these compounds cause similar

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toxicological effects, but that higher doses of these compounds are generally
required to cause effects of comparable magnitude to those induced by 2378-

     USEPA has determined that the critical end points of concern for purposes
of assessing risks associated with exposure to CDDs/COFs in the Midland area
are cancer and reproductive and teratogenic effects.  In addition, under
certain conditions, toxic effects on the liver and immune system may also
be significant in risk assessment.  The evidence for these health effects is
discussed in more detail in Chapter II of the Risk Assessment.

B.  Dose-Response Assessment for 2378-TCDD

     The evidence for the carcinogenic (cancer-causing) action of 2378-TCDD is
provided mainly by several  long-term studies of laboratory animals exposed to
the substance.  On the basis of these animal studies and associated factors,
USEPA has concluded that 2378-TCDD is an animal  carcinogen and should be
regarded as a probable human carcinogen (USEPA 1986).  Applying its
established procedures, USEPA used the experimental  animal  data to estimate an
upper bound on the cancer potency factor (referred to as "ql*") for 2378-TCDD
of 1.6 x 10*4 (pg/kg/day)~l.  Note:  "pg" stands  for picogram = 10~12 gram.

     While the above value  remains USEPA1s current position on the potency of
2378-TCDD, and,  therefore,  was  the one used in preparing the Risk Assessment,
a formal reassessment of its derivation is under way.  Final  results of  that
reassessment are not expected for at  least several  months.

     2378-TCDD has been shown to be  teratogenic  and  to cause adverse
reproductive effects in a number of  animal  species,  including subhuman  primates

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(USEPA 1985b). USEPA has examined the data in detail  and has selected a value

of 1 pg/kg/day as the Reference Dose (RfD)* for 2378-TCDD (USEPA 1987b).  This

value is used in the risk assessment to evaluate the potential  for non-cancer

effects resulting from long-term exposures to CDDs/CDFs.  USEPA is also

concerned about doses which pregnant women might ingest over a  short period at

a critical time in the development of the fetus.  USEPA therefore has adopted a

"health advisory" (HA) dose-level of 300 pg/kg/day for protection against

teratogenic effects.  This HA dose-level is appropriate for comparison with

single-dose intakes or short-term exposures lasting a few days, whereas the RfD

of 1 pg/kg/day is more appropriate for comparison with long-term or life-time


     Although USEPA has determined that reproductive/teratogenic effects are

the critical toxic effects for dose-response assessment of 2378-TCDD, based

upon a review of several animal studies, USEPA has concluded that the RfD of

1 pg/kg/day also is appropriate to protect against possible liver damage in all

populations experiencing long-term exposures to CDDs/CDFs (USEPA 1985b, 1988).

For short-term exposures (single dose), the animal data support an HA for liver

effects of 280 pg/kg, close to the single-dose HA derived for reproductive/

teratogenic effects. The toxicologic parameters used in the Risk Assessment are

summarized in Table III-l.

     All of the toxicological dose-response estimates described above—cancer

potency, Reference Dose, and Health Advisory--were derived by extrapolating
*The RfD, which is used for assessing toxic effects other than  cancer,  can  be
defined as an estimate (with uncertainty spanning perhaps an order of
magnitude) of the daily exposure (daily dose, e.g., in pg/kg/day)  of a  human
population (including sensitive subpopulations) that is likely  to  be without
an appreciable risk of adverse health effects even if exposure  occurs daily
during a lifetime.

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                                  TABLE III-l

Toxicologic End Point
Type of Parameter
Parameter Value
Dose-Response Slope
  Parameter (95%
 upper confidence
Teratogenesi s/Reproducti ve

    long-term exposures

    single-dose exposures

Hepatotoxicity (liver

    long-term exposures

    short  (10-day) exposures

    single-dose exposures



    1 pg/kg/day

    300 pg/kg/day

    1 pg/kg/day

    28 pg/kg/day

    280 pg/kg/day
*In USEPA's weight-of-evidence classification system for carcinogens,  B2
indicates that the evidence for carcinogenicity in animals is "sufficient",
while the human evidence for carcinogenicity is "inadequate."  B2  is  placed  in
quotation marks, because the classification was for 2378-TCDD alone,  whereas
total TEQs are being evaluated here, in accordance with USEPA interim science

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animal  test results to humans through the use of mathematical  models and/or
application of uncertainty factors.  This approach is necessary because
accurate data on actual  human exposures to CDDs/CDFs, and on the resulting
toxic effects, are not available.  USEPA believes that its methods for dose-
response assessment are conservative, and that the estimates so derived
are unlikely to be exceeded when humans are exposed to CDDs/CDFs.  The Agency
recommends that the estimates be used for assessing risks and for decision-
making related to the protection of human health, keeping in mind the
uncertainties inherent in their derivation.

C.  Dose-Response Assessment for CDD/CDF Mixtures

     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 potent.  USEPA has adopted as interim science policy the "toxicity
equivalence factor" approach for use until sufficient additional data are
available to derive a more accurate procedure that can be scientifically
validated (USEPA 1987c).  The TEF approach uses correlations between structure
and chemical activity to estimate the toxicity of any CDD/CDF mixture with
regard to both carcinogenic and noncarcinogenic endpoints.  The result is
expressed as an equivalent amount of 2378-TCDD.

     The TEF approach was used in the Risk Assessment to convert reported
quantities of CDDs/CDFs in environmental samples to "2378-TCDO toxicity
equivalents" (TEQs), which were then treated as if they were concentrations of
2378-TCDD.  The TEF approach and its limitations are discussed in more
detail in Part II.C of the Risk Assessment.

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0.  Exposure Assessment

     Quantitative estimates were developed for the significant routes of

exposure to CDDs/CDFs in the Midland area as outlined below.

1.  Exposure to Ambient Air

     Two scenarios were developed to estimate exposures of Midland area

residents to CDDs/CDFs in ambient air.  The "fenceline case" represents

exposure for a hypothetical individual  residing near the Dow Chemical plant

boundary at a location downwind (according to the prevailing wind direction)

from the incinerator and production areas; the "residential area case"

represents exposures further away from  the plant, nearer the higher-population-

density areas in Midland to the north of the facility.  For each scenario,

average exposure (dose rate) estimates  were derived for four specific age

ranges as well as for an entire lifetime.  The procedures used to develop the

air exposure estimates and their limitations and associated uncertainties are

described in detail  in Section III.B of the Risk Assessment.

2.  Exposure to Contaminated Soil

     The "lower estimate" and "upper estimate" of exposure were developed using

lower and higher estimates for (1)  the  frequency of exposure, (2) the amounts

of soil ingested as a result of outdoor activities, and (3) the fraction of

CDDs/CDFs absorbed into the body from the ingested soil.   Individual  lifetime

segment and lifetime average estimates  of exposure/dose rates were derived as

for air.  The methods used to derive these estimates  and  their  limitations and

associated uncertainties are discussed  in detail  in Section III.C of  the Risk


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3.  Exposure Through the Consumption of Contaminated Fish

     The five exposure scenarios which have been developed (see Table III-2)

vary with regard to the amounts and types of fish consumed (all fish is assumed

to come from the Tittabawassee River except for half of the fish eaten by the

"general consumer").  The long-term consumption rates were used to develop

CDD/CDF ingestion or dose rates to assess cancer risks and for comparison with

the RfD for non-cancer effects.  Single-meal CDD/CDF ingestion rates also were

developed to compare with the short-term Health Advisory (HA) values.

     The exposure assessment established that consumption of contaminated fish

was clearly the dominant route of CDD/CDF exposure for some populations, with

exposure and intake levels being as much as several  orders of magnitude higher

than those associated with other exposure routes.  The methods used to develop

these estimates and their limitations and associated uncertainties are

described in detail in Section III.E of the Risk Assessment.

4.  Other Routes of Exposure

     Several other potential routes of human exposure were evaluated in the

Risk Assessment (Section III.F).  Consumption of ground water or surface water

were found unlikely to be associated with CDD/CDF exposure.  Other routes that

were considered were exposure to potentially-contaminated house dust and

exposure of infants through breast milk.

     Since no measurements were available of the levels of CDDs/CDFs in

household dust in Midland, no quantitative estimates of exposure through this

route could be conducted.  It was concluded, however, based upon studies of

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                                  TABLE 111-2
                           FISH CONSUMPTION SCENARIOS
Scenario	Consumption Rate	Type of Fish3	

Plausible Maximum Consumer   Long-term: 100 g/dayb       50% Bottom feeders
                             Single Meal: 255 gc         -t- 50% Game fish

High Sports Fisherman

      — Level 1             Long-term: 100 g/dayb       100% Game fish
                             Single Meal: 255 gc

      -- Level 2d            Long-term: 48 g/daye        100% Game fish
                             Single Meal: 113 g?

Great Lakes Consumer9        Long-term: 16 g/day^        100% Game fish
                             Single Meal: 113 g?

General Consumer             Long-term: 7.8 g/dayi       50% Game fish
                             Single Meal: 113 gf         + 50% Clean fish

aAll fish are assumed to be from the Tittabawassee River except "clean" fish
 which are assumed to be free from COD/CDF contamination.  The following fish
 tissue concentrations are used in the Risk Assessment (1983-1987 data):

            Type of Fish        Partial TEQs (ppt)

           Bottom feeders               58
           Game fish                    13
           Clean fisn                    0

      percentile consumption rate for a cohort of Lake Michigan sports
 fishermen who ate more than 24 Ibs of fish per year (Humphrey et al.  1976).

C90th percentile fish meal size (USDA 1982).

dReferred to in Risk Assessment as "Median Sports Fisherman."

eMedian for a cohort of Lake Michigan sports fishermen who ate more than 24 Ibs
 of fish per year (Humphrey 1983).

fMedian fish meal size (USDA 1982).

9Added following completion of Risk Assessment, using the information  and
 procedures contained in that document.

"FDA-estimated upper 90th percentile consumption rate of freshwater fish in the
 Great Lakes area (USEPA 1984a).

''Average consumption of "finfish other than canned, dried, and raw"
 (USDA 1982).

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other situations where exposures to toxic pollutants in house dust had  been

measured, that this route of exposure could be comparable to some of the  other

exposures that were quantifiable.

     Similarly, CDD/CDF levels in breast milk from the Midland area have  not

been measured.  However, a simple model  was employed to estimate intakes

for nursing infants.

     Finally, while no data were available which would allow a quantitative

assessment of the exposures from consumption of CDDs/CDFs contained in  or

deposited on home-grown vegetables, a small number of samples are currently

being analyzed by USEPA, and the results should be available soon.

E.  Risk Characterization
     Quantitative estimates of the risks associated with CDD/CDF exposures by

the routes just discussed were developed by combining the exposure and intake

estimates with the toxicologic parameters discussed in the Dose-Response

Assessment. For long-term exposures to air and soil contamination, two measures

of risks were developed, an upper-bound estimate of the additional cancer risks

associated with lifetime exposures at the predicted levels, and a Hazard Index

(HI)* for non-carcinogenic effects.

     For a given exposure scenario, an HI of less than 0.1 indicates that

exposures are not likely to be associated with adverse non-cancer effects

(reproductive toxicity, teratogenicity, or liver toxicity).  If the HI

approaches or exceeds 10, the likelihood of adverse effects is  increased to the

point where action to reduce human exposure should be considered.  Owing to the

*Defined as the ratio of the estimated average daily dose to the previously
defined RfD (or HA for single or short-term exposures).

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uncertainties involved with these estimates, HI values between 1 and 10 may be

of concern, particularly when additional significant risk factors are present

(e.g., other contaminants at levels of concern).

     The risk levels predicted for each of the three major exposure routes are

summarized in Tables III-3 through III-6.  For air exposures, (see Table III-3)

the predicted incremental lifetime cancer risks (upper bound) range from

5 x 10-6["B2"] to 6 x 10-5["B2"], depending upon the exposure scenario and the

method used to calculate TEQs.  Many of the His for the various age groups and

scenarios are less than 0.1, and all  but one are less than 1.0.

     The upper-bound cancer risk estimates associated with exposures to

contaminated soil (see Table III-4) are slightly lower than those for the air

route; estimated lifetime risks are 5 x 10~7 ["B2"] for the "lower estimate"

scenario and 1 x 10~5 ["B2"] for the "upper estimate".   The His for non-cancer

effects are likewise lower than for air exposures.

     Both the cancer and non-cancer risks calculated for CDH/CDF exposures via

contaminated fish are much greater than for the other two pathways (see Table

111-5).  Upper-bound estimates of incremental  lifetime cancer risks range from

1  x 10-4 ["B2"] for the "general  consumer" to  1 x 10'2 C"B2"1 for the

"plausible maximum consumer".   The His  also exceed  10 for two of the scenarios.

The estimated single-meal CDD/CDF intake levels result  in His greater than 10

for meals comprising the maximum concentration bottom feeder (see Table III-6).

All  other single meal  His are  less than 1.0.   Note  that the risk levels

presented in Tables III-5 and  III-6 are for consumption of Tittabawassee River

fish contaminated with CDDs  and  CDFs.   Native  fish  from the river also  are

                              PUBLIC REVIEW DRAFT
                                  TABLE 111-3

                           Upper-Bound Cancer Riskb    Hazard Indexc(Long Term)

Exposure Scenario3	A-Methodd    B-Methodd	A-Methodd  B-Methodd

1.   Fenceline Case:
     Infants 0-1 year          --           --            0.4       0.1
       1-6 years               —           --             1        0.4
       6-12 years              --           —            0.7       0.3
     Adults (12-70)            --           --            0.3       0.1
     Lifetime               6xlO-5["B2"]e 2xlO-5["B2"]

2.   Residential Area
     Infants 0-1 year          --           —            0.05      0.02
       1-6 years               —           --            0.2       0.08
       6-12 years              —           —            0.1       0.06
     Adults (12-70)            —           —            0.05      0.02
     Lifetime               lxlO-5["B2"]  SxlO'6 ["82"]

aFrom Section II.B.6*.  All exposure estimates assume 24 hr/day exposure to
 outdoor concentrations, long-term residence (lifetime for cancer risks).

bUpper-bound estimate of lifetime cancer risk, obtained by multiplying exposure
 estimate in Table 111-12* by cancer potency factor of 1.6 x 10~* (pg/kg/day)-1
 and multiplying by relative bioavailability factor of 1.8 (see Section IV.C*).

cRatio of exposure estimate in Table 111-12* to RfD of 1 pg/kg/day, multiplied
 by relative bioavailability factor 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*).

eln USEPA's weight-of-evidence classification system for carcinogens, B2
 indicates that the evidence for carcinogenicity in animals is "sufficient",
 while the human evidence for carcinogenicity is "inadequate."  B2 is placed in
 quotation marks, because the classification was for 2378-TCDO alone, whereas
 total TEQs are being evaluated here, in accordance with USEPA interim science
*ln Risk Assessment

                              PUBLIC REVIEW DRAFT
                                  TABLE 111-4

                          IN SOIL IN MIDLAND, MICHIGAN
                              Upper-Bound Lifetime         Hazard Index0
Exposure Scenario3	Cancer Risk^	(Long Term)
Lifetime Average Exposure:

1.  Lower Estimate:
      Infants 0-1 year                 --                         0.02
        1-6 years                      --                         0.03
        6-12 years                     --                         0.009
      Adults (12-70)                   —                         0.0003
        Lifetime average            5xlO-7["R2"]d

2.  Upper Estimate:
      Infants 0-1 year                 —                         0.5
        1-6 years                      --                         0.6
        6-12 years                     —                         0.2
      Adults (12-70)                   —                         0.01
        Lifetime average            lxlO-5["B2"]
Assumptions and parameters are listed in Table 111-19*.  Note that the upper
 estimate does not include children with pica.  Individuals with this disorder
 could incur risks 10-fold higher.

bUpper-bound estimate of lifetime cancer risk, obtained by multiplying lifetime
 average TEQs dose rate from Table 111-20* by cancer potency factor of
 1.6 x 10~4 (pg/kg/day)~l, and multiplying by relative bioavailability factor
 of 1.8 (see Section IV.C*).

cRatio of adult TEQs dose rate from Table 111-20* to RfD of 1 pg/kg/day,
 multiplied by relative bioavailability factor of 1.8.

^In USEPA's weight-of-evidence classification system for carcinogens, B2
 indicates that the evidence for carcinogenicity in animals is "sufficient",
 while the human evidence for carcinogenicity is "inadequate."  B2 is placed  in
 quotation marks, because the classification was for 2378-TCDD alone, whereas
 total TEQs are being evaluated here, in accordance with USEPA interim science
*In Risk Assessment

                          PUBLIC  REVIEW  DRAFT

                                  TABLE 111-5


                              Long-Term Exposures
Exposure Scenar1oc	Cancer Riskd»e	Hazard  Index°»e»'

Plausible Maximum Consumer         lxlO-2["B2"]9                 50
 (bottom + game fish)

High Sports Fisherman
 (game fish only)
— Level 1
-- Level 2
Great Lakes Consumer
(game fish only)
General Consumer
(game + clean fish)
aOther contaminants such as PCBs, found in  the  fish,  add  to  the  toxicity
 (see Appendix B*).

bNote that Hazard Indices will  be about 2-3 times higher  for small  children
 (Table 111-32*).  Breast-fed infant could  be 10-times higher than  mother.

cFrom data in Section III.E.2* and Tables 111-30* and 111-31*.   Also  see
 Table III-2 in this document.   Long-term dose  rate for Great Lakes Consumer
 is 3.0 pg/kg/day.

^Upper-bound estimate of lifetime cancer risk,  obtained by multiplying  dose
 rate from Table 111-31* by cancer potency  factor of  1.6  x 10~4  (pg/kg/day)-l
 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 111-31* to RfD of 1 pg/kg/day.

9ln USEPA's weight-of-evidence classification system  for  carcinogens, 82
 indicates that the evidence for carcinogenicity in animals  is "sufficient,"
 while the human evidence for carcinogenicity is "inadequate."   B2  is placed in
 quotation marks, because the classification was for  2378-TCDD alone, whereas
 total TEQs are being evaluated here, in accordance with  USEPA interim  science
*Tn Risk Assessment

                              PUBLIC REVIEW DRAFT
                                  TABLE 111-6


                          Single Meal (Bolus) Exposures'3
Fish Meal  Size	Type of Fish	Partial  TEQsc    Hazard Indexd»e

 255 g (9  oz)         Bottom-feeder
                        — maximum             690 ppt            8
                        -- mean                 58 ppt            0.7

                      Game Fish
                      (walleye, etc.)
                        — maximum              39 ppt            0.5
                        — mean                 13 ppt            0.2

 113 g (4  oz)         Bottom-feeder
                        — maximum             690 ppt            4
                        — mean                 58 ppt            0.3

                      Game Fish
                      (walleye, etc.)
                        — maximum              39 ppt            0.2
                        -- mean                 13 ppt           <0.1

aOther contaminants such as PCBs, found in the fish, add to the toxicity
 (see Appendix B*).

bFrom data in Section III.E.2* and Tables 111-30*, 111-31*, and 111-32*.  Also
 see Table 111-2 in this document.

cNote that all estimates of intake are "partial  TEQs," including only
 2378-TCDD, other TCDDs, HxCDDs, HpCDOs, and 2378-TCDF (1983-1987 data).

dRatio of  bolus dose from Table 111-32* to single-dose HA of 300 pg/kg/day.

eNote that Hazard Indices will be about 2-3 times higher for small  children
 (Table 111-33*).
*In Risk Assessment

                              PUBLIC REVIEW DRAFT

contaminated with other toxic chemicals, including PCBs.  The presence of the

other toxic chemicals would result in increased calculated risk levels from

those presented in Tables III-5 and III-6.

     The cancer risk estimates calculated for all of the exposure routes are

summarized in Table III-7, and the His for non-cancer effects are summarized in

Table III-8.  Because of the overall uncertainty in the exposure and risk

estimates, cancer risk estimates are displayed only to the nearest order of

magnitude.  Non-cancer hazard indices less than 0.1 are rounded to "<0.1"

in order to simplify the table.  As previously noted these estimates are upper-

bound values that are unlikely to be exceeded by the actual  risks to humans.

                              PUBLIC REVIEW DRAFT

                                  TABLE III-7

Exposure Route   	Upper Bound Cancer Risk  (Exposure  Scenario)	

	Higher Estimate	Lower  Estimate	

Fish             10'2 (plausible maximum              10~3 (Great  Lakes
                       consumer)                            consumer)

                 10~3 (high sports                    10~4 (general consumer)
                       fisherman—level  1)

Soil             10~5 (upper estimate)                 10~6 (lower  estimate)

                 ID'4 (child with pica)

Air              10~4 (fenceline)                     10~5 (residential  area)
Notes: (1) 10'2, 10'3, 10'4, etc.,  indicate  risks  of  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 in  the Risk Assessment).

       (3) Sources: Tables III-3,  III-4, and III-5.

       (4) USEPA is currently Devaluating the  cancer potency  factor for
           2378-TCDD; a final determination  will  not  be available for at least
           several  months.

                              PUBLIC REVIEW DRAFT

                                  TABLE III-8

Exposure Scenario
                                                     Hazard Index (HI)a
Long-Term    Short-Term
Plausible maximum consumer
High sports fisherman--!eve! 1
Great Lakes consumer
Genera! consumer
Upper estimate young child
  — with pica
  — normal
Lower estimate young child
Upper estimate adult
Infant at fenceline
Child at fenceline
Child in residential  area
Adult in residential  area
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)
       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

CA11 HI values calculated using the "A method."  Infant exposure includes
 exposure from breast-feeding.
Note:  See Table III-6 for His for single meal  (bolus)  exposures.

                                   PUBLIC REVIEW DRAFT
IV.  Risk Management
     Collectively, the point source and environmental  studies conducted  by

USEPA, the State of Michigan, and Dow Chemical  over the past  several  years

clearly indicate that the Dow Chemical  Michigan Division plant at  Midland  has

been the most significant, if not the only significant, source of  CDD/CDF

contamination of the plant site and the general Midland area  environment.   As  a

result of these investigations Dow Chemical  has undertaken several  actions,

some unilaterally, some required by environmental  permits or  administrative

orders issued by the State of Michigan or USEPA, to minimize  emissions and

discharges of CDDs and CDFs and other toxic pollutants.  Dow  Chemical  has

completed or is implementing the following actions:

     o Terminated production of chlorinated benzenes,  and most chlorinated
       phenols, including 2,4,5-trichlorophenol and derivatives and
       pentachlorophenol  (late 1970s).

     o Installed a riverbank revetment system to collect contaminated ground
       waters from a significant portion of the plant  site (1979-1981);
       additional sections of the riverbank have undergone similar treatment

     o Upgraded air emission controls on the hazardous waste  incinerator (late
       1970s); landfilling rather than incinerating contaminated wastewater
       treatment sludges; upgrading operational controls and  practices at  the
       hazardous waste incinerator.

     o Undertook extensive point source and underground investigations of
       CDD/CDF contamination on the plant site (1983-1987).

     o Installed a wastewater effluent filtration  system for  the entire
       wastewater discharge to the Tittabawassee River (1985).

     o Replaced open wastewater ditches on the plant site with enclosed  sewers.
       Isolated high contamination areas of the plant  sewerage system from  the
       wastewater treatment system (1986-1987).

     o Implemented plant-wide dust-suppression program (1986).

                              PUBLIC REVIEW DRAFT
     o Capped areas in the plant with high levels of surface soil
       contamination; limited access to an area on the plant boundary with
       moderate levels of CDD/CDF contamination (1986).
     o Provided preliminary treatment of incinerator scrubber waters prior to
       commingling with other process wastewaters (1987).

     Recent data are beginning to show reduced incinerator emissions, reduced
wastewater effluent discharge levels and, to some extent, reduced  fish contami-
nation levels.  Overall, it appears conditions have improved significantly over
the last ten years.  Nevertheless, the levels of discharge and environmental
contamination as depicted by point source and environmental  data collected
during the 1983-1986 period indicate further remedial  work at the  plant site
and actions by the public to minimize exposures could  be helpful in reducing
the possible public health risks described earlier.

     The estimated risk levels presented in the Risk Assessment and summarized
in Section III are upper-bound cancer risks and upper-bound risks  of non-cancer
health effects based upon conservative assumptions regarding the toxicological
effects of 2378-TCDD, the possible toxicological effects of other  CDDs and CDFs
which have not been studied to the same extent as 2378-TCDD, and the exposures
of Midland area residents to 2378-TCDO and other CDDs  and CDFs in  their
environment.  Thus, the actual risks to Midland area residents are not likely
to be higher than those presented here, and they could be lower.  However,
USEPA believes it is prudent public health policy to consider actions to
mitigate or minimize exposures to contaminants when estimated excess lifetime
cancer risks exceed the 10-5 t0 ig-6 range, and when non-cancer health effects
are estimated to be significant through the use of a hazard  index  or other such
measures for comparing estimated exposures with reference doses and health

                              PUBLIC REVIEW DRAFT

     As highlighted in the preceding section,  the greatest potential  public

health risks (cancer and non-cancer health effects) are associated with

consumption of contaminated fish from the Tittabawassee River.   Possible public

health risks associated with ambient air contamination from current Dow

Chemical  incinerator emissions are estimated to be less significant.   Possible

risks associated with exposure to contaminated soils in the community, which

are related to current and past incinerator emissions, past process emissions,

and windblown dusts from the plant site, are estimated to be less than

estimated risks from consumption of fish or from exposure to contaminated

ambient ai r.

Even if USEPA adopted for use in risk assessments a potency factor an order of

magnitude lower (less conservative), the estimated cancer risks associated with

certain levels of fish consumption would still be quite high (10~3 to 10~5).

If one were to employ such a lower cancer potency factor in evaluating the

other routes of exposure, estimated risks for air and soil would be at or below

10~6 for all groups except children with pica, for whom the estimated risk would

be about 10~5.  Actions to minimize risk for fish consumers are thus the highest


     Also, the estimated non-cancer health effects, which would not be affected

by a change in the USEPA cancer potency factor for 2378-TCDD, are at a level of

concern for most rates of fish consumption, and are of marginal concern for

some worst-case air exposures.  (The worst-case air exposures are unlikely to


     Accordingly, it  is logical to focus additional remedial measures, to the

extent they are necessary, on those point and nonpoint Dow Chemical sources

                              PUBLIC REVIEW DRAFT

having the greatest impacts on the environment outside the plant.  Some of

these measures would be effective at reducing worker exposures in-plant as

well.  These proposed measures are described below, followed by recommended

precautionary measures that can be implemented by the general public and a

review of proposed supplemental point source and environmental monitoring

programs associated with the proposed remedial measures.

A.  Proposed Point and Nonpoint Source Controls at Dow Chemical

    1.  Wastewater Discharges

     Figure IV-1 presents a summary of monthly average Dow Chemical wastewater

discharges of 2378-TCDD for the period July 1984 to December 1987.  Dow

Chemical began full scale operation of the final effluent mixed-media

filtration system in November 1985 and began full-scale operation of an

incinerator wastewater pretreatment system in July 1987 (Dow 1988a).  The level

of discharge was initially reduced by about two-thirds upon operation of the

mixed-media filtration system.  Another significant reduction  (73%)  has been

realized after preliminary treatment for incinerator wastewaters was

instituted.  Overall, the average mass discharged has been  reduced by about 93%

from 1984 and 1985 levels.  The level of discharge for the past few months













                         FIGURE  IV-1

           Dow  Chemical  -  Midland Plant

                 2378-TCDD  Discharges
                 July  1984 - December 1987
                                   OJ i—i
                                   ro m
                                   i E:

                                PUBLIC REVIEW DRAFT
     Given the complexity of the wastewater treatment system and the sources

and sinks of 2378-TCDD and other CDDs and CDFs at Dow Chemical, it is not

possible to predict to what extent further progress in reducing the discharge

will occur without additional  remedial actions.  USEPA has evaluated alternate

end-of-pipe wastewater treatment technologies and supplemental  in-plant

controls for additional treatment of 2378-TCDD at Dow Chemical  and concluded

there are no available performance data for the treatment systems considered

and it is not possible to predict discharge reductions for either the treatment

systems considered or possible in-plant controls.  Accordingly, USEPA

recommended to MDNR a series of special NPDES permit conditions for the next

NPDES permit for Dow Chemical  (1987d).  These include:

     o Feasibility and end-of-pipe wastewater treatability studies for CDDs
       and CDFs.

     o An assessment of the amount of 2378-TCDD in tertiary pond sediments and
       a study to determine to what extent resuspended sediments containing
       CDDs and CDFs pass through the filtration system.

     o An evaluation of the effectiveness of the performance of the incinerator
       wastewater pretreatment system.

     Given the current levels  of discharge of 2378-TCDD, the continued progress

made toward reducing the levels of discharge, and the need to achieve lower

levels of discharge as determined by MDNR, USEPA recommends that the proposed

NPDES special conditions included in the above-referenced report be implemented

through the NPDES permit program.  The results from these special conditions

will allow a proper assessment of the extent to which additional  controls can

be installed to further reduce discharge levels.  Any further regulatory

actions would be implemented through the NPDES or RCRA permit programs.

                               PUBLIC  REVIEW  DRAFT
    2.  Incinerator Emissions
     The limited data available for Dow Chemical hazardous waste incinerator

emissions from 1978 through 1987 indicate that the emission rates of CDDs and

CDFs are considerably lower today than in the late 1970's.  Emissions testing

by USEPA in 1984 (Trembly and Amendola 1987) and Dow Chemical  in 1987

(Dow 1987a) indicate emission rates of 2378-TCDD (Partial  TEQs) have been

reduced by more than 90% from emission levels measured by Dow Chemical  in 1983

(Dow 1984).

     The investigations of air emission sources at the Midland plant conducted

by Dow Chemical clearly show the incinerator was the most significant point

source at that time (Dow 1984).  However, estimated cancer and non-cancer risks

for air exposures in the Risk Assessment are related more to the actual

measured ambient air concentrations than to the estimates of ambient air

concentrations resulting from dispersion modeling of the incinerator emissions.

These results suggest historical deposition from past incinerator emissions,

possible process emissions, and windblown dusts from the plant site impact the

ambient air around the perimeter of the plant and, to some extent,  out  in the

community more than the incinerator emissions.

Based upon these considerations and the estimated risks associated  with

incinerator emissions alone, there does not apppear to be sufficient

justification for requiring major changes in incinerator operations at  this

time (e.g., change in waste feeds, installation of additional  emission  control

technology).  However, additional  measures to optimize combustion conditions

within the incinerator and to optimize operation of the existing emission

                              PUBLIC REVIEW DRAFT
controls should be pursued to further reduce emissions below current levels to
the extent possible.

     At the present time it appears that the results from supplemental
monitoring of incinerator emissions and ambient air as described in Section
IV.C are necessary to determine whether, or to what extent, additional
incinerator emission controls are necessary.  The RCRA program can require
various incinerator emissions testing and ambient air monitoring programs for
final RCRA permits.

    3.  Dust Suppression Program

     A considerable portion of the Dow Chemical Midland plant site is either
paved roadway, paved open areas around process buildings, or paved parking
lots.  Some portions of the plant site are capped landfills with grass  cover.
The remainder of the site is occupied by buildings or is unpaved dirt or gravel
covered open areas.  Surface soil sampling conducted by Dow Chemical  and USEPA
indicate the entire plant site is contaminated with 2378-TCDD (and other
CDDs and CDFs) with a mean surface soil  2378-TCDD concentration of about
0.5 ppb (Dow 1984, USEPA 1985a).  During dry weather periods, vehicular traffic
through the plant has been observed to raise considerable particulate matter
from roadways.  Wind-blown dusts have undoubtedly contributed some CDDs and
CDFs to ambient air within the plant and around the plant perimeter.   Impacts
on nearby commercial  and residential  areas are determined by wind direction and

     In 1986,  Dow Chemical  began implementing a fugitive dust suppression
control program which calls for regular  flushing of paved roads  and parking

                              PUBLIC REVIEW DRAFT

lots, application of chemical  dust suppressants to unpaved roads, and controls

for storage piles and loading and unloading of materials from pollution control

equipment (Dow 1988b).  This program was revised in 1987 and appears to address

most sources of fugitive dusts from the plant site that may be contaminated

with CDOs and CDFs.  It is proposed that the effectiveness of this program be

evaluated through the proposed ambient air monitoring program presented in

section C.Z.c below.  Depending upon the results, all or some combination of

the following actions, or similar measures, could be implemented to further

minimize worker exposure levels and migration of CDDs and CDFs from

contaminated soils within the plant:

     o Paving or planting grasses over some of the remaining sand and gravel

     o Modified road dust suppression program or paving program for unpaved
       roads.  Modified spraying and sweeping programs for paved roadways to
       further minimize fugitive particulate emissions.

    4.  Ground Water Contamination

     Ground water and subsurface soil sampling conducted by Dow Chemical at the

Midland plant pursuant to Resource Conservation and Recovery Act  (RCRA)

requirements, revealed contamination with 2378-TCDD at a number of locations

(Dow 1987b).  Areas near former trichlorophenol production facilities were

found to be the most highly contaminated.  USEPA sampling of sediments from a

Mverbank revetment system collection sump revealed contamination with 2378-

TCDD and other CDDs and CDFs  (Amendola and Barna 1986).  Also, ground water

monitoring  by Dow Chemical near the Poseyville Road landfill has demonstrated

certain hazardous constituents emanating from the  landfill and migrating north

to northeast  (Dow 1987b).   (CDDs and CDFs have not been studied in the ground

                                 PUBLIC REVIEW DRAFT

water.)  Dow Chemical  has installed a purge system to clean up the release,  and

a slurry wall was constructed at the landfill  to prevent future releases.

     The contaminated ground water at the plant is largely contained within  the

site.  There are no potable ground water wells within the immediate area of  the

plant and monitoring of both public and private potable ground water wells near

the plant and near Dow Chemical  landfills showed no detectable CDDs or CDFs

(Barna and Amendola 1985).  The MDNR and USEPA Region V are currently

processing a RCRA permit for the Dow plant which has as a principal focus  the

issue of ground water contamination at the plant and at nearby landfills.

Accordingly, additional point or non-point source controls beyond those

required under the RCRA permit for the protection of ground water do not appear

necessary to protect public health.

B.  Precautionary Measures Recommended to the Public

     Although operations at Dow Chemical have caused widespread contamination

of the Midland area with 2378-TCDD and other CDDs and CDFs, USEPA believes that

the levels of contamination, with the exception of the Tittabawassee River

fish, do not present unacceptable or unmanageable health risks to the Midland

community.  USEPA does not believe that massive remedial measures such as  those

implemented at Times Beach, Missouri, or Newark, New Jersey, are warranted in

Midland.  There are, however, a number of actions people can take to minimize

exposures, and thus minimize possible health risks associated with CDDs and

CDFs.  Most of these recommendations focus on avoiding or minimizing ingestion

of materials that contain 2378-TCDD and other CDDs and CDFs.

                              PUBLIC REVIEW DRAFT
     1.  Tittabawassee River Fish

     In Michigan, legal responsibility for the evaluation of health risks and
issuance of health advisories resides with the Michigan Department of Public
Health (MDPH).  At this writing the MDPH has in place a fish consumption
advisory warning against consumption of catfish and carp taken from the
Tittabawassee River (MDNR 1987a).  These fish contain high levels of 2378-TCDD
and other organic chemicals.  As shown in the Risk Assessment, regular
consumption of even relatively small amounts of these fish over the long term
may pose substantial  risks of cancer.  Also, long-term consumption or, in
certain circumstances, short-term consumption of these fish may pose
significant risks of adverse impacts other than cancer.  The current Michigan
fish consumption advisory for catfish and carp is fully supported by the USEPA

     The Risk Assessment also highlights possibly significant risks from
consumption of game or sports fish (e.g., walleye, northern pike, smallmouth
bass, and white bass) by children and women of childbean'ng age, related to
possible reproductive effects, teratogenic effects, liver damage, and cancer.
These risks may be associated with both short-term and long-term consumption.
Risks from consumption of game or sports fish for other less sensitive groups
are also presented in the Risk Assessment.

     The MDPH has been conducting a creel survey to better define fish
consumption patterns  for Tittabawassee River fishermen and their families.   The
MDPH also has been actively participating in ongoing discussions with the other
Great Lakes states, USEPA, and the Food and Drug Administration regarding
establishment of a uniform basis for fish consumption advisories.   At this

                              PUBLIC REVIEW DRAFT
writing, the MDPH has decided to consider the results of its creel  survey, the

findings from this report, new data from the 1988 fish monitoring survey, and

the aforementioned discussions prior to determining whether or to what extent

to modify its fish consumption advisory for the Tittahawassee River.

     Individuals who choose to consume any fish caught in the Tittabawassee

River should clean them in accordance with MDPH recommendations to minimize

contaminant levels.  Fillets should he skinned, with all visible traces of

surface fat removed.  All  belly fat from the fillet should be removed, as well

as the dark tissue along the lateral line on each fillet.  Certain cooking

methods which permit fats  and juices to drain from the fish may result in lower

contaminant levels in the  cooked fish.

     2.   City of Midland  Surface Soils

     The overall estimated cancer and non-cancer risks from exposures to

surface soils in Midland are not considered to be significant except  possibly

for children with pica.  Children with pica are those who intentionally consume

inordinate amounts of soil.  Pica is considered a medical disorder.

     Some possible routes  of exposure to 2378-TCDD and other CDDs and CDFs in

City of Midland soils include direct ingestion by children at play outdoors;

ingestion of soil attached to home-grown vegetables, whether or not  the

contaminants were absorbed or transported into the edible portion of  the plant;

absorption through the skin which comes in contact with the soil  through play,

gardening, or other activities; inhalation of contaminated particulates

from the soil; and ingestion of household dusts which may be contaminated from

outdoor soils.  Note that  the results of the USEPA soil study showed  that

                              PUBLIC REVIEW DRAFT

2378-TCDD  (and other CDDs and CDFs by inference) tend to concentrate in areas

near roof  downspouts or driplines (USEPA 1985a).

     Although currently available information indicates that only children with

pica are at possibly significant risk from the soil contamination in Midland,

the commonsense practices presented below are recommended as generally useful

for minimizing exposure to soil  contamination or bacteria, whether the soil is

found in Midland or elsewhere:

     o Children at play, particularly toddlers and children with pica, should
       be  encouraged to keep soil or dirt out of their mouths.  Areas near
       downspouts and roof driplines are likely to have higher levels of 2378-
       TCDD and other CDDs and CDFs than open yard areas.

     o Children and adults should wash their hands after exposure to outdoor
       soils, particularly before meals.

     o Home-grown vegetables, both leafy vegetables and root crops, should be
       thoroughly washed prior to consumption to remove soil particles.
       Peeling root crops might be helpful  in removing 2378-TCDD which may be
       in  soil on the skins or absorbed into the skins.

     o Household interiors should be regularly cleaned to minimize contaminated
       dusts which can be inhaled or ingested.

C.  Proposed Point Source and Environmental  Monitoring Programs

     As noted earlier, there have been many  remedial  actions taken over  the

past few years to minimize emissions and discharges of CDDs and CDFs from the

Dow Chemical Midland plant.   The limited data collected recently indicate

contaminant levels outside the plant may be  declining.  Presented below  are a

series of proposed point source  and environmental  monitoring programs designed

to document the effectiveness of the remedial  programs and to characterize

other possible, but less likely, routes of  exposure which were not evaluated

initially.   Some of the proposed monitoring  programs  are current requirements

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of Dow Chemical  environmental  control permits or orders;  others  are new

programs that could be included in the RCRA permit now being developed or

required under other existing  regulatory mechanisms.

     Each proposed program is  described in the following  sections.   In all

cases, USEPA proposes that these monitoring programs  would be conducted by  Dow

Chemical in response to specific requirements placed  in environmental  permits

or administrative orders issued under the Air, RCRA,  or NPDES programs as

appropriate.  Study designs and sampling and analytical protocols would be

approved by MDNR, MDPH, and/or USEPA Region V.

     1.  Dow Chemical Point Source Monitoring

         a.  Wastewater discharge monitoring

     Dow Chemical currently monitors the outfall 031  wastewater  discharge to

the Tittabawassee River twice per month for 2378-TCDD as  required by NPDES

permit MI0000868.  The current discharge levels reported  by Dow  Chemical  are in

the range of less than 1 to 2 parts per quadrillion (ppq  or pg/1).   Data

collected for the last six months of 1987 indicate the discharge has been

fairly stable from month to month.  Dow Chemical should conduct  experiments to

determine what measures might be feasible to attain analytical method detection

levels of 0.1 ppq for 2378-TCDD (e.g., larger sample size, enhanced sample

cleanup, high resolution mass spectrometry).  MDNR has determined that 0.1  ppq

of 2378-TCDD in Dow Chemical's effluent would be protective of human health, by

minimizing bioaccumulation of 2378-TCDD in fish (MDNR 1987b).

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         b.  Incinerator emissions testing

     Over the past few years Dow Chemical has been modifying the operation of

its hazardous waste incinerator to optimize combustion conditions and minimize

emissions of 2378-TCDD and other CDDs and CDFs.  The most recent stack tests

were conducted by Dow Chemical  during June 1987 (Dow 1987a).  In Section

IV.A.2, USEPA proposes that Dow Chemical  continue efforts to optimize

incinerator emissions.  At some point over the next two years,  preferably

during the warm, dry-weather seasons of 1988 or 1989, another series of stack

tests should be performed to characterize the emissions of 2378-TCDD and other

CDDs and CDFs, and to determine the particle size distribution  of the stack

emissions.  The particle size data are useful for estimating incineration

emissions deposition for purposes of exposure assessments and for

distinguishing these emissions  from other sources of CDD/CDF contamination in

the ambient air.  Ideally, the  incinerator emissions testing would be conducted

concurrently with the ambient air monitoring program proposed below.  These

efforts should be coordinated with the incinerator emissions trial burns for

2378-TCDD required for RCRA permitting.

     2.  Ambient Ecological Effects and Food Chain Monitoring

         a.  Tittabawassee River native fish

     Dow Chemical is currently  required by the terms of a consent order with

USEPA to conduct monitoring of  Tittabawassee River fish every two years through

1991 (U.S. v. Dow 1984).  The most recent data were collected in 1987

(Dow 1987c).  The current sampling protocol calls for collection of three

bottom-feeding fish (carp or catfish) and three game or sports  fish (usually

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walleye) downstream of the plant.  The number of data points resulting from
this program is not sufficient to adequately characterize the fishery for
purposes of establishing appropriate fish consumption advisories.   Accordingly,
the MDPH, MONR, and USEPA have collaborated in developing an expanded fish
monitoring program for 1988.  That program will  include analysis of 20 walleyes
in 4 size classes and 10 carp.  The walleyes will be from the 1988 spring run,
and the carp will be collected during the summer.  All of these fish will be
collected downstream of the former Dow Dam, preferably in the vicinity of
Smith's Crossing Road.  A limited number of fish will also be collected
upstream.  All of the fish will be analyzed for 2378-TCDD and PCBs.  A limited
number will be analyzed for other CDDs and CDFs.

         b.  Tittabawassee River sediments

     Tittabawassee River sediments and the river flood plain, from upstream of
Dow Chemical to about five miles downstream from outfall  031, should be
thoroughly surveyed, evaluated, and classified in order to locate any pockets
of organic contamination or deposition zones containing clay, silt, or other
fine particles of a type with the potential to adsorb CDDs/CDFs.  The survey
should include extensive grab and/or core sampling with visual evaluation of
the samples by an experienced sediment classifier, supplemented by the
appropriate use of a gross measure of organic material such as TOC (total
organic carbon).  Samples with relatively high organic content or other
indications of potential contamination (e.g., large amounts of fine particles)
would be analyzed for 2378-TCDD and other CDDs and CDFs and other contaminants
to determine whether or to what extent sediment  removal might be appropriate.

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         c.  Ambient air monitoring program

     Concurrent with the incinerator emissions testing noted above, a limited

ambient air monitoring program should be conducted to determine particle size

distribution, particulate levels, and current concentrations of 2378-TCDO and

other CDDs and CDFs.  A network of at least seven monitoring sites (one upwind

of plant, three downwind near the fenceline, three downwind in the community)

would be necessary.  Two of the downwind sites should be located in the

vicinity of the estimated point of maximum ground level  impact of the

incinerator emissions.  An extended particulate monitoring program should be

conducted over a period of a few months.  COD and CDF determinations should be

made on at least three separate days with wind blowing from the upwind monitors

toward the the downwind monitors.  Analyses of CDDs and  CDFs under other

conditions could also be considered.  The specific monitoring protocols should

be developed by the MDNR and Region V air and waste management programs in

consultation with Dow Chemical.

         d.  Soil and dust monitoring program

     Surface soil sampling near each air monitoring station (10-15 samples,

total) should be conducted to reveal the presence of contaminated soils that

could influence the particulate samples through resuspension.  Limited surface

soil sampling throughout the community (20 samples) also should be conducted to

document current surface soil concentrations in Midland.  Selected sites

sampled in the 1983 USEPA survey should be resampled to measure changes that

may have occurred.  Appropriate control sites should be established for this

effort.  Collection and analysis of a limited number of household dust samples

would permit evaluation of the significance of this route of exposure.

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     3.  Food Chain Monitoring

         a.  Dairy sampling

     A limited screening sampling program (10 to 15 samples)  should be
conducted at dairy operations that may be located within 10 to 15 miles  of the
Dow Chemical plant.  Samples of whole milk, milk fat, and cheese should  be
collected and analyzed for 2378-TCDD and other CDDs and CDFs.

         b.  Garden vegetable sampling

     A limited garden vegetable and garden soil  sampling program (20 to  30
samples) should be conducted in 1988 to supplement the limited data collected
by USEPA for 1987 samples.  These data would be used to document whether,  or to
what extent, migration of 2378-TCDDs and other CDDs and CDFs  occurs from
contaminated soil into (or onto) garden vegetables.

         c.  Aquatic life, avian, and animal monitoring program

     A limited monitoring program should be conducted in 1988 or 1989 for
native bivalves or gastropods present in the Tittabawassee River as well  as
for native turtles, fish-eating birds that nest in the vicinity of the river,
and fish eating mammals such as the muskrat and raccoon.  About 20 samples
should be adequate for screening these organisms for 2378-TCDD and other CDDs
and CDFs.

                              PUBLIC REVIEW DRAFT

AMENDOLA, G.A.  and Barna, D.R.  1986.   Dow Chemical  Wastewater
     Characterization Study:  Tittabawassee River Sediments  and  Native  Fish.
     Environmental  Services Division,  Region V,  USEPA,  Westlake,  Ohio.   July.
     EPA 905/4-88-003.

BARNA, D.R., and AMENDOLA, G.A.  1985.   Screening survey of surface  water
     supplies, potable ground water, and Dow Chemical  brine operations.
     Environmental  Services Division,  USEPA, Westlake,  Ohio.  December.

DOW CHEMICAL COMPANY (Dow).  1978.   Letter from  E.H.  Blair, U.S.  Area  Research
     and Development, Midland MI, to Document Control  Officer,  Chemical
     Information Division, Office of Toxic Substances,  USEPA, Washington DC.
     June 28.

DOW CHEMICAL COMPANY (Dow).  1984.   Point sources and environmental  levels  of
     2378-TCDD (2,3,7,8-Tetrachlorodibenzo-p-dioxin)  on the Midland  plant site
     of the Dow Chemical  Company and in the City of Midland,  Michigan.
     Midland, Michigan.  November 5.

DOW CHEMICAL COMPANY (Dow).  1984-1987.  Discharge Monitoring Reports,  NPDES
     Permit No. MI0000868.  Environmental Services Division,  Region
     V, USEPA, Westlake,  Ohio.

DOW CHEMICAL COMPANY (Dow).  1987a.   Letter from J.M. Rio,  Manager,  Engineering,
     Computers, and Environmental,  Michigan Division, Dow Chemical U.S.A.,
     Midland, Michigan, to G.A. Amendola, Environmental Services  Division,
     Region V, USEPA, Westlake, Ohio.   October 20.

DOW CHEMICAL COMPANY (Dow).  1987b.   Michigan Division ground water  containment
     strategy: Investigation  of historical point sources of 2378-TCDD  to the
     Midland plant site wastewater system of the Dow Chemical Company
     (4 vols.).  Michigan Division,  Midland, Michigan.   June.

DOW CHEMICAL COMPANY (Dow).  1987c.   Letter from R.M.  Croyle,  Manager,
     Environmental  Services,  Michigan  Division,  Dow Chemical  U.S.A., Midland,
     Michigan, to G.A. Amendola, Environmental Services Division, USEPA,
     Westlake Ohio.  December 27.

DOW CHEMICAL COMPANY (Dow).  1988a.   Personal communication from  J.E.  Garvey,
     Environmental  Specialist, Environmental Services,  Michigan Division, Dow
     Chemical U.S.A., to G.A. Amendola, Environmental  Services  Division,
     Region V, USEPA, Westlake, Ohio.   February  24.

DOW CHEMICAL COMPANY (Dow).  1988b.   Letter from W.I. Delaney,  Environmental
     Services, Michigan Division, Dow Chemical U.S.A.,  Midland, Michigan, to
     G.A. Amendola, Environmental Services Division,  USEPA, Westlake,  Ohio.
     March 15.

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     (Foresight).  Citizens petition for an investigation and enforcement
     action.  A.K. Wilson, Director, ECOMM, and L. Fink,  Director,  Foresight.
     Filed with J.W. Hernandez, Acting Administrator,  USEPA, Washington  DC.
     March 16.

GENERAL SCIENCES CORPORATION (GSC).   1987.   GEMS multi-media modeling  of
     2378-TCDD at Midland, Michigan.  Prepared  for Office of Pesticides  and
     Toxic Substances, USEPA, Washington DC (Contract  No. 68-02-3970,  Task
     No. 3-11).  June 19.

HUMPHREY, H.E.B.  1983.  Population  studies of  PCBs in Michigan  residents.   In
     D'ltri, F.M., and Kamrin, M.A., eds.,  PCBs: Human and Environmental
     Hazards.  Butterworth Publishers, Boston.   Pp. 299-310.

HUMPHREY, H.E.B., RICE, H.A., and BUDD, M.L.  1976.  Evaluation  of  changes  of
     the level of polychlorinated biphenyls (PCB) in human tissue.   Final
     Report to FDA.  Michigan Department of Public Health, Lansing,  Michigan.


     Tanner, Director, to J.W. Hernandez,  Acting Administrator,  USEPA,
     Washington DC.  March 23.


     proposal to modify Final Order  of Abatement No. 2022 for Michigan
     Division, Dow Chemical U.S.A.,  Midland, Michigan.  Lansing, Michigan.
     September 25.

MICHIGAN WATER RESOURCES COMMISSION  (MWRC).  1984.  Final order  of  abatement
     no. 2022.  Cosigned by Michigan Department of Natural Resources  and
     Michigan Attorney General.  Lansing,  Michigan.  May  17.

TREMBLY, G.f and AMENDOLA, G.A.  1987.  Dow Chemical Building 703  Incinerator
     Exhaust and Ambient Air Study.   Environmental Services Division,  Region V,
     USEPA, Westlake, Ohio.  March.   EPA 905/4-88-004.

U.S. DEPARTMENT OF AGRICULTURE (USDA).  1982.  Foods commonly eaten  by
     individuals: Amount per day and per eating occasion.  Poa,  E.M.,  Fleming,
     K.H., Guenther, P.M., and Mickle, S.J.  Home Economics Research  Report
     Number 44.

     Midland Plant Wastewater Characterization  Study—Preliminary Summary of
     Results.  Region V, Environmental Services Division.  Westlake,  Ohio.
     March 28.

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U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).   1983b.   Dioxin Strategy.   Office
     of Water Regulations and Standards,  Office of Solid Waste and  Emergency
     Response, Dioxin Strategy Task Force.   Washington,  D.C.   October 20.

U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).   1983c.   Administrator's response
     to Central Michigan citizens petition  for investigation  and enforcement
     action.  W.D. Ruckelshaus, Administrator, Washington DC.  June 10.

U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).   1985a.   Soil  Screening Survey at
     Four Midwestern Sites.  Environmental  Services Division, Region V,
     Westlake, Ohio.  June.  EPA 905/4-85-005.

     Document for Polychlorinated Dibenzo-p-dioxins.  EPA 600/8-84-014F.
     Office of Research and Development,  Washington DC.   September.


U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).   1986.  Guidelines for carcinogen
     risk assessment.  51 FR 33992-34003.

     Study.  Report to Congress.  Office  of Solid Waste  and  Emergency Response,
     Washington DC.  August.  EPA/530-SW-87-025.

U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).   1987b.   Health Advisory for
     2,3,7,8-Tetrachlorodibenzo-p-dioxin.  Office of Drinking Water.
     Washington DC.

     for Estimating Risks Associated with Exposures to Mixtures of  Chlorinated
     Dibenzo-p-dioxins and Dibenzofurans.  Risk Assessment Forum, Washington DC,

U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).   1987d.   Technical support
     document for proposed best available technology effluent limitations
     and special NPDES permit conditions, NPDES permit MI0000868, Dow Chemical,
     Midland plant, outfall 031.  Environmental Services Division,  Westlake,
     Ohio.  June 3.

U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).   1988.  Risk assessment for
     dioxin contamination at Midland, Michigan.  Region  V, Chicago, Illinois.
     March.  EPA 905/4-88-005.

U.S. v. Dow.  1984.  Consent Decree, Civil  Action No.  83-CV7011BC,  United
     States of America, Plantiff, vs. the Dow  Chemical Company, d/b/a Dow
     Chemical, U.S.A., Michigan Division, Defendant.  March  30.