Proceedings: National Forum on Mercury in Fish, September 27-29, 1994 New Orleans, Louisiana


          United States
          Environmental Protection
          Agency
Office of Water
(4305)
EPA 823-R-95-002
June 1995
&EPA    National  Forum on
          Mercury  in Fish
          Proceedings
          Hg
      Hg
          Hg

                                         Hg

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National Forum on
Mercury in Fish
       Proceedings

 National Forum on
   Mercury in Fish
       September 27-19, 1994
       New Orleans, Louisiana
       Printed on Recycled Paper

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UNITED STATES ENVIRONMENTAL PROTECTION AGENCY
WASHINGTON, D.C. 20460
JUL
1995
OFFICE OF
WATER
Dear Colleagues and Interested Parties:
EPA OW Resource Center (RC4100)
401 M St. SW /
Washington, DC 20460

Phone Recording Order: (202) 260-7786
FAX Order: (202) 260-0386
Email: waterpubs@epamail.epa.gov
We appreciate the contributions of the speakers
workshop and we look forward to your continued
Sincerely,
and others who participated in the
interest in fish contamination issues.
Rick Hoffmann
Forum Organizer
Risk Assessment and Management Branch
Office of Science and Technology
(A. A)
X_J^7
Rocycled/Hecyclabte
Printed*i!hSoy/CanolaW
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National Forum on
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Contents
Abstract ^
Acknowledgments jx

DAY ONE

Welcome and Introduction 1
Mr. James Hanlon and Mr. Rick Hoffmann

Session One: Mercury Overview and Background

Biogeochemical Cycling of Mercury: Global and Local Aspects 3
Dr. William Fitzgerald

Aquatic Biogeochemistry and Mercury Cycling Model (MCM) 15
Dr. Donald Porcella

Mercury Methylation in Fresh Waters 23
Dr. Cindy Gilmour

Considerations in the Analysis of Water and Fish for Mercury 31
Mr. Nicolas Bloom

Bioaccumulation of Mercury in Fish 41
Dr. James Wiener

Mercury in Wildlife 53
Dr. Charles Facemire

Questions and Discussion: Mercury Overview and Background 63

Session Two: Florida Studies

Ecological Assessment of Mercury: Contamination in the Everglades
Ecosystem ....71
Dr. Jerry Stober

Atmospheric Deposition Studies in Florida „ 77
Dr. Thomas Atkeson

Watershed Effects on Background Mercury Levels in Rivers 83
Dr. James Hurley

Questions and Discussion: Florida Studies 89
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National Forum on Mercuiy in Fish
DAY TWO

Session One: Toxidty and Risk Assessment

Mercury Toxicity: An Overview [[[ 91
Dr. Thomas Clarkson

Neurobehavioral Effects of Developmental Methylmercury Exposure in
Animal Models [[[ 95
Dr. Deborah Rice

An Overview of Human Studies on CNS Effects of Methylmercury ............. 109
Dr. RobertaWhite

Exposure Assessment for Methylmercury [[[ 113
Dr. Alan Stern
FDA Perspective
Dr. Michael Bolger

EPA Perspective [[[ I23
Dr. John Cicmanec

Questions and Discussion: Toxicity and Risk Assessment ............................ 127
Session Two: Risk Management and Risk Communication

A Review of Fish Consumption Advisories [[[ 135
Dr. Robert Reinert

Different People, Different Approaches: Risk Management and
Communication in Minnesota [[[ 143
Dr. Pamela Shubat

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vii
Mercury Deposition and the Activities of the Clean Air Act of 1990 173
Ms. Martha Keating

Great Lakes "Virtual Elimination" Initiative 179
Mr. Frank Anscombe

Minnesota Mercury Reduction Activities 185
Mr. Pat Carey

Questions and Discussion: National Mercury Study and Mercury
Control Strategies ' 201
Speakers' Biographies 205
EPA Selected Publications 213
Attachments

Agenda
List of Attendees
Mercury Fact Sheets
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National Forum on
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Abstract
On September 27-29, 1994, the U.S. Environmental Protection Agency
sponsored a "National Forum on Mercury in Fish." Mercury is a ubiquitous
contaminant that occurs throughout the United States and the world Because
of mercury's potential to adversely affect human health, many state agencies
are monitoring fish tissues to determine how extensive mercury contamination
might be. More than 34 states have issued fish consumption health advisories
because of concerns about mercury contamination.

The primary purpose of the workshop was to transfer "state-of-the-art"
information about mercury to states and other parties involved with risk
assessment and fish consumption advisories. A variety of topics were pre-
sented in several sessions:
Session One
Session Two

Session Three
Session Four
Session Five
Mercury Overview and Background
Occurrence in Fish and Wildlife, Watershed Effects,
Florida Studies
Toxicity and Risk Assessment
Risk Management and Risk Communication
State Program Needs, National Mercury Study,
Mercury Control Strategies

Within each session, individual presentations were followed by questions
from the audience and responses by the speakers. The Proceedings document
contains a summary of each speaker's presentation, a selection of key graphics,
and a summary of audience questions and responses.
in
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National Forum on
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Acknowledgments
The National Forum on Mercury in Fish was funded by the U.S. Envi-
ronmental Protection Agency. The Standards and Applied Science Division in
the Office of Science and Technology (OST)—part of EPA's Office of
Water—sponsored the project. Mr. Rick Hoffmann, an environmental scien-
tist in OST, developed and organized the project. Ms. Charlie MacPherson
and Ms. Liz Hiett of Tetra Tech, Inc. provided essential logistical and editing
support throughout the project. Ms. Marti Martin (technical editor) and
Tetra Tech's Production Department provided editorial and production support.

Members of the Steering Committee provided valuable assistance by
helping to shape the agenda and recruit speakers for the Forum. Their help is
greatly appreciated. The Steering Committee members were Jerry Stober,
EPA Region 4; Philip Crocker, EPA Region 6; Martha Keating, EPA, RTP,
North Carolina; Brace Mintz, EPA OST; Mike Bolger, U.S. Food and Drug
Administration; Anna Fan, California EPA; Tom Atkeson, Florida Department
of Environmental Protection; Pam Shubat, Minnesota Department of Public
Health; and Don Porcella, Electric Power Research Institute. FDA also
assisted by providing supplemental funding.

Finally, the contributions of the invited speakers cannot be underesti-
mated since the success of the Mercury Forum depended on them. In later
evaluations of the Forum, numerous people complimented the high quality and
breadth of the presentations.
IX
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Welcome and Introduction
James A. Hanlon
Deputy Director, Office of Science and Technology
U.S. Environmental Protection Agency, Washington, DC
Rick Hoffmann
Environmental Scientist, Office of Science and Technology
U.S. Environmental Protection Agency, Washington, DC
James A. Hanlon

Mr. Hanlon welcomed the partic-
ipants to the workshop and re-
viewed some of the key aspects
of the mercury problem. He noted that
approximately 34 states had issued fish
consumption advisories at the time of the
conference; of those, advisories for 3 were
statewide in scope. At this point, research
is not complete enough to understand
completely how mercury reacts with the
environment. Consequently, mercury is a
"hot" topic in academic research, in pub-
lic debates, and in considerations by regu-
latory agencies. The public is pressing to
know what levels are considered safe.
Mr. Hanlon explained that the
purpose of the conference was to assist
states and others interested in the mer-
cury contamination problem. He said,
"We are going to share what we know
about biological and chemical facts of
mercury and fate and transport. We will
talk about what we do not know. And we
will discuss various risk-related issues,
including risk management and current
Agency guidance."
He further noted that the audience
was large and quite diverse. Many of the
participants were from state agencies, but
there were also representatives from a
large number of organizations.
Mr. Hanlon described the activities of
EPA's Mercury Task Force.
The Office of Science and Technol-
ogy is in the process of developing a four-
volume set of guidance documents
regarding fish consumption advisory
programs. The series is titled Guidance
for Assessing Chemical Contaminant
Data for Use in Fish Advisories. Volume
1 (Sampling and Analysis) and Volume 2
(Risk and Assessment and Fish Consump-
tion Limits) have been issued. Volume 3
(Risk Management) and Volume 4 are
being developed.

Rick Hoffmann

Mr. Hoffmann explained that the
conference was part of EPA's ongoing
commitment to assist states, which are
responsible for issuing fish advisories, by
providing timely and relevant technical
information and assistance about mer-
cury. The conference was designed with
two goals in mind: first, the immediate
needs of the end user and, second, the
broader national and international aspects
of the problem.
Mr. Hoffmann briefly described the
state-by-state mercury fact sheets. They
illustrate that the problem is widespread
and hard to ignore. The fact sheets also
show that 50 states have 50 somewhat
different responses to the issue. Many
states are moving toward a quantitative
risk assessment. Approximately 50
percent of the states issued risk-based
advisories, and the other half still used
advisories based on the FDA Action
Level for mercury. A map offish adviso-
ries shown by Mr. Hoffmann indicated
that 60 percent of the advisories were due
to mercury. An overlay of various poten-
tial sources of mercury illustrated that
mercury is pervasive in sediments.
Atmospheric sources are also important in
many locations.
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Biogeochemical Cycling of Mercury:
Global and Local Aspects
William F. Fitzgerald
Department of Marine Sciences, The University of Connecticut, Groton, Connecticut
Environmental and Human
Health Considerations

^^Biere is now much evidence docu-
• menting tissue concentrations of
M mercury (Hg) in marine and
freshwater fish that exceed local,
national, and international public health
guidelines (e.g., Wiener et al.,1990;
Eisler,1981). Moreover, nearly alt
mercury in fish flesh (>95 percent)
occurs as methylmercury (Westoo,
1966; Huckabee et al., 1979; Grieb et
al., 1990). Methylmercury compounds
are considerably more toxic than
elemental mercury and its inorganic
salts. Further, human exposure to
methylmercury comes almost exclu-
sively from consumption of fish and fish
products, and prenatal life is more
susceptible to brain damage than adults
(Fitzgerald and Clarkson, 1991). The
risk to public health is evident in the
fish consumption advisories that have
been issued by more than 30 states, the
U.S. Food and Drug Administration
(USFDA), the World Health Organiza-
tion (WHO), and numerous govern-
ments. Elevated levels of methylmer-
cury in marine and freshwater
piscivorous fish pose an economic threat
to commercial and sport fishing indus-
tries, and the potential to adversely
affect fisheries.
The environmental behavior and
accumulation of mercury in aquatic
organisms is subtly complex and driven
by chemical and biologically mediated
reactions involving exceedingly small
quantities of mercury in the atmosphere
and natural waters. Indeed, an insidi-
ously complicating feature of the
mercury cycle in aquatic systems is the
in situ bacterial conversion of inorganic
mercury species to the more toxic
methylmercury form. Recent work, for
example, suggests that in many natural
waters much of the methylmercury
accumulating in biota, especially large
fish, can be derived from the internal
biologically mediated syntheses from
inorganic mercury added to the aquatic
system from external sources (for lakes,
see Gihnour and Henry, 1991, and the
Mercury in Temperate Lakes Program
results as summarized in Hudson et al.,
1994 and in Watras et al., 1994; for
estuaries and the open ocean, see Mason
and Fitzgerald, 1990; Mason et al.,
1993; and Rolfhus and Fitzgerald,
1994). Atmospheric deposition is the
principal external source of mercury to
the oceans and most other natural
waters.
Atmospheric Cycling and
Deposition of Mercury

The prominence of atmospheric
mobilization and depositional processes
in the global biogeochemical cycling of
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T
i
AIR 25 Mmol
98% Hg° Hge
2%HgP 1
DEPOSITION HL,|j
|AU.fLUXESlNMmel/y |
Figure I. The modern global mercury cycle (adapted from Mason et al.,
1994).
The Global Mercury
Cycle: Contemporary and
Historical Views

A mass balance view of the
current global mercury cycle is
presented in Figure 1, where the
estimates for annual direct
anthropogenic mercury releases
to the atmosphere were averaged
and taken as 4000 tons or, in
megamoles (Mmol), 20 Mmol.
Total emissions were taken to be
7000 tons yr1 or 35 Mmol." A
premodern view of the global
mercury cycle is presented in
Figure 2 and corresponds to the
1890 period. These simulations
were adapted from Mason et al.
(1994).
Anthropogenic
Interferences
mercury is well recognized and described
in a variety of mass balance formulations
for the global mercury cycle. Environ-
mental assessments of source strengths
for natural and anthropogenic processes,
though often in error in early models, are
converging. Recently published budgets
for the atmospheric cycling of mercury, in
general, show human-related emissions of
mercury to the air as exceeding natural
inputs, with the principal sourcesbeing
coal combustion, smelting, and waste
incineration (Lindqvist and Rodhe, 1985;
Fitzgerald, 1986,1989; Nriagu and
Pacyna, 1988; Nriagu, 1989; Fitzgerald
andClarkson, 1991;LindqvistetaL, 1991;
Mason etal., 1994). Estimates for the
annual amounts of mercury released
directly into the air by human activities
rangebetween 3600 and 4500 tons, which
represents about 50 percent to 75 percent of
the total yearly input (6000 to 7500 tons) to
the atmosphere from all sources. This
adverse interference is larger because it is
now apparent that volatile elemental
mercury emissions from terrestrial and
marine systems include arecycled poll-
ution-derived component (Mason et al.,
1994).
A comparison of the models
provides a revealing and insightful
assessment of the extent to which
anthropogenic mercury emissions
have perturbed the mercury cycle over
for the past century. Firstly, it is
evident that terrestrial systems, ocean
waters, and the atmosphere are sig-
nificantly contaminated with mercury
released by human activities over the
100-year period considered in these
models. Secondly, the major role of
the atmospheric mobilization in the
mercury cycle and the associated
environmental impact is apparent
from the contemporary analysis
(Figure 1), where we find that local/
regional mercury emissions and
deposition (10 Mmol) are comparable
to the global contributions. That is,
about one-half of anthropogenically
related mercury emissions to the
atmosphere will be produced and
deposited on a local/regional scale,
while about one-half will contribute to
the global cycle. Local deposition is
most probably due to the presence of
reactive mercury species and particu-
late mercury in flue emissions.
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Figure
Mason
Elemental Mercury
Cycling

As illustrated, elemental
mercury cycling plays a central
role in dispersing mercury at the
earth's surface and in affecting
the synthesis and bioaccumula-
tion of methylmercury in aqueous
systems. Production and evasion
of elemental mercury in natural
waters is a major feature of the
biogeochemical cycling of
mercury in fresh and marine
waters. Our studies place oceanic
emissions of elemental mercury
at about 30 percent to 40 percent
(10 Mmol) of the annual mercury
flux to the atmosphere (Figure 1).
Aquatic elemental mercury
emissions are related to the
availability and supply of reactive
mercury (the Hg(II) substrate or
reactant, Hg?) and, as noted, the
atmosphere is usually the princi-
pal source. Biologically mediated
production of elemental mercury
appears to predominate over abiotic
mechanisms, and water-air recycling of
anthropogenically derived mercury is
significant. This reemission can exacer-
bate adverse environmental effects.
Indeed, the first-order view of the
modem mercury cycle shows that
approximately 70 percent of current
oceanic emissions are of anthropogenic
origin.
As part of the Hg(H) substrate/
reactant hypothesis, we proposed that
the in situ production and efflux of
elemental mercury could play a poten-
tial buffering and/or amelioration role in
aqueous systems (Fitzgerald et al.,
1991). We hypothesized that in-lake
biological and chemical production
processes for elemental mercury and
methylmercury compete with one
another for reactant (HgR), which we
suggest is labile Hg(II) species. Our
lacustrine and oceanic investigations
support this unifying physicochemical
paradigm. Evasion of elemental mercury
is balanced by total atmospheric deposi-
tion of inorganic mercury or reactant to
NATURAL
5
T
i
AIR 8 Mmol
98% Hg° H
DEPOSITION H
/
g"
(ID

| ALL FLUXES IN Mmol/y |
2. The pre-modera (ca. 1890) global! mercury cycle (adapted from
et al., 1994).
the oceans. 'The mechanisms by which
inorganic mercury is reduced to elemen-
tal mercury are poorly known. However,
the reduction appears to be biological
and involve microorganisms. In view of
the significance of elemental mercury
in affecting the speciation, behavior, and
fate of mercury in the environment, the
elemental mercury cycle in the atmo-
sphere and waters deserves much
scrutiny.
There is a rapid equilibrium
between the atmosphere and the surface
ocean. When this phenomenon is
coupled with the small sedimentation of
mercury in the oceans, deposition on
land becomes the ultimate sink for
atmospheric mercury. Since the oceanic
component is largely recycled, most of
the anthropogenic mercury added to the
system will be deposited on land and
sequestered Into surface soils. Accord-
ing to Lindqvist et al. (1991), surface
soils contain ca. 5,000 Mmol of mer-
cury. The model projects an anthropo-
genic mercury input at about 947 Mmol,
which would represent about 15 percent
of the total soil burden. Nater and
Grigal's (1992) estimates of the net
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National Forum on Mercury in Fish
increase in mercury in surface soils from
the north-central region of the United
States were between 2 percent and 20
percent, and comparable to the model
estimate. Mercury accumulating in soils
is released slowly to terrestrial waters.
Swedish studies (Lindqvist et al., 1991;
Johansson et al., 1991; Aastrup et al.,
1991) and the Swain et al. (1992)
research on lakes in Wisconsin and
Minnesota suggest that less than 30
percent of the atmospheric mercury
deposition to a watershed reaches a lake.
As the Swedish workers have stressed,
the effects from the anthropogenic
mercury loading will persist for a long
period after a reduction in mercury
emissions.
We estimate that atmospheric
emissions have increased by about a
factor of 4.4 over the last century as a
consequence of human activities. Notice
that the net increase in the atmospheric
burden is a factor of 3, due to the
predicted rapid removal near of the
source of mercury emissions in the form
of particles and ionic species. As a
consequence, 60 percent of the direct or
recycled component is contributing to
the mercury background in the atmo-
sphere even though 77 percent of the
present-day inputs might be directly or
indirectly of anthropogenic origin (27 of
the 35 Mmol yr1). The 25 Mmol
mercury in the atmosphere represents an
average concentration of 1.6ngm"3,
which is comparable to the average
concentration of mercury over the
oceans (see Pacific data in Fitzgerald,
1989). Given this contemporary con-
straint, we predict that the preindustrial
atmosphere contained 8 Mmol of
mercury with an average concentration
of 0.5 ng nr3.
Is Mercury Increasing in the
Atmosphere?

A present-day rate of increase of
atmospheric mercury at about 0.16
Mmol yr1 is predicted by assuming that
anthropogenic inputs have increased
linearly over the last 100 years. Accord-
ingly, 1000 Mmol were emitted
anthropogenically during the 100-year
period. Of those emissions, 17 Mmol
are now in the atmosphere, 36 Mmol are
in the surface ocean, and the remaining
947 Mmol have accumulated in surface
soils. About 500 Mmol came from the
rapidly recycled anthropogenic compo-
nent and 447 Mmol via the atmospheric
cycle. The prediction that the present
rate of increase of mercury in the
atmosphere is about 0.16 Mmol yr1
(i.e., 0.6 percent yr1) is testable. For
example, atmospheric carbon dioxide
has been increasing at about half this
rate (i.e., 0.3 percent yr1).
Summary

The elemental mercury and
methylmercury cycles are intimately
linked. Environmental studies of
mercury must view the biogeochemistry
of mercury as a unit and avoid a unilat-
eral focus on one aspect of the system.
For example, human exposure to
methylmercury in fish is related to
anthropogenic emissions of mercury,
especially elemental mercury, atmo-
spheric transport and deposition pro-
cesses, and in situ biological interac-
tions and chemical reactions that lead to
elemental mercury production and
recycling between water and air. Al-
though inorganic mercury reduction and
evasion remove mercury from the
waters where it might be methylated, the
recycling between surface waters and
the atmosphere will prolong the impact
of anthropogenically derived mercury
on aquatic systems. Present-day ocean
contains enhanced mercury levels that
promote increased methylation in the
water column. Oceanic emissions reflect
the presence of this increased burden.
About 70 percent to 80 percent of
today's emissions of mercury are related
to human activities. A substantial
portion of the emissions are predicted to
be deposited locally. Regional deposi-
tion would reflect the presence of ionic
and paniculate mercury species in
emissions. Elemental mercury emissions
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Conference Proceedings
contribute to far-field and more global
effects, although polluted terrestrial
atmospheric conditions with elevated
concentrations of particles, ozone, and
sulfur gases may enhance the oxidation
and deposition of elemental mercury
(Munthe, 1992). A 3X increase in the
mercury burden in the atmosphere and
surface ocean is predicted. Surface soils
contain most of the pollution-derived
mercury released over the past 100
years. Current emissions are exacerbat-
ing the problem by adding to seriously
contaminated active reservoirs of
surface soils, watersheds, the atmo-
sphere, and the oceans. As most mer-
cury deposited on the oceans is recycled
to the atmosphere, the terrestrial envi-
ronment becomes a principal sink.
Mercury deposited on land is mobilized
slowly to enter the watershed and
tributaries of fresh and coastal waters.
The insidious consequence of the
complex and interesting biogeochemical
cycling of mercury is to lengthen the
influence and active lifetime of anthro-
pogenic mercury in regions where
methylation can occur.
Future Research Directions

As shown, the atmospheric and
aquatic biogeochemical mercury cycling
will be affected not only by localized
processes and discharges but especially
by emissions, airborne transport, and
deposition of mercury from regional and
longer range sources. The linkages
between atmospheric mercury emissions
and the accumulation of methylmercury
in fish have been recognized and
included in the U.S. 1990 Clean Air Act
Amendments, which require an assess-
ment of health risk to humans and
wildlife caused by mercury emissions.
The potential adverse impact of atmo-
spheric mercury deposition to the fresh
and marine waters ("The Great Waters")
is contained in a recent EPA report to
Congress (EPA-453/R-93-055, May
1994). Currently, we are expanding and
refining the modeling of the global
mercury cycle. The Mason et al. (1994)
study outlined in this paper used a one-
box atmospheric model to develop the
time-dependent evolution of mercury in
the atmosphere and surface ocean over
the past 100 years. A Global Mercury
Cycling Model (G-MCM) that will
provide a more realistic simulation of
the global scale dynamics of the atmo-
spheric, terrestrial, and oceanic mercury
cycle is being developed (Hudson et al.,
1994a).
Increasingly, environmental mer-
cury research is speciation- and reaction-
oriented. For example, inorganic mercury
(Hg(H)), elemental mercury (Hg°) and
alkylated mercury species (methylmer-
cury (mmHg), dimethyl mercury
(DMHg)) are being measured at pico to
femtomolair levels in air, water, and
precipitation. A new wave of exciting
and important environmental mercury
studies are beginning to yield coherent
models for the principal species and
reactions governing the behavior and fate
of mercury in nature. Much needs to be
done, and critical research areas include
(1) establishing patterns of modem and
historic mercury deposition to provide an
essential foundation for detailed bio-
geochemical and ecological studies of
mercury; (2) assessing the contributions,
as well as the physical (i.e., particulate
mercury species) and chemical speciation
of global versus local/regional mercury
sources to terrestrial and oceanic regions;
(3) identifying the reactions associated
with cycling of elemental mercury in the
atmosphere and natural waters; (4) exam-
ining atmosphere-water coupling and its
influence on methylmercury and elemen-
tal mercury cycling; (5) investigating the
mechanisms leading to the post deposi-
tional in situ bacterial conversion of
mercury species to methylated forms in
natural waters, wetlands, and watersheds;
and (6) relating human exposure to
methylmercury with the levels of lowest
effect.
Acknowledgments

This work has been supported in
part by a grant from the National
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National Forum on Mercury in Fish
Science Foundation (Chemical Ocean-
ography Program) and partly by the
Wisconsin Department of Natural
Resources and the Electric Power
Research Institute.
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F.M. Morel. 1994. Biogeochemi-
cal cycling of elemental mercury:
Anthropogenic influences. Geo-
chemica Cosmochim. Acta
58:3191-3198.
Mason, R.P., and W.F. Fitzgerald.
1990. Alkylmercury species in the
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Conference Proceedings
1
9
equatorial Pacific. Nature 347:457-
459.
Mason, R.P., and W.F. Fitzgerald. 1993.
The distribution and biogeochemi-
cal cycling of mercury in the
Equatorial Pacific Ocean. Deep Sea
Res. 40:1897-1924.
Mason, R.P., W.F. Fitzgerald, J. Hurley,
A.K. Hanson, Jr., P.L. Donaghay,
J. Sieburth. 1993. Mercury bio-
geochemical cycling in a stratified
estuary. Limnol Oceanog. 38:1227-
1241.
Munthe, J. 1992. The aqueous oxidation
of elemental of mercury by ozone.
Atmos. Environ. 26A: 1461-1468.
Nater, E.A., and D.F. Grigal. 1992.
Regional trends in mercury distri-
bution across the Great Lake states,
north central USA. Nature
358:139-141.
Nriagu, J.O. 1989. A global assessment
of natural sources of atmospheric
trace metals. Nature 338:47-49.
Nriagu, J.O., and J.M. Pacyna. 1988.
Quantitative assessment of world-
wide contamination of air, water
and soils by trace metals. Nature
333:134-139.
Rolfhus, K.R., and W.F. Fitzgerald.
1994. Linkages between atmo-
spheric mercury deposition and the
methylmercury content of marine
fish. Water Air Soil Pollut. In press.
Swain, E.B., D.R. Engstrom, M.E.
Brigham, T.A. Henning, and P.L.
Brezonik. 1992. Increasing rates
of atmospheric mercury deposition
in midcontinental North America.
Science 257:784-787.
Trends '91. Carbon Dioxide Informa-
tion Analysis Center, Oak Ridge
National Laboratory.
Watras, C.J., N.S. Bloom, R.J.M.
Hudson, S.A. Gherini, R. Munson,
S.A. Claas, K.A. Morrison, J.
Hurley, J., J.G. Wiener, W.F.
Fitzgerald, R. Mason, G. Vandal,
D. Powell, R. Rada, L. Rislow, M.
Winfrey, J. Elder, D. Krabbenhoft,
A. Andren, C. Babiarz, D.B.
Porcella, and J.W. Huckabee.
1994.. Sources and fates of mer-
cury and methylmercury in Wis-
consin lakes. In C.W. Watras and
J.W. Huckabee, eds., Mercury as a
Global Pollutant: Towards Inte-
gration and Synthesis. Lewis
Press, Boca Raton, FL, pp. 153-
177.
Westoo, G. 1966. Determination of
methylmercury compounds in
foodstuffs I: Methyl mercury
compounds in fish, identification
and determination. Acta Chem.
Scand. 20:2131-2137.
Wiener, J.G., R.E. Martini, T.B. Sheffy,
and G.E. Glass. 1990. Factors
influencing mercury concentra-
tions in walleyes in Northern
Wisconsin lakes. Trans. Amer.
Fish.Soc. 119:862-870.
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10
National Forum on Mercury in Fish
Mercury in the Environment
Toxic
• Volatile
Readily mobilized

Significant anthropogenic interferences

Transformations to more toxic species,
e.g., Monomethylmercury

• Bioamplification, e.g., fish
• Human health hazard
Conclusions and Predictions

Anthropogenic activities have increased
atmospheric Hg emissions by a factor of
3 relative to natural emissions.
1/2 emissions—^-global atmospheric cycle
1/2 emissions—^-deposited locally/regionally

• Anthropogenic Hg emissions for past
100 years are contained in active
reservoirs at the Earth's surface. Of the
estimated 1000 Mmoles emitted, there
are:
17 Mm atmosphere! S:anificant
36 Mm oceans L Significant
947 Mm soils J Contaminant

»Terrestrial soils are the principal
repository for anthropogenic Hg—Hg is
slowly but continuously released to fresh
waters and the coastal zone.
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Conference Proceedings
11
Conclusions and Predictions
(conitiniued)

»Hg concentrations in the atmosphere and
ocean surface waters have increased by
a factor of 3. Soils have increased their
Hg content by about 15%.
Continued anthropogenic Hg emissions on
both a local and global scale are increasing Hg
in active reservoirs at the Earth's surface.

• Cessation of Hg fluxes associated with
human activities will lead to a relatively
rapid decrease in Hg contained in the
atmosphere and ocean surface waters.

••Unfortunately, the release of stored
anthropogenic Hg in soils will continue
for a long period—decadal time scale
after emission reductions are
implemented (cf. Swedish experience).
Taken from Hudson et.al., 1994.
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National Forum on Mercury in Fish
Little Rock Treatment Basin
Atmospheric Deposition
1.1 g/yr
Trophic Transfer
Phytoplankton/Bacteria
\
Zooplankton
|5 % of Total Inputs|
0.06 gfrr
Taken from Fitzgerald ct.al., 1991.
Methyl-Hg in Little Rock Lake, Wl (Bloom et al., 1991)
D.O. (met)
02411
10 13
I
10
June 15.1983
°2
11334
[CH9Hg](ng/L»«Ho)
D.O.(mg/t)
0 3 4 f 0 10 13
10
0 3 4 • 0 10 13
!
2 '

4 '

•

• •

10
Augusts, 1988
PHaHBt
s
October 9, 1989
•-icHH*
J^—l
°2
1 3 3
[CH3Hg](na/LHHg)
133
ICH3Hg](nefLuHg)
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Conference Proceedings
13
Who
Atmospheric Deposition
1 x 107 moVyr
e Ocean
River Inputs
1 x 106 moVyr
Upwelling
5.3 x 105 rnoj/yr
Trophic Tr.ansfer
Phytoplanktoii/Bacteria
I
Zooplankton
IL9 % of Total Inputs
2.2x10 maj/yr

Taken from Rolfhus and Fitzgerald, 1994.
Natural and Anthropogenic
Natural and Anthropogenic
40*S
Biological Incorporatic

Equator
40*N
Transport of atmospherically-derived H^2to the biologically
productive Pacific Ocean. Atmosphere/ocean circulation and
biogeochemical model for the production and accumulation of
* in oceanic fish.
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14
National Forum on Mercury In Fish
Equatorial Pacific Ocean
o
o 2BO 500 750 mnn
200 •
g 400-
£
**
a
[fMJ
MMHg
600+
PMHg
DGM
1 ? 3 4 5
Reactive Hg
Station 4
20 40
N03
35.5 37.S
'3
I
(uM)
• ^ r •
Taken from Maion aod Fitzgctald, 1990.
0 6.7
20
S (o/oo)
*TIC°1
Predictions—to Test

1. Atmospheric Hg concentrations are increasing
at about 0.6% (yr1)

2. On average, soils contain about 15%
anthropogenic Hg

3. Expect about a factor of 3 increase for Hg
deposition in locations that are relatively free of
localized emissions and deposition

4. Hg (MMHg) in ocean fish has increased by
about a factor of 3

5. Hg (MMHg) in fresh water fish has on average
increased by a factor of s£ depending on
location and type of water body (localized
impact and drainage)

6. About 1/2 anthropogenic Hg emissions enter
the global cycle as Hg°
About 1/2 anthropogenic Hg emissions are
deposited locally/regionally as Hg**
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National Forum on
Mercury in Fish
Aquatic Biogeochemiistry and
Mercury Cycling Model (MCM)
Donald B. Porcella
Electric Power Research Institute, Palo Alto, California
Mercury concentrations in
marine and freshwater fish
often exceed human consump-
tion health advisory limits, even in areas
remote from known mercury sources.
Atmospheric deposition, transformed to
methylmercury, can account for virtu-
ally all of the mercury in fish in these
environments. This is part of the natural
biogeochemical cycle of mercury from
the earth's surface to the air and back
again. Human activities have mobilized
much of this mercury, and sources to the
atmosphere include both natural and
anthropogenic components. Anthropo-
genic sources vary extensively histori-
cally as well as spatially and have
included waste incineration; fossil fuel
combustion; chloralkali plants; ore
extraction, roasting, and smelting;
precious metal extraction; and many
other activities.
These activities contribute addi-
tional mercury to the natural sources of
mercury. Not all of the mercury enter-
ing aquatic ecosystems is taken up by
fish. Most mercury enters the sediment
pool, and a small fraction is transformed
to methylmercury and enters the biotic
pool. Except when point sources
contribute excessive mercury, the
amount of mercury accumulated by fish
does not affect fish growth and survival,
but represents a risk to humans and
other organisms, especially bird and
mammal fish-eaters. To assess these
risks, we need to calculate the amount
of mercury accumulated by fish from
their aquatic environment, either via
uptake of aqueous mercury or via the
food chain.
As part of the Mercury in Temper-
ate Lakes (MTL) and Mercury Accumu-
lation Pathways and Processes (MAPP)
projects in northern Wisconsin, investi-
gators studied seven low-productivity,
dilute water seepage lakes that spanned
a range of pH and dissolved organic
carbon (DOC) concentrations. A major
objective was to develop a simulation
model to calculate fish mercury concen-
trations. This task required algorithms
to estimate net methylation of mercury,
especially since virtually all of the fish
mercury is present as methylmercury.
Among reasons for developing a simula-
tion model to assess mercury in fish, the
following seem most important:
(1) eating fish is the chief mode of
exposure for humans and animals;
(2) fish primarily accumulate methyl-
mercury, produced from a complex
mercury cycle with many influence
factors that vary widely in surface
waters; (3) water concentrations of
mercury represent many sources that
enter the surface water via multiple
pathways (ground and surface waters,
deposition); and (4) mercury is present
at ultra-trace concentrations (nano and
picomolar), and models can provide an
initial default assessment while helping
15
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16
National Forum on Mercury in Fish
Hg in fish, ug/g ww
0.3-
0.2-
0,1-
0.0-
r T r
Pallotlo Vandercook Crystal LRR
LRT
Max
Russett
Figure 1. One-year-old whole yellow perch from northern Wisconsin
lakes.
study
Dissolved methyl-Hg, ng/lifer
0.4
0.3
0.2-
0.1-
0.0
-0.13 + 0.19x RSQ = 0
i
2
Total Mercury, ng/liter
Figure 2. Mercury in seven northern Wisconsin lakes.

to define the most cost-effective sam-
pling design for studying a surface
water.
Seepage lakes are dominated by
atmospheric deposition and receive
virtually all of their water, nutrients, and
mercury from atmospheric deposition.
The MTL/MAPP lakes are close to-
gether, and we suspected that they
received the same mercury deposition,
but the mercury levels bioaccumulated
by fish varied over a factor of 10
(Figure 1). This observa-
tion reinforced the need
for a model capable of
dealing with the varying
conditions leading to the
tenfold difference in
mercury fish concentra-
tions. Simplistic relation-
ships such as regressions
between methylmercury
and total mercury in water
(Figure 2) or between fish
mercury and methylmer-
cury in water (Figure 3),
although applicable in
these seven lakes, were
not capable of application
to other sites. Further-
more, the results show
that the role of inputs, in
this case deposition,
remains unclear because
of the indirect nature of
transformation and
bioaccumulatiori. This
result is reinforced by the
observation in Minnesota
that while mercury
deposition has decreased
by a factor of 3 since the
1950s, fish mercury
concentrations have not
changed in response.
Intensive field
studies during MTL/
MAPP led to a conceptual
model (Figure 4) that
shows the importance of
loading (deposition, water
inflows), transformation
(presence of wetlands,
sulfate-reducing bacteria,
reduction, sorption, food chain dynam-
ics, water quality, and nutrient status),
and loss (evasion, sedimentation, and
outflows). This conceptual model was
codified in a mathematical model called
the Mercury Cycling Model (MCM)
(Figure 5). The MCM runs with a
monthly timestep and is bounded by the
atmosphere, the lake margins, and the
lake sediment margins at the deep
sediment layer. Reactions in the
watershed and the atmosphere are not
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Conference Proceedings
i7
0.0
modeled; concentrations
are measured to provide
input at the boundary.
All three major
species of mercury—
elemental mercury (Hg(0)),
inorganic mercury (Hg
(II)), and methylmercury
(CH3Hg+)— are tracked in
MCM in three physical
compartments: the mixed
layer (epilimnion), the
hypolimnion, and the
sediments. At one time
dimethylmercury was
considered as a possibly
important chemical
species, but so far, it has
only been observed in
marine environments.
Four biotic compartments
were defined, comprising a
linear food chain occur-
ring in the two layers of
water: phytoplankton,
zooplankton, a forage
fish, and fish that prima-
rily consume other fish.
Although simulation
output can include any
variable, the target of
interest is mercury in
predatory fish because
these fish represent the
greatest potential expo-
sure to other consumers
outside the model bound-
aries (birds, humans, other
mammals). Physical and
chemical influences on
mercury transport and
speciation are also mod-
eled. The MCM has a
user-friendly interface and
runs on a Macintosh
computer.
The model can
simulate the mercury
concentrations in the biotic compart-
ments quite well (Figure 6). Further-
more, in a more rigorous test, the model
can simulate the major mercury species
(elemental mercury, inorganic mercury,
and methylmercury) very accurately
mg/kilogram, wet weight
0.3
0.2-
0.4
methyl-mercury, ng/liter
Figure 3. Mercury in one-year-old yellow perch.
Figure 4. Important processes affecting mercury in surface waters.
(Figure 7). These results suggest that
the MCM provides a very accurate tool
for assessing the effects of mercury
deposition on mercury bioaccumulation
by fish in these lakes, thereby allowing
users to ask "what if questions that are
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18
National Forum on Mercury in Fish
Hypollmnion

Sediments
Figure 5. Mercury cycling model.
CH3Hg (ppm)
Predaceous fish QAge 4
(Yellow Perch)
Forage fish
(age 1 Yellow Perch)
Zooplankton
Phyloplankton
0.1
Simulate^ CH3H9
Figure 6. Mercury cycling model simulates biotic compartment concentrations.
difficult if not impossible to accomplish
experimentally.
Some of these questions are
illustrated in Figure 8. This figure
shows the baseline condition for mer-
cury in predatory fish, modeled in the
reference basin (unacidified) of Little
Rock Lake, one of the seven northern
Wisconsin lakes studied in MTL. The
annual cycle of mercury in fish repre-
sents the seasonal changes
hi the ratio of two pools—
fish biomass and the
mercury in fish. The
upper curve in Figure 8,
showing an increase in
fish mercury concentra-
tions, represents what
would happen if the
particulate matter in the
lake (clays, detritus, other
small particles) were
reduced by a factor of 10.
Less particulate matter
means that less mercury is
bound, making more
available for methylation
and subsequent uptake.
The lower curve in Figure
8, showing a decrease in
fish mercury concentra-
tions, represents what
would happen if we could
increase the rate of
demethylation by a factor
of 2. Faster demethyla-
tion would lead to less
methylmercury available
for uptake through the
food chain. The fourth
curve differs little from
the base case and results
from a 5 percent decrease
in deposition. Such a
decrease is the maximum
expectation of what might
result from control of
power plant emissions.
Although these
changes are apparent in
the simulations, they are
not substantial. In fact,
the changed fish concen-
trations do not begin to approach the
new steady state levels until after 7-8
years. One of the factors driving the
fish accumulation appears to be
sediments as a reservoir of substrate
for methylation and release to overly-
ing waters where biota can accumulate
the methylmercury. The mercury in
sediments has built up over time and
can affect rates of recovery when
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Conference Proceedings
loading is reduced. If
we simulate removal of
all mercury-containing
sediments from one of
the MTL lakes, a rapid
reduction in fish mer-
cury is observed, result-
ing in a 50 percent
reduction within 10
years (Figure 9). A new
steady state is not
reached for about 30-50
years, varying with lake
site-specific conditions,
like the rate of buildup
of mercury in the sedi-
ments.
The MCM has been
applied to a variety of
lakes: OnondagaLake
(using USEPA's
MERC4 model, a PC-
based version of the
MCM embedded in
USEPA's WASP4
modeling framework),
the seven Wisconsin
lakes, one of the
Adirondacks lakes, and
in the Great Lakes
(Superior and Erie).
New studies will apply
the MCM to a Florida
seepage lake, where a
subtropical climate will
be simulated. The
model has use in hypoth-
esis testing/definition,
constraining of rate
constants for different
processes, the evaluation
of alternatives, the
design of field studies,
and the evaluation of
uncertainty. Additional
applications will increase the robust-
ness of the model and its coefficients.
Modifications to the MCM presently
include use in global mercury cycling,
regional lake modeling, and more
complex food web/bioenergetics
simulation algorithms.
The field studies and model
results show the importance of mercury
Observed [HgfOfl and [CH, Hg]
0.1 0.2
Units, ng/Q
DHg(ll)
ACH3Hg
OHg{0)
1.0
Observed [Hg(U)]
Figure 7. Mercury cycling model simulates mercury species measured
Wisconsin lakes.
in seven
CH3Hg (ppm wet)
0.30
0.24
0.18
0.12
0.06
Decrease in
detrital particles
Base case
Increase in
demothylation
5% decrease -
2.5
5.0
Year
7.5
10
Figure 8. Piscivorous fish mercury—model result!!.
speciation and of site-specific factors in
controlling accumulation of mercury in
fish. Furthermore, sediments seem to
be the major factor controlling mercury
bioaccumulation by fish. The effects of
sediments and other site-specific factors
help explain why fish mercury concen-
trations are not directly coupled to
mercury inputs.
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20
National Forum on Mercury in Fish
CH3Hg (ppm wet)
0.5
0.45
0.4
0.35
0.3
0.25
0.2
0.15
0.1
0.05
0
/VAAAAAAAAA
0
1
2.5
5
Year
7.5
10
Figure 9. Piscivorous fish mercury.
References

Benoit, J.M., W.F. Fitzgerald, and
A.W.H. Damman. 1994. Histori-
cal atmospheric mercury deposi-
tion in the mid-continental United
States as recorded in an
ombrotrophic peat bog. In C. J.
Watras and J.W. Huckabee, eds.,
Mercury as a Global Pollutant, pp.
187-202. Lewis Publishers, Ann
Arbor, MI.
Fitzgerald, W.F. 1986. Cycling of
mercury between the atmosphere
and oceans. In The Role of Air-
Sea Exchange in Geochemical
Cycling, pp. 363-408. NATO
Advanced Science Institutes Series
C (P. Buat-Menard, ed.). Reidel,
Dordrecht, Netherlands.
Fitzgerald, W.F., R.P. Mason, and G.M.
Vandal. 1991. Atmospheric
cycling and air-water exchange of
mercury over mid-continental
lacustrine regions. Water Air Soil
Pollut. 56:745-768.
Hudson, R.J.M., S.A. Gherini, C.J.
Watras, and D.B. Porcella. 1994.
Modeling the biogeochemical
cycle of mercury in lakes: The
Mercury Cycling Model (MCM)
and its application to the MTL
study lakes. In C.J. Watras, and J.
W. Huckabee, eds., Mercury as a
Global Pollutant, pp. 473-523.
Lewis Publishers, Ann Arbor, ML.
Porcella, D.B.1994. Mercury in the
environment: Biogeochemistry. In
CJ.Watras, and J.W. Huckabee,
eds., Mercury as a Global Pollut-
ant, pp. 1-19. Lewis Publishers,
Ann Arbor, MI.
Watras, C.J., N.S. Bloom, RJ.M.
Hudson, S.A. Gherini, R. Munson,
S.A. Claas, K.A. Morrison,
J.Hurley, J.G. Wiener, W.F.
Fitzgerald, R. Mason, G. Vandal,
D. Powell, R. Rada, L. Rislove,
M. Winfrey, J. Elder, D.
Krabbenhoft, A.W. Andren, C.
Babiarz, D.B. Porcella, and J.W.
Huckabee. 1994. Sources and
-------
Conference Proceedings
21
fates of mercury and methylmer-
cury in remote temperate lakes. In
C.J. Watras, and J.W. Huckabee,
eds., Mercury as a Global Pollut-
ant, pp. 153-177. Lewis Publish-
ers, Ann Arbor, MI.
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National Forum on
Mercury in Fish
Mercury Methylation In Fresh
Waters
Cynthia C. Gllmour
Assistant Curator, Estuarine Research Center, The Academy of Natural Sciences
St. Leonard, Maryland
Mercury methylation is a pre-
dominantly microbial process
that occurs mainly in anoxic
sediments and waters, with maximum
intensity often at the interface between
anoxic and oxic conditions (O/A bound-
ary) (Gilmour and Henry, 1991; Winfrey
and Rudd, 1990). Understanding of the
geochemistry and microbiology of
methylation has progressed rapidly in the
last few years. Two major changes have
helped this progress: (1) the finding that
sulfate-reducing bacteria (8KB) are
important mediators of methylation; and
(2) improvements in mercury analysis that
have allowed measurement and speciation
of mercury at ambient levels.
Of critical importance in this
research is the relationship between
mercury inputs, or concentrations, and
resultant methylmercury concentrations
and bioaccumulation. However, mercury
concentration is only one of many
variables that need to be considered in
order to model methylmercury bioacc-
umulation. Have mercury levels in fish
increased as a result of increased mercury
deposition over time? Or does the
biogeochemistry of certain types of
aquatic systems predispose them to net
mercury production and bioaccumulation?
Are the changes in the biogeochemistry of
some lakes due to acid deposition the
cause of increased mercury
bioaccumulation? Each of these factors
no doubt plays a role. The following
discussion will highlight some of the
important factors in this very complex set
of relationships, particularly control of
methylation rates.
Methylmercuiy Budgets for
Three Lakes

Budgets have been constructed in
the past few years for a small number of
aquatic systems using appropriate
noncontaminating methods for mercury
speciation. New methods for estimating
reactions and fluxes have also been
applied as part of these studies. The
biogeochernical cycles put together for
these lakes demonstrate the state-of-the-
art understanding of mercury and meth-
ylmercury biogeochemistry.

Littie Rock Lake, Wisconsin

Little Rock Lake is a small, pristine
seepage lake. Studied intensely (e.g.,
Weiner et al., 1990; Watras et al., 1994),
the Little Rock Treatment (LRT) basin is
the lake on which the MTL model was
originally based. Little Rock Lake was
partitioned in 1984 and one basin acidi-
fied with sulfuric acid over 6 years. We
and others have developed methods in the
last year or two to fill in some of the
previously unmeasured parameters in the
methylmercury budget. These methods
include noncontaminating methods for
23
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24
National Forum on Mercury in Fish

Teplnvm
Tep4cnv*

FM
1»ng/s
0,1§o

A
n
u
Sosrmnl efflux
o.«u}Vtav
804 e*

IMftylaiKniaM
0,CUn»«8i),0-4em«vj.
ZAugAnZy
O-SSoV
tooutfmJy
10 OV

UTTLE ROCK TREATMENT
AJmotphere
<0,005ng/m3
II
II
V
Preoprtilion
0.1 ug/m2/y
0,01 o/»

Lake
dudved
0.12 ng/t
0.020

Scdlmer.lB
Scdfenent eccumuiatJon rate
O.Sua'mify
O.OSQV

Seston
5 ng/g
0.02 g

II
II
V
Sediment trap flux
5.4 ug/m2/y
0.3o/y

Sediment concentration
0.5 ng/g at surface
0.05 g
2o

Figure 1. Budget for methylmercury in Little Rock Lake treatment
basin modified from Watras et al., 1994. Modifications were based
on our measurements of nonadvective flux of methylmercury from
sediments and on methylmercury production rates and concentra-
tions within sediments. Sediment methylation rate, and methyl-
mercury concentration, accumulation, and efflux rate were modi-
fied; all other data are from Watras et al., 1994. Sediment
concentrations and methylation rate are given in ng/g wet weight
sediment. Rate calculations assume a 120-day warm season and
1 mm/y sediment accumulation rate. De novo methylation ap-
peared to occur to at least 8 cm depth although it was maximal in
the top 4 cm (Gilmour, 1994).

estimation of nonadvective flux from
intact sediment cores, and the use of
mercuric chloride with a specific activity
high enough to be used as a tracer (rela-
tive to bulk mercury) to estimate ambient
methylation rates for the first time.
A revised methylmercury budget for
LRT, based on a few estimates of methy-
lation rate and sediment/water methylmer-
cury flux in 1993, is shown in Figure 1.
The primary site of de novo methylmer-
cury production appears to be sediments.
Methylation rates in the top 1 mm of
sediments averaged about 2.5 ug/mVd in
mucky treatment basin sediments.
Sediments constitute the main pool of
methylmercury in the lake if the top few
centimeters are considered, and fish are
another important pool. Efflux of methyl-
mercury from sediments was a small
fraction of total methylmercury produc-
tion within sediments, suggesting intense
demethylation across the sediment/water
interface, or recycling of methylmercury
within sediments. Recycling of methyl-
mercury in the water column is very
important in its mass balance, with annual
sediment trap fluxes of approximately 10
times the level of methylmercury efflux
and approximately equal to de novo
methylmercury production in the top
1 mm of sediment. Although deposition
and de novo methylmercury production
are approximately equivalent in the top
1 mm of sediment, methylation occurs to
at least 8 cm sediment depth. In LRT,
sulfate stimulates sulfate reduction,
methylmercury production in and efflux
from sediments. In these high-organic-
carbon sediments, sulfate reduction is
limited by sulfate, as it is in most sedi-
ments.

Pattetie Lake, Wisconsin

Pallette Lake is a nearby pristine
seepage lake. As in LRT, the primary site
of de novo methylmercury production
appears to be littoral sediments. The oxic/
anoxic interface in the water column is
also a source of methylmercury, however.
De novo production occurs just below the
O/A interface in the zone of maximal
sulfate reduction (Figure 2) (Watras et al.,
1995). Methylation and sulfate reduction
do not occur in hypolimnetic waters or
sediments after sulfate is depleted in
spring. In epilimnetic and littoral sedi-
ments, sulfate reduction and methylation
are limited by organic carbon, not sulfate.
This is not generally the case. Because of
this limitation, sites of organic carbon
production and advection (such as ground
water inflow zones) and sites of high
photosynthetic production (like the
pycnocline) are primary sites of methyl-
mercury production in this organic-
carbon-limited system.
I want to emphasize the importance
of the O/A interface in methylmercury
production, and its location. A suite of
microbial processes occurs across this
gradient, with electron acceptors (e.g.,
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Conference Proceedings
25
oxygen, nitrate, sulfate) being supplied
from the oxic side, and organic substrates
being sequentially oxidized with depth.
Chemo- and phototrophic processes are
often maximal here, with the availability
of reduced substrates like HS-. Under
oxic waters, the O/A interface is usually
within a few millimeters to centimeters of
the sediment surface. With the formation
of a hypolirnnion, the O/A interface and
its microbial strata move into the water
column. Methylation occurs all along this
interface, and this is well illustrated in
Pallette Lake.

Onondaga Lake, New Yoik

Onondaga Lake is a very different
system. It is a large, eutrophic, alkaline,
heavily mercury-polluted drainage lake
(Henry et al., 1995). The main in-lake site
of methylmercury production is the
anoxic hypolirnnion. Sulfate concentra-
tions are extremely high for a freshwater
lake, and sulfate does not become de-
pleted in the hypolimnion over the
summer. External sources of methylmer-
cury, especially wastewater treatment
effluent, and streams flowing through
contaminated ground, are important
inputs. Efflux of methylmercury from
sediments, especially hypolimnetic and
contaminated sediments, is substantial
relative to the pristine lakes discussed
above, but is still a minor source to the
lake.
Microbiology of Methylation

Work in a number of lakes and
estuaries has shown that SRB are impor-
tant mediators of methylmercury produc-
tion in sediments and in anoxic waters.
Compeau and Bartha (1986) first showed
their importance in mercury methylation
in estuaries, and this was extended to
fresh waters in 1992 (Gilmour et al.,
1992). This work was done using specific
inhibitors (molybdate) and stimulants
(short-chain fatty acids) of SRB. The
distribution of methylating activity in
aquatic systems generally matches that of
sulfate-reducing activity—-just below the
-»- StiHato reduction
((jmo)9/m3-d)
0 tOO 200
50
| Bacteria
(10*ceHsAnL)
25 0
20-
C.
(I SO 100 2.0
MB methylation _o_
production
(rnmol C/m'-d)
SO 100
Phytoplankton
Figure 2. Biogeochemical process rates and microbial abundances
from in situ incubations in Pallette Lake.
O/A interfaces both in sediments arid the
water column, and in anoxic waters where
sulfate is available. Nevertheless, other
organisms may also contribute to mercury
methylation. Molybdate does not always
block all methylation; it does not affect
methylation at all in a few systems. The
role of other organisms in methylation
and the type of organisms involved are
poorly defined.
Why do SRB methylate mercury?
Mercury methylation is not a defense
mechanism against mercury for SRB.
Methylation is constitutive (not inducible
by mercury), and the ability to methylate
mercury does not confer added mercury
resistance among SRB. Only a subset of
SRB methylate mercury. We have
hypothesized that Hg-S species, which
generally dominate dissolved mercury
speciation in areas of methylation, are
available to SRBs for methylation,
possibly through metal uptake media-
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26
National Forum on Mercury in Fish
20
18
IB
io~

4-
2-
0-
nisms developed by these organisms for
sulfitic environments. SRB do not contain
the mer operon system, a plasmid-
encoded mercury defense mechanism
found in many aerobes that codes for
mercury and methylmercury uptake,
demethylation, and reduction (Henry,
1992). However, there is some evidence
that there is an oxidative methylmercury
decomposition system in 8KB (Oremland
etaL, 1991).
Factors That Affect
Methyimercuiy Production in
Lakes

1. Total mercury concentration.
Although increased mercury inputs to a
system generally result in increased
methylmercury in fish, the quantitative
relationship between mercury concentra-
tion and methylation is not linear. In one
type of bacterial culture, methylation is a
function of the log of the total mercury
concentration (Figure 3). This illustrates
that it is not the total mercury concentra-
tion, but the concentration of mercury
available for methylation, that needs to be
known to estimate methylation rates.
Mercury-sulfides are the dominant
dissolved Hg(E[) species in most waters;
even oxic waters often contain nM HS~.
Ionic Kg2*" concentrations are infinitesimal
i
0,1
1.0
10.0
100.0
Ho added, mgf
Figure 3. Concentration dependence of mercury methylation by
sulfate-rcducing strain ND132, in sulfate-reducing medium, which
can contain up to mM sulfide concentrations.
(< 10'30 M), and the free ion is probably
not the main biologically active species.
A comparison of mercury and
methylmercury concentrations and percent
methylmercury among the three lakes
(Table 1) shows that (1) mercury concen-
tration in the water column is not a linear
function of mercury in sediments and
(2) percent methylmercury in the water
column, either epi- and hypolimnia, is
similar among the lakes, but percent
methylmercury in sediments is not.
Clearly, there is not a linear relationship
between mercury loadings and methyl-
mercury concentrations among the
systems. Along with microbial activity,
mercury solubility and speciation in
sediment pore waters probably determines
methylation rate in sediments. We are
investigating sediment/pore water parti-
tion coefficients and mercury speciation in
pore waters in these and other lakes as a
tool to predict methylmercury production.
2. Lake chemistry/morphometry.
Factors that are predictive of mercury
levels in fish include low pH, high
dissolved organic carbon (DOC),
reservoir formation, and stratification.
The presence of an anoxic hypolim-
nion allows flux of inorganic mercury
from sediments; methylmercury
degradation is minimal in anoxic
waters; and methylmercury flux from
sediments appears to be increased. In
addition, methylmercury can be
formed in anoxic waters if sulfate is
not depleted (e.g., Onondaga). In
lakes where sulfate is depleted from
the hypolimnion, methylation may
occur at the O/A interface (e.g.,
Pallette). Methylmercury formed in
the water column may be more avail-
able for bioaccumulation than meth-
ylmercury formed within sediments.
There is little information on how
DOC may affect methylation rates
directly at this time, although DOC
amount and character do influence
dissolved mercury speciation and
hence availability for methylation.
Low-pH lakes are especially
susceptible to mercury problems. The
Little Rock Lake study showed that
sulfuric acid acidification alone resulted
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Conference Proceedings
27
Table 1. Comparison of total mercury (Hg) and methyhnercury (MeHg) concentrations, and methylmercury as
a percent of total mercury (%MeHg) in oxic and anoxic waters, and sediments of three lakes. Water column
values are for dissolved (<0.2 um) concentrations. Sediment concentrations are per g dry weight
Lake
Little RockTreatment
Pallette

Onondaga

Epilimmon
Epilimnion
Hypolimnion
Epilimnion
Hypolimnion

Water
HgD
ng/L
1
0.1-0.8
<0. 1-0.25
1-4
2-10

MeHg,
ng/L
0.06
<0.01
<0.01-2
0.05-0.2
0.3-10

%MeHg
6%
<10%
<10-50%
3-15%
up to 100%

Sediments
Hg
ng/g
80-140
0.8-1.3

1000-4500

MeHg
ng/g
3-10
0.02-0.05

3-11

%MeHg
3-7%
1-6%

0.02-0.3%

in increased mercury in fish (Wiener et
al., 1990). Increasing sulfate levels,
rather than pH per se, may be one
component of how pH influences
methylmercury production and bioacc-
umulation. The changes in mercury
accumulation in LRT were attributed to
increases in methylmercury production,
primarily in sediments (Winfrey and
Rudd, 1990). Increases in sediment
sulfate reduction rates in lakes impacted
by sulfate deposition are well docu-
mented, and this was also shown to
occur in LRT relative to LRL. It is
important to recognize that low pH in
lake water does not usually mean
decreased pH in sediment pore waters,
or inhibition of microbes. Sulfate
reduction is a strong alkalinity genera-
tor. In LRT sediments, we found that
increased sulfate levels stimulated both
production of methylmercury within and
efflux from sediments. However,
sulfate does not consistently stimulate
mercury methylation in sediments; in
some cases SRR is not sulfate-limited
(e.g., Pallette), and at high sulfate levels
sulfide production by SRB appears to
limit the availability of mercury for
methylation.
We have examined the relationship
between sulfate levels in lake water and
methylmercury levels in sediments in a
number of lakes and estuaries and have
found the pattern shown in Figure 4.
Methylmercury is plotted as a percent-
age of total mercury to compensate for
variations in total mercury among lakes.
The hypothetical relationship between
sulfate concentration and percent
methylmercury across a wide range of
sulfate and salinity is shown in Figure 5.
This is an evolving relationship. We are
in the process of adding information
from Wisconsin lakes to the graph to see
if the pattern still holds. We are also
examining other ways of looking at the
relationship, especially adding in more
details of mercury speciation and
solubility.
Reservoirs are also susceptible to
mercury bioaccumulation. Microbial
activity, and hence methylation, may be
high in newly formed reservoirs because
labile organic matter concentrations are
high. Reservoir formation and its
effects on the mercury cycle are cur-
rently being studied by a group in the
Experimental Lakes Area, Ontario.
Wetlands have recently been recognized

O>
I
m

11-
10-
9-
8-
7-
6-
5-
4-
3-
2-
1-
0-
C
O Hudson River Estuary
(• Mass. Reservoirs
13 Cape Cod Ponds
!• NC Reservoir
A Paliette Lake
A Little Rock Lake A
A A
A * A'
A A
• • * t o oo .
cF ' o R)
' • • • i ' • • • i i i 1 1 1 v> — iii| — i — i 1 1 1 — i — i 1 1 [
1 10 100 . 1000 10000 100000
Sulfate reduction rate, umoles m"2 d'1
Figure 4. Relationship between percent methylmercury and
sulfate reduction rate in the top 4 cm of sediment in eight lakes
and along the salinity gradient of an estuary.
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28
National Forum on Mercury in Fish
log sulfate reduction rate
Freshwater
Estuarine
Marine
Figure 5. Hypothetical relationship between sediment sulfate
reduction rate and the percent of total mercury hi the methylated
form.
as sites of high methylmercury produc-
tion, perhaps for the same reasons (St.
Louis et al., 1994).
Lake surface-to-volume ra,tio
affects methylmercury accumulation
(Bodaly et al., 1993). A relatively high
surface area of warm, shallow sedi-
ments increases microbial activity.
Temperature seems to affect methyla-
tion more strongly than demethylation.
Lake hydraulic retention time is also
important, with long-retention-time
lakes accumulating more methylmer-
cury from sediments.
References

Bodaly, R.A., J.M.W. Rudd, RJ.P. Fudge,
and C.A. Kelly. 1993. Mercury
concentrations in fish related to the
size of remote Canadian Shield
Lakes. Can. J. Fish. Aquat. Sci.
50:980-987.
Compeau, G. and R. Bartha. 1985.
Sulfate-reducing bacteria; principle
methylators of mercury in anoxic
estuarine sediment. Appl. Environ.
Microbiol. 50:498-502.
Gilmour, C. C. 1994. Comparison of
sediment Hg methylation rates and
the contribution of sediment MeHg
production to the MeHg mass
balance among ecosystems. Pre-
sented at the International Confer-
ence on Mercury as a Global
Pollutant, Whitsfler, B.C., British
Columbia, Canada, July, 1994.
Gilmour, C.C., and E.A. Henry.
1991. Mercury methylation in
aquatic systems affected by acid
deposition. Environ. Poll.
71:131-169.
Gilmour, C.C., E.A. Henry, and R.
Mitchell. 1992. Sulfate stimulation
of mercury methylation in fresh-
water sediments. Environ. Sci.
Technol. 26:2281-2287.
Henry, E.A. 1992. The role of sulfate-
reducing bacteria in environmental
mercury methylation. Dissertation,
Harvard U. 221 pp.
Henry, E.A., L. J. Dodge-Murphy, G.
N. Bigham, S.M. Klein, and C. C.
Gilmour. 1995. Total mercury and
methylmercury mass balance in an
alkaline, hypereutrophic urban
lake (Onodoga Lake, N.Y.) Water
Air Soil Pollut. In press.
Oremland, R.S., C.W. Culbertson, and
M.R. Winfrey. 1991. Methylmer-
cury decomposition in sediments
and bacterial cultures: Involve-
ment of methanogens and sulfate
reducers in oxidative
demethylation. Appl. Environ.
Microbiol. 57:130-137.
Ramlal, P.S., C.A. Kelly, J.W.M. Rudd,
and A. Furutani. 1993. Sites of
methylmercury production in remote
Candian Shield Lakes. Can. J. Fish.
Aquat. Sci. 50:972-979.
St. Louis, V.L., J.M.W. Rudd, C.A. Kelly,
K.G. Beaty, N.S. Bloom, and RJ.
Flett. 1994. The importance of
Wetlands as sources of methylmer-
cury to boreal forest ecosystems.
Can. J. Fish. Aquat. Sci. 51:1065-
1076.
Watras, C.J., N.S. Bloom, S.A. Claas,
K.A. Morrison, C.C. Gilmour, and
S.R. Craig. 1995. Methylmercury
production in the anoxic hypolim-
nion of a dimictic seepage lake.
Water Air Soil Pollut. In press.
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Conference Proceedings
29
Watras, C.J., and 21 others. 1994. Sources
and fates of mercury and methylm-
ercury in Wisconsin Lakes. In C.
Watras and J. Huckabee, ed.,
Mercury Pollution: Integration and
Synthesis, pp. 153-177. Lewis
Publishers, Boca Raton, FL.
Winfrey, M.R., and J.W.M. Rudd. 1990.
Environmental factors affecting the
formation of methylmercury in low
pH lakes: A review. Environ. Tox.
Chein, 9: 853-869.
Wiener, J.G., W.F. Fitzgerald, C J.
Watras, and R.G. Rada. 1990.
Partitioning and bioavailability of
mercury in an experimentally
acidified Wisconsin lake. Environ.
Tox. Chem. 9: 909-918.
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National Forum on
Mercuiry in Fish
Considerations in the Analysis of
Water and Fish for Mercury
Nicolas S. Bloom
Frontier Geosciences Inc., Seattle, Washington
This presentation will discuss
methods and relevant analytical
considerations necessary for the
accurate and precise determination of
total mercury and methylmercury in
aquatic organisms and the waters in
which they live. The topics that will be
discussed are (1) "ultra-clean" sample
handling; (2) methods and justification
for obtaining uiformation on mercury
speciation; and (3) typical results for
mercury speciation in a wide range of
aquatic organisms.
Ultra-Clean Sample Handling

Only in the last decade have
researchers been able to accurately
measure mercury in ambient environ-
mental media. Earlier limitations were
caused more by contamination than by
inadequate detection limits. With the
development of ultra-clean sample
handling, the average value and the
variability for the observed concentra-
tion of mercury in surface waters have
decreased dramatically over time
(Bloom, 1995; Fitzgerald and Watras,
1989). The ultra-clean techniques
discussed here were designed for and
apply most specifically to aqueous
samples, where the observed concentra-
tions might be in the 1-10 ng/1 range.
For biota samples, which contain
concentrations 105 to 107 times higher,
these rigorous techniques are not as
necessary (Bloom, 1992).
Ultra-clean sample collection
begins with processing of equipment in
a low-mercury environment. Particulates
are controlled by passing air through
high-efficiency (HEPA) filters. While
sufficient for all other trace metals, most
mercury is found in the gaseous phase,
thus requiring additional steps. Most
importantly, the level of mercury in the
air must be monitored. If total gaseous
mercury is -under 10 ng/m3, then the lab
is clean for low-level work, whereas if
the lab air has levels greater than 100
ng/m3 mercury, it should be considered
unacceptable. Reductions in gaseous
mercury levels can often be effected by
ventilating the space directly with large
volumes of outside air or by placing
mercury removal filters (gold or carbon)
on the intake to the HEPA filters. The
cleanroom must also be equipped with a
continuous source of low-mercury
reagent-grade water (< 1 ng/1 mercury).
Ultra-clean sample handling
mandates that the mercury concentration
of all reagents, gases, water, and room
air be known at all times and that
corrective action be taken if levels
become excessive. Often, reagents can
be used off the shelf or purified to the
point that they contribute less than 10
percent to the total signal obtained from
natural pristine samples. Gases can be
purified by passing them through gold
31
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32
National Forum on Mercury in Fish
traps prior to use. Some temperature-
resistant reagents (e.g., sodium chloride
(NaCl)) can be purified by heating to
>500 "C, whereas others (e.g., stannous
chloride (SnCl2) solution) can be
purified by purging with low mercury
nitrogen.
For water samples, the best
materials are hot-acid-cleaned Teflon®,
borosilicate glass, or quartz (Bloom,
1995). For temporary contact, acid-
cleaned hard plastics such as polycar-
bonate may be used, but specific items
should be tested for mercury contamina-
tion prior to use. Soft plastics such as
polyethylene and Tygon® should be
avoided. These materials allow diffu-
sion of gaseous mercury and are diffi-
cult to clean. Biota samples are col-
lected in polyethylene bags or
acid-cleaned glass jars with Teflon®
liners.
Handling of samples is undertaken
with the aim of maintaining a
"cleanroom" environment around the
samples at all times. In the clean
laboratory, this is relatively easy. The
major concern is to handle all containers
while wearing cleanroom gloves, and to
change gloves whenever they have
touched something that is not ultra-
clean. Except when samples are being
transferred for analysis, they should be
tightly capped to avoid diffusion of
mercury into the bottle (Gill and
Fitzgerald, 1985).
For field collection, a technique
called "clean hands-dirty hands" is
employed (Bloom, 1985; Fitzgerald and
Watras, 1989). The process starts in the
cleanroom, where the sample containers
are cleaned and double bagged. In the
field, the sample container is withdrawn
from the box by the person designated
"dirty hands," who opens the outer bag
only. "Clean hands," wearing a fresh
pair of cleanroom gloves, reaches into
the bag carefully, opens the inner bag,
and withdraws the bottle. "Clean
hands" then opens the bottle, pours the
acidified ultra-clean water out of the
bottle, rinses the bottle and cap with
sample water, and collects the sample.
The lid is replaced tightly, and the bottle
is returned to the inner bag. "Clean
hands" reseals the inner bag, and "dirty
hands" reseals the outer bag. The
samples are then returned to the labora-
tory or some other stable, clean area for
preservation.
Aqueous samples to be analyzed
for total mercury or methylmercury may
be stored longer than 4 months if
acidified with hydrochloric acid (HC1
(0.5 percent v/v)) and kept in the dark.
Aqueous samples to be analyzed for
methylmercury only, and all biota
samples may be stored frozen indefi-
nitely. Long-term storage should be in
Teflon® bottles, with the caps screwed
on very tightly using a wrench. Samples
stored in containers with loose lids or
made from polyethylene may gain a
mercury level through diffusion. For
short periods (days-weeks), aqueous
samples may be stored unpreserved in
Teflon® bottles. This allows better
preservation of the in situ speciation of
the labile chemical and physical mer-
cury speciation.
Analytical Methods for
Mercury Speciation

Because of the low detection limits
required, most ambient aquatic mercury
measurements are performed using
similar techniques, as was illustrated in
a recent intercomparison exercise
(Bloom et al., 1995). Almost univer-
sally, mercury is detected by one of the
three cold vapor atomic spectroscopic
methods—atomic absorption (AA),
atomic fluorescence (AF), or atomic
emission (AE). Until recently, AA was
by far the method of choice for mercury
determination due to its low detection
limits and simplicity of design. In the
past decade, however, many laboratories
have switched to AF, which offers a
wider linear range and is less prone to
interferences (Bloom and Fitzgerald,
1989). AF also offers an approximate
102 reduction in detection limit, thus
allowing the quantification of individual
mercury species, which in water might
exist in the pg/1 range. Although
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Conference Proceedings
33
sensitivity is not a limiting factor in
tissue analysis, the use of a more
sensitive detector allows the use of
smaller samples, thus reducing matrix
interferences.
To obtain sufficiently low detec-
tion limits (<0.1 ng/1) to quantify
mercury in ambient aqueous samples, a
large aliquot (50-1000 ml) is processed
and the mercury content preconcentrated
prior to injection into the detector. For
total mercury, this involves converting
all mercury present to volatile Hg°, and
then purging onto an amalgamation trap
(usually gold) for collection (Fitzgerald
and Gill, 1979). The mercury collected
on the trap is then thermally desorbed
into the analytical system as a single,
sharp pulse. Most laboratories now use
the method of bromine chloride (BrCl)
preoxidation (to break down organomer-
curials), followed by SnCL, reduction to
release the mercury (Bloom and Cre-
celius, 1983). Equally effective are
other preoxidation steps bromine (Br2),
potassium permanganate/potassium
chloride (KMnO4/KCl), potassium
chromate/potassiumperoxydisulfate
(KjCrO/K^Og, or ultraviolet (UV)
photo oxidation), or a one-step reduc-
tion, using sodium borohydride
(NaBH4) (GUI and Bruland, 1990).
These methods, when used with either
AA (200- to 1000-ml samples) or AF
(20- to 100-ml samples), have detection
limits that are ultimately determined by
the variability in the reagent blank,
rather than instrumental limitations.
Recently, several direct-purge (no gold
pretrapping) methods have been repor-
ted with detection limits of approxima-
tely 1 ng/1. These methods, while
offering the advantage of greater sample
throughput, have detection limits that
are too high to accurately quantify
ambient aqueous mercury concentra-
tions for research purposes.
Most ambient aqueous methylmer-
cury determinations are made using
aqueous phase ethylation and GC
separation, after a pre-extraction step to
separate the methylmercury from the
natural matrix. The most common
method involves partitioning into
dichloromethane (CH2C12) and then
back into water (Bloom, 1989), but
now, due to its greater simplicity,
accuracy, and reduction of hazardous
chemicals, distillation is becoming
favored (Horvat et al., 1993). To
quantify methylmercury in the ambient
concentration (0.01-1 ng/1) range, the
use of an AF detector is required. The
use of sulfhydryl-impregnated cotton
extraction, followed by traditional
GC/ECD detection of methylmercury as
the chloride, has been documented (Lee
and Mowrer, 1989), but the method
requires considerably larger sample
volumes and longer processing times
and is prone to positive interferences.
Because detection limits are not
critical in the case of biota, more
options are available for analysis. The
most commonly used technique is a
selective digestion method that allows
the determination of total mercury and
inorganic mercury Hg(II) directly, and
methylmercury by difference (Magos,
1971). In this method, the sample is
digested in.a strong alkaline solution,
and Hg(II) is determined by SnCl2
reduction and atomic spectroscopic
detection. If cadmium (Cd) is added
during the reduction, the methylmercury
is reduced as well. Alternately, a two-
digestion procedure may be used, in
which total mercury is determined on a
nitric acid/hydrogen sulfate (HNO3/
H2SO4) digested aliquot (Bloom, 1989),
and Hg(II) determined as above. Meth-
ylmercury is determined by difference.
This method, although it intercompares
well with more chemically specific
methods, is operationally defined, and
the results are thus always clouded by
ambiguity.
The most common technique used
to specifically determine methylmercury
in tissues involves extraction into an
organic solvent and then quantification
of the chloride by GC/ECD (Westoo,
1967). This technique is sensitive and
allows the identification of other niono-
alkyl species, but it risks positive
interferences from other halogen-con-
taining compounds. If methylmercury is
determined using this technique, then an
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34
National Forum on Mercury in Fish
additional digestion for total mercury or
Hg(H) is required. Recently, a method
was developed that allows the positive,
simultaneous determination of both
methylmercury and Hg(II) on the same
digest, using aqueous phase ethylation/
GC separation and CVAFS detection
(Bloom, 1989). This method also
affords the simultaneous determination
of dimethyl mercury, if present. The
sample is digested in a mixture of
potassium hydroxide (KOH) and
methanol, and then a small aliquot is
ethylated to obtain volatile ethyl analogs
of the compounds present. The species
are eluted in the order of dimethyl
mercury, methyl ethyl mercury (meth-
ylmercury analog), and diethyl mercury
(Hg(H) analog). The technique has a
detection limit of approximately 0.5
ng/g, and is not prone to matrix inter-
ferences.
Occurrence of Mercury
Species In Water and Biota

In most aquatic environments,
total mercury ranges in concentration
from approximately 0.5 to 5 ng/1, while
the fish living in those waters might
contain from 100 to 2,000 ng/g. The
methylmercury content of natural waters
is generally about 5-20 percent of the
total (Bloom et al., 1991), whereas in
free-swimming fish, it is approximately
95-100 percent of the total (Bloom,
1992). The methylrnercury content of
natural surface waters is positively
correlated with dissolved organic carbon
(DOC) content (Bloom et al., 1991).
Clear lake water and sea water contain
total mercury of approximately 0.2 to 1
ng/1 and methylmercury of <0.01 to 0.05
ng/1. Brown-colored lake waters often
have total mercury of approximately 2 to
5 ng/1, and corresponding methylrnercury
levels of 0.2 to 0.5 ng/1, while darkly
stained bogs may contain total mercury
>10 ng/1 and methylmercury >2 ng/1.
Most contaminated sites have surprisingly
low aqueous mercury concentrations (5 to
50 ng/1 total mercury, 0.2 to 5 ng/1
methylmercury) due to high particle and
biotic reactivity. Although these concen-
trations appear low given high levels of
localized mercury input, they are suffi-
cient to result in dangerously high meth-
ylmercury levels in fish (i.e., 1,000-
10,000 ng/g).
Recent analyses carried out under
strictly controlled ultra-clean conditions
have indicated that virtually all (>95
percent) of the mercury in the muscle
tissue of free-swimming fish is in the
form of methylmercury (Lasorsa and
Alan-Gil, 1995; Bloom, 1992). Earlier
reports of 10-30 percent inorganic mer-
cury may be biased by low-level Hg(H)
contamination and/or analytical proce-
dures that measure total mercury and
methylmercury or ionic mercury in a
separate analysis, with the remaining
species being determined by difference.
For whole fish, >90 percent is found to be
methylmercury although a general
dilution occurs due to lower mercury
levels in bone and skin. Some organs,
such as the liver, do contain higher levels
of Hg(II) but do not contribute signifi-
cantly to the overall body burden. For
aquatic organisms other than fish, the
mercury speciation varies significantly.
Generally, species such as crabs and
shrimp contain high fractions of methylm-
ercury (70-100 percent), whereas shellfish
such as mussels and clams often contain a
majority of their mercury burden (50-90
percent) as Hg(IT).
References

Bloom, N.S. 1989. Can. J. Fish. Aquat.
Sci. 46: 1131.
. 1992. Can. J. Fish. Aquat. Sci.
49: 1010.
-. 1995. Environ Lab. In press.
Bloom, N.S., and E.A. Crecelius. 1983.
Mar. Chem. 14: 49.
Bloom, N.S., and W.F. Fitzgerald. 1988.
Anal. Chim. Acta 209: 151.
Bloom, N.S., M. Horvat, and CJ.
Watras. 1995. Water Air Soil
Pollut. In press.
Bloom, N.S., CJ. Watras, and J.P.
Hurley. 1991. Water Air Soil
Pollut. 56: 477.
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Conference Proceedings
Fitzgerald, W.F., and G.A. Gill. 1979.
Anal. Chem. 55: 453.
Fitzgerald, W.F., and C.J. Watras. 1989.
ScL Tot. Environ. 87/88: 223.
Gill, G.A., and K.W. Bruland. 1990.
Env. Sci. Technol. 24: 1392.
Gill, G.A., and W.F. Fitzgerald. 1985.
Deep Sea Res. 32: 287.
Horvat, M. 1993. Anal. Own. Acta 282:153.
Lasorsa, B., and S. Allen-Gil. 1995.
Wat. Air Soil Pollut. In press.
Lee, Y.-H., and J. Mowrer. 1989. Anal.
Chim. Acta 221:259.
Magos, L. 1971. Analyst 96: 847.
West66, G. 1967. Acta Chem. Scand.
21: 1790.
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36
National Forum on Mercury in Fish
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38
National Forum on Mercury in Fish
Chromatogram Output from Ethylation/
GC/CVAFS Speciation System
(Bloom, 1989)
1000
750
5 600
JS
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250
5 10
Retention Timo. min
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-------
Conference Proceedings
Analytical Detection Limits for Hg Speciation
method
(typical level)
Au amalgamation/AS
Direct AAS
Direct AFS
Ethylation/CVAFS
Ethylation/CVAAS
GC/ECD
Headspace/CVAFS
LC/CVAFS
water (ng/L)
total
0.5-5
0.05
50
1
methyl
0.01-0.5
0.01
1
0.1
0.5
1
biota (ng/g)
total methyl
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0.01-2
0.001
o'.oos
0.001
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0.05
0.005

0.001
0.01
0.001
0.01
Schematic of Ethyla»ion/GC/CVAFS
System for Hg Spedatum
(Bloom, 19B9)
-------
40
National Forum on Mercury in Fish
Observed Total Hg in Surface Waters 1970 -1990
(Bloom, 1995)
Julian year
Analytical Method Requirements

> Sensitive

Water Fish
Total Hg 0.1 ng/L 0.01 ng/g
Methyl Hg 0.01 ng/L 0.01 ng/g

> Accurate (±10%)

> Precise (±10%)

> Generalizable (Water, Sediment, Tissue)

> Chemically Specif ic (Hg(II), MMHg, DMHg)

> Interference Free

> Non-Contaminating

> Economical
-------
National Forum on
Mercury in Fish
Bioaccumulation of Mercury
in Fish
James G. Wiener
National Biological Service, Upper Mississippi Science Osnter, La Crosse, Wisconsin
This presentation reviews the state
of our knowledge of the uptake,
tissue distribution, and bioac-
cumulation of methylmercury in fresh-
water fish. Environmental conditions or
situations associated with high mercury
(Hg) levels in fish are discussed, and the
range of concentrations in piscivorous
fishes under such conditions is de-
scribed. The toxicological significance
of methylmercury to fish is also exam-
ined.
Exposure to Waterborne
Mercury

In the past decade, the application
of clean techniques for sampling and
handling surface water, wet deposition,
and air, in conjunction with new meth- •
ods for the direct measurement of
methylmercury, have greatly advanced
our understanding of the biogeochemis-
try of mercury. Concentrations of total
mercury (unfiltered samples) range from
0.6 to 4 ng/1 for lightly contaminated
lakes and streams, but might seasonally
be much higher in very humic streams.
In directly contaminated waters, concen-
trations of total mercury vary from
about 5 to 100 ng/1 and are often in the
range of 10-40 ng/1. Methylmercury
concentrations in most oxic surface
waters range from about 0.01 to 0.8 ng
Hg/1. These waterborne concentrations
of mercury are probably much too low
to cause direct toxic effects, either in
adult fish or in the more sensitive early
life stages.
Uptake of Mercury in Fish

Nearly all (95 to 99 percent) of
the mercury accumulated in fish is
methylmercury even though very little
of the mercury present in freshwater
ecosystems exists as methylmercury.
The microbial production of methyl-
mercury by methylation of inorganic
Hg(II) in the environment is conse-
quently a key mechanism affecting
mercury concentration in fish. Fish do
not methylate inorganic mercury within
their tissues although methylation does
occur within the gut. Fish obtain
methylmercury from their diet and
from water passed over the gills.
Inorganic mercury is absorbed much
less efficiently across the gut and gills
and is eliminated more rapidly than is
methylmercury.
The diet is the primary route of
methylmercury uptake by fish inhabit-
ing natural waters, probably contribut-
ing more than 90 percent of the meth-
ylmercury accumulated. The
assimilation efficiency for uptake of
dietary methylmercury in fish is
probably 65 to 80 percent or greater,
whereas about 10 percent of the
methylmercury passing over the gills is
assimilated. In temperate waters, the
accumulation of mercury by fish seems
to be most rapid in summer, when the
41
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42
National Forum on Mercury in Fish
feeding and metabolic rates of fish and
the microbial production of methylmer-
cury are greatest. In the laboratory, fish
readily accumulate high concentrations
of methylmercury from water when
exposed to methylmercury concentra-
tions several orders of magnitude greater
than those in natural waters.
Tissue Distribution and
Retention

Methylmercury rapidly penetrates
and is cleared from the gut and the
gills, binds to red blood cells, and is
rapidly transported to all internal
organs, including the brain. The route
of uptake (gut vs. gill) has little influ-
ence on the distribution of methylmer-
cury among most internal organs and
tissues, except that concentrations in
the gills are much higher after
waterborne exposure (than dietary) and
concentrations in the intestines are
higher after dietary exposure. Concen-
trations of methylmercury are typically
greatest in the blood, spleen, kidney,
and liver in both laboratory tests and
field studies.
There is a dynamic internal
redistribution of assimilated methylmer-
cury among the tissues and organs of
fish exposed to methylmercury in
laboratory and field studies. The
concentrations and burdens (masses) in
the blood, spleen, kidney, liver, and
brain decrease after exposure to either
waterborne or dietary methylmercury
ceases, and skeletal muscle is the
primary "receiver" of the redistributed
methylmercury. Most of the methyl-
mercury in the body eventually accumu-
lates in muscle, bound to sulphydryl
groups in protein, even though concen-
trations are usually less in muscle than
in other tissues.
Fish do not readily eliminate
methylmercury. Estimated half-reten-
tion times of methylmercury in freshwa-
ter fish typically range from about 0.5 to
2 years. In some studies, there has been
no measurable excretion of methylmer-
cury from fish.
Effects of Diet, Food-Web
Structure, and Longevity

High concentrations of mercury
are sometimes observed in fish from
waters that lack direct sources of
mercury or conditions, such as low pH,
known to enhance the methylation or
bioavailability of the metal. In particu-
lar, mercury concentrations sometimes
exceed 0.5 or 1.0 ug/g wet weight
(values widely used as criteria in fish
consumption advisories) in the axial
muscle of long-lived, piscivorous fish.
This situation is partly due to the
influence of diet, food-web structure,
and longevity on the bioaccumulation
and concentration of mercury in fish.
Feeding habits and food-chain
structure influence methylmercury
uptake in fish, and piscivorous fishes
usually contain higher concentrations
than coexisting fishes of lower trophic
levels. Methylmercury biomagnifies in
aquatic food chains. In addition, the
fraction of total mercury that exists as
methylmercury in aquatic organisms
increases progressively from primary
producers to fish.
The structure of aquatic food webs
can influence mercury concentrations in
fish, particularly in species that are
typically piscivorous. For example,
lake trout Salvelinus namaycush and
northern pike Esox lucius have higher
mercury concentrations when forage
fish, such as rainbow smelt Osmerus
mordax or perch (Perca sp.), are
present. Concentrations in northern pike
in a Finnish lake lacking forage fish
were about one-fourth those in northern
pike in similar, nearby lakes with forage
fish.
Mercury concentrations in a fish
species within a given water body
generally increase with increasing age or
body size, partly because the rate of
uptake greatly exceeds the rate of
elimination. In addition, the methyl-
mercury content of the diet of some
fishes, particularly those which are
partly or totally piscivorous as adults,
increases as the fish grows larger. In
lake trout, for example, the rate of
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Conference Proceedings
43
mercury accumulation increases greatly
when the fish become large enough to
switch from a diet of invertebrates to
forage fish.

Effect of Lake Size

Lake size and temperature affect
the bioaccumulation of mercury in
fish. In northwestern Ontario, the
mean concentrations in axial muscle
of walleyes Stizostedion vitreum and
northern pike ranged about 0.7-1.1
jig/g wet weight in small (89-706
hectare) lakes but were less than 0.4
ug/g hi nearby, larger (2,219-34,690
hectare) and colder lakes. Specific
rates of mercury methylation in the
lakes were positively correlated with
water temperature, whereas specific
rates of methylmercury demethylation
(by microbes) were negatively
correlated with temperature. Scien-
tists attributed the differing mercury
concentrations in fish among the lakes
to temperature-related variation in
the microbial production of methyl-
mercury.
Point-Source Pollution

Many surface waters have been
contaminated by direct discharges of
mercury from point sources, including
chloralkali plants, pulp and paper mills,
and certain other industrial facilities.
Concentrations in axial muscle in
individual piscivorous fishes taken from
these contaminated waters were often in
the range of 1-10 ug/g wet weight, with
mean concentrations in piscivorous
species often hi the range of 1-7 pg/g
wet weight. High concentrations of
methylmercury (1-2.5 ug/g wet weight)
have also been observed in omnivorous
fishes from such waters.
Point-source discharges of mercury
to surface waters have declined in many
industrialized countries since the 1960s
and 1970s. Such reductions were
generally followed by decreased mer-
cury concentrations in aquatic biota. In
some waters, however, concentrations in
fish continued to exceed 0.5 or 1.0 ug/g
wet weight for several years after
mercury inputs were reduced or after
industrial-source plants were inacti-
vated.
Elevated Mercury
Concentrations in Fish

Many conditions can lead to the
bioaccumulation of high concentrations
of methylmercury in fish, including
anthropogenic discharges of mercury to
surface waters, flooding of new im-
poundments, and atmospheric deposi-
tion of mercury to low-pH and humic
waters. The most contaminated
piscivorous fish, with maximum
concentrations in axial muscle of about
5-15 ug/g wet weight, have been
associated with point-source discharg-
ers, such as chloralkali plants. Piscivo-
rous fish from newly flooded impound-
ments have maximum concentrations in
muscle of 3-4 ug/g wet weight or
greater. In piscivores from low-pH or
humic lakes, axial muscle generally
contains from 0.5 to 2 ug Hg/g wet
weight.
Gold Atoning

Gold-mining operations that used
the mercury amalgamation process have
caused long-term contamination of
sediment and fish in certain rivers.
Recent gold-mining activities have
caused substantial mercury pollution in
the Madeira River in the Amazon River
basin of South America. Mercury
concentrations in axial muscle of fish
from contaminated sites in the Madiera
River frequently exceeded 1.0 ug/g wet
weight.
Atmospheric Deposition to Low-pH
and Humic Lakes

Piscivorous fish in waters with low
acid neutralizing capacity (<60 ueq/1),
low pH (<6.7), or high humic content
often contain mercury concentrations in
axial muscle in the range of 0.5-2.0 ug/g
wet weight, even in waters far from
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44
National Forum on Mercury in Fish
anthropogenic sources of the metal.
This is a geographically widespread
pattern, observed in largemouth bass
Micropterus salmoides, smallmouth
bass M. dolomieui, walleye, and north-
ern pike. This pattern is also evident in
forage fishes, such as yellow perch
Percaflavescens. The greater accumu-
lation of methylmercury in fish in low-
pH waters has been attributed in part to
greater in-lake microbial production of
methylmercury. In regions of Sweden,
Finland, Canada, and the United States
that have many low-alkalinity and
humic waters, much of the mercury in
fish in remote or semi-remote lakes
seems to be derived from atmospheric
deposition.

Newty flooded Reservoirs

In newly flooded temperate and
subarctic reservoirs, concentrations in
axial muscle of piscivorous fishes often
average 0.6 to 3.0 ug/g wet weight;
maximum concentrations of 2-6 ug/g
can, in some cases, equal or exceed
concentrations in fishes from waters
heavily contaminated by direct
industrial discharges. For comparison,
mean concentrations in northern pike
and walleyes were typically in the
range of 0.20-0.35 ug/g in existing
surface waters before flooding by the
Churchill River diversion in northern
Manitoba, Canada. Nine years after
creation of the La Grande 2 reservoir
(part of the La Grande hydroelectric
complex) in the Canadian province of
Quebec, standardized concentrations of
mercury were 3.0 ug/g wet weight in
70-cm northern pike and 2.8 ug/g in
40-cm walleye; concentrations were
even higher (3.5 ug/g in 70-cm
northern pike) farther downstream, in
an unimpounded section of the La
Grande River. In comparison, concen-
trations in fish from 29 reference lakes
near the La Grande complex were 0.6
ug/g wet weight in 70-cm northern pike
and 0.7 ug/g in 40-cm walleye.
The rapid increase in bioaccumula-
tion of mercury after flooding is due to
the enhanced microbial methylation of
inorganic mercury present in the inun-
dated terrestrial habitats. In subarctic
reservoirs, the magnitude of the increase
in fish-mercury concentration after
flooding is positively related to the ratio
of newly flooded area to preimpound-
ment lake area. Mercury concentrations
in fish might remain elevated for
decades after flooding.
lexicological Implications for
Fish

Methylmercury exerts its most
harmful effects on the central nervous
system, even though other effects have
been observed in laboratory studies. In
the laboratory, long-term dietary expo-
sure to methylmercury has caused
inability to feed, incoordination, re-
duced responsiveness, and starvation.
These symptoms were also observed at
grossly polluted Minamata Bay, Japan,
where severely poisoned adult fish had
concentrations of 8 to 24 ug/g wet
weight in axial muscle.
Fish possess mechanisms to
protect against inorganic mercury, but
seem to have fewer defenses against
methylmercury. Methylmercury crosses
biological barriers (gills, intestines, and
internal cellular membranes) much more
readily than inorganic Hg(II) species.
Unlike inorganic mercury, methylmer-
cury in fish is neither effectively ex-
creted nor bound to metallothioneins.
Storage in the muscle, which seems to
be less sensitive to methylmercury than
other tissues and organs, may serve as
the primary detoxification mechanism
for methylmercury in fish. The binding
of assimilated methylmercury to pro-
teins in the skeletal muscle, even if
incidental, clearly reduces the exposure
of the brain to methylmercury.
The rate of accumulation in fish
seems to affect the toxicity of methyl-
mercury. If it is accumulated slowly,
fish can tolerate higher tissue concentra-
tions of mercury, presumably due to the
internal transfer and binding of methyl-
mercury to proteins in skeletal muscle
(the primary storage site), which de-
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Conference Proceedings
45
creases exposure of the central nervous
system.
The developing fish embryo can be
severely affected by a small quantity of
methylmercury or inorganic mercury.
Methylmercury derived from the adult
female, however, probably poses greater
risk than waterborne mercury for
embryos in natural waters, even though
the amount of mercury transferred to the
eggs during oogenesis is small. In
laboratory bioassays, maternally derived
mercury (both inorganic and methyl)
can adversely affect the survival,
hatching, and development of embryos.
The mercury content of eggs reflects the
maternal exposure history, with the
concentration in the egg increasing
concomitantly with parental exposure
and tissue concentrations.
The primary toxicological effect of
mercury on fish populations—if any, at
observed exposure levels—would
probably be reduced reproductive
success resulting from toxicity of
maternally derived mercury to embry-
onic and larval stages. Sublethal and
lethal effects on fish embryos are
associated with mercury residues in
eggs that are much lower than—perhaps
1 percent to 10 percent of—the residues
associated with toxicity hi adult fish. In
rainbow trout Oncorhynchus mykiss, for
example, mortality of embryos coin-
cided with total mercury concentrations
of 0.07-0.10 ug/g wet weight in the egg,
values less than 1 percent of the tissue
residues (10-30 ug/g) associated with
toxicity in the adult. Furthermore, some
data imply that for some fish popula-
tions, the margin of safety between
harmful and existing mercury residue
levels might be much less for embryo-
larval stages than for adults.
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Fudge, and C.A. Kelly. 1993.
Mercury concentrations in fish
related to size of remote Canadian
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Sci. 50:980-987.
Boudou, A., and F. Ribeyre. 1985.
Experimental study of trophic
contamination of Salmo gairdneri
by two mercury compounds—
HgCl2 and CH3HgCl—analysis at
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Cope. Water Air Soil Pollut.
26:137-148.
Effler, S.W. 1987. The impact of a
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Francesconi, K.A., and R.C.J. Lenanton.
1992. Mercury contamination in a
semi-enclosed marine embayment:
organic and inorganic mercury
content of biota, and factors
influencing mercury levels in fish.
Mar. Environ. Res. 33:189-212.
Putter, M.N. 1994. Pelagic food web
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Grieb, T.M., C.T. Driscoll, S.P. Gloss,
C.L. Schofield, G.L. Bowie, and
D.B. Porcella. 1990. Factors
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Harrison, S.E., J.F. Klaverkamp, and
R.H. Hesslein. 1990. Fates of
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Hecky, R.E., DJ. Ramsey, R.A.
Bodaly, and N.E. Strange. 1991.
Increased methylmercury contami-
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46
National Forum on Mercury in Fish
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St. Louis, V.L., J.W.M. Rudd, C.A.
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Verdon, R., D. Brouard, C. Demers, R.
Lalumiere, M. Laperle, and R.
Schetagne. 1991. Mercury evolu-
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Limnol. Oceanogr. 37:1313-1318.
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Conference Proceedings
47
Wiener, J.G., and D.J. Spry. In press.
Toxicological significance of
mercury in freshwater fish. In G.
Heinz and N. Beyer, eds.,
Interpreting Environmental
Contaminants in Animal Tissues.
Lewis Publishers, Boca Raton,
FL.
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48
National Forum on Mercury in Fish
Elevated Hg Levels in Game Fishes

Concentration (pg/g wet wt.)
Source or
habitat
Range in
means
Range in
maxima
Chlor-alkali plant
1 -5
Newly flooded reservoirs 0.7 - 3
2- 15
2-6
Low-alkalinity lakes
0.5 - 0.9
Source: Wiener & Spry 1995 (data for northern
walleye, largemouth & smallmouth bass)
Mercury Concentrations in
Intoxicated Rainbow Trout
Life stage Tissue
Hg cone.
(yg/g wet wt.)
Juvenile &
adult
muscle
whole fish
9-20
4-30
Embryo
eggs
0.07 - 0.10
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Conference Proceedings
Mercury in Northern Pike Finnish Lakes
(Rask & Metsala 1991)
1.5
O)

D)
^
•i
CD
0.5
Mekkojarvi

Majajarvi
No forage fish
^
9
0 10 20 30 40 50 60 70 80
Total length of pike, cm

Environmental Factors Linked to
High [Hg] in Fish

•Point-source discharges of Hg

% Atmospheric deposition of Hg

• Low-alkalinity or hurnic waters

% Enhanced microbial production of MeHg
Newly flooded reservoirs
Low-pH waters, acidified waters
Wetland ecosystems
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50
National Forum on Mercury in Fish
Biomagnification of MeHg
Australian
marine bay1
N. Wisconsin
lake2
Organisms
Piscivorous fish
Forage fish
Invertebrates
Plants
Water
iHg
(ng/g)
2,300
480
330
65
--
%MeHg
>95
93
45
10
~
(ng/g)
1,000
100
56
30
0.001
%MeHg
>95
>95
29
13
5
1 Francesconi & Lenanton 1992
2 Watras & Bloom 1992; Wiener et al. 1990
Mercury in Piscivorous Fishes

and Their Prey

Forage [Hg] ratio
Piscivore fish (predator/prey) Reference
Lake Trout rainbow
smelt

Walleye y. perch
7.7
6.4
MacCrimmon
etal. 1983

Cope et al.
1990
Bass
y. perch
5.1
Suns et al
1987
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Conference Proceedings
51
Mercury in Oxic Fresh Waters
Mercury fraction
Total Hg (unfiltered water)

Lightly contaminated

Direct Hg sources
Cone, range
(ng Hg/L)
Methyl Hg
0.6 - 4

5-100
(often 10-40)

0.01 - 0.8
(max. 2.0)
Intrinsic Factors Linked to High
[Hg] in Fish
~~^~~~^——————————_i__^
• Diet and trophic position

• Biomagnification in food chains

• Longevity (increased [Hg] with age)
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National Forum on
Mercury in Fish
Mercury in Wildlife
Charles F. Facemire
Senior Environmental Contaminants Specialist, Southeast Region, U.S. Rsh and
Wildlife Service, Atlanta, Georgia
Elevated concentrations of mercury
(Hg) have been found in virtually
all wildlife species. Although
each species tends to handle mercury
body burdens somewhat differently,
some generalities have been observed.
Figure 1 presents a simplified model of
mercury dynamics in birds and mam-
mals. Unlike fish and amphibians,
which may accumulate mercury directly
from their environment, mercury
accumulation in avian and mammalian
species is almost always via ingestion of
contaminated food.
Factors Influencing
Bioaccumulation
As illustrated by
Figures 2 and 3, total mer-
cury body burden is gener-
ally dependent on the type of
food ingested. (We are what
we eat.) Lowest concentra-
tions are usually found in
herbivores. As the diet
shifts toward the aquatic
food chain, concentrations in
body tissues increase.
Consequently, maximum
concentrations generally
occur in top predators within
the aquatic food chain. This
select group includes, but is
not limited to, predaceous
fish, fish-eating birds (including eagles
and ospreys), raccoons (Procyon lotor),
otters (Lutra canadensis), mink
(Mustela visori), and the endangered
Florida panther (Felis concolor coryf).
For example, mean mercury concentra-
tions in liver tissue and feathers from
great blue herons (Ardea herodius;
«=4) collected from a contaminated
area of northeastern Louisiana were
48.9 (range==20.1-109.6) ppm wet
weight (ww) and 27.6 (range=22.4-
33.8) ppm dry weight (dw), respec-
tively (USFWS, unpub. data). The hair
and liver from a Florida panther found
dead in Everglades National Park
contained concentrations of 130 ppm
FOOD
INTERNAL
TISSUES
URINE
Figure 1. Mercury dynamics in wildlife.
53
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54
National Forum on Mercury in Fish
Minamata, Japan
PISCIVOROUS
SEAB1RDS

OMNIVOROUS
WATERFOWL

PREDATORS
OMNIVOROUS
TERRESTRIAL BIRDS

HERBWORUS
WATERFOWL
012345678
Hg in Feathers (mg/kg)
Northwestern Ontario
SCAVENGERS
PISCIVORES
OMNIVORES
INSECnVORES
HERBIVORES
0 10 20 30 40 50 60
Liver Hg Concentration (mg/kg)
Date from Eisler, 1987
Figure 2. Mercury concentrations in birds from
contaminated areas.
Otter
Mink
Fur Seal
Sled Dog
Bobcat
Fisher
Marten
Arctic Fox
Raccoon
Polar Bear
Moose
Woodmouse hi
Opossum I
Bank Vole I
Wolf I
Skunk i
Red Fox p
Muskrat
Caribou
Cottontail Rabbit
Beaver
Roe Deer
White-tailed Deer
Squirrel
_L
_L
J_
_L
o.o
0.5 1.0 1.5 2.0
Mercury Concentration (mg/kg)
2.5
From Wren, 1986
Figure 3. Mercury concentrations in mammals.
dw and 110 ppm ww, respectively
(Roelke, 1990). Florida panthers are
exposed to mercury by eating raccoons
(Roelke et al., 1991). Mercury concen-
trations in raccoons collected in South
Florida range from 1.7 to 95.2 ppm dw
in hair and from 1.5 to 39.3 and 0.3 to
5.4 ppm ww in liver and muscle
tissues, respectively (USFWS, unpub.
data).
Tissue Distribution

In birds, feathers seem to contain
a significant amount of the total body
burden. Monteiro and Furness (1994)
reported that 93 percent of total mer-
cury in the adult Bonaparte's gull
(Lams Philadelphia) after completion
of molt was in the plumage. Mercury
is deposited in feathers as they grow,
and the first feathers developed receive
the greatest amount of mercury
(Braune, 1987). This is most evident in
species such as the Bonaparte's gull,
which have a sequential molt of the
primary feathers (Figure 4). Total
mercury distribution in some avian
species is shown in Figure 5, and it is
evident that there are interspecific
differences as well as differences
associated with age.
There are few data regarding
mercury contamination in amphibians
and reptiles, but the data that are avail-
able show some interesting trends.
Mercury distribution in the tissues of the
American alligator (Alligator
mississippiensis) appears to vary with
liver concentrations (Heaton-Jones,
1993; Figure 6).
In mammalian species (Figure 7),
there seems to be little difference in
distribution regardless of the level of
contamination. Concentrations (relative
to liver concentrations) in tissues of
raccoon collected at Okefenokee Na-
tional Wildlife Refuge, Georgia, which
had moderate mercury loads
(range=0.45-56.0 ppm dw in hair, 0.09-
9.9 ppm ww in liver; USFWS, unpub.
data), were not significantly different
(a=0.05)fromthosenoted in raccoons
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Conference Proceedings
55
fromSanibellsland, Florida, where
concentrations (range=l .2-8.1 ppmdw
and 0.21-2.8 ppmw win hair and liver,
respectively; USFWS, unpub. data) were
considered to be near background for this
species. As noted in Figure 7, the distribu-
tion of mercury in hair and soft tissues of
the Florida panther was somewhat similar
to that of raccoons.
Organic mercury distributions vary
greatly between and within species.
Thompson and Furness (in Monteiro
and Furness, 1994) reported that the
relative proportion of organic mercury
in liver tissue of 12 species of seabirds
varied from 3 percent to 100 percent,
and Norheim (in Monteiro and Furness,
1994) noted that organic mercury
constituted 20 percent to 100 percent of
total mercury in the livers of south polar
skua (Catharacta maccormicki). Or-
ganic mercury content in Arctic tern
(Sterna paradisaed) and Bonaparte's
gull muscle and liver tissues (Figure 8)
was apparently correlated with the
amount offish in the species' respective
diets (Braune, 1987). Virtually 100
percent of the mercury in feathers is in
the organic form.
Few data are available regarding
the distribution of organic mercury in
wild, free-ranging mammals. Virtually
all (99.8 percent) of the mercury in the
pelage of the Florida panther is organic
methylmercury. Distribution in hair and
other tissues of this species is shown in
Figure 9.
Depuration and Metabolism

Bioaccumulation of mercury is a
simple matter; disposal is generally not
as easy. Feathers appear to be the major
route of excretion in avian species.
Much of the dietary mercury accumu-
lated in soft tissues between molts is
mobilized into growing feathers, with
the result that soft tissue concentrations
decrease by more than half in many
species. Over 60 percent of the total
annual loss of mercury in the
Bonaparte's gull occurred during the
autumn molt (Monteiro and Furness,
Figure 4. Mercury concentrations in primaries.
Bonaparte's
Gull
Cory's
Shearwater
Great Egret
(hatchling)
From Monte/ro and Furness, 1994
Figure 5. Mercury distribution in birds.
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56
National Forum on Mercury in Fish
1.5
1.0
0.0
2,0

1.0

0.0
Everglades National Park Alligators
n=!2
Brain Uver Kidney Muscte Scales
Otter WiU Alligators
n=12
Brain Uver Kidney Muscle Scales
Farm-raised Alligators
Brain Uver Kidney Mujcle Scales

From HeatoH-Jiwes, 1993
Figure 6. Mercury distribution in alligators.
zs> p Raccoons, Ofefenofee NWR, GA
OJS
0.0
,2.0
1.6
! 1.0
'-O.S
0.0
Brain Uver Kidney Muscle Half Skin
Raccoons, Sanifie! Island, FL
n=10
Brain Uver Kidney Muscle Hair Skin
Florida Panther
n~7
Brain Uver Kidney Muscle Hair Skin

U.S. FWS, unpublished data
Figure 7. Mercury distribution in mammals.
1994). Other routes of excretion include
the feather sheaths and feces, the latter
accounting for the loss of about 22
percent of total dietary intake in
black-headed gull (L. ridibundus)
chicks. Evidence seems to indicate
that females may eliminate as much as
20 percent of their body burden of
mercury by sequestering it in eggs.
As in feathers, the first egg produced
receives the most mercury. Monteiro
and Furness (1994) reported a de-
crease in egg mercury concentrations
of nearly 40 percent between the
laying of the first and last eggs of
common tern (S. hirundo) and herring
gull (L. argentatus) clutches. The
half-life of mercury in birds appears
to be in the range of 35-90 days
(Stickel, 1971).
Mobilizing mercury into eggs
also might be a major route of excre-
tion for alligators. Heaton-Jones
(pers. comm.) indicated that female
alligators typically have lower body
burdens than males of the species. It
is evident from the data presented in
Figure 6 that alligators are using
some, as yet unknown, mechanism to
prevent excessive mercury buildup in
soft body tissues. Heaton-Jones
(1993) thought that scales might be a
major route of excretion, but he found
very low mercury concentrations in
scales. Joiris et al. (1991) have
proposed that marine mammals are
able to mineralize organic methylmer-
cury into the relatively nontoxic
inorganic form, which accumulates in
the liver of adult animals. This
appears to be what is happening in
adult alligators. Other data regarding
depuration in reptiles and amphibians
are lacking.
The half-life of methylmercury
in mammalian species is extremely
variable, ranging from about 3.7 days
in mice to as much as 74 days in man
(Stickel, 1971). Charbonneau et al.
(1974) reported a 39-day half-life for
methylmercury chloride in blood of
the domestic cat. Most mercury loss
appears to be in the hair, feces, and to
a lesser extent, urine.
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Conference Proceedings
57
Effects of Mercury
Contamination

Often, when dealing with
toxicants, we find that there is a
threshold level below which there are
no observable biological effects.
Methylmercury is among the most
potent known inhibitors of mitotic cell
division (Friberg and Vostal, 1972).
Friberg and Vostal (1972) also noted
that mercury compounds produce
chromosomal aberrations, polyploidy,
and somatic cell mutations. Thus, at
the cellular level, there is apparently
no threshold for methylmercury.
Mortality has been reported in
birds with total mercury concentrations
in liver tissue ranging from 17 (red-
tailed hawk, Buteo jamaicensis) to 752
ppm dw (grey heron, Ardea cinerea;
Eisler 1987). Sublethal effects reported
by Eisler (1987) include adverse effects
on growth, development, reproduction,
blood and tissue chemistry, metabo-
lism, and behavior. Some of these
effects have been noted at dietary
concentrations as low as 0.5 ppm dw
methylmercury (Heinz, 1979). Mer-
cury concentrations ranging from 5 to
40 ppm dw in feathers of adult birds
have been linked to reproductive
impairment (Eisler, 1987).
Laboratory studies using several
species of amphibians have demon-
strated mortality of 50 percent of the test
animals at inorganic mercury concentra-
tions in water ranging from 1.3 to
107 ug/1 (Birge et al., 1979). Concen-
trations of this magnitude are much
greater than those usually encountered
under natural conditions. However, one
should not assume that mercury is not a
factor in the decline of amphibian
populations worldwide.
It is difficult to document cases of
mercury poisoning in wild populations.
In most cases, wild animals seek a
place of shelter and seclusion when ill.
In addition, decay processes are rela-
tively rapid. Thus, dead or dying
animals are rarely found. But, in those
few instances when individual animals
are under a surveillance program, as in
I I Organic

^•i Inorganic
Arctic Tern
Muscle
Bonaparte's Gutt
Liver
Muscle
Liver
From Braune, 1987
Figure 8. Methylmercury in birds.
Ur«r
KUney
liarftnlc

Orymlc
S \
amln
Hfltr
OS. FWS taif»tVifttddata
Figure 9. Methylmercury in panther
tissue.
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58
National Forum on Mercury in Fish
the case of the Florida panther, dead
animals are easily found. In July 1989,
an otherwise healthy breeding-age
female panther was found dead in
Everglades National Park. As previ-
ously noted, mercury residues in hair
and liver were 130 and 110 ppm, re-
spectively (Roelke, 1990). As these
concentrations were well within the
range of those noted in dead domestic
cats during the incident in Minamata,
Japan, the cause of death was listed as
mercury toxicosis. Wren (1986) docu-
ments several cases of mercury
toxicosis in wild animals. Liver tissue
residues varied from 30 ppm in a fox
(Vulpes vulpes), which was observed
staggering and running in small circles,
to 96 ppm in an otter, which was acting
in a similar manner. Mercury concen-
trations in the brains of two domestic
cats, which subsisted on a diet of fish
entrails, small fish, and wild game
meat, were 16.4 and 6.9 ppm at death,
also within the range of mercury-
poisoned cats in Minamata. The be-
havior of both cats was similar: prior
to the onset of convulsions, the cats
frothed at the mouth, jumped into the
air, and ran in circles. Death in most
mammals, including humans, appears
to occur when mercury concentrations
in the brain approach 20 to 30 ppm
(Wren, 1986; Stickel, 1971). However,
mink seem to be the mammalian spe-
cies most sensitive to methylmercury
poisoning. Mink sustained on a diet
containing 5.0 ppm methylmercury
showed clinical signs of mercury
toxicosis within 24 days and died
within 30 days (Aulerich et al., 1974).
Outward clinical signs of methyl-
mercury poisoning, in addition to
those already noted, include incoordi-
nation, vertigo, anorexia, weight loss,
blindness, ataxia, paralysis, convul-
sions, and abnormal vocalization
(Wren, 1986). Internally, severe
lesions of brain nerve cells normally
result from lethal or near-lethal
concentrations (Wren, 1986; Eisler,
1987). Wren (1986) noted a few
factors, including bioaccumulation of
selenium and internal demethylation
of methylmercury to elemental mer-
cury, which may alter the toxicity of
mercury in mammalian species.
Animals as Monitors of
Mercury Contamination

In 1977, a symposium was
convened at the University of Con-
necticut to determine the potential of
wildlife species as models for the
detection and study of the effects of
environmental contaminants (NAS,
1979). Participants generally agreed
that much could be gained from this
approach. In the Southeast Region,
we have been using the raccoon to
assess risk to top predators such as the
Florida panther and red wolf (Canis
rufus) and to monitor environmental
trends. I have spoken with several
individuals or groups that are involved
in monitoring mercury concentrations
in fish, particularly largemouth bass
(Micropterus salmoides). In most
cases, they have stated that there is no
observable trend. Although analysis
of all our raccoon tissue samples is
not yet complete, some data are
available. As noted in Figure 10,
there has been more than a two- to
fourfold increase hi mercury concen-
trations in raccoons from southeastern
Georgia and South Florida.
Summary

Mercury continues to be a serious
threat to fish and wildlife resources, and
the magnitude and extent of mercury
impacts to wildlife might never be fully
elucidated. Although many of the
sources of mercury contamination have
been, or are now being, controlled or
eliminated, it might be several years
before we see any significant decrease in
mercury concentrations in tissues of
wildlife species. In the interim, it will
be to our advantage to try to minimize
future risks by eliminating point source
emissions in addition to cleaning up
presently contaminated sites.
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Conference Proceedings
59
References

Aulerich, R.J., R.K. Ringer, and J.
Iwamoto. 1974. Effects of dietary
mercury on mink. Arch. Environ.
Contam. Toxicol. 2:43-51.
Birge, W.J., J.A. Black, A.G.
Westerman, and J.E. Hudson.
1979. The effects of mercury on
reproduction of fish and amphib-
ians. In J.O. Nriagu, ed., The
Biogeochemistry of Mercury in the
Environment, pp. 629-655.
Elsevier/North-Holland Biomedi-
cal Press, Amsterdam.
Braune, B.M. 1987. Comparison of
total mercury levels in relation to
diet and molt for nine species of
marine birds. Arch. Environ.
Contam. Toxicol. 16:217-224.
Charbonneau, S.M., I.C. Munro, E.A.
Nera, R.F. Willes, T. Kuiper-
Goodman, F. Iverson, C.A.
Moodie, D.R. Stoltz, F.A.J.
Armstrong, J.F. Uthe, and H.C.
Grice. 1974. Subacute toxicity of
methylmercury in the adult cat.
Toxicol. Appl. Pharmacol. 27:569-
581.
Eisler, R. 1987. Mercury hazards to
fish, wildlife, and invertebrates:
A synoptic review. U.S. Fish
Wildl. Serv. Biol. Rep. 85(1.10).
90pp.
Friberg, L., and J. Vostal. 1972.
Mercury in the environment.
CRC Press, Cleveland, OH. 215
pp.
Heaton-Jones, T.G. 1993. Mercury
contamination in the American
alligator (Alligator missis-
sippiensis) in Florida. Report
submitted to Alligator Manage-
ment Section, Wildlife Division,
Florida Game and Fresh Water
Fish Commission, November 30,
1993.
Heinz, G.H. 1979. Methylmercury:
Reproductive and behavioral
effects on three generations of
mallard ducks. /. Wildl. Manage.
43:394-401.
Joiris, C.R., L. Holsbeek, J.M.
Bouquegneau, and M. Bossicart.
15

0
1971-73
1993-94
Southeast Georgia
Hair
Liver Muscle
25

0
South Florida
Hair Uver Muscle
m\97l-73—Bigleretal. 1975
ffl 1993-94—USFWS, unpuAllsfied data
Figure 10. Mercury concentrations in raccoons.
1991. Mercury contamination of
the harbour porpoise (Phocoena
phocoend) and other cetaceans
from the North Sea and the
Kattegat. Water Air Soil Poilut.
56:283-293.
Monteiro, L.R., and R.W. Fumess. 1994.
Seabirds as monitors of mercuiry in
the marine environment. Paper
presented at the 3rd International
Conference on Mercury as a Global
Pollutant, Whistler, British Colum-
bia, July 10-14, 1994.
NAS. 1979. Animals as monitors of
environmental pollutants. National
Academy of Sciences, Washington,
DC. 421pp.
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60
National Forum on Mercury in Fish
Roelke,M.E. 1990. Florida panther
biomedical investigation: Health
and reproduction. Final perfor-
mance report, Endangered Species
Project E-l E-E-6 7506. Florida
Game and Fresh Water Fish
Commission, Gainesville.
Roelke, M.E., D.P. Schultz, C.F.
Facemire, S.F. Sundlof, and H.E.
Royals. 1991. Mercury contami-
nation in Florida panthers. Florida
Game and Fresh Water Fish
Commission, Gainesville.
Stickel,W.H. 1971. Ecologic effects of
methylmercury contamination.
Environ. Res. 4:31-41.
Wren, CD. 1986. A review of metal
accumulation and toxicity in wild
mammals. I. Mercury. Environ.
Res. 40:210-244.
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Conference Proceedings
61
Hg Impacts on ¥isfi & Wildlife

• Reproduction
• Growth and Development
• Behavior
• Blood and Serum Chemistry
• Motor Coordination
• Vision
• Hearing
• Histology
• Metabolism
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National Forum on
Day One: September 27, 1994
Mercury in Fish
Questions and Discussion:
Session One
After each speaker's presentation,
an opportunity for questions and
answers was provided. Time
was also allotted for a group discussion/
question-and-answer session.
Aquatic Biogeochemistry and
Mercury Cycling Model

Dr. Donald Porcella, Electric Power
Research Institute
Blogeochemical Cycling of
Mercury; Global and Local
Aspects

Dr. William Fitzgerald, University of
Connecticut

Q: The global cycle suggests that a
large pan of the cycle is biologically
mediated. How much of this global
cycle is driven by biologically medi-
ated reactions, and how old are these
biological reactions?

Dr. Fitzgerald:
Most metals are involved in
biologically mediated reactions.
These processes have been around for
a very long time. Organisms in
general are not specifically trying to
reduce mercury for a purpose. The
mercury concentrations in water are too
low to turn on the "mer" gene, for
example, in bacteria.

Q: What about mercury in ocean
sediment?

Dr. Fitzgerald:
It is unlikely that open ocean
sediments play much of a role.
Q: Would the way that third world
countries use mercury affect your slide?

Dr. Porcella:
You would see a blip in my curve.

Q: What would be the small effect from
cutting emissions?

Dr. Porcella:
After 30-40 years you would see a
5 percent decrease.

Q (Deedee Kathman, Aquatic Resources
Center): You used a water-based food
web instead ofbenthic. Please com-
ment.

Dr. Porcella:
In the midst of the second phase of
model development, we are in the
process of incorporating a benthic food
web.

Q: Regarding use of coal combustion,
why the drop-off?

Dr. Porcella:
The peaik is caused by mercury use
for precious metal extraction from
Mexico and Central America.
63
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64
National Forum on Mercury in Fish
Mercury Methylation in Fresh
Waters

Dr. Cindy Gilmour, Philadelphia
Academy of Natural Science

Q (Trey Brown, U.S. EPA, Region 4):
Regarding biological disturbance, . . .
does that have an effect on methyl-
mercury?

Dr. Gilmour:
I'm not aware of any studies at this
time.

Q (Alan Stem, New Jersey Department of
Environmental Protection): How much
demethylation takes place in sediment?

Dr. Gilmour:
There is a significant rate of
methylmercury degradation going on in
sediment.

Considerations in the Analysis
of Water and Fish for Mercury

Nicolas Bloom, Frontier Geoscience

Q (Jim Wiener, National Biological
Survey): Regarding the possibility of
using preserved fish samples as a way to
estimate the magnitude of the increase of
mercury levels in fish, would it be possible
to do methylmercury analysis offish
samples as a way of getting around the
preservation contamination problem?

Mr. Bloom:
Possibly, but there is no way to
prove that over 100 years mercury is
stable at room temperature in a mu-
seum. You will have criticism no
matter what. We ran across a case
where somebody wanted to do bird
feathers that were preserved with
mercury chloride. When you have a
really high inorganic mercury-to-
methylmercury ratio, it's hard to quan-
tify the methylmercury.

Q (Rob Reash, American Electric
Power): You've given the fact that
historical mercury levels have been
biased due to contamination of water
samples. How long will it take or where
can we start to look at reliable mercury
data to see the trends showing where
mercury levels have been and where
they're going in surface waters?

Mr. Bloom:
Start in the late 1970s. Even
today, you only have the option to use a
peer review process to identify which
data sets are acceptable. Most data
collected routinely in the country are not
acceptable.

Q: Looking at larger fish, have you
recognized a variance in parts of the body
that may be carrying a body burden of
mercury? Do you have any recommenda-
tions or ideas on where you might take
subsamples of large fish, given the fact
that with ultra-trace capabilities we are
able to analyze less and less tissue, and
try to side-step this bottleneck that the
chemists get into if they have to grind up
the 5-pound fish? Do you have any ideas
where we can begin to look for a
subsampling technique?

Mr. Bloom:
That depends on the goal of the
project. I advocate taking muscle tissue
samples in the general case, except in the
case where you're doing a trophic study
where you need to have those whole
values as they go up the food chain. Most
mercury-in-fish numbers that are being
monitored are being looked at from the
standpoint of human consumption
advisories, as well as the fact that muscle
tissue is rather homogeneous. (If you take
10 samples of muscle out of a big fish,
you will come up with the same number.)

Q: You didn't present the intercompar-
ison results. Would you mind summariz-
ing those? They were interesting,

Mr. Bloom:
We did an international
intercomparison on mercury speciation
in water. A series of water samples were
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Conference Proceedings
65
collected from a well-mixed lake by
pumping sequentially and then the
samples were sent to laboratories around
the world to measure total and methyl-
mercury. The performance among the
labs was very good. I think 23 or so
laboratories returned results. Of those,
80 percent returned values that were
within 15 percent of the grand mean,
which coincided with the mean estab-
lished at our lab as the reference.

Q (Russell Isaac, Massachusetts Depart-
ment of Environmental Protection): I
am curious about the acids. The resins
•were the apparent reason for the
chloralkali. Sodium-hydroxide-gener-
ated material was the reason for the
water problem. Is that true for the
acids?

Mr. Bloom:
I can't say for sure. My guess is
that these ultrex acids and so forth are
purified using an industrial sub-boiling
distillation procedure. Unless you are
very careful how you apply that proce-
dure, which works extremely well for
nonvolatile metals, it can actually lead
to introduction of mercury into the
sample because of the large surface area
of acid exposed to the atmosphere.

Q: There has been some concern
expressed, in connection with chlori-
nated organic levels in fish, that some
Asian populations eat certain parts of
fish that other people do not consider
edible. Are those pans higher in
mercury than muscle?
Mr. Bloom:
I don't know that for sure. I know
that livers often have a higher mercury
content than muscle, although they don't
make up a very large mass compared to
the muscle. Jim Wiener might be able
to answer that better than I can.

Q: What about polycarbonate bottles?

Mr. Bloom:
They're probably good. The
problem with leaping out into other
kinds of bottles is that doing the ad-
equate storage tests at low concentra-
tions is very expensive. You're prob-
ably better off sticking with something
that you know works, rather than trying
to verify quantitatively that some other
container works. We use polycarbonate
bottles in our lab and anecdotally they
seem to work fine.

Group Discussion/Question-
and'Answer Session

Q (Pam Shubat, Minnesota Department
of Health): I was interested in the
seasonal variation in the mercury levels
in fish that you showed in your models.
What was the magnitude of that varia-
tion, and was it temperature-dependent,
light-penetration-dependent, or what?
Northern lakes, southern lakes, ocean?

Dr. Porcella:
In the model the fish are treated as
a "compartment," so all the mercury is
going into that compartment. The
amount of methylmercury produced
during the year changes with season.
During low temperature parts of the
year, there is not much production of
methylmercury, as I understand it. The
other variable is that the amount of fish
in the compartment also changes
seasonally. There are two things going
on at the same time, and that accounts
for the seasonal variation within the
year. Based on the model results, it
amounts to roughly 10-15 percent
variation over the year. Results were
from northern lakes. I would expect to
see it smoothed down in southern lakes,
but it is difficult to guess because you
have two nonlinear variables going on at
the same time. Biomass is not a fixed
number, and we measure it only once a
year because of the difficulty.

Q (Pam Shubat, Minnesota Department
of Health): Has that variation been
tested? Has anyone gone out and
collected the field data?

Dr. Porcella:
Yes, there is a very good data set
from Davis Creek Reservoir in Califor-
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66
National Forum on Mercury in Fish
nia. Darryl Sloten has collected data,
and they do show a variation in mercury
concentration in a fish compartment
within the year. I couldn't tell you
whether it's on that order or not.

Q (Alan Stem, New Jersey Department
of Environmental Protection): I've
heard some suggestions regarding the
possibility of methylation within fish. I
think these suggestions have come from
some calculations of mass balance,
which don't seem to be able to account
for the amount of methylmercury in the
biomass, given concentrations in the
water column and in the sediment.
Have any of you come across anything
like that or any speculation on the
possibility that it might be true?

Dr. Porcella:
This has been a bit of a contro-
versy. John Rudd raised this issue
based on measuring methylation rates in
fish. It can occur within the laboratory,
but John feels now that it's not an
important process in nature. Using
tracers, which generally free you from
the difficulty of contamination, there is
no evidence of appreciable methylation
or demethylation within the fish.

Q (Jim Wiener, National Biological
Survey): I think there have been some
applications ofbioenergetic models
where the modeler has been frustrated
by his/her inability to get enough
methylmercury into the fish to account
for the amount of mercury mass in the
fish. Some of the estimates of the
assimilation efficiency across the gut in
the earlier models were probably low
based on some of the laboratory-derived
data. But I think some recent applica-
tions ofbioenergetic models have shown
that more realistic estimates of assimila-
tion efficiency are on the order of 65-80
percent or greater. And some of the
estimated assimilation efficiencies used
in early models were as low as 20
percent. That may account for the
difference.

Q (Nicole Jurczyk, Environmental
Science & Engineering): Regarding
crayfish data—and I've had a hard time
finding crayfish data—do you see any
correlation between what's in the
crayfish for total mercury versus small
fish versus large fish? Are they about
the same as what's found in the small
fish, or do you notice that crayfish have
generally more mercury?

Mr. Bloom:
Data are limited, but within that
data set it does appear that crayfish
numbers are similar to small fish data.

Q (Arnold Kuzmack, U.S. EPA, Head-
quarters): You showed your estimate of
the proportion of anthropogenic mer-
cury emissions that were locally- or
regionally-deposited versus globally as
being the result of balancing your mass
balance. So as a residual it would
accumulate all of the errors in the rest
of your estimate. I wondered how
accurate is that? Could it be 20 percent
or 80 percent or 10 percent, rather than
50 percent?

Dr. Fitzgerald:
I think it's a factor of two that you
would have to worry about there. The
mass balance model provides a frame-
work for asking questions. I also wish
to clarify something in Don Porcella's
presentation. When Don was showing
decreases in deposition in Minnesota,
we must bear in mind that this would
reflect what's occurring on a local scale
and may not apply globally. I'm
concerned about mixing local issues
with global issues. Sometimes when a
small piece of the Earth's surface is
considered, it is not surprising to find
mercury deposition to have diminished
over recent times. But I suspect that on
a global scale that is not evident. There
is evidence for gaseous mercury con-
centrations in the atmosphere that may
have been increasing during the same
period of time over the Atlantic. Those
data are somewhat controversial.
Nevertheless, we have in one part of the
globe what appear to be increasing
concentrations, and in another part of
the globe we have decreasing concentra-
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Conference Proceedings
67
tions. We have to resolve the causes of
such variability.

Q (Arnold Kuzmack, U.S. EPA, Head-
quarters): This is significant from a
control strategy point of view since if
you're in an area where your lake
limnology is such that you get high
methylation rates, can you deal with
your problem by limiting regional
emissions, or would that be ineffective?

Dr. Fitzgerald:
I agree completely that you must
resolve local/regional effects in any type
of management strategy. Indeed, if you
could eliminate local deposition in
certain areas mercury concentrations in
fish should decrease.

Q (Russell Isaac, Massachusetts Depart-
ment of Environmental Protection):
Regarding your mercury model, in
looking at some of those variables, is
there something general you could say
about the sensitivity analysis of the
model in terms of helping direct field
investigations? Is the model based on
data from an ecoregion or a particular
part of the country where you wouldn't
necessarily want to extrapolate to
tropical climates?

Dr. Porcella:
In regard to your second question,
the model was developed in northern
Wisconsin and probably applies prima-
rily in that ecoregion for the coefficients
that we've obtained so far. One of the
tasks that I showed is that we are going
to begin to apply the model to Florida
data. It will be an important application
because it will allow us to test how
transferable that model is. We have
applied the model in other lake systems
and it seems to work reasonably well,
but we don't have the kind of data that
we had in Wisconsin to test them on.
In response to your first question,
we've felt that those variables were
important. One of them is pH. It's been
shown to be a factor that correlates with
mercury concentrations in fish. So when
we picked seven lakes, we picked seven
seepage lakes with a range of pH and a
range of DOC (dissolved organic car-
bon). There are other
local conditions that ______
affect mercury
uptake. One is
trophic levels. With
more productive
systems getting the
same amount of
mercury, you'll get
somebiodilution.
The amount of
mercury coming in —————
has an effect on the
response of the system, so you can't
ignore the loading, whether it comes
from the atmosphere or the drainage
system. We think that the amount of
mercury accumulated is to a large extent
driven by local conditions.

Q (Rick Hoffmann, U.S. EPA, Head-
quarters): Relating to sediment, if the
hypoxic zone is a narrow zone where
the methylation is taking place, is that
an important factor to consider when
you're sampling the sediments? In
other words, when you're doing sedi-
ment cores and trying to estimate
methylation, is the hypoxic layer really a
very thin layer or does it vary from
place to place?

Dr. Gilmour:
Yes, it's something important to
consider. When we've looked at depth
profiles of methylmercury in sediment,
the zone where you see high methylation
is generally right near the sediment
surface or within centimeters of the
sediment surface. If you take a bulk
sample that's 10 centimeters down,
you're certainly going to get a different
number than if you sample the top couple
centimeters of sediment. The zone where
methylmercury is highest does vary from
system to system. We generally take the
top 4 centimeters as a rough average,
although it does vary within the 4
centimeters. If you take a very deep
sample, you effectively dilute the meth-
ylmercury concentrations of the surface
sediments in almost every occasion.
**. . . we have in one part of
the globe what appear to be
increasing concentrations,
and in another part of the
globe we have decreasing
concentrations."
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68
National Forum on Mercury in Fish
Q (Mark Armstrong, Arkansas Game
and Fish Commission): You mentioned
in one of your slides the 28-day holding
period that EPA recommends and you
referenced it to your water samples.
Are you aware of anything that docu-
ments the decay of mercury over time
for holding periods for fish? Is that a
reasonable period? Are you aware of
any studies documenting that we need
to consider a [mercury decay rate] in
fish tissue analyses?

Mr. Bloom:
Fish tissues definitely do not
decay in 28 days. Studies to docu-
ment that have not been done because
they're expensive. There is anecdotal
evidence from Finland, however,
from samples that were stored frozen
that gave identical results after 3
years. Your biggest risk in storing
fish is losing water.

Q (Mark Armstrong, Arkansas Game
and Fish Commission): Regarding the
natural background variability that you
observe in fish tissue mercury concen-
trations taken from the same body of
water at the same time at the same age,
there were some age data on yellow
perch presented that were actually
pretty close together. What was the
spread over those same aged fish?

Dr. Porcella:
There was roughly a 10-15
percent coefficient of variation. But if
you went from the same 1-year yellow
perch and looked at it at different years,
you would see differences that were
driven probably by local conditions that
vary between the years; for example, a
drought year.
Bloaccumulation of Mercury in
Fish

Dr. James Wiener, U.S. Fish and
Wildlife Service
Q: How are you going to protect [water-
sheds] when the problem is basically
atmospheric? As managers, we look at
[the atmospheric contribution] and say we
have to build a roof over the place.

Dr. Wiener:
You need to go to your geochem-
ists and atmospheric people and ask
them the same question. I would be
concerned with mercury that's associ-
ated with particulates, for example.
The idea that you have more localized
deposition of certain mercury forms.
You might not want to site something
like an incinerator that puts out par-
ticulate mercury near a system.

Q (John Cicmanec, U.S. EPA): Re-
garding the slide where you contrasted
the marine ocean fish, the body
outside Australia, and the Wisconsin
lake, the top had a concentration of
2300 marine fish and then 1000.
Should we take those numbers literally
or are you just trying to point out the
contrast?

Dr. Wiener:
They analyzed several organisms
within each of those trophic layers, and
what I presented was the arithmetic
mean for the number of groups analyzed.
In marine systems we certainly have
longer food chains than we do in many
fresh waters. And we also have some
very large long-lived fish that are
capable of accumulating high concentra-
tions of mercury.

Q: I've analyzed a lot of prey organ-
isms in a contaminated bay in Texas,
and I don't see this big difference
between the predators and the prey
that you've pointed out for fresh water
and in the Australian case. I've
analyzed a large number of different
prey, and they are all very similar in
concentration to the larger fish for
total mercury.

Dr. Wiener:
It may be that you have lower
trophic levels. You may have a large
fraction of that mercury present as
inorganic mercury.
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Conference Proceedings
69
Q: But why don't you still see that
biomagnification that you're talking
about?

Dr. Wiener:
Methylmercury biomagnifies in
food chains. Inorganic mercury does not
biomagniry. My guess is that your data
would show biomagnification if the
analysis were limited to methylrnercury.

Mercury in Wildlife

Dr. Chuck Facemire, U.S. Fish and
Wildlife Service

Q (Rob Reash, American Electric
Power): Regarding your diagram of
Florida panthers showing methyl-
mercury to be the only form in the
hair, inorganic forms in liver, can you
try to speculate why this distribution
is the way it is? Is it because of
steady state condition—methyl going
to the hair has maxed out, is satu-
rated—or is it just a differential
affinity for various body parts for
different forms of mercury?

Dr. Facemire:
I think it is a steady state equilib-
rium condition, at least in the hair,
because they're constantly exposed.
However, total mercury in the liver, as
in the blood, is made up of both inor-
ganic and organic forms. This is due to
the fact that animals ingest both types.
Methylmercury is easily assimilated into
some body tissues, whereas inorganic
mercury, for the most part, is not. The
liver, blood, and kidneys work to
remove inorganic mercury from the
body via feces and urine. However,
some species appear to compartmental-
ize both inorganic and organic forms
differently. I don't really know why.

Q: I've seen reports of high mercury
levels in beluga whales in the St.
Lawrence River. Is there any evidence
that mercury can accumulate in fatty
tissues of marine mammals, and it has
any affinity for blubber or fatty tissue?
^Methylrnercury is easily
assimilated into some body
tissues, whereas inorganic
mercury, for the most part, is
not."
Dr. Facemire:
No, methylrnercury does not
accumulate in fatty tissues.

Q: Regarding marine fish meal used for
animal feeds, has there been a risk for
populations using that?

Dr. Facemire:
There have been studies looidng at
the impacts. For example there's a lot
of that going into cat food. A study
done in Canada demonstrated Minamata
disease in cats
fed with
contaminated
fish. There is
also a study
where mink
ranchers also
ended up with
contaminated
mink. It has .. . .
caused mortal-
ity problems. It is an important issue.
In Florida aibout 3 years ago someone
bought shark meat from the grocery
store and found 5-7 ppm. Also, tuna has
at various times contained very signifi-
cant amounts of mercury.

Q (Luanne Williams, North Carolina
Department of Environmental Health
and Natural Resources): Pertaining to
the percentage differences that you
referred to regarding the methylmercury
concentrations found in the fetus versus
the mother, are you referring to humans
or other animals?

Dr. Facemire:
It happens in both. As I men-
tioned, one study on humans showed 30
percent more methylmercury in the red
blood cells of the human fetus than in
the mother; however, there was less
mercury found in fetal plasma than there
was in the maternal plasma, but not that
much less. Overall, the fetal blood had
higher levels of mercury than did
maternal blood, so evidently mercury
crosses the placenta! barrier and very
easily.
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70
National Forum on Mercury in Fish
Q (Russell Isaac, Massachusetts Depart-
ment of Environmental Protection): Are
there regional influences that would
account for raccoon numbers?

Dr. Facemire:
Yes. Since the 1970s, for example,
in South Florida particularly, I mentioned
incinerators. Joe Delfino at the University
of Florida has been doing some work
looking at sedimentation rates in and
around some of these incinerators and
finds that there is in fact increased deposi-
tion in the sediments in the nearby areas.
So I think there are local sources that can
account for that.
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National Forum on
Mercury in Fish
Ecological Assessment of Mercuiy:
Contamination in the Everglades
Ecosystem
Jerry Stober
U.S. Environmental Protection Agency, Region 4, Environmental Services Division
Since 1989, mercury has been found
in elevated concentrations in
various biota of the Florida
Everglades, including fish, the Florida
panther, raccoons, wading birds, and
alligators. The State of Florida has
issued a fish consumption advisory due
to mercury contamination, banning or
restricting the consumption of large-
mouth bass and other freshwater fish
from 2 million acres encompassing the
Everglades and Big Cypress National
Preserve (Figure 1). Although highest
in the Everglades, mercury contamina-
tion in Florida also occurs in largemouth
bass in many other lakes and streams
across the state. Mercury in its most
toxic form, methylmercury, accumulates
in aquatic life and may pose increased
risks to consumers at the top of the food
chain (birds, mammals, and humans).
Scientists currently know little
about the sources, extent, transport,
transformation, and pathways of mer-
cury in South Florida ecosystems.
Possible mercury sources hi South
Florida include natural mineral and peat
deposits, atmospheric deposition (global
and regional), fossil fuel-fired electrical
generating plants, municipal waste
incinerators, medical laboratories, paint,
and agricultural operations. None of
these individual sources, however,
appears adequate to explain the vast area
apparently contaminated.
The Region 4 Regional Environ-
mental Monitoring and Assessment
Program (R-EMAP) study will identify
and coordinate research, monitoring,
and regulatory efforts to address this
issue, using EPA's ecological risk
assessment framework. The study
focuses on the Everglades ecosystem,
which is composed of the largest deposit
of near-neutral peat in the world and
encompasses a region about 60 km wide
by 160 km long (9,600 km2) from south
of Lake Okeechobee to Florida Bay. The
Study Area
Figure 1. Study area.
71
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72
National Forum on Mercury in Fish
study area includes the Everglades
Agricultural Area, three Water Conserva-
tion Areas including the Loxahatchee
National Wildlife Refuge, Big Cypress
National Preserve, Everglades National
Park, and other areas drained for urban
and agricultural development, resulting in
massive hydrologic modifications.
Seven policy-relevant questions have
been identified to guide the development
of this complex research and monitoring
effort:
• What is the magnitude of the
problem? What are the current
levels of mercury contamination in
various species? What ecological
resources of interest are being
adversely affected by mercury?
• What is the extent of the mercury
problem? What is the geographic
distribution of the problem? Is it
habitat-specific?
• Is the problem getting worse,
getting better, or staying the same?
• What factors are associated with, or
contribute to, methylmercury
accumulation in sensitive re-
sources?
• What are the contributions and
importance of mercury from
different sources?
• What are the risks to different
ecological systems and species
from mercury contamination?
• What management alternatives are
available to ameliorate or eliminate
the mercury contamination prob-
lem?
The Region 4 R-EMAP project is
focused on the first four questions above
and will initiate an ecological risk assess-
ment process. The project will integrate
and coordinate the efforts of various state
and federal agencies, including EPA's
Office of Research and Development and
Region 4 Envkonmental Services Divi-
sion; Florida's Department of Envkon-
mental Protection, Freshwater Game and
Fish Commission, Department of Health
and Rehabilitative Services, and South
Florida Water Management District; the
U.S. Army Corps of Engineers; the U.S.
Geological Survey; and industry repre-
sentatives. Dr. Ron Jones of the South-
eastern Environmental Research Pro-
gram at Florida International University
is cooperating closely with both the
Everglades National Park and Region 4
on this R-EMAP project.
Cycling of Mercury in the
Everglades System

Significant quantities of mercury
cycle through the air, water, and solid
phases of the global environment. Mer-
cury cycling through the atmosphere is
estimated at 6 billion grams per year.
Within this global background, certain
regional areas may have higher atmo-
spheric background concentrations due to
nearby urban or industrial activity. In
South Florida, the operation of solid waste
incinerators and fossil fuel power plants
has increased since 1940. It is possible,
therefore, that regional atmospheric
mercury might also have increased over
this time period. Figure 2 depicts atmo-
spheric deposition of mercury from urban
sources into the Everglades. Figure 3
shows a conceptual model of the bio-
geochemical cycling of mercury in the
Everglades ecosystem.
Activities

The Region 4 R-EMAP study is
designed to answer questions that focus
on the extent, magnitude, and trends of
the mercury problem, as well as to
provide information for the initial phase
of the ecological risk assessment process.
All the activities are part of a larger
interagency effort to study mercury
contamination in the Everglades. Habitat
types that will be sampled include canals,
ponds, sloughs, wet prairies, sawgrass
marsh, and hammocks/tree islands. Canal
sampling was carried out in September
1993, May 1994, and September 1994.
Four marsh transects that cross nutrient
gradients were sampled during April
1994. Seven canal structures have been
sampled biweekly since February 1994,
and the random marsh grid sampling is
scheduled to begin in spring 1995.
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Conference Proceedings
73
Figure 2. Atmospheric deposition of mercury from urban sources into the Everglades.
1. Global and regional
atmospheric input
Hg°, Hg", MeHg
4. Evasion Hg° nitrogen and phosphorus
9. Critical path analysis
(birds and mammals, etc.)
3. Surface inflow
Hg", MeHg
2. Peat soils
Hg", MeHg
Outflow Hg ,
MeHg transport
on/-^ -Nitrogen and-, • * '
Idemethylation J"^ ..... ", phosphorus ^
^.
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74
National Forum on Mercury in Fish
study. Finally, the Region 4 R-EMAP
study and other projects are jointly
developing analytical capabilities to allow
researchers to measure mercury at the
parts per trillion level in water and air.
Technical Approach

The Region 4 R-EMAP study will
test a number of hypotheses regarding
mercury contamination in the Everglades
ecosystem. These include the following:
• Mercury concentrations are
significantly increased by human-
induced (global and local) releases
to the air and subsequent wet/dry
deposition to the Everglades
ecosystem.
• The Everglades Agricultural Area
is loading the downstream Water
Conservation Areas and the
Everglades National Park with
mercury and/or methylmercury.
• Eutrophication of the Everglades is
resulting in conditions conducive
to the methylation of mercury of
geologic origin in peat soils.
The Region 4 R-EMAP results and
findings will provide a basis for defining
an ecological risk assessment of the
impact of mercury on the entire system, as
well as on selected rare and endangered
species. This assessment will help
researchers determine the factors and
processes to be incorporated into a
mathematical model of the mercury cycle
in the Everglades ecosystem.
Sampling Site Selection and
Indicators

Region 4 R-EMAP scientists are
using a random, probability-based
sampling strategy based on the EMAP
approach. The strategy is designed to
be integrated with the assessment
strategy of the South Florida Geo-
graphic Initiative, a Region 4 program
to address crucial environmental issues
in South Florida. The sampling grid is a
7x7-fold enhancement of the EMAP
base grid, resulting in a distribution of
points across the entire 9,600 square-
kilometer study area. The distance
between the individual points with the
full grid density is about 4 kilometers,
with a hexagonal area of about 13
square kilometers around each grid
point. Grid points in the Everglades
Agricultural Area, Water Conservation
Areas, and Everglades National Park
have an equal probability of inclusion.
The intensity of sampling will be
decreased in the areas outside this
primary study area.
Analytical Methods

To determine the sources and
fluxes of mercury in the Everglades
ecosystem, the investigators need to
measure mercury accurately at ultra
trace levels (parts per trillion) in air,
water, sediment, soil, and fish tissue.
To accomplish this, researchers will use
a technique called automated cold vapor
atomic fluorescence spectrometry.
The study employs "clean"
sampling protocols for air and water
to prevent contamination of the
samples during the collection, trans-
port, and storage phases. "Clean"
protocols for laboratory analysis of
total mercury and methylmercury in
air, water, soil/sediment, and tissue
are also being developed by related
projects.
Initial Results

The federal Central and South
Florida Rood Control Project (C&SF)
has sectioned the historic Everglades
with a system of canals and levees to
control water for urban and agricultural
development, resulting in pronounced
hydrologic modifications to the natural
system. As a part of this comprehensive
ecological risk assessment of mercury
contamination in the Everglades ecosys-
tem, a pilot study of canals was initiated
in September 1993 to determine the
extent and magnitude of total mercury
and methylmercury in water, sediment
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Conference Proceedings
75
and fish (Stober et al., in press). A
probability-based random sampling grid
was used to obtain consistent estimates
of mercury contamination over this large
geographic area. Two hundred canal
sampling locations were selected as
probability samples by associating grid
points on the sampling frame with
specific canal sections for independent
sampling cycles. Of this number, 50
locations were randomly selected for
sampling in this pilot study. The
selected canal points were sampled from
north to south during a 6-day period.
Cumulative distributions with 95
percent confidence intervals were
calculated and used to determine a canal
system median concentration for se-
lected water, sediment, and fish con-
stituents. The percent exceedance of
each median, by hydrologic subarea,
was determined to demonstrate the
existence and direction of spatial
gradients in the system. North to south
(high to low) gradients were apparent
for total phosphorus, sulfate, dissolved
organic carbon, conductance, total
mercury, and methylmercury in water.
However, the gradients were reversed
from south to north for total mercury in
sediments and fish (Gambusia sp.). The
greatest mercury concentrations in
Gambusia sp. occurred in the same
canals where largemouth bass had
previously been found to be most
contaminated. Additional information
collected during subsequent sampling
efforts will be reported as analyses and
interpretations are completed.
References

Stober, Q.J., R.D. Jones, and D.J.
Scheldt. In press. Ultra trace level
mercury in the Everglades ecosys-
tem, multi-media canal pilot
study. /. Water Air Soil Pollut.
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National Forum on
Mercury In Fish
Atmospheric Deposition Studies
in Florida
Thomas Atkeson
Florida Department of Environmental Protection, Tallahassee, Florida
We (the Florida Department of
Environmental Protection)
found an unusual thing on the
Chapola River, a panhandle river west
of Tallahassee. It had more mercury
than we thought should be there. It led
several of us from the agencies on a
long-term monitoring program around
the state to see if there were excessive
levels of mercury in Florida. We really
didn't find much until we got down into
the Everglades region, where fish
sampled from a variety of spots aver-
aged about 2.5 parts per million (ppm)
total mercury in the edible portion of
largemouth bass.
In about 1 million acres of the
Everglades—a large part of it compris-
ing water conservation areas 2 and 3 and
Everglades National Park—there was
mercury in the edible portions offish
exceeding 1.5 ppm. And in two sepa-
rate drainage areas, the Locksahatchee
National Wildlife Refuge and Taylor
Creek, the mercury concentrations were
somewhat lower, averaging a bit above
1 ppm.
Florida is a state with active
media, and they jumped on this story
and kept it on the front pages for 2
years. It certainly generated a lot of
attention among the agencies. It led us
eventually to work our way around the
state to describe the problem more
carefully. Today, most of the water
bodies of South Florida—particularly
the Everglades, where the problem is
worse—have come under these health
advisories. A number of waterbodies
are okay, such as Lake Okeechobee, and
typically these are the waterbodies in
Florida that are most "polluted" by
traditional standards. A smattering of
lakes and rivers from central Florida to
the Big Bend area and all the way out to
the panhandle are covered by these
health advisories. At least 1 million
acres of surface waters here are under
health advisories, and about another
million acres scattered about the state.
So, it is an extensive problem in our
state, defined by a threshold of 0.5 ppm
that results in the lower level of the
advisories being issued.
This issue has generated skepti-
cism. Mercury levels baffle experts.
Do we really know what we think we
know? There is also a good bit of
criticism of the response of government
to it. This sort of criticism gets a
response. Part of the response is to try
to fill some of the knowledge gaps in
terms of what is causing the problem
and what we will try to do about it.
We have been gratifyingly suc-
cessful over the last 2-3 years in putting
together an interagency approach to the
problem, destling primarily with four
entities: the Florida Department of
Environmental Protection, U.S. EPA,
the South Florida Water Management
District, and the Florida Electric Power
77
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78
National Forum on Mercury in Fish
Coordinating Group working through
the Electric Power Research Institute.
We are getting into various areas
of research: atmospheric, wetlands,
modeling. We are trying to do all of
this within the context of the ecological
risk assessment framework, trying to
define what outcomes we are interested
in as we look toward sometime being
able to manage the problem in our state.
My talk today will be limited to the
atmospheric part.
Why are we so interested hi the
atmosphere? We heard earlier speakers
address some of the larger, global
aspects of the mercury problem and how
the manifestation of the problem today
appears to be primarily driven by
atmospheric emissions, long-distance
transport, and deposition. There are
also some peculiarities to Florida. The
southeastern Florida coast has the
highest concentration of municipal solid
waste incinerators hi the country, five of
them just upwind of the Everglades.
There was a tremendous amount of
attention focused on that issue as soon
as the mercury problem became evident.
Environmentalists dropped dioxin like a
hot rock and used the mercury issue to
hang around the necks of the incinera-
tors.
But it's not at all clear that there is
a one-to-one relationship between the
presence of these incinerators and the
problem in South Florida. First of all,
we should mention that four of the five
incinerators were not even online at the
time we collected the original fish that
resulted in these advisories.
There are also some natural
processes that may have an effect. In
parts of southeastern Florida there is
often as much as 100 inches of rain hi a
year, most of it coming in the summer.
Mercury deposition is dominated by wet
deposition, and I think that in general
mercury deposition is proportional to
total rainfall.
What are the questions that we're
trying to answer with these atmospheric
studies? Into what sort of frame of
reference do you put it? First, if you
think the sort of general process operat-
ing in the environment is an atmo-
spheric one, we have to ask the ques-
tion: Is the problem of the Everglades,
where the problem is disproportionately
severe or unusually severe, caused by
disproportionate atmospheric deposi-
tion? Is atmospheric deposition in
South Florida about the same as it is
everywhere else, or is it higher? Sec-
ond, if it is higher, is this the product of
localized emissions and atmospheric
processes, or is it caused by something
else? Third, if it is not apparently a .
result of atmospheric processes, what is
it? Is it drainage and soil disturbance in
the Everglades agricultural area? Is it
hydroperiod alterations within the entire
Everglades system?
The first project to begin to look
into this, launched about 3 years ago,
was called the Florida Atmospheric
Mercury Study (FAMS). It is designed
to answer primarily one question: Is
mercury deposition in Florida different
from that in other parts of North
America? What are the loadings? I'm
not terribly interested in the atmosphere
as a complex phenomenon in and of
itself. I'm simply interested in it as a
loading term into the aquatic system.
I need to make it clear that I am
reporting on something that is not my
work. Don Porcella and I are project
managers on the various contracts. The
scientists involved are Curtis Pullman,
Gary Gill, and William Landing. The
first objective of the Florida Atmo-
spheric Mercury Study is to measure
mercury loadings into the Everglades
marsh, hi a fairly fine-scale, temporal,
and spatial way. We do this in compari-
son to a marine background site: is there
a difference between what we see
coming in off the Atlantic as it passes
over the urban area before it is deposited
out into the terrestrial part of South
Florida? Other objectives are to mea-
sure the spatial and temporal variability
in mercury vapor concentrations, to
measure wet and bulk deposition of
mercury species, to measure mercury on
particulates directly, and to take meteo-
rological measurements with which to
correlate all of this. They are doing this
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Conference Proceedings
79
by taking long-term, or monthly,
integrated deposition samples. (This is
done in an unattended and automated
mode.) They are also taking weekly
samples for mercury in the vapor phase
and mercury on particulates. And the
meteorology is being logged continu-
ously while these other instruments are
operating.
Lake Barko in northern Florida, a
small seepage lake, is proposed to be the
site where the mercury cycling model
will be brought to Florida and
re validated under Florida conditions.
This lake has been used in a variety of
hydrological and other atmospheric
surface water interactions. It is a very
well characterized waterbody, generally
similar to the waterbodies in the Mer-
cury in Temperate Lakes Project. So, it
is an excellent place to start to extend
the range of the Mercury Cycling
Model. The monitoring instruments are
set up on a 48-foot tower. We are not
interested in all the mercury that may be
traded around by local surface winds or
locally resuspended dust. We are trying
to look at the regional signatures
impinging on this area, so the tower is
put up high enough away from the
ground-level dust and the bugs and
other things that would contaminate
samples. The pumps, the electronics,
and the control equipment are in a small
portable building at the bottom of the
tower. At the top of the tower, there is a
standard atmospheric monitoring setup
based around an aerokometric sampler,
the workhorse of the acid rain studies.
It is extensively modified to make it
clean enough to take low-level mercury
samples. The dry bucket is not really
used for the mercury sampling, but the
wet bucket is equipped with some
Teflon® funnel/bottle combinations to
collect wet deposition.
A funnel made out of a bottle leads
to a Teflon® tube with a vapor lock into
a Teflon® receiving bottle to collect a
bulk mercury deposition sample. This
device is left out for a full month and
collects all of the rain and dry fall. It is
roughly similar to the way that mercury
monitoring was done in the Nordic
Monitoring Network, which the Swedish
ran for several years. It collects every-
thing that falls, as opposed to the
aerokometrics, which collect wet only.
You can infer something about dry
deposition from any difference that you
might see between these two collection
methods.
In the polycarbonate housing there
are several trains of mercury vapor
sampling equipment. There are silica
glass tubes, some of which have sec-
tions of gold-coated sand. (It's the
standard technique for taking mercury in
the vapor phase.) There are four of
these sampling trains within this hous-
ing, plus a blank. These are cut on one
each week of the month to collect a
long-term integrated sample for each
week of the month, plus a field blank.
On the other side of the tower,
there is a similar polycarbonate housing
piped to the bottom of the tower through
tubing that draws a vacuum through
several open-faced flat filters to collect
mercury in the particulate phase. This is
something that gave them a lot of
problems early on, but they've been
collecting particulate samples for about
a year now. Each one of these filter
systems is cut on sequentially for part of
each week, each of the four weeks of a
month.
These towers are to be located in
nine areais in Florida. We're putting
most of our money and effort into South
Florida to try to get a fairly fine-
resolution spatial picture to see whether
or not patterns of deposition in South
Florida can tell us anything about the
pattern that we see of mercury in fish in
sediments in water. What are the results
of FAMs after it's been in operation to a
limited degree for about 2 years and we
now have over a year at four sites in
South Florida and about 6 months at
another site in North Florida? First,
what are average annual deposition
rates? The one site in North Florida
seized deposition of approximately 10
micrograms per square meter per year.
This is very similar to what you'll see in
other parts of North America. South
Florida, however, is different. The
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80
National Forum on Mercury in Fish
average deposition among the sites'runs
about double that of the site in North
Florida, 20 micrograms per square
meter per year. In South Florida there is
a strong seasonality. Summer deposi-
tion accounts for about 95 percent of the
annual deposition. The rainfall concen-
trations are about 5-fold higher than
they are in the winter, and the amount of
rain is greatly elevated. The summer-
time deposition is exacerbated by both
the quantity of rain and the concentra-
tion of mercury in that rain, which is not
what we expected.
There is little correlation of
mercury with other trace elements that
are being analyzed in these samples.
Dr. Landing is doing extensive analysis
for other ions and trace elements in
these samples to attempt to correlate
these with fingerprints of certain
sources. You can see a clear sea salt
signature, for example, in the samples.
You can see the Sahara dust when it
blows over. You can occasionally see
some influence of other sources. But
these do not correlate with mercury
deposition.
The mercury vapor concentrations
in all of the sites, North and South
Florida, are very ordinary. The average
among all the sites is about 1.6 nano-
grams per cubic meter, plus or minus a
very small amount. The seasonality in
the North Florida site is not significant.
Within the South Florida region we do
not yet have enough sites running for a
long enough period of time to say
whether there are any spatial differences
there or not.
We've also had some other
projects running that are fairly small in
scope. We've been collaborating with
Jerry Keeler, University of Michigan,
who has been heavily involved in the
EPA Great Lakes studies. We've done
some limited monitoring in the urban
area of South Florida to answer the
question very much on people's minds:
Does the area source where 5 million
people live, plus a small number of
point sources—the southeastern coastal
area—contribute significantly to re-
gional mercury deposition out into the
Everglades? This question is frequently
asked. It is difficult to answer.
Jerry takes short-term event
rainfall samples, which allow you to
discriminate sources much better than
the long-term integrated samples of
FAMS. He also takes very high fre-
quency meteorological measurements in
conjunction with that, that allow you to
back-calculate wind trajectories and so
forth. He is doing both gas phase and
bulk mercury sampling. He can use this
to do source-receptor modeling.
The results from Jerry Keeler's
studies do not in all cases lead us to the
same conclusions that we see from
FAMS today. First, Jerry, who works
primarily in Michigan around some very
dirty sites, sees rain concentrations that
blow his mind. Broward County,
Florida, where he's done this work, is a
garden variety industrial area compared
to Detroit and Chicago. Yet rain
concentrations in his samples are as
high as 30-40 nanograms per liter. He
sees source signatures in some of his
samples. He sees some contribution
from wind trajectories in the Tampa Bay
area, and he can see signatures from
some of the individual sources in the
Broward County urban area. However,
the one thing he can't tell, using the
amount of data that he has at the present
time, is whether these sources appear to
be quantitatively significant for the total
long-term deposition.
This leads us to the point that
today there are several paradoxes, or
potential conflicts, among the various
work that we have going on. First, the
urban sampling shows correlation with
sources. The FAMS data, which smooth
out individual rain events, do not show
that these sources can reasonably be
seen to predominate the deposition.
Second, the FAMS marine background
site shows mercury deposition that is
approximately as high as what we see on
the mainland. We have to say that this
blows our minds. We expected to see
relatively clean air coming in off the
South Atlantic and the Gulf and that we
would look at the differences of those
clean air masses as they moved over the
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Conference Proceedings
81
urban area. But the fact is, where
FAMS has seen an average of about 20
micrograms per square meter per year,
in the first few months of the marine
background site you have to estimate an
annual rate of about 17 micrograms per
square meter. It is not much different.
It suggests that there may be some
source in the Caribbean region, some
unusual meteorology going on. No one
knows quite what to think of this.
A third paradox is that in some
sediment work that has shown long-term
increases in mercury deposition to
Everglades soils, The apparent mercury
accumulation rates of those soils, even
at depths where the rates are more
stable, are double to triple the highest
estimates that we have for the atmo-
sphere. This does not add up. I don't
know how we put those two things
together.
The upshot of all of this is that we
are trying to plan to do some coordi-
nated high-frequency sampling with the
higher density monitoring network in
the urban areas of Broward County and
Dade County next summer, involving
Dr. Keeler and the FAMS group. We
want to resolve some of these para-
doxes. We need to get a better answer
to the question of whether or not local
sources in this area are contributing
significantly to deposition in another
area.
South Florida is a good place to
address these questions. Where Jerry
Keeler works in Michigan, his ability to
discriminate sources and try to figure
out what's going on is compounded by
the fact that there are regionally elevated
mercury levels in the industrial heart-
land of America. Regardless of the
wind trajectory impinging on his
samplers, he is seeing a plethora of
sources and it's hard to separate them.
In South Florida the meteorology is
simpler hi that in the summer the
predominate wind trajectory is coining
from the east and south and there is not
presumably a regionally elevated
background concentration in this area.
What you're seeing is the uncorrupted
marine air coming in off the coast,
picking up whatever it will from purely
local sources. You can try to tease out
the local-scale contributions without the
interference of a regionally increased
background. I look forward to this
project next summer.
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National Forum on
Mercury in Fish
Watershed Effects on Background
Mercury Levels in Rivers
lames P. Hurley
Bureau of Research, Wisconsin Department of Natural Resources, Monona, Wisconsin, and
Water Chemistry Program, University of Wisconsin, Madison, Wisconsin
Water quality in individual
rivers results from both
natural and anthropogenic
influences in the watershed. Concentra-
tions of chemical constituents in a river
water sample reflect a net result of
specific processes such as chemical
weathering, adsorption/desorption to
various organic or inorganic matrices,
sediment resuspension, atmospheric
deposition, or direct point source inputs.
This is especially true for mercury,
which exhibits numerous transforma-
tions in atmospheric, soil, and aqueous
systems. Importantly, the methylated
form of mercury has been shown to
bioaccumulate in the aquatic food chain
and pose a significant risk to human
health. It is thus important to assess
factors that affect transformations and
bioavailability of mercury in aquatic
systems.
Our understanding of mercury
cycling in natural waters has been aided
by recent advances in low-level analyses
of total mercury, elemental mercury,
and monomethylmercury. Using these
techniques, investigators are currently
assessing complex mercury water
column cycling processes in lacustrine
systems. Specifically, a detailed study
of mercury cycling in lakes in northern
Wisconsin has helped identify pathways
and processes responsible for mercury
bioaccumulation through the food chain
(Watras et al., 1994). By using a mass
balance approach on seepage-type
(precipitation and groundwater-domi-
nated) lakes, investigators have identi-
fied that atmospheric deposition of
mercury was the predominant external
source of mercury to the lake, and that
this input was sufficient to account for
all of the mercury present in lake water,
seston, fish, and sediments (Fitzgerald
and Watras, 1989). This type mass
balance helped in understanding the
unusual observation of elevated levels
of mercury in fish from waters remote
from point sources. The mass balance
also identified significant internal
recycling of mercury. In predatory fish,
the predominant form of mercury
accumulating in fish tissue is in the
methyl form. In atmospheric deposi-
tion, methylmercury was low, typically
in the range of 1-2 percent or less of
total mercury (Fitzgerald et al., 1991).
Significant internal cycling and bio-
transformations were responsible for
conversion of total mercury to methyl-
mercury, leading to significant bioacc-
umulation in higher trophic levels. In
summary, these results demonstrated
that a relatively small amount of exter-
nally delivered mercury delivered to an
aquatic system can be rapidly transferred
through the food chain of seepage laikes.
In drainage lakes however, direct
atmospheric mercury sources might not
be the sole source of externally derived
mercury inputs. One must also consider
83
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84
National Forum on Mercury in Fish
riverine sources as input vectors.
Although the initial source of mercury
to some rivers might have been derived
as atmospheric deposition, significant
complexation and transformations might
occur prior to delivery to a receiving
water. The extent of these transforma-
tions may depend on the type of water-
shed that receives atmospheric deposi-
tion. For example, in watersheds that
exhibit high degrees of erosion, sus-
pended particle loads in an erosional
watershed might produce sites sufficient
for mercury sorption and transport. In a
separate watershed, high chloride levels
might be important for complexation
and transport hi the dissolved phase.
For these and related reasons, when
evaluating the importance of specific
transport processes of mercury in rivers,
it is important to limit variables such as
complexity of a watershed during site
selection.
Wisconsin Background Trace
Metal Study

lii 1991, the Wisconsin Depart-
ment of Natural Resources began the
Wisconsin Background Trace Metals

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Figure 1. Mercury in Wisconsin rivers, 1991.
Study. From a regulatory standpoint,
accurate assessment of trace metal levels
in rivers is extremely important when
issuing discharge permits for a given
waterway. The "background" trace
metal values obtained from upstream
river sites helps to determine discharge
levels that are based on dilutional
capacities or nondegradation levels of
receiving waters. Prior to this study,
however, strict adherence to trace metal
clean techniques had not been followed
when obtaining or analyzing the
samples used for calculation of dis-
charge limits.
The fkst phase of this study,
conducted in spring and fall 1991, was
limited to major rivers basins in the
State of Wisconsin. The results for
mercury, summarized by Babiarz and
Andren (1995), suggested that during
high-flow periods hi spring, mercury
levels in the rivers were higher than
during low flow in fall (Figure 1).
Interestingly, all mercury concentrations
measured in these rivers were below 10
ng/Lr1, a level that is at least 5-10 times
lower than the detection limit of previ-
ously used techniques.
Results of the first phase of the
study provided the groundwork for
future phases of the study.
Since site selection in
Phase I was based on
major river basins of the
state; the data produced
did not allow for a true
comparison of effects of
watersheds on trace metal
levels. Therefore, in
Phase II, we chose sites
nearer to headwaters to
enable the comparison.
Sites were chosen to
represent "Relatively
Homogeneous Units"
(RHU, from USGS
terminology) reflective of
individual land use
patterns in a given water-
shed. Sites selected
contrasted land use and
land cover among differ-
ent surficial deposits and
-------
Conference Proceedings
85
bedrock types. Land use/land cover
classifications (based on GIS data of
watersheds) were grouped as Forest and
Wetland, Agricultural/Forest, Agricul-
tural Only, Urban, and Integrator
(Integrator sites were a subset of six
sites from Phase I).
Similar to Babiarz and Andren
(1994), we observed an increase in
mean unfiltered mercury (total mercury)
in spring (7.9 ng/1) over fall (3.5 ng/1)
for all sites in the study. Classification
of sites based on watershed type yielded
interesting comparisons. Although all
site groupings showed an increase in
mercury during spring, major differ-
ences were observed among groups
based on particle partitioning and total
mercury levels (Figure 2). Highest
mean total mercury concentrations were
observed in Urban watersheds during
high flow in spring. Interestingly, the
lowest mean total mercury concentra-
tions were observed in Urban sites (and
Agriculture Only) during base flow in
fall. At Integrator sites, spring to fall
total mercury concentra-
tion differences were
slight and particle parti-
tioning was similar (60
percent and 67 percent in
dissolved form for fall and
spring, respectively).
Perhaps the greatest
difference among group-
ings was that in Wetland/
Forest sites, total mercury
was mainly in the filtered
phase during both sea-
sons. In contrast, in-
creased mean total
mercury levels in agricul-
ture-associated sites were
reflective of a greater
proportion of mercury
associated with particulate
matter.
Watershed yields,
calculated from concentra-
tion, flow, and watershed
area, provide a more
instructive tool than
mercury concentration for
comparison among
watershed types (Figure 3). Greater
differences exist between spring and fall
comparisons due to the inclusion of flow
as a factor in computing yield. The
differences between spring and fall in
Urban sites is particularly noteworthy.
Also important is the three- to five-fold
higher yield from Wetland/Forest sites
when compared to Agricultural/Forest
and Agriculture Only sites. These
observations of differences between
wetland/forest and agricultural sites are
most likely due to difference in organic
matter complexation and transport
among watershed types. In agricultural
areas, mercury deposited by atmospheric
deposition is most likely complexed
with particulate organic carbon in soil
zones. A small proportion probably
leaches through to ground water and
into streams. During high-flow periods,
mercury is mostly transported on the
particulate phase due to erosion. On the
other hand, in wetland zones, mercury is
probably complexed and transported in
the dissolved phase and transported with
90
80 -
•P 30
1 1 Fall 1992 j
Wm Spring 1 993
% as filtered
57%
1

2
Ol
20 -
10 -
80%
77%
37%
41%
49%
79%
50%
67%
60%
o
u.
s
2
bo
2
Land Use Type
Figure 2. Total mercury yields from various Wisconsin watersheds.
-------
86
National Forum on Mercury in Fish
dissolved organic carbon (DOC). DOC
is present at high levels in both surface
and pore waters of wetlands.
During our study, we also col-
lected samples for methylmercury at a
subset of sites. Similar to total mercury,
mean levels were higher in Wetland/
Forest than Agricultural/Forest sites.
Unlike total mercury, however, highest
methylmercury concentrations were
observed during base flow in fall at
Wetland/Forest sites. These observa-
tions are similar to those of St. Louis et
al. (1994) for watersheds in the Experi-
mental Lakes Area of Canada, where
investigators also found greater methyl-
mercury levels in the warmer months in
wetland zones. Their conceptual model
suggests that methylmercury is formed
within wetlands and transported either
downstream or to adjacent lakes. It is
suggested that for lakes that have
wetland influences, in-lake production
might not be the only site for methyla-
tion. Transport of methylmercury
produced within wetlands might be an
important delivery mechanism for
subsequent food chain bioaccumulation
in receiving waters.
A comparison of methylmercury
yield to percent wetland in watersheds
of our Wetland/Forest sites (Figure 4)
20-
15-
10-
5-
I 1 Fall 1992
Spring 1993
% as filtered
57%
49%
79%
50%
67%
60%
5f
o
Watershed Type
•S
Figure 3. Total mercury in Wisconsin rivers.
further shows the effects of wetlands on
methylmercury levels in rivers. During
both spring and fall, a significant
correlation existed between the two
factors.
Summary

The results of the Wisconsin
Background Trace Metal Study have
shown that partitioning and speciation
of mercury in Wisconsin rivers is
strongly influenced by land use and land
cover characteristics of the watershed.
Highest total mercury and methylmer-
cury yields were observed from sites
that passed through wetlands. Transport
of mercury through watersheds is most
likely affected by strong partitioning
with organic carbon. Our observations
of methylmercury yields concur with
those of other investigators and support
the hypothesis that wetlands are net
producers of methylmercury to aquatic
systems.
Acknowledgments

This Wisconsin Background Trace
Metal Study was funded by the Wiscon-
sin Department of Natural Resources,
Bureau of Water Resources Manage-
ment, David Webb, project liaison.
Laboratory analyses were performed by
Christopher Babiarz and Janina Benoit
at the University of Wisconsin-Madison,
Water Chemistry Program.
References

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Total concentrations of mercury in
Wisconsin lakes and rivers. Water
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Fitzgerald, W.F., and C.J. Watras.
1989. Mercury in surficial waters
of northern Wisconsin. Sci. Tot.
Environ. 87/88:223-232.
Fitzgerald, W.F, R.P. Mason, and G.M.
Vandal. 1991. Atmospheric
cycling and air-water exchange of
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Conference Proceedings
87
1.4 -
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continental lacus-
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Rudd, C.A. Kelly,
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Hudson, S. Gherini, R. Munson,
S.A. Claas, K.A. Morrison, J.P.
Hurley, J.G. Wiener, W.F.
Fitzgerald, R. Mason, G. Vandal,
D. Powell, R. Rada, L. Rislove, M.
Winfrey, J. Elder, A.W. Andren,
C. Babiarz, D.B. Porcella, J.W.
10
20
Percent Wetland Area in Watershed
Figure 4. Wisconsin rivers - Forest and Wetland sites.
Huckabee. 1994. Sources and
fates of mercury and methylmer-
cury in Wisconsin lakes. In C.J.
Watras and J. Huckabee, eds,.,
Mercury as a Global Pollutant:
Integration and Synthesis. Lewis
Publishers, Chelsea, MI. In press.
Zillioux, E.J., D.B. Porcella, and J.M.
Benoit. 1993. Mercury cycling
and effects in freshwater wetland
ecosystems. Environ. Toxicol
Chem. 12:2245-2264.
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National Forum on
Day One: September 27,
Questions and Discussion:
Session Two
After each speaker's presentation,
an opportunity for questions and
answers was provided. Time
was also allotted for a group discussion/
question-and-answer session.

Ecological Assessment of
Mercury: Contamination in
the Everglades Ecosystem

Dr. Jerry Stober, U.S. EPA, Region 4

Q (Nicole Jurczyk, Environmental
Science and Engineering): You have
both sediment and Gambusia data?

Dr. Stober:
Yes, we have water, sediment, and
Gambusia data for the canals.

Q (Nicole Jurczyk, Environmental
Science and Engineering): Have you
seen any trends between the sediment
and the Gambusia?

Dr. Stober:
Yes, they seem to co-occur; if
they're [mercury concentrations] high in
sediment, they're high in fish.

Q: What is the difference regarding
sampling between canals and marshes?

Dr. Stober:
I'm showing the first cycle of
canal samples. For the marsh data
we've sampled the transects once, but
the data still remain to be analyzed. I
think we'll be developing a model
specific to the marsh and another model
specific to canals. They are totally
different systems. The canals are
anthropogenic modifications of the
system, which set up a very good environ-
ment for mercury methylation to occur.

Atmospheric Deposition
Studies in Florida

Dr. Thomas Atkeson, Florida Depart-
ment of Environmental Protection

Q (Rick Hoffmann, U.S. EPA, Head-
quarters): I know, that when you worry
about atmospheric deposition for some
nutrients like nitrates, the issue always
arises about dry deposition and the
difficulties in accurately measuring it
(changes on the filters and so forth).
Have you looked at that for the dry
deposition of mercury?

Dr. Atkeson:

One of the other scopes of work
that we have done together (several
states) with the utility industry was to
pull together last spring an expert: panel
on atmospheric processes to try to sort
out: what we know, what we think we
know, and what we'd like to know. The
questions of: what is the speciation of
mercury emission sources, how these
species may change in the immediate
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National Forum on Mercury in Fish
vicinity of the plume, if you will, and
how that translates into both wet and
dry deposition down-field are questions
that are very much open at the time.
As was alluded to earlier by
Dr. Fitzgerald and his global mercury
model, there is sort of a working
assumption that approximately 50
percent of the emissions from a combus-
tion emissions source are mercury in the
vapor phase, which enters the global
circulation and travels long distances.
The other half of emissions may be hi
some more reactive phase—some ionic
mercury species—which would be
susceptible to being deposited locally or
regionally around the source. It has
enormous implications for how you
think about the problem and how you
might ultimately think about the solution
to the problem. However, there is
currently no technique that will allow
you to measure any of these ionic vapor
species. Will Straton is working with
Steve Lindberg to try to develop a mist
chamber sampling technique that would
capture the soluble species from the
atmosphere directly. That work is not
mature enough to report on at the
present time. Also, I'm sure there is a
great limitation in how any of these
samplers would sample those volatile
ionic species or how well they would
mimic natural dry deposition. It may
well be that the difference between what
we see in the mercury accumulation
rates for marsh land sediments (as
opposed to the deposition rates that we
see elsewhere) really relates to the
differing efficiency of vegetation in
scavaging dry deposition out of the
atmosphere as opposed to the very
artificial geometry of these collectors.
That is a central problem in any dry
deposition type of work. There's going
to have to be more work done to try to
develop the appropriate sampling
protocols.

Watershed Effects on
Background Mercury Levels in
Rivers

Dr. James Hurley, Wisconsin Depart-
ment of Natural Resources

No questions
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1
National Forum on
Mercury in Fish
Mercury Toxicfty: An Overview
Tom Clarkson
University of Rochester, Rochester, New York
Methylmercury is the predomi-
nant mercury species compo-
nent in fish and the main toxic
species we are dealing with in this
Forum. Divalent inorganic mercury may
also be important in the toxicology of
methylmercury to some extent. These
inorganic forms are very important in
the global distribution of mercury. I
would also like to talk about the body's
defenses against mercury and tolerance
mechanisms.
Mercury vapor goes into the
atmosphere and stays there for a long
time. The only way it gets back is to be
oxidized to the divalent water-soluble
form, and then it undergoes methylation
and bioaccumulation in fish. Some of
the highest levels of mercury in the
atmosphere must have occurred about 2
billion years ago, before oxygen was in
the atmosphere and before there was any
process of removal. Once oxygen
appeared, it is very likely that cells were
exposed to a divalent form of mercury at
the same time they were exposed to
oxygen.
Maybe it's no coincidence that the
defense mechanisms we have against
oxygen are also involved in the metabo-
lism of mercury. In particular, glu-
tathione plays a very important role not
only in the defense against oxygen but
against mercury itself.
The methylation of mercury
probably occurred a long time ago.
Jernelov, one of the discoverers of
biomethylation, suggested that it was a
detoxification mechanism for those
primitive methanogenic bacteria at that
time— divalent being more toxic. So,
this reaction also may go back to arcane
times.
It is a mystery why methylmercury
bioaccumulates to such a fantastic extent
on the aquatic food chain. (We heard
yesterday it was about a million-fold.)
Fish do not excrete methylmercury, and
that is presumably a big factor in the
accumulation mechanism. But we don't
know why fish fail to excrete methyl-
mercury.
The other interesting aspect of the
bioaccumulation process is that fish are
highly resistant to the toxic effects of
methylmercury. The levels in fish —
about 10 times what we can tolerate —
seem not to affect the performance of
the fish. Why do fish have this very high
level of resistance as compared to us?
Selenium has been suggested, but no
clear factor has been identified to
explain this higher resistance.
Then, of course, the methylmer-
cury gets to us. Methylmercury is
coming from fish into humans, and only
from fish or marine mammals. No
clinical cases of poisoning have resulted
yet from the input from fish in this
manner. The poisoning cases I'm going
to talk about are those which occurred
by accidental exposure to a fungicide or
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National Forum on Mercury in Fish
the release of methylmercury itself in
Japan.
It's clear that humans do have a
tolerance, although much lower than
that offish. It is clear also that the
tolerance does not lie in the ability of
humans to exclude methylmercury.
Methylmercury gets into mammalian
cells very readily. It plays a trick on us.
It combines with the amino acid cys-
teine to form a complex that has a
structure very similar to the large
essential amino acid, methionine. As a
result, it gets a free ride on the large
neutral amino acid carriers into mamma-
lian cells. Since these carriers are
ubiquitous, we can expect that methyl-
mercury will penetrate all mammalian
cells. Of course it crosses the blood-
brain barrier.
So, if we have a tolerance to
methylmercury, it must lie somehow
inside the cell. Once it enters the cell as
a cysteine complex, methylmercury has
the remarkable property of jumping
from one SH group to another with great
speed. There must be SH groups that are
targets inside the cell, but we have not
identified these despite 30 years of
research. There are so many proteins as
potential targets that we haven't been
able to identify a single target with great
confidence.
The good news is that inside cells
is glutathione, which has an SH group
and is present in cells at very high
levels. It's part of our oxygen defense
system. It also combines with methyl-
mercury and in doing so protects the
cell. Moreover, the methylmercury
complex itself is actively secreted out of
the cell on a glutathione conjugate
carrier. So from the point of view of the
cell, it's good news. From the point of
view of the blood-brain barrier, how-
ever, it's not, because the combination
of the cysteine and glutathione carriers
whips methylmercury very handily
across the blood-brain barrier so that it
enters the interstitial tissue of the brain.
Here, the glutathione complex encoun-
ters the extracellular enzyme gamma
glutamyltranspeptidase, resulting in its
hydrolysis and the release of the amino
acid cysteine. This allows the methyl-
mercury-cysteine complex to enter the
brain cells. This might be one explana-
tion for the peculiar finding that meth-
ylmercury seems to be selectively toxic
to the central nervous system. This is a
highly mobile, highly reactive chemical
and why it should just poison the central
nervous system is a bit of a mystery.
But ease of access to the brain might
have something to do with it. Further-
more, many nerve cells have lower
glutathione levels than other mamma-
lian cells in the body, and this may also
contribute to the sensitivity of the
central nervous system.
Another major detoxification
pathway is excretion. Methylmercury
enters the body as a cysteine complex,
forms the glutathione complex intracel-
lularly and is very rapidly and effi-
ciently secreted into bile as the glu-
tathione complex. It travels down the
biliary tree, enters the gallbladder and
again is hydrolyzed back to the cysteine
complex, which is reabsorbed. So we
have a large enterohepatic recirculation.
But some remaining methylmercury
finds its way into the GI tract, where a
group of microorganisms obligingly
demethylate it and form the poorly
absorbed inorganic divalent mercury,
which appears in the feces. Eighty
percent of methylmercury is excreted by
this pathway. It's really quite remark-
able that very few studies have been
'done on the microflora that are respon-
sible for detoxification. The
demethylation by microflora is very
important because it determines the half-
time of methylmercury in the body.
Antibiotics, for example, can affect that
population. It has been shown that if rats
are treated with antibiotics, the half-tune
of methylmercury increases.
The demethylation also occurs in
other parts of the body. We had the
fortunate opportunity, about a year ago,
to examine an autopsy brain from a
female who had been exposed 20 years
ago to methylmercury. We compared
the mercury levels in her brain to those
of a reference brain. Her brain had
mercury levels about 100-fold higher
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Conference Proceedings
93
than normal. And presumably that's
been there for the last 20 years. The
other astonishing thing is that the
mercury is not methylmercury although
she had been exposed to methylmercury;
it's all inorganic. So whether this
inorganic mercury, which clearly must
have been formed in the brain, is a
detoxification mechanism or whether it
itself is exerting some toxic effect
remains a matter of speculation at this
time.
When our defenses fail (as hap-
pened in the Iraq outbreak), terrible
things happen to the brain at very high
doses. Methylmercury in the adult brain
poisons certain areas. It has a focal
effect. The cerebellum, for example, is
affected, but only certain cells are
affected. The visual cortex is affected.
The neighboring cells are totally un-
scathed. This is also another mystery
about mercury. Why is it having this
focal effect?
One theory that's been around for
10 years or more, is that when methyl-
mercury first enters the brain it damages
all the cells. But certain cells, because of
their size and their repair capacity, can
overcome that damage, and these are the
ones that we see surviving. So this
pattern may not represent a property of
methylmercury, but a characteristic of
the nerve cells themselves—those that
can repair and those that cannot repair
this damage.
When this damage occurs, one sees
a fascinating and alarming sequence of
events, as we observed in the Iraq
outbreak. The period of ingestion of the
methylmercury-contaminated bread was
about six weeks. During the intake
period, no signs or symptoms of poison-
ing were experienced. Even after intake
had stopped, the first symptom,
paresthesia, did not appear for another
month or so. This was followed by the
insidious sequalae of more serious
effects such as ataxia, slurred speech
and the constriction of the visual fields.
Indeed, some victims ingested what
would ultimately result in a fatal dose
without any effects, not even stomach
irritation, during the intake period.
As opposed to the focal damage
seen in the adult brain methylmercury
appears to produce widespread damage
to the developing brain. Methylmercury
affects the development process. Prena-
tal exposure is particularly dangerous
because it is affecting a very basic
process in the brain. In a section of a
cortex of a child used as a control one
can see the ordered layers of cells.
However in a badly affected child from
Iraq, one can see that these ordered
layers are grossly disrupted.
There are cellular theories about
how this is happening. One of the
theories is that methylmercury affects
cell division, which is only occurring in
the developing brain. In a study on
neonatal mice where brain development
is still continuing, Sager and her col-
leagues demonstrated arrested cell
division in both sexes. However, at a
lower dose, only the male mice were
affected. This is interesting because in
Iraq it was the male infants who had the
more severe signs and symptoms versus
the female. The basis of this sex differ-
ence is a mystery.
The most susceptible structure
inside the cell is the microtubule system,
which is responsible for cell division, of
the separation of the chromosomes, and
is also responsible for cell movement.
Cell migration is another basic property
in the developing brain that is inhibited
by prenatal exposure to methylmercury.
The tubules are formed by a
treadmilling process. It is believed that
methylmercury combines with the SH
groups in the tubulin subunits and stops
the assembly end. And then, of course,
at the disassembly end the depolymer-
ization continues and the microtubule
disappears.
In conclusion, I do believe mat it is
very important to look into the mecha-
nisms of resistance and tolerance. If we
could understand what the mechanisms
of tolerance; are, we might be able to
understand when these are over-
whelmed. And it might be from this
biological point of view that we answer
the $60 billion question: "At what level
of methylmercury are our bodies safe?"
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National Forum on
Mercury in Fish
Neurobehavioral Effects of
Developmental Methylmercuiy
Exposure in Animal Models
Deborah C. Rice
Toxicology Research Division, Health Canada, Ottawa, Ontario
JA s a consequence of the tragic
£^k outbreaks of human methylmer-
M. Mkcury poisoning in Japan and
Iraq, substantial research effort has
focused on characterizing the develop-
mental effects of exposure to methyl-
mercury in animal models. Most of the
research has been performed in the rat,
including two large interlaboratory
collaborative studies, one in the United
States and one in Europe, in which the
effects of methylmercury were assessed
using a battery of behavioral tests.
Research in the monkey has focused on
characterization of sensory system
impairment produced by developmental
methylmercury exposure, in addition to
assessment of performance on measures
of cognitive function.
Methylmercury developmental
neurotoxicity was first identified in the
mouse by Spyker et al. (1972), who
reported retarded growth and increased
mortality in pups exposed in utero, with
no obvious effect on motor function.
Neurotoxicity was revealed when these
mice were forced to swim, however,
manifested as abnormal swimming
movements and posture. Abnormalities
of various sorts were also observed as
these animals aged, including kyphosis,
obesity, and severe neurological deficits
(Spyker, 1975).
A number of subsequent studies in
rats or mice exposed during several days
of gestation demonstrated gross neuro-
logical signs, changes in activity, or
impairment on simple learning tasks,
sometimes in conjunction with de-
creased maternal or pup weight, or
increased pup mortality (Geyer et al.,
1985; Cuomo et al., 1984; Eccles and
Annau, 1982a, b; Hughes and Annau,
1976; Inouye et al., 1985; Su and Okita,
1976). In a collaborative study involv-
ing six laboratories in the United States,
the effects of 2.0 or 6.0 mg/kg of
methylmercury on gestational days 6-9
were studied on negative geotaxis,
olfactory discrimination, auditory startle
habituation, activity, activity following
a pharmacological challenge, and a
visual discrimination task (Buelke-Sam
et al., 1985). Facilitation of auditory
startle at the high dose of methylmer-
cury was reliably observed across
laboratories, with inconsistent or
minimal effects on activity, pharmaco-
logical challenge, and the discrimination
task, in the presence of overt signs such
as decreased weight gain and delayed
developmental landmarks. Additional
research with a different battery of tests
using a subset of the rats from the U.S.
collaborative study revealed delayed
righting and swimming ontogeny,
decreased activity, and impaired com-
plex water maze performance (Vorhees,
1985).
In a collaborative study in Europe,
dams were exposed to methylmercury in
drinking water during pregnancy and
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National Forum on Mercury in Fish
lactation. Delayed sexual maturity and
impaired righting and swimming ability
were observed in the offspring (Suter
and Schon, 1986). Assessment of
complex learning as measured by visual
discrimination reversal and spatial
delayed alternation revealed increased
response latencies and an increased
incidence of failure to respond during a
trial, with no effect on accuracy of
performance (Schreiner et al., 1986;
Eisner, 1986). In addition, the pattern of
locomotor behavior in a complex
activity monitor differed between
control and methylmercury-treated
offspring, with treated rats exhibiting
less behavioral diversity. In a follow-up
study involving five European laborato-
ries, dams were exposed on days 6-9 of
gestation (Eisner et al., 1988). This
study in general confirmed results of the
previous study with respect to effects on
the spatial alternation and discrimina-
tion task, as well as the altered pattern
of locomotor behavior in methylmer-
cury-treated offspring. In a pair of
studies (Musch et al., 1978; Bornhausen
et al., 1980), rat dams were gavaged
with methylmercury on days 6-9 of
gestation. Offspring were impaired in
their ability to perform a DRH schedule
of reinforcement, in which a number of
responses on a lever were required in a
specified (short) period of time. This
paradigm detected effects at the lowest
dose (0.01 mg/kg) of any study. Little
research has focused on the effects of
methylmercury exposure on sensory
system function in the rodent. In utero
exposure results in changes in cortical
visual evoked potentials (Zenick et al.,
1976; Dyer et al., 1978). Other effects
on performance observed in rodents may
well be due at least in part to sensory
deficits, but this possibility has appar-
ently not been explored.
A considerable amount of research
on the neurotoxicity of methylmercury
has been performed in monkeys. This
was undoubtedly in part a response to
the tragic episodes of human methyl-
mercury poisoning, and the recognition
of the limitation of the rodent as model
of methylmercury intoxication. It is well
established that in the adult human,
methylmercury preferentially damages
the sulci, particularly but not limited to
calcarine fissure. As a consequence, one
of the hallmarks of methylmercury
poisoning in adult humans is constric-
tion of visual fields. The monkey, like
the human and unlike the rodent, has a
brain with deep sulci. Constriction of
visual fields is also observed in adult
monkeys following chronic methylmer-
cury exposure (Merigan, 1980). Other
functional deficits in visual function
have also been documented in adult
monkeys exposed to methylmercury.
Deficits in low-luminance form vision
were detected on a visual discrimination
task; these effects preceded more global
visual deficits (Evans et al., 1974).
Decrements in detection of a flickering
stimulus at low luminance have been
observed in monkeys, that also demon-
strated constriction of visual fields
(Merigan, 1980). Decreased flicker
sensitivity has also been observed in
squirrel monkeys exposed to methyl-
mercury (Berlin et al., 1975). Monkeys
in these studies had blood mercury
levels of 2.0-3.0 ppm. Hypesthesia
(impaired sense of touch), another
typical sign of methylmercury exposure
in adult humans, has also been observed
in adult macaque (Evans et al., 1975)
and squirrel monkeys (Berlin et al.,
1973).
Since it was clear from the episodes
of human methylmercury poisoning that
the developing organism is more sensi-
tive to the effects of methylmercury
intoxication than the adult, much of the
research in monkeys has focused on the
effects of developmental exposure. One
series of experiments was performed at
the University of Washington in macaque
monkeys (Macaco.fascicularis) exposed
to methylmercury in utero (Burbacher et
al., 1988). Females were dosed with 50,
70, or 90 ug/kg/day of methylmercury,
resulting in steady state blood mercury
concentrations prior to breeding of 1.3,
1.6, or 2.0 ppm for the three dose groups,
respectively. Reproductive success was
severely affected at the two highest
doses.
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Conference Proceedings
97
Methylmercury-exposed infants
exhibited impaired memory on a visual
recognition task during infancy
(Gunderson et al., 1986, 1988); perfor-
mance on this task is highly predictive
of later performance on intelligence tests
in humans (Pagan and McGrath, 1981).
At 9 months of age, these monkeys also
displayed retarded development of
object permanence (Burbacher et al.,
1986), which tests development of the
infant's ability to realize that an object
placed out of sight is still present. This
same group of monkeys also displayed a
decrease in social play and an increase
in nonsocial passive behavior when
tested between the ages of 2 and 8
months (Burbacher et al., 1990). In
these studies, none of the infants showed
overt signs of methylmercury toxicity,
including reduced birth weight. In a
follow-up study, this group of monkeys
was tested at 7-9 years of age on a
spatial delayed alternation task (Gilbert
et al., 1993). Monkeys exposed to
methylmercury in utero performed
better than control monkeys during the
initial phases of the experiment, with no
differences between groups by the end
of the experiment.
Studies in this same species of
macaque have also been performed at
the Canadian Health Protection Branch.
One group of five monkeys, presently
19 years old, was dosed with 50 ug/kg/
day of mercury as methylmercuric
chloride from birth to 7 years of age;
blood mercury concentrations during the
period of dosing were approximately
0.75 ppm. When these monkeys were 3
years of age, during the period of
methylmercury exposure, spatial visual
function was assessed under both high
(cone) and low (rod) luminance condi-
tions (Rice and Gilbert, 1982). Treated
monkeys were impaired under both
conditions in the absence of constriction
of visual fields. These monkeys also
exhibited impairment of high-frequency
hearing at the age of 14 years, 7 years
after cessation of exposure to methyl-
mercury (Rice and Gilbert, 1992).
Another study in the same labora-
tory examined the effects of in utero
plus postnaital exposure in the same
species of monkey. Females were dosed
with 10, 25, or 50 ug/kg/day of mercury
as methylmercuric chloride; blood
mercury levels averaged 0.37, 0.75, or
1.42 ppm during pregnancy. One, two,
and five infants were born from the
three dose groups, respectively. One
infant in the high-dose group was born
with signs of methylmercury poisoning
resembling those of human infants,
including motor impairment and nystag-
mus (Rice, 1983). Testing of these
monkeys during infancy and the juve-
nile period failed to reveal cognitive
deficits as measured on a discrimination
reversal task, although treated monkeys
performed differently from controls on
an intermittent schedule of reinforce-
ment (Rice, 1992). This group of
monkeys, including the monkey dosed
at 10 ug/kg/day, showed impaired
spatial visual function when tested
shortly after cessation of methylmercury
exposure at 4 years of age (Rice and
Gilbert, 1990).
When the group of monkeys
exposed only postnatally until 7 years
of age was 13 years old, they began
exhibiting clumsiness not present
previously (Rice, 1989). Further
exploration revealed that treated
monkeys required more time to retrieve
treats than did nonexposed monkeys
and displayed abnormalities on a
clinical assessment of sense of touch in
hands and feet, despite the fact that
routinely performed clinical examina-
tions during the period of dosing had
not yielded abnormal results. These
results are strongly suggestive of a
delayed neurotoxicity manifested, when
these monkeys reached middle age.
This observation was pursued in both
groups of monkeys by objective
assessment of somatosensory function
in the hands: both groups of monkeys
exhibited impaired vibration sensitivity
(Rice and Gilbert, 1994).
The only report of cognitive
impairment in adult monkeys exposed
to methylmercury developmentally is a
study in the squirrel monkey (Newland
et al., 1994), in which monkeys exposed
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National Forum on Mercury in Fish
during the last two-thirds of gestation
exhibited impaired ability to shift
response strategy on a complex test of
repeated learning.
The results from the animal data,
including studies in both rodents and
monkeys, suggest that tests of sensory
and/or motor function are more sensitive
indicators of methylmercury toxicity
than is assessment of cognitive end-
points. It is suggested that assessment of
sensory and motor function be included
in epidemiological studies exploring the
effects of developmental methylmercury
exposure.
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Berlin, M., G. Nordberg, and J.
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Dyer, R.S., C.U. Eccles, and Z. Annau.
1978. Evoked potential alterations
following prenatal methylmercury
exposure. Pharmacol. Biochem.
Behav. 8:137-141.
Eccles, C.U., and Z. Annau. 1982a.
Prenatal methylmercury exposure:
I. Alterations in neonatal activity.
Neurobehav. Toxicol. Teratol.
4:371-376.
Eccles, C.U., and Z. Annau. 1982b.
Prenatal methylmercury exposure:
II. Alterations in learning and
psychotropic drug sensitivity in
adult offspring. Neurobehav.
Toxicol. Teratol. 4:377-382.
Eisner, J. 1986. Testing strategies in
behavioral teratology: HI. Mi-
croanalysis of behavior.
Neurobehav. Toxicol. Teratol.
8:573-584.
Eisner, J., B. Hodel, K.E. Suter, D.
Oelke, B. Ulbrich, G. Schreiner,
V. Cuomo, R. Cagiano, R.E.
Rosengren, J.E. Karlsson, and
K.G. Halid. 1988. Detection limits
of different approaches in behav-
ioral teratology, and correlation of
effects with neurochemical param-
eters. Neurotoxicol. Teratol.
10:155-167.
Evans, H.L., V.G. Laties, and B. Weiss.
1975. Behavioral effects of mer-
cury and methylmercury. Fed.
Proc. 34:1858-1867.
Evans, H.L., V.G. Laties, and B. Weiss.
1974. Behavioral effects of meth-
yhnercury. Proceedings of First
-------
Conference Proceedings

Annual N.S.F. Trace Contami-
nants Conference, pp. 534-540.
U.S. Atomic Energy Commission,
Oak Ridge, TN.
Pagan, J.F., and S.K. McGrath. 1981.
Infant recognition memory and
later intelligence. Intelligence
5:121-130.
Geyer, M.A., R.E. Butcher, and K. File.
1985. A study of startle and
locomotor activity in rats exposed
prenatally to methylmercury.
Neurobehav. Toxicol. Teratol.
7:759-765.
Gilbert, S.G., T.M. Burbacher, and D.C.
Rice. 1993. Effects of in utero
methylmercury exposure on a
spatial delayed alternation task in
monkeys. Toxicol. Appl.
Pharmacol. 123:130-136.
Gunderson, U.M., K.S. Grant, T.M.
Burbacher, et al. 1986. The effect
of low-level prenatal methylmer-
cury exposure on visual recogni-
tion memory in infant crab-eating
macaques. Child. Develop.
57:1076-1083.
Gunderson, V.M., K.S. Grant-Webster,
T.M. Burbacher, and N.K. Mottet.
1988. Visual recognition memory
deficits in methylmercury-exposed
Macaca fascicularis infants.
Neurotoxicol. Teratol. 10:373-379.
Hughes, J.A., and Z. Annau. 1976.
Postnatal behavioral effects in
mice after prenatal exposure to
methylmercury. Pharmacol.
Biochem. Behav. 4:385-391.
Inouye, M., K. Murao, and Y. Kajiwara.
1985. Behavioral and
neuropathological effects of
prenatal methylmercury exposure
hi mice. Neurobehav. Toxicol.
Teratol. 7:227-232.
Merigan, W.H. 1980. Visual fields and
flicker thresholds in methylmer-
cury-poisoned monkeys. In W.H.
Merigan and B. Weiss, eds.,
Neurotoxicity of the Visual Sys-
tem., pp. 149-163. Raven Press,
New York.
Musch, H.R., M. Bornhausen, H.
Kreigel, and H. Greim. 1978.
Methylmercury chloride induces
learning deficits in prenatally
treated rats. Arch. Toxicol. 40:103-
108.
Newland, M.C., S. Yezhou, B.
Logdberg, and M. Berlin. 1994.
Prolonged behavioral effects of in
utero exposure to lead or methyl-
mercury: reduced sensitivity to
changes in reinforcement contin-
gencies during behavioral trainsi-
tions and in steady state. Toxicol.
Appl. Pharmacol. 126:6-15.
Rice, D.C. 1983. Nervous system
effects of perinatal exposure to
lead or methylmercury in mon-
keys. In T.W. Clarkson, G.
Nordberg, and P. Saaer, eds.,
Reproductive and Developmental
Toxicity of Metals, pp. 517-540.
Plenum Press, New York.
. 1989. Delayed neurotoxicity in
monkeys exposed developmentally
to methylmercury. Neurotoxicol.
10:645-650.
-. 1992. Effects of pre- plus
postnatal exposure to methylmer-
cury in the monkey on fixed
interval and discrimination rever-
sal performance. Neurotoxicol.
13:443-452.
Rice, D.C., and S.G. Gilbert. 1982.
Early chronic low-level methyl-
mercury poisoning in monkeys
impairs spatial vision. Science
216:759-761.
. 1990. Effects of developmental
exposure to methylmercury on
spatial and temporal visual func-
tion in monkeys. Toxicol. Appl.
Pharmacol. 102:151-63.
. 1992. Exposure to methylmer-
cury from birth to adulthood
impairs high frequency hearing in
monkeys. Toxicol. Appl.
Pharmacol. 115:6-10.
-. 1994. Delayed somatosensory
deficits in monkeys exposed
developmentally to methylmer-
cury. The Toxicologist 14:259.
Schreiner, G., B. Ulbrich, and R. Bass.
1986. Testing strategies in behav-
ioral teratology: II. Discrimination
learning. Neurobehav. Toxicol.
Teratol. 8:567-572.
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100
National Forum on Mercury in Fish
Spyker, J.M. 1975. Assessing the impact
of low level chemicals on develop-
ment: behavioral and latent effects.
Fed. Proc. 34:1835-1844.
Spyker, J.M., S.B. Sparber, and A.M.
Goldberg. 1972. Subtle conse-
quences of methylmercury expo-
sure: Behavioral deviations in
offspring of treated mothers.
Science 177:621-623.
Su, M.Q., and G.T. Okita. 1976. Behav-
ioral effects on the progeny of mice
treated with methylmercury. Toxi-
col. Appl. Pharmacol. 38:195-205.
Suter, K.E., and H. Schon. 1986. Testing
strategies in behavioral teratology:
I. Testing battery approach. Neruro-
behav. Toxicol. Teratol. 8:561-566.
Vorhees, C. 1985. Behavioral effects of
prenatal methylmercury in rats: a
parallel trial to the collaborative
behavioral teratology study.
Neurobehav. Toxicol. Teratol.
7:717-725.
Zenick, H. 1976. Evoked potential
alterations in methylmercury
chloride toxicity. Pharmacol.
Biochem. Behav. 5:253-255.
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Conference Proceedings
101
O
O
50

10
100/ugHg/gDIET
BODY POSTURE
•TAIL POSITION
HIND-LEG CROSSING
'RIGHTING REFLEX
GAIT
STAYING ON A ROD
HEAD MAINTENANCE
RIGHTING REFLEX
STAYING ON A ROD
31.5^gHg/gDIET

•RIGHTING REFLEX*
•TAIL POSITION
•HIND-LEG PARALYSIS
LIMB POSTURE
10/4 Hg/g DIET
29 36

EXPERIMENTAL DAY
Brain mercury concentrations associated with the appearance of neuroloeical
symptoms m mice exposed to methylmercury in the diet. Exposure stopped after da?4?fbr
*nhTefr^
death. (Reproduced with permission from Suzuki and Miyama (47).)
Biel Maze
- . Soe«0 Trials
*1
Bitl Mazt

Maz» Errors J
14
Maze Times
I'! J
60 i-
~.n l-
-o -
i
30 <-
1
20 1-
1
10 -
r

o
1
1
u
•

a
V
6
r

f
CM
T

a
a
120
i
i
1200J-
100- IOOOH
4

60 1-
4
20

I
o

c
•c
£
e
6
T

a
CM
T

a
o
800

800
4OO
200
-

-
-
'
T

Tl
!

•
J
6
f

a
JC
a
E

1
X

f
a
1

:8^
6 r-

Mean (±SE) swimming performance in a straight channel
.ml in a Biel maze summed across all test trials for errors
. and maze time (right). **p<0,()t. '/>
-------
102
National Forum on Mercury in Fish
DRH2/1
-ar-au-nt
llHC-induced levninc deviations of prenatally treated mate (a) and female (b) nit: percent-
afc* of operant behavior performance in three different test session of toe instrumental conditioning
protram "differential reinforcement of hifh ntes" (DRH). The percental deviations from controls
(-10096) art listed underneath the columns. All data are expressed as group means. Verticil brackets
iadkateSEs.
SUMMARY OF RESULTS OF U.S. COLLABORATIVE STUDY
NCTR battery (6 laboratories) -
2or6mg/kgGD6-9
maternal weight gain
physical landmarks
negative geotaxls
olfactory discrimination
auditory startle habituation
activity (1 and 23 hour)
discrete trial visual
discrimination/reversal
Cincinnati battery
physical landmarks
surface righting
negative geotaxls
pivoting
olfactory orientation
swimming ontogeny
activity
complex water maze
decreased
delayed
no effect
no effect
t high dose
t adult
i correct, high dose all labs combined
delayed
i high dose
no effect
no effect
no effect
delayed
minimal effect, high dose
Impaired, high dose
-------
Conference Proceedings
103
SUMMARY OF RESULTS OF EUROPEAN
COLLABORATIVE STUDIES
physical landmarks
righting
swimming
delayed
impaired
impaired
visual discrimination, delayed
alternation
i latency
4 no-response trials
no effect accuracy
locomotor/exploratory behavior
complex wheel
different pattern of alley entry
June 4. 1964
""July 10. 1968
July 31. 1969
Typical course of concentric constriction, which began with a unilateral deficit of the
temporal crescent
-------
104
National Forum on Mercury in Fish
LEFT EYE
HO 1M
nONKEY 82
Visual field chart for the left eye of monkey 82 that shows how the boundary of
field was determined from the pattern of detections and misses. Tha origin of the polar
represents the center of gaze.
100

70
100

55 "
gj 80

Vj 70
^ 100

|ii 90
80

70
100

70
(B8IGHIEST)
tf^mlanbtrt
(DIMMEST)
2 6 10 14 18 22 26 30

WEEKS SINCE METHYLMERCURY BEGAN

Effecti of a 29-wk exposure to
.uethyimercury on the viiual Hivriminarion
of macaque *81. The doling procedure and
blood Hg concentrations ire shown in Fig. 7.
Testing of some luminances did not begin
until blood concentrations had stabilized.
Symbols are the same as in Fig. 8. The arrows
in the two upper graphs signify a decline to
33% correct (chance). At the time of sacri-
fice in the 31st wk, the monkey had great dif-
ficulty in locating objects visually and finding
its way around the home cage. Motor inco-

to impairment of vision and touch
-------
Conference Proceedings
105
Object permanence apparatus.
monitor camera computer
monkey
periscope
-The apparatus and an example of die itimuli wed
-------
106
National Forum on Mercury in Fish
cnttlou. «K dnta tk> UmkoUt
SoUi kMl Of met dipt nrpmol cntioM o( UmlnUl fcr aanl
CONTROLS
JOCB9 40090 S 10000
035
10000 20900 MOO 40000
XOOO XGOD
0 10000 20000 30000

FREQUENCY(Hz)
20000 WOO 40000
Absolute detection threshold! (SPL (dB)) for control monkeys (top left) and each of five methyl mercury-treated monkeys. For treated
monkeys. X represents the right ear and Q the left. For control monkeys, each symbol represent! an individual: • 06, 0 117, and A 120. Dashed lines
represent the right ear, solid lines the left.
-------
Conference Proceedings
TABLE 1. Time to Complete Raisin Pick-up Test
——————.
Mean Time (sec)
Monkey
Number
—•—™—•»•
Control
06

10
Sex
male
female
female
Mathylmenury Exposed
male
male
male
male
35
36
39
46
34
female
Preferred
Hand
•
14.5
finger broken
straight
14.0
36.0
15.0
21.5
19.8
20.5
Nonpieferred
Hand
•
finger broken
straight
15.0
115.0
25.0*
20.5
37.0
18.0
22.5*
Mann-Whfoiey U test P - 0.047 for each hand.
Comment: Missed raisins; usod more than 2 fingers.
TABLE2. InddenceofNoResponse-onSensoryAssessment (Assessor 1/Assessor2,
Total* Prick Foot FtfckHand
Treated 35
36
39
46
Females
Control 02
10
0/4
2/4
1/1
3/0

0/1
0/1
2/2
0/0
1/0
1/0

0/0
0/0
0/1
0/0
1/1
0/0
0/0
0/1
9
6
5
4
1
2
0/0
0/0
0/2
0/0
3/1
4/0
0/0
0/0
3/3
0/0
0/0
0/0
0/0
4/0
1/0
0/0
0/0
0/0
0
0

2
0
4
5
0
0
5
1

11
6
9
9
1
2

11
-------
108
National Forum on Mercury in Fish
SUMMARY OF DEVELOPMENT EFFECTS IN MONKEYS
Exposure nnse Blood Ha Effects
Dose
(pg/kg/day)
Blood Hg
Concentration
(ppm)
In utero
50
1.3
postnatal only
(to 7 years)
In utero plus
postnatal
(to 4 years)
50
10.25. or 50
0.75
0.37.0.75.1.42
(maternal)
0.21.0.35.0.65
(postnatal)
during Infancy
- retarded object permanence
- Impaired recognition memory
- changes In social behavior

during adulthood
- facilitated delayed alternation
- Impaired spatial vision

- Impaired spatial vision
- Impaired high frequency hearing
- impaired somatosensory function
(delayed neurotoxlcity)

during Infancy
- overt toxicity (one at high dose)
- no effect - discrimination reversal
- changes on schedule-controlled
performance

during juvenile-adulthood
- Impaired spatial vision
- Impaired somatosensory function
-------
National Forum on
Mercury in Fish
An Overview of Human Studies
on CNS Effects of Methylmercury
Roberta f . White
of
Odense University, Department of Environmental Medicine

EnVJronmental ""»»* Center and Department of
Philippe A. Grandjean
Odense University, Department of Environmental Medicine
Pal Weihe
Department of Occupational and Environmental Health, Torshavn, Faroe Islands
paper will review the classic
literature on the central nervous
system (CNS) effects of exposure
to methylmercury, based largely on
studies carried out on individuals
exposed to mercury in Minamata and
Iraq. We will then proceed to discuss
some current epidemiologic studies
designed to investigate the relationships
between methylmercury exposure and
measures of CNS function.

Classic Studies:
Neuropathological Findings

The classic studies on the
neuropathological effects of methylmer-
cury intoxication have been well sum-
marized for the Iraq and Minamata cases
by Choi (1989). A more recent series of
case descriptions involves a family from
New Mexico (Davis et al., 1994).
Basically, these cases demonstrate a
relationship between age at exposure
and neuropathological outcome.
Prenatal exposure. Individuals
exposed to methylmercury in utero who
subsequently develop clinical disease
and who have undergone autopsy show
widespread brain damage extending to
the cerebral cortex and cerebellum with
remarkable reduction in brain size and
changes in the cytoarchitecture of the
brain (Eto et al., 1992; Matsumo et al
1965).
Childhood exposure. Children
exposed to methylmercury who develop
clinical disease and whose brains have
been studied have shown significant
neuropathological abnormalities in the
cerebellum and cerebral cortex with
widely distributed focal cerebral lesions
and some reduction in brain size.
However, brains were less reduced in
size than those of children exposed
prenatally and brain architecture was not
disturbed (Takeuchi et al., 1979).
Adult exposure. Brains of adults
with clinical disease showed cerebellar
changes, mild atrophy, and focal cortical
lesions at autopsy (Choi, 1989-
Takeuchi, 1968).
109
-------
Overview. The neuropathological
effects of methylmercury exposure of
sufficient severity to produce clinical
disease and/or death depend upon the
age of the affected individual at the time
of exposure. In general, the younger the
exposed individual, the greater the
extent of neuropathological damage and
the greater the number of sites within
the brain that are affected (Choi, 1989;
Davis et al., 1994).
Classic Studies: Behavioral
Evidence

Like the neuropathological studies,
the behavioral evidence from the Iraqi
and New Mexico cases and from studies
completed in New, Zealand suggests that
the younger the individual at the time of
exposure, the greater the impact on the
CNS.
Prenatal exposure. Prenatal
exposure to methylmercury resulting in
clinical disease is known to be associated
with intellectual deficits in multiple
cognitive domains. In addition, children
prenatally exposed to methylmercury at
levels insufficient to develop obvious
disease might exhibit changes in general
cognitive function on a delayed basis (i.e.,
they might later show deficits that are not
obvious at birth) (Marsh et al., 1980).
Childhood exposure. Exposure to
methylmercury in childhood both at
levels sufficient to produce obvious
disease and at lower levels is also
associated with multiple cognitive
deficits, which are also known to persist
(Kjellstrom, 1986; WHO, 1990). It
should be noted that childhood exposure
effects can be difficult to distinguish
from prenatal exposure effects due to
prevalance of exposure in populations
studied and persistence of mercury in
the brain.
Mult exposure. Exposure to
methylmercury in adulthood can produce
a variety of deficits, which have been less
intensively studied than those associated
with childhood exposure but seem to
include prominent visuospatial and motor
impairment (Davis et al., 1994).
Current Studies

Findings of functional deficits and
physical abnormalities from the
Minamata, Iraq, and New Mexico cases
reflect those seen largely in individuals
with obvious clinical disease who
demonstrate severe CNS damage. More
recent epidemiologic studies being
carried out by T. Clarkson and col-
leagues in the Seychelle Islands and our
group in the Faroe Islands focus on
exposure effects at the other end of the
health continuum, where subtle CNS
effects might be occurring in the ab-
sence of obvious clinical disease. These
studies focus on questions such as the
following:
1. Does exposure to methylmercury
at levels that are not associated
with obvious clinical disease
nonetheless produce target organ
system changes in the CNS that
are subtle but measurable using
sophisticated testing?
2. What levels of exposure are
required to produce behavioral
effects?
3. What are the relationships
between age at exposure, expres-
sion of behavioral changes, and
persistence of cognitive deficit?
Do different kinds of behavioral
changes appear at different ages?
The project in the Seychelle
Islands, for which T. Clarkson is
principal investigator, is a longitudinal
study of children evaluated at 6, 19, and
29 months of age who are now being
retested at about age 5.5 years. Expo-
sure measures include maternal hair
levels of mercury during pregnancy and
delivery and hair levels for the child at
each testing date. Physical, neurologi-
cal, and psychological examinations
were completed at each evaluation.
Results are pending (G. Myers, personal
communication).

Faroe Islands Study
This investigation focuses on the
relationship between prenatal exposure
to methylmercury (Grandjean, 1993)
-------
Conference Proceedings
111
and measures of CNS function 7 years
later.
Investigators are P. Grandjean,
Principal Investigator; P. Weihe, Co-
Principal Investigator; R.F. White and F.
Debes, Neuropsychology; K. Murata, K.
Yokoyama, F, Okajima, S. Araki,
Neurophysiology; and N. Sorensen,
Pediatrics.
Study subjects are about 1000
children born between 1986 and 1987
who were evaluated in 1993 and 1994
(about age 7 at time of testing). Results
presented in this paper reflect data
collected in 1993 on children belonging
to the oldest half of the cohort (N=443).
Exposure measures included cord
blood mercury levels (0-350 ug/1),
maternal hair mercury levels (0-40 ug/
g), maternal dietary histories during
pregnancy, and PCB levels in umbilical
cord (pending).
Outcome measures used in the
study included pediatric physical
examination; functional neurological
examination; electrophysiological
measures (visual evoked potentials,
brainstem-auditory evoked potentials,
computerized posturography, and EGG
R-R interval variability); and neuro-
psychological measures.
The neuropsychological test
battery included the following tests:
Motor:
• Neurobehavioral Evaluation
System (NES) Finger Tapping
Test
• NES Hand-Eye Coordination Test
Attention:
• NES Continuous Performance
Test (Child version)
• Wechsler Intelligence Scale for
Children-Revised (WISC-R)-
Digit Spans Forward
Verbal reasoning:
• WISC-R Similarities
Language:
• Boston Naming Test
Visuospatial:
• WISC-R Block Designs
• Bender Gestalt Test
Memory:
• Tactual Performance Test
• California Verbal Learning Test
Exposure measures from the Year 1 data
are summarized in Tables 1 and 2.
Results. The Year 1 data (N=443)
suggest that some neurobehavioral
dysfunction is related to maternal
seafood intake during pregnancy,
particularly on WISC-R Digit Spans
Forward and the Boston Naming Test
(see Tables 3 and 4). Though the
medians for the tests are similar or
identical, the upper exposure groups had
many more instances of scores in. the
lowest quartile. In addition to these
results, positive findings were seen on
the NES Continuous Performance Test
(child version) for the standard devia-
tions obtained for reaction time and the
number of false-positive errors. These
findings must be viewed with caution,
however, because residence in the
capital area of Torshavn is associated
with lower exposure levels and con-
founder analysis has not yet been carried
out. Also, PCB exposure levels are
being determined and could conceivably
explain some of the associations seen,
although mercury seems to be related to
some of the test results.
Conclusion

Classical studies of methylmercury
effects on CNS structure and function in
humans suggest that the extent and
severity of deficits are greater the
Table 1. Maternal marine food intake during pregnancy
Group
I
n
m

IV
Number
81
100
131

130
# whale dinners/mo
0
1-2
0
1-2
>3
# fish dinners/wk
0-3
0-2
>4
>3
(>1)
Note: Data incomplete for one case.

Table 2. Median mercury concentrations
Group
I
II
m
IV
Cord blood G-ig/1)
11.3
; 21.1
27.1
38.7
Maternal hair (jlg/g)
2.0
3.9
4.5
8.1
-------
Table 3. WISC-R Digit Spans Forward
Group
I
II
in
rv
Median
4
4
4
4
Range
1-8
1-7
1-7
0-6
Number (%) less than 3
12(15.4)
20(20.4)
27(21.8)
35(27.1)
Note: Spearman's r=-0.13; p=0.007.

Table 4. Boston Naming Test
Group
I
II
III
IV
Median
29
27
26
26
Range
12-38
13-40
16-38
11-39
Numb er (%) less than 23
14(19.4)
19(20.7)
23(19.8)
40(32.5)
Note: Spearman's r=-0.11; p=0.02.
younger the individual is at the time of
exposure. Preliminary results from the
first year of data collection in our study
of children in the Faroe Islands suggest
that there is a relationship between
maternal intake of seafood during
pregnancy and CNS function in children
7 years later. However, these data
cannot be directly related to mercury
exposure until further investigation of
potential confounders has been com-
pleted.
References

Choi, B.H. 1989. The effects of methyl-
mercury on the developing brain.
Prog. Neurobiol. 32:447-470.
Davis, L.E., M. Hornfield, H.S.
Mooney, K.J. Fiedler, K.Y.
Haaland, W.W. Orrison, E.
Cemichieri, and T.W. Clarkson.
1994. Methylmercury poisoning:
Long-term clinical radiological,
toxicological and pathological
studies of an affected family. Ann.
Neural. 35:680-688.
Eto, K., S. Oyanagi, Y. Itali, H.
Tokunagia, Y. Takizawa, and I.
Suda. 1992. A fetal type of
National Forum on Mercury in Fish
Minamata disease: An autopsy
case report with special reference
to the nervous system. Mol. Chem.
Neuropathol. 16:171-186.
Grandjean, P. 1993. Neurobehavioral
effects of intrauterine methylmer-
cury exposure. Proceedings of the
International Symposium on
Assessment of Environmental
Pollution and Health Effects from
Methylmercury. World Health
Organization and National Institute
for Minamata Disease.
Kjellstrom, T., P. Kennedy, S. Wassis,
and C. Mantell. 1986. Physical
and mental development of
children with prenatal exposure to
mercury from fish. Stage 1.
Preliminary tests at age 4. Report
3080. National Swedish Environ-
mental Protection Board,
Stockholm.
Marsh, D.O., GJ. Meyers, T.W.
Clarkson, L. Amin-Zaki, S. Tikriti,
andM.Majeed. 1980. Fetal
methylmercury poisoning: Clini-
cal and pathological features. Ann.
Neural. 7:348-353.
Matsumoto, H., G. Koya, and T.
Takeuchi. 1965. Fetal Minamata
-Disease: A neuropathological
study of two cases of intrauterine
intoxication by methyl mercury
compound. J. Neuropathol. Exp.
Neural. 24:563-574.
Takeuchi, T. 1968. Anthology of
Minamata Disease. In Minamata
Disease Study Group of Minamata
Disease, pp. 178-194. Kumamoto
University Press, Japan.
Takeuchi, T., N. Eto, and K. Eto. 1979.
Neuropathology of childhood
cases of methylmercury poisoning
(Minamata Disease) with pro-
longed symptoms, with particular
reference to the decortication
syndrome. Neurotoxicol. 1:1-20.
WHO. 1990. Methylmercury. Environ-
mental Health Criteria. World
Health Organization, Geneva.
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National Forum on
MercuiyinFish
Exposure Assessment for
Methylmercuiy
Alan H. Stem
Division of Science and Research, New Jersey Department of Environmental
Protection,* Trenton, New Jersey
What Questions Can Exposure
Assessment Data for
Methylmercuiy Answer?
ie key questions to be answered
include the following:
• To what extent is the (pregnant/
fetal) population at risk?
- What is the distribution of
exposures?
- What fraction of the popula-
tion is at risk?
• What priority should be assigned
to addressing methylmercury
exposure?
• What factors result in elevated
exposure?
- Fish consumption factors
- Other biologic and demo-
graphic factors
• Can the high-risk population be
identified in a way that allows it
to be targeted for intervention?
- Possible identifying variables:
geography, race/ethnicity, SES
Estimation of Methylmercury
Exposure Based on National
Data

Daily intake of methylmercury can
be calculated as follows (Stern, 1993):
This work does not necessarily reflect the policy or
views of the New Jersey Department of Environmen-
tal Protection.
I = MxCTxFxA
where I is the methylmercury intake
(ug/day); M is the mass offish/
seafood consumed per day (g/day); CT
is the concentration of total mercury
in fish (ug/g); F is the fraction of total
mercury present as methylmercury;
and A is fractional gastrointestinal
absorption of methylmercury.
Nearly all biological and human
activity parameters occur as distribu-
tions. In order for I to approximate
the true population distribution of fish
ingestion, input values must also be
distributions. Point value estimates
(e.g., means), no matter how reliable,
will not be useful in generating a
distribution. A Monte Carlo calcula-
tion approach is required.

Mass offish Consumed Per Day

Few data are in distributional
form. Data from Rupp et al. (1980)
are extensive, but from 1973-74.
Dietary habits have changed
since then. EPA estimates a 62
percent increase in consumption from
1960 to 1986.
The U.S. Food and Drug Ad-
ministration's 14-day Menu Census
Study results for consumers were as
follows:
mean = 32 g/day
90th percentile = 64 g/day
An underlying lognormal distribution
113
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114
30%

24%

18%
, i
J
12%
is assumed. The two resulting lognor-
mal distributions are averaged.

Concentration of Total Mercury
In Fish
This factor requires data on
concentration of mercury by species
weighted by consumption. A high
concentration in a species that is
rarely consumed will have little
influence.
Only one comprehensive database,
the National Marine Fisheries Service's
1978 study (Hall et al., 1978), is avail-
able. The database includes concentra-
tion by percent of catch from U.S.
coastal waters intended for human
consumption. Catch for human con-
sumption estimates species distribution
in the average diet. This distribution is
illustrated in Figure 1. There are,
however, caveats for the use of this
database. The data are only for U.S.
waters, and they reflect an average mix
of species hi the diet, not individual diet
variability hi species preference.

Fraction of Total Mercury Present
as Methylmercury
Earlier estimates (mean -70 per-
cent) apparently were influenced by
background inorganic mercury.
Current ultraclean estimates (Bloom,
1992) are available. These data are
©RISK Simulation
.469
.094 ' .188 .281 .375

Total Hg Concentration in U.S. Catch for Human Consumption
Figure 1. Distribution of mercury concentrations in the U.S. catch intended for human
consumption.
National Forum on Mercury in Fish

modeled as a normal distribution with
a mean of 95 percent and a standard
deviation of 0.063 percent. This
reflects a truncated distribution to
eliminate observations with methyl-
mercury >100 percent.

Fractional ClAbsorption of
Methylmercury
The fractional gastrointestinal
absorption of methylmercury is
assumed to be 90-100 percent. It was
-93 percent in rats fed fish with
intrinsic methylmercury (Yannei and
Sachs, 1993).
Results

The results of this Monte Carlo
simulation are presented graphically
in Figure 2. Numerical results for
selected percentiles of the fish-
consuming population are as follows:

mean = 3.7 ng/day
50% < 1.5 ug/day
75% < 3.7
90% < 8.7
95% < 15.4
99% < 33,2
These new estimates do not distinguish
by sex and can be adjusted as follows:
USFDA 1980-82 Total Diet Study:
Women (25-30)
eat fish portions
62-95 percent the
size of those
eaten by men.
Therefore,
estimates for
women of
childbearing age
can be reduced
by -20 percent.
The rela-
tionship of
adjusted exposure
estimates of daily
intake to possible
reference dose
guidance is shown
Sampling=Latin Hypercube "J_
.563 .656
.75
in Table 1. The
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Conference Proceedings
referencedoseincorporatesasignificant
margin of protectiveness. Therefore, this
comparison does not reflect the risk of
actual adverse effects, but an expression of
the estimated exposure relative toamargin
of safety. Given the quantitative uncertain-
ties in the model inputs, model predictions
should be viewed only as qualitative
predictions of exposures. When intake is
computed to an estimated threshold for
developmental affects (rather than a
reference dose with its attendant margin of
safety), less than 1 percent of women of
childbearing age are estimated to exceed an
estimated thresholdfor developmental
effects (-40 jug/day).

Ideal Characteristics of State/
Regional Exposure
Assessments

Ideal characteristics of state/
regional exposure assessments include:

• Direct measurement of methyl-
mercury biomarkers (hair, blood)
rather than estimates of food
intake.
• Speciation of mercury in
biological samples; contribution
of dental amalgams to total
mercury.
• Large sample size; adequate
representation of tail of the
distribution.
<> 3.125 6.25 8.375 1s7 15.625 18.75 21.875 25
Estimated Dally Mathylmerewy Int.*. for All U.S. Fiih Consum.rs
(ug/day)

A. Frequency distribution.
0 3.125 6.25 9.875 12.3 15.625 18.75 21.875 25
Estimated Daily MrtiyliMteuiy Intak. for All U.S. Hth Consum.rj
(uo/day)

B. Cumulative probability distribution.
Figure 2. Estimating daily intake of methylmercury among U.S.
fish consumers.
Cross-sectional population
sample. Currently, there is
insufficient information to
permit oversampling of "high-
risk population."
Table 1. Relationship of adjusted estimates to reference dose guidance
70-kg
adult
est%
Max consumers
Intake exceeding
(ug/day) maxintake
RfD 21 -w
, , *L 3%
based on
paresthesia
(0.3 ng/kg/day)
"RfD"
based on
developmental
effects
(0.07 ug/kg/day)
62-kg
woman
est%
max consumers
intake exceeding
(ug/day) maxintake
•
19 3%

4 18%

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116
National Forum on Mercury in Fish
Characterization of population
relative to fish consumption;
species, frequency, portion size.
Characterization of other demo-
graphic/lifestyle variables to
provide functional description of
high-risk population.
Sampling early in pregnancy
(first trimester) to avoid con-
founding due to pregnancy
related changes in physiology and
diet.
References

Bloom, N.S. 1992. On the chemical
form of mercury in edible fish and
marine invertebrate tissue. Can. J.
FishAquat.Sd. 49:1010-1017.
Hall, R.A., E.G. Zook, and G.M.
Meaburn. 1978. National Marine
Fisheries Service survey of trace
elements in the fishery resource.
NOAA Technical Report NMFS
SSRF-721. U.S. Department of
Commerce, National Oceanic and
Atmospheric Administration,
National Marine Fisheries Service.
Rupp, E.M., F.L. Miller, and C.F. Baes.
1980. Some results of recent
surveys of fish and shellfish
consumption by age and region of
U.S. Residents. Health Phys.
3:165-175.
Stern, A.H. 1993. Re-evaluation of the
reference dose for methylmercury
and assessment of current exposure
levels. Risk Anal. 13:355-364.
Yannai, S., and K.M. Sachs. 1993.
Absorption and accumulation of
cadmium, lead and mercury from
foods by rats. Food Chem. Tox.
5:351-355.
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National Forum on
Mercury in Fish
Methylmercury (MeHg) - Hazard
and Risk
Michael Bolger
U.S. Food and Drug Administration, Center for Food Safety and Applied Nutrition
Contaminants Branch, Washington, DC
Environmental Occurrence
and Exposure

Mercury (Hg) in the environ-
ment arises from both natural
and man-made sources, and
the global movement of mercury almost
exclusively involves the inorganic
forms, as shown in Figure 1 (IPCS/
WHO, 1990). It is estimated that
approximately 2700-6000 tons of
elemental mercury are released naturally
into the atmosphere by degassing from
the earth's crust and oceans. Human
activities, primarily the combustion of
fossil fuels and industrial production,
account for the release of 2000-3000
tons of mercury into the atmosphere.
However, these forms do not generally
accumulate in food. It is the conversion
of inorganic mercury to the methylated
form in the aquatic ecosystem that is of
critical importance in terms of the
presence of mercury in food.
With regard to environmental
transport, mercury (or more specifically
mercury vapor) is a highly mobile
metal. Mercury deposited on land or
water is in part re-emitted into the
atmosphere, and the bottom sediment of
the oceans and bodies of fresh water are
the ultimate sinks in which inorganic
mercury is deposited as the highly
insoluble mercury sulfide. The methyla-
tion of inorganic mercury, which takes
place via both nonenzymatic and
enzymatic pathways, occurs primarily in
freshwater and marine sediments, as
well as in the water columns of these
bodies of water, as a result of microbial
activity. Methylmercury (MeHg) Is
enriched to a high degree in aquatic
food, with the highest levels occurring
in predatory fishes, particularly those at
the top of the aquatic food chain. While
methylmercury is also incorporated in
the terrestrial environment, enrichment
does not occur to the same extent in the
terrestrial food chain. As shown in. Table
1, methylmercury in fish and fish
products is the predominant source of
methylmercury exposure. The estimate
of methylmercury exposure of 2.4 fig/
The Global Cycle of Mercury
TROPOSPHERE;
(2 x 10'12 g/l)
RAIN
(2 x 10'9 g/|)
SOIL
(20 x 10'6 g/kg)
OCEAN
(2 x 10'9 g/|)
BOTTOM SEDIMENT
(20 x ID'8 g/kg) HgS
Figure 1. The global cycle of mercury.
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118
National Forum on Mercury in Fish
Table 1. Intake of mercury (u,g/day)a in absence of
Exposure Source
Air
Fish
Other Food
Drinking Water
Dental Amalgams
Total
Elemental Hg
Vapor
0.03/0.02
0/0
0/0
0/0
4-21/3-17
4-21/3/17
Inorganic Hg
0.002/0.001
0.6/0.04
3.6/0.3
0.5/0.004
0/0
4.3/0.3
MeHg
0.008/0.006
2.4/2.3
0/0
0/0
0/0
2.4/2.3
intake, and second is amount retained in body (IPCS/WHO, 1990).

day is an estimate for the general
population. According to a 1982-87
survey by the Market Research Corpora-
tion of America (MRCA), about 77
percent of the U.S. population are
considered to be fish eaters. Thus, of an
estimated population of 250 million in
1990,192 million people ate fish or
seafood on a somewhat regular basis.
The 14-day consumption values from
the survey are 32 g/day for the mean and
64 g/day for the 90th percentile. The
frequency of the surveyed population
who reported shellfish eating was 13
percent for crustaceans and 4.8 percent
for molluscs. Using standard portion
sizes (USDA, n.d.), the estimated mean
and 90th percentile daily intakes varied
from 4 to 18 g for molluscs and from 9
to 19 g for crustaceans. The estimated
intakes of methylmercury resulting from
consumption offish containing an
average level of 0.3 ppm mercury
(NMFS, 1978) would vary from

Table 2. Mercury (ppm) in a variety of finfish and shellfish"
Catfish
Flounder
Lobster
Mackerel
Orange Roughy
Perch (freshwater)
Pollack
Shark
Shrimp
Swordfish
0.10 - 0.31
ND - 0.08
0.01 - 0.14
0.10 - 0.23
0.42 - 0.71
ND - 0.31
ND - 0.10
0.23 - 2.95
<0.10
0.26 - 3.22
• Summary of FDA analysis of mercury levels in species of fish and shellfish.
day (mean) to 19/ig/day (90th percen-
tile). A consumption study (National
Fisheries Institute, 1987) reported that
81 percent of the population eat tuna at
least once in a year, while shrimp, in
second place, is consumed by 38 percent
of the population.
As shown in Table 2, mercury can
be found in many finfish and shellfish
with mean levels generally below 0.3 ppm
and methylmercury generally comprising
90-100 percent of total mercury. Al-
though many species contain low levels of
methylmercury, long-lived, predatory fish
(e.g., swordfish) tend to have higher
levels (i.e., greater than 1 ppm). As a
result, the FDA published a consumption
advisory for women of child-bearing age
that recommended the reduced consump-
tion of species that routinely have elevated
levels of methylmercury.
Toxicokinetics and Toxicity

Methylmercury in the human diet
is almost completely absorbed into the
bloodstream. Age, including the neona-
tal stage, has little effect on gastrointes-
tinal absorption, which is usually more
than 90 percent of oral intake. Once
absorbed, methylmercury is bound to
sulfhydryl and disulfide groups of large
molecules, particularly those of proteins
hi the plasma and hemoglobin hi the red
blood cells, and is widely distributed to
all organs and tissues. Equilibration
between blood and organs and tissues
occurs in about 4 days. Organs that
accumulate and concentrate methylmer-
cury include the brain, liver, and
kidneys. Distribution of methylmercury
to the fetal and adult brain is somewhat
preferential, with about 10 percent of
the body burden localized in the central
nervous system. The concentration in
the brain is roughly six times that found
in the blood. Methylmercury readily
crosses the placenta, causing cord blood
levels to be somewhat higher than
maternal levels. The mercury concentra-
tion of human breast milk varies, but is
approximately 5 percent of the maternal
serum mercury concentration.
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Conference Proceedings
The demethylation of methylmer-
cury appears to occur in all tissues and
is an initial step in the excretion of
methylmercury. In humans the biologi-
cal half-life is approximately 70 days,
with the removal of mercury occurring
more slowly from the central nervous
system than from other tissues. The
primary route of excretion occurs
through the feces. The accumulation of
methylmercury in humans is best
measured by residues in hair and blood.
The concentrations in hair are propor-
tional to blood concentrations at the
time of formation of the hair strand. The
blood-to-hair ratio in humans is gener-
ally about 1 to 250. Once incorporated
into the hair strand, its concentration
remains unchanged and serves as a
biomarker of exposure that can be
recapitulated over time.
The toxicokinetics of methylmer-
cury are best described by a single-
compartment model in which a 70-day
half-life predicts that whole-body steady
state is achieved in about one year. The
relationship between the average daily
dietary intake and the steady-state
mercury concentration (C) in the blood
is described by the equation C (blood) =
0.95 x mercury (diet). A number .of
population studies of blood and hair
mercury levels have noted a fair amount
of overlap in these populations, and the
overlap includes those levels reported
for "fish-eating" vs."non-fish-eating"
populations. Many questions remain
concerning the interaction between
methylrnercury and essential dietary
nutrients, especially selenium. Some
studies have shown that selenium
ameliorates the adverse effects of
methylmercury, whereas others have
been less conclusive. The delineation of
the role of essential elements, such as
selenium, in the expression of the
toxicity of methylmercury is particu-
larly important because of the concomi-
tant exposure of methylmercury and
essential elements, like selenium, in a
fish-eating population.
The nervous system is the primary
target tissue for the toxic effects of
methylmercury. The sensory, visual,
and auditory functions and those areas
concerned with coordination, especially
the cerebellum, are the most affected.
Symptoms associated with methylmer-
cury in humans (Minimata and NMgata,
Japan and Iraq), include paresthesia,
malaise, blurred vision, concentric
constriction of the visual field, deaf-
ness, dysarthria, and ataxia. Methylm-
ercury poisoning has several important
features: (1) a long latent period lasting
several months; (2) damage limited to
the central nervous system; (3) highly
localized damage (e.g., visual cortex
and the granular layers of the cerebel-
lum); (4) irreversible effects in severe
cases, resulting from destruction of
neuronal cells; and (5) nonspecific
subjective early complaints, such as
paresthesia, blurred vision, and malaise.
The most sensitive neurological re-
sponse in adults, paresthesia, occurred
at an estimated hair mercury concentra-
tion of 50 ppm and a whole blood
concentration of 200 ppb. These levels
were attained with a minimum steady-
state, daily dietary methylmercury
intake of 300' jug.
During prenatal life and infancy,
humans are susceptible to the toxic
effects of methylmercury because of the
sensitivity of the developing nervous
system. Methylmercury has inhibitory
effects on neuronal migration and cell
division, which result in a deranged
central nervous system cytoarchitecture
and ectopic neurons. Methylmercury
crosses the placenta, and concentrations
in fetal red blood cells can be 30
percent higher than in those of the
mother. The effects of methylmercury
poisoning on the developing infant are
dose-dependent. Infants exposed to
high levels of methylmercury (e.g.,
maternal hair levels > 70 ppm) develop
cerebral palsy. Microcephaly,
hyperreflexia, and gross motor and
mental impairment, sometimes associ-
ated with blindness or deafness, are the
usual symptoms. Infants exposed to
lower levels did not develop overt
symptoms within the first few months
of life, but later displayed symptoms of
psychomotor impairment and persis-
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120
tence of pathological reflexes. Postmor-
tem observations indicate that damage
in prenatal exposure was generalized
throughout the brain in contrast to adult
exposure, where focal lesions were
predominant.
The tolerable daily intake (TDI)
for methylmercury is 30 fig/day
(weekly intake, 210 ^g). This is based
on a daily effect level of 300 fig/day,
which corresponds with the lowest
observed effect level in the adult
nervous system, paresthesia, and the
use of a 10-fold uncertainty factor. The
FDA's original action level of 0.5 ppm
was based on preliminary information
from the Japanese episodes and con-
sumption and exposure information
available at the time (1960s and early
1970s). The action level was subse-
quently reaffirmed by several expert
study groups, and in 1974 the FDA
proposed to establish the action level by
formal rulemaking. In 1979 this pro-
posal was withdrawn because of newer
information which showed that the
lowest dose associated with effects in
adults was greater than originally
estimated and methylmercury exposure
was lower.
Figure 2 is a graphical depiction
of the effects noted in children exposed
Methylmercury in Iraq: Effect on CMS
I
§
50 150 400
MATERNAL HAIR -CQN.C. (Hfl, JJBffl)
__———————————~—""—~~~~~~"~~~
Figure 2. Methylmercury in Iraq: effect on CNS.
National Forum on Mercury in Fish

in utero in the poisoning episode in Iraq
(Cox et al., 1989). On the basis of this
study, a "practical threshold" of 10-20
ppm was identified for the effect of
methylmercury on the fetus. Several
important points must be made regard-
ing this study. First, the number of
mother-infant pairs was fairly small, 84
mother-infant pairs. Second, most of
the mothers whose offspring were
observed to have decrements in nervous
system function had body burdens that
exceeded the lowest effect level for
adults (50 ppm mercury hair). Third,
the background incidence of either
delayed walking or CNS symptoms in a
population has a considerable impact on
the practical threshold for methylmer-
cury-induced effects. For example, if the
estimate of the background occurrence
of delayed walking is not 4 percent, but
rather 8 percent, then the "practical
threshold" is 119 ppm mercury hair
level. This would result in a correspond-
ing 10-fold increase in a TDI or refer-
ence dose (RfD) derived on the basis of
a 10-ppm hair mercury level.
The major flaw of the TDI or RfD
approach is that it is essentially an
attempt to identify a level of exposure
that is "safe" or "of negligible" risk. It
does not quantify what the risk is. It is a
qualitative description
of the risk that allows
us to conclude that an
exposure to a contami-
nant is not a problem.
With a contaminant
like methylmercury,
the answer we invari-
ably get from this
approach is that the
consumption of a
particular fish is
"unsafe" or the
population who
consumes it is "at
risk." The difficulty
with this answer is that
we do not know how
much of a problem a
particular exposure
represents. The TDI/
RfD approach should
ABNORMAL
NORMAL
1100
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Conference Proceedings
be the first step in an iterative process
that leads us to ask the question "what is
the level of risk." What is needed with
methylmercury is a quantitative estima-
tion of the variability in critical factors
like fish consumption, methylmercury
body burdens, rates of absorption, and
target organ sensitivity, so that we
derive ranges of risk and a quantitative
description of the uncertainty of our risk
levels. We should not ask the TDI/RfD
methodology to do something it was not
designed to do and can never do, namely
quantify risk.
The following conclusions can be
drawn regarding the potential hazard or
risk of methylmercury in fish and
shellfish. First, there is little demon-
strable risk to the general population
from methylmercury exposure through
the consumption of fish and shellfish.
Second, a certain segment of the popula-
tion who consume large amounts of fish
that contain methylmercury may attain
body burdens (e.g., mercury hair - 50
ppm) associated with a low risk of
neurological deficits in adults. Third,
the developing nervous system of the
fetus may be particularly sensitive to the
adverse effects of methylmercury.
However, pronounced neurological
damage has been reported only in the
offspring of women whose hair mercury
levels exceeded 70 ppm. Fourth, limited
evidence suggests that maternal hair
levels in the range of 10-20 ppm are
associated with subclinical neurological
effects (e.g., delayed walking and
central nervous system symptoms) in
their offspring. Finally, it is imperative
that these preliminary observations be
confirmed in well-designed and con-
ducted epidemiological studies of
children from a fish-eating population
and that a quantitative risk analysis that
quantitatively describes the risk associ-
ated with different levels of methylmer-
cury exposure be conducted.
References

Cox et al. 1989. Environ. Res. 49:318-
332.
Food and Drug Administration (FDA).
1979. Fed. Reg. 44:3990-3993.
Food and Drug Administration (FDA).
1994. FDA Consumer, Sept.:5-8.
National Fisheries Institute. 1987. Fish
consumption study.
NMFS. 1978. National Marine Fisher-
ies Service survey of trade ele-
ments in the fishery resource.
NOAA Technical Report NMFS
SSRF-721. National Marine
Fisheries Service.
USDA. n.d. 1987-88 national food con-
sumption survey. U.S. Department
of Agriculture, Washington, DC.
WHO. 1990. Environmental Health
Criteria No. 101. World Health
Organization.
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National Forum on
Mercury in Fish
An Approach for Noncancer Risk
Assessment of Methylmercury
John Clcmanec
U.S. Environmental Protection Agency, Office of Research and Development,
Cincinnati, Ohio
Msrcury is a significant pollutant
to which humans and animals
can be exposed via the environ-
ment. The most likely avenue of exposure
for humans is through consumption offish
that are contaminated with methylmercury
(MeHg).
A fairly extensive data base exists
for methylmercury, both for animal
species exposed within a laboratory
setting and for humans exposed through
accidental environmental contamina-
tion. In both settings, the neurological
effects on infants who have been
exposed in utero are the most critical
adverse effects.
Traditionally, the two most difficult
decisions to be made in noncancer risk
assessment are (1) to define the single,
most sensitive critical adverse effect and
(2) to define the dose level for which no
effect is seen (NOAEL) and the lowest
observed adverse effect level (LOAEL).
If extensive human data are available, the
choice is usually made to base the risk
assessment on human data rather than on
animal studies. However, this decision
usually presents two additional challenges
to the risk assessor: accidental exposure
of humans presents complications in
quantifying the dose level and complica-
tions that occur because of concurrent
exposure to other toxic agents.
Beginning in March 1993, the U.S.
Environmental Protection Agency
Interagency RfD/RfC Work Group
undertook the task of providing a quanti-
tative, noncancer assessment for meth-
ylmercury. Initial screening of the data
base narrowed the selection of a "critical
study" to two possible choices. The first
option was to use data from Iraq, collected
in 1971-72 following human exposure to
mercury-contaminated seed grain. The
second choice was to use data by
Kjellstrom et al. (1986,1989) for meth-
ylmercury exposure for children of
mothers in New Zealand who frequently
consume fish. The New Zealand data
were not used because the Agency felt
that the psychological and developmental
tests that had been chosen for evaluation
were inappropriate for the effects of
methylmercury.
The principal quantitative data
available for the Iraqi outbreak are from
the summary of 84 mother-infant pairs
provided in Marsh et al. (1989). To
establish a daily dose of methylmercury
that the mothers received, a daily dose
must be calculated indirectly from hair
concentrations of the mothers. This hair
concentration value is then converted to
a corresponding blood level, which is
then used to derive the daily oral
consumption dose. A number of
literature references are available to
calculate these conversion factors.
However, there is a range of normal
variation related to each of the conver-
sions that, through use of the formula,
results in greater variation than is
desired.
The exposure data for the Iraqi
population are presented in a continuous
fashion (as opposed to distinct dose
123
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124
National Forum on Mercury in Fish
groups resulting from animal studies)
with hair mercury concentrations
ranging from 0 to 674 ppm. To properly
evaluate these data, the use of a "bench-
mark dose" approach might prove to be
more useful than standard NOAEL-
LOAEL methodology.
It is likely that derivation of an
RfD for methylmercury based on devel-
opmental effects would be even more
conservative than the present value in
IRIS (1995) for adult effects of
paresthesia. Once a new RfD is de-
rived, it is important that a mechanism
be put in place to quickly accommodate
the new human data from the Seychelle
Islands and Faroe Islands studies as they
become available.
References

Kjellstrom, T., P. Kennedy, S. Wallis,
and C. Mantel. 1986. Physical
and mental development of chil-
dren with prenatal exposure to
mercury from fish. Stage 1:
Preliminary test at age 4. National
Swedish Environmental Protection
Board, Report 3080, Solna,
Sweden.
Kjellstrom, T., P. Kennedy, S. Wallis,
and C. Mantel. 1989. Physical
and mental development of chil-
dren with prenatal exposure to
mercury from fish. Stage 2:
Interviews and psychological test
at age 6. National Swedish
Environmental Protection Board,
Report 3080, Solna, Sweden.
Marsh, D.O., T.W. Clarkson, C. Cox, et
al. 1987. Fetal methylmercury
poisoning: Relationship between
concentration in single strands of
maternal hair and child effects.
Arch. Neural. 44:1017-1022.
USEPA. 1995. Integrated Risk Infor-
mation System (IRIS). U.S.
Environmental Protection Agency.
Office of Research and Develop-
ment, Environmental Criteria and
Assessment Office, Cincinnati,
Ohio.
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Conference Proceedings
125
A Reference Dose for Methytaiercury

Sources of Reduced Uncertainty

1. The critical study was performed in humans.
2. The critical study identified the sensitive subpopulation.
3. The data base is fairly extensive except for the lack of a two-
generation reproductive study.
4. Animal studies are generally supportive of the results in hu-
mans.
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National Forum on
Day Two: September 28, 1994^
Mercury in Fish
Questions and
Session One
After each speaker's presentation,
an opportunity for questions and
answers was provided. Time
was also allotted for group discussions/
question-and-answer sessions.
Mercury Toxicity: An
Overview

Dr. Thomas Clarkson, University of
Rochester

Q (Bruce Mintz, U.S. EPA, Headquar-
ters): You mentioned the importance of
glutathione in the excretion of methyl-
mercury. In the Iraq population, could
protein deficiencies have affected their
ability to excrete methylmercury and
made them more susceptible?

Dr. Clarkson:
There's no evidence of a pro-
longed half-time, although the half-
times in Iraq did cover a wide range.
The diet in Iraq was mainly cereal,
mainly bread, which is why they got
poisoned. Their diets are low in protein.
In general, we did not see starvation, but
no one conducted a detailed dietary
survey of this primitive countryside
population. There were a lot of disease
and a lot of parasites in this population.
It is not an average population for sure.
I can't answer your question on glu-
tathione, but certainly a carbohydrate
diet does not promote a high glutathione
level.
Q (Pom Shubat, Minnesota Department of
Health): Regarding the microflora you
discussed, does absence of microflora in
the fetus and then the infant help explain
the higher levels that are assumed to be
present in the developing fetus and then
the infant?

Dr. Clarkson:

They may. The system I described
for excretion was for adult animals. An
interesting phenomenon is that, in the
suckling animal, the glutathione secre-
tion does not occur. The secretion of
glutathione from the liver into bile starts
at the end of the suckling period. As a
result, methylmercury itself is not
excreted into bile in suckling animals.
So even if there were microorganisms in
the GI tract to break it down, it might
not even get there. We are trying to
check this by collecting hair samples in
infants about 6 months of age and
measuring the rate of decline in the hair
samples month by month. We have
enough children that are bottle fed so
they're not exposed to methylmercury
after birth. Right now we're having a
hard time determining the rate of growth
of hair in infants, and this is holding up
the study. If anyone has any informa-
tion on the rate of growth of hair in
infants, I would be grateful to know.
127
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128
National Forum on Mercury in Fish
An Overview of Animal
Studies

Dr. Deborah Rice, Health Canada

No questions

An Overview of Human
Studies

Dr. Roberta White, Boston University

Q (Deborah Rice, Health Canada): Are
you planning any functional testing of
sensory systems?

Dr. White:
No.
Group Discussion/Question'
' Answer Session
Q (Mike Bolger, U.S. Food and Drug
Administration): Regarding the results
of exposure analysis, it was my under-
standing that the primary methylmer-
cury exposure was coming from the
consumption of whale meat. In terms of
meat consumption and total methylmer-
cury exposure, is more coming from the
consumption of whale meat than from
consumption offish?

Dr. White:
Both fish and whale. Regarding
PCBs, meat has lower levels and blub-
ber has higher levels. Regarding smok-
ing and alcohol consumption, alcohol
affects toxicokinetics in breast milk.

Q (Luanne Williams, North Carolina
Department of Environmental Health
and Natural Resources): At public
meetings I've encountered questions
from people concerning fish consump-
tion by their cats. Do you have any
advice for how to respond?

Dr. Clarkson:
I know of studies in which cats
were fed pike with varying levels of
methylmercury. At high doses they
were severely affected.

Q (Alan Stern, New Jersey Department
of Environmental Protection): Regard-
ing the applicability of your findings...

Dr. Rice:
I try to make a point about rodent
literature that most has been aimed at
validating test batteries. No one has
pursued observations to interpret the
effects of methylmercury in the rodent.

Q: What is the relationship between
maternal hair and fetal brain levels?

Dr. Clarkson:
That is a good question. We are
attempting to answer it by measuring
brain levels in autopsy cases.

Q (Pam Shubat, Minnesota Department
of Health): What human age is compa-
rable to a 13- to 14-year-old monkey?

Dr. Rice:
A middle-aged, 40- to 50-year-old
human.

Q (Pam Shubat, Minnesota Department
of Health): Are there currently plans
for the Faroe Islands to look at geriat-
rics?

Dr. White:
People have always been exposed.
There are 50,000 people in the Faroe
Islands. It's a good place to look at
diagnostic outcomes.

Q (Jerry Pollock, California EPA): Is it
true that the younger you are, the
greater the effects?

Dr. White:
Yes.

Q (Bruce Mintz, U.S. EPA, Headquar-
ters): Factoring in meals per month, is
there any information that would tell us
anything about a single exposure in one
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Conference Proceedings
129
day that may be more or less significant
in terms of brain levels and potential
effects?

Dr. Clarkson:
We found in Iraq that maximum
brain level of methylmercury was the
best predictor of effects. The fact that
methylmercury is an irreversible poison
indicated that the maximum level is
very important.

Q (Tom Burbacher, University of Wash-
ington): Are you going to speciate?

Dr. Clarkson:
Yes.

Q (Tom, Burbacher, University of
Washington): Are you going to look at
different areas of the brain and follow
up with kids?

Dr. Clarkson:
Infants who have died within a few
weeks are all we've looked at.

Dr. White:
We'll follow up pending funding.

Q (Mike Bolger, U.S. Food and Drug
Administration): Regarding dental
amalgam, these kids don't have amal-
gams, do they?

Dr. White:
This is not seen as a problem.

Q (Mike Bolger, U.S. Food and Drug
Administration): Is there a connection
between dental amalgams and exposure
to different forms of mercury?

Dr. Clarkson:
It's an interesting question. There
was a study in rats or mice, in which
someone exposed one group to meth-
ylmercury, one group inhaled mercury
vapor, and one group was exposed to
both. There was another study in
which primates were given mercury
vapor. He found the same results,
more or less, with mercury vapor as
with inorganic.

Q (John Cicmanec, U.S. EPA): With
regard to the Faroe Islands study,
exposure during gestation is not con-
stant. Can you break it down between
trimesters?

Dr. White:
We do have dietary data. We don't
know if it's possible to have accurate
enough data. We can look at hair, and
hair tells you when the exposure was.

Q (Alan Stern, New Jersey Department
of Environmental Protection): Regard-
ing the effects of post-natal exposure,
what are the sources of data to draw a
conclusion of post-natal exposure
independent of pre-natal exposure?

Dr. Clarkson:
I don't know of any dose-response
data. I am reluctant to draw any conclu-
sions from lead experience.

Q (Alan Stern, New Jersey Department
of Environmental Protection): Regard-
ing animal studies, are there studies on
post-natal exposure?

Dr. Rice:
Data are lacking.
Exposure Assessment for
Methylmercury

Dr. Alan Stern, New Jersey Depart-
ment of Environmental Protection

Q (Arnold Kuzmack, U.S. EPA, Head-
quarters): One of the areas in which a
Monte Carlo analysis can go astray is if
your variables are not independent. In
particular with this case, it could well
be that the people who eat a lot offish
are a different population from the
average. They may eat different parts of
the fish, eat different species offish, and
get them from different places. [Such
differences] could lead to significant
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130
National Forum on Mercury in Fish
**... there is a tremendous dif-
ference among different species
for mercury bioaccumulation as
well as age and size."
differences in what the [statistical] tails
look like. There should be some way to
tease it out of surveys.

Dr. Stern:
I'm well aware of the problem you
describe, although I don't think that in
this case it has to do with correlations
within the analysis itself. I think the
problem arises with the data set we have
from the National Marine Fisheries.
The NMFS data which is reflective at
best of the
,^_____^^___ average
consumption
of the popula-
tion and the
high-end
consumers are
not likely to be
————^———— averaged in.
They probably
have very different characteristics from
the people in the middle of the curve.

Q (Bruce Mintz, U.S. EPA, Headquar-
ters): Have you thought about looking
at the exposure to children, and if so,
how would you handle the body weight
and consumption rate variables?

Dr. Stern:
I haven't given it much thought
because there are no data. But the data
that exist from the diet studies would
probably be the only data that are
relevant to children and those aren't
distributional. There's really no way to
get a handle on it. An exposure study
using biomarkers could be done with
children, and it could follow the same
parameters as for adults. That would be
an interesting thing to do.

Q (Russell Isaac, Massachusetts Depart-
ment of Environmental Protection):
Your concentration distribution was for
marine fish from coastal waters rather
than any freshwater fish?

Dr. Stern:
Yes, coastal marine fish. For
the general population, that's going to
be the great majority of fish consump-
tion. These data at very best are for the
population average and don't tell us
anything about the subgroups in the
population.

Q (Bill Hartley, Tulane Medical Cen-
ter): From an exposure standpoint, can
you comment on how important you
think a creel survey approach would be,
looking at what fish are actually caught
for each population? Because, as we
all know, there is a tremendous differ-
ence among different species for mer-
cury bioaccumulation as well as age
and size.

Dr. Stern:

I attended the International
Society of Exposure Analysis/Interna-
tional Society of Environmental
Epidemiology joint conference last
week in North Carolina, and there was
a paper presented there about the
discordance between creel surveys and
actual consumption. Apparently,
fishermen don't tell the truth about
what they catch, or they don't tell the
truth about what they eat from what
they catch. So, I would be a little
concerned about the reliability of creel
surveys. If that's the best data you
have, then go with it but realize there
will probably be some nonsystematic
sources of error in there.

Lee Weddig, National Fisheries Insti-
tute: I express caution about using the
data on the mercury levels in coastal
species to indicate the amount of mer-
cury in the total supply. You mentioned
the impact of imports and in fact the
consumption of commercial species in
the United States is roughly 70 percent
imported product. We export fully 30-
40 percent of what we catch ourselves.
The actual U.S. supply is predominantly
imported species, and so the levels in
the coastal survey done in the 1970s are
really not representative of what is in
the marketplace. Changes in composi-
tion can also have a profound effect on
it. For example, a level is indicated for
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Conference Proceedings
131
pollock. Back in the 1970s the pollock
available was Atlantic pollock, and
now the pollock that is in the market-
place is Alaska pollock. With 25
percent of the total catch being that
one species, it -will have a profound
effect on the total intakes you may
come up with.

Dr. Stern:
I agree that new data would
certainly be in order.

FDA Perspective

Dr. Mike Bolger, U.S. Food and Drug
Administration

Q: I've had 2 years' experience
dealing with mercury contamination
levels in Louisiana, and I recognize
that FDA and EPA and other scientists
understand the complexities of doing
an assessment when you 've got a site-
specific contamination problem. But
generally speaking we 've based our
advisories on the issue of critical
threshold for developmental. That
[value of] 0.07 micrograms per
kilogram per day is roughly what we
use. What that results in in our
exposure assessments is for pregnant
women and children an action level
kicks in at about 0.5 [ppm], based on
exposure assessment. We frequently
have people who oppose this level, and
I want to raise the problem of an FDA
legal standard that is an effect of 1,
and then when the health assessors are
pushed to the wall and asked what
level is safe for pregnant women and
children, and we finally come out with
something that is less than 0.1. Can
you tell us how to explain that to them?

Dr. Bolger:
It is a problem of comparing apples
and oranges. We continually box
ourselves in by forcing ourselves to
answer the question "Is it safe?" Then
we end up agonizing over the data
because we are trying to describe a level
that is "safe." When we talk about a
contaminant like methylmercury, and this
is the case with many contaminants
where we have a background level of
exposure in the
population of con- ______^^_
cern, the question we
should be asking
ourselves is "What is
the risk associated
with a particular
exposure?" Attempt-
ing to define a safe
level of exposure is not a useful exercise
on a population or individual basis. Is
the risk low or high or somewhere in the
middle? If we do not ask this question,
either as individuals or as a population of
consumers, then we cannot make rational
decisions as to the level of effort that will
reduce the risk in this most meaningful
way. In the end, it appears that there is a
discrepancy between what the FDA has
done in terms of its action level and what
the EPA has done in terms of the devel-
opment of a reference dose. This
difference is more apparent than real
because you are comparing two different
processes. The action level was devel-
oped for commercial species and in-
cluded considerations of not only the
available hazard information, but other
relevant information (e.g., background
environmental levels, analytical capabil-
ity, etc.). In contrast, fish advisories do
not include a consideration of the
consumption of commercial species, but
rather focus on the consumption of
recreational species and are designed to
deal exclusively with sport/subsistence
issues.

Mr. Hoffmann:
It is incumbent upon each of the
state regulators to try to explain, as
clearly as possible, the approach that
the state is using. To do this, you
must have a clear understanding of
what assumptions go into the FDA
national "action level." You must
recognize that FDA looks at the
commercial species and the impact
upon commercial fisheries when they
make their judgments. Some of their
key assumptions might not be appro-
box ourselves in by
forcing ourselves to answer
the question *Is it safe?' "
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132
National Forum on Mercury in Fish
priate for a state so a state may
choose to deviate from them. This
makes for a longer answer, and it's
one that people might not want to
hear. But nevertheless we need to
explain that one approach is based on
national averages assuming a mix of
different commercial species. For an
individual state or an individual water
body, there may be factors that are
different or unique to that area.
just averages. That was a probabilis-
tic analysis. Not everyone eats tuna
fish every day. There is a variety, and
the Monte Carlo approach attempts to
model the exposure pattern in the
population which more accurately
reflects what people actually consume,
how often they consume it, and how
the levels vary from day to day.
There is no average consumer. The
numerical average doesn't represent
anybody.
EPA Perspective

Dr. John Cicmanec, U.S. EPA

Q (Jerry Pollock, California EPA): Can
you estimate when the reference dose will
be available?

Dr. Cicmanec:
Hopefully by the next meeting, 1-2
months.
Group Discussion/Question'
and-Answer Session

Q (Jerry Pollock, California EPA): Is
your evaluation available in printed
form?

Dr. Bolger:
Yes, there is a manuscript and we
recently presented this risk analysis at the
international meeting on mercury which
took place in Whistler, Canada, this past
summer.

Q (Jerry Pollock, California EPA): In
my experience, it seems that any
individual eats only a limited variety of
fish. It's not a good idea to assume that
how much fish is sold is an indicator of
what people eat. Are there any studies
that indicate how many different species
offish an individual actually eats,
versus using these average numbers?

Dr. Bolger:
I was just looking at tuna con-
sumers, and we were not looking at
Q (Jerry Pollock, California EPA): The
point I'm trying to make is that, when we
look at the consumption of a low-fre-
quency species, there's only a limited
number of people who eat it. But for
those people who eat a lot of monk fish,
it's that number that we need to put in a
Monte Carlo distribution. It's not taking
monk fish and saying 194 million people
eat a few pounds of monk fish, coming up
with a low estimate, and then putting it in
the distribution. It's more like one million
people eat monk fish and that is what we
need to put into a model.

Dr. Stern:
Your point is well taken, and in
fact the Monte Carlo analysis was
modeling amount of the average mix of
species. I'm aware of no data that look
at the variability of the mix of species as
well as the variability in the consump-
tion of the overall mix. I would suggest
that a way of getting around that would
be looking at the biological indicators of
exposure.

Dr. Bolger:
I agree. That is a real problem for
us. When we look at a species like
shark, I have no data. I don't know who
eats it or how often.

Q (Jerry Pollock, California EPA):
There is going to be a consumption
study released from the Santa Monica
Bay Restoration Project that has some
distributions in it. Some of you may be
interested in that. I think the creel
information is useful in that regard.
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Conference Proceedings
I
133
When you look at creel, although it may
not be a good estimate of how much a
recreational type person is eating, it will
give you an idea about how many
species offish they eat. This must be
worked into the models.

Dr. Bolger:
We've talked about the need for
such studies on a federal level. There is
a new fish consumption survey from the
State of Florida where they're looking at
all the different species—commercial,
recreational, and subsistence—for the
entire state.

Q (Kim Mortensen, Ohio Department of
Health): Regarding the table John
[Cicmanec] showed on how many fish
can be eaten at safe levels, can you
comment on what you think you will be
coming out with in your final volume on
communicating risk and how to get
advice out to consumers?

Mr. Hoffmann:
As John showed, EPA is produc-
ing a four-part guidance series. The
sampling and analysis and consumption
tables are out already [Volumes 1
and 2]. Two other documents are under
way. One is for risk management. I
want to note that the consumption
recommendations in Volume 2 really do
not have a risk management component
built into them, so states should look
towards the risk management document
as well. It will address issues such as
appropriate fish consumption rates.
States often wrestle with this issue as do
we at the national level. The risk
management document should have a
comprehensive description of the
existing fish consumption surveys. The
document will be out in the next month
or two. [This has been delayed; it will
be out in 1995.] The other aspect is
how you communicate information that
is, to a large extent, site-specific. We
have a risk communication document
which is also under way. Dr. Barbara
Knuth from Cornell is the principal
author of this document, and she has
pulled together a lot of examples from
various state agencies. She has taken
general risk communication principles
and applied them specifically to fish
consumption advisories. The document
will include extensive appendices to the
document. They will include mainy
examples drawn directly from various
state agencies. We are sending out the
risk communication document to all 50
states for comment on the final draft.
[The final document will be available in
May 1995,]
"When you issue a public health
advisory, there are implications
beyond that public health advisory."
Q (Jerry
Pollock,
California
EPA): Rick,
regarding your
comment on ^———^^———
what EPA
provides and what FDA provides, I think
methylmercury presents a problem for us.
I'm going to have a problem when we issue
advisories if I use the lower RfD or lower
exposures for pregnant women and making
recommendations for fish that Jiave concen-
trations below 0.2 ppm, and not say
anything about commercial fish that have
high levels, like snapper.

Mr. Hoffmann:
A lot of the discussion on the RfD
choices has focused on what is an appro-
priate reference dose because the refer-
ence dose applies not only to fish con-
sumption advisories but to a whole
variety of other risk assessments. The
issue of the exposure comes later in the
process.

Dr. Bolger:
This is a constant problem. When
you issue a public health advisory, there
are implications beyond that public health
advisory. Whenever you say something
about methylmercury in bass, you're
really saying something about methyl-
mercury in tuna. I could take a fivefold
reduction in the RfD, which is what we're
looking at, and apply it to the action level.
I'm now down to 0.2, which is the average
for tuna fish. So, what conclusion do you
draw? We're going to take half the tuna
fish off the market? That's where you end
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134
National Forum on Mercury in Fish
up. It's a real problem and we are very
aware of it.

Q (Greg Cramer, U.S. Food and Drug
Administration): I think you 're
talking about the very heart of risk
management issues here. What do
you do in terms of this information?
Waiting for information from
Seychelle Islands to come up with an
answer that will help us with the fetal
outcome is very important. But if you
take the scenario that it says there are
real low-level effects, what do you do?
Do you tell everyone that we 're going
to ban all seafood because all fish
have mercury? The dietary changes
as a result of such a decision are
important. Perhaps we need to
provide information on how to make
informed decisions on how to change
your diet. These aren't easy issues.
-------
National Forum on
Mercury in Fish
A Review of Fish Consumption
Advisories
Robert £. Reinert
D.B. Wamell School of Forest Resources, University of Georgia, Athens, Georgia
Introduction

Transition from fish consumption
advisories based on U.S. Food and
Drag Administration (FDA) action
levels to advisories based on U.S.
Environmental Protection Agency
(EPA) risk assessment procedures has
caused confusion among fishery profes-
sionals, anglers, and the public. Why
do advisories always seem to be issued
for fish and not for terrestrial animals
such as squirrels or deer? How good are
our analytical techniques? What are the
differences between the older and newer
advisories? How are these recommen-
dations established, and how accurately
do they actually measure the health risk
associated with eating fish? Anglers
and the public deserve some basic
answers to these questions so they can
better understand this process that can
have a severe economic and social
impact on sport fisheries.
Fish—The Perfect
Biological Filter

If you asked a computer to design
the perfect system for filtering contami-
nants out of water, it probably would
come up with something that looked
like a fish or at least a fish gill. To
enhance the uptake of oxygen from
water, the surface area of a fish's gill is
many times greater than the combined
surface area of the rest of the fish. The
respiratory tissue of the gill is also
extremely thin—about 1/10 to 1/64 the
diameter of a human hair. This ex-
tremely thin tissue is all that separates
the water and the contaminants in it
from a fish's blood. Virtually all water
that is pumped across the gill contacts
this tissue, and most contaminants in
water rapidly pass from the water across
the gill membrane into the fish's blood,
which carries them to various parts of
the body. Add to this highly efficient
filter system the fact that fish, like
terrestrial animals, also accumulate
contaminants from their food and you
have an animal that has a high capacity
for concentrating contaminants from its
environment.
Not only are fish the perfect
concentrators, but their environment is
also the ideal collecting place for
contaminants. Runoff from land, direct
input from point sources, and input from
airborne pollutants add to the contami-
nant load in an aquatic system. Finally,
the solvent nature of water tends to keep
at least some of the contaminant in an
aquatic system in suspension hi the
water column, where it is available for
direct uptake by fish.
Differences Between FDA-
and EPA -Based Fish
Consumption Advisories

Although FDA action levels and
the EPA risk assessment procedures
135
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136
National Forum on Mercury in Fish
both use the principles of risk assess-
ment and risk management, they are
designed to protect different segments
of the population. The purpose of FDA
action levels established under the
authority of the Food, Drug, and Cos-
metics Act is to protect the general
public from contaminants in fish
shipped in interstate commerce
(USEPA, 1989). Action levels are
developed hi response to national needs
and are based on national patterns of
consumption that are often different
from those of local sport or subsistence
anglers (USEPA, 1989). In contrast, the
purpose of the EPA risk assessment
procedure is to provide the states with a
means for informing sport and subsis-
tence anglers about the health risks
associated with contaminated fish they
catch from local waters (USEPA, 1989).
These subpopulations of anglers are
potentially at greater risk than the
general population because they tend to
eat larger quantities of fish and because
they often fish the same locations
repeatedly.
For several reasons, fish consump-
tion advisories derived from the newer
EPA risk-based-assessment approach
generally give a much higher estimate of
health risk for a given level of contami-
nant than those based on the FDA
tolerance guidelines. The two agencies
use different risk assessment methodolo-
gies based on different assumptions
(USEPA, 1989), and fish consumption
rates vary in scope from national (FDA)
to local (EPA). Also, FDA action levels
are based not only on risk assessment
but also on risk management consider-
ations such as economic impacts likely
to accrue to the commercial fishing
industry (USEPA, 1889). For example,
the FDA clearly indicates that its
rationale for the current 2 ppm action
level for PCBs was a balance between
public health protection and the eco-
nomics involved in the loss of commer-
cial fish to the consumer (USFDA,
1984). In contrast, the EPA approach
for fish consumption advisories gives
full priority to protection of public
health. That some states use different
combinations of the FDA and EPA
procedures to formulate their advisories
further adds to the disparities in con-
sumption advisories among states.
How Low Can We Go?

During the past 30 years, develop-
ment of more sensitive analytical
instruments and better clean-up tech-
niques for samples have increased the
chemist's ability to detect contaminants
in fish and water about a million-fold.
In the early 1960s, the limit of detection
of many substances was in the parts per
million, which is equivalent to about
2 1/2 ounces of a substance in enough
water to fill a 20,000-gallon railroad
tank car. Now chemists can detect trace
amounts of most contaminants in the
parts per trillion, which is equivalent to
about 2 1/2 ounces of material hi
enough water to fill one million 20,000-
gallon railroad tank cars. This many
tank cars would make a train long
enough to stretch from the east coast to
the west more than three times.
With this increased analytical
ability, chemists now can find trace
amounts of contaminants in most bodies
of water and in most fish. For regula-
tory purposes, many times the question
no longer is whether a particular con-
taminant is in the water or fish, but
rather what effect if any these trace
amounts of contaminants have on the
fish and the animals, including humans,
that eat the fish. Unfortunately, our
ability to detect contaminants in the
envkonment has far surpassed our
ability to assess their effects.
Risk Assessment Models and
Calculation of Risk
Assessment Values

Because there is a lack of reliable
human epidemiological cancer data
involving environmental exposures,
animal bioassays provide most of the
information used to predict carcinogenic
effects on humans. Scientists use
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137
mathematical models to extrapolate
from effects of high doses administered
to experimental animals to effects of
low doses on humans corresponding to
levels found in the environment. There
are a number of possible models.
Depending on the one chosen, the
estimated increase in cancer incidence
can differ by several orders of magni-
tude (Brown, 1982; State of California,
1985). The model used by EPA is a
version of the linearized, multistage no-
threshold model developed by Crump
(USEPA, 1980). This model leads to
estimates of cancer risk that are very
conservative (i.e., it yields the highest
risk values) (USEPA, 1980, 1989). In
addition to its conservatism in extrapo-
lating from high to low doses, the EPA
model is also conservative in extrapolat-
ing from rodents to humans and differs
from the FDA in the approach used to
compensate for the size difference
between humans and rodents.
In any dose-response curve there is
a degree of uncertainty. Thus, scientists
calculate confidence limits, based on the
quantity and extent of the data, that are
the upper and lower estimates within
which the estimate of mean risk or "best
estimate" should fall. EPA reports the
increased cancer risk as the 95 percent
upper-bound estimate of the slope factor
(USEPA, 1980). This procedure
generally leads to the highest (most
conservative) estimate of the risk. If the
best estimate or the lower-bound
estimate were used, the risk value would
be much lower and could even be zero
or close to zero. Thus, the numbers
reported as an estimate of increased
cancer risk include margins of safety
and are conservative estimates of risk to
human health.
The 95 percent upper bound is
expressed mathematically as Ql*, the
carcinogenic potency factor or slope
factor (USEPA, 1989). The formula
P=(X)(Q1*) represents the increased
lifetime cancer risk (P) caused by
exposure to a daily dose (X) with a
potency factor (Ql *) for 70 years. The
daily dose is expressed as milligrams of
contaminant per kilogram of human
body weight per day. With the daily
dose, plus the size of each meal, the
concentration of contaminant in the
meal, an average size for the human
body, and a time factor in weeks or
months, one can calculate the number of
meals that, can safely be consumed over
a given time at a given level of in-
creased cancer risk.
For contaminants that do not
produce cancer but produce other health
effects such as nerve damage or birth
defects, the risks are not expressed as a
probability of occurrence but rather as
levels of exposure estimated to be
without harm. The daily dose for such
contaminants often is expressed as a
reference dose (RfD). Simply put, an
RfD is a rough estimate of daily expo-
sure to the human population (including
sensitive subgroups) that is likely to be
without appreciable risk of deleterious
effects during a lifetime divided by an
uncertainty factor (USEPA, 1993). The
magnitude of the uncertainty factor is
dependent on the quality of the toxicity
data. If there were a substantial amount
of good data on human exposures, the
uncertainty factor would be lower than
if the majority of the data were from
animal exposures. The risk manager
can use the RfD with the same elements
that were used above (i.e., human body
weight, time, meal size, and the con-
centration of contaminant in the meal)
to develop a fish consumption advisory
for noncarcinogens.
Questions About the Risk
Assessment Process

Animal bioassays that use high
doses of chemicals are coming under
increasing criticism because many
chemicals that cause cancer at high
doses might not cause cancer at the low
doses more comparable to human
exposure (Cohen and Ellwein, 1990).
Extrapolation from rodents to humans
has also been questioned because of
differences in life span and metabolic
rate, as well as biochemical and pharma-
cokinetic differences (State of Califor-
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National Forum on Mercury in Fish
ma, 1985; Ames et al., 1987). Also, the
actual shape of the lower end of the
carcinogen dose-response curve is hotly
debated. A noncarcinogen has a thresh-
old dose below which there is no
observable detrimental effect on the
animal. Conversely, a cancer might in
theory develop from a single trans-
formed cell. Therefore, cancer could
develop from a nonthreshold effect
initiated by very small doses of a
carcinogen reaching the right cell at the
right time (State of California, 1985).
However, even if there is no
threshold, marked alterations in meta-
bolic pathways that occur at high doses
but not at low environmental doses
could result in nonlinearity of the dose-
response curve for some animal carcino-
gens at low doses (Gehring and Blau,
1977; Hart and Fishbein, 1986). These
alterations could result in disproportion-
ately high incidences of cancer at high
doses. If a carcinogen does have a
threshold or if the dose-response curve
is not linear at low environmental
concentrations, the cancer risk could be
much less than that predicted by the
model.
About the only assumption on
which all factions involved in the risk
assessment controversy agree is that
decreasing the dose decreases the risk.
EPA's present conservative approach
assumes that any detectable amount of a
carcinogen has the potential for induc-
ing cancer (i.e., there is no threshold).
EPA takes this stance because cancer
researchers cannot determine with any
degree of certainty the minimum levels
at which substances cause cancer.
Another argument suggested in favor of
the conservative approach is that
exposure to low concentrations of a
variety of substances could have an
additive or synergistic effect (State of
California, 1985). Viewed in this
manner, EPA assumes that at low
environmental levels the dose-response
curve is linear and, therefore, no level of
exposure is free from risk.
Another conservative assumption
in the EPA risk assessment process is
that humans consume contaminated fish
for 70 years at a constant dose (USEPA,
1989). However, many compounds
listed as animal carcinogens (e.g.,
chlorinated hydrocarbon insecticides
and PCBs) have come into existence
only over the last 30-50 years. Also,
concentrations of many of these con-
taminants in aquatic systems are declin-
ing because of regulatory actions taken
over the last 25 years. For example,
average PCB levels in coho salmon
(Oncorhynchus kisutch) fillets from
Lake Michigan declined from 1.93 ppm
in 1980 to 0.39 ppm in 1984 (De Vault
et al., 1988). Using the EPA linear
model, this decline leads to about a five-
fold decrease in the estimated cancer
risk. Average DDT levels in Lake
Michigan bloater chubs (Coregonus
hoyi) declined from 9.94 ppm in 1969 to
0.67 ppm in 1986 (Hesselberg et al.,
1990). This decline would result in
about a 15-fold decrease in the esti-
mated cancer risk.
Because of the high degree of
uncertainty associated with the risk
assessment process, there is a tempta-
tion to delay issuing fish consumption
advisories until more reliable informa-
tion is available. Waiting, however, is
something agencies charged to protect
human health cannot afford to do.
Chemicals that cause cancer in experi-
mental animals and noncarcinogens that
cause a variety of deleterious effects are
in the environment and are accumulated
by fish. Because of the lack of knowl-
edge about the low-level effects of these
chemicals on humans, EPA has adopted
a very conservative approach to its
estimates of increased cancer risks and
other health risks in the interest of
public health. Despite the many short-
comings of interspecies extrapolation
models, at present they are the main tool
for predicting effects of environmental
and dietary levels of animal carcinogens
and noncarcinogens on humans.
Because use of the EPA risk
assessment process in state fish con-
sumption advisories is relatively new,
and because of the many associated
uncertainties, the process is under
constant review by EPA and the states.
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139
In the future, more states probably will
use some form of risk assessment
process in their fish consumption
advisories. Also, as new techniques for
predicting cancer risk and other health
risks such as developmental and repro-
ductive effects are developed, the states
will incorporate them into their fish
consumption advisories. Consequently,
even where concentrations of contami-
nants in fish remain the same, health
risks suggested by the advisories might
change.
Public Perceptions and Health
Advisories

State fish consumption advisories
can lead the public, and in particular
anglers, to the perception that fish are
the only food source that contains
contaminants. The sensitive instrumen-
tation now available makes it possible to
detect trace amounts of contaminants in
many other foods. Ames et al. (1987)
and Schuplein (1990) suggested that
dietary risks from natural carcinogens
might be much more important than
risks from synthetic pesticide residues
or contaminants in food. The same risk
assessment techniques discussed earlier
can be applied to any food. Based on
these calculations, the lifetime cancer
risk associated with drinking 1 pint of
milk per day is estimated to be 1 in
7,143 (Bro et al., 1987). One contami-
nant in milk is aflatoxin, produced by a
mold that grows on corn and peanuts
that may be used in feed grains. Simi-
larly, eating 4 tablespoons of peanut
butter per day, which also contains trace
amounts of aflatoxin, results in an
estimated increased lifetime cancer risk
of 1 in 1,666 (Bro et al., 1987). Risk
comparisons included in fish consump-
tion advisories should include dietary
risks from other foods, specifically
alternative protein sources. These
comparisons would be helpful to
persons who needed to replace sport fish
in their diet if they followed fish con-
sumption advisories (Wendt, 1986;
Clark et al., 1987).
Many anglers also perceive the
only risk Involved with fishing is the
health risk from eating contaminated
fish. Indeed, a risk factor can be
associated, with everything we do
including driving to the lake and going
fishing. Estimates of such risks are
derived from actuarial tables. Thus,
they are a different class of risk than the
lifetime cancer risks associated with
eating contaminated fish that are based
on extrapolations from animal data.
However, such risks do offer ang;lers a
way to place the health risks of eating
contaminated fish in perspective with a
variety of risks encountered in daily life.
The lifetime risk of death due to motor
vehicle accidents is 1 out of every 59
and deaths due to boating are 1 out of
every 400 (Clark et al., 1987). Thus,
driving to the lake and being out on the
water also involve risk.
A simple way anglers can decrease
contaminant-related health risks associ-
ated with eating fish is to trim and cook
the fish properly (Skea et al., 1979;
Foran et al.., 1989; Gall and Voiland,
1990). Because many organic contami-
nants are stored primarily in fish fat,
removing fatty areas can greatly reduce
the amounts of these contaminants
ingested and consequently reduce the
health risk. Skinning fish removes the
fatty layer between the skin and the
flesh. Filleting removes fatty areas
around the fins. Other fatty areas an
angler can remove are those along the
top of the backbone, the lateral line, and
the belly. Baking, broiling or grilling
fish on a rack drains off fats containing
organic contaminants. Puncturing the
skin also helps fats drain off. Although
these methods might also result in some
reduction of heavy metals in fish, the
reduction will not be as significant as it
is for organic contaminants because
heavy metals are more generally con-
centrated in muscle tissue.
In situations where there is an
advisory on a particular species or size
class, managers should make every
effort to let anglers know that other
species or size classes in that body of
water are safe to eat. Also, if strict
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National Forum on Mercury in Fish
advisories are being issued on stocked
fish, fishery managers might want to
reconsider their stocking program. An
alternative might be to stock fish with
less of a tendency to accumulate the
particular contaminant(s) causing the
problem.
Conclusions

Several strategies can be used to
increase the understanding of and
adherence to fish consumption adviso-
ries by anglers. First, the states need
to develop a more uniform approach
to their formulation of fish consump-
tion advisories. Anglers also need to
be made more aware of the assump-
tions used in the development of
advisories. For example, the EPA risk
assessment procedure assumes a 70-
year lifetime consumption of fish.
With this information, anglers might
choose to adjust their consumption of
fish according to their lifetime con-
sumption history. The use of a single
number as the estimate of health risk
(e.g., an increased cancer risk of 1 in
100,000) implies a degree of certainty
that, in fact, does not exist
(Fessenden-Raden et al., 1987). Risk
assessments that contain the full range
of risk estimates produced by
interspecies extrapolation models (i.e.,
upper-bound, best, and lower-bound
estimates) would provide risk manag-
ers with a more complete view of the
risk. However, risk managers must
find effective means of communicat-
ing this complex array of information
to the angler who only wants to know
if the fish are safe to eat. Television,
radio, newspapers, and magazines are
important sources of information for
anglers (Cable and Udd, 1990). Risk
communicators need to do a better job
of using these media to inform anglers
about fish consumption advisories.
Risk communication problems
associated with explaining fish con-
sumption advisories involve us in a
classic "bad news, good news" situa-
tion. The bad news is that we live in a
world contaminated with chemical
compounds. Aquatic systems are
sinks for these compounds, and fish
have a remarkable capacity to concen-
trate them. Relatively few of the
hundreds of chemicals that have been
identified in aquatic systems are
monitored routinely. Finally, we have
little information about the chronic
effects of many of these compounds
on fish and humans and even less
information about their additive or
synergistic effects. The good news is
that aquatic systems are remarkably
resilient. If a contaminant is pre-
vented from entering these systems,
its concentration in water, sediments,
and fish declines. Dramatic declines
in DDT and PCB concentrations in the
Great Lakes over the past 20 years are
good evidence of this (De Vault et al.,
1986, 1988; Hesselburg et al., 1990).
Further good news about fish
consumption advisories is that they
increase public interest in and concern
for water quality. Proper application
of risk communication can increase
anglers' understanding of fish con-
sumption advisories, keep them
interested in fishing, and help channel
their legitimate concern into actions
that will result in stricter water quality
regulations. The end result of such
actions will be improved water qual-
ity, which will benefit the health of
the fish and the health of the people
who eat them.
References

Ames, B.N., R. Magan, and L.S. Gold.
1987. Ranking possible carcino-
genic hazards. Science 236:271-
280.
Bro, K.M., W.C. Sonzagni, and M.E.
Hanson. 1987. Relative risks of
environmental contaminants in the
Great Lakes. Environ. Manage.
11(4):495-505.
Brown, C.C. 1982. High to low-dose
extrapolation in animals. In J.V.
Rodricks and R.G. Tardiff, eds.,
Assessment and Management of
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Chemical Risks, pp. 57-59. Ameri-
can Chemical Society, Washing-
ton, DC.
Cable, T.T., and E. Udd. 1990. Effec-
tive communication of toxic
chemical warnings to anglers. N.
Am. J. Fish. Manage. 10:382-387.
Clark, M.J., L. Fink, and D. De Vault.
1987. A new approach for the
establishment of fish consumption
advisories. J. Great Lakes Res.
13(3):367-374.
Cohen, S.M., and L.B. Ellwein. 1990.
Cell proliferation in carcino-
genesis. Science 249:1007-1011.
De Vault, D.S., M.J. Clark, G. Lahvis,
and J. Warren. 1988. Contami-
nants and trends in fall run coho
salmon. J. Great Lakes Res.
14(l):23-33.
De Vault, D.S., W.A. Willford, R.J.
Hesselberg, D.A. Nortrupt, E.G.S.
Rundberg, A.K. Alwan, and C.
Bautista. 1986. Contaminant
trends in lake trout, Salvelinus
namaycush, from the upper Great
Lakes. Arch. Environ. Contam.
Toxicol. 15:349-356.
Fessenden-Raden, J., J.M. Fitchen, and
J.S. Heath. 1987. Providing risk
information in communities:
Factors influencing what is heard
and what is accepted. Sci. Technol.
Hum. Val. 12:94-101.
Foran, J.A., M. Cox, and D. Croxton.
1989. Sport fish consumption
advisories and projected cancer
risks in the Great Lakes basin.
Am. J. Public Health 79:322-325.
Gall, K.L., and M. Voiland. 1990.
Contaminants in sportfish: Man-
aging risks. Cornell Cooperative
and Sea Grant Extension Fact
Sheet, Ithaca, NY.
Gehring, P.J., and G.E. Blau. 1977.
Mechanisms of carcinogenesis:
Dose response. J. Environ.
Pathol. Toxicol. 1:163-179
Hart, R.W., and L. Fishbein. 1986.
Interspecies extrapolation of drug
and genetic toxicity data. In D.B.
Clayson, D. Krewski, and I.
Munro, eds., Toxicological Risk
Assessment. Vol. I, Biological and
Statistical Criteria, pp. 3-35. CRC
Press, Inc., Boca Raton, FL.
Hesselberg, R.J., J.P. Hickey, D.A.
Nortrap, W.A. Willford. 1990.
Contaminant residues in the
bloater, Coregonus hoyi, of Lake
Michigan, 1969-1986. J. Great
Lakes Res. 16(1):121-129.
Jacobson, J.L., and S.W. Jacobson.
1988. New methodologies for
assessing the effects of prenatal
toxic exposure on cognitive
functioning in humans. In M.S.
Evans, ed., Toxic Contaminants
and Ecosystems Health: A Great
Lakes Focus, John Wiley and
Sons, Inc., New York, NY.
Schuplein, RJ. 1990. Perspectives on
toxicological risk—an example:
food-borne carcinogenic risk. In
D.B. Clayton, I.C. Munro, P.
Shubiik, and J.A. Swenberg, eds.,
Progress in Predictive Toxicology,
pp. 351-372. Elsevier Science
Publishers, Amsterdam.
Skea, J.C., H.A. Simonin, EJ. Harris,
S. Jackling, J.J. Spagnoli, J,
Synula, and J.R. Colghoun. 1979.
Reducing levels of Mirex, Aroclor
1254, and DDE by trimming and
cooking Lake Ontario brown trout
and smallmouth bass. /. Great
Lakes Res. 5:153-159.
State of California Health and Welfare
Agency. 1985. A policy for
chemical carcinogens: Guidelines
for chemical carcinogen risk
assessment and their scientific
rationale. Department of Health
Services, Berkeley, CA.
USEPA. 1980. Water quality criteria
documents. Federal Register
45(231):79318-79378. U.S.
Environmental Protection Agency
Washington, DC.
. 1989. Assessing human health
risks from chemically contami-
nated fish and shellfish: A guid-
ance manual. EPA-503/8-89-002.
U.S. Environmental Protection
Agency, Office of Marine and
Estuarine Protection and Office of
Water Regulation and Standards.,
Washington, DC.
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. 1993. ABCs of risk assessment.
USEPA Journal 19(1):10-15; 175-
N-93-014. U.S. Environmental
Protection Agency, Office of
Communications, Education, and
Public Affairs, Washington , DC.
USFDA. 1984. Polychlorinated
biphenyls (PCBs) in fish and
shellfish; reduction of tolerances;
final decision. Federal Register
49(10):21514-21520., U.S. Food
and Drug Administration Wash-
ington, DC.
Wendt, M.E. 1986. Low income
families' consumption of freshwa-
ter fish caught from New York
State water. Master's thesis,
Cornell University, Ithaca, NY.
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National Forum on
Mercury in Fish
Different People, Different
Approaches: Risk Management
and Communication hit Minnesota
Pamela J. Shubat
Environmental lexicologist, Minnesota Department of Health, Minneapolis, Minnesota
Introduction

A diverse population eats
Minnesota sport fish. Rates of
fish consumption range from
people who eat sport fish only a few
times each year to people who eat fish
several times a week during the height
of a fishing season. Populations differ
in their susceptibility to fish contami-
nants. As a result, there is a wide range
of risk associated with exposure to
contaminants hi fish. Many different
approaches in risk management policies
and risk communication practices are
required to address this diversity of risk.
Minnesota has issued fish adviso-
ries for the past 20 years and began
collecting data on methylmercury in fish
in 1969. Minnesota issued its first
mercury advisories in a 1977 press
release when levels that exceeded the
Food and Drug Administration's regula-
tory level of 0.5 ug/g were found.
Today the Minnesota Fish Consumption
Advisory program issues advisories in a
booklet and through specialized bro-
chures and supports these with a variety
of outreach activities. The "advisory" is
a booklet listing risk-based advice for
eating fish from 505 lakes and 66 sites
on 38 rivers and contains detailed
advice for specific sites, species of fish,
and sizes of fish. Other materials
targeting specific fish consumers
contain very simple guidelines. The fish
advisory program is flexible and adapt-
able to the needs of all Minnesotans.
Advice for Chronic
Consumption

The Minnesota advisory is in-
tended to keep a person's methylmer-
cury blood level below a threshold
associated with neurological effects.
For nonpregnant adults, the protective
level used in Minnesota is 20 ng/ml
methylmercury in blood, 10-fold lower
than the 200-ng/ml threshold associated
with parestliiesia in 5 percent of the
population studied in Iraq. According to
a pharmacokinetic model described by
Kershaw (Kershaw et al., 1980) and
the World Health Organization (WHO,
1990), this 20-ng/ml blood level corre-
sponds to a dose of 3 x IQr4 mg/kg/d
when intake and elimination are at
equilibrium. This is the same reference
dose the Environmental Protection
Agency has published on the Integrated
Risk Information System. To form an
advisory, this daily intake is converted to
the level of mercury in fish that is safe
to eat on a weekly or monthly basis. A
meal is defined as a 227-gram (0.5-
pound) meal offish for a 154-pound
person. A person can safely eat fish
with 0.16 to 0.65 ug/g methylmercury
once a week, can safely eat fish with
0.66 to 2.8 ug/g methylmercury once a
month, and cannot safely eat fish once a
month if it has more than 2.8 ug/g
methylmercury (Table 1).
This advice is communicated
through press releases at the opening of
the fishing season, published in a
143
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National Forum on Mercury in Fish
Table 1. Meal guidelines for persons eating methylmercury-contaminated fish. One meal is
assumed to be 0.5 pound cleaned fish (weight before cooking) per 154 pounds human body
weight
Exposure Duration
(1-year period)
ADULTS
1 to 3 weeks
3 weeks to 3 months
3 months or more
Methylmercury concentration in parts per million (ug/g)
<0.16
unlimited
unlimited
unlimited
0.16 - 0.65
unlimited
2 meals/wk
1 meal/wk
CHILDREN AND WOMEN IN CHILD-BEARING YEARS
1 to 3 weeks unlimited 1 meal/wk
3 weeks to 3 months 2 meals/wk 2 meals/mo
3 months or more 1 meal/wk 1 meal/mo
0.65 - 2.8
1 meal/wk
2 meals/mo
1 meal/mo
1 meal/year
0.5 meal/mo
do not eat
2.81 - 4.5
1 meal
1 meal/mo
eat none
do not eat
do not eat
do not eat
booklet, and summarized in the
annual fishing regulations guide. The
advisory booklet has meal advice for
fish in all of the water bodies that
have been tested to date, 505 lakes
and 66 sites on 38 rivers. This
booklet is available at state parks,
national forests, and natural resources
field offices, as well as at health
departments and university extension
offices throughout the state. The state
is now exploring options for a simple
and accurate advisory for untested
waters. Detailed advice for tested
waters (the current advisory booklet)
would still be used by anglers who
want to eat fish more frequently than
the recommendations in the proposed
general advisory.
Infrequent Fish Consumers

Many Minnesotans eat sport fish
only a few times a year and can use
advice that takes a short duration of
exposure into consideration. The
pharmacokinetic model allows for
calculations of acceptable doses for
less-than-chronic exposures. Exposure
durations of 3 weeks and 3 months were
used to develop fish advisories. Advice
is shown in table format and consumers
find the advice that matches then-
exposure pattern (Table 1). Anglers
eating sport fish for a few months of the
year are advised that it is safe to double
the amounts of fish considered safe for
chronic consumption. Anglers eating
sport fish for a few weeks are advised
that it is safe to eat four-fold higher
amounts of fish considered safe for
chronic consumption.
One important risk management
concern, so far unresolved in Minnesota,
is how to factor in consumption of
commercial fish. A short-term con-
sumer of sport fish who is eating a can
of tuna each week is chronically ex-
posed to mercury and should probably
be following advice for year-round
consumption.
Major communication concerns in
developing complex advice for short-
term consumers include questions of
how useful it is to people and whether it
conveys more certainty than what is
appropriate. In focus groups and
through written feedback, individuals
who have used the advisories in the past
say that they like more, not less, detail.
Minnesota will continue to evaluate
these concerns.
Advice for Fetal Protection

Methylmercury is particularly
harmful to the fetal nervous system.
In humans, the maternal blood level
associated with developmental delays
in Iraqi children is four- to five-fold
lower than levels associated with
paresthesia in adults. This implies a
woman can protect her fetus by
consuming one-fourth to one-fifth the
amount of methylmercury that is safe
for other adults.
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Four categories of advice are
used in the Minnesota advisory:
unrestricted, one meal per week, one
meal per month, and do not eat. For
any particular site, species of fish, and
size of fish, women of child-bearing
age are advised to use meal advice
4.3-fold lower than the advice for
other adults. For example, a woman
is advised to eat one meal a month of
fish that her male counterpart is
advised is safe to eat once a week.
Fish with less than 0.16 ug/g methyl-
mercury are safe to eat once a week, fish
with 0.16 to 0.65 ug/g are safe to eat
once a month, and fish with more than
0.66 ug/g mercury should not be eaten
(Table 1).
This advice is also offered to
women who may become pregnant. The
half-life of methylmercury in the
bloodstream is approximately 50 days.
Methylmercury uptake and elimination
reach steady-state after five to six half-
lives or about one year. The period of
time during pregnancy when the fetus is
most susceptible to methylmercury
toxicity is not known. That means a
woman should follow the fish advisory
for fetal protection at least one year
before conception.
After birth, an infant can continue
to be exposed to methylmercury through
nursing. Small amounts of mercury
pass into breast milk and form the only
source of exposure a child has until
weaned and eating fish. While it is not
clear what age is no longer particularly
sensitive to the developmental effects of
methylmercury, the nervous system is
still developing during infancy. Minne-
sota recommends that nursing mothers
and children under 6 years of age use
the more restrictive advice for fetal
protection.
One risk communication issue that
concerns us is that women ask for
information about commercially avail-
able fish. The Food and Drug Adminis-
tration found canned tuna averages 0.17
ug/g methylmercury (Yess, 1993). A
62-kg woman who wants to maintain
her blood mercury level at or below the
recommended 4 to 5 ng/ml should not
eat more than 7 ounces of canned tuna a
week. Shark exceeded 1 ug/g methyl-
mercury in 60 percent of 33 samples of
shark tested in Minnesota in 1991.
Tissue levels ranged from 0.2 to 4.9 ug/g
and averaged 1.4 ug/g methylmercury.
The safe fetal protection exposure level
for fish with this level of mercury is five
meals a year if that is the only source of
mercury during the year. The National
Fisheries Institute and the Food and Drug
Administration (1994) advise women to
limit meals of shark and swordfish to one
meal a month. Minnesota customarily
issues "do not eat" advisories when
methylmercury-contaminated fish cannot
safely be eaten at a rate of once a
month.
A risk communication challenge is
effective outreach to an audience that
has not traditionally used fish advisories.
Standard methods of outreach—keyed to
fishing openers and fishing regulation
guides—do not target women who do not
fish. The Minnesota Fish Advisory gets
media attention on the sports page, but
only recently has been covered in the
food section of newspapers. Primary
health care providers have been veiy dif-
ficult to reach. To meet this challenge, a
brochure intended for women who might
become pregnant was developed. It ex-
plains the health risks of contaminated
fish and directs women to the Minnesota
Fish Consumption Advisory. The bro-
chure also adlvises pregnant women not
to eat shark or swordfish and to limit
meals of canned tuna to one meal a
week. This brochure, An Expectant
Mother's Guide to Eating Minnesota
Fish, will be marketed to health care
providers through newsletters, through
health maintenance organizations, and di-
rectly to clinics.
Highly Exposed Population;;

It is not necessary to know how
much sport fish a population eats to issue
a fish advisory. However, these data are
useful in understanding the range of
consumption patterns and the impact of
the advice. This year 4,000 Minnesotans
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146
National Forum on Mercury in Fish
are being asked, in a random telephone
survey, how often they eat meals of
sport fish. Preliminary data suggest
approximately 2 percent of the general
population eats sport fish once a week or
more. During the height of the 1990
fishing season, about 5,000 anglers
answered similar questions in surveys
conducted at fishing sites around the
state (fisheries creel surveys). In these
targeted surveys anglers reported eating
32 grams fish per day (one 0.5-pound
meal per week). These surveys
oversample frequent anglers and might
represent a high-end exposure. In
surveys returned by 337 anglers who
received a 1993 Minnesota Fish Con-
sumption Advisory booklet, the average
consumption was 17 grams per day and
20 percent of those surveyed reported
eating fish at least once a week. Any-
one eating fish more than once a week
faces a potential risk of overexposure to
mercury since most game fish tested in
Minnesota have more than 0.16 ug/g
methylmercury.
Minnesotans with the greatest
potential of overexposure to contaminants
in fish include people who depend on sport
fish for food (subsistence anglers) and
people who eat highly contaminatedfish.
The fish advisory programcollects
anecdotalinformationabouttheseat-risk
populations from(l) otheranglers;
(2) fisheries personnelandconservation
officers; (3) social workers; (4) city,
county, and park officials; and (5) the
anglers or populations who identify
themselves as at-risk. Based oninforma-
tion from these sources, highly exposed
Minnesotans who havebeeneasily
identifiedincludeimmigrantpopulations
(primarily Southeast Asian), Native
American populations, and an indetermi-
nate number of urban poor or homeless
persons.
Minnesota has a large community
of Laotian (including Hmong), Cambo-
dian, and Vietnamese immigrants. Ap-
proximately 40,000 immigrants have
arrived in Minnesota since 1979, and
Minnesota has the second largest com-
munity of Hmong in the United States.
Southeast Asian anglers in Minnesota
tend to fish in large groups at some of
the most contaminated rivers in Minne-
sota. They are observed taking some of
the most contaminated fish, and they also
take home large quantities of fish. The
fish advisory program has collaborated
with the Minnesota Department of Natu-
ral Resources to conduct a limited survey
of fishing and fish-eating habits of this
population. Additional funding for more
work in this area is needed.
The risk management strategy for
this population has been to develop a
simplified version of the advisory that
focuses on the metropolitan area and
reduces the advice to two categories:
safe (eat all you want) and not safe (one
meal a month and clean the fish to
remove PCBs). The risk communication
strategy entails a combination of personal
interactions, written materials (including
translations), and visual materials. There
are cultural, economic, and language
barriers to communication that result in
poor access to this community. Due to
cultural practices and poor literacy, it is
difficult to reach this population through
health fairs, the mainstream media, or
mailed flyers. This audience is reached
through community meetings, demonstra-
tions at English and family education
classes, flyers posted at Asian food
stores, and the Asian community press.
Most recently, a Hmong-language video
on fish contamin' nts was produced by a
Hmong televisic producer, and it will be
shown on public television and distributed
to community organizations.
The Ojibwe or Chippewa of
Minnesota have identified themselves as
a potentially at-risk population. In
contrast to the Hmong or other Southeast
Asian communities, this population has a
sophisticated knowledge about environ-
mental health, health care, and health
care resources.
An exposure study was conducted
by the federal Agency for Toxic Sub-
stances and Disease Registry (ATSDR)
in northern Minnesota at the request of a
tribal government concerned about
overexposure to mercury. Fish adviso-
ries in the area cautioned anglers to limit
consumption of most game fish to one
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Conference Proceedings
meal a week. ATSDR conducted an
exposure assessment (asking about meal
type, frequency, and size) and measured
blood and hair mercury levels. ATSDR
found that only a few families ate fish
more than once a week and only one
individual had an elevated level of
mercury in blood (over 20 ng/ml).
This band and others innorthern
theirownfisheries. Abouthalfofthetribal
governments inMinnesotadistributefish -
advisories to their members. Therisk
managementissues associated with this
population arecomplex because insome
cases they arecollectingtheirown con-
taminant andhealth data. Theriskcommu-
mcationissuesforthis population are also
complexbecausecontaminationconcerns
andfishingpractices,suchas access to fish
andtribalrights to state waters, complicate
thehealthmessage.

Summary

The Minnesota Fish Consump-
tion Advisory has evolved to a flexible,
complex format as the needs of anglers
have changed over the years. Risk-
based advisories for methylmercury
allow for modifications based on duration
of exposure and reproductive status. As
new at-risk communities are identified,
the risk communication approach is
modified to tailor the advisory to their
needs.
References

FDA Consumer. 1994. Mercury in.
fish: Cause for concern? FDA
Consumer September 1994:5-8
Kershaw, T.G., P.H. Dhahir, and T.W
Clarksora. 1980. The relationship
between blood levels and dose of
methylmercury in man. Arch.
Environ. Health 35:28-36.
WHO. 1990. Environmental Health
Criteria 101. Methylmercury.
World Health Organization,
Geneva. 144 pp.
Yess,N.J. 1993. U.S. Food and Drug
Administration survey of methyl
mercury in canned tuna. J. AOAC
Int. 76:36-38.
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National Forum on
Mercury in Fish
Development of Risk-Based Fish
Consumption Guidelines in Georgia

Randall O. Manning
Environmental Protection Division, Georgia Department of Natural Resources, Atlanta, Georgia
As a result of the growing concern
regarding toxic contamination of
aquatic resources and the
increasing amount of information
available pertaining to toxicity of
different chemicals and risk assessment,
the Georgia Department of Natural
Resources (DNR) formed a committee
to develop guidelines for monitoring
fish tissue contamination and issuing
fish consumption recommendations.
Committee members included
R. Manning, Georgia Environmental
Protection Division; C. Coomer, Geor-
gia Wildlife Resources Division;
J. Crellin, Agency for Toxic Substances
and Disease Registry; R. Reinert,
University of Georgia; J. Stober, U.S.
Environmental Protection Agency; and
P. Winger, U.S. Fish and Wildlife
Service. The guidelines developed by
the Fish Tissue Advisory Committee
(FTAC) are for a systematic, ongoing
monitoring plan for rivers and lakes.
The monitoring strategy consists of two
tiers of studies.
Primary and Secondary Studies

The objective of the primary study
is to identify waterbodies where chemi-
cal contaminants are present in fish in
concentrations that might represent a
health threat to anglers while providing
sufficient data to issue specific con-
sumption recommendations for at least
two target species. Target species
recommended for the primary study are
one bottom-feeding species (catfish) and
one predator species (largemouth bass).
A list of recommended target
contaminants and detection limits,
including 13 metals and 30 organic
pesticides/PCBs, was developed.
Dioxins and dibenzofurans were not
included on the list of target contami-
nants. Currently, dioxins/dibenzofurans
are monitored in fish tissue (whole fish
and fillets) in the vicinity of five
bleached kraft pulp mills in Georgia.
The studies are conducted yearly by a
consulting firm following a study
protocol that was approved by DNR.
For the primary study, three sites
should be chosen to provide adequate
coverage of most lakes. More than three
sites might be needed in larger lakes to
define the geographic extent of contami-
nation adequately. Site selection in
rivers depends on the river reach to be
covered by consumption guidelines.
Sampling should be conducted on a
yearly basis in late summer through fall.
Compositing edible fillets from
individuals prior to analysis provides a
means of collecting information on
average contaminant concentrations
from a large number of fish with a
limited number of analyses. The vari-
ability among contaminant concentra-
tions in individual fish is lost by
149
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150
National Forum on Mercury in Fish
compositing. However, an accurate
estimate of individual variation is not
necessary to meet the objective of the
primary study. Therefore, composite
samples were recommended to reduce
the cost of analysis for the primary
study. An edible fillet is defined as the
fillet portion of the fish including the
bellyflap. For scaled fish, fillets should
be scaled but left with the skin on. For
fish without scales, the skin should be
removed from the fillet. Composites
should contain tissue from five indi-
vidual fish for a target species. Tissue
from different species of fish should
never be mixed to produce a composite.
Fish collected should be of a size
that is representative of what fishermen
are likely to catch in the area. Ideally,
the smallest fish in a composite should
be at least 75 percent of the size of the
largest fish. Composites should be
prepared with five fish of a similar
length representative of three size
classes (i.e., <12 in, 12-16 in, and >16
in). This will allow for the development
of consumption guidelines based on size
classes offish. Three replicate compos-
ites for a size class are needed to issue
consumption recommendations.
The objective of the secondary
study is to provide information regard-
ing additional fish species or to further
define geographic extent of contamina-
tion for water bodies where the primary
study resulted in restrictions on fish
consumption. Target species for the
secondary study should be chosen based
on site-specific information related to
fish populations and fishing preferences
of the local anglers.
Data Analysis and Fish
Consumption Advisories

In the past, DNR has based fish
consumption advisories on FDA action
levels or tolerances that have been set
for mercury, approximately 12 pesti-
cides or related degradation products,
and PCBs. In recent years, interest in
the use of risk-based approaches has
increased. With these methods, one can
calculate a quantitative value for risk
from consumption of fish containing
carcinogens. It should be emphasized
that risk calculations are only estimates;
the actual risk cannot be determined.
Currently, probability is not used
to express the potential for noncancer
toxicity. Instead, the potential for
noncancer toxic effects is evaluated by
comparing an exposure level for a
specified time period with a reference
dose or RfD (i.e., a level of exposure
below which it is unlikely that people
will experience any adverse health
effect). If this ratio, referred to as a
hazard quotient, exceeds unity, there
might be concern for potential
noncancer effects.
Dourson and Clark (1990) pro-
posed a method to improve the credibil-
ity of fish consumption advisories and
make them more useful for the average
fish consumer. The proposed model
accounts for the amount of fish con-
sumed (one of the most difficult param-
eters to determine) by making fish
consumption the dependent variable and
recommends that, where consumption
should be limited, advisory information
be provided as number of fish meals
allowed per month, week, or day.
The steps required for evaluation
of data with the Dourson and Clark
(1990) model begin with the calculation
of fish intake from the appropriate RfDs
for noncancer toxicity or potency factors
for cancer. The second step is to esti-
mate the amount of fish consumed per
meal. Dourson and Clark (1990) sug-
gested that a difference of approxi-
mately twofold (0.25 to 0.5 Ib) exists in
the size of individual fish meals. This
range of meal size and the frequency of
fish meals eaten over a given period
follow a logarithmic scale. That is, the
consumption of 3 to 10 grams of fish
per day is in the range of eating one
0.25- to 0.5-lb fish meal per month; the
consumption of 10 to 30 g/day is in the
range of eating one 0.25- to 0.5-lb meal
per week; the consumption of 30 to 100
g/day is in the range of eating three
0.25- to 0.5-lb meals per week; and the
consumption of 100 to 300 g/day is in
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Conference Proceedings
the range of eating one 0.25- to 0.5-lb
meal per day. The fish consumption
advisory proposed by Dourson and
Clark (1990) is developed from a direct
comparison of calculated fish intake
values to the estimated amount offish
consumed per meal and meal fre-
quency. However, in the interest of
simplicity, FTAC recommended
reducing the number of recommenda-
tions from six to four by categorizing
consumption greater than 30 g/day (3
meals/week and 1 meal/day) as nonre-
stricted.
The use of this model allows the
release of a gradient of recommenda-
tions ranging from unlimited consump-
tion to complete restriction with
intermediate recommendations based
on fish meals per week or month.
Another advantage of the method is
that it enables one to conduct risk
assessments for mixtures (i.e., assess-
ments when more than one chemical is
present in fish tissue) for either car-
cinogens or toxics with similar organ
effects.
Management decisions must be
made concerning appropriate inputs for
the basic model parameters. For
analyses of carcinogens, an appropriate
nsk level, a standard body weight, and
an exposure duration must be chosen.
For analyses of noncancer toxicity,
only body weight and exposure dura-
tion must be chosen. FTAC recom-
mended that in the model a risk level
of lO"4 be used for analysis of carcino-
gens, 30 years as the exposure dura-
tion, and 70 kg as the adult body
weight in evaluations for both carcino-
gens and toxics.
Special Considerations
Related to MethySmercury

Methylmercury presents a unique
problem when evaluated as a toxic in
the model described herein. The RfD
for chronic toxicity is 3 X 1Q-4 mg/kg-
day. Because of concerns of develop-
mental toxicity, U.S. EPA's Office of
Water has recommended the use of a
provisional RfD of 6 X 10-5 mg/kg-day
for women of reproductive age and
children.
In the interest of simplicity and
minimizing confusion when converting
to a new approach, FTAC recom-
mended that only one set of consump-
tion guidelines, for adult chronic
exposure, be produced. However, to
ensure that women of reproductive age
and children are adequately protected,
they should, be encouraged to limit
consumption to a greater extent than
recommended in the guidelines. For
example, women of reproductive age
and children should limit consumption
as follows:
If the guidelines
recommend:
no restriction
1 meal/week
1 meal/month
do not eat
Limit consumption
to:
1 meal/week
1 meal/month
do not eat
do not eat
To evaluate the degree of "protec-
tiveness" achieved with this strategy
compared to that using U.S. EPA's
provisional and chronic RfDs for
methylmercury, comparative values are
provided in Table 1.
Education/Communication
Strategies

DNR used a communications
consultant (Ringo Research Associates,
Atlanta, Georgia) to assist in acquiring'
public input for the proposed model
and developing a communication
strategy. In the fall of 1993, six meet-

Table 1. Ranges of allowable tissue concentrations for mercury
and categories of meal advice ««ry
Fish Intake and Meal Advice
Contaminant
^——,—,

Hg,T (chronic RfD)
Hg,T(subpopRfD)
Hg,T(G A advice)
>30g 30-llg
No restriction Imeal/wk
10-3g <3g
1 meal/mo Donoteat
<0.70
<0.14
0.70-2.10
0.14-0.42
<0.70
2.10-7.00
0.42-1.40
0.70-2.10
>7.00
>1.40
>2.10
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National Forum on Mercury in Fish
ings were held around the state to
provide the public an opportunity to
learn about the proposed method and
provide input. Several different types
of "stakeholders or customers" were
identified and invited to each meeting.
These included environmental activists,
lake association representatives,
owners of lakeside businesses (bait
shops, marinas), fishing guides, and
local sportfishermen. Meeting size was
limited to approximately 15 people so
that an informal discussion group
format could be used. A brief overview
of the proposed method (15 minutes),
prepared by the consultant for the
general public, was given and then the
floor was opened for discussion. Total
meeting time was limited to 2 hours. A
seventh meeting was held for Georgia
Power Company and the Corps of
Engineers, two major stakeholders
managing reservoirs in Georgia. The
format was similar with the exception
that more people attended (-30), a
more technical presentation was
presented, and time for discussion was
not limited.
The consultant facilitated the
discussions to ensure coverage of
several topics including first impression,
positive or negative; need for new
method, reasons for change; suggestions
for communication/education; media
exaggeration; the trust issue; putting risk
or hazard in perspective; and special
communication needs.
Responses during the meetings
were generally favorable regarding the
need for a more informative, easily
understandable system of conveying
consumption information, and the
format proposed. Some participants
had difficulty in understanding the
change in philosophy from the current
systems in which only "do not eat"
information is issued, to the proposed
systems in which different types of
information will be issued, allowing
the individual more latitude in deter-
mining how to restrict fish consump-
tion. However, as participants' ques-
tions were answered and discussed
openly, most people became comfort-
able with the concept by the end of the
meeting. Much of the discussion
focused on how to educate people to
understand the proposed system and
how to ensure that the information gets
to everyone.

General Recommendations for
Communication Strategy
1. Continue to involve stakeholders
in the process as the method is
refined and unproved.
2. Educate and use field personnel
(rangers, fisheries biologists, and
others) as front-line communica-
tors. They deal directly with the
public and their credibility is
often better than that of regula-
tors from DNR. The importance
of one-on-one communication
and communication to small
groups (fishing clubs, local
organizations, etc.) via field
personnel was mentioned fre-
quently.
3. Identify key local "communica-
tors" in lake areas. Educate them
and use them to convey informa-
tion. Examples of these people
include individuals who have
considerable influence on opin-
ions of fishermen, such as fishing
guides or marina and boat ramp
operators.
4. Different types of information
will be needed for different
customers. Identify those needs
and target information accord-
ingly- , ,
5. Keep information simple, clear,
and easy-to-understand. Be
prepared to repeat a consistent,
simple message over and over.
6. Put risk (or hazard) hi perspective
for people.

Specific Recommendations for
Implementation
1. Place articles, preferably written
by outdoorsmen, in sporting and
outdoor magazines to describe/
discuss new method in first year.
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Conference Proceedings
153
2. Produce a booklet with a brief
discussion of the process DNR
uses to monitor and assess
contamination, how DNR's
recommendations are developed,
what contaminants are found in
fish, and what the health risks
(and benefits) from consuming
fish are, followed by tables of all
the recommendations for differ-
ent water bodies.
3. The booklet should be updated
yearly and available where
fishing licenses are purchased, at
marinas and bait shops, and from
all DNR offices.
4. Produce color-coded tables
(signs) for posting at boat ramps.
5. Produce a short video and/or
slide set describing the program
that can be used by field person-
nel when speaking to groups.
Current Status

Sampiles of fish were collected
from 27 lakes and approximately 20
river reaches in 1991,1992, and 1993.
Collection sites have been designated
for the fall of 1994. Development of
educational materials and refinement of
a communication strategy are currently
under way. The system described herein
has not been officially approved by
DNR, but plans are continuing for an
implementation date of spring 1995.
References

Dourson, M.E., and M.J. Clark. 1990.
Fish consumption advisories:
Toward a unified, scientifically
credible approach. Reg. Toxicol.
Pharmacol. 12:161-178.
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National Forum on
Mercury in Fish
Managing and Communicating
Mercury Risks in Arkansas
Kent Thornton
Arkansas Mercury Task Force Coordinator, FTN Associates, Little Rock, Arkansas'
It is axiomatic that communication is
critical in all phases of risk assess-
ment and risk management. Yet, risk
communication is typically the last
activity considered as part of either risk
assessment or management. We found
that establishing lines of communication
early in the process was critical in
addressing the mercury problem in
Arkansas.
In the summer of 1992, Louisiana
issued a fish consumption advisory
because of mercury contamination
found in fish taken from the Ouachita
River just below the Arkansas-Louisiana
border. Historically, mercury concen-
trations were negligible in fish collected
in the Ouachita River in Arkansas, so
the fish consumption advisory was a
surprise. We had previously collected
fish from the lower portion of the
Ouachita River, but had frozen the
samples because funds were not avail-
able for a complete contaminate scan.
These fish samples were analyzed and
found to contain mercury concentrations
that were near or exceeded the FDA 1
mg/kg action level for tissue. Subse-
quent sampling offish tissue from the
Ouachita River indicated predator fish
exceeded the FDA action level, and a
fish consumption advisory was issued
'Contributing authors, by agency, include P. Burge
S. Evans and T. McChesney, Arkansas Department of
Health; J. Giese and A. Price, Department of Pollution
Control and Ecology; Mike Armstrong and Don
Turman, Game and Fish Commission, and J. Nix, Ross
Foundation and Chair, Arkansas Mercury Task Force
for the lower Ouachita River in Arkan-
sas (Figure I). Based on these findings,
we initiated a planned, systematic
approach for addressing the problem that
involved:
1. Developing a strategic approach
to address risks from mercuiy
contamination.
2. Boundingthescopeoftheproblem.
3. Managing and communicating
risks for fish mercury contamina-
tion.
Identifying the Strategy

The first activity was to address
initial public concerns about the health
risks from eating mercury contaminated
fish. A communication approach was
developed that included:
1. Public meetings.
2. Free blood screening for anyone
in the affected areas.
3. Fish consumption advisory
brochures.
4. Information dissemination at
county fairs, bass clubs, church
groups, Rotary and Kiwanis
clubs, and other civic organiza-
tions.
The Governor established a
Mercury Work Group that included
public and special interest group mem-
bers and was chaired by a well-known
scientist who was respected and trusted
throughout the state. This Work Group
kept the Governor, Legislature, press,
155
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National Forum on Mercury In Fish
and public informed on all aspects of the
mercury problem. The Work Group's
strategy was guided by a set of clearly
defined questions:
1. What is the extent and magnitude
of the problem?
2. What are the risks to human
health?
3. Why do we have the problem and
what are the sources of the
mercury?
4. What can we do to manage or
solve the problem?
5. Have we always had this problem
or did it develop recently?
An objective, scientific approach
was developed to answer these ques-
tions. The approach was designed to
provide incremental information on
these questions. The approach also was
prioritized to:
1. Continue to communicate infor-
mation and results to the public
on the mercury problem through
Figure 1. Shaded area of Ouachita River in eight southern Arkansas counties was
initial area for fish consumption advisories.
a Mercury Task Force and a
Mercury Advisory Committee.
2. Assess the magnitude and extent
of the problem and the potential
risk to public health.
3. Formulate initial management
actions to ameliorate the problem.
4. Identify possible sources and
causes of the problem.
5. Evaluate historical trends.
This strategic plan was submitted
to the Governor and subsequently
funded by the Arkansas Legislature.
The next step was to bound the scope of
the problem and establish a baseline for
future comparison.
Bounding the Scope of the
Problem

A systematic sampling approach
was used to implement the strategic
plan. This included sampling point
sources discharging
directly into the
Ouachita River or its
tributaries, sampling
from the border up-
stream to determine the
extent of the problem,
and sampling areas
where mercury contami-
nation might be ex-
pected based on stream
characteristics as well as
where it was not ex-
pected.
A two-phased
approach was followed,
with screening sam-
pling conducted as part
of Phase I (Figure 2)
and more intensive
Phase n sampling
conducted where
confirmation of screen-
ing results and/or
greater geographic
definition of the prob-
lem was needed. The .
largemouth bass was
used as the indictor
species for screening
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C....:,;c.ice Proceeciings
because it is a popular sport fish in
Arkansas, is at the top of the aquatic
food chain, and biomagnifies mercury
(Figure 3), with concentrations exceed-
ing FDA action levels in larger fish.
Fish composites were taken and grouped
by length class.
When fish mercury concentrations
exceeded or were near the FDA action
level of 1 ppm (mg/kg), confirmation
sampling was immediately conducted.
If the confirmation samples also ex-
ceeded the action level, a fish consump-
tion advisory for that body of water was
issued. Phase H sampling also included
developing fish length-mercury relation-
ships for selected species of popular
sport fish such as the white crappie and
sunfish (Figures 4 and 5). These fish
length-mercury relationships were
critical in reducing some of the fish
consumption advisories to include only
specific species such as the largemouth
bass greater than 16 inches in length
rather than all predator fish. This
reduction had important
economic consequences
for southern Arkansas,
particularly for fishing
license sales, bait shops,
fishing stores, and
associated businesses.
Without these relation-
ships, the fish consump-
tion advisories would
have been retained for
all predator fish, regard-
less of species or length
(age).
Good geographic
coverage of the Phase n
sites was ensured by
overlaying a random,
systematic sampling grid
on Arkansas and com-
paring the sites that had
been sampled in Phase I
with the randomly
selected sites. This
enhanced sampling grid
was provided by the
EPA Environmental
Monitoring and Assess-
and indicated there were geographic
areas that did not have adequate cover-
age. Additional fish samples were
subsequently collected in those areas.
In addition to the fish samples,
sediment and water samples also were
collected throughout the Ouachita River
basin and analyzed for total mercury. In
general, the concentrations of total
mercury in the water and sediment
samples were relatively uniform
throughout the Ouachita River basin,
being within a factor of 2 for all
samples. The average total mercury
concentration in sediments throughout
the Ouachita River basin was 0 11 mg/g
or ppm (sd = ± 0.21, n=l 11). In addi-
tion to sediment sampling, geologic
samples of rocks were collected
throughout the Ouachita Mountains.
These rocks were ground and analyzed
for total mercury. The average total
mercury concentration in 724 rock
samples from the Ouachita Mountains
was 0.17 ug/g (sd = ± 0.24). The
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158
o 350 400 450 500 5SO
Length (mm)
Figure 3. Increased mercury concentration in largemouth bass as a function ot
length (age) in Felsenthal National Wildlife Refuge.
'lOO 150 200 250 300 350
Length (mm)

Figure 4. Length-mcrcury relationship in white crappie in Felsenthal National
Wildlife Refuge.
National Forum on Mercury in Fish
frequency distributions of
total mercury in sediments
and rocks were remark-
ably similar (Figure 6).
While this does not
confirm geologic origin as
the source of the mercury,
it does indicate there
might be other sources in
addition to atmospheric
deposition. These studies
are being continued to
determine whether
geologic sources can be
readily methylated.
The information
collected as part of the
sampling effort was
communicated to the
public and used to initiate
management actions.

Managing and
Communicating
Risks from Fish
Mercury
Contamination

The strategic plan
proposed that two groups
be established to manage
and communicate the risks
from fish mercury con-
tamination. These two
groups are the Arkansas
Mercury Task Force and
the Arkansas Mercury
Advisory Committee.
The Arkansas
Mercury Task Force is the
coordinating group for
mercury studies in Arkan-
sas. The Task Force
consists of an independent
Chair and Coordinator, the
Directors of the respon-
sible state agencies—
Arkansas Department of
Health, Department of
Pollution Control and
Ecology, and Game and
Fish Commission—and
the Director of the Univer-
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""~~^^^^^

sity of Arkansas Water
Resources Research Center.
The Arkansas Mercury
Advisory Committee is one
of the principal vehicles for
communicating information
to the public. This commit-
tee is chaired by a knowl-
edgeable, respected layper-
son from southern Arkansas,
and has membership from
federal, state, and local
agencies such as the USDA
Extension Service, FDA, and
Arkansas Science and
Technology Authority;
private sector and civic
organizations such as electric
utilities; special interest
groups such as the Arkansas
Wildlife Federation; and the
press, including the Arkansas
Educational Television
Network. Each of these
members serves as a liaison
to communicate information
to their respective agencies/
organizations and their communities.
During the early stages of identify-
ing the mercury problem, it was obvious
that, while public meetings were very
important for conveying information,
these meetings were too time-consum-
ing and provided information to only a
small segment of the community. A
video, Mercury in Fish: A Problem We
Can Live With, was developed by the
Task Force for distribution throughout
the state. The Mercury Advisory Com-
mittee was one of the primary outlets
for distribution, but the video also was
provided to all county and regional pub-
lic health units, conservation offices,
wildlife refuges, state parks, schools,
and similar organizations. In addition
to being the medium watched by the
high-risk groups (young children, preg-
nant women, and women who might
become pregnant), it can be shown to
almost any audience. The county health
units, for example, put the video on
continuous loop in their waiting rooms,
particularly for the WIC and Prenatal
Health Care programs.
159
in Wuegillcrappie in Felsenthal National
Fish consumption advisory
brochures are prepared on at least a
quarterly basis and distributed through
all bait shops, sporting good stores, and
marinas. In 1995, the brochures also will
be distributed with both fishing and
hunting licenses. Special articles have
been prepared for outdoor magazines,,
newspapers, medical journals read by
Arkansas physicians, and newsletters of
special interest: groups and civic
organizations. Using multiple media is
critical because the high-risk groups
can be difficult to reach with informa-
tion on the risks from mercury contami-
nation.
Lessons Learned

The following lessons were
learned during the past 2 years of
experience in Arkansas:
1. Communication is the issue. It is
critical that a broad group of
communicators be trained and
used in communicating informa-
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National Forum on Mercury in Fish
tion on the risks of consuming
fish contaminated with mercury.
These communicators include the
following:
• Health officials.
• Fisheries and wildlife conser-
vation officers.
• Extension service personnel.
Physicians/nurses.
Scientists.
Community laypeople.
Public officials and other
individuals who have contact
with the public, in particular,
contact with the high-risk
consumer groups.
Rocks

Sediment
0.4 0.8 1.2 1.6 2.0
Mercury (ug/g)
i
Figure 6. Joint distribution of sediment mercury concentrations in the Ouachita River
and rock mercury concentrations in the Ouachita Mountains.
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Conference Proceedings
161
2. Keep the message the same and
keep it simple. Individuals need
to hear the same message 4-6
times before they fully under-
stand what is being said. Con-
tinually changing the message
confuses communication.
3. Use multiple media because the
high-risk group is hard to reach.
This should include:
• Videos
• County health unit handouts.
• School programs and
children's messages.
• Radio public service an-
nouncements.
• Television news reports and
public service announce-
ments.
• Educational television.
• County/state fairs.
• Bass tournament brochures.
• Newspapers and newsletters,
etc.
4. Develop an organized approach
to distributing information. Out-
reach committees are critical at
the local, state, and national levels.
5. Develop an approach to manag-
ing and communicating informa-
tion on the risks from mercury
contamination that is founded on
scientifically sound, strategic
approaches that have a clear set
of questions to be answered; that
are conducted through coordi-
nated, cooperative efforts of all
responsible agencies; and that
use a systematic sampling
approach.
6. Keep an open-minded perspective
on mercury sources and manage-
ment options and alternatives. It
is unlikely that there is a single
source or a single solution.
Focus on incremental increases in
information.
7. Identify interested, informed
people to participate. Do not
settle for the individual who
currently is not busy. We made
progress because we had indi-
viduals who were concerned
about the problem, aggressively
attacked it, and were not con-
cerned about agency affiliations.
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National Forum on
Day Two: September 28t199^\
Mercury in Fish
Questions and Discussion:
Session Two
After each speaker's presentation,
an opportunity for questions and
answers was provided. Time
was also allotted for a group discussion/
question-and-answer session.
A Review of Fish Consumption
Advisories

Dr. Robert Reinert, University of
Georgia

Q (Arnold Kuzmack, U.S. EPA,
Headquarters): Regarding your
experience of success communicating
with people by comparing [one type of
risk] to other risks, our experience
trying to do that is generally very-
negative. People are not reacting so
much to the quantitative information
as to the anger that somebody has
done this to them. This kind of com-
parison makes them more angry
because they perceive that you're
trying to minimize what they're
concerned about.

Dr. Reinert:
The worst way to do this is to have
an article pop up in the paper. You have
to go about it gradually, before these
things are released. Build a base. It
doesn't come easy. We're going to get
hit and we're going to get hurt. If you
work at it and build a base, you can
slowly educate the public. Look at
cigarette smoking as an example. We
can [talk about fish consumption risks]
without terrorizing people and having
them quit the sport.

Q (Kim Mortensen, Ohio Department of
Health): I disagree with you on parts of
your approach. I think you 've underes-
timated the rage factor. We must
understand how much rage people have
about imposed risk. There is a problem
of trivializing risk. When I go out to the
public and tell them I'm concerned
about a risk from PCBs or cancer, I go
out as an expert. They look to me for
advice. And if you go out there and
trivialize the risk, your message has
been severely undercut. From my
experience, you are putting across a
mixed message.

Dr. Reinert:
I'd never go out there and trivialize
what work has been done. I tell them
this is the best we're doing with what
we've got and that it is a problem. But,
pay attention to where the advisories are.
You always get two extreme groups with
a lot of power. One group will disregard
all the advisories, and the other group
will be terrified of them and quit. I think
we tend to underestimate the audience.
Be honest with the audience; get the in-
formation to them. I don't think we
should downplay, but I think you have to
bring them into some perspective. There
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National Forum on Mercury in Fish
*Our ability to detect things
has certainly surpassed our
ability to say anything about
the effects.9*
are many risks involved in things, other
than fish, that have contaminants in them.
Tell them that.

Q (Rob Reash, American Electric
Power): I thought your comment about
detection limits surpassing the ability to
elucidate effects in the real world was
very interesting. At this point we 're in
an era where that is not a theoretical
management
position, but is a
real one that's
happening. I'd
like to bring up an
example of
detection limits
__________ going down using
fish consumption
advisories to take water quality stan-
dards further down. I'm not talking
about subpopulations that are at risk.
My point is when agencies adopt these
very, very low water quality standards.
Take, for example, in the Great Lakes
where EPA has proposed 0.18 nano-
gram per liter wildlife criteria for
mercury. Now all of a sudden all these
health effect studies are going to be
done, which won't be completed for 3 to
4 years. Now all the agencies want to
study mercury levels in fish and see
where we've been. It seems that things
are a little backwards.

Dr. Reinert:
A lot of these advisories have led
people to think that water quality now
is getting worse and worse. I think
that for many things it's not. It's
getting better than it was. If you look
at fish populations, birds of prey
populations, they're coming back.
Now we're at a stage where it's not so
much from a point source, but from
airborne pollutants, and production
levels seem to be leveling off. Now
these animals that are reproducing, are
reproducing, but we're seeing some
effects. So we've gotten over one
layer, but we've gotten to the next
layer, which is developmental effects.
It's a touchy issue. Our ability to
detect things has certainly surpassed
our ability to say anything about the
effects. Anybody who talks about
zero guidelines or zero tolerances is
kidding themselves.
Different People, Different
Approaches: Risk Manage-
ment and Communication in
Minnesota

Dr. Pant Shubat, Minnesota Depart-
ment of Public Health

Q: What level of contamination are
you using to decide what is safe and
unsafe for the Hmong?

Dr. Shubat:
It's focused more on PCBs
because PCBs drive the urban area
advisories. We did bend the rules a
little, and we found out from people
who work with them regularly that it
is best to present things in a positive
way. For example, the brochure says
which fish are safe to eat, not what
fish not to eat. The fish that are the
most contaminated with PCBs we say
to eat once a month, whereas with
other anglers we say do not eat. We
also have detailed instructions on how
to clean and cook the fish to reduce
the PCB levels.

Q (Jerry Pollock, California EPA):
Did you quantify the level offish
consumed by the Hmong population?

Dr. Shubat:
Yes, as a prerequisite to the Hmong
video we did some interviews. We
interviewed 30 individuals and they don't
have that high a consumption. It looks
like they're doing a lot of fishing because
they are very visible, but they distribute
fish among themselves. They do eat
more than the average angler. We have
to do more work. What criteria did you
use for saying "Eat them, don't eat
those"? We said, "Eat all the pan fish you
want." For predatory fish, we said, "Eat
one meal a month if you clean the fish."
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Conference Proceedings
I
165
Q (Lee Weddig, National Fisheries
Institute): I think there is a great
distinction between saying "you can eat
six meals a year" and a "don't eat"
advice. The consumption data would
show that the typical number of meals
consumed for a various species is 5 or 6
times per year. You are cutting out
normal consumption.

Dr. Shubat:
People who are getting the
message about the tuna and shark
advisory are people who are pregnant
or are planning to be pregnant. Six
meals a year during pregnancy is a
more concentrated exposure. We
don't know if it's safe. It's probably
more than 1.5 ppm.

Luanne Williams, North Carolina
Department of Environmental Health
and Natural Resources: North Carolina
just completed a random sampling of
shark tissue from processing plants. We
collected 32 samples and the average
mercury level was greater than 1, which
has prompted additional concern for
other top predator marine species. I'm
interested in obtaining tissue sampling
results from the other top predator
marine species. This is a plea for
information. I'm also interested in
obtaining some information on adviso-
ries that have been issued from other
states on marine species where elevated
mercury levels have been detected.

Q (Gale Carlson, Missouri Department of
Health): Have you done any studies to
determine if people read and how well
they understand the advisories?

Dr. Shubat:
We have, and we've found that
50 percent randomly surveyed have
heard of the advisories. We asked
them in three different ways if they've
followed the advisories, and at least
half of those who answered do follow
them. However, there are many
people who answered "no" because
they know the advisory does not apply
to them or they are already fishing in
the right areas. Our brochures are on
different reading levels.

Q (Mike Armstrong, Arkansas Game
and Fish): I appreciated your com-
ments on the important role that the
DNR personnel can play in risk
communication. Please comment on
what role the Minnesota DNR has in
your process for establishing fish
consumption advisories. How well
have they received what you're doing?
What has been the economic impact of
your advisories on the recreation
fishing industry in Minnesota?

Dr. Shubat:
I started with the program the
year that we took out the short-term
consumption, and I got so many calls
from resort owners saying "you're
killing us." Then we did a lot of work
with them, traveling to the groups. We
worked with the Office of Tourism to
develop a specialized brochure for
short-term consumers, a simply, easy-
to-use piece that was not too scary. In
the succeeding years, I haven't re-
ceived any calls from resort owners.
Things have gotten better since we've
broadened the kind of advice that we
give, the different tools that we have
to communicate. DNR, Health, and
Pollution Control work collaboratively
to work out the advisories.

Q (Alan Stern, New Jersey Depart-
ment of Environmental Protection):
Regarding tuna, what considerations
were there within state government in
terms of the implications of this and in
terms of national policy ?

Dr. Shubat:
The group most impacted by this
is our State Department of Agricul-
ture. They are responsible for carry-
ing out inspection, etc.—for interpret-
ing FDA action limits. They did
contribute to the brochure. We've
talked about it at length with them
over the years. Our food inspection
people are satisfied.
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National Forum on Mercury in Fish
Q (Bruce Mintz, U.S. EPA, Headquar-
ters): Do you try to characterize the
risk associated with the contaminant?
Do you say that if you exceed the
guidance it's unsafe, or do you indicate
that if you exceed the guidance it
doesn't necessarily mean you're going
to experience harmful effects?

Dr. Shubat:
We try to do the latter, but I'm
sure we fail in communicating that to
most people. I recommend picking up
the Lake Superior Fish Advisory. It's
our best example. Its language was
crafted by the Great Lakes Advisory
Task Force, and a big part of the
advisory was how to communicate the
wide range of responses that the
human has to contaminants and how
that relates back to the advisory.
Development of Risk-Based
Fish Consumption Guidelines in
Georgia

Dr. Randall Manning, Georgia Depart-
ment of Environmental Protection
Q (Gale Carlson, Missouri Department of
Health): Why did you choose 1 in 10,000
as the [risk] cutoff level?

Dr. Manning:
I'll give you two reasons. One is
strictly a practical issue. If you look at
detection limits that are available out there
for a lot of chemicals in fish tissue, when
you look at 10'6 risk and 10'5 and do back
calculations, with 10'6 you get into trouble
with a lot of the detection limits. With 10'5,
it is less of a problem. After working with
the system and looking at the numbers, and
presenting some mock-ups, I knew that if
we didn't go with 104 it would be killed
from the beginning. If we look at the
numbers and toxicity and carcinogenicity
and think about conservativeness of the
procedures, it's better than not doing it.
Managing and Communicating
Mercury Risks in Arkansas

Dr. Kent Thorton, FTN Associates

No questions
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National Forum on
Mercury in Fish
Day Three: September 29, 19y4
State Assistance Needs
Rick Hoffmann asked the states
represented in the audience to
discuss their respective assistance
needs. The responses of the states are
presented in this section.

Stow Evans, Arkansas Department of
Health

Stan Evans briefly discussed the
Southern States Mercury Task Force and
its activities. He then listed a number of
ways in which the federal government
can assist state agencies in investigating
the mercury problem. The "federal
assistance needs" include (1) a federal
coordinator or point of contact for
coordination of state and regional
studies; (2) a bulletin board or similar
depository for exchanging information;
(3) studies on fish sampling/subsam-
pling to reduce the amount of tissue for
analyses and also holding time studies;
(4) deposition estimates and a deposition
monitoring network (revive NAAP for
mercury guidance); (5) tissue standards
for methylmercury, water standards for
methylmercury, and current tissue
standards from NRCC; (6) round robin
programs for sediment tissue and water
samples, including QA checks with state
participation; (7) financial support for
regional mercury task force efforts by
the states; (8) financial support for
outreach activities to reach impacted
segments of the public; (9) source
studies applicable to the southern United
States, including the role of southern
bottomland hardwood wetlands;
(10) continued dialogue between FDA
and EPA to achieve greater consensus
on risk assessment issues; and (11) alter-
native fish management programs for
impacted fisheries.

NOTE: The Southern States Mercury
Task Force is composed of Alabama,
Arkansas, Florida, Georgia, Louisiana,
Mississippi, New Mexico, North Caro-
lina, Oklahoma, South Carolina, and
Texas.
Jim Blumenstock, New Jersey Depart-
ment of Health

We're still formulating a multi-
regional approach. First meeting next
week. We are in our infancy, and being
here the past couple of days has cer-
tainly been very helpful to hear how
other states are addressing concerns.
Participating states are Delaware,
Maryland, Pennsylvania, New Jersey,
New York, and Connecticut. We have
invited participants from health agen-
cies, environmental protection and
conservation agencies, and departments
of agriculture. We've had a very good
response. Fish safety, food safety will
be represented.

Kirk Wiles, Texas Department of
Health

I applaud EPA for the guidance
documents they've developed. There
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National Forum on Mercury in Fish
has been a lot of response from
government in answering the ques-
tions laid out at the Pittsburgh meet-
ing. At this point we need to go a step
further. As I sit and listen to the
regional approaches being developed,
I'm a bit concerned. The docu-
ments—Volumes 1 and 2—are useful,
but they will need to be changed. I
propose that a national forum be
developed to discuss and implement
changes in the volumes as they come
out and as they become antiquated. It
could be necessary for a national
forum to look at each individual
volume and propose changes to it that
would be of usefulness to all of the
regions of the country. For instance,
if you look at the information pre-
sented here on the use of the Monte
Carlo approach to risk assessment,
there seems to be good acceptance
from some states. But if you look at
Volume 2, it's not going to be in-
cluded in there. The techniques and
technology will be changing in the
next few years. If we approach it on a
four- or five-region basis, I don't
think it's
_________^__ going to
solve the
problem.
We could
evolve the
volumes into
a useful,
———^———^——— working,
and chang-
ing document. In doing so we could
receive input from industry, states,
user groups, and federal agencies. We
need a national forum to discuss and
recommend changes to those manuals.
There is obviously usefulness in a
regional approach. But the question
here is national in scope, not regional
in nature.

Rita Schoney, U.S. EPA, Headquarters
There are some national efforts
that are under way, for example, the
Report to Congress, which is an interof-
fice, Agency-wide effort. There are
a. .. we've got to reach a good
balance between those risks
and the health benefits that
people gain from eating fish.w
other nationwide efforts. And there is a
meeting next week of a EPA-wide
Mercury Task Force.

John Hesse, Michigan Department of
Public Health
We've had a Great Lakes Task
Force in place since 1985, but we
haven't recognized mercury as a major
contaminant problem in the Great Lakes
waters. We've used PCBs as our
primary focus. Now that we focus more
on mercury, especially in our inland
waters, we recognize that we don't have
good background-level measurements of
what kind of exposure has occurred or is
occurring in our population in Michigan.
We're just gearing up to look at hair
levels. We have historic studies using
blood, but we'd like to get a better feel
for our general-population mercury
levels in hair so we can see how close
we might be to whatever threshold level
is determined. We're looking now at a
10- to 20-ppm level as the threshold
level of concern, based on the Iraq and
Japan studies. We're looking forward to
the Seychelle Island results. As a
reviewer of the first two volumes of the
EPA guidance documents, I'm looking
forward to seeing a more complete
health risk/benefit analysis. As we
tighten our advisories, we've got to
reach a good balance between those
risks and the health benefits that people
gain from eating fish. If we overlook
the health benefits, we may be doing the
public a disservice.

Jerry Pollock, California EPA
When we come out with a fish
advisory, it's very difficult to frame
what the benefits are. It's also difficult
to put it into perspective as to what else
people should eat. There are a limited
number of protein sources out there, so
if you are recommending that people
decrease their consumption of seafood
then you are essentially recommending
that they increase their consumption of
some other protein source. And that
may carry some risks with it, too. We
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Conference Proceedings
169
need an expanded database on exposure
to chemicals in these other food sources.
We can't ignore the associated risk of
increased consumption of saturated fats,
etc. I'm hoping that future documents
will put that in a tangible way. Right
now it's very abstract. A big uncer-
tainty I have is whether when I recom-
mend decreased consumption offish,
they actually carry a greater risk because
they increase their consumption of other
foods. We need a greater level of
certainty. Our recommendations could
have a serious impact on people if they
change their diet as a result of an
advisory. I need a greater amount of
insurance in my own heart.

Pat Carey, Minnesota Pollution
Control Agency

I want to thank EPA for efforts in
scoping out and addressing solutions to
the mercury problem. Martha Keating
has been invaluable to us in coordinating
our efforts as a state and through the
Great Lakes Initiatives as well. I hope
EPA continues to get the time to work on
this issue both on a regional and national
level. If the Southern States Task Force
or any other groups that are out there
would want to tie into our particular
workgroup, please contact Angela
Bandemear at Region 5, Air Division.

Russell Isaac, Massachusetts Depart-
ment of Environmental Protection
The issue is too large to manage in
isolation. The trade-offs must be consid-
ered to the extent that they can be. I urge
EPA to consider any financial support to
the Island studies. Our suspicion is that
our mercury is from our fallout. If that is
in fact true, it does suggest some things
we might do for going to low-mercury
fuels. Clearly, local conditions make a
big difference in many cases. Whether
the chemical erosion of local geology is
aggravated, acid precipitation is also a
major consideration. There are a lot of
scientific questions on sources, but if
we're ever going to go beyond managing
risk and actually try to do something
about reducing the problem, those are
obviously some of the questions that
need to be answered. Thanks for the
conference.

Greg Cramer, U.S. Food and Drug
Administration

In response to a previous question,
the Seychelle Islands studies have been
receiving financial support from NIEHS
and from FDA.. As people have talked
about regional activities and Stan
identified the needs for national data-
bases, one of the things that came to my
mind is that developing a national
database on hair levels would be very
valuable as we scope out and try to
describe the problem using first point
estimates to describe the level of mer-
cury exposure. As Monte Carlo simula-
tions come along, we see those numbers
characterizing potential exposures sort
of backing off as we take into account
some of the different distributions
instead of just assuming simple point
estimates. The corroboration with hair
levels would help us to describe the
extent of the national problem.

Alan Stern, New Jersey Department of
Environmental Protection
I want to add to Jim Blumen-
stock's comment regarding our interest
in a regional approach. In that respect, I
would like to invite the southern re-
gional group to get in contact with us.
They already have a head start so we
can find out what sort of things they
have been able to do and where their
thinking is.

Jim Hanlon, U.S. EPA, Headquarters
Let rne respond to the well-
thought-out comments in terms of where
we're at and where we should be going
in the next few year. This arena is
different from an EPA standpoint. It's
not rule making. We do not anticipate
any federal regulations that deal with the
fish contamination/consumption area. It
is particularly useful that where we are
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National Forum on Mercury in Fish
at now is based on a dialogue that the
Agency has carried out over the last 5
years with states and other customers in
this arena. It's a great idea that on a
regional basis states be in contact with
each other. It's easy to spot areas where
fish advisories run up on one state
border, then don't continue on the map.
States need ongoing dialogue with each
other to improve decision making and
public communication.
It also is advisable that the federal
government continue to get its act
together (EPA, FDA, and other part-
ners). We're moving in that direction
and plan to continue. At a similar
meeting a year ago, there were about
175 folks talking about PCB contamina-
tion in fish tissue (attendance was
limited by space). The turnout here is
overwhelming. The question is, rather
than try to identify another fish contami-
nant next year, recognizing the dynamic
nature of this part of the business that
we're in, given the ongoing island
studies, given the forthcoming Volumes
3 and 4 for risk management and
communication, given the developing
positions and advice from regional and
state task forces, doesn't it make sense
for the federal government to sponsor a
dialogue like this every 12 to 18 months
to sort of check hi and see where we are
with it? We will follow up as soon as
we can hi terms of the identified federal
points of contact, bulletin boards, etc. I
think it is invaluable to get the people
who are dealing with the issues on a
day-to-day basis to work in the same
place for a couple of days and do some
face-to-face coordination and communi-
cation. If you think that's a good idea,
we can take that back and put it in our
work plans. We are looking into 1995
and 1996 work plans. If you think this
kind of ongoing dialogue makes sense,
it's something we could respond to.
EPA can only handle so many
questions from the 50 states and tribes.
In all respects these are national issues,
and if there is a platform of understand-
ing or knowledge of where the other
states are at or where the federal govern-
ment agencies are at, I think it could
only put us all in a better position to
answer those tough questions over the
phone: "Is it safe to fish?" "What do I
do?" "What's your best advice?" To
the extent that we can be better in-
formed when answering questions to the
public, the better we'll be fulfilling our
mission to the general public.

RickHoffmann, U.S. EPA, Headquarters

The AFS meeting generated a list
of activities that the states said they
would like to see. We took that back
and formulated it into a federal action
plan, which to a certain degree
sounded more grandiose than it
actually was. It was sort of a work
plan for our group and it prompted a
lot of discussions among the other
agencies. In a similar vein, when we
get this type of information and
perhaps recommendations from the
other regional task forces and so forth,
we'll try to put them together and sort
them into different categories of
activities and then find some type of
mechanism for distributing that.
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National Forum on
Mercury in Fish
Mercury in Fish Tissue Projects
May 1995 Status Report
U.S. Environmental Protection Agency, Office of Water, Washington, DC
NOTE: Because the planning of the
Mercury Project has evolved since the
discussion of the project in September,
we have substituted a status report
current as of May 1995.

Background
Mercury Issue—Environmental
mercury contamination may pose human
health and ecological problems about
which there is still limited regional and
national understanding. The potential
adverse effects of chemical contami-
nants in fish is a recurrent Agency
concern; it is directly related to such
Clean Water Act responsibilities as
water quality standards, surface water
toxics, and EPA efforts to ensure that
waters of the U.S. are "fishable" and
"swimmable," etc.
Significant quantities of environ-
mental mercury cycle through air, water,
and solid phases of the global environ-
ment. Mercury is important because the
most toxic form, methylmercury,
accumulates in aquatic life. Public
concern stems from the tendency of
methylmercury to bioaccumulate in fish
tissue up to a million times or more
above concentrations found in the water
column. Although the degree of
bioaccumulation can vary from water-
shed to watershed due to various factors,
the problem appears to be a widespread
problem posing national concern. As of
September 1994, 34 states had issued
fish consumption advisories for one or
more waterbodies; several states had
issued statewide advisories.
Project
During 1995 and 1996, EPA will
be working with other agencies in a
cooperative effort to assemble a nation-
wide database on mercury in fish
tissues. The mercury project has two
parts: collection of mercury data and
database development. Mercury Data
Collection: During 1995, we intend to
identify and assemble data on mercury
concentrations in fish tissues throughout
the United States. As part of this effort
EPA will be working with state and
federal agencies and other groups that
have collected mercury data. Database:
EPA intends to eventually develop a fish
tissue database as a major part of the
STORET modernization efforts.
Planned Activities
The overall objective of this
project in 1995 is to assemble and
review data on the nature and nation-
wide extent of mercury contamination in
fish. To accomplish this, the following
approach is envisioned. It will be
modified depending on data quality and
availability.

Mercury Data Collection—
Preliminary Test

The first part of the data collection
effort will use EPA's EMAP stratified
sampling grid to specify sampling
locations within each state. If adequate
state-collected data exist for the speci-
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National Forum on Mercury in Fish
fied locations, the EMAP methodology
will be used to evaluate mercury con-
centrations on a nationwide basis.
Preliminary Review of Mercury Data

Another component of the project
is to make a qualitative evaluation of
the nature and extent of state-collected
mercury data. This review will be used
to derive an approximate sense of
existing data and determine what
additional work might be needed.
Working through EPA's regional
offices, we hope to assemble reports of
state fish mercury data and evaluate
data availability by state, region,
ecoregions, etc. "Snapshots" of the
data may be compiled to convey
approximate estimates of tissue con-
centrations, determine number and
frequency of mercury samples, etc.
Wherever available, statistics such as a
mean, median, range, variance, etc.
will be reviewed.
Mercury Data—Full-Scale Collection
and Storage

The long-term objective of the
study is to assemble a comprehensive
database of mercury fish tissue concen-
trations. This data collection will be a
multi-year effort. EPA's Office of
Science and Technology within the
Office of Water has already established
a National Fish Tissue Data Repository
(NFTDR). The objectives of the
NFTDR are to simplify data exchange
by improving the comparability and
integrity offish tissue data, encourage
greater regional and interstate coopera-
tion, and assist states in their data
collection efforts by providing ongoing
technical assistance. The NFTDR
currently is part of EPA's ODES
database; unfortunately, the ODES
database has not evolved into a widely
used database.
As part of this effort, EPA intends
to modify its existing National Fish
Tissue Data Repository (NFTDR) and
incorporate it as a major prototype
during the modernization (Phase III) of
the STORET database. During 1996, we
intend to convert the NFTDR to a
STORET-based fish tissue database.
The primary benefit of including the
NFTDR as a subset of STORET is that
one "platform" will be able to store both
water quality data and biological data,
such as fish tissue information. Existing
data sets would be able to easily migrate
to the new STORET system when it is
completed in early 1997. The use of real
fish tissue data during prototype devel-
opment should help us identify needed
data fields, test the data structure, etc.

Further Information
EPA recognizes that the mercury
study and database development project
will involve a large number of states.
Typically several different agencies
within the same state gather and analyze
fish tissue data. If you and/or your
agency might be interested in more
information about the project as it
develops, please send your name and
mailing address to the following ad-
dress. Information about the projects
will be sent out periodically.

National Mercury Fish Tissue Project
U.S. EPA/OW
Risk Assessment andManagementBranch
Rick Hoffman (4305)
401 M Street, SW
Washington, DC 20460
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National Forum on
Mercury in Fish
Mercury Deposition and the Activities
of the Clean Air Act of 1990
Martha Keating
Office of Air Quality Planning and Standards, USEPA, Research Triangle Park, North Carolina
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National Forum on Mercury in Fish
Clean Air Act of 1990
••^•^•••I^BHIMI
••Considerable debate in Congress over mercury emissions
and sources led to a number of provisions that specifically
address mercury.
••Congress recognized the scientific uncertainties about
whether mercury is a "local" or "global" pollutant, and also
discussed the implications of requiring additional control
technologies, particularly for utilities.
>-As a result, a number of Reports to Congress were
mandated as well as consideration of mercury in other
provisions.
Mercury Study Report to
Congress
National emissions inventory (snapshot ~ 1990)
> Exposure assessment- potential for public health and
ecological risk from inhalation and food chain
exposures.
- Long-range transport analysis
-Local impact analysis
- Human health benchmarks
- Wildlife criterion for trophic level 4
Risk characterization
Risk management
-Control technologies and costs
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Conference Proceedings
175
Mercury Sources and Emissions
HHBB^HH^BBRIHBBiBBBBBBBBHBi
Numerous source categories were examined,
included area sources,
•Biggest emitters are coal-fired utilities,
medical and municipal waste combustors,
chlor-alkali plants, copper and lead smelters,
cement manufacturers and secondary
mercury production.
-These sources, in the aggregate, comprise
98 percent of the inventory.,,.

But, what about impacts?
Some Factors Affecting Exposure
Results
Magnitude of emissions on a per-facility basis.
Proximity of the facility to a water body.
Stack parameters, including stack height and
exit velocity.
• Speciation of mercury emissions (greatly
affects predicted deposition).
• Fish consumption patterns of the exposed
population.
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National Forum on Mercury in Fish
Risk Management
Regulatory decisions combine the results of the risk
characterization with an assessment of control
options, and other nonrisk analyses (e.g, benefits
analysis).
The mercury study will address control technologies
and their costs for certain source categories.
It will also describe other provisions of the CM and
how they relate to mercury control, as well as
specific State and Federal actions that are also being
undertaken.
Important 112 Provisions for
Mercury Sources
•••^••HiHi^MB
• Utility Study - will include regulatory
recommendations for utility boilers.
- Section 112(c)(6) - requires EPA to list and regulate
sources accounting for 90 percent of the emissions
(except..)
" Great Waters Program - allows EPA to promulgate
any further control measures or standards to protect
public health and the environment.
• Urban Area Source Program - may identify mercury
as one of 30 priority pollutants in urban air.
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Conference Proceedings
177
Regulatory Activities Already
Underway
> Emission standards for municipal waste combutors.
»• Emission standards for medical waste incinerators.
> Advanced Notice of Proposed Rulemaking: lesser quantity
emission rate for mercury.
»Mercury source categories scheduled for regulation
-Chlor-alkali plants
-Commercial/Industrial boilers
-Primary lead smelters
-Primary copper smelters
-Portland cement kilns
-Sewage sludge incinerators
-Lime manufacturers
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I
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National Forum on
Mercury in Fish
Great Lakes 'Virtual Elimination'
Project
Frank Anscombe
Policy Analyst, U.S. Environmental Protection Agency, Great Lakes National Program Office,
Chicago, Illinois
Introduction

I am filling in for Jim Giattina,
Deputy Director of EPA's Great
Lakes Program Office in Chicago.
One reason that I regret that Jim could
not be here is that he recently called
up the Defense Department, which is
apparently the dominant supplier of
mercury within the United States, and
asked whether DOD could postpone
further sales, pending consideration of
their environmental ramifications.
Apparently, folks concerned about
mercury contamination have for years
been noting that the federal govern-
ment supplies the stuff. But, to my
knowledge, no one before Jim dialed
11 digits, reached the right people,
and asked, "Could you suspend this
practice?" They have, temporarily.
This fall our office will support an
EPA task force to consider what
recommendations to provide our
colleagues in DOD.
While I am sorry Jim cannot hear
your recommendations, I will certainly
pass along any you offer. We want to
know:
• If you just happened to own
11.5 million pounds of elemen-
tal mercury, what would you do
with it? This is actually a
serious question because the
simple fact is that as American
citizens we do own this much
mercury through our govern-
ment.
• As our society continues to
reduce its use of mercury, what
should we do with the resulting
excess?
We came across the federal sales
of mercury issue while working on a
project with the somewhat obscure
name "Virtual Elimination." I will talk
about this project and more broadly
about the efficacy of public policies
governing mercury, which is what the
project is really about. While not
directly part of the Administration's
Common Sense Initiative, our effort is
asking common sense questions, such
as: Should the federal government
supply a hazardous commodity that it
thereafter regulates from smokestacks
and pipes? We share with the Common
Sense Initiaitive a holistic perspective—a
whole systems approach—to environ-
mental protection. As we view mercury
this way, from cradle to grave, we can
consider whether the parts make an
efficient whole, which is cleaner,
smarter, cheaper.
Objectives

With this introduction, I am
organizing my remarks into:
• Mercury's environmental context
• Mercury's socioeconomic context
• Potential policy options
• What might our Virtual Elimi-
nation project suggest about
these?
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National Forum on Mercury in Fish
Mercury's Environmental
Context

The problem seems to be that
during this century humankind has been
busy, beavering away, extracting and
making much more use of mercury than
ever before, and then not disposing of
this mercury in an environmentally kind
way. The result is that some bit of it
converts to methylmercury, which
magnifies in aquatic food webs, posing
risks to Americans who rely on fish in
their diets.
When we look back at mercury
history as recorded in peat bog cores
and in sediment cores, we find that
mercury used to be much less present in
the upper Midwest:
• A peat bog near Duluth, Minne-
sota, has revealed that before
1900, mercury deposition was
about one-tenth of what it
became by mid-century (1935 to
1980); since 1980, levels have
fallen by a third.
• This trend is very much in
keeping with recent dated sedi-
ment cores from the Great Lakes,
which show that mercury levels
were extremely low before 1900,
surged greatly thereafter, peaking
between 1950 and 1970, and have
fallen back a bit since.
While bogs and sediment indicate
the general environmental abundance of
mercury, risks to human health are
posed by an apparently very small
percentage of this abundance—meth-
ylmercury in fish. Canadian researchers
have tracked methylmercury in several
Great Lakes fish species for a decade or
more. Their results generally mirror
the bog and sediment core trends, in that
they show a gradual decline in recent
years in methylmercury levels in lake
trout and smelt across the Great Lakes.
Yet, in recent years, public health
authorities in Michigan, Wisconsin, and
Minnesota have issued fish advisories
for thousands of lakes. Are new adviso-
ries reflective of a worsening problem
with mercury or of a growing awareness
of a long-standing problem? An answer
is complicated by the fact that many
factors seem to be involved in methyl-
mercury accumulation, including
differences in chemistry between water
bodies, differences between fish species
in vulnerability to mercury, and geo-
graphic variation in the distribution of
mercury and underlying geology. And
there are few data on year-to-year trends
in fish. If levels in the Minnesota peat
bog core and in Great Lakes fish and
sediments are indicative of a broad
national decline in methylmercury levels
in recent years, this is welcome.
It might be, however, that this
trend is a local anomaly, reflective of a
drastic reduction of mercury discharges
to the Great Lakes since the 1970s,
when chloralkali plants spewed mercury
into Lake Erie, closing fisheries there.
It might well be that atmospheric levels
of mercury over the upper Midwest
continue to increase, such that mercury
levels are still increasing in waters that
receive mercury only via the atmo-
sphere.
Whatever the recent national trend,
what is clear is that mercury levels in
many fish species across many waters
are near risk-based thresholds. There-
fore, it is prudent public policy to
increase the margin of safety for wildlife
and for human health by further reduc-
ing methylmercury levels in fish.
This leads to the central question
facing decisionmakers: How to do this?
Clearly the principal current
pathway for dissemination of mercury is
the atmosphere. While I regret missing
Prof. Fitzgerald's presentation on
Tuesday, I believe that he and his
colleagues are finding that mercury
levels in the atmosphere of the northern
hemisphere and in the world's oceans
are in the ballpark of three times those
of 100 years ago. They are also finding
that roughly one-half of anthropogenic
emissions enter the global atmospheric
reservoir of mercury, whereas the other
half is deposited near its source.
So the key to reducing methylmer-
cury in fish seems to be reducing
mercury emissions to the atmosphere,
both locally and internationally.
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Conference Proceedings
181
It is further my understanding that
the processes that convert mercury
forms to methylmercury are both
complex and insufficiently understood.
As a result, we must consider that all
emissions of mercury will potentially
yield methylmercury. If at some point
scientific understanding of methylation
is able to narrow our target from all
mercury emissions to just some, this
will be a welcome development, allow-
ing decisionmakers to focus on a more
narrowly defined problem.
Other key aspects to the environ-
mental context of mercury are that it is
both mobile and nondegradable.
• Mercury is mobile. It is a
volatile fluid at room tempera-
tures and reaches a gaseous state
at 300 °C. Any mercury released
to the environment can be a
"grasshopper pollutant," volatiliz-
ing from land to be redeposited
and revolatilized again. When it
enters water, it can be converted
to methylmercury.
• Mercury does not decay. If the
volume of mercury that mankind
uses and releases exceeds the
earth's capacity to rebury it, then
mercury levels will rise in the
atmosphere and the earth's
waters. In general, this rise has
been going on for the last 150
years, as evidenced in bog and
sediment cores. The world's
continuing use of mercury might
bequeath an inheritance to future
generations of rising mercury
levels in fish across the globe.
The only way to stop this out-
come—to break the mercury
cycle— is to convert unused
mercury and mercury waste to a
nonsoluble form, such as its
sulfide phase or cinnabar, and
dispose of this, perhaps by
reburial.
Socioeconomic Context

At this point, I will turn to the
socioeconomic context surrounding
mercury, which is a useful commodity
traded worldwide. Mercury usage in
both the United States and Europe has
significantly declined in recent years.'
Between 1980 and 1992, U.S. consump-
tion fell about 70 percent. The most
notable part of this decline in mercury
usage was in batteries. In 1980, batter-
ies accounted for 40 percent of mercury
demand; in 1992, battery making used
2 percent of domestic consumption.
Many other mercury uses have declined,
including measuring instruments (80
percent decrease) and chemicals and
allied products (95 percent decline),
because of the phaseout of mercury in
paints and reduced use in the chloralkali
sector.
Today, the leading domestic use
categories are chlorine and caustic soda
(32 percent of consumption); wiring and
switches (10 percent); followed by
electric lighting, measuring instruments,
dental supplies, and laboratory use.
This use reduction is welcome
news from an environmental point of
view. But substitution away from.
mercury has been followed by a surge in
exports from the United States to other
parts of the globe, including China,
India, South America, and South Africa.
I mentioned earlier that the U.S.
government auctions mercury from
holdings that are now regarded as
unneeded by the Departments of
Defense and Energy. In terms of our
domestic demand, these federal sales
are a big deal! In 1993, they were
about 625,000 pounds or two-thirds of
domestic demand. The remaining
stock of 11.5 million pounds is
equivalent to 10 more years of domes-
tic consumption.
A few more economic facts about
mercury:
• The going auction price is $1 a
pound or thereabouts. This low
commodity price is probably
attributable to the combination of
declining use in the United States
and Europe, coupled with the
availability of government-owned
stocks not merely in the United
States, but from the nations of the
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National Forum on Mercury in Fish
former USSR, which are making
all sorts of materials available.
• Because of this low price, mining
of mercury for profit is much
reduced. The largest mercury
mine in the world is owned by a
government (Spain's), so it might
not be exposed to profitability
pressures.
• There is no active mercury mine
in the United States, though there
are activities that yield mercury
as an incidental, recoverable by-
product, notably gold mining and
zinc operations and, to a smaller
extent, copper and natural gas
operations.
• Mercury's cheap price makes the
recovery or recycling of mercury
from products that contain it
financially unattractive. Recy-
cling is normally done because of
governmental regulations.
• This low price might favor
remaining uses because alterna-
tive products or processes might
be uncompetitive with mercury
on a cost basis.
• However, many remaining
deliberate uses of mercury
undoubtedly confer benefits to
society. Fluorescent bulbs save
energy and money. Many
valuable measuring instruments
use mercury.
Policy Options

Given these economic and environ-
mental contexts, what policy responses
could be considered? Emissions of
mercury are the key, and Martha Keating
has just mentioned the sectors that seem
to be the primary emitters: utilities,
municipal waste combustors, medical
waste combustors, chloralkali plants, lead
and copper smelting, among others. EPA
has recently proposed or will shortly
propose regulations governing both
municipal and medical waste combus-
tors. These requirements are not aimed
particularly at mercury, but at a host of
pollutants.
I understand that there will be
forthcoming air regulations for other
leading mercury emission sectors. It is
fair to say that utilities and smelters
cannot readily substitute away from
mercury since their mercury releases are
purely incidental to their businesses.
Their best opportunities to reduce
mercury emissions might be in capturing
mercury from their inputs, rather than in
product substitution, as was possible
with paint or batteries.
The newest technology for chlorine
and caustic soda production does not use
mercury. Most chloralkali plants still
using mercury are older facilities.
Switching to the new technology is very
capital-intensive and might not be eco-
nomically feasible for some firms.
Virtual Elimination Project
Lessons

At this point, I would like to apply
some lessons from our ongoing Virtual
Elimination project. This project is an
effort to assess the sources of mercury
and the regulatory structure surrounding
uses and releases, from cradle to grave,
so as to see whether governments can
improve their policies to spur ongoing
reductions—beyond compliance—in the
use and release of mercury.
"Beyond compliance" is a key
concept and is perhaps best illustrated by
what is going on in the hazardous waste
business. The costs of responsibly
dealing with hazardous waste are leading
generators to waste minimization so as
to save money. They are not merely
complying with RCRA; they are going
"beyond compliance" to prevent pollu-
tion. As a result, some waste disposal
firms face slowing demand for their
services, but waste minimization is good
for the environment.
The phrase virtual elimination is
taken from a U.S. policy statement on
the Great Lakes that is 16 years old. It
refers to persistent toxicants like mercury.
Our project is a work in progress.
Yet, we have some initial observations
and I will highlight a few:
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Conference Proceedings
183
Some states have banned the
deliberate use of mercury in
certain products. These bans
have generally happened where
alternatives are available or when
mercury use has been unimpor-
tant to society.
Banning is a very strong preven-
tion approach, which has yielded
the largest reductions in mercury
use in this country (dropping
mercury from paints and batter-
ies). When one or a few states
such as Minnesota, Wisconsin,
Michigan, and New York have
instituted product bans, there has
been a ripple effect, whereby
manufacturers then provide
mercury-free alternatives across
the Nation.
Many remaining uses are prob-
ably not amenable to bans. So in
addition, some states are trying
recycling requirements for
manufacturers. And I have heard
that some are considering taxes
on mercury uses to provide an
economic incentive for innova-
tion away from mercury use.
Such preventive measures are a
powerful supplement to federal
environmental approaches, which
tend to focus on regulating
pollutants at their point of release
or disposal.
Many regulatory requirements
levied at the release/disposal
point are not conveyed back to
those who initially decide to use
mercury in a consumer product.
Costs imposed on incinerators do
not necessarily encourage mer-
cury prevention by a manufac-
turer who sells this product to a
consumer, who hi turn sends the
product to an incinerator.
Many consumers are unaware of
the mercury content in products
at the moment of their purchasing
decision.
As said before, the federal
government auctions a lot of
mercury. We are looking into the
desirability of ending the federal
government's participation in
this. This would probably not
have a discernible impact on
price,, given the world surplus, or
on domestic use. But ending
these auctions might be grounds
for asking other governments that
sell mercury to likewise curtail
their sales. Ending sales would
exemplify "thinking globally,
acting locally" and would send a
clear message within our society
and to the world that this country
urges the prevention of mercury
use and release.
There might not be an exit plan
within the United States for mer-
cury, other than export. Sweden
has apparently banned recycling
of mercury on environmental
grounds. The United States may
want to consider doing the same
in this country for all but essen-
tial remaining uses of mercury.
EPA is respectful that much
further progress in preventing
pollution does not lie with
governments at all, but depends
on the expertise and innovatory
energy of the private sector.
Many industries are doing good
things to reduce their use of
mercury. A major light manufac-
turer is striving to develop a
mercury-free fluorescent bulb.
Chloralkali plants are doing more
recovery of mercury. Our
progress as a society in heading
toward final prevention of
mercury, virtual elimination, rests
on such efforts.
Conclusion

I will sum up:
• Mercury use and release lead to
an environmental problem—
methylmercury hi fish.
• Emissions are the most important
way that mercury contamination
is distributed.
• World releases of mercury might
increase because of the world's
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National Forum on Mercury in Fish
growing appetite for fossil fuels
to maintain the economic growth
unleashed by the collapse of
communism.
Our nation's use of mercury
seems to be declining and releases
might be as well.
But methylmercury levels in fish
are too high, and it is prudent to
strive for further progress toward
the holy grail of virtual elimina-
tion.
However, the abundance of mer-
cury and its relative cheapness
favor increased international use
and mercury-based technologies.
Bans on deliberate use of mercury
in products when alternatives are
available have been successful.
In addition, this nation might be
well served to consider an exit
plan for its growing surplus of
mercury, which could entail
returning mercury to the earth
whence it came, in a controlled
fashion.
Continued international attention
to mercury seems important,
given the global spread of
mercury contamination through
the atmosphere.
• Ending federal sales of mercury
might be a clear message to send
to the international community.
The Clinton Administration has
emphasized the reinvention of govern-
ment. This philosophy entails invest-
ing in prevention rather than cure. It
entails being guided by facts and
mission, rather than blindly adhering
to administrative rules of conve-
nience. It implies working with all
sectors of society, steering private/
public partnerships toward common
goals, like virtual elimination of
mercury. Our project is in keeping
with this spirit of reinvention.
Everything I have said is prelude
to the next speaker, who represents a
state that has been in the forefront of a
seismic shift toward mercury prevention
and the reinvention of environmental
protection. Pat Carey will discuss some
of the common-sense prevention
measures that Minnesota has taken to
reduce its mercury problem.
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National Forum on
Mercury in Fish
1
Minnesota Mercury
Activities
Patrick F. Carey
Principal Planner, Minnesota Pollution Control Agency, Hazardous Waste Division
St. Paul, Minnesota
Background

The Minnesota Pollution Control
Agency (MPCA) estimates total
anthropogenic mercury emissions,
excluding those resulting from latex
paint volatilization, to be about 7,700 lb/
year (White and Jackson 1992). The
MPCA finds that roughly half of these
mercury emissions are a result of energy
production (i.e., burning coal and other
fossil fuels that contain mercury) and
half result from the disposal of products
that are purposefully manufactured with
mercury (e.g., thermostats, fluorescent
lamps, dry-cell batteries, and thermom-
eters). Interestingly, water point-source
discharges account for only about 30 lb/
year of mercury.
Minnesota Strategy for
Mercury Emissions from
Energy Production

To address Minnesota's mercury
emissions from energy production, the
MPCA is intent on developing a long-
term state strategy based on federal
action resulting from two Clean Air
Act Studies, the Utility Air Toxics
Study and the National Mercury
Study, which are scheduled to be
completed over the course of the next
2 years. Until federal action occurs,
the MPCA will continue efforts to
work with the Minnesota Public
Utilities Commission to incorporate
the environmental costs of mercury
releases into utilities' energy planning
process and continue to promote
energy conservation, efficiency, and
alternatives to fossil fuels.
Minnesota Strategy for
Mercury Emissions from
Mercury Product Disposal!

To address Minnesota's mercury
emissions from the disposal of mercury-
bearing products, the Minnesota State
Legislature has passed a number of mer-
cury product laws over the last several
years. The following briefly summa-
rizes these laws, followed by a brief de-
scription of efforts to implement these
laws.

Minnesota. Mercury Product LAWS

Minnesota's mercury product laws
can be grouped into the following five
categories:

Product Labeling/Notification
Requirements

These laws include (1) a require-
ment that thermostats, switches, ther-
mometers, and scientific/medically
related equipment that contain mercury
be labeled to indicate the products
contain mercury and must be disposed
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National Forum on Mercury in Fish
of properly; (2) elemental mercury user/
handler notification requirements; and
(3) responsibilities for mercury lamp
sellers and replacement contractors to
inform the buyer/user of proper mercury
managementrequirements.

Mandated Collection Requirements

These laws include provisions
requiring (1) contractors removing
thermostats, switches, thermometers,
appliances, or medical or scientific
instruments from service to properly
manage removed products; (2) thermo-
stat manufacturers to provide incentives
to induce purchasers to properly manage
spent thermostats; (3) Northern States
Power (NSP), a major utility hi Minne-
sota, to collect fluorescent lamps from
households and small businesses located
in NSP service areas; (4) battery
manufacturers to ensure that mercuric
oxide batteries from businesses are
managed properly; and (5) lamps
removed from state-owned buildings to
be recycled.

Disposal Bans
These laws prohibit businesses and
homeowners from disposing of elemen-
tal mercury, mercury-containing lamps,
thermostats, thermometers, switches,
appliances, and medical or scientific
instruments in the solid waste stream or
sewer system.

Sales/Distribution Bans
These laws (1) prohibit the sale
of mercuric oxide batteries, fungi-
cides, and games, toys, and wearing
apparel containing elemental mercury
and (2) prohibit medical facilities
from routinely distributing mercury
fever thermometers.

Content Restrictions

These laws mandate the reduction
and/or elimination of mercury content in
certain dry-cell batteries, packaging,
pigments, and dyes.
Implementation Activities/Strategy

Minnesota, in general, has taken a
two-pronged approach to implementing
the mercury product laws and other
efforts for reducing mercury emissions
in Minnesota. The approach includes
(1) mercury product collection activi-
ties, the short-term solution/effort, and
(2) source reduction/elimination activi-
ties, the long-term solution/effort. The
following briefly summarizes activities
under both approaches.

Product Collection Activities

The MPCA's short-term goal is to
establish accessible and economical
collection systems for business and
household consumers to recycle mer-
cury products properly. To achieve this
goal, the MPCA established several
operating principles. First, don't
recreate the wheel. Work to tap into
systems that already exist for other
wastes in both the public sector (county/
municipal recycling programs and
household hazardous waste programs)
and the private sector (contractors,
reverse distribution, retailers). Second,
create partnerships by identifying
potential public/private sector partners,
understanding the impediments to
achieving their participation (regulatory
and economic), and removing unneces-
sary regulatory and economic impedi-
ments.
By applying these principles over
the last couple years, collection systems
for a number of mercury products have
been established with public and private
sector involvement:
1. Thermostats. Honeywell, a major
thermostat manufacturer, has
implemented a free take-back
program for-business and house-
hold consumers, which includes a
free reverse distribution system
(contractor to wholesaler to
Honeywell) and a prepaid mailer
system for those who replace
their own thermostats without a
contractor. Under the program,
Honeywell accepts any mercury
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187
thermostat, even those manufac-
tured by a different company.
2. Switches. A Minnesota switch
manufacturer is interested in
establishing a take-back program
similar to the Honeywell program.
3. Button Batteries. Proex, a major
photo-developing chain store in
Minnesota, will soon implement a
free counter-top drop box pro-
gram.
4. Mercury-Containing Lamps.
Three lamp recycling facilities
now exist in Minnesota. One of
these recyclers, Recyclights, has
installed a superior distiller in
order to recycle other mercury
products. There is a system of
about 50 transporters/contractors
in Minnesota. Northern States
Power is working to meet its
mandate to be involved in the
collection of lamps from
homeowners and small businesses
in NSP service areas.
5. Household Hazardous Waste Col-
lection Programs. All 87 Minne-
sota counties have established
household hazardous waste collec-
tion programs. Many of these
programs will accept mercury
products. One of the programs,
the Western Lake Superior Sani-
tary District (WLSSD) in the
Duluth, Minnesota, region, has
implemented the "Merc Alert"
Program, an aggressive program
for collecting mercury products
from citizens in the district.
6. Scrap and Auto Salvage Yards.
The MPCA is working with scrap
and auto salvage yards to employ
best management practices to
remove and recycle mercury-
containing items from autos and
other scrap.

Source Reduction/Elimination
Activities
The MPCA's long-term goal is to
source-reduce or eliminate mercury hi
products to the extent possible. To
achieve this goal, a number of activities
have been or will be conducted iin
Minnesota.
1. LA. Gear Mercury Switch
Shoes. Minnesota's 1994 sales
ban for mercury-containing
wearing apparel not only reduces
and eventually eliminates this
one source of mercury from the
waste stream, but it also
(1) sends a message to product
manufacturers to "design for the
environment" and consider the
appropriateness of using mercury
in products and (2) makes
consumers aware of the concerns
related to mercury-containing
products in order to help them
make purchasing decisions and
meinage these products appropri-
ately after use.
2. Mercury in Products Study. In
1995, the MPCA will conduct a
study of all products that contain
mercury to identify mercury
source reduction and elimination
opportunities. Legislation
governing mercury in products
might result from the findings of
the study. Conducting the study
will involve a substantial dialog
with product manufacturers to
define problems/solutions. The
MPCA will also investigate
innovative incentive-based
controls for mercury use reduc-
tions (e.g., use tax, deposit/
refund, others).
3. WLSSD''s Efforts with Dentists.
The Western Lake Superior
Sanitary District (WLSSD) has
worked aggressively with
dentists sewering to the WLSSD
wastewater treatment plant to
reduce mercury discharges
resulting from the sewering of
dental amalgam.
4. Hennepin County Collection
Programs. The municipal waste
combustor of the Hennepin
Energy Resource Corporation
(HERC) is located in downtown
Minneapolis, Minnesota. The
HERC facility, in conjunction
with Hennepin County, has
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National Forum on Mercury in Fish
established aggressive front-end
separation programs for mercury
products to control emissions.
After implementing these
programs, HERC's average
overall mercury emission
concentration was reduced by
over two-thirds.
References

White, D.M., and A.M. Jackson. 1992.
Technical work paper on mercury
emissions from waste combustors.
Prepared for Air Quality Division,
Minnesota Pollution Control
Agency, St. Paul, MN.
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Conference Proceedings
189
Estimated Atmospheric
Mercury Emissions in Minnesota, 1990
Annual Total about 7,700 pounds per year
Coal
(2,000 Ib, 26%)
Dentists, Hospitals, Labs (<1%) •
Cremation (<1%)
Petroleum Refining (1%)-^x'1
General Industrial Activity (3%r >
Fluorescent Lamps (300 Ib, 4%r
Sewage Sludge
(400 Ib, 5%)
x
Oil
(500 Ib, 7%)
Municipal Solid Waste
(1,500lb,19%)
Landfill volatilization
(880 Ib, 11%)
Wood (600 Ib, 8%)

Natural Gas (600 Ib, 8%)
Medical Waste (500 Ib, 7%)
Categories in Bold'have the highest degree of confidence;
additional data are needed for the other categories.
MPCA 12/92
MPCA
Estimated Mercury Emissions
by Source
General Industrial Activit;
Fluorescent Lamp:
Sludge Combustioi
Medical Waste Combustion
Puposeful
Use
Landfills
MSW Combustion
Coal
Energy
Production
Wood
Natural Gas
Oil
1— Petroleum Refining
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National Forum on Mercury in Fish
MPCA|
50 Percent Emissions from Energy

Production

• Develop state strategy based on federal
action from Clean Air Act studies; utility
air toxics study and mercury study
• Incorporate into energy plans the
environmental costs of mercury releases
• Promote energy conservation, efficiency
and fossil-fuel alternatives
MPCA
50 Percent Emissions from
Mercury in Products
• Mercury product laws
• Reduction activities/strategies
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191
MPCA
Minnesota Mercury Product Laws
• Labeling/notification requirements
• Mandated collection requirements
• Disposal bains
• Sale/distribution bans
MPCA
Minnesota Mercury Product Laws
• Labeling requirements for certain
mercury-containing products:
• Thermostats
• Switches
• Thermometers
• Appliances
• Lamps
• Medical/scientific instruments
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National Forum on Mercury in Fish
MPCA
Minnesota Mercury Product Laws

• Elemental mercury user/handler
notification requirements
• Seller provide MSDS
• Purchaser signs certification of
responsible use/disposal
• Lamp sellers and lamp-replacement
contractors inform buyer of mercury
management requirements
MPCA
Minnesota Mercury Product Laws

• Mandated collection requirements
• Contractors removing thermostats,
switches, thermometers, appliances, or
medical or scientific instruments from
service shall manage products.
• Thermostat manufacturers must provide
incentives to induce purchasers to
properly manage spent thermostats.
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J93
MPCA
Minnesota Mercury Product Laws
Mandated collection requirements continued
• Northern States Power to collect fluorescent
lamps from households and small businesses
in their service areas
• Battery manufacturers to ensure proper
management of mercuric oxide batteries from
•businesses
• Recycle lamps removed from state-owned
buildings
MPCA
Minnesota Mercury Product Laws
Disposal bans
• Elemental mercury
• Mercury-containing lamps
• Thermostats
• Medical or scientific instruments
Thermometers
Switches
Appliances
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National Forum on Mercury in Fish
MPCA
Minnesota Mercury Product Lews

• Sale/distribution bans

• Mercuric oxide batteries
• Games and toys containing elemental
mercury
• Wearing apparel containing elemental
mercury
• Medical facilities from routinely
distributing mercury fever thermometers
MPCA
Minnesota Mercury Product Laws

• Content restrictions
• Mandated reduction and elimination of
mercury content in dry-cell batteries
• Mandated reduction and elimination of
mercury content in packaging
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195
MPCA
Implementation Activities/Strategies

• Two-pronged strategy:
• Product collection - short-term strategy
• Source reduction/elimination - long-term
strategy

•
MPCA
Product Collection Activities
Goal: To establish accessible and
economical collection systems for business
and household consumers

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National Forum on Mercury in Fish
MPCA
es

• "Don't recreate the wheel"
• Public Sector
• County/municipal recycling programs
• Household hazardous waste programs
• Private Sector
• Contractors
• Reverse-distribution
• Retailers
MPCA
Principles Continued
Create partnerships
• Identify potential partners
• Understand impediments to participation
(regulatory and economic)
• Remove unnecessary impediments
• Pilot project for Special Hazardous Waste
• Work with manufacturers, retailers to
sponsor system
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Snap Shot of Collection Systems

• Thermostats
• Honeywell thermostat take-back program
« Free reverse distribution system
• Prepaid mailer for DIYers
• Any mercury thermostat accepted
Snap Shot of Collection Systems

• Switches
• Minnesota switch manufacturer interested
in establishing take-back program
• Button Batteries
• Proex to implement free couritertop drop
box program
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National Forum on Mercury in Fish
MPCA
Snap Shot of Collection Systems

• Mercury-containing lamps
• Three, lamp-recycling facilities
(250 to $1 per four-foot lamp)
• Fifty transporters/contractors
• NSP working to establish collection
system
MPCA
Snap Shot of Collection Systems

• Household Hazardous Waste Collection
Program
• All 87 Minnesota counties involved
• Most will accept mercury products
• Western Lake Superior Sanitary District's
"Merc Alert" Program
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Conference Proceedings
MPCA
Source Reduction/Elimination Activities
• Strategies for Reducing Mercury in Minnesota
Report
• Mercury in Products Report
• Dialogue with manufacturers to define
problems/solutions
• Innovative, incentive-based controls for
mercury-use reductions
• Two phases - legislative recommendations by
spring 1996
MPCA
Source Reduction/Elimination Activities
• WLSSD's efforts with dentists
• L.A. Gear mercury-switch shoes
• Federal mercury stockpiles

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National Forum on
Day Three: September 29, 1994
Mercury in Fish
Questions and Discussion
After each speaker's presentation,
an opportunity for questions and
answers was provided. Time
was also allotted for a group discussion/
question-and-answer session.
National Mercury Study
Dr. Jerry Stober, U.S. EPA, Region 4,
and Dr. Steve Paulson, U.S. EPA,
Newport

Q (Luanne Williams, North Carolina
Department of Environmental Health
and Natural Resources): Who do we
contact first for a listing of state adviso-
ries?

Mr. Hoffmann:
Jeff Bigler is the contact. We've
updated on an annual basis. We get
most data from 305(b) reports. Because
it changes so much, we try to do interim
updates. Contact our office. We have
money set aside for the next fiscal year
to update that database.

Q (Deedee Kathman, Aquatic Resources
Center): Steve, do you have any plans
for EMAP to do marine coastal waters?

Dr. Paulson:
Right now in terms of this study
we have not thrown that out. But the
estuaries program has been collecting
mercury data in fish, and those data will
be available. We haven't specifically
thought about how to incorporate the
estuaries into a concept like this, of
using existing data, but that's a good
suggestion.

Rob Reash, American Electric Power: I
would like to suggest that, for the Great
Lakes region, there exists a very sizable
database going back to the mid-1970s
for several standardized locations. For
four of the Great Lakes that the Ontario
Fish Contaminant Section has been
monitoring, you can call them and get
raw data from their standardized
locations. If you want to look at tempo-
ral trends and mercury residues in
various fish species that you do not
ignore this long-term database and
incorporate these historical data into
the data collected in future years.

David Sager, Texas Parks and Wildlife
Department: There are a lot more data
than just the 305(b) report and EMAP
data out there. There are long-term-
sampling programs that are not associ-
ated with EPA that I think need to be
incorporated into this. You need to
contact all of the agencies, not just those
major programs that report to EPA.

Q (Jim Wiener, National Biological
Survey): One of the problems that has
compromised the value of a number of
existing databases is the lack of rigor
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National Forum on Mercury in Fish
and the quality of the data. There was
some mention made of quality assur-
ance. Can you give more information
on that?

Dr. Stober:
That is a problem that we recog-
nize we are going to run into because
each state has its own protocol right
now and, even though there is a guid-
ance document out there, it takes time to
change over. Given the level and the
amount of data existing hi the states on
mercury, the challenge is to try to do
something valid with existing databases,
then move into some standard protocol
that cuts across all states so that we do
generate a rigorous database that moves
forward from here.
Dr. Paulson:
I'd add that while that is a real
concern, I think one of the values of
trying to look at data from across a
fairly broad spatial perspective is that
many of the patterns seem to show up
if they are there. (At least this is true
for other parameters that we've looked
at where there was similar concern
about the quality of individual mea-
surements and difference in protocols
across state lines, etc.) I do not want to
minimize that concern in trying to
move to a more standardized approach.
But I think first crack is that we'll see
some of the patterns—maybe not all of
them, and not defined at the level that
we'd like—but it will be useful to get
that started.

Mercury Deposition and the
Activities of the Clean Air Act
of 1990
Martha Keating, U.S. EPA

Q (Rob Reash, American Electric
Power): Utilities are gearing up for
compliance with phase 1 and 2 SO2
emissions. Given the fact that there will
be a lot of technology changes, how will
that incremental control of mercury by
these new technologies be factored into
your report for utilities that are switch-
ing to fuel gas desulfurization technolo-
gies, which will result in some incre-
mental decrease in mercury emissions?

Ms. Keating:
That will be in the Utility Study
Report. There have been a number of
projections about what utilities are
going to do—whether they're scrub,
whether they're going to fuel switch,
what they are going to do to meet the
acid rain provisions. All that will be
factored into the Utility Study for
mercury reductions. They are doing a
1990 base scenario and a 2010 projec-
tion to incorporate the acid rain technol-
ogy.

Q (Larry Fink, South Florida Water
Management District): Your work is so
important, I am ecstatic about it. Did
you attempt to mass balance the mer-
cury flow through the economy so that
you can validate emissions estimates,
less what's stored and/or in usable
forms, versus what's being used on an
annual basis?

Ms. Keating:
No. A lot of the mercury that is
used hi industry doesn't really become a
problem until the product is disposed of.

Q (Larry Fink, South Florida Water
Management District): Did you look at
area sources that have been created as
a result of historical reasons?

Ms. Keating:
No, there is no natural emissions
inventory. When we did a long-range
transport model, we factored in a
2-ng/m3 background.

Q (Larry Fink, South Florida Water
Management District): Did you cali-
brate and validate?

Ms. Keating:
We are comparing our model
results to measured data. There are not
a lot of data out there. There are not
enough data to validate our model.
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Conference Proceedings
203
Q (Larry Fink, South Florida Water
Management District): Can you use
data from Canada?

Ms. Keating:
No, we didn't feel it was complete
enough.

Q (Larry Fink, South Florida Water
Management District): Regarding
pollution prevention and risk manage-
ment options, is this part of this exercise?

Ms. Keating:
Pollution prevention options were
considered when we looked at control
options for a number of source catego-
ries. However, the data on both the
efficiency and costs of these types of
measures are very limited (for example,
battery recycling programs for munici-
pal waste combustors). Another ex-
ample of where we looked at pollution
prevention was switching from the
mercury cell process to a diaphragm
process for chlor-alkali plants. The
utility study will look at fuel switching
and other options for utility boilers.

Glenn Rice, U.S. EPA: I have been
working on this study. This is not a
site-specific study. It did not include a
lot of background levels. It did try to
come up with rigorously defined param-
eters that were used in the model. We
spent a lot of time focusing on param-
eters. We hoped it will be a resource to
the states who want to do site-specific
analysis.
Great Lakes "Virtual
Elimination" Project
Frank Anscombe, U.S. EPA, Great
Lakes National Program Office

Dr. William Fitzgerald, University of
Connecticut: I would like to clear up
any misconceptions about Factor 3 and
the changes that I spoke about on
Monday. I presented a modern and a
pre-modern view, and they are based on
average values and relatively simple
mass balances. The Factor 3 and the
other types of predictions should really
be used as guides provided with a
framework and a way of focusing
research. I would caution you not to
use a Factor 3 as a fact, but as a guide.

Mr. Anscombe:
I agree. I find it useful as a
general guide, while appreciating that it
cannot be a precise measure.
Minnesota Mercury Reduction
Activities
Pat Carey, Minnesota Pollution
Control Agency

Q (Jim Wiener, National Biological Sur-
vey): I applaud what you 're doing to
reduce emissions. There are a number
of examples of human activities that can
result in increased localized exposure of
populations to methylmercury. There
are human activities that don't neces-
sarily affect the supply of mercury to the
environment; for example, the creation
of new reservoirs, which is turning out
to be quite an issue in Canada, one that
greatly elevates the methylmercury ac-
cumulation in fish. What, if any, role do
you envision for regulatory agencies in
actions of this type that may influence
exposure to methylmercury?

Mr. Carey:
We would treat it as another
potential source and do an assessment
of whether it was something we should
be concerned about. We would deter-
mine how much of a contribution it is to
the overall problem and try to develop
corresponding solutions to deal with
that. A lot of our efforts up to this point
have been primarily focused on those
major sources.

Pom Shubat, Minnesota Department of
Public Health: There are a series of
reservoirs in Northern Minnesota, and
the utility's permit that allows them to
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National Forum on Mercury in Fish
*Using TCLP regulations,
you can essentially dispose
of pure elemental mercury
as a nonhazardous waste in
a nonregulated landfill.*
operate was held up because they were
required to submit a plan for monitor-
ing mercury and required to do some
experimental work in their reservoir
system.
Final Group Discussion/
Question-and-Answer
Session

Q (Cindy Gilmour, Philadelphia Acad-
emy of Science): Regarding TCLP
regulations for disposal of mercury as
hazardous waste, the TCLP extraction
procedures don't extract elemental
mercury out of
hazardous waste.
Using TCLP regula-
tions, you can essen-
tially dispose of pure
elemental mercury as
a nonhazardous
waste in a
nonregulated landfill.
< I was wondering if
anyone from EPA can
comment on that glitch in TCLP regula-
tion?
Mr. Hoffmann:
I'm not aware of anyone here
who can address that. I think that this
type of issue, where you have the
potential for conflicting goals and
mandates, is one of the reasons that
the Mercury Task Force is being
established. For example, if you
establish a policy to encourage the
collection and disposal of household
hazardous waste, what conflicts, if
any, might result?

Cindy Gilmour, Philadelphia Academy
of Science: There is a very common
impression among hazardous waste
contractors in the mid-Atlantic states
that people think elemental mercury is
neutral and it is not soluble, not volatile.

Martha Keating, U.S. EPA: The
Office of Solid Waste and Emergency
Response had come out with their
proposal on how to deal with fluores-
cent light bulbs—whether we should
exclude them from hazardous waste
regulations or recycle them. One of
the issues raised during comments on
that rule has been that there was not
an effective procedure for mercury.
The Office of Solid Waste is going to
be pushing research in that area.

Q (Greg Cramer, U.S. Food and Drug
Administration): Regarding the emis-
sions from wood sources, where are they
coming from and what are you doing to
control them?

Mr. Carey:
The wood sources are residential
burning. Our air quality folks are
looking at this component of the
emissions. They are considering
certain avenues to pursue.

Ms. Keating:
On a national level there is a 1
emission factor for wood burning. We
didn't use it in the national inventory
because it was based on only one test of
one type of wood. There are not a lot of
emissions data from wood stoves. We
also did not have a good handle on how
many wood stoves there were in the
country. We estimated about 12 mil-
lion, but it was a guess. Because of
these uncertainties, a national estimate
of mercury from woodstoves was not
included in the inventory.
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National Forum on
MercniryinFish
Speakers' Biographies
Frank Anscombe

Mr. Anscombe is a policy analyst
with EPA's Great Lakes Program Office
in Chicago, Illinois. He received a B.A.
from Yale College and an M.A. in pub-
lic policy from the University of Chi-
cago, concentrating in economic aspects
of government regulation. Prior to j oin-
ing EPA, Mr. Anscombe served as a
supply officer of a submarine and of a
shipbuilding program for the Navy.
With the Great Lakes Program, he has
led development of a Report to Con-
gress and is presently contributing to
the Virtual Elimination project, which
aims to promote public policies that
would spur prevention of bioaccumula-
tive pollutants.
Thomas D. Atkeson, Ph.D.

After 9 years with the Florida
Department of Health as Chief of the
Environmental Epidemiology Program,
where he was involved in a wide
variety of environmental contaminants
issues, Dr. Atkeson joined the Depart-
ment of Environmental Protection in
June 1992. His responsibilities are to
coordinate Florida's response to the
finding of high levels of mercury in fish
and wildlife. His primary efforts are
devoted to planning a long-term
research program aimed at defining the
causes of mercury contamination in
Florida and coordinating the activities
of a variety of local, state, federal, and
private agencies in pursuit of those
research objectives.
Dr. Atkeson's background is in
zoology and wildlife biology, with
education at Auburn University and the
University of Georgia.
Nicolas S. Bloom

Mr. Bloom is Chief Scientist and
Vice President of Frontier Geosciences
Inc., a small environmental research
corporation located in Seattle, Washing-
ton.
Mr. Bloom received his B.S. in
chemistry from the University of
Washington and his M.S. in oceanogra-
phy from the University of Connecticut.
He worked for 9 years at the Battelle
Pacific Northwest Marine Research
Laboratory, where he developed ultra-
clean sample handling techniques and
novel methods for the chemical specia-
tion of trace metals. In 1991,
Mr. Bloom and Ms. Sharon Goldblatt
established Frontier Geosciences, where
he and a staff of nine persons investigate
the speciation and biogeochemistry of
trace metals in the environment.
P. Michael Bolger, Ph.D.,
D.A.B.T.

Dr. Bolger is the Chief of the
Contaminaints Standards Monitoring and
Program Branch in the Center for Food
Safety and Applied Nutrition of the U.S.
Food and Drug Administration (FDA) in
Washington, DC.
Dr. B.olger received his B.S. in
biology from Villanova University and
his Ph.D. in physiology and biophysics
from Georgetown University. After a
2-year postdoctoral position with the
Department of Physiology in the
Georgetown University Medical Center,
Dr. Bolger became a staff fellow in
toxicology with the Bureau of Foods in
the FDA. Upon completion of the staff
fellowship, he accepted a position as a
toxicologist with the Contaminants
205
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National Forum on Mercury in Fish
branch at FDA. Over the last decade, he
has been involved in a number of hazard/
risk assessments of food contaminants,
including methylmercury. Dr. Bolgeris
board-certified as a toxicologist by the
American Board of Toxicology. He is
currently Chief of the Contaminants
Standards Monitoring and Programs
Branch, which is responsible for the
monitoring and hazard/risk assessment
of environmental contaminants in the
food supply.
for private animal research contract
firms in the Washington, DC, area.
During this time, as a study veterinarian,
Dr. Cicmanec conducted a subchronic
reproductive research study involving the
effects of PCBs on a large group of
rhesus monkeys. Dr. Cicmanec is a
Diplomate of the American College of
Laboratory Animal Medicine. In
addition to his veterinary training, he
received an M.S. from the University of
Michigan Medical School.
Pat Carey

Mr. Carey is a Principal Planner
for the Minnesota Pollution Control
Agency (MPCA), Hazardous Waste
Division, Program Development Section.
Mr. Carey received his B.S. in
government/political science from St.
Johns University in Minnesota. He
joined the MPCA in 1984. Over the past
decade, Mr. Carey has been involved in
developing waste management policies
and programs in Minnesota for a number
of special wastes, including used oil, oil
filters, vehicle batteries, dry-cell batter-
ies, used tires, PCB ballasts and capaci-
tors, and mercury-containing products.
He is currently a member of the MPCA's
Mercury Task Force, a multimedia effort
focused on developing strategies for
reducing mercury emissions.
John L. Cicmanec, Ph.D.

Dr. Cicmanec is a Veterinary
Medical Officer of the Systemic Toxi-
cants Assessment Branch in the Environ-
mental Criteria Assessment Office of
EPA's Office of Research and Develop-
ment in Cincinnati, Ohio.
Dr. Cicmanec is a research veteri-
narian who presently works as a risk
assessor. Prior to joining the staff of the
Environmental Criteria Assessment
Office, he directed the operation of the
research animal facility of EPA in
Cincinnati. Prior to the 8 years that he
has spent with EPA, he spent 16 years as
a clinical veterinarian and study director
Thomas W. Clarkson, Ph.D.,
M.D., h.c.

Dr. Clarkson is a graduate of the
University of Manchester, where he
received his B.Sc. and Ph.D. degrees.
He accepted a position at the University
of Rochester in 1957 as a research
fellow and, except for a 3-year period in
research institutes abroad, he has been a
member of the medical faculty at the
University of Rochester ever since.
Dr. Clarkson is currently Professor and
Chairman of the Department of Environ-
mental Medicine.
His research work is directed
toward understanding the toxicology of
heavy metals, especially mercury and its
compounds. His interest is in the
pathways and mechanisms of disposition
of toxic metals in the body. An under-
standing at the cellular level of how
metals cross diffusion barriers in the
body will give insight into the mecha-
nisms of toxic action, on factors that
influence their toxicity, and might lead
to the development of effective methods
of removing metals from the body.
Charles F. Facemire, Ph.D.

Dr. Facemire is the Senior Environ-
mental Contaminants Specialist for the
Southeast Region (Region 4) of the U.S.
Fish and Wildlife Service in Atlanta,
Georgia.
Dr. Facemire received a B.S. in
wildlife science from New Mexico State
University, an M.S. in biology from the
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Conference Proceedings
207
University of Illinois at Champaign-
Urbana, and a Ph.D. in zoology from
Miami University in Oxford, Ohio. After
a year as an Assistant Professor at South
Dakota State University, where he con-
ducted research on the impacts of agri-
cultural chemicals on migratory birds,
Dr. Facemire accepted a position with the
Vero Beach (Florida) Field Office of the
U.S. Fish and Wildlife Service. Prior to
accepting his current position, he served
as a Senior Staff Biologist with the Divi-
sion of Environmental Contaminants,
Arlington, Virginia.
William F. Fitzgerald, Ph.D.

Dr. Fitzgerald is a Professor of
Marine Geochemistry in the Department
of Marine Sciences at the University of
Connecticut. He has been at the Univer-
sity since 1971.
Dr. Fitzgerald obtained a B.S. in
chemistry from Boston College, an M.S.
in chemistry from the College of the
Holy Cross, and a Ph.D. in chemical
oceanography that was awarded jointly
by the Massachusetts Institute of Tech-
nology and the Woods Hole Oceano-
graphic Institution in 1970.
Professor Fitzgerald's general
research interests are in atmospheric and
marine chemistry, with particular
emphasis on global biogeochemical
cycles of trace metals and the environ-
mental impact resulting from metal
emissions associated with human en-
deavors. His current and long-term
research activities have been focused on
mercury in the environment, and he has
published more than 50 professional
papers dealing with various aspects of
the biogeochemical cycling of mercury.
At present, Professor Fitzgerald is
investigating significant aspects of the
biogeochemical behavior and fate of
mercury in the atmosphere and in natural
waters. This research is multifaceted
and often interdisciplinary and involves
international collaboration. For ex-
ample, these pursuits include a U.S./
French cooperative examination of the
historical record of interhemispheric
cycling and air-water exchange of
mercury over mid-continental lacustrine
regions as part of a multidisciplinary
program studying the pathways and
processes regulating the aquatic bio-
geochemistry of mercury in the temper-
ate zone; this work complements
ongoing investigations exploring the
aquatic biogeochemistry of mercury in
coastal and open ocean environments.
This research is supported by grants
from the National Science Foundation,
from the NATO Scientific Affaires
Division: Collaborative Research Grants
Programme, from the Wisconsin Depart-
ment of Natural Resources, from the
Electric Power Research Institute, and
from the Research Foundation of the
University of Connecticut.
Cindy C. Gilmour, Ph.D.

Dr. Grilmour is Assistant Curator at
the Academy of Natural Sciences'
Estuarine Research Center in southern
Maryland. She received her B.A. in
biochemistry from Cornell University
and her Ph.D. in marine, estuarine, and
environmental science from the Univer-
sity of Maryland. She joined the Acad-
emy after 3 years of postdoctoral work
with Professor Ralph Mitchell at
Harvard University. Dr. Gilmour's
research focuses on microbial mercury
methylation in fresh waters and estuaries
and on the microbial ecology of Chesa-
peake Bay,
Rick Irloiffmann

Mr. Hoffmann organized the
National Forum on Mercury in Fish. He
is an environmental scientist in EPA's
Risk Assessment and Management
Branch. The Branch is located in the
Office of Science and Technology within
the Office of Water. The Branch is
responsible for directing sediment
contamination programs and evaluating
risks associated with chemical contami-
nants in fish. Mr. Hoffmann works on
fish contamination issues.
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208
National Forum on Mercury in Fish
Prior to his current position,
Mr. Hoffmann worked in EPA's San
Francisco region, where he held various
positions relating to water quality
planning and pollution control as well as
overall environmental impact assess-
ments. He has also worked for the
Hawaii State Department of Health.
Mr. Hoffmann received a B.A. in
zoology from California State University
at San Diego and an M.P.H. from the
University of Hawaii's School of Public
Health, with an emphasis in environmen-
tal/occupational health.
James P. Hurley, Ph.D.

Dr. Hurley is a Chemical Limnolo-
gist with the Wisconsin Department of
Natural Resources, Bureau of Research.
He holds a joint appointment as an
Honorary Associate with the University
of Wisconsin-Madison Water Chemistry
Program.
Dr. Hurley received his B.S. in
chemistry and environmental analysis
from Nasson College and his M.S. and
Ph.D. from the University of Wisconsin
Water Chemistry Program. After a 2-
year postdoctoral position with the
Wisconsin Center for Limnology,
Dr. Hurley accepted his current position
with the Wisconsin Department of
Natural Resources. Over the past 6
years, he has worked with several
projects involving mercury cycling in the
environment. He has participated in two
phases of the EPRI-sponsored Mercury
Cycling in Northern Temperate Lakes
Project and 3 years of the Wisconsin
DNR's Background Trace Metals in
Rivers study. He is currently involved in
those two projects as well as the trace
metals in tributaries phase of the EPA-
sponsored Lake Michigan Mass Balance
Project.
Martha Keating

Ms. Keating received her B.S.
from the University of New Hampshire
and her M.S. in environmental science
from the School of Public Health at the
University of North Carolina - Chapel
Hill. She was employed as a staff
scientist by Radian Corporation until
1988, when she joined the U.S. Environ-
mental Protection Agency. Ms. Keating
has worked extensively with state and
federal air toxics programs and is
currently the project lead for the
Agency's Mercury Study Report to
Congress.
Randall O. Manning, Ph.D.,
D.A.B.T.

Dr. Manning is the Coordinator of
the Environmental Toxicology Program
in the Georgia Department of Natural
Resources, Environmental Protection
Division.
Dr. Manning received his Ph.D.
from the University of Georgia (UGA),
College of Agriculture, where he studied
the toxicity and metabolism of mycotox-
ins. After a 2-year postdoctoral position
with the Interdepartmental Toxicology
Program at UGA, Dr. Manning became
an Assistant Research Scientist in the
Department of Pharmacology and
Toxicology at UGA, studying the
toxicity of volatile organic chemicals
and the development of physiologically-
based pharmacokinetic models for use in
risk assessment. Dr. Manning joined the
Georgia Environmental Protection
Division in 1991 and was certified as a
Diplomate of the American Board of
Toxicology in 1992. He is currently the
Coordinator of the Environmental
Toxicology Program, which is respon-
sible for providing the Division with
support in toxicology and hazard/risk
assessment. One focus of Dr. Manning's
work has been the development of a
systematic monitoring program for
contaminants in fish and improved fish
consumption advisories in Georgia.
Donald Porcella, Ph.D.

Dr. Porcella is Project Manager,
Land and Water Resources Manage-
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Conference Proceedings
209
ment, at the Electric Power Research
Institute (EPRI), Palo Alto, California.
His current research activities at
EPRI include wetlands, carbon
mitigation and cycling, and the
biogeochemistry of selenium, arsenic,
and mercury. His previous positions
were at Tetra Tech, Inc., Utah State
University, the University of California
Sanitary Engineering Research
Laboratory, the Norwegian Water
Research Institute in Oslo as a Fulbright
Postdoctoral Fellow, and as a visiting
scientist at EPA's Environmental
Research Laboratory in Corvallis,
Oregon. His previous research interests
included lake and reservoir modeling,
bioassays, eutrophication, lake and
watershed liming, and radioecology.
Dr. Porcella has written more than 140
technical papers and books, has served
on many advisory committees, and has
been a technical reviewer for profes-
sional journals. He received
his B.A. and M.A. in zoology and his
Ph.D. in environmental hearth science
from the University of California at
Berkeley.
Robert £. Reinert, Ph.D.

Dr. Reinert is a Professor of
Fisheries in the D.B. Warnell School of
Forest Resources at the University of
Georgia.
Dr. Reinert received his B.S. in
biology from Ripon College in Wiscon-
sin and his M.S. and Ph.D. in fisheries
from the University of Michigan. He
worked on Great Lakes contaminant
problems for 9 years at the U.S. Fish
and Wildlife Service Great Lakes Fish
Laboratory in Ann Arbor, Michigan.
He then became the Unit Leader for the
Cooperative Fish and Wildlife Unit at
the University of Georgia, in Athens.
For the past 14 years Dr. Reinert has
been a faculty member of the D.B.
Warnell School of Forest Resources.
His main research interests are dynam-
ics of contaminants in aquatic systems,
development of biomarker techniques
for fish, and risk assessment.
Deborah Rice, Ph.D.

Dr. Rice is a Research Scientist
with the Toxicology Research Division,
Health Protection Branch, Canadiaoi
Department of Health, where she has
worked for 18 years. During that time,
Dr. Rice has been involved in determina-
tion of behavioral toxicity produced by
developmental neurotoxicants such as
lead and methylmercury, using the
monkey as a model. Her research has
focused on study of complex learning
and memory, and assessment of sensory
system function. She has served on the
National Institutes of Health Initial
Review Group (Study Section) for
Toxicology., as well as numerous ad hoc
committees for such agencies as the
Environmental Protection Agency and
the National Institutes of Environmental
Health Sciences.
Dr. Rice received a B.S. in biologi-
cal sciences from the University of
California, Irvine, and a Ph.D. from the
University of Rochester.
Pamela J, Shubat, Ph.D.

Dr. Shubat is an Environmental
Toxicologist with the Minnesota Depart-
ment of Health. She manages the
Community Environmental Health
Survey and Research program located in
Health Risk Assessment, Division of
Environmental Health.
Dr. Shubat received her B.S in
biology from the University of Minne-
sota, Duluth, and conducted aquatic
toxicity tests for many years at the Envi-
ronmental Protection Agency's Environ-
mental Research Laboratory in Duluth.
She received her M.S. in fisheries and
wildlife from Oregon State University
and her Ph.D. in pharmacology and
toxicology from the University of Ari-
zona. After a postdoctorate at Arizona,
Dr. Shubat took a research scientist po-
sition with the Minnesota Department of
Health in the area of risk assessment.
Dr. Shubat holds an adjunct appoint-
ment at the University of Minnesota,
where she lectures in risk assessment.
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210
National Forum on Mercury in Fish
Over the past 5 years, Dr. Shubat has
been responsible for the Minnesota Fish
Consumption Advisory program and has
been an active member of the Great
Lakes Sport Fish Advisory Task Force.
Alan Stern, Dr. P.H., D.A.B.T.

Dr. Stern received a bachelor's
degree in biology from the State Univer-
sity of New York at Stony Brook, a
master's degree in cellular and molecular
biology from Brandeis University, and a
doctorate in public health from Columbia
University. He is board-certified as a
toxicologist by the American Board of
Toxicology, adjunct assistant professor
in the Department of Environmental and
Community Medicine at the University
of Medicine and Dentistry of New
Jersey, and a Councilor of the Interna-
tional Society for Exposure Analysis.
After a brief stint with Region 2 of the
U.S. EPA, he was Chief Toxicologist in
the Environmental Health Services of
the New York City Department of
Health for 9 years. Since 1990 he has
been a Research Scientist in the Division
of Science and Research of the New
Jersey Department of Environmental
Protection, where he specializes in
human health risk and exposure assess-
ment. He is also a regular fish con-
sumer.
Jerry Stober, Ph.D.

Dr. Stober is a Fisheries Scientist
with the U.S. Environmental Protection
Agency, Region 4, Environmental
Services Division, Ecological Support
Branch, located in Athens, Georgia.
Dr. Stober received his B.S. in
1960, M.S. in 1962, and Ph.D. in 1968
from Montana State University. He was
a Professor of Fisheries at the Fisheries
Research Institute, University of Wash-
ington, for 18 years, where he conducted
aquatic environmental research in
freshwater and estuarine systems. Since
joining EPA in 1986, Dr. Stober has been
involved in assessing bioaccumulative
contaminants in fish and participating in
the development of national guidance
documents. Since 1992 he has been
conducting a R-EMAP study of mercury
biogeochemical cycling in the Everglades
ecosystem designed to culminate in an
ecological risk assessment
Kent W. Thornton, Ph.D.

Dr. Thornton is the Arkansas
Mercury Task Force Coordinator and a
Principal in FTN Associates, Ltd. in
Little Rock, Arkansas.
Dr. Thornton received his B.A. in
zoology and his M.S. in water pollution
limnology from the University of Iowa
and his Ph.D. in systems ecology from
Oklahoma State University. He spent a
year as a Postdoctoral Fellow in the
School of Electrical Engineering at
Oklahoma State and a year as Assistant
Professor in Biological Sciences at
Bowling Green State University. For 7
years, he conducted research on reservoir
water quality with the U.S. Army
Engineer Waterways Experiment Station
in Vicksburg, Mississippi. Dr. Thornton
has been a Principal with FTN for the
past 13 years. Over the past decade, he
has been involved in EPA aquatic effects
research, the NAPAP 1990 Integrated
Assessment, ecological risk assessment,
ecological restoration, and mercury
impacts on the environment. He is
currently serving as the Coordinator for
the Arkansas Mercury Task Force.
Roberta F. White, Ph.D., ABPP

Dr. White is Associate Professor of
Neurology and Environmental Health at
Boston University, Research Director of
the Boston Environmental Hazards
Center, and Director of Clinical
Neuropsychology at the Boston DVA
Medical Center and Boston University
Medical Center. She received her Ph.D.
in clinical psychology from Wayne State
University and did her postdoctoral
fellowship in neuropsychology at Boston
University School of Medicine, Depart-
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Conference Proceedings
211
ment of Neurology. For the past 14
years, she has done research in behav-
ioral toxicology and test development
and validation. She also trains students
studying neuropsychology at the gradu-
ate and postgraduate levels and works
with patients who have primary neuro-
logic disorders.
James G. Wiener, Ph.D.

Dr. Wiener is presently Leader of
the Section of Ecology at the National
Biological Survey's Fisheries Research
Center in LaCrosse, Wisconsin. The
Center does research on riverine and
aquatic ecology, ectotoxicology, and
habitat-restoration techniques for large
rivers.
Dr. Wiener has a B.S. in fish, and
wildlife biology from Iowa State Univer-
sity and a Ph.D. in zoology from the Oak
Ridge National Laboratory. He held a
position as a field station leader with the
U.S. Fish and Wildlife Service, National
Fisheries Contaminant Research Center.
During the past two decades, he has been
studying the bioaccumulation and fate of
potentially toxic metals in freshwater
ecosystems, with emphasis on mercury
and cadmium.
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-------
National Forum on
MercuiryinFish
Selected EPA Publications
J^Whe following listings are selected
I EPA publications related to
M. chemical contaminants in fish.
These documents were prepared by
EPA's Office of Water as part of a
Federal Assistance Plan to help states
and other interested parties implement
fish consumption advisory programs.
Guidance for Assessing Chemical
Contaminant Data for Use in Fish
Advisories: Volume I: Fish Sampling
and Analysis, EPA 823-R-93-002,
August 1993.
This document provides detailed
technical guidance on methods for
sampling and analyzing chemicals
in fish and shellfish tissues. It
addresses monitoring strategies,
selection of fish species and chemi-
cal analytes, field and laboratory
procedures, and approaches to data
analyses.
Guidance for Assessing Chemical
Contaminant Data for Use in Fish
Advisories: Volume II: Risk Assess-
ment and Fish Consumption Limits,
EPA 823-B-94-004, June 1994.
This volume provides detailed
guidance on the development of
risk-based fish consumption limits
for fish. In addition to methods, the
document offers specific toxicologi-
cal information on 24 potential fish
contaminants.
Guidance for Assessing Chemical
Contaminant Data for Use in Fish
Advisories: Volume III: Risk Man-
agement (being developed in 1995).
Guidance for Assessing Chemical
Contaminant Data for Use in Fish
Advisories: Volume IV: Risk Com-
munication, EPA 823-R-95-001,
March 1995.
The document begins with an
overview of the risk communication
process and its major components.
Subsequent sections provide in-depth
discussions of such topics as prob-
lem analysis and program objectives,
audience identification and needs
assessment, communication strategy
design and implementation, program
evaluation, responding to public
inquiries, and other topics. The
discussions are illustrated frequently
with "real life" examples drawn from
numerous state or regional fish
advisories.
Consumption Surveys for Fish and
Shellfish, A Review and Analysis of
Survey Methods, EPA 822-R-92-001,
February 1992.
This document contains a critical
analysis of methods used to deter-
mine fish consumption rates of
recreational and subsistence fishers,
groups that might have the greatest
potential for exposure to contami-
nants in fish tissues.
Proceedings of the U.S. Environmental
Protection Agency's National Techni-
cal Workshop "PCBs in Fish Tissue,"
EPA 823-R-93-003, September 1993.
This document summarizes the
proceedings of the EPA-sponsored
workshop held on May 10-11,1993,
in Washington, DC.
To Order Copies: Mail, call, FAX, or
Email a request to:

EPA OW Resource Center (RC4100)
401 M Street, SW
Washington, DC 20460
Phone recording order: (202) 260-7786
FAX order: (202) 260-0386
Email: waterpubs@epamail.epa.gov

Include the publication title and EPA
publication number.
213
-------
-------
National Forum on
Mereury in Fish
September 27-29,1994
New Orleans, Louisiana
Final Agenda
Tuesday, September 27
7:30-8:30 Registration

8:30-8:55 Welcome and Introduction
James A. Hanlon, U.S. EPA, Headquarters
Rick Hoffmann, U.S. EPA, Headquarters

MERCURY OVERVIEW AND BACKGROUND

9:00-9:30 Biogeochemical Cycling of Mercury: Global
and Local Aspects
Dr. William Fitzgerald
University of Connecticut

9:30-10:00 Aquatic Biogeochemistry and Mercury
Cycling Model
Dr. Donald Porcella
Electric Power Research Institute

10:00-10:30Mercury Methylation in Fresh Waters
Dr. Cindy Gilmour
Philadelphia Academy of Science

10:30-10:45BREAK

10:45-11:1 SConsiderations in the Analysis of Water and
Fish for Mercury
Mr. Nicolas Bloom
Frontier Geoscience

11:15-12:OODiscussion/Question-and-Answer Session

12:00-1:30 LUNCH (on your own)

1:30-2:00 Bioaccumulation of Mercury in Fish
Dr. James Wiener
U.S. Fish and Wildlife Service

2:00-2:30 Mercury in Wildlife
Dr. Charles Facemire
U.S. Fish and Wildlife Service
FLORIDA STUDIES

2:30-3:00 Spatial Distribution of Mercury in the
Everglades Canal System
Dr. Jerry Stober
U.S. Environmental Protection Agency,
Region 4

3:00-3:30 Atmospheric Deposition Studies in Florida
Dr. Thomas Atkeson
Florida Department of Environmental
Protection

3:30-3:45 BREAK

3:45-4:15 Watershed Effects on Background Mercury
Levels in Rivers
Dr. James Hurley
Wisconsin Department of Natural Resources

4:15-5:00 Discussion/Question-and-Answer Session

5:30-6:30 SOCIAL HOUR
Wednesday, September 28
TOX1CITY AND RISK ASSESSMENT

8:00-8:25 Mercury Toxicity: An Overview
Dr. Thomas Clarkson
University of Rochester

8:25-8:50 An Overview of Animal Studies
Dr. Deborah Rice
Environment Canada

8:50-9:15 An Overview of Human Studies
Dr. Roberta White
Boston University

9:15-9:45 Discussion/Question-and-Answer Session
-------
Final Agenda
9:45-10:00 BREAK

10:00-10:25Exposure Assessment for Methyl Mercury
Dr. Alan Stern
Newjersy Department of Environmental
Protection

10:25-10:50FDA Perspective
Dr. Michael Bolger
US. Food and Drug Administration

10:50-11:15EPA Perspective
Dr. John Cicmanec
U.S. Environmental Protection Agency

11:15-12:OODiscussion/Question-and-Answer Session

12:00-1:30 LUNCH

RISK MANAGEMENT AND RISK COMMUNICATION

1:30-2:00 A Review of Fish Consumption Advisories
and Their Impact
Dr. Robert Reinert
University of Georgia

2:00-2:45 Different People, Different Approaches: Risk
Management and Communication in Minnesota
Dr. Pamela Shubat
Minnesota Department of Public Health

2:45-3:15 Development of Risk-based Fish Consumption
Guidelines in Georgia
Dr. Randall Manning
Georgia Department of Environmental
Protection

3:15-3:45 Managing and Communicating Mercury Risks
in Arkansas
Dr. Kent Thornton
FTN Associates

3:45-4:15 Discussion/Question-and-Answer Session

4:15-5:30 Displays and Demonstrations in Nearby
Resource Room
• Demonstration of National Fish Tissue
Data Repository
• Demonstration of National Fish Advisory
Database
Thursday, September 29
8:30-9:00 National Mercury Study
Dr. Jerry Stober, US EPA Region 4
Dr. Steve Paulson, US EPA Newport

MERCURY CONTROL STRATEGIES

9:00-9:45 Mercury Deposition and the Activities of the
Clean Air Act of 1990
Ms. Martha Keating
U.S. Environmental Protection Agency

9:45-10:15 Great Lakes "Virtual Elimination" Initiative
Mr. Frank Anscombe
U.S. EPA, Great Lakes National Program Office

10:15-10:30BREAK

10:30-11 :OOMinnesota Mercury Reduction Activities
Mr. Pat Carey
Minnesota Pollution Control Agency

11:00-11:30Discussion/Question-and-Answer Session

11:30-11:45Conference Wrap up and Closing
Mr. Rick Hoffmann
U.S. Environmental Protection Agency
Resource Room Activities

There will be a resource room located nearby to the
main conference room where information will be
available. The resource room will provide an opportu-
nity for people to meet in small groups throughout the
conference. There will also be computer demonstra-
tions.
printed on recycled paper
-------
List of Attendees
A National Forum on Mercury in Fish
September 27-29, 1994
Assaf Abdelghani
Tulane University
School of Public Health
1501 Canal Street
New Orleans, LA 70112
504/588-5374
Michael Adams
U.S. Food & Drug
Administration
HFS-247, 200 C Street, S.W.
Washington, DC 20204
202/418-3041
Jeany Anderson-Labar
Louisiana Oept of Env Quality
P.O. Box 82215
Baton Rouge, LA 70884
504/765-0511
Frank Anscombe
USEPA (G-9J)
77 U. Jackson Blvd.
Chicago, IL 60604
312/353-0201
Tom Armitage
USEPA (4305)
401 H St., SW
Washington, DC
202/260-5388
20460
Mike Armstrong
Fisheries
Arkansas Game & Fish Commission
#2 Natural Resources Drive
Little Rock, AR 72205
501/223-6372
Tom Atkeson
Florida Department of
Environmental Protection
2600 Blair Stone Road
Tallahassee, FL 32399
904/921-0884
Tom Augspurger
U.S. Fish & Wildlife Service
P.O. Box 33726
Raleigh, NC 27636
919/856-4520
Alan Auuarter
USEPA
College Station Rd.
Athens, GA 30605
706/546-2209
Linda Bacon
Maine OEP
Station 17
Augusta, ME 04333
207/287-7749
Bev Baker
USEPA Headquarters
401 M St., S.U. (4204F)
Washington, DC 20460
202/260-7037
Alan Ballard
Gulf of Mexico Program
Bldg. 1103
Stennis Space Cr, MS 39529
601/688-7001
Lina Balluz
Louisiana Department of Health
234 Loyola Avenue
Suite 620
New Orleans, LA 70112
504/568-5967
Angela Bandemehr
U.S. EPA
77 W. Jackson Boulevard
Chicago, IL 60604
312/886-6858
Phil Bass
Field Services Division
Mississippi Dept of Env Quality
P.O. Box 10385
Jackson, MS 39289
601/961-5143
Terry Bassett
AKZO Nobel Chemical
P.O. Box 100
Axis, AL 36505
205/675-1310
Thomas Pride
Woodward-Clyde Consul.tants
9950 Princess Palm Ave.
Ste. 232
Tampa, FL 33619
813/626-0047
Michael Beck
LA DEQ
P.O. Box 82178
Baton Rouge, LA 70884
504/765-0251
Robert Benson, Ph.D.
U.S. EPA, Region 8
Water Management Division
(8WM-DW)
999 18th Street, Suite 500
Denver, CO 80202
303/293-1694
Gary Bigham
PTI Environmental Services
1601 Trapelo Road
Waltham, MA 02154
617/466-6681
Jeffrey D. Bigler
USEPA, 4305
401 M St., S.W.
Washington, DC 20460
202/260-1350
Chelie Billingsley
Tetra Tech, Inc.
10306 Eaton PI., Ste. 340
Fairfax, VA 22030
703/385-6000
Judith Black
U.S. EPA, Region 6
1445 Ross Avenue
Dallas, TX 75202
214/665-6739
Nicolas Bloom
Frontier Geosciences, Inc.
414 Pontius Avenue, N
Seattle, WA 98109
206/622-6960
Jim Blumenstook
New Jersey Department of Health
Division of Epidemiology
3635 Quacker Bridge Road
CN369
Trenton, HJ 08625
609/588-3120
Dr. Michael Bolger
Contaminants Branch
U.S. Food & Drug Administration
200 C Street, SW
(HFS-308)
Washington, DC 20204
202/205-8205
Lorna Bozeman
ATSDR, US Public Health Service
Executive Park, Building 33
1600 Clifton Road, E-56
Atlanta, GA 30333
404/639-6070
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List of Attendees
(continued)
Earl Bozeman
USEPA-Region 4 (4WD-UPB)
345 Courtland St.. HE
Atlanta, GA 30365
404/347-5065
Bruce T. Brackin
MS Department of Health
P.O. Box 1700
Jackson, HS 39215
601/960-7725
Duight Bradshau
Louisiana Oept of Env Quality
Office of Water Resources
P.O. Box 82215
Baton Rouge, LA 70884
Hirk Briggs
Minnesota Department of
Natural Resources
5463 U. Broadway
Forest Lake, HH 55025
612/464-1247
Trey Brown
U.S. EPA, Region 4
Federal Facility CRC
NOAA/HAZMAT
1 Tinet Drive
Pendleton, SC 29670
803/646-2335
Jim Brown
01 in Corporation
P.O. Box 248
Charleston, TN 37310
615/336-4308
Too Burbacher
University of Washington
Department of Env. Health
Seattle, WA 98106
206/788-0786
Clarence Callahan
U.S. EPA
(H-9-3)
75 Hawthorne Street
San Francisco, CA 94105
415/744-2314
Michael Callam
NE DEQ
1200 N St., Ste. 400
Lincoln, NE 68509
402/471-4700
Roxic Cantu
Texas Parks and Wildlife Dept
6200 Hatchery Road
Fort Worth, TX 76114
817/731-3713
Pat Carey
Hazardous Waste Division
Minnesota Pollution Control
Agency
520 Lafayette Road
St. Paul, HH 55155
612/297-8680
Gale Carlson
Missouri Department of Health
Bureau of Env Epidemiology
210 El Mercado Plaza
P.O. Box 57
Jefferson City, HO 65102
314/751-6404
John Cicmanec
U.S. EPA
26 U Martin Luther King
HS-190
Cincinnati. OH 45268
513/569-7481
Tom Clarkson
University Medical Center
University of Rochester
P.O. Box EHSC
Rochester, NY 14642
716/375-3911
Joe Clymire
Tulane University
Department of Chemistry
Box 26
New Orleans, LA 70118
504/865-5573
Paul Conzelmann
U.S. Fish and Wildlife Service
825 Kaliste SoIcom Road
Lafayette, LA 70508
318/262-6630
Barbara Cooper
OPH/SEE
234 Loyola Avenue
New Orleans, LA 70119
504/568-7036
Emelise Cormier
Louisiana DEQ
P.O. Box 82215
Baton Rouge, LA 70884
504/765-2765
Kirk Cormier
Louisiana Department of
Environmental Quality
804 H 31st Street
Monroe, LA 71201
318/362-5439
Greg Cramer
FDA/HFS-416
200 C St., S.W.
Washington, DC 20460
202/418-3160
Dr. Morris Cranmer
Cranmer & Associates, Inc.
P.O. Box 22093
Little Rock, AR 72221
501/224-0240
Philip Crocker
U.S. EPA
1445 Ross Avenue
Dallas, TX 75202
214/655-6644
Michael Crouch, PhD.
Terra Consulting Corp
P.O. Box 14207
Baton Rouge, LA 70898
504/769-1141
Art Crowe
Texas Natural Resource
Conservation Commission
2916 Teague Drive
Tyler, TX 75701
903/595-5466
Linda Cunnings, PhD.
Terra Consulting Corp
P.O. Box 14207
Baton Rouge, LA 70898
504/769-1141
William Danchuk
Environmental Affairs
Consolidated Natural Gas Co
625 Liberty Avenue, CNG Tower
Pittsburgh, PA 15222
412/227-1471
Charles Demas
USGS, Louisiana District
3535 S. Sherwood Forest Blvd
Baton Rouge, LA 70816
504/389-0391
-------
List of Attendees
(continued)
Dennis Demcheck
USGS
3535 S. Sherwood Forest
Baton Rouge, LA 70816
504/289-0281
Laura Dodge-Murphy
PTI Environmental Services
1601 Trapelo Road
Waltham, MA 02154
617/466-6681
Laurel Driver
USEPA MD-13
RTP, NC 27711
919/541-2859
Byron Ellington
TX Natural Resource
Conservation Connission
P.O. Box 13087
Austin, TX 78711
512/239-2253
Mary C. Evans
AR Department of He.ilth
300 Broopark
Little Rock, AR 72205
501/225-6613
Stan Evans
Arkansas Department of Health
4815 Harkham - Slot #32
Little Rock, AR 72205
501/661-2986
Chuck Facemire
U.S. Fish and Wildlife Service
1875 Century Boulevard
Atlanta, GA 30345
404/679-7081
Laura Fadil
LA Office of Public Health
234 Loyola Avenue
Suite 620
New Orleans, LA 70112
504/568-8537
Sharon Fancy Parrish
U.S. EPA, Region 6
1445 Ross Avenue
Dallas, TX 75044
214/665-7145
Joe Ferreri
57 Avila St.
San Francisco, CA
415/744-1922
94123
Larry Fink
South Florida Water District
3301 Gun Club Rd.
West Palm Beach, Fl. 33416
407/687-6749
William Fitzgerald
Department of Marine Sciences
University of Connecticut
Groton, CT 06304
203/445-3465
Henry Folmar
MS DEQ
121 Fairmont Plaza
Pearl, MS 39208
601/939-8460
Marilyn Fonseea
USEPA Headquarters
401 M St., S.W. (4305)
Washington, DC 20460
202/260-0593
Bradley Frazier
River Studies Center
Univ of Wisconsin - La Crosse
La Crosse, WI 54601
608/785-8259
Jane Fugler
LA DEQ
Office of Water Resources
P.O. Box 82215
Baton Rouge, LA 70884-2215
504/765-0511
Ed Gardetto
USEPA Headquarters
401 M St., S.W. (4305)
Washington, DC 20460
202/260-7035
Michael Gibertini
Midwest Research Institute
425 Volker Blvd.
Kansas City, MO 64110
816/753-7600
John Giese
Environmental Preservation Div
Arkansas Department of
Pollution Control and Ecology
8001 National Drive
Little Rock, AR 72219
501/570-2121
Dale Givens
Louisiana Department of
Environmental Quality
P.O. Box 82215
Baton Rouge, LA 70884
504/765-0491
Janice Gi Hi land
Alabama Department of
Public Health
434 Monroe Street
Montgomery, AL 36130
205-6135
Jennifer Goodwin
Louisiana Department of Health
234 Loyola Avenue
Suite 620
New Orleans, LA 70118
504/568-7309
Cindy Gilmour
Philadelphia Academy of Natural
Science
Benedict Research Lab
7311 Benedict Avenue
Benedict, MD 20612
301/274-3134
Ron Gouguet
NOAA HAZMAT
C/o U.S. EPA
1445 Ross Avenue
Dallas, TX 75202
214/665-2232
Jessica Graham
MA Department of Public Health
150 Tremont Street
7th floor
Boston, MA 02111
617/727-7170
Gary Gulezian
Air Toxics and Radiation Branch
U.S. EPA
77 West Jackson Boulevard
Chicago, IL 60604
312/353-8559
Arthur Hagar
LA Oept. of Health
New Orleans, LA
504/568-8229
-------
List of Attendees
(continued)
Douglas Hahn
Woodward-Clyde
2822 O'Heat Lane
Baton Rouge. LA 70816
504/751-1873
Hark Hale
NC OEHNR
4401 Reedy Crk. Rd.
Raleigh, NC 27607
919/733-6946
James Hanion
U.S. EPA, Headquarters
401 M Street, SW
Washington, DC 20460
202/260-5400
John Harju
IWO-EERC
lox 9018
Grand Forks. ND 85202
701/777-5208
Ruth Harper
HcNeese State University
Department of Biology and Env.
Lake Charles, LA 70609
318/475-5674
Dan Harrington
Tulane University
1430 Tulane Ave. SL29
New Orleans, LA 70112
504/588-5374
William R. Hartley
Tulane University
1430 Tulane Ave. SL29
New Orleans, LA 70112
504/588-5374
Beth Hassett-Sipple
USEPA MO-13
RTP, NC 27711
919/541-5346
Mary Heagler
HcNeese State University
Dept of Biol and Env Science
P.O. Box 92000
Lake Charles, LA 70609
318/475-5656
Hatthea Heinrich
LADEQ
Office of Water Resources
P.O. Box 82215
iaton Rouge, LA 70884-2215
504/765-0511
Thomas Herrington
U.S. Food & Drug Administration
Gulf of Mexico Program
Building 1103
Room 202
Stennis Space Cr, MS 39529
601/888-7941
John L. Hesse
Michigan Department of Public Health
P.O. Box 30195
Lansing, HI 48822
517/335-8353
Delbcrt Hicks
USEPA
College Station Rd.
Athens, GA 30605
706/546-2294
Albert Hindrichs
Louisiana Dept of Env Quality
P.O. Box 82215
Baton Rouge, LA 70884
504/765-0511
Rick Hoffmann
U.S. EPA, 4305
401 M Street S.W.
Washington, DC 20460
202/260-0642
David Hohreiter
01L
6723 Tcwpath Road
Sox 66
Syracuse, NY 13214
315/446-9120
Jeff Holland
Reedy Creek Imp District
2191 Bear Island Road
Box 10170
Lake Buena Vista, FL 32830
407/824-7301
Joe Hollouay
FDA
1110 Vermont Avenue
Suite 1110
Washington, DC 20005
202/418-3177
Scott Hopkins
Htw Mexico Environment Dept
Surface Water Bureau
1190 St. Francis Drive
Santa Fe, KH 87502
505/827-2814
Steve Houghton
Oklahoma DEO
1000 NE 10th
Oklahoma City, OK 73124
405/271-5240
James P. Hurley
Wisconsin ONR
VW Water Chemistry Lab
660 N. Park Street
Madison, WI 53706
608/262-3979
Diane Hyatt
Natural Res Damage Assessment
Texas General Land Office
1700 North Congress Avenue
Austin, TX 78701
512/475-1395
Russell Isaac
Massachusetts DEP
1 Winter Street
Boston, MA 02108
617/292-5559
John Jansen
Southern Company Services
P.O. Box 2625
Birmingham, AL 35202
205/877-7698
Dr. Betty K Jensen
Pubic Service Electric and
Gat Ccopany
80 Park Plaza
-------
List of Attendees
(continued)
Peter Jones
New York State Department of
Environmental Conservation
50 Wolf Road
Room 315
Albany, NY 12233
518/457-7470
Nicole Jurczyk
Env. Science & Engineering
P.O. Box 1703
Gainesville, FL 32602-1703
904/332-3318 ext.2278
R. Deedee Kathman
Aquatic Resources Center
P.O. Box 680818
Franklin, TN 37064
615/790-0172
Kenneth W. Kauffman
Oregon Health Division
State Office Building
800 NE Oregon St.
Portland, OR
503/731-4015
Martha Keating
U.S. EPA
MD-13
Research Triangle Park
Res Triangle, NC 27711
919/541-5340
John Kern
NOAA/Damage Assessment
9721 Executive Center Drive
St. Petersburg, FL 33702
813/893-3571
Patti King
MN Pollution Control Agency
520 Lafayette Road
St. Paul, MH 55155
612/296-6074
Barbara Klieforth
Tulane University
1430 Tulane Ave. SL29
New Orleans, LA 70112
504/588-5374
Doug Knauer
WI DNR
1350 Femrite Dr.
Monona, Wisconsin 53716
608/221-6354
Barry Kohl, Ph.D.
Department of Geology
Tulane University
New Orleans, LA 70118
504/865-5198
Fred Kopfler
U.S. EPA
Gulf of Mexico Program
Building 1103
Stermis Space Ct, MS 39529
601/688-3726
Paul C. Koska
US EPA, Region 6
1445 Ross Ave.
Dallas, TX 75202
214/665-8357
Napolean Kotey
USEPA-Region 4
345 Courtland St., NE 13th Fir.
Atlanta, GA 30365
404/347-2913
Arnold Kuzmack
U.S. EPA
401 M Street, SW
Washington, DC 20460
202/260-5821
A. J. Labuz
Allied Signal, Inc.
1700 Milton Avenue
Solvay, NY 13209
315/482-4078
Kenneth Landrum
P.O. Box 751
Gramercy, LA 70052
504/765-0330
Mike Ledet
Louisiana Dept of Env quality
Office of Water Resources
P.O. Box 82215
Baton Rouge, LA 70884
Felix Locicero
Technical Evaluation Section
U.S. EPA, Region 2
26 Federal Plaza
New York, NY 10278
212/264-5691
Dennis Logan
Coastal Environmental Services
1099 Winterson Road, Suite 130
Linthicum, MD 21090
410/684-3324
Brad Lyon
University of Tennessee
105 Mitchell Road
Oak Ridge, TN 37831 '•
615/241-2649
Charlie MacPherson
Tetra Tech, Inc.
10306 Eaton PI., Ste. 340
Fairfax, VA 22030
703/385-6000
Randall Manning
Georgia Department of Natural
Resources
Floyd Tower East, Suite 1152
205 Butler Street SE
Atlanta, GA 30334
404/656-4713
Tom HcChesney
Arkansas Department of Health
4815 W. Markham - Slot #32
Little Rock, AR 72205
501/661-2597
Moira McNamara Schoen
OPA/OPPE (2124)
USEPA Headquarters
401 M St., S.W.
Washington, DC 20460
202/260-2772
Terry D. Martin
Winston-Salem Journal
402 Desse Rd.
Monroe, NC 28110
919/833-9056
Malcolm Meaburn
Office of Special Projects
Natl Marine Fisheries Service
P.O. Box 12607
Charleston, SC 2942?
803/762-1200
Eugene Meier
Gulf of Mexico Program
U.S. EPA
Building 1103, Room 202
Stennis Space Cr, MS 39529
601/688-1233
-------
List of Attendees
(continued)
Phyllis Meyer
USEPA
960 College Station Rd.
Athens, GA 30605
706/546-2200
Larry Holcney
Ooherty, Ruable & Butler
150 Fifth Street Tower
Suite 3500
Minneapolis, HH 55402
612/340-5592
Steve Mierzykowski
U.S. Fish & Wildlife Service
1033 South Main Street
Old Town, HE 04460
207/827-5938
James K. Hoore
Asbury Park Press
703 Hill Creek Rd.
Manahawkin, NJ 08050
609/597-7000
Bruce Mintz, Chief
Environmental Fate Section
Office of Water
U.S. EPA, Headquarters
401 H Street, SW
Washington, DC 20460
202/260-9569
Kim Mortensen, PhD.
Bur of Epidemiology/Toxicology
Ohio Department of Health
246 N. High Street
Columbus, OH 43266
614/466-5599
Sarry Hower
Maine Dept of Env Protection
SHS 17
Augusta, HE 04333
207/287-7777
Ron Munson
Tetra Tech, Inc.
Pittsburg, PA
412/934-1120
Ismael Nava
Contaminant Assessment Program
Texas Parks & Wildlife Dept
4200 Smith School Road
Austin, TX 78744
512/389-4580
Steven Hewhouse
Indiana Dept of Environ Hgmt
100 H. Senate Avenue
P.O. Box 6015
Indianapolis, IH 46206
317/243-5114
AI Nissen
Louisiana Dept of Env Quality
Office of Water Resources
P.O. Box 82215
Baton Rouge, LA 70884
Toni B. Odom
01 in Corporation
P.O. Box 28-Olin Rd.
Mclntosh, AL 36553
205/944-3350
David Oge'
Louisiana Dept of Env Quality
Office of W»ter Resources
P.O. Eox 82215
iaton Rouge, LA 70884
Cheryl Overstreet
U.S. EPA, Region 6
1445 Ross Avenue
Dallas, TX 75075
214/665-6643
Heera Parab
Public Health Program Offices
DHH/OPH, Engineering Department
325 Loyola Avenue
Room 403
New Orleans, LA 70112
504/568-6504
Rindi Parks Thomas
U.S. Tuna Foundation
1101 17th Street, NW
#609
Uiihington, DC 20036
202/857-0610
Tonie Patterson
Governor Tucker's Office
State Capitol, Room 238
Little Rock, AR 72201
501/682-7527
Gary Pederson
USGS
3850 Holcomb Br. Rd.
#160
Norcross, GA 30092
404/409-7718
Steve Perry
6163 Brandy Run Rd.
Hobile, AL 36608
205/343-7425
Hark Peterson
Oak Ridge National Laboratory
P.O. Box 2008
ORNL, Building 1505
Oak Ridge, TN 37831
615-5763
Marjorie Pitts
U.S. EPA, Headquarters
OST/SASD
401 M Street, SW
Washington, DC 20460
202/260-1304
Jerry Pollock
06HHA/CA EPA
601 H. 7th St (HS 241)
P.O. Box 942732
Sacramento, CA 94234
916/327-7319
Don ForceUa
Studies
Electric Power Research
Institute
3412 Hillview Avenue
Palo Alto, CA 94303
415/855-2723
Donald Porteous
U.S. EPA
60 Westview Street
Lexington, MA 02173
617/860-4317
Bob Presley
Texas ASM University
Oceanography - HS 3146
College Station, TX 77843
409/845-5136
Drew J. Puffer
USEPA Gulf of Mexico Program
Bldg. 1103, Room 202
Stennis SpaceCtr, MS 39529
601/688-3913
Lori Rabuck
River Studies Center
Univ of Wisconsin—La Crosse
La Crosse, WI 54601
608/785-8259
-------
List of Attendees
(continued)
Lisa H. Ramirez
Applied Marine Res. Lab
1034 U 45th St.
Norfolk, VA 23529
804/683-3498
Dianne Ray
Louisiana Department of
Environmental Quality
8618 G.S.R.I. Avenue
Baton Rouge, LA 70310
504/765-2413
Rob Reash
American Electric Power
1 Riverside Plaza
Columbus, OH 43215
614/223-1237
Bob Reinert
School of Forest Resources
University of Georgia
Athens, GA 30602
706/542-1477
Vincent L. Reynolds
Radian Corp.
Austin, TX 78759
512/454-4797
Ken Rice
Texas Parks and Wildlife Oept
6300 Ocean Drive
Corpus Christi, TX 78412
512/993-4492
Glenn Rice
U.S. EPA
M.S. 190
26 U.H.L. King
Cincinnati, OH 45268
513/569-7813
Deborah Rice
Toxicology Research Division
Banting Research Center
Tuneys Pasture
Ohowa, Ontario
Canada, K1AOL
613/957-0967
Shano Rizvi
LA DEQ
Office of Water Resources
P.O. Box 82215
Baton Rouge, LA 70884-2215
504/765-0511
Barbara Romanowsky
LA Dept. of Env. Quality
P.O. Box 82215
Baton Rouge, LA 70884
504/765-0634
Lonnie Ross
U.S. EPA, Region 6
1445 Ross Avenue, Suite 1200
Dallas, TX 75126
214/665-6665
Alan Rovira
HcNeese State University
3145 O'Neil Road
Baton Rouge, LA 70809
504/753-5647
David Sager, Chief
Texas Parks and Wildlife Dept
4200 Smith School Road
Austin, TX 78744
512/389-4503
Jay Sauber
North Carolina Environmental
Management
4401 Reedy Creek Road
Raleigh, NC 27607
919/733-6510
Bobby Savoie
LA Department of Health
P.O. Box 629
Baton Rouge, LA 70821
504/342-6726
Julie Sbeghen
Hydro Quebec
75 Rene Levesgue Quest
Montreal, Quebec H2Z14A
514/289-5356
Rita Schoeny
US EPA/ECAO-Cin.
26 W. Martin Luther King Dr.
Cincinnati, OH 45268
513/569-7544
William Schramm
Louisiana Department of
Environmental Quality
P.O. Box 82215
Batch Rouge, LA 70884
501/765-0585
Bruce Schuld
Water Quality Compliance Office
Idaho Division of Env Quality
1420 N. Hilton
Boise, ID 83703
208/334-0550
Doug LaBar
Water Quality Division
C-K Associates, Inc.
17170 Purkins Roael
Baton Rouge, LA 70810
504/755-1000
Dave Serdar
Washington State Department
of Ecology
300 Desmond Drive
Box 4-7710
Olympia, WA 98504
206/407-6772
Walter Shepard
Allied Signal
P.O. Box 6
1700 Milton Avenue
Solvay, NY 13209
315/487-4403
Pam Shields
U.S. EPA, Rgion 1
Water Management division
HDA-CAN
JFK Federal Building
Boston, MA 02203
617/573-5730
Pam Shubat
MM Department of Health
P.O. Box 59040
Minneapolis, MN 55459
612/627-5048
Dennis Smith
Zeneca Inc.
P.O. Box 32
Bucks, AL 36512
205/675-0950
Stephanie Smith
CIS
OPH/SEE
234 Loyola Avenue
New Orleans, LA 70119
504/568-3588
Elaine Sorbet
Louisiana Department of
Environmental Quality
8618 C.S.R.I. Avenue
Baton Rouge, LA 70810
504/765-2406
-------
List of Attendees
(continued)
George Spencer
/ir..DaUy and Air Quality Week
4418 HacArthur Boulevard, NW
Washington, DC 20007
202/298-8201
Jerry Stober
U.S. EPA, Region 4
Environmental Services Division
College Station Road
Athens, GA 30613
706/546-2207
Alan Stern
Div. of Science and Research
CN409
Hew Jersey DEP
401 E. State Street
Trenton, NJ 08625
609/633-2374
Claus Suverkropp
Larry Walker Associates
509 Fourth Street
Davis, CA 95616
916/753-6400
Barbara Stifel
Oregon Dept of Env Quality
811 SW sixth Street
Portland, OR 97204
503/229-6982
Susan Svirsky
U.S. EPA, Region 1
JFK Federal Building
(HSS-CAN7)
Boston, MA 02203
617/573-9649
Jeff Swartout
USEPA (HS190)
26 U. Martin Luther King Dr.
Cincinnati, OH 45268
513/569-7811
Dr. Hark Tisa
Massachusetts Division of
Fisheries and Wildlife
29 Pheasant Hollow Run
Princeton, HA 01541
508/792-7270
Rani Thiyagarajah
921 Hesper Ave.
Metairie, LA 70005
504/588-6941
Kimberly Tisa
U.S. EPA, Region 1
JFK Federal Building
Boston, HA 02203
617/565-3257
Kent Thornton
FTN Associated, Ltd
3 Innwood Circle
Suite 220
Little Rock, AR 72211
501/225-7779
Don Tolbert
LeMoyne Citizens Advisory Panel
13040 N. Forest Dr.
Axis, AL 36505
205/675-1437
Don Turman
5^5°*.*? Caroe & Flsh Conraission
2320 Chidcster Road
Camden, AR 71701
501/836-4612
Steve Twiduell
Texas Natural Resource
Conservation Commission
P.O. Box 13087
Austin, TX 78711
512/239-4607
Steve Ugoretz
WI DNR
1350 Femrite Dr.
Honona, WI 53716
Yvonne H. Vallctte
USEPA Region 6
1445 Ross Ave.
Dallas, TX 75202
214/665-6420
John Villanacci
TX Department of Health
1100 W. 49th St.
Austin, TX 78756
512/458-7269
Dallas Wait
Gradient Corporation
Cambridge, MA 02138
617/576-1555
Jeff Waters
T-Utyne Environmental Law Clinic
7039 Freret Street
Hew Orleans, LA 20118
504/865-5789
Susan Wenberg
AHS
1777 H. Kent St.
8th Floor
Arlington, VA 22209
James Wiener, PhD.
Hationtl Biological Survey
Hatl Fisheries Research Center
2630 Fanta Reed Road
La Crosse, WI 54602
608/783-6451
Carl Watras
WI DNR
10810 Cty. N
Boulder Jet., WI 54512
715/356-9494
Linda West
U.S. Public Health Service
1600 Clifton Road, NE
MS-56
Atlanta, GA 30333
404/639-6070
Kirk Wiles
TX Department of Health
1100 W. 49th St.
Austin, TX 78753
512/719-0200
Lee Weddig
National Fisheries Institute
1525 Wilson Boulevard
Suite 500
Arlington, VA 22209
703/524-8880
Roberta White
Boston University
DVA Medical
150 S. Huntington Avenue
Boston, MA 02130
617/232-9500
Luanne Williams
North Carolina Department of
Environ Health and Natural Res
Env Epidemiology Section
P.O. Box 27687
Raleigh, NC 27611
919/733-3410
-------
List of Attendees
(continued)
Hark Wood
PPG
P.O. Box 1000
Lake Charles, LA 70602
318/491-4450
Jarrett Woodrow
Texas Parks and Wildlife Oept
P.O. Box 8
Seabrook, TX 77586
713/291-9914
Jay Wright
Oklahoma DEQ
1000 NE 10th
Oklahoma City, OK
405/271-5240
73124
Roger Yeardley
EHAP-SU
TAI/U.S. EPA
3411 Church Street
Cincinnati, OH 45244
513/569-7093
Carl Young
U.S. EPA, Region 6
1445 Ross Avenue
Suite 1200
Dallas, TX 75202
214/655-6645
Edward Younginer
SCDHEC
2600 Bull Street
Columbia, SC 29201
803/734-5401
Gary Zarling
Minnesota Department of
Natural Resources
5463 W. Broadway
Forest Lake, MM 55025
612/464-1247
David Zircmer
Bureau of Reclamation
1150 North Curtis Road
Boise, ID 83706-1234
208/378-5088
Jim Zarzycki
EA Engineering
2 Oakway
Berkeley Heights,
908/665-2440
NJ 07922
-------
-------
Mercury Advisory
Fact Sheet
Summary Informations
i.
Number of Water bodies
with Advisories 2
Basis of Advisory

Date Advisory Issued
FDA action level

1992
Advisory
Specifics:
Location
Olin Basin

Cold Creek Swamp

Waterbody
Type
65-acre
natural lake

Swamp area

Restrictions
Prohibits consumption of largemouth bass and
catfish

Prohibits the consumption of any fish

Possible
Sources
Point source inputs
from chemical
manufacturing
company (manu-
factured chlorine
and caustic soda)
Point source inputs
from chemical
manufacturing
company.
Comments: Further data is expected and will be released when received. Will update the advisories
as necessary.
Contacts Brian Hughes, Alabama Department of Public Health (205) 613-5347
-------
Mercury Advisory
Fact Sheet
Summary Information:
1. Number of Water bodies
with Advisories!
35. Basis of Advisory
3. Date Advisory Issued
18
FDA action level

First issued in August 1991; presently under review
Advisory
Specifics!
Location
Lake Columbia

Cut-off Creek
Bayou Bartholomew
Big Johnson Lake
Snow Lake
Grays Lake
Moro Bay Creek
Champagnolle Creek
Ouach'rta River
Felsenthal Wildlife Refuge
I All ox-bow lakes, backwa-
ters, overflow lakes, and
I barrow drtches formed by
JtheOuachitaRiver
I Saline River
(at 2 locations)
Dorcheat Bayou
Fouche La Fave River
I Johnson Hole
JNimrodLake
I Lake Wfnona
General Recommendation: "Pregnant women, women who plan to get pregnant, women
who are breast-feeding, and children under the age of 7 years are considered high risk
groups and should not eat fish from the consumption notice areas
Water-body
Type
Lake

Creek
Creek
Lake
Lake
Lake
Creek
Creek
River
Refuge

Mixed
Contacts
Restriction*
Possible
Sources
No more than 2 meals/month for mixed species
(8 ounces=1 meal); No restrictions on largemouth
oass 16". All
others, no more than 2 meals/month

Ni°«m°Aiith*un 2 meals/month of largemouth bass
>16". All others, no restrictions
No consumption of largemouth bass >16". All
others, no more than Zmeals/month
No consumption of largemouth bass >16". All
others, no more than ?meals/month
No more than 2 meals/month of black bass >1 6"
All others, no restrictions
Combination:
atmospheric deposi-
tion and naturally
occurring
Mike Armstrong, Arkansas Fish and Wildlife Service (501) 223-6300
-------
Mercury Advisory
Arizona
Summary Information:
Fact Sheet
1. Number of Water bodies
with Advisories

2. Basis of Advisory

3. Date Advisory Issued
3 (includes methyl mercury)

Risk-based

1989, reissued in 1994
Advisory
Specifics:
Location
Gila River to the Painted
Rocks Barrow Pit Lake,
Salt River below or west of
59th Avenue in Phoenix,
and Hassayampa River
from the Buckeye Canal to
the Gila River
Waterbody
Type
River flowing
into a Lake

Restriction*
Prohibits the consumption of any fish or other
aquatic animals

Possible
Sources
Methyl mercury
inputs from nearby
sewage plant.
Possible nonpoint
source inputs from
agricultural sources.

Comments! Data is currently under analysis.
Contacts
Marc Dahl, Arizona Department of Game and Fish (602) 789-3260
-------
Mercury Advisory

California

Summary Information:
Fact Sheet
1. Number of Waterbodlos
with Advisories

E. Basis of Advisory

3. Date Advisory Issued
On-site risk assessment for sport fish; FDA action level for
commercial fish

1st advisory issued in 1971; others issued in the mid to
late 1980's; most recent one in 1993
Advisory
Specifics:
General Recommendation: For the sites listed below, "Pregnant women, women who may
soon become pregnant, nursing mothers, and children under 15" should either eat reduced
portions or no fish from the affected areas.
Location
Waterbody
Type
Restrictions
Possible
Sources
Clear Lake
Lake
San Francisco Bay Delta
Region

Lake Nacimlento

.ake Berryessa
,ake Herman

Guadalupe River, Creek
nd Reservoir; Calero
leservolr; Alamaden
Reservoir; Alamftos Creek;
nd associated percolation
onds along the river and
reeks
Estuary

Lake

Lake
Lake

Reservoir
largemouth bass > 15" - no more than 11b/month, or
< 15" - no more than 2 Ibs /month; or
channel catfish > 24" - no more than 11b/month, or
< 24" - no more than 3 Ibs/month; or
crappie > 12" - no more than 1 Ib/month, or <12" - no
more than 3 Ibs/month; or
all white catfish - no more than 3lbs/month; or
all brown bullhead - no more than Gibs/month; or
all Sacramento blackfish - no more than 6 Ibs/month;
or
all hitch - no more than 10 Ibs/month

striped bass between 18-27" - no more than 4-7 Ibs/
month, or between 27-35" - no more than 2-4 Ibs/
month, > 35" - no consumption.

largemouth bass - no more than 4 meals/month

largemouth bass > 15"- no more than 1 Ib/month, or
largemouth bass < 15" - no more than 2 Ibs/month, or
all smallmouth bass - no more than 11b/month, or
all channel catfish - no more than 3 Ibs/month, or
all white catfish - no more than 2 Ibs/month, or
all rainbow trout - no more than 10 Ibs/month

largemouth bass - no more than 1 Ib/month

No consumption of any fish
Combination:
atmospheric
deposition and
naturally
occurring, mining
operations
Contacts
Anna M. Fan, Office of Environmental Health Hazard Assessment (510) 540-3063
-------
Mercury Advisory
Fact SIHeet
Sumnnary Informations
Number of Water bodies
with Advisories 3
Basis of Advisory

Date Advisory Issued
Risk-based

1st advisory issued in 1970's; others issued in the mid to
Iate1980's
Advisory
Specifics:
PW SB Pregnant women, nursing women and women who plan on being
pregnant and children under 9 years of age.
Location
Waterbody
Type
Restrictions
Possible
Sources
Navajo Reservoir
Reservoir
McPhee Reservoir
Reservoir
Narraguinnep Reservoir
Reservoir
Northern pike 30-36 in. Eat no more than 4 meals/
month, PW no mores than 1 meal/month; 36-42 in. no
more than 2 meals/month, PW Do not consume;
Smallmouth bass12-18 in. no more than 4 meals/
month, PW no more than 1 meal/month; Channel
catfish12-18 in. no more than 8 meals/month,, PW no
more than 2 meals/month.
Rainbow trout-6-12 in. Eat no more than 14 meals/
month, PW no more than 3.5 meals/month and 12-18
in. no more than 8 rneals/month, PW no more than 2
meals/month; Yellow perch-1-6 in. no more than 14
meals/month, PW no more than 3.5 meals/month and
6-12 in. no more than 8 meals/month, PW no more than
2 meals/month;Smallmouth bass 1-12 in. no more than
8 meals/month, PW no more than 2 meals/month;
Largemouth bass 12-18 in. no more than 2 meals/
month, PW Do not consume; Black crappie 6-12 in. no
more than 4 meals/month, PW no more than 1 meal/
month; Kokanee salmon 12-18 in. no more than 14
meals/month, PW no more than 3.5 meals/month.
Northern pike 12-18 in. Eat no more than 8 meals/
month, PW no more than 2 meals/month, 18-30 in. no
more than 4 meals/month, PW no more than 1 meal/
month, 30-36 in. no more than 2 meals/month, PW Do
not consume; Walleye 6-12 in. no more than 8 meals/
month, PW no more than 2 meals/month, 12-18 in. no
more than 4 meals/month, PW no more than 1 meal/
month, 18-24 in. no more than 2 meals/month, PW Do
not consume; Channel catfish 18-24 in. no more than 4
meals/month, PW no more than 1 meal/month; Yellow
perch 1-6 in. no more than 14 meals/month, PW no
more than 3.5 meals/month, 6-12 in. no more than 8
meals/month, PW no more than 2 meals/month.
Unknown
Contacts
Robert McConnell, CO Department of Health, (303) 692-2000
-------
Mercury Advisory

Connecticut

Summary Informations
Fact Sheet
Number of Waterbodles
with Advisories
Basis of Advisory

Date Advisory Issued
Risk-based

1st advisory issued in 1992; reissued annually
Advisory
Specifics:
Location
Dodge Pond
Waterbody
Type
Pond
Restriction*
Prohibits the consumption of any fish by pregnant
women, women who may become pregnant in the
near future or children under 1 5 years old. Others
should eat no more than 2 meals/month.
Possible
Sources
May be from indus-
trial sources. No
studies have been
conducted.
Contacts
Brian Toal, Connecticut Department of Health, (203) 240-9022
-------
Mercury Advisory

Florida

Summary Informations
Fact Sheet
1. Number of Watorbodies
with Advisories
68

Risk-based

1st advisory issued in 1989
Basis of Advisory

Date Advisory Issued
Advisory
Specifics:
General Recommendation: For the sites listed below, "women of childbearing
age and children should limit their consumption to one meal per month" from
waters where mercuiy concentrations in fish are between 0.5 ppm and 1.5 ppm.
Location
Majority of Everglades
National Park, and Water
Conservation Areas 2a
and 3
Evenly distributed over
the rest of the state
Waterbody
Type
Freshwater
marsh land
Rivers, creeks,
ponds, lakes
Restriction*
Prohibits any consumption of largemouth bass,
bowfin, and gar (where concentrations are above
1 .5 ppm). Approximately 1 million acreas affected.
For largemouth bass, bowfin, and gar (where
concentrations are between 0.5 ppm and 1.5 ppm),
consumption is limited to no more than one meal
per week (one meal = 8 ounces). Approximately 1
million acres affected.
Possible
Sources
Peat drainage,
hydrologic alter-
ation, and atmo-
spheric
Primarily from
atmospheric inputs
as well as lingering
point source inputs.
Comments: The Department of Health and Rehabilitative Services health risk assessment has
determined that fish having less than 0.5 ppm of mercury represent no dietary risk; fish containing 0.5 ppm to 1.5
ppm should be consumed only in limited amounts; and fish having greater than 1.5 ppm should not be consumed.

Over 50 percent of the State's water-bodies are currently under mercury advisories.
Contacts Tom Atkeson, Florida Department of Environmental Protection (904) 921 -0884
-------
Mercury Advisory
Summary Informations
1. Number off Waterbodl
with Advisories

St. Basis of Advisory

3. Date Advisory Issued
FDA action level (see comments below)

1989, reissued annually
Advisory
Specifics:
Location
Suwanee Basin
Purvis Creek, Gibson
Greek, and Turtle River
Waterbody
Typo
Swamp area
Riverine
Restriction*
Limits consumption of mixed species to 1
meal per week. Pregnant women, nursing
mothers, females of ohildbearing age, and
children under 15 years old should not
consume mixed species more than once a
month. Prohibits the consumption of large-
mouth bass entirely.

Prohibits the consumption of any seafood.
Possible
Sources
Naturally occurring.
Low pH.
Point source inputs
from chemical
manufacturing
company.
Comments: The state is converting to a new system that is risk-based. New data is being collected.
Contacts
Randall Manning, Georgia DNR, (404) 656-4905
-------
Mercury Advisory

Idaho
Summary Informations
Fact Sheet
Number of Waterbodl
with Advisories
Risk-based

May3,1994
Basis of Advisory

Date Advisory Issued
Advisory
Specifics:
General Recommendation: pregnant women, women planning a pregnancy and
children under 7 years old should consume one-fifth of the amounts listed below.
Location
Brownlee Reservoir

Waterbody
Type
Reservoir

Restriction*
For yellow perch, smallmouth bass, and large
crappie over 10" - no more than 60 7-ounce
meals/year.
For catfish and crappie less than 10 "• no more
than 120 7-ounce meals/year.
Possible
Sources

Naturally occurring;
Possibly historic
mining activities

Contact: Russell Duke, Idaho Department of Health and Welfare, (208)334-4964
-------
Mercury Advisory

Illinois

Summary Information:
Fact Sheet
Number of Waterbodles
with Advisories 2
Basis of Advisory

Date Advisory Issued
FDA action level (see comments below)

1994
Advisory
Specifics:
1: Lowest levels of contaminants, fish pose little or no hearth risks
Location
Kinkafd Lake
Cedar Lake
Waterbody
Type
Lake
Lake
Restriction*
largemouth and spotted bass** (Group 2)
largemouth and spotted bass >18"** (Group 2)
Possible
Sources
Unknown

: High levels on contaminants; no one should eat Group 3 fish.
EXCeedenCe °f FDA action level tri99ers further multi-disciplinary studies before
an
Contacts
Dr. Robert Flentge, Divison of Food, Drug and Dairy (217) 785-2439
-------
Mercury Advisory
Fact Sheet
Kentucky

Summary Information:
Number of Waterbodles
with Advisories 5
FDA action level

1993
Basis of Advisory

Date Advisory Issued
Advisory
Speclficss
Location
West Kentucky Wildlife
Management Area
(WMA)

Waterbody
Type
Ponds (i.e., Fire
Hydrant,
Horseshoe, New
Pond, Box
Factory and
Gravel Pit No. 1)
Restrictions
Prohibits the consumption of largemouth bass

Possible
Sources
Unknown

Contacts Michael Mills, Department for Environmental Protection, (502)564-3410
-------
Mercury Advisory
Fact Sheet
Summary Information:
1. Number of Watarbodles
with Advisories 1
Risk-based

1992, reissued 1994
2. Basis of Advisory

3. Date Advisory Issued
Advisory
Specifics:
Location

Ouachrta River

Waterbody
Type
River

Restriction*

Restricts the consumption of bass to no more
than 2 meals/month. All other species, no
restrictions.
Pregnant women and children under 7 years of
age should consume no bass and limit consump-
tion of other species to 2 meals/month (8oz. =
meal).
Possible
Sources
Unknown; possibly
atmospheric
deposition, natural
occurrence, or
discharge from old
mercury mines.

h nw °"T? SamP!l,n9 fe tar9eting baSS> Crappie' and catfish- statewide sampling to identify
extent of the problem is being conducted.
Contacts
Emelise Cormier, Louisiana Department of Environmental Quality, (504)765-051'
-------
Mercury Advisory
Fact Sheet
Maine

Summary Informations
Number of Waterbodles
with Advisories Statewide for lakes, ponds, and rivers

Basis of Advisory Risk-based

Date Advisory Issued June 1994
Advisory
Specifics:
General Recommendation: For the advisory listed below, pregnant women,
nursing mothers, women who may become pregnant and children under 8 years old
should not consume any freshwater fish species from state lakes, ponds, and rivers.
Location

Statewide for lakes, ponds,
and rivers

Waterbody
Type
All lakes, ponds,
and rivers

Restrictions

Consumption should be limited to 6-22 meals/
year for all freshwater fish species (number of
meals vary depending on the size of the fish).

Possible
Sources

In the past, point
sources were a
major contributor
to mercury
contamination.
Now mercury
concentrations are
most likely linked
to atmospheric
deposition.
Contacts Evangelos Dimitriadis, State Toxicologist, (207) 287-5378
-------
Mercury Advisory
Fact Sheet
Summary Information:
mfm
1
Number of Water-bodies
with Advisories
Basis of Advisory

Date Advisory Issued
18 waterbodies for specific advisories; statewide advisory
for pregnant women only

0.5 ppm for sensitive population;
1.0 ppm for general population

1986 to present
Advisory
Specifics:
Location
Statewide
All freshwater
bodies
Turner Pond
Walden Pond
Pepperell Pond
Pontoosue Lake
Powder Mill Pond
Quabbln and Wachusetts
Reservoirs
Quaboag Pond
South Pond
Sudbury River
Sudbury Reservoir
Mill Pond (above G.H.
Nfchols Dam)
Millers Rfver and tributaries
below the confluence
with the Otter River
Noquochoke Lake
Waite Pond
Cedar Swamp Pond
Concord River
Coplcut River/Cornell Pond
Factory Pond
Pond
Pond
Pond
Lake
Pond
Reservoir

Pond
Pond
River
Reservoir
Pond

River
Lake
Pond
Pond
River
River/Pond
Pond
Restrictions

—————————________
Advises pregnant women not to consume certain fish
from freshwater bodies. Does not apply to fish
stocked in freshwater bodies by the State Division of
Fisheries and Wildlife and does not apply to farm-
raised freshwater fish sold commercially.
Possible
Sources
All species (P1,P5)*
largemouth and smallmouth bass (P1, P3)*
largemouth bass (P1, P2, P4)*
largemouth bass (P1, P3)*
All species offish (P1, P5)*
lake trout > 24", largemouth and
smallmouth bass (1)*
largemouth bass (P1, P2, P4)*
All species of fish (P1, P5)*
All species of fish (P6)*
bass(Pl,P2)*
largemouth bass (P1, P2)*

brown trout and American eel (P1, P2, P4)*

largemouth bass (P1, P2, P4)*
All species offish (P1, P5)*
All species offish (P1, P5)*
largemouth bass (P1, P2, P4)*
largemouth bass (P1, P3)*
All species of fish (P6)*
Unknown
Unknown
Unknown
Unknown
Unknown
Unknown
Unknown
Unknown
Unknown
Point Source
Unknown
Unknown

Unknown
Unknown
Unknown
Unknown
Unknown
Unknown
Unknown
Elaine Kruger, Department of Health, (617) 727-7170

-------
Mercury Advisory
Fael Sheet
Michigan
Summary Informations
1. Number of Waterbodk
with Advisories

2. Basis of Advisory

3. Date Advisory Issued
Statewide

Risk-based
1st advisory in 1970 for selected waterbodies; statewide
advisory for all inland lakes in 1989
Advisory
Specifies:
Genera! Recommendation: For all inland lakes and reservoirs, the
advisory recommends that "nursing mothers, pregnant women, women
who intend to have children, and children under age 15 should not eat
more than one meal per month" of the fish species listed below.
Location
Statewide
Water-body
Type
All inland lakes
and reservoirs
Restriction*
No one should eat more than one meal per week
of fish of the following kinds and sizes from any of
Michigan's inland lakes and reservoirs: rock
bass, perch, or crappie over 9 inches in length;
largemouth bass, smallmouth bass, walleye,
northern pike, or muskie of any size.

Some species and sizes from a few lakes have
been found to contain mercury far above levels of
concern and the Health Department recommends
that no one eat the size and species of fish from
those specific areas.
Possible
Sources
Industrial,
naturally occur-
ring, atmospheric.
Comments: The Great Lakes are treated separately under different advisories. For specific
Great Lakes advisories and other specific waters, contact the Michigan Department of Public Health.

The Michigan action level for mercury is 0.5 ppm.
Contact! John Hesse, Michigan Department of Health, (517) 335-8353
-------
Mercury Advisory
Minnesota
Fact Sheet
Summary Informations
571

Risk-based

1st issued in 1975; Updated annually (May release)
1 • Number of Waterbodles
with Advisories

2. Basis of Advisory

3. Date Advisory Issued
Advisory
Specifics:
Location
Minnesota lakes and
rivers
"nr0nnal?eCOmrnend^tl0n: *?'the 5™ sites tssted-the advisory recommends that
pregnant women, nursing mothers, women who may become pregnant in the next several
!^!±!!^^
Waterbody
Type
•M^BMMBMB
lakes and
rivers
meal per week, one meal a month, and do not eat
Restrictions
—^•••m—^^m
Mercury levels of |ess than 0.16, 0.16 to 0.65, 0.66 to
2.8 and more than 2.8 parts per million in fish
correspond to meal advice categories of unlimited
meals, one meal a week, one meal a month, and do
not eat, respectively.

The most common species affected by the advisories
are the northern pike, walleye, crappie and bluegill.
Possible
Sources
^^••^^•^•"•^"i^w"***™

Estimated that 25%
of the mercury is
natural in origin.
The remaining 75%
comes from
airborne deposits
from burning of coal
and other fossil
fuels, burning of
municipal solid
waste, and from
fungicides that were
used in latex paints.
Contacts
Pam Shubat, Minnesota Department of Health, (612) 627-5479
-------
Mercury Advisory
Fact Slbeet
Nebraska
Summary Information:
1. Number of Water bodies
with Advisories 2
Risk-based

1st issued in 1993
2. Basis of Advisory

3. Date Advisory Issued
Advisory
Specifics:
Location
Merr'rtt, Oliver, and Box
Butte Reservoirs
Waterbody
Type
Reservoirs
Restrictions
These advisories are intended primarily for pregnant
or nursing women and infants and children under 15
years of age.
Possible
Sources
Unknown
Contact: Michael Callam, Department of Environmental Quality, (402) 471-4249
-------
Mercury Advisory
Fact Sheet
1
Summary Informations
FDA action level

1st issued in 1989; reissued annually
1. Number of Waterbodles
with Advisories 1

38. Basis off Advisory

3- Date Advisory Issued
Advisory
Specifics:
taMo ™f,Sndation: The advisory recommends that "children
under 12, pregnant women, nursing mothers and women who may soon
become pregnant should not consume fish from" either of the water
bodies listed below.
Location
Lahontan Reservoir
Carson River below
Lahontan Reservoir and
all waters in Lahontan
Valtey
Waterbody
Reservoir
Mixed
Restrictions
Adults should eat no more than one 8-ounce meal/
month; children 12-15 years of age should eat no
more than one 4-ounce meal/month; Gamefish over
21 inches in length should not be eaten.

Adults should eat no more than one 8-ounce meal/
week
Possible

Sources
T
Point source

contributions from
industries.
Contacts
Leroy McLelland, Division of Wildlife, Fishery Bureau, (702) 688-1500
-------
Mercury Advisory
ew Hampshire
Pact Sheet
Summary Information:
1. Number of Waierbodi
with Advisories

2. Basis of Advisory

3. Date Advisory Issued
1

FDA action level and Risk-based

June 10,1994
Advisory
Specifies:
Location
Horseshoe Pond
Waterboety
Type
Pond
Restrictions
The public is advised to not eat largemouth bass from
Horseshoe pond. This warning especially applies to
pregnant women, nursing mothers, women who may
become pregnant and young children.
Possible
Sources
Unknown
Contact: John Dreisig, NH Division of Public Health Services, (603) 271 -4664
-------
Mercury Advisory
New Jersey
Fact Sheet
Summary Information:
1. Number of Waterbodles
with Advisories

2. Basis of Advisory

3. Date Advisory Issued
Statewide

Risk-based

February 4,1994
Advisory
Specifics:
Location
Freshwater bodies
(Tested)

Pinelands area

Freshwater bodies (Non-
tested)

Waterbody
Typo
Lakes, Streams,
Rivers, and
Reservoirs

Lakes

Lakes, Streams,
Rivers, and
Reservoirs

Restrictions
People should limit their consumption of largemouth
bass and chain pickerel from several of New Jersey's
tested freshwater bodies to no more than one meal/
week. Pregnant women, women planning pregnancy
within a year, nursing mothers and children under five
years old are urged to limit consumption of these
species to one meal/month.
People are urged to limit their consumption of
largemouth bass and chain pickerel to one meal/
month. Pregnant women, women planning preg-
nancy within a year, nursing mothers and children
under five years old are urged to not consume the fish
at any time.
For the non-tested freshwater bodies, people are
urged to limit their consumption of largemouth bass
and chain pickerel to no more than one meal/week.
Pregnant women, women planning pregnancy within
a year, nursing mothers and children under five years
old are urged to limit consumption of these species to
one meal/month.
Possible
Sources
^B^

Unknown

MV«

•••••

Contacts
John Makai, NJ Department of Environmental Protection and Energy , (609) 748-2020
-------
I
Mercury Advisory
Fact Sheet
Summary Informations
1. Number of Water bod i
with Advisories

2. Basis of Advisory

3. Date Advisory Issued
24

FDA action level

1st issued in 1970; Last revision was in 1993
Advisory
Specifies!
Location
Waterbody
Type
Restrictions
Possible
Sources
Throughout the
State
Lakes,
reservoirs,
and rivers
Group 1: Pregnant women should eat no more than one
meal/month of fish of certain sizes. No other restrictions
apply.

Group 2: Fish of certain sizes in this group should not
be eaten by pregnant or breast-feeding women, women
who plan to have children, or anyone under 18 years of
age. Everyone else should eat no more than 26 meals/
year. Eat no more than 13 of these 26 meals in one
month. The remaining meals should be evenly spaced
over the remainder of the year.

Group 3: Fish of certain sizes in this group should not
be eaten by pregnant or breast-feeding women, women
who plan to have children, or anyone under 18 years of
age. Everyone else should eat no more than 13 meals/
year. Eat no more than 7 of these 13 meals in any one
month. The remaining meals should be evenly spaced
over the remainder of the year.
Group 4: Fish of this size should not be eaten by
anyone.
Unknown
Species affected: largemouth bass, channel catfish, bass, walleye, white bass, black bass, bluegill, crappie, carp, carpsucker,
bullhead, northern pike, trout, white crappie, black crappie, brown trout, Kokanee salmon, white sucker, lake trout, yellow
perch, black bullhead, river carpsucker

Group 1: Based on different sizes for different species; Skin-on fillet samples average 0.5 ppm mercury or less.
Group 2: Based on different sizes for different species; Skin-on fillet samples average 0.5-0.75 ppm mercury.
Group 3: Based on different sizes for different species; Skin-on fillet samples average 0.75-1.0 ppm mercury.
Group 4: Based on different sizes for different species; Skin-on fillet samples average >1.0 ppm mercury.

Contacts Steven Pierce, NM Surface Water Quality Bureau, (505)827-2800
-------
Mercury Advisory
New Yorlc
Fact Sheet
Summary Informations
1. Number of Water bodies
with Advisories

E. Basis of Advisory

3. Date Advisory Issued
14

FDA action level

1st issued in 1970; advisories are updated annually
Advisory
Specifics:
General Recommendation: For all waterbodies listed below, the
advisory recommends that "women of childbearing age, infants and
children under 15 should not eat any fish species".
Location
Big Moose Lake
Carry Falls Reservoir
Ferris Lake
Francis Lake
Hatfmoon Lake
Indian Lake
Lake Champlain
(Whole Lake)
Long Pond
Meacham Lake
Moshier Reservoir
Onondaga Lake
Round Pond
Stillwater Reservoir
Sunday Lake
Waterbody
Type
Lake
Reservoir
Lake
Lake
Lake
Lake
Lake
Pond
Lake
Reservoir
Lake
Pond
Reservoir
Lake
Restriction*
yellow perch - no more than one meal/month
(1 meal = Bounces)
walleye - no more than one meal/ month
yellow perch >12" - do not consume; <12" no more
than one meal/month
yellow perch - no more than one meal/month
yellow perch - no more than one meal/month
All species - no more than one meal/month
lake trout >25" , walleye >19" - no more than one
meal/month
splake >12" - do not consume
yellow perch >12" - do not consume; <12" - no more
than one meal/month
yellow perch - no more than one meal/month
All species - do not consume
yellow perch >12" - no more than one meal/month
splake - no more than one meal/month
yellow perch - no more than one meal/month
Possible
Sources
•MM

Combination:
atmospheric
deposition and
point source
contributions

Contacts
Larry Skinner, New York State Department of Environmental Conservation, (518) 457-1769
-------
Mercury Advisory
North Carolina
Pact Sheet
Summary Informations
1. Number of Water-bodies
with Advisories 5 active, 1 inactive
Basis of Advisory

Date Advisory Issued
Risk-based action level of 1 pprn

See below
Advisory
Specifics:
"General Recommendation: For all waterbodies listed below, the advisory
recommends that women of childbearing age, and children should eat none of the
specified species from areas listed.

"Date advisory issued.
Location
Abbotts Creek,
Leonards Creek
(6/81-3/92)**
Pages Lake (7/93)**
Pit Links Lake (7/93)**
Watson Lake (7/93)**
Big Creek/Waccamaw
River (7/93)**
Waterbody
Type
Creeks
Lake
. Lake
Lake
Creek,
River
Restriction*
Consumption of fish should be limited to no more than
8 ounces per person per week.*
Consumption of largemouth bass should be limited to
no more than two meals per person per month.*
Consumption of largemouth bass should be limited to
no more than two meals per person per month.*
Consumption of largemouth bass should be limited to
no more than two meals per person per month.*
Consumption of bass and blackfish should be limited
to no more than two meals per person per month.*
Possible
Sources
Industrial
manufacturing
«BHI

Unknown

<^^H

Contact:
Luanne Williams, NC Department of Environment, Health, and Natural Resources (919) 733-3410
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Mercury Advisory
Fact Sheet
North

Summary Information:
1. Number of Waterbodles
with Advisories 17

2. Basis of Advisory Risk-based

3. Date Advisory Issued 1992
Advisory
Specifics:
General Recommendation:
Women who plan to become pregnant, are pregnant or breast-feeding, or children who are
under that age of 15, are health sensitive and should consume no more than 2 meals per
month of any species if they are under a certain length. No restrictions for the general popula-
tion.

Women who plan to become pregnant, are pregnant or breast-feeding, or children who are
under that age of 15, are health sensitive and should not consume any of these species if they
exceed a certain length. The general population is then restricted for future intake of fish to
timeframes ranging from 10 to 22 days after consumption of the fish.
Location
Throughout the State
Water-body
Typo
dams, reservoirs,
lakes, and portions
of the Missouri and
Red River.
Restriction*
Species affected: brown bullhead, northern pike,
walleye, white bass, white sucker, yellow perch,
goldeye, carp sucker, sauger channel catfish, Chinook
salmon, crappie, paddlefisn, smallmouth bass,
bigmouth buffalo, rainbow trout, largemouth bass
Feasible
Sources
Naturally occurring:
probably some
atmospheric inputs
Contacts Mike Sauer, ND State Department of Health & Consolidated Laboratories, (701) 221 -5210
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Mercury Advisory
Oklahoma
Pad: Sheet
Summary Information:
1.

3.
Number of Waterbodles
with Advisories 1
Basis of Advisory

Date Advisory Issued
FDA action level

1st issued in 1992
Advisory
Specifies:
Location
McGee Creek Reservoir
Waterbody
Type
Reservoir
Restriction*
Prohibits consumption of largemouth bass
Possible
Sources
geologic sources
Contact: Judith Duncan, Oklahoma Department of Environmental Quality, (405) 271 -5240
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Mercury Advisory
Fact Sheet
Summary Information:
1. Number off Waterbodles
with Advisories

2. Basis of Advisory

3. Dale Advisory Issued
Risk-based

Cottage Grove 1987,1993; Antelope Reservoir 1988,1989;|
Jordan Creek 1988,1989; Owyhee Reservoir 1988,1994.
Advisory
Specifics:
Location
Waterbody
Type
Reatrletiom
Possible
Sources
Cottage Grove
Reservoir
Antelope Reservoir and
Jordan Creek
Owyhee Reservoir
Lake
Lake
Reservoir
Consumption of fish should be limited to no more than
8 ounces per week. General prohibition against any
consumption by children younger than 6 years or by
pregnant or nursing women.

Children between 6 and 16 years of age should not
eat more than 21/2 ounces of fish per month and
the general population should not eat more than 5.3
ounces of fish per month

Limit consumption of fish to no more than 8 ounces
six times a year. Prohibition of consumption by
children under 6, nursing women, pregnant women or
women planning to become pregnant.
Natural sources
and possibly past
mining activities
Contacts Ken Kauffman, Oregon Department of Human Resources, (503) 731 -4015
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Mercury Advisory
Pennsylvania
Fact Sheet
Summary Information:
1. Number of Waterbodies
with Advisories

S. Basis of Advisory

3. Date Advisory Issued
1

FDA action level

1st issued in 1991
Advisory
Specifics:
Location
Lake Wallenpaupack
Waterbody
Type
Lake
Restrictions
Anglers are advised to not eat walleye.
Possible
Sources
Atmospheric
Contact! Robert Frey, PA Bureau of Water Quality Management, (717) 787-9633
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Mercury Advisory
Fact Sheet
South
Summary Informations
Number of Water bod le
with Advisories
15

Risk-based

March 1994
Basis of Advisory

Date Advisory Issued
Advisory
Speclflce:
General recommendation: The advisory recommends that
"pregnant women, infants and children should avoid consuming
fish" trom the waterbodies listed below.
Location
Black River
Combahee River
Coosawhatchle River
Edisto River

Edisto River (North
Fork)
Edisto River (South
Fork)
Great Pee Dee River

Intercoastal Waterway
Little Pee Dee River

Lynches River

Pocotaligo River
Santea River

Vaucluse Pond
Waccamaw River

Waterbody
Type
River
River
River
River

River

River
River

River

River
River

Pond
River

Restriction*
bowfin-1/2 Ib/month; largemouth bass-3/4 Ib/month
largemouth bass-3/4 Ib/month
bowfin-1 1/2 Ib/month
bowfin-1 Ib/month; catfish-3/4 Ib/month; largemouth
bass-3/4 Ib/month
bowfin-1 Ib/month; largemouth bass 1 Ib/month

bowfin-1 1/4 Ib/month; largemouth bass 1/2 Ib/month

bowfin-1 1/4 Ib/month; catfish-1 3/4 Ib/month;
largemouth bass-1 Ib/month; red ear sunfish-2 3/4 Ib/
month
bluegill, sunfish-3 3/4 Ib/month; bowfin-2 Ib/month;
largemouth bass-1 Ib/month
bowfin-1/2 Ib7month; catfish-1/2 Ib/month; largemouth
bass-1 12. Ib/month
bowfin-3/4 Ib/month; catfish-1 1/2 Ib/month; large-
mouth bass-1 Ib/month
bowfin-3/4 Ib/month; largemouth bass 3/4 Ib/month
bowfin-2 1/4 Ib/month; catfish-5 1/2 lb./month;
largemouth bass-3 3/4 Ib/month
largemouth bass-1 1/2 Ib/month
bluegill, sunfish-3 1/2 Ib/month; bowfin-1 1/4 Ib/month;
largemouth bass-3/4 Ib/month; red ear sunfish-3 1/4
Ib/month
Possible
Sources
^••MB

Unknown; probably
atmospheric

Contacts
Russ Scherer, SC Department of Health and Environmental Control, (803) 734-5296
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Mercury Advisory
Tennessee
Fact Sheet
Summary Information:
1. Number of WaterbodU
with Advisor!*
Basis of Advisory

Dale Advisory Issued
FDA action level

1st issued in 1981
Advisory
Specifics:
Location
North Fork of the
Holston River

East Fork of Poplar
Creek

Waterbody
Type
Stream

Stream

Restrictions
Do not eat fish from these waters.

Do not eat fish from these waters.

Possible
Sources
An Industry with a
waste pond that
historically leaked
mercury.
Oak Ridge
Department of
Energy Reserva-
tion discharges
into the creek.
The facility is
leaking mercury.
Contacts
Greg Denton, TN Department of Environment and Conservation, (615) 532-0625
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Mercury Advisory
Fact Sheet
Summary Information:
Number of Waterbodles
with Advisories
FDA action level and risk assessment

1st issued in 1988
Basis of Advisory

Date Advisory Issued
Advisory
Specifics:
Location
LaVaca Bay
Waterbody
Type
Bay
Restrictions
Do not eat fish from these waters.
Possible
Sources
Industrial
(Superfund site)
Contacts David Sager, Texas Parks and Wildlife Department, (512) 389-4800
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Mercury Advisory
Vermont
Fact Sheet
Summary Informations
1. Number of Wfaferbodies
with Advisories
2. Basis of Advisory
3. Date Advisory Issued
1
FDA action level
May 4,1990
Advisory
Specifics:
Location
Lake Champlain and its
tributaries up to first
dams

Waterbody
Type
Lake

Restrictions
Walleye-No more than one meal/month. Women of
childbearing age, infants, and children under 15
should not eat any walleye.

Possible
Sources
Natural sources,
past industrial
discharges, and
atmospheric
Contacts
John Hall, Vermont Fish and Wildlife, (802) 241-3700
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Mercury Advisory
Fact Sheet
Summary Informations
i.
3.
Numbor of Waterbodles
with Advisories 2
Basis of Advisory

Dato Advisory Issued
FDA action level

1st issued in 1974
Advisory Specif less
Location
Waterbody
Type
Restrictions
Possible
Sources
North Fork of the
Hotston
South,
South Fork of the
Shenandoah, and
Shanandoah
River
River
Taking fish from Saltville to the VA/TN line for human
consumption is prohibited.
Limits consumption of fish to no more than one meal
per week from these waters (from footbridge at E.I.
DuPont at Waynesboro to the Page/Warren County
line). Small children and pregnant women should not
eat any fish from these waters.
Point source
contributions from
industries.
Contacts Dr. Peter Sherertz, Virginia Department of Health, (804) 786-1763
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Mercury Advisory
Pact Sheet
Wisconsin
Summary Informations
i.
Number of Water bodies
with Advisor!*
Basis of Advisory

Date Advisory Issued
230 waterbodies throughout the state including inland
lakes and rivers, and the Great Lakes

Risk-based

1st issued in 1971; Issued another advisory for inland
lakes in 1982, reissued in 1986; currently under review.
Advisory
Specifics:
Location
Waterbody
Type
Restriction*
Possible
Sources
Individual
waterbodies
statewide
Inland lakes
and rivers
Group 1: Pregnant women should eat no more than one
meal/month of listed fish. Everyone else may eat
unlimited amounts.

Group 2: Pregnant or breast-feeding women, women
who plan to have children, and children under 15 should
not eat listed fish. Everyone else should eat no more
than 26 meals/year. Eat no more than 13 of these 26
meals in one month.

Group 3: Pregnant or breast-feeding women, women
who plan to have children, and children under 15 should
not eat listed fish. Everyone else should eat no more
than 13 meals/year. Eat no more than 7 of these 13
meals in any one month.

Group 4: No one should eat these fish.
In the past,
sources may have
been from wood
pulp in paper mills
or industrial waste.
Currently, there
are two major
sources of
airborne mercury:
latex housepaint
and emissions
from coal-burning
power plants.
GommentSB Species affected: walleye, musky, largernouth bass, yellow perch, northern pike, smallmouth bass,
flathead catfish, sturgeon, black crappie, rock bass, channel catfish.

Group 1: Skin-on fillet samples average <0.5 ppm mercury; also can consider a certain length.
Group 2: Skin-on fillet samples average 0.5-0.75 ppm mercury; also can consider a certain lemgth.
Group 3: Skin-on fillet samples average 0.75-1.0 ppm mercury; also can consider a certain length.
Group 4: Skin-on fillet samples average >1.0 ppm mercury; also can consider a certain length.
Contacts Jim Amrhein, Wl Department of Natural Resources, (608) 266-5325
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