Greenpeace (Joe Thornon) testimony to Science Advisory Board

[IATP@iatp.org (IATP)]

Dear all:

This is a brief report on the meeting of the EPA Science Advisory
Board Dioxin Reassessment meeting, May 15 and 16, which I
attended.  My testimony is contained in a separate message.

The SAB panel is 41 persons, divided into two groups: one on
health effects, the other on sources and exposure.  The meeting
is two days and I attended only the first day.

The first half of the day was a plenary session and it made me
think a lot about Dante's Inferno.  The room was filled with
about two hundred reps of industry and its consultants, plus
three spectators from our side (EDF, CCHW, and the author Peter
Sills) and a handful of EPA people.

The agenda included public comment -- myself (15 minutes), and 13
industry presentations (3 hours and 40 minutes). This occurred
because EPA announced the meeting only in the Federal Register
(circulation: 11) in February, before they had selected a date
and a place, and accepted requests to testify only until March.
After that, EPA refused to make exceptions when EDF, Barry
Commoner, Arnold Schecter and others asked to speak.  Praise
Beatrice that Rick spends all his days reading the Federal
Register.

The endless industry testimony was your typical tide of crap, and
I was worried that since it was all but unopposed it might have
some effect on the panel.

My testimony went quite well; since I Didn't have time to discuss
in detail all the individual points industry made, I largely
tried to establish a framework for considering the issues in a
historical,  ethical, political and scientific context within
which all the  specific questions should be considered.  I also
addressed about  7 specific points that I felt it was essential
to touch on.   Overall, it was strange for me to give a speech
praising EPA,  but it had to be done.  I also submitted a letter
from Arnold  Schecter and referred to it extensively.

Afterwards quite a number of people approached me and said that
they thought the comments were very good, that these things very
much needed to be said, and that they thought our words had
affected the panel.  People from EPA seemed to like being praised
by Greenpeace.

The afternoon consisted of separate meetings of the two panels.
The exposure/sources panel is very sharp and straight, and
watching them operate made me feel better.  They quickly made
mincemeat of testimony by the CCC and by Greg Rigo on the
supposed  lack of relationship between chlorine feed and dioxin
emissions from incinerators, and they are solid on the issue of
"natural dioxin" (little or none; probably none).  I don't know
whether or not they will make any recommendations on the
chlorine-related issues on which we have pushed EPA.  I do expect
that their comments will not serve industry's agenda in any way
and that they will, from an objective perspective, strengthen the
document as a whole.

Can't say such nice things about the health panel.  This is the
more important group, because they ultimately have the power to
sink the entire reassesssment.  The panel contains some very good
people plus some middle-of-the-roaders, but there are also some
very aggressive bad ones (John Graham, Ronald Estabrook in
particular).  The discussion remained contentious throughout the
day, and no consensus was clear, even on issues that shouldn't be
controversial (i.e., use of animal models for judgments about
human health, use of TEQ to judge impacts of dioxin-like
mixtures).   There was even a long argument in which several
panelists insisted that EPA include extensive discussion of the
ways in which dioxin is good for you (it will protect you against
some cancers).  Ultimately,  the outcome will depend on dynamics
within the panel that I can't  predict, particularly the extent
to which an aggressive minority can determine a "consensus."

Next steps?  Individual panel members have been charged with
drafting consensus answers to the questions under discussion,
which will then be subject to more discussion.  By September, the
board is supposed to finish its report to EPA with comments and
recommendations on changing the reassessment. If they ask for
some clarifications and improvements in specific sections, this
is good for us.  If they say that the health assessment is
funda-mentally flawed and thus torpedo all the judgments EPA has
made about the public health risks of ubiquitous dioxin
pollution,  that's bad.

We'll see.

Joe















                       Greenpeace Testimony
before the U.S. EPA Dioxin Reassessment Science Advisory Board
May 15, 1995, Herndon, Virginia


submitted by

Joe Thornton
Research Coordinator, Greenpeace Toxics Campaign
462 Broadway, New York, NY  10013
212-941-0994, x208 (ph); 212-941-1928 (fax)


-----------------------------------------------------------------

Thank you for the opportunity to testify today.  My name is  Joe
Thornton, and I am research coordinator for the Greenpeace Toxics
Campaign.  We believe that this panel has an historic opportunity
to ratify and clarify a tremendously important and well-prepared
document.   Like it or not, EPA's dioxin reassessment now bears
the mantle of the world's definitive assessment of dioxin
pollution in the sphere of public policy.  The document -- and
this review process -- thus have profound implications for human
health and the integrity of the global environment.

I feel quite a burden as the sole representative of an
environmental or public health group in two full days of
meetings. The agenda shows that I will make a single
fifteen-minute presentation on behalf of the public interest
community.  No independent academics will speak at all.  There
are 12 presentations by dioxin-producing industries or their
consultants, totalling 3 hours and 40 minutes.  This does not
look good for this meeting, and it does not serve to enhance the
Science Advisory Board's credibility.

Dr. Arnold Schecter of the State University of New York, who has
published more than 100 scientific and medical articles on
dioxin, wanted to speak today but the SAB staff rejected his
request as tardy.  Dr. Schecter has provided me with written
testimony which I will distribute to the board and to which I
will refer in my comments.


HEALTH ASSESSMENT

We congratulate EPA for the reassessment's volumes on dioxin
toxicity and exposure. These sections are an important step
forward, because they address, for the first time, the sobering
public health implications of universal exposure to dioxin-like
compounds.  Previous approaches treated dioxin as a local
exposure problem and focused primarily on individual sources.
But these compounds are distributed globally, and exposure is
universal, and impacts upon the general population are of utmost
importance.

Because it was unprecedented for a U.S. agency to consider
background exposures, EPA had to devise a new framework in which
to ask and begin to answer these questions.  We believe this
framework is sound, although it has come under attack by the
industry.  Today, we'd like to address some of the industry's
arguments against EPA's approach.

First, we should clarify the purpose of the dioxin
reassessment. It must provide for policymakers an analysis of the
potential impacts of dioxin upon human health and ecosystem
integrity.  It must be a science-based description in the sphere
of public policy. This has very important implications for
reviewers, because the purpose determines the standard of proof
that must be satisfied.

Environmental policy must be based on the well-established
principles of public health practice: prevention of disease is
the highest mandate, and proof is not required before preventive
strategies should be pursued.  In "pure science" in an academic
setting, the goal is the search for truth, and the standard of
proof is very high, because the worst error would be to affirm a
false hypothesis.  Here, however, the ultimate error would be
failing to affirm a hypothesis that turns out to be true,
because the costs in terms of human suffering and environmental
degradation are terribly high.  It would thus be inappropriate
for scientists to be silent or disavow the information they have
because it is has not reached the standard of proof normally
associated with academic science.  As Dr. Schecter writes,  "I
would urge that if errors are to be made in characterizing the
health consequences of dioxins in this review, it is better to
err on the side of caution, to protect human health, than on the
side of allowing health impairment and death."

In this context, it is necessary and appropriate for EPA to
consider the full body of information and ask this question:
does the evidence make a plausible case that dioxin may pose a
health hazard?   This discussion must integrate data from a
variety of investigations that may not be conclusive in
themselves.  There is no reason that the case has to be
considered closed, and further information will certainly emerge
as investigation continues.  But uncertainty should not
undermine the effort to make judgments, as it would in "pure
science."  In this case, unknowns in the science may actually
mask a public health risk; uncertainty should strengthen a
statement of concern, rather than be used to justify silence.

Like the tobacco industry, chemical interests will always be able
to nitpick at individual studies in an effort to silence all
judgments. We hope that the board will keep in mind the goal of
this document: to provide a benchmark characterization of the
potential impacts of dioxin pollution on human health and the
environment.  This is what the world needs and what it is
expecting from these documents, not an ultimate statement of
scientific truth.

As for specific issues of contention, let's begin with toxic
equivalency factors.  Industry is arguing that EPA should not use
TEFs to make summary judgments about the cumulative impacts of
mixtures of hundreds of dioxin-like compounds.  These
substances clearly act together to exert their toxic effects.
The use of TEFs to describe the additive effect of mixtures is
internationally accepted, in both scientific and regulatory
communities, based on the common molecular mechanism of
toxicity.   As Dr. Schecter points out, TEFs have been
repeatedly justified in investigations on both animals and
humans.   Although far from perfect, TEFs provide a very
reasonable way of doing something essential:  considering the
hazard of the cumulative burden of dioxin-like compounds.
Industry's goal in criticizing TEFs is clearly to force EPA to
discuss these compounds one by one, because in isolation each
dioxin, furan and PCB cannot be related to a public health
hazard.

Second, the industry has argued that laboratory animal studies
are not an appropriate data source for considering human health
impacts.  Again, it is internationally accepted practice for such
data to play a role in public health judgments.  No
epidemiological study is perfect; only in the controlled context
of the laboratory can causality be examined with relative
precision.  Since it is unethical to experiment on people, we
must integrate epidemiological data with studies on lab animals.
In the case of dioxin, this is particularly appropriate.  As Dr.
Schecter writes, the "scientific literature strongly
documents that health consequences of dioxins are very similar in
humans to what is found in many other animal species,
inlcuding wildlife and laboratory animals."  We know that dioxin
causes a similar spectrum of effects via a common molecular
mechanism in a wide range of species, including humans.  The
science also tells us that humans in general do not appear to be
any less sensitive than other species1 -- in fact, we may be
fairly sensitive, given the longer half-life of dioxin in our
bodies than in many laboratory species.   There is no reason to
use the inherent inconclusiveness of epidemiological studies to
negate the valuable insights from the laboratory.

Third, the industry has argued that a recent EPA study of
dioxin levels in back fat from beef cattle indicates that the
reassessment's exposure estimates were too high. In fact, this
single study establishes no such thing.  First, when non-detects
are considered at half the detection limit, as is customary, the
total concentration in the fat are in the same range as EPA's
original estimate, though somewhat lower.  But most importantly,
people do not eat back fat, and there is no known relation
between contaminant levels in back fat and those in the food
supply.  In contrast, as Dr. Schecter details, actual market
basket studies from the U.S., Canada, Germany, the UK and
Netherlands all have established daily intakes of 2 to 8 pg
TEQ/kg/day -- the same range as EPA's original estimate.
Nursing infants receive an estimated 55 picograms TEQ per
kilograms per day -- over 9000 times the current ADI of .006
pg/kg/day.

Fourth, industry has argued against considering potential
health impacts on the general population based on body burden
data.   Clearly such data are the most appropriate way to
consider this essential question.  It is the body burden that
represents the total long-term cumulative dose, and biological
effects appear to depend less on dose than on concentrations in
the target organ over some critical length of time, and retained
compounds clearly cause biological impacts. Further, body
burdens are critical from a trans-generational perspective,
because the level in the mother's tissues determines the amount
passed to the child across the placenta and via breast milk.
Moreover, body burdens are the most appropriate data for
cross-species comparisons: because TCDD is far more persistent in
humans than in rats and many other laboratory animals, the same
daily dose will accumulate in humans to higher
concentrations in humans.2

We thus believe EPA's method was sound in coming to the
conclusion that background body burdens in the general
population are already in the same range at which effects are
known to occur in laboratory animals.  At body burdens at or
within a single order of magnitude of human background, studies
on a variety of species have documented clear effects on enzyme
induction, hormone levels, diabetes, immune system function,
endometriosis, and development of the reproductive and nervous
systems.

These calculations gain weight because other types of studies
support the same conclusion.  First, there is human evidence.
Dioxin exposure has been related to altered testosterone levels
in chemical workers with dioxin body burdens only slightly
higher than background.3  Dutch studies have related the dioxin
body burden of women from the general population to altered
thyroid hormone levels in newborns.4  Finally, a mother's
historical consumption of Great Lakes fish at background
environmental levels of dioxins, PCBs and other contaminants has
been related to persistent cognitive deficits in their children,
apparently due to cross-placental transfer of the mother's body
burden.5

Second, there is wildlife evidence.  A host of studies has
clearly established that environmental levels of dioxin-like
compounds are causing large-scale reproductive, developmental and
immunological effects on populations of marine mammals and
pisciverous birds in the Great Lakes, the Baltic, the Wadden Sea,
and elsewhere.6   Particularly notable is the recent study of
Ross et al which used controlled diets to link background levels
of dioxin-like compounds in fish from the Baltic Sea to immune
suppression and susceptibility to viral infection among Harbor
Seals.7 If background food contamination is high enough to cause
these effects in upper trophic wildlife, there is every reason to
believe that humans, who also sit high on the food chain, are
also at risk. It is unfortunate that the wildlife evidence was
not discussed in EPA's draft.

Overall, we believe evidence indicates that dioxin exposure is
already contributing to human disease and impairment on a large
scale and a long-term time frame.  The evidence does not permit
us to quantify that contribution.  But there is no doubt that
universal and constant exposure to these compounds places human
health at risk.  Highly exposed populations are at even greater
risk.  This is the core message that EPA's document justifies and
that the SAB should ratify.


DIOXIN SOURCE INVENTORY

As for the section on dioxin sources, we cannot offer such high
praise.8  As we have detailed in our comments to EPA, this
section obscures almost as much as it reveals.  Although much
improved over earlier drafts, this section underestimates
releases from certain identified sources and leaves out several
important sources altogether.

First, accidental fires.  Evidence from Europe indicates that
significant quantities of dioxin are produced in accidental home,
building and warehouse fires in which PVC is burned; this is no
surprise given sub-optimal combustion conditions and the
omnipresence of PVC in modern construction materials.  Given the
extraordinary number of these events -- over half a million in
the U.S. each year -- these appear to be a significant dioxin
source.

Second, EPA did not treat adequately the formation of dioxins in
the manufacture of feedstocks for PVC plastic -- particularly
ethylene dichloride produced through the oxychlorination
process. Numerous European studies have documented the formation
of high concentrations of dioxin in this process, their release
via air emissions, effluents, process wastes, and even the
products themselves, as well as the presence of dioxin in
environmental samples downstream from such facilities.  Our own
sampling program of wastes from US EDC facilities found
dioxin-like compounds in every sample analyzed; one sample from a
facility in Louisiana contained dioxin concentrations as high as
6.4 ppm TEQ  -- in the same range as the infamous wastes from
Agent Orange production.  Given the immense production of PVC
--some 6 million tons per year in the U.S. -- this process
appears to be a significant dioxin source that needs better
treatment in EPA's inventory.

In addition, EPA underestimates dioxin emissions from the
sources it does identify-- particularly certain types of
incinerators.  For instance, EPA's estimates for hazardous waste
incinerators were based entirely on so-called trial burns.  But
we know that these trial burns may underestimate actual
emissions by up to four orders of magnitude because they do not
reflect real-world operation:  human error is minimized, upsets
are avoided, equipment is new or tuned to minimize emissions,
simplified recipes of off-the-shelf chemicals rather than
real-world wastes are burned, delayed emissions due to the
hysteresis effect are ignored, and chemicals are burned in high
concentrations that lead to more efficient combustion than is
achieved on the lower concentrations found in real wastes.
Finally, EPA's estimate from these trial burns is not consistent
with the most recent trial burn data at the supposedly
state-of-the-art WTI incinerator, where dioxin emissions totaled
13,600 ng TEQ per ton of waste burned -- about 500 times greater
than the estimate EPA used in its inventory.

But a lack of data is not the fundamental problem with EPA's
discussion of sources.  EPA presents much information, but if
fails to organize it into a framework that revels the nature of
dioxin generation or allows us to formulate a meaningful
pollution prevention strategy.  Specifically, EPA's report fails
to state the obvious:  in virtually all cases, the essential and
preventable source of dioxin is a product or waste of industrial
chlorine chemistry.  The chemical industry is going to great
lengths to obscure the central role of chlorine chemistry in
dioxin formation, and we are afraid that EPA has fallen into this
trap.

EPA's presentation gives the impression that dioxin in the
environment comes from a large number of unconnected sources.
These can be tied together by the common chlorine-containing
feedstocks they share, but EPA spreads this information out over
hundreds of pages or omits it altogether.  The result is a
hodgepodge of data without an organizing principle.

For instance, the section on Motor Vehicle Fuels compared
dioxin in the exhaust of cars burning leaded gas to unleaded,
diesel to ordinary fuel, cars with a catalytic converted to those
without one.  Organized this way, the data appear
idiosyncratic. Only in passing does EPA mention that chlorinated
chemicals are added to gasoline and leaded gasoline contains far
more chlorine than unleaded gasoline.  Marklund has established
that fuels that do not contain chlorinated additives produce no
dioxin emissions.

EPA makes a similar mistake in its discussion of metallurgical
industries, which are organized into the categories ferrous,
nonferrous, primary, and secondary.  Again, EPA misses the key
factor: the introduction of chlorine-based chemicals into these
processes.  In metals recyclers, PVC is the major problem:  large
quantities of PVC enter as cable coatings, battery
casings, automobile accessories, and so on.  In primary
production, dioxin is generated because chlorine is deliberately
introduced as a solvent, cutting oil, or reactant.

In each case, EPA shies from the central role of feedstocks as
the cause of dioxin emissions.  Making dioxin requires three
things: organic matter, a chlorine donor, and an opportunity for
these to come together in a reactive environment.  Organic
matter and reactive environments are ubiquitous in industry and
nature.  The chlorine donor is the preventable factor that leads
to dioxin emissions.

For example, EPA lists incinerators for medical and municipal
waste as the two largest dioxin sources and admits that "dioxins
are formed in combustion processes when chlorine donor compounds
are present." But EPA fails to identify the chlorine donors that
turn combustion units into dioxin sources.  In medical and trash
incinerators, PVC supplies the vast majority of the chlorine.
Studies from Germany, the Netherlands, and Denmark have all found
that reduction of PVC input to incinerators reduces dioxin
formation when other factors are held constant.  At least seven
laboratory studies have found that burning organic matter in the
presence of PVC results in dioxin formation orders of magnitude
higher than burning organic matter in the presence of salt.  The
historical record is clear on this point as well: the levels of
dioxin found in ancient tissues and sediments indicate that
dioxin levels began to rise only in the century as the products
and wastes of chlorine chemistry began to proliferate.  In
contrast, the industry-sponsored reports that have found no
relationship between PVC feed and dioxin emissions have all
failed to hold combustion conditions constant as PVC feed
varied, so it is no surprise that a relationship would be
obscured.

This section of the reassessment should be reorganized to
identify the feedstocks that serve as chlorine donors in each
dioxin source.  This approach will reveal the preventable
factors responsible for all major dioxin sources.  And the
central role of chlorine suggests where EPA should look for the
sources of the remaining dioxin for which it has yet to identify
an origin: the lifecycle of other chlorinated chemicals.

There is no doubt, however, that certain identified sectors are
major dioxin sources -- particularly incinerators and pulp
bleaching.  There is no reason to wait to take action on these
established dioxin sources while texts are being redrafted,  and
the board should be clear about that if it recommends changes.
Otherwise, perfectionism in the drafting process and the need for
further study become excuses not to act.


HISTORICAL AND POLITICAL CONTEXT: ROLE OF THE SAB

Until the release of the 1994 reassessment, the history of
EPA's science on dioxin was stained by political tampering.  When
EPA last tried to reassess the hazards of dioxin, in 1987, it was
clear to all that the process was driven by a political agenda
for deregulation, although the document that emerged masqueraded
as science or, even worse, so-called "science-policy."  Only
after the SAB rejected that reassessment did EPA withdraw its
proposal to downgrade its estimate of dioxin's toxicity.  After
that, the record shows that the paper and chemical Industries
redoubled their lobbying effort to persuade EPA and the Bush
White House to revise the dioxin hazard assessment once again.
When the agency responded by announcing the reassessment in 1991,
we expected that this project, like the one before it, would be
designed to yield a predetermined outcome in the interest of
polluting industries.

It is thus with great surprise and sincerity that we
congratulate the scientists in EPA for their integrity in the
preparation of the documents released in September.  EPA built in
accountability and transparency by involving external authors and
expert review panels, publishing parts of the reassessment in
scientific journals prior to government publication, and holding
public hearings on the document.

EPA thus raised the public's expectations tremendously.  This
document has garnered worldwide attention and has catalyzed
recognition of the long-term health impacts of large-scale
dioxin pollution.  It has created a flurry of activity to
eliminate dioxin sources among grassroots communities in this
country, many of whom feel EPA has told them the truth for the
first time.  The world is eagerly awaiting EPA's final
commitment to the vision contained in the draft reassessment.

As we expected, however, the draft reassessment provoked an
aggressive counter-offensive by dioxin-producing industries.
Much of this effort, supported by tremendous financial
resources, you will see before you in the next two days.   Now
the ball is in the SAB's court:  the panel must help to clarify
the scientific basis of the message, but it must not shy from or
cloud the truth.  If at this point the SAB allows or forces EPA
to retreat in the face of political pressure, it will do
tremendous damage to the credibility not just of EPA but of
scientists in our society in general.  If EPA retreats now from
its position, everyone will know that the agency started to tell
the truth, but powerful political interests ultimately silenced
this voice, all under the guise of "scientific review."  The
public's trust in the integrity of science, currently at an
all-time low, will erode further.

Ultimately, the greatest cost will be the health of future
generations.  The reassessment and its review are not your
average government toxicology project.  At stake are issues that
pertain to the integrity of the human species -- and many
others, as well -- on a global basis.  At stake is our ability to
produce children who can develop normally and live full and
healthy lives in a world in which other species are also
healthy;  you are on this panel as leading scientists, but we
hope you will not forget your roles as parents, grandparents, and
guardians of the planet.  To  its credit, EPA has assumed a
leadership role in the dioxin debate.  We thank you for showing
courage, clarity and integrity as you address these profound
issues.

                            ###


NOTES

1 Lucier G (1991).  Humans are a sensitive species to some of the
biochemical effects of structural analogs of dioxin.
Environ. Toxicol. Chem. 10:727-735.

2 Webster T and Commoner B (1995).  Overview: the dioxin debate.
In: Dioxins and Health.  A Schecter, ed.  New York: Plenum Press.

3 Egeland G, et al. (1994).  Total serum testosterone and
goandotropins in workers exposed to dioxin.  Amer. J. Epidem.
139:272-281.

4 Pluim J, et al (1993).  Effects of pre-and postnatal exposure
to chlorinated dioxins and furans on human neonatal thyroid
hormone concentrations.  Environ. Health Perspect. 101:504-508.

5 Jacobson J, Jacobson, S. and Humphrey H (1990).  Effects of in
utero exposure to polychlorinated biphenyls and related
contaminants on cognitive functioning in young children.  J.
Pediatr. 116:38-45.

6 Reinjders P and Brasseur S (1992).  Xenobiotic induced
hormonal and associated developmental disorders in marine
organisms and related effects in humans, an overview.
Chemically-Induced Alterations in Sexual and Functional
Development:  The Human-Wildlife Connection.  Colborn T and
Clement C, eds.  Princeton:  Princeton Scientific Publishers, pp.
159-174.  See also, Fox G (1992).  Epidemiological and
pathobiological evidence of contaminant- induced alterations in
sexual development in free-living wildlife.  Chemically-Induced
Alterations in Sexual and Functional Development:  The
Human-Wildlife Connection.  Colborn, T and Clement C, eds.
Princeton:  Princeton Scientific Publishers, pp. 147-158.

7 Ross P, et al (1995).  Contaminant-related suppression of
delayed-type hypersensitivity and antibody responses in harbor
seals fed herring from the Baltic Sea.  Environ. Health
Perspect. 103:162-167.

8 These items are documented in detail in Greenpeace's
comments on the dioxin reassessment, submitted to EPA in January
1995.



Jackie Hunt Christensen
Institute for Agriculture and Trade Policy
1313 5th St. SE, #303
Minneapolis, MN 55414 USA
phone: 612-379-5980
fax: 612-379-5982
e-mail: iatp@iatp.org