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RESEARCH REPORTING SERIES
Research reports of the Office of Research and Development, U.S. Environmental
Protection Agency, have been grouped into nine series. These nine broad cate-
gories were established to facilitate further development and application of en-
vironmental technology. Elimination of traditional grouping was consciously
planned to foster technology transfer and a maximum interface in related fields.
The nine series are:
1. Environmental Health Effects Research
2. Environmental Protection Technology
3. Ecological Research
4. Environmental Monitoring
5. Socioeconomic Environmental Studies
6. Scientific and Technical Assessment Reports (STAR)
7. Interagency Energy-Environment Research and Development
8. "Special" Reports
9. Miscellaneous Reports
This document is available to the public through the National Technical Informa-
tion Service, Springfield, Virginia 22161.
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SYMPOSIUM ON ENERGY AND HUMAN HEALTH:
HUMAN COSTS OF ELECTRIC POWER GENERATION
Sponsored by
Graduate School of Public Health
University of Pittsburgh
and
Ohio River Basin Energy Study
March 19-21, 1979
Pittsburgh, Pennsylvania
OFFICE OF RESEARCH AND DEVELOPMENT
U.S. ENVIRONMENTAL PROTECTION AGENCY
WASHINGTON, B.C. 20460
U.S. Environmental Protection Agsncy
Region V, Library
230 South Dearborn Street
Chicago, Illinois 60604
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FOREWORD
The Ohio River Basin Energy Study is a multi-disciplinary project of con-
siderable magnitude, supported by a grant from the Environmental Protection
Agency. It is concerned with present and future energy - environmental re-
lationships in the Ohio River Basin: a tremendous resource which, as Senator
Bayh described it in his address, is shared by the people of six states;
Illinois, Indiana, Kentucky, Ohio, West Virginia and Pennsylvania.
The Ohio Valley is the acknowledged center of coal production in the
nation. Typically, five of the six valley states lead the nation in annual
coal production. However well known its coal production is, the valley also
has a unique nuclear history. The Shippingport Atomic Power Station, situated
a few miles down the Ohio from its beginning at the confluence of the
Monongahela and Allegheny Rivers in Pittsburgh, was the first commercial
nuclear power station in the world. Shippingport began to produce electric
power in 1957. The major thrust of the Ohio River Basin Energy Study (ORBES)
is the evaluation of the many possible consequences of present and projected
electric power generation in the valley. Its major objectives are to conduct
an assessment of the environmental, economic, social and institutional impacts
of all types of energy development along the Ohio River and within its basin.
A major concern of ORBES is the health component of energy resource
extraction, transportation, conversion (i.e. burning of coal and reactor
operation) and transmission. In order to establish a sound "state of know-
ledge" base it was decided to organize a three-day symposium devoted exclusively
ii
\J,S. Environmental Protection Agency
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to the energy-health relationship. The six sessions were devoted to:
I) occupational problems in coal and uranium mining;
II) methodological problems in detecting health effects;
III) health aspects of fossil-fueled power plants;
IV) health aspects of transportation *r ' transmission;
V) health problems in nuclear power generation; and
VI) future areas of concern.
The symposium was designed to provide ample time for discussion and the
record of the proceedings, included in this document, attests to the areas of
controversy and those deemed to require continuing investigation.
The future of electrical energy development in the Ohio Valley and
beyond hinges to a considerable extent on the environmental and health con-
sequences of its production, transmission, and utilization. We believe and
hope that this symposium has provided a firmer foundation for the health
assessment task of ORBES.
Dr. E.P. Radford
Prof. M.A. Shapiro
Graduate School of Public Health
University of Pittsburgh
iii
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TABLE OF CONTENTS
Foreword ....,..,,....,..,.,, , . , , ii
The Ohio River Basin Energy Study (ORBES)
Birch Bayh, U. S. Senator, Indiana 1
Session I: Health Problems in Extraction of Fuel 19
Occupational and Environmental Health Problems in Coal Mining
Curtis Seltzer, Ph.D. 21
Respiratory Problems in Coal Miners...W.K.C. Morgan, M.D. 61
Uranium Mining - Occupational and Other Health Problems
Joseph K. Wagoner, S.D.Hyg 71
Discussion 81
Session II: Special Methodologic Problems in Detecting Health
Effects From Fuel Cycle Pollutants 95
Measurement of Occupational and Environmental Exposures . . .
Morton Lippmann, Ph.D. . . . 97
Epidemiological Studies of Human Health Effects
Ian Higgins, M.D., Kathy Welch, MPH, and Jerel Classman,MPH 127
Role of Animal Experiments in Relation to Human Health Effects
Yves Alarie, Ph.D 143
Discussion 163
Session III: Health Aspects of Fossil-Fuel Electric
Power Plants 175
Air Pollution Benjamin G. Ferris, Jr., M.D., FACPM . . 177
Human Exposures To Waterborne Pollutants From Coal-Fired
Steam Electric Powerplants. . Jualian B. Andelman, Ph.D. . 205
Occupational Health Aspects of Fossil-Fuel Electric
Power Plants . . William N. Rom, M.D., MPH 231
Discussion 257
Session IV: Health Aspects of Transportation and Transmission m 275
Health Aspects of Fuel and Waste Transportation
S. C.Morris, Sc.D. ... 277
IV
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Health Aspects of Power Transmission . . Richard D. Phillips, Ph.D. . .303
Health Benefits and Risks of Electric Power Consumption
Ronald E. Wyzga, Ph.D 321
Discussion 343
Session V: Health Problems in Nuclear Power Development 363
Health Effects of Ionizing Radiation. . Edward P. Radford, M.D 355
Environmental Exposures from Nuclear Facilities, E.David Harward . . . 381
Occupational Health Experience in Nuclean Power
Robert B. Minogue 399
Discussion 425
Session VI: Future Areas of Concern 445
Potential Health Problems in the Production of Synthetic Fuels
From Coal. . Prof. M. A. Shapiro, C.S. Godfrey, J.K. Wachter and
G.P.Kay 447
Long Term Health Implications of Radioactive Waste Disposal
William D. Rowe, Ph.D 485
Areas of Uncertainty in Estimates of Health Risks
Leonardo. Hamilton, M.D., Ph.D 513
Discussion 581
v
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THE OHIO RIVER BASIN ENERGY STUDY (ORBES)
Birch Bayh
U.S. Senator, Indiana
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Chancellor Posvar, Dr. Radford, Dr. Shapiro, Dr.
Griffin, distinguished guests and participants in the symposium,
I'm glad to be here. I thank Dick Caliguiri for his
introduction, excessive as it was. I'm not too sure what the
heredity of this ORBES Commission is. I guess I have to claim
at least part of the bloodline.
I must confess to you I always think it's good for us to
have the kind of experience that makes it possible for us to
listen to that kind of introduction I got without inhaling.
Such as this morning's plane ride from Washington, the young
lady was going down the aisle taking our destination and name
and she got to me and she asked the destination, and I said
Pittsburgh, and gave my name. A big smile of recognition, "Oh,
that's just like Birch Bayh, isn't it?"
You know, Mayor Caliguiri and I were talking about the
environment which those of us as public officials serve. He has
the toughest job in the body politic in my judgment. Being a
Mayor he cannot afford the luxury of getting on a plane and
going back to Washington this evening and I'm sure that the job
has gotten even more difficult than it was at the time a certain
occurrence transpired in the southern part of our state several
summers ago, back when the trains were running reasonably on
time and most of them were carrying passengers. A new minister
arrived in a little southern Indiana town down close to the
river in the jurisdiction of ORBES and he had been expected for
a long period of time. In fact, they had about given up hope,
so there was nobody there to meet him. He looked around and
found no one and finally saw an old fellow sitting on the board
seat of his donkey cart, waiting over under the shade of a big
oak tree and asked the fellow if he'd carry him over to the
parsonage. And the fellow did, but the poor old donkey just
gave up the ghost and died right there on the parsonage lawn.
The minister got down and offered his sympathy to the gentleman
and went inside and immediately called the Mayor, "Mayor, this
is Parson Brown, I just arrived in town." The Mayor interrupted
and said, "Oh Parson, we've been waiting for you. I'm sorry I
wasn't there. I had some very important business. Is there
anything I can do to help you?" "Well, Mayor, you can. There is
a dead donkey on my front yard and I'd appreciate if you take
care of the remains." "Well," said the Mayor, "I'll take care of
that right away."
Well this is in the middle of the summertime down southern
Indiana and on the morning of the third day some of that pure
unpolluted southern Indiana air came into the bedroom of our
minister friend and it came to his attention that the Mayor had
forgotten his promise. So he bounced out of bed, whipped over
to the telephone and dialed the Mayor and said, "Mayor, this is
Parson Brown. Three days ago you told me you were going to
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remove the remains of that dead donkey. It is still there.
What's the matter, don't you politicians keep your promises?"
The Mayor answered rather hastily, he had been up the night
before dealing with some of the problems with his constitutents
and he said, "Well, Parson, I thought it was the duty of the
clergy to bury the dead." The Minister thought and said,
"Perhaps you're right, Mayor. I was just advising the next of
kin."
Mayor, I think you and I and any of us in the body politic
and the political hierarchy are living in a time when it is
difficult to get the benefit of the doubt. I must say the kind
of sensitivity you have shown, first as a council member, and
now as a Mayor of this fine city is an example I am sure others
would like to be able to follow.
I am glad to have a chance to be here, to share some
thoughts with you about the problems of environment and energy.
The reports that have reached me, perhaps not totally
accurately, but I think fairly accurately, about the environment
and atmosphere of the meeting this morning, makes me wonder if
I'm not like the early day Christian who was thrown into the
Colosseum and as he awaited the lion he got down on his hands
and knees and bowed his head and began to pray. After what
seemed like an endless period of time nothing happened and he
looked around and there the lion also was kneeling in prayer.
The Christian threw his head to the sky and said, "Thank you,
Father, for delivering me." Whereupon the lion opened one eye
and said, "Shut up. I don't know what you're doing but I'm
saying grace."
Perhaps some of you will agree and perhaps some will
disagree but I think the spirit of friendly controversy, the
spirit of prodding and the spirit of really searching for the
real answers to the problems of energy and environment, that is
the only kind of attitude, in my judgment, that is going to help
us solve both of these problems. Now what I would like to do,
this noon, is to perhaps go through some notes that I have
written down in consultation with my staff to try to sort of put
down a foundation, particularly for some of you who do not live
in the immediate valley area, to describe the way we got here as
far as the establishment of ORBES is concerned. I'd like to
discuss the origin of ORBES and, in general terms, the "politics
of policy." And then open for more specific questions. The
latter part will be the most beneficial for both of us.
I am grateful for this opportunity to speak before this
distinguished group brought together by Dr. Radford under the
auspices of the Ohio River Basin Energy Study, which most of us
who are at all familiar with this know that that is ORBES. We
appreciate the fact that we're here but I think Dr. Radford, as
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important a role that you played, I think the facts are that
neither you nor ORBES has actually brought us together, but it
was an act of nature known as the Ohio River, the nature of
which is very, very precious to all of us up and down this
river. It was that act that really brought us here, resulted in
this common resource shared by the people of Indiana,
Southwestern Pennsylvania, Ohio, West Virginia, Kentucky, and
Illinois, and there is no questioning the fact that it is an
extremely valuable asset.
But to share the river's assets is to also share her
problems. And her problems are not unique to this region.
Other places in the country may be represented here. I thought
that perhaps discussing how we got to the place of organization
where we are now, studying this problem with the regional
approach, that might be helpful as you apply this to other
places. We have all sorts of common strengths and weaknesses
here.
I recall some of the distillery workers in Lawrenceburg,
Indiana, having some friendly repartee with some of their
workers who live across the line in Hamilton County, Ohio, in
Cincinnati, and which starts out usually where Cincinnati people
say: "Ah-ha, to tell you what we think of your folks in
Lawrenceburg, we flush our toilets and dump our sewage in the
river and it goes down for you to drink it." And the people in
Lawrenceburg say: "Well, it's not quite that way. What we do
is bottle it up and sell it back to you." I'm not too sure that
settles the problem but we are inextricably bound together and
for that reason we have tried to approach this in a common study
vein .
I happen to believe that the energy-health dilemma, faced
by those of us in the Ohio River Valley, is indeed, if it isn't
already confronting, will soon confront most other areas of
America. ORBES, though regional in nature, is not provincial in
scope. We are facing a national challenge of unprecedented
complexity and I am proud of the fact that we in Ohio Valley
have taken the lead in developing new strategies to face this
challenge. I am extremely proud of the work that is being done
by ORBES and hope that we can conclude it as rapidly as
possible, and then be able to implement some of the findings.
If we look at the real historical foundation, on which
ORBES is based, it really didn't start here in the United
States. It started back in October, 1973, when a group of
non-industrialized countries in the Middle-East arrived at an
agreement to reduce the flow of crude oil to the United States,
Europe and Japan. The Arab oil embargo plus OPEC traumatized
this country because it struck two simultaneous blows from which
we are still reeling. And some of us are asking ourselves: is
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this really true? One of the blows was political. The American
public became aware for the first time, during the embargo, that
the country was now vulnerable in a vital matter, its energy
supply, really its economic jugular vein.
The other immediate impact was economic. Across the nation
the higher prices of imported and domestic petroleum worked
their way through the chain of economic interdependencies until
they appeared in the form of increased prices for other kinds of
energy and energy intensive goods and services. This economic
blow; this incredible inflation attendant to the high price of
energy which still dogs us politically and economically today.
The subject of OPEC, the merit or the fallacy of a so-called
free market for energy, the discussion of those issues it seems
to me can better take place at another time. But, I think it is
important to start out with the understanding that this is
really the first time in the entire history of this country that
we really began to worry about the cost of energy and the
availability of energy and what that can do to the entire
economic structure of this society and the way of life as we
have come to know it. It is the first time we have begun to
assess investments, lifestyles, in terms of their impact, and
the impact of energy on them. When you take this sudden
awakening to the costs and availability of energy and you lay it
on the foundation of a decade of concern and progress dealing
with the environmental problems that had gone long unattended in
the society, you bring us to the foundation, really the two
pedestals, on which the ORBES study was based.
A national consensus emerged during that period in which we
were trying to come to grips with reality-that an energy supply
was threatened. A consensus emerged that we must reduce our
reliance upon foreign oil and place greater dependence on
domestic fuels. In the electric power industry there was a
strong push that we must have a greater reliance on nuclear
energy and we must site more new coal fired plants near the coal
fields. I must say the closeness of coal is not the sole
criterion for plant sites as far as the utilities were
concerned. Water for transportation and cooling, as well as the
existence of these plants in reasonably sparsely populated
areas, were also required as people looked at the criteria of
development. Portions of Indiana and Kentucky along the Ohio
River between Cincinnati and Louisville apparently met these
specifications.
So we found the Arabs hardly lifted the embargo when
several utilities announced their intention to construct many
plants on both the Indiana and Kentucky sides of this reach of
the river. It was significant that certain of these plants were
long distances from the consumer-load centers of the utility.
In other words, we found unusually long spaces, great distances
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existing, between where the utilities are going to produce much
of this electricity and where it was ultimately going to be
consumed. Thus, it was clear that external conditions were
encouraging power plant construction in a scenic stretch of the
valley and that much of the power would be exported while local
residents were saddled with the liability of potential
environmental problems. It is not quite that simple, as some of
you know who have looked at the early results of the ORBES study
and who are familiar with the air currents, that indeed many of
the environmental impacts are going to follow, if not exactly,
at least a general direction of much of the use of the
electicity and it is that kind of problem we're trying to
dissect and have a better understanding of.
Citizens representing several environmental and public
interest groups called upon me early in the fall of 1974, to
report the problem and that more importantly they were unable to
get answers from the various government agencies on the impact
of these plants. Likewise, they were unable to find out just
how serious the environmental problems might be from such a
heavy concentration of facilities. Nobody seemed to have the
answer and so they asked for help. Thus the Senate
Appropriations Committee, of which I happen to be a member, did
act to direct the U.S. Environmental Protection Agency to
conduct a far-reaching study of energy development, including
power plant construction, in the lower Ohio River Basin. The
committee's action took the form of language which was added to
the report in the 1976 fiscal year funding measure for EPA and
the language added in July 1975 reads as follows, just to give
us a little idea to remind ourselves just exactly what the
legislative mandate for the Ohio River Basin Study was and is.
The committee is aware of plans in various
stages of development which could lead to a
concentration of power plants along the Ohio
River, in Ohio, Kentucky, Indiana, and
Illinois. Although the environmental impact
of such a concentration could be critical, the
decision making authority regarding the
construction of these facilities is dispersed
throughout the federal government and state
governments. The committee directs the
Environmental Protection Agency to conduct,
from funds appropriated in this account, an
assessment of the potential environmental,
social and economic impacts of the proposed
concentrations of power plants in the lower
Ohio River Basin. This study should be
comprehensive in scope- investigating the
impact of air, water, and solid residues on
the natural environment and residence of the
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region. The study should also take into*
account the availability of coal and other
energy sources in the region...
When the Appropriations Committee first headed the
mandate to EPA we were concerned about the concentration of
plants in the four states cited in the report: Illinois,
Kentucky, Ohio and Indiana. A number of factors, including
early findings which indicated that plants' air emissions
were carried hundreds of miles, led us to encourage EPA to
expand the ORBES region to include Southwestern Pennsylvania
and most of West Virginia. Thus, all six states, which
border the Ohio River are now included in the official areas
of the ORBES study.
Both EPA and the Appropriations Committee gave much
thought to the institutional structure which might best
carry out the energy assessment. I think we arrived at a
rare combination here. We encouraged EPA to consider a
framework which would include representatives from
University faculties in the Ohio River Valley. In an
innovative manner EPA sought proposals from major
universities on how they might cooperate in the
undertakings, and the ORBES study is the result. Most of
you know, researchers from nine university campuses in these
six states are engaged in a multidisciplinary endeavor.
I might add that one of the bonuses of expanding the
ORBES region was the opportunity to involve representatives
from the University of Pittsburgh's distinguished School of
Public Health. In the second and third years of this
activity we were grateful for that opportunity. Of course,
Professors Radford and Shapiro of the School of Public
Health are now participating in ORBES and have taken the
initiative in convening this symposium. Their examination
of the public health consideration is one of ORBES' most
important areas of inquiry, and I look forward to studying
their findings as quickly as we possibly can.
From the beginning, those of us in the Congress
realized that the assessment would have little credibility
unless the University researchers were given independence
from political and bureaucratic interference. Thus
researchers on an ORBES core team are participating in the
project under separate grants awarded directly to their own
universities by EPA. An EPA Project Officer, frankly an
internationally respected environmental scientist, Lowell
Smith, coordinates, as we know, the nine university
activities in an effort to guarantee that funds are being
administered in a manner consistent with federal guidelines.
But ORBES researchers are accorded freedom of inquiry in all
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respects. fn addition to the ORBES core team, more than one
hundred other faculty and staff members in the various
universities are providing support research to strengthen
the undertakings. Realistically, of course, there must be
coordination, guidance and direction in such a large
project. Such direction would be suspect if it came
directly from EPA itself. As we know, EPA is clearly not,
and frankly should not be a disinterested party.
To provide such direction in the university context,
EPA awarded grants to two University of Illinois members of
the core team to serve as a management team for the total
ORBES effort. I believe that the selections of Dr.
Stuckel, a distinguished engineer and Dr. Keenan with his
experience in political science, were outstanding. Their
task is, of course, to assure that the research process in
preparation of the final report be as objective as possible.
EPA and Congress have placed a heavy burden upon both the
management and research elements of the ORBES endeavor, one
that may be too heavy, according to some prophets of doom.
Indeed, they look at the past, and they say that in most
instances the record of inter-university cooperation and
research has not been overly impressive. Some say it is a
contradiction in terms for a federal agency and such a large
number of universities to attempt to cooperate in such a
fashion. After all, the main function of a federal agency
is to keep the wheels of government moving while a primary
purpose of university research is to criticize that
movement. Well, frankly, there may be some truth in this at
times. I think we should look at the positive side of this
marriage which I think can bring tremendous strengths to
bear and I am not willing to accept the conclusion as
inevitable from those who doubt whether we can succeed.
Neither am I willing to accept as inevitable that, because
EPA is coordinating ORBES, the agency is seeking only those
findings that conform with conventional EPA wisdom. I know
well that EPA has been criticized for such a policy in the
past. But, I am confident that this will not be the case
for ORBES.
I think it is important for us to see that the ORBES
study and those who are out looking for the answers and
putting together the data on which conclusions will be
based; that they be immune from political pressures. I
think so far we have been successful. We should take the
politics off finding out what the facts are. I have to say
that I think we have to distinguish that very important goal
on one side, from the very realistic assessment of how the
real world operates on the other. And that is that
political decisions are the way public policy is made in
America today and to expect that the so-called politicians,
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the elected public officials, will have no opportunity to
weigh the factors involved is to expect something that
cannot and, in fact, should not exist in our society. You
may want to get into a discussion of this in a little more
detail because I understand there may be some differing
opinions and that's what makes the world go around.
Now, I think it's important for us to have the benefit
of all this information as quickly as we possibly can. The
economics of environmental regulation and economics is one
of ORBES' major areas of inquiry, as we know has become a
very hot topic. Those of you who just came from the mining
seminar are undoubtedly aware of the recent fracas that
ensued in Washington when certain of the President's
economists were critical of the proposed surface mining
regulations on the basis that they were too costly.
For those in Congress, and I should say what I'm about
to say without relating that specifically to the assessment
that was made in Washington by some of the President's
economists, but looking at it more generally, there are
those in Congress and the agencies, probably some of you in
this room, who believe that money should not be a factor in
determining our national environmental quality goal. Let me
say as one of the original sponsors and continual protectors
of EPA, and the goals it was designed and is still designed
to accomplish, that I must say nevertheless that I disagree
with this point of view. I believe that environmental
decision makers, those in Congress, the agencies, the
research institutions, must be able, with some degree of
certainty, to have the sense of the cost associated with
their decisions. If I am to make any contribution to a
symposium such as this, I suppose, and I scratch my head to
see what kind of contribution I could make, in the presence
of those who are experts in the science of both energy and
environment, it seems to me if there is any contribution
that I as a United States Senator could make, it is to share
my very frank assessments, complete with their strengths and
their weaknesses, of the practical aspects of policy
implementation. And to do this in the general fashion and
then we can get into some of the specifics in the question
and answer part of the program this noon. Now, I confess
that I probably have already stepped on some toes and am
about to step on some more. I don't intend to apologize for
that; I found that in most of my lifetime in dealing with
public policy that probably we need a good deal more toe
stepping, because then you increase the circulation and you
get a little more action.
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In both this area of energy policy, and environmental
policy and particularly the coordination of the two
together, we are woefully short of action. If I may just
share some thoughts of my conscience with you: from a moral
sense I am not prepared to trade dollars or jobs for lives.
I find it very difficult to do that, impossible to do.
However, I am equally concerned over the fact that we've now
become polarized; those of us who were early on in the
movement trying to prick the national consciousness as far
as the environmental degradation that is going on, we are
polarized more and more from those in society who say we
must have more jobs, period. For those on the other side
who say no, the health question is the only question we must
consider. And it just seems that together we had to find
ways to stop this polarization because the real test of our
free society is how we can have enough jobs to accommodate a
growing society, at the same time we recognize the important
public responsibility of having a legislative policy that
will protect the health, not only of this generation but of
the next generation of Americans.
It is easy to say that, I have to confess to you. It
is much more difficult to implement that kind of policy and
to get the tradeoffs at an acceptable place on the scale.
It is complicated by the fact that the loss of jobs, the
cost of environmental protection, are immediate and obvious.
The loss of lives, more particularly the deterioration of
lives, which will be felt ten or twenty years from now, is
not immediately weighable. You can look at the admissions
to our hospitals of those who have respiratory ailments, and
you can chart the almost identical line with the particulate
matter in the air. But it is not the kind of fact that is
felt by those who are alive and working in a healthy way in
the workplace today. That is why I think it is extremely
important for us to look at the health factors and look at
the economic factors and do a better job of trying to mix
both of those together at an acceptable level.
I think we have to do a better job of articulating the
health realities, not just the immediate cost of environment
as they damage health, but the long range relationship of
environment to health. Secondly, I think we need to have a
better assessment of economic consequence, real economic
consequence—how they play on health, what dimensions the
health laws will really be. If you're going to really be
able to weigh this off we have to have all those facts so we
can make intelligent decisions. I think it is possible to
do that and ORBES is going to be very helpful to us. But
this is a critical kind of decision that we just have to be
prepared to make.
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We in Congress have to take better advantage of our
research arms such as the Congressional Budget Office, the
Office of Technology Assessment, to be able to assist us in
fixing a price tag to the environmental goals we legislate.
And as controversial as it is, there may be a point at which
a standard that makes one microgram increase in the
requirement, makes it that much more stringent, might be
incredibly costly without any real returns from the
standpoint of public health. I think we have to make those
decisions, and hopefully to make them accurately. I have to
say this from a practical standpoint, at a time when we are
not able to prove, as I think we can if we- do it the right
way, prove the real health benefits that are necessitated as
a result of certain environmental requirements then the
political, in the proper use of that word, the political
support for environmental protection is going to be gone and
the whole effort will be lost. So it is important for us to
have all these facts and be able to do a good job of
selling. This is true not only of Congress but the
regulatory agencies.
Another matter of some controversy, I think, causes me
to say to those of you who may think contrariwise that
design specifications often reduce the ability of the
marketplace to come up with alternative and more economical
ways to handle the waste products of our industrialized
society. I ask myself, "Isn't it far more prudent to set a
standard and allow the polluter to reach it within a
reasonable period, using whatever technology makes sense for
his individual enterprise?". I'm not so wed to the vehicle,
the technology, as I am to the results. And I think we need
to have enough flexibility to let each situation be resolved
on its own circumstance.
I have to say that as I've been personally involved in
this issue with some of my communities and some of the
interest groups that I represent that they are
characteristic of America. I find that the most frustrating
realism in public life today is to see that there tends to
be major conflicts, just irreconcilable conflicts, between
groups that really benefit or lose from the same set of
circumstances. You get industry on one hand and consumers
on the other, you get the auto industry, you get government
at loggerheads with one another. Somehow or other we have
not been able to get everybody together, and say okay, it
isn't good for industry to let the environment degrade to
the place that you have the kind of major movement that is
not going to consider any of the economics at all. It isn't
good for them, it isn't good for the automobile companies,
to have the kind of situation we had with the Clear Air Act
which I was and continued to be a strong supporter of that
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legislation. I have to confess to you that I don't think
any of us in 1970, when we sat there in all those hearings
thought we were really going to get an absolute decision
that Utopia is going to arrive in 1975. By the same token,
the people in the auto industry that had all the technology
to tell us to stop polluting, as we burn hydrocarbons in
internal combustion engines, they weren't willing to share
that information at all. They said, "We can't do it.",
period .
So we had to do something to get their attention. So
we established an arbitrary goal and said, "You better do it
by 1975." Well, industry rushed out here and instead of
government and industry and consumers and everybody sitting
down and saying, "Okay, here is the goal we're going to
reach. How is the best way to reach it?" You had industry
on one side, saying, "We can't reach it.", and government on
the other saying "You're going to reach it by 1975." We
ended up with a catalytic converter, which I think most of
us understand is certainly not the best long-range solution.
You know it doesn't help the purpose of our symposium
for me to pour out some of the frustrations in my heart as
far as I look at this as a policy maker. But some of you
who are providing these facts, I'd like for you to know it
is not always an easy solution as to how you get these
groups together to try to put together a policy that is
really in the long term national interest of the entire
society. You look at the ambient air quality problems that
we have right now, in which some of our communities are
going to be confronted in a relatively short period of time,
with major sanctions if they do not meet the standards that
have been established. I think in some communities this is
going to cause significant dislocations if they're not able
to reconcile the pollution with the standards. I have been
trying to deal with this and I must say as frustrating as
the first example is I have been heartened by the second.
If you live in Terre Haute, Indiana, you're not as concerned
at all with what the best way to solve the problem in
Buffalo or Detroit is, you're concerned with how you solve
it in Terre Haute, Indiana, or Indianapolis. Yet we had,
for a long period of time, EPA sitting there absolutely
unwilling to have any adjustments that would take into
consideration local situations. Well, we sat down with EPA
and we sat down with some of our institutions of higher
learning that had the technology and I must say I've seen an
amazing willingness on the part of EPA to say, "All right,
we're not going to say you have to do it our way as long as
you recognize the need to do it and are willing to commit to
reaching that goal." On the other hand, you have some in
industry who have been totally unwilling to recognize the
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fact that they're even polluting at all say, "All right, if
you let us have the chance to put this together in a
sensible way, we're going to sign off and we'll meet certain
standards." Now, I have to confess to you that the jury is
still out on that. Some of those people who had been the
major polluters may be using this as a guise, I don't know,
to put it off another year or two or three or four, five
years. I hope that is not the case. Although I am willing
to have a little give and take on how we reach a given goal
as long as we reach it, I'm not willing to let any of those
who are really destroying our environment and significantly
diminishing the lifespan of many of our citizens, hide under
a cloak of reasonableness to avoid what is their ultimate
responsibility.
Forgive me for sharing some of those personal
experiences with you but I think what we're trying to do in
ORBES is to get that information out there as quickly as we
can. I would hope that writing of the final report will
commence in January 1980. That is really just around the
corner considering the size of the job. I hope we can get
that out there as quickly as we can. Give us a set of
options; let us weigh the pluses and minuses and the
strengths and the weaknesses of these given options, and I
hope that we in the Congress, once we have the wisdom that
will come from knowing all the factors involved in the
development of energy and its impact on the environment of
this region, once we have the wisdom, I hope the good Lord
gives us the courage to do what is right. Right for the
health of our communities, really a significant section of
our country. At the same time we realized the importance of
providing sufficient energy for many other parts of the
country to meet the standards of living that they have
become accustomed to.
I may have had some pessimistic notes slipped in here.
I am normally an optimist, I still am an optimist. But I
think that optimism has to be laid on a realistic scale and
I am confident we can meet the dual goal of a good
environment and an economic plane that is acceptable to our
society. We cannot reach these two goals if we try to kid
ourselves, if we're not realistic. The costs involve both
failure to provide good environment and the cost of
providing good environment. We have to know both.
Now that is the end of this filibuster and this
rambling around. What's on your mind is of more
significance than what I've talked about.
Discussion
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Dr. H. Spencer, University of Louisville: I am one
of the ORBES core team members, also one of the citizens
that knocked on your door. We're grateful to you, Senator.
I have long said, and like to say here, that in those early
years we had more access to your office than we had to the
EPA.
Senator Bayh: I'd be glad to claim them; I just don't
want to claim all the credit. I think you fellows really
were the fathers. I was just offering the environment in
which you could do your work.
Dr . H. Spencer: I have one question which I think
you could give some answer to. There are a number of
industrialized countries that have no energy resources and
yet are economically strong. Those countries import
virtually all of their oil. We don't have quite that much
of a problem. Which means they must be doing something
right and we're doing it wrong. Answering those questions,
being able to get at that, is part of the ORBES charge.
What do you think we're doing wrong in the economic market
as compared to these nations?
Senator Bayh: May I just offer a little advice? Ask
another question. We haven't known each other long enough,
and we have ^ friendly repartee. The reason I say that is
that if ORBES tries, what are the consequences of what
happens out there? I think if we get ORBES into that area
you're getting it into an area from which you're never going
to be able to extricate it and we should stick to some of
the more immediate problems.
One of the most current problems is what's going on at
the multilateral trade negotiations. I am a trade man.
Looking at the value of the dollar—what that has done-- I
have to say that I hope we can balance our budget. I think
there has been far too much emphasis and far too much hope
placed on that because that is one of the parts of the
problem. But, if we look at the real problem of the deficit
balance, the real problem of the payments and you look at
the way our workers in our industry are treated one way when
we try to trade on someone else's turf and they're treated
another way when they try to trade on our turf. We have to
come to grips with that, because that is basic as far as the
strength of the dollar is concerned.
Here again I've asked myself the same question. The
other countries are not doing as much of this as I think
probably we are right now. One of the things I have deeply
regretted that we have not really been able to get geared
up, and we have started now and it's been woefully late in
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coming, is a major effort to try to provide alternative
fuels so we could get this oil monkey off our back. That
has a very insidious effect on us, not only from the
standpoint of energy, but also politics, national blackmail.
There are some things like that we just have to do more of.
I think ORBES lies in a more confined context and I
recognize that your question is right on target as far as
the complexity of the overall problem, the ORBES findings is
only a small sliver thereof.
Dr. Spencer: The health costs have escalated so
terribly in this country, and since we are debating health
here today which is such an integral part of the ORBES
project, I feel we cannot really dissociate ourselves that
easily from the subject. I know that you are not suggesting
that. I'm trying to reemphasize the complexity of the
health area in relation to the economic area and to the
world energy problem.
Senator Bayh: You're right. One other problem we have
is that we have demanded, I think rightly so, a higher
standard of living in the environmental sense, than any
other nation on the face of the earth. That is part of the
problem. That's one of the benefits of our society but
there are very few, if any, other nations, very few of any
other taxpayers, that have to bear the costs of quality of
life as far as environment is concerned in the production
process as we do here in our society. The irony of this is
if we look at a hundred years from now the global impact of
some of the environmental practices that we're pursuing or
not pursuing, this is going to come home to haunt everyone.
And to the extent we can do more to try to prick the
conscience of the industrialized world, all the industrial
communities of the world, that pollution of this society is
a world problem, not just an Ohio River Valley problem, or a
United States problem, then it seems to me we recognize the
environmental problem that is going to be confronting us a
couple or three generations away. We also recognize some of
the attendant economic problems that are a result of the
United States awareness of this problem before other
nations. I don't necessarily want to pass the buck to any
nation but I think if you look at what we're doing in our
society to try and deal with the environmental questions,
it's a generation or two ahead of where the other societies
are in most industrialized societies.
Question: Senator, you said that we have to have a
better handle than we now have on the cost of achieving the
environmental standard we have set for ourselvc lie have
certain very significant environmental stand en -- imposed
upon us by the Clean Air Act. And the Clean Air Act says
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nothing about how one can assess the cost to society of
achieving those standards. Would you favor an amendment of
the Clean Air Act, to impose that specific requirement upon
EPA?
Senator Bayh: Whether it takes an Amendment to the
Clean Air Act, or recognition of the real world in which the
Clean Air Act is being implemented, I am concerned about the
problem that once you start amending that Act you then open
it to those who are not really looking for realistic kinds
of weighoffs and tradeoffs, but many people who are looking
for loopholes so that they don't have to meet any standards
at all. I may be rather hard here. But here again I find
it very difficult on one hand, to say that we weigh dollars
against human lives. But in the long run, if we're talking
about a d_e minim is, or questionable increase and health
quality that hasn't been proven, hasn't been studied, versus
an economic dislocation that is rather quick and apparent,
then I think that it is an easy kind of a tradeoff to make.
Unfortunately, many of the decisions that have to be made
are not that easily recognizable.
Dr. Leonard Hamilton ,, Brookhaven National Laboratory:
I recognize that many socio-economic variables are very
important. The thing I do not understand is why
environmental controls necessarily mean a depreciation of
jobs or lack of jobs. The results suggest that they may
create more jobs.
Senator Bayh: There are some studies that do show
that, if you take the society generally, the studies that
I've seen as an environmentalist, and I like to believe
those studies, show that there are more people working now
to produce environmental protection equipment than have been
displaced by environmental requirements. I think we all
understand that many of those people are working in areas
where dislocation is not going to occur by the imposition of
the environmental standards. The difficulty is that you
have core areas of major dislocation. We try to go back and
see where could we have done better and if we don't learn by
our mistakes, particularly when we are pioneering in this
whole area of environment in the United States. I think we
have to get consideration of this now. ORBES is probably as
good an example as any where you have major pollution
problems created in one area to provide energy supplies to
others, but that pollution is not going to remain stable so
it is going to follow normal trends. I think we have to
look at a broader base of financing our environmental
requirements. I think we might have been better off if we
would have permitted a significantly higher tax writeoff to
get these things on stream quickly, so you don't have
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haggling that we're going to fight forever. Let's find a
way in which we can finance this situation out there
generally. The people that are going to be producing the
energy and have the environmental protection equipment
established, say in Madison, Indiana, since that is going to
benefit society generally to get that electricity. Maybe
society ought to generally help bear some of that and a tax
writeoff would help to do that. With what has happened to
utility rates, we see that the fact of life is that
consumers are going to pay for one end of the scale or the
other. And yet we are not being able, the way we are doing
it now, to get the systems implemented as quickly as we
otherwise could.
To get back to what we ought to be doing. We ought to
be doing much more than we have been doing in research as
far as combustion is concerned. Most of our research has
been directed at energy supplies, not the more efficient or
more environmentally sound combustion processes. We had two
or three of them, the fluidized bed combustion process, just
to name one, that is very close on, that can do a tremendous
job both as far as S02 and increased BTUs. Yet we have not
emphasized that part of the equation. Now I could have
answered your question in one word but a Senator never does
that when a five minute answer is there.
We are prepared to look at where the regulations have
us compared to what the original legislative intent was.
But I think we would be wrong if we looked at that from the
standpoint of retreat. Most of the goals that we originally
established were reasonable and we didn't have nearly as
much idea about how to get there, the cost attendant, the
time and dislocation involved in some instances as we do
now. So I think it is only fair and only wise to
periodically have oversight and look and see where these
regulations go. EPA is not the only government agency to
put out regulations. And as Dr. Bingham at OSHA will tell
you she couldn't see why her predecessor dealt with the size
of outdoor toilets and the reasonable proximity of (don't
get me started) wooden ladders and fire extinguishers and
things like that. I mean there is something about
regulators that tend to get carried away with dots and
tiddles instead of great announcements of public policy.
So I think it is important to reassess where we are.
But here again I would hope that we could find some way in
which we could get these near irreconcilable forces together
somehow. To get back to that auto thing, how you could have
gotten somebody to get the auto people that had the
technology and said, "Okay, we're going to make a major
innovation in this internal combustion engine and we're not
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going to say never.", and we're going to say "Okay, we'll
give you another four or five years." We're going to end up
giving you four or five years anyway and we're going to have
a mousetrap instead of a major change. So it is with some
of the other air pollution problems.
May I just make one more comment? I would hope that
those of you who are here and who obviously have deep
concern and interest as well as more than casual expertise
in this area, would let me know your assessment of this
problem. It is not an exact science and I'm sure that those
that are involved in ORBES are painfully aware that there
are going to be some tradeoffs that are not exactly certain.
And it is important for us to have the experience of benefit
of as many different aspects of this problem as we possibly
can, so we can make the right determination. As I say, you
can provide us the wisdom, I hope the good Lord provides us
the courage, because it is going to take a good dose of both
of those .
Dr. Edward Rad ford, University o_f Pittsburgh: Thank
you very much, Senator Bayh, and we appreciate your taking
the time to come to the symposium.
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SESSION I: HEALTH PROBLEMS IN EXTRACTION OF FUEL
Monday morning, March 19, 1979
Moderator: Edward P. Radford, M.D.
Professor of Environmental Epidemiology
Graduate School of Public Health
University of Pittsburgh
OCCUPATIONAL AND ENVIRONMENTAL HEALTH
PROBLEMS IN COAL MINING
By
Curtis Seltzer, Ph.D.
RESPIRATORY PROBLEMS IN COAL MINERS
By
W.K.C. Morgan, M.D.
URANIUM MINING - OCCUPATIONAL AND OTHER HEALTH PROBLEMS
By
Joseph K. Wagoner, S.D. Hyg.
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OCCUPATIONAL AND ENVIRONMENTAL HEALTH
PROBLEMS IN COAL MINING
By
Curtis Seltzer, Ph.D.
Office of Technology Assessment
U.S. Congress
Office of Technology Assessment
Washington, D.C.
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Coal-fired electricity is not made cheaply. The work-related
health and safety hazards of coal mining are well-known to miners
and operators alike. Even the general public has come to appreciate
the costs of "black lung1' disease and accidents that coal miners
experience. Many of the environmental health costs of coal mining are
less familiar although coalfields residents know them well. These con-
cerns range from acid mine drainage and fugitive dust to accidents from
coal^hauling trains and flooding from stream siltation in Appalachian
watersheds caused by years of contour strip mining.
Most major environmental health problems have been identified and
a sense of their magnitude, severity and remedies are known. Current
debate focuses on the level of magnitude, degree of severity and
applicability of certain solutions. In policy terms these issues
translate into a few simple questions,: 1) Are current federal occupa-
tional and environmental standards adequate?; 2) Are these standards
being complied with on a daily basis?; 3) Are the available compliance
data reasonably reliable?; 4) Are current monitoring strategies adequate?;
and 5) Are existing enforcement programs working well?
While most analyses discuss these questions and issues individually,
coalfield residents experience them holistically, cumulatively and,
in a sense, synergistically. Social turbulence in the coalfields is
likely to be related to the set of adverse environmental health conditions
miners experience in the course of their everyday lives. In these matters,
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scientific precision is often superseded by perceptions of reality. If
the creek in your backyard is the color of orange soda pop, whether its
pH is 3 or 6 is of little consequence.
Both the problems of and solutions to occupational and environ-
mental health in coal mining are related to supply-and-demand economics.
Tight markets and static prices determine the level of externalized
occupational and environmental costs. When demand was sluggish, concern
for environmental health was deemphasized as workers, environmentalists
and community activists feared that economic pressure on local mine
operators would affect their competitiveness and jeopardize jobs and
community welfare. When demand is rising steadily or when prices are
increasing (whether or not production is increasing), coal workers and
community activists are likely to push coal operators harder for pre-
ventive and compensatory programs related to occupational and environ-
mental health. As coal demand and production rises over the next 25
years, economic conditions will be created for increased demands for
occupational and environmental safeguards.
To understand the nature of coal mining's current occupational
and environmental health problems, it is necessary to understand some-
thing of the economics of the industry. Neither occupational health
and safety nor environmental quality exist independently of coal's
economics and politics.
The single most important economic fact about the American coal
industry is that for most of this century coal demand was stagnant.
The industry's capacity to produce did not change significantly after
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1918. In fact, as recently as 1975, coal operators produced less bitu-
minous and anthracite coal than they had in 1929; 658 and 655 million
tons respectively. In 1947, about the same amount of coal was produced
as in 1977.
Lack of demand, low prices and stiff competition forced coal
operators to cut production costs as much as possible to survive in the
1920-1970 era. During the first 30 years of this period, the operators
maintained competitiveness by holding down their labor costs despite
wage pressures by the United Mine Workers of America. Labor costs were
reduced by gradually introducing new labor-reducing technologies such as
mechanized cutting, drilling and loading machines. In 1920, 640,000 miners
were employed compared with 416,000 in 1950, a 35% reduction. After World
War II, the industry mechanized rapidly and comprehensively. The intro-
duction of continuous-miner technology, electric shuttle cars and roof
bolts in underground mines after 1950 enabled the industry to maintain
tonnage levels with even fewer miners. A section equipped with one con-
tinuous-mining machine could produce as much coal with 10 workers as a
hand-loading section with 80. Labor costs were also reduced by the steady
increase in the share of coal output mined by surface methods, which were
inherently more efficient and less costly than underground techniques.
The portion of total bituminous production mined by surface methods rose
from 24% in 1950 to about 60% today. Underground mechanization and
surface mining cut deeply into the workforce. The 416,000 bituminous coal
miners of 1950 were reduced to about 125,000 in 1969, a cutback of 70%.
Bituminous production, however, actually increased from 516 million
tons in 1950 to 561 million tons in 1969.
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This set of economic and technological changes carried grave
implications for occupational health, safety and environmental health
in coal mining. Weak coal demand and cost-cutting pressure meant operators
minimized health and safety expenditures. Occupational health and safety
costs were often externalized in whole or in part. (An externalized cost
of production is not paid by the mine operator. It is shifted in one
form or another to employees—as accidents or disease—the local environ-
ment, or adjacent communities.) The frequency of mine fatalities showed
no improvement between the early: 1950s and 1970,although the number of
fatalities fell as the workforce was reduced. Similarly, the frequency
of disabling injuries showed no improvement, although the number of injuries
fell. In terms of occupational health, continuous miners increased the
levels of respirable mine dust, which, caused many thousands of cases of
respiratory disease to appear by the latv. 1960s, No Federal dust standards
were established until the implementation of the 1969 Coal Federal Coal
Mine Health and Safety Act in 1970. In addition, the environmental costs
of surface mining were largely externalized in the 1950s and 1960s. A
few states enacted environmental controls in these years, but they were
inherently weak and enforced weakly. The environmental damage from
unfettered contour surface mining was considerable—naked high walls
run for 10,000 miles throughout Appalachia; overburden was pushed down
hundreds of slopes without regard for landslides, stream siltation or
water quality; blasting disturbed ground water and its noise aggravated
nearby residents; fugitive dust from mining and haulage nettled many;
finally, surface owners often had little say about how a coal company
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went about extracting the sub-surface coal it owned.
The economic conditions forcing coal companies to externalize
occupational and environmental costs were also handicapping the capacity
of coalfield communities to bear them. Hundreds of thousands of unemployed
union miners and their families were cut off from the health care and
retirement benefits they had earned. (Those union miners who were fortunate
enough to continue working enjoyed first-dollar coverage through the UMWA-
negotiated Welfare and Retirement Fund.) Federal "commodities11 (surplus
foodstuffs) became the dietary staples for many.
Most significant in terms of environmental health was the short
changing of local tax systems, which prevented communities from building
an adequate infrastructure of public services and facilities. Local
communities, counties and states had rarely taxed coal production or un-
developed minerals sufficiently. They feared that doing so would dis-
advantage local coal in competition with non-taxed coal from other areas.
The political influence of the coal industry was sufficient to beat back
efforts to impose higher local property taxes or state severance taxes.
The result was that coalfield communities lacked many facilities—such as
water and sewage treatment plants, recreation and adequate housing—and
services that make for community public health. The health consequences
of this syndrome were documented in a 1947 report on coalfield health
conditions prepared by Admiral Joel T. Boone for the Department of the
Interior.
The major consequence of this pattern—the cost externalization,
lack of infrastructure development, one-crop economies and undertaxation—
takes the form of a tremendous social deficit in the Appalachian coalfields.
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Current problems are compounded by the absence of tools to deal with the
legacy that carries over from the past. Future occupational and environ-
mental impacts from mining will be added to this existing deficit. In
many communities, the margin for additional damage is thin or nonexistent.
This implies that even small future increments of environmental degradation
will have very large social consequences.
In this context, an overview of coal mining's environmental health
implications can be focused in two separate but related areas. First, this
discussion will outline some of the direct health impacts of mining on mine
workers and environmental health in their communities. Second, a brief
discussion is presented of the direct impacts mining has had on the ability
of coal communities to cope with current and future occupational and
environmental health problems.
DIRECT HEALTH EFFECTS; OCCUPATIONAL AND ENVIRONMENTAL
A. Occupational Safety
Coal mining has never been a safe occupation. Since 19.00, mining
has killed a recorded 110,000 miners and, since 1930 alone? more than 1%
million disabling injuries have been reported. In 1977, coal operators
2
reported 139 fatalities and 14,933 disabling injuries to MESA. Fatality
frequency in 1977 was .36 per million worker hours and disabling injury
3
frequency was 37.77 injuries per million worker-hours. Summary accident
data for coal mining in 1977 is presented in Table 1. Trend data for
fatalities for 1952-1977 is found in Table 2. Little or no improvement was
recorded between 1952 and 1970 in fatality frequency for either underground
or surface mining. However, with the implementation of the 1969 Federal
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TABLEjj. - Number of injuries. Injury-frequency rates per million man-houra. persons working, man-hours, and production.
II
by kind of coal mined and work location, cumulative January-December 1977 —
Kind of coal and
work location
Number of injuries reported
to the Mining Enforcement
and Safety Administration
Fatal
All dis-
abling
A/
All ln)urles
5/
Injury-frequency rates,.
per million man-houra —
Fatal
All dis-
abling
4/
All in)urles
Average
numbe r
of
persons
working
6/
Man-hours
reported
3/
Production
reported
(short tons)
3/
Bituminous coal:
Underground mines:
Underground ~—-- 82
Surface 9
Total, underground mines— 91
Strip mines 26
AiiRer mines 2
Other surface TJ
Total, mirTing 119
Mechanical cleaning plants 8
Independent shops and yards 1
Total, bituminous coal— 128
Pennsylvania anthracite coal:
I Underground mines:
££ Underground — 9
I Surface
Total, underground mines-- 9
Strip mines—————--—™ 1
Other surface TJ •
Total, mining 10
Mechanical cleaning plants 1
Independent shops and yards
Total, anthracite coal 11
All coal:
Underground mines:
Underground 91
Surface 9
Total, underground mines-
All surface mining 29
Total, mining 129
Merhnnltnl denning plnnfs 9
Independent shops nnd ynrds 1
Total, all coal
10,911
713
11,624
2,142
29
2
13,797
733
110
14.640
66
1
67
101
7
175
105
13
293
10,977
714
11.691
2,281
13.972
838
123
14,933
(5,896) 16,807
(613) 1,326
(6,509) 18,133
(2,296) 4,438
(15) 44
(2) 4
(8,822) 22,619
(607) 1,340
(111) 221
(9,540) 24,180
(2)
(2)
(116)
(11)
(129)
(132)
(29)
(290)
68
1
69
217
18
304
237
42
583
(5,898) 16,875
(613) 1,327
(6,511) 18.202
(2,440) 4,721
(8,951) 22,923
(739)
(140)
(9.810) 24.761
1.577
261
0.40
.38
.40
.23
1.81
.35
.27
.15
.34
16.28
13.76
.47
3.33
.52
2.17
.45
.38
.44
.25
.37
.28
.15
.16
52.68
27.59
50.06
18.12
17.17
39.30
22.14
16.43
37.54
108.54
9.85
93.24
43.32
30.55
53.21
53.95
91.48
54.56
52.83
27.52
50.19
18.56
39.42
24.03
18.02
37.77
(28.48) 81.16
(23.76) 51.35
(27.99) 78.05
(19.37) 37.49
(8.13) 25.30
(5.04) 5.04
(25.04) 64.35
(18.89) 41.02
(16.28) 32.71
(24.40) 61.95
(3.62) 112.16
9.85
(3.06) 96.29
(53.68) 97.00
(48.01) 78.57
(42.23) 95.44
(68.61) 122.56
(204.07) 295.56
(56.74) 111.30
(28.41) 81.25
(23.66) 51.17
(27.92) 78.10
(19.91)
(25.19)
(21.85)
(20.26)
(24.81)
38.48
64.62
45.88
1R.28
62.59
126.722
14.541
141,263
61,887
1,294
134
204,578
17,670
3,854
226,102
415
74
489
1,267
171
1,927
1,107
76
3,110
127,137
14,615
141,752
64,753
206,505
18,777
I,1) 30
229,212
201.851,383
23,738,735
227.590,118
114,104,214
1.106,641
198,593
342.999,568
30,177,926
6,572,088
379,749,582
552,767
101,487
654,254
2.123.626
229,106
3.006,986
1,909,245
142,105
5,058,336
204,404,150
23,840,222
228,244.372
117,762,182
346.006,554
12,087.171
6.714.W
184,807,918
254,820.485
254.820.485
197.722.272
4.256,721
715.580
657,515.058
657,515,058
564,787
564,787
2.711,096
1,920,484
5,196,367
5,196,367
255,385,272
255,385,272
407,326,153
662,711,425
662.711,425
I/ Information presented In this table Is based on data on file February 11, 1978, and Is preliminary.
I/ Any Injuries from mines that have not reported man-hour data have not been Included In the computation of inlury-freqiiency rates.
T/ Based on recorded data from reporting mines; should be used only for the purpose of computing rates; does not constitute Industry total.
~kl Includes fatal injuries.
T/ Figures in parentheses are for nondlsabllng ln|urles and are Included in the accompanying figure.
~\>J Summary of average number of persons working for only those months during which each c»tabliiihiiient->|WBji_a
T/ Culm banks and dredges. ---si*.
-------
Table Z—Fatalities in U.S. Coal Mines, 1952-77
(hours of exposure)
Underground
Year
1952
1953
1954
1955
1956
1957
1958
1959
1960
1961
1962
1963
1964
1965
1966
1967
1968
1969
1970
1971
1972
1973
1974
1975
1976
1977
Fatalities
514
440
374
391
417
451
334
268
295
275
265
257
224
240
202
186
276
163
220
149
128
105
97
111
109
100
Rate*
.97
.96
1.10
1.06
1.11
1.30
1.26
1.11
1.29
1.34
1.34
1.28
1.12
1.21
1.12
1.05
1.63
.95
1.20
.86
.68
.56
.51
.47
.45
.43
Surface
Fatalities
33
21
22
25
28
22
19
20
24
17
20
22
15
18
23
22
24
28
29
23
20
16
24
32
23
27
Rate*
.55
.39
.48
.51
.52
.42
.39
.43
.52
.39
.46
.49
.33
.40
.55
.52
.57
.63
.55
.39
.38
.28
33
.33
.22
.23
Surface
fatalities as a
percentage of
underground
6%
5
6
6
7
5
6
7
8
6
8
9
7
8
11
12
9
17
13
15
16
15
25
29
21
27
a£xpressed in million nours of exoosure Data do not include auger mines, culm banks, dredges, preparation slants, shops, and contractors.
SOUPC£ Mine Safety ind Health Administration. 1978.
Coal Mine Health and Safety Act, the frequency of underground fatalities
has been cut by more than half. Fatal frequency in surface mining has also
been more than halved. The number of underground fatalities has fallen with
the reduction in frequency. However, the number of surface fatalities has
increased despite lower frequency as more surface miners were hired in the
1970s. When the data are examined closely, it is apparent that the act has
almost eliminated multi-victim underground disasters as a source of fatalities
by setting and enforcing standards for methane, combustible dust and electrical
equipment. Some improvement has also been recorded in reducing fatalities
from roof falls and haulage accidents.
On the other hand, little improvement has been recorded in reducing
disabling injuries since 1969. Underground disabling injury frequency was
53.26 per million hours worked in 1952 and 50.86 in 1977, according to data
-29-
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presented in table 3. Surface disabling injury frequency was 28.11 in 1952
and 18.91 in 1977. Overall, disabling frequency for all coal mining has
4
improved from 1952's 50.66 injuries per million worker hours to 37.77
injuries in 1977 (table 1). However, since 1969 little consistent improve-
ment has been recorded. The Act did not address injury prevention specifically
Table 3—Nonfatal Disabling Injuries in U.S. Coal Mines, 1952-77
(hours of exposure)
Underground
1952
1953
1954
1955
1956
1957
1958
1959
1960
1961
1962
1963
1964
1965
1966
1967
1968
1969
1970
1971
1972
1973
1974
1975
1976
1977
Injuries
28,353
22,622
16,360
17,699
18,342
17,076
12,743
10,868
10,520
9,909
9,700
9,744
9,692
9,705
8,766
8,417
7,972
8,358
9,531
9.756
10,375
9,206
6,689
8,687
11,390
11,724
Rate*
53.26
49.38
47.98
48.10
48.88
49.23
47.94
44.90
46.09
48.19
48.88
48.62
48.35
49.09
48.78
47.57
46.99
48.77
51.79
56.40
55.32
48.80
34.95
37.13
47.09
50.86
Surface
Injuries
1,698
1,604
1,342
1,140
1,318
1,339
1,150
1,054
1,125
1,052
1,027
1,099
1,116
1,178
1,043
949
1,039
967
1,346
1,564
1,305
1,208
1,229
1,714
2,071
2,246
Rate*
28.11
29.48
29.01
23.14
24.31
25.72
23.86
22.64
24.45
24.44
23.50
24.25
24.75
26.12
25.00
22.43
24.59
21.84
25.67
26.54
24.84
20.94
16.83
17.74
20.04
18.91
Expressed in million hours, of exposure Data does not include auger mines, culm banks, dredges, preparation plants, shops.
and contractors.
SOURCE. Mine Safety and Haaltn Administration, 1978.
One measure of injury is "severity," expressed as the number of calendar
days not worked by the injured worker because of the injury. On the average
each underground temporary total disabling injury resulted in an average of
73 lost calendar days in 1977. The average servity for surface miners was
58 days in 1977. Even more disturbing is' the fact that the average severity
for temporary total disabling injuries increased dramatically in 1977 over the
1950-1976 experience. In that 27-year period, average underground severity
-30-
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for temporary total injuries was 35 days for underground miners and 26 for
surface miners. These averages have been exceeded every year since 1974,
suggesting that reported accidents may be of an increasingly serious nature
and/or more time is spent recuperating from accidents than in the past—parti-
cularly in underground mining. Efforts by coal mine operators, labor and
federal enforcement agencies have not succeeded in substantially lowering
injury risk.
Estimates of future mine safety fatalities and injuries depend on the
level of coal production, the mix of mining methods (surface mining is
safer than underground), the number of miners employed, productivity rates
and accident frequency.
Most coal supply and demand forecasts predict greatly increased levels
of production over the next 20 to 30 years. Considerable disagreement
exists over how fast, how much, where and by what methods it will be
mined. Most observers say production will double and perhaps triple
mid-1970fs levels (650 million tons) by 2000; the ratio of surface - to
deep-mined production will not be any less than today's 60/40 division;
productivity (tons mined per worker per shift) will increase very slowly;
and most coal miners will continue to work in underground mines in the East
even as the locus of production shifts West. All of these factors will
affect coal mine injury and fatality experience. The more workers employed
in underground mines, the higher will be industrywide fatalities and injuries,
for example.
The Congressional Office of Technology Assessment recently prepared
production, employment and injury estimates through 2000. These estimates
suggest that coal production is likely to more than double and could possibly
•
triple 1977 tonnage (688 million tons) by 2000. Most production growth will
-31-
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occur after 1985 when production is estimated to better 1977 by between
39% to 66%. No net increase is predicted in production by 1985 for mines
east of the Mississippi River, and no increase is predicted for eastern
surface mines even by 2000. Almost all of the East's additional production
will come from underground operations.
The ratio of eastern to western production is shifting dramatically.
In 1977, western production of 166 million tons accounted for about 24%
of the nation's total. By 1985 this share is likely to rise to between
46% to 48% of the total, and by 2000, between 52% and 53%. In tonnage
terms, western production will increase over 1977 between 299% and 331%
by 1985, and by between 506% and 724% by 2000. However, most coal miners
will continue to be employed in eastern underground mines despite the
massive redistribution to western surface mined production. At both low
and high estimates of coal production, underground miners will represent
74% of the total workforce in 1985 and 79% by 2000. Employment is not
expected to increase significantly 1985 over 1977's 229,000 workers. By
2000, however, employment estimates range between 337,000 to 487,000 nation-
wide, depending on the level of coal production.
Probable health and safety costs of increased coal production can be
calculated using these estimates and current accident frequency rates.
Annual fatality and disabling injury forecasts are presented in table 4.
It may be argued that current accident rates overstate future costs since
they are likely to improve in the future. Perhaps. But trend data for
the last few years suggest that the rate of improvement in fatality
frequency has slowed almost to the point of stopping. Disabling injury
frequency has not changed much at all. Even if these frequencies are lowered,
-32-
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the number of actual fatalities and injuries may still rise due to higher
levels of employment.
Table 4 suggests the probability of a substantially higher number of
mine fatalities and disabling injuries in the future as production increases.
Fatalities are likely to increase to between 157 and 187 by 1985 (over 1977's 139)
and to between 259 to 371 by 2000. Disabling injuries are likely to rise from
1977's 14,933 to between 17,000 and 21,000 in 1985 and between 29,000 and 42,000
in 2000. Barring some unforeseen—and unlikely—breakthrough in mining technology
or safety practices, these estimates can be taken as representing a likely
range of human costs associated with increasing coal production.
Table 4—Mine Worker Fatality and Injury Estimates
Surface
Fatalities
Injuries
Underground
Fatalities
Injuries
Other Coal workers*
Fatalities
Injuries
Total
Fatalities
Injuries
1977
29
2.281
100
11 724
10
984
139
14989
1
Low
25
1 954
118
13 907
14
1 586
157
17447
985
High
30
2 401
140
16513
17
1 391
187
20 805
Low
32
2 515
203
24012
24
2 653
?S1
29 180
:ooo
High
46
3 634
291
34 405
14
3 804
171
41 H41
a 1977 data include workers in shops and cleaning plants, but not construction workers. Estimated data tor 1985 and 2000 include all other coal workers and uses a 10 percent
add-on to the total o< underground and surface accidents.
SOURCE: Office of Technology Assessment, The Direct Use of Coal; Problems
and Prospects of Production and Combustion (Washington. D.C.: U.S.
Caongress, 1979), p. 289.
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Occupational Health
The most serious occupational health hazard miners face is coal mine dust.
Respirable coal mine dust is retained in the gas-exchanging portion of the
lungs. Exposure to sufficient quantities of respirable coal mine dust over
a period of years can lead to coal workers' penumoconiosis (CWP), which, in
its most serious form, is fatal. Additional respiratory impairment may result
from one or more of the following: job exposure to "nonrespirable" dust (which
affects the upper respiratory tract) ; toxic fumes and gases (produced as com-
bustion products from fires in mine machinery, conveyor belts, lubricating oils
and the like); trace elements (as both respirable and nonrespirable dust particles);
and mines gases. Other health hazards include noise, hot and cold environments,
g
stress and whole-body vibration. The most recent mortality study found that
coal miners died more often than expected from a variety of respiratory diseases
such as influenza, emphysema and asthma. Penumoconiosis and bronchitis were
underlying causes of death in a significant number of deaths attributed to
nonmalignant respiratory diseases. Cancer of the lung and stomach were also
higher, which may or may not be related to work factors.
The 1969 Federal Coal Mine Health and Safety Act phased in a 2 mg./m standard
for respirable coal mine dust and established a "black lung" compensation pro-
gram. This standard is the strictest in the Western world. It is based
on British research done in the 1960s. Probability curves developed from the
British data suggest that at 2 mg., one to two percent of those exposed to no
9
more than 2 mg. of dust over 35 years would develop simple CWP. Recently
reported followup data suggests that the "risks of developing category 2 or
more coalworkers' simple penumoconiosis over a working life are one or two
percent {probability units} higher than earlier predictions."
-34-
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The 2 mg. standard may not prove to be as safe over time as the early
British research promised. A number of methodological questions can be
raised about the original research design and subsequent data manipulations.
Methodological criticism may be warranted on the data manipulation of both
11
sides of the dose-reponse relationship." No epidemiological study has been
done—or could be done—of miners actually exposed to 2 mg. over a working
life due to the newness of the standard. The second round of NIOSH's National
Study of Coal Workers' Pneumoconiosis done in 1973-1975 by the Appalachian
Laboratory for Occupational Safety and Health (ALOSH a facility of NIOSH)
found a 6% rate of disease progression among working miners x-rayed in both
j 12
rounds.
It is possible—and altogether likely—that future research will prove that
the 2 mg. standard is not as safe as originally believed. This implies
that CWP will continue in the future even if every mine complies with the
2 mg. standard every working day from now on.
Estimates of future prevalence of CWP can be made using available data.
Current NIOSH/ALOSH research suggests that a 10% to 15% prevalence rate
among working miners in the early 1970s is justified. Prevalence among
working miners in 1979 is probably lower inasmuch as about 40% of miners
working in 1969 have retired and almost 150,000 new workers have entered
the mines in the 1970s. Table 5 presents a set of CWP estimates associated
with increased coal production I developed for OTA. Under optimistic
assumptions of diligent dust control, as many as 10,000 miners would show
x-ray evidence of CWP in 2000. Under less optimistic assumptions, perhaps
18,000 cases would be detected. If the 2 mg. standard is not as safe as
as is currently assumed and if dust control efforts are not diligent, these
numbers will be higher.
-35-
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Table 5 —Estimates of CWP Among Working Miners, 1976,1985, and 2000
_. 4. ... Prevalence Rates
Optimistic Pessimistic
Underground Surface* Underground Surface3
Working miners tO% 4% js% 4%
1976 (208,000)
Underground (70%)
145,600 14,560 21 840
Surface (30%)
62,400 2,496 2,496
Total 17,056 24,336
Working miners 7% 3% 70o/o ,0/
1985(229,829)
Underground (74%)
169,922 11,895 16992
Surface (26%)
59.907 1,797 , 797
Total 13,692 18,789
Working miners 3% 7% 5% 2%
2000(410,893)
Underground (79%)
326,305 9,789 16,315
Surface (21%)
84,588 846 1.691
Total 10.635 18.007
a Prevalence rates for 1976 are consistent with the range ol current research findings. Tne 4 percent prevalence rate for surface miners comes from R Paul Fairman, Richard
J. O'Bnen. Steve SwecKer. Harlan Amandus. and Earte P Snoub. Respiratory Status ot 'he U S. Surface Coal Miners,' unpublished manuscript done for ALOSH NIOSH. 1976.
The ALOSH study used X-ray evidence to determine the prevalence of CWP Most of the surface miners had extensive experience in underground coal mining which contributed
to the prevalence of CWP Prevalence rates lor 1985 and 2000 assume that compliance with the current dust standard will lower prevalence In addition, increasing numbers
of older miners who h&d years of exposure before 1969 wiH retire, tnereby lowenng prevalence among working miners These prevalence rates have not been denved
_ mathematically, and should be seen more as possuMrues than as predictions.
SOURCE: OTA, Direct Use of Coal, p. 265.
CWP is one work-related disease process found in coal miners . "Black lung'
is the vernacular name miners use to describe all respiratory disability
associated with their trade. Black lung includes, CWP, as well as occupational
bronchitis and emphysema, severe dyspnea, airways obstruction and as yet an
13
unnamed disease process affecting the gas-exchaning portion of the lungs.
These various diseases may occur simultaneously in a single miner and in
different combinations. Cigarette smoking increases the risk of lung disease
among coal miners as in the population generally. Some of these disease
processes are probably related to nonrespirable coal-mine dust and to the
non-coal constituents of that dust (trace elements and quartz). No federal
-36-
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standards exist for nonrespirable dust or for toxic respirable substances
encountered in a mine environment. It is reasonable to assume that the
prevalence of black lung disability will continue to be significant among
coal miners in the absence of controls on these hazards. Emphasis on CWP
and respirable dust may have concealed meaningful dose-response relationships
between black lung and nonrespirable dust as well as other harmful air-borne
substances. Since many more cases of black lung appear today than of x-ray
14
diagnosed CWP, it is prudent ot suppose that a similar ratio will continue in
the future. In a rough way it can be said that for every case of CWP, at least
two cases of bronchitis, one case of severe dyspnea and one case of airways
obstruction will be found, although not necessarily exclusively.
NIOSH calculated future occupational health costs of increased coal
production in 1977. These estimates are presented in table 6. NIOSH's
prediction of CWP cases are considerable higher than those found in table 5.
Table 6 —Projected Health Effects of Increased Coal Production
Year
1975 estimates
Underground
Strip auger
Total
1985 estimates
Underground
Strip auger
Total
2000 estimates
Underground
Strip auger
Total
Millions of
tons produced
(quads)
279 ( 7.3)
332 ( 7.9)
611 (15.2)
395 ( 9.8)
735 (18.3)
1,130 (28.1)
630 (15.7)
1,170 (29.2)
1,800 (449)
Number of
employees
139,500
52,500
192000
197,500
116,000
313,500
315,000
185000
500000
Cases"
Of CWP
18 100
1 300
19400
25600
2900
28,500
40900
4600
45500
Cases of*
chronic
bronchitis
41 800
15 700
57 500
59200
34800
94000
94 400
66 300
160,700
Cases of"
severe
dyspnea
11 200
4 200
15 400
15 900
9300
25200
25 300
14800
40 100
Cases of"
airways
obstruction
41 800
10 000
51 800
59 200
22 100
81 300
94 400
35200
129 600
3 Not mutually exclusive.
3 Not necessarily due solely to coal dust nnala'.'On
SOURCE National Institute lor Occupatioral Saiery ana Health. Occupational Safety and Hearth Implications of Increased Coal Utilization," computer pnntout and attachments
(rev 'lov 4,1377 DistPDu'ed at a NiCSrt conference o( the committee on health and ecological ejects of increased coal utilization, Nov 21,1977
-37-
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NIOSH used a 10% CWP prevalence rate for working miners for 1975, 9% in !''•' ,
and 9% in 2000. These prevalence rates assume the current 2 mg. dust standard
will have little beneficial effect on CWP prevalence. NIOSH's assumption
may cast doubt either about the standard's inherent safeness or about thi> - •<•>
of compliance. NIOSH also used somewhat higher estimates of the future m'"»
worker labor force than OTA did (table 5). The OTA and NIOSH estimates rri.i.--
sent a band of possible occupational health implications of increased coal
production. As a matter of personal opinion, I believe the OTA estimate<:
will prove to be too low and the NIOSH ones too high. The range of likely
adverse health effects these two efforts present are: 1985, 13,700 to 28, ••""•
cases of CWP; 2000, 10,600 to 45,500 cases of CWP. Bronchitis, severe
dyspnea and airways obstruction should each occur in at least a 1:1 ratio
to COT.
Future prevalence of work-related lung disease among miners will be
determined in large part by the effectiveness of dust control measures
implemented by mine operators and coal miners. As there was no systematic
dust sampling and no standard before 1970, dose-response comparisons between
that era and now are difficult, if not impossible. The few dust surveys
done before 1970 found dust concentrations far in excess of the current
standard. For example Schlick and Fannick reported the results of 1968
Bureau took nearly 2,000 samples and found the mean dust concentrations oL"
0 1 f
the 16 occupation categories sampled exceeded 2 mg./m .
Miners who have worked in both periods say dust conditions are better now than
before. Clearly, the federal standard has forced mine operators to adopt
deliberate programs ot control respirable dust. It's fair to say that many
operators are making good-faith efforts to keep their working sections in
-38-
-------
compliance. Others, on the other hand, arent't.
The quantitative measure of this effort lies in the data accumulated
from the operator-submitted respirable dust samples submitted to MSHA several
(on the average) times a year. Miners performing certain jobs are required
to wear a personal sampler for a full shift at specified intervals throughout
the year. The samplers are turned into the company at the end of the shift,
and the company sends the sample to MSHA for weighing. Several weeks later
the results are sent back to the operator. If the sample exceeds the standard,
the miner is required to take 10 additional samples until the results indicate
compliance.
A number of flaws in this system have been pointed out.
First, the lag-time between when the sample is taken and when the results
are received is of great that the sampling has little relevance to daily dust
control efforts. Mining conditions change frequently. Without immediate
feedback from the monitoring, sampling results are useful mainly as a basis
for civil penalties and not for dust control. Second, incentives exist for
both miners and operators to falsify sample results. Samplers are noisy and
a nuisance to wear, especially in cramped conditions. Many miners believe
that operators only submit "good samples" and order retakes of the "bad" ones
(that is, those showing excessive dust). Some evidence is available to suggest
that this opinion is well-founded. Some miners report that their countries
weigh the entire sampler after each shift, rejecting those that are "too heavy."
Why, then they ask, should we bother taking samples when the company simply
redoes or falsifies "bad" results?" A "bad" sample means the miner is
required to take 10 more samples, a prospect that encourages him to go along
with falsification. Some miners believe that compliance samples will be used
-39-
-------
against them in future black lung eligibility determinations, and apparently
try to "stuff" the sample to record high dust concentration. MSHA has devised
methods to void samples showing extremely high concentrations of nonrespirable
dust, which, the agency believes, indicates "stuffing." Coal mine operators,
of course, have an interest in submitting compliance samples to MSHA. Such
samples minimize operator inconvenience and avoid the possibility of civil
fines, which, for respirable dust violations, averaged about $150 in 1978.
In one case, two management technicians with dust sampling responsibility at
a Consoldiation Coal Co. mine in Ohio were found guilty—and then innocent—
of deliberate fasification of sample results. Finally, MSHA has not been able
to establish adequate safeguards against sample falsification, which vary from
leaving the sampler in the dinner hole and sample stuffing to operator voiding
of samples. Samples taken by MSHA's own inspectors are even more infrequent
18
and often subject to the same kinds of distortions. While sample data from
operator submissions suggest a 90%+ compliance rate on the days the samples are
taken, MSHA inspectors cited 36% of the almost 5,000 underground sections they
sampled in 1976 for noncompliance. Further, MSHA issues an average of about
2,500 notices of noncompliance and 50 withdrawal orders annually for respirable
dust violations, casting further doubt on 90%+ compliance. As in any other
representative survey, dust sampling may or may not be good reflection of dust
exposure on the 200 or so days each year when sampling is not done.
Several studies have found such weaknesses in the federal dust sampling
program. The General Accounting Office reported:
"...many weaknesses in the dust-sampling program which affected
the accuracy and validity of the results and made it virtually
impossible to determine how many mine sections-were in compliance
with statutorily established dust standards."
GAO said factors that affected sample accuracy were: sampling practices
-40-
-------
used by operators and miners, dust sampling equipment, weight loss of sampling
20
cassettes, and weighting of cassettes by MESA and cassette manufacture's.
A National Bureau of Standards (NBS) study found:
...when the miners and mine operators perform and supervise
the sampling and when the weightings are made in the normal manner,...
the uncertainty (of accurate, actual measurements of dust concentrations)
is estimated to be as large as 31 percent..(Emphasis in the original.)
No follow-up study on the accuracy of the sampling program has been done
since the GAO and NBS reports were released in December 1975. Both investigations
noted that MSHA and NIOSH officials have made efforts to improve.
A recent study of underground mines in East Kentucky found:
Both the interview and the federal dust records suggest that
many dust samples are being collected incorrectly. In some instances,
extra dust has been added; but in substantially more cases, the samples
are too low. One explanation for inaccurrate sampling, of course, lies
in the fact that the mine owners control sampling in their own mines.
Since the penalty for exceeding federal standards may be close to mine,
coal operators have a strong incentive to err in the direction of samples
showing less than the actual dust levels. The 1969 law attempts to
circumvent this possibility by requiring that all samples be collected
by actual miners on the assumption that, since their own health is at
stake, coal miners will have a vested interest in insuring the accuracy
of samples taken at their work place. For various reasons, however,
that assumption has proven wrong."22
Sharp found 27 percent of the 680 face and high-risk samples he examined were
0.1 or 0.2 mg., which are generally considered to be impossibly low. (Those
readings represent dust levels in fresh air.) About 23 percent of equipment
operators' samples were also found to be too low to be realistic. Operator
attitude toward the sampling program has an important effect on sampling accuracy,
Sharp concluded.
These studies as well as anecdotal evidence suggests that the federal dust
sampling program is probably not a reliable indicator of daily respirable dust
exposures. The implication is that it is possible and probably likely—that many
miners are regularly exposed to illegal and unhealthy dust concentrations. It is
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impossible to say how high daily exposure is in every mine or how often compliance
is achieved. From the perspective of occupational health policy, it is unjustifiec
to believe that future prevalence of respiratory disease in coal miners can be base
on the assumption that most mines are in daily compliance with the federal standarc
For these reasons and others, MSHA has proposed shifting from personal to area
dust sampling. Some of the unreliability in dust data may be eliminated through
this change, MSHA believes. MSHA has not proposed that control of the sampling
program be altered or that the lag-time problem be addressed. In response, the
United Mine Workers (UMWA), has instead proposed to MSHA that a miner-elected,
MSHA-trained miner be in charge of sampling at each mine. The union has suggested
that area samples be taken by recording dust monitors capable of providing
instantaneous printed readouts. These monitors would enable miners and foremen
to immediately correct dangerously high exposures. Further, the union has
suggested that personal sampling be continued to determine compliance with
federal law. Miner control and immediate feedback would, the UMWA says, make
sampling more effective in protecting miners' health. The coal industry has
opposed area sampling and miner participation. MSHA has not yet reached a
final decision on the matter.
While respiratory disease is the most serious job-related health hazard
miners face, other exposures—to noise, fumes, gases, stress, whole-body
vibration, cramped conditions, hot and cold environments and wet working
conditions—also exist. Hearing surveys indicate that miners experience more
hearing loss than expected, although the degree to which hearing loss is
23
job related is disputed. Noise levels for certain mining jobs have been
found to exceed the 90 dba federal limit. Available noise sampling data is
not very accurate, MSHA officials admit. Often, many of the hazards noted
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above occur simultaneously. Occupational health research has not been able
to analyze the long-term effects (including synergisms) of multiple hazards.
Future investigation may begin to develop tools for multi-variable analysis.
The need for this kind of research is clear: it is how a coal miner is affected
by his work.
ENVIRONMENTAL HEALTH EFFECTS OF COAL MINING
Coal mining—as distinct from coal combustion—affects the air, land and
water where it occurs. In this discussion, a distinction is drawn between
mining's adverse effects on the environment and those on human health stemming
from environmental degradation. This overview is limited to the latter. ,
AIR
Fugitive dust is a problem in some surface mines. Recent federal regu-
lations require mine operators to develop fugitive-dust control plans and
24
implement them. Coal-truck haulage also creates fugitive dust, (as well
as significant safety hazards). Since much coalfield housing is squeezed into
narrow valley floors adjacent to coal-haul roads, fugitive dust is an import-
ant health issue to local residents. Often haulage-dust combines blow-off
or spillage from the coal with whatever dust (dirt and coal) is disturbed by
traffic flow.
Noxious fumes from burning coal-mine refuse piles are probably mining's
most substantial air-borne health hazard. A survey done by the U. S. Bureau
of Mines in 1968 found 292 fires burning in coal refuse banks, principally
25
in Appalachia. Most of these—132—were found in West Virginia. Smoke,
particulates, toxic and noxious gases are released by burning coal-refuse piles.
Gaseous emissions from these waste piles were surveyed in 1968. These data
are found in table 7. Coal-waste piles alone generated at least 1% of the
nation's total of all carbon monoxide, sulfur oxide, nitrogen oxides and
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particulates. As these piles are concentrated in the Appalachian coalfields—
and usually within steep-sided valleys—their potential health impact on local
populations is amplified. More than 90,000 persons, for example, lived within
26
three miles of burning gob piles in West Virginia alone. In 1940,
TABLE 7
GASES EMITTED INTO ATMOSPHERE FROM
BURNING COAL REFUSE BANKS IN 1968
Emissions Percent of
Gas (Million Tons) Total
Carbon Monoxide
Sulfur Oxide
Hydrocarbons
Nitrogen Oxides
Particulate
1.2
.6
.2
.2
.4
1.2
1.8
.6
1.0
1.4
SOURCE: Nationwide Inventory of Air Pollutant Emissions, 1968
National Pollution Control Administration, AP-73» August, 1970.
several doctors testified that sulfur dioxide emitted from burning piles located
1-1/4 miles from Triadelphia, W VA., was sufficient to cause severe problems
27
to the town's residents. The author is not aware of any current epidemio-
logical study of respiratory effects associated with burning gob piles. New
surface mining regulations require that coal-mine waste fires be extinguished
by the mine operator in accordance with an approved plan. Orphan piles may
continue to be a source of concern.
Blasting from surface mining is a third air-related hazard. Residents
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living adjacent to strip mines have been injured by rocks and debris striking
them or their homes. In one case, a 1000-pound boulder reportedly flew 50
feet and crashed into a Floyd County, Kentucky house injuring a woman's hand.
The Janis Grear Mine paid $4,700 in property damage, but nothing for personal
28
injury in this case. Blasting noise is also a nuisance. Mining noise has
been addressed in the final surface mining regulations which established noise
limits and for mining and set up other blasting restrictions.
LAND
The two most serious health hazards from mining's impact on land are
surface subsidence from underground mining and dangers related to the dis-
posal of coal-refuse.
Subsidence is a familiar problem throughout much of coalfield West Virginia,
Illinois and Pennsylvania. When underground mining occurs, pillars of coal are
29
left to support the roof. Over time, these pillars erode and weaken. When
deterioration is extensive, the strata above the mined-out area will collapse
into the void, lowering portions of the surface by the width of the coal seam
or less (a few inches to 6 feet or more). Property damage often results and
residents may be injured. A recent survey done by the General Accounting Office
reported that mine subsidence results in nearly $30 million in property damage
annually. GAO estimates that two of the 8 million acres undermined in the
U. S. have already subsided to some degree, and another 2 million acres will
subside by 2000 when total undermined acreage reaches 10.5 million unless adequate
preventive measures are taken. No reporting system exists to tabulate injuries
9AA
or pyschological stress related to subsidence. Subsidence-related injuries
are not reported to any federal agency. The always present danger of subsidence
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impedes the development of non-coal industry and community facilities in the
coalfields. The opportunity costs of subsidence are significant. Feasible
techniques are available to minimize subsidence by backstowing waste material—
either flyash from coal combustion or the coal mine waste itself. Coal operators
have not backstowed waste material because of the dollar costs involved.
Dr. Robert Erwin, head of the West Virginia Geological Survey, said
recently that thousands of West Virginian homes are being ruined and lives
30B
threatened by subsidence from abandoned underground mines. "'I wouldn't rule
out the chance of a youngster falling into a crevice caused by subsidence in
some places."1 A 7-year-old boy was reported drowned in Seneca, Illinois,
when "...an abandoned mine shaft filled with water collapsed in his back
yard."
Mining produces much refuse, which, in the past, has often been disposed
of haphazardly and with little attention paid to environmental or health
considerations. This refuse consists of materials extracted along with the
coal which are separated and discarded on the surface. (Other refuse is produced
from coal washing and preparation, together with sludge from treating acid-mine
waters and scrubbing coal's flue gasses.) About 107 million tons of mine refuse
was produced in 1975, (table 8). The fraction of run-of-the-mine material dis-
carded in preparation is now about 29%. Many coal consumers are demanding even
cleaner coal. More than 3 billion tons of mine waste are estimated to have been
piled on the surface over the years in some 3,000 to 5,000 refuse banks.
Apart from degrading surface water quality, the main hazard from refuse
piles comes from their physical instability. Erosion and landslides can result
when refuse is not graded, compacted and reclaimed. Few engineering or re-
clamation regulations applied to these banks—known as "gob" piles of "slag"
heaps—before the 1970s. In some cases, the refuse was heaped into jerry-built
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dams to create settling ponds used in coal preparation. Following the collapse
of a Pittston Corp.-owned gob dam on Buffalo Creek, W. VA in 1973 that killed
125, a survey found at least 30 other dams to be imminent flood hazards and
31
another 176 to be potential hazards. Federal agencies and coal operators
have made an effort to safen these dams since the survey. Existing and new gob
dams are now covered by recently promulgated OSM regulations. Existing impound-
ments are likely to present more of a hazard to human life than those built
in the future because of the new engineering requirements. The degree of danger
these dams present today is difficult to estimate. Fear of dam collapse is
often expressed by citizens living downstream from an impoundment. The lack
of housing options in the coalfields inhibits ready evacuation of downstream
areas.
Table 8—Mechanically Cleaned Bituminous Coal and Lignite'
(thousand short tons)
Year
19.10
1945
1950
1 °55
1S56
is 57
1658
1059
1950
1961
1962
1953
1964
1965
1966 ..:
1957
1968
1969
1970
1971
1972
1973
1974
1975
Total raw
coal
moved to
cleaning
plants
115.692
. . . 172.899
238.391
. . . 335.458
359 378
376,546
320.898
337.136
337686
328.200
339,408
362.141
388.134
. . 419.046
435.040
. . 448.024
438.030
435,356
. . 426.606
361.168
398,678
397,646
363.334
374,094
Cleaned
by wet
methods
87.290
130.470
183.170
252.420
268.054
279.259
240,153
251.538
255,030
247.020
252.929
269.527
288.803
306.872
316.421
328.135
324.123
315.596
305,594
256.892
281,119
278.413
257,592
260,289
Cleaned
by
pneumatic
methods
14.980
17.416
15,529
20,295
24.31 1
24,768
18.882
18.249
18,139
17.691
18704
19,935
21 ,400
25,384
24.205-
21,268
16.804
19,163
17,855
14,506
11,710
10,505
7,557
6,704
Total
cleaned
102,270
147,886
198.699
272.71 1
292.366
304.027
259.035
269 767
273 ".69
264,711
271,633
289,462
310.203
332.256
340.626
349.402
304.923
334.761
323,452
271.401
292,829
288,918
265.150
266.993
Total
produc-
tion
460.771
577.617
516.311
464.633
500,874
492,704
410,446
412.028
415.512
402.977
422.149
458,928
486.998
512.088
533.881
552.626
545,245
560.505
602,936
552,192
595,387
591,737
603.406
648,438
Percent
of total
production
mechanically
cleaned
22.2
25.6
385
58.7
58.4
61.7
63 1
655
657
657
643
631
637
64.9
63.8
63.2
62.5
59.7
53.6
49.1
49.2
48.8
43.9
41.2
Refuse
resulting
in
cleaning
process
13,422
25,013
39,692
62,743
67,013
72.519
61 ,863
67,351
65,517
63.489
67,775
72.679
77,931
86,790
94,414
98,624
97,107
100.593
103,159
89,766
105,850
108,728
98,184
107,101
Percent
refuse
of raw
coal
11.6
14.5
16.6
18.7
18.6
19.2
19.3
20.0
194
194
20.0
20.0
20.1
20.1
21.7
22.0
22.2
23.1
24.2
24.9
26.5
27.3
27.0
28.6
8 U.S Bureau of Mines Yeartxxx. various years
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WATER
Mining can seriously degrade the quality of ground and surface water in
mining areas. In addition, some evidence shows that stream siltation in
Appalachian watersheds caused by surface mining has increased the threat to
human safety and health from flooding.
Ground waters, which are often tapped for residential purposes including
drinking, can become contaminated from mining activity. When sulfur-bearing
coal is exposed to air and water, a chemical reaction occurs forming sul-
furic acid and iron. Heavy metals locked into the coal as trace elements tend
to dissolve in the lowered pH, adding metal ions such as aluminum, manganese,
zinc and nickel to the drainage. Acid mine drainage can contaminate ground
water when it seeps into acquifiers via joints and fractures in the rock or
through direct interception of the aquifierpi" When a mine is above the water
table, acid seepage can occur. When below, water can drain into the mine and
lower water tables and dry up wells. Mine-related blasting can dislocate
aquifiers. Mining and reclamation can change the permeability of surface soil
and rock strata, and alter the rate of groundwater replacement.
Acid mine drainage is a problem more commonly associated with surface
waters. The National Strip Mine Study prepared by the U. S. Army Corps of
Engineers in 1974 estimated that more than 10,000 miles of Appalachian streams
22
were significantly affected by mine drainage. About 6,300 miles of Appalachian
streams were continually polluted by acid drainage, representing about 93 percent
of the Nation's total. Northern Appalachia contains many of the polluted water-
ways. Acid drainage from underground operations—many of them abandoned—accounts
for pollution in the Basins of the Monongahela, Allegheny, Susquehanna, and North
Branch of the Potomac. The Environmental Protection Agency reported almost 20
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percent of the total stream miles in the Monogahela Basin are polluted by acid
drainage.
Acid surface water can be unfit for human consumption, expecially when
34
concentrations of heavy metals—some of which are carcinogenic—are high.
As water treatment and central water systems are not well-developed in many
coalfield areas, the health hazards of contaminated drinking water are signifi-
cant for many families. Compliance with recent regulations should minimize
acid drainage from operating mines, but abandoned mines will continue to
create acid drainage.
In mountainous regions, surface mining has frequently created substantial
siltation in adjacent watersheds. Before regulations were in effect, operators
often pushed unwanted soil, called "overburden" or "spoil," down the mountain
side. Rain eroded these unstable slopes causing landslides and stream siltation.
Research in Kentucky indicates that sentiment yields from strip-mined lands
35
were as much as 1,000 times that of undisturbed forests. In the Middle Atlantic
states, on the order of 30,000 tons per year of suspended solids have been
attributed to surface mining and 17,500 tons per year in the midwest. Re-
clamation of abandoned strip mines and compliance with OSM regulations in
active operations should reduce this impact. However, since much future
siltation from mining will occur in watersheds already heavily loaded by
past mining practices, the margin available for additional siltation may be
very small, particularly in many narrow Appalachian valleys.
Flooding, of course, is the principal danger from heavily silted streams
in that area. Much controversy exists over whether strip mining increases
surface runoff and amount, thereby silting stream channels and increasing
flooding potential and danger. Industry argues that surface mining often makes
affected land more permeable, reducing runoff and decreasing stream siltation.
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Steep terrain, forest fires, heavy rainfall, housing, roads and other construction
near natural stream beds are the principal causes of flooding in Appalachian
watersheds, industry argues.
Most state or Federally funded studies, however, suggest that surface
mining (as practiced before the 1977 law was enacted) contributes to stream
siltation and to flooding. The Kentucky Department of Natural Resources,
for example, studied the 1977 floods in East Kentucky and found:
The preponderance of evidence from previous studies indicates
that active, unreclaimed or improperly reclaimed surface mined
areas increase runoff.37
The claim that surface mining decreased flooding by increasing the porosity
of the affected land was challenged by Drnevich et. al:
One of the more startling findings was that the pereability
of the mine spoils was about four orders of magnitude lower
than what might be predicted based on particle size distri-
bution curves. This low pereability was attributed to the
breakdown and weathering of the soil during the compaction
and wetting processes.-'"
A recent case study of flooding in Harlan County, KY, acknowledged
that road construction, heavy rainfall and other factors contributed to the
devastating floods there in 1977, but found that these factors are "...small
39
in comparison to surface mining." Detailed examination of local watersheds,
Hardt says, indicates that "...surface mining has had a significant effect
on flooding in the county." This study suggests that surface mining increased
the April 1977 flood level at Harlan at least three feet and was responsible
41
for at least $3 million of the damage from the April flood. A preliminary
estimate of the dollar costs of the 1977 flooding in East Kentucky was $175.1
42
million.
Apart from the dollar costs incurred by public agencies and private
interests,local residents are killed, injured and psychologically affected
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by flooding. In the 15 East Kentucky counties flooded in 1977, the Red Cross
found 10 flood-related fatalities, 2,255 persons injured or made ill, and 132
persons hospitalized. More than 9,700 families suffered property losses
and more than 4,500 homes and businesses were completely destroyed or suffered
43
major damage. Several investigators have reported emotional traumas caused
44
by the Buffalo Creek disaster in Logan County, W VA. Children and adults
who have experienced flood trauma spend a great deal of energy and time
reconstructing their lives and coping with the stress of readjustment in
later years. Fears, phobias, sleeplessness, nervousness, irritability,
fatigue, physical illnesses (headaches, backaches, ulcers), depression,
marital tensions, and alcoholism have been identified as flood-caused
legacies among survivors.
!!• Mining's Indirect Effects on Health Care Capabilities in the.. Coal fields
The impact of occupational disease and injury and the impact of environ-
mental health hazards is determined in part by the facilities and services
that exist locally which are capable of preventing these problems and treating
them when they occur. This capability consists of a network of health-related
institutions, personnel, services and perspectives that plays an active role
in both prevention and treatment. Often, in coalfield Appalachia, a high level
of adverse health impact coexists with an underdeveloped infrastructure for pre-
vention and care. Both sides of the balance sheet are shaped by the general
quality of life—living conditions, housing stock, personal income, community
development and so on—that is found.
Some of these factors in Appalachia have changed markedly over the last
decade, while others remain the same.
-51-
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Substandard living conditions and inadequate public services have existed
in coalfield communities for decades. Journalists, novelists and social
scientists have all reported the dimensions and subtleties of the problems
45
there. It is also true, of course, that some conditions have changed for
the better within the last decade. Coal miners who work a full year can earn
$20,000 or more. The rise in coal prices that began in 1970 and increased
spectacularly in 1973-1974 following the OPEC embargo made rich dozens of
coal entrepreneurs. Federal disability benefits for black lung victims and
higher UMWA pension benefits. Spendable income in the coalfields has risen
since 1970 because of higher wages. The depression that beset Appalachia
throughout most of the 1950s and 1960s ended for many working miners and their
families, although this region continues to have a sizeable population of low-
and fixed-income citizens.
Yet, as in many countries of the Third World, indices of economic growth
such as personal per capita income do not necessarily reflect proportional
gains in public economic development (measure in terms of adequacy of community
services and institutions, public health, and long-term economic security). The
decoupling of economic growth from economic development in the Appalachian
coalfields may have significant consequences in the long-term future as coal
resources are extracted and economic diversification does not occur.
The role of coal production is central to the development of under-develop-
ment in Appalachia. Poor market conditions and cut-throat competition squeezed
the coal industry for most of this century leaving as a by-product severe under-
capitalization of private and public infrastructures in communities there.
Low wages and the company-town system prevented miners from purchasing and
building adequate housing. The lack of effective taxation on coal production
and undeveloped minerals prevented coal towns and counties from developing
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good schools, water and sewage services, recreational facilities and many other
public services.
Absentee ownership of coal resources and coal companies drew profits away
from the communities where they were made, leaving them starved for capital.
The most recent study of Appalachian capital needs found that energy development
is "...likely to be the source of about one-fourth of Appalachia's public
investment shortfalls ...somewhat less than $200 million..." during the 1977-
47
1985 period. Total private investment requirements to support adequately
Appalachian energy development will total about $6 billion, of which about 25%
will be demanded from local financial institutions.
This report said:
Serious shortfalls are likely to occur in the availability of
private financing for housing... and ...overall capital prob-
lems are most severe in the coal mining areas of eastern Kentucky,
the Central Appalachian portion of West Virginia, southwestern
Virginia and eastern Tennessee where the need is created by
nuclear power-plant construction rather than coal development.
...past deficits in public facility provision and maintenance
are not likely to be overcome by future Appalachian energy
developments. In some significant cases, new Appalachian
energy development will not generate enough revenue or tax
base—in the right places—to cope with near-term energy
accommodation problems.^
For these reasons and others, diversified economies never developed in
much of the Appalachian coalfields, thus chaining them to the whimsies of
coal's boom-bust cycle and protracted demand stagnation. Today, the con-
sequences of these patterns are apparent. Public services—roads, schools,
medical care, governmental capability—are frequently inadequate leaving
communities incapable to taking advantage of the benefits of future coal
growth. Where coal mining dominated local economies, the social and economic
problems seem more pronounced and the capability of responding to growth less
evident. Several recent studies have described the connection between con-
-53-
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centrated land ownership and inadequate taxation revenues on one hand with
49
extensive community needs on the other.
These larger social and economic patterns determine the kind of public
health measures and treatment capability available to coalfield residents.
For example, absence or inadequacy of water and sewage treatment facilities
is an important factor in preventive health. In Raleigh County, W VA, one
public health official told an interviewer from the University of Kentucky
that the only thing standing in the way of a typhoid epidemic breaking out in
some sewage-befouled hollows was the acid mine drainage that killed the bacteria.
The medical plan negotiated between the United Mine Workers of America
(UMWA) and the Bituminous Coal Operators' Association in 1978 instituted co-
payment on physician care. This change is likely to reduce doctor visitations
and preventive care. The UMWA Funds have also ended negotiated retainer re-
lationships with several dozen miner-oriented clinics and hospitals, forcing
them to cut services. Although West Virginia has begun to increase the
assessed value of undeveloped coal property, it is doubtful that this will be
able to produce enough tax revenue to help this network of health providers.
Coal companies are challenging higher tax bills in several counties.
Conclusion
Most observers feel that coal production will increase steadily over the
next 20 to 30 years, although demand limitations for certain kinds of coal will
continue intermittently. In light of this radical break with coal's past, it
seems imperative to mine coal differently than before. Many externalities have
been regulated by federal legistlation since 1969. But the adequacy of some
current occupational and environmental standards are questioned, and the degree
of compliance and enforcement is moot. Industry has not accepted occupational
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and environmental regulation gracefully. A spirited, well-financed campaign
against "excessive" regulation fills the coalfield media. The National Coal
Association recently submitted to the White House a 32-page list of federal
policies and regulations it wanted changed to unleash coal production and
combustion.
The patterns of the past need not—and should not—be repeated as coal
demand improves. Five general principles related to occupational and environ-
mental health can be set forth to guide responsible coal development. First,
production costs—occupational, environmental and social—should be fully
internalized. Second, it follows that coal prices—as well as the price of
other fuels—should not be artifically low and should reflect the true costs
of the product. Third, a different social calculus for apportioning economic
benefits between coal developers and local communities needs to be negotiated.
Fourth, momentary disruptions in oil and gas supplies should not be the pre-
text for turning the coalfields into a national sacrifice area through re-
laxing necessary occupational and enviornmental regulations on coal. Finally,
a wide spectrum of local citizens should participate in planning local coal
development—its extent, pace and conduct. In the past, these decisions were
made by private interests concerned only with their own ratios of costs to
benefits. Since mining scatters many kinds of costs and benefits in local
communities, those affected have a right to participate in the economic and
political decisions that shape the quality of their lives.
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REFERENCES AND NOTES
Mining, Enforcement and Safety Administration, Injury Experience
in Coal Mining, 1975. (Washington, D. C.: MESA/Department of the Interior,1978).
Mine Safety and Health Administration "Coal-Mine Injuries and Worktime,"
1978, p. 4.
3
When MESA was transferred from the Department of the Interior to the
Department of Labor in the spring of 1978, it was renamed the Mine Safety
and Health Administration (MSHA). The insertion of "health" into the agency's
name may indicate a renewed concern for the occupational health problems
in mining.
4
MESA, Injury Experience in Coal Mining, 1975, p. 125.
Ibid., The 1969 disabling freqency rate for all coal both underground
and surface was 41.76.
Data supplied by MSHA.
It should be added, however, that the federal accident reporting require-
ment was tightened in the 1970s so trend data may conceal real improvement.
On the other hand, it is difficult to estimate accurately the extent of under-
reporting and undercounting of accidents. Tighter reporting requirements may
actually stimulate less accurate reporting. Numerous other weaknesses in the
federal data harass those who have tried to make sense of it.
Q
Howard Rockette, Mortality Among Coal Miners Covered by the UMWA
Health and Retirement Funds, (Morgantown, W.VA: NIOSH/Alosh, 1977).
9M. Jacobsen. S. Rae, W.H. Walton, and J.M. Rogan, "New Dust Standards
for British Coal Mines," Nature, Vol. 227, August 1, 1970, p. 447.
M. Jacobsen, "Dust Exposure and Penumoconiosois at 10 British Coal
Mines," a paper presented at the Vth International Pneumoconiosis Conference,
Caracas, Venezuela, October 2 - November 3, 1978.
See OTA, The Direct Use of Coal for a brief discussion of some of these
questions. Also James Weeks, "Review of Scientific Data for the U.S. Standard
for permissible Exposure to Coal Mine Dust," OTA contractor report, November
1, 1978.
12Telephone interview with Harlan Amandus, ALOSH, April, 1979. Fifty to
sixty percent of the miners X-rayed in round 1 were not X-rayed in round 2.
Progression in those who were not X-rayed in round 2 is likely to be considerabl;
higher given the high rate of mine-worker retirement in these years. ALOSH has
not tried to evaluate the reliability of MSHA's dust samples, the majority of
which indicate compliance with the 2 mg. standard.
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13
Donald L. Rasmussen, "Breathlessness in Southern Appalachian Coal Miners,"
Respiratory Care, Vol. 16, No. 2, March-April, 1971.
14
The 1969 Coal Act—PL 91-173, Title IV, Part A~ provides "black lung
benefits" to "coal miners who are totally disabled due to pneumoconiosis
and to the surviving dependents of miners whose death was due to such disease."
"Black lung benefits" are awarded to victims of penumoconiosis, which is
defined as a "chronic dust disease of the lung arising out of employment in
an underground coal mine." (Surface miners and othe coal workers are also
eligible for benefits.) Between 1970 and December 31, 1977, 421,000
compensation awards were granted by the Social Security Administration and
Department of Labor. This represents a number equivalent to the entire
coal-miner workforce in 1950. Obviously, the number of awards for exceeds
the prevalence rates established for CWP by epidemiological surveys and
analysis. This suggests that federal officials have defined compensable CWP
to include "black lung disease." It may also imply that the accepted CWP
prevalence rates are far too low. And it may imply that the eligibility
standards have been stretched to include a very wide range of lung impairments
some of which undoubtedly, are made worse by cigarette smoking.
15
Both NIOSH and OTA excluded retired miners from their calculations.
If retired miners were included, the number of CWP cases would increase greatly.
16
Donal P. Schlick and Nicholas L. Fannick, "Coal in the United States,"
in Marcus M. Key, Lorin E. Kerr and Merle Bundy, Pulmonary Reactions to Coal
Dust (New York: Academic Press, 1971), p. 21.
17
Telephone interview with Larry Beaman, Office of Assessments, MSHA,
February, 1979.
18
For example, MSHA inspectors are often made victims of what is known
as "the penetration game." This occurs when a sample is being taken—either
by the worker or by the MSHA inspector—on a continuous miner machine. When
a foreman orders the operator to take abnormally shallow cuts into the coal
face, exposure to respirable dust will be lessened considerably. However,
since this technique—the penetration game—reduces production, it is only
used when samples are taken, miners and MSHA inspectors say. MSHA inspectors
do not have authority to order deeper—that is, normal cuts.
19
General Accounting Office, Improvements Still Needed in Coal Dusting-
Sampling Program and Penalty Assessments and Collections. December 31, 1975, p.
2°Ibid., p. 15.
21,
National Bureau of Standards, An Evaluation of the Accuracy of the Coal
Mine Dust Sampling Program Administered by the Department of the Interior, A
Final Report to the Senate Committee on Labor and Public Welfare. (Dept. of
Commerce, Washington, CD, 1975, p iii.
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22
Gerald Sharp, "Dust Monitoring and Control in the Underground Coal Mines of
Eastern Kentucky," Masters Thesis, University of Kentucky, November 1968, p. 4.
23
NIOSH, Survey of Hearing Loss in the Coal Mining Industry (Washington, D.C.:
HEW/NIOSH, 1976); J. A. Lamonica, R.L. Mundell and T. L. Muldoon, Noise in Under-
ground Coal Mines, (Washington, B.C.: Interior/MESA, 1971); and Thomas G. Bobick
and Dennis A. Giardino, The Noise Environment of the Underground Coal Mine (Wash-
ington, D.C.: Interior/MESA, 1976).
24
Regulations promulgated by the Office of Surface Mining Reclamation and
Enforcement, Title 30, Part 816.95.
25
U. S. Bureau of Mines, Coal Refuse Fires, An Environmental Hazard
(Washington, D.C.: Interior/USBM, 1971).
o /*
Ibid., p. 21.
27
From trial records, briefs of counsel, The Board of Commissioners of
Ohio County v. Elm Grove Mining Co., 122 W. Va. 422, 9 S.E. 2nd 20, 813 (1940).
28
"Conference Held on Strip Mine Blasting," Mountain Life and Work, May
1978, p. 27. A report of the proceedings will be available in June, 1979
from Appalachian Science in the'Public Interest, Corbin, Ky.
29
The exception to this pattern occurs when longwall mining systems—which
employ controlled subsidence as part of the extraction process—are used. Longwal]
mining accounts for only 4% of total underground production, however.
30
General Accounting Office, Alternatives to Protect Property Owners from
Damages Caused by Mine Subsidence, February 14, 1979. Much of the GAO's data
was derived from a 1977 contractor's report prepared for HUD.
30AAppalachian Research and Defense Fund, Disposing of the Coal Haste
Disposal Problem (Charleston, W.VA: Appalachian Research and Defense Fund, 1973).
30BErwin quoted in Steve Mullins, "Sinking Mine Tunnels Plague Homes in
W.VA," Charleston Daily Mail. January 15, 1979.
31U. S. Corps of Engineers, Department of the Army, The National Strip
Mine Study, Vol. 1. Summary Report, 1974.
31AOTA, Direct Use of Coal, p. 237.
32U. S. Army Corps of Engineers, The National Strip Mine Study (Washington,
D.C.: Department of the Army, 1974).
33Appalachian Regional Commission, "Challenges for Appalachia: Energy,
Environment and National Resources" (Washington, D.C.: Appalachian Regional
Commission, 1976), p. 497.
34Little, Inorganic Chemical Pollution of Freshwater, EPA, 1971.
35C. R. Collier, R. J. Pickering, J. S. Musser, "Hydrologic Influence of
Strip Mining," U. S. Geological Survey, Professional Paper 427-C, 1970.
36West Virginia Surface Mining and Reclamation Association, "Report on
the April Floods" (Charleston, W.VA: West Virginia Surface Mining and Re-
clamation Association, 1977).
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Kentucky Department of Natural Resources, "The Floods of April—A
Report on the April 1977 Flood in Southeastern Kentucky," (Frankfort,
Kentucky: Kentucky Department of Natural Resources, 1977).
38Vincent P. Drnevich, G. Perry Williams and Ronald J. Ebelhar,
"Geotechnical Properties of Some Eastern Kentucky Surface Mine Spoils,"
Proceedings of the Ohio River Valley Soils Seminars,Lexington, Kentucky, 1976,
39Jerry Hardt, "Harlan County Flood Report," (Corbin, Kentucky; Appalachia--
Science in the Public Interest, 1978), p, 42,
4°Ibid., p. 4.
41Ibid., p. 47.
42A1 Riutort, Randall Lawrence, and Janet C. McCarty, "Southeast Kentucky's
April 1977 Floods: The Cost of Recovery" (Frankford, Kentucky: Kentucky De-
velopment Cabinet, Governor's Economic Development Commission and the Appalachian
Regional Commission, 1977), p. 2.
43Ibid., p. 47.
44See, for example, Kai Erikson, Everything in Its Path (New York: Simon
and Schuster, 1976).
45
Among the most recent surveys of conditions in the Eastern coalfields are:
OTA, The Direct Use of Coal, Chapter VI; Kendrick and Company, "A Pleasing Tho'
Dreadful Sight": Social and Economic Impacts of Coal Production in the Eastern
Coalfields (Washington, DC: Office of Technology Assessment, 1978); Heln Lewis,
et al., Colonialism in Modern America; The Appalachian Case (Boone, NC:
Appalachian Consorium Press, 1978).
46
But thousands of miners worked short weeks or not at all in 1978 following
a 3-1/2 month-long contract strike. Poor market conditions for certain kinds of
Appalachian coals coupled with a prolonged strike by workers of the N&W Railroad—
the major coal-hauling line in central Appalachia—contributed to the layoffs.
A few companies shut down inefficient operations or laid off workers to increase
productivity. Underground miners worked an average of 220 to 225 days annually
in 1976-1977, but only about 200 days in 1978.
47
CONSAD Research Corporation and Denver Research Institute, Capital Impacts
of Energy and Energy-Related Development in Appalachia (Washington, D.C.:
Appalachian Regional Commission, 1978), p. pp. xvi-xvii.
Ibid., p. xxi.
AQ
Davitt McAteer, Coal Mine Health and Safety: The Case of West Virginia
(New York: Praeger, 1973); Tom Miller. Who Owns West Virginia? (Huntington,
WVA: Huntington Herald Dispatch, 1976); Appalachian Research and Defense Fund,
Coal Government in Appalachia (Charleston, WVA: Appalachian Research and Defense
Fund, 1972).
5°Kendrick and Co., "A Pleasing Tho Dreadful Sight," comment made to
Rand Bohren, Appendix El.
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One recent study of five clinics by the West Virginia University Department
of Community Medicine found that the financial conditions of the clinics worsened
measurably with the imposition of co-payments. As utilization fell, receivables
rose. Operating deficits were recorded in each quarter studied. Physican staffing
fell by 42% from July, 1977 through September, 1978. Non-physician staff de-
clined by 25%. Special preventive health programs were eliminated. See Depart-
ment of Community Medicine, (West Virginia University), William Kissick, and
American Health Management and Consulting Corp., West Virginia Primary Care
Study Group; Problems of Reimbursement, November, 1978.
52
Letter from Carl Bagge, National Coal Association to President Carter,
April 3, 1979.
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RESPIRATORY PROBLEMS IN COAL MINERS
By
W.K.C. Morgan, M.D.
Professor of Medicine
University of Western Ontario
Director of Chest Diseases Service
University Hospital London Ontario
London Ontario, Canada
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RESPIRATORY PROBLEMS IN COAL MINERS
An increased prevalence and higher mortality from bronchitis and other
chest diseases were noted in certain occupations including coal mining by
1 & 2
Thackrah and Greenhow in the nineteenth century. The term bronchitis as
used at that time was nonspecific, and in the case of coal miners undoubtedly
covered a variety of diseases including coal workers' pneumoconiosis (CWP),
silicosis, emphysema, tuberculosis, and bronchitis. It was the advent of the
chest X-ray and clinical pulmonary physiology, in conjunction with better
pathological and bacteriological techniques, which made it possible to define
and sort out the relative contributions of the various diseases to the morbid-
ity and mortality experienced by coal miners.
As a result of numerous epidemiological studies which have been carried
out in almost every coal mining country, a clearer definition of the respira-
tory problems seen in coal miners has emerged. It is apparent that the long
continued inhalation of coal dust in high concentrations may lead to two con-
3
ditions, namely coal workers' pneumoconiosis (CWP) and industrial bronchitis.
CWP is best defined as the inhalation of coal dust in the lungs and the tissue's
reaction to its presence. It can be divided into two forms - simple and com-
plicated, which is often known as progressive massive fibrosis (PMF).
COAL WORKERS' PNEUMOCONIOSIS
a) Simple
4
Simple CWP is response to the deposition of coal dust in the lungs. It
is recognized by a suitable history of exposure, usually at least 10 years
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underground, and by the presence of fairly distinctive radiographic appear-
ances. Pathologically it is characterized by the coal macule. This is a
stellate aggregate of dust situated round the respiratory bronchiole. With
prolonged and severe coal dust exposure, the body's defences are overwhelmed
and dust starts to accumulate around the second division of the respiratory
bronchiole. This is accompanied by a little reticulin and occasionally
minimal collagenous fibrosis. Later the smooth muscle in the bronchiolar wall
atrophies and the bronchiole dilates. The latter is often referred to as focal
emphysema and does not extend to the alveoli or major gas exchanging surface.
Simple CWP is divided into categories 1, 2 and 3 according to the profusion
of small opacities in the chest film. Postmortem studies have shown an ex-
cellent relationship between the coal contents of the lung and radiographic
category. Physiologically the high grades of simple CWP may lead to certain
very minor pulmonary function impairments. Thus the distribution of inspired
gas may be slightly disturbed, and the residual volume and alveolo-arterial
gradient minimally increased. Static lung compliance sometimes shows an
increase and in a few instances the diffusing capacity and the pulmonary
arterial tension for oxygen may be slightly reduced. These impairments are
usually only seen in categories 2 and 3 simple CWP, are unassociated with
symptoms and cannot be regarded as disabling.
The importance of simple CWP lies in the fact that it is a precursor of
the development of complicated CWP or progressive massive fibrosis (PMF).
The latter occurs on a background of category 2 or 3 simple CWP and if simple
CWP can be prevented, it follows there will be a decline in the incidence of
PMF. Simple CWP is unassociated with an increased death rate or disability
and is innocuous in itself.
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b) Complicated CWP or Progressive Massive Fibrosis (PMF)
4
This is a different and more serious form of CWP. Unlike simple CWP,
PMF is a response to coal dust plus some other factor or factors as yet
unknown, but possibly immunological. Necessary for its development is a
suitably heavy coal dust burden in the lungs. It will, however, only develop
when the lung has been suitably primed, that is to say when category 2 or 3 is
present. Unlike simple CWP, PMF may develop and progress after dust exposure
has ceased. PMF is characterized by the development of a large opacity greater
than 1 cm in diameter, plus the other changes of simple pneumoconiosis already
alluded to. The large opacity may slowly enlarge and in some instances other
large opacities develop elsewhere in the lungs. The earlier a large opacity
appears the greater the likelihood that it will progress and cause disability
and premature death.
The masses seen in PMF are partly collagenous but the centre is often
composed of calcium phosphates and glycosoaminoglycans, various proteins
4
including hydroxyproline, with only about 20 to 30 percent of collagen. As
the masses increased in size they obliterate the vascular bed and airways.
PMF is subdivided into stages A, B and C according to the size of the large
opacities. A is between 1 and 5 cm in size, B between 5 cm and a third of a
lung field, and C greater than a third of a lung field. Stages B and C are
associated with respiratory impairment and the latter leads to decreased
longevity. Physiologically PMF is characterized by a reduction in lung volumes
and in the diffusing capacity. The conglomerate masses also lead to ventilation
perfusion mismatching and a concomitant increase in the alveolo-arterial grad-
ient for oxygen which may be associated with arterial desaturation. Pulmonary
hypertension develops in stages B and C. Airways obstruction is frequent and
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occurs in the absence of cigarette smoking or concomitant emphysema.
The prevalence and incidence of simple CWP are related to a number of
factors of which the most important is exposure to high concentrations of
5
respirable coal mine dust. Long term studies by the National Coal Board
of Great Britain and by Reisner in Germany have done much to delineate the
6 & 7
risk for various levels of exposure. Jacobsen has looked into the
pneumoconiosis attack rate and likelihood of progression for various dust
levels and has been able to show that provided the dust levels are kept below
3
4.5 mg/M , less than 4 out of 100 miners starting off as category 0 will
6
develop category 2 or above over a period of 35 years. Similar findings
7
have been published by Reisner.
Aside from dust, individual susceptibility is important in the development
of CWP. Not all miners who are exposed to the same dust levels develop CWP.
in addition there are marked regional differences in the prevalence of CWP
which cannot be accounted for by the differences in dust exposure when the
latter is measured gravimetrically. Whether the difference in prevalence rate
is related to the chemical composition or rank of the coal mine remains un-
known but there is some evidence in favor of this hypothesis. Probably more
important is the propensity for certain coals to fragment into many smaller
particles of around 1 micron in size. Thus the mining of certain coals may
lead to a higher proportion of larger particles between 4 to 6 microns, while
other coals may fragment more easily and lead to a greater proportion of
smaller particles of between 0.5 and 2 microns. The latter are recognized
to be more dangerous as far as the development of CWP is concerned. Moreover,
when considering an eight hour dust measurement, it is important to bear in
mind that an almost infinitely greater number of small particles, e.g. around
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1 micron in size as compared to particles of 5 to 5 microns need to be present
to constitute the same gravimetric measurement.
Dust control is important in that it prevents the development of CWP.
Thus were it possible to prevent categories 2 and 3 simple CWP, then PMF
would be virtually eliminated, and it is for this reason that dust control is
essential. Nonetheless, no amount of dust control will lessen the effects of
cigarette smoke-induced disease, and it is pertinent to bear in mind that the
latter is still the main cause of respiratory disability in coal miners.
INDUSTRIAL BRONCHITIS
For many years it has been realized that coal miners have a greater
8
prevalence of cough and sputum than does a comparable population of non-miners.
Furthermore, most studies have shown that miners tend to have a slightly lower
ventilatory capacity than do non-miners. This reduction in ventilatory cap-
acity cannot be accounted for by the presence of pneumoconiosis and until the
last few years the explanation remained obscure. Thus, epidemiological studies
have failed to show a relationship between increasing category of simple CWP
and a decline in ventilatory capacity. Moreover, since there is a relation-
ship between X-ray category and the dust content of the lungs, it can be
inferred that the decrease in ventilatory capacity that is found in miners
cannot be explained by dust deposition, at least until PMF develops. These
apparent anomalies may be explained by two hypotheses:
a) That coal miners develop a form of airways obstruction which is
related to their occupation and dust exposure, but which is distinct from the
bronchitis that is induced by cigarette smoking. The cause of this airways
obstruction could be either emphysema or bronchitis.
b) That differential migration accounts for the differences. Thus were
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the more fit to leave coal mining within the first five or so years, those
who remain would have decreased pulmonary reserve, and this might account for
the lower ventilatory capacity observed.
The second hypothesis is considered first since it has been refuted.
Most studies have shown that it is not the fitter entrants who leave coal
mining, but the less fit and those with respiratory symptoms. The more fit
the man in general, the more likely he is to continue coal mining.
The first hypothesis therefore become more likely, and there is much
circumstantial evidence in its favor. There are a number of arguments which
have been marshalled against the suggestion that emphysema occurs more
8
commonly in coal miners, and these have been alluded to elsewhere. The
hypothesis that coal mining induces a nonspecific form of bronchitis is far
more attractive. Such a hypothesis would explain the observation that there
is often a poor relationship between the symptoms of bronchitis and CWP.
Without dwelling unduly on the methodology of several studies which indicate
that industrial bronchitis is the culprit, long-continued dust exposure has
been shown to lead to cough and sputum and also to decreased ventilatory cap-
8
acity. The airways obstruction which occurs in industrial bronchitis pre-
dominantly arises from involvement of the larger or central airways. Further-
more, there is further evidence to suggest it is the deposition of larger
particles in these airways that leads to the mucous gland hypertrophy and
excessive mucous secretion. Radiographic stigmata are not seen since the
particles deposited in the dead space are removed by the mucocilliary escaltor.
This entity which is a result of long continued deposition of dust in the dead
space is best referred to as industrial bronchitis and does not lead to the
development of emphysema. Finally it must be borne in mind that lowering of
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dust levels when such standards are measured in terms of respirable dust will
not necessarily affect the prevalence of industrial bronchitis, since most
of the evidence suggests that the nonrespirable fraction of dust between 5
and 10 microns is more likely responsible for the induction of industrial
bronchitis than is the respirable fraction of between 0.5 and 5 microns.
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REFERENCES
I. Thackrah, C.T. The Effects of Arts, Trades and Professions and of
Civic States and of Habits of Living on Health and'Longevity.
2nd Edition, Longman, 1832.
2. Greenhow, E.H. Report of the Medical Officer of the Privy Council
I860, Appendix VI H.M.S.O. London 1861.
3. Morgan, W.K.C. and Lapp, N.L. Respiratory Disease in Coal Miners.
Amer. Rev. Res. Dis. 114, 1047, 1976.
4. Morgan, W.K.C. In Occupational Lung Diseases. Chapter 12.
Morgan W. K. C. and Seaton, A. W. B. Saunders.1975.
5. Morgan, W.K.C. Burgess, D.B. Jacobson, G. et a I. The Prevalence of
Coal Workers' Pneumoconiosis in U.S. Coal Miners. Arch Envir. Health
27, 221, I973.
6. Jacobsen, M. Progression of Coal Workers' Pneumoconiosis in Britain
in Relation to Environmental Conditions Underground. Proceedings of
Conference on Technical measures of Dust Prevention and Suppression
in Mines. Luxembourg, October 1972.
7. Reisner, M.T.R. Results of Epidemiological Studies of Pneumoconiosis
in West Germany. Inhaled Particles Ml Vol 2 London Unwin Bros.
1970 Page 921.
8. Morgan, W.K.C. Industrial Bronchitis. Brit. J. Ind. Med. 285, 35, 1978.
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URANIUM MINING - OCCUPATIONAL AND OTHER HEALTH PROBLEMS
By
Joseph K. Wagoner, S.D. Hyg.
Special Assistant for Occupational Carcinogenesis
Office of the Assistant Secretary
OSHA
Washington, D. C.
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URANIUM MINING
OCCUPATIONAL AND OTHER HEALTH PROBLEMS
DR. JOSEPH K. WAGONER
It is appropriate to use as an analogy from the history of the develop-
of uranium bearing ores as an energy source, to look at it as a model for
how we should proceed in the future with regard to health research in re-
lation to energy technologies. I think it is a fair statement to say that
respiratory disease problems of underground miners have been with us since
ancient times. The first indication that there might be problems with
uranium-bearing ores dates from about 1546 when major respiratory disease
problems occurred in miners in the^Hartz Mountains of central Europe. The
specific nature of the respiratory disorder, however, wasn't suspected until
about 1887 when the first clinical evidence emerged that the disorder was
a malignancy. In 1913, about 30 years later, Arnstein reported that of
665 miners in the Schneeberg area who died during the period of 1875 through
1912, 276 or 40% of them died of lung cancer. In 1932, the physicians in
Joachimsthai reported that of 17 deaths among their miners in a one-year
period, 53% were due to lung cancer.
Now these investigators noted three characteristics of the disorder.
One, the long latent period between the onset of mining and death due to
lung cancer; two, the pathologic absence of silicosis; and three, the pre-
ponderance of undifferentiated small-cell carcinoma in the histology.
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They concluded that the most probable cause of these tumors was the radon
present in the air of the mines. They also made note at that time that the
miners themselves had stated that discovery of a rich uranium vein was
always followed some years later by a strongly increased mortality among
themselves. By the 1940's when large-scale mining and milling of uranium
bearing ores started with the United States, for nuclear weapons initially,
this lung cancer experience and its probable relationship to radioactivity
within the mines was fairly well accepted by the independent scientific
community, but little heeded by government or industry.
As a result the Public Health Service in the early 1950's initiated a
major epidemiologic program to delineate the magnitude of hazards associated
with health problems indigenous to the uranium-producing industry. During
the period of the 1950's and 1960's medical examination teams in the
Colorado plateau area of the United States examined about 5,370 miners and
millers. It was in the population of miners that as early as 1962, Archer,
Baldwin, and Cooper showed a statistically significant excess of lung
cancer among the subset of those uranium miners who had at least three or
four years of underground experience. In reviewing the study of the
methods of this study at the NIH in 1962, Dr. Brian MacMahon stated,
"If after the European experience there were any doubts as to the implica-
tion of radioactivity in the etiology of lung cancer, they surely have
been dispelled by the findings to date." Dr. MacMahon further stated that
the data therefore gave an indication that the problems of the American
uranium miners could become a medical disaster that in relative terms could
be as great as the European experience, because of the larger population
at risk.
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In 1964, however, the Surgeon General's Advisory Committee on Smoking
and Health concluded that, "Although the induction of lung cancer by radio-
nuclides is probable in man, the evidence is certainly not as firm as in
animals." It was in that same year that I and other members of the Public
Health Service reported a tenfold increased risk in lung cancer among long-
term underground miners and this excess could not be related to age, smoking,
nativity, heredity, urbanization, self-selection, diagnostic accuracy or
other variables in the mine. Furthermore, for the first time we were able
to show that the mean cumulative radiation dose of the uranium miners with
respiratory cancer was significantly greater than a matched control, matched
on the basis of age, year of initial examination and race and also other
kinds of non-respiratory disease. In 1964, Dr. Saccomanno of Grand Junction
reported that the lung cancer among the uranium miners, in contrast with
controls matched for age, smoking and residence, showed a peculiar distri-
bution with regard to histologic types. They were predominantly undiffer-
entiated small-cell carcinomas that occurred in the more proximal regions
of the lung. In 1965 we reported the demonstration of an exposure-
response relationship between air-borne radiation, as measured by the term
"cumulative working level months," and we demonstrated that this exposure-
response relationship persisted even after adjusting for cigarette smoking.
Now on the basis of these and other data the Department of Labor in
1967 issued an order under the Walsh-Healy Public Contracts Act to limit
the maximum permissible exposure to uranium miners to 3.6 working level
months during any 12-month period, or exposure limit of 0.3 working level
in the mines. This standard was to go into effect sometime in January,
1971. However, as has happened in the past as well as present, this
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proposed stricter standard led to a controversy, to say the least. The
Public Health Service and the Department of Labor were opposed by those
groups both within and without the Government interested in the continued,
uncontrolled exploitation of uranium ores. This debate and controversy
stemmed from two aspects of the data. First was that at that time there
were no data to demonstrate conclusively that anyone exposed to a few
working levels or less had any problem. Of course, there were as yet no
populations studied that experienced that limited exposure rate. The
other aspect was that the early studies had not demonstrated an increased
risk of lung cancer among the non-white miners, nearly all American
Indians, a group who because of their cultural, economic or religious
reasons, used very little tobacco. These findings led some to speculate
at that time that the induction of bronchogenic cancer by radiation in the
absence of cigarette smoking was either very unlikely or nonexistant.
It was speculation on those points that naturally led those with a
special interest in the continued uncontrolled exploiting of uranium to
suggest that maybe mining should be done either by non-smokers, or that if
smokers were to be permitted in the mines * that a low exposure standard
should only be set for those companies wh
-------
exposed at one working level for 12 months per year, within ten years had
accumulated enough exposure to lead already to a risk of lung cancer of
3 to 4 times. In 1971 Lundin also demonstrated that when you adjusted
for cigarette smoking patterns among the uranium miners, it was only
sufficient to account for about a 49% increased risk in the expectation,
yet there were still 62 observed deaths versus 11 to be expected or a
464% increase. At that time Lundin hypothesized that if the latent period
of radiogenic lung cancer was longer in the non-smokers as compared with the
smokers>due to the predominance of promoting effects of cigarette smoke,
that it might be too early to expect any problem in the non-smoking
proportion of the uranium group. Two more recent reports deal with efforts
to test this hypothesis among the U. S. uranium miners, one reported in
1974 at the International Cancer Congress and one by Dr. Archer reported
at the New York Academy of Sciences in 1976.
There were approximately 632 non-white Indian uranium miners, and out
of this group, as determined by the medical examinations and questionnaires
solicited in the period of 1950-51, 1954, 1957, and 1960, fully 437 of
those were reported to have never smoked cigarettes. The other clearly
obvious pattern for those who did smoke is that they smoked very little.
That group, when followed up through 1973, demonstrated eleven deaths due
to respiratory-tract cancer, whereas you would have expected only 2.5 to
occur. That 2.5 expected, I might comment, is fallaciously high due to
the fact that the rates used to generate them were from the Colorado
Plateau population, which had a component of non-white groups other than
Indian. Studies have shown that the Indian populations have a much lower
baseline risk of lung cancer. Among those Indians who had died due to lung
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cancer four had never smoked cigarettes, two had smoked cigarettes only
in the quantity of two or three cigarettes a week, four smoked two to six
cigarettes a day, and only one smoked a pack or more. The interesting
figures here show that the mean induction latent period for those who had
never smoked or smoked very little, that is less than one cigarette a day,
was 18.5 years. When we contrast that with the observations among the
white uranium miners who died from lung cancer, and who had smoked 20
cigarettes or more a day, the mean induction latent period was 13.7 years
for the smoking. Clearly, these results support the hypothesis that non-
smoking merely protracted the interval from the onset of mining to the
induction of the cancer.
These observations have now been confirmed by Axelson and Sundell
in their studies of the Swedish zinc miners, where they have shown an
association of radon-daughter exposure and lung cancer in non-smokers,
and a longer length of induction period for the non-smokers as opposed to
smokers. In 1974 Archer e^ al. demonstrated that, as opposed to matched
controls, matched on the basis of age and cigarette smoking, there not only
was an excess of small-cell undifferentiated tumors in this group but there
was an excess of epidemicid and adenocarcinoma also, but to a lesser degree.
More recently Dr. Archer and his group demonstrated an exposure-response
relationship for radiation and lung cancer for miners within the various
smoking and non-smoking categories, indicating that for each group there
is an increased risk associated with radon-daughter exposures that persists
in the absence of cigarette smoking. Recently, we have seen some more
definitive analysis from Czechoslovakia and these studies have demonstrated
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a statistically significant increased risk in lung cancer in each group
of radon-daughter exposure categories, down to and including 100 to 140
working level months.
Now, what can we say about the problem in uranium miners? We can say
that by 1974 we had a sizable increase of lung cancer; we can also say we
have a sizable increased risk of accidental deaths. More importantly, we
can see now what have been the devastating effects of the very lengthy
period of public debate and denial of the risks that have gone on. In the
same group studied and observed from 1950 through 1974 we now know that the
relative risk of lung cancer is very high. In terms of public health impact,
the cumulative risk has increased steadily: 9.2 excess deaths by 1962,
174 deaths by 1974. We have 114 excess lung-cancer deaths that have
occurred in the study population of 3,000. We now know that as of 1978
there are at least 35 more lung-cancer deaths and 25 have been diagnosed
among those 3000 miners systematically followed up.
Does the problem with mining uranium ores stop at the surface of the
mine? Obviously, we don't have all the data but the indications are that
it may well not. Our original concerns were restricted to the mining
population. However, in 1971 we started looking at what happens to the
group who were involved in milling. One significant finding was an
increased risk of lymphatic cancer in this group.
Finally, can we say that the problems of uranium as a source of energy
cease with milling? I think the evidence is now before us that the answer
to that question has to be no. During the late 1960's and the early 1970's
it became very widespread knowledge throughout the Colorado plateau
areas, that the tailings and waste materials from the milling of uranium
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ores have been used for landfill for housing developments in the Colorado
plateau area. At that time studies had indicated that the radon gases were
emanating through the surface foundations of the houses and that the con-
centrations of radon daughters in some of the buildings were similar to
what was being experienced in the underground mining. We now know that in
Colorado itself seventeen million tons of uranium mill tailings at inactive
and abandoned mill sites are sitting with no regulation. The long-term
health implications of this situation remains to be demonstrated, but from
the data at hand the implications are not reassuring. In that context I
think it is noteworthy that in 1978 the Congress finally passed the Uranium
Mill Tailing Radiation Control Act, which designated the Environmental
Protection Agency to set standards concerning control of past waste disposal
from these mills and earmarked the Department of Energy with responsibility
for implementing that. Recently, there has been a timetable set forth in
the Federal Register of Wednesday, February 28, 1979, with an announcement
by the Nuclear Regulatory Commission, giving the timetable for standards
that will be set to control the waste disposal problems associated with
past and current milling of uranium.
In the context of the underlying theme of this conference, human
costs of energy production, or an assessment of health effects associated
with energy technology, I think three points are clear. Due to the un-
controlled dissemination of waste materials, the human cost of energy
production is not restricted to and within the exclusive domain of the
working population. Due to protracted debate and the long period between
identification of health problems and subsequent control of exposures,
we have and will continue to have a legacy of health effects in the uranium-
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mining industry for years and years to come. The third point is that pre-
mature speculation, which seems to be prevalent in many studies of
occupational health, that the effects obviously have to be due to something
other than the industrial setting, in this particular case smoking, has led
to further delays in the suggestion that we set adequate standards in the
United States.
Two questions are now obviously before us as a society, if I may go
back to the original theme that I addressed. With the uranium-miner ex-
perience as a model, can we as a society afford the years of debate in
assessing the health consequences of future energy technology, while ex-
posures are allowed to take place? Certainly we should not. Second, can
our society any longer permit a lack of separation of powers in its govern-
ment, that is the separation of powers between those who promote a technology
and those who regulate it? The answer to that is certainly no, too. I think
also that the support of research concerning health effects, for example
with radiation, but I suggest in the whole energy technology field, should
no longer be in the hands of those who both promote and regulate a
particular technology.
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DISCUSSION
SESSION I
Dr. Leonard Hamilton, Brookhaven National Laboratory: I
would like to ask Dr. Morgan how he would have coped with
trying to predict the health effects in miners in the period
1985- 1990-2000, if he was involved in an exercise where one
would have to calculate these figures?
Dr. Morgan : That is a good question and I think one has
to consider the various health hazards to which miners are
exposed. If one starts off by considering coal workers'
pneumoconiosis, then there is enough information from the
National Coal Board of Great Britain and from Reisner of
Steinkohlenbergbauvereins of Germany, to calculate the
likelihood of a previously non-dust exposed new miner developing
simple pneumoconiosis. And from that, since the attack rate for
PMF is known for Category 2 and 3 simple pneumoconiosis, one can
predict with a fair degree of accuracy how many men are going to
develop PMF in those particular years. Such predictions always
assume that the dust measurements made by what used to be the
Bureau of Mines and now is MESA are accurate. We now know as a
result of a Congressional inquiry that something like 40% of the
measurements made between 1970 - 1976 were inaccurate. Clearly
there has to be some term of established dust sampling program
with valid measurements. The second thing one needs to consider
is, of course, industrial bronchitis. I really did not have
time to point out in my presentation that the type of dust which
is responsible for the induction of industrial bronchitis
differs from that which is responsible for the development of
coal workers' pneumoconiosis. We know that it is the respirable
fraction between 0.5 and about 6 microns which leads to the
development of coal workers' pneumoconiosis. The evidence would
suggest that it is larger particles, between 5 and 10 microns
which are deposited in the dead space and that lead to the
development of industrial bronchitis. But industrial bronchitis
is nothing like as much of a hazard as is cigarette
smoke-induced bronchitis. Nevertheless, one also needs to be
sampling different sized particles, or better still the total
airborne particulates, to obtain some idea of how to predict the
prevalence and effects of industrial bronchitis. So, there are
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two factors to be considered, both of which are likely to
produce occupationally related impairment, namely the size of
the particle, and the amount of dust that enters the respiratory
tract. The third thing one needs to know something about is the
cigarette consumption of the miners who are currently working.
If one knows this, I think one can draw the necessary inferences
from Fletcher and Peto's work in Britain which shows that about
13 to 15 percent of cigarette smokers will go on to develop
airways obstruction.* I forget the exact number who develop
severe airways obstruction, but these data can be found in the
monograph. Occupational exposure does not enter into this area.
Finally one must honestly think about accidents. This is not my
bailiwick, but clearly there does need to be some attempt made
to limit the number of accidents. Does that give you some idea
of how I would go about it?
Dr. Hamilton: Reasonable. There is a further point I
would like you to clarify and that is this. How would you go
about trying to predict what the effects of this 2 mg per cubic
meter standard is going to be? Given the uncertainty that you
would have stated about measurements. How does one cope with
that?
Dr. Morgan: Quite clearly, one has to have valid dust
measurements before you can make any accurate predictions. At
the time the Bureau of Mines introduced their dust sampling
program there were one or two of us in NIOSH, Dr. Marcus Key
and myself, who suggested that the personnel sampler
measurements should be supplemented by area sampling. We were
not too sanguine concerning the accuracy of the personnel
sampler, since this is dependent on the flow rate of the cyclone
and several other variables. To us some sort of check seemed
desirable. In the absence of valid dust measurements, one can
look at the attack rate and the progression rate of CWP over the
same period. Alternatively utilizing the dust measurements as
far as possible, and from the calculated attack rate and
progression index, one can try and calculate how many miners
will be affected over the next 30 years. In this regard, when I
was at NIOSH we used a group of radiologists for the most part
to look at progression rates. The only trouble was that there
were some radiologists who read twenty times as much progression
as did others, and all read about ten times as much progression
as did the British readers. While I have a feeling that the
British were under-read, I also have a feeling that
epidemiological studies cannot be carried out significantly and
properly in a situation where individualistic opinions reign
supreme. There has to be some standardization and uniformity
among readers. However, radiologists are not always susceptible
to standardization.
* The Natural History of Chronic Bronchitis and Emphysema,
Oxford University Press, 1976.
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Dr . Had ford ; I would like to ask Dr. Seltzer if he would
comment on the accident rate in coal mining. He gave some
numbers that sounded fairly horrendous to me in the area of
safety and accident rates, as they relate to morbidity and
mortality. Would you care to comment, Dr. Seltzer?
Dr. Seltzer: The mortality rate in coal mining, in
underground coal mining, has decreased significantly since 1969.
The main cause of this decrease has been that the multi-victim
disasters which plagued the industry throughout the 19th century
have been reduced significantly. What have not been reduced are
some of the other causes of accidents. What has not been
reduced at all since 1950 is the frequency rate of disabling
injuries. The 1969 Act did not address specifically the cause
of disabling injuries. Data from the Mine Safety and Health
Administration (DOL) in 1977 says that there were almost 15,000
disabling injuries which accounted for, on the average, two
months lost time, calendar tinre. If you take the current
fatality rate and the current disabling injuries rates, multiply
them by the expected number of miners for 1985 and the year
2000, divided according to surface and underground , you can get
the order of numbers I gave you.
I'd like to say something on the health question which is
Dr. Morgan's bailiwick and less so mine. To think that coal
workers' pneumoconiosis is a disease of the past, I think, is to
make a severe error. To say that you have to assume several
things. One is that the two milligram respirable dust standard
is inherently safe. It is not. That standard (2mg/m3) is based
on British research of the 1960's. It is based on a number of
statistical manipulations which do not look very sound in
retrospect. The probablity curves that were constructed with
these data suggested that at two milligrams, one to two percent
of the miners exposed would contract CWP (coal workers'
pneumoconiosis) over a 35-year period. Follow-up studies
released recently say that the probabilities are even higher by
one or two percentage points. The 2 mg standard is not
risk-free. Yet it is more stringent than any other standard in
the world. I think that before you can make the assumption that
CWP is a disease of the past you have to confirm the safeness of
the current standard. The second assumption that is made by Dr.
Morgan and others who think that CWP is a disease of the past,
is that every mine section meets the 2 mg standard every day.
That is, what the Marx Brothers used to call, horse feathers.
Any one who knows anything about coal mining knows that every
section does not meet the 2 mg standard every day. There have
been several studies that have confirmed this. The most recent
study—done at the University of Kentucky— indicated that 21%
of the dust samples surveyed were impossibly low. The study's
author, Gerald Sharp said such measurements were either lower
than or at the level of dust measurements taken outside the
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mine! If you have first-hand knowledge of the mining industry,
you know that there are various ways that both the company and
the miners can falsify dust level measurements. Everyone knows,
including MSHA, that the recorded dust measurements are too low,
and because of that knowledge, MSHA is now considering different
ways of measuring dust. The most important innovation, which
the Mine Workers' Union (UMWA) has proposed, is that miners
control the dust sampling. My hunch is that if that takes
place, you would see more effective dust control than you have
in the past.
Dr. Morgan; May I just comment on two portions of that
comment. If MESA has changed its name to MSHA or something else
then I apologize for being out of date. I don't doubt that by
next year it will have yet another name, another set of
initials, and another set of inaccurate dust data. I would
point out, however, that my figures were not based upon the 1969
data of Jacobsen. Had Dr. Seltzer been in San Francisco two
weeks ago at the International Conference on Occupational Lung
Disease, he would have heard Mike Jacobsen give follow-up NCB
data based upon complete dust sampling up to the end of last
year. He would also have heard Dr. Manfred Reisner do the same
thing for German coal mines. The relationship between the
likelihood of development of CWP and various dust levels as
derived from both the NCB and the German data, are very similar,
in fact they almost coincide despite the fact that the Germans
use a different method of measuring dust, vis. the
Tyndalloscope. Both mathematical models have hardly changed
since the first interim figures were presented at the European
Iron and Steel Community Meeting at Luxemburg in 1972.* The
present data that Jacobson and Reisner have described in the San
Francisco Meeting are in very close accord with those originally
published by the National Coal Board. Moreover, I did not say
that coal workers' pneumoconiosis was a disease of the past.
What I said was that the development of further CWP would be
highly improbable and almost negligible if the U.S. dust
measurements conformed to the standard. However, you are
absolutely right that dust measurements cannot be relied upon,
but that is your problem, sir, not mine.
Dr. George Moore (U.S. Department of Energy in
Pittsburgh): A couple of comments. I would say that coal
workers' pneumoconiosis is a disease of the past. Secondly, Dr.
Seltzer stated that miners' control of the dust hazard could be
a more effective way of dust hazard control. At no time should
an employee or miner be allowed to control the dust hazard. The
experts should control the dust hazard, for example, the people
who have been trained in occupational health and industrial
hygiene (MSHA. OSHA, etc.). They set the standards and at no
*Conference on Technical Measures of Dust Suppression in the
Mines, Luxemburg, 1972.
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time should employees be allowed to control the sampling because
if they do and eventually they come down with some type of coal
workers' pneumoconiosis or eventually black lung, that agency is
held liable. In reference to Dr. Wagoner: In the promulgation
of the rules for carcinogens, it was reported in the paper about
a week ago that you shouldn't have stringent standards for weak
carcinogens. In my opinion once a carcinogen, always a
carcinogen. There should be one standard for all of them. And
a second question, how much political or bureaucratic influence
has been brought to bear in handling of the carcinogens? For
example, some time ago, Dr. Bingham who heads OSHA and Ray
Marshall, the Secretary of Labor, have threatened to quit
because brown lung or byssinosis standard was somewhat
compromised. This was mainly due to the political implication.
So how much political implications have there been in the
setting of carcinogen standards? I ask this question because
the people who are responsible for the health and safety of the
workers should not compromise on an individual's health.
Dr. Wagoner: With reference to your first statement or
question, I'm not quite sure which it is. Yes, I strongly
support the position of making no distinction between a "weak
carcinogen" and a "strong carcinogen." I think it was Marvin
Schneiderman (NCI) who said that in terms of public health
practice if you make a distinction between "weak" and "strong
carcinogens," the "weak" ones will have the greatest public
health impact and if we don't do anything they are probably the
most pervasive in our society. The second point with regard to
the OSHA carcinogen situation and Dr. Bingham's situation, I
prefer to refer that question to Dr. Seltzer or Dr. Y.
Alarie. I clearly do make that statement on that, though. If
we as a society are going to perpetuate a concept of making
societal decisions, then those decisions should be made by
society with full knowledge of all data and with full disclosure
of those decisions out in a forum of society rather than behind
closed government doors. The reason there is no discrepancy
today, is that the tricks that are being used on the days when
the operators wear the samplers are not the same used when MSHA
samples are taken. The main point of the trick is called "the
penetration game," and since there are no coal mines in New
York, I will explain what "penetration game" is. Simply take a
narrower cut, a shorter cut into the coal,.and the miner or a
continuous miner is not exposed to the dust. MSHA has the right
to close something down but it does not have the right to start
something up. If an operator chooses not to run the machine in
the normal way, or chooses not to run the machine at all, MSHA,
on the day it did take the sample, cannot dictate to the section
working.
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On the other point that you raised, sampling is increased
with activity whether MSHA does it or whether the operator does
it. In an average mine only 3 or 4 samples on a given worker
will be taken. You cannot base any estimates of future disease
based on 3 or 4 samples a year, which every study that has been
done in this area says they have been inaccurate.
Ed Light (Appalachian Research and Defense Fund,
Charleston, West Virginia, also on the ORBES Advisory
Committee): I have one comment and one question. First, on Dr.
Morgan's topic, this is a little outside my area of expertise.
There is very strong disagreement with his opinions. Recently I
was in touch with Dr. Rasmussen who is with the Appalachian
Pulmonary Laboratory in Beckley, West Virginia. Dr. Rasmussen
has personally examined hundreds of coal miners disabled with
respiratory disease problems. He has given a statement which I
am submitting into the record of the meeting. "Emphysema among
coal miners is believed to be more frequent than among the
general population by some observers and may be a frequent cause
of disability among coal miners. The occupational versus
non-occupational factors in causing emphysema must be further
elucidated. It is true, for example, that cigarette-smoking
coal miners, on the average, have more loss of lung function
than non-smoking coal miners. On the other hand, there is no
proof that cigarette smoking is a greater hazard than exposure
to coal mine atmosphere. Some non-smoking coal miners are
severely disabled while some heavy smoking miners are healthy.
Smoking and moderate exposure may be additive. Much more
evaluations will be required to resolve these areas. Strict
enforcement of present regulations, careful health monitoring
with an effective transfer program with continuing study of the
bronchial disease problems offer the best means for preventing
the unwarranted suffering and excess mortality among miners
employed over the past several decades in the United States."
Now, my question which should be directed to Dr. Wagoner.
Is it possible to predict whether there will be additional lung
cancer cases from the future production of uranium in the United
States , both occupational for the miners and from the waste
disposal problem? And second of all, would there be some excess
lung cancer cases even if we meet the occupational and EPA
standards? Is it possible to make a judgment estimate as to,
for example, how many cases of lung cancer we may expect per ton
of additional uranium ore needed for power plants?
Dr. Wagoner; I think the current data would indicate two
things. Just because we lowered the concentrations, as
indicated by the standard, to 0.3 working levels or less than 4
working level months over a 12 month period, does not mean we
solved the problem arising because of what we failed to do in
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the past. That is going to be with us for a long, long period.
The second part of that question is—is the current standard
that good? Based upon the new data that have come from
Czechoslovakia and our own data, my personal opinion is that the
scientific data did not demonstrate and support the accuracy of
that standard in terms of being protective against future
introduction of lung cancer. I think the Czechoslovaks have
made some estimate of what they would consider to be the
contribution and I would refer the answer, after I get through
with this, to Dr. Radford who is probably much more
knowledgeable, with his responsibilities of the BEIR Committee.
But the Czechoslovaks indicated that they believe that the best
measure would be an additional 0.23 lung cancer per thousand
miners per working level.
Dr . Radford: I do think that we have a substantially
greater bodyof information on the problem of radon daughters
and cancer induction than we had even 3 or U years ago, because
of a number of new studies including further followup on
fluorospar miners in Newfoundland, Canada, and the uranium
miners in Canada, which, in my opinion, constitute probably the
most significant group in terms of defining the risk of any that
I know of. They have not, however, yet been followed up
adequately, it is pertinent to ask whether they will be. In
addition to the Swedish zinc miners that Dr. Wagoner mentioned,
there have been a number of other studies carried out on Swedish
iron miners, and I'm doing one of these myself. I think that
the Canadian miner data especially indicate that even for
exposures down in the range of 30 working level months, there
appears to be a doubling of the lung cancer risk. At least my
preliminary evaluation of the published Canadian miner data
suggests this. Thirty level working months: that means a tenth
of a working level for 300 months, which is 25 years exposure to
a 0.1 working level, almost doubles the cancer risk. Is that an
acceptable standard? I think more information is going to be
coming out in the next 3 or 4 years which will enable us to
sharpen that, but the point I wanted to add to this discussion,
is concerned with what Dr. Wagoner mentioned about the mine
tailings issue of uranium fuel sites. We have a problem right
here in Pennsylvania which is on the front page of today's
paper, about the Cannonsburg, Pennsylvania site. This area has
now been found to be heavily contaminated with uranium ore
tailings, and indeed if you visit the community, you find out
that they may have carried some of these tailings all over the
western part of the state, at least according to some anecdotal
statements. So, that here we have one such problem right in our
own back yard— it isn't just in Denver, Colorado, Grand
Junction, or elsewhere in the uranium mining areas, it's around
the U.S. The legislation referred to by "Y. Wagoner named 22
sites in the United States and the list is growing. These are
not particlarly related to energy production except that the
-------
mine tailings issue in the case of coal and nuclear fuel
that is going to be around for quite awhile.
is one
Jerry Fields (Pennsylvania Power and Light Co. in
Allentown): I have a question for Dr. Wagoner or Dr. Radford.
In a recent hearing we had for a nuclear plant that we're
building and also other hearings, the U. S. Nuclear Regulatory
Commission has prepared a Table S-3, that deals with the nuclear
fuel cycle. The question that generally comes up from
intervening groups are the effects of milling. My question is
of the total fuel cycle how significant is the milling portion
of it? Both from the environmental and the cost benefit
analysis points of view?
Dr
Radford
we have
probably not
than being
mechanism of
by different
Well, my answer would be that from the data
so far, the occupational health problem in the mills is
a major one. If indeed it is a problem then rather
lung cancer, the data suggest a very different
action, which will probably have to be controlled
techniques than eliminating radon daughters. But
the milling issue is intimately tied up
effects of the mine tailings. According to
believe this, but this is what they say) in
fuel cycle the exposures from mine tailings
single health impact.
with environmental
EPA (I'm not sure I
the whole nuclear
lead to the biggest
Dr. Hamilton: I would like to comment on that last point.
say something is the biggest part of the nuclear fuel
be biggest because all the rest is terribly
When you
cycle it could
small. Our group has done some calculations, in
mining and milling to the exposure
individual accumulating a dose to
a 50 year life period— any
eternity—developing lung cancer
operation is something
of developing a lung cancer from natural background, which is
something like 10 times greater. It only becomes a significant
risk if you take this dose and multiply it, as some people have
done, by the world population from now to the next 25 million
years and
lung cancer
that you get.
the bronchial
individual
that results
like 1 in 10, as compared
which we relate
The risk to an
epethelium over
from now to
from one year's
with the risk
calculate the number of people that would die from
Dr
Radford
I think your point is well taken. You may
have noticed that I was careful to say that I'm not sure I agree
with this assessment. But, this kind of evaluation is really
what the purpose of this symposium is all about. Can we make
predictions of this type in comparison with coal workers'
pneumoconiosis?
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Dr. Halen (Jones and Laughlin Steel Co.): Insofar as
accident statistics are concerned, a large number of variables
determine whether a man or miner loses time from work and how
much time he does lose. I wonder if the statistics that are
available today are responsive to the varying severity of
accidents as measured by an objective assessment of injury, or
do they report only total lost time?
Dr. Seltzer: I'm not sure of all the variables that
you're talking about. What I was referring to in the two months
figure, was the average lost calendar time of temporary total
injuries, not the fatal injuries and not the permanent partial
injuries. I'd like to add one other thing. These accident
statistics are probably as advanced as any you can find.
Informally, I am sure MSHA would admit that in the past, perhaps
as much as 60% underreporting and undercounting existed in
disabling injuries. With new regulations being promulgated
within the past year, MSHA now estimates about 20%
underreporting and undercounting. Thus, the available
information is not complete and is hampered by underreporting
and undercounting. The main variable in that equation is what
is called "Light Duty Policy." That is when a person gets
injured on the job and is encouraged not to record it. That
injury is not reported as a disabling injury. It is reported as
a nondisabling injury and that worker is kept on the payroll.
There are very substantial benefits, both from the company's
point of view and the worker's point of view to play along with
that game.
Dr. Halen; Well, let me answer that just for a minute. I
think there are ways of our objectively measuring the severity
of injuries, if one goes down the line of a computation,
fracture and so forth. What I mean, for example, in a recent
survey that I myself did prior to a strike, when we had some 100
coal miners off, there were three with fractures and 97 with
sprains and strains. I just wondered--is there a way—or do
these statistics address this sort of thing so that one can
determine more accurately what can be prevented and what cannot
be prevented?
Dr . K. Morgan: May I say something? I find myself in
agreement with Dr. Seltzer for once. If you consider fatality
rates in coal mines a relatively objective finding, the National
Academy of Sciences report indicated that the rate in the United
States is three times to seven times as high as in most European
coal mines. I think you have to distinguish between the
accident rates at large companies, such as that of Dr. Halen,
which have a good record, and the many small coal mines which
employ 15 or 20 miners in West Virginia and Kentucky. They're
the ones which have the bad accident record. It's not United
States Steel and Consolidation Coal Company, which have made a
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real effort to cut down accidents, but the small coal mines or
the relatively small coal mines, where the record is bad. I
don't think there's much doubt that this is where something
should and could be done.
Dr. Hugh Spencer: The recent discussion has brought up
one more issue that I want to address. The question of
radioactivity in the mine tailings of coal mines, has thus far
received only a brief comment. For example, in the Western
fields, some of the lignites are considered more valuable as a
source of low grade uranium ores than as a fossil fuel. In the
Eastern fields, coals are traditionally uranium poor, having a
very small quantity. But the shale overburdens are somewhat
hot. One question I'd like to address here is whether or not we
have any kind of statistical details or any knowledge of what
the radon daughter effect may be on the present population and
on the miner himself. There are some 2 million, perhaps 3
million acres of strip mined, unreclaimed land and tailings
containing these shales lying on the surface.
Dr . K._ Morgan: First, you'd have to show there is an
increased radioactivity in the coal mines and I don't think that
there is any evidence that this is so. I don't know about the
new lignite mines, but the measurements in established mines
have not shown any increased radioactivity. The other point is
that the coal miners, as a whole, have a lower death rate from
lung cancer than does the general population. Now, coal miners
are altogether different from the uranium miners of Ontario or
Utah. Somebody needs to make the measurements to see whether
there is an increase of radioactivity and I think this has been
done. To my knowledge, I don't think that there is any evidence
that there is any increased radioactivity.
Dr. Hamilton; There is good evidence that Dr. Morgan's
remarks are correct.
Dr_._ Spencer: Let me advise you that Exxon Company locates
seams by dropping a Geiger Counter down through the hole in
order to find them. And I am quite amazed at the amount of
radioactivity in coal.
Dr. Bad ford : I would like to follow up on Dr. Morgan's
response. The fact of the matter is that measurements have been
made in underground coal mines and the radon gas levels are not
high, and there is not as a result a large rise in lung cancer
rates in underground coal mines. I think Dr. Rockette is here,
and I believe he has shown a slight excess, nothing like the
kind of excess of lung cancer that is found in uranium mines.
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Dr. H. Spencer; I accept that that is quite correct. I
have no argument with that.
Dr. Morgan: Is Dr. Rockette here because I think it
would be very apropos for him to comment since in his report
which he provided to the Public Health Service, he had reported
an SMR of 112 and he very cautiously, (and he is often
misquoted,) put in a caveat that this slightly increased rate
could be due to different smoking habits or different
geographical locations. In this regard it subsequently turns
out that most of the miners who had an increased death rate from
lung cancer came from areas in the United States where lung
cancer rate is appreciably higher than elsewhere. In this case
it was Charleston, West Virginia, but one only need look at the
statistics to see that West Virginia, Kentucky, New Jersey and
New York for example, have a much higher death rate from lung
cancer as compared to Nebraska and Iowa.
Dr. Spencer: I come from the Johns Hopkins University
School of Hygiene and Public Health as a biochemist with a long
history of study in the field of molecular biology. And since
that time, it has been my conclusion that there is no such thing
as a safe dose of this sort of thing. The fact that there is a
small concentration only means that the impact may be small as a
result of only concentration alone. The pathways are still the
same. I think this means that zero dose is probably the only
safe dose.
Dr. Howard Rockette,, University o_f Pittsburgh: In
response to Dr. Morgan, I think the SMR of 112 speaks for
itself in terms of having not been able to take into account the
smoking history and geographical differences. In the report I
purposely pointed that out. Although the SMR of 112 was
statistically significant, statistical significance depends upon
the sample size also, as well as the actual difference being
observed. I think that on the basis of the study I have done,
it would be very difficult to go back, since I did not have
smoking histories, and attribute that excess, that 112 rather,
to be related to occupation. I might note that in the other
studies done in the United States, there are two contradictory
sets of results. There is the work by Ortmeyer and Costello
which obtained a very low lung cancer rate, and also there were
some previous studies done by Enterline which obtained a high
lung cancer rate. The current study is kind of intermediate
between the two, but as I indicated, without taking into account
the smoking histories, I don't see how one could attribute a
small excess to occupation.
Dr. Morgan: But Ortmeyer did take into account smoking
histories, all of which were available. His lung cancer studies
are still low.
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Dr. Rockette: Yes, that's true. Although I haven't
looked at that paper for some time, one thing that did confuse
me was that one age subgroup showed an unusually high risk. It
was the 65-69 age group. I'm not saying that this means there
is an excess risk but I thought there was a peculiarity in that
there would be one age group that would have that high of an
excess, and it merits further investigation.
Dr. Ian Higgins, University p_f Michigan: I want to
comment on this. In Britain during the 1930's through 1950's,
lung cancer death rates among coal miners were low or very low.
At that time coal miners tended to smoke less than the rest of
the population. This was probably the reason for their low
cancer death rates. Coal miners in Britain are now tending to
smoke much more heavily. This change is being reflected in the
Registrar General's Decennial Occupational mortality statistics
for 1970, which shows their lung cancer death rates to be
higher. It will be interesting to see what happens in 1980.
I also want to comment on the relative importance of mining
and smoking for bronchitis and disability. Comparisons of the
prevalence of respiratory symptoms, bronchitis and level of
ventilatory lung function in miners and ex-miners and non-miners
living in the same area have consistently shown a higher
prevalence of respiratory symptoms and chronic bronchitis among
miners. Miners and ex-miners also have a consistently lower
average lung function than non-miners. The magnitude of these
differences in different places has varied considerably.
Sometimes miners have appeared very little worse in either
respect from non-miners. Furthermore, it has not been very
clearly shown that the miners' excess symptoms and lower lung
function are due to their dust exposure, though this of course
seems likely.
In contrast, respiratory symptom prevalence and chronic
bronchitis are consistently related to smoking. Ventilatory
lung function is also lower in cigarette smokers than in
non-smokers. Thus both mining and smoking appear to contribute
to the excess symptoms and lower lung function of miners. My
view is that smoking does so rather more than mining; but I do
not think mining can be ignored.
In connection with Dr. Spencer's question, I believe it is
important to compare miners with non-miners in the same general
area where the miners.live. It is unsatisfactory to compare
miners in Utah with non-miners in the midwest.
Hamilton: Not a question, but just a comment to the
"who was worried about radioactivity in the coal. I have
a ball park figure that the worst could represent 2% of radon
exposure from uranium. So it is proportionally a great deal
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less.
Dr. Wagoner; I would like to make a few comments and I
hope Dr. Higgins would address some of these this afternoon.
In the whole discussion of the coal studies, the appropriate use
of regional versus a rather diluted national comparison needs
clarification. Also, I think, it is very important that we
define the concepts of the "healthy worker" and the "healthy
survivor", and our reliance, and I say this as a statistician,
on that magical test of significance which generates SMR of
around 100. I don't know what a normal SMR is. Certainly there
have been discussions where being normal is 60 and normal is 80.
I think also one has to consider with regard to the coal studies
that maybe they haven't proven the point that there is a
problem, but they certainly have not excluded the problem. It
is not a negative study.
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SESSION II: SPECIAL METHODOLOGIC PROBLEMS IN DETECTING
HEALTH EFFECTS FROM FUEL CYCLE POLLUTANTS
Monday afternoon, March 19, 1979
Moderator: Herschel E. Griffin, M.D., Dean
Graduate School of Public Health
University of Pittsburgh
MEASUREMENT OF OCCUPATIONAL AND ENVIRONMENTAL EXPOSURES
By
Morton Lippmann, Ph.D.
EPIDEMIOLOGICAL STUDIES OF HUMAN HEALTH EFFECTS
By
Ian Higgins, M.D.
ROLE OF ANIMAL EXPERIMENTS IN RELATION TO HUMAN HEALTH EFFECTS
By
Yves Alarie, Ph.D.
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MEASUREMENT OF OCCUPATIONAL AND ENVIRONMENTAL EXPOSURES
By
Morton Lippmann, Ph.D.
Institute of Environmental Medicine
New York University Medical Center
550 First Avenue
New York, New York 10016
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MEASUREMENT OF OCCUPATIONAL AND
ENVIRONMENTAL EXPOSURES
MORTON LIPPMANN
INTRODUCTION
This session is focussed on the detection of health effects associated
with the exposures of people to fuel cycle pollutants. While health effects
cannot be determined by measurements of occupational and environmental ex-
posures, such measurements can provide a rational basis for predicting the
extent and severity of the health effects resulting from the exposures when
the nature of the effects and the dose-response relationships are known.
The establishment of causal and temporal relationships between exposures
and effects must come from epidemiological studies and animal experiments
of the types to be discussed by Drs. Higgins and Alarie in the next two
papers.
The adequacy of measurement techniques for occupational and environ-
mental exposure evaluations can only be defined in terms of specific
contaminants. Thus, in order to define methodologic problems in the measure-
ment of exposures to fuel cycle pollutants, it is necessary to define which
contaminants are likely to be encountered in concentrations sufficient to
product effects.
Characterizing Exposures to Fuel Cycle Pollutants
For fuel with well-developed technologies, the exposures of concern
have been well characterized and techniques for their evaluation have, for
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the most part, been established. Thus, while the potential for excessive
exposures still exist in fuel oil refining, coal handling, and uranium
refining, there are no serious deficiencies in measurement and control
technology. The excessive exposures that still occur are due to failures
to apply the available technologies.
For the plutonium or thorium fuel cycles, i.e., breeder reactor
technologies, there are a number of aspects of the exposure control tech-
nologies which require considerably more development. These include capture
and disposal of the radioactive noble gas fission products, separation and
long-term storage of long-lived liquid and solid activation and fission
products, etc. On the other hand, there do not appear to be any major
technical deficiencies in the measurement technologies for characterizing
exposures to radionuclides or ionizing radiation.
The major methodologic problems in exposure evaluations for fuel cycle
pollutants are associated with the developing technologies for producing
synthetic liquid and gaseous fuels from coal and oil shale. One difficulty
lies in defining the compositions and strengths of the effluents and fugitive
emissions. There are complex mixtures of organics at various points along
the process streams. Furthermore, the stream composition varies greatly
from process to process, and with the compositions of the starting materials
and operating parameters in each process. The exposures of the refinery
workers will also depend on the number, distribution and magnitude of the
process leaks, while the exposures of downwind and downstream populations
will depend on the design and performance of the effluent recovery systems
and the extent of fugitive emissions.
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The only data currently available on exposures resulting from these
processes are from pilot-scale operations, and there are very few of these.
In any case, the results have limited predictive value for full-scale plants
because of likely variations in operating factors, and because the effluents
acceptable in a pilot-scale operation are likely to be unacceptable in a
full-scale plant. Thus, the controls specified on the basis of the pilot-
plant or demonstration plant experience should prevent the release of
hazardous effluents into the occupational or community environment of the
full-scale plant.
While the exact compositions of the process and waste streams from coal
conversion and oil shale processing plants will be highly variable, it is
clear that they will contain large numbers of hydrocarbons that are mutagens,
teratogens, whole carcinogens, co-carcinogens, initiators, and tumor pro-
motors. Thus, even if the compositions could be precisely determined, and
if the health effects of each alone were also known, it still would not be
possible to realistically determine the potential for adverse effects of the
mixture. The combined effects could easily be greater or less than the
aggregate of the effects produced by each of the components when acting
alone.
Use of Indicator Compounds
One approach to characterizing the hazard potential of such mixtures is
to select one or more individual components of the mixture to serve as
indicators. The presumption is that the concentration of the indicator(s)
varies directly with the hazard potential of the overall mixture. For
gasification plants, carbon monixide (CO) may serve as a suitable indicator
for most of the plant population. When the CO levels are monitored and
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results are used to ensure that the plant is operated in a manner that con-
trols the escape of CO, it can generally be- presumed that the concentrations
of other air contaminants will also be sufficiently low to satisfy occupa-
tional and environmental standards.
It is much more difficult to specify appropriate indicator chemicals
for the mixed contaminants which can escape or be released from coal liqui-
fication or oil shale processing. Concern for the carcinogenic potential
of the mixture is likely to force tighter controls than those needed for
the prevention of either acute or chronic chemical toxicity. Unfortunately,
there is no single chemical which can serve as an acceptable hazard indicator
for this type of process.
Some investigators have adopted or suggested benzo(a)pyrene (BaP) as an
indicator chemical, on the basis that: 1) it is likely to be present in
most mixtures, 2) it is a known and potent animal carcinogen, and 3) it
can be routinely analyzed by analytical techniques of proven reliability.
While it is likely to be present to some degree in most mixtures, its
contribution by mass or biological activity is likely to be highly variable.
Furthermore, its potency as a human carcinogen is uncertain.
An epidemiologic study of roofers exposed to very high concentrations
of BaP found some excess lung cancer among those exposed for more than 20
years ^ . The SMR's for those exposed for 9-19, 20-29, 30-39, and >_ 40
years were 92, 152, 150 and 247 respectively (the smoking histories of the
workers were not known). Airborne BaP concentrations measured in roofing
3 •}
operations range from 14 yg/m in the roof-tarring area, to 6000 yg/m" in the
coal-tar roofing kettle area (1,2). The amounts of BaP recovered from masks,
which were worn by a minority of roofers studied, indicated an average of
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16.7 yg BaP inhaled per day (1). Another group exposed to high concentrations
of airborne BaP were British gasworkers, who inhaled about 30 yg/day (3).
_2
The mainstream smoke of a cigarette contained 'v* 3.5 x 10 yg of BaP
(4)
in 1960, although the levels are lower now. Thus a 2 pack/day smoker
3 (2)
inhaled ^1.4 yg/day. Ambient urban air in 1958 contained about 6 ng/m ,
which could account for an inhaled mass of ^ 120 ng/day, i.e., 0.12 yg/day.
Rural ambient air has about 10% as much BaP
The lung cancer SMR's for rural non-smokers, urban non-smokers, light
smokers (< 1 pack/day), heavy smokers (> 1 pack/day), roofers (>_ 20 years
exposure, and including many smokers) and gasworkers (including smokers)
are 14(6), 16(6), 124(6), 502(6), 159(1), and 169(7), while their daily
BaP exposures are of the order of 0.012, 0.12, £0.70, 0.7 to *> 2.5, 17, and
30 respectively. Clearly, BaP exposures are not particularly good indicators
of lung cancer risks. All of the exposures cited involve a mixture of organic
compounds and other toxicants as well, but the influences of each, and their
interactions, cannot be determined.
Since there is potential for exposure to so many such substances in
coal and oil shale processing, it is impractical to routinely monitor for
more than a few indicator compounds. Furthermore, different indicators or
groups of indicators may be needed in different situations. Therefore,
research is needed on the unit operations and process streams in these in-
dustries, to identify chemical indicators whose biological effects are
similar to the mixtures in the expected exposure atmospheres. The strategy
/g\
recommended by a USDOE sponsored Working Group is to identify a variety
of potential indicators (perhaps 6 or 8), identify the places where each is
likely to be useful and the kind of monitoring required. They concluded
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that the state-of-the-art for monitoring each compound by the methods
needed should be assessed and, if necessary, that new instruments should be
developed. Since the final selection and evaluation of specific indicators
cannot be made until a commercial plant is built, it is necessary to be able
to choose among a number of indicators for which instrumentation is avail-
able. The Working Group also recommended that the instrumentation should
probably be non-specific, so that a common line of development will lead to
instruments capable of measuring several indicator compounds.
MEASUREMENT TECHNIQUES
Exposures to fuel cycle pollutants can take place via several different
pathways, i.e., inhalation, skin absorption or penetration, and ingestion.
There can also be exposures to excessive levels of physical agents, i.e.,
noise, ionizing radiations (x and y radiation, short A UV) and non-ionizing
radiations (long A UV, visible light, IR, microwaves). Most of the measure-
ments made to determine actual or potential exposures are made of the ex~
posure environment, e.g., concentrations of chemicals in the air, drinking
water, food, etc. These can frequently be supplemented by measurements
which determine toxicant accumulations or effects, e.g., measurements of
in-vivo burdens, concentrations in body fluids or tissues, and concentrations
in excreta such as urine, feces, hair, exhaled air, etc.
In-vivo measurements are practical when they can be made with external
detectors, as with radionuclides emitting penetrating radiations which can
be detected with solid-state and/or scintillation detectors. Population
estimates of accumulated chemicals and radionuclides can be made by measure-
ments of tissue burdens, when appropriate tissue samples can be obtained
from human accident victims at autopsy.
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Sensitive analytical techniques appropriate for determining the con-
tents of tissues, excreta, air and water samples are generally available,
although research and development on techniques for concentrating and/or
separating the contaminant from its matrix or sampling medium may be neces-
sary in many cases. There are relatively few cases where a judicious
selection of separation techniques and laboratory analytical techniques
fail to yield satisfactory analytical capabilities for an environmental
analysis of interest. However, there may frequently be cases where the
technology is too time-consuming and/or expensive for the particular
application.
One major area in which our capacity for environmental assessment is
technology-limited is in the evaluation of inhalation exposures to complex
mixtures of airborne organics. Another area is direct-reading instrumentation
for chemicals which produce effects more associated with their transient
peaks rather than their cumulative exposures. The need for direct-reading
instrumentation is greatest for chemicals present as aerosols. Great prog-
ress has been made in the past decade in the development of continuous direct
monitoring devices for specific airborne gases and vapors. By contrast,
there are no instruments available for the continuous measurement of the
airborne concentrations of specific chemicals present in the atmosphere
in aerosols. We cannot, for instance, currently monitor the concentration
of sulfuric acid mist. Our inability to do so has contributed to our fail-
ure to characterize the roles and effects of the various components of the
overall SO mixtures generally present in the ambient air.
X
The only direct-reading aerosol monitors currently available are those
which measure some physical parameters of the aerosol, i.e., size distri-
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butions, overall number or mass concentrations, and light scatter or ex-
tinction.
The adequacy of measurements made to evaluate the potential for health
effects in a given situation can be judged by a variety of criteria or
combinations of criteria.
These include:
1. Sensitivity, i.e., can the airborne concentrations capable of
producing the health effects be measured at an acceptable level of accuracy.
2. Specificity, i.e., can the contaminant of interest be measured in
the presence of co-contaminants and background contaminants.
3. Temporal resolution, i.e., can the peak concentrations of the
contaminant of interest be determined with a resolution appropriate to the
averaging time for the biological effect.
4. Temporal responses, i.e., what is the interval between the time of
air sampling and the availability of the concentration determined for the
sample. This can vary from instantaneous for direct-reading gas phase
sensors to months for laboratory evaluations of field-collected extractive
samples.
5. Spatial resolution, i.e., can the measurements be made at locations
suitable for exposure evaluations. In other words, can the measurements
be made using personal samplers or hand-held samplers or monitors at the
breathing zone of the individual whose exposure is being determined.
A complete discussion of measurement techniques for the determination
of chemical contaminants attributable to fuel cycle pollutants, and for
those released into the occupational environment, ambient air, and liquid
effluents would require a monograph, and are clearly beyond the scope of
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this paper. A recent reviev of the current status of the available measure-
ment techniques and some recommendations for research on environmental
measurements was prepared by the Second Task Force for Research Planning in
(9)
Environmental Health Science
The balance of this paper will consist of a review of techniques for
characterizing exposure atmospheres which are applicable to both ambient
air and workroom air. Within it, the emphasis is on recent developments
in direct-reading instrumentation.
Monitoring Exposure Atmospheres
There are various approaches to monitoring the exposure atmosphere and
characterizing the concentrations of the chemicals to which people are ex-
posed. The traditional and simplest monitoring technique is manual sampling,
where a known volume of air is drawn at a known flow rate through a collector.
For particles, the collector can be a filter; for soluble gases, it can be
a bubbler; for organics, it can be a charcoal trap. The appropriate collect-
or is used to trap particles with known, and presumably, high efficiency.
For gases and vapors, the collection efficiency needs to be known and
constant. If it is less than 100 percent, the amount collected can be
corrected to compensate for the lack of total collection. For aerosols,
on the other hand, there must be 100 percent collection efficiency, since
the collection efficiency is particle size-dependent, and the Investigator
wants to know the total amount, and not some estimate that varies with its
particle size distribution. In practice, this requirement doesn't cause
any great problem, since filters and other types of collectors with essentially
quantitative collection capabilities are readily available.
One advantage of sample collection and subsequent analysis is that there
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is almost no limit in the choice of sample processing that can be done, or
in the range of sophisticated and sensitive laboratory instruments that can
be brought to bear on analytical problems. The investigator can get the
ultimate in sensitivity and specificity, with correction for interferences.
On the other hand, there is a basic limitation in this procedure in that
there is a significant time lag between sample collection and the deter-
mination of what was collected. Manual sampling techniques may, therefore,
be used to back up continuous monitors, and perhaps, as the final arbiter
on a substance's exact concentration.
For a more complete discussion of the state-of-the-art of air sampling
technology and for descriptions of available sampling and monitoring in-
strumentation, the reader is referred to the latest edition of the ACGIH
reference book: "Air Sampling Instruments."
Intermittent/Continuous Instrumentation
There are two basic types of automated instrumentation. One is the
intermittent type of operation, and the other is continuous. For monitoring
particle size distribution, a combination of intermittent techniques is
generally used because there is a very large particle size range to be
covered, and there is no universal instrument that can indicate the con-
centration of each particle size interval over the entire range.
One of the instruments used to measure very small particles (0.08 ym
to 0.5 ym) is the electrical aerosol analyzer shown in Figure 1. It sorts
out the particles of a poly-dispersed aerosol according to their electrical
mobility. The particles are collected on a current collecting filter at
the end of the tube, and the amount of charge they deposit on that filter
is measured incrementally. The voltage gradient and/or the flow rate is
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changed sequentially to allow a different size-cut to reach the filter. In
this way, there is a progression of size increments. This technique can
provide an accurate size-distribution in a stable atmosphere. However, it
takes a finite amount of time to run through these increments and collect
the size band data to get the size analysis.
While the mobility analyzer can be used as a size analyzer for small
particles, it cannot be used to measure particles larger than approximately
0.5 vim in diameter. Fortunately, there are other techniques suitable for
measuring the size distribution of the larger particles.
The property of light scatter is used in measuring the concentrations
and size distributions of particles of 0.3 ym diameter and larger. When
light is focused on a particle in the instrument illustrated in Figure 2,
some of that light will be scattered. The amount of light that will be
scattered by a given particle depends on its size. A photomultiplier can
be used to detect the light output from each particle. The pulses can be
accumulated according to size intervals in a multichannel pulse-height
analyzer, and these intervals can be calibrated according to particle size.
Unfortunately, there are other properties of the particle besides its size
that affect the amount of light scattered, including the refractive index,
the color, the shape, and so forth, and reliable data depend on accurate
calibrations.
Intermittent techniques can also be used in monitoring gases. One
method for carbon monoxide involves a combination of gas chromatography and
flame ionization detection. The flame ionization detector is nonspecific,
but by coupling it with the holdup time in the chromatographic column,
specific analyses can be obtained since the carbon monoxide will pass through
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the column and move into the flame ionization detector at a characteristic
time.
The alternative approach, i.e., continuous monitoring, is more commonly
used for gases. For example, carbon monoxide can be monitored using an
infrared analytical technique which does not collect the sample at all. As
shown in Figure 3, the gas is directed through the sample tube. Infrared
radiation also passes through the tube at wavelengths that are sensitively
absorbed by carbon monoxide. There will be an attenuation of the infrared
because of the absorption of the carbon'monoxide in the sample tube, and
thus, the energy received on the detector will vary with the substance
concentration. Operationally, this technique is best implemented by using
a reference tube of clean air, and getting the difference in attenuation
between clean air and the air containing the carbon monoxide.
Other gaseous constituents absorb infrared energy; for example, water
vapor. However, these gases and vapors are wavelength-specific, so by
tuning to the wavelength at which carbon monoxide has preferential absorptive
capacity, the effect of interference can be removed, giving a sensitive,
accurate, and specific analysis of carbon monoxide. The only time lag is
the insignificant amount of time it takes to flush the sample through the
tube. This, then, is a commonly used method of monitoring carbon monoxide
on a continuous basis. The sensitivity is a function of the length of the
sample tube, which can be 10 or 20 meters with folded tubes. Similar in-
struments can also be used in measuring other gases by choosing appropriate
wavelengths free of significant absorption interferences.
The flame photometric detector illustrated in Figure 4 is commonly
used in measuring the concentrations of sulfur-containing gases. If a sulfur-
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bearing material is passed through a hydrogen burner, a light photon emission
will result that can be detected with sensitive photomultipliers. It is a
nonspecific technique in that it gives roughly an equivalent response for
hydrogen sulfide, sulfur dioxide and some of the mercaptans. If the only
sulfur gas present is sulfur dioxide, then the test is quite specific, but
if there are other sulfur gases, the test cannot be specific unless the
sulfur gas detector is equipped with a chromatographic column that will
feed the sulfur species into the flame-photometer in sequence. Such a
composite instrument is, of course, an intermittent sampler.
In most situations, it is desirable to have a built-in calibration
device on the concentration monitor to ensure that the concentration in-
dicated on the output chart or on the dial is correct. One of the more
common devices used for in-line continuous calibration is the permeation
tube. For the flame-photometric detector, the calibration device shown in
Figure 4 contains liquid sulfur dioxide sealed into a Teflon tube. The
tube is slightly porous to the saturated sulfur dioxide vapor above the
liquid in the tube. The rate of permeation of sulfur dioxide vapor out of
the tube is very much dependent on the temperature, but is constant at a given
temperature. When the permeation tube is held within a constant temperature
bath, a known emission rate can be obtained. With an accurately calibrated
dilution air flow, the concentration of the calibration gas can be deter-
mined, and it can be directed periodically into the analyzer to get a span
signal. This is a very convenient method of instrument calibration. There
are similar calibration tubes available for nitrogen dioxide, and for a
number of hydrocarbons that are readily condensed into liquids at room
temperature.
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Instruments that measure the light emitted during gas phase reactions
of nitric oxide and ozone are also used in monitoring contaminant concen-
trations in occupational and ambient atmospheres. If an excess of ozone is
mixed with the sample containing nitric oxide, as in Figure 5, the amount of
light is proportionate to the amount of nitric oxide. This technique can
be used for measuring nitrogen dioxide by passing the sampled air through a
chemical converter that converts the nitric dioxide to nitric oxide, which
can then be measured on a mole for mole basis. Nitric oxide and nitrogen
dioxide can be differentiated by sequential readings with and without the
converter in-line.
The same basic type of instrument can be used as an ozone monitor by
feeding an excess of nitric oxide into the reaction chamber. Other ozone
monitors are based on other chemiluminescent reactions of ozone, specifi-
cally, with ethylene and organic dyes.
Measuring Aerosol Mass Concentration
Both of the methods described for measuring particle concentrations
and size distributions, i.e., the small particle mobility analyzer and the
larger particle light-scatter analyzer, measure the diameters of particles
and sort them by so many numbers of particles in each size interval.
Number concentration is important in many studies, but in studying effects
on people or animals, the investigator generally needs to know the
aerosol's mass concentration. Since th3 mass of a particle varies with
the cube of the diameter and with the density, the investigator needs to
know more than number distribution. On the other hand, the automatic
machines accumulate a very good statistical base. Adequate approximations
of mass concentrations can sometimes be made by determining the volume
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distributions from the transformed number distributions. If the particles'
density is determined, then a mass median diameter distribution or a con-
centration can be calculated.
While such data transformations may be justifiable in some cases, the
property that is being reported is not being directly measured. It is,
therefore, sometimes necessary to determine the aerodynamic size distri-
bution, since this is the distribution of sizes that affects deposition in
the respiratory tract. If a system of somewhat redundant measurements can
be justified, it is best to use a variety of complementary aerosol measure-
ments involving light scatter, mobility, and aerodynamic properties.
The beta attenuation technique combined with a two-stage collection
system, as illustrated in Figure 6, sorts the particles by their aerodynamic
sizes and measures the mass in each fraction. Using this technique, the
air enters an impaction jet at the top, and particles below its aerodynamic
cutoff size will be collected on the back-up filter. The mass of accumu-
lated particles collected at each state can continuously be monitored using
the beta attenuation technique. A carbon-14 source is used as a beta emitter.
The amount of {5-radiation that reaches the detector depends on the $-
absorption in the accumulated sample between the source and the detector.
There is only about a 10 percent variation in beta attenuation with
mass number (Z), with the exception of hydrogen, and hydrogen does not
usually contribute much to aerosol mass. Thus, the amount of beta attenu-
ation by the impacted particles on the first stage indicates how much mass
of material has been collected in particles above the impactor's cutoff
size, and the attenuation of the particles on the second stage indicates
the mass of small particles below the cutoff size. However, the response
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time of this technique is not very rapid.
Another type of direct monitor of aerosol mass concentration utilizes
quartz-crystal oscillators as mass balances, and is illustrated in Figure 7.
Very small sample masses can be detected as they accumulate on the quartz
crystal oscillator. The quartz crystal is cut into a particular mode, and
electrodes are attached on each side. When a high frequency signal is
applied, the crystal oscillates, and its oscillation frequency depends on
the mass of the crystal.
When particles are deposited on the crystal, its mass increases and
the oscillation frequency decreases, therefore, the sample accumulation
can be measured by the change in the frequency of the oscillator. In
modern instrumentation, frequency counting is relatively simple and precise,
and very sensitive. Thus, infinitesimal masses produce readily measureable
signals.
However, this technique has its limitations. The sensitive zone does
not have a uniform sensitivity. It is greatest at the center of the electrode
and falls off toward the periphery. However, it does provide a sensitive
indication of mass, and with enough calibration to be sure of its perform-
ance under the given operating conditions, can be used as a sensitive mass
monitor.
Another instrument that can be used to provide an approximation of mass
concentration of particles in the one-tenth to one micron range is the in-
tegrating nephelometer, which is illustrated in Figure 8. This technique
measures the total scatter of an aerosol. The instrument discussed earlier
measures the scatter from individual particles. The nephelometer, by
contrast, measures the scatter of a cloud, i.e., the total scatter of all
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of the particles in the sensing zone.
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SUMMARY AND CONCLUSIONS
Existing measurement techniques for the evaluation of occupational and
environmental exposures to fuel cycle pollutants are generally adequate
for the more fully developed fuel cycles. These include the preparation
of coal and petroleum products for combustion, and uranium for nuclear
fission. Further improvements in measurement techniques for evaluating ex-
posures to the pollutants for these fuel cycles will be primarily concerned
with refinements in instrument convenience, performance and reliability.
In many cases, there is room for improvement with respect to size, port-
ability, cost, response time, sensitivity and specificity.
Entirely new measurement technologies need to be developed and refined
for some of the pollutants associated with fuel cycles currently under
active development, especially coal conversion and oil shale processing.
One major problem is that the mixtures of hydrocarbons within these processes
and in their effluents are so varied and complex that it is not possible to
characterize all of their individual and combined toxicities. A second
problem is that designs of commercial scale plants and their potential for
effluent and fugitive emissions cannot be determined at this time.
An attractive approach for effective hazard evaluations in the synthetic
fuels industry is to select one or more appropriate constituents of the
mixtures to serve as indicators. However, considerable research will be
needed to serve as a basis for establishing the feasibility and utility of
this approach for these processes.
Continuous, direct reading instrumentation for monitoring airborne
concentrations of many of the pollutant gases of interest are available.
Many of these instruments utilize sensors which respond to gas-phase re-
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action products and/or spectral absorptions. Direct reading aerosol moni-
tors are available for the measurement of mass concentration and particle
size distribution. However, there are no direct reading instruments for
measuring the concentrations of specific chemicals present in aerosols. The
development of such instruments, while admittedly difficult, represents an
area for productive research.
ACKNOWLEDGEMENT
This work is part of center programs supported by Grant No. ES 00260
from the National Insitute of Environmental Health Sciences, and Grant No.
CA 13343 from the National Cancer Institute.
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References
1. Hammond, E.G., I. J. Selikoff, P.L. Lawther, and H. Seidman. Inhalation
of Benzpyrene and Cancer in Man. Ann.N.Y. Acad. Sci. 271:116-124 (1976).
2. Sawicki, E. Airborne Carcinogens and Allied Compounds. Arch. Environ.
Health 14:46-53 (1967).
3. Lawther, P.J., B. T. Commins, and R. E. Waller, A Study of the Con-
centrations of Polycyclic Aromatic Hydrocarbons in Gas Works Retort
Houses. Brit. J. Ind. Med. 22_: 13-20 (1965).
4. Kotin, P., and H. L. Falk. The Role and Action of Environmental Agents
in the Pathogenesis of Lung Cancer. Cigarette Smoke Cancer 13:250-262
(1960).
5. Faoro, R. B. Trends in Concentrations of Benzene Soluble Suspended
Particulate Fraction and Benzo(a)pyrene. J. Air Poll. Cont. Assoc.
25_: 638-640 (1975).
6. Haenszel, W., D. B. Loveland, and M. G. Sirken. Lung-Cancer Mortality
as Related to Residence and Smoking Histories. I. White Males.
J.N.C.I. 28:947-1001 (1962).
7. Doll, R., R. E. W. Fisher, E. J. Gammon, W. Gunn, G. 0. Hughes,
F. H. Tyrer, and W. Wilson. Mortality of Gasworkers with Special
Reference to Cancers of the Lung and Bladder, Chronic Bronchitis, and
Pneumoconiosis. Brit. J. Ind. Med. 22_:1-12 (1965).
8. Working Group on Assessing Industrial Hygiene Monitoring Needs for the
Coal Conversion and Oil Shale Industries. Final Report to U. S. DOE
under Contract No. EY-76-C-02-0016, Brookhaven Nat'l. Lab., Upton, NY
(Feb. 1979).
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9. Second Task Force for Research Planning in Environmental Health Science.
Human Health and the Environment - Some Research Needs. DHEW Publ.
# NIH 77-1277, Supt. Doc., USGPO, Washington, D.C. (1977).
10. Air Sampling Instruments Committee, Air Sampling Instruments for
Evaluation of Atmospheric Contaminants-5th Ed., Cincinnati, American
Conference of Governmental Industrial Hygienists (1978).
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Charged
dean air ( aerosol
Figure 1. Schematic diagram of electric mobility analyzer tube as
used in mobility size analyzer. Source: Liu, B.Y.H., (Ed.)»
Fine Particles, Academic Press, 1976, p. 599.
INLET
LAMP
PHOTOMULTIPUER
Figure 2.
Schematic diagram of single particle optical particle size
analyzer. Source: Climet, Inc. literature.
-119-
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| LIGHT
• SOURCE
if en TI Ccccj
ROTATING ^^ 11 ^-^
VANE *~~
Slreom cr:
I
I
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TUBE
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i
i
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1 ., ,
ELECTRONICS
Figure 3.
Schematic diagram of infra-red gas analyzer. Source: Air
Sampling Instruments (5th Edition), ACGIH, Cincinnati, Ohio,
1978.
-120-
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L
1
* • • m • i
^V
T
J
\
FOUF ftAY VALVE
\ ROTAUETER
PERMEATION
TUBE
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'2 I
I
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A.
Figure 4. Schematic diagram of flame photometric analyzer for sulfur
gases, with permeation tube calibrator. Source: Air Sampling
Instruments (5th Edition), ACGIH, Cincinnati, Ohio, 1978.
-121-
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SAMPLE
PHOTOMULTIPLIER
SOLID
STATE
ELECTRO
METER
JU
HI LEVEL
OUTPUT
FILTER
FLOW REACTOR
RECORDER
MECHANICAL
PUMP
VACUUM
GAUGE
Figure 5. Schematic diagram of chemiluminescence NO/NOX analyzer.
Source: Scott Research Labs literature.
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IMPACTION
STAGE
0 T O
TO PUMP
>t DETECTOR
FILTRATION
STAGE
PREAMP
AMP/
0180.
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Figure 6. Schematic diagram of TWOMASS mass concentration analyzer.
Source: Liu, B.Y.H., (Ed.), Fine Particles, Academic Press,
1976, p. 551.
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Mass Sensitivity
Distribution
0.2mm
ELECTRODES
Figure 7. Schematic diagram of quartz-crystal oscillator used as a mass
balance, showing sensitivity over crystal face. Source: Liu,
B.Y.H., (Ed.), Fine Particles, Academic Press, 1976, p. 489.
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Aerosol In
Aerosol Out
Cleon
Durge Air
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Constant
Figure 8. Schematic diagrams of integrating nephelometer.
Source: MRI, Inc. literature.
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EPIDEMIOLOGICAL STUDIES OF HUMAN HEALTH EFFECTS
By
Ian Higgins, M.D.
Professor of Epidemiology
Professor of Environmental and Industrial Health
Kathy Welch, M.P.H.
and
Jerel Classman* M.P.H.
School of Public Health
University of Michigan
Ann Arbor, MI
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Introduction.
The task of the epidemiologist who is interested in the effects on health
of fuel cycle pollutants is to relate exposure to response in some definable
population. As you have just heard, he has first to measure exposure to
specified pollutants. He has to do this in the work place and elsewhere to
reach sound conclusions about the dosage received by each person in his study
group. He has then to identify and measure any effects, or responses, that
these exposures have caused. The relationship between exposure and response
should be quantified with as much precision as possible in the form of a
dose/response curve (or series of dose/response curves). Responses of in-
terest may be influenced by many factors other than pollution, by age, sex,
socio-economic status and smoking, for example. It is essential that due
allowance should be made for such confounding factors if erroneous conclusions
about the hazards of pollution are to be avoided.
As in any scientific endeavor, the epidemiologist can make observations
or conduct experiments. Broadly speaking, observations are of two kinds:
1) Persons with an effect of interest can be compared with persons
without it to see if their current and past exposure differs, and
2) Persons with known (or estimated) exposures are followed to see if
the frequency and severity of some effect can be related to the intensity
and duration of those exposures.
Experiments are also of two kinds:
1) Those based on "natural" changes, such as varying concentrations
arising from industrial emissions or accidents, and
. 2) Those based on planned change where the effect of control measures
is studied.
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Definition of the population for study.
The first problem is to decide what population we should study. Are
we more interested in the general population or should we focus on those
we suspect of being a high risk group? Patients with heart or lung diseases,
asthmatics, the young or the old, for example. Ideally, we should know
what proportion of the whole community the high risk group comprises. But
susceptible persons have seldom been identified in this way. More often,
patients on the lists of physicians have been recruited for diary, panel
or other special risk studies. The result has been that one has only a
vague idea of the prevalence of such persons in the community.
Instead of trying to study the whole community, which is a taxing
activity requiring an initial census, epidemiologists often select some
group (or groups) with'in the whole, which is assumed to reflect the behavior
of the whole reasonably accurately. Thus, persons employed in different
jobs, children in school, insured persons and so on are often selected as
being more readily accessible than members of the community at large.
Occupational groups sometimes offer advantages over community defined groups.
The late Professor Donald Reid originally conducted his studies of air
pollution among postmen (mailmen) because the occupation ensured a certain
socio-economic homogeneity.
It may be more practicable to study the effect of certain exposures
within a particular industrial group rather than in the general population.
Exposure to pollutants, which may occur when coal is converted into liquid
or gaseous fuel, and exposure to ionizing radiation are examples. There
are a number of problems with occupational groups. The disabled tend to
be under-represented. The heavier the exertion required, the less likely
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are the disabled to remain in the work force. Disabled persons may move
from heavier to lighter jobs. Persons with certain impairments and diseases
do not ever get into the work force either because they do not try to do so
or because they are rejected by a pre-employment physical examination.
These forms of selection result in most occupational groups being healthier
than the general community, a situation which is often referred to as "the
healthy worker effect."
Identification of comparison groups.
It is important to establish adequate comparison groups. Frequently
the population being studied can be subdivided into a number of exposure
categories (none, light, moderate, heavy; or, better, classes based on
pollutant concentrations or dosages). These internal comparisons form the
bases for exposure/response curves. In many studies, however, additional
external comparisons are important. This is particularly so when the
question posed refers to a possibly increased risk of some disease resulting
from occupational exposure. Does this group of men who are occupationally
exposed to this or that pollutant have an increased risk of dying of cancer?
Chronic respiratory disease? All causes? These questions imply some
standard of comparison or basis for expectation. The United States pop-
ulation, the population of the state or city where the industry is located,
some other industry, all persons covered by social security, are some of the
comparison groups which have been suggested and used.
Sources of information on population.
Information on the general population is available from routine demo-
graphic and vital statistics. Often, however, the detail one might like
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is insufficient for adequate comparisons. Occupational data is limited
and smoking habits usually nonexistent. If these important confounding
variables are to be dealt with adequately, a special effort will have to
be made to collect them. Usually an up-to-date definition of the population
will need a census.
Occupational groups can be defined by company or Union records. But
these may not always be available. They need to be checked for completeness.
This can be done through quarterly social security records. Any discre-
pancies between nominal lists and SSA records need to be resolved.
Measurement of exposure.
We need to decide first what pollutants to measure, how, where and
for how long. Often measurements will have been made at one or more sites.
But these will seldom be adequate for epidemiological needs. Nevertheless,
such measurements may be all that are available for estimation of past
1 2
exposures. The studies of Buechley and Schimmel and their colleagues on
daily mortality in relation to daily pollution in New York City have been
based on measurements of pollution made at a single sampling station in
uptown Manhattan. Clearly such limited data, while it may provide a
reasonable picture of overall change, is less than ideal. In the industrial
setting, measurements will usually have been made at sites where the risk of
exposure is particularly high.
In neither the general community nor the work place are people exposed
to these measured concentrations. In the community, people live at some
distance from the sampling station. They work somewhere else. They travel
between the two and move about elsewhere during the course of the day.
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More important perhaps, but increasingly recognized, they spend most of their
time indoors whereas pollution is measured out-of-doors. There are large
differences in pollutant levels indoors and outdoors. In the work place
employees may spend only a small fraction of the work shift exposed to the
pollutant concentrations which are measured. The rest of the time they may
be exposed to lower concentrations. An additional problem in assessing
exposure at work is that sampling is usually intermittent. The days on
which samples are taken may not be representative of all days.
In the general community samples are usually taken over 24 hours, though
continuous recording instruments are used for some pollutants. Personal
monitors provide an integrated exposure over a working shift or in the
case of a radiation badge over a longer period, usually a week. For many
exposures we may be more concerned with short peaks than with integrated
shift or 24 hour samples. Thus, deterioration in the respiratory condition
of patients with chronic bronchitis and emphysema or attacks of asthma may
depend more on transient short peaks of exposure than on 24 hour concen-
trations.
In assessing exposure, the epidemiologist has to be concerned with daily
patterns of movement. In the industrial setting this involves a time and
motion study. But in the general community this is difficult. Perhaps
personal monitoring provides the best way of obtaining reasonably accurate
estimates. To date, few such studies have been carried out.
If it is hard to estimate short (24 hour) exposures, it is of course
much harder to estimate exposures over the past 10 or 20 years or over a
lifetime. The difficulty is compounded by the fact that pollutant concen-
trations have nearly always changed over the years. What we measure now
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may have little relevance to pollution in the past. Inevitably we must rely
on historical information, work and residential histories and what is known
or believed about the way pollution has. changed.
Measurement of response.
Turning now to the response side of the equation. A variety of biological
indices can be used to study effects of exposure. These range from death,
severe disability and serious illness, through respiratory or other symptoms
and lung function to mild discomfort, unnoticed changes in physiological or
psychological function, or silent accumulation of chemicals in the body.
Some of these indices are routinely collected. For example, deaths, including
daily deaths, can be obtained from the National Center for Health Statistics
(or similar Offices of Vital Statistics in certain other countries). Illnesses
are available in insured populations. But many of these indices must be
obtained by the epidemiologist by means of a survey.
Death is a good epidemiological index, if somewhat terminal. Provided
the fact of death is confirmed by a death certificate there is not much
doubt about it. As soon as interest turns to specific causes of death, a
number of problems arise. Some of these are concerned with diagnosis.
They include such things as criteria for diagnosis, fashions in certification,
observer variation and error. Others reflect the ordering of potentially
killing illnesses on the death certificate into underlying and contributory
causes. Finally, people who die of heart disease do not remain in the
population to die of cancer or stroke. There is, as we say, a problem of
"competing causes of death."
When one collects ones own data, a clear statement of the biological
index used as a measure of the effect of pollution needs to be made. The
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index needs to be clearly defined and its degree or severity classified.
The reproducibility of symptoms, physical signs, special investigations
such as chest x-rays, lung function tests, blood and other laboratory tests
has to be carefully assessed. Needless to say, initial training is
important in ensuring that tests are correctly carried out and variation
between observers is reduced to a minimum.
A claim that is sometimes made for epidemiology is that it offers
an opportunity to identify persons with the earliest deviations from the
norm. While this is certainly true, it should be recognized that minimal
changes are often hard to differentiate from normal variation. Once
defined there may also be uncertainty about the future implications of
such deviations. For example, a modest rise in respiratory airways
resistance (50%) may be brought about by exposure to SOo or NOp at low
concentrations. A comparable rise can also occur from breathing cold
air, after coughing or even from taking a deep breath. In the case of
S02» the A.W.R. may revert to normal even while the subject continues to
breath SO^. Do these changes have any more serious implications? We
do not know. Yet there is a tendency to assume they do and to regulate
accordingly.
Again, in the search for sensitive indices of effects, subtle changes
in lung function have sometimes been used. An increased response to
carbachol, for example, has been shown to be brought about by prior
exposure to low concentrations of NOo. What such a response means is
at present uncertain. But in the present state of our knowledge, such
a test seems to me to be an inadequate basis for regulation.
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What should we measure?
The brunt of fuel cycle pollutants falls on the respiratory system.
It seems obvious, therefore, that our focus of interest should be on this
system, though not of course exclusively. We have fairly adequate and
reasonably extensive tested methods of Investigating the respiratory system.
Thus respiratory symptom questionnaires, spirometry, chest radiography and
measurement of sputum volume and quality have been extensively used. Recom-
mendations have recently been made by a task group of the American Thoracic
Society (ATS 1978). The search goes on for more and more sensitive tests;
but in my view, our problem is much more to apply those tests we already
have than to develop new ones.
Ionizing radiation and coal conversion products pose a potential
risk of cancer, respiratory and other. Collection of morbidity and mortality
statistics on cancer should presumably be one of the indices with which we
should be concerned. But relatively large populations must be studied if
sufficient cases are to develop in a reasonably short time. It is clearly
desirable to monitor other changes, which may occur more frequently than
cancer, changes in sputum cytology, fetal wastage and congenital malfor-
mations, for example, particularly if women are exposed.
The Medical Research Council's Clinical and Population Genetics Unit
has been monitoring lymphocyte cultures in 197 dockyard workers exposed
to low concentrations of ionizing radiation (cumulative dosages of from
1 to 30 rems). They observed a striking correlation between dose in
rem and aberration counts/1000 cells tested. The relationship was particu-
larly notable for cells with unstable aberrations (acentric elements,
dicentrics, rings). This suggests to me that lymphocyte cultures should
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be considered in radiation effects. As other bio-assay systems are
identified, consideration should be given to them as they can provide a
relatively inexpensive method of screening for harmful effects.
Equal treatment of study population and comparison group.
When an industrial population is being compared with the national,
state or other comparison group, it is of course important to avoid
introducing bias through greater attention to the group of greater interest.
There is a serious risk that this may happen. There is an almost irresist-
able tendency to correct deaths which one knows to have been wrongly
certified in the group of special interest, as a result of review of the
hospital records, for example. Clearly such "correction" is quite
improper unless a similar scrutiny of the deaths in the comparison
population is also made. A more subtle form of this bias is to increase
the autopsy rates in the population of interest (but not in the comparison
group).
There may even be problems resulting from the scrutiny and coding of
the death certificates in the population of interest but accepting the
original coding for the comparison group. This seems to me to be parti-
cularly likely to occur when the original coding would have been carried
out under a different revision of the international classification of
causes of death.
Confounding factors.
Many factors other than air pollution influence morbidity and mortality
from the respiratory diseases. Smoking, occupational exposures, infections,
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allergy, heredity, age and sex must be carefully considered before respiratory
disease is attributed to general air pollution. Climate, in particular
temperature level and short-term temperature changes, may also contribute
significantly to disease, both respiratory and other. There may also be
difficulty in separating one pollutant from others. In London, for example,
daily concentrations of smoke and SOp are so highly correlated that it is
impossible to separate their independent contributions to effects. In most
cities, poor people tend to live in areas where pollution is highest.
Inevitably, effects of pollution are therefore confounded with effects due
to low socio-economic status.
Many studies of air pollution have failed to allow at all for smoking,
occupation, ethnic origin and socio-economic status, making any conclusions
that are drawn ajbout the effects of pollution uncertain. Other studies
have made some allowance for some of these factors but this allowance may
not have been sufficient to eliminate the confounding effect.
Miscellaneous problems.
A variety of problems arise in studying effects in relation to short-
term changes in pollution. Studies using daily deaths have shown that the
date a death is registered may not be that on which the death occurred
(Sunday deaths may be registered on Monday and other day-of-the-week
effects may also occur). Place of death may not be that reported. Pol-
lution in most great cities varies considerably from place to place.
Attempts to improve dose estimates by considering areas within the city
lead to problems with small numbers and uncertainty with respect to how
the population at risk of dying may have varied throughout the 24 hours.
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Another problem with daily studies is that there is often a phase
shift between the measurements of pollution and the measurements of the
health effects. Pollution over the 24 hours may be measured from 8:00 a.m.
to 8:00 a.m. Whereas, health may be measured from midnight to midnight.
It is difficult to make personal observations or tests for many days
at a time. We tried to study a sample of elderly persons (over 65 years
of age) in Tampa, measuring their ventilatory lung function once a day.
The best we were able to achieve was to follow a small, declining sample
of persons for three two-week periods. Over six months diaries or telephone
interviews may be more successful, but these suffer from subjectivity and
the problem of remembering to fill in the daily record. Another problem is
the tendency of most large cities to announce their daily "murk" index on
the radio or television, with the possibility that knowledge of pollutant
concentrations to which subjects have been exposed may bias answers.
Problems of analysis.
There are many problems in analyzing data on pollution and health
effects. The studies of Schimmel and his colleagues, Lave and Seskin
and the E.P.A.'s CHESS studies and their critical reanalysis make these
clearly apparent. Most of these authors have discussed these problems.
I do not intend to do so in any detail here. It may, however, be worth
saying again that no amount of statistical sophistication (or juggling)
can compensate for poor, inaccurate or absent data. It may be very
difficult, indeed impossible, to draw conclusions about effects of indivi-
dual variables when these are highly correlated. Multivariate analysis
used to date in pollution studies have always assumed linearity of variates,
an assumption which is at least questionable.
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The most critical decision from an economic standpoint is, of course,
what concentrations should be selected as standards of air quality. On the
basis of past epidemiological studies, average 24 hour concentrations of:
i
3 3
250 yg/m of smoke (as measured by the British smoke filter) and 500 yg/m
of S02 are probably reasonable. Average annual concentrations are harder
to specify, if indeed such standards are useful. One approach might be to
select an annual concentration which experience shows would never permit a
3 3
24 hour concentration of more than 250 yg/m for smoke or 500 yg/m for SOp.
For London this would result in average annual concentrations of about
50 yg/m3 for smoke and 130 yg/m3 for S02> The main trouble with this
approach, however, is that 24 hour distributions of pollutants through
the year differ in different places. What might be appropriate for London
might not be so for New York City.
A serious problem arises when one tries to convert British smoke con-
centrations to equivalent total suspended matter (T.S.P.) as measured with
a hi-volume sampler, the usual method in the U.S. At relatively high
3
concentration (750 yg/m ) the two methods are roughly equivalent; but at
low concentrations T.S.P. measurements are roughly three times those measured
3
with a smoke filter. Thus an annual average concentration of 50 yg/m
3
smoke would translate to about 150 yg/m T.S.P., a concentration that is
about double the current U.S. standard. Most authorities would deprecate
relaxing the particulate standard to such a degree without better evidence
on the relationship between the two methods. Clearly additional research
on the two methods taking particle size into consideration is needed.
These are some of the problems which epidemiologists who are concerned
with pollution have to face. There are, of course, many others, such as
the cooperation of persons being studied, access to records, completeness of
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follow-up and so on. But these are general problems for all epidemiological
work and the title of the session does say Special. In conclusion, I hope
we have not succeeded in convincing you that the problems are so great
that epidemiological studies should not be attempted. Epidemiology is the
only way of obtaining answers to some of the questions being asked.
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REFERENCES
1. Buechley, R.W., W.B. Riggan, V. Hasselblad and J.B. VanBruggen. S02
levels and perturbations in mortality. A study in the New York-New
Jersey Metropolis. Arch. Environ. Health 27;134-137, 1973.
2. Ferris, B.G., Jr. Epidemiology Standardization Project. Amer. Rev.
Resp. Dis. 1118:1-120, 1978.
3. Lave, L.B. and E.P. Seskin. Air Pollution and Human Health. Baltimore:
The Johns Hopkins University Press, 1977. 368 pp.
4. Schimmel, H. and L. Greenburg. A study of the relation of pollution
to mortality. New York City, 1963-1968. J. Air Pollut. Control
Assoc. 22:607-616, 1972.
5. Schimmel, H. and T.J. Murawski. S02~Harmful pollutant or air quality
indicator? Air Pollut. Control Assoc. 25_:739-740, 1975.
6. Schimmel, H. Evidence for possible acute health effects of ambient
air pollution from time series analysis. Bull. N.Y. Acad. Med.
54:1052-1108, 1978.
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ROLE OF ANIMAL EXPERIMENTS IN RELATION TO HUMAN HEALTH EFFECTS
By
Yves Alarie, Ph.D.
Department of Industrial Environmental Health Sciences
Graduate School of Public Health
University of Pittsburgh
Pittsburgh, Pennsylvania
15261
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INTRODUCTION
When new chemicals are proposed for introduction on the market as
food additives, drugs, pesticides, etc., an important portion of the re-
search work done is devoted to evaluation of their possible toxic effects,
not only for humans, but also for the biosphere.
Thus, the role of animal experiments is crucial in preventing cat-
astrophic effects to occur. The second role of animal experiments is to
investigate and confirm, expand, or deny claims of possible effects on
humans of chemicals already on the market and for which epidemiological
evidence is introduced about their possible deleterious effects. The
most important role of animal experiments is concerned with accurate pre-
diction of safe levels of exposure for the human population.
Animal experiments are also conducted to probe the mechanisms by
which toxic reactions are produced, and how the chemicals are biotrans-
formed and eliminated. This established a sound basis for recommendation
of safe levels of exposure.
II. REQUIREMENTS OF AN ANIMAL MODEL
In order for animal models to fulfill their role, they must be
solidly based on fundamental sciences and provide:
1. Sound anatomical, physiological, or biochemical basis of the
measured toxic effects.
2. The response observed must be characteristic, easily recognized,
and amenable to quantitation.
3. Concentration-response relationship must be demonstrable.
••
4. The qualitative correlation between the effect observed in animals
and the effect observed in humans must be very high for a series
of related chemicals.
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5. From the concentration-response relationship, prediction of effects
to occur in humans should be made over a wide range of exposure con-
centrations as well as delineate safe levels of exposure.
Obviously, the above are not always fully obtained with each animal
model currently used. Nevertheless, animal experimentation will in-
crease in the coming years and will be refined so that better predic-
tions can be made.
III. SOME ANIMAL MODELS
This Symposium is concerned with health effects from fuel cycle
pollutants, both waterborne and airborne. By using some examples of
animal models, I hope to demonstrate how they can be used and what their
role is, in relation to human health effects.
A. Airborne Irritants
Of industrial and urban atmospheric contaminants, approximately
50% of them have irritating properties. First, they impinge on the
surface of the cornea and nasal mucosa and stimulate the nerve
endings. This stimulation evokes a burning sensation. Entering the
lower airways, these chemicals can also induce bronchoconstriction
and inflammatory reactions. Repeated exposure to these chemicals
induces chronic bronchitis. An animal model (1,2) has been developed
to first categorize airborne chemicals as irritating or not, evaluate
and compare their potency, and to predict safe levels of exposure.
a. Basis ot tne Moael
•«
Recognition that an airborne chemical is a sensory irri-
tant is accomplished by monitoring the breathing pattern of an
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animal, typically a mouse, as shown in Figure 1.
When inhaling an irritant, a characteristic pause occurs in the
breathing pattern due to stimulation of the trigeminal nerve
endings located in the nasal mucosa. A reflex respiratory inhi-
bition is initiated. This response is easily recognized and
can be monitored continuously, as shown in Figure 2.
Since the level of response, measured as a decrease in
respiratory rate, is related to the concentration of the irri-
tant, a concentration-response relationship can be developed,
as shown in Figure 3.
b- Comparisons to be Made
Since concentration-response relationships can be obtained,
it then becomes very easy to compare the potency of various chem-
icals. As shown in Figure 4, the potency of these airborne chem-
icals varies greatly.
c. Predictions for Human Health
Once concentration-response curves are obtained» a con-
venient point for comparison, provided the curves are fairly
parallel, is the half-way point between no response and maximum
response, which for this model can be taken as 50% decrease in
respiratory rate and has been termed RD50' The RD5Q values for
the chemicals shown in Figure 4 are listed in Table 1. From
these values, predictions of effects to be expected in humans
and establishment of safe levels of exposures can be attempted.
A list of various standards for exposures to airborne chemicals
is in Table 2. In Table 3 are the proposed relationships of RD™
-146-
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to expected human effects and to the standards presented in
Table 2. If we want to test how effective the model is, we can
compare the predictions with the current Threshold Limit Value
as done in Table 4. We find that for 9-11 chemicals, the TLV
is between 0.1 - 0.01 RD5Q. The two exceptions are for epi-
chlorohydrin and formaldehyde. The difference for epichloro-
hydrin is small, but for formaldehyde, the acceptable range for
TLV predicted by the model is much lower. This difference has
been discussed and is due primarily to the fact that the animal
model does not consider tolerance development to this chemical,
while in workers continuously exposed to formaldehyde, this
phenomenon occurs (3).
Another test of the predictions made by the model is to
evaluate how accurate the predictions are for the range of expo-
sure concentrations. This is presented for 2 of the 11 chemicals,
acrolein and chlorine in Tables 5 and 6 (see Reference 1 for
others). It can be seen that, in general, the predictions made
within each concentration range are reasonable. Unfortunately,
for the lowest concentration, with the exception of sulfur di-
oxide, there were no data in the literature to permit us to
present firm conclusions. However, as long-term chronic studies
on these chemicals are being conducted, these results should
complete the picture.
d. Difference in Sensitivity
In predicting levels of effects for humans, we must
take into account, the difference in sensitivity existing
-147-
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in the population. This is particularly difficult to take into
account in animal experiments since we are using fairly homog-
enous pupulations. Several species can be tested, or different
strains can be tested to obtain an estimate of the variation in
sensitivity. This has been done using the model described above
and some of the results are presented in Table 7. As can be
seen, there is a factor of 10 between the most and the least
sensitive strains. Such variations can then be taken into
account when making predictions of human reactions from animal
models.
B. Pulmonary Hypersensitivity
Many industrial contaminants can elicit bronchial hypersensi-
tivity. Reports of asthma-like attacks by workers exposed to simple
chemicals such as toluene diisocyanate, phtalic anhydride, trimellitic
anhydride, ethylene oxide, formaldehyde, ethylene diamine, etc., are
frequent. Exposures to these chemicals stimulate the formation of
reaginic antibodies.
a. Basis of the Model
Several animal species have been used to investigate the
sensitizing properties of airborne chemicals. When challenged
with an aerosol of antigen, a characteristic breathing pattern
results which can be quantitated so that the magnitude of the
response can be obtained (4). Using the challenging antigen,
sera from sensitized animals can then be tested for antibody
reactive toward the hapten groups (i.e., specific chemical) of
interest.
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b. Application in Humans
Once it has been demonstrated that the antigen prepared
can be used to detect antibodies in sera of animals, it becomes
very easy to apply the technique for evaluating sera from
workers exposed to the chemical, in this case, toluene diisocy-
anate (5,6). Such tests, as shown in Figures 5 and 6 can iden-
tify workers with elevated levels of IgE antibodies and permit
the follow of their disappearance, once the workers are removed
from exposures.
IV. CONCLUSIONS
Society is now entrusting toxicologists with the primordial re-
sponsibility to prevent entry on the market of chemicals which can lead
to disastrous effects on a very large scale. Often we read newspaper
accounts, as well as scientific reports of adverse effects of chemicals.
Have toxicologists failed to protect the public? What we do not read
about is the number of promising chemicals which are prevented from
entering the market because of what toxicologists found in their inves-
tigations using animals. It would be interesting to have some accurate
statistics in this area to determine the performance of toxicologists
and the animal models used.
It remains, however, that toxicologists will be at the front-line
of evaluation of new chemicals and it is only via toxicological testing
in animal models that we can prevent adverse effects to occur in man.
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REFERENCES
1. Kane, I.E., Barrow, C.S. and Alarie, Y. A short-term test to predict
acceptable levels of exposure to airborne sensory irritants. Am.
Ind. Hyg. Assoc. J. 40, 207, 1979.
2. Alarie, Y., Kane, I.E. and Barrow, C.S. Sensory irritation: the use
of an animal model to establish acceptable exposure to airborne
chemical irritants. In: Industrial Toxicology, Principles and
Practice. A. Reeves and H.N. MacFarland Eds. J. Wiley for 1979.
3. Kane, I.E. and Alarie, Y. Sensory Irritation to formaldehyde and
acrolein during single and repeated exposures in mice. Am Ind.
Hyg. Assoc. J. 38, 509, 1977.
4. Karol, M.H., loset, H.H. and Alarie, Y. Hapten-specific respiratory
hypersensitlvity 1niguinea-pigs. Am. Ind. Hyg. Assoc. J. 39, 546,
1978i
5. Karol, M.H., loset, H.H. and Alarie, Y. Tolyl-specific IgE anti-
bodies 1n workers with hypersensitivlty to toluene diisocyanate.
Am. Ind. Hyg. Assoc. J. 39_, 454, 1978.
6. Karol, M.H., Sandberg, T., Riley, E.J. and Alarie, Y. Longitudinal
study of tolyl-reactive IgE antibodies in three workers hypersensi-
tive to toluene diisocyanate (TDI). J. Occ. Med., 21,, 354, 1979.
-150-
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TABLE 1
"50
and 95% Confidence Limits for
Eleven Sensory Irritants
Compounds
Acrolein
Ammoni a
Chlorine
Chi oroacetophenone
Chi orobenzyli dene
malononltrile
Chloropicrin
EpichlorohydHn
Formaldehyde
Hydrogen chloride
Sulfur dioxide
Toluene diisocyanate
RD50
ppm
1.68
303
9.34
0.96
i
0.52
7.98
687
3.13
309
117
0.39
95% Confidence
Limit
ppm
1.2.6 -
159
6.64 -
0.766 -
0.429 -
6.22 -
633
2.54 -
281
107
0.345 -
2.24
644
14.1
1.26
0.677
10.6
748
3.97
410
128
0.446
Exposure concentration associated with a 50%
decrease in respiratory rate.
-151-
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TABLE 3
Proposed Relationships of RD5Q Concentration Values
to Industrial and Environmental Standards
Concentration
Designation
Expected Response
in Humans
Proposed Relationships
to Industrial Standards
Proposed Relationship to
Environmental Standards
I
(->
01
I
10 RD
50
Lethal
Lethal or extremely severe
Injury to the respiratory
tract
RD
50
Toxic
Intolerable sensory irri-
tation; respiratory tract
Injury may occur with
extended exposure
0.1 RD
50
Effective
Definite but tolerable
sensory irritation
Highest acceptable
concentration for TLV
0.2 RD5Q-basis for STEL
0.3 RD5Q-basis for EEL
0.01 RD
50
Ineffective
Minimal or no sensory
irritation
Lowest concentration
necessary for TLV
0.001 RD
50
Acceptable
"Safe" level of no
effect
Recommended highest
concentration for
Air Quality Standard
-------
TABLE 4
Prediction of Sensory Irritation Responses in Humans for
Eleven Sensory Irritants Evaluated in Mice, and
Relationship of RD5Q to Current TLV-TWA Values*
Sensory
Irritant
Acrolein
Ammonia
Chlorine
hi oroacetophenone
Chi orobenzyli dene
malononitrile
Chloropicrin
Epichlorohydrin
Formaldehyde
Hydrogen chloride
Sulfur dioxide
Toluene
diisocyanate
Predictions of Responses in Humans
Intolerable
at RD5Q(95%
C.L.)
PPm
1.68
(1.26-2.24)
303
(159-644)
9.34
(6.64-14.1)
0.96
(0.766-1.26
0.52
(0.429-0.677)
7.98
(6.22-10.6)
687
(633-748)
3.13
(2.54-3.97)
309.0
(281-410)
117
(107-128)
0.39
(0.345-0.446)
Uncomfortable
but Tolerated
at 0.1 RDcn
oU
pom
0.2
30.0
0.9
0.1
0.05
0.8
70.0
0.3
30.0
12.0
0.04
Minimal ,
No Effect
at 0.01 RD50
ppm
0.02
3.0
0.09
0.01
0.005
0.08
7.0
0.03
3.0
1.2
0.004
1977
TLV-TWA
ppm
0.1
25
1
0.05
0.05
0.1
5
2(0*
5(O*
5
0.02(0)"
Is Current
TLV-TWA betwee
0.1-0.01 RD5Q
yes
yes
yes
yes
yes
yes
no
no
yes
yes
yes
* (C) indicates'Ceiling Value
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TABLE 5
Acrolein (3)
Predicted Effect According
to Proposed Model
Lethal or extremely severe
injury to the respiratory*
tract.
Intolerable sensory irritation;
respiratory tract injury may
occur with extended exposure.
Definite but tolerable sensory
irritation.
Highest acceptable concentration
for TLV.
Minimal or no sensory irritation.
Lowest concentration necessary
for TLV.
Safe; level of no effect.
Recommended highest concentration
for Air Quality Standard.
Concentration
Factor in
Terms of RDg0
10
. 1
ID''
ID'2
lO'3
Corresponding
Concentrator
ppm
20
2
0.2
0.02
0.002
Reported Exposures to Acrolein
(Results are for humans unless otherwise noted)
21.8 ppm Intolerable.
10.5 ppm x 6 hr 1/2 rabbits died.
8 ppm x 4 hr 1/6 rats died.
5.5 ppm Intense Irritation.
1.2 ppm x 5 min Extremely Irritating - only Just tolerable.
1.2 ppm x 5 min 872 of test panel reported irritation.
1 ppro x 5 min 024 of test panel reported irritation.
1.8 ppm x 30 sec Odor detectable.
1.8 ppm x 4 win Profuse lacrimation, practically intolerable.
0.5 ppro x 5 min 19-351 of test panel repdrted Irritation.
0.5 ppm x 12 min 9U of test panel reported irritation.
0.3 ppm x 60 min Considerable acute Irritation after 10-20 min; decreased
respiration.
0.15 ppm Nasal Irritation.
0.09 ppm Eye Irritation.
0.06 ppm Eye Irritation 0.471 on scale of 2.0.
No data available.
I
M
Ln
I
-------
TABLE 6
Chlorine (1)
Predicted Effect According
to Proposed Model
Lethal or extremely severe
injury to the respiratory *
tract.
Intolerable sensory Irritation;
respiratory tract Injury may
occur with extended exposure
Cefinite but tolerable sensory
irritation.
•Highest acceptable concentration
for TLV.
Minimal or no sensory irritation.
lowest concentration necessary
for TLV.
Safe; level of no effect.
aeconimended highest concentration
-'or Air Quality Standard,
Concentration
Factor In
Terms of RD5Q
10
. 1
ID'1
Iff2.
i
ID"3
Corresponding
Concentrattor
ppm
90
9
0.9
0.09
0.009
Reported Exposures to 'Chlorine
(Results are for humans unless otherwise noted)
1050 ppm Lethal concentration.
1000 ppm Rapidly fatal.
105 ppm Tolerable for only a few seconds.
40-60 ppm Dangerous for even short exposure.
20(8.7-41) ppm Painful eye Irritation,
16.8 ppm Irritation of throat 1n 3 minutes.
14-21 ppm Dangerous.
9(2.6-41) ppm Intolerable respiratory Irritation.
5 ppm Chronic exposure caused premature aging; bronchial disease;
mucous membrane Inflammation; corrosion of teeth.
3-6 ppm Stinging or burning of eyes, nose, and throat; headache.
3.0(1.8-4.2)ppm Painful respiratory Irritation.
1-2 ppm Men can work.
1.3(0. 02-2. 9)ppm No eye or respiratory Irritation.
0.05 ppm Odor detectable.
No data available.
I
H
Ui
-------
TABLE 7
Results of Sensory Irritation Obtained in Various
Strains of Mice with Exposure to Sulfur Dioxide
Strai ns
A/HEJ
A/HEJ
BALB/O
BALB/O
BALB/C
C57/BL6
SJL/J
SOL/J
C3H/HEO
C57L/J
DBA2/J
DBA2/J
A/J
Swiss 0
Swiss
Swi ss
Sex
F
M
F
F
M
F
F
M
F
M
M
F
F
M
M
F
H-2
Haplo-
type
a
a
d
d
d
b
s
s
k
b
d
d
a
-
-
—
RD50*
(ppm)
41
69
75
78
106
80
104
320
125
200
321
445
> 450
117
117
133
95% C.L.
39-44
46-104
72-80
53-114
67-167
59-110
72-150
162-630
110-142
113-352
178-580
333-595
—
99-138
67-204
94-187
Value obtained from concentration-response relationship which
represents the concentration necessary to obtain 50% decrease
in respiratory rate. Least squares linear regression analysis
with F test for regression significant at 0.05 level for all
groups.
jJResults from previous report.
+Data obtained from two different shipments—six months apart.
From Alarie, Y., Oka, S. and Cypess, R., unpublished, under
NIEHS grant #ES-00872.
-157-
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sec
Figure 1 - Typical oscillograph display showing the respiratory cycle of
a mouse during normal control conditions (upper tracing) and
exposure to a sensory irritant (lower tracing).
Figure 2 - Average respiratory rate of 4 male Swiss-Webster mice prior,
during, and following exposure to formaldehyde (top) and
acrolein (bottom).
-158-
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80
at
O 60
oe
a.
to
Ul
06 40
U
ui
O
20
I I
RD50=1.7PPM
95%C.L. = 0.77 -3.6
j i
I I I I I I I 11 I I
0.1
1.0 10.0
CONCENTRATION OF ACROLEIN -PPM
Figure 3 - Concentration-response relationship obtained with
exposures to acrolein in male Swiss-Webster mice.
I I I II
CHlO«O»CtIOPH£HOHE
FOIMALDIHVDI
\
IFICNiOHOMYMIN
I I I I I I II I I I I I I I I ll I I 1 I I I I ll I I I I I I III II I I I I I II
100
- rut
100
10000
Figure 4 - Concentration-response relationships obtained for
eleven sensory irritants in male Swiss-Webster mice.
-159-
-------
20 0(H
1600-1
1200-
5
a.
800-
400-
A0300)
A(2500)
m
A •
D *
a
a a
P<.01
» immediate response confirmed by bronchial challenge;^ »
Immediate bronchial response; Q , delayed bronchial response; £| , cutaneous
response;Vj- , delayed bronchial and cutaneous responses; @ , no response.
Significant titers: > 456 net cpm (P <0.01), >535 net cpm (P< 0.001).
-160-
-------
3000-
I. ASTHMA
TDI
BRONCHIAL CHALLENGE
TDI
2500-
2000-
1500-
1000-
500-
CASE1
(.ASTHMA
TDI
(.ASTHMA,HIVES
MDI
CUTAN.
TDI H
D.ASTHMA
TDI
D.ASTHMA,HIVES
TDI
CASE 3
CASE 2
9-77
11-77
T
1-78
I
3-78
I
5-78
7-78
I
9-78
11-78
DATE (MONTH,YEAR)
Figure 6
RAST assay for tolyl-reactive IgE antibodies and clinical hypersensitivity
episodes in 3 workers with TDI sensitivity. Net cpm = cpm (T-HSA discs) -
cpm (HSA discs). I. Asthma: immediate bronchial reaction occurring within
15 minutes of exposure. D. Asthma: delayed-onset bronchial reaction
occurring more than 120 minutes following exposure.
-161-
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DISCUSSION
SESSION II
A_ question to Dr . Higgins; Regarding one of the areas of
the pure type of pollutants, that originally needs
epidemiological assessment. As you know, a cornerstone of the
national energy program is the dieselization of mines. Because
of substantial increases in coal mined daily, each mine has
opted for dieselization. However, the Unions have gone on
record against dieselization. Just last week the West Virginia
legislature passed a moratorium on all diesels in West Virginia
mines for two years or until such time as the health impact of
use of diesels in mines has been resolved. Since the health
effects of diesels may be a big problem I would like to solicit
from Dr. Higgins or other members of the panel any comments or
suggestions they may have in regards to this urgent problem.
Dr. Higgins: The use of diesels underground and elsewhere
has become a political rather than a scientific issue. This is
a pity because there are important scientific questions to be
answered about the hazards of diesel emissions. There are two
main worries: do the emissions cause cancer of the lung? and
do they result in chronic obstructive lung disease? The
evidence, such as it is, suggests that they are not serious
hazards for either of these conditions. No study of workers
exposed to diesel emissions has shown an excess cancer risk.
Some studies of chronic respiratory symptoms and disability have
suggested some effect; but others have not. In Dr. Rockette's
study of the mortality of miners, mortality from lung cancer was
highest in Charleston, West Virginia, an area where diesels are
not used.
Dr. Hamilton; I don't wish to change the topic
immediately on diesels, because I think there's an area of
uncertainty here. But I want to ask Dr. Lippmann a question
because I have the general impression from his talk that he felt
very comfortable with the current methods of assessing the
conventional air pollutants, the health effects of which we seem
to have a great debate about. One of the problems is
exemplified, for example, in the recent Congressional review, it
isn't so recent now, in a review of the CHESS study they were
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very critical of the methods of measurement. Do you feel that
existing methods of measurement of the conventional air
pollutants, particularly of the species of the oxidation
products of sulfates, are such that we can place reliance on
them and later judging about the possible health effects
assessment?
Dr. Lippmann: I think there are really several questions.
One, I indicated that the only sulfur oxide we know how to
measure reasonably well was sulfur dioxide. We don't know how
to make routine measurements of any of the sulfur oxide
particulates directly. In fact, we rarely measure them
effectively on collected filter samples. If you want to measure
sulfur ic acid, you have to use teflon filters and do chemical
separations prior to the analyses. Clearly, we don't have
adequate methods for many of the pollutants of interest. Now,
sulfuric acid is not currently a regulated material; i.e.,there
is no ambient air standard for it. That is perhaps one reason
why we have not seen any effective instrument development,
although EPA has supported several instrument development
projects which were unsuccessful. While I agree with you, in
general, that we don't have accurate measurements, the fact that
we don't end up with good measurement and data bases is seldom
the problem of the technology. It's having the foresight to
know what to measure, and to have the resources, financial as
well as technical, to make enough good measurements.
Question: My first question, for Dr. Lippmann, is really
a follow-on to the one he just answered. Would you comment on
the actual field experience in the use of measuring techniques,
going from the technological capability to what actually has
occurred? My second question is to Dr. Higgins. Would you
comment on the influence of the actual field experience in the
use of measuring techniques? The reason for this question is
clearly that if you are investigating diseases that have latent
periods of 20 or 30 years, and you do a ten year study, you're
clearly going to get nothing, but this fact does not prove
anything. You may have spent a million dollars of the
taxpayers' money with no result. The final question that I have
is for Dr. Alarie: Would he comment on the Ames test as a
method of detecting carcinogens, that being a kind of animal
model to which human experience is now being compared.
Dr. Lippmann : A real problem in any study involving human
investigators and technicians is misuse of instruments.
Instruments may have good designs and demonstrated feasibility,
but that doesn't mean that you can depend on the technicians who
are likely to be employed in moderately difficult situations to
use them properly. The only reliable data are from studies
where there are elaborate quality control programs behind them
to make sure that the calibrations are performed frequently and
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reliably and, if necessary, where corrections or adjustments can
be made in the instruments. There is one other point. I think
you can be misled by worrying about the precision of the data.
As Dr. Higgins pointed out, the sampler is seldom located in
the most appropriate place, and worrying whether you have a 10,
20 or 405& error in the measurement may be excessive. The
expense of improving the precision of measurement at that
particular site may not be worth it when the site is not
representative of the area in which it is located.
Dr. Higgins: Two years ago when we were studying air
pollution in Florida, we learned that the West Gaeke method for
measuring S02 could be completely invalidated if the temperature
in the sampling box rose to high levels. Here was an example of
a problem with a test which has been used for many years as a
standard method which had been completely ignored—until a
technician brought it to light.
With regard to duration of follow-up, clearly a long period
may be necessary if you are to identify cases of cancer with a
long latency. I have never been completely convinced, however,
that you will get nothing from shorter periods of follow-up. I
suspect that some more sensitive subjects should show up after
shorter periods. Clearly, if you are studying a population with
about 20 years since first exposure to a suspect carcinogen if
the average latency period is 25 years, 20 years will not be
long enough to identify all the cancer cases which may develop.
The next 10 or 20 years may be crucial. 20 years may, however,
identify some excess cases. It is clearly very important to
live long enough to do the further follow-up or at least to will
the data to someone who will do it posthumously for you.
Dr. Alarie; Well, I have no problem with the Ames Test.
I think it's entering into a sort of second generation now,
where potency response or dose response curves are being
obtained, which I have shown in the model we have. You can't go
anywhere in terms of prediction until these are done and you
have it for several carcinogens on which you have some human
data. We have several carcinogens, known carcinogens, in man
from extremely potent to moderately potent and some probable.
One would think that Ames is intelligent enough to recognize
that fact. As a matter of fact, I think he is doing just that
right now. So I predict that within two to three years it
certainly will be a quite useful test. Right now for yes or no
answers that is ridiculous. Secondly, there are a lot of idiots
running around dumping a lot of things on the Ames test knowing
absolutely nothing about what they're doing. And they're
publishing letters here and there and everywhere saying it's no
good. If you dump a highly reactive chemical in these nutrient
systems and then they come out negative; well, what you have is
a stupid test to begin with.
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Dan Swartzman, University of Illinois School of Public
Health; 1 have a question for the panel or the attendees or the
moderator. I am troubled by the use of indicators, although I
understand it is a rather useful scientific shorthand. I'm
reminded of the situation with guidelines on wage and price
control where you set a 7% ceiling, which all of a sudden
becomes the target that everybody tries to meet. In community
air pollution control we've found that setting an indicator for
ozone as the chemical indicator for the control of chemical
oxidants concentrated our efforts on solving the ozone problem,
not on solving the photochemical oxidant problem. To the extent
that recently USEPA has decided that, in fact, the photochemical
oxidant problem is an ozone problem. Similarly with the use of
sulfur dioxide as an indicator of whatever. The total suspended
particulates-sulfur dioxide complex problem, using the sulfur
dioxide as an indicator of that, has led to a lot of political
problems, particularly in my home state of Illinois where we're
trying to do the best to protect the public from health problems
but we are way below the sulfur dioxide levels. We get a lot of
people saying, "Well, you can have a great deal more sulfur
dioxide without doing harm to the general public. Look how far
below the levels we are." I'm troubled by the process, the
political process by which the indicator loses its effect as a
symbol and instead gains some respectability as the end in
itself. I was wondering if anybody has suggestions, aside from
just constantly reminding ourselves and the politicians and
bureaucrats that these were established for use as indicators.
Dr. Lippmann: I could not agree with you more—in fact, I
spent my time pointing out that the most commonly used indicator
for air pollution potential has no relevance. Sulfur dioxide is
the best example possible. Because we did not know what
component of the complex to measure, we measured the one that we
could most easily measure. On the other hand, what should one
do when you have such a complex mixture and you can't possibly
measure all the potential toxicants? The only useful thing to
do is to keep the limitations of the measurements in mind and to
pick an appropriate indicator. For example, ozone appears to be
an appropriate indicator for the photochemical smog mixture,
albeit with some limitations. S02 is a poor indicator for the
SOx-particulate complex because S02 is essentially non-toxic at
realistic ambient levels. I think having a group of indicators
specific to the process may be the most positive thing we can do
in the control sphere at this time.
Dr . Hamilton; I'd just like to ask Dr. Lippmann to
clarify his last remark. My understanding of S02 is that it is
a precursor of sulfate.
-------
Dr. Lippmann; Sulfates form continuously and gradually
over long distances and I think a rational national policy would
be to limit sulfur dioxide emissions over the whole Northeast in
a uniform way. To have certain cities use 0.3% sulfur fuel and
other cities use 3.0% sulfur fuel is completely irrational.
Dr. Hamilton; I couldn't agree with you more except that
you're limiting it to the Northeast. It seems to me that with
prevailing winds we should certainly put the major emphasis
further west.
Dr . Lippmann; I didn't mean the Northeast in a limited
sense--! meant the whole Northeast quadrant of the United States
from Minnesota eastward and perhaps we should include the
southeastern part of the country as well. We have a different
problem out west than we do in the east.
Swartzman; I'd like to just clarify the problem I see with
the sulfur dioxide particularly in our state, (Illinois). We're
probably on the western edge of prevailing winds that created
the sulfate problem in the rest of the country. We have a
number of power plants around the state that are located in
areas in which the ambient air quality is far below the sulfur
dioxide national ambient air quality standard that has been set.
There is a great deal of movement in our state, by the
utilities, by the coal industry, and some other right thinking
people, who feel we ought not to have that sort of "overkill"
because we're so far below the standard that these plants ought
to be allowed to emit more sulfur dioxide than they are
currently allowed to emit. The problem that faces public health
advocates is that now that we have got this wonderful indicator
that tells us what the problems are, we're stuck with it as the
problem itself. We're so far below the sulfur dioxide level in
some of these cases that it is absolutely impossible to argue
for lower emission levels on a particular plant. Particularly
when the people in the legislature are able to say, "Well,
-------
great mistake, which I suspect they will, about using total
sulfate as the next air quality standard to drive controls.
Because ammonium sulphate is innocuous and that's where most of
the measured sulfate will be. Sulfuric acid is something else
again, because of the very variable percentage of it. Sulfates
might be important , but we just don't have enough data base to
really know. But total SO1* measured on a filter, I think would
be just as misleading, and just as misguided, as an engine to
drive controls of S02 gas.
W. C^ Hamilton, Continental Oil Company; I wonder if Dr.
Higgins would expand on his asthma remarks.I talked to an asthma
specialist last week who pointed out that not only do foods and
pollens exacerbate asthma attacks but there is a strong
psychogenic component and temperature change that have an
effect. He said that while he did not know anything about
epidemiology, he did feel it would be very difficult to ascribe
any asthma attacks to air pollution per se. It might occur or
might not occur, but one could never tell.
Dr. Higgins: I agree, it is difficult to acsribe
asthmatic attacks to air pollution, but I don't believe it is
impossible. In fact, asthmatic subjects may respond rather
specifically to certain substances. The trouble is that most
asthmatics respond to many different stimuli. The problem is to
identify asthmatics who respond specifically to pollutants and
then try to assess the consistency of their response.
Another problem with asthmatics and air pollution is that
there may be a response to some pollen which has not been
measured but which may vary in parallel with pollution.
A further problem is that asthmatic attacks may be
triggered by short peaks of pollution which may have very little
effect of the 24 hour pollutant concentration. It might appear
in such circumstances that a very low 24 hour concentration is
causing attacks and that consequently no concentration of the
pollutant is acceptable. On the whole, asthmatic attacks are in
my view a dangerous way of reaching acceptable pollutant
concentrations.
Question: Is there any way you can measure the sulfuric
acid in the emissions?
Dr . Lippmann: From a point source, the answer is yes.
There are quite acceptable methods for stacks or other point
sources where you have relatively high concentrations. I am
less sanguine about the possibility of measuring a few
micrograms to 20 micrograms per cubic meter in ambient air;
there you may have some problems. If you are influenced by a
local point source it could be measured by available technology
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with pretty good precision by someone in your local health
agency who could help.
Fred Lippert, Brookhaven National Laboratory; I want to
continue this debate I thought we had started on the sulfur
dioxide standards. I am a little confused as to whether there
is a disagreement among members of the panel or not. Dr.
Higgins, I believe, said he could live with 100 micrograms
annual average of S02 . I presume that included the sulfate
that goes with it. And Dr. Lippmann, if I understood you
correctly, you want to put the whole country on 0.2% sulfur or
do you want to hold that to 2%1 I am not sure which you meant.
You're concerned about sulfuric acid, and as a result you are
willing, regardless of the cost, to eliminate all the sulfur in
the atmosphere. Can you straighten me out?
Dr. Griffin: To whom are you addressing the question?
Fred Lippert: I'd like to hear if they both agree on this
or if they disagree.
Dr. Higgins: On the basis of the epidemiological evidence
and even more from animal experiments it is difficult to support
an ambient average annual standard fo S02 of less than 100
microg/m3. Alone, S02 appears remarkably harmless. One must
remember, however, that such an average annual concentration is
compatible with a one to three hourly concentration of perhaps 2
mg/m.3. This puts a somewhat different complexion on the issue.
Furthermore, S02 does not usually occur alone, and may be
converted into other chemicals--sulfates, for example, which
have sometimes been thought to be more irritant, though there is
now doubt about this.
Dr. Schimmel has been studying daily deaths in relation to
daily S02 and particles in New York City. He believes S02 to be
not only harmless but even beneficial. I find it difficult to
go along with him on this. But it is clearly important to try
and resolve the issue.
Dr. Alarie: My grandmother knew that. Dr. Higgins, I am
against this primitive method of burning sulfur candles at the
wake as a sort of healthy activity of helping people to the next
wo r 1 d .
Dr. Lippmann: I was not advocating any particular
level—I was simply trying to get the thinking going in a
different direction. While S02 by itself is not really likely
to be important, it does act as a messenger. In the past we
attempted to control the messenger rather than getting at the
real problem. It is time to get past that type of thinking.
The visibility problem is largely a sulfur oxide particulate
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problem for the northeast quadrant of the United States and for
the southeast to some extent also. In terms of acid rain, we
also have a problem which has to be addressed by control of
sulfur emissions. What I'm saying is that it's not fair to put
the burden of emissions controls on areas of the country
selectively for what will turn out, in retrospect, to be
capricious reasons. I don't know what percentage of sulfur
emissions control is appropriate for this whole quadrant of the
country where more than 50% of the population lives. But, it
should be distributed more equitably than it is now. It is
likely that 2% is too high, and 0.3% is too low for all sources.
We will have to come to some compromise figure, which, as
Senator Bayh suggested, may not necessarily be a zero risk
level. But it, at least, should be more equitable than the
multiplicity of limits now used in the various local regions.
Dr . Griffin: Let me ask one clarifying question. Are you
suggesting that the control of air pollution should not be based
on attempting to deal with air quality standards of some sort
locally? Or rather, that our control should be on an
industry-wide basis, so that there should be a reduction in
emissions of all sorts? Is that the basis for your suggestion?
Dr . Lippmann; I won't say that across the board; I do
say so for sulfur dioxide which is transformed to sul fates
during long range transport. We, for instance, in our own air
pollution studies, find that a location at High Point, New
Jersey, a very lightly populated site at the confluence of New
York, New Jersey and Pennsylvania in the summer-time, has
sulfate levels which are 85% as high as they are in New York
City. Thus, the contribution of the metropolitan region to the
sulfates measured in New York City, is only about 15 to 25%. In
that kind of situation the concept of local air sheds is
completely inappropriate. For other pollutants, it may still be
appropriate.
Julian Andelman; I have a comment and a question. As far
as standards are concerned, in the water field they are
different and they can be useful, particularly for those
parameters that may not be getting to levels that could be
harmful regularly, but rather when they're normally low and then
become indicators of the central problem. I feel more
comfortable with using them not necessarily for control levels,
but as indicators of the problem; for example, carbon
chloroform extract as an indication of high levels of organics
in water.
In 1970 the World Health Organization adopted the guideline
for six polycylic aromatic hydrocarbons in drinking water, such
that when the total concentration exceeded 20 ug/1, this would
be reason for concern and further investigation. And today in
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the water field there is a lot of concern about chlorinated
organics, some of which one could readily measure but a full
scale set of analysis would be rather complex; thus people are
trying to find indicator parameters, like total organic
chlorine, which one could perhaps more easily monitor.
Hopefully, this would ultimately result in a set of standards,
but for now the measurement simply would be used as a guide for
levels of concern .
I have a question I'd like to address to Dr. Alarie to
perhaps expand on a major point he made. How valid might this
target be for those chemicals that are sensory irritants, but
might also have other toxicological properties, like latent
effects on the central nervous system, or might be mutagens or
carcinogens? In other words, might this be expanded to those
sensory irritants that have more serious or more variable human
effects?
Dr . Alarie: I'm talking about a concept of getting a
concentration response curve and obviously the concept applies
to any model system you want to use, not only the model we have
used. If you have a chemical, let's say carbon monoxide, and
this animal model is used, the animals will die and -no
irritation response will be seen. Any model has limitations.
However, basically any chemical can be placed into a
classification; I've shown one model for sensory irritants and
developed one for pulmonary hypersensitivity and one can be
developed for any endpoint that you are interested in. I
haven't talked about limitations of models. We're working on
this now with 11 very common solvents that are used in industry,
and where the RD50s are now in the thousands of parts per
million. At one point, I fully expect that the model will no
longer be useful since another toxic effect will predominate.
Dr . Lippmann: I think though that there is one point in
your comments which really does stand out and has to be
addressed. If the material is a sensory irritant, and only a
sensory irritant, the model is great. When the sensory irritant
is also something else, such as a carcinogen, clearly it is not
great. Epichlorohydrin, in particular, has been shown to be an
animal carcinogen by various routes of administration, including
inhalation, and I believe that the results from epidemiological
studies are pointing in this direction also.
Dr. Alarie; That's fine with us. We have no objection
that chemicals would have other effects--obviously we expect
that they will have other effects. What we are interested in is
predicting a level, a concentration, at which epichlorohydrin
will not induce cancer. At the Society of Toxicology last week,
there was a dose response relationship presented for the
carcinogenicity of epichlorohydrin. This came from a 90 day
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study and there is now a three year study going on. Therefore,
I'm looking forward to see at what level we are going to detect
cancer occurrence. This would be true also for
bischloromethylether. Bischloromethylether is an extremely
potent sensory irritant, also the most potent airborne
carcinogen known in man. But it also has a dose response
relationship. It also has a concentration at which you see no
cancer occurring, as has been shown in animal studies.
Dr . H. Spencer; One comment about laboratory animals.
Dr. Alarie, could you tell us what the impact on the public
would be if we used rabbits to test the edibility of mushrooms?
Dr. Alarie: I'm sorry, what do you want to test?
Dr . Spencer; I would like you to tell me what the impact
would be on the public if we used rabbits to test the edibility
of mushrooms?
Dr. Alarie; We use rabbits? Rabbits to test what?
Dr . Spencer; To test the edibility of mushrooms. What
would happen to the public?
Dr. Alarie; Why do we use rabbits to test the toxicity of
mushrooms?
Dr . Spencer; The point I was trying to make is that the
panel apparently assumed that the concept of biochemical unity
is infallable, which is obviously not correct. Rabbits can eat
toxic mushrooms and survive. The point being that some
chemicals you may test by animal model, and that animal could
well have no response whatsoever.
Dr. Alarie; You see the way you address it, of course, is
you don't pick up one single species of animal. We have a wide
variety of them. There is no problem whatsoever and I certainly
can find one man on the face of this earth who will look exactly
like your rabbit. But the problem is he will be the exception.
So what I want is an animal which will represent the human
population. I go searching for it by trials and errors. It is
not something I can guess.
Joe Banon, Chicago Lung Association; I was riding home in
my car from work about a month ago, and I heard a news report on
an air pollution study, to be done by the Yale Lung Research
group, where two towns in Connecticut, I believe, are used to
study the prevalence of respiratory diseases. Dr. Higgins, if
you are familiar with the study, can you comment on it?
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Dr. Higgins; Yes, I am familiar with the studies you
mention. I think one of the main difficulties is that the
differences in pollutant levels between the two towns was very
small. One would not expect to be able to show differences in
bronchitis, lung function, etc., due to pollution because even
the more polluted town was not polluted enough. We had a
similar problem in our studies in Florida.
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SESSION III: HEALTH ASPECTS OF FOSSIL-FUEL ELECTRIC POWER PLANTS
Tuesday morning, March 20, 1979
Moderator: James J. Stukel, Ph.D.
Professor of Civil Engineering
University of Illinois
AIR POLLUTION
By
Benjamin G. Ferris, Jr., M.D.
HUMAN EXPOSURES TO WATERBORNE POLLUTANTS
FROM COAL-FIRED STEAM ELECTRIC POWERPLANTS
By
Julian B. Andelman, Ph.D.
OCCUPATIONAL HEALTH ASPECTS OF FOSSIL-FUEL
ELECTRIC POWER PLANTS
By
William N. Rom, M.D., M.P.H.
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AIR POLLUTION
By
Benjamin G. Ferris, Jr., M.D., FACPM
Professor Environmental Health & Safety
Harvard School of Public Health
Harvard University
Boston, MA
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HEALTH ASPECTS of FOSSIL-FUEL ELECTRIC POWER PLANTS - AIR POLLUTION
Benjamin G. Ferris, Jr.
Fossil fuels used for electric power include coal, oil and gas.
Coal and oil make up the major sources of energy. As a result of their
combustion, particulates, sulfur oxides and oxides of nitrogen are pro-
duced. Coal can produce large amounts of fly ash and soot which in
turn can be largely controlled by various methods. Oil usually does
not produce so much. Sulfur dioxide production will vary with the sulfur
content of the fuel. This component is more difficult to control than
the fly ash. Nitrogen oxides are also generated and when diesel engines
are used they can make considerable impact on ambient levels. They are
even more difficult to remove from the emissions than S02- Control
has been directed to limiting the generation of N02«
These components consist of the major air pollutants from fossil
fuel. This presentation will discuss their apparent impact on the
health of human beings with special emphasis on levels at somewhat above
the present air quality standards.
OXIDES OF NITROGEN
NO and N0£ are produced due to the heat and pressure if present, as
in Diesel engines. NO appears to have little effect. It can be converted
in photochemical smog to N02 which is reactive. Thus this discussion will
be on.the effect of N02.
Chamber Studies - Short-term
A number of chamber studies for short-term exposures have been done.
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These are summarized in table 1. Most of these have involved healthy
subjects (1, 5, 6, 13). A few have used asthmatics (7) or "reactive"
subjects (3). Some have used mixtures of pollutants (4, 14). Most
of these studies have produced negative results if levels of N02 have
been below 2.82 mg/m3 (1.5 ppm). One study (7) did indicate that 3
out of 20 asthmatics showed a measurable increase in airway resistance
after a one hour exposure to 0.2 mg/m3 N02, and 13 out of 20 had an
increased sensitivity to carbacol. The subjects apparently did not
detect any change in their airway resistance. This study has been
criticized because of the varying levels of the baseline airway resis-
tance in the subjects. Furthermore, the relevance of these sorts of
observation to the real world conditions have also been questioned.
Certainly further studies of this sort and in this dose range are
warranted.
Kerr and coworkers (6) have exposed 13 asthmatic, 7 chronic
bronchitics and 10 normal adults to 0.940 mg/m3 (0.5 ppm) N02 for 2
hours in a chamber. A 15-minute period of moderate exercise was per-
formed during the first hour of exposure. Each person had a 2-hour
control period in the chamber on the day before the exposure. They
did a variety of tests of pulmonary function including airway resis-
tance. The study was not made double blind since N02 could be detected
by odor at this level. During the exposure to 0.940 mg/m3, 7 of the 13
asthmatics had varying symptoms - two burning of their eyes, one head-
aches, and from some, chest tightness on exercises; one normal and one
chronic bronchitic had a running nose. All of these symptoms were
felt to be slight. No delayed reactions were reported. No significant
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changes were noted in the various measured parameters (spirometry,
airway resistance, single breath N2 elimination or pulmonary mechanics.)
If they grouped the asthmatics and chronic bronchitics together then
they could show a significant increase in total lung capacity, functional
residual capacity and residual volume. Static compliance was slightly
decreased. The authors interpreted their findings as physiologically
not meaningful, and that they could have been due to chance. These ob-
servations should be repeated at this level as well as at lower levels.
One other study also needs discussion. This is a study by Von Nieding
et al (14) in which they exposed healthy subjects either to workplace
levels of N02 (9.4 mg/m3 - 5 ppm), 03 (0.196 mg/m3 0.1 ppm) and S02
(13.1 mg/m2 - 5 ppm) or N02 (0.1 mg/m3 0.05 ppm), 03 (0.049 mg/m3 0.025 ppm)
and S02 (0.262 mg/m3 0.1 ppm). Changes in airway resistance and arterial
oxygen saturation were observed at the higher levels, whether exposure was
to N02 or 03 singly or in combination with or without S02. The lower levels
produced no effect. Both groups were challenged with 1, 2 and 3% acetyl-
choline. Acetylcholine, after exposure to the mixture with the higher
concentration, produced markedly increased responses over the control
values. After exposure to the mixture at the lower levels, there was a
slightly increased response after 2% acetylcholine but no increase after
1 or 3% acetylcholine. In view of the lack of an increased response to
3% acetylcholine, the change at 2% does not seem so important. It would
have been more relevant if there had been a graded dose response. To
propose a hypothesis that the response might be a stepwise function that
responded at 2% but not at 3% does not seem to be tenable.
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There is no short-term federal standard for NC^. At this time it
does not seem appropriate to set such a standard for one hour at the
level of Orehek's study. It would seem to be more appropriate at a level
of 0.5-0.8 rng/m^ (0.266-0.425 ppm) as a one-hour average value.
Epidemi o1og i c Studies
There are rather few epidemiologic studies that have looked at
the possible effects of NCU. Those that have, have been compounded by
errors in analysis for NC>2 that were discovered later or there had been
increased levels of other pollutants along with the increased level of
NC-2- Attempts to attribute an effect or a portion of the effect to
N02 are difficult.
The various studies are summarized in table 2. The studies by
Shy et al (9, 10) and Pearlman et al (8) had the problem of a probable
error in the Jacob-Hochheisser method of measuring NCU as well as the
coexistence of elevated particulate levels in conjunction with the
elevated NC>2 levels.
The study by Cohen et al (2) was examining such a narrow range of
exposure that one might not expect to see much difference.
The studies of Spiezer et al (11, 12) deal with an occupational
group - policemen. It may not be appropriate to extrapolate their
results to the general public. Also, the areas with the higher levels
of N0« also had elevated levels of other pollutants. So how much of
the effect - if any - could be attributed to N0£ is not clear.
The Federal standard annual average of 100 mg/m^ (0.05 ppm) is
probably more than adequately protective. Certainly more studies are
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needed to evaluate the adequacy of this standard.
S0y and Particulates
These two pollutants will be discussed together because they
usually have a common source. In addition, sulfates occur in the
particulate phase, either as a tnist 0*2804) or as an actual particle
as various sulfate salts.
There are two fundamental problems with the category of partic-
ulates. One involves the size distribution and the method of
collection, the other the chemical composition.
In Europe and Great Britain, particles are collected at relatively
low flow rates, on filters that are then read by light reflectance.
The system has been calibrated against a standard black coal smoke so
that the reflectance units can then be expressed as mg/tn . This
method collects the small size or respirable fraction (<10-7 urn). The
conversion applies only to a special coal smoke and cannot be used for
oil-fired smoke or for general dusts, etc., that may have a wide range
of colors. This method is referred to as the British Standard Smoke
method.
In the United States, particulates are sampled by the so-called
hi-vol method. In this method, air is drawn through a filter in
large amounts (70 - 75 m^/min) and the amount of dust is measured
gravimetrically and referred to as the total suspended particulates (TSP)
This method can collect larger particulates that would not be deposited
in the lung, although elutriators or other devices can be used to
minimize this effect. There is a move to collect the mass respirable
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fraction (MRP below 10 um) as well as the total suspended particulates.
Present U.S. standards are based on TSP. Data are being collected so
that hopefully eventually a standard can be set for MRP.
All of these methods-standards imply that equal weight has equal
effect. This probably is not so since the chemistry of the particulates
needs to be evaluated. Some data have been collected on suspended
sulfates, nitrates and a few on the metals. This is an area that needs
much more attention. It will be an expensive study but one that needs
to be done. The MRP particularly need such analyses as this is the fraction
that is more likely to contain the sulfates and also to be deposited deep
in the lung. In addition, the hi-vol glass filters tend to collect S02
and convert it to sulfate on the filter, thus giving spurious values for
suspended sulfates. In due course we should also be able to characterize
the type of sulfate, since they do not have equal effect on the respira-
tory system (15).
Mortality
The effects of acute episodes with markedly high levels of S02 and
particulates as have occurred in London in 1952 and 1962, the Meuse
Vally and Donora are clear evidence that an increased mortality can result.
It has been more difficult and controversial to demonstrate an effect at
lower levels closer to those usually seen. Buechley et al (16) analyzed
mortality data from the New York - New Jersey metropolitan area. They
used only one monitoring station to estimate exposure. They did an
extensive analysis and controlled for a number of confounding variables.
They felt that at about 300 jig/m^ S02 there was an excess mortality.
Particulates, in this case coefficient of haze, did as well as a
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predictor. Buechley (17) reanalyzed the data later and added additional,
more recent years when the levels had fallen. He demonstrated a similar
correlation but with a much lower cross-over point. He concluded that
862 was acting as a surrogate for some other substance that had not
changed as much.
Schimmel and Murawski (41, 42) analyzed the same sort of data
using somewhat different methods. They also used a single monitoring
station as their indicator of the levels of pollution. They reported
that 80% of the effect was due to particulates and 20% to S02. In one
of their presentations they concluded that S0~ was relatively unimpor-
tant. They too noted no reduction in the mortality with the reduction
in pollution.
Lave and Seskin (34) have made extensive analyses relating
minimum sulfate and suspended particulate levels to mortality. Their
results have received considerable attention. In some cases the results
have been accepted and used to calculate the impact on health. Others
have been critical of their methodology and conclusion. These are
perhaps best summarized by quoting from a group of Biostaticians (43)
that reviewed the report of Lave and Seskin.
They were particularly concerned that Lave and Seskin had not
investigated as fully as they would wish how well their models fit
their data. To determine whether Lave & Seskin's estimates might be severely
distorted by outlying values, they undertook a robust analysis and
re-estimated the regression given in equation 3.1-1 of Lave and Seskin
after some data correction and removal of outliers. The estimates that
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they obtained for the air pollution regression coefficients are
presented in Table 3 along with those of Lave and Seskin. They
differ considerably from the values given by Lave and Seskin.
They went on to state:
"Our other area of concern is that the linear model may not
be the best-fitting model. Even if it is a good description of current
inter-relationships, it may not be suitable for predicting what would
occur if the value of the air pollution variables were changed."
"There are several reasons for doubting the suitability. One
reason is that a dose-response relationship that can be regarded as
linear over a particular range of values may not be linear outside
that range. Another reason is that no attention has been paid to the
competing risks that cause mortality — the authors assume that all
the other socio-economic factors would remain constant while the air
quality changed. A third reason is that association does not
necessarily imply causality."
"Our final conclusion is that Lave and Seskin have made a pioneering
effort in showing an association between mortality rates and air pol-
lution. The next steps — assuming a cause and effect relationship
and assessing the relative costs and benefits of reducing air pollution
cannot, in our opinion, be undertaken with any degree of confidence
given the quality and nature of the available data. This conclusion
seems to be very close to the Lave and Seskin's own views as expressed
in their last chapter, Chapter 11. We believe readers would be well
advised to read Chapter 11 before other chapters, because it not only
summarizes the rest of the book but also places the work in perspective
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as a first step in the solution of a complex problem."
It does not seem reasonable to conclude from these studies
that SOX or particulates are having an effect on mortality at the
levels usually measured at present. It is not possible to conclude
unequivocally that there may not be some effect, but this is probably
unlikely.
The report from CHESS, 1970 - 1971 (44) will not be discussed in
detail. Their best-estimated values tend to confirm the present
Federal standards. Their indictment of sulfates needs much more
verification and study. It is unfortunate that the studies were not
designed to look at differences between populations as related to
differences in the levels of pollution. Instead, they were grouped by
area or regions where comparable studies were done.
A number of the studies reported below have come from workers in
Great Britain or in Europe where the British Standard Smoke method
was used to estimate suspended particulates. Commins and Waller (20)
made a comparison of this method with the hi-vol method. Their data
have been used to correct the Black Smoke data to total suspended
particulates.
Acute or short-term effects
There are a limited number of studies that have looked at the
short-term effects on mortality. The effects of a relatively high
level on mortality have been well documented. The few studies are
summarized in Table 4. The data are spotty and variable.
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Jaeger et al (33) exposed 40 mild asthmatics and 40 "normals"
to 1300 pg/nr (0.5 ppm) SC^ for 3 hours. All wore nose clips during
the exposure so they were forced to breathe through their mouths.
The asthmatics showed a significant decrease in mid-maximal expiratory
flow during the exposure. The other tests showed a similar but non-
significant trend. Two of the asthmatics and one of the "normals"
developed wheezing in the chest during the night after the exposure
to S02- These were not interpreted as being an asthmatic attack and
were considered mild episodes. This study can be criticized in that
the battery of pulmonary function tests were not done in the chamber
but rather in another laboratory about a four-minute walk away. They
did not measure participates and there was a kerosene heater in the
trailer-chamber that could have contributed to the exposure. No
organized effort was made to query all the subjects concerning possible
symptoms on the night after exposure. This study deserves to be re-
peated with an improved protocol.
Lawther et al (35) have reported increased symptoms in chronic
bronchitics at moderate levels of exposure. Emerson (24) was not able
to show any change in pulmonary function in similar types of patients
at somewhat higher levels of SC^. This may have been due to the
relatively small number of subjects studied.
Van der Lende et al (45) reported a transitory fall in FEV-^ Q
in a relatively large population at levels below those reported by
Emerson. Cohen et al (19) noted a weak association of asthmatic attacks
with levels of S02 above 200 ug/m3 and TSP above 150 pg/m3. They
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reported that temperature acted much more strongly. This was similar
to the observation of Emerson.
It does seem that 3-hour exposure to 1300 pg/nH of SO^ can cause
mild symptoms in some sensitive asthmatics. Somewhat lower levels for
24-hour periods in conjunction with levels of TSP above 150 ug/m-^ cause
reversible decreases in FEV^ Q and FVC. Since these changes appear to
be reversible and their long-range significance is unclear, one
could conclude that these changes represent an acceptable change.
Long-term effects
Selected studies on the effects of long-term exposure to S02 and
particulates are summarized in Table 5. These levels refer to 24-hour
annual average values. Here,too, the data reported as black smoke
have been converted to TSP equivalents. In Fletcher's study (30)
the particulates only had changed markedly; SC>2 levels had not. This
was interpreted as emphasizing the role of the particulates. Lawther
et al (35) had made a similar observation and conclusion with respect
to the short-term exposures. The studies of Sawicki on adults (40)
and Lunn et al (36, 27), and Douglas and Waller (23) on children, tend
to confirm the levels of particulates.
Chapman et al (18) have also studied children. Their study focused
primarily on particulates. They shifted their instrument that they
used to measure the pulmonary function without reporting any tests to
show comparability. Also, there were differences in the socio-economic
status that could have accounted for the differences seen. A further
problem lies in the tacit assumption that equal weight of particulates
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means an equal effect. This is probably not true. There is a great
need to develop more information on the particle-size distributions and
the chemical characteristics of the various particle-size groups.
Hammer et al (31) did very extensive analyses to control for a
variety of confounding factors in two groups of children in Long Island
and New York City. They concluded that there was an excess of lower
respiratory disease mortality when SC^ levels were 175 - 250 jag/nr
(0.067 - 0.096 ppm), TSP above 115 pg/m^ and suspended sulfates of
13 - 14 pg/m^. As with all of these studies, the exposures are best
estimates from a single monitoring station. Their suggested levels are
consistent with observations of others. No analyses were done to try
to separate out the effects of S02, particulates or sulfates. Certainly
their data are not sufficient to use to set a standard for sulfates.
The last three studies represent a 12-year series of follow-up
studies, on a community in New Hampshire (26, 28, 29), where the main
source of pollution is a pulp mill. The same sample was followed and
as the levels of pollution fell an effect level appeared at about
130 ug/m: TSP. The total sulfur as measured by the lead peroxide candle
was low and underwent some fluctuations reflecting the closing of the
sulfite operation in 1963 and the expansion of the Kraft process in
subsequent years.
The results from the initial study have been compared with
comparable data from Great Britain (38) and with a cleaner community
in British Columbia (27). This comparison indicated a sort of a dose-
response effect in that more polluted communities in Great Britain had
-189-
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more symptoms than in Berlin, N.H. and the cleaner community had
better pulmonary function. Thus, the observation from the community
with a pulp mill may well be applicable to other communities. It
would have been good to have had information as to the chemical com-
position of the particulates, as they undoubtedly were different
in the three communities.
Sulfates
The Chess (44) studies have reawakened interest in sulfates as
possibly being more important than SC>2. A fundamental problem with
sulfates is that it is probably the cation that is more important.
There appears to be a gradation of effects in animals (15) with
sulfuric acid being the most irritating and sodium sulfate being
relatively innocuous. We are not yet able to characterize the type
of sulfate. Thus, a general standard for soluble sulfates does not
seem to be warranted given the range of irritancy for the different
sulfate compounds.
An assessment of the effects of microparticulate sulfates on
human health has been prepared (25). It is appropriate to comment
on some of the studies reported there as well as some more recent
work.
Dohan (21) and Dohan and Taylor (22) looked at the prevalence of
respiratory disease in a number of cities related to levels of
suspended particulate sulfates. They showed an increased prevalence
with rising levels of sulfates. This was exacerbated during a flu
epidemic. Their threefold rise in suspended sulfates was accompanied
-190-
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by an increase in total suspended particulates from something over
O o
100 ug/m to 188 ug/m . They concluded that sulfates were the active
component. However, they had not controlled for the various con-
founding variables.
A similar study was undertaken by Ipsen et al (32) in which
much more detailed and sophisticated analyses were done to control
for the auto-correlation between pollutants and season of the year.
When they controlled for the auto-correlation, they were not able to
show that the levels of pollution were having any effect on respiratory
disease. Their studies emphasize the need to control for such phenomena
in order not to be tempted to make incorrect conclusions.
Sackner et al (39) have been exposing animals and human beings
to submicronic sulfuric acid mist. Human beings have been exposed
up to 1000 ug/m^ for 10 minutes without demonstrating any effects on
a variety of tests of pulmonary function. This has included some
asthmatic children. These results are encouraging as to the toxicity
of sulfuric acid mist but they need to be replicated and also for
longer periods of exposure. Exercise should also be added to the
protocol.
Miscellaneous
Some of the combustion products that are emitted from coal-
fired plants have carcinogenic capabilities. These materials, like
the variety of metals that can also be emitted, are probably in too low
a concentration to be having an effect. Careful studies to evaluate
this potential problem still need to be done to have better quantified-
-191-
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tion of the risk and also to determine whether there may be synergism
with such exposure and occupational exposure as well as with cigarette
smoking.
No discussion is planned of the role of sulfur oxides and oxides
of nitrogen to the formation of acid rains. These may well turn out
to be the controlling factor in control of emmissions.
Summary;
The most significant potential contributions to air pollution
from fossil-fuel-fired power plants are N02> sulfur oxides and
particulates. Their possible effects on health are discussed.
Acknowledgement;
This paper has been supported in part by Grant ES 00002 and ES 01108 from
the U.S. Public Health Service and EPRI Contract NO RP 1001-1.
-192-
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Table 1
Selected Summary of Results of Chamber Studies (short-term)
on Human Beings Exposed to N02
Concentration
3
mg/m
(ppm)
Duration of
Exposure
Effects
References
4.5 (2.5)
<2.82
1.316- (0.7-1.0)
1.880
plus other
smog compon-
ents
1.166
(0.62)
0.940
(0.5)
0.564 (0.3)
added to 63
exposure
0.200
(0.11)
0.10 (0.05)
(also ozone
| 0.05, S02
0.26)
2 hrs.
0.25 hr.
Not specified
until pulse 150/
min on exercise
2 hrs. exercise
0.2 - 1 hr. ven-
tilation incr.
4 x
2 hrs.
2 hrs.
1 hr.
2 hrs
Incr. Raw normals
to incr. to Ach
response
No change Raw
health subjects
No significant change
in reaction time or
cardiorespiratory
work efficiency in
healthy subjects
No change; no diff.
exercise healthy
subjects
13 asthmatics, 7 chr.
br.» 10 health nor-
mals; 7/13 asthmatics:
slight burning eyes (2)
headache (1) and chest
tightness exercise (4);
no significant change
in pulm. function unless
comb, patient groups;
changes very slight
No increased response in
"reactive" subjects
3/20 asthma inc. Raw
13/20 increased sensitiv-
ity Carbacol; no symptoms
No effect gas exchange
or Raw» 2% Ach incr. Raw
1% & 3% no effect; heal-
thy volunteers
13
14
-193-
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Table 2
Selected Summary of Epidemiologic Studies on
Concentration mg/m^
Mean
0.15 - 0.28*
(0.08 - 0.15)
Same
0.096 vs 0.043
(0.051 vs 0.023)
0.103
(0.055
(ppm)
90th Percentile
0.28 - 0.94*
(0.15 - 0.54)
0.188 vs 0.113
(0.10 vs 0.06)
Maximum
0.263 - 0.654
(0.140 - 0.30
Effects
Slight increase in respiratory symptoms and
slight decrease in pulmonary function
Slight increase in bronchitis morbidity -
No effect on croup, pneumonia or hospitalizations
No effect healthy non-smoking adults
Questionable small Increase in respiratory
symptoms. No difference in pulmonary function;
Policemen.
|
References
9, 10
8
2
11, 12
I
M
VO
I
* Data from Jacob-Hochheiser method. Later shown to be in error (low); values probably should be higher.
-------
Table 3
Comparison of Regression Coefficients (b - values) Calculated
by Lave and Seskin (34) and Thibodeau et al (43)
Minimum
Mean
Maximum
Sulfates
Lave &
Seskin
0.473
0.173
0.028
Thibodeau,
et al
0.08
0.26
0.08
Particulates
Lave &
Seskin
0.199
0.303
-0.018
Thibodeau,
et al
0.57
0.01
0.01
-195-
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Table 4
Selected Summary of Effects of Short-Term Exposures to S0?
and/or Particulates - 24-hr Level Unless Otherwise Specified
S02
ug/m3
1300
722
300-200
250
200
(ppm)
(0.5) 3 hrs
(0.276)
(0.114 - 0.070)
(0.095)
(0.076)
Suspended Particulates
S}
pg/nr
*"~
350a
230a
350a
150
Effects
Chamber exposure, mouth
breathing, Resting, Sit
deer. MMEF asthmatics;
2/40 asthmatics wheezed
in night; 1/40 "normals"
wheezed in night
No change in pulmonary
function in patients
w/ chronic bronchitis
Reversible
Decreased FEV^Q
Increased respiratory
symptoms in patients
w/ chronic bronchitis
Weak association
asthmatic attacks
Ref .
33
24
45
35
19
a Corrected from orginal data to TSP equivalents (20) .
-196-
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Table 5
Selected Summary of Effects of Long-Term Exposures
to SC>2 and Particulates; Levels Refer to
24-hour Annual Averages
SO 2
jjg/m3 (ppm)
250
130
120
120
23
250-175
55
37
66
(0.095)
(0.05)
(0.046)
(0.046)
(0.009)
(0.096-0.067
(0.021)b
(0.014)b
(0.025)b
Suspended
Particulates
250a
24 Oa
200a
230
110
115
180
131
80
Effects
Increased phlegm production
Increased respiratory disease
Increased respiratory illness
and decreased pulmonary function
Increased lower respiratory
illness
Decreased FEVQ_75
Increased lower respiratory
disease and morbidity
Increased respiratory symptoms
Decreased pulmonary function
No effect
No effect
Refs.
30
40
36,37
23
18
31
26,27
28
29
a Corrected from original data to TSP equivalents (20)
Equivalents calculated from lead peroxide data
-197-
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HUMAN EXPOSURES TO WATERBORNE POLLUTANTS
FROM COAL-FIRED STEAM ELECTRIC POWERPLANTS
By
Julian B. Andelman, Ph.D.
Professor of Water Chemistry
Graduate School of Public Health
University of Pittsburgh
Pittsburgh, Pennsylvania
-205-
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HUMAN EXPOSURES TO WATERBORNE POLLUTANTS
FROM COAL-FIRED STEAM ELECTRIC POWERPLANTS
by
Julian B. Andelman, Ph.D.
Professor of Water Chemistry
Graduate School of Public Health
University of Pittsburgh
The focus of this paper is the evaluation of the potential impact on
human health from waterborne chemical pollutants emitted principally at
coal-fired steam electric powerplant sites. Coal is the primary fossil
fuel used for electric power generation in the Ohio River Basin, which is
the major reason for its emphasis in this paper. Nevertheless, such plants
have substantial emissions in common with other fossil-fueled and nuclear
powerplants, and thus, where applicable such as for cooling water effluents,
some of the total impacts of these common emissions will be considered when
assessing total wastewater flows. Although many of the chemicals which are
constituents of the coal itself will also be emitted as waterborne wastes
due to coal mining, preparation, and transportation, the possible impacts
of these activities will not be considered specifically.
It is not the intention of this paper to exhaustively present the full
range of chemical pollutants emitted by the water route at these powerplants,
Such information can be found in mimerous articles and reports. Rather,
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-------
using a few specific examples, an attempt will be made to assess some of the
likely human exposures that may occur, principally through the drinking
water route, once these chemicals are emitted to surface receiving waters,
primarily rivers, and assuming that they act as conservative pollutants.
In this context, and perhaps somewhat unusually, the term conservative will
signify: first, that they do not degrade, which certainly applies to
trace elements in stable oxidation states; that they are not released by
the natural water system, such as by precipitation or volatilization; and
finally that they are not affected by municipal water treatment processes.
It is safe to say that it is unlikely that one could find any water pollu-
tant that meets all of these conditions, but, as a preliminary worst-case
analysis, this is certainly a conservative set of conditions in two senses
of the term.
After initially describing briefly the kinds of sources of wastewaters
associated with fossil-fueled steam electric powerplants, two broad classes
of chemicals will be considered: trace elements and organics. Some of
their uses and origins at these sites will be reviewed, along with some of
their quantities emitted, and possible impacts on surface water quality, and
ultimately, possible human exposures. Although it is well known that such
human waterborne exposures can be considerably amplified, such as for mer-
cury, via concentration and accumulation in the aquatic food chain, because
of limited quantitative information this possible route will not be evaluated.
Nevertheless, any conclusions based on assessments of waterborne exposures
that do not consider such additional routes must be regarded as incomplete.
There are a variety of wastewater streams associated with powerplants
and these are shown schematically in Figure 1 (1). They vary considerably
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-------
in flow volumes, ranging from as much as 1 MGD/Mw typically for once-through
cooling, to just a few gallons per day per megawatt for some cleaning operations
with recirculating cooling water blowdown and once-through ash sluicing
systems being intermediate in flow at several thousand GPM/Mw. The compo-
sition of the intermittent smaller flows of run-off from coal piles, as
well as that of the bottom and fly-ash wastewaters, is largely determined
by coal composition, while many other wastes, such as cooling water, waste-
water from boiler water treatment and boiler condensate blowdown are
strongly influenced by added chemicals. The categories of these wastewaters
by relative volumes and rainfall runoff influence are listed in Table 1.
A large variety of organic and inorganic chemicals are utilized for
water treatment, cleaning, and the control of corrosion and biofouling of
cooling water systems, many of which are shown in Table 2. These additives,
along with coal constituents can and do appear in these cooling water and
wastewater effluents. Because of the very large volumes from once-through
cooling, which is estimated to be used currently in about two-thirds of
the steam electric powerplants in the U.S., a portion of this paper will con-
sider the potential impact of the formation of chloro-organics in such
systems due to the wide use of chlorine to reduce bio-fouling.
Many trace elements, including heavy metals, can appear in virtually
every wastewater and cooling water effluent stream of powerplants at con-
centrations higher than those in the source water. Such chemicals can ori-
•
ginate from the coal itself, from corrosion products at the plant, and from
chemicals used for such purposes as cleaning agents, corrosion inhibitors,
such as zinc and chromium, and water and wastewater treatment chemicals,
such as alum,used as a coagulant in water treatment,and contaminants of
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-------
lime. In some cases there is the potential for reducing their emissions
by using alternative chemicals, such as the possible substitution of
molybdate as a corrosion inhibitor instead of chromium or zinc. However,
when the trace element originates from the coal itself, it may be possible
to reduce its emission only by modification of the wastewater flow systems
or treatment of their effluents. Thus, for example, the diversion of run-
off from a coal storage pile to an ash lagoon can reduce its impact.
Unlike the trace organics, considerable data are available regarding
the concentrations of trace elements emitted in wastewater flow, streams at
powerplants. To obtain a perspective on the possible impact of a few such
metals in wastewaters of powerplants, Table 3 presents estimates of their
daily quantities discharged compared to those from all other industrial
sources. It is clear that for these four metals, powerplants constitute a
significant, if not substantial source. In the case of chromium this 1973
estimated discharge rate was perhaps 0.5 percent of all chromium actually
used by industry in the U.S. Similarly, it was recently estimated by the
E.P.A. that during the period 1975 to 1990 electric utilities would dis-
charge about 50 percent of all the lead emitted to water. It is, therefore,
apparent that there is a need to assess the possible impacts of the emissions
of these and other trace elements as possible agents of waterborne disease.
Some typical concentrations of zinc and chromium applied as corrosion
inhibitors in cooling towers are shown in Table 4, along with information
about a few other chemicals. It should be emphasized that these typical
concentrations in the circulating water are in units of mg/1, and are quite
substantial should they ultimately appear in a receiving stream and remain
relatively undiluted. However, the volumes of such blowdown flows are
-209-
-------
much smaller than those from once-through cooling, and do in fact often re-
ceive considerable dilution by receiving waters. Where there may be
reason for concern, in spite of the high dilution, is the possible pre-
cipitation and incorporation of these and other heavy metals into sediments,
which can then constitute a major sink and act as a substantial source in
the aquatic food chain, such as for shellfish. Thus, where an analysis
indicates that the average impact of such effluents on receiving waters and
ultimately drinking water is small, other warerborne routes of exposure
should be considered before a hazard is judged to be unlikely.
TO obtain an additional perspective on some of the wastewater streams
from a coal-fired powerplant, Table 5 shows some typical flows in gallons
per day per megawatt (GPD/Mw) from several plant operations. It is apparent
that there is a considerable range of flows as discussed earlier, as well
as concentrations of trace and macro constitutents within them. The flows
shown there are substantially lower than the typical value of 1 MGD/Mw for
once-through cooling, which is also much larger than, perhaps typically ,
10,000 GD/Mw for blowdown from a recirculating cooling water system. How-
ever, the latter flow and that from a once-through ash pond overflow are of
the same order of magnitude.
In all of these wastewater streams one can find a full range of
trace elements, and these have been studied extensively. Some examples of
their concentrations in coal pile leachates are shown in Table 6 (2). It
is apparent that the concentrations of many of these chemicals can be quite
high compared to typical concentrations in the Allegheny River, as well as
drinking water criterion limits. However, because of the relatively low
average volumes of these leachates, they are unlikely to constitute a hazard
-210-
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except for a local situation, such as due to non-dilution or contamination by
infiltration into a water supply aquifer. Another possible route of im-
pact on water quality of these trace elements is by the ultimate settling
of particulates from stack emissions at powerplant sites, and their subse-
quent leaching into surface or ground waters. No such direct assessment of
this route will be presented here, but it is incorporated into the following
regional assessment.
It is useful to consider a possible future impact of trace element
eniiw«5ions from increased power utilization in a specific region. One such
analysis by the Regional Studies Program of the Argonne National Laboratory
did such a projection to the year 2020 for several areas, including four
counties in the Illinois River basin in Illinois (3). As part of the
National Coal Utilization Assessment they projected the emissions of trace
elements in a combined high coal electric and accelerated synfuel scenario.
This region was chosen as a case study because of the large amounts of
accessible coal reserves and the potential for increased coal-fired power
generation and synthetic fuel production. It should be emphasized that their
projected emissions include those related to several phases of coal utiliza-
tion, including the possible impact of urbanization. Also particulate atmos-
pheric emissions that are settleable were included. In this case they assum-
ed that 50 percent of the deposited atmospheric trace elements are trans-
ported to the river via surface run-off. Although it is apparent that their
analysis encompasses much more than impacts of the coal-fired electric
powerplant itself, to the extent that it assesses the full range of sources,
it can indicate whether indeed there may be cause for concern-about operations
at the powerplant site.
-211-
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As an example of their approach we shall examine their analysis for
Jersey county, one of four they considered in the Illinois River basin.
Table 7 presents their data for eight trace elements that have potential
impacts on human .health. In each case average concentrations in the river
in the absence of increased coal utilization are shown, as well as some
current "drinking water standards or criterion limits. Incidentally, the
average values for arsenic and cadmium in the river exceed these limits.
However, water treatment will often reduce concentrations of trace elements.
Table 7 indicates that there are substantial projected increments under
average flow conditions due to the 2020 scenario, at least for some of the
trace elements, including selenium, mercury and beryllium. And, of course,
under the 7-day 10-year low flow condition, there is a substantially greater
impact, by a factor of about 8. In this case the increments compared to
]•'
background concentrations become important for the other elements as well.
It should, however, be emphasized that where the human effects of these
elements are chronic, the short period low-flow higher exposure becomes of
lesser concern. Finally, the last column considers the relative body
burdens due to drinking water intake under low flow conditions compared to
typical dietary sources. For mercury and lead the water constitutes a sub-
stantial source, but again these would be reduced by a factor of about 8
under average flow conditions. It should also be noted that their assessment
also indicates that the air contributions to these body burdens are much
lower than those of water. One can thus conclude that, to the extent that
the assumptions are valid, it is unlikely that there is a substantial impact
from most of these trace elements on the human health of the general popula-
tion in the year 2020 scenario in Jersey County, Illinois. Where the
analysis indicates that an element like mercury may be of concern, there may
-212-
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je need to refine the assumptions and examine further the extent to which,
for example, the mercury may be behaving as a conservative pollutant in
the river and water treatment systems.
One can at least make several preliminary judgements and conclusions
ibout the possible waterborne route impact on human health from trace elements
arising from steam electric coal-fired powerplants. There can be substantial
quantities of such trace elements emitted, even when compared to those
associated with other anthropogenic activities. Some of these emissions are
due to the use of chemicals at the plant and can be limited by the judicious
use of alternative chemicals. However, a large number of trace elements are
present in coal and will necessarily appear in wastewater streams, although
their impact can be reduced. These trace elements are naturally present in
the hydrosphere and in many cases and at most times the incremental loads
from powerplants are very small. However, for some elements, such as mer-
cury, selenium, arsenic, chromium, and lead, the added waterborne load could
be substantial compared to background concentrations. In particular, situa-
tions could be encountered where there are localized impacts, such as due to
low dilution, groundwater contamination, or concentration in sediments. In
general, however, the concentrations of trace elements in water are such that
potable water sources constitute a relatively small fraction of the contri-
butions to human body burdens compared to dietary sources. Where there is a
potential increase from powerplant emissions, it is unlikely that they
will constitute a danger of acute human toxicity. However, there is a need
to fully and continually assess their potential chronic effects as such
powerplants become regionally concentrated and their emissions become highly
localized.
-213-
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Next we shall address the organic chemicals that can appear in waste-
water effluents at coal-fired steam electric powerplants, and these can
be attributed to four basic sources: those present in the raw source water,
either of natural or anthropogenic origin; those orginating from the coal
itself, ultimately appearing, for example, in ash pond effluents or run-off
from coal storage piles; chemical additives, such as corrosion inhibitors
and cleaning and dispersing agents; and.products from the reactions of
chemicals in the v-cster and wastewater systems, such as those from chlorine,
added to cooling water au'1 then reacting either with natural or synthetic
organics already present in or added to the water. Serious concern about
such chlorination reactions has developed in relation to the formation of
trihalomethanes in drinking water disinfection, but many other products,
depending on the nature of the organic precursor, can form as well. The
E.P.A. list of 129 priority pollutant chemicals consists mostly of organic
chemicals and includes several of these trihalomethanes that can form in
water and wastewater chlorination. All of priority pollutants are now
being addressed for possible control in the proposed revision of steam elec-
tric powerplant effluent limitations guidelines (4).
Only sparse data seem to be available on the nature and concentration
of organics actually present in wastewater or cooling water from these
powerplants. A compilation of some such measurements reported recently by
the E.P.A. for several powerplants is shown in Table 8 (4). In addition to
the organics listed there, others were detected frequently, such as unchlorinated
phenol at concentrations of a few yg/1 in cooling tower blowdown, several
phthalates, and several polycyclic aromatic hydrocarbons, which as a class
are frequently associated with coal process wastes and contain some highly
potent animal carcinogens.
-214-
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Of the organics listed in Table 8, benzene can be categorized as a
suspected human carcinogen and chloroform as an animal carcinogen. For
almost all the other listed chemicals there are either very little or no
available data on chronic toxicity, although acute human toxic effects are
known at much higher levels of exposure. Several of these chemicals have,
however, unpleasant taste and odor characteristics, and at the concentrations
shown can impart unpleasant taste to fish or similarly taint drinking water.
As a class halogenated organics are responsible for adverse biological
reactions and are the subject of regulatory initiatives.
Although the concentrations shown in.Table 8 are in the ;g/l range,
in most cases they typically are at least comparable to and often substanti-
ally larger than the highest concentrations found in drinking water (5).
Whether they will result ultimately in significant waterborne human exposure
depends on dilution of the wastewater streams, their ability to concentrate
in the food chain, their movement and fate in natural waters, and their
ability to survive drinking water treatment.
In an attempt to assess the possible impact of the reactions of
chlorine with organic precursors in powerplant cooling water, Jolley and
co-workers in the laboratory exposed untreated cooling water sources to the
chlorine doses they would receive typically in practice, using radiotracer
chlorine-36 and assessing its incorporation into the gross organic load, as
well as measuring some specific chloro-organics that were formed (6). Chlo-
rine is frequently used in such cooling water to prevent bio-fouling of the
cooling water system. The tentative identification and quantification of
several of the compounds found is shown in Table 9, along with comparable
results for a chlorinated secondary sewage effluent. There is considerable
-215-
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concern about the possible adverse effect of chlorine residuals and such
chloro-organiccompounds on aquatic biota, and it .is interesting to note
that the concentrations in the chlorinated secondary sewage effluent were
comparable to those in the other chlorinated waters. Many of these compounds
are known to kill or otherwise affect fish or zooplankton. For example,
it has been reported that 5-chlorouracil and 4-chlororesorcinol can signi-
ficantly lower the hatching success of carp eggs at concentrations as low
as 1 yg/1 (7). Nevertheless, aside from organoleptic characteristics of
the chlorophenols showu in Table 9, any possible adverse chronic human effects
at these concentrations are generally not known. However, they are of
interest as an indication that a wide variety of chloro-organics can be
formed in chlorinated cooling waters at powerplants.
In these chlorination studies it was observed that the range of incor-
poration of chlorine into chloro-organic matter was .0.5 to 3 percent of the
applied chlorine dose of approximately 3 mg/1, which is typical of that
used in chlorinating secondary sewage effluents and in once-through cooling
water systems at powerplants, although the latter usually receive inter-
mittent doses. From these results one can infer that there was an incorpor-
ation of a range 15 to 90 yg/1 of chlorine into organic matter in the cooling
water. The actual quantity of organic matter thus ending up as chloro-or-
ganics would, of course, be highly dependent on their nature. Taking chlor-
obenzoic acid as a model, this range of chlorine incorporation would
generate 65 to 390 ug/1 of total chloro-organics. If, however, all the
chlorine were incorporated into the highly chlorinated chloroform, this
would generate 17 to 101 yg/1.
In order to evaluate the possible ultimate human exposures to these
-216-
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chlororganics from powerplant effluents it is useful to first assess their
potential impacts on surface water quality, particularly in comparison to
the loads generated by chlorinated municipal sewage. This is addressed in
Table 10 for four segments of the Ohio River and two of its major tributaries
in the greater Pittsburgh area. The quantities of power generated along
these river segments are shown, along with the estimated or known cooling
water effluent flows (including both once-through and other types), chlorina-
ted sewage effluent flows, and average and recent minimum river flows. It
is apparent that, except for the Ohio River from Pittsburgh to the Beaver
River, the ratio of cooling water effluent flow to that from chlorinated
sewage is quite high. On the average for the region, this ratio is about 8
to 1. It is interesting to note that in the lower Allegheny and Mononga-
hela Rivers the cooling water effluent flows are about 40 and 60 percent,
respectively, compared to recent minimum river low flows, although they are
substantially smaller than the average river flows. It is thus apparent
that the chlorinated organics in these cooling water effluents could appear
in the surface receiving waters relatively undiluted at times. Also, be-
cause the doses of applied chlorine are comparable for the cooling wal.er and
secondary sewage effluents, it is reasonable that they may be generating com-
parable loads of chloro-organics when their relative volumes and frequency
of chlorination are considered, at least in the Pittsburgh area described.
in Table 10.
One can make several generalizations and conclusions from these various
sources of information regarding the possible impacts of organics from steam
electric powerplants. Measurable concentrations in the region of 1 to
of a large variety of organic chemicals can be found in the wastewaters of
-217-
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such powerplants, although the available data are quite limited. In addition
to the organics from the coal itself and those added in the plant, such
as for water treatment, corrosion inhibition and cleaning, chlorination of
cooling water can result in quantities of chloro-organics comparable to
those generated by the chlorination of municipal sewage, and in some areas,
possibly even much greater quantities. The possible impacts on water quality
will be highly site-specific, and under some low flow conditions the dilutions
of these cooling water effluents may be very small. Although a few of the
identified organics are likely to be human carcinogens, most occur at con-
centrations well below known acute toxic levels, and at the same time
little or no information is available regarding their chronic human effects.
In addition to human exposure via drinking water, they could also affect
human health by concentration in the aquatic food chain. However, it is a
reasonable judgement that there is no need for alarm about their possible
impacts. At the same time it would be highly desirable to obtain additional
information about the full range of organics in these effluents and their
likely concentrations. Such evaluations could then be put in the perspective
of the variety of information now being developed about the possible human
health effects of such compounds in water, and a better assessment then made
as to the contributions and impacts from powerplants.
REFERENCES
1. U.S. Environmental Protection Agency, Development Document for Effluent
Limitations Guidelines and New Source Performance Standards for the
Steam Electric Power Generating Point Source Category, EPA 440/1-74
029-a, October 1974.
2. Cox, D.B., T.Y.J. Chu, and R.J. Ruane, in Proceedings of NCA/BCR Coal
Conference, Louisville, Ky., October 1977.
-218-
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3. Regional Studies Program, An Integrated Assessment of Increased Coal
Use in the Midwest; Impacts and Constraints, ANL/AA (DRAFT), U.S.
Department of Energy, Argonne National Laboratory, October 1977.
4. U.S. Environmental Protection Agency, Technical Report for Revision
of Steam Electric Effluent Limitations Guidelines (DRAFT), Effluent
Guidelines Division, Washington, D.C., September 1978.
5. Safe Drinking Water Committee, Drinking Water and Health, National
Academy of Sciences, Washington, D.C.,1977.
6. Jolley, R.L., G. Jones, W.W. Pitt, and J.E. Thompson, "Determination
of chlorination effects on organic constituents in natural and process
waters using high-pressure liquid chromatography, " in Identification
and Analysis of Organic Pollutants in Water, L.H. Keith (Ed.), Ann
Arbor Science, 1976.
7. Gehrs, C.W., L.D. Eyman, R.L. Jolley, and J.E. Thompson, "Effects of
stable chlorine-containing organics on aquatic environments," Nature, 249,
575 (1974).
-219-
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•CAW
O
I
LABoEAfOE-l' ^ SAMPUM3
WA«>TE«i, IUTAML& sceea
COOllUti VVATEE. SV&TEWS
FIGURE 1. TYPICAL WATER AND WASTEWATER FLOW DIAGRAM FOR FOSSIL-FUELED STEAM ELECTRIC
POWERPLANT (FROM EPA JUn/l-7ii
-------
TABLE 1 . CLASSIFICATION OF VARIOUS WASTEWATER SOURCES FROM
STEAM ELECTRIC POWER PLANTS (FROM EPA ^0/1-7^ 029-a)
Class
Source
High Volume
Nonrecirculating main condenser
cooling water
Intermediate Volume
Nonrecirculating house service water
Slowdown from recirculating main
cooling water system
Nonrecirculating ash sluicing systems
Nonrecirculating wet-scrubber air
pollution control systems
Low Volume
Clarifier water treatment
Softening water treatment
Evaporator water treatment
Ion exchange water treatment
Reverse osmosis water treatment
Condensate treatment
Boiler blowdown
Boiler tube cleaning
Boiler fireside cleaning
Air preheater cleaning
Stack cleaning
Miscellaneous equipment cleaning
Recirculating ash sluicing systems
Recirculating wet-scrubber air
pollution control systems
Intake screen backwash
Laboratory and sampling streams
Cooling tower basin cleaning
Rad wastes
Sanitary system
Recirculating house service water
Floor drainage
Miscellaneous streams
Rainfall Runoff
Coal pile drainage
Yard and roof drainage
Construction activities
-221-
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TABLE 2 .- CHEMICALS USED IN STEAM ELECTRIC POWER PLANTS
(PROM EPA 4 Jl 0/1-7*1 029-a)
i
to
to
10
Coagulant in clarification
water treatment
Regeneration of ion ex-
Chang* water treatment
Ll.-ne soda softening
water treatment
Corrosion inhibition or scale
prevention in boilers
pH control in boilers
Sludge conditioning
Oxygen scavengers in boilers
Boiler cleaning
Kegenerants of ion exchange
for condensate treatment
Chemical
Aluminum sulfate
Sodium aluminat*
Ferrous sulfate
Ferric chloride
Calcium carbonate •
Sulfuric acid
Caustic soda
Hydrochloric acid
Common salt
Soda ash
Ammonium hydroxide
Soda ash
Line
Activated magnesia
Ferric coagulate
Oolomitic lime
Disodiw phosphate
Trisodium phosphate
Sodium nxtrate
Ammonia
Cyc lohexy laroi rat
Tannins
Lignins
Chelates such as EDTA,NrA
Hydrazine
Morphaline
Hydrochloric acid
Citric acid
Formic acid
Hydroxyacetic acid
Potassium bromate
Phosphates
Thiourea
Hydrazine
Ammonium hydroxide
Sodium hydroxide
Sodium carbonate
Nitrates
Caustic soda
Sulfuric acid
Ammonex
Corrosion inhibition or seal*
prevention in cooling towr.rs
Biocides in cooling tower*
pH control in cooling towers
Dispersing agents in
cooling towers
Biocides in condenser cooling
water systems
Additives to house service
water systems
Additives to primary coolant
in nuclear units
Numerous uses
Chemical
Organic phosphates
Sodium phosphate
Chromates
Zinc salts
Synthetic organics
Chlorine
Hydrochlorous acid
Sodium hypochlorite
Calcium hypochlorite
Organic chromates
Organic zinc compounds
Chlorophenates
Thiocyanates
Organic sulfurs
Sulfuric acid
Hydiochloric acid
Lignins
Tannins
Polyacryloni trile
Polyacrylamide
Polyacrylic acids
Polyaerylie acid salts
Chlorine
Hypochlorites
Chlorine •
Chromates
Caustic soda
Borates
Nitrates
Boric acid
Lithium hydroxide
Hydrazine
Numerous.proprietary
chemicals
-------
TABLE 3 . TOTAL METALS DISCHARGED PROM POWERPLANTS IN THE
U.S. (1973) COMPARED TO OTHER INDUSTRIAL SOURCES,
INCLUDING COOLING WATER DISCHARGES
(FROM EPA 4HO/1-74 029-a)
.Pollutant
Chromium
Copper
Iron
Zinc
Total
Discharges by Major
Steam Electric Power-
plants, Ib/day
15,365
2,739
20,683
20,099
58,886
Percentage of
All Major
Dischargers
50
14
10
21
14
-223-
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TABLE 4. WASTE DISPOSAL CHARACTERISTICS (WITH CONCENTRATIONS
IN mg/1) OF TYPICAL COOLING TOWER INHIBITOR SYSTEMS
(PROM EPA MO/1-71! 029-a)
Inhibitor
System
Organic only
Organic
Biocide
Concentration in
recirculat ing
water
Chromate only
Zinc
Chromate
Chromate
Phosphate
Zinc
Phosphate
Zinc
Phosphate
Phosphate
Organic
200-500
8-35
17-65
•10-15
30-45
8-35
15-60
8-35
15-60
15-60
3-10
as
as
as
as
as
as
as
as
as
as
as
Cr04
Zn
Cr04
Cr04
P°4
.Zn
P04
Zn
P°4
P04
organic
100-200 as organic
10 est. as BOD
100 est. as COD
50 est. as CCl,
4
extract
5 est. as MBAS
30 as chlorophenol
5 as sulfone
1 as thiocyanate
-224-
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TABLE 5 . TYPICAL CHEMICAL WASTES FROM A COAL-PIRED POWERPLANT
(FROM EPA 440/1-7^ 029-a)
Waste Stream
Ion exchange
Boiler blowdown
Boiler cleaning
Boiler fireside cleaning
Air preheater cleaning
Miscellaneous cleaning
Laboratory operations
Floor drains
Recirculating bottom
ash sluicing blowdown
Ash pond overflow (once-
through fly ash)
Coal pile drainage
Plow,
GPD/Mw
88
52
0.25
4.44
11.7
1.11
10
30
400
5000
60
Typical Concentrations of Major Pollutants ,mg/l
TSS
46
25
127
582
1882
1000
100
100
1000
60
864
Iron
_
-
2100
142
1610
•»
-
'-
-
-
-
Copper
_
-
380
-
-
-
-
-
-
-
—
Sulfate
2085
-
-
1650
1130
-
-
-
-
510
6880
Hardness
_
-
520
4661
3700
-
-
-
-
244
1025
I
ho
f-0
Ln
I
-------
TABLE 6 . COMPARISONS OF SOME TRACE ELEMENT CONCENTRA-
TIONS IN COAL PILE LEACHATES WITH THOSE IN
THE ALLEGHENY RIVER AND HEALTH AND OTHER
DRINKING WATER CRITERION LIMITS (yg/1)
Element
Cu
Zn
Ni
Cr
Hg
As
Se
Be
Leachate,
Plant la
400
2,000
700
< 5
< 0.2
5
< 1
30
- 1,000
- 16,000
- 5,000
10
_ o
600
30
70
Leachate, in/-/-
1966 mean,
Plant 2a Allegheny R.
10 -
1,000 -
200 -
< 5 -
3 -
6 -
< 1 -
< 10 -
500 30
4,000 90
500 20
10 5
7
50 60
i _
30 0.1
EPAb
criterion
limit
1,000
5,000
-
50
2
50
10
0.2C
aFrom D.B. Cox, T.Y.J. Chu, and R.J. Ruane, in Proceedings of NCA/BCR Coal
Conference, Louisville, Ky., October 1977.
U.S.E.P.A. Interim Primary Drinking Water Regulations and Proposed Second-
ary Regulations.
°U.S.S.R. Drinking Water Standards
-226-
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TABLE 7 . YEAR 2020 PROJECTION OF TRACE ELEMENT
IMPACT FROM A COMBINED HIGH COAL ELECTRIC
AND ACCELERATED SYNFUEL SCENARIO: WATER
QUALITY IN ILLINOIS RIVER (JERSEY COUNTY)
AND BODY BURDEN*
Concentration - yg/1
Year 2020 coal
utilization increment
Trace
element
As
Be
Cd
Cr
Hg
Ni
Pb
Se
*Adapted
Impacts
River
average
44
0.10
12.7
7.4
0.0
12.9
28.3
0.01
Average
Flow
0.6
0.13
0.7
1.1
0.4
2.5
2.9
0.5
7- day
10-year
low flow
5
1.0
5.7
8.4
2.9
19.8
22.7
4.1
from An Integrated Assessment of Increased
and Constraints,
ANL/AA-11
(Draft), Argonne
Drinking
water
criterion
10
0.2
10
50
2
1000
50
10
Coal Use in
Water
vs. diet
body
burden
0.23
0.11
0.03
0.32
2.3
0.08
0.73
0.02
the Midwest:
National Laboratory,
October 1977.
^Comparing projected 7-day 10-year low flow concentration in river (assum-
ing same in drinking water) with typical diet intake.
-227-
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TABLE 8 . SOME REPORTED CONCENTRATIONS (yg/1) OF ORGANIC
CHEMICALS IN WASTEWATERS FROM STEAM ELECTRIC
POWERPLANTS*
Once -thru
Chemical cooling
Benzene
Toluene
2,4-dinitrophenol
Dichlorobenzene (isomers)
2 ,4-dichlorophenol
2 . 4 . 6 -trichlorophenol
Cooling tower Ash pond
blowdown effluent
2-45 1
24 4
50
20 35
83
35
- 2
- 64
-
1,2-dichloroethane 44
1,1-dichloroethylene 16
1,2-dichloroethylene 11
1,1,1-trichloroethane 12 - 27
Tetrachloroethylene 78
Chloroform - 2-26
Bromoform - 13 - 154
Chloiodibromomethane - 59
*
From Technical Report for Revision of Steam Electric Effluent
Limitation Guidelines (Draft), U.S. Environmental
Protection Agency, September 1978.
-228-
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TABLE 9 . TENTATIVE IDENTIFICATION AND CONCENTRATIONS
(yg/1) OF CHLORO-ORGANICS IN LABORATORY-
CHLORINATED SAMPLES OF SEWAGE EFFLUENT AND
STEAM ELECTRIC POWERPLANT COOLING WATER
INFLUENT3
Sewage
Effluent
Watts Bar
Lake
Sample
Mississippi
River
Sample
Nuclt^ide
5-chlo?-ouridine
1.7
0.6
Purine
8-chlorocaffeine
6-chloro-2-aminopurine
8-chloroxanthine
1.7
0.9
1.5
1.1
1,
3
0
6
3
Pyrimidine
5-chlorouracil
0.6
Aromatic acid
2-chlorobenzoic acid 0.3
3-chlorobenzoic acid 0.6
4-chlorobenzoic acid 1.1
3-chloro~4-hydroxybenzoic acid 1.3
4-chloromandelic acid 1.1
4-chlorophenylacetic acid 0.4
5-chlorosalicylic acid 0.2
Phenol
4-chlorc-3-methylphenol 1.5
2-chlorophenol 1.7
3-chlorophenol 0.5
4-chlorophenol 0.7
4-chlororesorcinol 1.2
1.1
0.2
0.3
0.8
1.8
3
3
0.2
0.2
0.2
0.2
0.5
10
8
8
3
6
20
18
0.7
4
6
2
7
From R.L. Jolley, G. Jones, W.W. Pitt, and J.E. Thompson, "Determination of
chlorination effects on organic constituents in natural and process waters
using high-pressure liquid chromatography," in Identification and Analysis
of Organic Pollutants in Water, L.H. Keith (Ed.), Ann Arbor Science, 1976.
-229-
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TABLE 10 . COMPARISON OF ESTIMATED STEAM ELECTRIC POWER
COOLING WATER AND CHLORINATED MUNICIPAL SEWAGE
EFFLUENT FLOWS WITH THOSE OF THEIR RECEIVING
WATERS IN MAJOR RIVERS OF SOUTHWESTERN PENNSYLVANIA'
River segment
Lower Allegheny
Lower Monongahela
Ohio-Pittsburgh
to Beaver R.
Ohio-Beaver R.
to Pa. border
Total
Power
generated
Mw
1,150
3,620
530
2.590
7,890
Cooling
water
effluent
MGD
750
720
400
150
2,020
sewage
effluent
MGD
25
17
195
9
246
Avge.
river
flow
MGD
12,500
7,900
20,900
23,350
Recent
minimum
river flow
MGD
2,000
1,150
3,160
3,715
-230-
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OCCUPATIONAL HEALTH ASPECTS OF FOSSIL-FUEL ELECTRIC POWER PLANTS
By
William N. Rom, M.D., M.P.H.
Rocky Mountain Center for Occupational and Environmental Health
University of Utah
Pulmonary Disease Division, Department of Medicine, and
Division of Occupational and Environmental Health,
Department of Family and Community Medicine
Salt Lake City, Utah
84132
-------
OCCUPATIONAL HEALTH ASPECTS OF FOSSIL-FUEL ELECTRIC POWER PLANTS
Analyses of occupational health risks in fossil-fueled power plants have
concentrated on raw material extraction (e.g. underground coal mining), trans-
portation of the raw materials, and the health consequences of the air pollu-
tion from electricity generation. There is little information concerning
occupational safety and health risks of the power plant workers.
The Edison Electric Institute estimates there are 1,000 fossil-fueled
power plants in the United States, and that they employ approximately a half-
million workers. A typical fossil-fueled power plant will have three to four
units, each capable of generating fifty to one-hundred Megawatts. Most power
plants are now using coal or are in the process of converting from oil and
natural gas to coal for economic reasons and encouragement by the U.S. Depart-
ment of Energy. This will result in greater occupational and environmental
health risk because coal-generated power entails greater risk than oil or
natural gas.
For a 1,000 Megawatt power plant, coal has a two to three times greater
health risk (occupationally-related deaths) than an oil-fired plant, and a
thirty-six to 1,120 times greater health risk than natural gas.
From 1967 to 1971 at two 1,000 Megawatt TVA power plants (Colbert and
Gallatin) there were 665,000 man-hours worked annually at each plant with
2
388.5 days lost because of accidents. There were no fatalities. By con-
trast, in 1969 in coal mining there were thirty-two disabling injuries per
million man-hours worked versus eight for all industries. There were 2,000
days lost per million man-hours worked which compares to approximately 258
for power plants.
-232-
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Over half the health costs associated with the generation of electrical
energy comej f rom coal mining; these risks will be only about 10 to 15% with
strip mining. Coal transport by railroad may also represent hazards, parti-
cularly accidents, since 10% of all railroad cars are hauling coal to power
2
plants (approximately five million carloads of coal in 1970).
In comparing estimates of the health effects for alternative fuel cycles
for equivalent 1,000 Megawatt electric units (Table 1), coal greatly exceeds
oil and natural gas for occupational and nonoccupational deaths and occupa-
tional impairments. ' The occupational death and impairment risks from coal
are magnified (Table 2) when one considers the greater number of millions of
Kilo-watt hours are generated by coal-fired plants compared to oil and natural
gas in 1975. (844 X 106 for coal vs. 292 X 106 and 297 X 106 for oil and
gas respectively). In evaluating the coal fuel cycle (Table 3), coal mining
accidents and disease were the highest with power generation accidents very
low, and power generation disease not even listed.
The future portends dramatic increases in coal production to meet energy
needs, both in electricity and liquid/gaseous fuels. Coal mining will undergo
major expansion in the Rocky Mountain states (Table 4) with a doubling of the
number of existing mines over the next ten years with a four-fold increase in
production. Major power plants are planned (e.g. Intermountain Power Project
in Utah) to produce power primarily for transhipment, or schemes (railroad,
slurry pipeline) to ship the raw products to the Far West or Midwest. Con-
siderable health risk and environmental degradation will likely occur from
these energy needs - all of which will not be accomplished without considerable
controversy.
The National Occupational Hazard Survey has provided a modicum of informa-
tion on power station health hazards. The National Occupational Hazard Survey
was a two-year field study initiated by NIOSH in 1972, intended to describe
-233-
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the health and safety conditions in the American work environment, and to de-
termine the extent of worker exposure to chemical and physical agents. The
sample of businesses in the survey was selected by the Bureau of Labor Statis-
tics and consisted of approximately 5,000 establishments in sixty-seven
metropolitan areas throughout the U.S.
Hazard exposure data was provided for 453 occupational groups, including
#433 - Electric power linemen and cablemen (43,433 workers) and #525 - Power
station operators (3,340 workers). Table 5 illustrates the number and per
cent of workers exposed to the more prevalent five individual hazards from
the survey (continuous noise, mineral oil, ethanol, isopropanol, and tri-
chlorethylene). Eighty percent of power station operators were exposed to
continuous noise, and 23.5% were exposed to trichlorethylene.
Using the "Occupational Mortality in Washington State 1950-1971" study
by Dr. Samuel Milham (NIOSH contract) as the reference, public utility
workers have increased proportional mortality ratios (PMR) of cancer of
the rectum (191), asthma (184), coronary heart disease (112), and accidents
caused by electrical current (449). (Table 6) Possible etiologies for
such elevated PMR's other than chance or bias could be social class, sulfur-
dioxide - particulate in-plant air pollution, electromagnetic radiation, sol-
vent exposure, etc. An increased pulmonary embolism PMR in linemen may be
secondary to traumatic injury.
In understanding the occupational health and safety problems of fossil-
fueled power plants, two tours were arranged through electric generating
stations. One was a public utility that burned coal, oil and/or natural gas,
and the other was an industrial utility burning coal and natural gas. These
tours provided practical experience in viewing the processes and work situations
of power plants. Generally, the work environment did not appear particularly
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hazardous, although the noise level appeared excessive at numerous sites,
and several of the maintenance jobs may be especially hazardous. One power
plant was twenty-five years old with three units generating over 240,000 kilo-
watts, and the other was slightly older generating 175,000 kilowatts. Both
employed over 100 workers with one-third to one-half working on maintenance.
Coal arrived in railroad cars from nearby coal fields - one unit
consumed 1700 tons of coal per day. Inside a separate building, coal is
shaken out of the railroad cars exposing the operator to coal dust and noise
levels as high as 115 decibels. Ear protection was mandatory, and the building
had been insulated with an acoustical material. No dust respirators were
worn. Coal is transported by conveyor to a storage area; it is loaded and
transported from here to a secondary storage area where coal is stockpiled
(Figure 1). The conveyor belts may create a coal dust problem, particularly
near adjacent walkways. The coal pulverizer is enclosed and utilizes large
steel balls or a hammer mill. The powdered coal is blown into the boiler.
Compared to natural gas, coal dust causes greater wearing of the pipes carrying
steam in the boiler and results in greater maintenance problems (Figure 2).
In the boiler, air and coal are mixed to heat distilled water into super-
heated, pressurized steam (1005°F, 1,525 pounds pressure). Heat may be a prob-
lem, expecially if the boilers are inside a larger building. The steam is then
transported to the main engine room to drive the turbines and generators to pro-
duce electricity. The turbine room was very noisy (estimated 85 decibels) (Fig-
ure 3). Nearby is the control monitoring headquarters. Older switches may con-
tain mercury and present a mercury hazard to control monitor workers.
Flyash from the boilers may be a problem. It is considered a nuisance dust,
and has a fine, sand-like quality with a variable silica content depending on
the coal (17% at one of the power plants visited). Flyash exposure may occur
at the base of the boiler when various doors are opened; a slight negative
-235-
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pressure within the boiler reduces dust exposures to flyash. A positive pres-
sure would increase the dust exposure hazard. The flyash is conveyed to a sepa-
rate building where it is moistened and hauled away via truck by contractors
(Figure 4). Loading flyash may lead to excessive dust exposures, especially for
farmers removing it to place on their fields to melt snow and hasten the plant-
ing season. Farmers prefer to load it dry to facilitate unloading. Electro-
static precipitators are used to remove particulate from flue gases going up
the stack. Neither power plant had scrubbers to remove sulfur dioxide since
they burned low sulfur (<0.5%) coal. A comparison of stacks from two units of
one power plant illustrates the differences in smoke from natural gas (left)
and coal (right) fuels (Figure 5).
Power plants have two closed cycles for water use and re-use - condensors
are used to condense the steam returning from the turbines. The water in the
steam cycle is distilled and kept free of impurities to reduce scale formation.
Cooling water from cooling towers passes through the condenser; this water is
also purified - a large water treatment plant exists which may entail exposures
to chlorine gas, sulfuric acid, and sodium hydroxide. Settling ponds are used
prior to any water discharge. A wet chemistry laboratory is used to monitor
water purity.
Maintenance work may prove particularly hazardous since it is an ongoing
activity throughout the plant. Exposures are usually intermittent, but may
be quite heavy. One of the generators was being overhauled on one tour; sol-
vent and oil exposures may occur here (Figure 6). Trichlorethylene and methyl
ethyl ketone exposures are not unusual. Insulation on pipes may contain asbestos;
this is more common in power plants built in the pre-1970 era (Figure 7). Re-
moval of the asbestos may generate a hazardous dust exposure. Scale and plaque
that accumulates on steel parts may be sandblasted resulting in a silica hazard.
A welding shop on the premises has exposures to various welding fumes.
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The electricity generated passes through transformers prior to distri-
bution. The transformers may contain polychlorinated biphenyls, and an expo-
sure may potentially occur during maintenance. The electricity then passes through
a sub-station where electromagnetic radiation exposures may occur.
A list of the safety mishaps at one power plant was available for Feb-
ruary - it provided a typical listing of power plant injuries: An apprentice
mechanic received a hairline fracture to his right arm when the sump pump he
was removing slipped and fell on him. A test and instrument journeyman re-
ceived medical attention for inhalation of chlorine gas. A serviceman received
flash burns to both eyes when a flash occurred as he was installing jumpers
in a meter base. A skilled helper received a laceration to the two middle
fingers on his left hand when he caught them between the forks on a fork-
lift. Five meter readers received medical attention for dog bites.
Measurements of crystalline silica, respirable coal dust, total coal dust,
and fly ash were made at three coal-fired power plants in Colorado by NIOSH.
Only a small number of workers were in direct contact with coal or flyash.
Personal samplers were used; coal handlers were exposed to excessive total
coal dust at all three power plants and to excessive silica at two. (Tables
7 and 8). One of the power plants required NIOSH-approved respirators for
its coal handlers. Most coal handlers worked outside on a high stockpile of
coal where engineering controls were not feasible. Excessive flyash exposures
occurred at one utility plant among utility men cleaning baghouses (Table 9).
Professor N. LeRoy Lapp has reported pathological findings on a lung
biopsy of a forty-two year old boiler repairman who worked at a power genera-
g
ting station that burned bituminous coal. He was a nonsmoker who had been
employed for twenty-four years. His chest x-ray (Figure 8) was read as normal.
The lung biopsy was obtained at the time of mitral valve replacement. Light
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microscopy (Figure 9) revealed mild-moderate thickening of the walls of pul-
monary arterioles, and focal areas of thickening and fibrosis of alveolar
septae. There were also a moderate increase in the number of pigment-laden
alveolar macrophages. Electron microscopy (Figure 10) revealed thickening
of the basement membrane in the alveolar walls by fibrous material and colla-
gen fibers. Four types of particulate matter were found in the intersti-
tium (Figure 11): 1) dense needle-like material, 2) smooth, angular pieces,
3) larger rectangular chunks, and 4) granular aggregates of the previous three
types of particle. Also, small, round debris (probably silica) and a few
asbestos bodies within macrophages were noted. Presumably, this particulate
material represented an occupational exposure to mixed dusts (flyash, as-
bestos, silica, coal dust) in a nonsmoking boiler repairman.
The Federal Power Commission estimated 3,607,000 tons of flyash were
9
released to the atmosphere in 1972 from 696 major steam plants. This re-
sulted from the combustion of 350 million tons of coal with an average ash
content of 13.4 percent (by weight). Recently, flyash has been reported to
be mutagenic. Both organic and inorganic compounds were found in a res-
pirable fraction of coal flyash that caused frameshift mutations in a bac-
terial strain lacking normal excision repair (positive Ames test). A
horse serum filtrate had approximately a tenfold greater activity than a
saline filtrate of coal flyash suggesting this increased the sensitivity of
the Ames technique in detecting mutagenicity of complex mixtures, or enhanced
solubility of mutagenic compounds, or provided serum proteins for complexes to
be formed increasing mutagen detection. Substances on the surface of flyash
deposited deep in the lung could be similarly soluble in alveolar fluid. The
surface of flyash may contain polynuclear aromatic hydrocarbons (shown to be
-238-
-------
mutagenic and may bind serum proteins), and may condense many metals, e.g.
cadmium, selenium, arsenic, antimomy, molybdenum, lead, nickel, beryllium,
manganese, and iron.
Coal-fired power plants may result in population doses of radioactive
particles and daughters of uranium 238 and 235 and thorium 232 that exceed
those of a comparably-sized nuclear plant. These particles are primarily
attached to flyash. Radium-226 and radium-224 are the major contributors
to the whole-body and most organ doses from the coal-fired plant, and in-
gestion is the main exposure pathway.
Coal and oil-fired power plants are responsible for nearly two-thirds
of the nation's sulfur dioxide emissions. Seventy-four percent of 623 large
coal and oil-fired power plants are currently in compliance with sulfur dio-
12
xide limitations. Sulfur dioxide is an irritant to the respiratory mucosa,
primarily to the upper respiratory tract where it is absorbed as sulfurous
acid or one of its ionization products. In high concentrations, it may cause
a chemical pneumonitis. Frank and associates studied acute changes in pul-
monary flow resistance after ten to thirty minute exposures in healthy human
13
volunteers. Pulmonary flow resistance increased significantly in 39%
exposed to five ppm, 72% to thirteen ppm, and in only one of eleven exposed
to an average level of one ppm. The change occurred within one minute of
exposure, increased after five minutes, but on the average, showed no further
increase after ten minutes. The cause of these changes appeared to be broncho-
constriction rather than tissue swelling or edema. Smith and Peters assessed
the effects of chronic, low-dose sulfur dioxide exposure on pulmonary func-
14
tion. In studying 113 copper smelter workers, they noted that at average
levels of 1.0 and 2.5 ppm, sulfur dioxide was associated with an excess loss
of FEV.. over one year and an increase in respiratory symptoms after controlling
for smoking. No exposure to respiratory particulates on pulmonary function was
-239-
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found. Workers with FEV.. less than the predicted values based on age and
height showed evidence of even greater losses of pulmonary function related
to sulfur dioxide exposure.
Trichlorethylene exposure may occur among maintenance employees; the
main physiological response is central nervous system depression, especially
from acute exposure. Other effects include visual changes, confusion, euphoria,
incoordination, nausea, skin irritation and alterations in hepatic and renal
function. Liver cancers in mice fed trichlorethylene by gastric intubation
have been reported by the National Cancer Institute.
Exposures to polychlorinated biphenyls may occur to workers repairing
electrical capicitors and transformers. About 95% of the 100 million capaci-
tors produced annually in the U.S. contain PCB's, and the 135,000 PCB-containing
transformers represent 5% of all transformers in the U.S. The Toxic Substances
Control Act of 1976 has now banned manufacture, processing, and distribution
in commerce of PCB's. Health effects of PCB's were best described from the
Japanese Yusho incident in 1968 where 1,200 cases were reported from persons
exposed to up to 3,000 ppm of Kanechlor 400 in rice bran oil contaminated by
PCf's during a heat exchanger leak. Signs and symptoms included darkened
skin, acneiform eruptions, including chloracne, eye discharges, nausea, visual
changes, neurological changes, and edema and/or low birth weight among infants
born from women exposed to PCB's during pregnancy. PCB's may induce hepatic
microsomal enzymes, and in animals, may cause hepatic necrosis, hepatic
tumors, and an altered immune response.
Power plant workers may be exposed to electromagnetic radiation since
there are sixty Herz electric and magnetic fields in several locations on the
power plant premises. Electromagnetic radiation may cause biological effects
from tissue heating, or by membrane excitation which occurs earlier. Studies of
electromagnetic radiation effects have directed attention to growth and develop-
-240-
-------
ment of plants and animals, cellular and molecular aspects of cell metabolism
and physiology, chromosomal changes, alterations in behavior, and the health
-I "7_~| Q
of utility linemen. The Johns Hopkins University nine-year study of
utility linemen working on energized high voltage transmission lines found no
19-20
physical, mental, or emotional changes attributable to the exposure.
Soviet studies of workers exposed to electromagnetic radiation in substations
and switchyards found increased subjective findings, e.g. headache, fatigue,
neurological and cardiovascular changes, hematological changes, and decreased
21-23
sexual potency. Marina and Becker have found that rats exposed to a sixty
Herz electric field for one month exhibited hormonal and biochemical changes
24
similar to those caused by stress. In another experiment they continuously
exposed three generations of rats to the same electric field and found in-
24
creased infant mortality and stunted growth.
A preliminary study in man showed that a 1-G (45 Herz) magnetic field
has a slight but statistically significant effect on dognitive skill assessed
25
by the Wilkinson Addition Test and Response Analysis tests. Constant magne-
tic fields are reported to slow wound healing by a delay in fibrosis and
9 f\
fibroblast production.
In summary, there are multiple potential and real hazardous exposures
for fossil-fuel electric power plant workers. There is a paucity of published
information on the prevalence of occupational disease and injury rates among
these workers. The working population is generally stable, and would provide
ample opportunity for research. An important study design feature would be
to isolate the many potential exposures, in order to study workers exposed to
single hazardous agents. This may be particularly difficult to achieve in
maintenance workers. Further studies on the health status of power plant
workers are needed.
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BIBLIOGRAPHY
1. American Medical Association Council on Scientific Affairs. Health evalua-
tion of energy-generating sources. JAMA 1978;240:2193-2195.
2. Sagan LA. Health costs associated with the mining, transport, and combus-
tion of coal in the steam-electric industry. Nature 1974;250:107-111.
3. Comar DL, Sagan LA. Health effects of energy production and conversion.
Annual Rev of Energy 1976;1:581-600.
4. Guidotti T. Health implications of expanded coal utilization in the western
states. 1978 (unpublished)
5. National Occupational Hazard Survey. Survey analysis and supplemental
tables. USDHEW PHS CDC NIOSH, December 1977;3.
6. Milham S. Occupational mortality in Washington State 1950-1971. CDC
Contract No CDC 99-74-26.
7. Gunter BJ. Health hazard evaluation determination report 78-50 (A,B, and C)-
517. NIOSH August 1978.
8. Harrison G, Lapp NL. Electron microscopic findings in the lungs of miners.
Ann NY Acad Sci 1972;200:73-93.
9. Federal Power Commission. Steam-electric plant air and water control data
for the year ending December 31, 1972. Washington, D.C., 1975. (FPC-S-246).
10. Chrisp CE, Fisher GL, Lammert JE. Mutagenicity of filtrates from respirable
coal flyash. Science 1978;199:73-75.
11. McBride JP, Moore RE, Witherspoon JP, Blanco RE. Radiological impact of
airborne effluents of coal and nuclear plants. Science 1978;202:1045-1050.
12. Fishbein G. Environmental health letter. Washington, D.C., February 1, 1979.
13. Frank NR, Amdur MD, Worcester J, Whittenberger JL. Effects of acute controlled
exposure to S09 on respiratory mechanics in healthy male adults. J Appl
Physiol 1962;17:252-258.
-242-
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BIBLIOGRAPHY (continued)
14. Smith TJ, Peters JM, Reading JC, Castle CH. Pulmonary impairment from
chronic exposure to sulfur dioxide in a smelter. Am Rev Resp Dis 1977;116:
31-39.
15. Industrial Union Department. Trichlorethylene: a cause of occupational cancer?
Washington, D.C.: I.U.D. Facts and Analysis - Occupational Health and Safety
July 1975;24.
16. USDHEW PHS CDC NIOSH. Occupational exposure to polychlorinated biphenyls (PCB's)
criteria for a recommended standard. Washington D.C., September 1977.
17. Miller M, Kaufman GE. High voltage overhead: a health hazard? Environment
1978;20(l):6-36.
18. Young LB. Danger: high voltage. Environment 1978;20(4):16-38.
19. Kouwenhoven WD, Langworthy OR, Singewald ML, Knickerbocker GG. Medical evalua-
tion of men working in AC electric fields. IEEE Trans, on Power Apparatus and
Systems 1967;PAS86:506-511.
20. Singewald ML, Langworthy OR, Kouwenhoven WD. Medical follow-up study of
high-voltage linemen working in AC electric fields. IEEE Trans, on Power
Apparatus and Systems 1973;PAS92:1307-1309.
21. Asanova TP, Rakov AI. The state of health of persons working in the electric
field of outdoor 400 and 500 kV switchyards. Gig Trud Prof Zabolev 1966;10:50.
(Translated by GG Knickerbocker).
22. Sazanova TE. A physiological assessment of work conditions in 400 to 500 kV
open switching yards. Scientific Publications of the Institute of Labor Protec-
tion of the Ail-Union Central Council of Trade Unions 1967;Issue 46, Profizdat.
23. KorobkovaAP, Morozov YA, Stolarov MD, Yakub YA. Influence of the electric field
in 500 and 750 kV switchyards on maintenance staff and means for it's protec-
tion. In: Int Conf on Large High Tension Electric Systems (CIGRE). Paris:
August-September 1972.
-243-
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BIBLIOGRAPHY (continued)
24. Becker RO, Marino A. Electromagnetic pollution. The Sciences 1978(Jan);18:11
25. Gibson RS, Moroney WF. The effect of extremely low frequency magnetic fields
on human performance: a preliminary study. Pensacola, FA: Naval Aerospace
Medical Research Laboratory 1974.
26. Gross W, Smith LW. Wound healing and tissue regeneration, biological effects
of magnetic fields. M. Barnathy, ed. New York: Plenum Press, 1964.
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TABLE 1
I
ro
Ui
i
Occupational impairments; 26.0-156.0 ! 12.0-94.0 4.0-24.0 4.0-13.0
COMPARISON OF HEALTH EFFECTS FOR ALTERNATIVE FUEL CYCLES*
i
Effects
Occupational deaths
Nonoccupational deaths
Total deaths
Coal
0.54-8.0
1.62-306.0
2.16-314.0
Oil
0.14-1.3
1.0-100.0
1.1-101.0
: - . .- ,'
Natural
Gas
0.06-0.28
• • *
0.06-0.28
. - i. .- - . .. i
Nuclear
0.035-0.945 !
0.01-0.16
0.045-1.1
*For electric power production per 1,000 megawatt electric units.
-------
TABLE 2
I
10
COMPARISON OF HEALTH EFFECTS FOR ALTERNATIVE FUEL CYCLES*
Fuel
Coal
Oil
Gas
Nuclear
Total**
1975 kW-hr,
Electric ,
Units X 10
844
292
297
168
1,601
Equivalent No. of
1,000-Megawatt
Electric Plants
128
44
45
26
243
Estimated Deaths
Occupational Nonoccupational
69.0-1,024
6.0-57
3.0-13
0.9-25
79-1,119
207.0-39,168
44.0-4,400
• * •
0.3-4
251-43,572
Estimated
Occupational
Impairments
3,330-20,000
530-4,100
180-1,080
100-340
4,140-25,000
*For electric power production in the United States in 1975.
**Some totals do not add up because of rounding.
-------
TABLE 3
ESTIMATES OF HEALTH EFFECTS
Occupational
Procedure Deaths*
Coal fuel
Extraction
Accidents 0.45-1.24
Disease 0.00-4.8
Transport
Accidents 0.055-1.9
Processing
Accidents 0.02-0.05
Power Genera-
tion Accidents 0. 01-0. 03
Air Pollution
TOTAL 0.54-8.0
OF COAL FUEL CYCLES
Occupational
Injuries and Nonoccupational
Disease* Deaths
22.0-80.0
0.6-48.0
0.33-23.0 0.55-1.3
2.6-3.1 1.0-10.0
0.9-1.5
0.067-295.0
26.0-156.0 1.62-306.0
*Per 1,000 megawatt electric units per year.
Some totals do not add up because of rounding.
-247-
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Table 4 The magnitude of the expansion of coal mining in far Western states.
Number of Number of Annual Coal Increases in
State Existing Mines* Planned New Mines Production** Production**
Arizona
Colorado
Montana
i New Mexico
M
-P-
" North Dakota
2
33
8
5
10
20
4
20
102
(0)
(18)
(0)
(0
(0)
(20)
(0
(5)
(45)
0
37
6
3
5
25
2
23
10 1
10.2
9.4
26.1
9.8
11. I
7.9
4.1
30.9
109.5
5.0
45.6
48.2
77.7
42.6
64.5
2.0
139.8
425.4
Utah
Washington
Wyoming
Total, 8 states
* Numbers in parentheses indicate underground mines; remainder are strip mines.
** Annual production in millions of short tons per year. A short ton, the industry
standard measure, is very nearly equal to a metric ton, or 1000 kg. Data are
current for 1976.
-------
TABLE 5 NATIONAL OCCUPATIONAL HAZARD SURVEY
#
1) Continuous Noise
433 Electric power linemen 2,881
and cablemen
525 Power station operators 2,673
2) Mineral Oil
433 26,988
525 1,159
3) Ethanol
433 1,984
525 209
4) Isopropanol
433 ' 3,229
525 488
5) Trichlorethylene
433 11,595
525 789
% of the occupa-
tional group
6.6%
80.0%
62.1%
34.7%
4.6%
6.3%
7.4%
14.6%
26.7%
23.6%
TABLE 6
CAUSES OF DEATH OF ELECTRIC UTILITY WORKERS
Cause of Death
Public Utility Workers
Cancer of the rectum
Asthma
Coronary heart disease
Accidents caused by electrical current
Proportional
Mortality Ratio
191
184
112
449
Linemen
Cancer of the large intestine
and the rectum
Cancer of the respiratory system
Pulmonary embolism
Accidents due to falls
Accidents caused by electrical current
157
129
278
239
2,657
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TABLE 7
BREATHING ZONE AIR CONCENTRATIONS OF
TOTAL COAL DUST
NIOSH Health Hazard Evaluation
Report
* J
f
i ', Sample ; i
jn Number ' \ Location
r3 1!
Job Classification
i !
61 , ; Basement Equipment Operator
115 ; <
111 ! i
: 64 ' M
117
60
Bag House Cleaner
Utility
Heavy Euqipment Operator
Utility
"
Time
8:12
8:28
8:17
8:20
8:30
12:30
i
of Sample
am - 2:30 pm
am - 3 : 02 pm
am - 9:20 pm
am - 2:25 pm
am - 12 : 00 noon
pm - 2 :30 pm
" ~ f
Total Coal Dust
0.7
0.5
56.0
64.0
39.0
1.6
EVALUATION CRITERIA
10.0 I/
JL/ = the nuisance dust TLV of 10 mg/M« was used, since these were not respirable samples
-------
TABLE 8 BREATHING ZONE AIR CONCENTRATIONS OF RESPIRABLE CRYSTALLINE SILICA (QUARTZ & CRISTOBALITE) AND
RESPIRABLE COAL DUST NIOSH Health Hazard Evaluation Reoort
Sample
Number
.
r — •• -"
2381
Location
Coal Handling
Job Classification
Coal Handler
Time of Sample
8:07 am - 3:00 pm
EVALUATION CRITERIA
LABORATORY LIMIT OF DETECTION
CRYSTALLINE SILICA
Quartz Cristobalite Coal Dust
(mg/M3) (mg/M3) (mg/M3)
0.14 * 3.0
0.05 0.05 2.0
0.03mg/sample 0.03mg/sample
I
K;
Oi
TABLE 9 BREATHING ZONE AIR CONCENTRATIONS OF FLY ASH
NIOSH Health Hazard Evaluation Report
Sample
Number
Location
Job Classification
Time of Sample
Fly Ash
(mg/M3)
110
59
Outside Coal Handling
Bag House Cleaner
Welder (Cleaning Bag)
8:20 am - 2:25 pm
8:17 am - 9:20 am
1.7
83.0
EVALUATION CRITERIA
10.0
-------
Figure 1 Coal conveyer, loading,
and storage processes
Figure 2 Coal-fired boiler
Figure 3 Turbine and generator
room of a fossil-fuel
power plant
Figure 4 Flyash disposal loading
facility
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Figure 5 Smoke from a stack from a boiler burning natural gas (left) compared
to smoke from a stack from a boiler burning coal (right)
Figure 6 Maintenance workers overhauling a turbine
Figure 7 Older pipe insulation may contain asbestos posing a hazard during
replacement
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Figure 8 PA chest rnd lo-f r:\u\- •,>£ 42 year old nonsmoking boiler repairman
(read as U/l on the ii.O/UC 1971 classification of the radiographs of
the p n e urao c o n i o s e.--,)
2d
Figure 9 Lung biopsy spt-cirncn denionstrating mild-moderate thickening of the
walls of pulmonary arcerioles, and focal areas of thickening and
fibrosis of alveol/n septae
-------
Figure 10 Thickeninq of alveo^r s
and fibrous material ( Hh
^e Hue to collagen fibers
?0.,UOO)
Figure 11 Particulate matter found in "lift pulmonary interstitium:
N-needle-like material, An-ar.cu'Iar pieces, R-rectangular
chunks, and Aq-granular aqqregdces (x 9,400)
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DISCUSSION
SESSION III
Dr. L. Hamilton: I would like to make a general
clarifying comment particularly in view of the remarks that have
just been read into the record. Particularly in the light of
Dr. B. Ferris's presentation because I think that some
confusion could arise. You know there is no evidence that S02
does anybody any harm. Of course, we accepted that in the light
of present day epidemiology that indeed harm is from the
particle material. But S02 is mainly oxidized to another
material, sulfate or sulfuric acid; and it is these materials
that are harmful. But S02 is the harmful precursor; it isn't
the material itself. In essence, I think it would be very
hazardous to give the public the impression that we are seeing
no effect of S02, and that we don't have to worry about the
material itself—it is what S02 turns into. Now there is
another very important consideration that we have to keep before
the public and that is when S02 leaves the stack as a gas, in
the process of being oxidized to sulfate, it forms a respirable
particle. This is another important matter. The very best
particulate removers in the world will not remove the S02 and
prevent the occurrence of this respirable particle in the
atmosphere. And a third important point is that, if it is a
sulfate particle, it's capable of being carried over many
thousands of miles. To give you an example, it has been shown
that in Europe, long-range transport of the acid material has
been amply demonstrated by European workers. Now, this is a
very important problem; the fact that you have long-range
transport. It means that if you have a 50% reduction in S02
emissions in New York, you can do the sort of study that has
just been reported, in which the S02 levels apparently have gone
down and one hasn't seen any concomitant change in health. It
is easy again by just focusing sometimes on isolated studies, to
draw misleading conclusions. I mention these things in a very
simplistic way, at this time, because I would like the ORBES
study, which is going to be the subject of consideration, to
take these into account. I feel it is necessary that these
considerations be clearly enunciated at this time. But, of
course, tomorrow I would like the opportunity of dealing with
these uncertainties more fully.
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Dr . H. Spencer; I think in all fairness I should respond
to and compliment Dr. Ferris and his analysis of the work of
Lave and Seskin in discussing the regression correlation
techniques used. I respond by saying that the classic
misstatements and mis-use in that technology exist in
engineering literature in the classic textbook by Metcalf and
Eddy on Water and Wastewater Treatment, and the text by Nemerow
on Industrial Wastewater Treatment. I think that they take a
stand on the issue mentioned, that certain regressions did not
show any relationships, and all of these regression techniques
take a partial of the sum of the squares which, in turn, makes
the assumption that the variables therein hold constant relation
to each other, which is totally wrong. I have a question I'd
like to address to the group. That is in relation to, not
knowing what sulfur dioxide does except that in sulfuric acid
there is another gaseous component which was passed by rather
lightly this morning, the subject of nitrous oxides--better
known as NOx. Among that family of compounds it is quite
reasonable to write equations about the formation of nitrous
acid which, in times past, in the good years of molecular
biology, since it was written as HONO was known as "Oh NO."
Nitrous acid is a powerful mutagen. That is a known fact. It
is a fact in molecular biology and has been for many years. We
need not argue that. I would like to hear an answer to the
question: what is the effect of nitrous acid, through
inhalation into the alveoli of the lung?
Dr . Ferris: I don't know that there have been any
measurements of nitrous acid per se. By and large, NO has been
felt not to have any health effects. It is oxidized to N02, and
that in turn is hydrated to H2N03 so it's usually the nitric
acid that is of concern.
Dr. H. Spencer: The problem I have with that is the long
term laterfcfy of cancer and the fact that we cannot show an
effect by respiratory volume or irritation of anaphylactic
shock, of which the person may be suffering. To me it is a
meaningless measure of the possible impact of that one
particular thing.
Dr . Ferris: But if you are talking about the carcinogens,
we are faced with all sorts of competing factors and, with the
long latent period, it is awfully hard to look back in your
"Retrospectroscope" to determine which is the initiating agent,
agents, or co-agents.
Dr. H_._ Spencer: I can't argue with that.
John Blair, EvansvilleL Indiana; One of the things I'd
like to hear this panel address, both on air and water
pollution, is the synergistic effects of all these chemicals
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forming together, and what effect do these have on health
problems of people? Also one other question about power plants,
loss of fuel in power plants and its relation to ozone
productions. That seems to be one of the major elements and the
EPA saw fit to change the standards.
Dr. Andelman; I hesitate to really comment very much
about the synergistic health effects. That's certainly not my
area. I have been somewhat familiar with polycyclic aromatic
hydrocarbons and their possible influence on waterborne disease,
and have been looking at some of the health effects that other
people measure. Of course, some of these chemicals are potent
carcinogens. There have been a number of studies which not only
have attempted to determine their carcinogeniclty on an
individual basis, but on some of the mixtures of polycyclic
hydrocarbons as well. In some such studies that have been
recently reviewed, it has been shown for some of the potent
carcinogens like benzopyrene and dibenzanthracene that, if
indeed you put these in with mixtures of other polycylic
aromatic hydrdocarbons, there doesn't seem to be either
potentiation or cocarcinogenicity.
Dr. Rom; I'm not aware of any measurements of ozone on
the premises of power plants. Most of the ambient ozone
measurements are made in communities. It generally has been
ascribed that most of this ozone has been due to various
transportation systems and reactivity from sunlight. Ozone may
have acute respiratory effects. Most of these effects have been
demonstrated by the investigators of the Los Angeles Basin.
There have been several recent studies that are probably worth
commenting on and would certainly warrant further discussion.
One is whether there is acclimatization to ozone, whether people
who live in high ozone environments for an extended period of
time have less of an acute response to experimental ozone
exposures than those who live in areas with less ozone. I would
think that is a recent finding that would warrant further
discussion.
Dr. Ferris: I would like to amplify on what Dr. Rom
said. The NO-N02 interaction in the presence of ultraviolet can
release atomic oxygen which then reacts with molecular oxygen to
form the ozone. This is part of the photochemnical reaction and
requires sunlight (ultraviolet) to cause the interaction. The
effect of tolerance to ozone has been demonstrated in chamber
studies that have compared Los Angelenos, who had lived there
for some time, with Canadians, who came to Los Angeles for the
study. The Canadians showed much more reaction to the chamber
exposure than the Los Angelinos who had been exposed to it over
a period of time. This tolerance has been used as an
explanation as to why we have not seen much of any effect of
ozone increases during alerts in the Los Angeles area. To speak
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more specifically to possible interactions, this of course, is
of great concern because frequently in the laboratory you give
gas A; then you give compound B; you don't usually give them
as a mixture. It is only just recently that some of the chamber
studies have used various mixtures. We also have to refer to a
certain number of animal studies to assess this and to identify
synergism or antagonism. Dr. Amdur in Boston, Dr. M. Corn
here in Pittsburgh, and others have looked at the interaction
between S02 and particulates. They have shown that with
hygroscopic type particulates and certain chemicals, such as
metals that can act as a catalyst, they can augment the effect
of the S02. Presumably the S02 is absorbed on the particle, and
then with the catalyst and water vapor it is converted to
sulfuric acid, which is much more toxic than the S02. Related
studies have looked at the interaction of S02 with ozone and S02
with hydrogen peroxide and in both instances presumably the end
product has been a sulfuric acid mist which again apparently is
more toxic than the original S02 gas. I certainly underscore
what Dr. Hamilton said that the S02 is a precursor and probably
its end product in the final common pathway is its appearance as
a sulfate that we have to be concerned about. But do not fall
into the next trap which says that all sulfates are equally bad,
because they are not. I think that is why we should not set a
sulfate standard, until we can improve our chemical techniques
so we can specify the type of sulfate we are talking about.
Dr. Stukel: There are documented cases of elevated
oxidant levels due to the long range transport of power plant
emissions. In a recent study, the pollutant concentrations in a
St. Louis area power plant plume were monitored, over a long
distance, using plume tracking aircraft. It was found that the
oxidant levels in the plume increased over time, and that a
large fraction of the elevated oxidated levels measured in
Springfield, Illinois, could be attributed to this plume.
Springfield is more than a hundred miles north of St. Louis.
Dr . Ferris: Is this not due to interactions of oxides of
nitrogen in the plume?
Dr. Stukel: Yes, that's correct. The point is that
oxidant levels are usually thought to be only due to automobile
emissions. I wanted to make the observation that this is not
always the case.
Dr . Si._ Ali, Public Service p_f Indiana: I have a question
for Dr. Rom. The material that was shown was on smaller units
which were 25 years or older. I wonder if he intended to show
the worst case situation rather than the actual situation which
exists in most power plants constructed and in operation?
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Dr . Rom: Of the two power plants that I toured, the worst
case was the industrial one for which I didn't have any slides
illustrating the problems there. They would not allow
photographs. The other one, a public utility, had two of its
units that were very old; the newest was the largest of the
three and was constructed during the early seventies. The other
two plants were built in the 1951-1955 era. It reflects the
technology that existed 20-25 years ago. And in that sense, I
would say it is more of a worst case example than a "best case
example. There are quite a few large coal-fired power plants
being built in our region, and I'm told that many of the
problems that I illustrated no longer exist. For example, they
don't use asbestos-containing insulation on the pipes; that's
being taken over by fiberglass. Also I was told that they have
electric switches that do not use mercury so that there is no
mercury hazard. I am not sure about the sandblasting
operations. They are, however, having a lot of coal dust
problems, and I'm told that their primary concern is now the
dust hazard in the new, large power plants. I think what may
happen in many of these cases is that as we advance with our
newer technologies, we have new problems to solve.
Dr. Ali; Another question I have for you, Dr. Rom, is
that you're trying to show here that smaller units are prone to
more problems. This is somewhat contrary to the objective of
EPA "Prevention of Significant Deterioration" which encourages
going to smaller noncentralized units. Do you have any views on
the subject? And have you provided your views to EPA?
Dr. Rom: The answer to the second question is no. To the
first part of your question--True, smaller plants may have more
problems. I think that is more in terms of how new a plant is
and newer plants tend to be larger plants. Many of the older
problems are solved with newer technologies.
Dr. Ali; The trend would be to smaller units if
"Prevention of Significant Deterioration," especially in the
midwest and east, becomes the main consideration.
Dr. Radford: I have a couple of comments and then a
question for each of the panelists. With regard to Dr. H.
Spencer's question about nitrite arising from oxides of nitrogen
when the nitric acid or N02 hydrolizes, it is my understanding
you get both nitrite and nitrate molecules, which might suggest
that nitrite could be significant. We have some unpublished
data on smokers, who inhale a lot of oxides of nitrogen too,
along with all the other stuff. One would predict that if
nitrite were a significant product in a smoker, you would get a
very definite relationship between the production of the
methemoglobin, which is generated by nitrite in the body, and
the amount of exposure to other agents such as carbon monoxide.
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We found very slight effects in a very large sample. We are
currently working on people taken from all over the United
States. We are finding a very slight effect of levels of
smoking on the production of methemoglobin in the body. It has
been a much argued point. But, it is extremely small and it
suggests to me that however the chemistry goes, the nitrite
component must be extremely small. This fits with what Dr.
Ferris said about NO also being present because we find no
physical logical evidence. That's the comment I wanted to make.
I'd just like to make a quick question. Dr. Ferris. Would you
like to say anything about the Six City Study you're currently
doing? Would you want to make any comments or preliminary
statements, or have you said enough?
Next question is to Dr. Andelman: Is there any extensive
use of river water for irrigation purposes where some of these
contaminants in the river, before treatment in water systems,
might get on to food crops and therefore have a pathway into the
human population? Finally to Dr. Rom, and I guess it's really
relevant to the point made by a previous discussant about the
age of power plants. There was a technology—it may no longer
exist—where in coal-fired power plants, the feeding of the fuel
into the boiler was under positive pressure. I have been in one-
such plant, and those are extremely dusty because we have the
fuel fed at higher pressure at any place in the working area.
Does anybody have any idea how frequently this positive pressure
technology is being used?
Dr. Ferris; Reluctantly I will make some preliminary
comments recognizing that we are still finding and collecting
data much faster than we can analyze it. One of the things we
are finding which is extraordinarily important, which others
have commented on, is that the levels that to which we are
actually exposed are much more influenced by the indoor
environment. If you want to predict what a person's exposure is
going to be, you have to measure the indoor environment, which
is much more likely way to give an accurate exposure estimate
than the outdoor environment. Yet the outdoor environment is
what we are controlling. Also, when we selected our cities, we.
had a nice gradation of exposures to total suspended
particulates, from very low to quite high which is one of your
neighboring communities, Steubenville, Ohio. We started
collecting mass respirable particulates and find that this nice
separation no longer exists. At this time, the cities are very
similar in mass respirable particulates and Steubenville, Ohio,
sticks out as the only one high in mass respirable particulates.
So this is another factor that needs to be taken into account.
Although there may be a lot of big stuff in the total suspended
particulates, they may be having no effect on the health. We
have finished analyzing some data from Steubenville, Ohio, which
involves hospital admissions over four months per year, over a
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four year period, and tried to link this to levels of pollution
on the alert days. There were days when the pollution levels
ran over 300 to 400 micrograms, total suspended particulates and
S02. We were not able to demonstrate any association between
levels of pollution and non-traumatic hospital admissions. We
also looked at oxides of nitrogen and some spotty ozone data.
We were not able to see that they were having any influence on
hospital admissions. This study can be criticized that perhaps
the population base is too small to show anything, or that we
are using too coarse an endpoint for this since all we could
look at were the total nontraumatic hospital admissions. The
other intriguing thing that has come out is that if homes are
using gas stoves for cooking, as other people have shown, there
are higher levels of oxides of nitrogens throughout the home.
This is so even though the stove is being used only three or
four hours in the course of the day. It affects the 24-hour
level. Other people have looked at the instantaneous values and
they have been as high as almost 1 part per million over 15
minute periods of time. It may very well be that these peaks
are much more important because the levels that we see in the
homes are way below the 24 hour annual standard for N02. There
are some suggestive data that this may be having some effect
upon the respiratory symptoms and tests of pulmonary function in
the children who live in those homes. These are very, very
preliminary and we need to have further evaluation of it. We
are not seeing marked differences in respiratory symptoms or
pulmonary function in the adults across the six cities. I think
we need to look at these on a longitudinal basis so we don't
have the high inter-city variability to mask intra-city effects.
The analyses are still in a very preliminary stage.
Dr. Andelman; I have no factual information about the
possible use or impact of the use of wastewater from power
plants or cooling water in terms of their ultimately being used
as irrigation water. There are a couple of people at the
Graduate School of Public Health attempting to develop
information about the possible impact of power plant effluents
on health. I wonder if any of them know of papers reviewing the
subject since they have been reviewing this literature much more
extensively than I? Do any of you have any ideas about this?
J. Bern, Student, University of Pittsburgh: With regard
to irrigation use of power plant effluents, the many studies
done by EPA, Corps of Engineers and DOE were concerned with the
release of heavy metals from the ash, as well as from
FGD-scrubber sludges. There has been some concern with the
uptake of cadmium and vanadium by plants. The researchers were
concerned with plant health rather than with the problem of
heavy metals entering the food chain. With regard to sewage
effluents, there are limitations placed on the spraying of
sewage effluents or digested sludge or untreated wastewaters on
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food crops. The limiting factor used is cadmium concentration.
This limitation is due to the expected uptake by the plants as a
result of a specific concentration of cadmium. There are a
number of studies with a great deal of information with regard
to heavy metal uptake. Now, as far as organics are concerned, I
believe that very little information is available in literature
or in the reports of actual operations.
Dr. Rom; The power plant I toured had negative pressure
rather than positive pressure for its coal dust. And I don't
know how prevalent positive pressure is throughout the country.
Perhaps the utility industry has information on that. At a
number of coal fired power plants in the west, I'm aware of some
irrigation experimentation that has occurred with wastewater.
This has been done in Utah by Utah State University. They have
been concerned more about the effects on the plant rather than
toxic products entering the food chain. Their primary concern
has been with vanadium. However, toxic effects have been
observed .
Dr. Stukel; Are there any comments on positive pressure
technology that any of you would like to make?
Dan Swartzman, University of Illinois School o£ Public
Health: Professor Shapiro mentioned that you were hoping to
have a document to represent the state of knowledge at this
time, and so I would like to offer some results that were
obtained by a colleague of mine at the University of Illinois,
School of Public Health, with two very important caveats. One
is that at this time the report which has been done under
contract with the United States Environmental Protection Agency
has not been approved and released by EPA, although a public
presentation of the data was made. Secondly, this is based on
my understanding of that public presentation and if you are
willing to accept my understanding of it, then I don't want to
trust your judgment too far. I offer this not as expert
testimony but just pointing out some information that does
exist. And what ought to happen is that somebody ought to look
into it if there is any interest after my presentation.
Professor Tsukasa Namikata was asked to look at a 1M%
reduction in the mortality rate that occurred in the Chicago
area between 1971 and 1975. Specifically, he was asked whether
or not he could associate any of that reduction with reduction
in air pollution levels in the city. He divided the city into
76 recognized community areas. He then took results from 28
particulate monitors and 24 sulfur dioxide monitors and
extrapolated air pollution results for the community areas that
did not, in fact, contain monitors. He noted in the
presentation that that was probably not too bad for
particulates. That sort of extrapolation got a little bit
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tenuous when you dealt with S02. He then did a similar linear
regression technique to what was done by Lave and Seskin, and
controlled for socioeconomic variables, educational levels and
an index of other environmental stresses. He had three indexes
which he gave the sources for, and I'm afraid I do not have them
at this time, what the indexes were or where he got them. He
looked at the total suspended particulates, sulfur dioxide, a
combination of total suspended particulates and sulfur dioxide,
and a complex of total suspended particulates and sulfur
dioxide. So, there are four different categories of pollution.
He also looked at a wide variety of causes of death, including
just about everything I could think of as a non-doctor other
than accidents; he excluded accidental deaths and homicides.
The findings on mortality rates of the study were that 5% of the
14? drop in mortality rate from 1971 to 1975 was associated, at
a statistically significant level, with a 25% reduction in total
suspended particulate levels. I don't know about the morbidity
aspects of the study—he didn't present them at the presentation
I attended—but I understand in discussing this with some of the
people who worked with him, that they did find some significant
associations with reduction in pollution levels and hospital
admissions. I just offered that for the sake of the record and
those interested should contact Dr. Tsukasa Namikata. Again,
I'm not sure whether the study has been released yet. In fact,
when EPA reviews it, they may decide they should not release the
study.
Dr. S^ Morris, Brookhaven National Laboratory;_ I have
two questions'^ One for Dr. loirf: yo~u start by pointing out
that in the estimates of health effects throughout the total
fuel cycle, there were no estimates that had been previously
made for occupational disease in power plants. Now that you
have gone through this, do you have any preliminary estimate of
the incidence of occupational disease—say, per power plant per
year, or something—that might be put in there. The second
question is to Dr. Ferris: in your discussion of the
statistical reanalysis of the Lave and Seskin data, I understood
that in general the result was to confirm the association that
Lave and Seskin found, but then you followed by saying that your
conclusion was there was not any likelihood there of an effect
at current levels of air pollution. What I'd like to ask is, is
that conclusion based on your thinking that the association of
Lave and Seskin is not causal, or because of the nonlinear
damage functions you mentioned, or for some other reason?
Dr. Rom; I don't have any preliminary data on the
prevalence of occupational disease in power plants. I think
this would relate again, as would the previous question asked,
to the age of the plant and length of duration exposure of power
plant workers. There probably is no such thing as "power plant
disease;" there are a number of exposures and a number of
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potential problems. I would not even hazard to guess what the
prevalence of disease may be for morbidity or mortality. I
would mention some studies that I am aware of, that may be
addressing this problem. First of all, Dr. Selikoff at Mount
Sinai has done a survey of workers in the Tennessee Valley
Authority. I am not aware of this being published anywhere, so
I don't know the exact statistics. However, that prevalence
survey addressed the prevalence of asbestos-related disease
among asbestos insulators who work for the Tennessee Valley
Authority. The prevalence of asbestosis by chest radiograph
among these asbestos insulators may be similar to other studies
of asbestos insulators in New York and New Jersey. The other
studies that I'm aware of are those that have been done by the
Tennessee Valley Authority. They have been looking at
respiratory effects of dusts, particularly coal dust. However,
I am very interested in studying power plant workers to see if
we can address your question in particular, "What is the
prevalence of disease and what diseases are these?"
Dr . Ferris: I gave you, if you recall, the data that were
reported. The association from the reanlysis was much, much
lower, and it did not reach a level of significance. Those who
did the reanalysis felt the observations could have occurred by
chance alone. So, on this basis we exclude these as being
causally related. I think if there were causality, one would
have to be careful about the range over which these observations
were made and I think we would all agree that at high levels
there is a definite effect of this mixture of S02 and
particulates. But, which is the active ingredient? I don't
think we know. I think it very unwise to take data from one
level and extrapolate it down to the lower level. This may not
be defensible at all. At the levels of pollution we are seeing
in most instances around here, there may be a very minimal
effect, if any, upon mortality. It may be having an effect upon
symptoms but not mortality.
Ray Gordon, West Virginia State Coordinator for EPA: Last
May 1978, in Phase I, the ORBES did the first year's interim
report. One of the very exciting portions of that presentation
involved the Teknekron work. That seemed to indicate the long
range transport mechanism and the causative factors for acid
rain consideration of a very serious nature. In my role, I've
had an opportunity to be approached and deliberate at great
length whether, in fact, we should be concerned about the acid
rain phenomenon. In addition, since that time, the study
indicated that this could be a very large impact area, sort of a
funnel effect. Western Pennsylvania, Northern West Virginia,
and Eastern Ohio seem to be the receptors of these problems.
There have been a number of supportive activities since May
1978. A number of subtle and some very dramatic matters have
occurred since the first finding. The EPA office which is not
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too far from Pittsburgh—in Wheeling, West Virginia—has
unoffically observed some phenomenally low pH readings
associated with rainfall, in particular with the inversion that
occurred last fall, in late October or November, 1978, which was
declared to be the worst in the past three years. So it was
more than a coincidental relationship. I would like very much
to have the panel discuss the acid rainfall. I don't want to
reveal the pH readings we get until I hear what you have
experienced across the board and particularly the lowest
readings that you have seen. We have done some quick literature
research and the values we found are startling. I don't see
anything in the literature close to what we found. Although it
is unofficial data, we have a lot of confidence in it's
validity.
Dr . Rom: Acid rain.s have occurred in the northeastern
part of the U.S. This has had some effect on some of the lakes.
I do not think we have quite as bad a situation as has occurred
in Scandinavia where they had serious effects on lakes such that
they had reduction of fish population. I think probably in most
of the areas where there are woods or vegetation there is enough
buffering capacity to tolerate the acid rains, unless they are
at an extremely low pH.
Dr . Stuckel: What's extremely low there?
Dr. Ferris; The low pH's are 3 to 4. Most of this has
been attributed to sulfuric acid although the nitric acid
probably contributes some. With respect to the alert you talked
about, we collected base-line pulmonary function data on the
children in Steubenville and followed them during the period of
that alert. We are just in the process of analyzing the
pulmonary function data to see if it had any effect upon their
health. We have not fully completed that analysis as yet.
Dr . And elm an : I think that it would be very difficult to
assess health impacts from acid rainfall in this part of the
country where we have a lot of acid mine drainage. We certainly
have very low pH's in some of the rivers, like the Kiskiminitas
or the Monongahela. Sometimes we get pH's as low as three. One
question is what is the possible impact of such a lower pH on
human health through the route of affecting water treatment or
mobilizing trace metals from sediments and things like that. If
I had to conjecture, I'd say it's going to be very difficult to
assess. What you have to try to do is see if, in fact, you can
measure some high levels of metals and if you can do that, then
the next step is assessment of the impact on human health. I
think that, as Dr. Ferris indicated, probably the greatest
concerns about acid rainfall are ecological ones.
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Ed Light^ Appalachian Research and Defense Fund in West
Virginia: I think it's appropriate to make a statement at this
point. The key environmental health question ORBES needs to
answer is what is the best judgment of dose-response range for
sulfate. This conference will be a real disappointment to me as
an advisory committee member if information isn't generated to
help make this decision. First of all, it appears to be
relatively unlikely that S02 direct health effects below
standards are significant. Hopefully, but maybe this is too big
a hope, EPA will soon get its act together to enforce the
existing ambient 802 standard. As a member of another advisory
committee on increased coal utilization to the office of
Technology Assessment of Congress, I was most impressed by a
conclusion of our team of researchers from Harvard School of
Public Health under John Spangler on the sulfate question.
After a very thoughtful review of all the relevant data, they
told us that the epidemiological work on sulfate indicates that
some pollutants or combination of pollutants emitted by coal
burning power plants poses probable health risks at ambient
levels. Increasing emissions will probably increase this risk.
Total sulfate isn't necessarily the definite culprit, but it is
a valid indicator. They said some of the CHESS findings are not
inconsistent with other independent research. Sulfate-effect
thresholds concluded by CHESS are basically restated by OTA as
its current best estimates, i.e. seven or eight micrograms per
cubic meter for asthma aggravation, around twenty-five
micrograms per cubic meter for increased mortality. They
debunked the common criticisms of epidemiological studies
implicating sulfates after a thorough and thoughtful analysis.
On smoking, it is important to note that a very high correlation
between air pollution and smoking habits of the entire urban
population would be required to account for the mortality
differences now attributed to air pollution. It is unlikely
that this is true. The report generally endorses the Brookhaven
approach to estimating the range of sulfate effects. I
understand Dr. Hamilton will give detailed discussion of this
tomorrow and, in my opinion, this will be the real heart of this
environmental health conference. I'd like to make one brief
comment on the University of Illinois' unpublished study that
was just mentioned. I think this would be a very important
contribution to the data ORBES needs to make its decision. It
will be helpful to estimate the trends in Chicago sulfate levels
and maybe try to work this into the analysis.
Dr. Stuckel: Before there are other questions, are there
any statements in response to that?
Dr_. Lippmann, New York University: As has been brought
out by several speakers and comments at this meeting, there are
good reasons not to rush into a sulfate standard. It's quite
clear that the bulk of sulfate that we measure most of the time
-268-
-------
is ammonium sulfate which is innocuous. Sulfuric acid is much
more hazardous, but it forms a very variable part of the
measured sulfate. While I'm up, if I may, I'd like to respond
to something Dr. Hamilton just said about concentrated sulfuric
acid depositing in the alveoli. Fortunately, that is physically
impossible, primarily because sulfuric acid and other acid
droplets are hygroscopic. They can't get to the alveoli in
concentrated form even if they're inhaled in the concentrated
form, because of the enormous uptake of water vapor .as they
penetrate through the conductive airways. They have to deposit
as very, very dilute droplets.
One thing which the directors of this conference have not
addressed is related to the necessity for SOx control. I'd like
to refer to something that we saw in a slide projected on the
screen yesterday showing haze. Now the S02, as a gas, does not
scatter light. However, when it is oxidized, it forms particles
which are acidic. These particles scatter light and produce
haze. Haze may be very important, and not only in terms of
visibility reduction. It was demonstrated quite effectively by
several presentations at a recent Atmospheric Aerosol Conference
sponsored by the New York Academy of Sciences in January—that
the haze reduces the actinic radiation reaching the ground.
Some fairly convincing data is coming to light which indicates
that the Ohio River Valley Basin may need to be concerned about
the effect of the haze on productivity of crops. I suspect that
these considerations, i.e. agricultural productivity, acid
rain, and visibility are perhaps the really significant problems
resulting from the sulfur oxide emissions in the environment.
Perhaps we should deemphasize the search for health effects
which may not be there and devote more research to other aspects
of the pollution problem which may show effects at lower levels.
Dr. Hamilton; A quick correction, sir. One of the
problems of uncertainty is clearly that even when we have a
meeting like this, people don't listen to your remarks, or if
they do, they mishear them, because I distinctly remember saying
that sulfuric acid didn't get neutralized.
Dr. Satl Mazumdar, Department of Biostatistics, University of
Pittsburgh": Yesterday and today" Dr". Herbert Schimmel' s work"
has been discussed several times. Dr. Schimmel wanted to come
to this meeting to discuss a few things and share a few thoughts
Due to personal reasons, he could not make it. As I am quite
familiar with his study, he requested that I present his slides
and bring out a few highlights of his study. He sent me some
reprints of his paper in the Journal of The New York Academy of
Medicine. If some of you are interested you can take a copy.
-269-
-------
This is the first slide (Figure 2c) . His study covers the
time period 1963-1976 in New York City. He was investigating the
possible association of sulfur dioxide with mortality and also
possible associations of particulates with mortality. The time
period is 1963 through 1976. He analyzed data for three
sub-periods: 1963 to 1969, 1970 to 1976, and the combined
period. Tne average level of sulfur dioxide in the first time
period was 0.16 ppm and in the second time period, 1970 to 1976,
0.04 ppm. So you can see there was a multiple reduction in the
level of S02. Now in this first slide there are tvrc sets of
figures, one at the bottom and one at the top. The four numbers
represented in each time period (each figure) of a set are the
magnitude of the mortality variate in the four quartiles. This
is the quartile classification of mortality based on S02. The
values, the solid lines, are the magnitude of the adjusted total
mortality variate. What Dr. Schimmel wanted to show in this
figure, without any numbers, was that using a time series
methodology which he developed over ten years, if you only
account for seasonal variation, or long term variation (that is
what he called filtered only) we see a kind of dose-response
relationship that is about the same in the two time periods. So
if there is a causal relationship we cannot see it because in the
first time period the level of S02 is very high, about four time?.1}
higher on the average than in the second time period. He implies
there cannot be a causal relationship, if the results for the two
tine periods are so similar and the levels of S02 so dissimilar.
If we go to the upper set of three figures where the variates arc
filtered and temperature corrected, that is when the effect of
temperature, as well as seasonality on mortality has also boon
taken into account, we see that all the effects of S02 on
adjusted Total Mortality are nonsignificant. There is no dose
response relationship suggested.
The slide (2d) shows the same adjusted Total Mortality whore
the quartile classification is based on Smoke Shade. Here" we see
the Filtered and Temperature Corrected set of results. Some
association between smoke shade levels and adjusted Total
Mortality still remains after correcting for temperature and
seasonal variation. The results still suggest a possible dose
response relationship between Smoke Shade and adjusted Total
Mortality unlike the situation for S02. Dr. Schirnmel has other
analyses. This is only one way of looking at the data. In his
paper he also presents a two-way classification where he shows
that any synergistic effect of the two pollutants is not
apparent.
His conclusions from his study are that there is no effect
of S02 on mortality and this is consistent with human and animal
experiments where no acute adverse effect is found below 1 ppra.
-270-
-------
REFERENCES
Schimmel, Herbert. Evidence for Possible Acute Health Effects of
Ambient. Air Pollution from Time Series Analysis: Methodological
Questions and Some New Results Based on New York City Daily
Mortality, 1953-1976. Bull. N.Y. Acad. Med. Vol. 54, No. 11:
1052-1108, 1978.
-271-
-------
i
Ni
vj
to
i
1963-69
I97O-76
1963-76
2o-
I
1%
2a 4—1-
t
FF
i
I-
r±
f1
FILTERED
AND TEMPERATURE
CORRECTED
FILTERED
ONLY
Fig. 2c. Ml()= Adjusted Total Mortality: Quartile classification based on SO....
-------
1963-69
I97O-76 1963-76
»*
2
-------
SESSION IV: HEALTH ASPECTS OF TRANSPORTATION AND TRANSMISSION
Tuesday afternoon, March 20, 1979
Moderator: Hugh T. Spencer, Ph.D.
Professor of Chemical Engineering
University of Louisville
HEALTH ASPECTS OF FUEL AND WASTE TRANSPORTATION
By
Samuel C. Morris, Ph.D.
HEALTH ASPECTS OF POWER TRANSMISSION
By
Richard D. Phillips, Ph.D.
HEALTH BENEFITS AND RISKS OF ELECTRIC POWER CONSUMPTION
By
Ronald E. Wyzga, D.Sc.
-275-
-------
HEALTH ASPECTS OF FUEL AND WASTE TRANSPORTATION
By
S.C. Morris
Biomedical and Environmental Assessment Division
National Center for Analysis of Energy System
Department of Energy and Environment
Brookhaven National Laboratory
Upton, Long Island, New York 11973
-277-
-------
INTRODUCTION
Energy resources are frequently not found where we could like
them to be. We thus expend considerable effort in transport. Living
on Long Island, I am reminded of the cost involved every time I
buy gasoline for my car or oil for my furnace. I do not find much
solice in the knowledge that 200 years ago, when we were on a wood
economy, the area on Long Island where I live was a major supplier
of energy to New York City. As a sidelight, if you have ever
wondered what happened to all the horse manure generated in New
York back then, it was sent to Long Island on the same boats that
brought wood to the city. Unfortunately, today we have not been able
to find a profitable return cargo for most of our energy transport,
so the round trip cost, in dollars, health and environmental impact,
must be charged against the transported fuel.
What are the health costs of energy transport? Accustomed
as we are to the carnage on our highways, we should not be
surprised that there are some. In the U.S. we move around
o q
annually about 6.5 x 10 tons of coal, over 4 x 10 barrels of
Q
crude oil and over 5 x 10 barrels of refined products, and over
12
2 x 10 cubic feet of natural gas. Most health damage is due
simply to the trauma resulting from accidents which accompany the
handling and movement of such a large mass of material. Some of
the health risk, however, stems from the unique nature of the
fuels transported. Table 1 summarizes estimates of the health
damage of energy transport in several fuel cycles on a unit energy
basis. Since coal has the highest health risk and nuclear the
most controversial, I will go through these two in some detail.
-278-
-------
. Health
Fuel Cycle
Coal
Oil
Natural Gas
LNG
Nuclear
Table 1
Damage in Energy
per GWe-yr
Deaths
0.5
0.08
0.004
10"6tolO-1
0.02
Transport
In j ury
2
7
1
0.3
Latent
Cancer
_
-
—
0.002
COAL TRANSPORTATION
Coal is transported by rail, water (rivers, Great Lakes, and
intercoastal waterways), truck, and/or conveyer belt. One slurry
pipeline is in operation and pipelines are a potentially significant
mode of coal transport in the future.
Most coaff moves by rail. Coal constitutes 29% of all rail
freight in the U.S. and 13$ of all freight revenue. By comparison,
coal transport makes up 20$ of all rail freight in the USSR. Coal
is moved in hopper cars which are unloaded by turning the car
itself over, by opening bottom hoppers, or, more rarely, by
unloading from the top. The cars are generally loaded at mine
sidings or tipples which collect from several mines. The average
hopper car carries 75 tons of coal, older cars 55 tons and newer
ones 100 tons. Size of hopper car used depends on the condition
of the track. Modern unloading facilities are frequently trestles
running over storage piles into which coal is dumped from moving
cars. Many have loading and unloading rates of thousands of tons
per hour. _2?9_
-------
Statistics are not maintained for accidental deaths and
injury in railroad transportation by type of freight carried;
thus, it is not possible to determine directly from available
data the mortality effects of transporting coal by rail. There
are several ways to estimate this value. The simplest is to
assign a proportionate share of all railroad deaths to coal
transport. This apportionment may be on the basis of total
weight or bulk of material transported, train-miles traveled,
or ton-miles traveled. Over 60 percent of accidental deaths
associated with freight traffic result from rail-highway grade
crossing accidents, primarily due to collisions between trains
2
and motor vehicles. The number of intersections crossed and the
characteristics of each, crossing (e.g., highway vehicle and train
traffic density, type of crossing protection) are crucial
parameters. Several models have been developed to predict the
accident risk at grade-crossings based on such factors. Rogozen,
o
et al., use such a model to estimate the impact of specific
unit train routes compared to coal slurry pipelines. They conclude
that an increase in train traffic is non-linearly related with
statistics such as train-miles or ton-miles. In a typical example,
as the average number of trains per day increased by 7Q%, the
predicted accidents increased'by only 30%. While there are many
factors which cannot be considered in these models, it seems clear
they offer the best approach to quantifying impacts for particular
cases. A great deal of information is required, however. The
routes to be followed must be specified; for each grade-crossing
-280-
-------
on route, the following data is needed: average daily highway
*
traffic, average daily train traffic, type of crossing protection,
urban or rural location, and single or multiple tracks. For
broad assessment purposes in which specific routes are unknown,
a simpler approach is required. Estimates below are based on
ton-mile and train-mile apportionment. Since the detailed models
indicate a non-linear response, these are average, rather than
marginal, estimates. Examples cited by Rogozen, et al., suggest
the marginal estimates may vary downward from the average by as
much as a factor of 5- Since coal represents a substantial share
of all rail transport, and an even greater share in areas with
heavy coal traffic, the average figure may be reasonable when
estimating effects of total U.S. coal transport. When estimating
the incremental effect of a single plant or a perturbed scenario,
a marginal estimate would be desired. All grade-crossing accidents
involving trains have been charged against coal transport in
calculations made below. One might argue that since the fault
frequently lies with the motor vehicle, that only a portion (and
perhaps a small portion) should be charged to coal transport.
There is some reason to believe that unit coal trains may
create different exposure situations than the average freight
train. Coal has a greater density than average freight, coal
cars are generally bigger and heavier and coal trains longer than
average. Train velocity may be different. Unit trains generally
operate on well used and maintained lines and it has been
suggested that they may be less likely than average freight trains
-281-
-------
to pass non-signal crossings. Concerning the 40 percent of
•
accidents not at grade-crossings, unit trains generally can avoid
hazardous switching and yard operations. While one might suspect
that unit trains are less likely to be involved in fatal accidents
than are average freight trains, there is no quantitative basis in
available data on which to base an adjustment. Occupational
accidents associated with unit trains seem likely to be
concentrated at on- and off-loading facilities.
Schoppert and Hoyt, in a sample of grade-crossing accident
reports from six states, found that grade-crossings have a
turbulent effect on motor vehicle traffic resulting in accidents
l\
not involving a train. Accidents not involving trains were
twice as frequent as accidents involving trains and motor vehicles,
Of the accidents not involving trains, half occurred when a train
was present but not involved and half when a train was not even
present. Based on detailed data from 16,000 crossings in
Illinois, it was found that the fatality rate was much higher in
accidents involving trains but the non-fatal injury rate was
higher in non-train crossing accidents (Table 2). These accidents
Table 2
Accidents and Health Damage at Railroad
Grade-Crossings by Train Involvement^a'
Accidents Deaths Injuries
Train Involvement No« % No., Per Accs NO. Per Accs
Train Involved 1113 30.7 290 0.26 738 0.66
Train Not Involved 2514 69-3 25 0.01 1707 0.68
Total 3627 100.0 315 2445
(a) Based on Illinois data for 1962-1964. From Schoppert and
Hoyt, National Cooperative Highway Research Program Report
50, 1968, pp. 20-21.
* Accidents
-282-
-------
not involving trains have not been included in calculations below.
In cases where a crossing exists solely for the benefit of a
unit train such accidents should be charged against coal transport
to the same extent as accidents involving trains. In the
majority of cases, however, where crossings have mixed use, it is
not clear to what extent non-train accidents should be charged
against coal transport. Lorber has extensively reviewed Schoppert
and Hoyt and developed a statistical model of grade-crossing
accidents based on their data.
In unit trains, and for the most part in non-unit trains also,
the cars must return to the mine empty. Thus, train mileage refers
to the round-trip distance per trip times the number of trips
while ton-mileage is calculated as tonnage hauled per trip times
one-way distance (no ton-miles are incurred on the empty return
trip) times the number of trips.
There were 6.95 x 10 ton-miles of freight movement on U.S.
railroads during the period examined, 1966-74. Freight trains
Q 6
logged 3.97 x 10^ train-miles. Statistics for total deaths and
injuries, deaths and injuries among employees and among the public
are given in Table 3 per ton-mile and per train-mile.
The basic data from which the statistics are calculated are
given in Table 4. The annual statistics show a slight downtrend
*
in public deaths and injuries. Given that both railroad and
*The 1973 deaths and injuries among the public seemed anomalously
low. The data for 1973 were rechecked with DOT to assure they
were correct (personal communication with M. Snellings, 6/8/78).
-283-
-------
Table 3
Deaths and Injuries Associated vrith Railroad Freight
Operations per Ton-nile and Train-mile
Year
1966
67
68
69
70
71
72
73
74
66-74
Deaths
per 10
ton mi
2.16
2.08
1.98
1-95
1.95
1.94
1.82
0.38
1.62
1.74
data
PUBLIC
Q Deaths,- Injuries
y per 10 per 10?
train mi ton mi
3
3
3
3
3
3
3
0
2
3
from
-65
.55
.43
.45
.50
.33
.14
.68
.95
.05
Table
4
4
4
4
3
4
3
0
3
3
4'
-30
'.26
.50
.86
.05
.99
.45
.56
.66
Injuries
per 106
train mi
7.25
7.65
7-38
7.97
6.90
6.97
6.E7
0.61
6.45
6.42
Deaths-
per 10
t on mi
0.050
0.060
0.059
0.072
0.077
0.041
0.048
0.068
0.055
0.059
-;,*•?
Dea-hs,-
per 106
train ni
0.385
0.102
0.103
0.127
0.128
0.070
0.3S2
0.124
0.100
0.103
LDYFt
.'0
Injuries
per 109
ton mi
5.
4.
5-
4.
4.
3.
3.
3-
4.
4.
33
41
13
94
50
89
56
54
02
44
j_n j u r i o o
per 1G'J
train :r.i
9.00
7.55
8.83
8.75
8.06
6.69
6.14
6.44
7.28
7.78
Table 4
Railroad Freight Statistics 1966-74
PUBLIC
Year
1966
67
68
69
70
71
72
73
74
66-74
Ton mi
x 109
738
719
744
768
765
740
111
852
851
6954
Train mi
x 106
437
420
429
433
427
430
451
469
469
3965
Deaths
1595
1493
1474
1456
1495
1432
14H;
321
1353
12103
Injuries
3173
3214
3168
3455
2949
2994
3099
381
3027
25460
EMPLOYEE
Deaths
37
43
44
55
53
30
37
58
47
410
Injuries
3933
3783
3814
3790
3443
2874
2767
3019
3418
303^6
xon-mile and train-mile data frcm Yearbook of rlailroad Pacts,
Association of American Railroads, Washington, DC, 1977, PP• 29
and 37.
Injury and death data from U.S. Dept. of Transportation, Federal
Railroad Administration, Office of Safety, Accident Bulletin
Nos. 135 through U'3, 1966-7'-:. Data for 1975 and later years ar--i
not available in this form.
-284-
-------
automobile traffic is increasing, this must reflect the effort
of the railroads, state highway departments, and Department of
Transportation to reduce accidents, particularly at grade-crossings.
Statistics were not calculated later than 197^ since accident data
were no longer reported separately for freight traffic by DOT after
that year.
The average haul length for the industry as a whole is over
500 miles, but coal shipments have an average haul length of
•7
300 miles. Assuming 1 GW"e-yr electrical output requires 3«4 x
6 9
10 tons of coal, this yields 1 x 10 ton-miles.
Assuming an optimum unit train size of 15,000 net tons,
annual round trips required would be 3_.4 x 10 tons = 227 train
T.SxlO^tons/train
trips.
227 trips x 600 miles round trip = 1.4 x 10^ train miles per
GWg-yr.
Non-unit train movement would involve more train miles to
deliver the same amount of coal, but only a share of the effort
can be charged to coal transport. If one takes these results and
applies the average figures over the 1966-7*1 interval from
Table 2:
cases per GWe-yr
Train-mile
basis
public deaths O.^ll
public injuries 0.86
employee deaths 0.014
employee injuries 1.0
-285-
Ton-mile
basis
1.8
3.8
0.06
-------
The estimates from the train-mile approach give a closer fit
with the results of the more detailed approach in Rogozen when
compared in actual cases. For haul distances other than 300
miles, the estimates are linearly proportional to changes in
haul distance. Note that accidents involving the public, mostly
collisions between motor vehicles and trains, have a high death
to injury ratio, while occupational accidents involve many more
injuries than deaths.
Since the bulk of the effects involve collision with
automobiles, one would expect variation by region due to
differences in the density of automobile traffic and driving
patterns. Table 5 provides estimates of the variation in
accident rates by railroad district. These tables combine data
on all rail traffic, both freight and passenger. The difference
in deaths per train-mile among regions is less than a factor of
2 and in injuries less than - 105S.
Potential health effects not quantified result from the
contribution of diesel exhaust from coal unit train locomotives to
air pollution and to the possible impairment of emergency medical
service in communities where major streets are frequently blocked
by unit trains.
Barge transport of coal is estimated to be an order of
magnitude less hazardous than rail transport and slurry pipeline
(based on experience with oil) a further order of magnitude
8
safer.
-286-
-------
Table 5
Casualties by Railroad District 1575
(Class I Railroads, Line-Haul)
Eastern Southern
Train Miles x 10
Train Accidents-Class I Line-Haul
killed
injured
Train Incidents-Class I Line-Haul
killed
injured
Non-train Incidents-Class I Line-Haul
killed
injured
Total All Casualties
killed g
deaths/10 train-miles
(1
in j ured g
injuries/10 train-miles
(84
276. 4 113.4
56 23
464 345
416 285
4138 2413
' 46 84
18990 7141
518 357
1.87 3.35
.7-2. 0> (3.0-3.7)
23592 9859 '
85.4, 83.6
•3-86.5) (82.0-85-3)
Source of data is for Class I railroads, line-hauls fros USDOT,
Railroad Administration Accident/Incident Bulletin Mo. 145 , pp.
70.
Western
329.4
68
425
575
5493
87
19346
730
2.22
(2:i-2. 4)
25269
76.7
(75.7-77.7)
Federal
64, 68 and
*Range in parentheses is 95$ Poisson confidence interval.
Truck transport has been the most rapidly growing coal transport
IT
mode. Twelve percent of total coal production, cr about 8 x 10'
tons, is delivered by truck. Haul distance averages 50 to 75
q
miles. This does not include truck-haul of coal to tipples for
loading on rail or barges. Assuming a 30 ton load of coal per
trip, 3.4 x 10 tons requires 1.1 x 105 trips. For a 100 mile
7
round trip, this yields 1.1 x 10 vehicle-miles. Common carrier
r-287"
-------
truck fleets average 7 accidents per 10 vehicle miles, resulting
in 79 accidents per GWe-yr. Assuming 0.03 deaths and 0.5 injuries
per accident results in 2.4 deaths and 40 injuries per GW -yr.
The principle waste products in the coal fuel cycle subject
to transport are fly ash and scrubber sludge. In general, these
wastes are maintained on or near the plant site to avoid
unnecessary transportation. Current designs use slurry pipelines
which are expected to produce minimal health effect.
NUCLEAR FUEL CYCLE
Transport is much more complex in the nuclear fuel cycle than
for coal because there are many more steps in the cycle. The mass
of nuclear materials required per GW -yr is much less than for
coal, however. Even with the elaborate precautions required in
the shipment of nuclear materials, transport is a minor part of
the cost of entire fuel cycle. Because of this, other factors
predominate in processing facility location leading in some cases
to cross flows of material or longer hauls than would otherwise
be required. Figure 1 illustrates the transport steps in the
full nuclear fuel cycle. These are detailed in Table 6 and its
accompanying notes for the steps needed to support 1 GW -yr
C
production of electricity in the nuclear fuel cycle the way it is
currently operated in the United States, although including
shipment of spent fuel assemblies to interim storage. Later
introduction of a federal waste repository would require an
additional 7 trips by rail from interim storage to the repository.
-288-
-------
Fuel Elements
L
Nuclear
Power
Plants
Fuel
Element
Fabrication
Fuel
Material
Preparation
Conversion
U3°8
Mills
Spent Fuel
Uranium
Enrichment
Ore
Mines
Reprocessing
r~
f
~~
Deoleted UP,
o
Depleted U
Th
J 1
QQ - —
Waste
Repository
FIGURE 1 Full Nuclear Fuel Cycle
-289-
-------
TABLE 6. NUCLEAR FUEL CYCLE TRANSPORT (NO RECYCLE)
per GW -yr
M.i tori ft! Form
crjs Sclid Bulk
Concentrated !i inular or
I'jOg ("yellow cake") powder ir.
5 "> gal steel
diums
IT, Stlid in 10
tc 14 ton
t-jlinders
1 r:-.iriched VS. Eclid ln(n)
£ 2.5 ton
O cylinders
"JO I'cwder or
2 ;.ellet in
i;tcel pails
supported in
r^ gal drums
Unirradiated Type B Con-
Fuel Assemblies IE in era
Irradiated Fuel V 'pe B Con-
Afsesblies t liners
Lou Level baste
Low Level Vtaste
Low Level Vast a Solids packed
i.i dmiis
rron
Mine
Mill
Cor version
Plant
Enrichment
Plant
Fuel Prepara-
tion Plant
Fabrication
Plant
Reactor
Conversion
Plant
Fabrication
I'lant
Keactor
To Mode
Mill Truck
Conversion Truck
Plant
Enrichment Truck
Plant
Fuel Prepare- Truck
tlon Plant
Fabrication Truck
Plant
Reactor Truck
Storage Truck
Rail
Burial Site Truck
Burial Site Truck
TlitrOiJ. Ground
QUANTITY
Mass
1.7xl05KT(a>
340 KT(f)
,..
394 Kl"'
-64 OT(0>
49 MT(s)
43 MT U*W)
., ._ (aa)
16 W Ian)
24 HI (aa)
280 M3(cc)
180 H3^ff^
100-1000 n3 ^8)
SHIPPED DISTAJJCE SHIPPED „ t
Activity K.les Shipments
1.4xl03Cl(b) 0-40 (5){c'd) b3fO(e)
360 Ci<8) 275-2200(1000) ('!) 20^ 1}
tlf\ (1\ fr»)
62l ' 20-900 <500)1 ' 22 3'
62 l?tv)
62(x) (1000) (y) 7(l>
7.6E6 (5«>) ^ 2o[aa).
1.1E7 (1000) l ' 5 ;
20-900 (iOO)(dd> 25-38(ce)
20-900 (500)(dd) 19-:S<8>?)
2R3 Ci ~ ( "iOO) 6^ * '
-------
Notes to Table 6:
a. Calculated from GESMO, p. IV J (E)-17. 1.77E6/(4732 x 1.1) = 340.
MT U30g. An ore grade of 0.2% this yields 1.7E5 MI ore. Note WASH-1238 &
WASH 1248 (p. K-7)have a much lower fuel requirement since they
assume recycle and only 0.8 GWe-yr.
b. Calculated from GESMO p. IVH 14, 4.51E5 x 14 = 6.31E6 ci 1975-2000 total
from GESMO p. IVJ (E) 17, 6.13E6/4.732E3 = 1.33E3 ci/GWe-yr.
c. WASH-1248, p. H-7.
d. Number in parenthesis is the distance used in the models of WASH 1248 and
GESMO.
e. Scaled from WASH 1248, p. H-7, 182 MT U308 and 3350 trips. (340/182 x
3350 = 6258.
f. From GESMO, p. IV-J (E) 17, 1.6E6/(4732 x 1.1) = 307 MT U308. Assuming
yellowcake is 90% t^Os, 307/0.9 = 341 MT yellowcake.
g. Following calculation was provided by J. Nagy. The activity of a mass
of radionuclide is given by:
C [Ci] - 3.5768 x 10U M_ [Mass (metric tons)]
AT [atomic wt] [half life yrs]
For Unit Mass
Nuclide U-235 U-238
M 11
A ^235 ^238
T 7.04 x 108 4.468 x 109
C [ /tonne] 2.162 0.336
The activity of nuclear fuel is given by:
2.162 f d + 0.336 f g d „ ci/tonne
where,
f = parent nuclide fraction by weight
d = number of main sequence daughters in equilibrium
plus parent
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f and d depend on before/after milling and before/after enrichment.
Rough values are given below:
before milling
after milling/
before enrichment
after enrichment
f235 d235
0.007 11
0.197
(4.0%)
0.007 2
0.030
(4.0%)
0.032 2
0.138
(9.6%)
f238 d238
0.993 14
4.671
0.993 4
1.335
0.968 4
1.301
OV_ U JLV JH-J
(Ci/MT-u)
4.84
1.36
1.44
h. WASH 1248, p. H-9.
i. Scaled from WASH 1248, p. H-9, 307 x 12 = 20.
182
j. From GESMO, p. IV-J (E) 17, 1.21E6/(4551 x 1.1) = 266 MT U.
or 340 MT UF&.
k. See note g.
1. WASH 1248, p. H-10.
m. WASH 1248, p. H-10.
n. Shipped as Class A, fissile material (NUKEG-0170, p. A-6)
o. Calculated from GESMO, p. IV-J (E) 17, 1.89E5/4346 = 43 MT U
or 64 MT
p. See note g.
q. WASH 1248, p. H-12.
r. Scaled from WASH 1248, p. H-12
(64/52) x 5 = 6.2
s. See note o. 43 MT U = 49 MT U02.
t. See note g.
u. WASH 1248, p. H-14.
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v. WASH 1248, p. H-14, 40 MX U02 requires 9 Shipments.
(49/40) x 9 = 12.3
w. See note o.
x. See note g.
y. GESMO, p. IV-G 4.
z. From GESMO p. IV-G 4 - 30,800 shipments
From GESMO p. IV-F (E) 17 4346 GWe yr equivalent 30,800/4346 = 7
aa. From GESMO, p. IV-G 4
50,200 MT Uranium + Plutonium by truck in 61,400 shipments
75,200 MT Uranium + Plutonium by rail in 15,300 shipments
From GESMO, p. IV-F (E) 17 3072 GWe yr equivalent.
bb. GESMO, p. IV-G 4.
43 3
cc. From WASH 1248, p. H-13, Scaled to 1 GWe yr 8000/0.8 =10 ft = 280 m
dd. See note cc.
ee. See note cc.
3 3
ff. See note cc 5000/0.8 = 6250 ft = 180 m .
gg. USEPA, Environmental Analysis of the Uranium Fuel Cycle (EPA-520/9-73-003-B,
Part I, 1973, p. 138 gives 3000 - 55 gal. drums (620 m ). WASH-1238, p. 49
gives 3800 ft3 (100 m3). The SDG and E Environmental Report for Sundesert
Nuclear Plant Fig. 3.5-4, gives 300 - 55 gal. drums plus 483-50ft3 containers
(1000 m3).
hh. WASH-1238, p. 49.
ii. EPA 520/9-73-003-B, p. 139.
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Introduction of reprocessing and recycling, of either uranium or
of uranium and plutonium introduces some additional transport
steps, but reduces the flows in others. The differences are
estimated in detail in GESMO.
Although the quantities shipped are much lovrer than in the
coal fuel cycle, there is greater concern due to the intrinsic
risk of exposure to radiation both routinely and in accidents.
Workers involved in transport are not classed as radiation workers
and not subject to individual monitoring. Thus, occupational
exposures of transport workers cannot be obtained directly from
available data. A recent surveillance program showed that some
transport workers receive a higher annual dose than permissable
12
for the general public. As a result, there are plans to require
individual exposure monitoring for certain classes of transport
workers.
Dose calculations have been made in several reports based on
assumed dose rates and time spent by workers at various locations.
Table 7 summarizes the collective radiation dose and the expected
latent cancer fatalities associated with transportation between
various stages of the nuclear fuel cycle. The cancer estimates,
i
based on health damage functions developed by the BEIR committee,
are very small; the total estimated exposure in all transport for
1 GWe-yr might lead to 1 cancer in 1000 years. In 1975, fuel
cycle related transport contributed less than 10% of the
population dose from transport of all (non-military) radioactive
materials. This is expected t'o grov; to 15% by 1985- A more
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TABLE 7
ROUTINE RADIOLOGICAL RISKS Qg TRANSPORT IN THE
NUCLEAR FUEL CYCLE
MATERIAL
ORE
INTERMEDIATE
MATERIALS **
UNIRRADIATED FUEL
IRRADIATED FUEL
Low LEVEL WASTE
FROM REACTOR
TOTALS
POPULATION
WORKERS
CORKERS
PUBLIC
WORKERS
PUBLIC
WORKERS
PUBLIC
WORKERS
PUBLIC
CORKERS
PUBLIC
TOTAL
MAN-PEN
PER GK'E-YR
0.06
0,23
0,04
8:ffli
B
1:2
. LCF* '
E-5
*E-5
7E-6
0.11
2E-4
3E-J*
2E-4
2E-4
/!£-/!
m
*LATENT CANCER FATALITIES,
**INCLUDES ll^Oo, IJP , !!09 AND LOW LEVEL WASTES FROM "FRONT END"
OF FUEL CYCLE,0 b L
BASED ON RASH 1233, p, 8 AND WASH 1?M, p. H-21, ADJUSTED FOR
NO-RECYCLE AND SCALED TO 1 G'-'-YR,
important concern is the risk of larger potential exposure in the
event of an accident. Both the Nuclear Regulatory Commission and
the Department of Transportation have promulgated regulations
aiming to minimize the chance of an accident involving a radiation
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release and minimizing the impact were a release to occur. The
United Nations Scientific Committee on the Effects of Atomic
Radiation (UNSCEAR) concluded that the annualized exposure from
transport accidents is an insignificant addition to normal
transport risk. A WHO working group examined the risk of spent
fuel accidents and reported that, "as the fuel assemblies are
stored for extended periods before shipment, most of the
radioactivity will be due to the longer lived strontium-90 and
caesium-137j which are not volatile in an accident causing
rupture of the shipping container, any radioactive contamination
occurring would be localized. Although in extreme cases evacuation
of people in the immediate vicinity might be desirable, more
general evacuation, although common in accidents including other
17
toxic materials such as noxious gases, would not be necessary."
The most extreme case would be an accident involving a large
release of radioactive material in a high population density area
such as Nev; York City or Chicago.
Table 8
Results of Low Probability/High Consequence Accident Analysis
Latent
Cancer Early Early
Material Fatalities Morbidities Fatalities
Spent Fuel (3000/2.I?xl05ci) 10 6 0
Plutonium (l.lSxlO^ci)** 3964 952 18
, . - —
*Truck shipment through NewwYork City. 3000 dispersible/2.17x10^
non-dispersible.
**New York City air cargo of overseas fuel. 100 kg of Pu02, 100$
released, 5% aerosolized.
From A.R. DuCharme, et al., SAND77-1927, pp. 113-120.
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Taylor, et_ al. , in a study of potential accidents in New York
City found that time of day and routing restrictions significantly
affect accident impacts and that buildings significantly limit
1 R
radiation exposure. In a later, more detailed report, the
largest domestic fuel cycle related accident (spent fuel) examined
was calculated to produce only 10 latent cancer fatalities
(Table 8). y Urban accidents involving recycled plutonium have
20
been estimated to result in less than 100 latent cancer fatalities.
Although the transport of fuel cycle materials prior to
enrichment has generally assumed to pose insignificant radiological
hazard, a recent accident in Colorado (September 1977) involving
a spill of several tons of yellow cake resulted in extensive
clean-up and review of possible regulatory action covering future
shipments by NRC and DOT, and has been cited in a recent HEW
report as one example raising pressing questions on the need for
25
emergency response planning.
Finally, transport of nuclear material also involves the
common accident risks faced by coal. The shipments detailed in
Table 6 sum to over 300,000 vehicle-miles per GW -yr, including
C
— 8
return trips. If fatality and injury rates are 5 x 10~ and
— 7 22
8.7 x 10""' respectively, expectation is 0.02 deaths and 0.2
injuries per GW -yr.
v*
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SUMMARY
Coal transport accidents raise almost no concern, yet can
involve more loss of life than any other step in the fuel cycle.
Perhaps the reason is that the accidents are common, every day
auto accidents - or that the biggest imaginable catastrophy
would be a school bus being hit by a train. Yet perhaps the
level of attention given this subject is appropriate to the level
of risk. If one were concerned with grade-crossing accidents, they
would be better addressed in the whole, rather than restricting
interest to accidents involving coal trains. In contrast,
transport of nuclear fuel cycle materials raises widespread
concern - despite the fact that all assessments show minimal
effects - order of magnitude less than the corresponding effects
from coal transport. Even the largest calculated accidents in
nuclear transport have a lower cost in life than the annual damage
from coal transport, although the clean-up costs in nuclear transport
accidents can approach $10 . It is interesting to note that despite
the low risk of radiologic exposure, the nuclear fuel cycle
involves more vehicle-miles of travel than coal. Injury from
common accidents is estimated to be lower in the nuclear cycle
only because of the lower accident rate associated with the
transport of hazardous materials.
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ACKNOWLEDGEMENTS
Work supported by USDOE, ASEV, Office of Technology Impacts
Assistance from colleagues in the Biomedical and Environmental
Assessment Division at Brookhaven, particularly J. Nagy and
L.D. Hamilton.
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REFERENCES
1. Congressional Research Service, National Energy Transportation,
Vol.x I, Committees on Energy and Natural Resources and Commerce,
Science and Transportation, U.S. Senate (publication 95-15),
1977, PP. 56-58.
2. Federal Railroad Administration, USDOT, Accident Bulletines
No. 135 through No. 141, 1966-1972, Table 108.
3. M.B. Rogozen, L.W. Margler, M.K. Martz, and D.F. Hausknecht,
Environmental Impacts of Coal Slurry Pipelines and Unit Trains,
Office of Technology Assessment, U.S. Congress (OTA-E-60-PT2),
1977, PP. 72-73 and B-28 - B-35.
4. D.V7. Schoppert and D.W. Hoyt, Factors Influencing Safety at
Highway-Rail Grade-Crossings, National Cooperative Highway
Research Program Report 50, Transportation Research Board,
National Research Council, 1968, pp. 20-21.
5. W.H. Lorber, draft report, Los Alamos Scientific Laboratory,
1979.
6. Association of American Railroads, yearbook of Railroad Facts,
1977, PP- 29, 35, and 37-
7. National Coal Association, Coal Traffic Annual, Washington, DC,
1976.
8, S.C. Morris, K. Novak, and L.D. Hamilton, National Coal Assess-
ment, Health Effects of Coal in the National Energy Plan,
Brookhaven National Laboratory, Upton, NY, 1979-
2. Congressional Research Science, p_p_ sit, p. 62.
10, Congressional Research Service, National Energy Transportation,
Vol. I, U.S. Senate Committees on Energy and Natural Resources
and on Commerce, Science, and Transportation, 1977, PP- ^50-452.
11. U.S. Nuclear Regulatory Commission, Final Generic Environmental
Statement on the Use of Recycling Plutonium in Mixed Oxide Fuel
in Light Water Reactors (GESMO), NUREG-0002, 1976.
12. U.S. Nuclear Regulatory Commission, Summary Report of the State
Surveillance Program on the Transportation of Radioactive
Materials, NUREG-0393, March, 1978.
13. Interagency Task Force on Ionizing Radiation, Report of the
Work Group on Radiation Exposure, U.S. Dept. of Health,
Education, and Welfare, Center for Disease Control, February,
-i 079.
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14. National Academy of Sciences, The Effects on Populations of
Exposure to Low Levels of Ionizing Radiation, Report of the
Advisory Committee on the Biological Effects of Ionizing
Radiation, (BEIR) Washington, DC, 1972.
15. USNRC, Final Environmental Statement on the Transport of
Radioactive Material by Air and Other Modes, NUREG 0170,
1977, PP. 4-37.
16. United Nations Scientific Committee on the Effects of Atomic
Radiation (UNSCEAR), Sources and Effects of Ionizing
Radiation, 1977, p. 211.
17. Health Implications of Nuclear Power Production, Report of a
Working Group, WHO Regional Office for Europe (ICP/CEP 804(1))
Copenhagen, 1977, p. 42.
18. J.M, Taylor, e_t al., A Model to Predict the Radiological
Consequences of Transport of Radioactive Material through
an Urban Environment, Proceedings, 4th Conference on
Sensing of Environmental Pollutants, New Orleans, 1977-
19. A,R, DuCharme, et al., Transport of Radionuclides in Urban
Environs: A Working Draft Assessment, SAND 77-1927,
Sandia Laboratories, 1978, pp, 118-120.
20. USNRC, NUREG 170, O£ sit, pp. 5-46.
21, Interagency Task Force on Ionizing Radiation, pp. 211 and
214. Report of the Work Group on Radiation Exposure,
U.S. Dept. of HEW, Center for Disease Control, February,
1979, PP. 211 and 214.
22. USAEC, Environmental Survey of Transportation of Radioactive
Materials To and From Nuclear Power Plants, WASH-1238, 1972,
p. 105-
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HEALTH ASPECTS OF POWER TRANSMISSION
By
Richard D. Phillips
Biology Department
Battelle
Pacific Northwest Laboratory
Richland, WA 99352
Operated by
Battelle Memorial Institute
Work supported by the U.S. Department of Energy under contract EY-76-C-06-1830,
and by the Electric Power Research Institute under contract 23112-02714.
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Health Aspects of Power Transmission
Richard D. Phillips
Biology Department
Battelle
Pacific Northwest Laboratory
Richland, WA 99352
There has been a rapid growth of power transmission systems in the United
States over the last several decades and this growth is expected"to con-
tinue. There are currently more than 40,000 circuit miles of overhead
ac (60-Hz) transmission lines in the United States operating at extra-
high-voltage (EHV), 345,000 to 765,000 volts, and many more miles are
planned over the next several years. In addition, ultra-high-voltage
(UHV) transmission systems are now being developed that will operate at
1,100,000 to 1,500,000 volts.
Considerable controversy has developed over the past several years con-
cerning the health aspects of existing EHV and proposed UHV transmission
lines. Several scientists and concerned groups claim that the electro-
magnetic fields in the vicinity of these power lines produce adverse
biological effects and are hazardous to man (132). Other scientists
state that such claims lack scientific support (3,4). Legal proceedings
have been unable to resolve this issue because of the lack of reliable
data. In recognition of the need for scientifically sound data to make
a risk assessment and to insure public health and safety, research pro-
grams have been initiated by the Department of Energy (DOE) and Electric
Power Research Institute (EPRI) to assess the health aspects of power
transmission systems.
Four research projects are in progress at Battelle Northwest as part of
the DOE and EPRI programs. In one of the DOE projects, a multidisciplinary
research team, consisting of physical and biological scientists, is con-
ducting a broad and comprehensive study to screen for effects on rats and
mice of acute and chronic exposure to 60-Hz electric fields. In a compan-
ion project, supported by EPRI, miniature swine are being exposed chroni-
cally to a 60-Hz electric field over two generations to assess possible
effects of exposure on clinical parameters and on reproduction, growth
and development. A third project is examining the potential of static
(dc) and 60-Hz electric fields to induce genetic changes in fruit flies
and bacteria. The fourth project is evaluating the ecosystem in the
vicinity of a 1,100 kV test transmission line at Lyons, Oregon.
The small and large animal studies were started in 1976 and a large amount
of data has been generated from these projects during the past three years
(5-11). This paper will summarize the results of the small animal project
and relate our findings to the results of other studies reported in the
literature.
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EXPOSURE SYSTEMS
The environment in the vicinity of high voltage transmission lines is
complex and includes many factors that might be sources of biological
effects (Table 1). For the purpose of controlled laboratory studies
we chose to retain only those which dominate in the transmission line
environment and which, based on existing literature, have been reported
by some laboratories as having produced effects. This decision led to
system design criteria which eliminated or minimized all the factors in
Table 1 except the external electric field and the unavoidable conse-
quences of physical interaction between this field and the exposed
subject (internal fields and currents; field perception).
Table 1. Possible Electromagnetic Field-Related Sources
of Biological Effects in the Vicinity of ac
Transmission Lines
Primary Field Effects
Large External Electric Fields
Small Internal Electric Fields
Electric-Field-Induced Body
Currents
Small External and Internal
Magnetic Fields
Magnetic-Field-Induced Body
Currents
Field Perception
Hair Stimulation
Other Modes?
Secondary Factors
Spark Discharges
Steady-State Currents
Corona Discharge
Ozone
Audible Noise
Radiofrequency Fields
Hum and Vibration (of significance
mainly in laboratory simulations
of the transmission line fields)
Higher-Frequency Harmonics in the
Electric and Maanetic Fields
The maximum electric field encountered by man under EHV transmission lines
is about 9-12 kV/m. The currents and electric fields induced within the
body are a function of the field intensity and the body shape. Values are
quite different for man (biped) than those for rodents and swine (quadru-
peds). Accordingly, considerable care must be exercised in designing
animal experiments and using data from such studies to predict possible
effects on humans in the same situations. This is illustrated in Figure
1, which shows a man, a pig, and rat placed in a uniform 60-Hz electric
field of 10 kV/m. The strongest surface electric field generally occurs
at the top of the body and is enhanced over the uniform field value by a
factor of 15-20 for man (12], 7 for the pig (13) and about 4 for the rat
(ll). Estimated current densities are shown at two locations within each
body, the trunk and lower limbs, and illustrate the strong dependence on
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body shape. 'The total current between each body and ground, the short-
circuit current (Isc), is also shown. Based on these data, a much higher
unperturbed field would have to be used with pigs or rats to produce
surface fields and internal current densities comparable to those in a
man exposed to 10 kV/m. Scaling factors between rat and man are: en-
hancement, ^ 4:1; average trunk current density, ^ 15:1; average current
density in the lower limbs, ^ 5:1. Comparable scaling factors between
pig and man are about 2.5, 7 and 2.5, respectively.
We selected 30 kV/m for the pig exposures and 100 kV/m for the rat and
mouse exposures in the biological experiments. Assuming a scaling factor
of 3 between pig and man, and a factor of ^ 10 between rat and man, the
field strengths used in the experiments would be equivalent to exposing
man to about 10 kV/m.
Three systems were built for exposing small laboratory animals to uniform,
vertical, 60-Hz electric fields: a rat exposure system, capable of sim-
ultaneously exposing 144 rats individually housed in plastic cages; a mouse
exposure system in which 288 mice, 3 per cage, can be exposed simultaneously;
and a special test system for experiments requiring direct data acquisition
from individual or small numbers of animals during or immediately after
exposure. The same numbers of rats and mice are sham-exposed under envir-
onmental and housing conditions identical to those of the exposed animals.
One of the four racks used for exposing rats is shown in Figure 2. Each
rack consists of four electrodes, with the rats individually housed in
plastic cages located in the three lower electrodes. The animals are in
electrical contact with a metal mesh floor that forms the top layer of
each two-layered electrode. Animal excreta falls through the mesh floor
onto absorbent paper in a field-free region on a lower metal plate. The
water system is located in this space between the mesh floor and the lower
plate, with a small demand-type water nozzle located at the floor level of
each cage. This design eliminates possible perturbation of electric field
uniformity by the watering system, eliminates shocks to the animals during
drinking, and minimizes mouth-to-nozzle steady-state currents during drink-
ing. Pellet food is provided ad libitum in slot hoppers at the front of
each cage. The profile of the food delivery system is low to minimize any
potential perturbation of field uniformity by the food.
The mouse exposure rack (not shown) is identical to the rat exposure rack
except for a lower cage height, a small vertical separation between elec-
trodes, and an additional electrode.
Extensive measurements have been made to characterize the three small animal
exposure systems. Electric field uniformity is +_ 4% over the total cage
area in the rat and mouse exposure systems. The exposure systems are free
of detectable levels of audible noise and ozone, and there is very little
harmonic distortion. Animals do not receive spark discharges or other shocks
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from the housing system or from other animals during exposure to electric
fields.
Photographs of the system used to expose miniature swine to a vertical,
60-Hz electric field are shown in Figures 3 and 4. Exposed and sham-exposed
pigs are housed in separate, environmentally equivalent buildings (Figure
3). The overhead electrode and individual animal stalls are shown in
Figure 4. Electric field uniformity over the area of a stall is about
+_ 2.5%. No levels of audible noise, hum, vibration or ozone have been
detected with the high-voltage system operating.
BIOLOGICAL EXPERIMENTS
Experiments are being conducted in 11 major biological areas to screen for
effects over a wide range of parameters in rats and mice exposed to 60-Hz
electric fields for up to 120 days. Experiments in each major area use
separate animal groups and are directed by professionals with specialties
in the areas under investigation.
Experimental Design
Several features of experimental design are common to all the biological
experiments. All experiments use Sprague-Dawley rats and/or Swiss Webster
mice. All animals received from the supplier. Hilltop Laboratories, are
carefully examined before being used in experiments to assure that they
are healthy. A sample population from each shipment is sacrificed at
delivery for virology screening and histopathologic examination. The
remaining animals are maintained in standard cages in an isolation room
for 1-3 weeks, earcoded, then acclimated for 14 days in cages identical
to those used in the electric field exposure systems. During exposure
or sham-exposure, the environment, housing and husbandry are identical
for both groups of animals except for the presence or absence of the
electric field. This design reduces the risk of obtaining false positive
results and increases the ability to detect subtle effects of exposure.
In addition, animals maintained in standard cages ("cage controls") are
used in many of the experiments to verify that the exposure cages do not
produce effects that might mask subtle effects of exposure.
In most of the experiments the animals are about 60 days of age at the
start of exposure. Except for several cardiovascular and behavioral
experiments, the field strength used for all exposures is 100 kV/m. The
exposure period is about 21 hours/day; this allows about 3 hours/day for
scheduled measurements, cage cleaning, feeding and watering.
With few exceptions, experiments are double-blind: the principal investi-
gator is unaware of which animals are exposed and which animals are sham-
exposed until the measurements have been completed. Most experiments are
replicated to insure that the results of a single experiment are not due
to some unidentified systematic error in that experiment, or to statistical
chance. Our statistical criterion for positive effects is p < 0.05.
-307-
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The results of the biological experiments with small animals that have
been completed to date are summarized below. The swine study is still
in progress and results are not available at this time.
Metabolic Status and Growth
In eight separate experiments, body and organ weights were determined
in juvenile (age, 26 days) and young adult (age, 56 days) male and female
rats, and in young adult (age, 60 days) male and female mice that were
exposed or sham-exposed to 60-Hz electric fields at 100 kV/m for 30 or
120 days. In addition, food and water consumption was measured daily
during the 30- to 120-day exposure periods. In other experiments, a
number of parameters related to metabolism and growth were measured in
rats that had been exposed to 100 kV/m for 30 or 120 days, including:
oxygen consumption and carbon dioxide production rates; metabolic rates;
circulating concentrations of thyroxine, thyroid stimulating hormone
and growth hormone; lipid, protein, and glycogen levels in liver; and
serum concentrations of glucose, urea nitrogen and triglycerides. There
were no reproducible, significant differences between exposed and sham-
exposed animals in any of the parameters measured in any of the experi-
ments. These experiments failed to confirm effects reported by other
investigators: increased pituitary and adrenal weights, reduced water
consumption and lower body weights in rats exposed to 15 kV/m for 30
days (14); transitory, enhanced growth rate in mice exposed to 25 and
50 kV/m for 6 weeks (15); reduced growth rate in rats exposed to 50 kV/m
for 100 days (16).
Bone Growth and Structure
Bone growth and structure were assessed in juvenile male and female rats
that were exposed to 100 kV/m for 30 days starting at 28 days of age.
To differentiate any possible direct effect of exposure on bone growth
from that of an indirect effect on the general growth pattern of the
animals, body weights, kidney weights and liver composition (fat, glyco-
gen, protein and moisture) also were determined. Exposure had no effect
on growth rate of the tibia, morphology of lumbar vertebrae or the tibia,
or on cortical bone area and marrow space in the tibia. No alterations
in the general growth pattern were observed.
Reproduction, Growth and Development
A series of three replicated experiments were undertaken to determine the
effects of exposure to 60-Hz electric fields at 100 kV/m on reproduction
and on fetal postnatal growth and development in the rat. In the first
experiment, a 6-day exposure prior to and during mating did not affect the
reproductive performance of either males or females. Continued exposure
of the mated females through 20 days of gestation did not affect the
viability, size, or morphology of the fetuses. A similar 30-day exposure
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of the males and unmated females did not affect their mating performance
or fertility on subsequent testing. In the second experiment, exposure
of the pregnant rats was begun on day 0 of gestation and continued until
the resulting offspring reached 8 days of age. There were no differences
between exposed and sham-exposed groups in litter sizes or survival of
offspring. Body weights and subsequent growth through 42 days of age
were the same for both groups. The only differences observed between
exposed and sham-exposed animals were in tests of neuromuscular and neuro-
logical development through 42 days of age. A higher percentage of
exposed offspring showed motile behaviors (moving, grooming and standing)
and a lower percentage exhibited righting reflexes at 14 days of age. The
results of the two groups were indistinguishable upon retesting at 21 days
of age. Tests of the reproductive integrity of the offspring have not
disclosed any deficits. The third experiment involved a 30-day exposure,
beginning at 17 days of gestation and continuing through 25 days of post-
natal life. There were no significant alterations in growth or develop-
ment of the offspring. In another experiment mice conceived, born and
raised in a 100 kV/m, 60-Hz electric field for three successive generations
were compared to identical sham-exposed groups. Exposure had no apparent
effect on conception, litter size, mortality or body weights up to 10
weeks of age in any of the three generations. These findings fail to
confirm a report by Marino ejt al_ that exposure to electric fields of three
generations of mice increases mortality and rate of growth of offspring.
Hematology and Serum Chemistry
Clinical pathologic evaluations were made in female rats exposed to 60-Hz
electric fields at 100 kV/m for 15, 30, 60 and 120 days, and in female
mice exposed at 100 kV/m for 30, 60 and 120 days. All experiments were
replicated and used exposed, sham-exposed and cage-control animals. Hema-
tology parameters measured included volume of packed red cells, red cell
count, mean corpuscular volume, hemoglobin concentration, white cell count,
distribution of leukocyte cell types, reticulocyte concentration, platelet
concentration, bone marrow cellularity, red cell osmotic fragility, pro-
thrombin time and iron uptake from plasma. Serum chemistry parameters
measured included urea nitrogen, alkaline phosphatase, glutamic oxaloacetic
transaminase, glucose, triglycerides, iron, total iron-binding capacity,
total proteins, and protein fractions as determined by electrophoresis.
Exposure of rats and mice to 100 kV/m for 15-120 days did not cause repro-
ducible changes in any of the hematologic or serum chemistry parameters
assayed. Several investigators have reported effects of electric field
exposure on hematologic and serum chemical parameters (14-16, 18-21). The
failure of this study to substantiate these reported effects may be explained
by one or more of the following: 1) our exposure systems and conditions are
very well defined, and eliminate secondary influences of the electric field,
such as spark discharges, ozone, and noise; 2) our exposures have been rep-
licated for each time period, whereas most other studies reporting effects
have not been replicated; 3) our sham-exposed animals are more valid controls
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than "cage-controls" used in some studies; and 4) our electric field
strengths and durations of exposure were, in many cases, different from
those used by other investigators.
Immunology
A series of experiments were conducted to quantitatively assess humoral
and cellular components of the immune system. Serum immunoglobulin levels
were measured in rats exposed to 100 kV/m for 15 or 30 days and in mice
exposed to 100 kV/m for 30 or 80 days. Complement activity and peripheral
blood T- and B-lymphocytes were measured in mice exposed to 100 kV/m for
30 and 60 days. No significant differences were observed between exposed
and sham-exposed rats or mice in any of the parameters measured. In the
second phase of this study, we assessed functional immune responses by
measuring serum antibody levels in response to a specific antigen and by
in vivo assays of cell-mediated immunity. To assess the primary immune
response, the serum antibody levels were measured in mice exposed to 100
kV/m for 30 or 60 days and challenged with keyhole limpet hemocyanin (KLH).
No significant differences in the amount of precipitating antibody for KLH
were observed between exposed, sham-exposed and cage-control mice. Cell-
mediated immunity was evaluated in mice after 30 days of exposure to 100
kV/m by determining the delayed hypersensitivity to KLH and the contact
sensitivity to dinitrofluorobenzene (DNFB). Exposure had no effect on the
response of sensitized mice to DNFB. In exposed mice, however, there was
a significantly reduced response to KLH as measured by skin thickness at
the site of injection. The mean reaction diameters for the two groups were
not significantly different. Other experiments have been made in which
cell-mediated immunity was tested in mice exposed for 30 to 180 days by
examining the response of lymphocytes stimulated with mitogens. No effects
were observed.
Endocrinology
Plasma hormone concentrations, and endocrine gland and reproductive organ
weights were examined in rats after exposure to a 60-Hz electric field at
100 kV/m for 30 days. In addition, a detailed examination was made of male
reproductive endocrinology. This included plasma gonadotrophin levels,
plasma testosterone, testicular vein androgens, blood flow rate through
the reproductive tract and androgen secretion rates. Exposure of rats to
electric fields had no effect on body weight, weights of endocrine organs
or plasma levels of corticosterone, thyroxine, thyroid stimulating hormone,
follicle stimulating hormone, testosterone or luteinizing hormone. Testicu-
lar weights were unaffected by the treatment, and there was no effect on
testicular b.lood flow rates, androgen levels, or testosterone secretion
rate. These data are in conflict with previous studies (14,20) where much
lower field strengths were employed, and suggest that secondary factors
(electrical discharges, corona and ozone) may have had a major influence
on those experiments. Our results are in general agreement with those of
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the Italian (ENEL) studies summarized by Cerretelli and Malaguti (22),
where field strengths of 80-100 kV/m were used.
Cardiovascular Function
A series of experiments were conducted to determine whether exposure to
60-Hz electric fields alters cardiovascular function in the rat. Para-
meters assessed included electrocardiograms (ECG), heart rate, blood
pressure and vascular reactivity. In addition, the cardiovascular and
endocrine responses of rats to acute cold stress were determined in
animals that had been exposed to 60-Hz electric fields. Electrocardio-
grams and heart rates were evaluated in male rats exposed to 80 kV/m for
8 hours or 40 hours (8 hours/day for 5 consecutive days), and to 100 kV/m
for 1 month (^ 21 hours/day). The same evaluations were made on female
rats exposed to 100 kV/m for 1 or 4 months (21 hours/day). ECG analysis
consisted of measuring the durations of the PR interval and the QRS complex.
Recordings were made during the first hour after the completion of electric
field exposure. No differences were seen between exposed and sham-exposed
animals in any of the experiments. These results failed to confirm the
findings of Blanchi e_t a\_ (23), who reported that exposure of rats to 100
kV/m slowed electrical conduction in the heart. Systolic, diastolic, pulse
and mean systemic blood pressures, and vascular reactivity were measured
in rats that had been exposed to 100 kV/m for 35 or 120 days. Vascular
reactivity was quantified by measuring the change in pulse pressure in
response to an injected dose of phenylephrine, a vasoconstrictor that
produces an elevated pulse pressure by increasing peripheral resistance
to blood flow. No significant differences were observed between exposed
and sham-exposed animals in any of the measures. Cardiovascular and endo-
crine responses to cold stress were measured in rats that had been exposed
or sham-exposed to 100 kV/m for 30 days. Plasma corticosterone and thyroid
stimulating hormone levels were determined in the animals prior to and after
being subjected to acute cold stress (-13 +_ 1°C) for 1 hour. No significant
differences were found between exposed and sham-exposed rats before or after
cold stress. In a parallel experiment heart rate, skin temperature and deep
colonic temperature were measured during cold exposure in rats that had been
exposed or sham-exposed to 100 kV/m for 30 days. Values of both groups were
essentially identical.
Pathology
Complete gross and histopathologic examination of approximately 30 selected
tissues per animal were performed on groups of male rats and both male and
female mice exposed or sham-exposed to a 100 kV/m, 60-Hz electric field for
30 or 120 days. Animals were weighed after sacrifice, and selected organs
from each animal were weighed. No histopathologic effects of exposure were
observed, and exposure had no significant effect on body or organ weights.
The results of these studies fail to confirm a report by Soviet scientists
(19} that exposure of rats to electric fields at 5 kV/m produces vascular
damage and atrophic changes in brain and liver.
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Central Nervous System
A detailed histologic examination was made of the brains of mice exposed
to 100 kV/m for 30 days. Results failed to reveal any differences between
exposed and sham-exposed mice.
Neurophysiology
Synaptic transmission and peripheral nerve function were assessed in male
rats that had been exposed to 100 kV/m for 30 days. Immediately following
exposure or sham-exposure, superior cervical sympathetic ganglia, and
vagus and sciatic nerves were removed from rats anesthetized with urethan,
placed in a temperature-controlled chamber (37.5 +_ 0.4°C) and continuously
superfused with a modified mammalian Ringer's solution equilibrated with
95% 02 and 5% C02. Parameters used to characterize synaptic transmission
and peripheral nerve function were: 1) characteristics of the postsynaptic
or whole-nerve compound action potential (including amplitude, area, config-
uration, rate of rise, and rate of fall); 2) conduction velocity of the
postsynaptic or whole-nerve compound action potential, measured at the
beginning of the compound action potential (inflection conduction velocity)
and at the peak of the compound action potential (peak conduction velocity);
3) absolute and relative refractory periods; 4) accommodation; 4) stimulus
strength-duration relationships; 6) changes in poststimulus excitability
(e.g., conditioning-test response); 7) frequency response; 8) post-tetanic
response; 9) high-frequency-induced fatigue. The only consistent difference
observed between exposed and sham-exposed animals was a shift in the con-
ditioning-test response curve for exposed animals that suggested increased
synaptic excitability.
Behavior
A series of experiments were conducted to assess the effects of various levels
of 60-Hz electric fields on the behavior of rats. These experiments have
focused on perception and passive avoidance behavior, activity during exposure
and performance of a learning task immediately after exposure. In the passive
avoidance experiments, rats were given the option of being exposed to or
shielded from various field strengths during short- (45-minute) and longer-
duration ( ^ 24-hour) tests. Rats were placed in a shuttlebox, one end of
which was shielded and the other end visually identical but unshielded from
the 60-Hz electric field, and scored for activity (number of end-to-end
traverses) and time spent in each end of the shuttlebox. In short-duration
tests (45 minutes), rats exposed to field strengths ^90 kV/m spent signifi-
cantly more time on the shielded side of the shuttlebox than did the sham-
exposed controls. Repeated tests over 4 weeks, one test per week, did not
modify this behavioral response. However, exposure of the rats to 100 kV/m
for 30 days (630 hours) prior to the test, attenuated this behavioral res-
ponse. Activity during the 45-minute tests was significantly greater in
exposed rats than in sham-exposed controls. This higher activity was seen
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at field strengths as low as 50 kV/m and increased with repeated tests.
In longer-duration tests ( ^ 24 hours, 12 hours light:12 hours dark),
rats exposed at 75 or 100 kV/m spent more time in the shielded end of
the shuttlebox than did controls during both the light and dark periods.
However, rats exposed at 50 kV/m spent more time ir± the field than controls,
but only during the 12-hour light period. The results of the longer-duration
tests confirmed the results of the 45-minute tests in which exposed rats
showed an increased activity. This effect was observed in rats exposed to a
field as low as 25 kV/m and occurred only during the first hour of exposure.
An experiment was conducted to assess the performance of rats in a learning
task after exposure to 60-Hz electric fields at 0, 50 or 100 kV/m for 23.5
hours. After exposure, each rat was placed in a two-compartment shuttlebox
and learned to move from one compartment to the other in response to an
80-dB tone in order to avoid a 20-second shock to the feet (an avoidance
response). If no avoidance response was made by the rat, it could escape
the ongoing shock by moving to the other compartment (escape response).
No consistent differences were observed between exposed and sham-exposed
rats in avoidance or escape responses.
SUMMARY
Exposure of rats and mice to 60-Hz electric fields at 100 kV/m for up to
120 days had no statistically significant, reproducible effects on a number
of measures of metabolic status and growth, bone growth and structure, re-
production, hematology and serum chemistry, endocrinology, cardiovascular
function, nerve function, or organ and tissue morphology. An effect on
cell-mediated immunity was detected and is being evaluated further in addi-
tional experiments. Exposure of rats in utero (day 0 of gestation to 8 days
of age) had a transient effect at 14 days of age on motile behavior and
development of the righting reflex. Significant effects were observed
in synaptic transmission and behavior. Exposure to 60-Hz electric fields
may increase the excitability of the nervous system of rats. Experiments
are in progress to obtain a better understanding of these effects and their
potential consequences.
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References
1. Marino, A. A. and R. 0. Becker. 1978. High-voltage lines: hazard
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Strength Electric Fields.
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CONS/1830-2, Conservation
Biological Effects of High
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Springfield, VA.
Phillips, R. D., M. F. Gillis, C. H. Allen, J. L. Beamer, R. L.
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Phillips, R. D., M. F. Gillis, J.
J. R. Decker, T. W. Jeffs, and R.
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L. Richardson. 1977c.
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D. L. Hjeresen, R. A. Jaffe, W. T. Kaune, B. J. McClanahan, J. E. Morris,
H. A. Ragan, R. P. Schneider, and G. M. Zwicker. 1978. Biological Effects
of High Strength Electric Fields on Small Laboratory Animals. Annual
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12. Deno, D. W. 1977. Currents induced in the human body by high voltage
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tribution and dose. IEEE Trans. Power Appar. Syst. PAS-96: 1517-1527.
13. Kaune, W. T., R. D. Phillips, D. L. Hjeresen, R. L. Richardson, and
J. L. Beamer. 1978. A method for the exposure of miniature swine to
vertical 60-Hz electric fields. IEEE Trans. Biomed. Eng. BME-25(3):
276-283.
14. Marino, A. A., T. J. Berger, B. P. Austin, R. 0. Becker, and F. X. Hart,
1976. Evaluation of electrochemical information transfer system. I.
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development of plants and animals. J. Microwave Power 12(1): 41-42.
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17. Marino, A. A., R. 0. Becker, and B. Ullrich. 1976. The effect of
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18. Bayer, A., J. Brinkman, and G. Wittke. 1977. Experimental research
on rats for determining the effect of electrical AC fields on living
beings. Elektrizitaetswirtschaft 76(4): 77-81. (In German).
19. Blanchi, D., L. Cedrini, F. Ceria, E. Meda, and G. G. Re. 1973.
Exposure of mammalians to strong 50-Hz electric fields. I. Effects
on the proportion of the different leukocyte types. Arch. Fisiol.
70: 30-32.
20. Dumansky, Y. D., V. M. Popovich, and Y. V. Prokhvatilo. 1976.
Hygienic evaluation of electromagnetic field generated by high-
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613-647).
21. Knickerbocker, G. G., W. B. Kouwenhoven, and H. C. Barnes. 1967.
Exposure of mice to a strong ac electric field - An experimental
study. IEEE Trans. Power Appar. Syst. PAS-86(4): 498-505.
22. Cerretelli, P. and C. Malaguti. 1976. Research carried out in Italy
by ENEL on the effects of high voltage electric fields. Rev. Gen.
Electr., Special Issue, July: 65-74.
23. Blanchi, D., F. Cedrini, F. Ceria, E. Meda, and G. G. Re. 1973.
Exposure of mammalians to strong 50-Hz electric fields. II. Effects
on the heart's and brain's electrical activity. Arch. Fisiol. 70:
33-34.
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i
U)
UNIFORM FIELD = 10 kV/m
J ~ 2000 nA/cm2
E~175kV/m
J-175 nA/cm2
J ~ 900 nA/cm2
E ~70kV/m
J ~ 25 nA/cm2
E ~ 40 kV/m
J~12 nA/cm2
J~ 400 nA/cm2
lsc~180juA
•sc ~ 70
sc
Figure 1. Interaction of man, pig and rat with a uniform, 10 kV/m electric field. E represents the
enhanced field strength at the highest point on the surface of the subject; J is the cross-
sectional current density at the trunks and lower limbs of the subjects; Ic_ is the short-
circuit current between the subject and ground.
sc
-------
ZH-09 oq. S^BJ asodxa o^ pasn
'2
r-t
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I
u>
(-1
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I
Figure 3. Exterior view^of buildings used to house sv;ine during exposure or sham-exposure to 60-Hz
-------
I-1
VO
I
mmmm>*mmmmmmmmm*t
Figure 4. Interior view of exposure building showing overhead electrodes and stalls for individual
swine.
-------
HEALTH BENEFITS AND RISKS OF ELECTRIC POWER CONSUMPTION
By
Ronald E. Wyzga*
Program Manager
Integrated Assessment Department
Environmental Assessment Department
Electric Power Research Institute
Palo Alto, California
*The contents of this paper are the responsibility of the author and should
not be attributed to EPRI.
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So far we have concerned ourselves with a traditional
environmental view of electricity generation: the health
and environmental costs of fuel extraction and transport,
electricity generation with its accompanying air pollution,
solid waste disposal, and electricity transmission. Tomorrow
we will discuss those environmental concerns peculiar to
nuclear power generation. As we discuss these issues, I
can't help but think that somehow we're missing a fundamental
aspect in the current environmental debate, that of how much
energy we should consume. Environmental regulations are seen
as tools to help limit the consumption of energy, even though
they were created for other purposes.
There is no doubt that environmental concerns are justified.
The serious air pollution episodes of Donora, London, the
Meuse Valley have had environmental consequences that should
never be repeated, and we now have laws to insure against a
reoccurrence. SC>2 and particulate levels have declined
considerably in our cities as air pollution control measures
have been taken. We spend much time debating over appropriate
levels of S02 and whether sulfates are injurious to health,
but new and existing regulations are observed. Certainly
there is a need to review these and all regulations periodi-
cally as required by the Clean Air Act. It is encouraging
that the 24-hour ambient standard for photochemical oxidant
was recently relaxed. The fact that standards can be relaxed
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as well as tightened may suggest that we are approaching
socially optimum standards rather than seeking an unrealistic
environmental perfection.
Despite the original importance of health issues in develop-
ing environmental standards, the most recent controversies
over proposed power plants avoid debates about health effects,
This is certainly true for the substances most commonly
emitted by fossil fuel power plants. Current issues of
concern are visibility degradation, acid rain, socio-economic
impacts, aesthetic impacts and impacts upon non-human species,
It is noteworthy that the Seabrook controversy did not focus
upon health and safety risks of nuclear power, but upon the
fate of a clam population. Health effects of air pollution
were all but ignored in the Kaiparowits debate. It was to be
the cleanest coal-burning power plant ever built. Health
effects were not an issue; concern for visibility, aesthetics
and water quality were most often voiced.
The Kaiparowits debate does in fact provide an important clue
to what may be a new and important environmental issue. The
Environmental Protection Agency (EPA), in its critique of the
Environmental Impact Statement (EIS), focused attention on
the need for Kaiparowits (1). The EIS, according to the EPA,
did not consider the impacts of conservation measures being
implemented by the State of California. These included manda-
tory insulation standards, a partial ban on electric heating
in new commercial buildings, appliance efficiency standards,
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and commercial lighting standards. Moreover, the EPA was
concerned that the EIS failed to address the possible demand-
reducing effects of peak-load pricing and other load-management
techniques. Environmentalist and other groups agreed. Friends
of the Earth criticized the methods used to forecast electricity
demand and argued that "financial incentives and disincentives
combined with regulations concerning electrical power use
could limit electric power demand to the point where new
generation capacity would not be required" (2). The California
Governor's Office of Planning and Research asked "if demand
forecasts overestimate the actual electricity need and a
surplus of electric energy is available, growth will be encour-
aged to fulfill the demand forecasts and proposed conservation
efforts will be curtailed" (3). In other words, growth should
be curtailed in order to encourage conservation.
It is my argument that one of the most important current
objectives of environmental concerns is the desire to impose
a conservation program upon society. The origin of this-
attitude may be environmental, as one way to preserve our
environment is to allow no new intrusions and to redistribute
existing resources to meet current needs. What better way to
•
achieve this goal than to control energy growth.
NEPA or the National Environmental Policy Act and other
regulations force us to scrutinize every action or development
and to list all conceivable environmental impacts. If any-
thing is scrutinized, some impacts will be found. Such
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scrutiny is useful to identify potentially important impacts,
but it can also divert our attention from the fundamental
issues which underlie societal concerns. Such I believe is
the case of Seabrook; very few members of the Clamshell Alliance
worry about the future population of the seaclam; nuclear
power and level of energy consumption are the unspoken issues.
I don't argue here that NEPA should be abolished or amended,
but while attending to the risks of electricity generation,
we must remember the total picture. It is important to
foresee impacts on clam populations, but we must at the same
time ensure that we are providing enough energy for our society.
'nvironmental regulations are not the appropriate tool to
achieve the universally-accepted goal of energy conservation.
There are two ways in which environmental policy can lead to
reduced electricity consumption: (1) it can impose environ-
mental constraints which increase the costs of electricity
and therefore reduce demand; (2) it can use environmental
regulations to restrict the the development of new energy
facilities and thereby reduce the supply.
Electricity costs can be increased in many different ways
through environmental regulation: air and water control
equipment, higher-priced fuels, environmental siting and
permitting procedures, delays in construction and operation.
All of these costs must be weighed against the environmental
benefits they yield, but we must also weigh these benefits
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against the social consequences of the higher costs. Higher
electricity costs contribute to inflation, that problem which
troubles the U.S. public most according to the several public
opinion polls reported in our newspapers. Inflation itself
spawns many socio-economic impacts, also cited frequently
these days in our newspapers. Some attention is presently
being paid to this issue. It has been raised by the Council
of Economic Advisers, dismissed by the EPA, and is now under
study by a commission responsible to Alfred Kahn, our national
inflation fighter.
It may be difficult to weigh environmental concerns against
inflationary concerns, particularly when there is uncertainty
and debate about both. The two are certainly intertwined;
better estimates of their association are needed so that
our policy decisions can reflect them judiciously.
Price increases of electricity can achieve conservation, but
responses are limited, particularly in the short-run where
voluntary restraint or changes in lifestyle are the only
significant options. There is little opportunity to introduce
technical innovations through equipment modification,
alternative production cycles and technical systems in the
short-run. Ten years as a minimum are required for these
innovations to come to pass. Other responses such as fuel
substitution or changes in the industrial mix take even
longer to implement.
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As an energy conservation tool, price increases induced by
environmental regulations will impact the residential sector
the greatest. Little immediate conservation will take place
in the industrial and transportation sectors because the
potential for conservation in these sectors resides largely
in technical innovation (which requires a lead time of at
least five years). There may be some possibility for conser-
vation in the commercial sector, but it is the residential
sector who will respond the most, and since taxes on energy
are regressive, it is the lower income groups who will be
the most affected by increases in energy prices.
Figure 1 demonstrates the increase in fuel costs resulting
from environmental regulation according to Consolidated
Edison of New York (4). These costs represent the difference
in cost between high and low sulfur fuel. Similar cost
differentials exist for other fuel uses; i.e., residential
and commercial boilers. Environmental benefits may have been
achieved as a result of these costs; certainly SC-2 levels have
been reduced significantly in New York City over this period.
(See Figure 2)(5). There has incidentally been no concommitant
measurable change in the health status of New York City during
this period (6).
Dr. Lawrence E. Hinkle, Director of the Division of Human
Ecology at the New York Hospital-Cornell Medical Center
worries about the health effects of increased energy costs.
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He writes that "in the past few years, as the cost of home
heating and electricity have gone up, an increasing number of
landlords of the poor have reduced or abolished the heating
of dwellings and have turned off the electric power of those
who could not pay their bills. In New York we actually have
poor old people dying from cold and exposure in unheated
apartments, and we have people of all ages dying from accidental
fires, smoke inhalation, and carbon monoxide poisoning because
they have attempted to supplement the inadequate heat in their
apartments by turning on the oven or by using a charcoal
brazier or a kerosene space heater." Dr. Hinkle adds, "It
seems quite possible that further efforts to lower the SC>2
content of the outdoor air to produce health benefits that
are probably illusory may in fact increase morbidity and
mortality from smoke fires, and carbon monoxide"(7).
Writing in the Annals of Internal Medicine, Dr. John E.
Milner, Department of Environmental Health, University of
Washington, reports of several British studies which demonstrate
a high incidence of hypothermia among the elderly poor, who
cannot afford to heat their homes to adequate temperatures (8).
One British study in fact suggested that between "20,000 and
100,000 hypothermia deaths occurred yearly in Britain".
Hypothermia is the failure to maintain a body temperature
adequate for optimal physiologic functioning, and it can
result in depressed respiration and consequent pneumonia,
pancreatitis, heart failure, and cerebrovascular accidents.
There is no information about the incidence of hypothermia in
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the U.S., but the British experience should cause some concern
about the potential for hypothermia in the U.S., particularly
in an era of rapidly-rising energy prices.
I or no one else knows for certain how many deaths or health
effects can be attributed to hypothermia or unsafe heating
resulting from high energy costs. We have ignored these
impacts to date and have certainly not considered their
possibility in our framing of regulations. Everything is more
complicated than previously thought to be; environmental
policy-setting is no exception. These policies can have
negative impacts as well as benefits.
Environmental regulations may yield some conservation results
as a side-effect, but they are not designed for that purpose
and are not the most suitable tools for achieving conservation;
their results may in fact be counterproductive, yielding
more societal harm and discomfort than intended. The tools
for implementing conservation need to be designed and evaluated
for that purpose alone.
Environmental regulations can yield some conservation by
limiting supply as well as limiting demand. Availability of
supply was an issue in the Kaiparowits debate. The cancellation
of a power plant can lead to environmental benefits and
possibly to some conservation. But as a conservation measure,
the most significant response possible in the short-run to
the non-building of power plants is the voluntary change in
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lifestyle which will take place largely in the residential
sector. Some of the drawbacks associated with this
approach were cited above; others are a result of a general
shortfall in electricity generating capacity.
The amount of conservation possible is limited. A detailed
study of the potential for technological conservation
suggested that a seventeen percent reduction in anticipated
energy use could reasonably be attained through conservation
measures by 2000 (9). (See Table 1.) With extreme efforts
this reduction could be as high as 34%. Demographics favor
an increase in total energy consumption. According to the
Bureau of Labor Statistics the total number of Americans
expected to be in the labor force in 2000 A.D. is 119 million
contrasted with the 102 million in the labor force today. Past
increases in productivity have generally occurred as a result
of replacing manpower by machine power which requires a greater
per capita energy consumption. It is increased productivity
which generally contributes to our increased per capita incomes,
The larger share of elderly in our 2000 A.D. population will
also lead to greater energy requirements.
Environmental requirements in themselves will demand additional
energy. For example, a change from water-cooled to air-cooled
condensers, in order to reduce the detrimental effects upon
water resources would require increased fuel consumption
of 6-10% for fossil fuel plants and 7-13% for nuclear power
plants. Flue gas desulphurization will require about 5-10%
-330r-
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of the input heat of a fossil fuel power plant.
In addition the extraction of energy fuels will require
more energy as they become less readily available and as
environmental measures are needed to restore the land. All
of these factors lead us to estimate that by the year 2000,
we would need significant additional energy to maintain our
standard of living. Our current consumption is about
75 quads a year. One can argue about forecasts of the
energy demand for the year 2000, but no one argues that our
energy supply must increase between now and then if we are
to improve or even maintain our standard of living. Even
Lovins estimates that we will consume 95 quads of energy in
the year 2000, although Lovins would suggest that very little
of this energy would be in the form of electricity (10). Given
that the year 2000 is but 21 years away, and that the existing
trend is towards electrification, a significant share of the
energy growth will be in the electricity sector.
Insufficient electricity supply can create severe problems.
We noted above some of the problems which could occur in the
residential sector. In addition, decreased capacity will
provide a smaller reserve margin and reduced reliability of
service. Certainly the probability of blackouts and brown-
outs would increase. An improbable combination of natural
phenomena, improperly operating protective devices, and
communication difficulties all led to the New York City blackout
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of July 13, 1977. Constraints on electricity supply will
certainly increase the probability of such events. The events
of the catastrophic New York City blackout are well-known.
In a study for the Department of Energy (11), Systems Control,
Inc. estimated a lower bound of $345 millions damage. (Note
Table 2.) The greatest losses were those which received little
publicity: loss in business activity and losses to the
utility, Con Ed. Vandalism, crime, and food spoilage contributed
only a small part of the total damage.
There may have been significant health effects, also. Table 3
gives mortality by cause of death for several days around the
blackout. We note that the blackout itself began at 9:36 p.m.
on July 13 and enrded in most areas the evening of July 14.
The most striking statistic is the increase in cardiovascular-
renal deaths among those 65 years or older during the day after
the blackout began. With only one data point, no adjustment
for weather, and no consideration of the usual variance in the
New York City daily mortality rate, it is dangerous to draw
any conclusions. Nevertheless the figures are consistent with
a hypothesis that blackouts can lead to increased mortality.
The damage associated with the New York City blackout was not
unique; cost estimates of other power outages have been made
and are given in Table 4. The higher costs of the 1977 New
York City outage may reflect its long duration, but all of the
estimates suggest that blackouts can be costly.
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The other danger associated with a shortfall in capacity is
that inadequate supply will stunt economic activity. This
can happen in two ways: In periods of inadequate supply,
the industrial sector is often the first to whom supply is
curtailed. This *was the case with the recent natural gas
shortage. In the face of an uncertain supply, no industry
will locate in a given area. Secondly, frequent curtailments
or outages can create a generally unfavorable economic climate
with little confidence for investors. In both cases, limited
or lessened investment will have its effects on the economy.
It will result in higher unemployment which is far less benign
than the monthly figures often bandied.about. A study
undertaken by Dr. Harvey Brenner, School of Hygiene and
Public Health, The John Hopkins University, relates national
health statistics to unemployment(12). The results of his
study are summarized in Table 5. We see that general mortality,
infant mortality, cardiovascular mortality, cirrhosis mortality,
suicide rates, homicide rates, imprisonment rates, and mental
hospital admissions rates are all statistically significantly
and positively associated with higher unemployment. General
mortality, infant mortality, suicide rate, imprisonment rate,
and mental hospital admission rates were all positively
and statistically-significantly associated with inflation
rates. Brenner replicated his results for three states
(California, Massachusetts, and New York) and for two countries
(England and Wales, and Sweden). There is a need to scrutinize
Brenner's data and methodology, but his results suggest that
we pay close attention to how we impact our economy.
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My underlying concern in this paper is that we pay full
attention to both the risks and benefits of electricity
consumption. At present we highlight the environmental
risks associated with electricity generation and we applaud
the generation of less electricity in the name of conservation.
Conservation is a worthy goal, but reduced electricity
use is not equivalent to conservation. Measures aimed
merely at restricting energy use may have public health
consequences.
Environmental policy is naturally directed towards protecting
all site-specific and regional environments. When it is
applied in the energy sector, it is applied on an incremental
plant-by-plant basis. The results are that the broader policy
issues of adequate energy supply are not addressed. We
desperately need an energy policy with an important conservation
component so that our society and its regulations can address
energy concerns along with environmental concerns in order to
develop solutions which minimize the total social impact.
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Figure 1
O
160
140
120
100
= 80
60
40
20
67 68 69 70 Tl 72 73 74 75 76 77
YEAR
ANNUAL COST OF SULFUR DIOXIDE CONTROL IN POWER AND STEAM PLANTS
LOCATED IN NEW YORK ClTY
Source: Reference (4).
-335-
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CO
o
c:
H
O
(D
(D
Hi
0)
H
(D
3
O
n>
Concentration (ppm)
O
m
cz
>
m
p
2
OO
en
O
Q
ro
T"
p
CT)
T"
P
8
p
g
T"
i
to
OJ
CO
o
ro
o
o
•z.
o
m
n
(D
CD
CD
O
-------
Table 1
YEAR 2000 END USE CONSERVATION POTENTIAL PERCENT SAVINGS
(IN PERCENT)
CONSERVATION PROGRAM
ELECTRIC NONELECTRIC
ENERGY ENERGY TOTAL
SECTOR SECTOR ENERGY
NONE
REASONABLE
EXTREME
0
17
34
0
25
50
0
20
Source: Reference (9).
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Table 2:
SUMMARY OF ECONOMIC IMPACTS1
Impact Areas
Businesses
Government
(Non-public services)
Consolidated Edison
Insurance"
Public Health
Services
Other Public
Services
Westchester County
Direct ($M)
Food Spoilage
Wages Lost
Securities Industry
Banking Industry
$ 1.0
5.0
15.0
13.0
Restoration Costs
Overtime Payments
10.0
2.0
Metropolitan Trans-
portation Authority
(MTA) Revenue
Losses 2.6
MTA Overtime and
Unearned Wages 6.5
Food Spoilage
Public Services
equipment damage,
overtime payments
TOTALS
0.25:
0.19
$55.54
Indirect ($M)
Small Businesses $155.4
Emergency Aid 5.0
(private sector)
Federal Assistance
Programs 11.5
New York State
Assistance Program 1.0
New Capital Equipment 65.0
(program and
installation)
Federal Crime Insurance 3.5
Fire Insurance 19.5
Private Property
Insurance 10.5
Public Hospitals--
overtime, emergency
room charges
MTA Vandalism
MTA New Capital Equip-
ment Required
Red Cross
Fire Department
overtime and damaged
equipment
Police Department
overtime
State Courts
overtime
Prosecution and
Correction
1.5
.2
11.0
.01
.5
4.4
.05
1.1
$290.16
Estimate based on aggregate data collected as of May 1, 1978. See
previous page for discussion of limitation of these costs.
2Overlap with business losses might occur since some are recovered by
insurance.
^Looting was included in this estimate but retorted to be minimal.
These data are derivative, and are neither comprehensive nor definitive.
Source: Reference (10).
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Table 3
Cause of Death July 12-15, 1977
Cardiovascular
Total Respiratory Renal Homici
Date July 12
i 64~ —
u> »
f Age *
65+ —
Total 212
13
72
104
176
14
77
157
234
15
68
139
207
13
6
14
20
14
11
15
28
15
8
12
20
13
24
51
75
14
25
100
125
15
20
87
107
13
4
14
6
jde
15
5
Oth
13
39
38
77
14
37
42
79
er
15
36
39
75
Blackout began 9:36 p.m. July 13, 1973; power restored c. 10:30 p.m., July 14, 1977
Source: Reference (11) .
-------
Table 4
COMPARATIVE COST! ESTIMATES OF POWER OUTAGES
Hauugard1
NYEDA1
Shipley1
Telson1
NERA1
Gannon 3
Geographic Scope
New York State
NYC
U.S.
New York State
U.S.
U.S.
Ontario Hydro2 Canada
Present Study^ New York City, 1977 $4.11/kwh
Estimated
Cost Date
$2.17 million/hr 1971
$2.5 million/hr 1971
$.60/kwh 1971
$.33/kwh 1973
$l/kwh 1976
$2.68/kwh(ind), 1976
$7.21/kwh{comm)
$15/kwh(15min), 1977
$91/kw(l hr)
1978
*As reported in Myers
20ntario Hydro, "Ontario Hydro Survey on Power System Reliability:
Viewpoint of Large Users", April, 1977.
3P. E. Gannon, "Cost of Interruptions: Economic Evaluation of
Reliability", May, 1976.
Direct plus indirect costs divided by estimated kwh sales lost due
to the blackout (see Section 4). Disaggregated, direct.was $.66/fcwh
and indirect was $3.45/kwh.
Source: Reference (11).
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Table 5:
MULTIPLE REGRESSION OP NATIONAL ECONOMIC INDICES ON SELECTED MORTALITY RATES, UNITED STATES
(t — Statistics in parentheses)
Time Log Time Per Capita Unemploy-
Dependent Variable Years Intercept Trend Trends Income ment rate
GENERAL MORTALITY RATE1
(Lag 0-5)
(1) Mortality rate, fo/m ,„
(2)
(3)
(4)
(5)
(6)
(7)
(8)
(9)
total whites "™ " ™'" *(1 92)
Mortality rate, 1940-74 116 4 - — I?F i
total nonwhites 194° 74 136'4 M6 55)
LT 1 whites M7.06)
LT 1 nonwhites M10.48)
Cardiovascular
disease mortality iyiu-/J -^,8Jt>.a -I/.B i,o//.o
rate2 M4.70) M4.76)
(Lag 1-4) 4
Cirrhosis mortality
(Lag 0-5) 3 M8.99)
Suicide rate
t(1.50)
Imprisonment
45) M3.14) M3.48)
(Lag 0-2)
Mental hospital
LT 65 *(8.69)
(Lag 0-5)
0.62
M5.05)
1.68
M6.95)
12.65
M8.01)
17.74
M10.69)
2.85
Ml. 83)
.14
M4.21)
.42
M14.23)
— 1 <^Q
M5.92)
3.11
M8.92)
Inflation _
Rate R F
0.87 0.89 *21.9
M2.96)
2.83 .96 *74.1
M5.16)
3.59 .97 *98.6
M5.44)
30.77 .99 *199.6
M6.49)
1.04 .74 *6.50
(.78)
.16E-2 .98 *114.4
(.01)
.27 .91 *26.2
M4.23)
.64 .76 *10.4
*3.35)
2.19 .97 *63.4
M3.21)
D.W.
1.93
1.67
2.11
2.40
2.36 .
1.65
1.80
1.87
1.85
1 Per 10,000 population
2 Per 100,000 population
3 2d degree, polynomial distributed lag equation.
4 Ordinary least squares equation.
Source: Reference (12).
tailed tests:
tsicjnifirant at 90 percent level of confidence;
t=31.1; FM.B9
•significant at 95 percent or greater levels
of confidence, i.e.: at 95 percent level of
confidence.
t=1.71; F=2.28; at 99 percent level of confidence,
t=2.49; F=3.31; at 99.9 percent level of confidence,
t=3.45; F=4.71.
-------
References
(1) United States Environmental Protection Agency, letter from
Administrator Russell E. Train to Secretary of the Interior
Thomas S. Kleppe, June 4, 1976.
(2) Friends of the Earth, Inc., letter to Paul Howard, State
Director, Bureau of Land Management, Utah, November 13, 1975.
(3) United States Department of the Interior, Final Kaiparowits
Program Decision Option Document, April 30, 1976.
(4) Freudenthal, Peter C. (December, 1978) "Discussion of Paper
of Vaun A. Newill, R. Wyzga, and James R. McCarroll",
Pull. M. Y. Academy of Medicine, 54 (11), 1249.
(5) Eisenbud, Merril (December 1978) "Levels of Exposure to
Sulfur Oxides and Particulates in New York City and Their
Sources", Bull. N. Y. Academy of Medicine,54(11), 1012.
(6) Schimmel, Herbert (December 1978) "Evidence for Possible
Acute Health Effects of Ambient Air Pollution from Time
Series Analysis: Methodological Questions and Some New
Results Based on New York City Daily Mortality, 1963-1976,"
Bull. N. Y. Academy of Medicine, 54 (11) , 1052.
(7) Hinkle, Lawrence, Jr. (1978) "Health Benefits and Health
Costs of Controlling Sulfur Oxides in Air", Bull. N. Y. Academy
of Medicine, 54(11), 1257.
(8) Milner, John E. (October 1978) "Hypothermia", Annals of
Internal Medicine, 89(4) , 565.
(9) Smith, Craig, editor (June 1978) Efficient Electricity Use,
Pergamon Press, Inc.
(10) Starr, Chauncey (April 1977) "Energy Planning—A Nation at
Risk" in Hearings before the Subcommittee on Advanced Energy
Technologies and Energy Conservation Research Development
and Demonstration, Ninety-fifth Congress, first session,
April 4, 5, 1977, U.S. Government Printing Office,
Washington, D.C.
(11) Systems Control, Inc. (July 1978) Impact Assessment of the
1977 New York City Blackout, Final Report prepared for
U.S. Department of Energy, Washington, D.C. 20545 under
contract No. EC-77-C-01-5103.
(12) Brenner, Harvey (1976) "Estimating the Social Costs of
National Economic Policy: Implications for Mental and
Physical Health and Criminal Agression", a study prepared
for the use of the Joint Economic Committee, Congress of
the United States, October 26, 1976, U.S. Government Printing
Office.
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DISCUSSION
SESSION IV
John Blair, Evansville, Indiana: Most of my remarks are
going to be addressed to Dr>. Wyzga from the Electric Power
Institute, and if he would like to'respond, I would appreciate
it. It seemed to me as he was talking, that I was going to go
back to Evansville, Indiana, and watch the 20 or so power plants
that are going up around my home with a lot different light
because I was hoping that they would put out pollution so my
electrical costs could stay down. It seems as though he failed
to recognize one very essential element of economics, as far as
electric power production is concerned, and that is, according
to the New York Times yesterday, we are 36/& over the peak load
capacity needed in this country. Now 36/S over our peak load
need says that there is an inflation built in, in economic
aspects of utilities in this country, that is totally
unnecessary. Any time you are operating 36% over peak load
capacity, that means you are paying for power plants that aren't
needed. I'd like to point out two examples of this, the fact
that power plant construction is what causes the price of
electricity to go up. One of them is the Marble Hill Plant
which is being built on the Ohio River at Madison, Indiana, at
the cost of approximately two billion dollars. It is a nuclear
plant. That is doubling the capital base of the company that is
building it, the Public Service Company of Indiana. Doubling
it! Their rates are based upon their capital base. That looks
to me like it is going to double their rates. And it is not
pollution control equipment that is going to cause the rates to
double .
I would also like to point out the example of the
Indiana-Michigan Electric Company Power Plant, which is owned by
the American Electric Power, that is going up in Rockport,
Indiana, which is also a 2,400 megawatt unit. It also is going
to double Indiana-Michigan's capital base. That is why electric
rates go up; not just becase* scrubbers or precipitators or
whatever, are put on these. I would also like to point out that
conservation does work. As a matter of fact, conservation has
taken place so much in Indiana over the last year that the
construction of several power plants has been delayed. The
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Indiana-Michigan Plant, for instance, has been delayed by at
least a year because Indiana-Michigan misprojected their
electrical needs. And also, during the coal strike in 1977-78,
we found that in Indiana a 25% reduction in electrical usage was
accomplished with the lay-off of 6,000 people under an emergency
situation. Now 25% electrical reduction in the state of Indiana
was a pretty massive reduction. Those 6,000 people who were
laid off, had adequate planning taken place, probably would not
have been forced to be laid off. Also another thing is that
peak load demand is hardly a way to run this country whenever we
are having a real serious environmental problem. Peak load says
that you can build and accomplish the needs of whatever you
want. Environmentalists, it seems, would say, let's go with
peak load pricing and make people pay for those. When I have a
business, which I do, and my capital runs out, I stop expanding.
I can't just arbitrarily say I want to build more and more and
more, and expand when the capital runs out. That is the same
thing that should happen with people using electricity. If
there is none left to use at peak load times then there should
be no more use of it. And then Dr. Wyzga said — this is a
quote: "In the face of uncertain supply, no industry will
locate in a certain area." Well, I would like to speak from the
hear't here, because in my area with all these power plants going
up around me, we are seeing a mixing zone. You can fly any day
and see a mixing zone of varying depths in the atmosphere. We
are seeing our air turn brown and orange and whatever other
color. And why are we seeing this? The utility that services
my particular area has a total generating capacity of about
1,000 megawatts. That's Southern Indiana Gas and Electric. In
that same area that Southern Indiana Gas and Electric serves, we
have Indianapolis Power and Light, which has a major electrical
facility which serves Indianapolis. We have the
Indiana-Michigan Electric Company which is building the plant in
Rockport, which I mentioned earlier. We have the Public Service
Company of Indiana, just 25 miles north of Evansville, which is
going to have a 3,250 megawatt station when it's finished. It
seems that, with the Clean Air Act Amendments of 1977 and the
fact that economic sanctions are placed upon places that don't
comply with the Clean Air Act standards, the economic arguments
that he mentioned do not hold water because of one very
significant thing. If our air is clean today and not clean
tomorrow, and we have a non-attainment status as a result of
that, and all the electrical production that's going on in the
area which is dirtying our air, causing us to be on
non-attainment status, is going to places like Fort Wayne,
Indiana; Muncie, Indiana; Indianapolis, Indiana; and
Plainfield, Indiana; we are not receiving any of the benefits
from it. All we are receiving is the pollution. So it is very
simple if you are going to look at things on a national level to
say yes, we need to build more and more power plants to supply
clean energy growth. But for those of us who are in the lower
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end of the valley, we don't want to see it happen like it has
happened here in Pittsburgh. I took a drive up the Ohio River
Boulevard yesterday and I've never been so appalled in my life!
Thank you.
Dr. Hj_ Spencer; I would like to announce some ground
rules for this debate. First of all, I'm not involved in it. I
am sure that many of you realize that that requires the exercise
of some considerable restraint. Secondly, I feel that the
presentation was a side of a controversial issue, or many such
issues, and I think it would be appropriate if anyone who feels
to be on the opposite side, be given equal time. The panel
first, please.
Dr. R_._ Wyzga: I think the question probably was directed
more at me than my colleagues, although if they want to take a
stab at the answer I would be happy to let them. Let me first
of all say that I did not argue that we should dismiss
environmental protection. I think environmental protection
should, in fact, be implemented when it is needed. All that I
simply argued is that when we consider environmental control
measures, we should look at what the total impacts are. There
are environmental benefits; there are conservation benefits;
but there are also some social impacts. I ask that we examine
these social impacts, something that we have ignored heretofore.
Secondly, I have not argued against conservation. I think that
everyone agrees that conservation is necessary. What I am
arguing for is some resolution of the dilemma we now face
because we are working on one hand with, I guess, the
incrementalism of environmental policy versus the need for some
type of an overall comprehensive energy policy. We somehow have
got to learn to resolve these two policy directions. I don't
really know your specific area so I can't comment on it, but I
will say that having excess capacity is something that no one
wants, even utilities. It costs them money, and if there is one
thing that motivates utilities , it is money, economics. And I
would add that, as part of the measures to try and insure that
we don't have excess capacity, we have Public Service
Commissions and Public Utility Commissions. If they are doing
their jobs correctly, and I think in many states they are doing
their jobs correctly, it is they who examine the need for
electricity or energy in a given area and try to ensure that
these needs are in fact met. I think even they are frustrated
and have difficulty in dealing with some of the environmental
policies at the same time.
Dr. H_._ Spencer ^ Does anyone else on the panel wish to
respond to the remarks of Mr. Blair? Who feels to be on the
other side of that debate from the audience?
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John Campbell, New York: I am from New York and I don't
want to talk too much because my situation is a lot different
from the Ohio River Basin. However, we do have in New York,
purportedly, according to a lot of people, something like a 35%
reserve margin, and the idea that that is surplus power, beyond
what is needed to insure a reliable service, has stopped a lot
of power plants.
In my state, and it is certainly one consideration that is
important here, M5% of our electricty is generated with oil. It
results in tremendously high rates in my area, having nothing to
do with the capitalization of the utilities.
The capital portion of a utility rate base is not the
entire rate base. It also has operations and maintenance and
labor, and an assortment of other expenses. In particular in
New York State, we spend about 1.2 billion dollars a year for
oil. In the future, if new plants aren't constructed, whatever
additional demand occurs in my state, however small, is going to
be met with oil and it is going to be met at ever increasing
cost. We've done a study on the economics of power in New York
State and we found that if we build power plants in large
numbers, the savings to our utility customers run into the
billions of dollars.
What hasn't been seen is that the number of plants and the
virtues of conservation are not entirely unmixed. We live in a
world where we are affected by other people: by Arabs, by wars
in Iran, and by a whole variety of other effects. We also burn
a lot of oil in New York City, and it adds a tremendous amount
to the sulfur burden in the city and on Long Island.
I haven't been exactly organized here but to sum up—when
you are considering whether or not to build a power plant, you
have to look at the entire picture—all the economic effects and
not only one small facet of it, which is whether you have
surplus power or not. The one-facet approach is a very obtuse
way of doing energy planning and it has cost me and my neighbors
in New York State well into the area of 2 billion dollars or so,
and it is going to continue to cost them more in the next few
years.
Dr. H^_ Spencer; The gentleman in the blue sweater is
next, and then Dr. Blome, and then the two right in the middle.
I'd like to ask the panel if there is any response to the
previous comment that you would like to make. I would prefer
that we try to conduct this as smoothly as possible, but it's
probably not going to be easy. I'll give you about five minutes
and that's it.
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Dan Swartzman, University of Illinois School of Public
Health: I've been debating with myself whether to get up here
and say anything or not. I don't feel that I am particularly on
the other side of whatever issue it is exactly that we are
trying to put our finger on. In fact, I see myself on a
parallel line with the gentleman from the Electric Power
Research Institute, certainly heading in the same direction,
hopefully lines that will never meet. The reason why I say we
are heading in the same direction is that the question he
addresses is an extremely important question for all of us to be
asking ourselves. If there is any group of people who ought to
be willing to examine the other side of the coin, it is those of
us who consider ourselves environmental advocates. We are the
ones who have been saying for many years that there is no such
thing as a free lunch. It behooves those of us who spend some
time doing this, particularly those who get paid to do it, as I
do, to sit back and see what is the total impact of what we do
and of what we are advocating. It is terribly important to look
at all of the social costs, all of the both quantifiable and
nonquantifiable societal impacts of the actions that we propose
that society take. Because of that I have, in the past,
advocated a number of times that environmentalists should be
behind the push towards cost-benefit analyses. Once we are able
to really get a handle on some sort of assessment of the
benefits of the programs we advocate, we will be in a much
better position to achieve the goals that we have been fighting
for. My concern is the way in which this issue was addressed,
not the fact that it was addressed. I think it has a very
proper place in the program. I am concerned about a few points
that were raised, and I would just like to briefly hit each of
those points. I think, however, that I commend to those who
read this record sometime in the future--! assume you are going
to put it in a time capsule or something—I feel they will be
capable of judging Mr. Wyzga's work on its own merit, and I am
not going to presume to tell them how they ought to read that
work. But I do have a couple of points that I think we ought to
think about in the work. First is the concept that health is
not a significant issue in the development of new power plants.
The reason why a lot of the arguments have centered around
visibility and esthetics and costs, is because we don't have a
lot of the data we need to argue the health point. For
instance, in the New Source Performance Standards that are being
considered by EPA and debated by people in front of them, there
is a concern for pollution from coal burning. I feel that is
implicit, in where a lot of the environmentalists are coming
from, is a concern for the health of our population. But since
we don't have the sulfate information or the secondary impact,
and we are stuck with a fairly poor indicator like sulfur
dioxide, we are not in a position to be able to forcefully
advocate the health side of these things. But I take fairly
strenuous objection to the concept that the only thing we're
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debating is economics and esthetics, although I think those are
extremely important, as one of the previous discussants
mentioned. I also just want to point out that I didn't hear,
during the presentation, any kind of association between
hypothermia and higher energy costs. In fact, if I'm not
mistaken, I heard, although it went by very quickly, that no
association was possible at this time and so that all we have is
that sort of anecdotal presentation that yes, in fact, it has
happened. It is interesting to note, as was pointed out to
me—this is not my thought-- that this supposedly has happened
in England where we don't have the same sort of strenuous
controls that we are asking the utilities to meet here in the
United States. Also, I would like to point out to the
representative of EPRI, and maybe he can take it back to his
colleagues, that if, in fact, they're concerned about
discriminatory burdens on individuals who have difficulty
meeting high electrical rates, that maybe they ought to consider
supporting rather than opposing inverted rate structures. That
might get them to the same place that they're concerned about
here. Also the gentleman pointed out that a number of the
studies that he looked at were rather facile. After looking at
his description of the situation in New York after the
"blackout," I am quite certain as to his qualifications to make
that judgment. I would just like to end by reinforcing what I
said at the beginning. It is a terribly important question, and
we lose all credibility as environmental health advocates if we
don't examine this question, but I don't think this record
reflects the kind of examination that is needed. Thank you for
this opportunity.
Dr . FL_ Spencer: D. Blome is next, and I would like to
have someone following that who would talk about some issues
related to the other two papers, which were very good.
Do n Blome, University p_f Kentucky: I would like to address
this question to Dr. Morris. You showed some very impressive
films concerning the safety of nuclear transport, at least on
land surfaces. There is going to be an increasing amount of
nuclear traffic, both spent fuel and new fuel, along waterways.
Will you comment on the safety and potential hazards of nuclear
transportation accidents with regard to waterways and the
integrity of those canisters in water?
Dr . Morris: I guess the only comment I can make is that
the NuclearRegulatory Commission standards for the casks that
the spent fuel is shipped in do specificy standards for
immersion that they must meet. They have to be able to stand up
to tests of being immersed in water.
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Dr. HL_ Spencer: Next person, please.
Jerry Fields, Pennsylvania Power and Light Company,
All en town: I would like to respond to the gentleman from
Evansville--a personal response; I don't want to respond for my
company. In Pennsylvania a utility is required under the Public
Utility Commission Act Section 401 to provide reliable, safe
electrical generation. Also your reference that projections of
utilities were way off base is correct. In the early 70's, our
company, for example, suggested that the demand in the future
would increase approximately 1% per year. However, this has
decreased sharply and now we estimate about 2.5/& demand increase
per year .
You mentioned your local electric utility company is
doubling its size. Our company is, also. Our investment over
the first 50 years is about 2 billion dollars and at the present
time we are building a 2-unit thousand megawatt nuclear reactor
which costs also about 2 billion dollars. But one thing you
must remember is that for each year a nuclear power plant, for
example, is delayed, the construction and interest costs will be
higher by about 150 to 250 million dollars. This will then be
passed onto the customer. In addition to that, each day that
this new plant is delayed, we will be using approximately
100,000 barrels of oil. It should be noted that with high
energy prices for all fuels that we have right now there is an
additional dependence on oil for gasoline, tires, clothing, and
other substances. Since there is a shortage of oil we are
compounding the problem by using oil for power. In addition, if
a new plant is delayed we may have air pollution problems by
continuing to use old plants which are allowed to operate
instead of being retired. Even though there may be an
additional amount, let's say 36% electric above the demand, you
really can't talk about that per company. Most companies work
on interconnection and they work by economic dispatch which
means that if you can produce electricity for three cents per
kilowatt per hour, and another company can produce it for two
cents, you are not going to operate your plant. In the
interconnection that our company is in, the Pennsylvania, New
Jersey, and Maryland interconnection, there is a lot of oil.
These are basically older plants. For example, Philadelphia
Electric has a lot of oil units. That is one reason to go to
new plants, possibly coal and nuclear. This means a utility,
like our company, will be having excess electrical generation
even though we prepare environmental reports for fossil and
nuclear plants and simultaneously talk about conservation. For
example, we talk about insulation, storm windows, purchasing
appliances that use less electricity. So on one hand, we are
building power plants, and on the other hand we are talking
about the conservation. It seems like we are in a vice that we
are trying to do as much as we can for our community, for the
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public, to make certain they have safe and reliable electricity.
And yet once you start building a power plant, as it was
mentioned, I believe this morning, it takes about 10 to 12 years
for planning and construction. You just can't stop and wait a
few years until electricity is needed. You have got to continue
your programs and try to provide a good environment for the
community living around the power plant, and also you have to
try to give the consumer the best rate possible. I just wanted
to give a little information on that. Thank you.
Dr. E_._ Spencer; Thank you. Now did anyone on the panel
wish to speak to any of that? Dr. Radford, and Dr. Hamilton.
Then I will try to assess the crowd at that point.
Ed Light, Appalachian Research and Defense Fund and also
ORBES Advisory Committee: I feel there is a very important
issue relating to the health effects of electric power
transmission which wasn't covered, and I really feel that ORBES
has an obligation to get information on this topic. I'm not
sure that many members of the panel would be involved in this
issue, but perhaps other people in the audience would have
information and I would urge ORBES to go into this further with
perhaps people who aren't here. This has to do with the effects
of spraying herbicides under the electric power transmission
lines. In West Virginia we have had complaints for several
years from people all around the state concerning problems
caused by this application. Up to now, it has been mainly
2,4,5-T used on these electric power transmission lines. The
concern for health effects ranges from birth defects, skin
irritation and cancer. EPA, in just the past weeks placed a ban
on 2,4,5-T, which for years the power companies kept telling us
was safe. Of course, the manufacturers of the chemical will
challenge this and the decision could possibly be overturned.
Probably more significant, in terms of what we ought to consider
for the future, is that the companies will try alternative
sprays, i.e. 2,4-D and tordon, which also would have a range of
possible human health effects in addition to ecological effects.
Another problem I have is with Dr. Phillips' presentation. He
summarily wrote off the school of thought which has concluded
that there are possible health effects, based on research up to
date, from very high voltage transmission lines. I don't have
any expertise in this area, myself, but again feel that ORBES
has an obligation to get information from somebody with
expertise from the other point of view on this. I'm not sure
there's anyone here that can speak to that side of the question
but obviously there is animal data and Russian research data to
the other point as Dr. Phillips just said he disagreed with it.
I would have liked to see him go into specifics as to why he
disagreed with it. He didn't choose to do that. I'd like to
make one observation on Dr. Wyzga's presentation. I was
fascinated by the industry's willingness to accept the
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epidemiological work on the unemployment and blackouts question.
Yet you talk about the epidemiologic work on sulfates and
they're not quite so ready to accept it.
Dr. H_._ Spencer: I have already asked the panel
members—perhaps I have not gotten to all of them. About the
Agent Orange question, I'll give a one sentence response to that
if they don't feel there's anything they can say about it. Dr.
Phillips, would you like to respond to the question about the
Russian data base in relation to what you said?
Dr. Phillips: First I will respond to the second question
concerning other studies which have been conducted in the United
States, and then answer the first question concerning the
Russian data base. I did not have the opportunity in my 30
minute presentation to discuss the value and shortcomings of
earlier studies that have been done in this research area. I
did not mean to give the impression that earlier research has no
value. This is not the case, of course. There have been
several rather extensive critical reviews of past research.
Some of these appeared within the last year in the open
literature. It is not possible to discuss the rather massive
amount of research that has been conducted on biological effects
of ELF electromagnetic waves. It would require more time than
we have available in this discussion period. In response to the
first question concerning Soviet research in this area, during
the past year I had the opporunity to visit the Soviet Union and
talk with their scientists as a U.S. participant on two
different U.S.-USSR exchange programs. I briefly summarized
some of their findings in my presentation. I had an opportunity
to talk to the group at an institute in Leningrad who published
some of the work at the 1972 Cigre meeting, the group doing the
animal experimental work at Kiev at the Communal Hygiene
Laboratory and to several groups of scientists at institutes in
Moscow. We can't ignore the Russian results. Data is data. I
would be the last one to say that their data are not valid.
Philosophically data is data; it's neither good nor bad. How
you interpret the data is another issue. There are two
potential problems with the Soviet research that has been
conducted to date. First, they use experimental designs and
procedures that are somewhat disparate from acceptable Western
standards. For example, they do not always use appropriate
control groups in their studies. This makes it difficult to
determine whether the effects they observe (i.e. 60 Hz fields,
or whatever) are the result of the agent in question or due to
some secondary factor (i.e. temperature, humidity, noise,
etc.). One starts to wonder how one can claim an effect when
there is no appropriate control available to make such a claim.
This situation was not evident at several laboratories in
Moscow. Unfortunately, the results of studies from these
laboratories have not been published yet. There appears to be
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within the
the earlier
My present
data are in
some disagreement among various scientific groups
Soviet Union concerning the validity of some of
research on effects of 50-Hz electromagnetic fields.
position is neutral. Let us wait till all the
before we make judgments. There will be a meeting with the
Soviet scientists this June in Seattle, as part of this
U.S.-USSR Exchange Program. Both U.S. and USSR scientists will
present their latest results. We should have more information
available at that time concerning the most recent Soviet
findings.
Dr
issue?
H. Spencer: Did anyone else wish to speak to this
Dr. Wyzga: I think there was a comment made about
qualifying some of the results of those other studies.
my not
I think
if you read my paper carefully, you will see that, in fact, I
did qualify them. Professionally I am a statistician and I
believe it is an obligation to my profession to scrutinize any
result before I formally declare whether or not I believe it. I
simply made observations of these results and indicated that
they need scrutiny before we can determine whether or not we can
accept them. Perhaps they generate hypotheses which should be
tested in other studies.
Dr . PL_ Spenc er: Dr. Radford and Dr. Hamilton;
policy of trying to allow all persons to speak.
hav e a
already had
immediately
raised.
something to say,
but I haven't
I'm not going to come back
I do
If you
to you
forgotten that your hand has been
Dr . RadI ford: I have a
transportation issue, a question
further comment on what we
con ser vat ion/environmental argument
earlier question about the shipping
materials by barges. I was a few minutes
and I may have missed it, but if you didn't
comment concerning the
for Sam Morris, and then a
can perhaps call a
The comment relates to the
of wastes, coal or other
late coming in
comment on
, Sam ,
the use
of river traffic for handling waste or fuels, I wish you would.
It is my understanding that there are definite health costs
involved in that, too. Barges do get loose and cause various
problems. It is particularly relevant to this part of the
country where a lot of fuel is transported by barge. The
question I have has to do with your statement. If I interpreted
you correctly, you said that the occupational accident mortality
in the transportation of coal created more deaths than in the
mining of coal. Is that a correct statement?
Dr
S. Morris: It depends on the situation. If you look
at a strip mine situation, I think that is true
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Dr . Radford : You can qualify it if you like but I would
just like to ask the question,: In reviewing that conclusion
where do you see the preventive strategies? I mean, a lot of
what we are discussing in this symposium has to do with
historical things that have gone on now for the last several
decades, and may involve technology that may be out of date.
One of the things, obviously, we all hope to do by uncovering
these problem areas is to prevent them. In other words, we
don't have to accept the fact that, say, 5,000 men die each year
moving coal around this country. In the future maybe there are
things we can do and maybe that is part of the cost we are going
to build into the fuel, too. That's what we are talking about
when we protect the environment. So my question is, would you
address that?
Now a final comment with regard to Ron Wyzga's
presentation. What I am hearing is not so much the
confrontation that some people seem to feel. In other words, I
don't think that the separate courses are necessarily parallel,
never to meet. It sounds to me as though what we are really
saying here on this conservation versus environment argument is
that, I think, we are almost at a point where we can uncouple
environmental control and environmental costs from the ultimate
societal cost or benefit of generating electricity. In other
words, I don't see that there is a one-to-one correspondence
between protecting the environment and the final cost that is
going to go to the consumer. It is relevant to some of the
things that the critics have just raised. I wish perhaps you
might speak to that.
Dr. J5^ Morris: I appreciate your question very much
because it gives me an opportunity to push a point that I try to
make as frequently as I can. I think there are two criteria
that we have to consider when we decide how much prevention we
want to have. After all, just because we can calculate what the
health effect is, really doesn't say anything about how much you
should then do to try and reduce that health effect. Maybe it
is already reduced to the maximum feasible amount. The first
criterion is the total impact, and those are the numbers that I
was showing, so we can compare how many deaths per gigawatt
electric year in transport, as compared to mining, as compared
to air pollution, and give us some idea of where the biggest
effect is. That gives us some basis of deciding where we want
to put our emphasis on prevention. But there is another
criterion also, and that is the level of individual risk. I
think that that difference is very clear when you compare coal
mining, with the transportation effects. Although our
calculations show that the per gigawatt year total effect of
transportation accidents and coal mining accidents are roughly
the same, that is within a factor of two or three or something,
the individual risk to the coal miner is much higher because the
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number of coal miners involved in producing that coal per
gigawatt year is much less than the number of people who are at
risk of being hit by freight trains. At least that is true on a
national average basis. There are probably local situations
where the individual risk in a local community that has a lot of
unit train traffic is perhaps higher. I could envision that
there are such local situations. One indication of that is that
the Department of Transportation keeps records on railroad
employees who are killed at grade crossing accidents-off duty,
in their private life, not occupational. It is hard to
calculate a rate but there are enough of them so that the
individual risk must be high. I assume it is just because those
people live and travel around railroad crossings more than the
average person. I hope that answers that part of the question.
On barge transport, the data we have been able to look at from
the coast guard on water transport would indicate that the
deaths and injuries in accidents in barge transport are
considerably lower than in railroad transport. There is quite a
variation between inland river rates and Great Lakes transport,
though. Great Lakes transport has a higher risk, particularly
occupational risks. I'm not sure, offhand, of the difference in
risk to the public, like small boats being run down.
Dr. H_._ Spencer; I would like just very quickly to answer
Mr. Light on behalf of this question to Agent Orange. Mr.
Light, the ORBES Project personnel will not let that go
unnoticed. We are working on it. We have a good deal of data
on the pharmacological effect of that compound which goes back
to 19^0 up to the present. Now Dr. Hamilton and then Dr.
Zeller, and this gentleman right here, and I think John Blair,
have been patient long enough. I'll recognize John if there is
still some time left.
Dr. L_._ Hamilton, Brookhaven: I have several questions
for Dr. Phillips. The first question is: Are the effects that
you describe linked by some change in the membranes of cells and
I wondered whether they are all recoverable or whether they are
permanent? Have you any observations on the recoverability from
these effects--in other words—their duration? That is the
first question. The second question is this: In assessing the
health and environmental impacts of energy we would like to
include some quantitative data from this question of power
transmission effects. So for this purpose it would be very
helpful if you would tell us if you have done any thinking about
the numbers of workers that might be exposed to these sort of
effects, and whether or not the public is inevitably exposed, or
whether they can be adequately protected by eliminating them
from coming anywhere near these rights of way? I mean, what
hazards are the public and occupational people really going to
be exposed to? Thank you.
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Dr. Phillips: Unfortunately, I could only spend 30
minutes to cover the tremendous amount of research. To date we
have found very few effects. Of the many systems we have
examined, the few effects appear to involve the nervous system,
behavior, and immunology. Our plans in the immediate future are
to investigate the relationship between effects and magnitude of
field strength and/or duration of exposure, and to examine
recovery from effects to determine whether such effects are
transitory or permanent. Such data are not available at this
time.
Concerning the mechanism of interaction of fields with
biological tissue, I believe research on membranes may be a
fruitful area. We currently have a study in progress that is
addressing potential membrane changes by exposure to 60-Hz
electric fields. These are in vitro studies—experiments in
which cells are removed from the body, exposed to fields, and
then studied. The major issues of concern in terms of human
health are occupational and general public exposures.
With regard to occupational exposures, the population
exposed to the largest electromagnetic fields are people who
work in switchyards. Just recently, within the last year, some
very valuable data have become available concerning the
durations and intensities of exposure to some of these workers.
Much of these data have not been available earlier because the
worker is exposed to various field intensities at various
durations of exposure throughout his workday in the switchyard.
Recently, a personnel monitor has been developed by Dr. Deno at
Project UHV which gives cumulative exposures within various
bands of field strengths. Data they are now collecting with
this new device should provide us with a better estimate of how
long workers are exposed to electric fields and at what
strength. Public exposure is normally very small. Only a few
people walk under EHV transmission lines. These are the hunters
and campers who sometimes follow the transmission line
rights-of-way because it it easier to walk along these cleared
areas. There are farmers, of course, who grow crops under EHV
transmission lines. The general population, aside from those
mentioned above, are seldom exposed to electromagnetic fields of
EHV lines. There is not a good quantitative estimate of the
durations and intensities of exposure to such groups as hunters
and campers who walk the transmission corridors.
Dr . H. Spencer^ Based on some recent literature, I think
the membrane question is a dynamite issue. It truly is. Mr.
Zeller, would you go ahead, and then John Blair.
Tom Zeller, Ind iana State University: One point I just
want to point out. We have heard a lot of epidemiological
studies--animal studies--shot down for statistical reasons, etc.
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and I just want to point out that works both ways. If the
effects are derived from animal studies you can't necessarily
conclude that there are no effects in humans. Currently the
policy is that man-made substances have full constitutional
rights and are deemed innocent until proven guilty. If the
burden of proof is on the consumer, the only advantage I can see
is that it makes for great material for epidemiological studies
in the future.
My questions are as to the separation of conservation and
environmental control-- that's a good point and I think we need
to do that as much as possible, but I want to point out that
there is one place in which they are really connected and you
can't separate them. It's the whole issue of placing the true
cost on the product, itself, instead of part of the cost of
production being born as social costs and health costs, which is
what this meeting is all about. Until you do that, I don't see
how people can make true conservation decisions. When I flip on
a light switch, I'm thinking I am creating air pollution and
nuclear waste by doing this and I take that into account because
I know that. But the general public doesn't know that, and the
people in Fort Wayne, Indiana, do not know that when they turn
on their switch, they are polluting my air due to the
Indiana-Michigan Plant down near Evansville, Indiana. So that's
one place where, until those environmental controls are put on
that plant, those people in Fort Wayne are not being made to
bear the full cost of consuming their product and therefore
cannot make a reasonable conservation decision. But otherwise I
agree with that point.
I would like to ask Dr. Morris about the impressive film
of the transportation of radioactive waste. I am impressed by
the efforts that have been made to contain these wastes during
transportation, and I am not sure what else you can ask them to
do. But I do want to ask, since we have been talking about
statistical reliability of tests--how statistically significant
were those tests? Did they do one casket a couple of times?
Did they do it several times? How significant is one test under
ideal conditions at the Sandia laboratory without taking into
account human error? Was it statistically significantly done?
Can you answer that?
Dr. Morris: I am not sure exactly how to evaluate the
statisticalsignificance of it. Those tests were in the context
of a much larger testing program which involved computer
simulation and scale model tesfls. I believe the ones shown were
the only ones done of the full scale tests. You say that they
are sort of ideal conditions. I don't really know that they
were ideal conditions. I think they were purposely designed to
be extreme conditions. In other words, most of the trucks that
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are carrying spent fuels are not going to be traveling at 80
miles an hour. It is very unlikely that they are going to find
as solid a concrete wall to crash into as they did at Sandia. I
don't think they are ideal conditions. I think they were done
as sort of verification tests to determine whether the findings
from the scale model testing and the computer studies actually
held up in a full scale test. I'm sorry that, at least right
now, I can't really give you a statistical evaluation of what
that means.
Tom Zeller: I just wanted to ask Mr. Phillips about the
effects of farming under those high voltage lines. Are there
any problems with that or are there just no problems, so that
you can go ahead and farm as normal?
Dr. Phillips; I can only answer that question from what I
have read both in the popular press and from the very few
scientific papers that have appeared in the literature. There
have complaints by farmers, even in the area where I live. They
complain of spark discharges. For example, they drive tractors
under the transmission line, and may receive spark discharges
when they get on or off the tractor under the line. There may
be complaints in some areas by people who are doing farming,
i.e., picking crops under a EHV transmission line, especially if
they are using any kind of wire support for the crop. They may
experience spark discharges. All the complaints that I am aware
of have been directly related to the spark discharge problem,
and of course, to the land utilization issue.
Dr. PL_ Spencer: The gentleman in the light tan coat?
I'd like to ask the panel, to stay another five minutes. Is
that all right with you people? There seems to be a
considerable amount of interest here. Go right ahead.
Richard Ulrich, Group Against Smog and Pollution (GASP)
Pittsburgh: The first comment is concerning Dr~. Phillips'
results that he presented from the Battelle labs. There were
numerous effects that were not found in the studies so far but I
think that it may be very important to notice that one effect
can be enough if that effect is a serious enough effect. They
have found two different things right now, the immunology and
the nervous system. If these are serious enough, it doesn't
matter that they have't found a list of 20 different things. I
think this issue is reflected in other things that have been
said, both this afternoon and earlier, about the size of the
effects that are being measured or not measured. The animal
studies, Dr. Phillips told me, involved usually about 20
animals. To see an effect with 20 animals, it sometimes
requires a rather large effect. The effect of pollutants in
epidemiological studies, partly because the pollutants,
themselves, are measured very badly, and partly because the
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individual exposures are measured very badly, as Dr. Ferris
said, from the Six-City Study where the indoor levels are quite
different from the outdoor levels. My own assessment of the S02
data is that the health cost of S02 could be anywhere from
nothing to 20 billion dollars. This is about the confidence
limit that we can place on it, or maybe you could even put it on
the other side, it could be helping 10 billion dollars worth.
The size of these effects are not known and this relates to that
kind of control. We don't know the cost of these health effects
and the size they could be is a lot bigger than the point
estimates that get made of them.
Dr . ,H_._ Spencer; Does anyone on the panel wish to respond
to that? Dr. Philips, you're nodding your head aggressively.
Dr. Phillips: You addressed two very important issues,
and we are acutely aware of these issues. Let me address the
second question first, about the sensitivity of our tests. In
the biological screening experiments, we are using a very broad,
screening approach. If an effect is seen in a particular study,
then we look at the system in much more depth. Each
investigator from past experience in his research area, knows
what size population he needs by having knowledge of the test
sensitivity and variance. He will know how. many anmimals he
needs to show an effect, with 95% confidence. Of course, one
has to be realistic and weigh cost and effort against the
probability of detecting an effect with a certain test system.
Some biological systems may be more sensitive than others.
Other systems may not be very sensitive, partly reflecting the
fact that some biological systems have high variability or are
protected by compensatory mechanisms; this can "hide" effects.
In our studies, each investigator is using the most sensitive
tests he has to detect effects. This relates directly to your
first question: whether one effect can be as important as, or
more important than, 20? Of course. What a scientist must do
is first to identify the effects — what biological systems are
sensitive. The existence of such effects have to be confirmed
by others in independent studies. Once an effect has been
found, you attempt to determine the consequences of the effect.
This is, you start in-depth studies to obtain a better
understanding. For example, in our study we see a change in
synaptic excitability. This is an extremely sensitive test.
This effect may not be reflected in the behavior or function of
the whole organism. However, such sensitive tests as this may
provide important insight into the mechanism of interactions of
electromagnetic fields with biological tissue. Such information
is needed to design specific tests for possible effects that may
be harmful. Also, data from such studies may provide the
foundation for epidemiological and clinical studies on humans.
Eventually we need to examine either volunteers or
occupationally exposed groups. This issue addresses a previous
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question from the audience: can effects occur in humans and not
in experimental animals? Yes. The human species is very
complex, especially behaviorally. What we do in laboratory
studies on animals is model biological systems and, hopefully,
obtain the basic information that is needed to relate this
information to the human exposure situation. Eventually,
however, you have to be able to relate research results from the
laboratory to humans by conducting studies (assessments) on man.
Dr. H^ Spencer: The gentleman at the fourth table here,
and then Mr. Blair in overtime.
Jay Henry, Illinois Power Company; I'd like to just clear
up something for the record as far as the gentleman from the
Appalachian Research is concerned. It wasn't clear to me that
it was pointed out exactly, what happened with the two
herbicides, 2,4,5-T and 2,4-D. It wasn't a proposed ban or
anything like that. It was an absolute prohibition of using
those two herbicides immediately effective when Barbara Blum
made the announcement about three or four weeks ago. I'd like
to point out that it was only the second time that the EPA has
done something like this without any detailed statistical
epidemiological studies. Clearly the EPA thought that there was
enough evidence to take this type of action based on some
observations that were made on miscarriages in women living in
areas where these two agents were broadcast for "right of way"
control. The ban went on a little further than just broadcast
applications and completely banned the use of them. Our
particular company has not been broadcasting herbicides for some
20 years now, although that is not the case with everybody. But
it was an absolute ban and even removes the use of them from
selected basal spraying. I think that's possibly unfortunate
because these two agents might possibly be used in that type of
application in an environmentally acceptable manner. But at any
rate, it is a complete ban until further notice. I just wanted
to clear that up. The other thing I would like to speak to, and
this may surprise him a little bit, but many of the things Dan
Schwartzman spoke about earlier, I am in complete agreement
with. And I think it's good that the two sides, if you can
categorize people into environmentalists and industrialists for
the time being, their disparity in viewpoints is getting a lot
closer together. The
-------
terms of "time of day metering," and load management, to try to
spread out the peak loads and drop the peak load a little bit.
Those types of things are being actively pursued by the
industry, as well as institutes such as EPRI and others. I
think that all these things are being considered. They are
looking not only at what they do for the load, but also the cost
of those types of services or those types of metering devices.
The industry is doing its part in those areas.
Dr. H^ Spencer: Allright, thank you. I'll add to that
as John is coming to the microphone. EPA is concerned, as is
the air force, particularly about the cockpit crew of the
Ranchand Aircraft. These persons engulfed considerable amounts
of Agent Orange during the Vietnam war and, of course, suffered.
Mr . J_._ Blair: A couple of points. One of them I would
like to ask is about the transportation of nuclear waste. The
subject was brought up about barge transportation. Well, the
Hoosier National Forest has been mentioned as a possible
permanent storage site for radioactive waste. And that sits on
the Ohio River in Perry County, Indiana. What are the prospects
for barge transportation of radioactive wastes? And if they use
a cask—like the tow boat that recently sunk in the Ohio River
near Evansville--that took more than two weeks to raise, what
kind of contingency plans are involved in something like that?
Dr . S^ Morris:: I am not sure that I can immediately
answer the question. You want to know what kind of planning is
done in case a barge were to sink?
Mr. Blair: Well, essentially the first question is: are
barges one transportation mode for radioactive waste?
Dr. S_._ Morris^: Yes.
Mr . Blair^ Okay. What kind of contingency plans? I can
see these films and they are truly impressive and it does make
me a believer. But it also makes me wonder about the human
error that is involved in something like that, once one of these
casks sink to the bottom of the Ohio River. Is it going to stay
intact for the duration of the time it is going to take to raise
it; does it take a couple of weeks or a couple of months?
Dr. H^_ Spencer: I might give you fair warning that Mr.
Blair is a Pulitzer Prize winner in news photography and I think
he is waiting. He is looking for a subject. You had best be
careful with your answer.
Dr. S_._ Morris:: I can't say specifically what the
contingency planning for something like that is. It would
depend on the situation, I guess. As far as whether the cask
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would stay intact for the time it would take to raise it, I have
every reason to believe that there is no difficulty there. But
I can't say from any specific knowledge what difficulties there
might be.
Mr . Blair: Okay. What prompted my question is the fact
that originally we were told that it was safe to put this stuff
in 55-gallon drums and dump it in the ocean. Then we were told
it would be okay if we put it in storage tanks or, better, in
underground salt formations. I'm just wondering, when the whole
nuclear waste question is really going to be solved?
Dr. H._ Spencer: Did you want to respond to that, Dr.
Morris?
Dr. Morris: I think that at this point I don't
necessarily want to respond directly to the question of when are
we going to find a final resting ground for nuclear wastes. I
might say, just on a specific point, that there has recently
been a program at Brookhaven to try to recover some of the 55
gallon drums that were dumped in the ocean during the 50's.
They have successfully recovered a few drums and the idea was to
see whether there is any problem; whether the drums, in fact,
leaked. The answer is no, they didn't. They didn't find any
problem with the drums that they did recover. But that is just
a sort of side-light issue.
Dr. H^ Spencer; Dr. Hamilton, did you want to speak to
this or some other issue?
Dr. L_._ Hamilton: Yes. I just wanted to speak to this
issue because I think it is terribly important, first of all, to
separate transportation from the question of ultimate waste
disposal. I think those are two separate issues. I think that
before anybody would decide on using a site, they would have to
do a very thorough specific environmental analysis of all the
routes to that site. I assume that would be part of the
process. Now you mentioned several things that lead me to
believe you are confusing a low-level waste with high-level
waste. For example, the stuff that was dumped in the ocean in
55-gallon drums was low-level waste. They have never dumped
high-level waste in 55-gallon drums in the ocean. And West
Valley, or whatever it is, I always get confused about this
place in New York, the problem there is of low-level waste. It
is a low-level waste problem that they haven't been able to
handle. I think the whole question of the storage of high-level
nuclear waste in this country is something that hasn't been
settled, as you point out. There never was a decision vis-a-vis
Lyons, Kansas. There was a decision, if my memory serves me
correctly, that the Atomic Energy Commission had decided to go
to "over-ground engineered storage," just at the time Mr.
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Schlessinger took over the agency. And then to show that he was
a really big, tough administrator, he was going to shake things
up. I believe this is a fair appraisal of that. He said, "No,
we are going to start again." So he bears a very heavy burden of
disrupting that particular analysis and decision. And the next
thing that happened is, again if my memory serves me correctly,
this question of underground storage at Kansas was raised as a
possibility, but when they looked into the area, apart from the
public opposition, the important thing is that it turned out to
be not as geologically stable as they first thought. So it was
never really seriously thought of as a solution. It was raised;
there was a lot of public debate about it; but it was never put
forward as a definite proposition. And there has been a further
consideration, as you know, in the New Mexico area and those
things are still under consideration. I think if you look at
the latest report that has been issued by the Deutsch Committee,
you will find that they say, very specifically, that before they
choose any individual site, and they decide to go to that
particular site, they are going to have to do some further
corroborative measurements before they make the ultimate
decision. I think that is the status of it—of the nuclear
waste disposal problem. What we have had, unfortunately, is
what happens frequently when you have a sort of changing
bureaucracy and you have not exactly the best brains of the
country concentrating on the problem of high level waste
disposal from nuclear power plants because it has not been an
overriding pressing issue. They have been able to cope with it
on a temporary basis. I think everybody feels this has led,
unfortunately, to a great deal of confusion in the public's
mind. There has been a great misperception of what this whole
thing is about. But I think that is really a record of
bureaucratic bungling, rather than the technological problem.
However, technological problems still do remain to be solved and
demonstrated and shown. I think that is a very pressing issue.
Dr. HL_ Spencer: Allright, Dr. Radford, would you like
to call it quits on this process?
Dr . £_._ Radford: I think we ought to put a lid on it and
give our panel a chance to take a break. We are going to be
discussing this very issue tomorrow. Bill Rowe will be here to
talk about EPA's view, for example.
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SESSION V: HEALTH PROBLEMS IN NUCLEAR POWER DEVELOPMENT
Wednesday morning, March 21, 1979
Moderator: Niel Wald, M.D.
Chairman Department of Radiation Health
Graduate School of Public Health
University of Pittsburgh
HEALTH EFFECTS OF IONIZING RADIATION
By
Edward P. Radford, M.D.
ENVIRONMENTAL EXPOSURES FROM NUCLEAR FACILITIES
By
E. David Harvard
OCCUPATIONAL HEALTH EXPERIENCE IN NUCLEAR POWER
By
Robert B. Minogue
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HEALTH EFFECTS OF IONIZING RADIATION
By
Edward P. Radford, M.D.
Professor of Environmental Epidemiology
Graduate School of Public Health
University of Pittsburgh
Pittsburgh, PA
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HEALTH EFFECTS OF IONIZING RADIATION
Edward P. Radford, M.D.
Professor of Environmental Epidemiology
Graduate School of Public Health
University of Pittsburgh
In this presentation I shall restrict my remarks to the health effects of
low doses of ionizing radiation, such as those associated with most medical
uses as well as exposures occuring to workers in nuclear industries. In
general these cumulative exposures are well below 100 rem, or about 50 times
background or less.
The two effects of interest in this dose range are genetic mutations
resulting from irradiation of the germ cells in the gonads, and cancer production
from irradiation of cells distributed throughout the body. Genetic damage will
be expressed only in the offspring of the irradiated persons; for some types
of mutations these may be manifested several generations after the event.
Cancer arising from irradiation, in contrast, affects directly the individuals
exposed. Another difference between the genetic and somatic effects is that
cancer (a somatic effect or one affecting all body cells except the germ cells) is
usually life - threatening, whereas genetic effects may involve health impacts
that range from mild disturbances in specific body functions to crippling
though not necessarily life - threatening mental or physical disability.
These are some of the reasons that comparison of the health significance
of cancer induction with the genetic effects of radiation is difficult. Another
important factor is that we have virtually no direct evidence of genetic effects
on man, most of the evidence being derived from animal experiments. In the
case of cancer induction,on the other hand, we have a substantial body of
evidence obtained from study of human populations exposed to radiation for
various reasons.
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I shall not discuss the genetic effects of radiation in detail, but 1t is
important to note that whereas in the 1950's genetic effects formed the chief
basis for radiation exposure limits to the general population, since the BEIR I
report in 1972, genetic effects have been considered to be of less importance
than cancer in terms of the total public health impact of radiation. This
circumstance arises not so much because genetic risks are now perceived as less
serious than was thought, but more because the cancer risks are recognized as more
significant now than previously. The chief reason for the rise in risk estimates
for cancer is the longer follow-up of exposed populations, which has brought
to light those radiation-induced cancers with long latent periods to development.
Ionizing radiation is not only the best-documented environmental human
carcinogen, but it also induces a wider range of cancer types than any other
single known agent. We now have about 40 studies of radiation-induced human
cancer which have shown an increased risk of cancers of many kinds. For each
of the most important types of cancer induced by radiation we generally have
several separate studies, which permits comparisons of the excess cancer risk
per unit dose among these studies. By and large the different studies corro-
borate each other with respect to the particular cancer types under investiga-
tion, a circumstance that adds weight to the resulting risk estimates, especially
in view of the fact that the populations that have been studied are of different
ethnic backgrounds and the radiation exposure conditions have been different.
Current estimates indicate that about 1 to 3 percent of all cancers in
the U.S. arise from background radiation exposure, on the basis that the linear
no-threshold dose-response curve applies. One to six percent of new genetic
mutations each generation are also ascribed to effects of background radiation.
This quantitative similarity between somatic and genetic effects of background
radiation is consistent with, but does not prove, the idea that mutation of
somatic cells is an important step in cancer induction.
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The sensitivity of various tissues of the body to cancer induction by
radiation varies considerably, but no obvious generalizations emerge in regard
to this sensitivity. Some cancers at sites known to be influenced by hormonal
factors are readily induced by radiation, e.g., female breast and thyroid, but
others are not, e.g., prostate and uterus. Tissues of mesodermal origin are
generally resistant to cancer induction by radiation, but myeloid leukemia is
an exception. Nor does the induction of cancer correlate well with the normal
rate of cell proliferation; for example, the small intestine with its high
epithelial turnover rate is relatively resistant to radiation-induced cancer.
Cancers associated with suppression of the immune system are not especially
radiation-sensitive, indicative that such suppression by radiation is not
criT.ial to radiation carcinogenesis. Considerations such as these emphasize
the complexity of the disease or diseases we know as cancer.
The major radiation-induced cancers are defined by their relative sensitivity
to radiation induction, and by their natural frequency in the human population.
Rare cancers that are highly sensitive to radiation induction may be less
important that more common cancers that are only moderately sensitive to radiation.
Thus far, five types of cancer are the major factors in the cancer risk from
radiation exposure. These are cancers of the female breast, thyroid and lung,
leukemia and cancers of the alimentary tract, especially of the stomach and colon.
In addition, there are a number of cancers whose induction by radiation is well-
documented, but the risk is relatively less important. These are cancers of the
pharynx, salivary glands, liver and biliary tract, pancreas, urinary tract,
nervous system, bone, skin and the lymphomas. For an additional group of sites
the magnitude of the radiation-induced cancer risk is uncertain. These include
the larynx, ovary, uterine cervix and connective tissues. Finally there are a
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number of cancer types for which there is no evidence of an effect of radiation,
including cancers of the prostate, testis, corpus of the uterus, the mesentery and
mesothelium, and chronic lymphatic leukemia. The fact that such a large array
of types of human cancer have been shown to be induced by radiation suggests
that at high enough exposure and with long enough follow-up essentially any
cancer can be shown to be induced by radiation.
Fetuses irradiated in utero are highly sensitive to development of certain
cancers, but this increased risk persists after birth only until about the age
of puberty. After a brief radiation exposure to children or adults, granulocytic
and acute lymphatic leukemia as well as osteosarcomas (bone cancers) induced by
radiation have a short minimum latent period to appearance of the cancer of
two to five years, with eventual dying out of the effect in about 25 years. In
contrast all other radiation-induced cancers in adults have minimum latent periods
of about ten years or more, and with follow-up to the present, excess cancers
continue to appear as long as 50 years after radiation exposure.
The excess cancer risk from radiation is not necessarily proportional to
the "natural" risk, that is the relative risk model does not apply in general,
but the effect of age at irradiation or age at cancer development is very impor-
tant, an observation suggesting that radiation enhances or triggers the action
of age-specific factors related to cancer induction, factors which are widespread
in the population. Figure 1 shows a schematic way of explaining the concepts of
absolute and relative cancer risks, as well as the concept of "expression time,"
that is the time that the excess risk is present during the life of the irradiated
person. .In each graph the curved solid line is taken as the "normal" or spontaneous
cancer rate related to age. The upper graphs illustrate the change in risk for
a cancer, such as leukemia, which is expressed only for a limited time. After
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Irradiation and a minimum latent period, the canc-er rate In the irradiated popula-
tion then deviates from the spontaneous rate, but eventually returns back to it.
This difference 1n cancer rates permits us to calculate the increased lifetime
risk for that particular radiation dose, the right upper graph shows that if
the individuals are irradiated at an older age the risk may be greater, that
is, proportional to the spontaneous risk at that age. In this sense the risk
is "relative," in that it is proportional to the spontaneous rate.
The two lower graphs illustrate the case where the expression time is
assumed to last for the lifetime of the Irradiated population. As in the first
graph, upper left, irradiation is at a young age. In one case, at the left,
the risk is assumed to stay constant, in terms of an elevated cancer rate,
throughout the rest of life. In the other, on the right, the risk is elevated
in proportion to the natural cancer risk. This latter model of the cancer effect
is called the "relative risk model" and gives higher estimates of the cancer
risk than the former, called the "absolute risk model."
Age at irradiation is thus an important factor affecting radiation risk.
Figure 2 shows this effect for the Japanese A-bomb survivors. On the right,
the excess cancers per unit radiation dose is plotted against age at irradiation.
The excess for leukemia is shown as well as the excess of all cancers except
leukemia. For leukemia the risk is high in childhood, decreases to a minimum
and then increases with advancing age. A similar pattern is shown for other
cancers. On the left the risk relative to the spontaneous rate is shown. This
decreases from the childhood period and then remains relatively constant, indica-
ting that the relative risk model is appropriate.
Figure 3 shows the same type of information for a group of British patients
with an arthritic disease, ankylosing spondylitis, given deep x-ray therapy to
the spine for treatment of their symptoms. These patients have now been studied
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for over 20 years, and have been found to fjave an increase in cancers of various
types. This increase is shown plotted against age at irradiation, and also
relative to the spontaneous rate (observed over expected ). A pattern similar
to the Japanese A-bomb survivors is evident.
Recent evidence from human follow-up studies.continue to be consistent with
the dose-response relationship for cancer induction being linear without a thres-
hold; new data showing excess risk of several types of cancer are now available
in the range of doses from a few rads to 50 rad. The evidence for a linear dose-
response curve for leukemia is less certain. Women have a greater total radiation-
induced cancer risk than men because of their greater sensitivity to breast and
thyroid cancer. We have reason to suspect, moreover, that some subsets of the
population are more sensitive to cancer induction by radiation, but the significance
of such groups on dose-response data for whole populations is not known at present.
Figure 4 shows recent dose-response data on lung cancer in Chechoslovakian
uranium miners, with excess cancer per 1000 miners plotted against radiation
exposure in terms of "working level months." This unit expresses the product
of the duration of underground exposure in months, times the concentration of
daughters of radon gas present at the work sites, given in a standard unit
called the "Working Level." It is the short-lived daughters that irradiate the
bronchial tissue with alpha radiation and initiate bronchial cancers.
If you look carefully at the points at the lower doses, you will see that
they can be fitted with a curve that bends over slightly and is concave downward.
That is, lower doses are somewhat more effective per unit dose than the higher
doses. It is also of interest that recent data from other miner groups and the
Japanese"A-bomb survivors indicate cigarette smoking acts primarily to shorten
the latent period to onset of bronchial cancer, and that the combination of smoking
and radiation exposure leads to a cancer risk that is not much more than additive
for those two cancer inducers.
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Finally, I present dose-response data for the Japanese A-bomb survivors,
primarily because the information at low doses of radiation is quite extensive.
Figure 5 shows the data for leukemia in Hiroshima obtained from the Leukemia
Registry. Excess risk is plotted against the mean dose to the bone'marrow,
with a correction to take account of the greater cancer-producing effect of
neutrons compared to gamma rays. The best fit to the data in the lower dose
range is a line with a slight upward curvature.
Figure 6 is the same plot for the Nagasaki survivors, with identical
lines drawn through the data points. Because the study group in Nagasaki is
so much smaller than in Hiroshima, the error limits for Nagasaki are larger,
and thus the precise dose-response relationship is less certain, but the curve
in Figure 6 is identical with that for Figure 5.
Figure 7 shows the dose-response data for the incidence all the major
radiation-induced cancers in Hiroshima and Nagasaki for the period 1959-1970,
or from 14 to 25 years after exposure. The straight lines are weighted regression-
lines, and fit the data well.
In summary, we now have have a substantial body of human data which permits
us to estimate cancer risks from irradiation, at least under conditions similar
to those of the groups that have been studied. Our knowledge of possible genetic
effects of radiation is limited to extrapolation of results from animal studies,
but the numerical estimates of risk at low doses are similar for those of cancer.
In both cases we apply the linear, no-threshold dose-response curve, not because
the data conclusively prove its applicability, but because of experimental
support for this model and because DO other approach fits the facts better at
this time..
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FIGURE 1
FINITE EXCESS RISK
RADIATION
INDUCED
CANCERS
RADIATION
INDUCED
CANCERS
MINIMUM
LATENT
PERIOD
IRRADIATION
UJ
Sc
oc
cc
UJ
u
<
o
" ABSOLUTE RISK"
IRRADIATION
AGE
LIFETIME EXCESS RISK
" RELATIVE RISK'
MINIMUM
LATEND
PERIOD
RADIATION /
INDUCED /
CANCERS/
^
RADIATION- /
INDUCED^/
CANCERS 7S^
MINIMUM f
IRRADIATION
LATENT
IRRADIATION
AGE
Some models of the effects of radiation exposure in relation to age. In
each of the four graphs, the spontaneous cancer rate for a group is assumed
to increase progressively with age, with the total age range covering the
lifetime of the individuals exposed.
Upper graphs, Left: Irradiation at a young age, and with the excess
cancer risk increasing and then decreasing after a period of time (finite
excess risk model). After a minimum latent period, usually several years,
before any cancer excess is observed, the excess number of cases is given
by the area under the dashed line.
Right: Irradiation at an older age. The same time course of excess
cancers is observed but a greater effect is present because the older
individuals are more susceptible to radiation-induced cancer.
Lower graphs: Two possible results for radiation-induced cancers which
have an increased risk lasting for the individuals' lifetime. Left: After
the minimum latent period the cancer rate rises above but parallels the
spontaneous rate. Right: After the latent period the cancer rate increases
in proportion to the rising spontaneous rate. The former situation implies
that the excess risk does not change with the rising sensitivity to spon-
taneous development of cancer, and is sometimes referred to as the "absolute
risk" model. The latter case implies that those factors responsible for the
increasing spontaneous cancer rate are also active in enhancing the radiation.
effect, and is referred to as the "relative risk" model. We do not yet know
which of these two models may apply for those cancer types that may show a
lifetime increased cancer risk after irradiation.
-373-
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FIGURE 2
34 r
20
. 16
£
c
III
tu
c 8
RELATIVE RISK
ABSOLUTE RISK
LEUKEMIA
ALL CANCER
ALL EX. LEUKEMIA
12
10
8 1
_1
-J
I
UJ
o
u
X
Ul
0102030405060 0102030405060
AGE ATB
• Rl*k of 10O» rad ralativ* to 0-9 rad
Effect of age at radiation exposure on the subsequent cancer risk. Data
for leukemia (heavy solid lines), all cancer (light solid lines) and all
cancers except leukemia (dashed lines) for survivors of the atomic bombing
of Hiroshima and Nagasaki. Followup 1950-74. The data are plotted against
age at the time of the bombing (ATB) in 19A5.
Right graph: Excess cancer deaths per million person-years per rad for
.all exposed groups. Both for leukemia and for all cancers except leukemia
the minimum excess risk is observed in the 10-19 age group, .and rises
progressively with age, in accord with the spontaneous rate among Japanese.
Left graph: Cancer risk for the heavily exposed group (100+ rad)
relative to the risk for the low-dose group (0-9 rad), equivalent to a
control group. For all cancers, the relative risk is highest in children
and remains comparatively unchanged in adults, although for leukemia there
is a suggestion of a minimum among the 35-50 year-old group. These results
support the relative risk model at least for the effect of age at the time
of radiation exposure.
Data from: Beebe, G.W., Kato, H. and Land C.E. "Mortality Experience of
Atomic Bomb Survivors, 1950-74." Radiation Effects Research Foundation,
Life Span Study Report 8, 1977.
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FIGURE 3
29
BO
69
no of
"""deaths
I
250
fP
X
200 S
OL
ro
ft*
150 J
°u
w S
Of
50 *'
age at first treatment (years)
Effect of age at irradiation on subsequent cancer risk. Data are for
British patients with ankylosing spondylitis given x-ray treatment to
the spine and pelvis 1935-54. Follow-up to 1970. Data are plotted by
age at time of x-ray treatment; number of observed deaths along top of graph.
Closed circles and solid line, right ordinate: Excess cancer deaths
per 100,000 person-years at risk. The excess risk rises progressively
with age at exposure, in the same way that the spontaneous rate in the
general population does.
Open circles and dashed line, left ordinate: Ratio of observed number
of cancer deaths to number expected from age-specific rates for British
population. The relative risk is highest for the youngest group, but is
relatively constant for the older groups. Again the data support the
relative risk model applied to the age at irradiation.
Data of Smith, P.G. and Doll, R. Age and time-dependent changes in the
rates of radiation induced cancers in patients following a single course
of x-ray treatment. Proc. Int. Atomic Energy Agency Symposium on late
biological effects of ionizing radiation. Paper 1AEA-SM-224/711 Vienna,
1978.
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FIGURE 4
100 200 400 6C
Cumulottd txpoturt In WLM
Excess lung cancer risk from inhalation of radon daughters. Czechoslovakian
uranium miners studied from 1950 to 1973. Ordinate: Excess lung cancers/1000
miners. Abscissa: Exposure to inhaled alpha radiation in units of "Working
Level Months," a unit which takes account of the radon daughter concentration
times the number of months of exposure -during the work. Error bars represent
90% confidence limits.
Data of Sevc, J., Kunz, E. and PlaSek, V. Lung cancer in uranium miners,
and long-term exposure to radon daughter products. Health Physics 30;
433-437, 1976.
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FIGURE 5
CONFIDENCE LIMITS 80 %
(NEUTRON RBE=10)
100 200 300 400
MEAN BONE MARROW DOSE (REM)
Dose-response relationship between radiation exposure and leukemia risk,
Hiroshima atomic bomb survivors, Leukemia Registry data. Abscissa: Mean
bone marrow dose in rem, with assumption of a quality factor (RBE) of 10
for the neutron component of the exposure. Error bars are 80% confidence
limits for each point. Ordinate: Leukemia rate, cases per thousand
exposed. The straight line is fitted by eye, as is the curved line, which
appears to fit the data better. The point for the highest dose is not
included because it is probably in the dose range where cell-killing may
reduce the leukemia risk per unit dose.
Data from: Beebe, G.W., Kato, H. and Land C.E. "Mortality Experience of
Atomic Bomb Survivors, 1950-74." Radiation Effects Research Foundation,
Life Span Study Report 8, 1977.
-377-
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FIGURE 7
HIROSHIMA 1959-1970
BOTH SEXES
CONFIDENCE LIMITS 80 %
NEUTRON RBE = 5
2t
NAGASAKI 1959-1970
BOTH SEXES
0 100 200 300 400 0 100 200 300 400
MEAN TISSUE DOSE ( REM )
Dose-response relationship between radiation exposure and total cancer
incidence for both Hiroshima and Nagasaki. Data from tumor registries in
both cities, but ascertainment of cases more complete for Nagasaki than for
Hiroshima. Followup 1959-1970. Abscissa: Mean tissue dose in rem, with
assumption of a quality factor (RBE) for neutrons of 5. Ordinate: age-
adjusted cancer incidence, cases/lOOO/year. Error bars are 80% confidence
limits for each point. Straight lines through the points are weighted
regression lines.
Data courtesy of Dr. C.E, Land
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I
OJ
oo
o
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ENVIRONMENTAL EXPOSURES FROM NUCLEAR FACILITIES
By
E. David Harvard
Environmental Projects Manager
Atomic Industrial Forum
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Environmental Exposures from Nuclear Facilities
E. David Harward
Environmental Projects Manager
Atomic Industrial Forum
Presented at the
Symposium on Energy and Human Health:
Human Costs of Electric Power Generation
Pittsburgh, Pennsylvania
March 19-21, 1979
After Dr. Radford asked me to speak at this conference the
other day, I started looking for the data which I thought might
best represent the environmental radiological impact of the nuclear
power industry. I came to the realization that radiation protection
now suffers from paper proliferation the way everything else does
with the enormous quantities of data now available. At that point
I also wondered whether I had contributed to the current flood of
data in my former role of bureaucrat with the Public Health Service
and EPA. In a paper before the 1970 Annual Meeting of the Health
Physics Society, I had uttered the phrase"... It is my opinion that
some of the public relation problems the nuclear power industry is
now facing could have been lessened if early in the game detailed
data from operating nuclear power plants had been made available
to the health and scientific community for interpretation to the
public in terms of radiation dose to people."
Now hopelessly caught up in a web perhaps partially of my own
spinning, I will attempt to bring you a perspective as to the
radiological impact of the generation of electric power by nuclear
energy. None of the data I am using have originated with the nuclear
industry; it is largely from the Environmental Protection Agency,
the Nuclear Regulatory Commission and the recent draft Interagency
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Radiation Task Force Report by the Department of Health, Education
and Welfare. At the risk of involving you in a numbers game, I
feel compelled to use these data as the only way in which such an
impact can reasonably be demonstrated. Qualitative comparisons are
helpful but generally inconclusive. Both quantitative and
qualitative analyses are, of course, open to argument. I have
attempted to use data that are representative and I believe, within
the range of values that are accepted by the majority of the
knowledgeable scientific community.
I would like to show you a table that hopefully will help
place in perspective the total contribution of nuclear power
generation and its component parts to the total United States
population radiation exposure. The sources and the corresponding
cumulative doses in person-rems per year are from a table in the
recent HEW draft report of the Interagency Task Force on the
Health Effects of Ionizing Radiation. I have added two columns:
potential health effects and percent of total U.S. cancer deaths
that might be attributed to various sources of radiation using the
linear non-threshold concept. A conversion factor of 100 potential
health effects for each million person-rems was used? Please note
that I carefully use the word "potential" when speaking of health
effects throughout these remarks. From this table, perhaps one
percent of the total of 390,000 U.S. cancer deaths per year might
be statistically attributable to radiation, of which roughly half
might be natural background related and nearly half related to the
healing arts, largely from the use of diagnostic X-rays. I say
this realizing there may be certain synergistic effects that are
not yet fully understood between radiation and other substances.
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My remarks will be addressed to the nuclear power industry com-
ponent of this table which might account for some one-thousandth
of the total radiation-induced health effects to the general
public.
I would like to review the environmental radiation protection
standards and regulations that are applicable to the nuclear power
industry. Perhaps after this discussion, when you read the many
reports of federal agency overlaps in the control of radiation,
you will have a better understanding of what the problem is.
Table 2 shows the present basic U.S. radiation protection
guidance for the public developed by the former Federal Radiation
Council whose responsibilities were given to EPA with formation
of that Agency in 1970? These guides, in existence for many years,
are used by all federal agencies involved in protecting the general
public from radiation. Guides are also available for occupational
radiation exposure.
Table 3 shows the NRC objectives for light water reactor
waste treatment system design, Appendix I to 10 CFR Part 505
These guides were promulgated in 1975 after some three years of
public hearings. The NRC implements these numerical values as
operating limits in the technical specifications of the license
for each nuclear power plant in addition to reviewing the capability
of radwaste treatment systems design during the licensing process.
In addition, NRC regulates licensees according to 10 CFR Part 20,
Standards for Protection Against Radiation.4 Part 20 contains the
detailed regulations which must be followed by a licensee during
operations to assure public health and safety. Accompanied by
detailed isotopic analyses of effluents, a comprehensive environ-
mental surveillance program and reporting mechanism is provided.
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After some seven years of development, the Environment
Protection Agency in 1977 promulgated their environmental
standards for the uranium fuel cycle (40 CFR 190) which are
being implemented by the NRC.5 These are shown in Table 4.
These standards are effective December 1, 1979, except for
uranium milling operations (December 1, 1980) and krypton-85
and iodine-129 which are effective January 1, 1983. These
latter two standards (krypton-85 and iodine-129) apply generally
to the fuel reprocessing component of the nuclear fuel cycle
which, of course, is currently non-operable under U.S. policy.
Another applicable EPA standard is the regulation for
public drinking water which is shown in Table 5. This is a
regulation to be implemented by state authorities but has been
incorporated into NRC model radiological technical specifications
as guidance to NRC licensees.
Table 6 shows two EPA authorities that are potentially
of real significance. Another layer of regulation was applied
to many industries including nuclear power in the Clean Air Act
Amendments of 1977 when radiological provisions were included
for the first time. The inclusion in the amendments of radiation
was not well-known at the time but the wording of the Committee
report made it clear that it was intentional.7 EPA is now in the
process of determining how to implement this Act and certain
administrative actions must be taken by them by August, 1979.
Hopefully, NRC will be the regulating agency for this Act under
EPA auspices in the case of nuclear facilities; this appears to
be the direction things are headed. However, the Act also makes
it possible for states to control air emissions from these facili-
ties, undoubtedly a complicating factor. One state has already
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taken initial steps to control such emissions.
Finally, the Federal Water Pollution Control Act contains
provisions for providing water quality guidance to states. An
example of the regulatory complication that could result is a
recent radioactivity guide for Great Lakes water developed by
EPA and the Canadian authorities under the aegis of the Inter-
national Joint Commission.9 A radioactivity objective of one
mrem per year was written for Great Lakes water based on a con-
sumption of 2 liters per day. This objective potentially can be
used by states under FWPCA to establish water quality criteria,
thus inserting an additional regulatory layer.
Now that we have reviewed the various regulatory controls
imposed on nuclear facilities, let's look at some of the estimated
radiological impacts associated with the various components of
the nuclear fuel cycle listed in Table 7. These are listed in
their general order of occurrence during the operation of the
fuel cycle. You can see that over half of the impact might result
from fuel reprocessing which, as I mentioned earlier, is not
operating at the present time. The next highest impact results
from the mining of uranium, primarily through the release of radon.
Radon also is the major emission from the tailings resulting from
milling operations. If one uses the linear concept, the potential
health effects for each 800 MWe reactor and its part of the sup-
porting total fuel cycle are about 0.056 per year although this
number probably needs additional scrutiny... It might be slightly
higher. If one extrapolates this to the current number of operating
nuclear plants in the U.S., there is very close agreement with the
HEW draft report table which indicated some 5.6 potential health
effects in 1978.
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It is of interest to discuss several specific radionuclides
resulting from the production of nuclear power because of their
unique properties and characteristics. The first radionuclide
in this category is radon-222, a naturally occurring radioactive
gas having a half-life of 3.8 days. It has been estimated that
some 100 million to 240 million curies are released to the U.S.
atmosphere each year, normally through the earth's crust. Many
factors influence the exposure of people to radon. Homes built
of concrete, stone or brick can have concentrations of radon three
to seven times greater than typical outside air. Things such as
agricultural practices, closing of windows in homes, home insula-
tion, whether the home uses natural gas or ,not (which contains
radon) may influence the levels of radon to which one is exposed
Dr. Leonard Hamilton of Brookhaven National Laboratory"has estimated
incremental doses from the fuel cycle using doses to the bronchial
epithelium reported by the United Nations Scientific Committee on
the Effects of Atomic Radiation (UNSCEARf2 He has estimated that
the one year's operation of a 1,000 MWe nuclear power plant at a
capacity factor of 65 percent would result in an increased dose
to the bronchial epithelium of less than one-thousandth of a
mrem/year (2.5 x 10 ) from the mining and milling of uranium to fuel
the plant. If one follows through Dr. Hamilton's assessment, the
risk of developing lung cancer from naturally emitted radon is
about 1.5 x 10 times greater than developing lung cancer from
radon resulting from the fuel cycle.
These data were presented before an NRC Atomic Safety and
Licensing Board at a hearing on the Perkins Nuclear Station in
May, 1978. The Board ruled that the release and impact of
radon-222 associated with the uranium fuel cycle were insignificant
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in striking the cost-benefit balance for the Perkins Station.
Nevertheless, there does remain some concern about the national
average impacts of radon resulting from man's disturbances of the
earth's surface from various activities such as mining of minerals
EPA did not include radon in their uranium fuel cycle standard
mentioned earlier. However, that Agency is, evaluating radon from
the standpoint of the Clean Air Act Amendments and the story on
that still remains to unfold. It should be mentioned that the
radiological impacts within close proximity of uranium mills are
of more concern because of the presence of tailings, and consider-
able effort is underway by NRC to control this source of radiation
exposure through stabilization of the tailings. I did not have
available to me a new report which should be issued shortly by
NRC which was prepared by Oak Ridge National Laboratory!3 This
report will assess the radiological impact of radon-222 from
uranium mills and other sources and should be an important reference
on this subject and may clarify some of the uncertainties in this
area.
Another radionuclide of some interest is carbon-14 which is
produced in nuclear reactors, largely in the fuel, but also in
primary coolant. This nuclide may be potentially of greater dose
significance than krypton-85 for which EPA has established a
standard. However, since it is largely released during fuel
reprocessing which is not now being performed, there would be
time to more fully evaluate control techniques^. Although there
is no present cost-effective control technology for carbon-14
removal, it is belived that certain existing krypton-85 recovery
systems can be used for its removal. There has been some concern
about the cost-effectiveness of krypton-85 control technology.
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However, this doubt may completely vanish if these systems are
shown to have the capability for removing carbon-14 which is of
potentially greater dose significance. Carbon-14 and radon-222
achieve their importance despite low per-capita doses largely
through the exercise of multiplication of these extremely small
doses by billions of people over long periods of time. Some
people believe it is necessary to consider these materials for
long periods because today's activities in the fuel cycle result
in continuing releases of radon-222 and the persistance of the
long-lived carbon-14.
I would like to leave with you some comments on the high-level
radioactive waste issue. Although Dr. Rowe will be addressing
this subject in depth later in the program, I think those aspects
relating to the radiological impact should be mentioned in this
review of nuclear facility impacts. EPA is now in the process of
completing a detailed impact analysis of high-level waste disposal
in connection with the development of an environmental radiation
standard. To my knowledge, it is the most detailed analysis
undertaken to date. They have evaluated the total radiation
impact over a period of 10,000 years in a geological formation
under very pessimistic assumptions and have found that there
might be a potential 100-1,000 health effects as a "high value"
over that period of time, with a "low value" four orders of
magnitude less. These were the numbers reported to the House
Subcommittee on Energy and the Environment by EPA staff in
16
January. Discussions with EPA staff personnel since that time
have indicated that their "high value" is probably closer to
50-100 potential health effects over 10,000 years or somewhere
in the order of one one-hundredth of a health effect per year.
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Furthermore, EPA has reported what everyone with a knowledge of
Plutonium behavior has known, that plutonium is highly immobile
in geologic formations and, as such, contributes less than one
percent to the total health impact of high-level waste disposal.
Thus, one of the most rigorous analyses available has shown that
geological storage of high-level wastes can be achieved safely
even under adverse conditions, although all efforts will be made
to choose the safest site possible. It appears that the major
remaining hurdle is to somehow get the U.S. waste disposal
project moving in a forward direction.
In closing, I would like to state that much has been done
to make nuclear power safe from an environmental and health
standpoint. The potential impacts are small and indeed at
least as small as other electrical energy alternatives. In
this connection, it is my opinion that comparative risk analyses
of the various energy options should be continued and refined.
From my experience in environmental health, I believe that
nuclear will come out well. However, whatever options are
chosen to generate electricity, I am convinced that this nation
will need the energy and need it badly in the near-term as well
as the long-term and is in every sense of the word a public
health benefit. The continued protection of the public health
in the process is uppermost as a priority, but the general
welfare of the public is also important, and that is coupled with
the availability of energy at a reasonable cost. I believe the
health impacts of all viable forms of energy can be made acceptable,
but without the necessary energy available, many people both here
and abroad may suffer needlessly.
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,
u>
IABLLJL
U,S, GENERAL POPULATION EXPOSURE ESTIMATES - 1978
PERSON-REMS PER YEAR POTENTIAL PERCENTAGE OF
SOURCE (WHOLE BODY) _ HEALTH EFFECTS TOTAL CANCER DEATHS
NATURAL BACKGROUND 20,000,000 2,000 0,5
TECHNOLOGICALLY ENHANCED L 000, 000 100 0,025
HEALING ARTS 18,000,000 1,800 0,46
NUCLEAR WEAPONS
FALLOUT 1,000,000-1,600,000 100-160 0,025-0,04
WEAPONS DEVELOPMENT, „,.,_ ,,. _
TESTING AND PRODUCTION 165,000 16,5 0,004
NUCLEAR ENERGY 56,000 5,6 0,0014
CONSUMER PRODUCTS 6,000 0.6 0,00015
POTENTIAL HEALTH EFFECTS TOTAL 4,023-4,083
NUMBER OF ANNUAL CANCER DEATHS 390,000
ADAPTED FROM DRAFT REPORT OF THE WORK GROUP ON RADIATION EXPOSURE REDUCTION,
INTERAGENCY TASK FORCE ON IONIZING RADIATION
-------
TABLE 2
FEDERAL RADIATION COUNCIL
w
RADIATION PROTECTION GUIDES FOR GENERAL POPULATION
INDIVIDUALS IN GENERAL POPULATION 500 MREM/YEAR
SUITABLE SAMPLE OF EXPOSED POPULATION
NEAR A RADIATION FACILITY 170 MREM/YEAR
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TABLE 3
NUCLEAR REGULATORY COMMISSION REGULATIONS
APPENDIX I TO 10 CFR PART 50
NUMERICAL GUIDES FOR DESIGN OBJECTIVES AND LIMITING CONDITIONS FOR OPERATION
FOR MEETING ALARA IN EACH LIGHT WATER REACTOR EFFLUENTS (APPLIED ABOVE
BACKGROUND)
>, LIQUID EFFLUENTS
f>
? DOSE TO TOTAL BODY FROM ALL PATHWAYS 3 MREM/YEAR
DOSE TO ANY ORGAN FROM ALL PATHWAYS 10 MREM/YEAR
NOBLE GAS EFFLUENTS (AT SITE BOUNDARY)
GAMMA DOSE IN AIR 10 MRAD/YEAR
BETA DOSE IN AIR 20 MRAD/YEAR
DOSE TO TOTAL BODY OF AN INDIVIDUAL 5 MREM/YEAR
DOSE TO SKIN OF AN INDIVIDUAL 15 MREM/YEAR
RADIOIODINES AND PARTICULATES
DOSE TO ANY ORGAN FROM ALL PATHWAYS 15 MREM/YEAR
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TABLE 4
ENVIRONMENTAL PROTECTION AGENCY GENERAL
ENVIRONMENTAL STANDARD FOR THE URANIUM FUEL CYCLE
40 CFR PART 190
DOSE TO TOTAL BODY OF AN INDIVIDUAL 25 MREM/YEAR
DOSE TO THYROID 75 MREM/YEAR
DOSE TO ANY OTHER ORGAN 25 MREM/YEAR
TOTAL QUANTITY OF RADIOACTIVE MATERIALS TO
GENERAL ENVIRONMENT PER GIGAWATT OF ELECTRICAL
ENERGY TO BE LESS THAN:
50,000 CURIES OF KRYPTON-85
5 MILLICURIES OF IODINE-129
0,5 MILLICURIES OF PLUTONIUM-239 AND
OTHER ALPHA-EMITTING TRANSURANIC
RADIONUCLIDES WITH HALF-LIVES
GREATER THAN ONE YEAR
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TABLE 5
ENVIRONMENTAL PROTECTION AGENCY REGULATIONS
FOR RADIONUCLIDES IN DRINKING WATER
MAXIMUM CONTAMINANT LEVELS
COMBINED RADiuM-226 AND RADiuM-228
GROSS ALPHA ACTIVITY
(EXCLUDING RADON AND URANIUM)
AVERAGE ANNUAL CONCENTRATION FROM
MAN-MADE RADIONUCLIDES (EXCLUDING ALPHA)
SHALL NOT PRODUCE DOSE TO TOTAL BODY OR
ANY INTERNAL ORGAN GREATER THAN
5 PCl/LITER
15 PCl/LITER
MREM/YEAR
(BASED ON 2 LITER PER DAY WATER INTAKE)
TABLE 6
OTHER EPA AUTHORITIES
WHICH IMPACT ON NUCLEAR FACILITIES
• CLEAN AIR ACT AMENDMENTS OF 1977
• FEDERAL WATER POLLUTION CONTROL ACT
GUIDANCE.TO STATES FOR WATER QUALITY CRITERIA
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TABLE 7
ESTIMATED U,S, POPULATION 100 YEAR
DOSE COMMITMENT PER 800 MWE-YEAR
NUCLEAR FUEL CYCLE COMPONENT
MINING
MILLING
UFg CONVERSION
ENRICHMENT
U02 FUEL FABRICATION
LIGHT WATER REACTOR EFFLUENTS
IRRADIATED FUEL STORAGE
REPROCESSING
TRANSPORTATION
WASTE MANAGEMENT
OFF-SITE TOTAL BODY DOSE
COMMITMENT (MAN-REMS)
110
39
6,9
0,022
0,48
61
0,0035
330
1,1
8,9
INDUSTRY TOTAL
558 MAN-
0,056
OR
_OTENTIAL HEALTH
EFFECTS PER 800 FiWE
LANT PER YEAR
FROM NRC STAFF RESPONSE TO HONICKER PETITION
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REFERENCES
1. U.S. Department of Health, Education and Welfare. Draft
Report: Interagency Task Force on the Health Effects.of
Ionizing Radiation, February, 1979.
2. The Effects on Populations of Exposure to Low Levels of
Ionizing Radiation. Report of the Advisory Committee on
the Biological Effects of Ionizing Radiations. National
Academy of Sciences National Research Council. November
1972. (BEIR I).
3. Background Material for the Development of Radiation
Protection Standards" Report No. T~. Federal Radiation
Council. May 13, 1960.
4. Code of Federal Regulations. Title 10. Energy (Regulations
of the Nuclear Regulatory Commission). Revised as of
January 1, 1979.
5. Code of Federal Regulations. Title 40. Protection of
Environment. (Regulations of the Environmental Protection
Agency). Revised as of July 1, 1977.
6. National Interim Primary Drinking Water Regulation. EPA-
570/9-76-003. Office of Water Supply. U.S. Environmental
Protection Agency. 1977.
7. Conference Report. Clean Air Act Amendments of 1977. U.S.
House of Representatives Report No. 95-564. August 3, 1977.
8. Clean Water Act of 1977. Public Law 95-217, December 27,
1977.
*
9. Federal Register, Volume 42, No. 65 - Tuesday, April 5, 1977,
pp. 18171-18172. Department of State notice of report of the
International Working Group on Radioactivity Objective for
the Great Lakes Water Quality Agreement.
10. Nuclear Regulatory Commission Response to the Jeannine
Honicker Petition for Emergency and Remedial Action: An
Overview Regarding Radiation Exposure as Related to the
Nuclear Fuel Cycle. 1978.
11. Testimony before the Nuclear Regulatory Commission Atomic
Safety and Licensing Board in the matter of: Duke Power
Company, Perkins Nuclear Station, Docket Nos. STN 50-488,
50-489 and 50-490. May, 1978.
12. Sources and Effects of Ionizing Radiation. United Nations.
Scientific Committee on the Effects ot "Atomic Radiation.
1977 (Report to the General Assembly).
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13. Travis, C.C. et al. A Radiological Assessment of Radori-222
Released from Uranium Mills and Other Natural and Technologi-
cally Enhanced Sources. NUREG/CR-0573. Oak Ridge National
Laboratory report for U.S. Nuclear Regulatory Commission.
14. Public Health Considerations of Carbon-14 Discharges from
the Light-Water-Copied Nuclear Power Reactor Industry.
Technical Note ORP/TAD-76-3.U.S. Environmental Protection
Agency, July, 1976.
15. Final Environmental Statement: 40CFR190 Environmental
Radiation Protection Requirements for Normal Operations
of Activities in the Uranium Fuel Cycle. EPA 520/4-76-016,
U.S. Environmental Protection Agency, Office of Radiation
Programs. November 1, 1976.
16. Testimony before the Subcommittee on Energy and the
Environment, Committee on Interior and Insular Affairs,
U.S. House of Representatives, January 25, 1979. Dr.
James E. Martin and Mr. Daniel J. Egan, Jr., Waste Environ-
mental Standards Program, Environmental Protection Agency.
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OCCUPATIONAL HEALTH EXPERIENCE IN NUCLEAR POWER
By
Robert B. Minogue, Director
Office of Standards Development
and
Abraham L. Eiss, Technical Assistant to the Director
Division of Engineering Standards
Office of Standards Development
U. S. Nuclear Regulatory Commission
Washington, D. C. 20555
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Occupational Health Experience in Nuclear Power*
Robert B. Minogue, Director
Office of Standards Development
and
Abraham L. Eiss, Technical Assistant to the Director
Division of Engineering Standards
Office of Standards Development
U. S. Nuclear Regulatory Commission
Washington, D. C. 20555
Introduction
This symposium is addressing a question of great national concern:
"What are the public and occupational health aspects of relying on coal
and nuclear power for the generation of electricity?"
This morning's session is devoted to health problems in nuclear
power. Our earlier speakers (Dr. Radford and Mr. Harward) have
presented information on how radiation exposures are translated into
health effects and about the public health effects of nuclear power.
I have been asked to discuss occupational health experience in nuclear
power from the perspective of a regulator.
In considering occupational health aspects of any fuel cycle, one
should address all activities that must take place to obtain the fuel,
generate the power, and dispose of any waste materials. In nuclear power,
the principal activities are uranium mining, ore processing or milling,
fuel fabrication, power generation, and fuel storage and ultimate disposal,
*Presented at the Symposium on Energy and Human Health: Human Costs of
Electric Power Generation, sponsored by the University of Pittsburgh
and the Ohio River Basin Energy Study, held in Pittsburgh, Pennsylvania
on March 19-21, 1979.
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In nuclear power, we can further divide occupational health effects
Into two categories: radiation hazards and more conventional non-radiological
effects. Many of the non-radiological risks of the work place are comparable
regardless of the method used for power generation. Examples include
scalding* electrocution, exposure to toxic chemicals, falls from ladders
or scaffolds, and dropping of heavy loads. Others are not comparable.
For example, most of the non-radiological hazards from the mining and
transportation of any fuel are basically a function of the tonnage handled
and are therefore greater for fossil-fuel than for nuclear energy generation.
Exposure to airborne radioactivity in uranium mines has no direct counterpart
in fossil power generation, just as black lung in coal miners has no analog
in the nuclear area.
Since we in the Nuclear Regulatory Commission are much more concerned
with radiological health and because the public interest and mine as well
is largely focused on the same area, I plan to spend most of my time this
morning discussing occupational radiation exposures to workers in the
nuclear field.
10 CFR Part 20 (Reference 1) contains NRC's standards for protection
against radiation. Under this rule, whole body doses are limited to
1.25 rem per calendar quarter unless the licensee has determined a worker's
lifetime accumulated occupational dose. In this case, the whole body dose
is limited to 3 rem per calendar quarter provided that the worker's
accumulated dose does not exceed 5(N-18) rems, where "N" is the worker's
age (SLIDE 1). You will recognize this as the basic Federal Radiation
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Council standard, now under the cognizance of the Environmental Protection
Agency (EPA). Last month NRC published (Reference 2) a proposed rule
that woule eliminate the 5(N-18) dose averaging formula. The quarterly
dose limit would be 3 rem but the annual limit would be 5 rem in all
cases.
More important than these limits is the requirement that all doses
must be As Low As Reasonably Achievable (ALARA). This basic concept
of ALARA is recognized in all radiation standards — whether they are
set by international bodies such as the International Commission on
Radiological Protection (ICRP) or U. S. authorities.
In nuclear power plants the ALARA requirement translates Into a
broad program of actions and controls all directed toward reducing worker
exposure. A good ALARA program Includes such things as plant design
and layout to facilitate maintenance; requirements on fuel cladding, water
treatment and purification systems to inhibit corrosion or reduce deposition;
controls on access to radiation areas; worker training; radiation surveys;
use of remote and semi-remote maintenance equipment; local decontamination
of surfaces; special ventilation systems; protective clothing, etc.; etc. --
in short a complex wide-ranging exposure control program.
In fact, ALARA programs are effective in these highly disciplined
engineering activities and very few workers receive doses that approach
the limits. The next slide (References 3 and 4)(SLIDE 2) presents some
recent figures that show where we are. It is obvious that nuclear power
plants represent the major source of occupational exposure associated
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with energy generation -- both in the number of workers affected and 1n
the average dose received. Workers at fuel fabrication and processing
facilities also receive significant doses, although they average less than
one-third those at nuclear power plants. Perhaps as Important as the
average dose is the distribution of actual dose received by individuals.
This is shown for workers at power reactors and fuel facilities tn the
next slide (Reference 3)(SLIDE 3). From this one might conclude that
there is no cause for concern since of the tens of thousands of workers
In the nuclear field only a few hundred approach the exposure limits of
NRC's regulations.
However, I believe it Is safe to say that most of us here do not
accept this view. Recent studies of the incidence of cancer among workers
exposed to radiation point to the possibility that the limits may be less
conservative than previously thought. While the data are not conclusive
on the quantitative effects of low-level radiation, I am personally
convinced that 1n the range of occupational exposures, say from 100 mllllrem
to 5 rem per year, there 1s no threshold for radiation effects. We do
not know the precise relationship between dose and risk at low levels
of radiation. However, I believe it 1s wise that public health officials
concluded some years ago that there is a risk, and based exposure standards
on assumptions of a linear non-threshold dose response curve. The perception
that no radiation dose level Is without risk is a key concept underlying ALARA.
Therefore, the regulatory requirement that exposures be kept as low as
reasonably achievable 1s of great importance. Simply stated, NRC's aim is
to eliminate unnecessary exposure and limit necessary exposures.
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The ALARA control program can stress reduction of exposure to Individuals
or total population exposure (Zdose x persons exposed) or both. The regulatory
approach to achieving ALARA depends on what relationship between exposure
and risk 1s assumed. This sketch, which was prepared by Dr. K. I. Morgan
for recent testimony before a U. S. Senate Subcommittee, may help me to
Illustrate some of the possibilities. (SLIDE 4)(Reference 5). It Illustrates
approaches to extrapolating data from observed effects on those exposed at
Hiroshima and others who have received high radiation doses, and from
limited ep1dem1olog1cal studies, animal studies, studies of the Interaction
of radiation with body tissues, and observations on behavior of radioactive
material within the body. Beginning with data at high radiation levels,
the curves show extrapolation down to lower exposures assuming three possible
relationships. If the relationship 1s linear (Curve A), any reduction in
total man-rem would be accompanied by a reduction 1n health effects. If it
Is subHnear (Curve B), reduction of Individual doses at the higher levels
would yield health benefits even If this were accompanied by some Increase 1n
total man-rem. If, however, the relationship Is superllnear (Curve C), the
greatest health benefit would be achieved by reducing total man-rem rather
than Individual doses. And, one would expect for Curve C as well as Curve A,
the so-called linear hypothesis, 1n the case of at least some activities, to see
an increase in health effects if the exposure limits were lowered since this
could result 1n more individuals being exposed and, as a result of expected
inefficiencies, more total man-rem. This would likely be the case in some
nuclear power plant activities such as maintenance and inservice inspection;
whereas one would expect little or no Increase in total worker dose in
the field of nuclear medicine.
-404-
-------
In effect, the NRC's regulatory stragety reflects an assumption
of a linear or superllnear relationship. That is we are encouraging the
reduction of both individual doses and total man-rem.
From the data I showed earlier (SLIDE 2), it is obvious that
the greatest room for improvement is in nuclear power plant operation
since it accounts for more than 902 of the total dose in the nuclear
power cycle. Also, the average exposure 1s three times that in any other
stage of the cycle. As more reactors have come on line, the total number
of man-rem has increased rapidly - from 14,000 in 1973 to 21, 000 in 1975,
and over 32,000 in 1977, the latest year for which data have been analyzed.
The exposure data can be expressed in man-rem per megawatt year
(SLIDE 5)(data from Reference 3). This has been relatively constant
with a small increase in exposure at boiling water reactors (BWRs)
being balanced by a decrease at pressurized water reactors (PWRs).
The radioactivity in nuclear power plants is initially confined
to the core - that is, within the fuel elements housed inside a shielded
pressure vessel. With time two things occur. First, the intense neutron
radiation in the core converts atoms of material in the structure and 1n
the coolant to radioactive species. A certain fraction of both these is
carried outside the pressure vessel in the coolant to other parts of
the reactor system where they tend to be deposited on whatever surfaces
are present. Second, some percentage of the fuel elements will develop
small leaks with time, and some of the radioactive fuel and fission product
atoms in these fuel elements will also find their way into the coolant stream
and will be deposited on the reactor system surfaces. In general, the
more surface area exposed to the coolant in any reactor component, the
more important a radiation source it will become. Thus steam generators
-405-
-------
and other heat exchangers that may have thousands of square feet of surface
area are particularly likely to contain large amounts of radioactive material.
Dem1neral1zer resin beds used to maintain the purity of water in the
core also become a major source of radioactivity. These highly
radioactive components are a key element 1n occupational exposure.
Close approach by workers to perform maintenance or Inspection could
result 1n significant exposure.
All of this was well known and was taken Into account by the
designers and builders of nuclear power plants. The areas of high
radioactivity were shielded; and those areas routinely occupied by
plant personnel such as the control room were further shielded and/or
were located as far as possible from the major sources of radiation.
The next slide (SLIDE 6)(Reference 3) listing the percentage of
personnel dose by work function shows this. Routine operation and
refueling were recognized as important by the plant designers and the
ALARA approach was generally applied. Therefore, the doses received
1n performance of those functions have been constant and relatively
smal1.
In the case of routine maintenance (for example, the repairing
of Instruments and repacking of valves), control of exposures by the design
of nuclear power plants and by careful practice proved more difficult.
As a result, for several years this activity was the greatest contributor
to occupational exposure 1n nuclear power plants. By the mld-1970's
-406-
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Industry and regulators alike recognized the need for action. Consequently,
by Improving shielding, equipment* and procedures, industry has substantially
reduced exposures from routine maintenance.
Exposures from three activities, however, have doubled in the past
few years. These are special maintenance (now the greatest contributor
to occupational exposure), inservice Inspection, and waste processing.
There have been several occurrences at nuclear power plants that
required special maintenance activities. For example, when 1n 1974 cracks 1n
stainless steel pipes were observed at the Dresden nuclear station, the
NRC ordered all operating BWRs to be shut down for inspection of similar
piping. Cracks were found at several other reactors. The affected piping
had to be repaired or replaced. And in each case the workers involved in
the Inspection and repair received exposures.
Pressurized water reactors have had a history of corrosion-related
failures 1n the steam generators. This has resulted in the need for
workers to plug failed tubes and to remove some tubes for study. In
addition, this will shortly result in the full replacement of steam
generators in at least four units at two plants. Surry Unit 1 is
already shut down for this purpose. The extent of these failures
appears to have been unanticipated by the designers. They have been
one of the factors that caused the NRC to increase the required frequency
and extent of inservice inspections; this in turn has contributed to
the doubling of exposure from inservice inspection.
-407-
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I mentioned that at least two utilities are planning to replace
steam generators. Although the principal driving force for these
replacements is economic, an important consideration is minimizing
radiation exposure to workers at those plants. At the Surry plant,
for example (SLIDE 7)(Reference 6), steam generator maintenance accounted
for more than 60% of all radiation exposure during 1977. The comparable
figure was 40% in 1975 and 1976 and only 6% in 1974, which was before the
problems had been observed. The total dose related to steam generator
maintenance had risen to 1400 man-rem in 1977. The plant's owners
estimate that replacement of the steam generators in both reactors at
Surry will result in about 4300 man-rem total exposure. If this number
is correct and it has the desired effect of eliminating exposures from
steam generator maintenance, the payback time for that 4300 man-rem dose
will be about 3 years. Doses not suffered after that time will be the
"benefit" of the steam generator changeover. The replacement is therefore
claimed to be consistent with ALARA principles.
The NRC staff is taking a hard look at all the proposed activities
involved in the steam generator replacements to make sure that all
possible sources of exposure have been taken into account in the planning
and analyses and that the worker dose due to the replacement is in fact
ALARA.
The increase in worker exposure from waste management resulted directly
from an NRC decision in 1975 to establish ALARA guidelines for effluents
-408-
-------
released from nuclear power plants. These guidelines were issued as
Appendix I to Part 50 of the regulations (Reference 1). In order to
meet the Appendix I requirements, nuclear power plant operators have had
to retain more radioactive waste within the plant for longer periods; hence
the increase in worker exposure.
Although the examples I have given are from our experience with
nuclear power plants, NRC's approach to occupational exposure and its
use of the ALARA concept applies to all the facilities and activities
that we regulate. As the earlier slide indicated, exposures are
relatively low at the fuel preparation and fabrication stages and, since
we have no active licensed reprocessing facilities in this country at
present, there are no exposures associated with that activity. In nuclear
power plants, the principal radiation hazard is exposure of the body
or parts of the body from an external source. In some fuel cycle
activities, a second potential hazard exists to a much greater degree
than in nuclear power plants; that is, inhalation or ingestion of
radioactive particles into the body by breathing or swallowing fine
particles dispersed in the air. This is of particular concern in fuel
facilities processing plutonium. In these facilities special precautions
are taken, including isolation of the material in glove boxes or similar
enclosures, continuous monitoring, and the use of special clothing and
respirators.
-409-
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Another problem that I would like to mention is how to control
exposures to workers employed at more than one facility during a quarter.
NRC deliberately places the burden of controlling access, monitoring workers.
and reporting exposures at a facility on the facility licensee. This,
however, does not take into account employees who moonlight on a second
job or who may leave one employer and go to work for another within the
same quarter. The records of each employer may show that the worker's
exposure is within acceptable limits; but the sum of all the exposures
may show that the worker has been exposed beyond the limits.
The Commission is now considering issuing a rule that would require
licensees to control total occupational dose for workers at their
facility. The licensee would be required to get from workers a statement
of exposure from outside sources during the quarter. Each terminating
worker would be furnished, on request, an estimate of the doses received.
The worker could then make this available to his next employer to help
ensure that he is not overexposed.
The Department of Health, Education, and Welfare (HEW) recently
published the data presented in the next two slides (Reference 7)
(SLIDES 8 and 9). These data show that the radiation exposure received
by workers and the public from nuclear power 1s a small fraction of
the total received from other sources. Nevertheless, we believe that
any exposure may result in some risk and accordingly try to reduce
exposure to the lowest levels reasonably achievable.
-410-
-------
Occupational exposure to radiation is a health hazard. As with
other public health hazards that cannot be completely eliminated, a
judgment must be made as to what level of exposure is acceptable.
Affected workers must have a basis for informed acceptance, that is,
workers should be aware that risks exist and of the extent of those
risks when they accept employment at nuclear facilities just as workers
at mines, steel mills, chemical plants, and so on should be aware of
the different risks facing them in their employment. Open discussion
of these risks, including meetings such as this, helps to contribute
to the informed judgments that must be made.
I would like to conclude by responding to a question that has been
asked several times of late; that is, In light of the current uncertainty
regarding the health effects of low-level radiation exposure, why doesn't
the NRC reduce the existing permissible radiation dose limits?
It is important to understand that dose levels such as the 5 rem per
year standard for workers, as used in regulatory practice, are upper
limits of permissible doses to individuals which, if exceeded, set off
a chain of regulatory actions such as investigations, reports, mandated
corrective actions, and possibly penalties. These levels should not be
taken as acceptable or safe in themselves; that is, a person is not in
immediate danger if he receives slightly more than the permissible level,
nor is he perfectly safe from adverse effects if he receives slightly
less than the permissible level.
-411-
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Radiation dose standards, as applied by the NRC, are more correctly
characterized as a broad range of radiation control measures intended
to assure that actual doses received by individuals remain far below the
prescribed permissible dose limits. Experience has shown that these control
measures have been effective in keeping occupational exposures well
below the limits.
Even so, we have noted that the total collective dose to workers
in NRC-licensed activities has been steadily increasing during the past
few years. Further, we are aware of recent health studies that raise a
question as to whether current estimates of health effects are as
conservative as previously assumed. Because of these two points, we
have initiated several actions aimed at tightening up our radiation
standards to further reduce the collective dose.
We have proposed a rule change that would eliminate the special
provision that currently allows some workers to receive as much as
12 rem per year. We are in the final stages of a rule change that
would provide more effective control over doses received by workers who
move from one licensed facility to another and those who work at more
than one licensed facility at the same time. We are considering a rule
change that would strengthen our commitment to the "As Low As Reasonably
Achievable" (ALARA) concept for occupational exposures.
The NRC staff is also in the process of issuing a series of regulatory
guides to describe acceptable ALARA techniques for different types of
licensed activities and to help achieve better radiation exposure control.
-412-
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We believe that it is these types of regulatory standards actions
that will be most meaningful, in a practical sense, in reducing radiation
exposures. Lowering of the existing permissible dose limits is also
under consideration. However, by itself, such an action may not be
as effective as the tightening of radiation control measures discussed
above.. In fact, for some regulated activities lowering the limits might
be counterproductive, that is, it might increase the collective dose.
With respect to the permissible dose levels, we are currently
cooperating with EPA in its development of Federal guidance on
occupational exposures. We anticipate joint participation with EPA
and OSHA in a public hearing to be held later this year on the adequacy
of the present standards.
In summary, we are taking action to tighten up our regulatory
requirements to further reduce occupational exposures. We have not
concluded that the evidence presently available indicates an immediate
need to lower the present permissible dose levels; but we are, along
with EPA and OSHA, examining the adequacy of these present standards.
-413-
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REFERENCES
1. Code of Federal Regulations, Title 10 - Energy, Chapter I - Nuclear
Regulatory Commission, revised as of January 1, 1978, Washington,
D. C., U. S. Government Printing Office (1978).
2. 44 FR 10388. Federal Register. Volume 44, No. 35, February 20, 1979.
3. "Occupational Radiation Exposure, Tenth Annual Report, 1977,
NUREG-0463, U. S. Nuclear Regulatory Commission (1978).
4. EPA data from report to be published.
5. K. Z. Morgan, "Radiation Induced Cancer in Man", presented to the
Subcommittee on Energy, Nuclear Proliferation and Federal Services,
U. S. Senate, March 6, 1979.
6. Data compiled by NRC staff.
7. Summary of Work Group Reports of the Interagency Task Force on
Ionizing Radiation, Department of Health, Education and Welfare,
February 27, 1979.
-414-
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SLIDE 1
NRC REGULATIONS LIMITING RADIATION DOSE
Ln
I
1.25 REM/CALENDAR QUARTER
OR
3 REM/CALENDAR QUARTER
IF ACCUMULATED DOSE IS KNOWN TO BE
<5(N-18) REM
(N = WORKER'S AGE)
-------
SLIDE 2
RADIATION EXPOSURE OF U.S. NUCLEAR FUEL CYCLE WORKERS
NUMBER OF WORKERS MEAN WHOLE BODY COLLECTIVE
I
-O-
/-IVs 1 1 V 1 1 1
URANIUM MILLS^/
URANIUM ENRICHMENT 2/
FUEL FABRICATION AND
PROCESSING ^
NUCLEAR POWER PLANTS-^
TOTAL
300
7,471
11,496
71,904
EXPOSED
100
5,664
7,004
44,233
L^VJOL. rv/rt i i titShJi.
EXPOSED (REM)
0.050
0.070
0.246
0.740
MAN-REM
5
400
1,725
32,731
NRC LICENSEE DATA FOR 1977.
EPA ESTIMATES FOR 1975.
-------
SLIDE 3
DISTRIBUTION OF WORKER EXPOSURE IN 1977
POWER REACTORS
FUEL FABRICATION AND PROCESSING
DOSE RANGE
REM
NOT MEASURABLE
MEASURABLE BUT
<0.10
0.10-0.25
0.25 - 0.50
0.50 - 0.75
0.75-1.0
1-2
2-3
3-4
4-5
>5
NUMBER OF
WORKERS
27,671
15,523
6,750
5,179
3,300
2,500
6,174
2,838
1,130
569
270
PERCENT OF THOSE
RECEIVING
MEASURABLE DOSE
—
35.0
15.0
12.0
7.0
6.0
14.0
6.0
3.0
1.0
0.6
NUMBER OF
WORKERS
4,492
4,533
1,057
571
315
179
205
91
28
25
0
PERCENT OF THOSE
RECEIVING
MEASURABLE DOSE
—
65.0
15.0
8.0
4.0
3.0
3.0
1.0
0.4
0.4
0.0
PERCENTS DO NOT ADD TO 100 DUE TO ROUNDING.
-------
3D
rn
PERCENT INCREASE IN CANCER RISK
p
b
p
CO
p
CO
en
8 M
CO o
m
O
z
N
Z
O
DO
O
00
o
o
o
O
ro
00 ->
CO
*
o
o
N —
23
So
O
oH
oz
oO
O Tl
3JO
mo
O
Tl
-------
SLIDE 5
AVERAGE MAN-REM/MW-YR
4.0
111
cc
3.0
2.0 -
1.0
0
1969
1970
1976
-------
SLIDE 6
PERCENTAGES OF PERSONNEL DOSE BY WORK FUNCTION
I
.p-
o
I
WORK FUNCTION
REACTOR OPERATIONS
AND SURVEILLANCE
ROUTINE MAINTENANCE
IN-SERVICE INSPECTION
SPECIAL MAINTENANCE
WASTE PROCESSING
REFUELING
1974
14.0%
45.4%
2.7%
20.4%
3.5%
14.0%
PERCENT OF DOSE
1975 1976
10.8%
52.6%
3.0%
19.0%
6.9%
7.7%
10.2%
31.0%
6.0%
40.0%
5.0%
7.9%
1977
1 0.6%
28.9%
6.6%
41.4%
5.9%
6.6%
-------
SURRY IN-PLANT DOSES
ALL OPE RATIONS
1
-O
YEAR
1974
1975
1976
1977
YEAR
1974
1975
1976
1977
iwnTwmMAiQ DOSES AVERAGE
EXPOSED (MAN-REM) REM/INDIVIDUAL
1,715
1,948
2,753
1,860
STEAM
TOTAL
INDIVIDUALS
EXPOSED
26
393
711
GENERATOR
DOSES
(MAN-REM)
54
638
1,287
1,410
844
1,649
3,164
2,307
0.5
0.8
1.2
1.2
MAINTENANCE
AVERAGE
REM/INDIVIDUAL
2.1
1.6
1.8
TUBES
PLUGGED
200
500
1,750
1,525
REPLACEMENT OF, STEAM GENERATORS 4,336 (EST.) MAN-REM.
-------
ro
ro
U.S. GENERAL POPULATION EXPOSURE
ESTIMATES - 1978
Qni .ppc PERSON-REMS PER YEAR
bUUKU: (IN THOUSANDS)
NATURAL BACKGROUND 20,000
TECHNOLOGICALLY ENHANCED 1,000
HEALING ARTS 17,000
NUCLEAR WEAPONS
FALLOUT 1,000-1,600
WEAPONS DEVELOPMENT, TESTING,
AND PRODUCTION 0.165
NUCLEAR ENERGY 56
CONSUMER PRODUCTS 6
m
oo
-------
U.S. OCCUPATIONAL EXPOSURE ESTIMATES - 1975
PERSON-REMS PER YEAR
(IN THOUSANDS)
HEALING ARTS 40-80
MANUFACTURING AND INDUSTRIAL 50
NUCLEAR ENERGY 50
RESEARCH 12
NAVAL REACTORS 8
NUCLEAR WEAPONS
DEVE LOPMENT AND PRODUCTION 0.8
OTHER OCCUPATIONS 50
O
m
-------
DISCUSSION
SESSION V
Jerry Rosen, University of Pittsburgh: I have two brief
questions. Dr. Radford, you indicated in your talk that the
incidence of cancer from natural background would be in the
order of one or three percent and Mr. Harward indicated, on his
first slide, that about 1/2% of the cancers in the population
would be due to natural background. I'd like you to address
that. Another item for any of the panel members would be that
on many of the graphs we've seen here today we see error bars on
measured health effects; for example, incidence of leukemia.
We very rarely see error bars associated with the delivered
doses. Could you indicate what order of magnitude these errors
might be?
Dr. Radford: I'll take the first part and possibly Dave
Harward might want to comment. The estimates I gave are based
on more recent data than the 1972 data. In part, these data are
now published in the 1977 UNSCEAR Report which is in the open
literature. I think they indicate the impact of the "further
follow-up effect," if I can call it that. One of the big
problems in defining the cancer risk from radiation exposure has
been, as I tried to indicate in my presentation, how long is the
effect going to last within the population. If it lasts
throughout the lifetime of the individuals, it means that the
risks are substantially higher than if, as in the case of
leukemia, it doesn't last for the lifetime of the individual. I
think that previous risk estimates have, to a considerable
extent, made the assumption that the risk will last only for a
finite period of years and now we think that most cancers will
not. Mr. Harward, do you want to comment on that?
Dave Harward; I think the table you're referring to is the
one that I got out of the HEW Draft Interagency Report, where it
indicated something like roughly 50% of the radiation induced
cancers in the United States, might be due to natural
background. As to your comment on the error band being rather
sizable, I think this is generally the case with this kind of
thing and error bands with a factor of two when trying to
interpret some of these numbers is certainly not uncommon.
-425-
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Dr . Radford : Just to correct you, Dave. You meant a
1/255, not
Dave Ha r ward : 1/2% of the total cancer deaths, but about
50? of the total radiation induced deaths. If you look at the
HEW figures with about 4,000 theoretically radiation induced
cancers per year, roughly 2,000 are from natural background.
Dr . Radford : Can I just respond to the dose issue. The
speaker, Mr. Rosen, is quite correct that one of the problems
that we have in the epidemiology of almost any environmental
agent, is to define what the exposure has actually been. Now,
the dose data that I used for the Japanese is based on the most
recent tissue doses obtained by the Oakridge National
Laboratory. For the low dose end of the curve I think the error
bars are relatively small, becauses it was much more possible to
define the shielding characteristics of the individuals who are
out away from the bomb epicenter, in contrast to the higher
doses where I think the uncertainties remain somewhat high. So
I agree with your general point and maybe we should, if we had
the information, put error bars on the doses.
Mr . R_._ Minogue : I'd like to add to what Dr. Radford has
said, looking at a different exposed group. First of all, I
think there is always a difficulty in trying to relate some of
the epidemiological studies of exposed workers, or some of the
studies planned on soldiers, to the medical exposure that the
people studied may have received. This is a matter of some real
concern .
Even as to the radiation exposure involved in the
activities of these various groups, there's a lot of
uncertainty. For the soldiers and other personnel involved in
the weapons test program, the external dosimetry was at best
limited and the internal dosimetry verged on nonexistent. Thus
there's a great deal of uncertainty as to what the exposures
really were, at least in my opinion.
Even among the industrial radiation workers that are
involved in highly disciplined activities where the ALARA
concept has been applied, there is a great deal of uncertainty
as to the doses received. Let me just tick off some of the key
points. First, the low exposed part of the group yo.u almost
have to drop from your data base because among them may be many
workers who received no exposure or some indeterminate low
exposure. Below about 30 millirem on the film badge, the data
verges on indeterminate. Even above that level there's a great
deal of variation in the data that one gets back if you use one
of the commercial dosimeter processing services, in terms of the
doses reported. This is a matter that we're giving a great deal
of attention to right now in the context of an epidemiology
-426-
-------
feasibilty planning study which we've been mandated by Congress
to do. I think it may be a statistical variation, but it's
fairly wide. The point I'm trying to make is there is, in fact,
a fairly large plus or minus on the external exposures measured
by the film badges and other personnel dosimeters used in the
industry.
The last point I'd like to make, in brief, relates to
internal dosimetry. That type of exposure is quite limited in
the regulated industry because it's generally been regarded as
somewhat of a "no no" because of the recognized high level of
uncertainty. There are a number of techniques that are applied,
bioassay techniques, for example, for workers who may have been
exposed to internal doses that I think are quite good. The
dosimetry, in fact, is probably rather good between measurements
of air sampling systems and bioassay.
Dr. Wald: We'll take somebody from the front. While he's
getting there, let me mention that the Ichiban program, the
Japanese reconstructed dosimetry program, felt that they had
arrived at something that was approximately plus or minus 25 to
50% of each individual's exposure. The other point I think has
to be recognized is that the medical exposure risk was as great
for people who received insignificant weapons radiation in
Hiroshima and Nagasaki because they all came under an A-bomb
Survivors Compensation Law which provided for medical
examinations, so the lower the exposure from the weapon, the
proportionately greater influence the medical x-ray in the
following would have been.
Dr. Had ford; If I may, Neil, I just want to point out
that very careful assessment of what the medical X-ray
contribution has been to various tissues-- and it's by no means
uniform—has shown it's not the whole body approach that has
been taken into account. I'm not sure that all the data I
showed has built that in, but I think we can .
Dr. Wald: Yes. Usually it just shows the weapons
exposure, but I think that's a good point.
Dr. H. Spencer, one of the QRBES researchers: I am
interested particularly in the Ohio River Basin. In the basin
we consume something on the order of 400 million tons of coal a
year. Coals in the basin contain one to two parts per million
uranium and thorium oxides, in equilibrium with their decay
daughters. Upon combustion the gaseous components, thoron and
radon, go out immediately. Some of the other daughters
apparently evaporate but the uranium and thorium appear to
remain with the ash. The question I'd like to direct to the
panel can be answered yes or no. Should we now begin looking at
these ash pits the same way we're looking at mine tailing areas
-427-
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across the country?
Mr. Harward: I can take a stab at what I know is going on
about the subject. I mentioned earlier the EPA implementation
of the Clean Air Act Amendments of 1977. They are looking at
this very closely through a series of contracts and have a
substantial background of data over roughly 10 years from fossil
fuel plants. I do know they are considering whether or not to
include fossil plant radioactive emissions within the Clean Air
Act. By August of 1979, they have to construct some lists of
various pollutants that would be covered under the Clean Air
Act. I won't go into what they are, but there are three
sections in the Clean Air Act under which pollutants can be
listed. This is under consideration. I don't know at what
point they are in their work on it.
Dr . H_._ Spencer: I would like the NRC representative to
answer the~~question .
Mr. Minogue: I really don't feel that falls within the
range of my regulatory expertise. I think Mr. Harward is
better qualified to answer that.
Dr. Wald: I think we have to allow yes, no or none of the
above"
Dr. £._ Hartnett, University p_f Illinois, Chicago: I have
two questions that are directed to the last two speakers. I was
somewhat confused by what I thought were different statements.
I thought I heard the second speaker, Mr. Harward, say that the
uranium mining and milling pose greater hazards with respect to
radiation than did the nuclear power plant. And I thought I
heard the last speaker, Mr. Minogue, say just the opposite.
I'd like to have that question clarified. The second question
is directed to the last speaker, Mr. Minogue. I believe on the
last slide, if I read it right, it said that other occupations
show 50,000 person-rems per year, while nuclear energy showed
50, nuclear reactors 8, and nuclear weapons 0.8. Does this
suggest that a worker in a candy factory or a professor in a
classroom is exposed to more radiation than a worker in the
nuclear industry or in the nuclear weapons industry?
Mr. Minogue: Let me answer the second question first
because it is pretty straightforward. What it suggests is that
there are a number of people, far larger numbers of people, in
some of these other occupations who are not generally regarded
as radiation workers but who are exposed in the work place to
radiation at levels greater than that which arise from natural
background. Because there are so many of these, and if you
recognize the no-threshold concept, the total number of man-rem
they receive is quite significant. This would include phosphate
-428-
-------
workers, it would include the airline stewardesses and so on
There are large numbers of these people.
Dr. J. Hartnett: You did
occupations"-- you are talking
that correct?
not mean by that "all other
about selected occupations. Is
Mr. Minogue; The data I'm referring to is from the HEW
Report. My understanding of the groups that they looked at was
that they were all workers who are exposed to radiation at
higher than background levels because of the nature of their
occupation. There are many of these workers. The data is not
terribly good, but there are very large numbers of these
workers.
Dr
as it' s
"other
J. Hartnettj_ You clarified that slide, but I think
the slide it is misleading because it says
stated on
occupations."
Mr. Minogue; Let me now reply to
question. Certainly I intended in no
public exposure problem from mill tailings
sorry if you read that into what I
occupational exposure and the occupational
of mill workers is a very minor
occupational exposure to nuclear power
part of the first
way to imply that the
is trivial. And I 'm
said. My topic was
exposure to radiation
problem compared to the
plant workers. First,
there is a large number of those people in the nuclear power
plants; and secondly, they are inherently exposed to very high
radiation levels. The work they do in which they receive
exposure is primarily related to maintenance of critical safety
equipment; nonessential exposures are rather easily eliminated.
They are, as a group, exposed to quite high radiation levels. I
associate with them; I've been exposed to those radiation
levels myself, and they're quite high.
Harward
_:_ Well, just to further amplify.
the screen was for environmental
NRC data
that I had on
according to the NRC data, the combined mining
population dose represents a little better than a
total dose from the entire nuclear fuel cycle. The
that was higher was the fuel reprocessing
I indicated, of course, is nonexistant at
the lack of fuel reprocessing.
The table
exposure and
and milling
l/3rd of the
only thing
public exposure which
present, because of
Mr
Olson , Westinghouse
address to Dr. Radford
definition of low level radiation
you said from 10 to 100 rads.
Minogue was talking about
talking about five to
have two
First of all,
As I
Just a
questions I'd like to
I'm surprised at your
think I understood you,
minute ago, though, Mr.
high levels of radiation, he was
fifteen. So my question is what about
levels less than, say, ten rad. What are the effects there?
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Secondly, at these exposures of ten to one hundred rads, is
there any difference in the rate of exposure? That is, is it
the same getting a 50 rad dose in a few seconds, or a few
minutes, as it is getting a fifty rad dose spread over a year?
Dr . Radford: Right, good questions. Really, the second
question leads into the first. The question of dose rate has
been one that has been of considerable interest and importance
in the radiation protection field. In other words, the point
you raised, if you get the radiation stretched out over time,
let's say accumulate 50 rads that way, compared with getting
zapped with 50 rads all at once, does it make any difference in
the long term effect? For the kinds of radiation represented by
alpha radiation, the human evidence suggests that stretching out
the dose increases the risk per total accumulated dose. That's
for so-called high LET radiation; that is, radiation with a
high linear energy transfer. For low LET radiation, the
experimental data strongly suggests that stretching out the dose
reduces the risk per rad per total accumulated unit of dose.
And until comparatively recently this has been rather the
accepted view in interpreting risks of relatively low doses. If
we use the linear hypothesis, and if we take no account of the
so-called "dose rate effect" we will be overestimating the risk
for low LET radiation, and possibly overestimating it by a
significant amount. I think follow-up of the occupational
groups which has now been stimulated by a number of these recent
studies is going to help us out a lot on this. We have some
evidence which suggests that the dose rate effect for even low
LET radiation is not as significant as we thought it was, based
on the animal data, and there are theoretical reasons why the
animal data might have shown this more readily than the human
data. Briefly, these are the comparisons of the cancer risk
arising in the women who were radiated by fluoroscopy repeatedly
over many months or years, turn out to be almost identical with
the risks per unit dose that were obtained from women who were
treated for other conditions and received a single dose of
radiation, in the order of 100 rads or so, to the breast tissue,
compared with the Japanese A-bomb survivor data when again it
was a single dose at relatively high doses in this case, too.
So, the previously thought to be applicable "dose rate effect
for low LET radiation" is not strongly supported by the human
data at this time. In either case, both for the high LET
radiation which leads to an underestimate of the risk at low
dose rates, let's say, and the low LET radiation which might
lead to an overestimate of the risk, the uncertainty probably is
not very much greater than a factor of two. So, if you'll
accept that degree of uncertainty, which I think we have to
because of the data, then the dose rate effect becomes
relatively minor .
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Dr. N. Wald: Are you specifically addressing the
endpoint of cancer induction?
Dr. Rad ford: Yes, strictly cancer induction. Obviously
for other end points such as the kind that Dr. Wald is
particularly interested in, dose rate makes a big difference.
Mr. Minogue; I'd like to make a point in this-connection.
I appreciate the questioner raising this. I noted the same
difference in point of view when I listened to Dr. Radford's
speech and meant to comment on it in giving my own remarks, and
then neglected to. He and I don't cut off at the same point.
When I talked about occupational levels or low-level exposure,
recognizing what the averages are and recognizing the turnover
in job assignments and so on, I am definitely thinking of a
range that cuts off from 10 to 20 rem lifetime exposure. And
it's clear that Dr. Radford is looking at a much broader span,
that is much higher lifetime exposures.
Dr. E._ Radford: Well, I'd like to comment on that. I'm
sorry I dTdn't answer that question because I think it's an
important one. If the dose rate effect is minor, as I have just
indicated, then it doesn't matter. What we're talking about is
total cumulative dose up to particular age or time. And there
is I think, for example, from background radiation exposure up
to age 50, you've accumulated five rads. Well, you're already
at five and you're going to add to that from your medical
exposure another four or five rads. So you're up to ten
already, and now we're going above that with these other
exposures. So, with regard to the general population, yes, we
are concerned in the range of an extra added dose of, maybe over
the lifetime of an individual, a few rads. I agree that in the
epidemiologic data literature, we don't have a lot of hard data
at those doses, and therefore we are extrapolating downward
using one of these models in order to get an indication of what
effect there will be, say from 10 to 20 to 30, to 50 rads, where
we do have some data and where the data are actually becoming
quite good.
Now with regard to Mr. Minogue's statement about the
occupational exposures, this gives me an opportunity basically
to ask the other panelists a question. They used aggregated
data. In other words, they averaged over the industries. I
would like to have them comment on the fact, and it's my reading
of the NRC reports, that the performance of different reactors
within the same type of design and everything else, is widely
variable; I mean by a factor of almost 10. So that some plants
are restricting their exposures to workers very markedly and
indeed are achieving what I consider to be an admirable record,
whereas other plants are not. When you average them all out,
obviously then, you set an intermediate value. The second thing
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is that if you look at the aggregated data in the UNSCEAR Report
last year (1977), worldwide, but even in the United States, you
find that there are substantial subsets of the occupational
groups that have now already accumulated 50 to 60 to 70 rads,
and presumably they are going to continue working. There are
some of the foreign plants that aren't doing as well. They are
up over 100 rads to individual workers and I don't mean only one
worker — I mean a few, at least perhaps 1% of the total work
force. So when we talk about occupational exposures, we're not
talking about five rads or ten rads. We're talking about 50
rads or 100 rads over the work life of the individual. You
disagree, Bob?
Mr. Minogue: Let me take the last point first. Yes, I
definitely disagree. There may be a few individuals who receive
those levels but that's simply not true of the vast majority of
the workers. The other comment you made is, I think, an
important one. There are differences among plants. Some of
these are clearly due to different operating experiences; some
have had more problems than others. The older plants have had
some build-up of activity. Some plants have had more
modifications imposed by the regulators than others. And many
of the differences can be attributed to this. But there are
differences that relate to the -- let us call it -- "the level
of conviction" with which ALARA is applied, and because of this
the staff of NRC has recommended to the Commission that we find
a regulatory framework to put more teeth in ALARA. Not from a
perception that many of the companies haven't done a very good
job, because they have, but to get hold of the people who aren't
measuring up and bring them into line as well. That element is
clearly there. It isn't all attributable to differences in the
operating experience or maintenance requirements for the plants.
Tom Zeller, Indiana State University: I have two questions
for Dr. Radford. I walked in a little late on your talk, so if
you addressed these, I apologize. First of all, your figure of
half a percent of cancers, I hear you mentioning half the
percent of the cancers are due to the background radiation, is
that what I was picking up?
Dr. Radford; No, I said one to three percent.
Tom, Zeller: One to three--!'m wondering how you could ever
get that number without just plain guessing. Secondly, I'm
really interested where you got that number. Dr. Goffman's
study, which is about ten years old now, estimates that the
total United States population is exposed to five millirem
dose--you'd end up with thirty-two thousand excess cancers per
year or excess deaths, I don't remember which. Now you're
saying that this is three orders of magnitude too large a
figure?
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Dr. Radford; I'm not sure where the three orders of
magnitude came from.
Tom Zeller: You're saying a thousand or two thousand at
background, which is two millirems, and he's talking five
millirems.
Dr. Radford: Five millirems he calculated? No, I don't
think so. I worked with Dr. Goffman closely at various times
when he was generating those numbers and I don't think that's
correct. We can come back to that point. I would prefer simply
to say that the estimate that I derived is based on the linear
hypothesis, and I was careful to say it. In other words, taking
the data we have at the higher doses and extrapolating them
downward to what the individual gets over his life span from
background radiation, leads to one to three percent of the
cancers. In terms of incidence that's around 600,000 cancers a
year, so 1% to 3% is 6,000 to 18,000 that would be due to
background radiation.
Tom Zeller:
numbers,
radiation
millirem?
When Dr. Goffman was generating those
I thought it was with regard to the acceptable
limit around the fence of the plant. Isn't that five
Dr. Radford: No, that's five hundred millirem.
Tom Zeller; Okay, so was that the figure he was using?
Dr. Radford: 1 believe so.
Tom Zeller: Is that figure in the ball park with what he
comes up with? I've heard that figure disputed, is why I ask.
Dr . Radford: I think his estimates were too high and the
principal reason was that he made the assumption that all
cancers induced by radiation had the same sensitivity; that the
percent increase in risk of cancer of any type was proportional
to the dose and was equal for all different cancers. I think
that assumption has been very thoroughly contradicted by the
human data.
Tom Zeller
this also—I
and the
both cases, very
My second question is--and maybe you mentioned
didn't hear anything about the recent Mancuso study
study of the Naval Shipyard workers that involved, in
low dosages. It's been in the media, but I
don't have the data on what
significant were the number
information on that? Thank you
they were
of cancers
exposed to or how
Do you have some
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Dr. Had ford: Okay, I'll take that one, and I'll let the
other panelists add any comments they would like. I've
discussed this with Dr. Mancuso so this is, in no way, telling
a tale out of our school. In my opinion, the Mancuso study
shows a relationship of risk of cancer to radiation exposure in
the work place, at the levels at which those workers were
exposed, but only for one cancer type, namely multiple myeloma,
which is a relatively rare, although rapidly increasing in
importance, type of bone marrow cancer.
The other putative effect, an increase in pancreatic cancer
in these workers, I do not believe can be adequately ascribed to
the radiation exposure. I think it's a linked effect and it's a
problem in our methodology of epidemiology that we frequently
cannot assign a single cause or even a direct cause to a
particular agent.
If you take the excess risk that these workers had, and I
agree that there was a small excess risk, and compare it to the
expected risk on the linear hypothesis that would be derived
from the figures that I used, it comes out very close to what
you would have expected. Indeed, you would not have expected
all to be in multiple myeloma, but you would have expected a
scattering of cancers, but unfortunately the epidemiologic
technique is just not capable of detecting it.
So my first conclusion is that the Hanford data did not
show any unusually high risk in these workers. The second
point, and I believe Dr. Mancuso agrees with me on this, and I
have repeatedly said this in public, my interpretation of the
Hanford Study is that the exposures were remarkably good,
remarkably low. Here you had a plant that started out making
plutonium for military purposes way back in the forties and went
through the whole range of nuclear technology including peaceful
uses and military uses and everything else, starting from
absolute scratch with relatively untrained personnel, and yet,
when you look at the exposure data in that plant, it is
extremely good. The average dose over the working span of the
individuals, many of which were short, I agree, because they
were construction workers and they left, was only 1.8 rads. And
Alice Stewart herself has commented to me her surprise that so
few workers ever got more than five rads a year. Very few ever
did. So my conclusion is that this plant was extremely well run
from the health physics point of view, and I have had occasion
to congratulate Mr. Herb Parker who was the chief health
physicist at that plant for this fact. And indeed if anybody
were here from the union, I would tell them you've got a
well-run plant. All you have to make sure of is that it keeps
being well run. So with regard to the Hanford Study that's my
bottom line and maybe some of the other panelists would want to
comment on this.
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The second point is the Portsmouth Navy Yard Study. Drs.
Najarian and Colson were very careful in their paper, published
in Lancet, to point out that it was a preliminary study; they
had no dosimetry. There is no possible way you can compare,
let's say, the risks that we would derive from the other studies
where we do have dosimetry. They are now in the process of
collecting the dosimetry data and bringing together the data on
mortality. I hope that it will be possible for NIOSH and other
groups that are involved in this study, to blend their data
together. So the Portsmouth Yard Study in no way says anything
about whether the risk is higher, lower or what.
The same thing can be said for the Utah children who have
recently been studied from, and whose exposure to radiation was
from fallout from bomb testing. Again, no dosimetry is adequate
and it is premature to say anything about that result except for
one important thing. And that is they have found an excess of
leukemia in the children. This result suggests that the dose
response curve in children might conceivably be different in
shape from the dose response curve in adults. As you noticed, I
used the curvilinear dose response curve for the adults,
primarily adults in the Japanese data.
So I conclude that of all the, "recent studies that show an
increased risk" none of them really do. The only one is Dr.
Bross's reanalysis of the Tri-City Study of children irradiated
in utero. I simply do not agree with Dr. Bross that his data
shows what he says it shows.
Dr. Wald: Do any of the panelists want to respond?
Panelist: I'd like to make a comment about the first
question from the gentleman from Indiana State. I am familiar
somewhat with Dr. Goffman's projections. These were made
approximately ten years ago. And I think the key thing to keep
in mind is that those projections, of total cancer deaths, were
based on two hundred million people in the United States, each
being exposed to the five hundred millirem per year. If you
look at the actual exposures of the public, and I presented
these in another format in one of my slides, you'll find that
the exposure, per capita, in the United States historically has
been well less than 1 millirem per year which is akin to riding
an elevator maybe ten times a year in terms of the change in
background. I think you've got to keep in mind these
projections of a lot of people to doses which can get
astronomically big, but it has to be kept in perspective.
Dr. Wald: I think the fatalities from the crowding at the
fence post, if you put the whole United States population in,
will be much higher than anything Dr. Goffman contemplated.
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Mr. Minogue; I'd like to comment on the work of Drs.
Mancuso, Bross and Alice Stewart, and others, from a little
different perspective from that of Dr. Radford. I'm a
regulator and I have to make some immediate decisions with the
industry that I'm regulating now. As these studies began to
come out, certainly from the beginning I recognized the kind of
methodological challenge that has been raised to some of the
conclusions. Dr. Radford has identified a number of them here,
and the statisticians, from a mathematical point of view, have
raised equally sharp challenges. However, the fact does remain
that these studies would indicate, and I referred to this twice
in my remarks, that the basis of the present radiation
protection standards perhaps is not quite as conservative as
some of the regulators thought it was. In other words, let's
say it gives a lot more emphasis to the importance of applying
the linear hypothesis literally as if you really mean it. So I
would say as far as what we on the NRC staff have done, between
the trend analysis of exposures that I covered in my remarks in
some detail, and looking at these data and considering
discussions we've had, particularly with Drs. Bross and Alice
Stewart—that these were factors in leading us to conclude that,
even though there may still be uncertainty and there certainly
is not widespread scientific acceptance of the findings of these
researchers, there were enough indications here that we as
regulators should look hard to redoubling some of our efforts to
control exposure, which is what we're doing.
John Blair, Evansville, Indiana: Concerning day workers in
nuclear plants and how that practice is going today where a
worker can come in and receive his yearly dose of radiation one
day and then not work in the plant any more. Just what is
happening in that level?
Dr. Radford: I did address the genetic effects of
radiation, and I do think they are important. You were
apparently not here when I did address it. I think my position
on the genetic effects is that you cannot really add them
directly to the somatic cancer effects, the way the ICRP has
done, for example. They equate "health effects from genetic
damage" with the "health effect from cancer induction." This a
real problem and I know the geneticists share this concern.
That does not mean that the genetic effects are ignored, far
from it. I think what it tells me is that we must be especially
conservative in restricting exposures, especially to individuals
who will be in the child-bearing age or up to the time of the
usual reproductive span of the individual. One way to interpret
this is to restrict very sharply the exposures of young
individuals working in association with the radiation, whether
it's in the nuclear industry or whether it's in general industry
as we've heard about, or whether it's in medical uses,
restricting exposures of individuals who are under the age of 35
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as sharply as you can. I think there is going to be undoubtedly
a lot of discussion in this area as Mr. Minogue's review gets
under way. So I don't mean to play down the genetic effects; I
think they're very real and, as I try to indicate
quantitatively, they look as though they are in the same ball
park in terms of percent effect. But you just can't compare a
genetic change directly with a cancer change.
John Blair: Have there been studies done about the genetic
effects to date that adequately addressed the problem, in your
v iew?
Dr. Radford: The human studies are plagued by the fact
that we don't know what the natural genetic load is in the human
population to begin with. So if you don't know what the "normal
level" is, which we know very accurately for cancer, you see,
then if you look at a population like the Japanese bomb
survivors or any other population of human subjects, it's almost
impossible to detect whether environmental agent A, B, C or D
has been having an effect of a genetic nature, in part, because
it may be expressed only in two or three generations away and
that's 60, 80 years from now. So we're very seriously limited
by that problem. The spiderwort: I'm familiar with Dr.
Ishikawa's work. The studies of plant cells have shown that you
get detectable genetic effects down in the range of a few rads.
And it's one of the experimental pieces of evidence that
convinces us that the "linear no-threshold dose response curve"
is not just a mathematical convenience but it has some substance
in the biological sense. And it's not the only data, by any
means.
Dr. Wald; Bob, do you want to take the other question?
Mr. Minogue: I'd like to comment on the genetic question.
I didn't mention it in my talk because Dr. Radford had covered
it. I wouldn't want to leave anybody with the impression that
we, as regulators, discount the genetic problem. There is a
tendency, I think, because of the relatively easier experimental
problem that the researchers in this area tend to talk mostly
about cancers, but the regulators recognize that there are other
adverse effects. In fact, I think it's true that some of the
decision makers among my predecessors back in the 50's were more
concerned with genetic effects in considering how to treat low
levels of exposure. One of the reasons they adopted this
principle of assuming the linear no-threshold model was more
because of their concern about genetic effects rather than
somatic effects. As to the other question, I'll try to answer
it briefly. It's a complex issue. I touched on the transient
worker issue—people moonlighting and moving from job to job in
my remarks. But there's another element of this short-term
contract workers. I do not like the term, and I don't like to
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use it, the idea of "burning out people." That is something that
if it involves using inexperienced or unqualified workers is not
really tolerable just on safety grounds, because the operations
that people do on these plants that involve exposures typically
are involved in the maintenance or repair of essential safety
equipment. There is really no trivial exposure. So you want
highly qualified workers to do these jobs. If a licensee began
to run through unqualified workers, just piling up bodies to do
jobs, it would be counter to safety in the first place, and
secondly, would involve unduly large collective doses. If the
regulatory strategy that's adopted emphasizes reducing
collective doses, you would tend to catch this practice in that
context, that is, the total number of men involved in doing a
job is focused on and controlled, as well as exposures of
individuals; you tend to root out this sort of practice which
has occurred from time to time in the past of "burning out"
individual workers.
Question: How did the NRC take that? Was that something
they slapped the company on the wrist and said you shall not do
this anymore?
Mr . E_._ Minogue: No, it's not contrary to the present
regulations. I don't mean to give that impression. Let me give
you a specific example. I think President Carter took part in
an operation like this many years ago. It's conceivable that
there might be some operation involved that required little
specialized skill where a worker might be called on to go in and
do one job, and then move out again and go back to his normal
job outside the radiation field. It would be completely
acceptable if that was part of a program that led to the minimum
number of total man-rem, which, in my mind, I equate to total
cancers. It's not that simple of a question to say, "Well, you
should never do this." That, I think, is not a sensible answer.
But rather to select whatever mode causes the least public
impact. That's the basic bottom line. What is the best way to
do a job that involves the least public health impact and
accomplishes the safety goal? That's the test we use.
Dr . N_._ Wald: Excuse me, I think we'll have to let some
other people ask questions.
John Blair: I'd just like to say one brief thing. It
seems what I have heard today, as far as health effects of
nuclear energy, is that's okay to shoot now and ask questions
later because so much of this stuff we really don't know, and it
seems that even this distinguished panel which is made up of
academic and industry and government people doesn't have very
many of the answers that the public is crying out for. With
this kind of policy of making plenty of nuclear energy today,
and not knowing what's going to happen with it in 10 years, is a
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policy that may get us into a lot of trouble in the long run.
I'd like to make a brief comment, if I may. I've been very
impressed with what I've heard today in an area that is very new
to me. However, I have to admit that the statistical
projections that you gentlemen are forced to make, are forced to
rely on, leaves me a little bit cold. It's not something I feel
I can snuggle up with and really get to know. I am concerned
about an area that I think is raised specifically by the nuclear
power question and that's the area of health economics. I'm
going to just scratch the surface in my comments, because if I
do anything more, I'll reveal my profound ignorance of the
subject matter. I am concerned with the extreme costs that
appeared to be associated with nuclear power generation,
particularly capital outlay, operating and maintenance, and also
some of the internalized costs; hopefully, the costs to be
internalized, such as waste disposal and the potentially
staggering costs of decommissioning plants 30 or 40 years from
now. There are two effects of that enormous cost. One is
potential raising of the cost of electricity. I would refer
anyone interested in that to the remarks made by the gentleman
yesterday from the Edison Power Research Institute Electric
Power, ^EPRI. Although I don't necessarily agree with the
conclusions he drew, he did raise some questions about what are
the societal and health impacts of increased electrical power
costs. But mostly I'm interested in the fact that making the
determinations as to what are the health impacts of nuclear
power generation, can't be made in a vacuum that this discussion
has been contained in. I'm not saying that that is a fault of
the people who put together the program. It's inevitable what
you're trying to do, but I think it is important to point out
that we, as a society, have very limited resources and that if
we decide to spend hundreds of millions of dollars or billions
and billions and billions of dollars on nuclear power
generation, that is money we're not going to be able to spend on
health issues— health promotion, other areas of health
prevention, some of the fairly staggering cost of environmental
control. I guess what I just want to point out is that the
issues of human health costs of nuclear power generation are not
just related to occupational and community safety, but also
raise the issue of resource allocation as a determinant of
health. I think that's a consideration of everything we've
talked about in the last three days. But I think that, given
the staggering costs that nuclear power may result in, that it
is most sharply raised in this issue. I just wanted to point
that out. Thank you.
Dr. N. Wald; Does anyone want to comment?
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Panelist: I'd like to make several comments. I'm not sure
that was a question. I think it was a short speech. First,
I'll challenge the assumption that the cost of decommissioning a
nuclear power plant is staggering in terms of the cost of the
plant. That's simply not true. Much of the technology of
decommissioning these plants is already established and, in
fact, several have been decommissioned. But more important, the
basic issue here that I am going to talk as a public health
regulator. I found this conference an extraordinarily
interesting experience. I had no idea how severe the health
problems were in the coal industry until I came to this meeting.
I would agree with and support any argument that said the public
health impact of producing electrical energy and the use of
electrical energy should be fully considered before one goes
forward. But that means fully considered in all modes, and I've
heard nothing to persuade me that the issues I try to grapple
with in my day-in-day-out job, in terms of controlling radiation
exposure both to the workers and the public, are being handled
any less well than those associated with coal. I have had
exactly the opposite impression. I've sat here and listened to
people talk about sulfates and a complete uncertainty as to what
the effects are, and some suggestions that "so let's not set any
standards. We'll just keep on doing it." I've been a regulator
for a long time, and I found that sort of discussion quite
disturbing, personally.
John Blair: May I ask a follow-up question?
Dr. N_._ Wald; Let's give the panel a chance to respond.
I really can't let anyone monopolize the question because there
are other questions.
Panelist: I'd like to also respond to the decommissioning
issue. There have been a number of studies by industry and by
others about the cost of decommissioning and I have never seen
anything that I consider to be a solid technical study that
doesn't put the decommissioning cost of a nuclear power plant at
a very, very low level when compared to the total capital outlay
that you're talking about in a plant. As far as the economics
of nuclear power, I think this is certainly variable, depending
on where you are in the country, what the cost of coal, what the
cost of hydro, the availability, etc. I don't see a lot of
nuclear power plants being built where they're not economical.
In fact, we don't see very many nuclear power plants being
built, period, right now. And I believe if we don't get some
built, I think we're going to have serious shortages in this
country. And I say this also as a public health person and not
just as a representative of the industry. I think that the
public health benefits of adequate energy is an essential
ingredient to the United States, and to our welfare and health
overall. I guess that's about it.
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Dr. E. Had ford: I'd just like to add a very brief
comment—not to prolong this discussion. It is absolutely true
that the economic aspects of all these alternatives are
important. This symposium was not designed to address these
except in a very limited way, deliberately because we wanted the
health implications given the prominence we think it has. I
would agree that ultimately all of our activities that impact on
either the general public or the workers, ought to be
internalized in the cost of that activity. And I agree that
it's far from being internalized. I don't think it's adequately
internalized in the nuclear industry, for one case. For
example, look at the mining problem which is still with us, and
which is not being adequately factored into the equation, any
more than the coal mining issue is in the coal cycle. So I
think we've got to do it and one of the ways we do it, is by
getting a better handle on the health effects, and that's what
we're trying to do here.
Richard Ulrich, Group Against Smog and Pollution,
Pittsburgh; I have a question concerning the exposure
information for the people employed in the plants. Out of
70,000 workers, I think, the slide shows 11,000 workers
receiving more than one rem. Now, I think, there are some
people who do believe that one rem could be a sufficient
standard, that is the standard should be lowered from 5 rems to
1 rem per year. Now, with those 70,000 workers, there were
30,000 or 25,000 who didn't get any exposure and certain others
who are probably not working in the critical areas. Are these
11,000 out of a much smaller group of critical workers—are
there steam fitters or some other group of whom there are only
10,000, and right now 8,000 or 9,000 of them actually are
getting the 1 rem exposure or more. The implication of this
health thing, if the standard is lowered, can nuclear power
plants keep running or can most of them keep running, all of
them keep running, or will they run out of workers?
Dr. N^ Wald: Whom are you addressing? Whose slide was
it you described? I think it was in the regulation.
Panelist: I think I can answer the question rather
briefly. I think it's correct that of the group exposed to
greater than the 1 rem cutoff, a large percentage of those are
highly skilled workers that are associated with some of the
critical welding and inspections operations. These skills are
rather widely available throughout the country. It's a high
level of skill that is relatively available, I think.
Richard Ulrich: So there will be workers available in
other industries that the nuclear industry would be able to
hire?
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Panelist; The trouble is that I looked at this issue more
from the point of view of what it is that produces the least
public health impact. Running through more workers, if you
could somehow make them available, might increase the total
collective exposure. The perspective you're asking me to answer
is more that of industry. I would assume they could train
welders if all else fails. That wouldn't accomplish any public
health goal.
R. Ulrich: I kind of suspect it's going to be hard to
keep an industry going if it requires a heavy turnover of highly
skilled individuals.
Panelist: I really doubt that very much. The cost of
these repairs in terms of the worker cost is miniscule compared
to the investment in these plants.
Ulrich: So they could keep a larger permanent work force?
Maybe that would be a solution--it would have extra workers who
• * •
Panelist: Workers of this type typically work for various
contractors. They're not necessarily the employees of the
util ity.
Dr . N_._ Wa 1 d: We have time for one more question.
Jerry Rosen, University o_f Pittsburgh: My question to the
panel is about the differences in estimated health effects from
natural background which I raised earlier. I got the answer I
expected from the panel. What concerns me is that a new
interagency report which is in draft form, makes use of
information on biological effects which is several years behind
the times. It doesn't draw on the UNSCEAR Report of 1977. It
obviously cannot draw on the new BEIR Report which, I belive, is
due shortly. This is a document which I believe will be used
strongly in the political decision making process related to
future changes in radiation exposure limits. People like Mr.
Minogue do not have some of this information available to them
unless they go outside of their own agencies to gather it. I
feel that this is detrimental to future policy making.
Dr . N_._ Wald: Anyone care to comment?
Dr . _£_._ Radford: I'll just comment to your first point.
I'm not quite sure what your last point was--that because we
know more about radiation we should be less concerned about it,
more concerned about it, or what? To answer your first
question, I do agree that the decision on the part of the
technical staff who prepared the Libassi Report to use BEIR I
risks estimates was, in my opinion, a mistake. I'm not quite
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sure why they did it, except perhaps it was available to them in
a form that they could use in their computer runs more readily
than perhaps some of the other data that was possibly available
to them. I think you're right. It is out of date and it is
unfortunate that the BEIR report did not come out before the
Libassi Report. In fact, I'm told that one of the reasons that
the Libassi Report was delayed was because they were waiting for
the BEIR Report to come out. I'm chairman of the BEIR
Committee, and therefore I carry the onus of the fact that it
isn't out. But we're doing our utmost.
New Speaker: The second point wasn't to say that we should
go ahead with nuclear power or coal power, I think most of the
decisions ahead of us are not really scientific. They are going
to be political. I see issues being raised here by some of the
questioners that are purely political and I don't think that the
questions are very healthy in nature. Let's put it that way—at
least the reasons for them being formulated.
Dr. j*L_ Wald, moderator: I think we've run out of our
time for questions and answers and I want to thank the speakers
for their very lucid presentations and the audience for its
contributions to the discussion. Thank you.
T-443-.
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SESSION VI: FUTURE AREAS OF CONCERN
Wednesday afternoon, March 21, 1979
Moderator: Wesley W. Posvar, Ph.D.
Chancellor
University of Pittsburgh
POTENTIAL HEALTH PROBLEMS IN THE PRODUCTION
OF SYNTHETIC FUELS FROM COAL
By
Maurice A. Shapiro, Professor
LONG TERM HEALTH IMPLICATIONS OF RADIOACTIVE WASTE DISPOSAL
By
William D. Rowe, Ph.D.
AREAS OF UNCERTAINTY IN ESTIMATES OF HEALTH RISKS
By
Leonard D. Hamilton, M.D., Ph.D.
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POTENTIAL HEALTH PROBLEMS IN THE
PRODUCTION OF SYNTHETIC FUELS
FROM COAL
By
Maurice A. Shapiro, Professor
Carole S. Godfrey
Jan K. Wachter
and
George P. Kay
Environmental Health Engineering
Graduate School of Public Health
University of Pittsburgh
Pittsburgh, PA 15261
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Introduction
The first commercial coal hydrogenation (liquefaction) plant was
built at Leuna, Germany in 1926. With the evolution in design improvements
for this plant, liquid fuel products were generated which were comparable
in composition to those derived from petroleum. Twelve additional German
coal hydrogenation plants were eventually built so as to compensate for
the lack of that country's oil and gas supplies. It was these hydrogenation
plants that during World War II supplied over 85% of the aviation gasoline
used by the Luftwaffe. On March 8, 1979, the N.Y. Times reported that
the Sasol plant under construction in Secunda, South Africa will, in
1982, process 27 million tons of coal a year and produce 500 million
/•
gallons of liquid fuel per year. The plant will employ 7,500 workers.
One of the key goals of the Administration's energy planning has
been the achievement of greater American independence from foreign oil
and gas supplies. The United States currently utilizes oil for 46% of
its energy needs, natural gas for 32%, while coal provides only 17% (.1).
Since our known U.S. coal reserves (8000 x 10 Btu) far outweigh, the
U.S. oil reserves (200 x 1015 Btu), it is evident that the United States
will have to use coal or coal conversion products as a major means of
reaching such energy independence (2).
Several governmental agencies have reported that the U. S. coal
reserve base is approximately 400 billion tons. The Department of Energy
has estimated that by the year 2000, high- Btu gasification will supply
6.8 x 1015 Btu's and low-Btu gasification 1.8 x 1015 Btu's of energy (3).
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Approximately 176 sites have already been Identified in the U.S. each of
which have sufficient coal and water (large quantities of water are
required in the conversion process) to support the operations of a gasi-
fication plant (250 Mscf/day) for twenty years. If coal gasification and
liquefaction processes are expected to supply such vast quantities of
energy in the near future, it is imperative that potential health impacts
associated with synthetic fuel production be determined.
The aim of this paper is to evaluate the potential impacts of coal
conversion derived pollutants as they are transported and transformed in
air, water and soil and to ascertain the public and occupational health
consequences.
DRINKING WATER - POSSIBLE HEALTH EFFECTS
The effluents from coal conversion processes are numerous, with
the majority of streams being relatively clean and thus amenable to
recycling and/or safe disposal. Some of the residues are contaminated
by toxic and mutagenic substances and must be treated before discharge.
The generation of these by-products depends upon the interactions of ma.ior
factors in the design and operation of the coal conversion plant, such as
operating temperature, method of coal injection, and coal type. These
factors will affect the composition and ultimately the potential health
impacts of effluent streams derived from gasification and liquefaction
facilities. Based upon information obtained from existing pilot plants,
a full scale commercial gasification plant (250 Mscf/day of pipeline gas)
may be expected to generate between 0.4 and 1.2 million gallons of liquid
discharge per day. As an example of the range of contamination loadings,
a coal gasification plant generates approximately 50-100 Ibs of tar,
30-70 Ibs of oil and naptha, and 8-12 Ibs of phenols per ton of coal (4).
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Some other constituents expected to be present in the wastewater include
ammonia, cyanates, thiocyanates, arylamines, aliphatic hydrocarbons,
mono- and polycyclic hydrocarbons, organic-sulfur compounds, carboxylic
acids, esters, furans, tetralins and organometallic complexes.
To assess possible pollutant concentrations which may enter potable
water supplies and thereby affect health, it is necessary to investigate
pollutant removal efficiencies of various treatment methodologies. Methods
which could be utilized to treat coal gasification wastewater include:
ammonia stripping, solvent extraction of phenols, biological oxidation of
phenols and other organic constituents, and possibly carbon adsorption
and chlorination. Ozonation will probably not play a major role in the
wastewater treatment scheme due to its high cost and low efficiency (5).
The concentration of pollutants remaining after wastewater treatment
are shown in Table 1. This information is based upon data obtained from
operating pilot coal gasification wastewater treatment plants or by
extrapolation of results derived from treatment plants serving similar
industries. Using the concentrations in Table 1, it is possible to calcu-
late constituent concentrations of pollutants when dispersed and diluted
in specified receiving streams (Table 2). We chose specific locations on
the Allegheny and Monongahela Rivers to reflect possible future sites for
coal gasification facilities. As can be seen in Table 2, during average
flow conditions, the constituents will probably be diluted to such an
extent that their contribution to environmental concentrations will be
negligible. However, during 7-day, 10-year low flow conditions, some
constituents will not be sufficiently diluted so as to comply with various
stream quality standards. For instance, during the 7-day, 10-year low flow
of the Monongahela River at Charleroi, Pa., the increase of phenol concen-
tration above background in the receiving water exceeds the recommended
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Ippb standard for surface waters (6). Table 2 does not take into account
the background levels of constituents in receiving streams. It is possible
that the increase of some constituents due to coal conversion wastewater
when added to background concentrations may cause them to exceed water
quality standards.
Even though the load of pollutants, when diluted with receiving stream
water will generally be reduced to very low levels, review of the literature
indicates that there are some classes of compounds which warrant concern.
The classes of major concern are organic contaminants, cyanate and
thiocyanate, ammonia and hydrogen sulfide.
Organic Contaminants. Monohydric and dihydric phenols are major
organic compounds in wastewater generated during coal gasification.
These phenols can be reduced to trace concentrations by biological
oxidation. Phenols in drinking water lead to significant taste and odor
problems and possible health effects. It should be noted that chlorination
of phenol containing water usually increases taste and odor problems due
to the lower odor thresholds associated with chlorinated analogs of
certain phenols. Polycylic phenols are present in lower concentrations
than monocyclic phenols. The efficiency of removal of polycyclic phenol
by biological oxidation is less than that obtained for mono-and dihydric
phenols.
Monocyclic and polycyclic N-aromatics are present in small quantities
in coal gasification wastewater. The ingestion of pyridine (a major compound
in this class of organics) has been shown to cause liver and kidney damage (9).
Aliphatic acids may be present in coal conversion wastewaters at concen-
trations up to 700 mg/1, with acetic acid comprising approximately 85% of
this aliphatic acid section. In sufficiently dilute form, acetic acid is
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not toxic nor are its acetates, such as potassium a-nd sodium acetate.
Cyanide and Thiocyanate. Data on cyanide and thiocyanate concen-
trations in processed coal gasification wastewater is needed because of
these compounds' toxic properties. There are inconsistencies in the
literature regarding cyanide and thiocyanate quantities generated by
gasification operations. The same is true of the cyanide removal ef-
ficiencies of several treatment methods. Cyanide is present in coal
gasification wastewater at concentrations ranging from 0.01 and 2.28 mg/1,
and thiocyanate is present in raw coal gasification effluent in concen-
trations ranging from 20 to 400 mg/1. Given an average concentration of
thiocyanate (150 ppm) and a practical removal efficiency of 70%, then
approximately 45 ppm of thiocyanate ts expected to be present in treated
coal gasification wastewater. The average concentration of cyanide in
such treated wastewater is 0.6 mg/1. Reduction of cyanide concentrations
in wastewater has been reported to be as high as 90%. In general practice,
reduction of cyanide by biological oxidation is approximately 60%. Cyanide
at low concentrations [10 mg/1 or less] is converted in the human body to
the less toxic thiocyanate species (8). Upon chlorination, either at a
coal gasification plant or at a municipal water .treatment plant, cyanide
"is easily oxidized. The remaining concentration is below the health
effect threshold level.
Ammonia. Approximately 80% of the nitrogen in the feed coal is
converted to ammonia during coal gasification. Some 20-22 Ib of ammonia
are generated per ton of coal gasified. The average concentration of
ammonia in gasification wastewater is 7500 mg/1. Ammonia stripping, lime
treatment and biological oxidation are expected to reduce ammonia concen-
trations in treated coal gasification wastewater to a range of 5-15 mg/1.
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The presence of ammonia, nitrite and nitrate in potable water supplies results
in a variety of pollutional problems. Ammonia and its oxidized analogs
are potential algal and microbial nutrients in water distribution systems.
Ammonia also increases the chlorine demand at water treatment plants which
practice free-residual chlorination. In addition, ft increases the
biochemical oxygen demand in receiving waters.
The conversion of ammonia to nitrite and nitrate is a significant
occurrence due to the potential adverse effects of these compounds on
human health. The well known health hazards of nitrites and nitrates in
drinking water are the induction of methemoglobfnemia (especially in
infants) and the potential formation of carcinogenic nitrosamines.. In
infants, nitrite acts In blood to oxidize hemoglobin to methemoglobin, a
form which cannot act as a carrier of oxygen to the tissues leading to
anoxia and possible death. The reported concentration of nitrate in water
needed to induce methemoglobinemia varies from reference to reference.
However, very few cases have been related to drinking water containing less
than 10 mg/1 nitrate as nitrogen Ql). It is known that infants have been fed water
that contained larger amounts of nitrate without developing methemoglobinemia,
To assess the impact of nitrate in drinking water as a causal agent
of methemoglobi.nemia, one must determine what other sources of nitrate in
the environment will be ingested. An "average" person has a total daily
nitrite-nitrate intake of approximately 110 mg, with vegetables contributing
over 80% of the total input (.12). Water, on the other hand, contributes
no nitrite and 0.7% nitrate as compared to other sources.
Upon dilution with stream or process, water, the concentration of
ammonia would be considerably less than the 5-15 mg/1 present in the
treated coal gasification wastewater. Assuming that all of this ammonia
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is converted to nitrate, it is likely that the resulting concentration
would be below the threshold for methemoglobinemia. However, when the
contributions of nitrate and nitrite from diet, air and water supplies are
added, the amount of ammonia present in coal gasification effluents which
is then converted to nitrate and nitrite may exascerbate existing problems.
Adverse health impacts may also ensue when nitrates are converted to
carcinogenic N-nitroso compounds in water. The contribution of nitrate
transformed to N-nitroso compounds in water compared with the amount
contributed by food ingestion has not been sufficiently well determined.
However, epidemiological studies have correlated the increased incidence
of gastric cancer with elevated nitrate levels (90-110 mg/l)in drinking
water 03).
Hydrogen Sulfide. Hydrogen sulfide ^S) has been reported as being
present in untreated coal gasification wastewater in a range of concentrations
from < 5 mg/1 to 250 mg/1. Biological oxidation and acid gas stripping have
been reported to be 97% and 99% effective in removing H2S from wastewater.
The toxic properties of H2S are exerted in the undissociated form.
The extent of dissociation is largely dependent upon pH, with approximately
50% dissociation occurring at pH 7.0. If oxygen is present in the water
at concentrations above 0.025 mg/1, then HpS will probably be converted
into sulfate. If sulfide is not converted into sulfate, it would most
likely form insoluble metal sulfide complexes due to its strong ligand
properties.
SOL mi WASTES - POSSIBLE HEALTH EFFECTS
Solid wastes along with contaminated liquids are generated during
coal conversion operations. Solid residues from coal gasification include
ash and char from the gasifier, desulfurization and wastewater treatment
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sludges, and disposable catalysts. The volume of solids generated depends
on the characteristics of the feed coal and the conversion process. The
literature reports that typically a 250 Mscf/day gasified will produce
3000-4000 tons/day of ash and char (14). These gasification solid wastes
contain higher concentrations of trace elements than the feed coal.
Somerville et_ al_. (15) have shown that 81% by weight of the major and
trace inorganic elements in the feed coal exit with the ash. In the coal
ash, the major constituents are complexes of aluminum, calcium, iron,
potassium, magnesium, sodium and silicon.
The potential for trace element contamination of ground or surface
water by leachates derived from land-filled or ponded ash depends on the
chemical and physical characteristics of the stored sludge and ash, its
rate of application, the soil characteristics and the hydrological regime
of the area. Uptake and toxicity to flora and fauna (especially micro-
organisms) must be considered. The transport of trace elements in the
soil depends upon the rate of water movement, adsorption capacities and
chemical reactions taking place within the soil profile.
Trace elements sorbed on soil will be strongly held by some soils
and thus prevent rapid leaching of many elements into surface and ground
waters. Factors affecting trace element attenuation by soil include pH,
oxygen availability, soil particle size distribution, cation exchange
capacity, amount and type of hydroxides and oxides of Fe, Mn, and Al,
pore size, and concentration of organic material, salt, and microorganisms.
The literature emphasizes a concern about the presence and behavior
in coal gasification ash of the following elements: arsenic, cadmium,
chromium, fluorine, mercury, sulfur, and selenium.
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Arsenic. Health effects have been associated with the ingestion of
drinking water with high concentration of arsenic. In Antofagasta, Chile,
a city with a population of 100,000, drinking water was reported to contain
a weighted average arsenic concentration of approximately 600 g/1 (16)..
This high arsenic concentration was linked to a high incidence of cutaneous
skin lesions (145.5/100,000 for males and 168/100,000 for females). After
the installation of a water treatment plant, the arsenic content of the water
was reduced to 80 ug/1, while the incidence of cutaneous skin lesions
dropped to 9.1/100,000 for males and 10/100,000 for females. Pue to the
low concentration of arsenic present in coal gasification ash, it Is
expected that most soils will have the ability to attenuate arsenic
sufficiently through, such mechanisms as, copreclpitati.on with, sulflde,
ferric hydroxide, ferric chloride, and ferric sulfate.
Cadmium. Food is the primary source of cadmium intake for man.
The total daily intake of cadmium from air, water, food, and tobacco
ranges from 40-190 ug/day. Drinking water contributes only a small
fraction (/less than 5%). of the total (.11). A variety of disease states
are thought to be influenced or caused by high levels of cadmium in
various organs. Chronic ingestion of cadmium at levels of greater than
600 ug/day has been reported to be responsible for the onset of
"Itai-Itai" disease in Japan (.11). Along with its kidney toxi.city, there
has also been some indications in animal studies that cadmium is
carcinogenic and/or teratogenic. Cadmium is present in gasification ash
at a concentration of approximately 0.2ppm. Cadmium also has a very low
solubility in water. Due to these two factors, it does not seem likely
that cadmium in coal gasification and liquefaction ash would contami-
nate drinking water su'pplies at levels which cause disease.
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Chromium. Concentrations of chromium in natural waters are limited
by the low solubility of chromium (III) oxides. Very little infor-
mation is available on the average total daily intake of chromium, although
it appears to be slightly lower than the intake for cadmium. On the average,
approximately 0.04% (400 ppm) of coal gasification and liquefaction ash
is composed of chromium. This is a significant fraction given the huge
amount of ash expected to be generated. There are many inconsistencies in
the literature regarding the renovatton potential of soil for chromium.
However, even though chromium is relatevely insoluble in water, it is
considered a potential hazardous compound In ash due to the many
uncertainties about its behavior in the environment.
Fluoride. Fluoride, due to its anionic nature, is not attenuated
to any great degree by the soil. The lethal dose of sodium fluoride for
man is 5 g CI7). We know that teeth and bone are the most fluoride
sensitive tissues. National Academy of Sciences (11) have concluded that
symptomatic skeletal fluorosis can occur at a level as low as 3 ppm.
They have also concluded that the possibility of fluoride causing adverse
effects such as allergic responses, mongolfsm, and cancer has not been
adequately documented.
Sulfur. Sulfur is one of the major components of coal gasification
ash. In anaerobic environments, sulfur is usually present as sulfide
(S~). In this species, it can easily form insoluble precipitates.
However, under aerobic conditions, sulfur is oxidized to sulfate (SO/"}.
National Academy of Sciences (11) have concluded that no adverse health
effects have been noted when the concentration of sulfate in water is less
than 500 mg/1. The observed physiological effect at concentrations
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greater than 1,000 mg/1 is the induction of diarrhea.
Selenium. Selenium is easily volatilized during gasification and emitted
to the atmosphere. Therefore, the amount of selenium in coal gasification
ash is very small and other sources of selenium (e.g. diet) will over-
shadow the possible contribution of selenium from coal gasification solid
residue. Mercury, likewise, is easily volatilized and can be emitted as
a vapor from coal gasification stacks. Therefore, its environmental effect
due to its presence in ash or sludge will be minimal.
HEALTH IMPLICATIONS OF AIR POLLUTANTS
Potential atmospheric pollutants from synthetic fuel production arises
from the auxiliary operations as well as the actual conversion process.
A list of some of the potentially hazardous substances follows in the
section dealing with occupational health problems. These substances
may be present in coal conversion process streams; however, because of the
enclosed and pressurized nature of a gasification or liquifaction system,
air emissions during regular plant operations are expected to arise
mainly from the auxiliary operations. During startup or in an emergency,
emissions could be of high rates but of short duration and, for
high-BTU gasification, are expected to be less than one percent of
the total plant air emissions. Emissions from the gasification process
itself would arise mainly from leaks in pump-seals, joints, flanges,
compressors, etc., and from venting operations (18). Quantities of the
major gaseous effluent streams from the various processes are compared in
Table 3 with the corresponding streams from a large power plant using
recycled cooling water (19).
Because published data on emissions from coal conversion plants is
sparse (20) only auxiliary operations were considered in the ERDA
Synthetic Fuels Commercialtzation Program Report (21) which estimated air
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emissions from coal conversion plants. In order to make the resulting
pollutant loads meaningful, they were calculated for a conversion facility
that would produce enough fuel to support a 1000 MW power plant operating
at 33 percent efficienty. Table 4 indicates ambient air quality contribu-
tors of such a plant. National Ambient Air Quality Standards are shown in
the headiros (21). Of interest is the relative contribution of gasification
plants to ambient air quality. The ratio of sulfur dioxide derived from the
gasificiation plant to the Annual Average Standard ranged from.0.01 to 0.24;
the N0? ratio ranged from 0.01 to 0.22; particulates from 0.0 to 0.3; and
hydrocarbons ranged from 0 to 0.04 of the Three Hour Maximum Standard.
Some of these amounts are important contributions to the ambient load.
The median and 90th percentile values for total suspended particulates
gathered by State and local air pollution control agencies are presented
in Table 5 along with the secondary National Ambient Air Quality
Standard Values (22). Since the ambient air quality in certain
situations already exceeds the standard, the contribution of such a
gasification plant could add to the already high ambient levels.
Experimental "Hygas" bench scale results indicate that much of the
total flow of trace elements would get into downstream process systems
and eventually be removed in the gas quench, shift conversion, acid-gas
removal, or-on catalyst surfaces. However, data from the Synthane pilot
plant gasifier indicate that a major fraction of trace elements concentrate
in the char residue which may be burned in the utility boiler, releasing
them to the atmosphere upon combustion. Therefore, the amount of trace
element concentration would be increased 4 to 5 times over that normally
emitted by a coal fed boiler of similar-size (23). The background concentration
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of several metals and the contribution from possible coal use projected
in the year 2020 is given in Table 6; potential violations of suggested
acceptable atmospheric trace element concentrations are primarily due to already
higher background levels. In a report of the Argonne National Laboratory on coal
utilization in the Illinois River Basin, it is stated that the gastro-
intestinal tract, rather than the respiratory system, could be the most
significant route of entry for coal related air and waterborne trace ele-
ments. The significance of the gastrointestinal tract is further enhanced
if dietary trace element intake were added. Moreover, uptake of trace
elements in food materials due to higher ambient levels in air may increase
such a contribution. In spite of this, projected coal utilization is not
anticipated as a prime contributor of trace element body-burden, but it
could account for as much as one-third of the vanadium and one-tenth of
the chromium body burden in exposed populations (24).
Combustion of fossil fuels accounts for a substantial portion of
atmospheric contamination by mercury. Studies of persons occupationally
exposed indicated a dose-response relationship involving the nervous
3
system starting with concentrations as low as 0.1 mg/m . Mercury, there-
fore, in ambient air probably represents little if any health problems for
the general population (25).
Also to be considered is the radiological impact of emissions due
to conversion processes. Based on results of analyses of coal, SRC solid
fuel, and flyash samples from both, the following observations were made:
1. Uranium levels were less than thorium in
all cases except for SRC particulates
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2. Uranium and thorium were more concentrated
in particulate samples than in the coal
and SRC solid fuel
3. Literature cited in the report (26) indicated
that at least 90 percent of the uranium is
expected to be retained in the bottom ash and
collected fly ash
The estimated level of U-238 expected to be discharged from a power
plant which combusts SRC solid fuel is 0.2 ug/m3 which is an order of
magnitude less than the 7 ug/m3 "general public" exposure standard for
air (26).
Although many potentially hazardous materials are residues of the
coal conversion process, there is no direct, continuous atmospheric
emission of these substances (27). Concentrations of some organic com-
pounds found in an urban atmosphere, and also suspected present in coal
conversion process streams are shown in Table 7. Polycyclic aromatic
hydrocarbons (PAH) can be readily absorbed by animals through ingestion,
inhalation, or skin contact (29); the carcinogenicity of PAH adsorbed onto
polycyclic organic material (POM) through inhalation has been documented
with experimental animals (30). However, in 1970,BaP concentrations in over
100 United States cities were one to two orders of magnitude less than 0.12
ug/m3, the suggested maximum concentration of atmospheric BP (31). Since
the coal conversion process is expected to be a more controlled system
than coking, its pollution contribution should be less.
OCCUPATIONAL HEALTH CONSIDERATIONS
The first occupational cancers were reported as far back as 1775,
when the prevalence of scrota! cancer among British chimney sweeps was
determined to be eight times that of the general populace (32). Chimney
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soot was identified as the suspected carcinogen. One hundred and thirty-two
years later, England officially acknowledged epitheliomatous cancer or
ulceration from exposure to pitch, tar, and tarry compounds as valid grounds
for workmen's compensation (33, 34). Today, industrial materials such as
soot, shale oil, certain aromatic amines, coal tar, and isopropyl oil,
among others, are recognized occupational carcinogens (35, 36).
Fpidemiological evidence has conclusively shown that workers routinely
exposed to the combustion and/or distillation products of bituminous coal
run an increased risk of developing cancer of the skin or viscera
(37, 38, 39).
Although large-scale coal hydrogenation plants were operated in
Germany in the 1920's, Britain in the 1930's and South Africa in the
1950's, the best insight we have into the potential health effects of
coal conversion is the result of a pilot plant operated at Institute,
West Virginia during most of the 1950's. This Union Carbide
facility produced chemicals via coal hydrogenation (liquefaction) with
a design capacity of 300 tons coal/day. Even before the Institute Plant
"went on Tin?" in 1952, it was known that the facility would generate a
wide variety of chemicals, many which would pose potential acute or chronic
health hazards to the workers. Over two hundred individual chemicals were
eventually identified from the Institute plant (40), the majority of which
fit into the following six classes of compounds:
a. ) aliphatic hydrocarbons
b. ) single ring aromatics
c. ) polynuclear aromatics
d. ) phenols
e. ) aromatic amines
f. ) N-heterocyclic aromatics
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However, several inorganic gases as well as dusts and particulates were
also found to be present in the plant environment.
During the first two years of operation several intermediate and
final products of the Institute facility were painted on the skin of mice
to test for tumorigenicity (41). The light oil stream and its eight
fractions did not exhibit any tumorigenic activity. As a rule, these
light oil stream fractions have relatively low boiling ranges, phenolic
pitch being the only component separating above 260°C. Conversely, the
process streams and residue boiling at higher temperatures (middle oil
stream, light oil stream residue, pasting oil stream, and pitch product
stream) were all demonstrated to be highly carcinogenic to the skin of
mice. Carcinogens implicated by these results include polycyclic aromatics
such as phenanthrene (bp 339°C), perylene(sub 350-400°C), picene (bp 520°C),
and pyrene (bp 404°C) (42). The structural formulae of these and other
high boiling, polycyclic aromatic constituents of coal-tar are depicted
in Figure 1.
The Institute work force was thoroughly warned of the results of the
animal studies in late 1952 and 1953. Moreover, the workers were provided
with safety education and changes of clothing during work. Despite these
precautions, cases of skin cancer were discovered among the work force.
Dr. R.J. Sexton, the plant's medical director, examined for five years
the 359 men regularly assigned to work the plant area. Sexton found nine
workers with one cutaneous cancer each and one worker with two cutaneous
cancers as shown in Table 8. He also found forty workers with one cutaneous
precancerous lesion each as shown in Table 9 (34, 44). This incidence of
skin cancer is many times that of either West Virginia or the United
States (34). These skin abnormalities were believed to have resulted
-463-
-------
from occupational exposure to coal tar, pitch, or high boiling-polycyclic
aromatics primarily via air-borne Cvapor or condensed droplet)
contamination routes (45, 46).
In a study conducted by the Stanford Research Institute (44) nine of
i.K ten workers described in Table 8 and all forty workers listed in Table
9 were follcwed-up in order to determine their vital status as of July
1977. Of the ten workers originally diagnosed with skin cancer, two died
in the intervening period from causes other than cancer, two retired
(one of whom is ill with lung cancer), five were still working, and one
subject could not be found. Of the forty workers diagnosed with pre-
cancerous skin lesions, three died from causes other than cancer,
thirteen retired, twenty-three were still working, and one retiree was
hospitalized with Parkinson's disease and prostate cancer. The Stanford
researchers note:
that the available data do not support the
initial hypothesis; that those workers exposed to
heavy streams of toxic materials from the coal hy-
drogenation process, with evidence of cancerous
skin lesions, may be at increased risk of developing
systemic carcinoma. This observation is based upon
a marked lack of cancer-related deaths or morbidity
in both the confirmed skin cancer group and the pre-
cursor group, after a latency period of 18-20 years.
Nonetheless, two additional facts merit consideration - a. ) that the
cohort under examination was small; and b. ) that the 309 workers who
did not exhibit lesions in the Sexton study (34) were not examined in
the Stanford study (44). Few health effect studies, other than the one
conducted at the Institute facility, have been reported. Hueper (47,48)
tested the carcinogenicity of Bergius and Fischer-Tropsch oils obtained
from the experimental coal hydrogenation-liquefaction facility at
Bruceton, Pennsylvania. Fractions were tested by repeated application
-464-
-------
to the skin of mice and rabbits, and I.M. injections to the thighs of rats.
Eight of nine Bergius oil fractionation products were found to be
carcinogenic, the degree of carcinogenicity usually increasing with
boiling points. Fischer-Tropsch products were less carcinogenic and seemed
to have a narrower species and tissue susceptibility spectrum.
Epidemiological studies of gasworks and coking operations (38, 39, 49, 50)
have provided some insight into the potential health effects of coal conversion
plants because the types of toxic chemicals present are similar. However,
coal conversion plants operate by necessity with good containment and
worker exposure to these agents is projected to be much less than in the
aforementioned industries (42).
Researchers at Battelle-Columbus Laboratories (43) examined the potential
occupational health effects of three gasification processes: the high-pressure,
fixed-bed system; the atmospheric-pressure, entrained-suspension system; and the
atmospheric-pressure, fluidized bed system. In all of the gasification schemes
the greatest carcinogenic potential was determined to exist in the early process
stages, when the complex organic constituents of coal undergo structure! degrad-
ation. It is during these early operations that the risk of spills or leaks
must be minimized. In the later stages, the output of the gasifier approaches
a typical gas in composition and the carcinogenic potential is eliminated or
minimized. Coal liquefaction processes pose a greater danger to the workers.
Sophisticated engineering and industrial hygiene programs will be required in
order to minimize worker contact, both dermal and respiratory, with organic
compounds such as phenanthrenes, pyrenes, 1, 2-benzanthracenes, chrysenes, and
five-ringed compounds.
-465-
-------
We believe that worker exposure at future commercial-scale,
conversion facilities will be maximal during shutdowns or equipment
modifications/replacements attempted during periods of operation. Under
such circumstances workers may be required to open process lines or enter
vessels. It is worth noting that most of the skin cancer subjects
reported by Sexton and shown in Table 8 were engaged in plant maintenance
at the Institute, W. Va. facility. Our major concern is the exposure of
such maintenance workers to the known carcinogens and cocarcinogens listed
in Table 10. Most of the other chemicals present, as well as physical
agents (heat and noise), can be dealt with by good industrial hygiene
practice.
-466-
-------
-J
I
Table 1. Representative Water Pollutant Loadings from a 250 Mscf/day Synthetic Natural Gas
Plant Using Illinois H Coal
Untreated
Treated(a)
Efficiency of
Treatment Based
on Loading Reduction (%)
Parameter
TSS
pH
Phenols
Oil
COD
BOD
NH3
Cyanide
Total Solids
Thiocyanate
Phosphate as P
Chloride
Fluoride
S04
Fe
Pb
Mg
Zn
As
Cu
Cr
Cd
Mn
Ni
Al
Se
Ba
Cone, (mg/1)
600
8.6
2,600
7,500
15,000
2,300
8,000
0.6
1,400
150
2.5
500
56
-
3
3
2
0.06
0.03
0.02
0.006
0.006
0.04
0.03
0.8
0.36
0.13
Loading (Ib/day)
16,500
-
71,500
13,800
413,000
62,400
220,000
16.5
38,500
4,130
6.9
13,800
1,540
39,000
82.5
82.5
55
1.65
0.83
0.55
0.16
0.16
1.1
0.83
22
9.9
3.6
Cone, (mg/1)
20
8.5
0.4
5
90
14
7.5
0.1
12
45
0.3
25
6
12.1
-
-
-
-
-
-
-
-
—
-
-
-
•"
Loading (Ib/day)
550
-
10
138
2,500
375
206
2.75
330
1,239
8.3
688
165
334
-
-
-
-
-
-
-
-
-
-
-
-
™~
97
—
99+
99+
99
99
99+
83
99
70
88
95
89
99
-
-
-
-
-
—
—
—
-
"-
-
-
~~
(a) Flow of condensate is approximately 5.0 cfs
Source: Adapted in part from Argonne National Laboratory (7).
-------
Table 2, Coal Gasification V/astewater Constituent Reduction Via Receiving Stream Dilution
Constiiuent
TSS
Phenols
Oil
COD
BOD
NU
Cyanide
Total Solids
Thiocyanate
Phosphate as P
Chloride
Fluoride
Treated
Condensate
Concentrations
20
0.4
5
90
14
7.5
0.1
12
45
0.3
25
6
Concentration (rog/1) of
streams of the following
constituent after dilution with receiving
flov/ rates ( c ) :
Monongahela River at Charleroi, PA
7-day, 10-year low flow
(420 cfs)
0.23
0.005
0.06
1.0
0.16
0.087
0.001
0.14
0.52
.0.003
0.29
0.07
Average flow
(8975 cfs)
0.0010
0.0002
0.003
0.05
0.0077
0.0041
0.00006
0.0066
0.025 '
0.0002
0.014
0.003
Allegheny River
7-day, 10-year low
(2,700 cfs)
0.037
0.0007
0.01
0.2
0.026
0.014
0.0002
0. 022
0.083
0.0007
0.047
0.01
at Kit tanning , PA
flow Average flov;
(15,570 cfs)
0.0063
O.CC01
0.002
0.03
G.G04.4
O.CC24
0.00003
O.C033
0.01/1
0.0001
O.OOol
0.002
oo
I
(a) Assumed condensate flov/ of approximately 5,0 ofs
(b) Values obtained from Reference (7)
(c) Receiving stream water assumed to contain zero concentration of parameter before addition of condensate;
complete dispersion is also assumed; 7-day, 10-year low flow and average flow values were obtained
from Kay et al. (8).
-------
TABLE 3, MAJOR GASEOUS EFFLUENT STREAMS (19)
PROCESSES GASEOUS EFFLUENT STREAMS, TON/DAY
C02 + FLUE GASQ C,T, AiRb NITROGENC
'LOW- AND MEDIUM-
I BTU GASIFICATION 4,900-19,200 600,000-2,221,000 0-38,000
HlGCA?ioNGASIFI~ 45,000-94,000 546,000-3,264,000 0-21,000
LIQUEFACTION 39,000-66,000 1,250,000-2,655,000 6,000-16,000
1,000 MI'/E POWER
PLANT (EXAMPLE) 110,000 3,500,000 0
SOURCE: Magee [19}
a Contains combustibles, sulfur.compounds, and oxides of nitrogen,
b Effluent cooling tower air may contain volatile organic or inorganic
compounds present from leaks or other sources,
c Waste nitrogen streams from oxygen plants are usually clean.
-------
TABLE 4. AMBIENT AIR QUALITY CONTRIBUTIONS OF UNIT
HIGH-BTU FIXED-BED GASIFICATION PLANT (21)
Region/Distance
Appalachia
1 km from plant
Stability Class B
Stability Class D
5 km from plant
Stability Class B
Stability Class D
Eastern Interior
1 km from plant
Stability Class B
Stability Class D
5 km from plant
Stability Class B
Stability Class D
Ambient Air Concentration (ug/m )
Sulfur Dioxide
Annual Avg.
(STD 80)
yg/m3)(a)
19
1
8
11
19
1
8
11
24-Hr. Max.
(STD 365)
ug/m3)(a)
61
3
23
34
65
3
27
34
3-Hr. Max.
(STD 1300
Ug/m3)(b>
92
4
34
50
99
4
38
53
Nitrogen
Dioxide
Annual Avg.
(STD 100
Pg/m3)(b)
19
1
3
10
22
1
4
11
Particulates
Annual Avg.
(STD 60
ug/m3)^
4
18
Q
3
5
16
1
2
24 -Hr. Max.
(STD 150
Ve/J)w
12
60
1
9
16
52
2
9
Hydro-, ^
carbons ;
3-Hr. Max.
(STD 160
Vg/m3)(b)
4
0
1
2
6
1
1
3
O
.1
(a) These values are the primary '/ational Ambient Air Quality Standard values,
(b) These values are the secondary National Ambient Air Quality Standard values.
(c) Hydrocarbons are a precursor to the formation of photochemical oxidants. The 1-hour secondary National
Ambient Air Quality Standa.u for Oxidants is 160 yg/m ,
Stability Classes refer ^o atmospheric stability; Class B is unstable; Class D is neutral.
Highest pollutant emission rates which resulted from various coals were used in these cal-
culations of ambient a-r concentration. Possibly used control efficiencies of 99,7% for
particulate removal, 23% NOX removal, 85% FGD, 95% for sulfui- recovery,
—^~, T?T»nA f)'\
-------
TABLE 5, 1976 CONCENTRATIONS OF TOTAL SUSPENDED PARTICULATES (22)
(UG/M3)
ANNUAL MEAN (2350 SITES)
PEAK DAILY (2350 SITES)
REGION III ANNUAL MEANA
REGION V ANNUAL MEANB
ANNUAL AVERAGE (SEC, NAAQ STD)
24-HouR MAXIMUM ( " )
MEDIAN
66
365
55
60
60
150
90™
90
325
90
95
A PENNSYLVANIA, WEST VIRGINIA, VIRGINIA
B OHIO, INDIANA, ILLINOIS, ETC,
Adapted from U.S.E.P.A. (22).
-------
TABLE 6. BACKGROUND URBAN AND NON-URBAN AIR QUALITY AND PROJECTED
3-HOUR AND 24-HOUR AIR QUALITY DUE TO PROJECTED 2020 COAL
UTILIZATION IN THE ILLINOIS RIVER BASIli (ug/m3)
As
Continuous Exposure
Standard 0.17
Annual average
N> Urban Air
Non-urban Air
Be
0.0066
.00002
.00001
Cd
0.17
.0025
.0001
Cr
Cu
0.33 0.33
Background
.0054
.0028
.106
.1264
Concentrations due
24-hr, maximum .00056
3-hr, maximum .029
.000064
.0033
.00015
.008
.00056
.029
.00012
,0063
Fe
Hg
0.03 16
Concentrations
1.17
,24
to 2020
.21
10.9
-
-
Mn
,5
.032b
.007
Ni
3.3
,082
,001
Pb Se
0,5 0,66
.886
.578
V
0.17
,010
,001
Zn
3,3
.32
.10
Coal Utilization
.000013
,0067
.00098
,051
.00054
,028
.0029 ,00032
.152 ,017
, 00087
.046
.0058
.304
Q
From G. Ackland et al., "Air Quality Data for Metals 1970-1974 from the National Air Surveillance Networks,"
Environmental Monitoring and Support Lab, Research Park, North Carolina, EPA-600/4-76-041, August 1976.
b o
Environmental Health Resource Center suggests a 24 Hour Average of 0.006 ug/m based on synergram with
sulfur dioxide.
Adapted from Argonne National Laboratory (24).
-------
TABLE 7, CONCENTRATIONS OF SOME LARGE ORGANIC COMPOUNDS
IN THE AVERAGE AMERICAN URBAN ATMOSPHERE (28)
COMPOUND AI-RBORNE PARTICULATES PG/M
BENZO (A) PYRENE 0,0057
BENZO (E) PYRENE 0,005
FLUORANTHENE 0,004
PERYLENE 0,0007
BENZO (G, H, i) PERYLENE 0,008
CORONENE 0,002
SOURCE: Sawicki (28)
-------
TABLE 8 : CUTANEOUS CANCER CASES IN 359 COAL HYDROGENATION WORKERS* EXAMINED FOR FIVE YEARS
Subjects
Case Age
1 30
2 33
3 29
4 37
5 43
5 43
6 34
7 46
8 40
9 33
10 38
Job
Assignment
Operations
Maintenance
Maintenance
Maintenance
Maintenance
Maintenance
Operations
Operations
Operations
Maintenance
Maintenance
Length of
Exposure
( months )
41
62
12
48
108
132
83
83
116
60
72
Diagnoses
Body Site
Forearm, right
Cheek, left
Cheek, left
Buttock, left
Hand, left
Ear, right
Hand, left
Neck, postero-
lateral, right
Ear, right
Leg, left
Leg, right
Local Pathologist
Basal-cell
carcinoma
Basal -cell
carcinoma
Squamous-cell
carcinoma
Squamous-cell
carcinoma
Squamous-cell
Mixed basal and
Squamous-cell
carcinoma
Intraepithelial
squamous-cell
carcinoma
Squamous-cell
carcinoma
Squamous-cell
carcinoma
Keratosis
Keratosis
Out-of-Town Pathologist
Malherbe's calcifying
epithelioma
Basal -cell epithelioma
No pathology done,
clinical diagnosis only
Inverted follicular
keratoma type of sebor-
rheic keratosis
Squamous-cell carcinoma.
Metatypical carcinoma
Bowenoid keratosis
Prickle-cell epithe-
1 i oma
Keratoacanthoma
Intraepithelial
squamous-cell
carcinoma
Squamous-cell carcinoma i
* White Males Only
Source: Sexton (34)
-------
.c-
•vj
TABLE 9
SIW\RY OF PRECANCEROUS CUTANEOUS
LESIONS AMONG 359 COAL HYDROGENATION' WORKERS*
FOR FIVE YEARS
Histological Diagnoses
Pitch Acne1
Chondrodermatitis
helicis
2
Keratoses
Keratoses
Acanthoses and hyper-
keratoses
Number
of
Cases
3
3
17
8
9
Mean
Subject's
Age
30
33
39
44
40
Length of
Min.
10
3-5
• 10
17
5
Exposure (months)
Max.
74
52
116
96
108
* White Males Only
1. Clinical Diagnoses Only
2. Diagnoses by a single pathologist only
SOURCE: Sexton (34) and SRI International (44),
-------
TABLE 10
MAJOR CONSTITUENTS OF COAL CONVERSION PROCESS STREAMS AND EMISSIONS
CONSTITUENTS
PHYSICAL STATE
OSHA STANDARD*
OCCUPATIONAL SIGNIFICANCE
ALIPHATIC HYDROCARBONS
AMMONIA
AROMATIC AMINES
SINGLE-RING AROMATICS
CARBON DISULFIDE
CARBON MONOXIDE
CARBONYL SULFIDE
HETEROCYCLIC AROMATICS
HYDROGEN CHLORIDE
GAS OR VAPOR
GAS
LIQUIDS OR SOLIDS
LIQUIDS AND SOLIDS
LIQUID
GAS
GAS
LIQUIDS AND SOLIDS
GAS
50 PPM
5 PPM FOR ANILINE AND
TOLUIDENE; NO SAFE LIMIT
FOR B-NAPTHYLAMINE AND
BENZIDENE
10 PPM FOR BENZENE
20 PPM
50 PPM
NO STANDARD
5 PPM FOR PYRIDINE; NO
STANDARD FOR ACRIDINE
5 PPM CEILING
UNLIKELY THAT MOST WILL PRESENT
SIGNIFICANT HAZARD, EXCEPT FOR
DODECANE - A POTENTIATOR OF SKIN
TUMORIGENESIS BY BaP
NO EVIDENCE OF ILL EFFECTS FROM
PROLONGED EXPOSURE TO SUBIRRITANT
CONCENTRATIONS
ANILINE & SUBSTITUTED BENZENES AR2
HIGHLY TOXIC; B-NAPTHYLAMIiJE AND
BENZIDENE ARE POTENT CARCINOGENS
VAPOR HAZARDS ARE ONLY LIKELY WITH
BENZENE AND RELATED COMPOUNDS OF
RELATIVELY LOW MOLECULAR WEIGHT
ACUTE EFFECTS WOULD ONLY BE RESULT
OF LARGE LEAK IN PROCESS STREAM;
CHRONIC POISONING IS MORE SERIOUS
HAZARD
CHRONIC LOW-LEVEL EXPOSURE EFFECTS
ARE CONTROVERSIAL
LITTLE EVIDENCE OF HUMAN TOXICITY
ALTHOUGH IT IS PROBABLY LESS
HAZARDOUS THAN HgS
N-HETEROCYCLIC COMPOUNDS ARE THE
ONES OF MAIN INTEREST (SKIN AND
MUCOUS MEMBRANE IRRITANTS,
POSSIBLE POTENTIATORS
IRRITANT
-------
TABLE 10 (CONT.)
CONSTITUENTS
PHYSICAL STATE
OSHA STANDARD*
OCCUPATIQNAL SIGNIFICANCE
1
•vj
--J
1
HYDROGEN SUXFIDE
MINERAL DUST & ASH
NICKEL CARBONYL
NITROGEN OXIDES
NITROSAMINES
PHENOLS
POLYCYCLIC
ARffi/ATICS
TRACE ELEMENTS - As,
Be, Cd, Pb, Mn, Hg,
Se, and V&
SULFUR OXIDES
GAS
PARTICULATE
LIQUID
GASES
LIQUIDS & VAPORS
SOLIDS OR LIQUID
MIXTURES
SOLIDS
SOLIDS
GAS OR AEROSOL
20 PPM CEILING;
50 PPM 10 MIN. PEAK
—
Vug nf 3
5 PPM FOR N-DIOXIDE
EXCEPTIONALLY
DANGEROUS
CARCINOGEN
5 PPM
NO SAFE LIMITS '
2(Be) - 500 (As, Va)
ug m~3
5 PPM
STRONG IRRITANT; POSSIBLE
COAGENT FOR CARCINOGENS
POSSIBLE VEHICLE FOR PAH
VAPOR INHALATION AFFECTS CNS
& MAY INDUCE CHEMICAL
PNEUMONITIS
SOURCE OF NOX (SEE NEXT LINE)
IT HAS BEEN HYPOTHESIZED THAT
NOX FROM COMBUSTION MAY REACT
WITH VAPOR FROM GLYCOLAMINE
SCRUBBERS TO YIELD THESE
CARCINOGENS.
POTENTIAL ENHANCEMENT OF
SKIN AND RESPIRATORY CARCINOGENS
WELL ESTABLISHED AS SKIN CARCINO-
GENS, LESS SO AS RESPIRATORY
CARCINOGENS. BaP IS HIGHLY
CARCINOGENIC
PROBABLY NO ATMOSPHERIC HAZARD
IN VICINITY OF PLANT, BUT THEY
MAY POSE HAZARD TO WORKERS
CLEANING FILTERS & STACK
DEPOSITS AND MAINTAINING
TOPS OF GASIFIERS
POSSIBLE COCARCINOGEN
*- TIME-WEIGHTED AVERAGE UNLESS OTHERWISE SPECIFIED
ADAPTED FROM ENVIRO CONTROL (42)
-------
FIGURE 1
POLYCYCLIC AROMATIC CONSTITUENTS OF COAL-TAR
BOILING POINT RANGE
ABOVE 300' C.
oo
I
NONADE.CANE
b «8
-------
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-479-
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Carolina; June 1976.
20. Cavanaugh, G., et al. Potentially Hazardous Emissions from the
Extraction and Processing of Coal and Oil, EPA-650/2-75-038,
U.S. EPA; Washington, D.C.; 1975.
Hittman Associates, Inc. Environmental Impact, Efficiency
and Cost of Energy Supply and End Use, Volume II. Columbia,
Maryland, 1975-
Radian Corporation. A Western Regional Energy Development
Study (Draft); Austin, Texas. 1975.
-480-
-------
21. ERDA Syn. Fuels Com. Prog. Draft Env. Prog. ERDA
U.S. Gov. Ptg; Wash., D.C.; Dec. 1975-
22. U.S. EPA. National Ambient Air Quality and Emissions Trends
report 1976, EPA-450/1-77-002 . U.S. Gov. Prtg Office;
Washington, D.C.; December 1977.
23. Argonne National Laboratory. National Coal Utilization
Assessment - An Integrated Assessment of Increased Coal
Use in the Midwest: Impacts and Constraints. Volume II.
ANA/AA-11, (Draft), Argonne, Illinois, October, 1977-
24. Ibid
25. American Thoracic Society, Medical Section of American Lung
Assoc. Health Effects of Air Pollution. 1978.
26. Koester, Pamela A. and Warren H. Zieger. Analysis for Radio-
nuclides in SRC and Coal Combustion Samples. EPA-600/7-78-185.
U.S. EPA. Washington, D.C. September 1978.
27. ERDA. Syn. Fuels Com. Prog. (Draft) Env. Prog. ERDA-15^7. U.S.
Gov. Prtg. Off.; Washington, D.C.; Dec. 1975-
28. Sawicki, E. et al. "Quantitative Composition of Urban Atmos-
phere in Terms of Polynuclear AZA Heterocyclic Compounds
and Aliphatic and Polynuclear Aromatic Hydrocarbons," Int.
J. Air Water Pollution. 9, 515. 1965.
29. EPA. "Scientific and Tech. Assessment Report on Particulate
Polycyclic Organic Material (PPOM) . EPA-600/6-75-001 . 1975.
30. Braunstein,H.M. et al. eds. Env., Health, and Control Aspects
of Coal Conversion: An Info. Overview, ORNL/EIS-94 . ORNL;
Oak Ridge, Tennessee; April 1977.
31. Sawicki, E. et al . As in 28.
32. Pott, P. ChiurglcaU Observations. London: Hawes, Clarke, and
Collings, 1775.
33. Henry, S.A. Cancer of the Scrotum in Relation to Occupation.
London: Oxford University Press,
3^. Sexton, R.J. The Hazards to Health in the Hydrogenation of Coal -
IV. The Control Program and the Clinical Effects. Arch.
Environ. Health 1: 208-231 (I960).
35. Eckardt, R.E. Industrial Carcinogens. New York-: Grune and
Stratton, Inc., 1959-
36. Weil, C.S. Quest for a Suspected Industrial Carcinogen A.M. A.
Arch. Indus. Hyg. 5: 535, (1952).
-481-
-------
37. Schwartz, L. Occupational Dermatoses. In: Industrial Hygiene
and-Toxicology, Vol. I-General Principle's. F.A. Patty (ed.).
New York: Inter-science Publishers, 1958.
38. Redmond, O.K., Cloccl, A., Lloyd, J.W., and Ruch. H.W. Long-
Term Mortality Study of Steelworkers: XI. Mortality from
Malignant Neoplasms Among Coke Oven Workers.
-------
49. Mazumdar, S.C., Redmond, C., Sollecito, W. , and Sussman, N.
An Epidemiological Study of Exposure to Coal Tar Pitch
Volatiles Among Coke Oven Workers. J. Air Pollut. Control
Assoc. 25(4) 382-89 (1975)
50. Doll, R., Fisher, R.E.W., Gammon, E.J., Gann, W., Hughes, G.O.,
Tyrer, P.H., and Wilson, W. Mortality of Gasworkers with
Special Reference to Cancers of the Lung and Bladder, Chronic
Bronchitis and Pneumoconiosis. Br. J. Indust. Med. 22: 1-12
(1965) ~ ~
-483-
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*-
oo
-p-
i
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LONG TERM HEALTH IMPLICATIONS OF RADIOACTIVE WASTE DISPOSAL
By
William D. Rowe, Ph.D.
Former - Deputy Assistant Administrator for
Radiation Programs - EPA
Present - Visiting Professor Operations and
Analysis Department, School of
Business Administration
The American University
Washington, D. C.
-485-
-------
The Long Term Health Implications of Radioactive Waste Disposal
Introduction
Any projection into the future is an extropolation
based upon experience and models or clairvoyance. In the
absence of reliable application of the latter, projections
will be no better than the models used. Thus any discussion
of the long term health impact of radioactive wastes depends
upon a sequence of models from source terms to exposed popu-
lations and their capabilities.
The time interval of interest is that after institutional
controls are no longer expected to be maintained and longer.
That is, about 100 years to 10,000 or 100,000 years from the
present. Models for projections over such time periods
depend on major assumptions regarding the size and nature of
future societies as well as estimates of the future behavior
of nature and ecological systems. Thus the uncertainties in
such projections will be large; the question of whether the
uncertainties are critical can only be ascertained after
analysis is complete. The uncertainty of critical parameters
will, therefore, be dominant; but a limit analysis, i.e.,
estimation of minimum, best estimate, and maximum ranges can
be very informative and useful. An attempt at this is made
here.
-486-
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Models for Estimation
The array of models used for estimation of long term
impact begins with estimation of source terms for all forms of
waste, i.e. high level and transuranic, mill tailings, and other
wastes. High level wastes consists of fission products from
fuels reprocessing and unreprocessed spent fuel, or any other
materials whose activity level is high enough to cause acute ef-
fects with only ordinary precautions. Transuranic elements are
considered as a part of the high level waste problem since simi-
lar disposal methods may be used. Mill tailings are the residues
from the milling of uranium and thorium. Other wastes are all
those whose effects are primarily chronic with ordinary precau-
tions, and includes such things as "low level wastes," material
and rubble from decomissioning, or any thing else. Table 1
characterizes these by their volume and activity levels.
The second model involves the pathways to the environment
over time. There are three parts, 1) the selection of a dispo-
sal method and site with specified design objectives, 2) pathways
to the environment allowed by the design, 3) and pathway to the
environment from external events caused by man or nature. A
third model is required to convert exposure to health effects
for individuals and generic populations, and finally a fourth
model is required to specify the size and behavior of future
populations and societies.
-487-
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Each model is inter-related to assumptions in the
others and cannot be developed without such recognition.
Table 2 summarizes these models, the details will be
covered when the models are applied.
Source Terms
The long term impact of radioactive waste disposal
must be measured after repositories are sealed or institu-
tional controls ended. Further, the impact of the total
practice must be ascertained, not that of a single
repository. For energy production by fission the amount
of waste generated for a typical 1000 MWe*/yr plant is summar-
rized in Table 3.More detailed estimates are available such as
those by Blomeke and Lee(l)}but are not required for the
limit analysis attempted here. OECO and UNSCEAR esti-
mates based upon uranium reserves at reasonable cost, that
about 10,000 GWe years are available from fission energy.
This may be increased by a factor of about three for use
of thorium and higher priced uranium. Use of breeder
reactors can extend this to about a million GWe years to
a first approximation. Thus, the total practice for a
world population of 10 Billion (2 1/2 times our present
population) represents one kilowatt per person,
-488-
-------
not per year, but totally, for uranium fission. This is
equivalent to 2 watt-years per year for 500 years. For
breeders this goes up to 200 watt-years per year for 500
years.
Table 4 estimates the total wastes from these prac-
tices. They provide a first cut for describing a total
health impact limit. However, they can only be used with
more detailed estimates. So far only one estimate of
health impact has been made for advanced disposal practices
for exposure at a significant level of detail. This is the
Environmental Protection Agency analysis of impact from
high level wastes for the purpose of establishing regulatory
standards. This analysis is based upon a base line, deep
geological repository with no planned releases, and forms
the basis for health impact estimates made here.
High Level Waste Analysis
The objective of the EPA study was the synthesis of
the probabilities and consequences all significant events
that might occur over a substantial period of time. The
results shown here are from congressional testimony given
by Dan Egan (21 .
-489-
-------
The analysis is based upon a model deep geologic reposi-
tory with no planned releases over its lifetime. Impact will
depend upon the designed repository to perform not as planned
or disturbances by external forces. Thus, only impacts from
"unplanned" inadequacies in repository design or "accidental"
disruptive events have been addressed. Only impacts which
might occur after final backfilling and sealing of the reposi-
tory have been investigated. Sealing of the repository is
established as the initial point of the time scale in which
the potential impacts are considered. The analysis addresses
total amounts of radioactivity which might be released to the
environment over various long time periods after repository
sealing. Most attention has been devoted to calculating
total impacts incurred over the first 10,000 years after
sealing. Radionuclide concentrations in various geologic or
environmental pathways are generally not calculated. Thus,
this analysis is not directly relevant to determination of
radiation doses or health risks to individual members of a
population.
"Definition of a baseline geologic setting. Initially
this has been chosen as a bedded salt repository, with over-
and underlying aquicludes (relatively impermeable strata)
immediately adjacent to the repository strata, and aquifers
on the other side of both aquicludes.
Definition of a baseline repository design. The details
of the baseline repository design selected for analysis are
-490-
-------
shown in Table 5. The repository was assumed to be a spent
unreprocessed fuel repository containing about 100,000 metric
tons of heavy metal (MTHM). It was also assumed that all the
spent fuel would have aged for approximately ten years after
reactor discharge before the repository was sealed " (2) .
Sequences of events or process which could initiate
releases of radionuclides were identified by an extensive
study undertaken for EPA by Arthur D. Little, Inc. The events
were identified and the range of the rate of occurrence for
each event were made. Upper bound estimates and more realistic
lower value estimates were made for some 60 different sequences
of events and are categorized as shown in Table 6.
For releases to the air or land surface, the fraction is
the portion of the repository inventory directly expelled.
For releases to ground water pathways, the fraction represents
the portion of the inventory subjected to contact with, and
potential transport by, ground water. In addition, for releases
to ground water pathways, either the permeability of the flow
path resulting from the event is estimated or a water velocity
through the affected area was provided. A simple one-dimen-
sional ground water transport model, neglecting axial disper-
sion, was employed to approximate the flow of radionuclides
from the repository to surface water bodies. This model was
determined to be adequate, compared to more sophisticated
techniques, for the purpose of calculating total radioactivity
reaching the environment over long periods of time. Figure 1
-491-
-------
depicts the geometry employed in the model. Table 7 indicates
the various parameters used in the calculation, including the
retardation factors initially assigned to the various radio-
nuclides.
The radioactive releases have been translated to health
effects incurred by an assumed average population. Person-
rems to the various organs were calculated using average path-
way and population models developed by the EPA staff. These
were then converted to health effects using the 1972 BEIR
estimates (4).These models are intended as representations of
pathways as they are currently understood. The health impacts
indicated are not intended as predictions of future effects,
unless future pathways and populations are assumed to be
reasonably similar to those of today.
In order to develop probability and consequence data a
set of hypothesized event times was selected, based upon
establishing appropriate "event time periods." The occurrence
rate for each event chain was then integrated over this event
time period at arrive at a probability of that event occurring
within the period, with the specific event time being taken
as the midpoint of the period.
-492-
-------
Consequences are developed with respect to the time over
which the environmental impact is being considered. For re-
leases which involve sudden removal of material from the
repository (releases to either air or land surface) the con-
sequences are assumed to occur at the event time. Releases
through ground water pathways would be drawn out over time
due both to the slowness of the ground water transport and
the dissolution of the radioactive waste. Dose commitments
over the time period of interest are then calculated.
Using the techniques outlined above, probability/
consequence data points are generated. These data have been
summarized in two ways. First, the sum of the products of
these data points is calculated. This result, which is
variously called the "expected value" of the environmental
impact, or the "risk", is an estimator of the health effects
"expected" within the dose commitment period of interest.
Second, the probability/ consequence points are depicted
graphically through the use of a "cumulative complementary
distribution function (ccdf)". Figure 2. indicates the two
methods used to summarize the analysis.
"Figures 3 and 4 depict the format of the results
obtained by applyimg the above methodology to the "high
value" and "low value " occurrence rates provided by A. D.
Little. A primary purpose of this presentation is to focus
upon the format of this analytic methodology and its potential
usefulness for environmental standards, as opposed to the
numerical values off preliminary results which are still being
-493-
-------
extensively reviewed. As a tool to encourage this, several
of the numerical parameters have been deleted from Figures
4 and 5. However, it can be noted that the sum of the pro-
ducts of probability and health effects (which will be termed
the "expected value" risk) for the 10,000 year period has been
in the range of 100-1000 for the "high value" rates, with the
"low value" rate results being about four orders of magnitudes
smaller'.'(2) .
There are several observations which can be drawn from
Figure 3. First, over this 10,000 year period, with the
"high value" event chain rates estimated by A. D. Little,
it is virtually certain that some health effects will be
incurred from radionuclide releases. Thus, although no
"planned" releases are forecast, "unplanned" events or
"accidents" are expected sufficiently often that releases
u.p to a certain level could still be projected with a
probability approximating one. As Figure 4 indicates,
the situation relative to the "low value" rates is quite
different"(2) .
Further, the bulk of the "expected value" risk is
attributable to ground water related pathways.
"This "expected value" risk can also be subdivided
according to the radionuclide causing the impact, and pre-
liminary results of such analyses are indicated in Table 8.
-494-
-------
The dominance of technetium-99 is surprising only until one
considers its relatively high fission yield (on a gram-atom
basis), its long half-life (213,000 years), and its assumed
lack of sorption in geologic media. Many radionuclides
which have often been considered more characteristic of the
hazards of high-level waste (strontium-90, cesium-137,
plutonium-239, etc.) do not appear to be significant in
this analysis because either their short half-life (strontium-
90, cesium-137) or their assumed strong sorption in geologic
media (plutonium and other actinides) prevent them from
reaching the accessible environment through ground water
pathways within 10,000 years (4) •
The base line system used by EPA will accommodate
100,000 MTHM as shown in Table 5. Three such repositories
of this type would suffice for disposal of the total high
level waste of 10,000 GWe-years of uranium fuel cycle
operation. (See first row and column of Table 4.) This
would mean an upper limit of 3000 health effects for the
total cycle and about 0.3 for the most optimistic estimate.
Table 9 summarizes this data.
In order to put these risks in perspective they may be
compared to a number of bench marks: which are shown in
Table 10. Even the upper level of risks from waste disposal
(0.3 per year for 10,000 years) is small compared to the
benchmarks.
-495-
-------
Low Level Wastes
There have been no extensive studies conducted on the
long term impact of disposal of low level wastes or mill
tailings to the extent carried out by EPA for hich level
waste disnosal. Thus, only a limit analysis can be made for
low level and mill tailings wastes.
The IRG report indicates that there are 16 x 10 ft of
low level waste at the six commercial sites in the
United States. About 35 times this volume of waste would
need to be disposed of under current schemes for 10,000
GWe years of operation although advanced volume reduction
would reduce this by a factor of 10. Greater amounts are
required for expanded fuel cycles.
Some of six commercial sites have been closed down
because releases to the environment have been greater than
expected. Thus some level of "planned" release may exist
if present methods are used for low-level disposal. More
important after institutional control lapses these sites
are subject to internal design failures and a whole array
of external factors, including erosion and human intrusion,
which are not as important in deep geological disposal.
This is also true for mill tailings disposal if by present
practices as well.
Without evaluation of all of these factors for different
disposal methods, no health impact evaluation is possible.
What I have chosen to do instead is to use Blomeke and Lee's (1)
estimates of the volume of air for dilution of a given
-496-
-------
volume of material to concentrations specified in DOE (ERDA)
concentration guides as a measure possible impact, and then
to determine the decontamination (or retention) factor, d.f.,
needed to bring the impact into the same ball park as those
for high level waste disposal. Thus, the "d.f." will be a
measure of the "effectiveness of containment" needed for a
repository.
The total mass of the atmosphere has been estimated at
5.2 x 10 gms.{5)with a density of .00122 gms/m at sea
level. This would indicate that a total volume of air at
f\ A ~\
about 4 x 10 m . Blomeke and Lee have used dilution factors
as follows.**
Non Transuranic Low
93 3
Level Wastes 1 x 10 m of air/m waste
Mill Tailings 1.6 x 10 m of air/m waste
8 3
For 10,000 GWe years, about 5 x 10 m of low waste dis-
14 3
posal and 8 x 10 m for mill tailings accumulate for the
uranium fuel cycle (Table 4). For dilution this would re-
quire 5 x 10 m of air for low level waste and 1.3 x 10 m
19 3
of air for mill tailings. For breeders 5 x 10 m is required
-497-
-------
for low level waste while tailings stay about the same. The
mill tailings dilution volume exceed that available in atmos-
phere just to meet DOE standards. Thus a retention factor of
three is required for mill tailings just to keep it at DOE
maximum levels. Mpc value for DOE standards are based upon
concentration guides of 500 mrem/yr to an individual, and
10 9
exposure to 10 people of this level is 5 x 10 man rems/yr
or about 10 health effects per year based upon ICRP models.
This is a factor of 3.3 x 10 higher than the upper limit
estimate for the fuel cycle in Table 9. To achieve these
levels a retention factor of about 10 per year is required
for mill tailings over their lifetime. Low level waste
retention cannot be adduced in this way.
Thus in summary the retention factor for mill tailings
indicates that this may be the key disposal problem. Whether
the d.f. level can be achieved has yet to be determined. It
may be quite easy to do so, but at least this provides an
initial target for disposal retention capability. Retention
requirements for low level wastes may have to consider indi-
vidual exposures as a limitation.
This paper does not give definitive answers. There are
none. But high level wastes have limited health impact. Low
level waste impact has yet to be determined. Mill tailings
may be the real problem for waste disposal.
-498-
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TABLE 1
Some Generic Waste Classifications
Waste
Type
Relative
Volume
Exposure
Activity
High Level
Fission products
from Reprocessing
Spent Fuel Rods
Discrete Sources
Small
Acute
Transurancies
Small to
Medium
Chronic
Mill Tailings
Large
Chronic
Other Wastes
Low Level Waste
Rubble, etc.
Medium
Medium to
Large
Chronic
-499-
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TABLE 2
Models Required for Health Impact Estimation
1. Source Terms
High Level - spent fuel or reprocessed
Low Level
Tailings and diffuse wastes
2. Pathways to the Environment
Disposal Method and Site
Designed Pathways
Unplanned Events
3. Exposure Health/Effect Determination
Dose Estimation - Internal and External
Population Commitments
Individual Doses
4. Future Population Model
Size and Growth
Protective Capability
-500-
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TABLE 3
ANNUAL WASTE GENERATION RATES (3)
(Normalized to an Average 1000 MWe
Light Water Reactor)
Spent Fuel Discharged
Low Level Waste, Generated Onsite I/
a) Present Experience
b) Design Basis
c) Advanced Volume Reduction 2/
Low Level Waste, Generated Offsite
-a) Uranium Mill, Tailings Solutions 3/
Tailings Solids 3/
b) UF3 Conversion
c) Enrichment- 3/, 4/
d) Fuel Fabrication
Transuranic wastes/ Generated Onsite and
Offsite
25.4 MT HM/yr
(332 ftVyr)
45,000 ft /yr
15,000 ft3/yr
5,000 ft3/yr
254,000 MT/yr
96,000 MT/yr
1,200 ft3/yr
50 ft3/yr
750 ft3/yr
0
NOTE: MT = Metric Tons
HM = Heavy Metals
I/ Roughly 40% of current volumes generated is contaminated
trash.
2/ This estimate reflects the use of methods which are pre-
sently not economical Current, allowable activity levels
per package may preclude actual achievement of this level
in the future.
3/ These wastes are currently disposed of at the processing
facility sites,
4/ This value is based on gaseous diffusion technology. The
new centrifuge process could potentially generate more
(up to 2900 ft3/yr.
-501-
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TABLE 4
SOME ROUGH ESTIMATES OF THE TOTAL RADIOACTIVE WASTES
FROM FISSION ENERGY PRODUCTION
i
Ui
o
N5
I
Type of Waste
Spent
Fuel
Uranium
lO^GWe-yrs.
3xl06
3xl05
AMOUNT PRODUCED
Uranium & Thorium
SxlO^GWe-yrs.
IxlO7
IxlO6
Breeders
106GWe-yrs.
3xl08
3xl07
Units
ft3
MT(HM)
Low Level Wastes-on site
A.
B.
C.
Present Practice
Design Basis
Advanced Volume
5xl08
2xl08
5xl07
2xl09
6xl08
2xl08
5xl010
2xl010
5xl09
ft3
ft3
ft3
Reduction
Low Level Wastes-off site
A. Uranium (Thorium)
Tailings
Solutions
Solids
B. UF Conversion
C. Enrichment
D. Fuel Fabrication
r3x!09
xlO1
lx!09
IxlO7
5xl05
IxlO7
IxlO10,
2xl015'
3xl09 .
6xl011+'
2xl07
IxlO6
3xl07
SxlO1 *
6xl016'
IxlO11.
2xl016>
IxlO9
MT
ft3
MT
ft3
ft3
ft3
ft3
-------
TABLE 5. PARAMETERS FOR BASELINE REPOSITORY (2)
High-Level
Solidified Waste Spent Fuel
Depth of Repository Horizon (feet) 1,500 1,500
Mined Area (acres) 2,000 3,500
Capacity (canisters) 35,000 320,000
Total metric tons heavy metal
(MTHM) charged to reactor 100,000 100,000
Specific Heat Input
(lew/acre) - maximum 150 50
-503-
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TABLE 6. CATEGORIZATION SYSTEM FOR EVENT CHAINS
AND SOME TYPICAL EVENT CHAIN PARAMETERS (2)
Event
'High Value"
Occurrence
Rates
(per year)
DIRECT ATMOSPHERIC RELEASES (AIR)
Meteorite Impact 3 x 10'10
DIRECT RELEASES TO LAND SURFACE (LS)
0 for 0-100 yrs
9 x ID'6
after 100 years
ranges from
2 x 10'6 to
4 x 10-8
"Low Value"
Occurrence
Rates
(per year)
3 x 10~u
Gas/011 Exploration
CONVECTIVE RELEASES TO AQUIFER (AQ)
Se1sm1city/Fault1ng
CONVECTIVE RELEASES DIRECT TO SURFACE WATER (SW)
Breccia Pipes
ranges from
1 x lO-4* to
2 x 10'9
always 0
ranges from
4 x 10~nto
1 x 10"13
ranges from
5 x 10"loto
8 x 10"15
Fraction of
Repository
Involved
0.20
0.00002
0.01
0.002
-504-
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TABLE 7. - PARAMETERS USED IN GROUND
WATER PATHWAY CALCULATIONS (2)
Permeability along Aquifer
or through fractured overburden:
Flow Gradient along Aquifer:
Flow Gradient through fractured overburden:
Retardation Factors for
Significant Radionuclides:
1 X
C - 1"
SR- 90
CS-137,135
I -129
TC- 99
NP-237
PU-238,239,2^2
AM-2U1
CU-2'4"
•JQ..U cm/sec
0.1
0.01
10
100
1000
1
1
100
10000
10000
3300
TABLE 8
- BREAKDOWN OF "EXPECTED VALUE" RISK
BY RADIONUCLIDE (2)
Radionuclide
TC- 99
C - 14
AM-2U1
I -129
SR- 90
PU-239
remaining
radionuclides
Per cent of Impact
88
7
•3
j
1
less than 1
less than 1
much less than 1
-505-
-------
I
Ui
o
TABLE 9
RANGES OF HEALTH EFFECTS FROM HIGH LEVEL RADIOACTIVE
WASTE DISPOSAL FOR THE
TOTAL FISSION ENERGY PRACTICE
1 Repository Uranium Cycle Uranium & Thorium Breeders
Cycles
105 MTHM 3x105 MTHM 6x105 MTHM 3x107 MTHM
Upper Limit
Health Effect 1000 3000 9000 100,000
Lower Limit
Health Effects 0.1 0.3 0.9 10
-------
I
Ui
o
^J
I
TABLE 10
Some Radiation Risk Benchmarks
(Based upon EPA calculations)(3)
Risks From Nuclear Weapons Fallout
(Tritium, Cesium-137, Carbon-14, Plutonium)
700 health effects/yr,
One Percent of Natural Background
100 health effects/yr,
Risks From Undisturbed Natural
Uranium Ore Bodies
10-15 health effects/yr,
Risks From Nuclear Energy Operation
(10,000 GWe years based upon 40 CFR 190)
200 health effects/yr.
(First 100 years)
30-60 health effects/yr.
(Next 10,000 years)
-------
o
oo
1
AQUIFER
AQUICLUDE
REPOSITORY
STRATA
fr :--; ^v y-*-^
AQUICLUOE
AQUIFER '•
U •: JJ 1. f V: .-.
FIGURE 1. Schematic of Ground Water Flows (2)
-------
THE PROBADILITY AND CONSEQUENCE. CALCULATED FOR EACH SUCH EVENT SCENARIO
ARE THEM COMBINED AND EXPRESSED IN'TWO WAYS: (2)
'EXPECTED VALUE'
'COMPLEMENTARY CUMULATIVE
DISTRIBUTION FUNCTION (CCDF)'
FIGURE 2
-509-
-------
-OTS-1
PROBABILITY
o, S S
u> oo ••*!
en
tn
° °.
i. 01
•
N>
•««j.•'.'.mr^arrv, Vivi^_. .MMIEAU. MiKi-m
BBC
M
3
o
it
X
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5
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•n
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PROBABILITY
CO 00
-------
References
1. J.O. Blomeke and C.W. Lee, "Projections of Wastes to Be
Generated" Proc. Management of Wastes from the LWR Fuel
Cycle", ERDA CONF 76-0701.
2. Joint Statement of Dr. James E. Martin and Mr. Daniel J.
Egan, Jr., Waste Environmental Standards Program, Environ-
mental Protection Agency; before the Subcommittee on
Energy and the Environment Committee on Interior and Insu-
lar Affairs, House of Representatives, January 25, 1979.
3. Report to the President by the Interagency Review Group on
Nuclear Waste Management, TID-28817 (Draft), October 1978.
4. The Effects on Populations of Exposure to Low Levels of
Ionizing Radiation, Report of the Advisory Committee on
The Biological Effects of Ionizing Radiation, National
Academy of Sciences - National Research Council, November
1972.
5. Handbook of Chemistry and Physics, 56th. Edition by A:
Poldervarte.
*Calculated from Tables 11 and 12 of Blomeke and Lee, (1).
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AREAS OF UNCERTAINTY IN ESTIMATES OF HEALTH RISKS
By
Leonard D. Hamilton, M.D., Ph.D.
Biomedical and Environmental Assessment Division
National Center for Analysis of Energy Systems
Brookhaven National Laboratory
Associated Universities, Inc.
Upton, New York 11973
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INTRODUCTION
-Confusion is engendered in estimates of energy-entailed health risks by
the misundertstanding between objective measures of risk - which describe the
estimated real or actual risk of a process-and the subjective perception of
these risks; the subjective perception of risks colors much of the thinking of
most decision-makers and the public. The situation is worsened by propaganda
from special-interest groups. In assessing health risks from energy production
and use, one must map where are the gaps in knowledge, yet necessarily basing
the assessment on state-of-the-art- information.
Another uncertainty is engendered by confusion as to how health assess-
ment enters into energy assessment. Estimates of health risks and their costs
are an essential in energy-policy along with (a) direct costs of energy produc-
tion; (b) other costs generated in a way similar to the assessment of health
costs; and (c) other politico-societal considerations. Figure 1 diagrams the
position of biomedical assessment in overall energy assessment. The demand for
energy by the consumer is the starting point. Nationally or regionally, this
demand can be met by varying combinations of existing energy-generating systems.
Or, if assessment of research on new energy systems is at the forefront of in-
terest and necessity, one must foretell how best to mix existing energy-genera-
ting systems and alternatives arising from research and development.
To measure the real health costs of various energy sources, one needs to
put them in the framework of logical, comprehensive energy analysis. Accord-
ingly, Figure 2 diagrams stages in energy production, distribution and use;
it permits coherent analysis of costs and hazards at each state. The diagram
includes: (1) hydropower; (2) nuclear fuel; (3) coal; (4) oil; (5) natural gas
and (6) new technologies to be developed. The steps in the fuel cycles com-
prise: (1) exploration and extraction; (2) refining and conversion; (3) trans-
port; (4) central station conversion; (5) transmission and distribution; (6)
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decentralized conversion; (7) conversion by final energy users. Most
of these process steps entail unique biomedical, environmental, and other
costs, some direct (e.g., risks of injury or death in mining), some in-
direct, (e.g., release of pollutants into air, water, thence into food chains,
etc.).
Such analysis helps: (1) to evaluate alternative energy policies with
due reference to health costs; (2) determine where money must be spent to re-
duce health costs; and (3) decide where to allocate research and development
funds for determining health and environmental costs.
This paper is concerned with several currently prominent uncertainties
in estimating health risks from electric-power generation: (1) health effects
of air pollution, especially acid sulfates and respirable particulates; and
(2) low-level radiation effects. With these uncertainties in mind, state-of-
the- art current assessments of various fuel cycles on a unit plant basis are
given and a method outlined for using these results in national or regional
energy assessment.
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HEALTH EFFECTS OF AIR POLLUTION
Coal combustion produces a wide range of air pollutants, including
particulates — S02> NOX, CO; polycyclic aromatic hydrocarbons (PAH); and
trace metals, e.g., iron, mercury, and cadmium. These primary pollutants
contribute to atmospheric chemical reactions producing secondary pollutants
such as ozone, sulfate, and nitrates. Because exposures to many pollutants
are simultaneous, it is difficult to assign damage by air pollution to
individual agents. Considerable evidence links sulfur-particulate air
pollution with health damage. *"•* It is currently hypothesized that the
causative agents are sulfate compounds produced by oxidation of S02 in the
atmosphere. Table 1 summarizes the mechanisms that convert S02 to sulfates.
As seen, oxidation of S02 to sulfates depends on the presence of other
pollutants such as NOX, oxidants, heavy metal ions, and particulates.
There is much uncertainty in understanding the mechanisms by which S02 is
oxidized to sulfate: the role of heterogeneous transformation processes (S02
oxidation, S02"03-liquid-water interaction, S02"H202-liquid-water
interactions, S0£ oxidation of graphitic materials and other aerosols, etc.);
aerosol transformation (nucleation growth, gas-aerosol reactions); and
S02~free-radical reactions (OH, H02, organic radicals) all need research. The
fact that presence of other pollutants determines the formation rate and the
final form of sulfate is important in underscoring the difficulty in ascribing
the health effects of air pollution to individual agents.
Particulate emissions from combustion are today largely controlled by
mechanical devices, e.g. , cyclone, electrostatic precipitators, and,
occasionally, fabric filtration. The chemical composition of emitted aerosols
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(particulates), especially surface composition, depenas on their chemical
history and is poorly understood; the smaller sizes present disproportionately
more surface, and thus serve as an adsorption site for effluent species in
post-combustion gases. An important consideration is that even after removal-
of most of the particulates, the oxidation of SC>2 to sulfates in the atmosphere
results in the formation of secondary particulates in the respirable range
«2ym down to submicrometer range). These persist longest in the atmosphere
and penetrate most into human airways since particle size is an important
variable that affects the site of deposition of sulfur oxides in the
respiratory tract and the size of the response. Figure 3 diagrams the effect
of particle size on deposition of particles in the respiratory tract. Small
particles are deposited deeper in the respiratory tract than large particles.
Support for the hypothesis linking sulfur-particulate air pollution with
health damage comes from many sources, the most dramatic from the major, amply
documented episodes of air pollution — Meuse Valley in Belgium; Donora,
Pennsylvania; and London — which clearly showed that air pollution, when
severe, caused widespread illness and death.
One of the worst air pollution disasters was in December 1952. A dense,
cold fog settled on London for four days, suddenly increasing deaths. Excess
deaths during the fog or shortly afterwards were estimated at 2,500-4,000 in
greater London (population 8.3 million). Table 2 gives figures for the
smaller area of the county of London. Deaths from bronchitis contributed most
to the rise in deaths. Deaths from other diseases with impaired respiratory
function also increased. There were increased deaths from heart disease,
presumably due to strain from impaired respiratory function or to a direct
effect. Death from other causes also increased; this residual mortality was
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significant; it is unlikely that it was due to respiratory impairment. The
increases in mortality in London in 1952 were correlated with vast increases
in smoke shade and S02> measured at the same time. Concentrations of smoke
shade were too great to be measured accurately; the 48-hour average of
~ 4.5 cig/m^ at a central site is thus a conservative estimate.
Concentrations of SC>2 were as high as 3.7 rag/mr (48-hour average). Smoke
shade and 862 were monitored in the United Kingdom since 1912; their choice
reflected the view that these were the important pollutants.
Figure 4 relates the incidence of chronic bronchitis to SOX precipitation
for several Japanese cities. There is a linear correlation between chronic
bronchitis and SOX precipitation present even in the absence of smoking.
Smoking 11-20 cigarettes/day (curve a) or 1-10 cigarettes/day (curve b)
clearly exacerbates the effects of the SOX.
Figure 5 plots deaths in Oslo, Norway against weekly S02 concentration.5
The relationship is linear. Since we know that S02 by itself does not kill or
cause chronic bronchitis, it is probably a chemical transformation product of
the S02 that is the crucial factor. The fact that Britons, Japanese, and
Norwegians succumb to damage from air pollution indicates the absence of
specific ethnic resistance. This is amply confirmed by results from the
United States Environmental Protection Agency's CHESS (Community Health and
Environmental Surveillance System) studies."
Figures 6-8 give examples of the results of the CHESS studies. Figure 6
plots the percent excess acute lower respiratory disease in children against
annual average suspended sulfates concentration (Ug/nr) (studies in six
areas). Figure 7 plots aggravation of heart and lung disease in the elderly
(given as percent excess) against the 24-hour suspended sulfates concentration
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(yg/m^) (studies in two areas). Figure 8 plots the percent excess mortality
rate in New York City in the 1960's against the 24-hour suspended sulfates
concentration (yg/nH). For comparison, the figure includes data on excess
mortality in London in the 1950's and Oslo in the 1960's.
Although many have criticized these epideraiological studies and their
pollution measurements, and because of the uncertainties emphasized by these
criticisms, one cannot use the results of the CHESS studies to estimate
dose-effect relationships. Yet, despite all their limitations, the CRESS
studies provide weighty evidence that "sulfates" — or something closely
related to them — damage health. The data are compatible with the notion
that the more sulfate, the more damage.
A vast literature associates air pollution (smoke shade, total suspended
particulates, and SOX) with sickness and death.^"^ Again, since one now
knows that it is not the SC>2 which damages it is probably some chemical
transformant of S02 that is responsible: this is the material that forms a
respirable particulate that probably constitutes most of the smoke shade and
most of the noxious material in the respirable fraction of total suspended
particulates. This body of evidence supports the hypothesis that sulfates as
respirable particulates or something closely associated with them does the
damage.
Impressive evidence for damage by sulfates has come from laboratory
studies in animals. The acid sulfates proved the more irritating and toxicity
was also related to particle size (Table 3).°>^
For perspective, Figure 9 plots the incidence of leukemia at Hiroshima
and Nagasaki against radiation (90% confidence limits). The incidence of
various cancers in the atom-bomb survivors is among the most significant and
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widely used data on current risk estimates of damage to health. Despite its
wide uncertainty (indicated by the spread in the 90% confidence limits and in
the uncertainties in the dose actually received by survivors), the data are
roughly compatible with linearity between dose ana effect. Use of these data
for risk estimation of the health damage from the nuclear fuel cycle
necessitates extrapolation of damage induced by high doses given at high dose
rates down to extremely low doses of radiation given at low rates. Such
doses usually comprise a tiny fraction of a'percent of natural background
radiation; it is impossible to discern any damage to health directly from this
natural background. In contrast, the addition £f sulfates or related material
from fossil fuel combustion, especially in the United States east of the
Mississippi, adds to an ambient concentration of sulfates already very close
to the level at which clinical damage has been seen. There is thus less
uncertainty in this regard in the application of a sulfate-damage function
than in the application of the frequently very precisely calculated risk made
from radiation.
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CRITICISMS BY OTHERS OF THE MULTI-CITY EPIDEMIOLOGICAL STUDIES
Despite the overwhelming evidence linking air pollution and ill-health,
many uncertainties still attend the individual studies. Some have argued that
certain air pollutants are not bad for health. Special-interest groups have
focused on the weaknesses of one or more of these studies. Thus critics
analyzing regression studies of city (SMSA) mortality rates, typically of the
classic studies of Lave and Seskin, have discussed most of the formal
statistical difficulties attending any observational study. The most
important criticism is that an observational study only shows association, not
causation. The case for the quantitative relation between air pollution and
mortality rests on broader studies than observational studies. Eight types of
studies connect air pollution and mortality:
1. Multi-city regression studies^-12 (Lave and Seskin,
Hickey et al., Schwing and McDonald);
2. Detailed studies of mortality in a particular cityl3-15
(Winkelstein et al. in Buffalo, Zeidberg et al. in
Nashville, and Gregor in Pittsburgh);
3. Studies of daily mortality and the association with daily
pollution levels in single cities^* 16,17 (Lave and Seskin,
Schiminel et al. , Buechley);
4. Studies of disastrous air-pollution episodes and consequent
increased mortality*^' *-° (London air pollution episodes);
5. Animal studies showing damage from air pollution
exposure8>^0,21 (^m^ur, Frank, and others);
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6. Morbidity studies — in general these have dealt with
individuals rather than aggregates^,23 (Ferris et al. ,
Douglas);
7. Occupational studies (see N10SH criteria documents on
sulfur dioxide and sulfuric acid);
8. Experiments with human subjects^~2o (Amdur, Frank).
Each type of study has its limitations. However, if one selects a
particular limitation, one can find other studies that do not have this
limitation.
Table 4 lists some issues that qritics can raise. These include presence
or absence of randomization, population variables, socio-economic variables,
controls for smoking, confounding by "regional effects," and direct
applicability to the general population. One row in the table is devoted to
each problem, and a column to each method. The code P in a row and column
means that the problem specified by this row is not dealt with satisfactorily
directly or indirectly by the method specified in this column.
In human epidemiological studies, while experimental randomization (i.e.,
deciding what pollution conditions an individual will be exposed to without
regard for his personal preference but solely on the basis of an arbitrary
mechanism, e.g., dice throwing) is necessary for valid causal inference, such
randomization is virtually impossible in large-scale, long-term studies
because one cannot dictate an individual's living conditions vis-a-vis
pollution so arbitrarily. Animal experiments and short-term human studies,
however, can be randomized. Such analyses, in fact, show that exposure to
specific pollutants damages health in animals and man.
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The next three rows in Table 4 exemplify adjustments which, if made in
the analysis, might clarify the relationship between air pollution and
ill-health: adjustments for the racial and age-sex structure of the
population, possible socio-economic variables, and smoking. Since these
particular variables are reasonably constant from day to day, the daily
studies and studies of air-pollution episodes do not have these as serious
limitations, hence have adequately dealt with these problems. These factors
are irrelevant in animal studies and in experiments on human beings because
appropriate randomization eliminates these issues directly.
The "regional effects" variables only affect the following studies:
multi-city,"some morbidity, and some occupational. The single-city, daily
mortality, and episode studies deal with this problem by being
region-specific. The problem is irrelevant in experimental studies on animals
and man.
Only the occupational and experimental studies have problems with their
direct applicability to the general population.
In sum, there are two or more study methods that address each problem.
Workers who have applied the methods in the studies cited above overwhelmingly
agree in finding health damage. That human beings are, indeed damaged is
dramatically shown by air-pollution episodes, by the association between daily
pollution levels and mortality, the multi-city regression studies, and
experiments on human volunteers. This consistent mass of evidence impels the
assertion that air pollution injures health.
Criticisms of the Lave and Seskin work have raised two questions about
the sulfate data. First, that the "1960" data set includes data from earlier
years (back to 1957) to fill in missing data for many SMSA's. This is not a
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problem. Were one studying the relation between daily air pollution peaks and
mortality on a given day, substitution of a different day's pollution data
would be unacceptable. Lave, however, examines differences in long-term
(annual) mortality rates among cities. The effect of pollution on the annual
mortality rate of a city depends on the long-term effect of pollution over
several years on the general health of the population. Lave's pollution data
are an index rather than a specific measure of pollution levels during the
year of death.
The second criticism of sulfate data is that bi-weekly and quarterly data
are mixed, causing a potential bias in the use of minimum and maximum numbers.
This is a valid criticism of Lave and Seskin, but not of the health-damage
functions derived by the Biomedical and Environmental Assessment Division
(BEAD) at Brookhaven. As documented, ' the BEAD health-damage function is
based on annual average sulfate pollution levels — an index unaffected by use
of bi-weekly or quarterly data. In the BEAD health-damage function, only
average sulfate levels are included because our analysis lead us to believe
that this was a better base than the minimum or maximum values reported by
Lave. Thus, many of the caveats of the critics of Lave and Seskin have
already been incorporated in the BEAD analysis.
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BEAD PROBABILISTIC ANALYSIS
To mass all uncertainties underlying the quantitative relationship
between the operation of a coal-fired power plant and damage to health, Morgan
and Morris made a comprehensive probabilistic analysis.^" Sulfur air
pollution transport, dispersion, and impact were modeled from a 1,000-MWe coal
power plant to the population within an 80 km radius. A gaussian plume
dispersion model with linear sulfur chemistry was used with a linear
health-damage function. Important features of the model involving uncertainty
were: fraction sulfur emitted as 804, S02 loss rate, SO 4 loss rate, S02 to
SO^ conversion rate, 'health-damage function, the meteorological model. The
uncertainty in each of these variables was characterized by a probability
density function based on best available scientific judgment. This provides
not only the "estimate" but the estimate of a probability that a variable's
actual value may be given in amounts higher or lower than the "estimate."
Essentially, these distributions are a description of the odds a knowledgeable
scientist might calculate if asked to bet on the outcome of a series of
definite experiments which would, at a future time, determine the true value
of the variables. These probability density functions (pdfs) were then
combined in a simulation analysis to produce estimates of population exposure,
premature deaths (Figure 10), and person-years lost.
What are the advantages of characterizing uncertainty as pdfs based on
best scientific judgment over the use of classical statistical methods on
available data? Several:
1. In many instances, the best data comes from studies which have (often
unavoidably) serious flaws, e.g., design problems, unaccounted for variables,
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etc. Classical statistical methods cannot clearly interpret results from such
studies.
2. Available data are often based on a subset of the total possible
universe that may not be representative, e.g., epidemiological studies on
certain population subgroups, airborne air chemistry studies on days when the
plane can fly, etc.
3. The need to combine results from various kinds of studies, e.g.,
taking laboratory studies as well as those conducted in. the "real world" into
account. Extrapolation from laboratory results demands more than classical
statistics can provide.
What important uncertainties were not quantified? The model itself and
the form of the parameters were assumed to be known. Both may be quite
different from that assumed. This was not explicitly dealt with and adds
uncertainty beyond that characterized. For example, a linear damage function
is assumed and no uncertainty due to possible alternative damage function
shape is considered.
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THE DEFINITION OF THE HLALTH-DAMAGE FUNCTION
The health-damage function used links annual average sulfate exposure
with increased annual mortality rate. It does not represent the acute effects
of episodes but the long-term impact on the population of a continuing
environmental exposure. Although the sequence of events leading to this
impact on the population is unknown, long-term exposure to air pollution,
particularly in childhood, presumably increases susceptibility to respiratory
infection. A history of repeated respiratory infection, possibly coupled with
continued air pollution exposure, increases the prevalence of chronic
respiratory disease. This leads to more deaths from a broad range of
cardio-pulmonary diseases. Thus increase in air-pollution exposure degrades a
population's health; this is eventually reflected in mortality rate. Deaths
attributable to an air-pollution exposure in a given year do not necessarily
occur that same year, but are distributed over the lifetime of the exposed
population. We cannot yet estimate how these deaths are distributed in time.
Mortality estimates not only represent premature deaths, but years of
decreased respiratory function, perhaps disability before death. Since not
all induced respiratory diseases may result in premature death, the annual
incidence of new-disease cases is undoubtedly higher than the annual number of
deaths. Since the health-damage function is based on annual mortality rates,
each death attributed to air pollution represents at least one year of life
lost. Reasonable estimates of the age distribution of the deaths leads to the
conclusion that 5 to 15 years lost per attributed death are likely.
Under steady-state conditions, the deaths occurring over future years
attributable to pollution exposure this year equals the number of deaths
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occurring this year, due to the summated pollution exposure of all previous
years. Based partly on this, a linear health-damage function was drawn from
cross-sectional studies as a simplified way to estimate effects of alternative
energy strategies. By this simplified linear damage function, incremental
sulfate exposure this year inevitably increases health damage and premature
deaths. The incremental health damage is proportional to incremental sulfate
exposure and is independent of the total sulfate exposure under the linear
assumption. These estimated premature deaths may be compared with total
deaths annually in the exposed population; this imparts perspective to the
estimates. This fraction might be taken as a rough estimate of the eventual
contribution to mortality of a continuing air-pollution exposure of that
level; it is not the fraction of total deaths attributable to this level of
exposure occurring in the same year.
It seems doubtful that the damage function is truly linear with no
threshold over the entire range of exposure. More likely, at low absolute
levels of exposure, the health impact of a unit increase in sulfate is
reduced. There may be a threshold below which there is no detectable health
damage. The data on which the dose-response function is based are from urban
areas with generally high background sulfate levels but, significantly, the
linear function is consistent with data from urban and rural areas with high-
and low-pollution levels. Use of a linear function to estimate effects of
small changes in sulfate levels in areas with high background levels seems
reasonable. Estimates of the effects of sustantial changes in background
levels, or of small changes in areas with low initial background levels,
increase the uncertainty in estimation of damage.
The health damage function described by Morgan et al.^8 ranges from 0 to
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12 deaths per 10^ per yg/m^ sulfate, with a median value of 3.7 (95%
confidence interval 0-11.5). These estimates were derived by a subjective
analysis of data principally from correlation studies of the type conducted by
Lave and Seskin. These studies are subject to methodological and data
problems discussed in detail elsewhere. Standing alone, these studies are
inadequate to ascribe the observed effect to sulfate air pollution. In
concert with toxicological and epidemiological studies, however, they provide
a useful means of estimating the magnitude of the damage.
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BEAD'S OWN ANALYSIS OF AIR POLLUTION AND ILL-HEALTH
Now at the same time as our re-analysis of data available in the
literature on the relationship between air pollution and ill-health, we have
developed our own data base for this purpose. This includes the total
mortality records in the United States for the years 1969, 1970, and 1971 from
the National Center for Health Statistics. There are roughly 2 million deaths
a year in this file; one is analyzing a total of 6 million deaths for the
entire 3,100 counties of the United States, in contrast to the much smaller
number of deaths in the standard metropolitan statistical areas (SMSA's) in
the Lave and Seskin study. Moreover — again in contrast to the SMSA studies
— our data include the entire urban and rural portions of the United States.
We have also used the 1970 Census Data as a source of some socio-economic
variables, especially income. By including three years' total U.S. mortality,
and studying people exposed to a wider range of air pollution, one can be that
much more confident of the significance of the effects observed.
Our analysis, using these data on the relationship between air pollution
and health effects, has proceeded in three stages. In stage 1 all 3,100
counties in the United States were aggregated into 192 groups based on 17
levels of income of the 1970 census and 21 levels of pollution expressed as
emissions per square mile. Income variables were represented by race-specific
median family income data from the 1970 census. Ideally, in relating air
pollution to health effects, one would like to know the actual dose to which
the population was exposed. Unfortunately, the dose of air pollution to the
population is not available; Lave and Seskin and other studies have used air
quality data (concentration of pollutant/m ) as surrogate for dose. The
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incompleteness of the air quality data reduces their usefulness initially for
a nationwide study of health damage of air pollution. Thus, at this stage in
our analysis, we have used estimated emissions as surrogate for dose. This
variable varies by five orders of magnitude over urban and rural regions in
the United States. Thus, the "pollution" variable was represented by the
decimal logarithm of the calculated sulfur emissions (SOX) in tons per square
mile for 1970. This logarithmic transformation of emission has a more normal
distribution than the raw estimates and was therefore preferred. The
mortality variable was represented by age-, race-, sex-, and cause-specific
mortality rates for 1969-1971. The multivariable statistical techniques
(multiple regression and path analysis) used provided distinct estimates of
the relationship of income level and pollution to mortality. The effects of
pollution and income were observed by age cohorts because it was then possible
to compute age-, race-, and sex-specific relationships that address the issue
of cost in terms of reduction of life span — not simply total attributable
deaths.29
A striking feature of the analysis of the relationship of family income
to mortality-^* is seen in Figure 11. The average family income in the 3,100
counties for non-whites is less than the average given for whites. This is
why we have concentrated in deriving our damage function from data on whites
only. One cannot include the non-whites: the impact of income on non-white
mortality is just overwhelming. In the 0-4, 5-14, as well as 45-54 age groups
there is a striking effect of family income on mortality rate with a notable
sex difference in all age groups applicable to non-whites and whites. In the
65-84 age group, as one might expect, the effect of income has leveled off,
although the differences in rates between males and females are still
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apparent.
Figure 12 shows the relationship of income and pollution to mortality for
white males and females at all ages. The X-axis contains midpoints of
five-year age cohorts. The beta coefficient values for income and pollution
as predictors of mortality are graphed on the Y-axis. The beta coefficients
— a standardized regression coefficient in a multiple regression equation —
quantify the strength of the relation between mortality at each age and the
indicated variable (income or pollution). A positive coefficient indicates
that an increase in the variable goes with increased mortality at that age,
while a negative coefficient indicates that increase in the variable goes with
a decrease in mortality at that age. Values near 1 or -1 typically represent
high association (the beta coefficient may exceed 1 in absolute value, so that
beta coefficients should not be interpreted as correlation coefficients). The
cross-hatched area indicates where the coefficient is not statistically
different from zero. ^
Income generally tends to be negatively associated with mortality with
increasing age. This is particularly evident for white males, in whom income
maintains — and in fact increases — protection against mortality with
advancing age. Pollution for both sexes becomes more strongly associated with
mortality as age increases. The only exception is the 0-4 cohort where a
positive association with pollution is suspected. This finding suggests that
pollution may be especially damaging to infants, as measured by their
mortality, and deaths of the very young. Further research is needed.
Comparison of our calculated excess deaths with other research shows
striking similarities. 9 Winkelstein et al.*3 attributed approximately 14
deaths/100,000/yg TSP/m3. Lave and Seskin10 calculated an order of magnitude
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lower estimates of 0.9 deaths/100,000/pg TSP/m3 for white males 55-74. Since
both estimates are based on a measure of TSP rather than SO^, certain
modifications of our data were necessary for comparison. The issue of
pollution equivalence was a difficult problem. Recent studies have estimated
that the 804 part of TSP varies by a wide range.32'33 By assuming 25 to 80
percent to be a reasonable conversion range, we can convert our excess death
estimates to figures comparable with the Winkelstein and Lave and Seskin
numbers. By a completely different approach, Morgan et al. ° also calculated
excess deaths, however, since their estimates are based on an 804 measure of
pollution, no modification beyond differentiating between the relative
proportion of 802 and 804 in SOX was necessary. A modified version of the
Finch and Morris2? comparison of excess deaths is found in Table 5.
Since emissions are not an ideal criterion of air quality in the second
stage of our analysis, we have used the air-quality data available in 1970
from the 248 EPA air-quality measurements for three pollutant species: S02,
804, and total suspended particulates (TSP). As we have already noted, these
248 measuring stations fall far short of covering all 3,100 counties in the
United States — the county was the unit of analysis in the first stage of our
analysis; and while major urban areas are monitored by one or more measuring
stations, rural areas are sketchily monitored. In an attempt to surmount this
problem, i.e., that only 221 counties had one or more EPA air-quality
measuring stations in 1970, we have assumed that each EPA measuring station
provides good estimates of the pollution level for all those counties which
have similar emission and socio-economic characteristics. For this purpose we
have used the original 192 groups in the first stage of our analysis to
aggregate our data to give a population size large enough to calculate
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statistically significant mortality rates. ^
Of these original 192 groups, 92 county groups contained at least one EPA
measuring station. In 44 of these 92 county groups, 50% or more of the
population reside in counties containing one or more measuring station.
Unfortunately, these 44 groups are more representative of polluted urban areas
in the U.S. and caution must be exercised when extrapolating these results to
the more sparsely represented rural populations. Nevertheless, as will be
seen from Figures 13-15, there is, in general, good agreement between the
age-specific damage function derived from the emission-mortality analysis from
stage 1 of our analysis and that obtained by using EPA measuring stations and
grouping emissions in counties without measuring stations with these, stage 2
of our analysis. The data agree reasonably with those derived by Lave and
Seskin and Morgan et al. for SO^ and with Winkelstein and Lave and Seskin for
TSP. The difference in the damage function for 804 exposure derived from
stage I and stage II in age groups over 60 may be related to differences in
the size of the populations included in each stage, and the
underrepresentation of the rural population in stage II.
For perspective, it is worth noting that the National Academy of
Sciences, in its report on saccharin, estimated the risk associated with the
equivalent of the consumption of one can of diet soda per day. Depending on
different mathematical models used, the estimate of risk varied by five orders
of magnitude.
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LOW-LEVEL RADIATION EFFECTS
Except for accidental cases of acute high-level exposure, worries about
nuclear facilities center on possible damage by airborne or liquid effluents
and resultant low radiation doses to people nearby. Note almost all delayed
cancers from power-plant accidents in WASH-1400 are calculated to be also due
to low radiation doses «1 rad).
What — if any — are levels "safe," "acceptable," and understandable to
the public? But neither term can be quantitatively defined. In practice both
imply a definite but extremely small probability of risk.
There are now three ways of determining what dose-levels may be
considered tolerable. One determines at what dose level the risk of
detectable somatic or genetic radiation damage becomes low enough to be
vanishingly small in comparison to the summated environmental insults
to somatic and gonadal cells due to "normal" causes encountered in a person's
lifetime, including background radiation, i.e., to nuclear radiation that
forms part of our natural environment, e.g., froia potassium and cosmic rays,
and determines below what level any additional radiation exposure would result
in an insignificant increment in dosage. A cut-off or de minimus level of
risk (and therefore of dose) has also been suggested for general application
to the general population. Deaths of 1 x 106 to 1 x 10~5 per individual per
year have been proposed.
The difficulties in defining the effects of very low levels — a few
millirem per year or less — on the general population from the nuclear-fuel
cycle are two-fold. For one, no statistically valid experimental work is at
hand because of the virtually insurmountable difficulties imposed by the
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necessarily large-scale, long-term nature of such experiments, e.g., a popula-
tion of P million will have about P million live born children per generation
with ~3.5% of them obviously genetically defective. Thus in several, say 3
generations there will be 10 P such defectives in the control population.
The population exposed at a few, say 3, mrem y will have had an excess ex-
posure of 0.10 rem by the mean age of child-bearing or conception (~30 y).
With an induction rate of genetic defects by radiation of 80 x 10 rem , a
population of P million will in 3 generations have had an excess of induced
defectives of 3P x 10 x 80 x 10~ x 0.1 = 24 P extra defectives. For detec-
tion of this excess at 2 standard errors 24 P = 2 , / (10 + 24) P. Hence
P = 700 million. Conditions on a very large, genetically extremely homogeneous
population would have to be rigorously controlled and over several generations
to detect significant genetic changes. Even epidemiological studies on compara-
ble populations living exposed to different natural radiation levels have
proved inconclusive. It also would be imperative to establish a unique cause-
and-effect relationship—even were correlations between morbidity and radiation
exposure apparent—in order to rule out other causes, such as economic conditions,
nutritional factors, or improved diagnostic facilities due to better medical ser-
vices.
Another problem arises from the fact that, although it is easy to observe
deaths and malignancies such as observable at dose levels above 50-100 rad, it
is more difficult to observe minor incidences of illness in a much larger
population, such as might result from low-level exposures, and to distinguish
them unambiguously from similar illnesses that could be caused by a host of
other causes.
Due to these difficulties, a conservative approach is to take the
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dose-effect values obtained at high-dose levels and to extrapolate them down
to low-dose levels. What is usually assumed is a linear relationship between
dose and effect, independent of dose rate, an assumption that appears to be
amply justified for acute high dose levels.
Several recent reports (Bross;-*5 Mancuso, Stewart and Kneale;-*6 and
Najarian^7) have been interpreted by some people to indicate that the
commonly employed risk estimates, which are based on the UNSCEAR and BEIR
Committee Reports, underestimate the risk of radiation at all levels. They
especially emphasize that the linear theory (that the risk per unit dose as
derived from available data at high levels of radiation dose holds all the way
down to zero exposure dose) is not sufficiently conservative in estimating
risk at low doses but rather underestimates it.
Bross believes he has identified subgroups in the population which are
espcially sensitive to radiation damage. His belief derives from his analysis
of the Tri-State Leukemia Survey, wherein he studied an association between
some "indicators of susceptibility" (viral infections, bacterial infections,
and allergy) shown by the leukemic child from birth until diagnosis of
leukemia. He concluded "the apparently harmful effects of antenatal
irradiation are greatly increased in certain susceptible subgroups of children
possessing the indicators associated with a slightly higher intrinsic risk of
leukemia." However, reanalysis^° of his findings shows that children with
leukemia are simply more prone to viral and bacterial infections and allergies
before the clinical onset of the disease, i.e., these indicators characterize
the disease itself and do not relate to the child's inherent susceptibility to
leukemia. The incidence of these diseases as part of the pre-leukemia phase
of leukemia in children is well known in clinical hematology. Analysis of
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Bross' data shows that the incidence of these indicator diseases before the
clinical onset of leukemia is the same in children who had received no
irradiation in utero as in those who had.38 xhe hypothesis of Bross, that
there is a susceptible portion of the population at higher risk of leukemia,
has also been challenged on the grounds that Bross' methods yield no way to
identify susceptible individuals ahead of time and so no way to test his
thesis.39
More recently, Bross has suggested that the relatively small radiation
exposures from diagnostic X-rays in adults significantly increases the risk of
leukemia. 0 It appears that Bross assumes, in coming to this conclusion, that
in the absence of diagnostic X-rays, the incidence of heart disease and
leukemia is zero. 0>41 Were this not the case the fact that the
"dose-response" curves of adults exposed to diagnostic X-rays are flat below
10 rad exposure would suggest a threshold. Indeed, a more conventional
relative risk analysis^ found little or no increase in risk of leukemia from
a small number of diagnostic X-rays. Bross also assumes here that relative
risks are fixed and that the percentage of the population affected varies with
dose, i.e., the basic response variable is the proportion of the irradiated
population affected by radiation. Conventional relative risk analyses assume
that everyone is affected and that the relative risks vary with dose. The
improvement made by Bross et al.'s approach is unclear. The position taken
here by Bross appears to be at odds with his earlier paper, in which he
postulated the existence of a sensitive subgroup of fixed size whose relative
risk of leukemia increased rapidly with increasing X-ray dose.
Finally, one should note that the leukemia risk (or "percent affected")
does increase dramatically in males (females appear to be unaffected) after
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large numbers of diagnostic X-rays. However, the cause-effect relationship is
uncertain in that large numbers of diagnostic X-rays — *** 40 or more within 10
years — implies the presence of a disease state perhaps deriving from heart
disease or a preleukemic sensitivity to infections.
Mancuso, Stewart, and Kneale^" have reported preliminary findings on the
work and survival experience of 24,939 male workers with 3,520 certified
deaths and of an unspecified number of female workers with 412 certified
deaths at the Hanford Works, Richland, Washington between 1943 and 1971, The
preliminary report, largely limited to analysis of data on the 3,520 male
deaths for which death certificates were available, claim to demonstrate a
radiation-induced excess of cancers, greater than linear models would
indicate. Their analysis has been widely criticized. Their report does not
state the actual individual doses received by Hanford workers who died of
cancer, only mean cumulative radiation doses. Besides, their study did not
take into account the calendar year in which the cancer began and made no
correction for the fact that the incidence of the cancers they were observing
in the Hanford workers also increased during the period of the study in the
population at large. Thus, Table 11 in their publication, showing an increase
in cancer with increasing dose accumulated over increasing time, fails to take
into account that even in the absence of the increasing dose of radiation,
there is a similar increase in cancers they were finding in the U.S. as a
whole when plotted against increasing time. Other analyses of the same data
published by Marks et al.^3 and by Hutchinson et al.^ point to the
possibility of an association with the work experience for two cancer types:
cancer of the pancreas and multiple myeloma (multiple myeloma in whites is
increasing in the U.S. for no known reasons). There is no reported radiation
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relationship for lymphatic or haemopoietic cancers other than myeloma, i.e.,
no excess of leukemias (which previous experience suggests should have been
most observable where radiation is a factor).
Since the specified radiation doses were very small, perhaps on the order
of a few rads, the cancer-doubling estimates found in the Mancuso, Stewart,
and Kneale paper have been strongly disputed. If the postulated small dose
actually caused a doubling of the spontaneous rate of cancers, then background
radiation would produce more than the numbers of cancer observed in the
population. It therefore appears that if these doubling doses are correct,
something other than radiation was the cause of the observed cancers. In the
light of these criticisms, Mancuso et al. now appear to have modified their
estimates of doubling doses and are quoting doubling doses of 2-150 rem.
Najarian and Colton-^' estimated that since the Portsmouth Naval Shipyard
(PNS) in New England began to service nuclear-powered ships in 1959, 20,000
people were employed there, of whom about 20% were exposed to radiation. From
a search of death certificates 1959-77, 1,450 former PNS employees who had
died below age 80 were identified in New Hampshire, Maine, and Massachusetts.
To ascertain whether these ex-employees were radiation-exposed workers,
attempts were made to contact near relatives by telephone. This was
successful in 525 cases and it was established that 146 were probably exposed
to radiation during their working life.
The authors show that, compared with mortality in U.S. white males for
1973, the observed numbers of cancers and leukemias were considerably greater
than those expected: for example, 56 cancer deaths were found in death
certificates of 146 ex-workers exposed to radiation; only 34.5 were expected.
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In non-exposed workers there were 88 cancers; 79.7 were expected. For
leukemias there were 6 in the former radiation workers; only 1.1 were
expected.
Najarian and Colton listed some inadequacies in their survey. It was an
analysis of deaths only; no information was available on the total population
at risk. There could be a bias in the information supplied by relatives.
They had no information on how long workers worked at the shipyard, how long
nuclear workers were exposed to radiation, and the amounts of radiation they
received. Consideration was not given to other toxic agents, such as
asbestos, smoking, industrial solvents which could have acted alone or
synergistically with radiation to cause the apparent excess deaths from cancer
and leukemia.
There are other inadequacies in this survey. To exclude some of the
effects of other carcinogens, one raust show that cancer frequencies increase
with increasing radiation exposure, but knowledge of the lifetime accumulated-
doses of the former employees was not available. More importantly, if the
radiation work at PNS began only in 1959, it is unlikely that changes in
overall cancer frequency induced by radiation would appear before at least 10
years after exposure, or after 5 years for leukemia, these being roughly
minimum latent periods for cancer induction. The data given in Najarian and
Colton can be divided into deaths during the periods from 1959-69, when
radiation effects would not be expected to appear, and 1970-77, when effects
might be expected. In 585 death certificates of persons who died between
1959-69, 24.6% had cancer listed as the cause of death. Considering the 33
radiation-exposed workers who died during this period, 13 or 39.4% of the
deaths were recorded as due to cancer. In 865 death certificates 1970-77,
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25.7% had cancer as the cause of death; hence there was no significant
difference between the percentage of cancer deaths between the two periods for
all workers. For the 113 radiation-exposed workers, 43 or 38.1% of deaths in
the later period where due to cancer — no more than in the earlier period
(39.4%).
RADIATION EXPOSED
CANCER % CANCER CANCER % CANCER
ALL DEATHS DEATHS DEATHS ALL DEATHS DEATHS DEATHS
1959-69
1970-77
585
865
1,450
144
222
366
24.6
25.7
33
113
13
43
39.4
38.1
The absence of any apparent latent period effect casts doubt on
conclusions about the contribution of radiation to the curiously high numbers
of cancer deaths among the radiation workers.^
In the meanwhile, NIOSH made available to Drs. Najarian and Colton
radiation exposure data supplied by the U.S. Navy. On February 2, 1979, at a
symposium sponsored by the Johns Hopkins School of Public Health, Baltimore,
Maryland, Drs. Najarian and Colton introduced these radiation exposures into
their PNS Study. At this time, they announced that in contrast with the
original Lancet data, where 6 leukemia deaths were observed instead of 1.1
expected, it was found that two of the cases of leukemia had no history of
radiation exposure. One had less than 0.1 rem, which is what one receives
after one year's natural background. One received 15 rem, one 5 rera, and one
"not numbered" — probably less than 5 rem. The number of leukeiaias is now 3
instead of 1.1 expected. For all cancers the new data are:
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CANCERS
EXPOSURE NUMBER OBSERVED EXPECTED RATIO
Less than 0.1 rem
From 0.1 to 0.99
Greater than 1
64
50
49
17
16
19
13.5
10.5
10.2
1.26
1.53
1.58
No exposure 358 92 7.49 1.24
Chi-square test shows no significant difference in the ratio among the
exposed levels at p = 0.10. Cochran's chi-square test for a linear
regression, which considers that the ratios increase in the expected direction
shows no statistical significance at p =» 0.05 but is significant at p = 0.10.
Early verification of these data is urgent.
A tentative list* of chemical and physical agents probably present at the
Portsmouth Naval Shipyard during the past 25 years includes:
Acetone Chlorinated Diphenyls
Alcohols Chlorinated Napthalenes
Amines Chromic Acid
Ammonia Chromium
Ammonium Hydroxide Coal Tar Volatiles
Amyl Acetates Epichlorohydrin
Antimony Oxide Ethyl Acetate
Asbestos Ethylenediamine
Benzene Fibrous Glass
1, 3, Butadiene Fluorides
Cadmium Fungicides
Carbon Monoxide Hydrogen Chloride
Carbon Tetrachloride Hydrogen Cyanide
* Personal communication: R.D. Zumwalde
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Infrared light Sodium Hydroxide
Lead Titanium Oxide
Methyl Ethyl Ketone Toluene
Methyl Isobutyl Ketone Trichloroethylene
Mineral Wool Tri Sodium Phosphate
Nickel Turpentine
Phenols Ultra Violet Light
Polyvinyl Chloride Wood Preservatives
Radiofrequency (Microwave) Kylene
Silica (Quartz) Zinc Chromate
Comparison with Table 6, taken from Table 25: Common Occupational
Carcinogens from Health and Work in America: A Chart Book, American Public
Health Association, Washington, D.C., 1975, underscores the difficulty in
assessing the effects of low levels of radiation in this worker population.
One must await the results of the complete survey being carried out by
the Center for Disease Control and National Institute for Occupational Safety
and Health before any conclusions can be drawn between exposure to radiation
at PNS and risk of cancer.
Thus, although these claims of higher risks from the levels described by
Bross, Mancuso, Stewart, Kneale, and Najarian have become the subject of
considerable public debate, examination to date of their work does not support
these claims.
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BEAD'S APPROACH TO ASSESSMENT IN THE FACE OF UNCERTAINTIES
BEAD at Brookhaven is assessing the health and environmental costs of
energy production and use. BEAD's methodology is straightforward. One starts
with compilation of pollutants from the energy system, then the various
pathways to man are traced. This task entails definition of transport
mechanisms, including chemical and biological conversions and varous transfers
through the biosphere to man. A quantitative evaluation is then made of
effects. This evaluation relies on information from epidemiological data,
field and laboratory studies, and biomedical research designed to elucidate
molecular and cellular mechanisms underlying responses to pollutants. Once
given the magnitude of energy flows through the system and the size of the
populations exposed, total health damage can be estimated. The framework of
the evaluation is provided by the energy-system models of the National Center
for Analysis of Energy Systems, of which BEAD is a part; this provides the
resources (including the required energy-flow projections) and the means of
integrating the results with a national energy policy.
Most energy models are based on aggregated national data or on large
regions, such as census regions. Health and environmental effects, however,
are highly location-dependent. The need for a high degree of geographical
disaggregation of emission data led us to develop a county-level energy and
emissions data base. " We maintain a file on sites of planned future energy
facilities. For assessment, the Regional Studies Division at the Center has
developed methods for siting future energy facilities associated with
long-term energy projections. Data on emissions from these sites are then fed
into large-scale meteorological-air chemistry transport models*^ to estimate
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likely ambient air quality.
Risk assessment aims at improving the base for decision-making for policy
makers and public. The information upon which to base risk assessment is
often scanty. Even so, assembling available data, organizing them so as to
clarify choices among energy options, and gauging the uncertainties is a
useful aid to decision-making. Since decisions mean choices among different
technologies, standardized comparisons are essential to avoid poor choices.
For technologies producing the same form of energy, e.g., electricity, a
standardized unit of production or production rate can be used, e.g., a 1,000-
MWe power plant-year. When comparisons must extend across technologies
producing different energy forms, e.g. coal-electric vs. coal-gasification vs.
coal-liquefaction, the proper comparison is not always obvious. Indeed, there
may not be a totally satisfactory basis. Streams of electricity, gas, and oil
with the same energy content are not really equal: they are used by the
consumer for different purposes and with different efficiencies. As discussed
in the Introduction, this difficulty can be largely overcome by examining
different technological choices within the entire energy system meeting all
demands (Figure 2). Risk assessment must quantitatively assign risk to each
component of the energy system; valid comparisons can be made only between
entire fuel cycles or between entire alternative energy systems. While we are
not yet able to analyze completely environmental and health impacts with
quantitative data for the entire energy system, current economic- and
technology-oriented models use this integrated framework.^"
The main difficulty in risk assessment lies in comparison of
qualitatively different risks. There may be trade-offs among air, water, and
land impacts; between short-term and long-term risks; or between extraordinary
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and routine risks. In comparing coal and nuclear fuel cycles, for example.
the high probability of air pollution impacts from coal (although uncertain in
magnitude) must be compared with the low probability of catastrophic events
from nuclear energy. Quantitative analysis alone cannot tell how large a
certain, routine impact one is willing to accept to avoid an unlikely
catastrophe. Risk assessment would help separate scientific issues from value
issues in these very thorny technological problems, thus helping the public
and political decision-makers clarify key value decisions.
Until recently, we concentrated on comparisons of the main sources of
electric power. Tables 7 and 8 summarize our preliminary estimates of health
effects on a unit-plant basis, * assuming currently mandated environmental
controls. Table 7 shows a summary of the nuclear cycle effects on a
unit-plant basis. Table 8 shows our current estimates of the health effects
of the coal fuel cycle on a unit-plant basis. Most of our attention has been
directed to quantifying coal-mining accidents and occupational disease, coal
transport accidents, and air pollution from coal combustion.
Detailed Approach to Assessment
Some of the results of our assessments are incorporated into a
coordinated effort of several groups within the national laboratories in
support of a U.S. Department of Energy program called the National Coal
Utilization Assessment (NCUA).^ The complete project is wide-ranging. It
may be useful to the Ohio River Basin Energy Study (ORBS) to examine what —
from our point of view — is the main theme of the exercise, since the course
of ORBS must be somewhat similar. It consists of six steps:
1. Scenarios which span the range of energy policies to
be analyzed for specific future reference years were
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designed.
2. Energy technology-economic analysis at the regional
level resulting in estimates of energy supply,
conversion, and use by fuel, sector, and region was
carried out.
3. Specific energy facilities were sited within each
region. This was done with models which consider
historical trends, resource availability, end use,
etc.
4. Environmental transport models were run to convert
air-pollutant emissions to ambient concentrations.
The result was a geographical distribution of
air-quality contributions from energy use in each
scenario-reference year.
5. Population exposures were determined by overlaying the
pollution distribution produced in step 4 on mapped
population distribution. The result was the number of
people exposed to various levels of energy-generated
pollution. Although this has been applied only to
man, the same approach is expected to estimate
pollution exposure to crops and various natural
ecosystems.
6. Using dose-response functions developed independently,
the impact of population exposure was estimated.
Several aspects of this approach are under further study. Some examples:
(a) background pollution exposures from non-energy sources are an important
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consideration that should be projected and analyzed — attempts have been made
to do this but it greatly enlarges the required effort; (b) more opportunity
to consider environmental factors and alternative emission controls within the
technology-economic modeling of step 2; (c) opportunities to allow changes in
the technology-economic modeling based on the impacts calculated in step 6;
(d) expansion of the kinds of environmental modeling — we are now working on
water-quality modeling; (e) expansion of receptor categories - mappings of
agricultural crops and endangered species are being integrated with pollution
level and siting mappings to identify potential impacts; (f) flexibility —
each step is an independent process, products are available for review after
each step, and revision of the models in any one step can be easily
incorporated.
Simplified Approach to Assessment
The comprehensive approach requires much time, personnel, and
coordination. Frequently, quick, first-cut estimates must be made of the
effects of various policy options. To meet this need, we have used a unit
effects approach. Based on detailed case studies, we have developed impact
estimates for typical unit facilities, particularly power plants. If a
scenario calls for the equivalent of 50 1,000-MWe coal power plants, we assign
the impact to be 50 times the impact of our unit plant. We have used the unit
effects approach on national, regional, and multi-regional studies.
Acknowledgements
This research was supported by Office of the Assistant Secretary for
Environment, U.S. Department of Energy under contract EY-76-C-02-0016.
I thank my colleagues in the Biomedical and Environmental Assessment
Division (BEAD) Dr. S.R. Bozzo, Dr. S.J. Finch, Mr. K.M. Novak, Dr. S.C.
Morris, and Dr. J. Nagy for their work and helpful discussions.
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Soc. Sci. and Med. Geog., 13D(2), pp.95-109, 1979.
32. Tanner, R.L., and Marlowe, W.H., Size Discrimination and Chemical
Composition of Ambient Airborne Sulfate Particles by Diffusion Sampling
(in press), Atmospheric Environment, 1977.
33. Weiss, R.E., et al., Sulfate Aerosol: Its Geographical Extent in the
Midwestern and Southeastern United States, Science, 195:979, 1977.
34. Bozzo, S.R,, Novak, K.M., Galdos, F., and Hamilton, L.D., A Comparative
Study of Air Pollution Health Damage Using Different Pollution Data, in
preparation.
-553-
-------
35. Bross, I.D. and Natarjan, N., Leukemia from Low-Level Radiation:
Identification of Susceptible Children, New England Journal of Medicine
287:107-110, 1972.
36. Mancuso, T.F., Stewart, A., and Kneale, G., Radiation Exposures of
Hanford Workers Dying from Cancer and Other Causes, Health Physics
33:369-85, 1977.
37. Najarian, T. and Colton, T., Mortality from Leukemia and Cancer in
Shipyard Nuclear Workers, The Lancet, May 13, 1978, p. 1018.
38. Smith, P.G. , Pike, M.C., and Hamiton, L.D., Multiple Factors in
Leukaemogenesis, Letter to Editor, Brit. Med. J. 2:482-483, 1973.
39. Rothman, K.J., Review of Dr. Irwin Bross' Presentation on Radiation
Exposure and Cancer Risk, prepared for a public meeting of the low-level
effects of ionizing radiation sponsored by the U.S. Nuclear Regulatory
Commission, Washington, B.C., April 7, 1978; see also Letters to Editor,
Journal of the American Medical Association 238(1):1023-1024, 1977.
40. Bross, I.D.J. and Natarjan, N., Genetic Damage from Diagnostic Radiation,
J. Amer. Med. Assoc. 237:2399-2401, 1977.
41. Bross, I.D.J., Ball, M., Rzepko, T., and Laws, R.E., Preliminary Report
on Radiation and Heart Disease, J. of Med., 9:3-15, 1978.
42. Ginevan, M.E., Nonlymphatic Leukemias and Adult Exposure to Diagnostic
X-rays: The Evidence Reconsidered, Health Physics, in press.
43. Marks, S., Gilbert, E.S., and Breitenstein, B.D., Cancer Mortality in
Hanford Workers, IAEA Symposium on the Latent Biological Effects of
Ionizing Irradiation, March 1978, IAEA SM-224.
-554-
-------
44. Hutchinson, G.B., Jablon, S., Land, C.E., and MacMahon, B. , Review of
Report by Mancuso, Stewart, and Kneale of Radiation Exposure of Hanford
Workers, Health Physics, in press.
45. Reissland, J.A. and Dolphin, G.W., A Review of Mortality from Leukemia
and Cancer in Shipyard Nuclear Workers by T. Najarian and T. Colton, The
Lancet, VI, p. 1018, 1978, National Radiology Protection Board (NRPB),
Harwell, Didcot, England, May 18, 1978.
46. Drysdale, F.R. and Calef, C.E., The Energetics of the United States of
America: An Atlas, BNL 50501-R, Brookhaven National Laboratory, Upton,
N.Y., 1977.
47. Meyers, R.E., Cederwall, R.T., and Ohmstede, W.D., Modeling Regional
Atmospheric Transport and Diffusion: Some Environmental Applications, in
Advances in Environmental Science and Engineering, in press.
48. Seller, M. et al, Energy Systems Studies Program Annual Report — Fiscal
Year 1976, BNL 50539, Brookhaven National Laboratory, Upton, N.Y., 1976.
49. Hamilton, L.D., Testimony on Comparative Health Effects of the Coal and
Nuclear Fuel Cycles, in the Matter of the Power Authority of the State of
New York (Greene County Nuclear Power Plant), No. 50-549, Case 80066,
June 5-6, 1978, before the U.S. Nuclear Regulatory Commission, transcript
pp. 18810-19130.
50. Morris, S.C., Novak, K.M., and Hamilton, L.D. , Health Effects of Coal in
the National Energy Plan, in An Assessment of National Consequences of
Increased Coal Utilization Executive Summary, U.S. Department of Energy,
Office of the Assistant Secretary for Environment, Washington, D.C.,
TID-2945 (Vol. 2), pp.12-1 to 12B-3, February, 1979.
-555-
-------
Table 1 MECHANISMS THAT CONVERT SULFUR DIOXIDE TO SULFATES
i
Ln
Ui
Mechanism
1. Direct photo-
oxidation
2. Indirect photo-
oxidation
3. Air oxidation in
liquid droplets
4. Catalyzed oxidation
in liquid droplets
5. Catalyzed oxidation
on dry surfaces
Overall reaction
S02
S02
light, oxygen
water
smog, water, NOX
organic oxidants,
hydroxyl radical (OH*)
H2S04
H2S04
SO-
liquid water
NH3 + H2S03
Oxygen
S02
S02
oxygen, liquid water
H2S03
'+ S0|
S04
Factors on which
sulfate formation
primarily depends
Sulfur dioxide concen-
tration, sunlight
intensity.
Sulfur dioxide concen-
tration, organic oxi-
oxidant concentration,
OH', NOX
Ammonia concentration
Concentration of heavy
metal (Fe, Mn) ions
heavy metal ions
oxygen, participate I Carbon particle concen-
""carbon, water ' 2 4 « tration (surface area)
-------
TABLE 2
INCREASE IN MORTALITY IN THE LONDON FOG OF DECEMBER 1952
CAUSE
OF
DEATH
Bronchitis
Other lung diseases
Coronary artery dis-
ease, myocardial
degeneration
Other diseases
Total
SEASONAL
NORM
(DEATHS
PER WEEK)
75
98
206
508
887
DEATHS
IN WEEK EXCESS
AFTER FOG DEATHS
704 629
366 268
525 319
889 381
2484 1597
PERCENTAGE
OF TOTAL
EXCESS
DEATHS
39
17
20
24
100
Table 3 — Ranking of sulfates for irritant potency.
Compound % Increase Resistance/^ SO4,'m3
H2SO4
Zn(NH4)!(S04)1'
Fe2(SO4)a*
ZnSO/
(NH4)2SCV
NH4HSO4
CuSO,
FeSO4»
MnSO42
0.410
0.135
0.106
0.079
0.038
0.013
0.009
0.003
-0.004
1 Data of Amdur and Corn (1963).
1 Data of Amdur and Underbill (1968).
-557-
-------
TABLE 4
Enumeration of Strengths and Weakness Study Designs
for
Air Pollution Health Effects
t-l
^
JJ
>
•H
CJ
£
s
Randomize
Population
Socio-Economic
Smoking
Direct Applicability to
General Population
Regional Effects
P
P
P
P
N
P
•H
O
•
•u
•H
^
•H
O
P
N
N
N
N
K
ti
•H
ft
t-t
O
a
p
p
p
p
N
P
o
C
O
0
N
N
N
N
P
N
r-1
CO
5
S
N
NA
NA
NA
P
N
P = possible problem area
N = design directly or indirectly controls for this factor
NA = not applicable
-558-
-------
TABLE 5
Comparison of Attributable Pollution Death Estimates
by' Various Researchers
Researchers
Excess Deaths
(death x 105/ug
pollution type)
95% Confidence Limit
Minimum Maximum
Winkelstein (1967)***
white males and females
ages 50-69 ug/TSP/m3
Eozzo et. al.
white males and females
ages 50-69
ASSUMPTION: 25% SC>4/TSP
80% SO4/TSP
Lave and Seskin (1977)*
white males and females
ages 45-64 ug/TSP/m3
14.00
2.29
7.34
0.90
Lave and Seskin (1977)
white males 45-64, (ug SC>4/m3) 4.41
white females 45-64 (ug SC-4/in3) 8.10
Bozzo et. al.
white males and females
ages 45-64
10.00
0.91
2.91
0.40
-5.80
2.20
18.00
3.67
11.76
1.40
14.60
14.00
ASSUMPTION: 25% SO4/TSP
80% S04/TSP
Lave and Seskin (1977)
All ages, white male
All ages, white female
Morgan et, al . (1977)
all ages (ug S04/m3)
Bozzo et. al. (1977)
all ages (ug S04/m3)
1.68
5.38
4.80
9.35
3.71**
3.56
0.68
2.16
-0.50
4.50
0 .00
1.16
2.69
8.59
10.10
14.20
11.47
5-95
* Personal communication to S. Finch (in Finch and Morris 27)
** Median value
*** As calculated by Finch and Morris from Winkelstein ' s data
-559-
-------
Common cancer inducing agents have been linked to various occupational
groups.
Table 6
COMMON OCCUPATIONAL CARCINOGENS
Agent
Wood
Leather
Iron oxide
Nickel
Arsenic
Chromium
Asbestos
Petroleum, petroleum
coke, wax, creosote,
shale, and mineral oils
Mustard gas
Vinyl chloride
Bis-chloromethyl ether,
chloromethyl methyl
ether
Isopropyl oil
Coal soot, coal tar,
other products of coal
combustion
Benzene
Auramine, benzidine,
alpha-Naphthylamine,
magenta, 4-Aminodiphenyl,
4-Nitrodiphenyl
Organ Affected
Nasal cavity and sinuses
Nasal cavity and sinuses;
urinary bladder
Lung; larynx
Nasal sinuses; lung
Skin; lung; liver
Nasal cavity and sinuses;
lung; larynx
Lung (pleural and peritoneal
mesothelioma)
Nasal cavity; larynx; lung;
skin; scrotum
Larynx; lung; trachea;
bronchi
Liver; brain
Lung
Nasal cavity
Lung; larynx; skin;
scrotum; urinary bladder
Bone marrow
Urinary bladder
Occupation
Woodworkers
Leather and shoe workers
Iron ore miners; metal grinders and polishers
silver finishers; iron foundry workers
Nickel smelters, mixers, and roasters;
electrolysis workers
Miners; smelters; insecticide makers and
sprayers; tanners; chemical workers; oil
refiners; vintners
Chromium producers, processors, and users;
acetylene and aniline workers; bleachers; glass,
pottery, and linoleum workers; battery makers
Miners; millers; textile, insulation, and
shipyard workers
Contact with lubricating, cooling, paraffin or
wax fuel oils or coke; rubber fillers; retort
workers; textile weavers; diesel jet testers
Mustard gas workers
"Plastic workers
Chemical workers
Isopropyl oil producers
Gashouse workers, stokers, and producers;
asphalt, coal tar, and pitch workers; coke oven
workers; miners; still cleaners
Explosives, benzene, or rubber cement workers;
distillers; dye users; painters; shoemakers
Dyestuffs manufacturers and users; rubber
workers (pressmen, filtermen, laborers);
textile dyers; paint manufacturers
SOURCE: National Cancer- Institute.
-560-
-------
TABLE 7
NUCLEAR FUEL CYCLE EFFECTS SUMMARY
EFFECTS PER 0,65 GWY(E)
DEATHS DISEASE/INJURY
MINING
PUBLIC
WORKERS
RADIATION INDUCED CANCER
NON-RADIATON INDUCED
OCCUPATIONAL DISEASE
OCCUPATIONAL ACCIDENTS
SUBTOTAL
PROCESSING
PUBLIC
WORKERS
RADIATION INDUCED CANCER
OCCUPATIONAL ACCIDENTS
0,08
0,06
0,07
0,31
0,52
0,002
0,034
0,004
0.08
0.03
0,14-2.8*
11.96
12.21-14,87
0.002
0.034
1.3
SUBTOTAL
0,04
1.34
ELECTRICITY GENERATION
ROUTINE PUBLIC
WORKERS
RADIATION INDUCED CANCER
OCCUPATIONAL ACCIDENTS
CATASTROPHIC ACCIDENTS
0,017
0,07
0,013
0,1
0.017
0.07
1.13
SUBTOTAL
0,20
1.217
*BASED ON RATIO OF OCCUPATIONAL DISEASE/DEATH IN COAL MINERS,
LOWER ESTIMATE IS USED IN TOTAL,
-561-
-------
TABLE 7
NUCLEAR FUEL CYCLE EFFECTS SUMMARY (CONTINUED)
WASTE MANAGEMENT
PUBLIC 5,1 x 10"5 5,1 x 10""5
WORKERS 7,45 x HP1 7.45 x
SUBTOTAL 7,96 x 10"4 7.96 x
TRANSPORT
ROUTINE PUBLIC 6,1 x 10^ 6,1 x 10"^
WORKERS
RADIATION INDUCED CANCER 8,5 X 10~^ 8,5 X 10"^
OCCUPATIONAL ACCIDENTS 0,01 0,1
CATASTROPHIC ACCIDENTS
CANCERS 8,3 x 10~5 TO 8.3 x 10"5 TO
7,1 x HH 7,1 x 1^
PROMPT DEATHS 2,1 X 10"' TO
9,3 x 10"5
SUBTOTAL 0,01 0.10
DECOMMISSIONING
PUBLIC 5,3 x 10"9 5.3 x 10~9
WORKERS
RADIATION INDUCED CANCER 4,2 X 10~* 4.2 X 10~^
OCCUPATIONAL ACCIDENTS 8,0 X 10~^ 0.07
SUBTOTAL 5 x 10"3 0.07
TOTAL 0,77 14.9-17,6
-562-
-------
TABLE 8
COAL FUEL CYCLE EFFECTS SUMMARY
(PER 1,000 Fiw PLANT-YEAR, 65% CAPACITY)
DEATHS
DISEASE/INJURY
MINING1
PUBLIC
WORKERS
ACCIDENTAL INJURY2
OCCUPATIONAL DISEASE
PROCESSING
PUBLIC
WORKERS
ACCIDENTAL INJURY
OCCUPATIONAL DISEASE
0,6
0,02-0,1
0,05
42
0,5-1,0
2,9
TRANSPORT
PUBLIC AND WORKERS
ACCIDENTAL INJURY
ELECTRICITY GENERATION
PUBLIC
AIR POLLUTION (50 MI RADIUS)^
AIR POLLUTION (TOTAL U.S,)^
WORKERS
ACCIDENTAL INJURY
TOTAL
0,3-1,3
0,6 (0-3)
6 (0-30)
0.1 (0.02-0.3)
7,7-9,1
1,2-5,9
NOT ESTIMATED
NOT ESTIMATED
3,3 (2.7-4,0)
-563-
-------
TABLE 8
COAL FUEL CYCLE EFFECTS SUMMARY (CONTINUED)
NOTES;
1, ASSUMES 62% UNDERGROUND., 38% SURFACE MINING (THE RATIO OF
APPLACHIAN COAL PRODUCTION, SOURCE U,S, BUREAU OF MINES, MINERAL
YEARBOOK 1974, U,S, GOVERNMENT PRINTING OFFICE, 1976, VOL. 1,
pp. 367-76),
2, COAL MINERS ACCIDENTAL (NON-FATAL) INJURY (1965-73 MEN)
c
UNDERGROUND MINING - 27,6 INJURIES PER 10° TONS
SURFACE MINING - 5,2 INJURIES PER 1(T TONS
[(27,6 x 0,62) + (5,2 x 0,38)] x 2,2 x 106 = 42 INJURIES PER
PLANT-YEAR
FROM MORRIS AND NOVAK (REF, 61, p,13)
3, ASSUMES RAIL TRANSPORT, 300 MILE TRIPS. RANGE is DUE TO
DIFFERENT METHODS OF ESTIMATION,
4, ASSUMES 3 MILLION PEOPLE WITHIN 50 MILE RADIUS, SULFUR OXIDE
EMISSION RATE OF 0,12 LBS. $02 PER 10 BTU INPUT (LOW SULFUR
COAL COMBINED WITH 90% REMOVAL OF SULFUR IN FLUE GAS. RESULTS
ARE APPROXIMATELY LINEAR FOR S02 EMISSIONS.
5, ASSUMES TOTAL EFFECT lOx LOCAL EFFECT,
6, ESTIMATES FROM BERTOLETT AND Fox, WITH POISSON 95% CONFIDENCE
LIMITS,
-564-
-------
LEGENDS TO FIGURES
1. The position of biomedical assessment in overall energy assessment.
2. Reference energy system, 1977, diagramming stages in energy production,
distribution and use.
3. Deposition in various portions of the lung and respiratory tract for
various size particle populations. Nasal-P stands for the nasopharyngeal
compartment, T-Bronchial for the tracheobronchial compartment, and
Pulmonary for the alveolar compartment.
4. Correlation between the prevalence of chronic bronchitis and sulfur oxide
precipitation (measured by Pb02 method) for differing smoking rates in
the subjects after correction for sex and age.
5. Total number of deaths for 156 winter weeks in Oslo, Norway (1958/9 to
1964/5) plotted against weekly mean concentration of S02-
6. Excess acute lower respiratory disease in children plotted against annual
average suspended sulfates concentration.
7. Aggravation of heart and lung disease in the elderly plotted against
24-hour suspended sulfates concentration.
8. Excess mortality rate in New York City in 1960 plotted against 24-hour
suspended sulfates concentration (includes data on excess mortality in
London'in 1950's and Oslo in 1960fs).
9. Excess leukemia mortality at Hiroshima and Nagasaki plotted against the
dose in rem (with 90% confidence limits). Kerma dose was converted to
effective absorbed dose. (The line is a least-square fit forced through
the origin deleting the two negative Nagasaki points. The slope is 49.90
deaths/10^ person-rem with a standard deviation of 4.27.)
-565-
-------
10. BEAD probability density functions representing the uncertainty in the
slope of the assumed linear damage function. The solid curve is the
subjective distribution. The dashed curve is the classical estimate
(student's jt_ distribution with three degrees of freedom) obtained by
treating the results of four regression studies as independent
observations of the same slope.
11. Sex-, race-, age-specific mortality rates and family income, 1970.
12. The combined effects of income and pollution by age for white males and
females, total mortality.
13. Total deaths associated with 804 exposure (deaths/100,000/yg/SOA/year),
U.S. 1969-71 white males. Stage 1: Analysis based on emissions data.
Stage 2: Analysis based on air quality and related emissions data. Note
the average values given by Lave and Seskin and the results of the
probabilistic study from Morgan et al. for both sexes at all ages.
14. Total deaths associated with 804 exposure (deaths/lOO.OOO/pg/804/year),
U.S. 1969-71 females. Stage 1: Analysis based on emissions data. Stage
2: Analysis based on air quality and related emissions data. Note the
average values given by Lave and Seskin and the results of the
probabilistic study from Morgan et al. for both sexes at all ages.
15. Total deaths associated with total suspended particulates exposure
(deaths/100,000/ug/TSP/year), U.S. 1969-1971 white nales. Stage 1":
Analysis based on emissions data assuming TSP contains 25% 804. Stage 2:
Analysis based on air quality and related emissions data. For comparison
note values given by Winkelstein for age 50-69 and Lave and Seskin for
age 45-64.
-566-
-------
ENERGY POLICY ASSESSMENT STRESSING BIOMEDICAL EFFECTS
1^Bl^r--_/ „ \-orBR*
I ENERGY
POLICY
SSESSMENT
DAMAGE
AND COST
RELATION
SHIPS
ENERGY
SYSTEM
MIX
EXISTING
SYSTEMS
(ALTERNA-
TIVES)
RESIDUALS
(POLLUTANTS)
DIRECT EFFECTS
SOURCES OF
BIOMEDICAL
EFFECTS
TRANSPORT
AND
FATE
ENERGY
DEMAND
ENERGY R&D
(NEW OPTIONS)
TECHNOLOGY ASSESSMENT
FIGURE 1
SOURCES OF EFFECTS ON
AESTHETICS
ANIMALS
VEGETATION
SOILING
LAND USE
RESOURCE DEPLETION
MATERIALS
BIOMEDICAL ASSESSMENT
-------
FIGURE 2
REFERENCE ENERGY SYSTEM. YEAR 1977
RESOURCE
NUCLEAR FUELS
une U2»
RENEWABLES
HYOROPOWER
GEOTHERMAL
SOLAR
FOSSIL FUELS
COAL
Ln
cr>
00
NATURAL CAS
EXTRACTION
& TRANSPORT
" & STORAGE
I 1
CENTRAL rrRANSMSSKDN DECENTRALIZED
STATION DISTRBUT1ONI CONVERSION
CONVERSION & STORAGE
UTUZNG
DEVICE
ENERGY
SERVICES
ENRICH B FABRICATE* TRUCK ' LWR
** i- i- i i i •- ™ >°«2
DAM ' HYDROELECTRIC " 765 K VAC
LONGDISTANCE
1 '•MH^M* • -** fe *BI^HM( 'Z) 1 f CAS 8I"E mnm"
1831 . (93) . 390 „ fj 361(32) . Z2O
Kygffl
<7 24(91^^^^ 659
ELECTRICITY
_£°°g_» —
^
^*^
^\v....
y \
...JL^-Ui'.
; / ^xx-4«
•• /.rvv"
;/7 ,%
/ WFNE /
MBBMM^ f
RTS (CRUDE) /
472 /
^J///
IMPORTS (REFINED)
18.61 „
NATIONAL CENTER FOR ANALYSI9OF ENERGY SYSTEMS,
j)ltI BHOQKH AVE>J^ATJg^ LABORATORY
nit i TesocWEtruwvEteJTies.THC
UNECR DOC CONTRACT NO EY-Tt-C-Ot-OOW
A07Z5/ LEGEND:
t SOLID £l£WiVr DENOTES A REAL ACTIVITY
EACH ELEMENT CONVERSION EFFICIENCIES ARE
INDICATED IN PARENTHESIS
3, INDUSTRIAL PROCESS HEAT DEMAND INCLUDES
AtmCULTURE AMD WNIN6 AS WELL AS ALL
OTHER INDUSTRIAL REQUIREMENTS
4 HVODANOmSTE NOT INCLUDED IN TOTAL ENERGY
OF THERMODYNAMICS
6. SOME Ni*ieERS ON TftSCHAItr ARE
G ANALYSES.
DEMAND
SECTOR
RESIDENTIAL 8> COMMERCIAL.
MISCELLANEOUS ELECTRIC
- INDUSTRIAL,
ELECTRIC DRIVE
INDUSTRIAL,
Al UMINUM
. INDUSTRIAL,
IRON ft STEEL
ELECTRIFIED MASS
TRANSPORTATION
RESIDENTIAL » COMMERCIAL,
AIR CONDITIONING
RESIDENTIAL 8 COMMERCIAL
SPACE HEAT
NO OF HOUSEHOLDS 741 10* BTU/UNIT 50 » 10'
COMM FLOOR SPACE 27»IO*FT' BTU/5Q FT 26,000
RESIDENTIAL 9 COMMERCIAL.
MISCELLANEOUS THERMAL
INDUSTRIAL,
PROCESS HEAT a MISCELLANEOUS
. INDUSTRIAL,
PETROCHEMICALS
, TRANSPORTATION.
PIPELINES
GASOLINE ENGINE (I-C)
220(10)
TRANSPORTATION.
AurOMOBL-F
GAS TURBINE
6,17(13)
. TRANSPORTATION,
AIRTRANSPORT
PASSENGER Mi 193x10* PASS MPG 169
TON Mi 8«K>* TONMPG 46
08° _^ TRANSPORTATION,
ELECTRICITY
cutter SEIMCES
(l-C) ENGINE
090(10)
BUSPAS5M.. 95x10* 8U8.TRUCK fl RA.L
TRUCK TON M' 525 x |0»
VEH Mi 263 x 10*
009 TRANSPORTATION.
•M^MMH^^^^^ SHIP
TOTAL ENERGY, 1977
7M4K»"Btu
AVAILABLE ENERGY. 1977
ST24»IO"Blu
S0.6TxlO"Btu
29.73 «10* Btu
14.59.10" BtG
-------
-------
PREVALENCE OF CHRONIC BRONCHITIS (•/.)
I
On
^J
O
Number of deaths
70
p
HIGASHl"
SUMIYOSHI
(I)
S
HIGASHI-
SUMIYOSHI
(H)
FUKUSHIMAg;
(I) ta
in
KONOHANA
TAISHO
u
NISHI-
YODOGAWA
o>
—r
00
—I—
K>
—T~
cn
-------
FIGURE 6
EXCESS ACUTE LOWER RESPIRATORY DISEASE IN CHILDREN
100
I I
BASED ON1 STUDIES IN
SIX AREAS.
UJ
o
><
UJ
fc: 50
LU
O
Di
UJ
CU
Gn \
I
10
15
20
25
30
ANNUAL AVERAGE SUSPENDED SULFATH
-571-
-------
PERCENT EXCESS
I
Ul
CD
-------
PERCENT EXCESS
Ui
OJ
sc
o
a
-a
i<\
rj
CO
c:
r-
71 |N*
2; -
ni
*x>
fs>
O
J-
.1
3-
)
O
— O\
a o- o'
i2 o fn
H- ^i o
••o ^~ za
m -^M
C» Ji *^
v>
"' ~{
~n
(—4
cn
oo
_L L
-------
FIGURE 9
25,000 -
CD
O
20,000
(T
O
15,000
UJ
:*:
ID
UJ
LU
o
X
UJ
10,000
5,000
• HIROSHIMA
* NAGASAKI
90 % CONFIDENCE LEVEL
/
_L
100
200
REM
300
400
-574-
-------
PROBABILITY DENSITY, I04
O — no CM
m
m
C/)
o
m
O)
rn
o
01
rn
C/)
o
•p
(Q
\
-------
Figure 11
0-4 YRS.
5-14 YRS.
10.0-
M
0
R
T
A 7.5-
L
I
T
Y
R
A ,
1 5.0—
E
P
E
R
0 2.5-
0
0
0 9
+
r x**i
******* ^ +
** *4
** * .** t
*t* ;
*
*
*
vx ^
*^«^ ,** "•
S-II'-" \,_L
OCXDOOOOOQQ ^
^^QOQ) O
1 1 !
J. * ^~—
M
0
R
T
A .9-
L
T
Y
R
A
T .6—
E
IHM*M«a
!- P
rO E
OC*5^ R
0 .3-
0
0
0 0
1 B-°"
+•
+
*
* + ^-v.
*********** ^ ^.
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-576-
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FIGURE 13
'iotai deaths associated with S04 exposure. b.S. 1969-71
(aeaths/100,000/ug/so5/year)
Vvhllt hALES
46t
So-
30-
D
t,
A
T
22-
6-
STAGE II
(Concentration,
+ Emission)
STAGE 1
(Emission)
Morgan et al. (both sexes)
15
30
45
AGE
60
75
90
-578-
-------
62 +
54-
46-
A
I
h
30-
22-
u
6-.
FIGURE 14
Total deaths associated with 50^ exposure. U.S. 1969-71
(deaths/100,000/ug/Son/year)
VihlTE FEMALES
STAGE II
(Concentration
+ Emission)
STAGE I
(Emission)
Morgan et al. (both sexes)
I
15
\
30
60
75
90
AGE
-579-
-------
FIGURE 15
lotal deaths associated vvith ISP exposure.
(deaths/100,000/ug/lSP/year]
U.S. 1969-7 1
WhlTL KALtb
1 1-
b
t,
K
1
n
'kvinkelstein
SlAGh, II
(Concentration
+ Emission)
STAGL I
(hmis eion)
Lave it Seskin
15
30
45
AuL
60
75
90
-580-
-------
DISCUSSION
SESSION VI
Dr . Hartnett , Energy Jte£o.ur_c_es Center , ]^ILiY.£L§i^y P_£
Illinois , and _a member o_f the ORB ES Core jJLfLEi This question is
addressed to Dr. Hamilton. Yesterday we heard from Dr.
Mazumdar, reporting on the work of a colleague, that studies in
New York City showed that even though the S02 level decreased by
a factor of five, there were no significant changes in deaths
related to S02. Can you rationalize that with the results that
you showed?
Dr_._ Hamilton ; That's a very good question and I'm afraid
I didn't make myself clear yesterday when I intervened after she
spoke. I think the reason for the lack of change in New York
City is due to the long-range transport of sulfate or some
chemical transformation product of the S02. 80% of sulfate in
New York City is foreign. Very careful study has been done on
this. 80% is imported from areas of the United States west of
the Hudson River, unfortunately. Again, there's another point I
think you have to have some perspective on: we're looking at a
very tiny proportion of the annual death rate. The worst sort
of figures that we're getting from air pollution is only about
2% to 3% of the annual death rate. You'd be looking for a very
tiny change on that particular point.
Dan Swartzman , University o_f Illinois Sc_hool p_f _
Health: To the great relief of everybody present I have a
question, not a comment. Dr. Rowe, I just wond er ed--you used
the term "worst case assumption" in dealing with the deposition
of high level radioactive materials into salt caverns. I was
wondering if anybody has looked at the worst case assumption of
finding out that, in fact, it doesn't work. And, in fact, we
may be stuck with holding the high level wastes as we currently
are, in temporary storage facilities. Has anybody done the sort
of in-depth analysis that you did, which I was terrifically
impressed with, for that sort of "worst case" analysis?
Dr . Rowe : Let me say, first, that I didn't do the
analysis--Tt was done by the professional while I was heading
the Office of Radiation Programs of EPA. They did look at worst
case consequences. The event might be a failure of a certain
kind where 50% of the total material could be released to the
-581-
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environment, by the worst possible pathway. This was then used
as a consequence measure. An even more extreme case would
involve releasing all -the available material. Then they worked
backwards, and tried to determine what kinds of events could
cause that kind of consequences. They then began to try to base
the probability of such events upon historical data and models
to get some idea of their relative frequency. In a sense they
ha^e looked at some worst cases of having this material reach
the environment. Now then, you ask what is the problem if we do
nothing. Remember, I only stated conditions from the time the
repository was closed. There are also conditions up to the time
that you put the material in the repository. The major
difference in concept between those is that if we do the work to
put it in the repository in our generation, we are taking risks
in our generation for benefits gained in our generation. But in
the long term, other than the intangible benefit of the
continuity of society, there is really no benefit to the future
generations, so a legacy remains. If we do nothing, we leave it
as a liability for the future. Once produced, wastes are
nonproductive in our society. Under inflation, the worth of
productive items goes up at the same time the costs go up to
handle them. But for nonproductive items such as wastes, the
costs escalate and become a significant part of the economy
without any productivity. A good example, I think, are the 22
abandoned mill tailing piles in the West where Congress now has
voted 130 million dollars to clean them up. That's a
significant amount of money considering how little was spent to
put them there. Another example is the culm piles in eastern
Pennsylvania. These were put there at a very low cost—now we
can't afford to move them and the land is not usable. The
problem is further exacerbated in that the balances we make have
to take into account not only the economic and the health impact
aspects, but also the equity aspects.
Dan Swa_r.t^zm_an_:_ May I just ask one quick follow-up question
becau¥e"l'm not quite sure if I was understood. What I'm asking
is that implicit in your analysis and much of the analyses I've
seen, is the assumption that there is a method for storing
high-level radioactive materials. What I'm saying is, "Has
anybody done the projected health effects into the future not
using that assumption?" In other words, using the assumption
that, in fact, we never find a satisfying way of storing high
level materials? Has anybody done the same sort of projection
into the future of the health effects of that? That's what I
was asking.
£r_. ]to_we_: I don't think such projections have been made
for the total practice as I did. I think they've done it for
waste we have already accumulated, a relatively a small amount,
but I don't know what the effect would be for total practice.
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Dr . Swartzman_:_ Would you care to speculate?
Dr. Rowe; I only can speculate on the social system
involved. We would require institutional controls to preserve
the integrity of present wastes, if we leave them in the form we
have now. If we did nothing, and the institutional controls
broke down to some extent, we would end up with cathedrals and
high priests around each repository to keep it safe. I don't
know the answer.
Dr. H_._ Spencer, one p_f the ORBES Core Team members: I
have worked hard in this conference to try to see to it that
issues that I felt relevant and important were not overlooked.
I have one more I think we passed by. It goes as follows, very
briefly. The San Diego air crash, Pacific Airlines Flight 182,
cockpit crew contained three pilots and one flight engineer. At
the time of the crash all three pilots, one of whom was just on
a jump ride, were looking for the light plane. They missed it,
obviously. PSA since has flown two test flights under the exact
same conditions on the same route, using a 172 separated by 1000
feet in air space for safety purposes. On both occasions, with
four people in the cockpit, they could not pick out the light
plane against the background which was into the sun with smoke
and haze, and six miles of visibility. I want to show you
people in a very quick set of slides, what six miles visibility
looks like, and then I have a question to ask the group in
relation to the health impact of this problem. (FIRST SLIDE)
That's Madison, Indiana from an altitude of 5,500 feet, the very
dead center of the American Midwest, and the visibility recorded
on that day was six miles. It seems to me that from the
standpoint of airline safety alone, and esthetics, this question
of air pollution need not be debated or argued any further. My
question is why have we not in this health analysis taken this
risk to air travelers into account?
Dr. Rowe: I'll make an attempt to address the problem.
If you look at the total perspective of risks in society and
control of those risks, especially the involuntary . ones which
are imposed inequitably on people, we tend to emphasize all our
efforts on those which we can do something about. Either
because they're institutionally controllable or because they're
technically controllable. We tend not to deal with those which
are less tangible. Often for these the manner in which we do
something about it requires changes in lifestyle, or changes in
our whole economic structure, and in the way we live. I think
this problem occurs throughout our society, not just in the
particular case you cited. This is a case in which technology
has fixes, and we know how to impose those fixes. We impose
them through the FAA on particular air control towers in air
traffic control. They are measurable and do-able. Now, I'm not
suggesting that's the right approach. All I'm suggesting is
that the institutions address that which they can control, as
opposed to those they cannot, such as the case for sulfur
-583-
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dio xide.
Dr. Spencer: I want to answer that. I am an
instrument-rated pilot certified for high performance aircraft
and I don't agree with a thing you've said.
Dr. Hamilton: I don't want to get involved in that sort
of controversy because I'm very mindful of Birch Bayh. I was
very impressed by his feeling that we should try to understand
what's going on, and I'm delighted at your intervention because
what you've shown is, of course, exactly the distribution of
sulfates in the United States. I've got a couple of slides. We
don't have the time to see them but I can assure you you could
superimpose "sulfates," whatever they are, on those things.
And, of course, we do know that they are responsible for loss of
visibility. It is a well-established fact. There have been
some beautiful studies done on this, and again I think that is a
very powerful argument for reducing the precursor of sulfates,
which is S02. I would think, in the light of this and the long
range transport, it's a powerful argument for new source
performance standards, being established.
Dr. Rowe; I just have one response. Namely, I didn't say
it was the correct thing to do. I happen to agree with you
because I also fly a high performance aircraft myself, open
cockpit as well. I happen to agree with you—I'd like to see it
cleaned up. But I was just trying to give an explanation of why
society doesn't seem to give equal weight to these things.
That's all.
Professor Shapiro: I feel completely out of place here.
I'm justbetween two pilots and facing one here. I am without
any apology for the program, what's on here, but I would presume
that if we really went into meteorology and all of the other
aspects that are related to this view, we would have to have had
not three days but 30 days of symposium. Hence, I would be
happy if we should have another symposium on that particular
subject in relation to the Ohio River Basin Study because this
is of fundamental importance, but we restricted ourselves. I
believe we should show more concern for accidental injury and
death and agree with the need to evaluate such impacts. I
happen to believe that that is also an area our school, for
example, doesn't emphasize enough, and yet from the point of
view of public health has tremendous impacts.
Mr. Olson, Westinghouse; I have two questions for Dr.
Rowe. First, I have a comment. Dr. Rowe, you said that there
is no benefit to future generations. I take issue with that
because the benefit I see is that we are leaving our future
generations more oil, gas, and coal by burning uranium today.
My questions are both on the same slide. You showed 10,000
gigawatt years of electricity by burning uranium. Is that with
or without plutonium recycle? Secondly, then you showed only 10
-584-
-------
times as much for light water reactors. Why shouldn't that be
more like 60 times as much?
Dr. Rowe: The 10,000 gigawatt years are for the burning
of uranium in our present fuel cycle operation. With plutonium
recycle and thorium, I extended that by a factor of three. With
the use of breeder reactors, I extended that by a factor of 100.
The idea being that with the breeder reactor we may or may not
get the breeding ratios we are talking about; so assuming one
order of magnitude of uncertainty here is not going to affect
the five orders of magnitude uncertainty that I was talking
about at the endpoint. Regarding your first question, I think
you misunderstood me. I didn't say there was no value. I said
there was a value to the continuity of society with or without
gas and oil.
jjci Light, Appalachian Research and Defense Fund; I have a
couple of questions for Dr. Hamilton. First of all, if ORBES
is able to come up with some estimated sulfate concentrations
for projected power plant emission scenarios for the next 20 or
30 years, and have estimates as far as the populations residing
in different areas of different sulfate concentrations, could
they use your estimates of sulfate mortality effects to come up
with some projected mortality in this area?
Dr . Hamilton: Yes, very definitely.
Ed_ Light: The other question is: Could you suggest to us
how we could estimate the morbidity factors of having these
various sulfate levels in the different areas around the power
plants?
D r. Hamilton: Yes, I'm very glad you've asked the
morbidity question because I didn't touch on that. I think that
you can use several methods. First of all, we do have a rough
factor by which we multiply mortality. If people are going to
die from air pollution, our view is that it is not a harvesting
effect, our view is that it is a chronic effect and we do have
some estimates on person-years lost. The other point of view is
that one should try to use some of the best EPA estimates,
guesses, for shorter periods for acute effects. They don't have
such things for chronic effects but they have them calculated
both for TSP and for sulfates and, with all the caveats that one
wishes to include in them, I believe OTA has suggested that
they're reasonable to use. I feel we're going to start trying
to use them, examining the uncertainties involved with them very
clearly.
Prof. Shapiro; I'd like to ask Dr. Hamilton to address
the problem that can be seen in the studies that he referred to
and studies in other areas of health effects which exhibit a
similar kind of problem. Namely, that when we conduct the
analysis on a global basis, as when we evaluate relationships
-585-
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between "sulfates" and the whole population of the United
States, or a very large population, you obtain these
relationships which indicate a health damage due to "sulfates."
But when you start analyzing smaller aggregates, those kinds of
effects seem to vanish or at least are reduced. What is the
reason for such findings?
D_r._ Hamilton ; You're not referring now to the actual use
of the damage function; you are referring to its derivation.
The question is a very interesting question that Professor
Shapiro has raised, and it is one that was demonstrated very
sharply by Lipfert's reanalysis of Lave and Seskin's work using
the same air pollution monitoring stations, and the data from
that for the inner city portion of the standard Metropolitan
Statistical Areas. Lipfert demonstrated that when you restrict
the mortality to consideration of only people in the central
city,' this apparent correlation between "sulfate" and mortality,
this association, disappeared. You want my explanation for
that? My explanation is very straightforward and simple, as far
as Lave and Seskin's work and its reanalysis. It is that when
you restrict yourself to the inner city, you have very
powerful— particularly for the period that we're dealing with—
socio-economic impacts of the inner-city poor. That was a
period, by the way, when there was tremendous non-white
in-migration into those areas. I have already shown you that
the economic variable, as a matter of fact, is a very powerful
variable. I believe that is why it disappears. It is
interesting that the association between total suspended
particulates and mortality does not disappear in the inner city.
I am not able to explain that differential thing. This Lave and
Seskin's type of analysis, which is a multi-regression analysis,
is very sensitive to the weight of the different variables. If
you have a very powerful variable, which obviously comes out
when you go to the inner-city, I think that explains why that
disappeared. That objection, by the way, doesn't apply to the
work of Bozzo, Galdos, Novak and Hamilton, which covers the
entire country.
Professor Shapiro^ But when you use the Standard
Metropolitan Area as an area of study, you're including a
tremendously variable set of circumstances, both from
meteorological and from population density points of view.
Where you locate your measuring devices seems to me very
important. So I can't see how you can, on one hand, have it
disappear and explain it on an economic basis, but then it
appears when you use this tremendous area. It just somehow
doesn't make sense to me.
DrA Hamilton: Well, you made a very good point of
uncertainty here because we are using a single station; but
we're increasing the sensitivity of the analysis to pollution
because we are using a larger area, a larger mortality base, and
we're damping out the effect of poverty. That would be the
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explanation. Let me just say you've put your finger on a very
important area of uncertainty. The use, for example, in our
analysis of only 248 stations for the entire 3,100 counties,
even though we've gone through a very deliberate aggregation
analysis based on our previous work on emissions for all the
counties, is not a desirable thing. We already know that there
is great uncertainty anyway from one single air pollution
monitor in an area and people's outdoor and indoor exposure.
But, you know, that's the best analysis we can come up with at
the present day. Until we have studies where you have personal
monitors attached on people, and follow them for the next 20 or
30 years, we're not going to have any better analysis. That's
my point. You've got to have some assessment.
Dr . Had ford; Well, it seems to me that to rely for damage
functions on a very blunt tool, which the multiple regression
analysis is, and which, as you know, is fraught with a great
deal of controversy and question as to whether, in fact, it
shows any correlation or not, and to ignore what I would call
much more specific studies, in which an attempt has been made to
directly relate exposure to sulfates, sulfur oxides, and so
forth, in areas in relatively small populations where you can
have single exposures, I think that is scientifically not very
sound. The impression I have been left with, especially by data
from multiple regression analysis, the damage functions are just
not known. To assume that we can regulate sulfur emissions on
the basis of health effects when there is that much uncertainty,
I think from a regulatory standpoint, would be a disaster
because it would be shot down in the courts in nothing flat. A
point that Dr. Lippmann made yesterday was really reinforced by
what you just said. We may be barking up the wrong tree. What
we should be concerned about are some of these broader effects,
the impact of sulfur oxides combined with ozone on plant life,
as well as things like visibility, etc. These may be where the
action is in terms of controlling power plant pollutants from
coal burning. I would just like to leave it on that note and
maybe get a reaction from the panel, as to whether we can at
this stage in our regulatory process, do anything on the basis
of other than putative health effects, which a lot of us are
very uneasy about.
Dr . Hamilton: Well, I'd like to answer Dr. Radford in
this area. There are an overwhelming mass of independent
studies, independent of these cross-sectional city studies, the
Lave and Seskin work, and our own massive work in this area.
They point undeniably to the fact that some transformation
products of S02 in urban atmosphere is harmful to health. Now,
the fact that Dr. Ferris hasn't seen it in his small sample in
the Six-City Studies, he has not been able to pick up anything
yet so far, doesn't negate the fact that air pollution is bad
for you. There have been all these episodes. It raises some
questions about dose/effect relationships. But he hasn't given
us any figures for what would be the lower limit of risk, as a
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matter of fact, that you might be able to derive from his
studies. So, it seems to me that if you need some quantitative
measure of damage, and I think one does in any assessment, and
we're not talking about instituting sulfate standards or any
other, suppress the precursor of this material, which is the
S02. And I don't think anybody denies that. Dr. Ferris
himself said that he wanted to live with the present standards,
apparently. I don't know what that meant, rnind you, since I
don't know whether he meant he was against new source
performance standards or what? He seemed to avoid the issue as
to whether or not sulfates or some
oxidation of S02, is harmful to
I'd like to hear from somebody else
material, related to the
human health. I don't know.
on this.
Dr. Andelman, Graduate School o_f Public Health, University
of Pittsburgh: I'd like to ask
highly rated rower of boats, and
water field today, there is a
criteria. EPA is going through
their 129 priority pollutants,
greatest majority, are, in fact,
health point of view. Now, much
all, in relation
been focused on
a question as a non-pilot, as a
a peruser of water. In the
considerable problem in setting
this exercise right now for
not the
chronic
many of which, if
of concern from a
of the discussion, although not
to air pollution for the past three days, has
such things as sulfur dioxide, nitrogen oxides,
and particulates, presumably based on their more acute effect
concerns. I'd like to ask perhaps Dr. Hamilton or the others,
what might be the area of concern on air pollution exposures for
these many emissions of varying kinds of pollutants from power
generation, about which we probably similarly have very little
good information regarding their health effects; and might
these ultimately prove to be of such considerable concern that
even when we can control some of the more acute kinds of
pollutants, these others might still end up being very massive
in terms of their possible impact.
Dr
Hamilton
[ assume you are referring
pollutants, such as polycyclic
and trace metals, etc. Well, let me put
we have been advocating in dealing
reduce particulates and S02, you
non-criteria
hydrocarbons
way. The strategy
thing, is that if you
reduce the trace metals and polycyclics that are going
out too (and also nitrogen oxides). As long as
thorough job in minimizing those things, you should
reduce these other possible potential bad actors.
modeling studies that have been done on trace
association with burning larger amounts of coal from
power plants, and for that matter, from the
aromatics, have indicated that we don't anticipate
would be large amounts.
to the
aromatic
this
this
also
come
do a
metals, in
fossil fuel
polycyclic
that there
Dr . Rowe
he was
separate
Dr. Hamilton used the word
talking about. I think that'a a
the technical information knowledge
"strategy" in what
good opportunity to
and certainties we
-588-
-------
have from what I would call the social or political ones. You
brought up the problem of water pollution. It seems to me in
the area of water pollution we spend more money than any place
else in our economy for pollution control, and very little of it
is for health effects—except for the drinking water problem and
perhaps some particular contaminated areas. Most of it is for
maintaining or reclaiming our resources. I'm not indicating
whether this expenditure is good or bad, but a tremendous deal
of money is spent in this area for municipal treatment plants or
maintenance of existing resources. The problem is, we do have
limited amounts of resources that we can put into taking care of
pollution. I think it is possible to begin to take our resource
estimates and to look at our technical uncertainties and to
determine, based upon the range of 'our uncertainties and the
cost of control at different levels, where we can best spend our
resources; even to make judgments about the uncertainties. The
problem is that at the present time all of our various pollution
laws are set up under different acts and we're constrained by
the institutional constraints. We haven't looked across our
society to find out how to best allocate our resources. We can
possibly begin with the technical uncertainties. It's not just
the problem here for energy development by itself; I think it's
across the board, a measure of how we address society in a
cost-effective manner.
Professor Shapiro: I'd like to take, if I understood you
correctly, slight issue with you and point out that in this area
of synthetic fuel production, or coal conversion to liquid fuels
and gases, where we know that it produces damaging material, and
therefore we start not with the assumption of the . cost of how
much it will cost to control, but that if we don't institute
truly preventive measures, then we'll be way off beam when it
goes on stream. So I think there are areas, especially where we
start de novo, of a need of instituting the best, and even in a
sense an over-control, rather than an under-control.
Dr. Ro we; I'm not necessarily in disagreement with you,
except I recognize the fact that it's much more effective to be
able to regulate at the beginning than it is to try to retrofit.
Even for that reason alone I might agree with you. But as a
second aspect, I think some of the practices that we've accepted
in the past have been perhaps lax in terms of pollution control.
Any new process coming in, no matter what it is, is now subject
to a different scrutiny; and no matter what we do, I suspect
our society will be more conservative. For right or for wrong,
I think it's a fact of life.
Ed Light; I would like to bring up an issue which I
haven't heard addressed yet, but since one of the topics on the
program this afternoon is remaining areas of uncertainty, I
think it is very relevant. That is the question of the risk of
an accident from a nuclear power plant. I think this is a very
important issue for ORBES to address in terms of what are the
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health effects and what is the probability of this occurring.
One of the primary reasons for ORBES being formed, and one of
the primary uses of the information which will be generated by
ORBES, is to help decide how much we want to go towards nuclear
and how much we want to go towards coal burning power plants in
the region. The expert opinion we have received so far in this
conference, are suggestions that if all segments in the fuel
cycle go according to standards, there really aren't very
significant health problems. I mention here that I am somewhat
leery because we've gotten mainly one side of the expert view on
this issue, and perhaps we have excluded a body of opinion from
people with maybe an equal stature as experts, which may have
different ways of looking at some of the same data. But if this
is true that the well-run nuclear plants are not much of a
health risk, what is the best information we can develop in
terms of -the risk of some type of accident developing where
things don't go according to standards and we have a big release
of radiation from the plants?
Dr . Hamilton; I'm very glad you have asked that question.
I want to apologize. The shortage of time prevented me from
following the example of my colleague from Brookhaven, Dr.
Morris, and showing you a film clip from the China Syndrome;
but I understand the film is on locally, and I recommend that as
the first move in answer to this question. But now, seriously,
I was involved, my group was involved, and we had Dr. Wald who
was also involved, in the revision of the consequences of the
reactor safety report. I actually played a very interesting
intermediary role between the reactor safety report group and
the American Physical Society group that was criticizing the
reactor safety report. I think we arrived, as far as the
biological consequences were concerned, at some reasonable
meeting of the minds and very fortunately we have on the panel,
today, Dr. Bill Rowe, because he was the chap who wrote the EPA
criticism of that part of the report. In any case, we now have
to live with the fact that the report has been reviewed by yet
another group, the Lewis Committee, and essentially what the
Lewis Committee said is that, on the whole, the methodology was
fine, but they felt the limits of uncertainty were greater. I
mean that is the key issue that they raised. They also attacked
the use of these probabilities when you were very uncertain,
when you really didn't know whether there was any truth in it or
not, and I think that was a very serious criticism. Now, with
that point, I'd like to turn it over.
Dr . Rp_we_j_ Let me just say I was a member of the Lewis
Committee also. You stated your position very clearly. The
problem that I wanted to address in my talk is one problem, that
of high level waste for a nuclear situation. There are lots of
problems in nuclear energy. There are lots of problems in coal
and oil as well. The problems may not always be commensurate on
the same scale. On the other hand, for the nuclear case, I
brought up a different problem: namely, that of the problem of
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disposing of uranium mill tailings. I think that's an area that
hasn't yet been solved. In the area of the accident situation,
the Lewis Committee did state that the uncertainties were
greater than were stated in WASH-1400. But they could be either
way; they could be lower as well as higher. I think we have to
do some more work in that area.
In the case of oil, for example, I think this is where we
have our highest death rate per whatever energy measure you want
to use. This occurs in the occupational area, because of loss
of tankers at sea, especially those under flags of convenience,
where the counting of the number of people versus the use of
oil, has never really been statistically added up in useful
ways .
Dr . Spenc_er;_ Once again I want to go along with what Dr.
Hamilton said earlier. We've looked at some of the sulfate
data, and up through 1977 the smear of haze does superimpose
over the sulfate distribution. That's not my reason for coming
here at the moment. Let's suppose that we don't have the
Mancuso, Stewart, Nealy Report, or the study of the ship-yard
workers, or the problem of the children in the desert subjected
to fallout from the bomb test. Do you feel, Dr. Hamilton,
based on our state of knowledge, that the regulations are weak,
strong, or somewhere in between? What is your professional
opinion on that question?
Dr. Hamilton: Well, my reaction was that I have always
felt rather uncomfortable with this business of dividing the
year into quarters and allowing people somehow to get 12 rems a
year. I only discovered that relatively recently in my life, as
a matter of fact. I feel that somehow or other we should have a
5 rem a year standard. I like the principle of as low as
reasonably achievable, whatever it is. But I like even more
what I've learned about the naval ship yards activities insofar
as they have had a forcing operation and I've seen them reduce
the level down to, I think the figure sticks in my mind, about 2
rem a year per person. I mean, that's my off-the-cuff reaction
to that question.
Dr. Posvar: May I suggest, since we're losing a lot of
our audience, and I believe our speakers would be willing to
stay for further informal discussion, that we we limit ourselves
to one or two more questions in this formal part of the
presentation.
John Campbell: There was a little talk about the Rasmussen
Report and I just wanted to ask and see if I can get my
impression of it confirmed. Is it true that the Rasmussen
Report is still just about the most reliable accident safety
study available at this time?
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Dr . Hamilton: Well, it is the most because it's the only
one. It's also the least; whichever way you want to look at
it.
John Campbell: Okay, now on the upper bounds of the
uncertainty; can you, on the basis of reactor operation to
date, set an upper bound on the probability of an accident?
Dr . Rowe: There are two ways of looking at this problem
and the first is to recognize that there are different kinds of
reactors operating under different conditions. The question is,
can you lump them all together, including naval reactors, for
example, and use that as an upper limit? I don't know if you
can or not. I don't think the differences have been looked into
in far enough depth yet to know if this is feasible. I could
take, perhaps, a group of reactors, operating under similar
conditions, and be able to set upper limits for that particular
set of reactors with some confidence--but to lump them all
together, I don't know yet if this is proper or improper.
Secondly, there is something else going on which we have yet to
measure. This is the whole operation imbedded in a regulatory
process. When something occurs, a fix is made. This fix may
even lower the probability for the very low probable accidents.
So we don't know yet what the effects of an ongoing regulatory
process are on safety. Until we know that, we may find that
even our history of data bases is getting better — so it could go
either way. My answer would be that, in terms of upper limits,
we can take the history of collected data we presently have and
lump it together and get some figure. Whether that's a good
estimate of what is really going on or not is another question.
I think it is premature to say.
Hamilton: I'd like to tell a little story about the
word, "both." The use of the word, "both", I found
this country, is grossly abused 'by many people;
s real academese. The only correct use is illustrated by a
marvelous movie in which Humphrey Bogart played, called "Beat
the Devil." Humphrey was asked by a North African Potentate
which he thought was more chic, a Rolls Royce or a Cadillac.
Bogart said, "you should have both." That epitomizes my attitude
toward this question of nuclear and coal, by the way, that I
wanted to get into the record. From the health point of view, I
think you can have either. I see nothing preventing control of
both of them equally well. It seems to me on the health point
of view, I would like to leave it on the record that I see
nothing to choose with them. It's possible with proper controls
for both to reduce the health effects to really trivial
proportions.
Dr_^ Posvar: I think that's a good moderate tone on which
to en~cT~this dTs~c~ussion. I want to thank Professor Shapiro, Dr.
Rowe and Dr. Hamilton for their excellent presentations. I'm
sure you will all join rne in this sentiment. As a layman, I
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must say I haven't heard much here this afternoon to give me
good cheer, but I am very much impressed by your concerns and by
the expertise of the people in this group. Now I would like to
call on Dr. Radford to close the meeting.
Dr . Radfordj^ Thank you, Chancellor Posvar. I will put it
in the record, and it is really relevant to a point that Ed
Light asked. I don't think everything is peaches and cream in
the nuclear fuel cycle anymore than I think it's peaches and
cream in the coal or oil or any of the others. I think we have
a lot of problem areas. One of the things that I sense, at
least speaking personally, is that I can now sharpen my focus on
certain areas. For example, specifically, the occupational
hazards in the nuclear fuel cycle. I think they are relatively
out of control, notwithstanding what Bob Minogue said today. I
think they have exemplified the fact that the sort of sense,
"well, everything is O.K., so we can go on doing things the way
we have been doing" has been worn out by history; that a number
of the reactors, as well as perhaps even some of the nuclear
facilities other than reactors, are not achieving what I
consider to be a safe level for the workers, while some of the
others are. Once you find out that some are, you ask the
question why aren't all of them? On that note, I think it is
appropriate to perhaps close the formal portion of the session.
I want to thank all of the audience and all of the speakers and
moderators personally for their good work, and I personally am
looking forward to a review of this transcript because we do
want to incorporate all of this material in the final report,
and it will influence the ORBES Report when it finally comes
out . Thank you all .
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