From: dave@ratmandu.esd.sgi.com (dave "who can do? ratmandu!" ratcliffe)
Newsgroups: misc.activism.progressive,alt.censorship,alt.activism
Subject: "Deadly Deceit," Afterword and Methodological Appendix
Summary: an essential democratic tradition -- open access to sensitive info
Keywords: measuring statistically significant excess death rate change
Date: 15 Dec 92 01:19:00 GMT
Followup-To: alt.activism.d
Organization: Silicon Graphics, Inc.
Originator: daemon@pencil.cs.missouri.edu


  Unless "we the people" conduct our own research and learn for ourselves the 
  actual state of public health in this technocratic, industrialized culture--
  what the true risks are and who benefits from taking such risks--we will 
  otherwise be lulled into permanent sleep by official myths serving interests
  other than those of the children and all life yet unborn.  One of the many 
  fission products created in the nuclear fuel cycle and in the detonation of 
  nuclear bombs is strontium-90 which has a half life of almost 30 years. 
  From the Methodological Appendix, below Dr. Gould writes:

        Strontium-90 is chemically similar to calcium and, therefore,
     concentrates in the bone of the developing infant, child, and
     adolescent.  Once in the bone, strontium-90 irradiates the marrow
     where the cells of the immune system originate at a low rate over a
     period of many years.  As first discovered by Dr. Stokke and his co-
     workers at the Oslo Cancer Hospital in 1968, extremely small doses of
     only ten to twenty millirads can produce visible damage to the blood
     forming cells of the bone marrow, probably via the production of
     free-radical oxygen.[209]  This can lead to the development of bone
     cancer, leukemia and other malignant neoplasms both directly by
     damaging the genes, and indirectly by lowering the ability of the
     immune system to detect and destroy cancer cells.[210]

  Back in 1943 Robert Oppenheimer, Enrico Fermi and Edward Teller all knew 
  that atomic radiation was a biological weapon and, if the bomb failed to 
  work, they could still poison the German food supply with "radioactive 
  fission products bred in a chain-reacting pile. . . .  The radioactive 
  isotope the men identified that `appears to offer the highest promise' was 
  strontium, probably strontium 90, which the human body takes up in place of
  calcium and deposits dangerously and irretrievably in bone." [Richard 
  Rhodes, "The Making of the Atomic Bomb," Simon and Schuster, 1986, p. 511]

  Excerpts follow from the Afterwood written by Dr. Gould in the first edition
  of "Deadly Deceit" appearing in the summer of 1990:


      . . .  I believe there is now a great need for the expert testimony 
     of statisticians in evaluating the significance of another ratio, 
     which lies at the heart of toxic tort litigation.  The key ratio to 
     study when a population is exposed to an environmental risk is the 
     "observed" number of deaths in a given area and period compared with 
     the "expected" number based on national norms.  We then seek to 
     ascertain whether the ratio of the two numbers is too great to be 
     attributed to chance.  It is this measure of a statistically 
     significant excess death rate change which lies at the heart of the 
     demonstrations in this book of excess deaths following releases of 
     low-level radiation.
      . . .  After more detailed examination of our databases, I began to
     believe that most of the excess mortality I had found may have been
     associated with a few major accidental nuclear releases, especially
     the accident at Three Mile Island (TMI).
        Concerned Harrisburg residents urged us to present our TMI findings
     to the Senate Public Health Committee, with a plea for public debate.
     At this time I first learned that there were 2,500 lawsuits in
     progress against the local utility, of which 300 had already been
     settled on condition that no details of the settlement would ever be
     revealed.  All this despite the claim that "no one died at TMI." . . .
        Why were birds so affected?  Why had AIDS-related deaths in the
     U.S. doubled in May of 1986?  Why were human immune systems so damaged
     by the Chernobyl fallout?  All these were questions we wanted to
     answer.  So we started to investigate the major nuclear releases in
     the past--from atmospheric nuclear bomb tests in the fifties and the
     sixties to civilian and military reactor accidents such as those at
     Savannah River, Millstone, and recurrent releases at TMI and Peach
     Bottom reactors.
        Beginning in 1945, the superpowers released massive quantities of
     fission products into the biosphere from above- and below- ground
     explosions of nuclear devices with yields of about 600,000 kilotons,
     according to estimates by the National Resources Defense Council.
     This was the equivalent of 40,000 Hiroshima-sized bombs.  Emissions
     from nuclear reactors, including major accidents such as Three Mile
     Island and Chernobyl, added to the total, much of which was composed
     of long-lived radioactive isotopes that will remain in the
     stratosphere for millennia. . . .
        In this book we have drawn heavily on the databases created by
     Public Data Access, Inc., described in the methodological appendix.  I
     regard these databases as our major achievement, for they represent a
     wonderful public resource, and a tribute to an important democratic
     tradition of open access to sensitive information.  These databases
     enable us now to examine, in great detail, clusters of excess deaths
     from any cause, in any county or groups of counties, anywhere in the
     U.S., at any time since 1968.  While we have focused attention in this
     book on the long neglected factor of low-level radiation, we fully
     recognize that all environmental abuses should be analyzed in the same
     spirit of open public inquiry.


  Even before the explosion of the first atomic bomb at Alamogordo--long 
  before the 600,000 kilotons of short and long -lived fission products were 
  released into the biosphere of our Earth--the creators of this technology 
  understood its lethal effects as a devastating biological weapon.  Yet this 
  knowledge was assiduously covered up and denied to the public at large.  It
  is still being denied today by the public relations arm of the nuclear
  industry through organizations like the U.S. Council for Energy Awareness
  which makes statements like "All the medical and scientific evidence gives
  nuclear power plants a clean bill of health. . . . the radiation from 
  natural and man-made scources presents little or no risk.  Scientific 
  studies over several decades show no health effect on people from exposures 
  below about 10,000 millirem."  Whose interests are being served by the 
  promulgation and perpetuation of such "knowledge"?  We must all ponder 
  deeply and consider this critical question of our times.  Preventing the
  exposition and understanding of such crucial information reduces the general
  public to an infantile status and paves the way to oblivion.
                                                                 -- ratitor


              "It is not enough for a handful of experts 
               to attempt the solution of a problem, 
               to solve it and then to apply it.  
               The restriction of knowledge to an elite group 
               destroys the spirit of society 
               and leads to its intellectual impoverishment."

                                             -- Albert Einstein
                                        


 the following is taken from the revised and updated softcover 1991 edition of 
 "Deadly Deceit, Low-Level Radiation, High-Level Coverup" by Dr. Jay Gould and 
    Benjamin A. Goldman with Kate Millpointer, published by Four Walls Eight 
     Windows, New York, and reprinted here with the permission of Dr. Gould.
  ___________________________________________________________________________



                          Afterword By Jay M. Gould


        As I now see it, a curious twist of fate was responsible for my
     embarking on this controversial voyage of discovery, in such sharp
     contrast to my professional interests as an economist and
     statistician.
        I was retained by Westinghouse Electric Corporation in 1979 as an
     expert antitrust statistician in a suit involving the price-fixing of
     uranium by a so-called "international uranium cartel."  My job was to
     ascertain whether forces of supply and demand could justify a six-fold
     rise in the price of uranium in the wake of the oil embargo of the
     early seventies.  It became clear to me that uranium shortages could
     not have been a factor in the rise in the price of uranium.  Because
     of frequent shutdowns, the performance of civilian nuclear reactors in
     the seventies fell far below expectations, and thus so did their
     demand for uranium.  I was also surprised to find that the monthly
     reports of reactor operations in the nuclear trade press were more
     realistic than the contradictory statistics available on the
     consumption of uranium from the Atomic Energy Commission.
        My interest in nuclear problems began with that assignment,
     especially as I had been appointed to the Science Advisory Board of
     the Environmental Protection Agency in 1977 as a result of my
     discovery of a way to estimate regional concentrations of toxic
     wastes.  This, in turn, led me to reflect on possible linkages of
     environmental problems with effects on public health.
        It was in this connection that I first read "Secret Fallout," by
     Dr. Ernest Sternglass, which I found to be most provocative and
     disturbing.  Here was an eminent professor of radiology at the
     University of Pittsburgh Medical School, and a former senior physicist
     at Westinghouse Research Laboratories, who had become convinced,
     against his will, that the government was lying about the mortality
     impacts of an early accident at the Shippingport reactor near
     Pittsburgh.  I felt there could be no question about his honesty as he
     described the process by which he was forced to assume the role of an
     anti-nuclear whistle blower.  But I never dreamed that someday I, too,
     would be impelled, out of what was only a modest degree of
     intellectual curiosity, to confirm his findings and play a similar
     role.
        My career as an expert statistical witness began, quite by chance,
     when I was retained by the Department of Justice in 1955 to prepare
     statistical exhibits for a small antitrust suit.  To the surprise of
     all concerned, the suit went all the way to the Supreme Court and
     became the famous Brown Shoe Case.  In addition to establishing
     precedents for all postwar antitrust litigations, it established the
     role of a statistician as an expert witness in evaluating the
     significance of estimates of a company's "market share."
        As a result of this case, my career as a statistical expert
     blossomed.  For the next two decades I participated in more than two
     dozen antitrust cases involving many major American companies,
     including IBM, Beatrice Foods, Greyhound, Armour, Occidental
     Petroleum, R. J. Reynolds, Emerson Electric, North American Phillips,
     and Westinghouse.  Many of these companies have disappeared in the
     "merger mania" of the Reagan years so that antitrust litigation is
     today merely a historical footnote.
        While there may no longer be a demand in antitrust litigation for
     the analysis of market share ratios, I believe there is now a great
     need for the expert testimony of statisticians in evaluating the
     significance of another ratio, which lies at the heart of toxic tort
     litigation.  The key ratio to study when a population is exposed to an
     environmental risk is the "observed" number of deaths in a given area
     and period compared with the "expected" number based on national
     norms.  We then seek to ascertain whether the ratio of the two numbers
     is too great to be attributed to chance.  It is this measure of a
     statistically significant excess death rate change which lies at the
     heart of the demonstrations in this book of excess deaths following
     releases of low-level radiation.
        My active antitrust practice led me to establish Economic
     Information Systems Inc., a company which successfully developed large
     computer databases for the analysis of the market shares of major
     companies in all industries.  After the sale of my company to Control
     Data Corporation in 1981, 1 felt free to use my special database
     expertise to explore environmental problems.  In the course of this I
     came across a remarkable book, "The Next Nuclear Gamble," by Marvin
     Resnikoff, published by the Council On Economic Priorities.
        From Dr. Resnikoff, I learned that highly radioactive used nuclear
     fuel assemblies were piling up in refrigerated pools at each reactor,
     awaiting the time, presumably early in the next century, when a "Great
     Nuclear Cemetery" would be built to receive them.  Resnikoff estimated
     that the task of transporting the hundreds of millions of tons of
     radioactive materials away from the reactors was likely to involve an
     average of sixteen nuclear accidents each year, each of which could
     spew as much radioactivity into the environment as had the Three Mile
     Island catastrophe of 1979.
        The Resnikoff book was so impressive that I paid a visit to the
     Council on Economic Priorities (CEP), and accepted an invitation from
     CEP to continue my environmental research at the Council when my
     responsibilities to Control Data ended in 1984.
        My first research project at CEP affirmed the National Cancer
     Institute's 1977 findings that cancer mortality at the county level
     was correlated with concentrations of petrochemical activity.
     Reasoning that environmental pollutants, initially at least, were
     highly localized, and remembering that the 1980 Census had for the
     first time included the five-digit ZIP code area as a geographic unit,
     I made some calls to the Census Bureau and other federal agencies.  To
     my surprise, I discovered that at very little cost (and with help from
     the Freedom of Information Act) I could purchase computer tapes from
     the Census Bureau, the EPA, the National Cancer Institute, and the
     National Center for Health Statistics, containing unpublished but
     politically sensitive information that had cost the government an
     estimated $40 billion to collect!
        This treasure trove of environmental and public health data had
     never been integrated and analyzed comprehensively.  I can only
     speculate that epidemiologists, mainly employed by state departments
     of health, rarely investigated the causes of wide variations in local
     mortality rates, perhaps because of the political consequences of
     finding a correlation with some local environmental abuse.  I believe
     most environmental epidemiological studies are self-limiting as a
     result.
        For someone with a database background like myself, these unused
     files were a researcher's paradise.  It proved to be relatively easy
     to find statistically significant differences in geographic mortality
     rates because the official U.S. mortality databases were based on all
     death certificates filed in a given year.  Even small differences
     might prove to be significant because of the large numbers involved.
     However, processing such large databases requires a professional staff
     of computer programmers and analysts.
        So, in 1985 I helped organize a small company called Public Data
     Access, Inc. (PDA) in the hope that it could eventually serve as the
     computer research arm of the environmental movement.  It was in this
     context that I first worked with Ben Goldman, who at the time was a
     project director at CEP.  He had discovered the same need to integrate
     diverse government data sources for a study of the hazardous waste
     industry, and had ventured into the world of micro-computers to
     accomplish the task.  In fact, the database he developed on a personal
     computer for "Hazardous Waste Management:  Reducing the Risk" (Island
     Press, 1986) ended up being PDA's first commercial product, available
     through a computerized information network called Chemical Information
     Services, Inc.  Ben helped me start PDA, and eventually became its
     president.
        This fledgling effort received generous support from environmental
     foundations and concerned individuals.  Even more important was the
     "sweat equity" contribution of a small group of enthusiastic young
     analysts, who in time became adept in interfacing large mainframe
     computers with the increasingly powerful and flexible personal
     computers, which among their other effects have made possible a
     decentralizing of data processing and great cost reductions.
        Since 1986, PDA has helped produce numerous environmental research
     studies.  "Quality of Life in American Neighborhoods:  Affluence,
     Toxic Waste and Cancer Mortality in Residential Zip Code Areas"
     (Westview Press, 1986), was a "database publication" with data for
     each of some 35,000 residential five-digit ZIP Code areas taken from
     EPA and Census Bureau databases.  Although the 1980 Census cost about
     one billion dollars, the Reagan Administration decided that it would
     be too expensive to publish results for small areas such as ZIP codes,
     so this book remains the only public source for such localized
     information.  PDA also produced in 1987 "Toxic Wastes and Race in the
     United States" for the Commission for Racial Justice, which showed
     that a significantly disproportionate number of toxic waste facilities
     were located in African-American neighborhoods.  "The Philadelphia
     Toxics Story," for the National Campaign Against Toxic Hazards, and
     "Toxic Waste and Cancer Mortality in Michigan," for the Public
     Interest Research Group in Michigan, also were produced by PDA in
     1987.  In 1988, PDA completed "Mortality and Toxics Along the
     Mississippi" for Greenpeace USA.
        In all of these publications, the focus was on geographic areas
     with significantly high mortality rates and the extent to which these
     were correlated with exposures to toxic chemicals.  Although
     frequently the correlations were good, in important cases they were
     poor.  This apparent paradox was only resolved for me by discussions
     with Dr. Ernest Sternglass, who pointed out that a large culprit in
     the mortality situation might not be toxic chemicals, but low-level
     nuclear radiation.  He argued that at least some part of the positive
     correlations we were obtaining between toxics and mortality were due
     to the overlap of nuclear pollution and toxic pollution in industrial
     areas, and also that where we were not getting a good correlation it
     might be because our studies did not contain a nuclear pollution
     variable.
        Dr. Sternglass also realized that our large mortality databases
     would overcome earlier criticisms of his research that had used small
     bodies of data to show that low-level radiation had a major impact on
     mortality.  In response to his challenge, I decided to examine recent
     mortality trends in areas most exposed to nuclear emissions since
     1975.  In this work I did find small but statistically significant
     increases in total mortality, cancer mortality and infant mortality,
     for the period 1975-82 (compared with 1965-69) for "nuclear" as
     compared to "non-nuclear" areas.  Nuclear areas were defined as the
     160 counties which either had at least one commercial nuclear power
     plant or were downwind of such a county.
        After months of recalculation and checking, CEP published the
     nuclear county results in its December 1986 newsletter, entitled
     "Nuclear Emissions Take Their Toll."  In the months that followed, I
     was disappointed with the complete lack of U.S. news coverage.
     However, it became a front-page story in Italy in January of 1987.
     Fabrizio Tonello, who reported on my findings for the Italian news
     weekly "Il Mondo," told me that his story played a significant role in
     generating the 80 percent referendum vote to halt work on Italy's two
     proposed nuclear reactors.  Later that year the Italian cabinet
     accepted the popular decision, and Italy today has banned the
     construction of new nuclear reactors.
        European environmentalists were not the only people who were aware
     of my findings, however.  I learned the CEP newsletter was making
     waves in Italy after I received a telephone request from the Italian
     Atomic Energy Commission for a copy.  Only a few hours later, I
     received a call from a Philadelphia engineering firm involved in the
     construction of nuclear reactors.  My caller seemed somewhat flustered
     at reaching me directly, as I had no secretary at the Council.  I
     asked whether he wanted a copy of the report.  "No," he replied, the
     question he wanted answered was, "who authorized this report?"
        In the U.S., various anti-nuclear groups throughout the country,
     disturbed by the CEP newsletter, clamored for detailed reports on each
     reactor.  After more detailed examination of our databases, I began to
     believe that most of the excess mortality I had found may have been
     associated with a few major accidental nuclear releases, especially
     the accident at Three Mile Island (TMI).
        Concerned Harrisburg residents urged us to present our TMI findings
     to the Senate Public Health Committee, with a plea for public debate.
     At this time I first learned that there were 2,500 lawsuits in
     progress against the local utility, of which 300 had already been
     settled on condition that no details of the settlement would ever be
     revealed.  All this despite the claim that "no one died at TMI."
        I presented our TMI findings to staff members of the Committee
     twice in the Spring of 1987.  Early in 1988, Senator Edward Kennedy,
     Chair of the Public Health Committee, requested that the National
     Institutes of Health conduct a study of mortality near nuclear
     reactors.  Senator Kennedy cited reports of high leukemia rates found
     by epidemiologists of the Harvard School of Public Health near the
     Pilgrim reactor in 1982-84, which were published in a letter to the
     British medical journal "The Lancet" on December 5,1987.  "The New
     York Times" on July 7,1988, reported that the National Cancer
     Institute (NCI) had agreed to study cancer deaths among people living
     near nuclear plants.  The "Times" quoted Dr. John Boice, chief of
     radiation epidemiology at NCI, who said "the study was prompted by a
     British survey completed last year . . . [that] found a higher
     incidence of leukemia among children and teenagers living near nuclear
     plants."
        We expect that this book may contradict the NCI findings, promised
     for 1990.  Our hypothesis suggests that many more counties need to be
     studied than the number proposed by NCI.  Dangerous fission products,
     particularly radioactive iodine and strontium, can be borne by winds
     and waterways for hundreds of miles and then come down in the rain,
     contaminating sources of fresh water and milk far from the reactor
     site itself.  These ingested fission products can then wreak serious
     damage on immune systems.  All of this was suggested by our Chernobyl
     findings.
        We began our Chernobyl study after an invitation to present our TMI
     findings at the European Conference on Chernobyl Radiation in
     Amsterdam at the end of May 1987.  While there, I not only gained much
     anecdotal knowledge about the impact of Chernobyl radiation in Europe,
     but also learned that no European nation publishes monthly mortality
     reports similar to the "Monthly Vital Statistics Report" of the U.S.
     National Center for Health Statistics.  I wondered whether mortality
     in the U.S. could have been affected by the small percentage of
     Chernobyl radiation that drifted over in the stratosphere and came
     down in the May 1986 rains.
        We began our research on this question when I returned to New York
     in June 1987, and were intrigued to find that abnormally high levels
     of radioactive iodine had been detected by Environmental Protection
     Agency milk-monitoring stations in almost every state beginning on
     about May 9th, 1986.  We also found that significant mortality
     increases had occurred in May for which the Chernobyl fallout seemed
     to be the only plausible explanation.
        We revealed our Chernobyl findings in two papers delivered at the
     First Global Radiation Victims Conference held in New York City in
     September 1987.  As we had come to expect, the U.S. press did not
     cover the story, but it was front-page news in the Japanese and
     Canadian press.  This was followed by major stories in leading English
     papers such as the "Independent" and the "Economist."  Finally, almost
     six months after we presented our findings, "The Wall Street Journal"
     broke the silence in the U.S. by reporting on our results on February
     8, 1988.
        A few weeks after the publication of "The Wall Street Journal"
     story, I received a fascinating letter from Dr. David DeSante, a
     researcher at the Point Reyes Bird Observatory in California,
     enclosing an article he had published in an ornithological journal
     early in 1987.  He had recorded a 62 percent drop in the number of
     newly hatched landbirds during the period from mid-May to mid-August,
     1986.  The only explanation he could find for the landbird
     reproductive failure was the radiation fallout from Chernobyl.
        Why were birds so affected?  Why had AIDS-related deaths in the
     U.S. doubled in May of 1986?  Why were human immune systems so damaged
     by the Chernobyl fallout?  All these were questions we wanted to
     answer.  So we started to investigate the major nuclear releases in
     the past--from atmospheric nuclear bomb tests in the fifties and the
     sixties to civilian and military reactor accidents such as those at
     Savannah River, Millstone, and recurrent releases at TMI and Peach
     Bottom reactors.
        Beginning in 1945, the superpowers released massive quantities of
     fission products into the biosphere from above- and below- ground
     explosions of nuclear devices with yields of about 600,000 kilotons,
     according to estimates by the National Resources Defense Council.
     This was the equivalent of 40,000 Hiroshima-sized bombs.  Emissions
     from nuclear reactors, including major accidents such as Three Mile
     Island and Chernobyl, added to the total, much of which was composed
     of long-lived radioactive isotopes that will remain in the
     stratosphere for millennia.
        In the Fall of 1988, the Senate Government Operations Committee,
     under the leadership of Senator John Glenn, held hearings about a
     series of accidents and safety problems at military nuclear facilities
     operated by the Department of Energy.  It turned out that crucial
     information about some of these accidents had been withheld from the
     public and the Congress for as long as 25 years.
        We immediately realized that our mortality database, with its
     ability to yield calculations of excess mortality at any place and at
     any particular time, could be brought to bear to illuminate the health
     consequences of these incidents.  In late 1988, we joined efforts with
     the Commission for Racial Justice of the United Church of Christ (CRJ)
     in creating the Radiation and Public Health Project (RPHP).  The
     project grew out of a long-standing relationship between PDA and CRJ.
     Since 1982, CRJ has investigated the presence of toxic substances in
     residential communities across the country, and has challenged the
     disproportionate impact on racial and ethnic neighborhoods.  This
     pursuit lead CRJ to engage PDA in 1986 to prepare the ground-breaking
     study "Toxic Wastes and Race in the United States," which was the
     first comprehensive empirical study of race and toxics in the U.S.,
     and which has been instrumental in influencing the Centers for Disease
     Control to undertake epidemiologic studies in this area.  The function
     of RPHP is to extend our studies of the health effects of nuclear
     releases, and to stimulate public debate on these controversial
     issues.
        In this book we have drawn heavily on the databases created by
     Public Data Access, Inc., described in the methodological appendix.  I
     regard these databases as our major achievement, for they represent a
     wonderful public resource, and a tribute to an important democratic
     tradition of open access to sensitive information.  These databases
     enable us now to examine, in great detail, clusters of excess deaths
     from any cause, in any county or groups of counties, anywhere in the
     U.S., at any time since 1968.  While we have focused attention in this
     book on the long neglected factor of low-level radiation, we fully
     recognize that all environmental abuses should be analyzed in the same
     spirit of open public inquiry.


  ____________________________________________________________________________



                            Methodological Appendix




     Statistical epidemiology, the study of the distribution and
     determinants of disease among human populations, goes back many years.
     Indeed, as John Allen Paulos notes in his book "Innumeracy,"
     probability theory began in the seventeenth century with gambling
     problems and "statistics began in the same century with the
     compilation of mortuary tables, and something of its origins stick to
     it as well."[202]
        Epidemiologists emphasize the fact that statistical correlation
     cannot prove causality.  Indeed, they have coined the phrase
     "ecological fallacy" to indicate cases where people have mistakenly
     drawn the conclusion that A caused B from parallel movements of
     factors A and B.  Every epidemiology textbook is full of examples of
     how one can make this erroneous conclusion.
        Common sense tells us the same thing.  Any baseball fan knows that
     if a team won 15 out of 18 games (factor B) in August, this probably
     has less to do with the fact that the temperature on the winning days
     was over 90 degrees (factor A), than with a star pitcher or hitter
     returning to the lineup (factor C).  We would reach this conclusion
     even if 90-degree days correlate better with winning, because the star
     player may have been in the lineup on losing days too.  Thus, if there
     is a plausible theoretical mechanism by which factor A could cause
     factor B, then their correlation is much more plausible than one with
     some factor C for which there is no obvious causal connection to B.
        Statistical correlation has always been used to help identify
     potential causal factors.  The search for statistical correlation is
     not meant to replace causality studies, but rather to provide clues
     where to look.  For example, if one finds an outbreak of sickness in a
     local community, the epidemiologist would look at many factors, trying
     to identify which correlates with the illness.  If it turns out that
     most of the people in the community who became sick had eaten dinner
     at Tom's Restaurant within the last week, it would be a reasonable
     first step to examine the restaurant or something in it for a causal
     factor.  Follow-up studies scrutinizing the restaurant's cleanliness,
     food packaging, etc., could ultimately prove that something at Tom's
     caused the outbreak.
        However, an examination of the people who became ill in that
     community may also show a statistical correlation between the illness
     and wearing the color red.  The sensible epidemiologist, faced with
     two factors to investigate, factor A (eating at Tom's restaurant), or
     factor C (wearing red), would undoubtedly put his/her resources into
     investigating factor A.  Common sense suggests that eating at a
     restaurant is a much more plausible candidate for causing the illness
     than is wearing red;  though, a curious epidemiologist might also
     check out the possibility that people were wearing clothes dyed red
     with a harmful chemical.
        In this book, the causal hypothesis linking factor A (low-level
     radiation) with factor B (excess deaths) is the "Petkau effect,"
     discussed in detail below.  The Petkau effect offers a plausible
     explanation that suggests low-level radiation may in fact cause excess
     mortality, and this hypothesis is supported by the statistically
     significant correlations.
        This brings us to the important notion of "excess death" used
     throughout the book.[203]  Epidemiologists use the concept of excess
     death to show that certain geographic areas and demographic groups
     suffer from unexpectedly high mortality rates.  Excess deaths may be
     roughly defined as the difference between the number of deaths
     observed in a given population and the expected number.  It is
     relatively easy to measure the observed number of deaths using
     government tabulations of death certificates.  The more difficult
     question is:  how do we know how many deaths to expect?
        The most common method epidemiologists use to estimate expected
     deaths is to compare the population of concern, for example, residents
     in counties surrounding the Savannah River nuclear plant, with a much
     larger population, such as all residents of the United States.  The
     basic idea is that the much larger U.S. population experiences a
     "normal" or average rate of mortality that can be used as a yardstick.
     Thus, the observed mortality among the smaller population, be it a
     locality, a particular age cohort, or other grouping, is tested to
     determine if it is significantly different from the national norm.
     The smaller group is often called a "sample" taken from the "universe"
     of the U.S. as whole.
        To make this comparison, epidemiologists first "standardize" the
     population of concern to rule out the influence of peculiarities in
     age, gender, and racial composition.  These three characteristics are
     most commonly standardized, partly because such data are
     systematically collected on death certificates.  For example, if a
     county has a much higher proportion of older people, then it is
     natural to expect a higher mortality rate.  Similarly, since women
     tend to live longer than men, if a county has an unusually high
     proportion of men, this too might account for a higher mortality
     rates.  In addition to classifying deaths according to age and sex,
     the government differentiates between "whites" and "nonwhites," with
     the latter including a wide mix of African Americans, Spanish
     Americans Asian Americans, Native Americans, and so on.  Although
     "non-whites" is thus a very imprecise category, it generally has been
     observed to have significantly higher rates of mortality than the
     category "whites."
        Epidemiologists deal with these variations by first dividing the
     population of concern into the different age, gender, and race groups,
     and then calculating the expected mortality rates of each age-sex-race
     group based on the corresponding national rate.  The calculation of
     theoretically expected mortality can then be compared with the
     mortality rate that is actually observed in each group to yield the
     difference.  Thus excess death is defined as the number of observed
     deaths that are significantly higher than expected for each race-sex-
     age group based on their corresponding national average;  although,
     sometimes, only adjustments for age are used.
        It is important to note one flaw in the conventional
     standardization technique used by government epidemiologists, and
     employed here.  By standardizing for the vague racial categories of
     white and nonwhite, this technique underestimates the excess deaths
     suffered by people of color.  Rather than considering the cause of
     higher mortality among nonwhites, this technique simply defines it as
     expected.
        There are clear biological and behavioral explanations for
     expecting higher mortality among certain sex and age groups;  the same
     cannot be said for the multi-racial grouping called nonwhite.  A
     person over eighty is more likely to die than a young adult.  Females
     are more likely to get breast cancer than males, and males are more
     likely to have a heart attack than females.  The majority of
     differences in mortality among racial and ethnic groups, on the other
     hand, are caused by environmental factors, including living
     conditions, diet, pollution, etc.  Only a very few diseases have been
     genetically linked to certain racial and ethnic groups, Tay-Sachs
     among Jews, for example, and sickle-cell anemia among African
     Americans.
        Defining higher mortality among nonwhites as expected is thus
     similar to saying that society expects nonwhites to be exposed to
     unhealthy environmental factors.  Future research should adjust for
     this distortion;  however, this was not done here.
        What elevates an excess death to the level of being "statistically
     significant?"  In rough terms, an event is statistically significant
     when it is "improbable" that it would be observed in the real world if
     merely the laws of chance were operating.  Epidemiologists seek
     fluctuations in mortality that exceed the limits of chance variation.
     They do this by determining the "improbability" of the difference
     between observed and expected mortality.  A difference so great that
     it is improbable that it results from chance means the observed
     mortality increase or excess is "significant."
        Throughout this book, an increase in mortality is characterized as
     significant if the probability that it could be due to chance is less
     than one out of 100 (a "P value" of less than 0.01).  This judgement
     can be made precisely, because variations in mortality conform to the
     bell-shaped "normal" curve.  Because the statistical demonstrations
     are intended to develop hypotheses rather than to prove their validity
     definitively, significant divergences have been identified
     occasionally with P values of less than 0.05 (less than five percent
     probability of a chance result).  Both confidence levels are commonly
     used by statisticians.  Any individual case that passes a significance
     test may still reflect a random variation.  But the cumulative
     significance of the five sets of correlations between low-level
     radiation and increased mortality, considered in Chapters Two, Four,
     Five, Eight and Nine, means that the likelihood that they are all
     chance occurrences is remote.
        Imagine repeatedly tossing one hundred coins and recording the
     percentage of heads that turns up in each repetition.  The following
     sequence could result:  51 percent heads, 48 percent heads, 50 percent
     heads, 47 percent heads, 52 percent heads, 50 percent heads, etc.  If
     we keep tossing the one hundred coins one thousand times and then plot
     the number of times each percentage appears, we would generate the
     bell-shaped normal curve, and 50 percent heads would be the most
     frequently recorded, or "mean," result.
        Statistical theory enables us to determine that the "standard
     deviation" of this distribution is plus or minus five percent heads.
     This means that about two-thirds of all results are expected to fall
     within one standard deviation on either side of the mean result (from
     45 or 55 percent heads).  About 95 percent of all possible results are
     expected to fall within the interval between 40 and 60 percent heads,
     or two standard deviations on either side of the mean.  Most
     statisticians would regard the remaining possible outcomes (i.e., less
     than 40 or more than 60 percent heads) as highly improbable and thus
     statistically significant.  The following table indicates the P value,
     or degree of statistical improbability associated with three
     increasingly improbable outcomes:

        PERCENT                STANDARD                 P
         HEADS                DEVIATIONS              VALUE
          65%                     3                   0.001
          70%                     4                   0.0001
          75%                     5                   0.000001

        When an increase in mortality has a P value of less than 0.001,
     that is, less than one out of one thousand, this is equivalent to the
     highly improbable act of tossing one hundred coins and getting 65
     heads and 35 tails.
        The formula used in this book for computing the significance of
     mortality phenomena is the standard one described by the National
     Center for Health Statistics in the annual volumes of the "Vital
     Statistics of the United States:"

                       (O - E) / SQRT ( (O^2 + E^2) / N)

     where O = observed mortality rate;  E = expected mortality rate;  SQRT
     = the square route of;  and N = observed number of deaths.  Expected
     rates are calculated as a function of the original observed rate
     multiplied by the change in the U.S. rate.  This formula is based on a
     Poisson distribution, which is appropriate for statistically rare
     events such as mortality.  The formula yields that number of standard
     deviations by which the observed rate differs from the expected rate.
     This value can be converted to a probability estimate with a table of
     the area under the normal curve, which can be found in the back of any
     statistics textbook.
        Since we calculated that it is highly unlikely that the excess
     deaths found in the case studies were due to chance, what could have
     caused them?  The hypothesis proposed here is that they were caused by
     a biochemical mechanism whereby ingested fission products promote the
     formation of "free radicals" that damage the immune system.  This
     mechanism was discovered in 1972 by Abram Petkau.[204]  The
     statistical tests in this book demonstrate that there were highly
     significant events among large human populations, each of which
     requires a reasonable explanation.  The Petkau effect is a plausible
     biochemical mechanism (though significance tests cannot prove it was a
     cause), and thus must be considered.
        Dr. Abram Petkau is a Canadian physician and biophysicist who until
     recently managed the Medical Biophysics Branch of the Whiteshell
     Nuclear Research Establishment, located in Pinawa, Manitoba.  While
     studying the action of radiation on cell membranes in 1971, Dr. Petkau
     conducted an experiment never done before.  He added a small amount of
     radioactive sodium-22 to water containing model lipid membranes
     extracted from fresh beef brain.  To his surprise, the membranes burst
     from exposure to just one "rad" (a measure of the amount of radiation
     absorbed) over a long period of time.  Conversely, Dr. Petkau had
     previously found that 3,500 rads were required to break the cell
     membrane when X-rays were applied for only a few minutes.  He
     concluded that the longer the exposure, the smaller the dose needed to
     damage cells.
        After several more experiments, he discovered the cause of this
     surprising effect from low-level radiation.  The irradiation process
     was liberating electrons, which were then captured by the dissolved
     oxygen in the water, forming a toxic negative ion known as a free-
     radical molecule.  The negatively charged free-radical molecule is
     attracted to the electrically polarized cell membrane.  This causes a
     chemical chain reaction that dissolves the lipid molecules, which are
     the principal structural components of all membranes in cells.  The
     wounded and leaking cell, if unable to repair the damage, soon dies.
     If the free radicals are formed near the genetic material of the cell
     nucleus, the damaged cell may survive, but in mutated form.
     Subsequent research by Dr. Petkau and other scientists ultimately
     demonstrated that this process occurs even at background radiation
     levels.[205]  At high levels of radiation, Petkau found less cellular
     damage from free-radical production per unit of energy absorbed than
     at low levels of radiation.
        Free radicals are so dangerous to living systems because they form
     in water, and water comprises eighty percent of a cell.  Free radicals
     not only destroy healthy cells, but also affect normal cell function
     in a way believed to speed the aging process.
        Nature has provided some protection from free radicals, probably
     because they are normally produced by the oxygen metabolism within the
     cell.  The protector, superoxide dismutase, quenches the chain
     reaction.[206]
        It is now believed that superoxide dismutase is found in all cells
     which use oxygen in their life processes.  For example, human tissues
     that contain naturally high levels of superoxide dismutase, such as
     the brain, liver, thyroid, and pituitary, are more resistant to the
     effects of radiation than tissues low in superoxide dismutase content,
     such as the spleen and bone marrow.  Apparently this enzyme evolved to
     protect biological systems from superoxide, or free-radical, damage
     caused by ultraviolet light, background radiation, and the result of
     normal energy production in the cell.  However, radiation which is
     produced by fission products and ingested through the food chain, or
     applied externally, can produce more free radicals than the body can
     deactivate (or "dismutate"), resulting in gross damage that may be
     irreparable.  Furthermore, Dr. Petkau and others have found that only
     ten to twenty millirads will destroy a cell membrane, in the absence
     of the protective superoxide dismutase.
        The free-radical reaction can be quenched in another way.  At
     higher intensities of radiation, the free-radicals become so
     concentrated that they tend to deactivate each other.  If this were
     not so, medical X-rays would cause far greater biological damage than
     they do.  A simple analogy, first used by Dr. Sternglass, can explain
     this phenomenon.  Think of the free radicals as individuals in a
     crowded room.  A fire starts and everyone tries to get out at the same
     time.  As a result, everyone bumps into each other and very few
     escape.  If only a few people are in the room when the fire occurs,
     however, everyone leaves easily through the door.  The rate of escape
     is very high, and therefore, efficient.
        Chronic exposure to low-level radiation produces only a few free
     radicals at a time.  These can reach and penetrate the membranes of
     blood cells with great efficiency, thus damaging the integrity of the
     entire immune system although very little radiation has been absorbed.
     In contrast, short, intense exposures to radiation, as with medical
     X-rays, form so many free radicals that they bump into each other and
     become harmless ordinary oxygen molecules.  Short exposures thus
     produce much less membrane damage than the same dose given slowly over
     a period of days, months, or years.
        More recently, Charles Waldren and co-researchers have found that
     when a single human chromosome is placed in a hybrid cell and
     irradiated, the ionizing radiation produces mutations much more
     efficiently at low than at high doses, as in the case of cell membrane
     damage.[207]  They found that very low levels of ionizing radiation
     produce mutations two hundred times more efficiently than the
     conventional method of using high dose rates, or brief bursts from X-
     ray machines.  They found that the dose-response curve exhibits a
     downward concavity (logarithmic or supra-linear relationship) in
     mammalian cells, so that the mutational efficiency of X-radiation is
     maximal at low doses, exactly as was found by Petkau for free-radical
     mediated biological damage.  Thus, their findings contradict the
     conventional scientific dogma that the dose-response curve is linear,
     and that a straight line can be used to estimate low-dose effects from
     studies of high doses.
        A protracted exposure to ingested beta emitters can be one thousand
     times more harmful to cell membranes than a brief external exposure to
     X-rays, because DNA repairs itself relatively efficiently after an X-
     ray hit compared to the damage caused by oxygen free-radicals at very
     low doses.[208]  This type of exposure may thus account for the jump
     observed in mortality immediately after nuclear plant accidents, or
     after fallout from atmospheric bomb tests.
        Strontium-90 is chemically similar to calcium and, therefore,
     concentrates in the bone of the developing infant, child, and
     adolescent.  Once in the bone, strontium-90 irradiates the marrow
     where the cells of the immune system originate at a low rate over a
     period of many years.  As first discovered by Dr. Stokke and his co-
     workers at the Oslo Cancer Hospital in 1968, extremely small doses of
     only ten to twenty millirads can produce visible damage to the blood
     forming cells of the bone marrow, probably via the production of
     free-radical oxygen.[209]  This can lead to the development of bone
     cancer, leukemia and other malignant neoplasms both directly by
     damaging the genes, and indirectly by lowering the ability of the
     immune system to detect and destroy cancer cells.[210]
        A peak accumulation of strontium-90 in the body after two or three
     years could explain the delayed peaks in total mortality as observed
     after the Savannah River Plant accidents described in Chapter Four.
     This accumulation results from the combination of growing uptake and
     slow excretion, and the consequent mortality primarily involves deaths
     from heart diseases, as well as from cancers and other causes.  Free-
     radical oxygen, produced most efficiently by internal beta emitters
     such as strontium-90, may be a factor in coronary heart disease as
     well as cancer.  The theory is that the free radicals oxidize the
     low-density cholesterol and cause it to become more readily deposited
     in arteries, thus blocking the flow of blood and inducing heart
     attacks.[211]
        Recent medical research from across the country has provided new
     evidence linking cancer to impaired immune systems.[212]  The studies
     have focused on transplant patients, who as a group suffer from
     extremely high rates of a variety of cancers.  Their cancers
     diminished rapidly when the doses of immunosuppressive drugs were
     reduced.  (Such drugs are given to stop normal immune systems from
     rejecting the transplanted organs.)  The researchers suspect two types
     of cells in the immune system of playing major roles in this
     phenomenon:  natural killer cells and cytotoxic T-cells.  They found
     evidence that during immunosuppression, these cells were more depleted
     among the transplant patients who developed skin cancers than among
     those who did not.[213]  Earlier research published in 1977
     demonstrated that bone-seeking isotopes such as strontium-89 and
     strontium-90 deactivated precisely such natural killer cells in
     laboratory mice.[214]  These new findings linking cancer to
     immunodeficiencies, combined with the earlier findings of Petkau and
     others of higher-than-expected cell damage from low radiation doses,
     point to a possible explanation for the rapid increases in mortality
     rates after low-level radiation releases.
        The correlations of health effects with low-level radiation that
     are discussed throughout this book may thus be caused indirectly by
     chronic low-level exposures to ingested radiation through hormonal and
     immune system damage from free radicals.  Low levels of strontium-90
     and iodine-131 ingested in food, milk, and water, and breathed in air,
     may damage the ability of the body to detect and destroy infected or
     malignant cells.  Such damage may occur even if radiation is present
     at concentrations far below existing standards.  These standards were
     set on the basis of a quite different biological mechanism:  cancer
     cell production caused by the direct impact on genes of high doses of
     external radiation.



 [203]  For a more technical description of the methodology for calculating
        excess deaths, see Public Data Access, Inc., "Mortality and Toxics
        Along the Mississippi River," Washington, DC:  Greenpeace USA, 1988.
        The method used here is fully documented in the Greenpeace report
        with the one addition that race has been figured into the adjustment
        process.

 [204]  A. Petkau, "Effect of 22 Na+ on a phospholipid membrane," "Health
        Physics," Vol. 22, 1972, p. 239.  See also A. Petkau, "A Radiation
        carcinogenesis from a membrane perspective," "Acta Physiologica
        Scandinavia," Suppl. Vol. 492, 1980, pp. 81-90.

 [205]  A. Petkau and W. S. Chelack, "Radioprotective effect of superoxide
        dismutase on model phospholipid membranes," "Biochemica et
        Biophysica Acta," Vol. 433, 1976, pp. 445-456.  See also A. Petkau,
        W. Kelly, W. S.  Chelack, S. D. Pleskach, C. Barefoot, and B. E.
        Meeker, "Radioprotection of bone marrow stem cells by superoxide
        dismutase," "Biochemical and Biophysical Research Communications,"
        Vol. 67, No. 3, 1975, pp. 1167-1174;  A. Petkau, W. S. Chelack and
        S. D. Pleskach, "Protection of post-irradiated mice by superoxide
        dismutase," "International Journal of Radiation Biology," Vol. 29,
        No. 2, 1976, pp. 297-299;  A. Petkau, "Radiation protection by
        superoxide dismutase," "Photochemistry and Photobiology," Vol. 28,
        1978, pp. 765-774;  A. Petkau, "Protection and repair of irradiated
        membranes," in "Free Radicals, Aging, and Degenerative Diseases,"
        Alan R. Liss, Inc., 1986, pp. 481-508;  and A. Petkau, "Role of
        superoxide dismutase in modification of radiation in jury," "British
        Journal of Cancer," Vol. 55, Suppl. VIII, 1987, pp. 87-95.

 [206]  Irwin Fridovich, "The biology of oxygen radicals:  the superoxide
        radical is an agent of oxygen toxicity;  superoxide dismutases
        provide an important defense," "Science," Vol. 201, 1978,
        pp. 875-880.

 [207]  Charles Waldren, Laura Correll, Marguerite A. Sognier and Theodore
        T. Puck, "Measurement of low levels of X-ray mutagenesis in relation
        to human disease," "The Proceedings of the National Academy of
        Sciences," Vol. 83, 1986, pp. 4839-4843.

 [208]  T. Stokke, P. Offedal, and A. Pappas, "Effects of small doses of
        strontium-90 on the ratbone marrow," "Acta Radiologica," Vol. 7,
        1968, pp. 321-329.

 [209]  Ibid.

 [210]  Peter A. Cerutti, "Prooxidant states and tumor production,"
        "Science," Vol. 227, 1985, pp. 375-381.

 [211]  See New York Academy of Science, "Antioxidants may prevent or slow
        down heart disease," "Science Focus," Vol. 3, No. 4, Spring 1989,
        p. 8, and Jane E. Brody, "Natural chemicals now called major cause
        of disease," "The New York Times," April 26, 1988 and Jean L. Marx,
        "Oxygen free radicals linked to many diseases," "Science," Vol. 235,
        1987, pp. 529-531.

 [212]  Elizabeth Rosenthal, "Transplant patients illuminate link between
        cancer and immunity," "The New York Times," December 5, 1989.

 [213]  Ibid.

 [214]  O. Heller and H. Wigzell, "Supression of natural killer cell
        activity with radioactive strontium:  effector cells are marrow
        dependent," "Journal of Immunology," Vol.110, 1977, pp. 1503-1506.
        Also, E. Sternglass found in 1973 that significant changes in
        cervical cancer incidence and mortality in Baltimore women were
        directly correlated with changes in concentrations of the short-
        lived strontium-89 found in milk.  See "Epidemiological studies of
        fallout and patterns of cancer" in "Radionuclides and
        Carcinogenesis, U.S. AEC Symposium Series 29, Conference-720505,
        edited by C. L. Sanders, et al., Washington, DC:  U.S. Atomic
        Energy Commission, June 1973, pp. 254-277.



--
     "We are able to inform you that ancient grandfathers, the great stands
   of cedar and redwoods, are in danger of extinction by chainsaws.  The 
   maple, chief of trees, is dying from the top down, as was prophesied by
   Ganiodaiio, Handsome Lake, in 1799.  Great rivers and streams are filled
   with chemicals and filth, and these great veins of life are being used 
   as sewers.
     "We were told the female is sacred and carries the gift of life as our
   Mother Earth, the family is the center of our life and that we must build
   our communities with life and respect for one another.
     "We were told the Creator loves children the most, and we can tell the
   state of affairs of the nation by how the children are being treated.
     "When we return to Onondaga, we will begin our Great Midwinter
   ceremonies.  We will tie the past year in a bundle and give thanks once
   again for another year on this earth.
     "This was given to us, and we have despoiled and polluted it.  If we are
   to survive, dear friends and colleagues, we must clean it up now or suffer
   its consequences.
     . . .  But Lyons also remembered turning to Leon Shenandoah, chief of 
   the Grand Council of the Six Nations Confederacy.  "My chief, he doesn't 
   say much, but I asked and he said, `They're not taking it serious enough.  
   I don't think they realize what's going to happen to them.  What's coming.'
   He would have liked to see less posturing.  We have our prophecies.  We 
   know what is coming down the road.'"
                        -- Onondaga Chief Oren Lyons, on the Global Forum he 
                           helped organize on Environment and Development for 
                           Survival held in Moscow, January 15 to 19, 1990.
Newsgroups: misc.activism.progressive