1

Unpublished, additional supporting materialfor the submitted paper,

Lessons to be learned from a contentious challenge to mainstream radiobiological science(the linear no-threshold theory of genetic mutations).

By Jan Beyea, Ph.D.

Comprising,

Additional responses, section by section, to defenses by Edward J. Calabrese made in a 2016paper1 (herein, “Calabrese II”),

which responded to my 2016 critique2 (herein, “Beyea I”)

of an earlier 2015 paper3 (“herein, Calabrese I”),

Revision 2

(Changes since Revision 1 appear in red)

September 30. 2016

Consulting in the Public InterestLambertville, NJ

jbeyea@cipi.com

This project has been a pro bono effort.

1 Calabrese II: LNTgate: How scientific misconduct by the U.S. NAS led to governmentsadopting LNT for cancer risk assessment, Environmental Research, Vol. 148, 535-546

2 Beyea I: Response to, "On the origins of the linear no-threshold (LNT) dogma by means ofuntruths, artful dodges and blind faith," Environmental Research, Vol. 148, 527-534

3 Calabrese 1: "On the origins of the linear no-threshold (LNT) dogma by means of untruths,artful dodges and blind faith," Environmental Research, Vol. 142, Pages 432-442.

2

Preface: I have submitted a paper (Beyea, 2016a) and supporting online material for publicationentitled, “Lessons to be learned from a contentious challenge to mainstream radiobiological science.”The bulk of the paper addresses the state of knowledge in the 1930-1956 time period about the geneticimpacts of ionizing radiation. It supplements an earlier paper, Beyea-I (Beyea, 2016b), critiquingEdward J. Calabrese’s conspiracy, corruption and misconduct theories about prominent geneticists,the community of geneticists around the world, the US National Academy of Sciences, theRockefeller Foundation and others in the pre-1960 period. It was prepared after Professor Calabreseoffered his defense (Calabrese, 2016), which I call Calabrese-II. However, there was not space, ineither the new paper (Beyea-II) or its online supporting material (Beyea-II, SI), to respond to all of the13,000 words that Calabrese made in defense of my original critique. Thus, I have prepared thisproject report, which will be available on the web, as an additional supplement(www.cipi.com/PDF/MiscSupplementaryResponsesByBeyeaToCalabrese2016.pdf).

Calabrese had an introduction and 22 numbered sections in Calabrese II. I use the same numberingsystem in analyzing his writing. I note that, because Professor Calabrese repeats himself many times,I must do the same with my response. Also, because he usually repeats what he said earlier inCalabrese-I (Calabrese, 2015) without addressing what I said in response, I again have to repeatmaterial, although I have tried to minimize such repetition.

The audience I have in mind for this report includes potential future investigators of Calabrese-likecharges about the linear no-threshold theory of ionizing radiation.

3

My abstract for Beyea-II serves as an introduction to this project report:

“There are both statistically valid and invalid reasons why scientists with differing defaulthypotheses can disagree in high-profile situations. Examples can be found in recentcorrespondence in this journal, which may offer lessons for resolving challenges tomainstream science, particularly when a scientific minority attempts to elevate the status ofoutlier studies and/or discredit default theories by alleging self-interest of proponents.Edward J. Calabrese and I have been debating the historical origins of the linear no-thresholdtheory (LNT) of carcinogenesis and its use in the regulation of ionizing radiation. ProfessorCalabrese, a supporter of hormesis, has attempted to discredit the LNT theory by accusing acommittee of scientists of misconduct in their preparation of a 1956 report on the geneticeffects of atomic radiation. Specifically he claims the report mischaracterized the researchrecord that supported the genetic LNT and suppressed calculations of some committeemembers. After reviewing the available scientific literature, I found that thecontemporaneous evidence overwhelmingly favored a (genetics) LNT and that no calculationswere suppressed. Calabrese’s claims do not hold up primarily because of his lack of attentionto statistical analysis. Ironically, outlier studies were more likely to favor the antithesis of hisposition, supra-linearity. Finally, the claim of investigator bias, which underlies Calabrese’sattacks, is based on misreading of text. Attention to partisan charges, early on, may help seeda counter narrative explaining the community’s adoption of a default hypothesis and may helpfocus attention on valid evidence and any real weaknesses in the dominant paradigm.”Beyea-II.

The essence of Professor Calabrese arguments are that the current acceptance of the LNT for cancercan be attributed to scientific misconduct on the part of a 1956 genetics panel (not the cancer panel) ofthe National Academy of Sciences, who were supposedly driven by hopes of financial gain and byunspecified ideological interests. Fraudulent data and cover-ups are part of the story. Thismisconduct according to Calabrese extends to major scientific and funding institution and theirleaderships. A key element of Calabrese’s logic is that subsequent panels went in lock step with this1956 panel, regardless of subsequent scientific data, such that if the panel never existed, then the LNTfor cancer would never have been accepted by US scientific and regulatory bodies. This is what, Iguess, can be called an infection theory of scientific advising. Once in contact with geneticists whoCalabrese does not like, scientists become infected, as do those they subsequently come into contactwith as mentors or fellow panel members, thereafter unable to think for themselves, following the“geneticist creed” and infecting others, ad infinitum. An alternate view, to which I am partial, is thatwhen exposed to convincing ideas and data that are continually supported, scientists do tend tocontinue to support the ideas of the discoverers, albeit with significant modifications as the scienceadvances. And, if the science does not support the standard paradigm over a 50 year period, there arelegions around to point that out and argue for modifications, in hopes of advancement and fame, ifnothing else.

Professor Calabrese is a fierce advocate of theories other than the cancer LNT. In effect, he accuseshis competitors of fraud and misconduct, which makes him far from an objective source. Thispartisanship should not be forgotten in judging his claims, which are almost entirely based onmisreading of report texts and interpretations of correspondence that he has sampled from a largebody of private papers, previously reviewed by historians, who do not draw the same conclusions thathe does.

4

As I shall show, little attention is paid to what the panel’s report actually said, rather than the disputesthat were being discussed in transcripts prior to final publication. For instance, recommendations areattributed to them that they never made in the report, e.g., that the LNT should be used instead of athreshold model for genetic assessments, let alone cancer assessments. They are accused of leavingout material that the report actually contains, such as the different views held by panelists on the LNTslope, both qualitatively and quantitatively. What Calabrese said the panel should do, the panellargely did. Similarly, with scientific papers, Professor Calabrese reads into them things that I cannotfind there and misses sections that contradict his thesis.

Having immersed myself in both his writings and the relevant scientific literature, I have gotten the(admittedly subjective) impression that he reads too quickly, sometimes missing key information, andseems to only search for statements that support his contrarian views. He also does not seem to checkhis inferences for statistical fluctuations. However, I am only making an inference here; there couldbe lots of alternate explanations. Since Professor Calabrese does not hesitate to make inferencesabout his scientific competitors, I am sure he cannot object to my doing so in his case.

In reading Calabrese’s work, the reader should be alert to the rhetorical techniques used, namely longchains of inference, attributing motives, use of scornful language, defining standards of conduct,repetition of charges, assumptions built into sentences rather than derived from evidence, assumingthe worst interpretation, and only mentioning things that sound negative. To me, it is the language ofelectoral politics and will likely end up finding a home there, just as has the contrarian climatescience.

Note that in the following sections, I have Calabrese’s words in italics.

5

Calabrese-II, section 1. Title and Abstract.

With his new title listed below, Professor Calabrese has doubled down, with ever stronger pejorativelanguage:

“LNTgate: How scientific misconduct by the U.S. NAS led to governments adopting LNT forcancer risk assessment”

In the abstract, he continues:

“…….reaffirming the conclusion that the Genetics Panel should be evaluated forscientific misconduct for deliberate misrepresentation of the research record inorder to enhance an ideological agenda.” (Calabrese, 2016)

This ideological agenda is never spelled out, which is an amazing omission. Could hesimply be referring to the scientific views of geneticists of the day as an ideology? Or, didthe agenda have something to do with the worries of some of the panelist that fallout andother radiation could be a threat to the population if doses got too large and lasted too long?Or, did he have something else in mind? We are not told.

Calabrese says that he has provided newly uncovered evidence, but never tells us what that is. Hedoes refer to some earlier papers, which may be his meaning.

As I have shown in detail in my latest paper, Beyea-II, the research record overwhelminglysupported the NAS panel. Professor Calabrese’s scientific claims do not hold up. Heexpresses consternation that the panel did not debate and document the basis for itsunanimous adoption at the very start of the first meeting of the genetic LNT. Well, by 1956,this was old science. He should have looked back at the material in the 1940s and early1950s, when the theory was being debated and the data checked.

The panel report turned out to largely reflect the contemporaneous scientific record andconsensus in the US and internationally. There was one dispute that did not affectacceptance of LNT as a theory, with its zero threshold and linear dose-response function.Professor Calabrese will not address this distinction, implying in many sections thatdisagreements existed about the entire LNT, not just its slope.

In the abstract, Calabrese goes on to state:

“This critique documents numerous factual errors along with extensive anddeliberate filtering of information in the Beyea letter (2016) that leads toconsistently incorrect conclusions and an invalid general perspective.” (Calabrese,2016)

Note the use of the unnecessary word, “deliberate,” in front of filtering, which suggests afalsification of the truth, without explicit statement. As for the factual error claims, I foundno merit to them. I have dealt with some in Beyea-II, Supporting Information, and deal withmore in this report, with still more to follow, in what is obviously going to be a continuingdebate. As for incorrect overall conclusions, I, of course disagree. Readers will have todecide.

6

Calabrese-II, Section 1 (introduction).

He begins with a succinct discussion of the dispute between us.

“Beyea (2016) offers a series of alternative interpretations to my conclusions (Calabrese,2015a) on the acceptance of the LNT by the regulatory and public health communities andthe role of the radiation genetics community and the U.S. NAS BEAR I Committee,Genetics Panel in this process. The principal claims of Beyea are that the BEAR ICommittee, Genetics Panel was not biased, despite being portrayed this way in my series ofpapers (Calabrese, 2013b, 2014a, 2015a, 2015b, 2015c), that the Genetics Panel was notparticularly influential to subsequent NAS committees dealing with the issue of the effectsof low doses to mutagens and carcinogens, especially the BEIR committees, and that LNTwould have emerged as the default assumption in cancer risk assessment even if BEAR IGenetics Panel had not been convened.” (Calabrese, 2016)

He then goes on to categorize my work in language that I found to strikingly match his own:

“ In making these claims he creates his own narrative, a mixture of filtered information withthe end result resembling a type of historical novel with a blend of facts, fiction, numerousfactual errors, revisionist history and wishful thinking.” (Calabrese, 2016)

Readers will have to decide whose narrative most closely matches the evidence.

7

Calabrese-II, Section 2 (Biased or not).

Attributing statements to the panel that they never made:

“The Genetics Panel recommended that the dose response model for genetic riskassessment be switched from a threshold to a linear model in 1956 without discussion ordebate based on meeting transcripts.” (Calabrese, 2016)

In fact, the genetics panel report said nothing about switching models, let alone making any suchrecommendation. There were no recommendations made by the panel to use a linear model. Thereport made recommendations only about setting a threshold standard for dose to the entirepopulation. Professor Calabrese offers no information about when genetic risks had ever beenassessed with a threshold model. Genetic calculations played no role in the recommended standards,which were set with respect to natural background.4

What is true is that prior to the report, genetic risks were not considered in policy settings; the 1956panel recommended that omission be corrected. The report was largely successful in making thathappen. In addition, the panel report did make a series of what would now be called findings in amodern NAS report. These findings included a zero genetic threshold and linear response. AsProfessor Calabrese correctly notes,

“Despite a Panel of 17 outstanding researchers and leaders, including 13 nationallyrecognized experts in radiation genetics, no dissent was offered.“ (Calabrese, 2016)

I add the fact that a similarly expert panel in the UK came to similar findings. Most readers I thinkwould presume that this was a reflection of the historical scientific record that preceded them, as Iconfirmed in Beyea II. However, Professor Calabrese does not see it that way. To him, the panelmust have infected the UK panel through the conversations that leaders of the panels had(unsuccessfully) in trying to get full agreement. At least so far, Calabrese has not accused the UKpanel of bias, fraud and/or self-interest.

I often find some element of truth in Calabrese, but it takes a lot of reading into the material.Although the panel did not recommend any switching or use of the genetic LNT, the fact that it had aunanimous finding about the genetic LNT would give others solid ground for using it in any geneticrisk assessment, although they would have to fend for themselves in justifying a slope to actually docalculations. As for cancer LNT, the word cancer or somatic injury is not mentioned in the report, sothere is no basis in the report for anyone to rely on it as justification for cancer dose-response modelshaving a zero threshold or linear response. In fact, a different 1956 panel, the pathology panel, wasassigned to deal with cancer, and they happened to be prone to a threshold model it appears, but said

4 James Crow, who I quoted in my first response to Calabrese, thought it was ironic that the decision aboutstandards was based on other principles, having nothing to do with the debate, but it is typical in my experience,when there is no consensus on a contested issue. “…in the end the numerical recommendation was based almostentirely on the amount of background radiation. Genetic calculations had little influence.” (Crow,1989). The adhoc NCRP report indicated that, “The previous recommendation of the National Academy of SciencesCommittee and the National Committee on Radiation Protection for a maximum average-per-capita-dose to thegonads of 10 roentgens of manmade radiation per 30 years is roughly three times the background level...”NCRPM, 1960. Somatic radiation dose for the general population. Science. 131, 482-486..

8

the cancer threshold could be zero.5 Calabrese does not mention the existence of a panel assigned todeal with cancer.

By 1972, genetics no longer dominated concern about radiation and cancer induction became the bigconcern, as I stated in Beyea I.

Calabrese express his surprise at not finding what he expected about low dose response:

“This lack of discussion/debate was unexpected as I was hoping to learn how leaders of thepast wrestled with the key issue of the nature of the dose response in the low dose zone.“(Calabrese, 2016)

To this end, he would have done better to read the pre-1956 literature on hit (target) theory, as well asthe reports of linearity in single chromosome breaks that could be counted in the microscope (SeeBeyea II). That is when the “wrestling” was taken place. By 1956, the evidence was overwhelmingto geneticists, with very few exceptions (see Beyea-II). By this time, they were fighting ferociouslyabout something else, namely the cumulative impact across generations, which defined the slope ofthe linear model. Were the negative mutations dramatically reduced by a weeding out process or not?

Target theory had its weaknesses, which Calabrese is free to criticize. He is free to criticizegeneticists for accepting it, but he should at least be aware of its existence and use.

Calabrese goes on to attribute goals and motives to the panel as a whole or as individuals, one of thecommon inferences he makes. In doing so, he steps outside of both science and his expertise andenters the world of history and political science, without either academic training in those fields orpublications in historical journals. He also makes assertions about what those goals and motivesshould have been, and then criticizes the panel for not meeting his goals.

The genetics panel was one of six panels that made up the NAS study on the biological effects ofatomic radiation. It was the pathology panel that had been given the responsibility for radiationinduced somatic diseases, e.g cancer.6 The expectations of the NAS for the six 1956 panels wasdescribed in the foreword to the summary reports by Detlev W. Bronk, President National Academyof Sciences.7 He stated that the six summarized reports were the first findings and recommendations

5 “In consideration of animal experiments, uncertainty exists as to whether or not there is a true dose thresholdfor the production of malignant tumors by irradiation. The answering of this question wouldrequire an extremely expensive, massive experimental program employing very large numbers of animals andmuch time. ….. If the fundamental cause, or one of the indispensable factors, in radiation carcinogenesis is theinduction of somatic mutations, it would appear possible that radiation carcinogenesis, or perhaps the inductionof precancerous states by irradiation, has no dose threshold. … In any event the incidence of cancer in exposedpopulations is not sufficiently great to be regarded as an important contribution to the degree of premature deathoccurring in a group such as that of the American physicians discussed above.” This quotation is from the fullpathology report NAS, Report of the Committee on Pathologic Effects of Atomic Radiation(www.cipi.com/PDF/BEAR1956_pathology_panel_report.pdf). National Research Council of the NationalAcademy of Sciences, Washington, 1956b..6 The pathology panel in is full report indicated its belief in a threshold model, while recognizing that thethreshold could be zero ibid..7 “The reports published in this volume summarize the first technical findings and recommendations of sixcommittees established to carry on a continuing study of the biological effects of atomic radiations from thepoints of view of genetics, pathology, meteorology, oceanography and fisheries, agriculture and food supplies,and the disposal and dispersal of radioactive wastes. The members of these committees, numbering more than

9

of committees “established to carry on a continuing study of the biological effects of atomicradiation.” The goal was analysis – analysis to make available the “facts about the biological effectsof atomic radiations based on all existing knowledge available to us.” This left considerable freedomfor the panels to choose particular aims for their reports.

In particular, the genetics panel summary report focused on possible hazards:

“In fact, the National Academy study, as its title indicates, is concerned with the possiblebiological hazards due to atomic and other radiations. And the present report, made by theGenetics Committee, is concerned with the genetic aspects of the possible biologicalhazards.” (NAS, 1956a)

The panel focused on reaching the general public, not the scientific public,

“The problems of the Atomic Age affect every man, woman, and child - in fact, every livingthing - in our country, and of course in the whole world as well. Although many of theseproblems are technical in character, it is nevertheless of importance to our democracy thatthese matters be as widely understood as possible. Therefore every e££ort has been made thatthis report be generally understandable.” (NAS, 1956a)

The panel report went on to offer further explanation if desired by government agencies:

“The later sections of the present report will be supplemented by more detail and factualjustification if this is later desired by any of the agencies (as for example, the NationalCommittee on Radiation Protection, the Atomic Energy Commission, governmental andindustrial groups concerned with radiation hazards, etc.), which have responsibility for theprocedures and standards to which our recommendations apply.” (NAS, 1956a)

As far as I have been able to learn to date, no such request was made.

Calabrese says,

“Their foremost goal was not to address how genetic risks from exposure to ionizingradiation should be assessed, but how to implement their dose response mantra intopolicy and risk assessment practices.” (Calabrese, 2016)

100, are among the most distinguished scientists in their fields in the United States. They have given generouslyof their time and talents in making this analysis during the past several months because they are convinced thattheir fellow citizens should have the facts about the biological effects of atomic radiations based on all existingknowledge available to us. The members of the committees served as individuals, contributing their knowledgeand their judgment as scientists and as citizens, not as representatives of the institutions, companies, orGovernment agencies with which they are associated.” NAS, 1956a. The biological effects of atomic radiation,summary reports (www.cipi.com/PDF/BEAR1956Summaries.pdf). National Resarch Council, NationalAcademy of Sciences, Washington.

10

(The person with the goal of getting his theories (hormesis) into policy and risk assessmenthas been Calabrese (Calabrese et al., 2016).)

Calabrese provides no basis for saying that the foremost goal of the panel was to implement adose response model into policy and risk assessment. It is an assertion of Calabrese’s beliefs.

In fact, the genetics report was mainly concerned with an assessment (aimed at the public) ofgenetic risks from ionizing radiation. And, what Calabrese pejoratively calls the dose-response mantra (particularly, the LNT) was ironically not used in making anyrecommendations in the report, including the recommendation for a threshold standard forthe average dose to the general population, as will be discussed later. To add morebackground, according to historian, Hamblin, it was the USAEC, which was intimatelyinvolved in all the deliberations, who wanted a dose standard with the support of researcherslike Muller. The committee eventually went along.

Calabrese understanding of what the report says is not correct. The linear and no thresholdpart of the LNT was a finding of the report, one of the facts on which there was substantialagreement. (No panel finding was made about the strength of the LNT, i.e., the slope of thelinear term, because consensus could not be reached on this topic.) The panel made norecommendation about risk assessment practice or use of the LNT by anyone. The reportclearly wanted genetic considerations to be considered in policy, but its recommendation wassimply to keep doses low to the population, specifically not too much greater than naturalbackground radiation and towards the low region of their estimated range for the mutationdoubling dose.

Conspiracies in the panel formation?

Continuing in the same vein, Calabrese makes conspiratorial claims with no foundation.Assertion after assertion.

“This specific group of radiation geneticists was convened to create a dose responserevolution and this process started with decisions concerning who would comprisethe Panel.” (Calabrese, 2016)

So, a conspiracy was created to bring together a group of panelists, who Calabrese himselfcalls, “… outstanding researchers and leaders, including 13 nationally recognized experts inradiation genetics.” It is standard NAS practice to bring in the major researchers. Where isthe evidence that the goal was to create a dose-response revolution? Let’s review the originof the NAS study:

The conspirators in Calabrese’s mind appear to be the NAS, the Rockefeller Foundation andpersons associated with these organizations, such as the former head of the AmericanAssociation for the Advancement of Science (AAAS), Warren Weaver, who chaired the NASpanel. According to Jolly, Weaver had wanted to start such a committee within the AAAS,but agreed to combine with the NAS panel.

11

“In December 1954, at roughly the same time that trustees of the Rockefeller Foundationdecided to approach Eisenhower about the possibility of setting up an NAS committee onradiation effects, AAAS members suggested forming a committee to investigate the biologicaleffects of radiation. As current president of AAAS and an official of the RockefellerFoundation, Warren Weaver was aware of both these efforts and sought to negotiate acompromise between the two efforts in order to avoid unnecessary duplication. Weaveragreed not to pursue the formation of an AAAS study until the NAS had decided on its courseof action; however, he also wrote to Dean Rusk, who had first written to Eisenhower onbehalf of the Rockefeller Foundation, to outline possible roles that an AAAS committee mightplay. One reason Weaver mentioned as a reason for an AAAS study was that it would be"useful to have an independent study carried out by the AAAS (of a somewhat differentcharacter in that the AAAS study would be relatively brief, wholly unclassified, free fromGovernment connection and possible influence. The Rockefeller trustees concluded that theradiation study should be carried out under the auspices of the NAS, as it was the officialscientific advisory body to the government, and that it was essential that such a study have theapproval of the "highest authorities" (by implication, the President) and the AEC.”(Jolly, 2003)

Cynthia Jones identifies the USAEC as the requestor of the study,8 which it may have formally been.Certainly, the UASEC was heavily involved in the studies, as Hamblin has indicated. Yet,government influence, (e.g., that of the USAEC), plays no role in Calabrese’s narrative.

As for the USAEC’s interest,

"....with the public controversy over radiation hazards, it became the undeviating goalof the AEC to justify scientifically the position that fallout and low levels of radiation pose nothreat to humans, and might even be beneficial genetically." (Seltzer, 2007 at 290).

Seltzer goes on to state that, in general, the USAEC "... sought to dominate all the relevantcommittees, government and independent, that were formed to study and/or recommend policy onradiation exposure limits."

In a similar vein, Hamblin argues that this attempt to dominate committees extended to theBEAR-I panel; he claims that the panel was not truly independent of the USAEC, with USAECscientists on many panels and subpanels and holding the keys to much important data (Hamblin,

8 “Due to the number of new scientific recommendations and interest by Congress and the public regardingradiation and the effects of radioactive fallout, the AEC, in 1955, requested the National Academy of Sciences-National Research Council (NAS/NRC) to undertake a major study of the effects of low-level radiation.Although not directly involved in setting radiation protection standards, the NAS/NRC appointed a Committeeon the Biological Effects of Atomic Radiation, which became known as the BEAR Committee (NAS/NRC1956). Years later, this Committee would be renamed as the Biological Effects of Ionizing Radiation (BEIR)Committee. In addition, the NCRP and ICRP cooperatively worked with the BEAR Committee and alsoundertook extensive evaluation of the concerns associated with population exposure from fallout, especiallywith respect to genetic effects. Although different groups conducted these studies, they arrived at essentially thesame conclusions because the database was the same for all and there was membership overlap between theorganizations. More specifically, they agreed that there could be possible genetic consequences of exposing theentire population to both medical and occupational sources.” Jones, C. G., 2005. A review of the history ofU.S. Radiation protection regulations, recommendations, and standards. Health Phys. 88, 105-24..

12

2007). In direct contradiction to Calabrese's claims about the direction of NAS bias, Hamblin arguesthat the NAS staff was too solicitous of the USAEC; that the staff allowed the USAEC to negotiatewith the panel about content (e.g. commenting on drafts). Calabrese continues to ignore the influenceof the USAEC on the NAS panel, directly and indirectly, including the fact that the USAEC was afunder of many of the current panelists, had funded many in the past, and might do so in the future.Calabrese continues to ignore the political role of the USAEC and geneticists reaction to suchinfluence. This is an example of what I meant in Beyea-I, when I claimed that Calabrese presented anincomplete narrative.

The NAS certainly represents the scientific establishment, but to claim that they andthe Rockefeller Foundation were after more than advancing science and the human conditionrequires extraordinary evidence. There was great concern about the advancing move towardsatomic power and concern about weapon’s fall out. Not in Calabrese’s narrative, though.

The Rockefeller foundation had been supporting genetic research, along with the USAEC, the Carnegie Foundation, and the US National Institute of Health. It would be naturalto want genetic effects to be considered when addressing the biological effects of radiation.Genetics was one of six committees. Calabrese does not discuss these other committees. Ithas fallen to my role to list the factors that Calabrese leaves out of his narrative.

Calabrese continues with his mischaracterization of the situation:

“Creating a Panel that uniformly agreed on the central issue of a highly contentiousdebate…..” (Calabrese, 2016)

There was no contentious debate in the genetics community about the LNT as a theory.Calabrese has himself conceded this in past writings. The contested issue was not thethreshold or linearity in genetic effects. It was about the strength of the association, a subjecton which the panel was strongly split and could never reach consensus. It is unfathomable tome how such statements that confuse the situation can be made.

To quote Calabrese’s full sentence:

“Creating a Panel that uniformly agreed on the central issue of a highly contentiousdebate was biased from the start, denying a fair and legitimate process to properlyassess what is the nature of the dose response in the low dose zone.“ (Calabrese,2016)

By 1956 no one was interested in going back to the issue of threshold and linearity at low doses. Thiswas settled science to geneticists, as I discuss in Beyea II. The issue had long ago gotten a fair andlegitimate hearing in the literature. This is a big issue to Calabrese, but he didn’t go back far enoughand never considered target theory and its history. All he can focus on is outlier views on plantgenetics such as held by Ralph Singleton, who was on the agricultural panel. I have discussedSingleton’s research and views in Beyea I and II, and how he had moderated his views by 1956describing his past research as indicating non-linearities, not a threshold. (Other plant researchers,Sax at Harvard, Stadler at U Mo, Giles at Yale, were firmly in the hit theory camp.)

More out-of-date thinking:

13

“The end result was a self fulfilling prophesy. Selection of individuals with uniform beliefcore on this issue precluded the search for truth.” (Calabrese, 2016)

Incorrect premise. As the work of Jolly, Seltzer, and others has indicated this panel was deeplydivided on the core issue of the time, the strength of the association, namely, would genetic mutationsbe weeded out or not? The “search for truth” on the lesser issues had been carried out in the scientificliterature.

It was certainly not a surprise that geneticists had some basic common beliefs. No more of a surprisethan finding out that physicists in 1956 didn’t bother to debate relativity by that late date, althoughthere have always been some relativity doubters. Opponents of relativity could also think thatmainstream physicists were biased.

Funding pressures?

Calabrese implies funding pressures played a role:

“Some of the Panelists had been/were being funded by the Rockefeller Foundation, thesame organization that was also funding the BEAR Committee activities and selecting themembers.“ (Calabrese, 2016)

And some panelists were funded by the USAEC. Researchers have to be funded by someone. NASstaff are responsible for selecting members, not the funders. No doubt NAS staff paid attention torecommendations from the chair, Warren Weaver, and the USAEC. What is strange is to think thatthe Rockefeller foundation, NAS staff, and Warren Weaver would have a nefarious agenda. Mereassertion won’t work; nor will back inference from the pick of an establishment group of scientists.There was a shortage of plant geneticists on the panel, such as Sax of Harvard and Stadler of U ofMissouri and Giles at Yale, but the relevance to humans of plant studies is not as clear and theseresearchers were on board with target theory, anyway, so would not have added any questioning of thezero threshold and linear slope for single hit mutations i.e. at low doses.

Calabrese continues,

“The President of the Rockefeller Institute for Medical Sciences (later to becomeRockefeller University) and the President of the NAS at this time was the same person, Dr.Detlev Bronk. President Bronk would ensure the creation of a Genetics Panel and that theperson (i.e. Dr. Warren Weaver) overseeing the funding of the geneticists' grants from theRockefeller Foundation would chair the Genetics Panel. Thus, organizational andleadership structure of BEAR I, as well as the Genetics Panel selection and functioning,displayed an improper inbreeding relationship between the funder and recipient organizationwith the potential for undue influence of the funding organization over Panelists who werehighly dependent on grant funding from the Rockefeller Foundation.” (Calabrese, 2016)

Note the addition of the opinionated and gratuitous word, “improper,” and the addition of the word,“highly” in front of dependent. The authority here is Calabrese, himself. He uses, “highly” fordramatic effect, but with no evidence of such a dependency. In fact, a broad mix of funding had cometo geneticists on the panel from the Rockefeller Foundation (Muller, Sonneborn, Beadle), the USAEC

14

(Neel, Hollaender, Muller, Crow, Russell, Warren, possibly Wright), the Carnegie Foundation(Kaufmann, Demerec), the National Institute of Health (Glass), University of Wisconsin AlumniResearch Foundation (Crow), Wallace C. and Clara A. Abbott Memorial Fund of The University ofChicago (Wright).9 Sturtevant only lists his Cal Tech affiliation; presumably Little was retired fromactive research. Here is another example of Calabrese leaving out the full story. He cites one correctpiece of information (funding by the Rockefeller Foundation), leaving out any mention of (at least)five other funders. This kind on innuendo may be common in partisan political politics, but it is rarein scientific journals.

The conflating by Calabrese of the Rockefeller Institute for Medical Sciences (RIMS) and itspresident, Bronk. with the Rockefeller Foundation is an attempt at guilt by linguistic association. TheRIMS had a long record of scientific achievement (http://www.rockefeller.edu/about/history).Calabrese is grasping at straws here. In any case, one wonders who the evil folks were at theRockefeller Foundation who wanted to deceive the world about the genetic dangers of exposure toionizing radiation. John Bugher of the Rockefeller Foundation was a member of the pathology panel,which did not support the LNT for cancer (although recognized the threshold could be zero).

Although having a potential funder (Weaver) as chair of a committee was undesirable, all things beingequal, the presence of the biggest genetics funder of all, the USAEC (Jolly, 2003), was comparablyundesirable and in need of balance. The USAEC was heavily represented in the room, with the panelessentially monitored by the, non-geneticist and AEC stalwart, Shields Warren. And, the USAECcommented on panel drafts, according to Hamblin. Calabrese does not discuss the AEC’s funding ofgenetic research. As I said in Beyea I:

“Anyone at the time who took a view opposite to the USAEC on fallout risk was potentiallyvulnerable to loss of funding or loss of future opportunity of funding. And, the USAEC wouldhave appeared to have been watching, given the USAEC-friendly scientists on the geneticspanel, including Shields Warren, the former head of the USAEC’s Division of Biology andMedicine (1948–1952), who had "authored the USAEC's basic assumptions" (Hamblin,2007). From this broader viewpoint the panel exhibited courage in my view when it deviatedfrom the USAEC party line by insisting that the potential genetic risks of radiation exposurehad to be stressed in the report.” (Beyea, 2016b)

9 Based on acknowledgements on papers, statement of Dobzhansky in 1957 Seltzer, M. W., The technologicalinfrastructure of science. Science and Technology Studies, Vol. Ph.D. Virginia Polytechnic Institute and StateUniversity, Virginia, 2007. and statements in a paper by Gray from the Rockefeller Foundation: “Thebiological specialty which has received probably the largest proportion of support is genetics. Soon afterThomas Hunt Morgan went to the California Institute of Technology, a grant was made to assist hisresearch, and almost con- tinuously since that time genetics at Caltech has been sup- ported-in addition toother biological studies there. H. J. Muller's distinguished work has been assisted through a series ofgrants-first at the University of Edinburgh, then at Amherst College, and more recently at IndianaUniversity. An appropriation now current at Indiana is divided among Muller, Ralph E. Cleland, and T. M.Sonneborn. Among other geneticists whose programs have attracted Foundation support are L. C. Dunnand Th. Dobzhansky at Columbia University, Albert L. Blakeslee at Smith College, Curtis and Stadler atthe University of Missouri, J. T. Patterson and his associates at the University of Texas, Joshua Lederbergat the University of Wisconsin, and E. L. Tatum and George W. Beadle on the Pacific Coast. A recentcheck through the records shows that assistance has been given to genetics in fifty-three institutions, andthe Foundation itself has directly engaged in experimental genetics on a large scale through its agriculturalresearch program in Mexico.” Gray, G. W., 1954. The Rockefeller Foundation and the biological sciences.AIBS Bulletin. 4, 13-15..

15

Manipulation?

Calabrese continues with his negative assertions:

“From the start, the process would be susceptible to manipulation, coercion and bias, as wellas timing pressures.” (Calabrese, 2016)

Other than from the USAEC, I have found no historians reporting attempts to affect the outcome otherthan by intellectual arguments. Calabrese tries to infer that there were such attempts based on hisconspiracy theory, but provides no backup. The situation here was no different from any NAS study,where NAS leadership picks panel members, fully aware of multiple interests and where there aremultiple constituencies among the panelists to balance out biases of concern. Calabrese’sconstituency of threshold and sublinearity was not represented and had no business being represented,given the state of knowledge at the time, as I discuss in Beyea II. Calabrese ignores the pressure fromUSAEC discussed by Hamblin, despite citing Hamblin’s article for other purposes. Timing pressuresare always an issue with NAS panels; here there were 100 scientists to deal with among the entiregroup, including 17 on the genetics panel. Not surprisingly, the NAS is led by the scienceestablishment and it wants to keep government agencies as happy as possible, which may explain whythe USAEC was given such unusual access to the process. In this case, as often happens, panels gotheir own way. It is true that the NAS is an organization of the scientific establishment, which meansit can sometimes be slow to recognize the young disruptors who may soon shake up a field, but thatdidn’t happen here. Subsequent geneticists held to the same views.

Calabrese continues:

“While the complexity of these inter-relationships makes their dissection extremelydifficult…

But not too difficult for Calabrese to ignore the full set of players or infer conspiracy.

…too much power, control and influence was rested in Bronk and Weaver … (Calabrese,2016)

Hmm. Was not too much power in the hands of the USAEC? As it turns out there were a lot ofcompeting, and somewhat balancing influences.

“This type of organizational framework, functional control and funding manipulation,created the likelihood that the funder would get what it wants.” (Calabrese, 2016)

Which funder would get what it wanted? The USAEC, who had a policy interest in the report, or theNAS establishment, with its reputation on the line, or the Rockefeller Foundation, with itsestablishment credentials? And, we are never told exactly what the “funder” wanted. Calabreseassumes the Rockefeller Foundation wanted what the panel produced, but that is circular reasoning.By the way, panelists do not get paid for their time. Their travel and accommodations are covered bythe funding source, as are staff expenses.

16

Panel report content

Calabrese claims that alternative dose response models were ignored. I have dealt with this in BeyeaII, where I state:

“In contrast to Calabrese’s claim, dose response functions other than linear were considered,studied in detail when they occurred (primarily in chromosome or chromatid aberrations), andinterpreted theoretically in terms of multiple hits. Examples in plants are: (Conger and Giles,1950; Lea and Catcheside, 1942; Rick, 1940; Sax, 1938; Sax, 1939; Sax, 1940).Chromosome and chromatid aberrations were considered to be one pathway to actualmutations, distinct from possible point mutations.” Beyea-II.

Calabrese claims that the panel hid profound disagreements of the panelists over the transgenerationalgenetic risks from radiation exposure.10 While no Table appeared, the final report is quite clear aboutthe disagreement,11 with multiple disclaimers, while also being clear on the much broader agreementthat existed. As I stated in Beyea I and II, it is a difficult decision for all panels as to how to handledisagreement. How much should go into a report so as to be clear, while not distracting from theconsensus findings and recommendations. As I said in Beyea II, Supporting Information:

“As for how much discussion of disagreements should be dwelled upon in any NAS-typereport, it is necessary to bear in mind that the excitement of disagreements can drive attentionaway from recommendations and consensus findings…..The panel was addressing a report-writing problem that remains today for scientists assembled to advise on issues of interest topolicy makers and to the public.” Beyea-II, SI.

As I know from experience, often a single word change will eliminate major disagreements. Othertimes multiple views must be presented in the text. In the worst case, such as the 1980 BEIR report,minority reports are required, which renders a report of reduced use due to the distraction. Panelistsare right to worry about too much dissent weakening the message. Had the panel report not discussedthe disagreement, Calabrese would have a point, but they did. No one could claim based on the reportthat the full effects of the damage was known. And, as I have already said, recommendations do not

10 “Such leadership failures are also seen in a decision (i.e. the Panel voted) (Weaver memo to Panel, June 5,1956d (Weaver. 1956d)) to hide profound disagreements of thePanelists over the estimation of radiation induced population based transgenerational genetic damage risks inthe U.S.”11 Some key quotes: “…..it becomes most clearly evident that different geneticists find meaningful ratherdifferent approaches to the problem of genetic damage. “

“This calculation …. is, to some geneticists, not a very meaningful way of looking at the problem. To others itadds up to something at least reasonably clear, and in any event very serious.”

“Their principal reservation is doubtless a feeling that, hard as it is to estimate numbers of mutants, it is muchharder still, at the present state of knowledge, to translate this over into a recognizable statement of harm toindividual persons. Also they recognize that there is a risk involved in extrapolating from mouse and Drosophiladata to the human case.”

17

follow from contested findings. No recommendations were made by the panel based on geneticdamage calculations.

Calabrese claims the panel failed after the report to explain a switch to LNT.12 It never recommendedsuch a switch as I have previously discussed. This is another place where Calabrese colors thelanguage. There never had been a threshold theory of genetic damage. The panel wanted to getgenetic concerns taken into account. There were some non-geneticists who wanted an explanation ofthe consensus findings on the LNT. The panel could indeed have helped their cause among thesequestioners by pointing to the literature reviews on the subject (Beyea II), but they would have had notrouble providing the references, as I discuss in Beyea II. The panelists were authors of much of it.The report did indicate that supporting information would be provided on request to governmentagencies that dealt with standards.

Lack of familiarity with the historical literature, especially the theoretical literature, coupled with hisincorrect views of what the panel did and said in the report, has led Calabrese to drastic inferences.13

He apparently thinks the documentation did not exist (which I have listed in Beyea II). He also thinksthat he can set the policies for the National Academies of Sciences.

Calabrese raises the issues of peer review:

“The process also failed to offer an independent peer review, resulting in the reinforcing andensuring of biased perspectives.” (Calabrese, 2016)

I do not know what kind of review the panel reports got. Specific peer reviewers were not listed asthey are today in NAS reports, as required by Congress in 1997 under Section 15 of the FederalAdvisory Committee Act.14 In the 1972 BEIR I report, the existence of a review process wasdescribed, although no names were listed. I do not know when the Academy first instituted such aprocess and noted it in reports. Regardless, according to Hamblin, the USAEC was reviewing paneldrafts, so, at a minimum, it was giving peer review. It would be hard to argue that views close to thoseof Calabrese would not have been raised by the USAEC, if they were deemed credible. When thereport was reprinted by Science Magazine, there would have been some review, but possibly cursory,since they were reprinting an NAS report.

As far as I can tell, a biased perspective to Calabrese is one that does not accept a threshold and non-linear response for genetic effects.

12 “Similarly flawed leadership is also displayed in the Panel's subsequent refusal, again by a vote, toprovide a written scientific basis for why it recommended the switch to LNT (G.B. Beadle memo).”Calabrese-II. I note that no such switch was recommended.

13“Such arrogance with its lack of scientific, societal and historical documentation responsibilities, andimproper manipulation of scientific and public policy issues was permitted by NAS president Bronk.”Calabrese-II.

14 “An Act to amend the Federal Advisory Committee Act to clarify public disclosure requirements that areapplicable to the National Academy of Sciences and the National Academy of Public Administration..”http://www.nasonline.org/about-nas/leadership/governing-documents/federal-advisory-committee.html?referrer=https://www.google.com/.

18

Possible alternative experts

It is hard to know who could have given the kind of critique that Calabrese seems to want beyondpeople who commented on the drafts for the USAEC. If Singleton were to bring up his plant work, itwould have been, I think, categorically rejected for the reasons I give in Beyea II.15 Later in his paper,Calabrese brings up a 1962 paper by Plough as evidence that I mischaracterized the scientific situationin 1956. Calabrese did not quote Plough closer in time to 1956, for instance, in 1954:

“The genetic effects of neutrons from the detonations require separate extensive tests, sincethey are not identical with the somatic changes. For one thing, the organism as a whole mayrecover from single or even repeated exposures to low level radiation, yet the same radiationdosages will cause increases in mutation frequency which are permanent and cumulative.”(Plough, 1954)

Thus, in 1954, Plough took a conventional position. What about in 1962? Putting the time mismatchaside, Plough who had been an administrator in the USAEC from 1951-1953, still reported linearitydown to 100-r in his work and noted the visible changes in fruit fly bristle mutations down at 5-rshown in the 1961 work of Glass and associates.

Unlike Calabrese, he considers earlier NAS panels as conscientious, specifically the 1960 report,which had stated agreement with the 1956 report,

“With these figures and the evidence of linear dose-mutation curves a conscientiouscommittee on radiation projection recommended the limits to radiation exposure alreadynoted.” (Plough, 1962).

Plough in 1962, in partial agreement with many of the 1956 NAS panelists, thought that selectionwould reduce the really harmful effects in later generations and prevent them from persisting16 Heobjected to the term “genetic death,” which he thought had greatly disturbed people. This is faircriticism of the subset of the 1956 panel members who believed in this approach and got it discussedas one possibility in the report, but it is not what Calabrese has complained of. I acknowledged inBeyea I that the 1956 report, unnecessarily as it has turned out, probably contributed to increased fearof radiation, but this is not fraud or scientific misconduct. (It also likely helped to some degree inbringing about the atmospheric weapons test ban treaty.)

In addition to matching the view of some 1956 panelists on the likely reduced strength of the long-term association, Plough also took note of post-1956 work on possible repair. “There is moreoversome reason to believe that minor genetic changes are corrected at the cellular level.” Of course,repair is not necessarily 100% effective, so it may only reduce the percentage of damage per unit dose,which is what Russell had found in male mice after 1956. So Calabrese is incorrect to think that

15 For instance, the lack of replication by Nybom and the lesser relevance of plants to humans, as well as thefactor of 4 difference in the supposed threshold between two different measurement years. Nybom reference:Nybom, N., et al., 1956. The genetic effects of chronic gamma irradiation in Barley(http://onlinelibrary.wiley.com/doi/10.1111/j.1601-5223.1956.tb03012.x/epdf). Hereditas. 42, 74-84.16 “These isolated observations give grounds for questioning the common view that low level radiation actuallyresults in any persistent increase in harmful mutations as required by the linear mutation-dose curve. Moreprobably they are painlessly eliminated by selection in earlier stages.” Plough, H. H., 1962. The harmful geneticeffects of radiation. Journal of the National Medical Association. 54, 652-657..

19

Plough is arguing for a biologic threshold of the standard form. Plough concludes his 1962 paper bysaying there is little evidence of a permanent increase in the harmful genetic effects, which might bedifferent from his 1954 position, but it is hard to know.

Certainly Plough sees the situation as having changed, because of new data, so an evolution in histhinking may have occurred. It looks like he found the 10-r recommended limit as too restrictive, butit is not clear what he would have thought in 1956. Based on his 1954 paper, quoted above, Ploughwas not thinking about repair, apparently. Still, he probably would have speculated then, as he did inhis 1962 paper that mutations might lead to an improvement in the population, which was an AECposition during the panel’s deliberation.

“In addition there are studies in population genetics which suggest that mild radiation mayeven be advantageous, at least to the immediate offspring, due to the production of geneticheterosis. We all know that hybrid corn and hybrid chickens give better yield.” (Plough,1962).

On balance, I don’t see Plough as giving any different comments from what the panel already hadreceived. The heterosis argument from the USAEC was well known. Plough did not contest linearityor threshold. His position on the low risk of damage in 1962, especially permanent damage acrossgenerations, would have put him in the balance camp, along with Wright, although his position mighthave been stronger than Wright’s. It is possible that Plough was one of the AEC reviewers whocommented on drafts.

Had Plough been chosen as a panelist, he might have made up in part for the absence of Dobzhansky,who, although appointed, did not serve on the panel. More discussion of the balance view wouldlikely have been necessary for sign-off. However, when it came to choosing panelists, it must benoted that the USAEC was already heavily represented on the panel, so adding another panelist withan AEC connection would have been unlikely. (Singleton was also funded by USAEC.)

As I have said above, it is hard to tell how much Plough’s views might have changed between 1956and 1962, when his article cited by Calabrese appeared. By 1960 even the second BEAR geneticsreport was criticizing the genetic death hypothesis.

“There are, however, several considerations that make this point of viewunsatisfactory….“Even conspicuously unfavorable effects of mutations in particularcombinations may be balanced by favorable effects in others. In the next place, the equatingof all unequivocally injurious mutations is very unrealistic without consideration of thepersonal and social impact. It will perhaps suffice here to note that the occurrence of adominant mutation, lethal in the first week of development, will produce no appreciabledamage to the population or to any one in it.” (NAS, 1960).

The omission of these more explicit counterarguments to the genetic death concept from the firstBEAR report was a mistake. I doubt it would have happened, if Dobzhansky had served on the firstpanel, not just the second, but I also doubt it would have made any difference in the reception of thereport, whose magnitude calculations were not used in any recommendations. Nor, would fear havelikely been reduced as a result.

Calabrese continually changes the subject from threshold and linearity to slope magnitude, withoutnoting the shift. Discussion of the slope of the LNT and relevant arguments like Plough’s are

20

interesting, even if after the fact in his case, but such discussions are a distraction from Calabrese’sthesis of misconduct and fraud. He claims the panel knew or should have known that zero thresholdand linearity were wrong. (They weren’t wrong then and they aren’t today, according to the latest USNAS committees. See Beyea II.)

21

Calabrese-II, 3. Did the Genetics Panel have long term influence?

I never said the panel did not have long-term influence. It had an impact on radiation standards, butCalabreses thesis is that the 1956 panel brought on the adoption of LNT by regulators, particularly forcancer assessment. I said the LNT concept for cancer had already been implicitly adopted by theNCRP in 1954, citing as evidence a 1995 study by Kathren, who didn’t even mention BEAR I.

"In place of the tolerance dose, Report No. 17 introduced the concept of the maximumpermissible dose (MPD). Implicit in the MPD was the idea of acceptable risk, and hence anonthreshold model, the basis for which were the observations of linearity in geneticmutations in Drosophila melanogaster which, for protection purposes, were assumed to alsoapply to somatic mutations." (Kathren, 1996)

Calabrese does not address this predating of the 1956 BEAR-I report by NCRP Report No. 17.Kathren’s history essentially falsifies Calabrese’s claim, unless Calabrese can claim that the MPDintroduced in Report 17 would have been abandoned without BEAR-I. So far, he has not made thatclaim.

Thus, in this section about long term influence, Calabrese is fighting a straw man. Nevertheless, heconstructs his own motivated reasoning. For instance, he points to a later NCRP ad hoc committeereport (“NCRPM”),17 which generalized the LNT to cancer two years after the BEAR report. It citedthe earlier, 1954 NCRP report mentioned by Kathren.

Here is a misleading sentence by Calabrese on this subject:

“The most significant long-term influence of the BEAR I Genetics Panel occurred when theU.S. National Commission for Radiation Protection and Measurements (NCRPM)generalized the application of the LNT for reproductive to somatic cell mutation withinapproximately two years after the BEAR I report (NCRPM, 1960; Whittemore, 1986).”(Calabrese, 2016)

The BEAR-I committee did have influence on the NCRPM committee according to his citation,Whittemore, but not in the way Calabrese states. As I have stated, the BEAR-I report influencedstandards. The NCRPM report was influenced by the BEAR-I study, according to Whittemore(Whittemore, 1986) and according to the NCRPM report itself,18 but only in terms of loweringstandards, not adopting an LNT, a difference that Calabrese does not acknowledge. The only role forBEAR I, along with the MRC report, that Whittemore describes is pressuring the NCRP to lower itsstandards.

17 NCRPM, 1960. Somatic radiation dose for the general population. Science. 131, 482-486..18 “The committee would like to note that if the National Committee on Radiation Protection chooses amaximum permissible dose of man-made radiation, exclusive of medical and dental sources, in the generalvicinity of the background level, there will be an order of agreement with the recommendations of other groupsthat have studied the problem. The previous recommendation of the National Academy of Sciences Committeeand the National Committee on Radiation Protection for a maximum average-per-capita-dose to the gonads of10 roentgens of manmade radiation per 30 years is roughly three times the background level, and theserecommendations include the estimated contribution from medical and dental radiation.” Ibid..

22

“Nevertheless, it was clear that the driving force behind both the ICRP and NCRP actionswere the study done by the National Academy of Sciences. The Executive Committeeformally agreed that "a lowering of the limits is called for in line with the NASrecommendations." (Whittemore, 1986).

As I indicated above in my citation of the Kathren conclusion, the LNT itself implicitly predatesBEAR-I in the NCRP by two years.

Calabrese introduces an aphorism, saying that I failed to “to grasp the key concept that "as the twig isbent, so grows the tree." True, I didn’t recognize this aphorism as a valid scientific or political scienceprinciple. As for what Calabrese doesn’t seem to grasp with his analogy is that there are multipletwigs and trees here: multiple reports, with different mix of scientists, with different charges, eachplanted in soils with successively new nutrients of research data. A bent 1956 twig does not benddifferent twigs plotted later. He would have had better luck with an aphorism about contaminatedsoil.

Infection theory

Caabrese’s sole evidence for influence is temporal and even that doesn’t work, as I have noted,because of NCRP committee reports earlier than the 1956 genetics report that crossed the no-thresholdbarrier. And, he brings back the infection theory, 19 namely that if a committee member from BEAR Ior a former student of a BEAR-I panel member was on a later committee that meant that the LNTwould not have been adopted without BEAR-I.

In this section, he claims in effect that this NCRPM committee, infected by BEAR-I, led the way forinfection of the 1972 NAS committee. He does not acknowledge, as I indicated in Beyea-I that the1972 NAS committee was charged with looking afresh at radiation effects. Nor, does he recognizethat the pathology panel in the second, 1960 BEAR report recommended against using the LNT at lowdoses for cancer risk.20 When boiled down, the Calabrese argument is that the BEAR-I genetics reportcame before regulatory adoption of the LNT for cancer, so such regulatory adoption would not haveoccurred without BEAR-I. Event A precedes B, therefore B would not occur without A.

Calabrese states that,

“LNT based cancer risk assessment would continue in each of the subsequent BEIRCommittee reports over the next forty years.” (Calabrese, 2016)

19“It is important to note here that James Crow, a BEAR I Genetics Panel member from the University ofWisconsin, was also a member of this NCRPM committee.” Calabrese-II.20 “In view of the many uncertainties, the Committee does not consider it justifiable to predict human tumorincidences from small radiation doses based on extrapolation from the observed incidences following highdosage.” NAS, 1960. The biological effects of atomic radiation, summary reports. National Academy ofSciences, National Research Council, Washington.. However, the 1960 pathology panel still considered itprudent to adopt a zero threshold model. “Some members of the Subcommittee believe, on the basis of analogyto radium data and chemical poisons, that there must be a threshold; however, no member of the Subcommitteefeels that he can estimate the size of the threshold or, for that matter, even prove its existence. Accordingly, theSubcommittee believes it is prudent to assume that there is no threshold.” Ibid..

23

Yes, this is how they assessed the then current evidence on cancer, which was more exhaustive eachdecade than in 1956. No infection here, straight science. He has repeated what was in Calabrese-I,without addressing the history that I presented in Beyea-1, where I wrote:

“As for cancer induction, successive NAS BEIR committees (NAS, 1972; NAS, 1990; NAS,2006; Reissland, 1981) have become increasingly supportive of the LNT model, first treatingthe LNT model for cancer as a conservative approach for characterizing risks for radiationprotection purposes, and today treating it as the best biologic model for characterizing bothsolid cancer and genetic risks in humans.”(Beyea, 2016b)

However, I am pleased to note that in a later section in Calabrese-II, he now implicitly acknowledgesthat there was controversy over the cancer LNT within successive NAS committee reports, whichundercuts the infection thesis.

How does Calabrese deal with the fact that the 1956 genetics report did not discuss cancer risk? Hesays it is “the widely recognized catalyst that led to the LNT’s adoption and use in carcinogen riskassessment.” Yet, he does not present any citations to such a “widely recognized” situation.Certainly, Ron Kathren in his review of the history of the LNT did not think so for radiation, failing toeven mention BEAR-I.

Later on, Calabrese repeats his attribution of goals to the genetics panel, namely claiming that its goalwas the adoption of the LNT. For genetics? For cancer? He does not say. I have dealt with thisincorrect assertion above. As with most panels, the panelists had many goals, one of which here wasgetting genetic impacts considered and taken into account. The 1956 genetics panel had norecommendations about use of the LNT for either genetic or somatic effects.

Calabrese then continues with more assertions that border on the political or reflect some angeroverriding objectivity: “For more than a decade…the Panel used every conceivable means to ensureits adoption and continuance.“ (I wonder, did those “every conceivable” means not includeintellectual argument?) In fact, the panel paid little attention to the LNT.

He seems to think that some of the panel members accepted requests to testify before Congress was anact of conspiracy. NAS panel members are routinely asked to testify before Congress. And, it is nosurprise that panel members published articles after the 1956 panel was finished. It is also notsurprising that geneticists recommended their students and colleagues for committees. Certainly, theywould want the genetics perspective represented. Memberships should not be left up to the USAEClobbying.

More infection theory:

“BEIR I (1972) Committee, Genetics Subcommittee of 10 was comprised of threemembers from the BEAR I Genetics Panel (i.e. Crow, Neel and Russell) with James Crowserving in the important role of Chairman for this subcommittee.“ (Calabrese, 2016)

Calabrese has this view that the 3 of 10 panel members from BEAR_I infected all others with whomthey came in contact. This is a key part of his long arm of inference. What about the other 7 panelmembers? Were they sheep?

24

He blames the 1972 report for coming to the same conclusions on genetics as the 1956 genetics panel,after their fresh view of the evidence. He does not criticize the evidence on which they relied, nordoes he mention that the 1972 report rejected the genetic death arguments of the 1956 panel, makingtheir views consistent with the latest NAS panel on genetic risks. It is a very strange mode ofargument.

He then implies, based on his assertions alone, that the 1972 report served as the key guidancedocument for the 1980 BEIR I report. Moreover, he fails to mention that the 1980 BEIR report fellapart due to the inability to reach consensus on the shape of the cancer dose response (Fabrikant,1980), as I discussed in Beyea-I. He also fails to mention that the 1972 report dealt separately withgenetic and cancer risks and that it discussed in detail the many uncertainties involved in trying toquantify cancer risk at low doses.21

It did not give a ringing endorsement to the cancer LNT:

“At this time, then, the linear hypothesis, which allows the mean tissue dose to be used as theappropriate measure of radiation exposure, provides the only workable approach to numericalestimation of the risk in a population. Further, since there is no means at present ofdetermining the value of the dose-effect slope in the low-dose region of interest, use of thelinear extrapolation from data obtained at high doses and dose rates may be justified onpragmatic grounds as a basis for risk estimation.” (NAS, 1972 at 89)

Calabrese is surprised that a precautionary philosophy was based on an LNT, with the idea that alinear no-threshold model would be conservative. That in itself assumes that supralinearity does nothold. As stated in the 1960 BEAR report of the pathology panel, no member could identify where thethreshold might lie.22 So, there is this parallel track among those focused on cancer, which is basically

21 ….however, it must be borne in mind that the foregoing estimates of mortality from radiation exposure maybe too high, or too low, for a variety of reasons: (1) the carcinogenic effects of a given dose of low- LETradiation may be lower at low dose rates than at the high dose rates on which these estimates have been based;(2) conversely, the carcinogenic effects per unit dose may be higher at low doses and low dose rates, owing toless killing of cells susceptible to cancer induction; (3) insofar as high dose data have provided a basis for theestimates given here, the risks may have been overestimated, owing to side effects at high dose level s whichenhance the carcinogenic action of radiation under certain conditions; (4) longer periods of follow-up may leadto estimates of risk that differ in magnitude from those above; (5) none of the estimates of risk used by theCommittee derives from a sufficiently large experience to be free of sampling variation; i.e., the data on mostradiation-induced tumors are too scanty to allow construction of dose-incidence curves adequate forextrapolation; (6) uncertainty attaches to the RBE values which must presently be used for alpha and neutronradiations; and (7) further uncertainty attaches to the relevant organ or tissue dose, owing to attenuation of theradiation with depth in the body and to other sources of nonuniformity in the spatial distribution of the doseNAS, 1972. Effects on populations of exposure to low levels of ionizing radiation. Advisory Committee on theBiological Effects of Ionizing Radiation, Division of Medical Sciences; National Research Council, NationalAcademy of Sciences..22 In consideration of animal experiments, uncertainty exists as to whether or not there is a true dose thresholdfor the production of malignant tumors by irradiation. …... If the fundamental cause, or one of the indispensablefactors, in radiation carcinogenesis is the induction of somatic mutations, it would appear possible that radiationcarcinogenesis, or perhaps the induction of precancerous states by rrradiation, has no dose threshold. NAS,Report of the Committee on Pathologic Effects of Atomic Radiation(www.cipi.com/PDF/BEAR1956_pathology_panel_report.pdf). National Research Council of the NationalAcademy of Sciences, Washington, 1956b..

25

a threshold model, with no knowledge of where the threshold lies, necessitating for precautionarypurposes a no-threshold model. One possibility would be that cancer was caused by somaticmutations, which would lead to linearity for single hit mutations. But this is not in the germ line.Geneticists sometimes studied somatic mutations, but such mutations have nothing to do with passingon detriments to future generations (putting aside modern ideas of epigenetics).

After 1956

Later in this section, Calabrese looks to the post-1956 period to find justification for his views aboutdose response--- specifically information that panel member, Russell, published later about dose anddose rate effects in mice, with separate results for males and females. This is irrelevant to the 1956panel’s conduct, plus he does not describe the situation correctly, as I discuss in Beyea II.

“…..his interpretation of post-1956 studies is not complete. He avoids mentioning thedominant signal and linearity found in male mice (irradiated spermatogonia and spermatazoa),implying that the weak signal and non-linearity in females (irradiated oocytes), discussed inone paper (Russell, 1977), was the whole story.” Beyea-II

The female signal was so weak than the response of a mixed population would follow the male signal.Calabrese in this section also raises the Capspari and Stern studies to which I have dealt withextensively in Beyea II. He then claims that Russell’s work supported a dose rate effect for Caspariand Stern. However, he misses the fact that it would not apply to the spermatozoa studied by Caspariand Stern, as I discuss in Beyea II.

Here is another non-sequitor:

“….. the BEIR I Genetics Subcommittee (1972) would not veer from the LNTrecommendation of the BEAR I Genetics Panel, again showing its long term impact.”(Calabrese, 2016)

The fact that A preceded B does not show that A caused B.

And, they actually did veer, as I have indicated above, after looking at the issues afresh as was theircharge. They also took their own views on cancer, and where particularly harsh on using a cancerthreshold in radiation protection.

“The concept is an attractive one because there are well-confirmed non-linear responses toradiation in the experimental literature. In radiation carcinogenesis the concept may havevalue in the design and interpretation of experiments, but its applicability to the setting ofguidelines for human exposure is highly questionable. There is no sufficient theory ofradiation carcinogenesis from which the concept may be deduced, and an empiricaldemonstration has not been made (NAS, 1972 at 94).

“Some human populations are so large that even very small linear estimates of risk, in theregion of dose prescribed by current guidelines, yield finite estimates of induced cancers , i.e.,deaths. These estimates of risk are beyond empirical demonstration. It is unlikely that thepresence or absence of a true threshold for cancer in human populations can be proved. If theintent of authorities is to minimize the loss of life that radiation exposure may entail, they

26

must, indeed, be guided by such estimates, and will not rely on notions of a threshold.” (NAS,1972 at 95).

The 1972 report, however, did not want the LNT to be treated as dogma.

Calabrese notes that the FRC radiation protection guidelines say their general population guidelines,based on genetic considerations, conforms to the BEAR recommendations. These are standards, notLNT guidelines, and “conforms to” indicates that the FRC has support for its decision in a past study.The FRC made its own assessment.

Thus, in contrast to Calabrese’s claim, it is not I who have incorrectly characterized the impact of theBEAR I genetics panel; it is Calabrese.

He also claims that the ICRP in 1966 discussing Muller’s genetic death calculation was an indicationof the BEAR-I panel’s influence. Muller had his own large influence before and after BEAR-I. Forinstance, his concept of genetic death was discussed before and after the BEAR-I panel report. Thepart of the 1956 BEAR I report that relied on the genetic death concept was not a consensus statementof the panel and affected no recommendation. Moreover, genetic death is about the slope of the effectof the LNT, not the linearity and no-threshold part, which is what Calabrese objects to in his claims ofscientific misconduct.

Calabrese continues to come up with nefarious goals for the genetics panel.

“The Genetics Panel …… goal was about controlling and directing the future national riskassessment and management agenda.“ (Calabrese, 2016).

This is worthy of a spy thriller. As justification, he talks about post-panel efforts by Muller incorrespondence. Is this about the panel, or about Muller, one of 13 geneticists appointed to the panel?

That Calabrese actually does recognize the consensus in the genetics community comes out in thevictory language tucked into the following quote.

“BEAR I provided the radiation genetics community a major victory along with a platformto secure and extend their influence in affecting textbooks, the research agenda, andnational risk assessment policy even as the science would progress.“ (Calabrese, 2016).

I could find no basis for the claim that the US EPA used recommendations of the genetics panel toadopt two decades later the LNT for radiation and chemical carcinogens risk assessment. The 1994reference by Albert that Calabrese provides (Albert, 1994) does not cite BEAR-I, instead Albert citesonly a precedent of an USAEC study of cancer risk assessment of strontium and iodine, whichsupposedly provided justification for use adoption of a cancer LNT. What all this has to do withBEAR-I is a mystery. Moreover, as far as I can tell in tracking down the study, it was completedyears before the 1956 report.

Calabrese then thinks out loud about what might have happened had the BEAR-I report rejected theLNT theory (and thereby gone against the consensus of the genetic community). In his view, future

27

panels would then not have been corrupted and would therefore not have adopted LNT (whichhappened, at first, as a precautionary approach and then as the best science):

“Lacking a precautionary principle based foundational belief such as LNT, the field wouldhave soon had to incorporate fundamental biological concepts such as DNA repair,adaptive response, apoptosis, bystander effects, hormesis and non-stochastic-relatively high threshold dose-based impacts (e.g. promotional stimulation) oncarcinogen dose responses, amongst other developments into dose-response modeldevelopment, all of which have the capacity to significantly affect carcinogen doseresponses in the low dose zone often leading to non-linear dose responses.“ (Calabrese,2016).

Putting aside the fantasy elements of the above wishful thinking, all of these concepts were consideredafter BEAR I, including such possibly supralinear concepts as genomic instability not mentioned byCalabrese. Scientifically, these aspects of dose response may already be incorporated into the linearresponse. Why this consideration of concepts (largely rejected as modifying linearity in humancarcinogenesis from ionizing radiation) would have been any faster with BEAR I abandoning geneticprinciples of the day is not explained. And, conspicuous by its absence is the possibility ofsupralinearity. The latest NAS BEIR (500+ Page) report still sees linearity as the best biologic modelfor cancer causation. Calabrese ideas have never been accepted by NAS committees.

Next, Calabrese proceeds to accuse James Crow of backpedaling when he served on futurecommittees that changed views from BEAR-I in terms of the genetic death calculation included. Whyis that not a good thing, responding to the latest evidence? Calabrese also criticizes Crow, ageneticist, for backpedaling as a member of a committee that took LNT as conservative for cancer.23

Taking LNT as conservative for cancer did not compromise positions on genetic impacts, especiallyconsidering the existence of studies I mentioned in Beyea-II for supralinearity in genetic doseresponse, e.g., (Bonnier and LüNing, 1949).

Calabrese attempts to tie the 1956 genetics committee to a committee of the Environmental MutagenSociety by its use of the doubling dose:

“On the Committee were James Crow, James Neel, and Alexander Hollaender.Committee 17 drew heavily on both the BEIR I (1972) committee for guidance onexposure limits and the BEAR I Genetics Panel's use of the doubling dose conceptwhich itself was based on its LNT assumption and recommendation.”

In addition to serving on Committee 17, Crow and Neel were on the BEIR I (1972) panel. They andHollanender were on the 1960 NAS report. So the only direct connection Calabrese has to the 1956genetics panel is its use of the doubling dose. Very thin, for a number of reasons. The doubling doseis a simple concept that was invented before the 1956 panel. It was used in 1949, for instance, byphysicist Robley Evans to analyze mutation risk (Evans, 1949). Muller used it in 1951 and 1954,

23 “The committee concludes that the present data are still insufficient to establish the character of the doseresponse curve for somatic effects. Nor is there sufficient knowledge of the mechanisms to serve as a guide inareas where the data are not available. In the absence of such information, the committee believes that it isprudent to be conservative and choose a premise which, if in error, would be likely to overestimate the effect oflow doses rather than underestinmate it. The committee decided to adopt as an assumption that a proportionalrelationship between dose and effect exists, as briefly outlined above.” NCRPM, 1960. Somatic radiation dosefor the general population. Science. 131, 482-486..

28

getting credit over Evans for the formulation in geneticist circles (Sankaranarayanan and Chakraborty,2000). Doubling dose was also used in the 1956 report from the UK (MRC, 1956). By definition, thedoubling dose does not depend on the LNT or any dose-response model, although it is a way ofcharacterizing the slope of the LNT. As I have stated, the 1972 NAS committee were tasked withlooking at all of this afresh. They used the most current data that went beyond the informationavailable to the 1956 genetics committee; they were not very flattering to the 1956 committee. Noinfection.

29

Calabrese-II, section 4. Beyea's historiography: information filtering

Calabrese claims that I filtered out his charges about Muller. Muller in my view acted, at worst, muchlike Calabrese does in favoring studies that conform to his strong beliefs. A temptation that is hardnot to give into. I have discussed the mischaracterization that Calabrese has made of the Uphoff 1-day replication report in Beyea II. Calabrese’s claims of bias and fraud are false, as I have indicated.The data looked at as a whole are supportive of the LNT in fruit flies down to doses of the order of50-r and lower. Calabrese claims that Muller in his correspondence admits to all sorts of bad things,but after checking claim after claim made by Calabrese about documents that turn out to be wrong, Ican put no credence in any of such claims. I do not find Calabrese an objective reader of documents.He finds material that he can interpret as negative, without looking for other interpretations supportedby other portions of the document. His spin also tends to go beyond what is in the document,requiring a number of inferences to justify. I have given repeated examples of this in Beyea II. Inaddition, Calabrese’s one-sided characterizations of panel members do not square with those made byhistorians.

Muller’s work was replicated over and over again.

30

Calabrese-II, section 5. “Curt Stem: the hand is quicker than the eye”

Here we have Calabrese at his pejorative best; the language of scorn.

As I have discussed in Beyea II, Calabrese has misread a section in a 1947 report (Uphoff and Stern,1947), which leads him to claim that the work of Uphoff and Stern was flawed. There was nostatement by Stern that there was bias; there was no claim that the results were uninterpretable, onlythat additional replication was in order.24

I find it incomprehensible how Calabrese can justify assigning guess-work motives to Stern such assabotaging Caspari’s chances of being widely cited. It would have been inappropriate for Stern andCaspari to have claimed that this one study refuted an entire body of theoretical and experimentalfindings. A cautious approach would be standard. There were no flagrant actions by Stern; they existonly in Calabrese’s mind.

For everything Calabrese claims, there is either an error on his part or there is a simple standardexplanation in terms of what goes on in science all the time.

24 Calabrese claims that the Uphoff manuscript was available only to the Stern research team. I found it listed inan Oak Ridge biography, ORNL, Bibliography of classified documents. Health Physics Education and Training(ORNL-502 (Pt. 1) (http://web.ornl.gov/info/reports/1949/3445605703959.pdf). Oak Ridge NationalLaboratory, USAEC, 1949. It was also cited in the Science Magazine article, Uphoff, D. E., Stern, C., 1949.The genetic effects of low intensity irradiation. Science. 109, 609-610..

31

Calabrese-II, section 6. “Bentley Glass…”

I have dealt with some of this discussion of Bentley Glass in Beyea-II, Supporting Information. AsCalabrese does in many places, he conflates disagreements over the total damage calculations with theconsensus numbers, such as the zero value for the threshold, the doubling dose, and the estimate ofvisible damage. Glass in his 1991 paper repeats the information about the six-geneticist total damagecalculation that appears in the 1956 report, although he gets the differences in the best estimateswrong. (The factor of 2 should have been referenced to the central value, the geographic mean, noteach value.)

In an earlier section in this report and in Beyea II, I have dealt also with the six-geneticist calculation.I add a few additional comments here.

Calabrese writes:

“Glass (1991) wrote that Dr. Weaver inspired the radiation geneticists of his Panel toestimate the population risk of a gonadal dose of ionizing radiation for up to the next tengenerations.” (Calabrese, 2016)

No, Glass did not write that. He wrote about the total damage calculation. Calahrese misses or forgetsthat the 10-generation calculation is different from the total damages passed on to the next generation.

Glass described Weaver’s charge as:

“Let each member of the committee retire to his room and make the best calculation he could,relating a particular low dose of atomic radiation, such as 10 roentgens, to the number ofdamaging mutations such as recessive lethals, sublethal effects, and chromosomeabnormalities that would be expected in the entire population of the United States.” (Glass,1991)

No mention of 10-generations. He is referring to the total damages passed on to the next generation.Next, Calabrese shows his conflating of the LNT with the damage calculations:

“Glass sought to sustain the myth that scientific consensus had emerged and that LNThad become the default because independent experts had all converged on the sameanswer-suggesting that they must all be correct.” (Calabrese, 2016)

The LNT was a finding of the report. It had emerged as a consensus among geneticists by at least the1940s. Consensus on linearity and no-threshold had nothing to do with convergence or lack of it onthe damage calculations and the magnitude of the LNT slope, but Calabrese cannot see this.

“This is the illusionary belief that must be sustained because it hides the scientificmisconduct of the entire Genetics Panel.” (Calabrese, 2016).

The illusionary belief is not that of Bentley Glass; the illusionary belief is Calabrese’s idea that thedebate in the genetics panel about the linear slope had something to do with the LNT as a theory, withzero threshold and linear dose-response function. The debates in the 1956 panel about slope camelong after the consensus among the genetics community on the LNT, as even Calabrese has written,albeit in criticism.

32

Calabrese-II, section 7. “Deception at the highest level”

I have dealt in detail with this claim about the genetic calculations in Beyea-II, SupportingInformation: Calabrese is wrong to conclude that some of the nine estimates made by geneticists wereexcluded from the report. He either doesn’t realize that there were two presentations of estimates inthe report, or he thinks the panel should have combined estimates for tangible mutations, with thosethat included lethal and detrimental mutations, which would have biased the resulting total damagenumber. In any case, when I mixed up the two types of estimates, the total damage number went from5 million to 1 million, which would have remained, a “sobering” result, as the panel reportcharacterized the number. The resulting uncertainty as measured by geometric standard deviation wasa factor of 13-14, higher than the 10 listed in the report, which would have made the result more, notless, sobering.

Calabrese focuses his attention on correspondence, but not the language of the final report, with itscaveats and representation of the differing views of panelists, which was necessary to get sign off.Calabrese claims:

“Beyea's inaccuracies are strikingly emphasized by the following additional information.While a February 8, 1956 Weaver memo charged the experts to provide genetic damageestimates out to ten generations, the Science journal Genetics Panel publication clearlyindicates that the estimates actually addressed those only for the "next" generation, withno mention of ten-generation estimates (page 1163, column 3, Genetics Panel, Anonymous,1956).” (Calabrese, 2016)

In fact, Weaver’s challenge to estimate out to 10 generations was only taken up by a few geneticistsand mentioned neither in the report nor the reprint in Science.

There were actually three types of genetic damage estimates that were either mentioned in a transcriptor cited in the report:

a) Tangible mutations passed on to the next generation. These included “such things as mentaldefects, epilepsy, congenital malformations, neuromuscular defects, hematological andendocrine defects, defects in vision or hearing, cutaneous and skeletal defects, or defects inthe gastro-intestinal or genitourinary tracts.” The estimated number, 50,000 per 100 millionoffspring per 10-r to the parents, was presented in the report.

b) All mutations passed on to the next generation, including lethal and other detrimental effects,such as reduced IQ. Under the genetic death model, each one of these would remain in thepopulation until removed by some “tragedy.” The estimated number, 5,000,000 per 100million offspring per 10-r to the parents, was presented in the report as the calculation of sixgeneticists; not a number to which all panelists agreed. The uncertainty was given as a factorof + - 10 (a factor of 100 range).

c) Damage accumulated out to ten generations. No estimate was presented in the report.

The discussion in the report of the challenge taken up by six geneticists was specifically restricted tothe total damage calculation, namely, item b above. Thus, the number of total mutations (5 million)

33

passed to the first generation is different from the number of what the report calls, tangible geneticdefects, in the first generation (50,000). Under the genetic death model, not mentioned directly byname, each one of these 5-million must eventually be extinguished out of the population throughtragedy.” The report calls this “another way of looking at the problem”:

“…another way of looking at this problem of genetic damage, and that consists of trying tomake some useful sort of really long-term, fully complete estimate. This consists ofestimating the total number of mutant genes which would be induced in the whole presentpopulation of the United States and passed on to the next appearing 100 million children,were this whole population to receive a certain total radiation dose to the gonads.” (NAS,1956a)

The report then stated the limitations of such an approach:

“First, they are clearly not really satisfactory to any geneticist. Too much has to be assumed,too little is dependably known. Second, this kind of estimate is not a meaningful one tocertain geneticists. Their principal reservation is doubtless a feeling that, hard as it is toestimate numbers of mutants, it is much harder still, at the present state of knowledge, totranslate this over into a recognizable statement of harm to individual persons. Also theyrecognize that there is a risk involved in extrapolating from mouse and Drosophila data to thehuman case.” (NAS, 1956a)

The bottom line here is that Calabrese has not carefully read a historical document, although I mustconcede that the wording was not very clear in the report, as Beatty has also noted (Beatty, 2006).

Calabrese makes the following statement:

“In a substantial misrepresentation of the record the Panel reported in the Science paperthat the uncertainty range of the remaining six estimates was 100-fold; yet it was actually750 fold.“ (Calabrese, 2016).

The factor of 750 is based on an average of the individual panelist ranges. If the geometric mean isused, which is most appropriate when numbers range over orders of magnitude, the value is 212, notthe big difference that Calabrese calculates. I note that the panel used the geometric mean to computethe best estimate for the group as a whole. That also appears to be the measurement of choice for thebest estimate of tangible mutations in the first generation (50,000). I expect they would have takenthis approach in evaluating ranges. A factor of 212 would mean a factor of 15 up or down, not the 10listed in the report. Calabrese, here, is worrying about uncertainty in uncertainty.

Interestingly, when I tried the average approach that Calabrese used, I found the values were ratherskewed. The average range from the best estimate to the lower value was a factor of ten, consistentwith the report’s estimate. From a precautionary point of view, that is the most important direction.The average range from the best estimate to the high estimate was a factor of 30.

In any case, Calabrese does not put the uncertainty statement in context by showing theapologetic paragraph that follows. Here is what the report states:

34

“The most probable estimates as thus calculated by the six geneticists do not differ widely.They bunch rather closely around the figure 5, 000, 000. Four of the six estimates are veryclose to that figure, and the other two differ only by a factor of 2.

“These six geneticists concluded, moreover, that the uncertainty in their estimation of themost probable value was about a factor of 10. That is to say, their minimum estimates wereabout l / l0, and their maximum estimates about 10 times the most probable estimate. Thiscalculation assumes a stable value for the total population.

“This calculation is admittedly somewhat complicated and disappointingly vague. It is, tosome geneticists, not a very meaningful way of looking at the problem. To others it adds up tosomething at least reasonably clear, and in any event very serious.”(NAS, 1956a).

By signing off on the report language, the six panelists implicitly agreed that their original rangeswere somewhat high. And, the first estimate of uncertainty listed above, namely the small spreadamong the best estimates of those elicited, is also a meaningful piece of information about uncertainty.

Calabrese also fails to note that this calculation was never used in any recommendation; it could notbe used, because there was not a consensus.

So let us consider the grounds on which Calabrese claims it is appropriate to support an investigationinto fabrication and falsification:

First, he makes the claim that the report said only six geneticists provided genetic damage estimates?Well, the report didn’t say that. It said six geneticists provided total genetic damage estimates. And,it provided earlier a 50,000 estimate for tangible defects, which is what the “missing” panelistscalculated. So this first claim goes away.

Second he says that the report reported a range of 100 for these numbers that the report callededucated guessing, when he thinks they should have reported a range of 750 based on his decision totake averages. Instead, the use of the more appropriate geometric mean for a set of widely varyingnumbers gives a value of 212.

Good luck with getting anyone interested in such an investigation based on such a weak claim.

Finally, I note that Calabrese seems to think that publishing the Table of the six estimates completewith minima and maxima would have undercut the panel. Actually, to the extent that anyone paidattention (The NY Times didn’t mention the numerical damage estimates in its news stories), the highranges would have led to greater fear, not less.

35

Calabrese-II, section 8. “Muller: more problems, more errors”

I dealt with this fully in Beyea II SI. Calabrese mixed up some dates, thereby undercutting hisinferences.

36

Calabrese-II, Section 9. “James Crow”

Calabrese refers to “long standing” risk assessment practices, but provides no citations as to what theyare. He is again getting into the uncertainty of uncertainty. I have been on several NAS panelsdealing with risk assessment. There are lots of ways to make such error bounds, but with limited dataall methods are rough. You do whatever you can do to try to span the uncertainty. Calabreseprovided no alternative for Crow, just as he has provided no alternative to the LNT for making riskestimates in 1956.

In this case, Crow used results from different species to provide the span. The biological plausibilityis that there are likely to be differences between species and that humans are likely to fall within therange. Any particular non-human animal is likely to differ from the human result. Differencesbetween fruit flies and mice give one estimate of species difference. Crow needed another species onthe other side of the mouse side to get an estimate of the full range. That’s where humans came in.If the available results from humans were valid, the doubling dose could be quite high, so Crowreasonably, in my view, uses human data to get the missing side of the species range. Crude, butplausible in my view.

The data from the Japanese A-bomb survivors was preliminary at this point, so could not be used as acentral estimate. As Neel and Schull themselves indicated, the doses and population numbers meantthey did not expect to see much above background (Beatty, 1991), but the data could still be used as alimit. There was another reason why the A-bomb data available at the time would have tended to givea low risk slope. There would be detriments that the A-bomb studies could not detect.

37

Calabrese-II, Section 10. (BEAR I must be correct, the UK Panel agreed)

In this section, Calabrese claims that because the UK and US panels collaborated on some issues (notsuccessfully by the way, as I discussed in Beyea-I), the agreement on the scientific genetic issues issomehow compromised. This is a non-sequitor, whose only support is Calabrese’s infection theory,namely that scientists once infected by contact with anyone from the NAS panel became sheep andtook orders, having lost their capacity for independent thought.

Both reports agreed on zero threshold for genetic effects and a linear dose response. The UK reportgave the discussion and references that Calabrese wants to see. And, as I discuss in Beyea-II, SI, thebasis for the LNT was vast in terms of studies showing linearity, with theoretical support from targettheory. This had all been worked out years before the 1956 panel. As I discuss in Beyea-II, SI, areport under the auspices of the US NAS had come out in 1954 covering all the LNT topics, with theexception of the classical/balance controversy (which happened to underlay the dispute on the ’56panel over the slope of the LNT).

Calabrese stated:

“Furthermore, since the Genetics Panel failed to provide a written scientificjustification for their LNT recommendation, it is not possible to understand thebiological basis for their decisions, let alone directly compare it with other reports.”(Calabrese, 2016)

.

The panel made a recommendation about standards; it did not make a recommendation aboutuse of the LNT. They made a series of findings about linearity, zero threshold and thegeneral negative effects of mutations. The biological basis can be found in the many reviewsthat were written from the 1930s on, as I discuss in Beyea-II.

The report indicated that it would provide further material, if agencies responsible forstandards so requested.

38

Calabrese-II, Section 11. (“It starts at the top”)

Calabrese complains about the absence of a full report. I have dealt with this in detail in Beyea-II,Supporting Information.

Calabrese-II, Section 12. (“Stacking the deck”)

I dealt in Section 2 of this report with Calabrese’s claim that NAS president, Bronk, and othersstacked the composition of the panel.

Calabrese-II, Section 13. (“Hormesis..”)

There are a number of reasons that in Beyea-I I mentioned Professor Calabrese support and lobbyingfor the dose-response of hormesis. First, to indicate that he has had issues with the National Academybefore, as he further makes clear in this section. Second, to indicate that he is not a disinterested partywhen it comes to dose-response, which is something he did not disclose to readers. He is an opponentof the LNT. I have no hesitation in indicating my prior beliefs: I happen to believe that the LNTforms a good mid-point between sublinear and supralinear dose responses at very low doses, withuncertainty on both sides, at which point all models predict low risk. I do not think I should keep suchinformation from readers.

39

Calabrese-II, Section 14. (“Self interest”)

Calabrese states, ignoring what I wrote in Beyea-I:

“Beyea plays down the fact that correspondence between BEAR II Genetics PanelistsDemerec and Dobzhansky discussed how members of their research community,including themselves, may intentionally overstate potential harm to frighten the public inorder to enhance opportunities to acquire grant support (Calabrese, 2014b ). It is statedin these letters that "stretching the truth" would be acceptable if it helped to ensure suchawards. “(Calabrese, 2016).

The only quote along these lines was made by Dobzhansky, as I have previously written, who did notserve on the first panel and was therefore not a party to the NAS panel’s deliberations. It is anincredible stretch to claim that someone (Demerec) is nefarious, because he received a letter in whichsomeone else makes a statement that is criticized. Note that Calabrese says that the stretching thetruth concession is contained in letters, plural, linking Demerec. It is not, based on the extensivecorrespondence quoted in the Seltzer thesis (Seltzer, 2007 at 305), on which Calabrese admittedlyrelied (Calabrese, 2014).

Here is the quote from Dobzhansky:

“Let us be honest with ourselves. we are both interested in genetics research, and for the sakeof it we are willing to stretch a point when necessary. But let us not stretch it to the breakingpoint! Overstatements are sometimes dangerous, since they result in their opposites whenthey approach the levels of absurdity.” (Seltzer, 2007 at 305)

In the latest discussion of this issue by Calabrese, “stretching a point” has grown to “stretching thetruth.”

Here is what I wrote in Beyea-I about this topic:

“I have never been on a panel of scientists who didn't think that more research was a socialgood. That does not translate into corruption. Furthermore, the disparaging quotes fromDobzhansky and Demerec used in the article, which contained talk of bending views toincrease research dollars, were made a year after the BEAR-I report was published, makingthem of questionable relevance. And Dobzhansky did not even serve on the first BEARpanel, only the second one. In addition, the quotes cited in Calabrese came from one faction inthe debate, namely those who supported low risk numbers, not from panel members likeMuller and others who supported high risk numbers.

It should also be noted that the research fund being discussed in the correspondence was aproposal of one of the correspondents, namely Demerec, who wrote that he thought moreresearch was necessary before geneticists should give risk estimates (Seltzer, 2007), p 305.He worried that traditional funding would lead to a dissipation of effort. It was Dobzhansky,Muller's main scientific antagonist, who wrote about a willingness to bend his views a bit. Incontrast to Dobzhansky, Jolly argues that Muller was concerned in the debate about the effecton the public and policy debates over radiation exposure, not funding (Jolly, 2003), p 305.Moreover, it was Dobzhansky who was charged at the time to have "bent [his] interpretationof experimental results to get money out of the AEC [U.S Atomic Energy Commission]."

40

(Lewontin et al., 2001; Seltzer, 2007), p 450. (Readers should be skeptical of all suchmutterings about the ethics of scientific competitors, whether expressed in the past or today.)”(Beyea, 2016b)

Resignation of Warren Weaver.

Calabrese writes:

“Beyea (2016) asserts that "Calabrese also charges, without any evidence or citation. thatWeaver resigned from the Committee (Pa• nel) after it issued its report to be able, (to avoid)an obvious conflict of interest, to give grants from the Rockefeller Foundation, of which hewas a division head." “ (Calabrese, 2016).

He makes my point in what he next writes by listing three additional reasons that Weaver gave in aletter.

“ 1) it required too much time, 2) he was not qualified, since he was not a geneticist, 3)his relationship might be strained, having served as a referee for intense dispute…. and,finally, 4) the possibility of conflicts of interest relating to the Rockefeller Foundation'sproposed funding of research by some Panel members.

Had Calabrese said that a potential conflict of interest was one reason that Weaver had resigned, hewould have been on safe ground. And, to be fair to Weaver, he should have mentioned the otherreasons that have been written about Weaver’s departure.

“The resignation from the Genetics Panel of its chairman, Warren Weaver, showed thebreakdown of consensus most clearly. Although he had not resigned in protest, his subsequentactions betrayed his sense of dismay and frustration at the AEC, particularly ChairmanStrauss.” (Hamblin, 2007).

Later in this section, Calabrese repeats his claim about a distortion of the research record. This isfalse, as I have indicated in Beyea II.

41

Calabrese-II, Section 15. (“History of science perspective”)

Calabrese cites some material from historian John Beatty about Beatty’s concern that expert groupslike the NAS panel understate their disagreements in the hopes of being taken more seriously, whichmay be problematic in a democracy. Certainly, legitimate questions to raise. I have pushed back onthis in Beyea-II, SI, based on my experience with NAS panels, indicating first of all that thedisagreements were (calmly) stated in the genetic panel’s report and that no recommendations cancome out of a disagreement, which is why disagreements are routinely de-emphasized in Academyreports. I point out that focus on disagreements distract from areas of agreement, most importantlythe findings and recommendations.

In any case, Beatty, unlike Calabrese, is not charging scientific misconduct.

I repeat that Calabrese’s claim that the research record was distorted is false (Beyea II).

Calabrese-II, Section 16. (Challenges by geneticists)

Calabrese claims that there was ample scientific record for non-linear dose responses in the pre-1956literature. My article, Beyea-II is largely devoted to refuting that claim, where I went back through allthe papers that Calabrese cites and many others that he did not discuss.

Calabrese-II, Section 17. (“Beyea states that "NAS panels have never doubted linearityof radiation Induced genetic mutations.”)

Calabrese heads this section with a title that refers to genetic mutations, but then proceeds to discussin the body of the section the issue of linearity of cancer dose response, which was heavily contestedover the years. This is the very point I made in Beyea-I. I am sorry that he didn’t read that sectioncarefully, but glad that he recognizes that future NAS panels did not march in lockstep with the 1956panel. Future panels did, however, continue to support linearity in genetic impacts, albeit with a dose-rate reduction factor of three for low dose rates.

I have also dealt with this topic in Section 3 of this report.

Calabrese-II, Section 18. (no hormesis possibility statement by the USAEC)

I actually gave the quotation in Beyea-I.

"....with the public controversy over radiation hazards, it became the undeviating goal of theAEC to justify scientifically the position that fallout and low levels of radiation pose no threatto humans, and might even be beneficial genetically." (Seltzer, 2007) p. 290.

There was no word, hormesis, defined in 1956, but the above sentence discusses a possible beneficialeffect from low level radiation.

42

Calabrese-II, Section 19. (documents used by Calabrese)

As I have shown in Beyea I and II, Professor Calabrese should not be regarded as an objective sourceof historical information. Too many times when I checked sources that were available I found majorleaps in interpretation. When he relies on material that is not easy to obtain by a reviewer or reader,including defamatory material that supports his view as a stakeholder, he loses credibility. I havemade an effort to get new materials into the publicly available record, by digitizing out-of-copyrightmaterial that is linked in Beyea I and especially Beyea II. I am sorry that he has not done the same.

Calabrese-II, Section 20. (incomplete assessment of historical record)

Calabrese claims I did not back up my claim that his assessment of the historical record wasincomplete. I thought that was what I did in Beyea-I, for instance, when I discussed his omittingcoverage of the USAEC influence on the panel and omitting providing the fallout context. I pointedout that he did not mention the MRC report from the UK, where a panel of scientists supportedlinearity and zero-threshold for genetic effects. He also did not mention a UN panel concluding thesame in 1957. He left out the historical development of NAS panels on the cancer and genetic LNT.He did not compare the numerical estimates of BEAR-I with modern day assessments. He nevermentioned the possibility of supralinearity, only thresholds.

In Beyea II, I expand the list of omissions to the realm of scientific papers.

Calabrese-II, Section 21. (Discussion)

In the discussion section, Calabrese repeats themes he raised earlier and which I have dealt with inthis report or in Beyea II, including the six versus nine geneticists, Bentley Glass, the Stern group’spapers, Muller’s dose rate figures, Weaver’s resignation, and the long-term influence of the NAS,BEAR-I panel. Having dealt with them elsewhere, I do not repeat my comments here.

43

22. Conclusions

Calabrese concludes:

“The letter by Beyea is highly filtered and contains multiple significant factual errors. Noneof its arguments are sustained upon analysis.” (Calabrese, 2016)

I, of course disagree, and think the sentence would best apply to Calabrese’s work, as I have indicatedin Beyea I & II. Readers will have to decide.

“The evidence strongly supports the conclusion that the U.S. NAS BEAR I CommitteeGenetics Panel should be evaluated for scientific misconduct as a result of its deliberatemisrepresentation of the scientific record to mask expert uncertainties in their genetic riskassessment estimates.” (Calabrese, 2016).

In my view, if anyone is to be evaluated for misconduct, it is Calabrese who should be investigated for(prosecutorial) misconduct.

Calabrese now cites a paper of Carter.

“..the comments of Carter et al. (1956) are in striking agreement with the deliberatelyhidden view of the Genetics Panel that there was much uncertainty in the radiationgenetics community concerning the estimation of genetic risks in the low dose zone fromionizing radiation.” (Calabrese, 2016).

However, there was no uncertainty about linearity for single hit mutations and for zero threshold, as Ihave repeated again and again. The uncertainty about LNT slope was not hidden at all. Thedisagreements were stated in the NAS report. As for uncertainty in the total damage calculation,Calabrese overestimated it as I have discussed earlier, by using an arithmetic mean, rather than ageometric mean, which would have been appropriate for quantities that vary by orders of magnitude.

“The significant perspective is that Carter et al. (1956) had the intellectual and moralcourage to express this situation…..” (Calabrese, 2016).

Hmm. Carter et al. discussed both supralinearity and sublinear dose response. They indicated thattheir low dose mutation results on mice were consistent with linearity and with Russell’s data.25 So,

25 “Our control mutation rate is clearly of the same order as Russell's; and our 40 r mutation rate is compatiblewith that expected on a linear law. On the other hand, the present data are also still compatible with a muchhigher rate.” So, here is support for the linear law down at the dose range that Calabrese thinks is not there infruit flies. I have not yet been able to find a report of what the data eventually showed after this preliminaryreport. Supposedly, the results were incorporated into “widely used textbook on human genetics by Curt Sternthat from its first edition in 1949, contained a whole chapter on ‘The genetic hazards to radiations’ that wasupdated in later editions to incorporate the latest findings; see Stern, 1949; 2nd edition, 1960; 3rd edition, 1973.”de Chadarevian, S., 2006. Mice and the Reactor: The “Genetics Experiment” in 1950s Britain. Journal of theHistory of Biology. 39, 707-735..

44

they apparently had the courage to state views with which Calabrese disagrees, while acknowledginguncertainty as did the 1956 BEAR report, which included many caveats.26 The panelists did not,however, consider that uncertainty left them nowhere.27 The BEAR report also called for furtherresearch. Carter, by the way, was a scientific secretary for the MRC report, which agreed with theBEAR report on the LNT linearity and zero threshold principles. (The report did not get into totaldamage; nor did the MRC group propose standards.)

Calabrese goes on:

“….whereas the geneticists of the BEAR I Genetics Panel, not only failed to state what theytruly believed, they hide this belief and deliberately mislead the scientific community topromote their agenda and careers.” (Calabrese, 2016).

This is incorrect as I have indicated in Beyea-I and II; it is slander of dead scientists, in my view. Itshould be noted that when Carter et al. wrote their statement, they were not a disinterested party inthat they were building a research program involving mice, which would benefit from showing a lackof existing knowledge. Given Calabrese’s interest in such potential conflicts of evidence, he wouldhave been thorough to point this out. Here is a discussion of their work (de Chadarevian, 2006):

“The Genetic Section under Carter used the increased public awareness of the threat ofradiation and the policy developments at the MRC to propose an ambitious 10-yearprogramme involving another five-fold expansion of the genetics work at Harwell.”

“The plans had been in the drawer since 1955 but the MRC wanted to postpone the decisionon the proposal until after the general revision of its genetic programme undertaken by theGenetics Panel of the committee drafting the White Paper. It now looked favourable at theproposal. “

“Before the new facilities were inaugurated, Carter had decided to leave the unit and take up aposition in the poultry industry.”

26 26 Some key quotes: “Concerning these estimates of total number of mutants, three things should be said,First, they are clearly not really satisfactory to any genetecist. Too much has to be assumed, too little isdependably known.”

“…..it becomes most clearly evident that different geneticists find meaningful rather different approaches to theproblem of genetic damage. “

“This calculation …. is, to some geneticists, not a very meaningful way of looking at the problem. To others itadds up to something at least reasonably clear, and in any event very serious.”

“Their principal reservation is doubtless a feeling that, hard as it is to estimate numbers of mutants, it is muchharder still, at the present state of knowledge, to translate this over into a recognizable statement of harm toindividual persons. Also they recognize that there is a risk involved in extrapolating from mouse and Drosophiladata to the human case.”

27 “In other words, there are many situations in which science can give only rough estimates. These estimatescan nevertheless be very useful. No one should disdain such an estimate because it is rough, norshould anyone consider such estimates unscientific.

45

“With Carter’s departure his ambitious project was never realised as such, but the miceirradiation studies at Harwell continued under John Searle’s and Mary Lyons’ supervisionwell into the 1990s.” (de Chadarevian, 2006).

46

Citations.

Albert, R. E., 1994. Carcinogen risk assessment in the U.S. Environmental Protection Agency. Critical Reviewsin Toxicology. 24, 75-85.

Beatty, J., Genetics in the atomic age: the Atomic Bomb Casualty Commission, 1947-1956. In: K. R. Benson, etal., Eds.), Expansion of American biology. Rutgers University Press, 1991, pp. 284-324.

Beatty, J., 2006. Masking disagreement among experts. Episteme. 3, 52-67.Beyea, J., 2016a. Lessons to be learned from a contentious challenge to mainstream radiobiological science (the

linear no-threshold theory of genetic mutations), submitted.Beyea, J., 2016b. Response to, 'On the origins of the linear no-threshold (LNT) dogma by means of untruths,

artful dodges and blind faith'. Environ. Res. [doi:10.1016/j.envres.2016.01.039]. 148, 527-534.Bonnier, G., LüNing, K. G., 1949. Studies on x-ray mutations in the white and forked loci of Drosophila

melanogaster. I. a statistical analysis of mutation frequencies(http://onlinelibrary.wiley.com/doi/10.1111/j.1601-5223.1949.tb02868.x/epdf). Hereditas. 35, 163-189.

Calabrese, E. J., 2014. The Genetics Panel of the NAS BEAR I Committee (1956): epistolary evidence suggestsself-interest may have prompted an exaggeration of radiation risks that led to the adoption of the LNTcancer risk assessment model. Arch. Tox. 88, 1631-1634.

Calabrese, E. J., 2015. On the origins of the linear no-threshold (LNT) dogma by means of untruths, artfuldodges and blind faith. Environ. Res. 142, 432-442.

Calabrese, E. J., 2016. LNTgate: How scientific misconduct by the U.S. NAS led to governments adopting LNTfor cancer risk assessment. Environ. Res. 148, 535-546.

Calabrese, E. J., et al., 2016. The Integration of LNT and Hormesis for Cancer Risk Assessment OptimizesPublic Health Protection. Health Physics. 110, 256-259.

Conger, A. D., Giles, N. H., 1950. The cytogenetic effect of slow neutrons(http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1209493/pdf/397.pdf). Genetics. 35, 397-419.

de Chadarevian, S., 2006. Mice and the Reactor: The “Genetics Experiment” in 1950s Britain. Journal of theHistory of Biology. 39, 707-735.

Evans, R. D., 1949. Quantitative Inferences Concerning the Genetic Effects of Radiation on Human Beings.Science. 109, 299-304.

Fabrikant, J. I., 1980. The BEIR III controversy. Rad. Res. 84, 361-368.Glass, B., 1991. The Rockefeller Foundation: Warren Weaver and the launching of molecular biology. The

Quarterly Review of Biology. 66, 303-308.Gray, G. W., 1954. The Rockefeller Foundation and the biological sciences. AIBS Bulletin. 4, 13-15.Hamblin, J. D., 2007. ‘A dispassionate and objective effort:’ negotiating the first study on the biological effects

of atomic radiation. J. Hist. Biol. 40, 147-177.Jolly, J. C., Thresholds of uncertainty: radiation and responsibility in the fallout controversy. History of Science,

Vol. Ph.D. Oregon State University, 2003.Jones, C. G., 2005. A review of the history of U.S. Radiation protection regulations, recommendations, and

standards. Health Phys. 88, 105-24.Kathren, R. L., 1996. Pathway to a paradigm: the linear nonthreshold dose-response model in historical context:

the American Academy of Health Physics 1995 radiology centennial Hartman oration. Health Phys. 70,621-635.

Lea, D., Catcheside, D., 1942. The mechanism of the induction by radiation of chromosome aberrations inTradescantia. J. Genetics. 44, 216-245.

Lewontin, R. C., et al., Interview of RC Lewontin. In: R. S. Singh, et al., Eds.), Thinking About Evolution:Historical Philosophical and Political Perspectives. Press Syndicate of University of Cambridge,Cambridge, 2001, pp. 22-61.

MRC, The hazards to man of nuclear and allied radiations (Cmd 9780)(www.cipi.com/PDF/MedicalResearchCouncil1956HazardsToMan.pdf). Medical Research Council,London, 1956.

47

NAS, 1956a. The biological effects of atomic radiation, summary reports(www.cipi.com/PDF/BEAR1956Summaries.pdf). National Resarch Council, National Academy ofSciences, Washington.

NAS, Report of the Committee on Pathologic Effects of Atomic Radiation(www.cipi.com/PDF/BEAR1956_pathology_panel_report.pdf). National Research Council of theNational Academy of Sciences, Washington, 1956b.

NAS, 1960. The biological effects of atomic radiation, summary reports. National Academy of Sciences,National Research Council, Washington.

NAS, 1972. Effects on populations of exposure to low levels of ionizing radiation. Advisory Committee on theBiological Effects of Ionizing Radiation, Division of Medical Sciences; National Research Council,National Academy of Sciences.

NAS, 1990. Health effects of exposure to low levels of ionizing radiation. Committee on the Biological Effectsof Ionizing Radiation (BEIR V), National Research Council, National Academy Press, Washington.

NAS, 2006. Health risks from exposure to low levels of ionizing radiation: BEIR VII Phase 2 (Committee toAssess Health Risks from Exposure to Low Level of Ionizing Radiationl). National Research Council,National Academies Press, Washington, D.C.

NCRPM, 1960. Somatic radiation dose for the general population. Science. 131, 482-486.Nybom, N., et al., 1956. The genetic effects of chronic gamma irradiation in Barley

(http://onlinelibrary.wiley.com/doi/10.1111/j.1601-5223.1956.tb03012.x/epdf). Hereditas. 42, 74-84.ORNL, Bibliography of classified documents. Health Physics Education and Training (ORNL-502 (Pt. 1)

(http://web.ornl.gov/info/reports/1949/3445605703959.pdf). Oak Ridge National Laboratory, USAEC,1949.

Plough, H. H., 1954. Introduction to the Symposium. Amer. Naturalist. 88, 209-213.Plough, H. H., 1962. The harmful genetic effects of radiation. Journal of the National Medical Association. 54,

652-657.Reissland, J. A., 1981. BEIR III, 'The effects on populations of exposure to low levels of ionising radiation'. J.

Soc. Rad. Protection. 1, 17.Rick, C. M., 1940. On the nature of x-ray induced deletions in Tradescantia chromosomes

(http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1209103/pdf/466.pdf). Genetics. 25, 466-482.Russell, W. L., 1977. Mutation frequencies in female mice and the estimation of genetic hazards of radiation in

women. Proc. Nat. Acad. Sci. 74, 3523-3527.Sankaranarayanan, K., Chakraborty, R., 2000. Ionizing radiation and genetic risks: XI. The doubling dose

estimates from the mid-1950s to the present and the conceptual change to the use of human data onspontaneous mutation rates and mouse data on induced mutation rates for doubling dose calculations.Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis. 453, 107-127.

Sax, K., 1938. Chromosome aberrations induced by X-rays(http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1209022/pdf/494.pdf). Genetics. 23, 494.

Sax, K., 1939. The time factor in x-ray production of chromosome aberrations. Proc. Nat. Acad. Sci. of theUSA. 25, 225-233.

Sax, K., 1940. An analysis of x-ray induced chromosomal aberrations in Tradescantia(http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1209078/pdf/41.pdf). Genetics. 25, 41.

Seltzer, M. W., The technological infrastructure of science. Science and Technology Studies, Vol. Ph.D.Virginia Polytechnic Institute and State University, Virginia, 2007.

Uphoff, D. E., Stern, C., 1947. Influence of 24-hour gamma-ray irradiation at low dosage on the mutation rate indrosophila (http:\\www.cipi.com\PDF\uphoff1947.pdf). Atomic Energy Commission, Oak Ridge,Tenn.

Uphoff, D. E., Stern, C., 1949. The genetic effects of low intensity irradiation. Science. 109, 609-610.Whittemore, G. F., National committee on radiation protection, 1928-1960: from professional guidelines to

government regulation. Harvard Univ.,Cambridge, MA; Harvard Univ., Boston, MA (USA), 1986, pp.Medium: X; Size: Pages: 696.