Another example of improper selection of relevant data is that full information is not provided on the rate of spontaneous DNA damage in mammalian cells (70 million per cell per year) against that induced by radiation (2 per cell per 1 mSv) (Billen 1990), and also a one-sided discussion of double-strand breaks of DNA. In Chapter 4., p. 31, quoting after Ward (1990) that double-strand breaks (dsbs) "induced by ionizing radiation, in contrast (to spontaneous dsbs) have unusual end groups, often accompanied by bds (base damages), the Report states: "the dsbs ... induced by ionizing radiation ... are peculiarly difficult substrates for the cell to cope with and ... endow ionizing radiation with its uniquely toxic effects." The Report assumes also that the formation of spontaneous double-strand breaks is extremely rare. However, according to UNSCEAR (1994) the radiation induced dsbs were found to be error-free repaired. The toxic uniqueness of ionizing radiation postulated by Ward 1990, as well as the extremely low rate of dsbs formation were refuted by Stewart 1999. Stewart found that the rate of spontaneous base alterations in double-stranded DNA is about 700 per hour per cell. Stewart also found (1999) that about 40 spontaneous double-strand breaks occur in each mammalian cell in a year, about 1000 times more than after a ionizing radiation dose of 1 mSv. Among all complex damages induced by ionizing radiation, double-strand breaks are only about 20%, with other clustered damage constituting some 80%. The clustered damages are regarded as critical lesions producing lethal and mutagenic effects of ionizing radiation (Sutherland et al. 2000). Normal cells are able to repair these damages with fidelity, as recently confirmed by (Moustacchi 2000). Moustacchi stated that comparison of mutants and wild-type organisms pragmatically suggests that, for many genotoxins and agents, very low doses may have no effect at all in normal cells. The papers by Moustacchi, Stewart and Sutherland et al., along with many others that are in disagreement with the NCRP line, well-known in the radiobiology science literature, are not cited in the Report.

The Committee's conclusion to some chapters and the final conclusions frequently do not follow logically from the evidence provided. Papers quoted as supporting LNT often contain data to the contrary and evidence against LNT is often downplayed. The Report states that ecological studies in epidemiology "cannot be regarded as trustworthy and should not be relied upon to assess either the presence or absence of excess radiation-induced cancer at low doses" (page 136) - if they provide evidence against LNT, e.g. Cohen 1995, yet they are acceptable otherwise, for example to show that the increase of thyroid cancer reporting in Belarus is due to Chernobyl fallout, and that it is supposedly directly proportional to radiation dose (e.g. Demidchik et al., 1996, at page 161). No in-depth discussion of screening effect, the most probably cause of the increase in this registration, is provided. This topic is extensively documented in the 115 page thick Scientific Annex J of UNSCEAR 2000, which is well-known as the primary scientific assessment of the effects of the Chernobyl accident. As appears in UNSCEAR 2000, the highest thyroid cancer incidence of 0.027% appeared in the Bryansk region of Russia, where the average thyroid dose was 380 mGy. The highest incidence in Belarus of 0.018% was found in the Gomel region (thyroid dose 177 mGy), and in Ukraine of 0.005% in the Kiev region (thyroid dose of 37 mGy). The incidence is not seen to be directly proportional to dose. The normal incidence of occult thyroid cancers, which while not causing any visible clinical disturbance, are histologically malignant and aggressive, is very high in most countries. They are usually discovered in the course of post mortem pathological examination or an imaging study. The autopsy prevalence of occult thyroid cancers in various countries ranges from 4.5% to 36% (Moosa and Massaferri 1997, Tan and Garib 1997). The potential of the screening effect of the occult thyroid cancers, the number of which is about 1000 times higher than the number of reported thyroid cancers in post-soviet countries, should be discussed in the Report.

This greatest manmade exposure of a large population to low doses of ionizing radiation following the Chernobyl accident (with more than 5 million people exposed) was not treated correctly by the Committee. Omission of the important information from UNSCEAR 2000, that during 15 years after the accident there was no increase in leukemia incidence or any solid cancers (except thyroid cancer, which, arguably, is a screening effect), indicates the way and degree in which the Report is biased. The Report also does not inform the reader about a lack of radiation induced hereditary disturbances both in the Chernobyl population, and among the progeny of survivors of atomic attack in Japan.

The Committee reports on an exceptionally high risk of radiation induced leukemia is presented for the SMOKY nuclear test, where the average dose was 4.66 mSv and the Observed/Expected number of leukemia cases was 10/4.0 (standard mortality rate, SMR = 2.5), yet contradictory data from OPERATION GREENHOUSE with an average dose of 13 mSv, where 1.0/4.4 cases were found (a deficit of leukemia of 73%, SMR = 0.23) (Robinette et al. 1983), are not presented. The substantial evidence, and consensus, that there are no adverse effects to the populations of nuclear weapons observers, was not reflected in the Report.

The above examples show that the Committee does not even try to objectively present the scientific evidence related to the validity of the LNT, but instead merely propagates the LNT by errors of omission and commission. The method used throughout the report is the following: (1) selecting the material so that the many important papers that contradict the LNT are not presented at all; and (2) presenting the pro-LNT work in great detail, while merely providing references to a few papers that disagree with these publications, without presenting their data, or arguments.

After our critical comments of December 1998, the text of the final version of NCRP Report No. 136 did not improve in this respect, but rather worsened. For example in Table 9.2, p. 142 on cancers in humans exposed to low or fractionated irradiation, four papers of ten presented in the draft version of this table are eliminated, those that show a decrease of cancers after low doses. In paragraph 9.3.5.1 on lung cancer, on page 171 of the Report its draft statement: "in none of the studies was cigarette smoking information available to control for its potential confounding effects," has now evolved into "only the Hanford study has collected data on smoking so as to be able to control for its potential confounding effects (Petersen et al., 1990)." In our 1998 criticism we noted that this statement in the draft version "is again a biased selection of literature and downplaying the data which are against LNT." We cited the paper by Tokarskaya et al. (1997) in which the smoking confounding factor is fully accounted for in a study on a unique group of the Mayak (Eastern Ural) nuclear reprocessing plant workers, exposed to plutonium. This extremely professional paper is not cited here probably because of its two conclusions: (1) "Dose-effect for smoking had a linear character," and (2) "dose-response relationship for plutonium incorporation corresponded to the non-linear threshold relationship" with a threshold at 0.80 Gy, and also because it shows a clear evidence for hormetic effect at low radiation exposure.

But the authors of the final NCRP Report No. 136 gave the paper of Tokarskaya et al. an even worse deal: they stated incorrectly on page 171 that it "showed an excess of lung cancer down to levels of about 1 Sv." They confused here the unit Gy with the unit Sv. In fact in the paper of Tokarskaya et al. Gy and not Sv was used for the lung dose from plutonium alpha radiation, which ranged between 0 to 17.0 Gy. This corresponded to summary equivalent dose (SED) range (including internal alpha and external gamma radiation) of 0 - 344 Sv. An excess of lung cancer incidence was observed by Tokarskaya et al. only between 1.01 and 17.0 Gy or 20.1 to 344 Sv of SED, not "down to levels of about 1 Sv" as stated in the Report. But between 0.81 to 6.0 Sv a 21% decrease in lung cancer incidence was found, and between 6.1 and 20.0 Sv 28% decrease. This important finding is ignored by the Committee. We observe here not just incompetent and careless presentation of published data, but also concealing important information that strongly refutes the LNT. This is a pattern that is unfortunately typical for the Committee in producing the NCRP No. 136 Report.

Detailed comments

Page 1, footnote 2: In the definition of "stochastic (probabilistic) effects," the premise of a "no threshold" response, and linearity as well, are arbitrary. The definition of "stochastic" effects, the severity of which allegedly does not vary with dose, and which distinguishes them from "deterministic" effects, the severity of which increases with dose, seem to be empty and obsolete in view of the current voluminous information on the mechanisms of carcinogenesis and genetics. The lack of dose related severity in stochastic effects - the main difference between them and deterministic effects, is simply not true. As demonstrated by Walinder (1995) many radiogenic cancers in man and in experimental animals show greater histologic and clinical malignancy after high radiation doses than after smaller ones. Also latency time is shortened when the dose increases, so malignant tumors can have time to develop during a lifetime. Medicine does not know such a distinction. The notion of "stochastic" and "deterministic" effects was a tacit introduction of the LNT thinking template into radiation protection, that occurred in the late 1970s.

Page 3 line 3 from the bottom to page 4 line 2: "it appears likely that this adaptive response acts primarily to reduce the quadratic (two-hit) component of the doses response curve, without changing the slope of the linear component." Why so? How can this be? Why not the linear component, or any other combination, since hormesis must surely be a non-linear effect with dose. If one believes in power expansions, surely positive and negative terms of up to three orders in power may be involved, not just the "linear component". This is not only a technical, and contorted, argument, but it is not explained nor followed up in the main text (where "two-hit" is not explained either), nor is there any substantiation of this statement by reference from the literature. There is a conceptual difference between "linear" and "quadratic" (aD+ßD²) parametrisation and a "single-hit" and "two-hit" description, e.g. of a survival curve, in that no linear component in a pure "two-hit" system is required for the "c-hit" or "m-target" (c> 1 or m>1) model to be able to satisfactorily describe RBE-LET relationships in cell cultures, for instance by Katz's track structure theory. On the other hand, the (aD+ßD²) description of the survival curve, combined with "classical" microdosimetry, is unable to make any prediction as to the value of ß with dose or LET, so how can a statement relating hormesis with a change in ß ever be verified basing on the microdosimetric arguments the Report is so fond of?

Page 6, line 5 to 1 from the bottom: "... for some types of cancer there may be no significant departure from a linear-nonthreshold relationship at low-to-intermediate doses above the dose level where statistically significant increases above background levels of radiation can be detected." - but this Report does not discuss natural radiation levels at all. Thus the question arises what did the authors have in mind: The low dose range above 2.4 mSv per year? (which is the global average whole body dose for man); or that above about 50 mSv per year? (which is the background dose in many high natural radiation areas), or above 700 mSv per year? (as in a house in Lodève, France (Delpoux et al. 1996), and in Ramsar Iran); or above lifetime natural doses often reaching several thousands of mSv? The Committee does not acknowledge that there are no increases in cancers in such high background radiation dose areas, nor that in some of these areas there are significant reductions in cancers. This is another instance in which the Committee has failed to provide the relevant scientific evidence which disproves the very premise of the LNT.

Page 6, line 2 from the bottom to page 7 line 8: From the statement the "The existing epidemiological data on the effects of low-level irradiation are inconclusive, however, and, in some cases, contradictory, which has prompted some observers to dispute the validity of the linear-nonthreshold dose-response model..." the conclusion that: "...no alternate dose-response relationship appears to be more plausible than the linear-nonthreshold model on the basis of present scientific knowledge" - cannot be logically deduced. To the contrary, the voluminous evidence that demonstrate beneficial effects in response to low dose radiation produces consistent and confirmed quadratic dose-response.

Page 20, line 1-5: The key issue, both theoretical and experimental is whether a single electron can produce a biological effects (e.g. kill a cell). The Committee dwells here on the well-known fact that a high-LET particle can kill a cell. In principle, if a single electron cannot kill a cell, but two or more can, one is led to non-linear (e.g., quadratic) extrapolation in the low-dose region.

Page 23, Conclusions: These conclusions are justified solely on the basis of argument from "classical microdosimetry", which has so far been unable to make any quantitative prediction in radiobiology, therefore could hardly be expected to be more reliable than the Katz model, in the "untestable" extrapolated region of low dose in radiation protection. The track structure perspective (Katz's model) leads to very different conclusions. Therefore, that model can not be ignored in Chapter 3 (as it is), if the Committee's aim were to objectively present the evidence based on current knowledge.

Page 74, line 7 from the bottom to page 75, line 13: The study on unstable chromosome aberrations in the peripheral blood lymphocytes of 31 Chernobyl cleanup workers, which show linear dose-response curves, is reported here (Semov et al., 1994). However, a new much larger study on 4,833 cleanup workers, with more than a quarter of a million metaphases examined (Littlefield et al. 1996), is not presented. Littlefield et al. data demonstrate that the translocation frequency is lower among the exposed workers than among the controls, and that there is no increase in the mean, median or range in chromosome aberrations in lymphocyte cultures. These results are consistent with negative results of several studies of cancer incidence in Chernobyl cleanup workers. Ignoring this information attests to the biased style of the Committee's Report.

Page 115, line 8-10: The statement that "thyroid cancer induction is heavily dependent on the hypothalamic-hypophyseal-thyroid feed-back system" is correct. But then, on page 155, in discussion of radiation induced thyroid cancer incidence after x-ray irradiation of the scalp, the Committee ignores the possibility that not irradiation of the thyroid, but rather irradiation of the hypophysis, is the cause.

Page 123, line 13 to125 line 4 from the bottom, Chapter 8.4 Life Shortening: The title of the chapter precludes objectivity. It shows that the authors are biased toward assuming that radiation effects cause "life shortening" rather than reporting on evidence of changes in the duration of the life span. Low doses are well-known to cause life-span increases. The Committee cites Walburg, 1975 that in experimental animals "shortening of life span by low-to-intermediate doses of whole-body radiation has been observed to result primarily from increased or accelerated rates of neoplasia." But it does not cite the same author that "when only non-neoplastic causes of death were considered, there was no significant effect on life shortening, and the mean age at death increased in irradiated animals relative to controls."

The improved immunity after low-dose irradiation which influences an increased life span is not reported; and no mention is made that "aging" is not an effect of low doses. After detailed presentation of few papers showing life shortening due to neoplastic causes, the Committee does not present the results of 16 papers that failed to show life shortening at low doses in experimental animals. Instead, the Committee characterizes them only as "ostensibly at variance" with the linear increase of life shortening with dose. The Committee did not present the important study on the effect of chronic irradiation on the human embryo cells at a dose rate corresponding to about 3.65 Gy per year, in which the life-span of cells was longer by a factor of 1.2 to 1.6 than of unirradiated cells (Suzuki et al. 1992). The Committee did not quote the summary statement from UNSCEAR 1994, paragraph 232: that "the mean life-span of male, but not female, mice could be increased if the animals were exposed daily to low-LET radiation from a few milligray to several hundred milligray per year above the level of background radiation." Neither did it take the neutral, or carefully weighed, stance of UNSCEAR 1994: "Taken together, the results of these experiments could be interpreted as demonstrating that, compared with the pattern observed in unirradiated controls, there was no significant effect on mean life-span following exposure to accumulated doses up to a few gray, at dose rates between 0.005 to 0.3 Gy d^-1, or on the time of appearance of tumors or on tumor incidence among irradiated animals. Why some experiments resulted in an increase in life-span is not easily explained. While the observed increase in life-span could be due to random variability, it is possible that the effect is real. If so, it is important to understand the precise conditions under which life-span is increased."

In Chapter 8 the Committee does not present the beneficial effects of whole- or half body fractionated irradiation to about 1.5 Gy cumulative dose of patients with tumors, 90% of which showed complete or partial remission (UNSCEAR 1994).

Page 134, line 13 to page 136, line 6, Ecologic Studies: This presentation is exceptionally biased. The arguments of only one side are presented. The Cohen study (1995) demonstrates that LNT predictions of lung cancer mortality due to residential radon are not confirmed by the highly statistically significant results of the epidemiological study of large populations that are exposed to moderately large variations in radon. In this chapter, four papers are cited to support a statement that ecological studies, such as performed by B.L. Cohen, are intrinsically biased. Cohen refuted these rather shoddy unfounded arguments through rigorous scientific analysis in his numerous publications. Yet none of these Cohen's publications are even mentioned by the Committee. A striking example of the biased treatment is that the paper by Lubin (1998) in which Cohen's work is criticized (in general rhetoric about "the kinds of errors that could affect an ecologic study," but ignores that Cohen has produced tens of independent studies all of which demonstrate consistent results), is cited here twice. However, Cohen's substantial reply in the same issue of Health Physics (p. 18-23) is not presented. In this reply Cohen analyzed the actual data to show that the so called "Lubin's effect" contributes very little to the huge discrepancy between the Cohen's rigorous results and LNT predictions, and does not offer a plausible explanation of this discrepancy. The same, biased treatment of the available information is continued on pages 171-177 where the Committee passes its final sentence upon Cohen's work: His study of health effects of radon (in fact, the largest and producing the best statistics ever done, which most carefully accounted for 54 confounding socioeconomic factors, including smoking) produced "the result (which) cannot be relied upon." This unfounded discrimination against an excellent scientific study, which does not fit the LNT model, is not something NCRP can be proud of. Neither does the Committee present any of the many studies by others that, although not as comprehensive as Dr. Cohen’s studies, consistently confirm his results, especially by Bogen (1998) in which all lung cancer deaths in women by U.S. county in 1950-1954, correlated with EPA’s environmental radon level data, confirm Cohen’s results.

From among very many important papers by Professor Cohen, on the subject of radon and lung cancer, from 1987 to 2000, the Committee cites only one. On the other hand, nine papers of his principle opponent, Dr. J.H. Lubin, are in the list of references. In none of these papers does Dr. Lubin present an analysis that supports the presumption that there COULD be effects that MIGHT cause an ecological study to produce an erroneous result. We doubt these nine citations reflect an effect of the name of Dr. Lubin being listed on page 265 of the Report as the Member of NCRP, as well as the ex aequo record nine citations of another Member of NCRP, Dr. J.D. Boice Jr. The reason is rather their pro-LNT stance, as suggested by a fact that the important paper by another Member of NCRP, Dr. Marco Zaider (Rossi and Zaider, 1997), presenting a comprehensive review of all studies of the dose-response relationship between external low LET radiation and lung cancer, which strongly refutes the LNT assumption, is not cited at all.

Page 137, line 11 - 28: The Committee states that "healthy worker effect" is ubiquitous in occupational studies. But it was excluded in the Smith and Doll study (1981) on British radiologists, for which the controls were other medical practitioners. One cannot suppose that radiologists were self-selected for initial or later good health in a different way than other medical practitioners. Also in the study of nuclear shipyard workers (Matanoski 1991) this effect was explicitly excluded. From both these occupational studies it is apparent that low doses of radiation are beneficial for the workers (in nuclear shipyard workers: about 24% less mortality due to all causes, and even statistically significantly less all-cancer mortality in nuclear vs. non-nuclear workers; in British radiologists in 1936-1954: 39% less cancer death); data that was not revealed in the Committee’s Report. If, however, the induction of radiogenic cancers were really a "stochastic" phenomenon (as postulated in this Report), depending simply on the probability of radiation changes in DNA, then the stochastic chance of cancer should be the same for a "healthy" and a "less healthy" worker. It seems, therefore, that promoters of the LNT and "stochasticity" should desist in using an ambiguous "healthy worker effect" concept to discount many cases in which the data shows decreases of cancers in workers exposed to low-dose irradiation.

Page 138, line 21-34: The Committee fails to express here at least the reservation as to whether health effects in atomic bomb survivors in Japan are relevant to estimating the risk of chronic or highly fractionated exposures, e.g. lifetime exposures from Chernobyl fallout or fractionated occupational exposures during a few decades, because of a factor of 10¹⁵ difference in the dose rates. The biological responses to such essentially "instantaneous" high doses, from mixed gamma-neutron sources, can not be, and are widely known to not be, a sound foundation to assess health effects of low level protracted irradiations, typical for the realm of radiation protection and natural background.

Page 145, line 15-26: Here are two examples of biased selection of publications, and of a distortion of information. The Committee cites Smith and Doll (1981) as having "reported excess of total cancers." In fact, this paper shows a deficit of deaths due to all neoplasms for the period 1936-1954, and 21% deficit for the period 1921-1954. The Techa River data of Kossenko and Degteva (1994) are presented to show "a statistically significant exposure-response (LNT) relationship" in the exposed general population. However, a study by Kostyuchenk and Krestinina (1994) of the tumor-related mortality of the Techa River population from 22 contaminated villages, shows a statistically significant decrease of this mortality from 28% to 39% for dose categories of less than 500 mSv. The same holds for the Techa River discussion in p. 153.

Page 146, line 8 - 10: The statement that "In summary the atomic-bomb study provides evidence suggestive that acute exposures, even at low doses, increase the risk of solid malignant tumors" is in disagreement with statements in p. 144, line 18-37, that for the atomic- bomb survivor data "the fit of the linear curve and curves with a threshold of 100 mSv fit about equally well for the incidence data...", and that "The results suggest that the low-dose data are too imprecise to definitively rule out one type of curve versus another." In fact, below a dose of 100 mSv, the causal link between radiation exposure and the increase of cancer is entirely speculative, whereas the statistically significant epidemiological data from numerous studies on occupational, natural and accidental exposure strongly suggest the decrease of neoplasms. The discussion of the latter evidence in Chapter 9.3.8.1. Hormesis is limited to two papers, of the several hundred references and paper abstracts and summary data provided by Radiation, Science, and Health to which the Committee refers.

Also the Committee does not present here a generalized view and theory of hormesis (for example, from a paper by Calabrese (1999), or at least some of many hundred papers reviewed recently in 26 papers published in Calabrese 2001, which includes one by Arthur C. Upton, the Chairman of the Scientific Committee 1-6, that prepared the Report. Hormesis (or the beneficial effects of low doses) in which ionizing radiation is not a subject of some miraculous exclusion, is a phenomenon observed for virtually all kinds of chemical and physical agents, and is well known in pharmacology, toxicology and general medicine.

Page 146, Figure 9.2: This is a report to evaluate the applicability of the LNT in the context of radiation protection policies and regulations, i.e., on the effects of low doses. Why then does this figure prominently show the leukemia mortality as the result of high doses in Japanese atomic-bomb survivors, and not from doses below 0.5 Sv? Why does the Committee not follow, e.g., Shimizu et al. 1992, or Figure XXI in UNSCEAR 1994, where the deficit of leukemia below 200 mSv is clearly seen, and presented in great detail? Why, for the most important dose category of 1 to 200 mSv, are only 3 millimeters given at the dose (X) axis of Figure 9.2, and 73 millimeters for the largely irrelevant doses of 500 to 5000 mSv? This again demonstrates the strong bias in the scientific evaluation by the Committee to mislead the reader to accept the LNT and to reject the scientific data that demonstrate the beneficial effects of low doses.

Page 154, line 4-6: It is true that in early British radiologists, irradiated between 1921 and 1935 with doses estimated to be about 3.8 Sv , the standard mortality rate (SMR) for leukemia was about 2.5 (Smith and Doll 1981). But why does the Committee stop at this point, and not present the data from the same paper that shows that, in the period 1936 - 1954, the British radiologists irradiated with doses estimated to be a mean of about 1.25 Sv, had an SMR for leukemia of 0.77, and for other neoplasms of 0.53?

Page 154, line 19-24: Why after presenting data for workers from facilities of DOE or Navy Nuclear Reactor Propulsion Program, showing a leukemia SMR of 0.47, and for workers in US nuclear shipyards – an SMR of 0.87, does the Committee state: "No excess of leukemia was observed," when in fact a deficit of leukemia of 53% and 13%, respectively, was observed?

Page 160, line 9 to page 162, line 5: This is an unbalanced discussion of thyroid cancers reported from Belarus, Russia and Ukraine after the Chernobyl accident. The data on increased reporting of thyroid cancers is limited exclusively to children, whereas since the studies of V.K. Ivanov et al. in 1996 and 1997, reviewed in UNSCEAR 2000, it is well known that, the increase was similar in those adults that were screened similarly as children: i.e. recovery operation workers. Most of the epidemiological studies reviewed here are of the "ecological" type, which as discussed in General comments, in the case of Cohen's studies that refute the LNT, the Report condemns as "not trustworthy" and which "should not be relied upon". However, when arguing that thyroid cancers are caused by low doses of Chernobyl radiation, this condemnation is forgotten, and results of ecological studies are defined as "convincing", and "conform(ing) reasonably well to the magnitude of dose by region" (in fact there was a lack of reliable personal thyroid dosimetry and the estimations of thyroid doses are highly uncertain - as opposed to high quality dosimetry in Cohen's studies). The Committee states that "the excess of histologically confirmed thyroid cancer has been so large that it cannot be attributed only to increased surveillance" This statement does not seem to be correct. According to the Report, "... during 1990 and 1994 a total of 315 thyroid cancers in children were observed in Belarus, which was a 30-fold excess over the numbers observed there in the previous 10 y." A similar 21-fold excess of thyroid nodules due to screening effect was observed in the United States between 1974 and 1979 . One should also note that a similar screening effect was found for chronic lymphocytic leukemia (deemed not increased by radiation exposure) among the Russian recovery operation workers (standardized incidence ratio, SIR, of 3.11, compared with SIR of 3.94 for thyroid cancer in children from the Gomel region) (UNSCEAR, 2001 - unpublished). The screening effect and the influence of occult thyroid cancers on it are practically ignored by the Committee.

Page 162 - 166, Chapter 9.3.4 Breast Cancer: The paper by Miller et al. (1989) on breast cancer mortality in Canadian tuberculosis patients should be discussed here, not only in the Chapter 9.3.8.1 Hormesis, page 195-197. This paper shows a 27% deficit of breast cancer in women in the 0.10 - 0.19 Gy dose category as compared with 0 - 0.09 Gy category. This deficit was not noticed by Miller et al., who interpreted their results as dictated by the LNT paradigm, as a straight line from high doses, even though the line falls many standard deviations outside the data points at lower doses. In the Chapter Hormesis, the deficit found by Miller et al. in population of patients from the years 1930 - 1952, is downplayed as "a statistical anomaly", on the grounds that an update of this study led by the second author (Howe and McLaughlin, 1996) "lumped" all of the low dose data into a single data point to eliminate the possibility of demonstrating the reduced breast cancer in these women. To further compound the misrepresentation of the results in the Miller study, the Committee references a later, unpublished study by G.R. Howe which is claimed to confirm these results. This study was claimed to be "in press" in the October 1998 draft NCRP Report, and is claimed to be "to be published" in the June 2001 final Report. However, no presentation or discussion of the results of this unavailable study is provided by the Committee. The study by Matanoski (1991) of the US nuclear shipyard workers, showing a strong hormetic effect of their low radiation doses for lymphatic and haemopoietic cancers and for all causes (and for all-cancers) is disqualified on the false ground that it was caused by a "healthy worker effect" factor. However, as discussed in General comments, and as stated in UNSCEAR 1994, this statistically significant decrease in mortality ratio in shipyard workers cannot be due to the healthy worker effect. The Committee makes the wholly unfounded statement that "a difference for total mortality, and not just for radiosensitive cancers, supports the interpretation that (worker) selection factors were operative." This effect indicates only that enhanced immunity induced by low radiation doses had a general character, and was active not only for cancers but, as well-documented in the medical literature and in in vivo animal studies, immunity enhanced by low dose radiation reduces infections, inflammations, and many other ailments.

Page 171, line 38-42: The papers of Hohryakov and Romanov, 1994, Koshurnikova et al., 1997 and Tokarskaya et al., 1997 are cited here as showing "an excess of lung cancer down to levels of about 1 Sv" in workers of the Russian plutonium facility. Why does the Committee not inform the reader that in all these three papers a deficit of lung cancers was observed at doses below 1 Sv? The first two papers did not account for confounding factors such as smoking, but the paper by Tokarskaya et al., 1997, the best of them, did, and clearly demonstrated that "the dose-response relationship for plutonium incorporation corresponded to the non-linear threshold relationship," and that the threshold for plutonium-induced lung cancers was 3.7 kBq or 0.8 Gy.

Page 176, line 10 to page 177 line 6: This is a continuation of an attack on Cohen’s study (1995) which demonstrates that residential radon cannot be a causal factor for lung cancers in the United States. As noted above, the results of this study, which directly contradicts the LNT "predictions," was statistically much more robust than results of any other study on the relation between lung cancer and residential radon, and it meets the most rigorous methodological criteria. For example, the slopes of this relationship, as found by Cohen, are inconsistent with the LNT predictions of BEIR IV by more than 20 standard deviations. In its attempt to disqualify the methodically meticulous work of B.L. Cohen, the Committee cites five papers criticizing Cohen's result (Greenland & Morgenstern, 1989; Lubin, 1998; Smith et al., 1998; Stidley & Samet, 1994; and NAS/NRC, 1999 BEIR VI). Cohen thoroughly responded to all of these rhetorical discussions of possible areas of discrepancy, and also other criticism, refuting the validity of the technical arguments used against his work (Cohen 1988; Cohen 1994; Cohen 1997; Cohen 1998a; Cohen 1998b; Cohen 1998c; Cohen 2000a;Cohen 2000b; Cohen and Colditz 1994). None of these papers by Cohen are even mentioned in the Report.

In the case of Cohen and Colditz, the second author, Dr. Graham Colditz of Harvard University, is one of the most highly regarded epidemiologists in the world. Dr. Colditz’ rigorous evaluation and analysis in this paper confirms that the analysis of Cohen’s data produces a highly significant negative correlation with radon levels according to the highest standards of epidemiology practice. Yet this paper is never addressed by those who claim that some undefined condition MIGHT cause an ecologic study to produce erroneous results. A statement in page 177, line 6 that the result of Cohen's study "cannot be relied upon", should perhaps end with: "because it does not support LNT". At least this would be a frank statement by the Committee on the basis for the conclusions in this part of the Report. It is sad and discouraging that the Committee, following the same rationale of the BEIR VI Committee, seeks to misrepresent the results of such an enormous and excellent testing study (of about 90% of the entire U.S. population), and fail to consider the basis for the huge discrepancy between the observational data and LNT predictions, which clearly shows that LNT fails the experimental test. This is a severe violation of the Scientific Method.

References

          Bogen, K.T., (1998). "Mechanistic model predicts a U-shaped relation of radon
          exposure to lung cancer risk reflected in combined occupational and US residential
          data." Human and Experimental Toxicology, 17(12), 691-6; discussion 701-4, 708-18

Billen, D. (1990). "Spontaneous DNA damage and its significance for the "negligible dose" controversy in radiation protection." Radiation Research, 124(242-245).

Cohen, B. L. (1988). "Dissociation between lung cancer and a geological outcrop." Health Phys., 54(2), 224-225.

Cohen, B. L. (1994). "Invited Comentary: In defence of ecologic studies for testing a linear-no threshold theory." American Journal of Epidemiology, 139(8), 765-768.

Cohen, B. L. (1995). "Test of the linear-no threshold theory of radiation carcinogenesis for inhaled radon decay products." Health Phys., 68(2), 157-174.

Cohen, B. L. (1997). "Problems in the radon vs lung cancer test of the linear no-threshold theory and a procedure for resolving them." Health Physics, 72(4), 623-628.

Cohen, B. L. (1998a). "The cancer risk from low-level radiation." Radiation Research, 149(May), 525-528.

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