Part 1 of 5

Comments on ICRP-2005
C-1 Task Group Report

The report states in its Executive Summary, page 9, lines 16-20:

The present document has been preceded by other, recent reports, notably those of the UNSCEAR and the US NCRP.  These reports recommended that radiation protection be guided by the LNT hypothesis.  The task group concurs with those recommendations.

Thus, this report, like the NCRP reports it cites, does not examine, or even reference, the massive body of work that has demonstrated the lack of harmful effects and the presence of beneficial effects from low dose irradiation, for example the work of those scientists listed in the example references.  These scientists are highly respected by their peers, work at creditable institutions, and their reports are published in mainstream peer-reviewed science journals.   This evidence has not been refuted.  The Task Group, by ignoring and discounting this scientific evidence, does not present a valid basis for its conclusions.

In addition to ignoring the most relevant evidence, the ICRP and similar advisory reports do not even demonstrate that their self-restricted data pool and analyses support their conclusions.  They speculate that various processes and phenomena have been “suggested” or “postulated” that “may induce” or “would enhance” various effects and “thus facilitate the accumulation of the requisite number of genetic events to produce a cancer.”  Then they quickly add that “most types of cancer have not been associated with specific DNA repair defects.” (page 115, line 21).  And in “Conclusions” (p.189, lines 16-18) they assert:

There is no direct evidence, from either epidemiological or experimental carcinogenesis studies, that radiation exposure at doses on the order of 1 mGy of less is carcinogenic, nor would any be expected…

But, content with that degree of support, they state (page 12, line 9) as “The conclusions of this report” that “there seems to be no particular reason to factor the possibility of a threshold into risk calculations for purposes of radiation protection.  The LNT hypothesis…remains a prudent basis for radiation protection at low doses and low dose rates.”

To repeat:  The Committee 1 Task Group report does not even claim to have reasonably established that low-dose radiation is harmful.   In this, it is in full accord with previous advisory reports on the subject.   For example, NCRP-121, states:

Few experimental studies, and essentially no human data, can be said to prove, or even provide direct support for the concept…It is conceptually possible, but with a vanishingly small probability, that any of these effects could result from the passage of a single charged particle…It is a result of this type of reasoning that a linear non-threshold dose response relationship cannot be excluded.  (p. 45, emphasis added)

 

The French Academy of Medicine states:

The hypothesis of the risks of cancer induced by low doses and dose-rates is founded on…the linear no-threshold (LNT) assumption. This hypothesis conflicts with itself and has many scientific objections  and it is contradicted by experimental data and epidemiology. ..[the Academy] denounces utilization of the linear no-threshold (LNT) relation to estimate the effect of low doses… (Dec 2001)

The relevant professional societies, the American Nuclear Society and the Health Physics Society, have also supported this stance in carefully considered Position Statements:

 

It is the position of the American Nuclear Society that there is insufficient scientific evidence to support the use of the Linear No Threshold Hypothesis in the projection of the health effects of low-level radiation. (PS-41, June 2001)

In accordance with the current knowledge of radiation health risks, the Health Physics Society recommends against quantitative estimation of health risks below 5 rem in one year.  (Public Statement on Radiation Risk in Perspective, Jan 1996)

Both societies agree that: “Below 10 rem…risks of health effects are either too small to be observed or are non-existent.”

 

The fact that low-dose radiation is harmless and often beneficial is not a new or minority opinion.  

It has been widely reported in the science media, and recently in the general media, e.g., Fortune (Jun 03), Discover (Dec 02), American Spectator (Jul/Aug 02), Crisis (Jun 02), Wall St. Journal (Dec 19, 03), and Boston Globe (Dec 12, 03).  The proto-scientist Paracelsus said in 1540, “Nothing is poison but the dose makes it so.” 

Within months of Roentgen’s discovery of x-rays, reports began appearing in scientific journals on the use of x-rays to cure infection.  It was found even then that the radiation was not strong enough to kill the bacteria directly, and that its effectiveness results from stimulation of the immune system. 

This phenomenon—toxicity at high levels and stimulation of healing at low levels—is a nearly-universal biological process, which has been called hormesis.   Low dose radiation consistently shows that it acts to reduce cancer incidence.

Calabrese and Baldwin report (Nature 421, 691, 2003) “thousands of studies demonstrating hormesis…we see it across the whole plant and animal kingdom… and at essentially every endpoint…the hormetic model is not an exception to the rule—it is the rule. 

Jocelyn Kaiser’s four-page News Focus on hormesis (Science 302, 376, 2003) contained a full-page sidebar documenting the phenomenon’s occurrence with ionizing radiation.

 

There is voluminous data showing the beneficial effects of low-dose radiation.  

T.D. Luckey, Chairman Emeritus, Biochemistry, U. Missouri-Columbia, wrote two books, Hormesis with Ionizing Radiation (1980) and Radiation Hormesis (1991) with more than 2000 references validating hormesis in plants, animals and humans. 

James Muckerheide, as Chair of the ANS Biology and Medicine Division Committee on Low Level Radiation Health Effects, organized a series of sessions on Low-Level Radiation Health Effects at ANS annual meetings, 1994-2003.  (See http://www.radscihealth.org/rsh/realism/ANSsessions1994-1999a.doc)

Radiation, Science, & Health, has amassed and evaluated several thousand documents on the health effects of low-dose radiation (See http://www.radscihealth.org/rsh/docs ). 

Edward Calabrese and colleagues at the Northeast Regional Environmental Public Health Center,  U Mass School of Public Health, publish a newsletter, Biological Effects of Low-Level Exposures, and run an annual international conference on Non-Linear Dose-Response Relationships (See http://belleonline.com ). 

Evidence that radiation may be essential to life is shown by experiments in which organisms were shielded from background (e.g., H. Planel et al., Health Phys. 52, 571, 1987) and in which organisms  were cultured in potassium with the K-40 depleted (T.D. Luckey, Radiat. Res. 108, 215, 1986).

Populations that live at the lowest levels of natural background radiation have higher cancer rates and shorter lifespans than populations that live in areas with moderate and high background radiation levels. 

 

The nuclear medicine pioneer, Rosalyn Yalow, Nobel Laureate in Physiology or Medicine, asserted:

No reproducible evidence exists of harmful effects from increases in background radiation three to ten times the usual levels.  There is no increase in leukemia or other cancers among American participants in nuclear testing, no increase in leukemia or thyroid cancer among medical patients receiving I-131 for diagnosis or treatment of hyperthyroidism, and no increase in lung cancer among non-smokers exposed to increased radon in the home. 

The association of radiation with the atomic bomb and with excessive regulatory and health physics ALARA practices [As Low As Reasonably Achievable] has created a climate of fear about the dangers of radiation at any level.  However there is no evidence that radiation exposures at the levels equivalent to medical usage are harmful.

The unjustified excessive concern with radiation at any level, however, precludes beneficial uses of radiation and radioactivity in medicine, science and industry.  (Mayo Clinic Proc 69:436-440, 1994)

Hugh F. Henry at Oak Ridge summarized the then known low dose research data in 1961 in the Journal of the American Medical Association:

A significant and growing amount of experimental information indicates that the overall effects of chronic exposure (at low levels) are not harmful…The preponderance of data better supports the hypothesis that low chronic exposures result in an increased longevity… Increased vitality at low exposures to materials that are markedly toxic at high exposures is a well-recognized phenomenon.  (JAMA 176, 27 May 1961)

The “Wingspread Conference” August 1-3, 1997, concluded:

In a surprise move, leading US and international scientific experts agreed in an historic accord that an increase in cancer has not been observed at radiation exposures below 10,000 millirem given to the whole body in a short time.

Prof. W.V. Mayneord, former member of UNSCEAR and ICRP, wrote:

I have always felt that the argument, because at higher values of dose an observed effect is proportional to dose, at very low doses there is necessarily some effect of dose, however small, is nonsense (Radiation and Health, p.140, 1964).

These and many other reports also establish that attributing damage where none exists can cause, and has caused, serious harm in a number of ways. 

Telling people who have received trivial doses of radiation working with radioactive materials, or from radon in their homes, or from mammograms and or medical procedures, has already caused untold damage and initiated extensive legal proceedings and damage compensation program based on false scientific premises. 

Attributing a special hazard to any hypothesized terrorist action that might involve radiation converts a relatively harmless situation into a potentially life-threatening panic and invites the very situation it claims to protect us from..

Robert Brent, in “Commentary on JAMA article by Hujoel et al.” in the current Health Physics (2005 Vol. 18, No. 4, pp. 379-381)  addresses the false premises  in the subject JAMA article (2004 Apr 28;291(16):1987-93) that applies the ICRP claim that even trivial radiation doses can be harmful in assessing the risk to the fetus of dental x-rays.  Brent states, correctly, that “the extensive animal and human literature refutes the claim of the authors…”  Brent deplores the harm caused by such premises. 

It will promote anxiety in the dental patient population, provide the news media with alarming information, and provide American trial lawyers with another area of litigation.

Such false claims are repeatedly made, demonstrating the high cost of presenting this false premise of harm as scientific fact, where none has been shown to exist.  It is disingenuous of ICRP to “see no particular reason” to refrain from promulgating such false premises.

 

The Harmful Fallacy of Collective Dose

 

Once one assumes that any small amount of radiation is harmful, then the concept of “Collective Dose” arises.  Small individual doses received by a large population are added up, and hundreds or even thousands of radiation-induced deaths are “predicted.”  So, radiation protection policy uses collective dose as a prime measure of the severity of a casualty, or the efficacy of “good plant operation.” Such use of collective dose has been repeatedly condemned as scientifically indefensible.  Yet current policy presumes that, in the absence of more data, this is the prudent course.   

NCRP-121 specifically warns that collective dose should not be used to predict death or injury from low-dose radiation:

The summation of trivial average risks over very large populations or time periods…has produced a distorted image of risk, completely out of perspective with risks accepted every day, both voluntarily and involuntarily.  (p.58)  

And again:

…it is recommended that regulatory limits not be set in terms of collective dose…When the uncertainty in the number of individuals …is large… collective dose should not be used as a surrogate for risk, even at relatively high levels of individual radiation dose. (p. 62)

And the Health Physics Society, in its March 1993 Position Statement, emphasized in bold-faced type:

We strongly recommend that dose limits be applied only (sic) to individual members of the public, not (sic) to the collective dose to population groups.

The French Academy of Medicine quoted and concurred with the above statement from NCRP-136, and stated in a press release 4 Dec 01:

[the Academy] associates with many international institutions to denounce improper utilization of the concept of the collective dose to this end. These procedures are without any scientific validity, even if they appear be convenient to administrative ends.

Zbigniew Jaworowski, MD, PhD, the noted member and former chair of UNSCEAR, wrote in “Radiation Risk and Ethics” (Physics Today, Sept 1999, 24-29) that use of collective dose:

…was introduced in the early 1960s…the concept is still widely used, although both the concept and the concern [about harmful hereditary effects] ought to have faded into oblivion by now…Individual doses cannot be additive over generations, simply because humans are mortal and the dose dies when an individual does.  Similarly, individual doses cannot be added for individuals of the same generation because we do not contaminate one another with a dose that we have absorbed…

If harm to the individual is trivial, then the total harm to members of his or her society over all past or future time must also be trivial—regardless of how many people are or will have been exposed.

 


 

Part 2 of 5

 

The Committee 1 Task Group Report explicitly establishes common purpose with the recent NCRP-136. NCRP-136 report uses the same methods to scientifically justify the LNT.  Our comments on that report apply equally to this report:.

NCRP Committee 1 has misrepresented the scientific data to support its false premise that low-dose radiation (LDR) might be harmful.

But the data say otherwise.  The Committee:

1.         Produced voluminous irrelevant and misleading data to support the linear no threshold (LNT) premise.

2.         Selectively misrepresented and obfuscated data that do provide highly statistically significant and consistent evidence of LDR benefits, and null dose-response effects, that contradict the LNT. 

3.         Failed to consider the voluminous scientific literature, submitted to them by the scientific community, including RSH, that consistently contradicts the unsupported LNT premise. 

 The NCRP’s position leads to extreme radiation protection policies requiring enormous public expenditures for no public health benefit. 

 

The C-1 Task Group Report promulgates false and misleading claims.   For example (p. 10 lines 2-6): 

There is some evidence of increased cancer risk associated with exposures on the order of 10 mGy… Also, the risk of mortality and morbidity from all solid cancers combined is proportional to radiation dose down to about 100 mGy, 

Results from few, unconfirmed, studies indicate harm in cases of very high, instantaneous, dose rates, in the range of 100 mGy.  This is primarily from the weak, unconfirmed, epidemiological study of the atomic bomb survivors, and the claims of damage to fetuses from moderate x-ray doses. 

However, hundreds of medical and biological research experiments consistently demonstrate that whole-body x-ray and gamma ray doses in the range of 5 to 500 mGy, that are extended over a minute or more, consistently stimulate positive biological responses.  These responses are shown to consistently cause medical and health benefits.  Somewhat higher doses have been used to consistently enhance immunological capability to successfully treat infections and inflammatory diseases.

These results have been demonstrated since the 1910s, although accurate doses at the applicable low doses were then not well defined.  However, such results have been confirmed thousands of times over the last 80+ years, with hundreds of experiments in recent decades, which apply current molecular biology, immunology, physiology and epidemiology to demonstrate stimulatory, generally beneficial, effects. 

For example, J.B. Murphy, in the Proceedings of the US National Academy of Sciences (PNAS) in 1920, in one of many reports by Murphy and others in the 1910s and ‘20s, in studies of immunology in preventing cancer, moderate doses of radiation were shown to suppress lymphocytes, which caused increases in cancers.  Increasing doses caused increasing suppression of lymphocytes, and increasing cancers.

However, at low doses, the lymphocytes were stimulated.  This caused DECREASES in cancers compared to unexposed controls – in one case, 96.5% ‘takes’ in controls from inoculations with cancer cells vs. 50% in the exposed groups, and another case, 75% in controls vs. 25% in exposed.

Such results have also been consistently reported and confirmed in recent decades.  E.g., studies by K. Sakamoto and colleagues demonstrated enhanced stimulation of mice and humans with doses in the 5 to 30 cGy range.  Hundreds of experiments by S.Z. Liu and colleagues have consistently produced equivalent results. [See examples in references below.]

The “data” on epidemiology and biology presented in this report (Chapters 2-5) reference many papers that are not relevant to the evaluation of the health risks of low-dose radiation.  Many describe in vitro studies that report results in cells that are not relevant to the dose response in immunologically whole organisms. 

Others address high-dose and high-dose-rate conditions.  But organisms respond totally differently than they do to low-dose irradiation. 

In addition; the report suppressed the thousands of relevant results of research that demonstrate and repeatedly confirm actual biological and epidemiology dose responses in whole organisms, which are conducted at relevant doses and dose rates.  See, for example, a few of the references to more extensive work by Ed Calabrese and colleagues.  These papers document the importance, the many studies, the consistent results, and the failure to adequately consider the research that addresses the relevant doses and sample sizes, and the appropriate animal models and human exposure data.

 

The TG Report also provides false premises.  For example, it states, (p. 10 lines 12-15):

The fundamental role of radiation-induced DNA damage in the induction of mutations and chromosome aberrations and the apparent critical involvement of aberrations and mutations in the pathogenesis of cancer provides a framework for the analysis of risks at low radiation doses and low dose rate exposures (Chapter 3).”

 

This premise has been repeatedly and consistently demonstrated to be false in recent decades. [See examples in references below] 

Direct and indirect radiation-induced DNA damage has been shown to be irrelevant in assessing radiation risk because, in the biology of immunologically whole organisms and animals, the amount of DNA damage from background radiation up to about 100 times background radiation levels is insignificant compared to the normal metabolic DNA damage rates, for both single and double strand breaks. 

This damaged DNA is continuously and consistently repaired, or in very few cases is not repaired.  However, this is a function of the damage control system, not of low radiation doses.  The chance that a radiation-damaged cell would progress to cancer remains an insignificant fraction of the normal quantity of damaged cells.  

Damage to the damage-control and repair systems are primarily due to high stress events and conditions. This does apply to high-dose-rate radiation among many other stressors.  Or it is due to reduced repair capacity caused by aging or other limitations in the organism from disease or genetic conditions. 

At high doses, the damage control and repair system are affected.  Specific genes and other response factors are stimulated to undertake “emergency repairs” which are error-prone.  This is the same as the toxic effect of essential nutrients at high doses.  Recent data demonstrate that there are different subsets of genes expressed than are stimulated by low radiation doses. 

At low doses, the organism delays cell cycles and initiates other factors to produce error-free repairs, and to eliminate damaged cells that strengthen the organism immunologically and physiologically. This is equivalent to essential nutrients, exercise, heat and other factors.

Of course, damage control fails to prevent damage in some instances, but a healthy organism or animal prevents such cells from affecting the organism by eliminating them (through apoptosis or necrosis) or preventing cell cycle progression to division.  Although such cells do occasionally “escape” such controls, there are an insignificant number of such damaged cells caused by radiation-induced damage from low doses (i.e., less than about 1 Gy) than from normal causes.

The above quoted TG Report statement further begs the issue of the known lack of the linkage between mutations and chromosome aberrations to cause cancer in its use of “apparent” as a qualifier.  In fact, there is no causal linkage beyond the equivalent traditional case that “galoshes cause colds.”  This is a misleading presentation to foster a perception to justify the LNT.  People in high natural background areas and occupationally exposed populations have shown increased mutations and aberrations with NO increase in cancers.

This false premise substantially misleads persons concerned about radiation protection to believe that a low dose of radiation can be hazardous in a linear relationship from high dose experience. It fails to reflect the fact that biology cannot have an adverse linear response to low doses of toxins or physical stressors such as heat and ionizing radiation to which whole organisms are normally exposed.  Such a condition would make life unsustainable.

In the case of radiation, it would indicate that life could not have succeeded in prehistoric times, when background radiation was much greater, and that high dose areas of the world would destroy or debilitate populations.  But in fact, people living in these areas do not have chronic illnesses or conditions. They are not deformed or short-lived. Their health conditions are consistently better where background radiation is higher. 

This is necessarily true when such stressors are essential to biological functions.  This is the case with radiation since “radiation protection” from background radiation to levels at and below low natural background levels, at roughly 1 mGy, has been shown by e.g., H. Planel and colleagues in Comptes Rendus in the 1960s-1980s, summarized in 1987 (Health Phys, 52:571-8), and many others to cause physiological debilitation in such organisms.

However, even with stressors that produce purely damaging insults, the biological response at the lowest doses that would cause a response is to initiate an “over-compensation” to the damage.  This results in a net increase in health and physiological conditions, not unlike the damage caused by “low to moderate doses” of physical exercise.

The fundamental response to radiation is not related to direct or indirect radiation-induced DNA damage.  The fundamental response to radiation is the biological stimulation of enzymes, genes, proteins, cytokines, and other biological control molecules and cells that constantly attempt to maintain optimum biological conditions. 

Any DNA damage from low and moderate radiation doses is completely incidental to the primary and highly significant biological response effects in immunologically whole organisms directly caused by low- and high-dose radiation exposure.

Just as Murphy showed in the PNAS in 1920 with the difference in low-dose and high-dose response of lymphocytes, current molecular biology has repeatedly shown and confirmed that there are completely different responses to high-dose and low-dose radiation exposures.  These conditions alone establish that there can be no “linear” response that provides a continuous response between these wholly different biological processes.  This is, in fact, consistent with the current biological knowledge that demonstrates that bi-phasic responses are the default condition in biology, physiology and health.

Recent studies have shown that there are substantially different sets of genes and other molecules that are stimulated at high-doses vs. low-doses; in addition to specific genes, enzymes and other factors that respond in completely opposite directions (either stimulation or suppression) when doses at moderate dose-rates are higher or lower than a dose in the range of 20-50 cGy.  These differences are equivalent to the stimulation vs. the suppression of lymphocytes shown by Murphy in the 1920 PNAS report, and in hundreds of studies since.  This includes the successful treatment of infections, etc., before the advent of antibiotics and other drugs that were favored by the commercial medical establishment and government agencies. 

This is similar to (and anticipates) the current Codex effort to ignore evidence of the health benefits of vitamins and minerals and nutritional supplements.  These initiatives will similarly constrain access to these supplements in favor of dispensing by medically-controlled prescription at high cost, and to limit quantities to “minimum daily requirements” which are generally considered to be less than adequate to stimulate immunological and physiological conditions that are known to prevent disease and recover health.

 

In addition, the Task Group Report uses the results of many in vitro studies to claim that their response supports the justification of a linear dose-response for cancer and other adverse health effects. 

Cells in culture do not have the immunological functions and cellular repair capacities of immunologically whole organisms.  Therefore, their response to radiation doses does not reflect the response of living organisms.

There are dozens, if not hundreds, of factual errors and misrepresentations that could, and should, be addressed with specific applicable contradictory scientific references that have not been included in the report. But this cannot be achieved in this limited context.

It is also useful to consider that there are hundreds of active scientists that have published the current literature that contradict the results and conclusions contained in this report.  Despite the hundreds of such papers in mainstream radiobiology and other major biology and medicine journals, they have chosen NOT to comment on this report. 

It is reasonable that they see this report as having no interest in addressing the relevant science.  It is seen instead, as with the NCRP-136 Report, a biased exercise to rationalize and fabricate support for the LNT; and that questioning this mandate may be hazardous to their government-supported research and institutions.  It may be seen as “trying to teach a pig to sing.”  It is not only a waste of time, it annoys the pig.

 


 

Part 3 of 5

Comments on ICRP’s
Proposed New Radiation Regulation Guidelines

 

The ICRP report will be considered by many people to be the ultimate authoritative judgment of the international scientific community on the matters it discusses.  It is important to recognize that this is simply not true.  ICRP reports express the opinions of a self-selected group of radiation protection specialists whose scientific judgment differs markedly from mainstream biologists and medical researchers.  It is neither appropriate nor necessary to speculate as to the biases or agendas of the ICRP committee members.  But it is vitally necessary to view the conclusions of the ICRP reports in light of relevant research findings and conclusions of the broader scientific community.  Our comments are presented in that context. 

It is also pertinent to note that ICRP has no competence or responsibility to consider the practical or economic impact of its recommendations.  When it concludes that “The LNT hypothesis…remains a prudent basis for radiation protection” we should note that this sentence is preceded, not by a statement that this conclusion is derived from the scientific evidence, but by the casual rationale that “there seems to be no particular reason to factor the possibility of a threshold into risk calculations for purposes of radiation protection.”   That is an opinion that calls for input from outside the expertise of the ICRP.

Moreover, the question of whether or where to apply a threshold is less important than the need to repudiate the false idea, now being promulgated as official scientific truth that even the tiniest amount of radiation poses a threat that must be reduced if at all possible.  ICRP tells us its mission is to create a mindset that makes us ask of every radiation exposure, “Have I done all that I reasonably can to reduce these doses?”   That question puts radiation reduction, which it misleadingly calls “optimization,” ahead of public health and safety.  We should not concur in that mission.

 

ICRP-2005 is Harmful and Unnecessary Step Backwards

The proposed ICRP 2005 document is ill-advised and harmful, both in concept and detail.  It makes no mention of the vast amount of literature that shows, to quote NCRP-136, “it is important to note that the rates of cancer in most populations exposed to low-level radiation have not been found to be detectably increased, and that in most cases the rates have appeared to be decreased.”  Supporting data for this statement have been published in the professional literature and presented repeatedly to various regulatory bodies.  See, for example, http://www.radscihealth.org/RSH/docs  

Perhaps mindful of this fact, ICRP drops all previous effort to justify its requirements on the basis of risk.  In fact, it offers little justification at all for extending its regulatory arm down to a fraction of a percent of natural background.

It concedes that “there is no major problem identified with the practical use of the present system of protection in normal situations.”  Despite this fact, the report virtually scraps all previous guidance and proposes a new system, based on new principles, with new terminology and more complex and more burdensome requirements.  No justification is given for these changes

It disguises the concept of ALARA by calling it “optimization,”  stating that ICRP’s mission is to create a state of mind that looks at every radiation exposure situation with the question: “Have I done all that I reasonably can to reduce these doses?”  Since radiation dose generally results from people attending to operations and equipment in a radiation zone, a regulatory incentive to minimize such critically important safety functions actually works against safety without producing any health benefit. We have many examples of this.

ICRP’s phobic attitude toward radiation is shown by its continued insistence on treating even natural radiation as a hazard, requiring that natural radiation be regulated when it is considered “controllable” (e.g. radon and mill tailings) while ignoring even higher doses (e.g. airplane passengers; dwellers in, or visitors to, high natural radiation areas; medical therapy) that, for the present, it calls “uncontrollable.” 

The report warns against misuse of collective dose, but then sets up requirements that will inevitably increase its use in falsely “predicting” thousands of deaths were none would realistically be expected.  This is particularly harmful in dealing with emergencies, where a minor event can be made into a life-threatening panic, and rescue workers prevented by unwarranted fear of radiation from doing their duty.

As a final insult to science and common sense, the report suggests that regulatory authorities set even lower values “but probably not by as much as a factor of ten.”  This is after suggesting that where there may be multiple dominant sources, still further restraints are advised.

The report also recommends that a vast new research program be set up to determine the effects of low-dose radiation on all non-human species, which would lead to waste of public resources and even further constraints on our use of technologies involving radiation.

We strongly recommend that this entire report be rejected out of hand.  It is a scientific embarrassment and a harmful and unnecessary assault on all beneficial uses of radiological technologies.

 

Recommendations

All that is really needed is to clarify current regulations by adding a statement such as “Doses below 50 or 100 mSv/year are not harmful and may be beneficial.  ALARA below those levels serves no useful purpose and can be detrimental.” 

Merely setting a threshold radiation dose is not enough.  It is important to repudiate the false dogma that a single gamma ray can kill.  Nearly every responsible organization writing on radiation protection—the UK NRPB, the US NCRP, the Health Physics Society, the American Nuclear Society, the French Academies of Medicine and of Science—all have stated that in the presence of a large and widely varying natural radiation background, it is clearly absurd to argue that even the tiniest increase in radiation dose will cause a numerically predictable increase in cancer and death, and must be avoided.  Yet this repudiated argument is what we are asked to accept in ICRP-2005.  That argument is at the root of the radiophobia that blocks rational discussion of radiation protection.  It must be squarely faced and publicly be put to rest.

In addition, the concept of collective dose itself must be repudiated.  Amending current regulations to add a phrase such as: “Collective dose should not be used as a measure of excellence in radiation protection, nor should it be used to predict detrimental effects such as illness or death.  The only meaningful doses are those to individuals.”  The Chairman of the ICRP, Roger Clarke, has often asserted unambiguously (e.g., 1 Oct 98 at http://hps.org/documents/controllable.pdf) : 

If the risk of harm to the health of the most exposed individual is trivial, then the total risk is trivial—irrespective of how many people are exposed.

It is essential that this important principle be made crystal clear in all relevant regulations, standards and practices.

 


 

Part 4 of 5 – References 1

 

Comprehensive assessments of the scientific literature and current biology refute the biased misrepresentation of selected “facts” and the suppression of valid data provided in the Task Group report.  For example:

 

Calabrese, E.J. (2005). “Hormetic Dose-Response Relationships in Immunology: Occurrence, Quantitative Features of the Dose Response, Mechanistic Foundations, and Clinical Implications,” Critical Reviews in Toxicology, 35:89–295. [207 pages]

   Immune-system-related biphasic dose-responses occur extensively, with over 90 different immune response-related endpoints, induced by over 70 endogenous agonists, over 100 drugs, and over 40 environmental contaminants, including radiation, reported in over 30 animal models, over a dozen mammalian and human cell lines. Immune-system-related hormetic-like biphasic dose-response relationships are common and highly generalizable. These findings were generally recognized and explicitly discussed by the original authors, often with consideration given to possible mechanistic foundations as well as numerous clinical implications. Despite this recognition, the overall widespread nature of immune-related hormetic responses has been only little appreciated, with a general lack of insight into the highly generalizable nature of this phenomenon as well as the complex regulatory networks affecting biological switching mechanisms that result in the hormetic responses.

 

Calabrese, E. J. and R. Blain (2005). "The occurrence of hormetic dose responses in the toxicological literature, the hormesis database: an overview." Toxicol Appl Pharmacol 202(3): 289-301.

   This database of studies includes ~5600 dose-responses satisfying criteria for hormesis of over 900 agents, of which radionuclides/radiation constitute 29% of the results.  Hormetic dose-response occurs in animal models in all age groups, across species, with a broad range of toxic susceptibilities, in plants, viruses, bacteria, fungi, insects, fish, birds, rodents, and primates, including humans. Endpoints include growth, longevity, metabolic parameters, disease incidences (including cancer), performance endpoints such as cognitive functions, immune responses, and others. Quantitative strength of the evidence supporting hormesis is based on study design, magnitude of the response, statistical significance, and reproducibility. Comprehensive biology/toxicology evidence shows hormesis to be the biological default condition.

 

Calabrese, E. J. (2004). "Hormesis: from marginalization to mainstream: a case for hormesis as the default dose-response model in risk assessment." Toxicol Appl Pharmacol 197(2): 125-36.

 

Calabrese, E. J. (2004). "Hormesis: a revolution in toxicology, risk assessment and medicine." EMBO Rep 5 Spec No: S37-40.

 

Calabrese, E. J. (2004). "Hormesis--basic, generalizable, central to toxicology and a method to improve the risk-assessment process." Int J Occup Environ Health 10(4): 466-7.

 

Calabrese, E. J. and L. A. Baldwin (2003). "The hormetic dose-response model is more common than the threshold model in toxicology." Toxicol Sci 71(2): 246-50.

 

Calabrese, E. J. and L. A. Baldwin (2003). "Toxicology rethinks its central belief." Nature 421(6924): 691-2.

 

Calabrese, E. J. and L. A. Baldwin (2003). "HORMESIS: The Dose-Response Revolution." Annu Rev Pharmacol Toxicol 43: 175-97.

 

Calabrese, E. J. and L. A. Baldwin (2002). "Applications of hormesis in toxicology, risk assessment and chemotherapeutics." Trends Pharmacol Sci 23(7): 331-7.

   “…in properly designed studies the U-shaped hormetic response predominates and is more fundamental.”

 

Calabrese, E. J. and L. A. Baldwin (2002). "Radiation Hormesis and Cancer." Human and Ecological Risk Assessment 8(2): 327-353.

   Data on radiation hormesis and cancer exist consistent with and/or supportive of radiation hormesis. Biomedical research provides mechanistic insight: low dose exposures activate immune functions to prevent tumor development and metastasis; low doses of radiation reduce mutagenic responses and induce endogenous antioxidant responses. This is consistent with epidemiological data showing inverse relationships between background radiation and cancer incidence, and with occupational epidemiological investigations in which low-dose exposure groups display markedly lower standardized mortality rates (in excess of the “healthy worker effect”) than controls.

 

Calabrese, E. J. and L. A. Baldwin (2001). "Hormesis: U-shaped dose responses and their centrality in toxicology." Trends Pharmacol Sci 22(6): 285-91.

   The fundamental nature of the dose-response is neither linear or threshold, but rather U-shaped. When studies are properly designed to evaluate biological activity below the traditional toxicological threshold, low-dose stimulatory responses are observed with high frequency and display specific quantitative features. …mechanistic evidence indicates that hormetic effects represent overcompensation in response to disruptions in homeostasis that are mediated by agonist concentration gradients with different affinities for stimulatory and inhibitory regulatory pathways.

 

Calabrese, E. J. and L. A. Baldwin (2001). "Hormesis: A generalizable and unifying hypothesis." Critical Reviews in Toxicology 31(4-5): 353-424.

 

Calabrese, E. J. and L. A. Baldwin (1999). "The marginalization of hormesis." Toxicologic Pathology 27(2): 187-194.

 

Calabrese, E. J., L. A. Baldwin, et al. (1999). "Hormesis: a highly generalizable and reproducible phenomenon with important implications for risk assessment." Risk Anal 19(2): 261-81.

 

Calabrese, E. J. and L. A. Baldwin (1998). "Hormesis as a biological hypothesis." Environmental Health Perspectives 106(Suppl 1): 357-62.

 

Calabrese, E. J. (1999). "Evidence that hormesis represents an "overcompensation" response to a disruption in homeostasis." Ecotoxicology and Environmental Safety 42(2): 135-137.

 

Liu, S. Z. (2003). "On radiation hormesis expressed in the immune system." Crit Rev Toxicol 33(3-4): 431-41.

   For mouse and human T lymphocyte functions in the dose range of 0.01 to 10 Gy a J or inverted J-shaped curve is usually observed. The cellular and molecular mechanisms of the enhancement of immunity induced by low-dose radiation are analyzed on the basis of literature published in the last decade of the past century. Intercellular reactions among the APCs and lymphocytes via distinct changes in expression of relevant surface molecules and secretion of regulatory cytokines in response to different doses of radiation were described. The major signal transduction pathways activated in response to these intercellular reactions were illustrated. The suppressive effect of low-dose radiation on cancer induction, growth, and metastasis and its immunologic mechanisms were analyzed. The present status of research in this field gives strong support to radiation hormesis in immunity with low-dose radiation as one of the mechanisms of cancer surveillance.

 

Tubiana, M. (2000). "Radiation risks in perspective: radiation-induced cancer among cancer risks." Radiat Environ Biophys 39(1): 3-16.

   …the use of the linear no threshold (LNT) hypothesis… gives credence to the concept that even the smallest doses are harmful. There are a number of scientific and epidemiological data currently under debate that are not consistent with the LNT hypothesis. For example, no difference in the incidence of cancers or of birth defects has been observed between regions with low or high natural irradiation.

 

Jaworowski, Z. (1995) “Stimulating effects of ionizing radiation: New issues for regulatory policy, Regulatory Toxicology and Pharmacology,” 22:2.

   UNSCEAR 1994 concentrates on the elucidation of mechanism by which radiation hormesis acts at the level of cell control systems such as protein synthesis, gene activation, DNA repair, stress-response protein production, radical detoxification, activation of membrane receptors, proliferation of splenocytes, and stimulation of the immune system.

 

Townsend, J.F. and Luckey, T.D. (1960) “Hormologosis in pharmacology,” J. Am. Med. Assoc., 173: pp44-48.

   While studying fermentation in milk, Richert (1906) noted that heavy metals were stimulatory at concentrations lower than those which gave the harmful "oligodynamic action." Schulz (1888) and Branham (1929) have shown that most of the classic bactericidal agents exhibit hormesis in yeast. Antibiotics frequently cause a zone of accelerated growth in bacteriological assay work. Garrod's evidence (1951) indicates that this may have a direct effect on the cells. The antibiotic growth stimulation of laboratory and farm animals has recently been reviewed in full (Luckey 1959a).

   Since pharmacology is the department of medicine which deals most directly with such chemical effects on cells and tissues, a survey of hormetics is appropriate in this field. From the generalized viewpoint of hormology, a study of the action of a variety of drugs in animal systems may add further evidence to the validity of the thesis and illustrate a common denominator in drug action. Goodman and Gilman (1955) recognize the phenomenon of hormesis as being of a general nature as is shown by the following statement: 'Quinine affects such a large variety of biological systems that it has been called a general protoplasmic poison; with some reservations this appraisal is probably correct. Like many other poisons of this sort, it may stimulate in low concentrations but depress in higher concentrations.'

   A possible mechanism of action at the cellular level has been suggested (Luckey 1959b) as follows:  The stimulation reflects limitations in the ability of the organism to equate or modulate its response to a given stimulus at the lowest threshold of perception. If we assume that the response involves a chemical reaction, then the response of the organism is a unit (discontinuous) response, in which the lowest possible reaction would require one or more molecules to be changed. The release of an enzyme, proenzyme, hormone, or ribonucleic acid information molecule could quickly change the internal character of cells. The minimum response is an apparent overcompensation at the sensing threshold of the organism.

   The complexities of higher organisms lead to interactions between different cells and tissues. This allows a more complex reaction mechanism to be visualized. In spite of this, the over-all patterns of response are similar to those seen with micro-organisms. Irrespective of mechanism, common denominators evidently exist in the response of organisms to drugs at the threshold of perception and response levels.

   The fact that so many apparently unrelated stimuli produce the same general response (for example, stimulation followed by depression) at least suggests that there are a few fundamental processes by which the cell responds to all such stimuli rather than myriad processes by which it responds to a wide variety of compounds. The complete pattern of drug response patterns should be known. Demonstration of the uniformity of response in the face of diversity of stimulation ...should point the way to a better understanding of drug action and allow some generalization in basic cellular physiology.

 


 

Part 5 of 5 - References 2

 

These references are a few examples of studies that consistently find and confirm that low dose radiation stimulates immune functions, and reduces cancer incidence.

 

Liu, S.Z. (1997), “Cellular and molecular basis of the stimulators effect of low dose radiation on immunity,” In: Wei, L., Sugahara, T. and Tao, Z., High Levels of Natural Radiation 1996: Radiation Dose and Health Effects, Beijing, Elsevier, pp341-353. 

   It has been observed in human populations and animal studies that low dose radiation (LDR) could stimulate the immunological responses.  The up-regulation of immunity following LDR involves a series of cellular and molecular reactions as well as their systemic regulation.  The studies in our laboratory and elsewhere in recent years have convinced us that whole-body irradiation (WBI) with X- and gamma-rays in the dose range within 0.2 Gy has definite positive effect on the immune system which can be considered as beneficial to the organism.

 

Liu, S.Z., Liu, W.H. and Sun, J.B. (1987) “Radiation hormesis: its expression in the immune system,” Health Phys 52:pp579-583.

   The effects of low-dose single and continuous whole-body irradiation on immune functions were studied in C57BL/6 mice. Plaque-forming cell reaction of the spleen was found to be stimulated by single doses of x rays in the range of 0.025 to 0.075 Gy and by continuous exposure to gamma rays with a cumulative dose of 0.065 Gy. The reactivity of thymocytes to interleukin 1 showed a dose-dependent depression in the dose range of 0.025 to 0.25 Gy, but there was an increase in cell number in the thymus between doses of 0.025 and 0.10 Gy, resulting in enhancement of reaction of the whole organ. Unscheduled DNA synthesis of spleen cells was stimulated by single irradiation with 0.05 Gy and continuous irradiation with a cumulative dose of 0.13 Gy. The implications of these immunologic changes under low-dose radiation are discussed."

 

Kojima, S., K. Nakayama, et al. (2004). "Low dose gamma-rays activate immune functions via induction of glutathione and delay tumor growth." J Radiat Res (Tokyo) 45(1): 33-9.

    …immune functions were enhanced through the induction of cellular glutathione after low-dose irradiation …in Ehrlich solid tumor-bearing mice. Tumor growth after inoculation was significantly delayed by the radiation.

 

Kojima, S., H. Ishida, et al. (2002). "Elevation of glutathione induced by low-dose gamma rays and its involvement in increased natural killer activity." Radiat Res 157(3): 275-80.

 

Kojima, S., S. Matsumori, et al. (2000). "Possible role of elevation of glutathione in the acquisition of enhanced proliferation of mouse splenocytes exposed to small-dose gamma- rays." Int J Radiat Biol 76(12): 1641-7.

   The glutathione level in mouse splenocytes increased 2 h after whole-body gamma-ray irradiation at 50 cGy… is at least partially responsible for the enhancement of immune function, and may throw light on the mechanisms of carcinostatic effects induced by low dose ionizing radiation.

 

Takahashi, M., S. Kojima, et al. (2000). "Prevention of Type I Diabetes by Low-Dose Gamma Irradiation in NOD Mice." Radiation Research 154: 680-685.

 

Kojima, S., S. Matsumori, et al. (1999). "Elevation of glutathione in RAW 264.7 cells by low-dose gamma-ray irradiation and its responsibility for the appearance of radioresistance." Anticancer Res 19(6B): 5271-5.

 

Mitchel, R. E., J. S. Jackson, et al. (2003). "Low doses of radiation increase the latency of spontaneous lymphomas and spinal osteosarcomas in cancer-prone, radiation-sensitive Trp53 heterozygous mice." Radiat Res 159(3): 320-7.

 

Safwat, A., N. Aggerholm, et al. (2003). "Low-dose total body irradiation augments the therapeutic effect of interleukin-2 in a mouse model for metastatic malignant melanoma." J Exp Ther Oncol 3(4): 161-8.

 

Safwat, A. (2000). "The role of low-dose total body irradiation in treatment of non-Hodgkin's lymphoma: a new look at an old method,." Radiother. Oncol. 56(1): 1-8.

 

Smirnova, O. A. and M. Yonezawa (2003). "Radioprotection effect of low level preirradiation on mammals: modeling and experimental investigations." Health Phys 85(2): 150-8.

 

Yamaoka, K., S. Kojima, et al. (2000). "Inhibitory effects of post low dose gamma-ray irradiation on ferric- nitrilotriacetate-induced mice liver damage." Free Radic Res 32(3): 213-21.

   A single post whole-body low-dose irradiation (50 cGy of gamma-ray) on mice with …induced transient hepatopathy…accelerated the rate of recovery… This may be because of the enhancement of antioxidant agents such as total glutathione (GSH + GSSG), glutathione peroxidase (GPX), glutathione reductase (GR) and gamma-glutamylcysteine synthetase (gamma-GCS) by low-dose irradiation. These findings suggest that low-dose irradiation relieved functional disorders at least in the livers of mice with active oxygen species related diseases.

 

Yamaoka, K. and Y. Komoto (1996). "Experimental study of alleviation of hypertension, diabetes and pain by radon inhalation." Physiol Chem Phys Med NMR 28(1): 1-5.

 

Ohnishi, T. (1997). “The induction of a tumor suppressor gene (p53) expression by low-dose radiation and its biological meaning,”. Low Doses of Ionizing Radiation: Biological Effects and Regulatory Control: 406-409.

 

Shen, R. N., L. Lu, et al. (1997). "Murine AIDS cured by low dosage total body irradiation." Adv Exp Med Biol 407: 451-8.

 

Shen, R. N., L. Lu, et al. (1996). "Curative effect of split low dosage total-body irradiation on murine AIDS induced by Friend virus: the results and the possible mechanism." In Vivo 10(2): 191-9.

 

Shen, R. N., L. Lu, et al. (1991). "Effect of split low dose total body irradiation on SFFV mRNA, genomic DNA and protein expression in mice infected with the Friend virus complex." Leukemia 5(3): 225-9.

   DBA/2 mice infected with lethal dosages of Friend virus complex (FVC) can be 100% cured by split-dose total body irradiation (TBI) at 150 cGy, an effect associated with the restoration of the cellular immunity which is compromised by the virus.

 

Shen, R. N., L. Lu, et al. (1991). "Cure with low-dose total-body irradiation of the hematological disorder induced in mice with the Friend virus: possible mechanism involving interferon-gamma and interleukin-2." Lymphokine Cytokine Res 10(1-2): 105-9.

 

Shen, R. N., N. B. Hornback, et al. (1988). "Curative effect of split low dosage total-body irradiation on mice infected with the polycythemia-inducing strain of the Friend virus complex." Cancer Res 48(9): 2399-403.

   All FVC-P injected mice were dead within 40 days; however, infected mice receiving TBI on days 5 and 12 exhibited long- term survival. FVC-P-injected mice receiving TBI treatment on days 5 and 12 had normal leukocyte counts, normal spleen weights, and no detectable spleen focus-forming virus. Although the FVC-P-infected mice had decreased proportions of L3T4+ cells and increased proportions of Lyt-2+ cells, these were returned to normal following TBI treatment. …The inability of in vitro irradiation doses of up to 1000 cGy to inactivate FVC-P which was subsequently injected into murine hosts suggests that the effectiveness of the TBI treatment in vivo is not due to a direct radiation effect on the virus.

 

Miyamoto, M. and K. Sakamoto (1987). "Anti-tumor effect of total body irradiation of low doses on WHT/Ht Mice." Jap. J. Cancer Clin. 33(10): 1211-1220.

 

Sakamoto, K. and M. Miyamoto (1987). "Tumor control effect by total body irradiation,." Oncologia, 20(2): 86.