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Excerpts from: Some Non-scientific Influences On Radiation Protection Standards And Practice

by Laursiton S. Taylor

[The original article appeared in Health Physics 1980; 32, pp 851-874. The excerpts were chosen by John Cameron with verbal approval from the author.]

I. Introduction:
Today, we know all we need to know to adequately protect ourselves from ionizing radiation. What is the problem and why is there one? [The problem] is not a scientific one. Rather, it is a philosophical problem...Or perhaps it may be a political problem ... or perhaps the problem may not be as much protecting ourselves against radiation as protecting us against ourselves. I shall mention, at least briefly, several non-scientific factors which may influence protection practices .... and thus, in turn, influence the setting of our numerical protection standards.

II. Biological Effects of Radiation:
Collectively there exists a vast array of facts and general knowledge about ionizing radiation effects on animal and man. ... the depth and extent of this knowledge are unmatched by any of the myriads of other toxic agents known to man. .... the public has come to expect sharp, clear, definitive, and undisputed answers to any questions involving radiation. This leads to the difficulty that when there is ... disagreement among scientists the public feels ... let down .. by the scientific community. A good example is the current so-called "controversy" ... centering around the effects of radiation delivered in low doses at low dose rates. Radiation effects are generally proportional to dose when delivered acutely in moderate amounts, say 100 rads and upwards. Precise proportionality is difficult to establish. The problem becomes especially critical in the low dose region say below 25 or 50 rads, delivered acutely, for which the latent period may be three or even four or more decades. During that long a period any individual would be subjected to hundreds of other insults, any number of which might produce the same effect as the radiation. There is uncertainty about the existence of threshold effects for ionizing radiation. There are very few threshold effects, although there are clearly some.

If one is concerned about the degree of hazard in the region where effects cannot be found or identified, to what extent should an attempt be made to further "reduce the hazard" to some fraction of what could not be found in the first place? The question is "how large is half of something that cannot be measured?"

Today we know enough about dose-effect relationships to state unequivocally that at least for low-LET (Linear Energy Transfer = dE/dx) radiations the relationships cannot be strictly linear over the whole dose range and that even for high doses they are probably not linear.

The difficulty is that since we do not know the precise relationship - it is assumed as a matter of cautious procedure, that the dose-effect relationships are linear throughout the entire dose range. This assumption -- taken too literally -- may lead to unnecessary and unjustifiable restrictions on the use of ionizing radiation. From the mere fact that radiation may cause some identifiable effect, it does not follow that the effects are necessarily detrimental.

III. Non-Scientific Aspects Of Radiation Protection:
In the late 1940's it was clear to the NCRP (National Council on Radiation Protection and Measurements), and probably to other bodies, that non-scientific factors would be involved in permissible dose standards. Why are people willing to accept any risk at all? This argument applies to practically everything we do in life, with radiation being perhaps one of the smallest risks that we normally have to contend with.
The past supply of wisdom has come mostly from the scientists themselves, who consciously, or unconsciously, recognizing the limits of their knowledge, have made strong and important judgment actions regarding their knowledge and the amount of radiation considered to be acceptable for radiation workers or the public or the patient.

No one has been identifiably injured by radiation while working within the first numerical standards set by the NCRP and the ICRP (International Commission on Radiological Protection) in 1934. The theories about people being injured have still not led to the demonstration of injury and, if considered as facts by some, must only be looked upon as figments of the imagination.

a. Politics:
From about 1946 to 1977, practically all federal matters in the United States relating to ionizing radiation were handled through the Joint Committee on Atomic Energy. The joint committee, with a stable membership from both the House and the Senate, was dedicated to developing facts and an understanding of atomic energy, rather than looking for newspaper headlines and votes.

Now, in its place there are some two dozen congressional committees, lacking in stability and without an overview power. Rarely does the chairman or staff of these committees have any knowledge in depth of the broad subject of ionizing radiation.

In spite of technical shortcomings in the political arena, both federal and state legislatures exert strong influences on the development of numerical radiation protection standards. Because of the likely influence on governmental committees by vocal but prejudiced witnesses or witnesses having some personal case to plead, we are today faced with the possibility of unreasonably restrictive limitations being placed on legitimate uses of ionizing radiation.

b. The Media:
One of the first political needs we must always recognize in dealing with groups of people is education. The prime agents of education (outside of formal schools) in these times are the radio-television, newspapers, comic books, books generally and books written by scientists. Of these, the "news media" clearly dominate, and here lies one of our most critical problems and the most fruitful area in which the radiation protectionist must assist in the education of the public. First, however, we have to persuade the media (and I use the term rather broadly now) that they have a national obligation to assist the country in educating its public about radiation matters.

Attacks on the news media for one reason or another are common as is their own defense under the First Amendment. However, in my opinion, the First Amendment .. is an essential bulwark of freedom....[but] the First Amendment also carries with it an obligation on the part of the press to completely and properly report the news.
In the case of ionizing radiation .... there are constant and continuous violations of this principle... The fact remains that we need greater responsibility on the part of the news media in the objective presentation of uneditorialized news.

c. Laws and Regulations:
There are at least fourteen agencies of which six have regulatory responsibilities. Six have research and development responsibilities and three have advisory roles. In the legislative branch of the government, there may be some twenty-four House or Senate committees playing some role in radiation matters (the exact identification of these is not easy).

d. Economics:
There is constant pressure to lower protective standards by some radiation protectionists as well as "consumer advocates" and generally concerned members of the public. Too often their arguments are based mainly on theoretical arguments of effects that have never been observed .... So this is a case of reducing by some factor something that you did not know in the first place. If someone were today to decide on a reasonable de minimis level for radiation exposure, it would probably be found that most of our radiation installations are already well below it.

e. Education:
We need two things: (1) better communication within and between scientific and technical groups on the one hand, and the general public on the other; and (2) much broader education of information to the public. These communication and educational projects should be carried out basically by non-governmental organizations, aided and assisted, however, by some limited government support. In the matter of communication, the radiation protectionist profession must play a stronger role ...

It is my belief that much of the blame for the public's fears and apprehensions with respect to radiation matters are due to our media. There is another criticism that must be directed to the media, namely, their constant use of a small number of individuals who are clearly out of step with the radiation protection community. In the U.S. alone there are some 3500 health physicists and 1800 radiological physicists. Yet the media will, for some newly breaking news story, seek out some of a half a dozen individuals who are willing to make willfully deceptive statements regarding radiation.

f. Scare Books and Articles:
Of a collection of "popular" books published over the last decade or so dealing with radiation matters there is not a single one which is not riddled with half-truths, untruths, and evidence of basic lack of knowledge of nuclear energy or radiation. ... another insidious practice designed to keep the public alarmed about radiation matters .... the constant linkage made between the atomic bomb and any discussions about radiation, including medical and industrial applications.

I plead that we cease the seemingly endless procession of studies, congressional committees, and hearings on the problem of "low level ionizing radiation" .. About this we know what we know and we know what we do not know; there is reasonable and rational agreement as to the degree of disagreement. Either we forget the whole "problem" or we theorize or postulate a dose-effect relationship.

However, .... these technical concepts have been grasped by the press, by the congress, by some government agencies, and hence by the public as established facts, rather than as the scientific ruminations, which they are.
Somehow, we as radiation protectionists must develop an unassailable counter force against such misguided actions as outlined above. This counter force should act with such strength and integrity and persistence as to compel public attention and respect.

John Cameron is an emeritus professor at the University of Wisconsin

jrcamero@facstaff.wisc.edu

Can Low Level Radiation Protect Against Cancer?

Ludwig E. Feinendegen, Victor P. Bond, Charles A. Sondhaus.

Abstract
Effects of ionizing radiation in living tissues are generally viewed in terms of damage. However, low doses of ionizing radiation also cause changes in normal intra- and extracellular signaling, with potentially beneficial consequences.

Cellular signaling is triggered in part by reactive oxygen compounds and may result in the protection of cells against molecular damage, especially that to DNA. As shown in various rodent and human cell systems, radiation induced protective mechanisms serve the cell to defend against, repair, and remove damage to cells. Most of this damage comes from oxidative byproducts of normal metabolism. Only a relatively small fraction of the damage in tissues is caused by ionizing radiation, even at many times the dose from normal background radiation.

Protective responses in various cell systems increase initially with dose up to about 0.1 - 0.2 Gy and then decrease and disappear. These responses are analyzed here in microdosimetric terms. The result contradicts in principle the linear nothreshold (LNT) hypothesis for radiation carcinogenesis. In fact, the incidence of spontaneous cancer may decrease at radiation doses below about 0.1 - 0.2 Gy. This is compatible with epidemiological data.

Introduction
The risk RE of detrimental effects such as cancer induction from exposure of multicellular tissues to low doses of ionizing radiation is conventionally assumed to be proportional to the absorbed dose[21] D: R = alpha D (1) The expression in equation (1) formalizes the "linear nothreshold" (LNT) hypothesis. It states that even the smallest dose of radiation has a risk of causing cancer. The proportionality constant alpha has the dimension of inverse dose, Gy^-1 and is assumed to be of the order of 10^-4 Gy^-1 for cancer in human tissues exposed to low LET radiation. The average dose from background radiation at sea level is about 2 mGy per year.
This paper analyses various effects of ionizing radiation in living tissues [15], and uses published data on low dose responses of tissues and cells in rodents and humans. The conclusions of this analysis contradict the LNT hypothesis. Living tissue is a nonlinear dynamic system, for which it would indeed be strange if such a simple expression of linearity were true over several orders of magnitude of dose.

Absorbed Dose to Tissue (Macrodose) and to Cells (Microdose)
The absorbed dose D expresses energy/mass. In a macroscopic sense, the SI unit of dose is the gray, Gy, where 1 Gy = 1 J/kg. It has the convenience of being easily measured. However, at low values this macroscopic dose is inappropriate for estimating risk at the cellular level where cancer is induced. Thus, absorbed doses to individual cells, or microdoses, need to be considered.

Ionizing radiation is absorbed in matter by the deposition of discrete amounts of energy along the tracks of charged particles that arise throughout the exposed matter [22]. The amount of energy absorbed from such tracks in a defined microvolume of tissue is here called a microdose. The microvolume of tissue is here taken to have the mass of a typical mammalian cell, 1 ng [3, 8, 12, 16, 28]. The mean microdose from a single interaction is calculated from the frequency of track events, or hits, in the defined micromass. Its value, z1, also called mean specific energy [22], hit-size or cell-dose, is a constant for a given type of radiation. For example, the z1 from 100 kV x-rays is about 1 mGy. According to microdosimetry theory [22], the tissue-absorbed dose D is equal to the product of z1 and N_H/N_e with N_H being the number of hits of any size, and N_e the number of exposed micromasses:

D = z1 (N_H/N_e) (2)

For the same macrodose from any type of radiation, N_H/N_e and z1 are reciprocally related. That is, for as given dose D of high LET radiation the average microdose z1 is proportionately greater and there are fewer hits for the same D than from low LET radiation. Substituting equation (2) into equation (1) gives

RE = alpha . z1 . (N_H/N_e),

and with RE being equal to the measured number of cancerous tumors N_q induced in the exposed tissue composed of _e cell-equivalent micromasses:[4]

N_q/N_e= alpha z1 (N_H/N_e)

This is known as the hit-number-effectiveness-function [4]. Multiplying each side of this equation by_ Ne yields:

N_q = alpha . z1 . N_H. (3)

Note that if the LNT hypothesis is correct, the proportionality constant alpha has the same value from equation 1 to 3.

The Meaning of Dose Rate
It has long been known that effects in irradiated living tissues depend on the rate at which the dose is absorbed. In microdose terms, the macrodose rate, Gy/unit time, allows one to determine how often on the average an individual cell is hit by a single average track event. The calculation [17] uses equation (2). Thus, D per unit time t is:

D/t = z1 (N_H/N_e) 1/t

or D/t = z1 /(t N_e/N_H)

The denominator (t N_e/N_H) defines the average time interval between two consecutive hits per individual cell. This time interval also gives the average time available for repair of the cell prior to a second hit. This paper only considers short term exposures. A dose rate of 2 mGy per year from 100 kV x-rays would bring a hit to each individual cell in a 70 kg human on average once every 6 months. This may be viewed as two short term exposures of individual cells, 6 months apart. Since z1 from 100 kV x-rays is about 1 mGy, 2 mGy/y = 1 mGy/(y . 0.5)

Cellular Responses to Microdoses
The response of living tissues to ionizing radiation in the low dose region involves various cellular responses [15] that are triggered mainly by hits in cells. Hit cells may also cause responses in non-hit cells by releasing signal substances and toxic, so-called clastogenic factors [9]. Moreover, hits in the extracellular matrix of the tissue may form products that interact with the cells [6] Indeed, the extracellular matrix may even reduce the natural incidence of cancer [2]. The response of tissues to low level radiation is, naturally, affected by tissue complexity.

The quantification of cellular responses to hits in tissue is important for evaluating tissue risk at low doses. Cellular responses in tissue can be observed even after single hits per cell from low LET radiation [33]. These responses may have the following consequences [15]:

a) Induction of damage:
Radiation may change the structure of DNA and cause cancer. This is a major concern in radioprotection. High doses of ionizing radiation are known to increase the probability of cancer in the exposed tissues. The greater the dose, the larger is the risk. At low doses, less than 0.2 Gy of low LET radiation, no statistically significant increase of cancer is seen in mammalian tissues [35, 36]. 0.2 Gy corresponds to about 100 times the annual dose from background radiation at sea level and still causes about a 100 times less damage to the DNA than does normal cell metaboli[31].

The probability per average hit of inducing a cell in the exposed tissue to cause cancer is assigned the term p_ind. High-dose and high dose rate exposure exceeding about 0.3 Gy induces human leukemia proportionally to dose; at this high dose, p_ind is estimated to be approximately 10^-14 per average hit from low LET radiation in human blood forming stem cells [15]. Interestingly, p_ind per average hit in tissue culture cells [19] is about 10^-5 Thus, the difference between the two p_ind is a billion and is not readily explained only by the difference between the cellular mechanisms of malignant transformation in tissue and in culture.

In this paper, p_ind is assumed to be constant over a wide range of doses from low LET radiation. If an enhancement of _ind were to result from an increase in the number of hits, then the enhanced probability of cancer per hit would then become p_ind (1+p_enh). For low LET radiation, p_enh per hit average is assumed to be zero.

b) Activation of damage control:
Low doses below about 0.2 Gy of low LET radiation affect physiological signaling within and between cells. This effect is due to chemical substances involving oxygen-containing radical compounds that are produced in the irradiated tissue. Altered signaling may change cellular metabolism in a variety of ways and trigger what can be viewed either as physiological responses of complex systems to toxic agents [10], or as adaptive responses [30]. They protect cells against damage to DNA and other biologically important molecules in the exposed tissue, irrespective of the cause of such damage. These protective responses may be grouped into four categories:

1. Damage prevention by temporarily stimulated detoxification of molecular radical species [11, 13, 14, 20]. This temporary protection of cellular constituents against toxic oxygen-containing radicals was found in mouse bone marrow at a maximum at 4 hours after short-term, i.e., acute, exposure to low doses of y-radiation; the degree of protection increased with dose up to about 0.1 Gy and then disappeared as a function of dose exceeding about -0.1 0.2[17,18].
2. Damage repair by temporary stimulation of repair mechanisms. Low dose x-irradiation stimulated, i.e., conditioned the reduction of chromosomal aberrations that occur in cultures of human lymphocytes following large, so-called challenging doses [5, 30, 31, 33, 34, 38]. The degree of protection varied from zero to a maximum with individual donors of these cells. Protection was seen when the challenging dose of 2 Gy was given between about 4 and 70 hours after the conditioning dose of 0.005 - 0.01 Gy. It was not seen when the conditioning dose of 0.01 Gy was given at the very low dose rate of 0.0064 Gy/minute, or when the conditioning dose exceeded 0.1 Gy [32, 33], or when the challenging dose was 4 Gy instead of 2y [34].
3. Damage removal by induction of apoptosis [23, 29]. Apoptosis is cell death in response mainly to DNA alterations; it is triggered by intracellular signals and eliminates damaged cells from tissue. At low doses of x-radiation, removal of damaged cells outweighed the induction of tissue damage from lost cells [23]. In one study, the incidence of this protective cell death in cultures of human lymphocytes rose up to day 4 after exposure to low LET radiation; it appeared linear with dose between about 0.1 and 2 Gy with a slope of 0.08 per 0.1 Gy [27].
4. Damage removal by stimulated immune response [1, 26]. Cells of the immune system in rodents responded by stimulated production of Tcells during fractionated gamma-irradiation with 0.01 - 0.04 Gy per day for a total of 20 days [26]. The maximum response to acute whole-body gamma-irradiation was at doses between 0.1 - 0.3 Gy. This reponse improved surveillance of damaged cells over periods of weeks, and eliminated cancerous cells [1, 26]. An improved immune response may result in an increased resistance to common infections and prolong life [37].

The four protective responses all activate cell damage control and are here summed up by a cumulative probability p_prot per average hit. Damage to cells results mainly from oxidative byproducts of normal metabolism and not from low dose irradiation[31]. Thus, radiation-induced protection acts mainly by preventing such damage. Also, existing damage may be eliminated by protective responses. Because protection may be mediated by way of intercellular signaling and by the extracellular matrix, nonirradiated cells may also benefit.

Since DNA damage may induce cancer [7, 37], the radiation-induced protective responses may also protect against spontaneously occurring cancer [37]. The probability of a spontaneous malignant transformation per cell is denoted here by p_spo. In the human blood forming stem cells, about 10^9 in the adult, p_spo per cell causing leukemia is approx^-11 throughout life [17].

As stated above for the human blood forming stem cell, p_ind per average hit is about 10^-14. Hence, the ratio p_spo/p_ind is about 10^3. This is a factor of ten smaller than the ratio of metabolically produced DNA damage and that due to background radiation per cell per day [31].

Regardless of the mechanisms involved, the values of p_spo, p_ind and p_prot are likely to vary with the organism, cell type, and z 1. This emphasizes the principal difficulty of predicting the risk of cancer for an individual from a given dose of radiation. Nevertheless, in contrast to _ind, in different cell systems p_prot decreased when D exceeded about 0.1 to 0.2 Gy of low LET radiation, as was discussed above [17,32,33,34].

The observed detrimental and protective responses in the exposed tissue operate transiently over different time spans. Thus, in order to compare the various p-values numerically, their averages need to be established and normalized to their time of duration. Moreover, a radiation-induced malignant transformation in a single cell may eventually cause a tumor to develop only over a period of perhaps several decades and following a series of subsequent DNA mutations. Therefore, in order to offset one randomly occurring spontaneous transformation leading to later tumor development, either the respective cell must experience a temporary protective response often or an accordingly large number of respective cells must each be temporarily protected once.

Tissue Response as the Sum of Microdose Effects
The preceding section indicates that low doses of low LET radiation that result in single or few hits per cell may initiate cancer and also produce various protective effects against both spontaneous and radiation induced cancer. The following probabilities per cell are here defined:

p_spo = spontaneous malignant transformation throughout life,

p_ind = radiation induced malignant transformation per average hit,

p_enh = enhancement of p_ind per average hit,

p_prot = protection that will prevent cancer from developing in the exposed tissue, per average hit.

The total probability per average hit of causing a cancer in the exposed tissue can then be expressed as [18]:

N_q/N_H = [p_ind + p_ind p_enh - p_prot p_spo - p_prot p_ind- p_prot p_ind p_enh] (4)

With N_q/N_H = alpha . z1 (see equation 3)

and rearranging equation (4) :

alpha = [p_ind (1 + p_enh)- p_prot(p_spo+p_ind+p_ind p_enh)](1/z1) (5)

In Figure 1, equation (5) is abbreviated to

alpha = [{P_ind} - {P_prot}] (1/z1) (6)

with { P_ind} = p_ind (1 + p_enh) ; and {P_prot} = p_prot(p_spo+p_ind+p_ind p_enh).

For low LET radiation, p_enh is taken to be zero. {P_prot} increases up to a dose of about 0.1 - 0.2 Gy. At higher doses it decreases gradually to zero. Since the protective term goes through a maximum in the low dose range, it is impossible for alpha to be a constant as required for the LNT hypothesis [15, 17, 1].

The various p-values estimated above may be used for a crude approximation of the probability of radiation induced leukemia. Thus, the value of p_ind for blood forming stem cells is about 10^-14 per hit average of low LET radiation [15]; p_enh is considered zero for low-LET radiation; p_spo for the same cell type has been estimated to be about 10^-11 throughout life [17]; thus, the value of the negative term in alpha, p_prot (p_spo + p_ind +p_ind p_enh) would become equal to the value of the positive term p_ind (1 + p_enh) if p_prot were 10^-3 at some dose of low-LET radiation. At this dose, there would be no increase in leukemia and a threshold would exist. With higher values of p_prot the leukemia incidence would be lower than in the control population; conversely, RE in equation (1) would only increase with D, as p_prot decreases following a maximum (see Fig. 1).

Thus, with regard to radiation-induced cancer, at least two different dose effect curves must be considered. According to equation (6) and as seen in Figure 1, the sum of these dose effect curves generates the net dose effect curve. In Figure 1, D is the product of N_H and the constant z1/N_e making N_H = c' . D. On the vertical axis is the increase (+M) or decrease (-M) of cancers in the exposed tissue compared to the background cancer incidence. Most of these background cancers are due to DNA damage resulting from normal cellular metabolism.

Components of p_prot are easily measured at low doses in various cell systems whereas _ind is not [37]. If cancer is induced at low doses, i.e., below about 0.2 Gy, it is lost in the statistical noise of spontaneous cancer incidence. Indeed, a lack of statistically significant changes in N_q after exposure of mammalian tissues to low LET radiation below 0.2 Gy makes it impossible to determine whether detrimental, beneficial, or no effects occur [36, 37]. However, epidemiological and many experimental data support the existence of a threshold or even beneficial (hormetic) effects at low D and low LET radiat[24,25].

Regarding the term alpha for high LET radiation, the relatively high value of z1 may cause p_prot for the exposed cells to be so small as to be ineffective. However, p_ind, p_ind p_enh and p_spo might be offset by a larger p_prot if it is initiated in non-hit cells by intercellular signal substances and specific toxic factors stemming from irradiated cells. Stimuli that are induced by high LET radiation in the extracellular matrix might also affect nonhit cells.

Conclusion
For assessing the probability of radiation induced cancer at low doses, the absorbed dose of importance is that to individual micromasses, the microdose. The macrodose, D, has limited applicability in estimating cancer risk at low doses. The macrodose from a given type of ionizing radiation in tissue is equal to the product of the number of microdose events, or hits, N_H, per number of exposed micromasses, N_e and the average energy absorbed per hit micromass, z1, i.e., the mean microdose for that radiation. For the calculation of z1 for any type of radiation, the micromass in tissue is taken to be 1 ng and corresponds to the mass of a typical cell in mammalian tissue. For the same macrodose from any type of radiation, N_H/N_e and z1 are reciprocally related. That is, for a dose D for high LET radiation, the average microdose z1 is proportionately greater with fewer hits than for the same D of low LET radiation.

The structure and function of tissues are determined by cells, the elemental units of life. Cells respond to hits. Adjoining cells may be affected by signal substances from hit cells and irradiated extracellular matrix.

One type of response to low LET irradiation initiates cellular damage, especially to DNA. Other responses protect against or remove DNA damage by way of stimulating existing cellular mechanisms for DNA damage control. The mis- or unrepaired DNA damage that is constantly caused by oxidative by-products of normal metabolism is estimated to be about 10,000 times greater than DNA damage from background radiation [31] Mis- or unrepaired DNA damage may cause cancer. It follows that the protection produced by hit cells mainly operates against spontaneous cancer from normal metabolism.

Low dose of low LET irradiation of different mammalian cell systems shows that the protective mechanisms increase initially with dose up to about 0.1 Gy. As the dose increases above 0.1 0.2 Gy, the protective action decreases and eventually disappears. The biphasic response of the protective action of radiation is in marked contrast to the assumed linear increase of cancer with low doses predicted by the LNT hypothesis. The incidence of radiation induced cancer may be zero at low doses and the spontaneous cancer incidence may even fall in the dose region around about 0.1 Gy. Many epidemiological and experimental data support this conclusion.

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31. Pollycove M., Feinendegen, L.E. Quantification of human total and mis/unrepaired DNA alterations: intrinsic and radiation induced. To be published
32. Shadley J.D., Wolff S. Very low doses of X-rays can induce human lymphocytes to become less susceptible to ionizing radiation. Mutagenesis 2: 95-96 (1987).
33. Shadley J.D., Afzal V., Wolff S. Characterization of the adaptive response to ionizing radiation induced by low doses of X-rays to human lymphocytes. Radiation Res. 111: 511-517 (1987)
34. Shadley J.D., Wienke, J.K. Induction of the adaptive response by X-rays is dependent on radiation intensity. Int.J.Radiat.Biol. 56: 107-liB (1989).
35. Shadley J.D., Dai G. Cytogenetic and survival adaptive responses in G phase human lymphocytes. Mutation Res. 265: 273-2B1 (1992)
36. UNSCEAR. Ionizing Radiation: Sources and Biological Effects. United Nations, New York, N.Y.: 19BB.
37. UNSCEAR. Sources and Effect of Ionizing Radiation. United Nations, New York, N.Y.: 1994
38. Wei Q., Matanoski G.M., Farmer E.R., Hedayati M.A., Grossman L. DNA repair and aging in basal cell carcinoma: A molecular epidemiologic study. Proc.Natl.Acad.Sci.USA 90: 1614-161B (1993)
39. Wolff S., Afzal V., Wienke J.K., Olivieri G., Michaeli A. Human lymphocytes exposed to low doses of ionizing radiations become refractory to high doses of radiation as well as to chemical mutagens that induce double-strand breaks in DNA. Int.J.Radiat.Biol. 53(1): 39-49 (1988).
40. Zamboglou N., Porschen W., Muehlensiepen H., Booz J., Feinendegen L.E. Low dose effect of ionizing radiation on incorporation of iododeoxyuridine into bone marrow cells. Int.J.Radiat.Biol. 39: 83-93 (1981).

The Rise and Fall of the Linear No-Threshold (LNT)

Theory of Radiation Carcinogenesis

Myron Pollycove, M.D.

Physics, together with its sister Chemistry and daughter Biology, furnish knowledge of the laws of Nature. The welfare of society depends upon a harmonious interaction between the natural laws governing our environment and physical body and human actions of conscience and integrity. I fully believe in the Hippocratic Oath of the physician to act "for the benefit of my patients, and abstain from whatever is deleterious." Growing together with Nuclear Medicine since 1953, I was concerned with radiation's health effects on our patients and staff. We held to the conservative threshold limits of the Atomic Energy Commission. Later, we adhered strictly to further reductions of exposures to "as low as reasonably achievable," ALARA. The latter reductions were associated with the Linear No-Threshold (LNT) theory that all radiation doses, even those close to zero, are harmful. In other words, Low doses are held to have the same effects as high doses, but with lower incidence.

Fully involved with clinical research, teaching, and the diagnosis and treatment of patients in both Nuclear Medicine and the Clinical Laboratory, it never occurred to us to question radiation regulations. These regulations are based upon recommendations of International and National Radiation Protection Committees composed of eminent radiation science specialists. Nevertheless, after 35 years of complete trustful acceptance of radiation protection policy, in the late 80's and 90's peer reviewed publications and conferences began to present data that were incompatible with LNT theory.

Upon retirement, I accepted the position of Visiting Medical Fellow with the US Nuclear Regulatory Commission. I began a careful examination of some published epidemiologic low-dose radiation studies. No statistically significant low-dose radiation study (<20cGy) was found to support the LNT theory of carcinogenesis and mortality risk. This was confirmed by the National Council of Radiation Protection and Measurements (NCRP) Report 121 (11/30/95) that summarizes the current status of LNT theory:1

"...essentially no human data, can be said to prove or even to provide direct support for the concept of collective dose with its implicit uncertainties of nonthreshold, linearity and dose-rate independence with respect to risk. The best that can be said is that most studies do not provide quantitative data that, with statistical significance, contradict the concept of collective dose...

Ultimately, confidence in the linear no threshold dose-response relationship at low doses is based on our understanding of the basic mechanisms involved. ...[Cancer] could result from the passage of a single charged particle, causing damage to DNA that could be expressed as a mutation or small deletion. It is a result of this type of reasoning that a linear no-threshold dose-response relationship cannot be excluded. It is this presumption, based on biophysical concepts, which provides a basis for the use of collective dose in radiation protection activities".

Dr. Feinendegen has presented microdosimetric evidence of cell and tissue low-dose stimulation of the DNA damage control biosystem. This stimulation is confirmed at the level of the organism as well as the cell by the 1994 report of UNSCEAR. Why, then, aren't we aware of corresponding beneficial effects in humans who have been exposed to low-dose radiation? Regrettably, presentation of this data has been suppressed, deleted, discounted as unreasonable, and unscientifically criticized as implausible or invalid. Concurrently, efforts to present low-dose data that support the LNT theory have led to misrepresentation of their data by authors of four studies:

• The 1989 Canadian Fluoroscopy Study2 discards the most statistically significant data demonstrating large decreases of breast cancer mortality at 0.15Gy and 0.25Gy cumulative exposures. The study retained insignificant higher dose data so that "The best fit for the data was provided by the linear model..."
• The 1996 revision of the Canadian Fluoroscopy Study3 states that since low-dose data is uninformative, it is necessary to extrapolate from high-dose data. The authors then lumped together 5 dose categories to form a single 0.01-0.49 Gy dose category.
• The 1995 Cardis, et al. Study of Nuclear Industry Workers in three Countries4 reports that non-chronic lymphocytic leukemia was significantly associated with chronic low-dose occupational exposure. The authors apply one-sided methodology to their 7 dose categories with a total of 119 deaths in order to discard 86 deaths in the 4 dose categories with fewer observed leukemia deaths than expected. A computer simulation of 5000 deaths was then used to simulate statistical significance for the remaining 33 deaths in the 3 dose categories selected.
• The 1996 RERF Life Span Study Report 12.5 This report was used in November 1996 to mobilize support for the LNT theory. The International Commission on Radiation Protection (ICRP) under Chairman Roger Clarke and the French Society for Radioprotection reviewed this Life Span Study of Atomic Bomb Survivors which includes the 1985-1990 mortality data.5.6 The ICRP claimed that analysis of this new data shows a statistically significant increased solid cancer mortality at doses as low as 5 cSv. According to Warren Sinclair, President Emeritus of the NCRP and Chairman of the ICRP Committee 1 which analyzes results of health-effects studies, the new results "vindicate" previous recommendations to lower permissible dose limits. "The combination of more data points and a more precise analysis," Sinclair said," allowed the RERF researchers to state with confidence that excess cancer risk due to radiation was observed at doses as low as 50 mSv."6 The "more precise analysis" does not use the observed excess solid cancer deaths but substitutes estimated excess deaths derived from a model fit that assumes linearity.
• The report omits statistical analysis of the observed excess solid cancer deaths following exposures of 5 rem (P=0.25) and 15 rem (P=0.56) that demonstrates they are not statistically significant; the lowest significant dose for increased solid cancer mortality is 35 rem (P=0.03). The correct dose for this increased mortality is considerably greater than 35 rem. The revised DS86 dosimetry used gives estimates for neutron radiation from the Hiroshima atomic bomb that are lower by an order of magnitude than both the original T65D dosimetry and the experimental values obtained from neutron activation measurements at the distances from the hypocenter that correspond to low-dose exposures.7

While no statistically significant data support the assumption of monotonic increased risk of cancer with increased low-dose radiation, in recent decades a considerable body of contradictory scientific epidemiologic data has accumulated.

Increased longevity and decreased cancer death rates have been observed in populations of the U.S., China, India, Austria, and the United Kingdom exposed to high natural background radiation. Several recent epidemiologic studies with high statistical significance have reported that exposure to low or intermediate levels of radiation are associated with decreased mortality and/or decreased incidence of cancer:

• Cancer Mortality in an Irradiated Eastern Urals Population (1994)8 This study reports statistically significant 28% and 39% decreases of cancer mortality in the 50cSv and 12cSv dose groups.
• Atomic Bomb Survivor Mortality from All Causes (1993)7 Longevity is significantly greater in the exposed survivors than in the unexposed.

University of Pittsburgh Residential Radon Study (1995)9

A comprehensive survey that includes the effect of smoking and more than 60 other confounding factors, analyzes 89% of the U.S. population, many exposed to high residential radon concentrations, shows with very high statistical significance, the strong tendency for lung cancer mortality to decrease as radon exposures increase, in sharp contrast to the increasing mortality expected from the LNT theory.
U.S. Nuclear Shipyard Worker Study (1991)

The UN Scientific Committee on the Effects of Atomic Radiation (UNSCEAR) 199411 reports, "The statistically significant decrease in standardized mortality ratio for deaths from all causes [0.76+0.015] cannot be due to the healthy worker effect alone, since the non-nuclear workers and the nuclear workers were similarly selected for employment and were afforded the same health care thereafter." "The type of work carried out by the three groups was identical, except that the nuclear workers were exposed additionally to 60Co gamma-radiation."11

The Canadian Fluoroscopy Study (1989)2

Breast cancer mortality is statistically significantly decreased to 0.66 in women exposed to cumulative doses of 10-20 cGy and is decreased to 0.84 in women exposed in the 20-30 cGy dose range.
Despite almost 40 years of intensive search, the LNT theory is not supported by any statistically significant quantitative low-dose (e.g.<20 cGy) data. On the other hand, this "presumption, based on biophysical concepts," is contradicted by the emergence during the past two decades of significant data demonstrating risk decrements in response to low-dose radiation exposures. Risk increments in response to high doses (e.g., > 1Gy) are well documented. The matter is clearly more complex than a simplistic biophysical presumption of linearity. These observations require careful realistic scientific and public policy discussion based upon current epidemiology and molecular biology.

The complex cell circuitry signaling for growth, division, and death includes both extracellular factors and transcription factors. "...the extraordinary detail and duplicate functions of these circuits are designed so that single disruptions here and there do not create malignant growth. A cell divides without restraint only when its circuitry has been disrupted at a number of key points: multiple mutations are required."12 Intrinsic metabolic mutations occur with very high frequency. "...by fundamental limitations on the accuracy of DNA replication and repair, ...in a lifetime, every single gene is likely to have undergone mutation on about 1010 separate occasions in any individual human being..."13 The additional relentless continual damage of DNA by reactive oxygen metabolites (02 , ^OH, H2O2), comprising 2-3 percent of all oxygen consumed, and thermal instability, increases this number to more than 1011 mutations per gene.14.15

"From this point of view, the problem of cancer seems to be not why it occurs, but why it occurs so infrequently. Evidently, ...if a single mutation in some particular gene were enough to convert a typical healthy cell into a cancer cell, we would not be viable organisms."13

Our survival depends on effective defense mechanisms that prevent (anti-oxidants, cell cycle control) and repair (DNA repair enzymes) DNA damage, and remove about 102 mis/unrepaired DNA alterations/cell daily by cell cycle diierentiation, programmed cell death (apoptosis), necrosis, and the immune system (Figure 3).11.14.15 Low dose radiation stimulates and increases the effectiveness of this DNA damage control biosystem.

The progressive accumulation of metabolic mutations and an age-related decline of biosystem effectiveness is associated with an exponential increase in the incidence of cancer with the third to the fifth power of age.13.16-20 The low incidence of cancer under the age of 50 is usually associated with genetic defects of the biosystem controlling DNA damage.

A whole body radiation background of 1mGy/year would produce about 10-7 mutations/stem cell/day.15.21 Exposure to 20cGy/year would produce 2x10-5 mutations/stem cell/day. Though this is insignificant compared to the intrinsic metabolic background of ;1 mutation/stem cell/day,15 a very small linear incremental risk of cancer would result theoretically, assuming that the effectiveness of the biosystem controlling DNA damage remains constant. During the past 15 years studies have shown that biosystem control of DNA damage does not remain constant, but adaptively responds with beneficial increased activity to low-dose (e.g.,<20cGy) radiation as well as to low-dose toxic chemical agents11.16.22. As the dose is increased to high dose (e.g.,>1Gy) radiation levels, the DNA damage control biosystem is progressively suppressed and fails.

LNT theory applied to the risk of cancer is based on two assumptions: 1) the biological response of cancer to radiation dose monotonically increases, and 2) all mutations, whether induced by ionizing radiation or other agents, produce a corresponding increase in the risk of cancer, assuming the fraction of DNA damage repaired is constant with dose. These assumptions are not valid. They are contradicted, with no support, by all statistically significant low-dose epidemiologic data and they ignore the operative effect of ionizing radiation on the DNA damage control biosystem. Emphasis is placed on the relative difficulty of repairing infrequent double strand breaks (0.4/cell/cSv low-LET radiation),21 while ignoring the daily removal and control of the unrepaired breaks, together with trillions of other metabolic misrepaired or unrepaired DNA alternations, by the adaptive responses of differentiation, self programmed cell death (apoptosis), necrosis, and the immune system. Disregarded are the extremely high background of spontaneous metabolic mutations and the adaptive responses to radiation that, until they diminish with age, very effectively prevent, repair, and remove both the spontaneous and the relatively few low-dose, low-dose-rate environmental mutations.

Contrary to the increased risks associated with injury to the DNA damage-control biosystem by high-dose radiation, this biosystem is stimulated by low-dose radiation to function even more effectively and decrease the risks of mortality and cancer. These observations of fundamental biologic cellular functions and corresponding epidemiologic studies contradict the theoretical assumptions based on biophysical concepts and exclude a LNT dose-response relationship.

Nevertheless, since 1959 the LNT theory has remained the basic principle of all radiation protection policy. This theory is used to generate collective dose calculations of the number of deaths produced by background radiation. The increase of public fear through repeated statements of deaths caused by "deadly" radiation has engendered an enormous increase in expenditures now required to protect the public from all applications of nuclear technology: medical, research, energy, disposal, and cleanup remediation. These funds are allocated to appointed committees, the research they support, and to multiple environmental and regulatory agencies. The LNT theory and multibillion dollar radiation activities have now become a symbiotic self-sustaining powerful political and economic force.

Scientific understanding of the positive health effects produced by adaptive responses to low-level radiation would result in a realistic assessment of the environmental risk of radiation. Instead of adhering to non-scientific influences on radiation protection standards and practice23 that impair health care, research, and other benefits of nuclear technology, and waste many billions of dollars annually for protection against theoretical risks, these resources could be used productively for effective health measures and many other benefits to society.

Myron Pollycove is a Visiting Medical Fellow at the U.S. Nuclear Regulatory Commission and Professor Emeritus of the Laboratory Medicine and Radiology at the University of California in San Francisco.

A Partial Solution to LLW Siting?

John F. Ahearne

"...a radioactive waste dump...will endanger the Colorado River and the people, animals and vegetation which depend upon it -- all the way to Los Angeles."

"What's at stake? Nothing less than the drinking water supply of 12 million Southern Californians...."

"..it is highly unlikely that significant amounts of radioactive material...Will reach the ground water...and an even smaller chance of reaching the Colorado River."

These widely different statements do refer to the same site, and do not refer to high level radioactive waste. They refer to the proposed low-level radioactive waste (LLW) site in Ward Valley, in the Mojave Desert. The first two statements are from the Executive Director of Greenpeace and Sen. Barbara Boxer . The last is from the Chair of the National Research Council Ward Valley Committee.

While some of the debate about radioactive waste has focused on geologic repositories proposed for New Mexico (the Waste Isolation Project Plant, WIPP, for transuranic waste, TRU) or Nevada (the Yucca Mountain repository for high level waste, HLW), more prevalent are arguments in several states about siting low level waste sites. Low level waste is different from that destined for WIPP and Yucca Mountain in several aspects. First, the responsibility for disposal of commercial LLW rests with the states, not with the federal government. The Department of Energy (DOE) does have a substantial amount of LLW generated by defense and DOE research, but it has been and is planned to continue to be disposed of on DOE sites. Second, unlike HLW and TRU, LLW was thought to be relatively easy to handle. This has turned out to be a monumental misjudgment.

Six commercial sites were developed to receive LLW. By the end of the 1970's, three had been closed because of environmental problems, primarily concerns about the possibility of waste leaking off site. The governors of the states with the remaining three sites became concerned that no new sites were being developed but they must allow waste to come in from any other state. This led to an initiative in Congress in 1978 for the federal government to take over responsibility for siting new disposal facilities. The National Governors' Association opposed federal control and the Waste Policy Act of 1980 retained state control. This Act established a process by which groups of states could band together in "compacts" which could restrict waste disposal to members of the compact.

The compacts were to be in place by 1986, when states could begin barring waste generated outside the compact regions. In 1985, with no new sites being developed, Congress slipped the deadline but added that each compact's facility was expected to be operational by 1993. When one of the three original sites closed in 1993, no new sites had been developed, leaving only two for the entire United States, one at Richland, Washington, and one at Barnwell, South Carolina. The Washington site was closed in 1993 to any state outside of 11 states in two compacts and the South Carolina site was closed in 1994 to all states but those in the 8 state southeastern compact.

Thus, although by 1995 47 states were members of compacts, and 11 states had plans for disposal sites, only Barnwell and Richland were operating. This led to considerable turmoil as waste generators in the states barred from the two sites tried to find alternative disposal methods. The medical community was particularly upset. An NIH official said "Biomedical investigators will have to substitute new and perhaps less effective research procedures which do not rely on radioisotopes. Some may be forced to abandon research projects." Another result, he said, would be "soaring costs" as hospitals try to store wastes on site.

There is now a temporary reprieve. The South Carolina site has been reopened because of a dispute within the compact. The compact agreement was that South Carolina would close its site when the next state opened a LLW site. North Carolina was to be that state. However, North Carolina has been unable (or unwilling) to develop a site, which led to South Carolina requesting North Carolina be removed from the compact. When the compact states declined to eject North Carolina, South Carolina reopened its site to all states except North Carolina, while increasing its disposal cost. (In the 1970's, disposal cost was less than $5/ft3; it now is $350/ft3 at Barnwell, of which $235 goes to the state.) Also, a non state-related commercial facility, Envirocare, in Utah, accepts a limited set of LLW.

In October, the compact agreed to give North Carolina another $6.5 million. The local press reported: "The funds would give new life to a project that already has cost $90 million over eight years and has produced only an undeveloped site...." The governor of North Carolina recommended that the other states in the compact share the costs of further studies. The compact rejected this proposal and gave the state until 1 December to accept the existing proposal, which included NC utilities putting up $7 million, or offer another proposal. The state did neither and, in December, the compact cut off funding to North Carolilna. The state then began "the orderly shutdown of the project." Through December, $106 million had been spent on the project. This cost and time, as well as the result, are not unusual. In 1992, Illinois rejected a site that had been studied for 8 years at a cost of $85 million. New York halted its search for a LLW site after 8 years and a cost of over $55 million. The contentious Ward Valley site received a license from the State of California (but a license that cannot be exercised until the land is transferred from the federal government) that lasted eight years and cost $45 million.

What goes into these LLW sites? A 1995 Government Accounting Office (GAO) report on LLW status described the commercial uses of radioactive materials that lead to LLW:

• operations at nuclear power plants.
• more than 100 million annual medical procures.
• testing and development of about 80% of new drugs.
• sterilization of consumer products.
• production of commercial products, such a smoke detectors.

Data on actual disposal is poor. The best is that compiled by the DOE, which divides commercial LLW into five categories:

• Academic, which includes university-related hospitals and medical research as well as other research facilities.
• Government, which includes state and non-DOE federal agencies, including NIH.
• Industrial.
• Medical, which includes the non-university related hospitals and research facilities.
• Utilities.

Thus, it is not possible to separate out medical wastes in the DOE compilation. But utility waste has been separated. In 1994, utility waste represented 44% of the volume of radioactive material sent to the two operating LLW sites, but 91% of the radioactivity as measured in curies.

For some states, utilities represented even a larger fraction of the radioactive materials: of the waste shipped in 1995 by New York state generators, 5.3% of the volume and 99.3% of the curies were shipped by power plants.

"...two activities leading to major concern and dread are radioactivity and nuclear power. LLW sites...with waste from nuclear power plants, combine both factors...[they] need not...[if] LLW material from power plants [is stored] on site."

While many states have plans to site and construct a disposal facility, in almost all cases these plans have been halted or delayed. The GAO noted that between 1991 and 1995 all but one compact plan slipped by several years, in all cases to beyond 1996. (The one exception is the compact for a site in Texas, a compact which involves the interesting combination of Texas, Maine, and Vermont -- there is no Congressional requirement that the states in a compact be contiguous.) The reason, of course, is the opposition to siting a radioactive "dump' in a local area. A study by the National Research Council of the aborted effort in New York state concluded that public acceptance is key to success, but also noted that "...some opponents clearly and vocally stated they would not accept any site, regardless of the technical justification...." A Nuclear Regulatory Commission study in 1993 concluded seven factors negatively affected siting a LLW site, including perceptions that the regulations are inadequate and that long-term storage is more desirable than disposal. However, public and political concern appeared to be a major factor and were linked to many of the other factors.

I believe a partial solution can be found to the LLW dilemma for a substantial part of the problem. Public opposition to LLW sites has been studied by sociologists such as Paul Slovic, who attribute public opposition to activities they dread. These studies indicate that two activities leading to major concern and dread are radioactivity and nuclear power. LLW sites, being predominantly filled wi