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.]

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.

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.

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.

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.

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.

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).

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.

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.

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

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

This article presents arguments and data from rodents and humans to support the thesis that low level radiation (< 0.2 Gy) may be beneficial to the health of the exposed individual. Our conclusions contradict the assumption that radiation induction of cancer follows a linear-no-threshold (LNT) function of the dose. Living tissue is a nonlinear dynamic system. The functions of both normal and cancer cells, as well as their interaction, are complex biological processes. It would indeed be strange if radiation induction of cancer were linear over many orders of magnitude of dose.

Body tissues have the capacity to prevent, repair and remove damage to their cells from any cause, whether by chemical or physical injury, by toxic substances from normal metabolism, or by radiation. We will present evidence that four protective mechanisms can be stimulated by small doses of radiation. Three of these protective mechanisms have been shown to increase in effectiveness up to about 0.1-0.2 Gy, after which they begin to decrease and gradually disappear with increasing dose. Studies of A-bomb survivors in which essentially all the radiation induced cancers involved doses above 0.5 Gy would not be expected to give evidence of a health benefit of low dose radiation. Most of the A-bomb survivors had doses less than 0.5 Gy. The fact that the incidence of leukemia in the A-bomb survivors has been shown to be reduced below that of the control population when the absorbed doses were below 0.2 Gy, and that no significant increases in any form of cancer could be seen below 0.3 Gy can alone be considered as an argument against the general validity of the LNT hypothesis.

In radiation dosimetry it is customary to use the macroscopic quantity energy/mass, called the absorbed dose. The SI unit of absorbed dose is the gray (Gy) where 1 Gy = 1 J/kg . With decreasing doses this macroscopic quantity becomes increasingly inappropriate as a measure of damaging agent to cells. At low doses, the absorbed dose to individual cells, or the microdose, needs to be considered. Ionizing radiation is absorbed in matter by the deposition of discrete amounts of energy along the track of charged particles throughout the exposed matter; the lower the dose the more spaced apart are these energy deposition events and vice versa. The amount of energy absorbed from a track in a micromass of tissue is denoted a microdose. The micromass of tissue is assumed to be 1 ng, the mass of a typical mammalian cell. The microdose is also called cell-dose, hit-size, or, more formally, specific energy. The mean microdose, z1, from a single energy deposition event, i.e., from a hit, is calculated from the frequency of such events in the defined micromass. The spectrum of microdoses, and thus the mean microdose, is constant for a given type of radiation. For example, the z1 from a 100 keV photon is about 1 mGy. For densely ionizing radiation z1 is larger. It follows that for a given type of radiation, only the number of hits per micromass and not the hit-size changes with dose. In this article we only consider exposure to radiation with a low linear energy transfer, LET - better known in physics as dE/dx.

It has long been known that the response of irradiated tissues depends on the rate at which the dose is absorbed. Repair of damaged tissue takes time. This is the basic reason that radiation therapy is protracted over many weeks rather than being given in a single dose. The extra time allows exposed normal tissues to recover. From the dose rate one can calculate how often, on the average, an individual cell is hit by a track, or energy deposition event. Natural background radiation gives a macrodose of about 2 mGy/y. Since a single hit from 100 keV photons delivers a mean microdose of about 1 mGy, it means that on the average each cell gets struck about twice a year.. From a cellular viewpoint, background irradiation can be regarded as two short exposures of 1 mGy twice a year, allowing a long time for repair to take place. Areas in the world with high background levels do not show an increase in cancer incidence; even decreases have been reported.

The risk of damage to tissues from ionizing radiation results from responses triggered in cells by microdoses in tissues. With many hits per cell, damage is overwhelming. In the low dose region with hits occurring more rarely, as is true in the low dose region, different kinds of cellular responses must be balanced against one another.

Cells respond biochemically directly to being hit and may also induce responses in neighboring non-hit cells through the release of chemical (signal) substances, so-called clastogenic factors. In addition, hits in the extracellular matrix of a tissue may form products that alter cellular metabolism. These cellular responses may not only produce damage, but also need to be considered as stimulating mechanisms that can counteract damage to cells that have not been damaged excessively. Indeed, evidence is accumulating that low dose irradiated cells not only may produce cancer, but may also respond with mechanisms that initiate protection against cancer from any cause, especially from normal metabolism. In nature, competing processes are common, some causing damage but at the same time initiating mechanisms serving to protect against the same or similar damage. Infectious diseases and immunity against them are well known examples.

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Depending on dose, radiation is known to change the structure of DNA in the cell and initiate cancer at a later date. Doses of low LET radiation higher than about 0.3 Gy given in a short period of time to a large human population significantly increase the incidence of cancer in the exposed people at a later date, in a dose related fashion. However, at lower doses, no statistically significant increase is seen. The damage to DNA by a dose of 0.2 Gy, about 100 times the annual dose from background radiation at sea level, is less than one hundredth of that caused by normal cell metabolism in one day.

On the other hand, low-LET radiation at low doses below about 0.2 Gy, but not at higher doses, has been shown to change physiological signaling in various cell systems. This effect is at least partly due to chemical substances involving reactive oxygen species, ROS, resulting from radiation absorption by the water in tissues. However, ROS are also constantly generated as toxic by-products of normal metabolism, causing tens of thousands of DNA lesions per average cell per day.. Normal cells possess mechanisms that counteract excess ROS and their effects on DNA in an attempt to prevent cellular damage. A radiation induced rise in the level of ROS affects these balancing mechanisms.

Altered signaling following low dose irradiation has been shown to affect cellular metabolism in a variety of ways and trigger what can be viewed as physiologically adaptive responses of complex systems to toxic agents. They appear to protect against damage to biologically important molecules including DNA in the exposed tissue, irrespective of the cause of such damage.

In various cells and tissues of rodents and humans, such protective responses lasting from hours to days have been experimentally observed after low doses of low LET radiation. These responses appear to vary with cell type, organism and species. The examples described below for low dose exposures may be grouped into four categories: 1) damage prevention; 2) damage repair; 3) damage removal by apoptosis; and 4) damage removal by a stimulated immune response.

Damage prevention operates through temporarily stimulated detoxification of reactive oxygen species. This temporary protection of cellular constituents against ROS in mouse bone marrow reached a maximum at 4 hours after short-term (i.e., acute) exposure to low doses of gamma radiation. The degree of protection increased with dose up to about 0.1 Gy and then disappeared at doses exceeding about 0.2 Gy .

Damage repair results from temporary stimulation of repair mechanisms. A low dose of x-radiation (5 to 10 mGy) was observed in human lymphocytes, in many but not all individuals, to stimulate protection against a large challenging dose (2 Gy) given 4 to 70 hours later. Repair was not seen in the responders when the small dose was given at the very low dose rate of 6.4 mGy/minute, or when it exceeded 0.1 Gy, or when the challenging dose was 4 Gy instead of 2

Damage removal by apoptosis, or programmed cell death, occurs mainly in response to DNA alterations and, of course, removes carcinogenic potential. It is common in many tissues and can be triggered by radiation through cascades of intracellular signals. In one study, the incidence of apoptosis in cultures of human lymphocytes rose up to day 4 after exposure to low LET .

Damage removal by stimulating an immune response was reported in rodents following low doses of low-LET radiation. The immune system responded maximally to acute irradiation at doses between 0.1 to 0.3 Gy. This caused an enhanced surveillance of damaged cells over periods of weeks, and eliminated cancer cells. An improved immune response commonly leads to an increased resistance to common infections and may prolong life.

The four protective responses all activate cell damage control in the exposed body and are here summed up by a cumulative probability P(prot) per average hit. We define the probability of spontaneous cancer as P(spo) and the probability of radiation induced cancer as P(ind). Damage to cells results mainly from reactive oxygen species, ROS, produced by normal metabolism and, much more rarely, from low dose irradiation. Thus, low level radiation, on balance, is expected to rather protect against, than augment, damage caused by normal metabolism. Because DNA damage is known to induce cancer, the radiation-induced protective responses tend to reduce the incidence of spontaneously occurring cancer, as well. Also, existing damage may be eliminated by these protective responses. Because protection may also be mediated by way of intercellular signaling and by the extracellular matrix, non-irradiated cells may also benefit.

The values of P(spo), P(ind) and P(prot) are likely to vary with the organism, cell type, and the type of radiation. Thus it is impossible to predict the risk of cancer for an individual from a given dose of radiation. Nevertheless, as was discussed above, whereas P(ind) appears constant in different cell systems, three of the above named components of P(prot) are not constant but were found to decrease when D exceeded about 0.1-0.2 Gy of low LET radiation,.

The probability of cancer after radiation exposure involves two different dose effect functions. One describes the occurrence of adiation induced cancer as a linear function of dose. The other represents the radiation induced protective responses against DNA damage mainly from metabolic ROS and probably its ensuing cancer, as a multi component function of dose. These functions are shown schematically in Figure 1. The sum of the dose effect functions generates the net dose-effect curve shown, which reduces the incidence mainly of spontaneous cancer at low doses. On the horizontal axis, D is the product of the microdose per hit, a constant for a given type of radiation, and the number of hits in the exposed cells. The dashed line shows the increase of cancer (+M) due to radiation if there were no protective mechanisms. The background (Bkgd) line shows the spontaneous cancer incidence, most of which is due to DNA damage resulting from normal cellular metabolism. The light solid line indicates the effect of the damage control response, which is mainly on the background cancer incidence. The heavy solid line shows the combined effects ofcancer induction and prevention. The shaded region represents the probable reduction of cancer incidence due to protective effects which have been also termed "radiation hormesis". The evidence of protection against DNA damage discussed in this paper in principle contradicts the LNT model of radiation risk. The "threshold" shown for observable radiation-induced cancer, 0.2 Gy, complies with epidemiological data.

Figure 1

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Figure 1. Schematic diagram showing the combined effects of low dose irradiation in causing and protecting against cancer. The heavy solid line is the sum of the two dose-effect functions. The shaded area illustrates the effect of the postulated radiation-induced reduction in the incidence of spontaneous cancer which has been also termed "radiation hormesis". The "threshold" shown for observable radiation-induced cancer, 0.2 Gy, complies with epidemiological data (see text for details).

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The components of P(prot) are easily measured at low doses in various cell systems, whereas P(ind) is not. These two P-values in the low-dose irradiated organism have been estimated to differ by a factor of more than a billion. If cancer is induced in humans by low doses of radiation, i.e., below about 0.2 Gy, it is lost in the statistical noise of spontaneous cancer incidence. Indeed, the lack of observed statistically significant changes in radiation induced cancers after exposures of mammalian tissues to low LET irradiation below 0.2 Gy makes it impossible to determine whether detrimental, beneficial or no effects occur. However, both epidemiological and many experimental animal data support the existence of a "threshold" or even beneficial effects of low level radiation. Further experimental work on the various P-values in different mammalian cell systems would permit a risk assessment that is more realistic than that obtainable from epidemiological studies.

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The authors deeply appreciate the most effective editorial help from Dr. John R. Cameron, University of Wisconsin, Madison WI.

Ludwig E. Feinendegen

Medical Department, Brookhaven National Laboratory, Upton, NY and Office of Biological and Environmental Research, U.S. Department of Energy, Washington, DC.

Ludwig.Feinendegen@mailgw.er.doe.gov

Victor P. Bond

Research Faculty, Washington State University, Richland, WA.

Charles A. Sondhaus

Radiology Department, University of Arizona, Tucson, AZ.

Feinendegen L.E., Loken M., Booz J., Muehlensiepen H., Sondhaus C.A., Bond V.P.

"Cellular mechanisms of protection and repair induced by radiation exposure and their consequences for cell system responses." Stem Cells 13(1): 7-20 (1995)

Feinendegen L.E., Bond, V.P., Sondhaus C.A., Muehlensiepen H."Radiation effects induced by low doses in complex tissue and heir relation to cellular adaptive responses." Mutation Res. 358: 199-205 (1996)

Kondo S. Health Effects of Low Level Radiation.,Kinki Univ.Press, Osaka, Japan; Medical Physics Publishing, Madison, WI; 1993.

Sugahara T., Sagan L.A., Aoyama T., Eds. "Low Dose Irradiation and Biological Defense Mechanisms." Proceedings of the International Conference on Low Dose Irradiation and Biological Defense Mechanisms, held in Kyoto, Japan, 12-16- July, 1992. Excerpta Medica, Amsterdam, London, New York, Tokyo; 1992.

UNSCEAR. Sources and Effects of Ionizing Radiation. United Nations, New York, NY; 1994

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.

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:

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:

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.

Figure 3

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.

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"...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.

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.

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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