RADON EXPOSURE AT LOW DOSES: EPIDEMIOLOGICAL RESULTS
All epidemiological evidence dealing with lung cancers resulting from radon exposure points away from the existence of a "safe threshold", and towards the conclusion that the linear hypothesis is non-conservative at low doses. Regarding the concept of a safe threshold, the Ham Commission concluded:Dr. Victor Archer, M.D., Medical Director of the U.S. National Institute for Occupational Safety and Health (NIOSH), has recently reviewed the epidemiological evidence for fifteen different groups of uranium miners, and has concluded that the linear hypothesis seriously underestimates the risk of cancer at low doses in every single case. In other words, the existing epidemiological evidence on uranium miners fully supports the evidence mentioned earlier about alpha-induced cancer at low doses. Dr. Archer has only reached this conclusion in the last two or three years, although he has twenty years experience in the field of lung cancer epidemiology for uranium miners.  (Archer et al., ref. 3; see exhibit 3 below)
"Since the Commission's Study of data based on the Ontario Uranium Nominal Roll provides no evidence supporting the hypothesis of a threshold of exposure below which there is not significant excess risk, the concept of a maximum safe exposure is not tenable on the basis of these data." (p.95, Ham Commission Report)
A B S T R A C TArcher, V.E., Radford, E.P., and Axelson, O. Radon Daughter Cancer in Man: Factors in Exposure-response Relationships. Radiation Research -- to appear.
Lung cancer among fifteen different mining groups exposed to radiation from radon daughters was analyzed to determine what factors influence incidence and induction latent period. As the exposure rate decreases, cancers per unit of radiation increases. The induction-latent period is shortened by increased age at start of mining, by cigarette smoking, and by high exposure rates. For follow-up periods of 20-25 years, the incidence increases with age at start of mining, with magnitude of exposure, and with amount of cigarette smoking. For very long follow-up periods, the incidence among nonsmokers sometimes exceeds that among smokers. Both lung cancers per year per WLM and relative risk were found to vary greatly with exposure rate, age of cohort at start of mining and with length of follow-up period. Lifetime risk per WLM, adjusted for exposure rate, was proposed as the best statistic for use in predicting lung cancers among other groups exposed to radon daughters. These findings are consistent with the theory of radiation carcinogenesis which postulates that cancer is caused by a series of changes in chromosomal proteins (some of which occur with increasing age) followed by a promoting factor.
Key words: Radiation, radon daughters, miners, lung cancer, carcinogenesis.
In fact the epidemiological evidence has always been there, but until recently it was ignored because it did not conform to the linear hypothesis. In 1970, for example, Gofman and Tamplin published a paper reviewing the evidence of lung cancer incidence among uranium and hard rock miners who began working on the Colorado Plateau before 1955. Dr. Gofman's arithmetic, using data provided by the U.S. Federal Radiation Council, clearly demonstrated the increasing effectiveness of radon exposure at low doses in causing lung cancer. His calculations are graphically presented in Figure 6 (based on reference 4). 
Graphical Summary of Dr. John Gofman's Calculations (Reference 4)
The radiation dose required to double the natural incidence of cancer is called a "doubling dose". For uranium miners on the Colorado Plateau, Gofman's evidence shows that -- to double the incidence of radon-induced lung cancers -- fewer accumulated WLM are required in the lower exposure categories than in the higher exposure categories.
The exposure categories are:
A: miners exposed to less than 120 WLM (4 cancers)
B: miners exposed to less than 359 WLM (11 cancers)
C: miners exposed to less than 839 WLM (16 cancers)
D: miners exposed to less than 1799 WLM (27 cancers)
E: miners exposed to less than 3719 WLM (37 cancers)
F: total population of 1981 miners with 49 lung cancers
Category A is of dubious significance because of so few cancers.
Category B was corrected for possible additional radon exposure due to previous hard rock mining experience.
MINISTRY OF HOUSING DATA: Lung Cancer Deaths Caused by Radon
Let us now turn to the data supplied by Dr. Muller in the MOH Report. An examination of Dr. Muller's first four tables -- reproduced here -- confirms Dr. Archer's observations and Dr. Gofman's conclusions: in each case, the greatest risk (per unit dose) occurs at the lowest exposures.
In each table, the first and last columns are the important ones to look at;
- the first column gives the degree of exposure to radiation, and
- the last column gives the number of radiation-caused cancers expected per unit dose at that exposure level.
In Table 1 (Exhibit 4) and in Table 2 (exhibit 5), both dealing with the Colorado Plateau data, a marked increase in excess cancers per WLM is observed at exposures below 359 WLM (Gofman's categories A and B).
The last column of Table 2 tells the story:
- the average of the last four entries in this column is 5.25 excess cancers per WLM, but
- the second entry shows that the number of excess cancers per WLM is almost three times larger for exposures between 120 and 359 WLM, and
- the first entry shows that the cancer risk is almost six times larger for exposures between 0 and 120 WLM!
- The overall average risk of 5.7 excess lung cancers per WLM (given at the bottom of the last column of Table 2) greatly underestimates the risk for those exposed to less than 120 WLM (given at the top of the last column of Table 2).
Similar observations can be made about Table 3 (Exhibit 6) dealing with Czechoslovakian data.
- Notice first of all that the exposures in this table are in the range from 0 to 600 WLM for the most part, corresponding to only the first two or three entries in Table 2. In other words, the Czechoslovakian miners received considerably less exposure to radiation than the American miners.
- And, sure enough, the average risk of 11 excess lung cancers per WLM in Table 3 is twice the average of 5.7 from Table 2, thus confirming once more that lower exposures correspond to larger risks per unit dose.
- Moreover, within Table 3 itself, the number of excess cancers for exposures below 50 WLM is twice the average number of excess cancers from 50 WLM to 600 WLM, in full agreement with the doubling indicated between the first two entries of Table 2.
- Once again, in Table 3, the overall average of 11 excess cancers per WLM seriously underestimates the risk for those with low exposures (in this case, those with less than 50 WLM).
The same relationships can be observed in Table 4 (exhibit 7) which is based on data from Hiroshima. Using the correspondence 1 WLM = 4 rem to the lungs (which is even more establishment-oriented than Dr. Muller's conversion factor -- 1 WLM = 4.42 rem -- given on page 5 of Appendix 1 of the MOH Report), we see that
- the first two entries in Table 4 fall in the "below 50 WLM" range;
- the second two entries lie between 50 and 300 WLM (equivalent) exposure;
- the average of the first two entries (4.5 excess cancers per rem) is triple the average of the last two entries (1.5 excess lung cancers per rem);
- the first entry (7 excess cancers per rem) is four times as large as the average of the other three entries (1.7 excess cancers per rem).
Thus, the Ministry of Housing data, assembled by Dr. Muller, is entirely consistent with the evidence cited earlier which suggests that the linear hypothesis seriously underestimates the risk of lung cancer at low exposures to radon. In fact, the relative risk seems to get consistently worse as the exposures get progressively smaller
All of this evidence points away from a safe threshold and away from the linear hypothesis, contrary to what is stated on page 5 of the MOH Report. 
INTERPRETATION OF MOH ESTIMATES: Anticipated Lung Cancer Deaths
The Ministry of Housing is recommending a standard of 0.02 WL of radon in buildings. If one were to spend one's lifetime in such a building, what would be the risk of getting lung cancer as a result of this radon exposure? Table 6 from the MOH Report, reproduced below, summarizes the Ontario government's risk estimates for a lifetime exposure at 0.02 WL of radon at the rate of one hour's exposure per day. These are based on the average cancer risk values presented in Table 1, Table 2, Table 3, and Table 4, with some additional assumptions. As the MOH Report explains, "increasing or decreasing the hours of exposure per day will increase or decrease the risk (as given in Table 6 below) by the same factor." (MOH Appendix, page 6)
|Model Used||Number of Radiation-Induced |
Cancers per 100,000 Persons
|Mean Loss of Life Expectancy at birth, per person (days)|
|Absolute Risk Model|
|Relative Risk Model|
|Uranium Miners |
|Relative Risk Model|
|Hiroshima||Relative Risk Model|
We will limit ourselves to the male risk figures in Table 6, since almost all of the epidemiological evidence is based on male populations, and it is not clear how the female figures are arrived at.  As the MOH Report refers to "the fact that people spend no more than half their time outdoors during the course of a year" (accompanying the Summary of Clean-up Criteria in the Appendix), let us assume a minimum of 12 hours per day exposure indoors. We then arrive at the following risk figures for males (making use of Table 6 and the natural incidence of lung cancer in Ontario males of 54 per 1000, given in the MOH Report.)
ESTIMATES OF MALE LUNG CANCER RISK
FROM A LIFETIME EXPOSURE TO 0.02 WL
per 100,000 men
per 100,000 men
per 100,000 men
from Table 6
(Appendix, p. 91)
from Table 6
from Table 6
from Table 6
Note that if radon exposure is more effective in producing cancer at lower doses, as the evidence indicates, then one would be tempted to rely more heavily on the low-exposure populations of Czechoslovakia and Hiroshima -- thereby arriving at a risk estimate two-and-a-half times larger than Dr. Muller's estimate.
But even this does not fully reflect the risk at low exposure levels, because table 6 is based on average risk values and does not use the low-exposure data from Table 1, Table 2, Table 3, and Table 4. What happens if we take this low-exposure data into account?
CORRECTIONS TO THE MOH ESTIMATES: Probable Lung Cancer Deaths
By definition, 1 WLM is the accumulated exposure of an average adult male individual spending 170 hours in a radon environment of 1 WL.
Exposure to 0.02 WL for one hour per day over a lifetime of 70 years leads to an accumulated exposure of 0.02 x (365 / 170) x 70 = 3 WLM ; over a lifetime of 50 years, the accumulated exposure would be only 2 WLM.
So, for 12 hours per day exposure, the accumulated dose would be 36 WLM for a 70-year life span and 24 WLM for a 50-year life span.
The only purpose of this little calculation is to demonstrate that the persons at risk in homes with a 0.02 WL radon environment will be in the low-exposure, high-risk categories previously identified in the text.
The risk estimates in Table 6 are based on the average risk figures from Table 1, Table 2, Table 3, and Table 4; but those averages systematically underestimate the actual risk to the low exposure groups in each case. If we make the appropriate adjustment to account for the low-dose risk data in the tables, we arrive at the following corrected estimates:
Corrected Estimates of the Low Dose Cancer Risk based on MOH Data
Notice that this adjustment brings the three relative risk figures into much closer agreement. (The first entry, based on a different model known as the "absolute risk model", is not really comparable with the relative risk figures since it is calculated in a different fashion -- see note 3 for both Table 1 and Table 2 )
The average number of excess lung cancers per 100,000 given by the relative risk model is therefore 140 -- exactly seven times larger than the risk figure cited by Dr. Muller. But this is for only one hour per day exposure; multiplying by 12 and dividing by 100, we get 16.8 excess lung cancer cases per thousand for 12 hours per day exposure. This represents a 31 percent increase over the normal lifetime lung cancer rate for Ontario males (54 per 1000) as given in the MOH Report. COMMENTS ON THE CALCULATIONS
The risk figures calculated from Table 6 (and subsequently reflected in my corrected estimates) may be wrong for a number of reasons. The method of calculation has both conservative and non-conservative factors built into it. A brief summary of these is given below. a) Non-Conservative Factors
- The number of excess cancers per WLM may be even greater than indicated by the previous calculations at the low doses and low dose rates which are actually involved. This possibility is suggested by both experimental and epidemiological evidence on alpha-emitters. For example, if we had used the appropriate data (reproduced below) from "Radon Daughter Cancer in Man" (by Victor Archer et al.) as the basis for our calculation, we would have arrived at something like a 45 percent increase in lung cancer as a result of 0.02 WL at 12 hours per day, assuming only a 50-year lifetime. It may be that the MOH data is just too coarse to reveal the true hazard at very low dose rates.
ESTIMATION OF LUNG CANCER RISKS FROM
RADON DAUGHTERS AT DIFFERENT EXPOSURE RATES
(per year, per WLM,
per million persons)
(per lifetime, per WLM,
per million persons)
needed to produce
one lung cancer
per million persons
per WLM of exposure
a) Non-Conservative Factors (continued)
"It is not clear how long after start of exposure the incidence of lung cancer continues to increase; certainly no one has yet observed a decrease with increasing time, as has been observed for radiation-induced leukemia" (page 5).The gradual build-up of long-lived radon daughters in the lung, such as lead-210 with its 21-year half-life, makes it highly unlikely that extra cancers would stop appearing after 20 years.  Lead-210 gives rise to polonium-210 as a daughter product; the potent carcinogenic properties of polonium-210 are well documented (see Figure 5).
In addition, epidemiological evidence reveals that non-smokers who started mining at an early age are only now beginning to show dramatic increases in lung cancer some 40 or 50 years after initial exposure ("Radon Daughter Cancer in Man", page 21).
Nevertheless, I have been informed that 50 out of 58 new homes recently tested in Elliot Lake showed levels in excess of 0.02 WL before fans were installed to provide extra ventilation. Of a total of 1900 older homes tested in Elliot Lake since 1976, about 325 were found to be over the 0.02 limit. This fraction (1/6) is not very reassuring -- if 1/6 of the planned population of 30,000 were exposed to 0.02 WL, we could have over 80 radon induced lung cancer deaths just from breathing radon gas at home.
However, the risk is additive, and the ICRP recommends that all unnecessary exposure to radon be avoided.
Such a turnover of population will not reduce the total number of expected cancers however (even according to the linear hypothesis -- see pages 103-105 in The Ham Commission Report). The cancers will just be diluted in a larger population -- the human tragedy will be undiminished, but the statistical percentage will look smaller.
According to the non-linear hypothesis described in this paper, a turnover in population may actually increase the number of cancers by decreasing the individual exposures without diminishing the total dose to the entire population -- thereby bringing about an increased risk per WLM because of the lower individual exposures.
The Atomic Energy Control Board has laid down annual dose limitations for whole-body exposure, and for various organs of the body.
For whole-body exposure to penetrating radiation, AECB limits are 5 rems per year for atomic workers and 500 millirems per year for members of the General public; however, AECB policy is to aim for no more than one percent of the Maximum Permissible Dose of 500 millirems per year as an official guideline -- in other words, members of the public should not be exposed to more than 5 millirems per year.
For the lungs, AECB exposure limits are set at 15 rems for atomic workers and 1. 5 rems for members of the general public.
Let us deal with the lungs first.
Whole-body exposure results primarily from gamma radiation.
ESTIMATING THE RISK FROM GAMMA RADIATION
The health risk from exposure to low level gamma radiation includes not only cancers and genetic defects, but also possible increases in such diseases as diabetes milletus, cardiovascular disease, mental retardation, stroke, hypertension, and a great many infectious diseases. These somatic risks are discussed in some detail in the Proceedings of a Congressional Seminar on Low-Level Ionizing Radiation (Chapter III). Such adverse health effects should definitely be included in any risk assessment associated with setting housing standards for gamma radiation.
There are many well-qualified and well-respected people in the field of health physics or radiation biology who believe that current risk estimates are understated by about a factor of ten.  As Dr. Morgan says on page 84 of the Proceedings, "the somatic risks and in particular the risk of radiation-induced cancer of almost every type are more to an order of magnitude [i.e. ten times greater] -- than we considered them to be some time back." A more detailed discussion of the controversy is given in "The Biological Effects of Radiation: Ten Times Worse Than Estimated".
There is also some evidence which seems to indicate that low dose rates may be more harmful than high dose rates in producing cancer, even in the case of gamma radiation; hut the evidence is quite confused on this subject and I am not able to form a professional judgment as to what the correct risk factor might be (see Proceedings of a Congressional Seminar on Low-Level Ionizing Radiation, Chapter IV). When it is a matter of life and death, however, I believe that the standards must be made as stringent as possible. It is far better to overestimate the risks than to underestimate them -- standards can always he relaxed later on, hut dead people cannot be resurrected so easily. Moreover, if the housing standards are tightened up at some future date, it will be very difficult and costly to do the remedial work needed to bring older buildings into conformity with the new standard.
CONCLUSION AND RECOMMENDATIONS
Radon is a very potent carcinogen, mainly because of the radon daughters which inevitably accompany it. Even if we use the linear hypothesis, it has been estimated that about 8 percent of all spontaneous lung cancers in the United States are due to naturally-occurring radon gas, and that is at an average level of exposure (0.001 WL) which is only 1/5 of the proposed housing standard.  Allowing a twenty-fold increase in public exposure to such a potent carcinogen seems a very questionable policy. The U.S. Environmental Protection Agency has calculated that outdoor exposure to radon gas emitted by a typical tailings pond, even with five metres of earth covering it, would cause from 60 to 200 extra deaths in the surrounding population per century, due to radon-caused lung cancer (see "Health Effects of Radon-222 from Uranium Mining" for details.)
In this paper, I have argued that
Two recommendations suggest themselves. The first is that people should be told that there is a very real risk of excess lung cancer from radon exposure in homes, and that the proposed housing standard could, under the worst conditions, lead to a substantial increase in lung cancer rates. This may not be a pleasant thing to do, but it must be done. People deserve to know the worst, since they are the ones who will be taking the risks -they certainly deserve more than soothing reassurances which make the problem seem to be non-existent. The second recommendation which I would like to make is that every effort should be made to prevent excess radon in Elliot Lake buildings, if necessary by building them above ground without basements, elevated by means of cinder blocks or other props under the foundations. If all else fails, serious consideration should be given to having workers live away from Elliot Lake and commute to work.
When there is conflicting testimony on the nature of a public health hazard with a high degree of credibility on both sides, it seems to me that the standards should be set on the assumption that the more pessimistic estimate may in fact be the true one. Certainly my training as a mathematician tells me that when this kind of conflicting evidence exists, it can be dangerously misleading to rely on one simplistic mathematical model which incorporates only one narrow view or version of the truth. As Fred Knelman has said, when human life is at stake, the "magic numbers" provided by a calculational model can turn out to be "tragic numbers" for the people involved.
Now Medical Director at the U.S. National Institute for Occupational Safety and Health, Dr. Archer (MD) has been engaged in studying lung cancer among uranium miners for over twenty years. He worked very closely with J. K. Waggoner (author of the famous Waggoner Report on Uranium Miners in the United States, 1967, which led to a drastic reduction in the maximum permissible radon exposure for U.S. miners in 1971 -- from 12 WLM to 4 WLM annually. The Canadian standard of 4 WLM was not adopted until four years later.)
Dr. Archer has played a major role in the field of radon carcinogenesis epidemiology. The Ham Commission Report (reference 1) cites six papers co-authored by Dr. Archer out of a total of about twenty papers on the subject.
John Gofman and Arthur Tamplin
In 1963, the U.S. Atomic Energy Commission appointed Dr. Gofman as Assistant Director of the Lawrence Radiation Laboratory in Livermore, California. His mission was to head up a team of experts to investigate the biological effects of radiation on man. After seven years of intensive study of all existing experimental and epidemiological evidence on the subject, Dr. Gofman and his colleague Dr. Tamplin published results which showed that the health effects of radiation were very much higher than official estimates indicated. The research program of Drs. Gofman and Tamplin was terminated not long afterwards, to the mutual dissatisfaction of all parties.
Dr. Gofman is an M.D. and a Ph.D. in nuclear physical chemistry. He is co-discoverer of U-232, U-233, Pa-232, and Pa-233. He is Professor Emeritus in Medical Physics at the Berkeley Campus of the University of California, and Lecturer in Medicine at the San Francisco Campus of the same university. His medical researches are well known; for example, in 1972 he won the Stouffer Prize (one of the most prestigious awards in the field of heart research, carrying a $50,000 cash award) for his work on the role of lipoproteins in arteriosclerosis.
Dr. Tamplin is a Ph.D. in biophysics; he served as a group leader under Dr. Gofman in the Biomedical Division of the Lawrence Radiation Laboratory from 1963 to 1969, when funds for the project were terminated. He is currently a staff scientist at the Natural Resources Defense Council, 917 15th Street NW, Washington DC, 20005.
Karl Z. Morgan
Click here for photograph.
A world-renowned pioneer in the field of Health Physics, often referred to as "the Father of Health Physics", Dr. Karl Morgan was Director of the Division of Health Physics at the Oak Ridge National Laboratory for over 30 years. He was one of the original members of the International Commission on Radiological Protection, and was editor of the professional journal Health Physics until quite recently.
In 1971, Dr. Morgan was prevented by his superiors at Oak Ridge from delivering a paper on the health hazards of plutonium (an alpha-emitting transuranic element -- see reference 10). That was only one of several instances of suppression of scientific results at Oak Ridge (referred to by Dr. Morgan in reference 8, reprinted here as Exhibit 12). Dr. Morgan left Oak Ridge in 1972 and is now Professor of Health Physics in the School of Nuclear Engineering at the Georgia Institute of Technology.
Alice Stewart and George Kneale
Click here for photograph.
In the 1960's, Dr. Alice Stewart (MD) did an epidemiological study of childhood cancers and leukemias caused by obstetric x-rays in England. Her work showed that a single x-ray to the abdomen of a pregnant woman during the first six weeks of pregnancy would result in a 50 percent increase in childhood cancer and leukemia among the offspring. She also verified the linear hypothesis for x-rays down to very low doses in the range from 0 to 1.5 rads (low doses, but high dose rates).
When her results were greeted with skepticism, she and her statistician colleague George Kneale undertook a far more ambitious study which took in the entire British Isles. The results of this second study, the largest ever done in the field of radiation carcinogenesis epidemiology up to that time, were printed in Lancet (the British Medical Journal) in 1970. They fully confirmed her earlier findings. A similar study was done by Dr. Brian McMahon of Harvard University using U.S. data, and it gave additional confirmation to Dr. Stewart's results.
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