Canadian Coalition
for Nuclear

Regroupement pour
la surveillance
du nucléaire

Estimating Lung Cancers


It's Perfectly Safe,
But Don't Breathe Too Deeply

Part 2

Estimating Lung Cancer Deaths
Caused by Permissible Radon Exposures
in New Homes in Elliot Lake, Ontario

by Dr. Gordon Edwards

a summary of testimony presented to
the Ontario Environmental Assessment Panel
on permissible levels of radon contamination
for new homes in the town of Elliot Lake


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:

"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)

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. [17] (Archer et al., ref. 3; see exhibit 3 below)



Archer, 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). [18]


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;

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:

Similar observations can be made about Table 3 (Exhibit 6) dealing with Czechoslovakian data.

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

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. [19]


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)


Effects of Exposure to   0.02 WL   for   one hour per day   over a lifetime

Model UsedNumber 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
in Czechoslovakia
Relative Risk Model
HiroshimaRelative 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. [20] 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.)



Source of
Extra Cancers
per 100,000 men

(1 hour/day)
Extra Cancers
per 100,000 men

(12 hours/day)
Extra Cancers
per 100,000 men

(17 hours/day)
Increase in
Cancer Rate

(12 hours/day)
Increase in
Cancer Rate

(17 hours/day)
Minimum Risk
from Table 6
2.7 percent
3.8 percent
Muller's Estimate
(Appendix, p. 91)
4.4 percent
6.3 percent
from Table 6
5.6 percent
7.9 percent
Overall Average
from Table 6
7.5 percent
10.6 percent
Relative Risk
Data (averaged)
10.4 percent
14.8 percent
Maximum Risk
from Table 6
11.8 percent
16.7 percent

A glance at the right hand column shows that there is a very wide spread in the risk estimates that one might make on the basis of the MOH data, even if we only use the averages given in Table 6, and that Dr. Muller's estimate is toward the low end of this spectrum.

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?


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.


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

  1. 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.


Table III from "Radon Daughter Cancer in Man" by Victor Archer et al.


Mean Exposure Rate
(in WL)
Up to 0.01
0.01 to 0.36
0.36 to 1.09
1.1 to 2.5
2.6 or more
Cumulative exposure
(in WLM)
Up to 3.0
3.1 to 100
101 to 300
301 to 700
701 or more
Attributable cancers
(per year, per WLM,
per million persons)
Attributable cancers
(per lifetime, per WLM,
per million persons)
Average WLM exposure
needed to produce
one lung cancer
Relative risk factor
per million persons
per WLM of exposure

  1. At 12 hours per day exposure, 0.01 WL yields a lifetime dose (over a period of 50 years) of about 12 WLM. Excess cancers, according to this table, would then be 12 times 1170 = 14,040 cases per million, or 14 extra cases per thousand -- a 26 percent increase in the Ontario male lung cancer rate.
  2. At 12 hours per day exposure, 0.02 WL yields a lifetime dose (over a period of 50 years) of about 24 WLM. Excess cancers (using this table) would then be at least 24 times 1020 = 24,480 cases per million, or 24.5 extra cases per thousand -- representing a 45 percent increase in the Ontario male lung cancer rate.

a) Non-Conservative Factors (continued)

  1. Dr. Muller assumes that all lung cancers will appear within a 20 year period following a single exposure (see his comment, reproduced under table 6 on page 27). There is no epidemiological evidence presented to support this assumption. In fact, no less than 11 of the Colorado Plateau miners studied in John Gofman's paper developed cancer more than 20 years after initial exposure -- and this number, 11, is almost double the expected number of lung cancers for the entire population of 1981 miners (using U.S. data on lung cancer incidence in those age groups.) As Victor Archer points out,
    "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. [21] 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).

  2. Children are known to be more radiosensitive than adults. In the late 1960's, Dr. Alice Stewart showed that a single diagnostic x-ray to the abdomen of a pregnant woman in the first six weeks of pregnancy leads to a 50 percent increase in childhood cancer and leukemia among the offspring [22] -- a risk factor which is in turn higher than the relative risk for children up to nine years of age, which is in turn greater than the relative risk for adults (see "The Cancer and Leukemia Consequences of Medical X-Rays", especially table 1 therein). This extra sensitivity of children to radiation-induced cancers may be compounded by heavy juvenile exposures to radon, as a result of

    1. children crawling or playing on the floor or close to the walls, where the radon concentrations are often higher than elsewhere in the house;

    2. children spending more than 12 hours per day inside the house and/or spending more time in the basement;

    3. children playing outside close to the outer walls of the house, where the radon gas rises from under the house.

    4. Mothers and invalids may spend much more time indoors than able-bodied men and older children, thus giving rise to proportionately greater doses.

    5. Mechanical problems or structural deterioration may incapacitate protective systems (such as fans or sealants) within the buildings, resulting in indoor radon levels above 0.02 WL. [23]

    6. Atmospheric radon gas from uranium tailings in the Elliot Lake area will contribute an outdoor component of radon exposure which is by no means insignificant and which should also be evaluated (see "Health Effects of Radon-222 from Uranium Mining", which is based on data from the U.S. Environmental Protection Agency). [24]

    b) Conservative Factors

    1. Not all buildings will approach the 0.02 WL limit.

      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.

    2. For uranium miners, the additional radon exposure in the home will be a relatively small augmentation to the exposure which they receive in the mines.

      However, the risk is additive, and the ICRP recommends that all unnecessary exposure to radon be avoided.

    3. Most people will not spend their entire lives in Elliot Lake; there will be a considerable population turnover.

      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.

    • Using Dr. Muller's equivalence of  1 WLM = 4.42 rems  (page 5, Appendix, MOH Report), it is easily seen that one year's accumulated dose at 0.02 WL for 12 hours per day amounts to almost 2.28 rems, which is far in excess of the 1.5 rem limit set by the AECB.

    • Even if we use 1 WLM = 4 rems, the annual accumulated exposure at 0.02 WL for 12 hours per day is just over 2 rems, which is 33 percent higher than the maximum permissible exposure for members of the public.

    • As the BEIR Commission Report notes, typical conversion factors are  1 WLM = 5 to 6 rems , which makes the situation even worse: see the Ham Commission Report, page 116.

    Whole-body exposure results primarily from gamma radiation.

    • The MOH Report advocates a standard of 0.05 millirems per hour (gamma) at a height of one metre above the centre of the floor (where your gonads might be when you stand up).

    • With 12 hour per day exposure, this will produce an accumulated annual dose of 219 millirems, which is more than 40 times larger than the AECB Guideline of 5 millirems per year.

    • Recent standards laid down by the U.S. Environmental Protection Agency limit the exposure of any member of the general public from any U.S. nuclear facility to an absolute maximum of 25 millirems per year.

    • Thus, on a 12 hour per day basis, the proposed housing standard of 0.05 millirems per hour will lead to an annual accumulated dose which is 8.76 times higher than the Maximum Permissible Dose from a nuclear facility in the United States.


    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. [25] 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.


    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. [26] 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

    1. there is good scientific evidence that alpha radiation is more effective in causing cancer at low dose rates than at high dose rates

    2. using data provided by the Ministry of Housing, one can reasonably estimate a 31 percent increase in the incidence of lung cancer among people who spend a lifetime in buildings having a 0.02 WL radon environment.

    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.



    Victor Archer

    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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