|
Our current estimate is that about 75% of the current annual incidence of
breast cancer in the U.S. is being caused by earlier ionizing radiation, primarily from medical sources.
Mammography - radiation induced breast cancer.
John W. Gofman, M.D., Ph.D., Committee for Nuclear Responsibility, P.O. Box 421993, San Francisco, CA 94142, in Preventing Breast Cancer: The Story of a Major, Proven, Preventable Cause of This Disease.
Mammography and ionizing radiation received on the chest leads to an increased breast cancer risk. A study reports for instance that
Young women with Hodgkin's disease treated with high levels of radiation to the chest are much more likely to develop secondary breast cancer than women on less aggressive radiation regimes... .
The study found that the breast cancer risk was eight times higher among women exposed to the highest levels of radiation than women who were given the smallest doses, where those women
were treated before age 30. The risk persisted years after treatment, with the high-dose group still more than twice as likely to develop breast cancer than the low-dose group 25 years later, according to
the study in the Journal of the American Medical Association.
The findings by researchers at the National Cancer Institute in Bethesda, Maryland,
confirm the thinking that women with Hodgkin's disease (cancer of the lymphatic system) should be given only as much radiation as is necessary to eliminate the
primary cancer. Survival rates for Hodgkin's disease (HD) have increased significantly in the last 50 years - the five-year survival rate in the United States is now 85
percent, according to the Institute. But the improvement in treatments has been accompanied by an increased risk of secondary cancers, with breast cancer the most
likely form to strike women. ... Increased rates of breast cancer have been generally attributed to chest irradiation for HD, consistent with the known sensitivity of the
breast to ionizing radiation at young ages. The evidence "supports the notion that 'lower is better' as long as the radiation dose used augments the cure rate for HD,"
wrote Joachim Yahalom, an expert in radiation oncology with New York's Memorial Sloan-Kettering Cancer Center in an accompanying editorial. ... Researchers based
their findings on a study of 3817 women diagnosed with HD at age 30 or younger between 1965 and 1994, 105 of whom went on to develop breast cancer. (Sapa-AFP)
Ionizing Radiation (X-Rays, Fluoroscopy, Mammograms) as a Preventable Breast Cancer Cause
excerpted from the book Preventing Breast Cancer: The Story of a Major, Proven, Preventable Cause of This Disease, (1996), by John W. Gofman, M.D., Ph.D. This
book uncovers the major cause of the recent breast cancer incidence in the USA. The author shows that past exposure to ionizing radiation --- primarily medical x-rays ---
is responsible for about 75 percent of the breast cancer problem in the United States. The good news: Since the radiation dosage given today by medical procedures can
be significantly reduced without interfering with a single useful procedure, numerous future cases of breast cancer can be prevented.
The author recommends specific actions to start breast cancer prevention now, not
ten years from now.
The Master Table referred to in these extracts can be seen at www.ratical.org/radiation/CNR/PBC/chp39.html#MasterTblA-J.
CHAPTER 1: Our Conclusion: A Large Share of Breast Cancers Need Not Occur
Part 1. The Bottom Line
We begin this book with our bottom line, because we think the advice of Sara Jeannette Duncan is good: "If you have anything of
importance to tell me, please, PLEASE begin at the end!" So here is our conclusion:
Breast cancer is a largely PREVENTABLE disease, and we reach that good news because of our finding that a large share of recent and
current breast cancer in the United States is CERTAINLY due to past medical irradiation of the breasts with x-rays at all ages, including infancy and childhood. Much of today's radiation dosage is
preventable, without any interference with necessary diagnostic radiology, and hence many future breast cancers need not occur.
What do we mean by "a large share" of recent and current breast cancer?
Our estimate is that about three-quarters of the current annual incidence of breast cancer in the United States is being caused by earlier ionizing radiation, primarily
from medical sources. We will show that the recently growing incidence is not mysterious, and that if we wish to understand why the incidence has been growing, we must look to radiation events in
the life of women 15-25-35-45 and more years before breast cancer diagnosis. Moreover, there is recent evidence about induction of EARLY-onset breast cancer by radiation (Chapter 3).
There are many stories in this book, but no villains. The cast of historical characters is interesting, impassioned, and sometimes very wise.
No one meant to do any harm. On the contrary. After discovery of the x-ray in 1895 and of radium in 1898, radiation was tried out
widely in medicine, right up to recent times, in the hope of RELIEVING a great variety of human afflictions. Some radiation therapies were (and are) clearly effective (and this book is highly
complimentary about such uses). Some other therapies, clearly not effective, have been discontinued. But usefulness is not always clear-cut in medicine. For example, users reported benefits which
others could not see, regarding one type of x-ray therapy which was used for infants and children from 1911 to almost 1960.
The finding of this book constitutes an example of what can happen from exposing people to new agents, such as x-rays, when no one
KNOWS the long-term consequences. Readers will see the innocent enthusiasm, the repeated assurances that the procedures were safe, and the power of the "technological imperative" to suppress the idea
that there might be a problem with anything as wondrous and potentially useful as x-rays. This is a story of "disaster creep" - a massive problem creeping up on society without any recognition.
In science, every important discovery should be challenged and checked by others, and our finding certainly will be. We will welcome
the genuine, thoughtful critiques. And we expect our finding to be validated. We arrive at our startling conclusion after UNDERestimating the past dosage of x-rays, and after using
conversion-factors (conversion from dose to subsequent cancers) which derive from real-world observations. There is just no doubt that past radiation exposure accounts for a major share of our recent
and current breast cancer problem. The evidence for our finding is overwhelming if one simply looks.
Many will look thoughtfully at the input to this study but there will be exceptions. We expect our finding to be automatically rejected by
some who merely WANT it to be faulty and who will comment upon it without even reading this book.
If breasts could talk, they might say, "Read first, judge second, and please start now!"
Part 2. For Whom Is This Book Intended?
This book is intended for anyone interested in breast cancer, and its prevention. Interest in the problem is the only requirement. The
book is for medical professionals AND for individuals with the greatest personal concern: Women in general and their families. Readers do not need to know every medical term in the stories,
because the MEANING of the stories will be clear anyway. No medical skill or knowledge is essential to understand what will be presented.
Many chapters will begin with a description of what happened, and will end with specific calculations based on the events. Of course,
many readers will skip the numbers. The "easy readers" should feel no guilt for skipping the latter part of various chapters. Lots of professionals, also, read scientific journals without ever examining
the calculations and tables there. But numbers are in journals, and also in this book, for a very important reason: To ALLOW people to check for themselves exactly how the quantitative conclusions were
reached, and to evaluate the validity for themselves.
Part 3. An Astonishing Statement in a Fund-Raising Appeal
I've recently received in the mail a request for funds to help breast cancer research. It said: "Breast cancer is THE most commonly
diagnosed cancer in American women today. It is THE leading cause of death among women ages 40 to 44, and the leading cause of cancer death in women 20 to 54." No argument about that. Every
part of that statement makes it all the more important for women to know precisely why we say that breast cancer is largely preventable. Then the letter added:
"What's worse, even the best doctors have no idea what causes breast cancer or how to cure it." Cure is indeed problematical, and
when successful, the process itself can be highly unpleasant. All the more reason why prevention is so very important.
But how can anyone in 1994 say that "even the best doctors have no idea what causes breast cancer"? This error also went out over NBC
national news during October 1994, in the television network's coverage of Breast Cancer Month. In reality, medical science has clearly known for some 20 years already that ionizing
radiation is a prominent and proven cause of breast cancer. Ionizing radiations include x-rays and gamma rays, as well as beta, alpha, and some other high-speed particles. (Radium is used in
medicine as a source of powerful gamma rays.)
We think "the best doctors" do indeed know about the role of ionizing radiation as a prominent, proven cause of breast cancer, but
it is astonishing that both lay and medical sources COMMONLY fail to mention this outstanding fact of medical science: Past medical exposure to ionizing radiation, 10, 20, 30, 40, and more years back
in a woman's life, can cause breast cancer.
Radiation exposure in the first few months of life may be the most serious in causation of later breast cancer. In fact, irradiation of the
breasts between age 0 (newborn) and age 9-years may cause MANY-fold more cases of breast cancer, over the subsequent lifetime, than does irradiation of women over 40 years of age with
the same amount (dose) of ionizing radiation.
The Current Size of the Problem, USA
Today, it is estimated that one woman out of every nine in the USA will develop breast cancer sometime during her lifespan. The breast
cancer problem is reflected in the estimates below, of breast cancer incidence in the USA (derived by the American Cancer Society from government data). The numbers exclude "in situ" cases. The rapidly
rising numbers below reflect diagnosis, not death. As so many families know already, diagnosis in itself brings severe consequences, even if a woman dies of something else in the end. The numbers on
the right show that the growth of the female population can explain only a small part of the rising incidence of breast cancer. (The tabulation below is expanded in Tables 1 and 2, which are located after the final chapter.)
1970: 68,000 cases diagnosed; females of all ages = 104,309,000
1975: 88,000 cases diagnosed; females of all ages = 110,401,000 est.
1980: 108,000 cases diagnosed; females of all ages = 116,493,000
1985: 119,000 cases diagnosed; females of all ages = 122,474,500 est.
1990: 150,000 cases diagnosed; females of all ages = 128,454,000
1994: 182,000 cases diagnosed; females of all ages = 133,194,000
Part 4. How Do We Know that Radiation Is a Cause of Breast Cancer?
Every once in a while, a massive step forward in medicine is taken by the oldest technique in medical practice the careful taking by a
physician of a patient's medical history. Such an event of landmark proportions is represented by the observations of Dr. Ian MacKenzie, a physician in Nova Scotia, Canada.
In 1961, a woman with a rapidly growing breast cancer came to his office. He noticed that her cancer had occurred in the upper inner
quadrant of her right breast, and that her skin over the right chest wall, breast, and sternum showed signs of dermatitis (skin inflammation).
MacKenzie questioned her carefully about her history, and learned that she had been treated 14-15 years earlier for pulmonary (lung)
tuberculosis. In those years, a common practice was to let one of the lungs rest, by collapsing it with an injection of air between the chest wall and the lung. This procedure was called artificial pneumothorax
therapy, and in her case, it took place over 46 months. Each time she had a re-fill of air into the chest, the status of the lung was checked with fluoroscopy, before and usually after.
Fluoroscopy is also called roentgenoscopy, in honor of Wilhelm Konrad Roentgen, who discovered x-rays in 1895. In
roentgenoscopy, examination of a patient with x-rays takes place while the x-ray beam stays "on," so that the physician can observe what happens when the patient or the patient's
organs are in motion. Roentgenoscopy is thus very different from roentgenography, which is the use of x-rays to expose a sheet of film (or other types of image-receivers) to
produce the usual x-ray picture. Roentgenoscopy, requiring no development of film, produces information immediately.
When Dr. MacKenzie obtained his patient's sanitarium records, he learned that she had had at least 200 fluoroscopic examinations
during her treatment. The patient remembered that her skin changes began during this period, too. Dr. MacKenzie recognized that she had radiation dermatitis, and he began to suspect that breast
exposure to x-rays might also account for her breast cancer.
To check on this idea, Dr. MacKenzie studied almost 800 women who had been treated for tuberculosis in one sanitarium during
1940-1949. The startling results were published in 1965. Of 510 women who did NOT receive artificial pneumothorax treatment and therefore did not have repeated fluoroscopies, one woman had
subsequently developed breast cancer by the time of Dr. MacKenzie's study. This is a rate of (1 woman / 510 women), or 0.00196. Of 271 women who DID receive artificial pneumothorax treatment with
multiple fluoroscopies, 13 had developed breast cancer by the time of Dr. MacKenzie's study. This is a rate of (13 / 271), or 0.04797. The breast cancer rate in the irradiated group was (0.04797 /
0.00196), or 24.5 times the rate in the non-irradiated group. In his paper (p.7), Dr. MacKenzie said:
"From the evidence presented, it would appear to be a reasonable conclusion that the well-recognized role played by ionizing radiation
in the development of certain other forms of malignant disease can be extended to include carcinoma of the breast in the circumstances presented by these cases." If pulmonary tuberculosis itself were the
cause of the breast cancers, then the irradiated and non-irradiated cases should have had similar breast cancer rates, as Dr. MacKenzie commented. Dr. MacKenzie's finding caused quite a "stir" in radiation circles.
1965 (March): Ian MacKenzie, "Breast Cancer Following Multiple Fluoroscopies," British Journal of Cancer 1965, Vol.19: 1-8.
Soon thereafter, C.K. Wanebo and colleagues, studying the survivors of the atomic bombings at Hiroshima and Nagasaki, and stimulated
by the MacKenzie work, launched an investigation of breast cancer in those survivors. In 1968, they published confirmatory evidence of human breast cancer induction by ionizing radiation. In 1969,
Myrden and Hiltz extended the follow-up time for MacKenzie's 1965 study. And in 1970, Arthur Tamplin and I used the MacKenzie and Wanebo data to quantify the dose-response for radiation-induced breast cancer. We showed in The Lancet that the breast cancer risk
from ionizing radiation was quite serious indeed.
Proven, and Then Forgotten?
In the years which have followed MacKenzie's 1965 paper, numerous studies have confirmed and quantified the induction of breast cancer
by ionizing radiation. For the convenience of readers, we have identified a number of those papers by prominently flagging them with the symbol "#" in our list of references. Many of these studies
have been analysed in Gofman 1981 and in Gofman 1990. In 1994, even further confirmation became available in the latest reports on cancer incidence in the A-Bomb Survivors (Mabuchi; Thompson; Tokunaga).
The radiation-causation of human breast cancer is not in dispute. Nonetheless, it is commonly forgotten in discussions about the
alleged mystery of breast cancer causation.
Part 5. What about Other Potential Causes of Breast Cancer?
Cancer - not breast cancer alone - is now considered to be a genetic disease. It is thought that a tumor develops in stages from a single
cell, as the cell and some of its descendants accumulate a set of several "genetic lesions." A lesion is an injury or loss of function. Genetic lesions are those which occur in the genetic molecules
- namely, in the DNA molecules which control a cell's proper operation, including the accuracy and appropriate rate of the cell's division. Genetic lesions in a cell can occur at any age.
Inherited diseases are properly called genetic diseases. They occur because offspring receive certain genetic lesions in the DNA which
they inherit from their parents. (Mother and father do not often transmit the SAME lesions, however.) Inherited genetic lesions are present in the fertilized human egg. Since every cell we have is
descended from the fertilized egg, the lesion is present in every cell. By contrast with an inherited lesion, a genetic lesion which occurs in childhood or adulthood is present only in the cell where it took place,
and in cells descended from the altered cell, but it is not present as an all-cell lesion. So, inherited diseases are genetic, but not all genetic diseases have to be inherited. The responsible genetic lesions
can occur after conception.
With respect to cancer, it is thought that cells become malignant only after they have accumulated several carcinogenic lesions (many
estimates range from four to ten lesions). Some of the lesions may be inherited, and others may occur at any age after conception. Individuals who inherit one or more carcinogenic lesions in EVERY
cell, have an increased chance that SOME of their cells will accumulate a complete set of the necessary lesions during their lifetimes. Such people are born "predisposed" to develop full-blown, clinical cancer.
Interaction of Inheritance and "Other Forces"
Almost certainly, inherited carcinogenic lesions have a range from weak to strong. The famous lesions are the rare inherited ones which
confer a high chance of cancer in a specific organ, with the clinical cancer often occurring at a very early age. We call those "destiny" lesions, and the weaker ones "predisposing" lesions.
The inherited "destiny" lesions are estimated to account for five to ten percent of human cancer. For breast cancer, the estimate is about
ten percent. Even a "destiny" lesion may need help from other forces, in order to create some cells with the COMPLETE set of genetic lesions required for full-blown cancer. By "other forces," we mean to
include agents such as x-rays, viruses, or certain chemicals.
An inherited "predisposing" lesion, by definition, needs help from other forces in order to cause a cancer.
Do such other forces, acting in the absence of INHERITED carcinogenic lesions, ever produce the complete sets of lesions
required for malignancy? At this time, there is no way to know how often this happens, if ever. It may turn out that cancer almost NEVER develops in the absence of an inherited "head start" ... and almost
ALWAYS requires the interaction of inherited lesions with other forces.
The bottom line on inheritance and other forces is this:
A very large part of the cancer problem can be eliminated, if people CORRECTLY identify and eliminate the non-inherited forces which act
alone or act in concert with inherited genetic lesions, in producing malignancy. This book shows that past exposure to medical x-rays is a MAJOR non-inherited cause of the breast cancer which has
occurred, is now occurring, and is already committed to occur in the future in the USA. Readers who follow the stories, chapter by chapter, will end up realizing that medical radiation is surely a
non-inherited cause of OTHER cancers, also. How large the share is, for other cancers, remains to be evaluated.
And What about Pesticides, Hormone Pills, Diet, and EMFs?
There is nothing about the finding of this book to imply that ionizing radiation is the ONLY cause of recent breast cancer.
Many non-inherited forces, including pesticide by-products, hormone pills, diet, exercise, EMFs (electro-magnetic fields and "transients"),
and several additional factors, have been implicated by epidemiologic studies as potential contributors to recent rates of breast cancer. (Epidemiology is a science which tries to find the causes of diseases,
by comparing their frequencies in various groups of people.)
Do we dismiss these other forces? Not at all. Even agents and behaviors which cause no permanent genetic lesions may accelerate
a developing cancer in several ways without casting any doubt upon the multi-step genetic model of cancer development. The power of such promoters may depend on the presence of genetic lesions.
Indeed, we take this opportunity to say that we are particularly concerned about the question of EMFs, to which human exposure is
likely to INCREASE in future years. We highly recommend a collection of papers on EMFs and breast cancer (Slesin 1994).
With respect to ionizing radiation, the proof that extra exposure is a cause of cancer (including breast cancer) comes from studies where
all sorts of ADDITIONAL non-inherited causes may have been operating too. The point is this: In any valid epidemiologic study, those other carcinogens are acting EQUALLY upon the irradiated
groups and upon the non-irradiated groups. Thus, the EXTRA cancers in the irradiated groups can be attributed to the extra radiation, but the REST of the cancers are due to something else
(such as equal exposure, on the average, of all the study-groups to chemicals, EMFs, or prior exposure to radiation-sources other than the source studied).
There is no inherent conflict or competition between carcinogens. The multi-step genetic model of cancer development "permits"
contributions even to a SINGLE CASE of cancer, from heredity, ionizing radiation, viruses, and chemicals (for example). It is correct to say that each contributor CAUSED the cancer, if the case would
not have occurred when it did, without that contributor.
The finding of this book is that an estimated 75 percent of recent and current breast cancer cases would not have occurred as they did, in
the absence of earlier medical (and other) irradiation.
CHAPTER 3: Early-Onset breast cancer: Evidence on Radiation-Induction
Recent evidence, discussed below, underscores the importance of acting upon the finding of this book, if prevention is everyone's goal.
So that all readers (including the "easy readers") can contemplate the meaning of this new evidence, we introduce the units in which radiation doses are measured.
Part 1. Dose-Units, Especially "Medical Rads"
The term "medical rad" is the one which we use in reaching the finding of this book. To show what it means, we have to cover some other units.
RADS. The "rad" is a unit in which amounts (doses) of ionizing radiation are measured, the way "dozen" measures an amount of
eggs. Rad is the abbreviation for "radiation absorbed dose." A rad is really just a ratio of energy delivered by ionizing radiation, per gram of irradiated cells or tissue. A rad is 100 ergs of energy per gram a
definition which NO reader needs to remember. One thousandth of a rad, or 0.001 rad, is a milli-rad. An effort is underway to re-name the rad as a centi-gray (cGy) and to call 100 rads a gray (Gy). We
and many others prefer to stick with rads.
ROENTGENS. The Roentgen is a unit for measuring ionization in air; a few reports also use it for doses inside the body. The abbreviation
for Roentgen is R (but a small "r" was customary in the older literature). Under common medical circumstances, an entrance dose of 1 Roentgen at the skin gives a breast-tissue dose of about 0.69
rad, when the beam is traveling from front-to-back of a patient. The Roentgen is the dose-unit often used to describe x-ray dosage from fluoroscopy. In the 1930-1935 era, many fluoroscopy machines
could generate beams with dose-rates like 100 Roentgens per minute (Braestrup 1969).
REMS. Another unit is called the rem, an abbreviation for "roentgen equivalent, man." The rem can indicate that adjustments have been
made for the non-standard "quality" of some radiations. Usually (but not always) the standard is an x-ray of 100 to 400 KeV. An effort is underway to re-name the rem as a centi-sievert (cSv) and to call 100
rems a sievert (Sv).
MEDICAL RADS. Per rad, gamma rays from an atomic bomb are about half as harmful as x-rays from medical irradiation, so 1.0 rad
of A-bomb gamma radiation could be called 0.5 rem. We avoid rems in this book by converting all doses into "medical rads." Hence, 1.0 rad of A-bomb gamma radiation is called 0.5 medical rad.
Some Very Common Radiation Dose-Levels
NATURAL BACKGROUND RADIATION. The typical annual dose from natural background radiation, excluding doses from inhaled
radon, is about 0.1 rem or 100 milli-rems (BEIR 1972, p.50; BEIR 1990, p.18). The dose per year rises with altitude. Because the natural background dose is mostly from gamma and cosmic
radiation, its medical equivalent per year is about 0.05 medical rad (50 medical milli-rads). In a 70-year lifespan, the cumulative dose is about 3.5 whole-body medical rads. A whole-body dose is received
by all parts of the body, in contrast to a partial-body dose.
The natural dose-rate per MINUTE is of interest, for comparison with dose-rates from fluoroscopy. Nature's dose-rate per minute is (0.05
medical rad / year) times (1 year / 525,600 minutes), or 0.000000095 medical rad per minute from natural background radiation. If we round this off, it is about one ten-millionth of one
medical rad per minute. At this dose-rate, only a tiny fraction of cells is irradiated per minute.
AIRLINE TRAVEL. The extra radiation dose, from flying between the east and west coasts of the USA, is about 0.3 milli-rem (0.0003
rem) per HOUR of commercial flying. For a ten-hour roundtrip, the extra dose would be about 3 milli-rems (0.003 rem). It would require about 3,300 flying-hours to receive 1.0 extra rem of
whole-body irradiation --- equivalent to about 0.5 extra medical rad. Dose-rates from flying vary with altitude and latitude.
Part 2. The Dose Which Doubles the Rate of Early-Onset Breast Cancer
Ordinarily in epidemiological studies of cancer development from radiation, one faces the "small numbers problem": An insufficient
series of cases in the relatively EARLY follow-up period to permit a reliable conclusion. So time is allowed to run, to accumulate additional cases ("statistical power"). And then all the cases --- short
latency and long-latency cases, combined --- are examined together for such issues as cancer increase per rad of dose. But WHAT IS LOST, within the accumulated total, is any evaluation of whether the
"early-onset" cases are different from the other cases. From here on, the cases diagnosed before age 35 will be called "early-onset" cases.
With follow-up of the A-bomb survivors now complete for 1950 through 1985, there may be enough total cases of breast cancer to
separate the early-onset cases from the others, and to compare them for induction-rate per rad of irradiation. In 1993, Charles Land, Masayoshi Tokunaga, and additional RERF analysts, made a brief
report in the Lancet, entitled "Early-Onset Breast Cancer in A-Bomb Survivors" (Land 1993). By extracting the pertinent data from the figure in their 1993 paper, we can tabulate their findings in the
nearby box. They are remarkable results, to say the least!
In their 1993 paper, Land et al. are reporting exclusively on female A-bomb survivors who received the bomb exposure before the age
of 20 years. Although Land et al. do not say so, the number of females who were exposed by the bombs below age 20 was approximately 12,000, and their average age at the time of bombing
was about 10 years old (calculated from Gofman 1990, Table 26-F). There are 205 incident cases of breast cancer, reported between 1950-1985 for this group. The cases are segregated by Land et al.
into two main groups: Women whose breast cancers occurred before age 35 years constitute one group, and women whose breast cancers appeared after age 35 years, the other group. We repeat: All the
women were less than age 20 at the time of exposure.
In the boxed tabulation, the entries for "fractional increase ... per rad" indicate a spectacular difference between early-onset cases
versus cases occurring at age 35 and beyond. The difference is treated as real (not spurious) in both Land 1993 and Tokunaga 1994. We shall propose an explanation of the difference in Part 4.
But here, we will focus on the breast-dose which, if delivered sometime before age 20, can DOUBLE the rate of early-onset breast cancer. This value can not change with any future observation of the
A-bomb survivors, because the story for EARLY-onset cases was over when the youngest survivors (newborn in 1945) passed the age of 35 in 1980.
TABULATION BASED UPON LAND ET AL., 1993.
|
|
Average Age When Breast Cancer Occurs
|
Number of Breast Cancer Cases
|
Fractional Increase in Breast Cancer Rate over Spontaneous
Rate
per rad
|
|
Breast Cancers Occur Before Age 35 years
|
32 years
|
27
|
0.136 13.6 %
|
|
Breast Cancers Occur After Age 35 years
|
41 years
49 years
57 years
|
80
85
13
|
0.013 1.3 %
0.024 2.4 %
0.017 1.7 %
|
|
Sum of cases,
|
bomb-exposed
|
women
|
205 cases.
|
|
The "Doubling Dose" for Early-Onset breast cancer
The dose which doubles the spontaneous frequency of early-onset breast cancer is the dose which causes a 100 % increase in its
spontaneous rate. Therefore, to estimate how many rads would cause a 100 % increase, we divide 100 % by 13.6 % per rad (from the boxed tabulation). Thus, 7.35 rads, received before age 20, is
the approximate doubling dose for early-onset breast cancer.
The doubling dose for early-onset breast cancer is even lower when we consider medical x-ray radiation, or beta particles of energy
comparable to such x-rays. The medical rad has approximately two times the effectiveness of A-bomb radiation from which Land, Tokunaga, and colleagues developed their findings. Therefore, we
must warn that the dose of medical rads required to double the spontaneous rate of early-onset breast cancer must be in the neighborhood of only 3.68 medical rads, received sometime before
age 20. As readers will see in Sections 2 and 3 of this book, such doses and far higher ones have been commonly received during childhood from certain medical procedures and we do NOT mean
doses from radiation therapy after a cancer has already occurred.
Part 3. A Test for Agreement about the Magnitude of Risk
Below, we will show the good agreement between RERF's quantification of risk (by Land, Tokunaga, et al) and our own
independent analysis of 1990. The "easy readers" of this book may wish to skip to Part 4 or Part 5, but others will find Part 3 very interesting.
Our analysis used the data on cancer deaths (all types) from 1950-1982 in the A-Bomb Survivors, and the RERF analysis used
exclusively the breast cancer incidence from 1950-1985 among the A-Bomb Survivors. Both analyses (Gofman and RERF) are finding out the "fractional increase or percent increase above the spontaneous
rate, per rad" a concept which we named "the K-value" simply for the sake of brevity. Tokunaga et al. call the same thing "Excess Relative Risk," or ERR.
Based on the linear dose-response in Tables 15-G and 15-H of Gofman 1990, our K-value estimate for females exposed at ages 0-9
years is 0.01922 (the same as 1.922 %). Age 0 means from birth to the first birthday. For exposure at ages 10-19, the K-value is 0.01097 (or 1.1 %). When the two values are weighted by the number of
cases, the average is 0.01265, or 1.265 % per rad for exposure at ages 0-19. This value is for ALL types of cancer, combined. For breast cancer alone, the K-value is 2.524 times the value for
combined types (Thompson et al 1994, pages S26, S49, S61). Multiplying the 1.265 % per rad for all cancers, by 2.524 to adjust for breast cancer alone, we obtain a K-value of 3.2 % per rad for
breast cancer, when bomb-exposure occurred at ages 0-19 years.
The comparable K-value from RERF's own analysis is 2.41 % per rad from Tokunaga 1994, p.215, Table VI. RERF's value is derived from
observations of cancer incidence, whereas our value is derived from observations of cancer mortality. When our 3.2 % is divided by their 2.41 %, we see that one estimate differs from the other by only 33
% . The two separate analyses are in remarkably close agreement.
The similarity in estimates is supportive of the concept that, when extra radiation induces extra cancers, it induces cancers which are
fatal and non-fatal in the same proportion as occurs without the extra exposure to radiation.
Part 4. Early-Onset Cases vs. Later Cases: Why Such a Difference?
If readers look back in Part 2 at the boxed tabulation, they will see the column for "average age when breast cancer occurs" for 205 of
the A-bomb survivors irradiated between birth and age 20. For cases diagnosed at an average age of 32, the percent increase per rad above the spontaneous rate is 13.6 %, whereas the percent increase
per rad is DRAMATICALLY LOWER if diagnosis occurs at the average ages of 41 years, or 49 years, or 57 years.
What accounts for the striking difference? Is there some big biological difference between the radiation-induction of breast cancer
for cases which appear before age 35, compared with the radiation-induction of cases which appear after age 35? Is there some altered response (to irradiation during childhood) in the
irradiated HOSTS after they pass age 35? Various possibilities are discussed in Tokunaga 1994 (pp.221-222).
We propose a relatively simple explanation. Our figure, "Three Curves with a Story," demonstrates how the observed difference could arise.
Three Curves with a Story
Curve B = breast cancer rate in women irradiated below age 20, by an unspecified dose.
Curve A = spontaneous breast cancer rate in comparable non-irradiated women.
Curve C = relative risk (Curve B / Curve A).
Age at breast cancer Diagnosis, in Years.
|
Age
|
A
|
B
|
C
|
|
Age
|
A
|
B
|
C
|
|
29
|
0
|
0
|
|
|
50
|
42.5
|
102
|
2.4
|
|
30
|
0.1
|
1
|
10.0
|
|
51
|
44.0
|
104
|
2.4
|
|
31
|
0.2
|
2.5
|
12.5
|
|
52
|
45.0
|
107
|
2.4
|
|
32
|
0.2
|
4.0
|
20.0
|
|
53
|
46.5
|
108
|
2.4
|
|
33
|
0.6
|
7.5
|
12.5
|
|
54
|
47.0
|
110
|
2.4
|
|
34
|
1.0
|
11.0
|
11.0
|
|
55
|
47.5
|
112
|
2.4
|
|
35
|
2.0
|
14.0
|
7.0
|
|
56
|
48.0
|
113
|
2.4
|
|
36
|
3.5
|
20.0
|
5.7
|
|
57
|
48.5
|
114
|
2.4
|
|
37
|
5.05
|
25.5
|
5.0
|
|
58
|
49.0
|
114
|
2.3
|
|
38
|
7.5
|
32.0
|
4.3
|
|
59
|
49.3
|
114
|
2.3
|
|
39
|
9.5
|
39.5
|
4.2
|
|
60
|
49.6
|
114
|
2.3
|
|
40
|
12.0
|
45.5
|
3.8
|
|
61
|
49.7
|
114
|
2.3
|
|
41
|
15.0
|
54.0
|
3.6
|
|
62
|
50.0
|
114
|
2.3
|
|
42
|
18.0
|
61.0
|
3.4
|
|
63
|
50.0
|
114
|
2.3
|
|
43
|
21.5
|
68.0
|
3.2
|
|
64
|
50.0
|
114
|
2.3
|
|
44
|
25.0
|
75.0
|
3.0
|
|
65
|
50.0
|
114
|
2.3
|
|
45
|
28.0
|
80.0
|
2.9
|
|
66
|
50.0
|
114
|
2.3
|
|
46
|
32.5
|
86.0
|
2.6
|
|
67
|
50.0
|
114
|
2.3
|
|
47
|
35.5
|
90.0
|
2.5
|
|
68
|
50.0
|
114
|
2.3
|
|
48
|
38.5
|
94.0
|
2.4
|
|
69
|
50.0
|
114
|
2.3
|
|
49
|
41.5
|
98.0
|
2.4
|
|
70
|
50.0
|
114
|
2.3
|
|
Who Are These Curves?
CURVE A: In the nearby figure [above], Curve A depicts a SPONTANEOUS breast cancer rate beginning to rise when women
reach the age of about 30. We wish to emphasize that Curve A is a "generic" or illustrative curve, with imaginary rates of new cases (per 10,000 women) on the vertical axis. The reality-based aspect of
Curve A is its depiction of a rise which is gradual, then steep, and then gradual again.
For ages 20 through 29, the spontaneous frequency of breast cancer is very low (shown as "zero" rate). Then, for ages 30, 31, and 32, we
have elevated each data-point (really, data-symbol) SLIGHTLY above the baseline. At age 33, we show the rate of new cases starting to increase in each successive year, with the amount of annual increase
greater (steeper) between ages 35 and 50 than between ages 50 and 60, for example. The rates plotted as Curve A are tabulated in the box underneath the figure.
CURVE B: Curve B depicts the corresponding breast cancer rate in a comparable group of women who received breast irradiation
between birth and age 20. Again, we show IMAGINARY rates of new cases (per 10,000 women) on the vertical axis, and we have not specified any particular radiation dose. What we are showing,
however, is reality-based: Starting at age 30, the irradiated group shows a rate of breast cancer which is HIGHER than the spontaneous rate. The real-world observations of a higher rate were discussed in
Part 2. Among the irradiated A-bomb survivors who were ages 0-19 during the bombings, there are 27 cases of early-onset breast cancer --- and all but 2 or 3 of those cases were diagnosed when the
women were ages 30 through 34 (Tokunaga 1994, p.214). There are 178 additional cases diagnosed after age 35 in that group.
What we want to explain is why the percent increase per rad is so much higher for the cases diagnosed at the average age of 32 (the
early-onset cases) than for cases diagnosed later. Curve C depicts the question.
CURVE C: Curve C shows the result when each cancer rate of Curve B, for irradiated women, is divided by the corresponding (and lower)
cancer-rate of Curve A, for non-irradiated women. The values are also tabulated beneath the figure. These ratios are the relative rates, or Relative Risks (RR), which quantify how many TIMES higher the
exposed rate is than the spontaneous rate. We plot the RR values as Curve C, which uses the scale of the vertical axis as an "all-purpose" scale (just don't say "per 10,000 women").
At age 32, the tabulation shows that the irradiated rate is 20 times higher than the spontaneous rate. To transform this Relative Risk of
20 into percent increase per rad (K-value), we just subtract 1.0 from the Relative Risk and then divide 19 by the dose in rads. Example: If the average dose which produced Curve B were 110 rads, then the
fractional increase per rad for cases diagnosed at age 32 would be (19 / 110 rads), or 0.173 per rad which is the same as 17.3 % per rad.
What Is the "Story" of A, B, and C?
Curves A and B are nice, smooth curves suggesting nothing biologically EXOTIC. Nonetheless, their relationship generates a
stunning PEAK in Relative Risk, and therefore in percent increase per rad, for early-onset cases diagnosed at an average age of 32. After its peak value of 20, Relative Risk declines dramatically --- down to
4.3 for diagnosis at age 38, down to 3.0 for diagnosis at age 44, and then remaining above 2.0 for diagnosis beyond age 44.
What is the meaning of this peak for early-onset cases?
When two curves (for irradiated and non-irradiated groups) have been near the zero-rate during a follow-up study, the addition of just
a few cancer cases to one curve earlier than to the other curve has to cause very high Relative Risks --- even when the higher rates are not very high at all. Such events are illustrated for ages 30, 31, and 32 at
diagnosis. At age 29 and younger, the breast cancer rates are shown as equal in the irradiated and non-irradiated groups. Curves A and B are right on top of each other, at the zero-rate. At age 30, both rates
increase a LITTLE (see the tabulated values): Non-irradiated moves to 0.1 case per 10,000 women, and irradiated moves to 1 case per 10,000 women --- a very low rate compared with what is coming
later. Nonetheless, this slight change means that the risk goes "overnight" from being equal in both groups, to being 10-fold higher in the irradiated group --- all because of 1 case per 10,000 women.
At ages 31 and 32, additional small changes drive the Relative Risk to its peak at 20.
In computing Relative Risks, the spontaneous rates are the denominators of the fractions. As long as the spontaneous rates
remain near zero, even modest growth in the exposed rates will generate enormous Relative Risks. The phenomenon does not happen when analysts look at the women exposed at older ages,
because the spontaneous rate is already well above zero when analysts begin comparing the irradiated and non-irradiated groups.
The Key: A Baseline Rate Near Zero
For A-bomb survivors irradiated below age 20 and diagnosed with early-onset breast cancer before age 35, the exceedingly high
Relative Risks (and percents increase per rad) are real --- but their initial magnitudes turn out to be temporary. Relative risks compute at a less spectacular level as soon as the spontaneous cancer-rates
have their own rapid climb (away from zero) in the denominator of such ratios. We have been able to mirror these observations, in a generic way, with Curves A and B, which generate Curve C. The
three curves also mirror the observation that the less spectacular Relative Risk (for cases diagnosed after age 40) persists at an approximately constant level through the 1985 follow-up (see Land's
data in Part 2; confirmation in Tokunaga 1994, p.221).
In our opinion, "Three Curves with a Story" means this: Analysts of the A-Bomb Study need not invoke special concepts about the
cancers or the hosts, in order to explain the much higher Relative Risk observed for early-onset cancer-cases than for the cases diagnosed at older ages. The observed difference in Relative Risk,
due to radiation, can be explained by the fact that both curves rise from a baseline rate which is very close to zero.
True Meaning of "Less Spectacular"
The "less spectacular" Relative Risk really reflects a much greater number of radiation-induced breast cancers than the peak Relative
Risk. In figures like ours, it is the AREA under a curve which reflects the aggregate number of cases observed. The area under Curve B minus the area under Curve A reflects the EXCESS number of cases
induced by radiation. Clearly, the difference in the two areas for ages 30 through 35 is very small compared with the difference in the two areas beyond age 35. The "less spectacular" Relative Risk not only
endures much longer, but it reflects the multiplication (by radiation exposure) of a much higher spontaneous cancer-rate.
Part 5. The Need for Action
How many women who have developed early-onset breast cancer over the past half-century KNOW whether or not they were irradiated in infancy?
We wonder. Readers of this book are going to learn about a very large number of female children who suffered the fate of such
undesirable irradiation of the breasts --- even before they left the nursery of hospitals where they were born. Others suffered nearly the same fate in their first few years of life.
No one can alter the past. But from the past, we can learn the key to preventing many, many cases of early-onset and later breast cancer. Prevention.
Time Would Tell ... And Time Has Told
Once upon a time (1977), the United Nations Scientific Committee on the Effects of Atomic Radiation, known as UNSCEAR, speculated
that breast-irradiation during infancy and childhood might have "minimal" cancer consequences because "only a few breast cells" exist to be irradiated before puberty (UNSCEAR 1977, p.389). Since
these few cells must be the progenitors of all future breast-tissue cells, we rejected that line of reasoning (Gofman 1981, p.249-250).
In 1994, the issue seems settled. Tokunaga et al (1994, p.215, Table VI) report statistically significant excess breast cancer rates in the
bomb-irradiated women who were ages 0-9 years old in 1945 --- as well as in the group which was 10-19 years old in 1945. Both groups, each analyzed separately for the period 1950-1985, show
the excess. And both groups have much higher risks per rad than risks for women who were 20 years of age and older at the time of the bombings.
The Irradiation of Children Today
The era of irradiating children is far from past. The diagnostic use of x-rays can be extremely helpful in pediatric medicine. For example,
we are aware that a high number of x-rays may be taken of premature infants and others in neonatal intensive care units (NCRP 1989). The use of x-rays is also high in association with birth defects
(especially heart problems). The use of x-rays for children involved in automobile and other accidents can also be high, especially if there are insurance battles and lawsuits.
The task mandated by the evidence in this chapter is not to stop such examinations, but rather, it is to make sure that the frequency and
doses are kept to the minimum really NEEDED. In Section 4 of this book, we have some suggestions about what concerned parents, physicians, and medical schools can do.
CHAPTER 9: Thymus Irradiation to Reduce Sudden Death in Children
Part 1. The Thymus and Sudden Death: A Pervasive Fear in Medicine
and in the Public
"A thymic death is one of the supreme tragedies of surgery. An apparently healthy child dies during the administration of an
anesthetic, during or after an uncomplicated tonsil and adenoid operation, or, as recently happened, during a simple circumcision. Again, as reported by one of our medical examiners [coroners], a
child was standing on the edge of the sidewalk. A runaway horse dashed by and the child dropped dead. At autopsy the condition known as status lymphaticus was found; that is, there was an
enlarged thymus and a hypertrophy of all the lymphoid structures of the alimentary canal, these structures being the solitary follicles Peyer's Patches and the mesenteric glands. This slight pathology
was all that was found to explain the unexpected death." This statement in 1926 is from Dr. Harris P. Mosher, Dr. Alexander S. MacMillan, Dr. Frederic E. Motley (Mosher 1926).
By no means was the concern about disorders of the thymus gland confined to infants under one year of age. Indeed, as we shall see in
this chapter and the next, such concern was evident for all ages up through the 'teens. There were long-standing ideas concerning the thymus gland and sudden death; the availability of x-rays did not
help to dismiss these long-standing worries, particularly in situations of stress, of which anesthesia and surgery were prime examples.
We continue with a quote from M.L. Janower and O.S. Miettenen, concerning policy at a major institution in Boston, Massachusetts (Janower 1971, p.753):
"From 1924 to 1946, it was the policy of the Massachusetts Eye and Ear Infirmary in Boston to apply prophylactic irradiation in every case
in which an enlarged thymus gland was diagnosed in infancy. The assessment of the size of the thymus gland was based upon an anteroposterior roentgenogram of the chest taken in expiration with
the patient in the supine position. Whenever the width of the superior mediastinum was at least half the width of the heart the gland was characterized as `enlarged' or `suspicious,' and the child
was given radiation treatment; if the gland was less than half the width of the heart the child was not given radiation. On the basis of these criteria, 1,131 children received thymus gland radiation in the
22-year period." Despite one use of the phrase "in infancy," the irradiated children were an average of 4.7 years of age at exposure.
At the end of this chapter, we will evaluate annual average breast-dose from such treatment of children, ages 1 through 9, for Column M of our Master Table.
Part 2. Enlarged Thymus, with and without Symptoms: Dr. O'Brien
The issues surrounding such treatments were succinctly and well stated by Dr. Frederick W. O'Brien in 1929, at the annual meeting of
the American Roentgen Ray Society. We quote O'Brien (1929, p.271):
"For some years now, it has been the routine in certain hospitals to examine all children roentgenologically before submitting them to a
general anesthetic. If there is found what is thought to be an enlarged thymus gland, a prophylactic roentgen treatment is given, because of the rather well-entrenched belief that an enlarged thymus
gland is an integral factor of the syndrome of so-called status lymphaticus, a reputed cause of otherwise unexplained sudden death." He also described the controversy:
"An enlarged thymus as a symptom-producing organ, and the roentgenologist's ability to diagnose it, has not gone unchallenged.
Status lymphaticus, indeed, as a pathologic entity is declared a misconception."
And the two propositions posed by Dr. O'Brien:
1. Is there a symptom-producing enlarged thymus in infants that can be diagnosed by the roentgen ray and relieved by irradiation?
2. Is there an enlarged thymus without symptoms in infants, children, and young adults, which represents objective evidence of
status lymphaticus, and which can be diagnosed by the roentgen ray and should receive prophylactic radiation?"
Uncertainty about Where the Truth Lay
Dr. O'Brien appeared uncertain about where the truth lay. With respect to mortality, he divided the cases as follows (1929, p.273):
"Cases of thymic death are readily referred to two distinct groups, those with and without symptoms." About cases with symptoms:
"Accepting the concept of the evolution of the thymus, I do not find any student of the subject who does not concede the existence of a
symptom-producing thymus at least in infants. The groups with symptoms usually display the so-called syndrome of thymic asthma, characterized by attacks of inspiratory dyspnea, inspiratory stridor
and the so-called Rehn's symptoms, the expiratory swelling of a tumor [meaning a fulness, not a real tumor], the cranial thymus-end in the jugulum." And about cases without symptoms (p.274):
"The other group of so-called thymic deaths occurring in older children in an apoplectiform manner without premonitory symptoms
is the one responsible for the current hospital practice to which I have referred of roentgenographing all children before anesthesia." And:
"It has been suggested that these sudden deaths have been due to improper anesthetization and poor operative judgment and technique
[see Part 3]. But they occur even without anesthesia and following minor or no surgical procedure at all. These are the cases that are the tragedies of practice and if personal, or under one's immediate
authority, cause one to pause."
Prophylactic Irradiation: Claims of Success vs. the Skeptics
Dr. O'Brien continued (p.274):
"Mosher, well aware of the newer concepts, clings to the old idea that the thymus is involved in these sudden deaths, and he has the added
argument of no sudden death in his great clinic since his study with MacMillan and Motley (Mosher 1926). They found out of a total of 2,344 children, a positive thymus shadow in 7.5 per cent. Of the
positive cases treated by roentgen radiation all were successfully operated on and since employing the routine roentgen examination of the mediastinum, they have had no sudden unexplained death
under anesthesia." And (p.274):
"This has been the practice for two years at the Boston City Hospital and the Cambridge Municipal Hospital with both of which I am
connected. At the Boston City Hospital, out of a total of more than 2,000 children, there has been but one unexplained death under anesthesia, which occurred recently. There had been no prior
roentgen examination and there was no autopsy. At the Cambridge Municipal Hospital, in 526 cases, there have been no deaths. A survey of the chests showed a broadened mediastinal shadow' in +6 percent."
We will return to Dr. O'Brien's conclusions in Part 4.
Others were much more skeptical about the 1926 report by Dr. Mosher and colleagues, on the grounds that the absence of deaths
was not proof that the roentgen treatment of ostensibly enlarged "silent" thymuses was the real reason for such absence.
Boston: "Nearly All Infants Are X-Rayed Promptly"
During the discussion of Dr. O'Brien's paper, Dr. R.D. Leonard of Boston commented as follows (in O'Brien 1929, pp.276-277):
"We have to construct some theory along which to work, and as our empirical results and our interest and enthusiasm in this theory
develops we subconsciously forget that we are working simply on a hypothesis. I think this is something we need to bear in mind in relation to this thymus problem. As we see from these two papers,
we know what is generally thought about the thymus gland, but very little has actually been proven." And:
"In Boston, as in various other places, the thymus gland is at the present time a popular subject for discussion. Our obstetricians are
very much interested in the thymus gland. Nearly all infants are x-rayed promptly and if any sort of a shadow is seen in the mediastinum, treatment is instituted. In the sudden, unexplained
deaths, we recognize the thymus gland as a probable cause. Therefore on account of the present popular interest in the thymus gland, I would add this word of caution that, as far as possible, we
as roentgenologists should be sure we know what we are talking about."
The statement by Dr. Leonard strongly indicates that the practice of roentgenographing "nearly all infants" was not confined to research
studies. One implication: Our estimate of breast-dose from the screening-process itself in Chapter 8, Part 2, Item 10 is almost certainly a serious underestimate.
Part 3. The 1914 Edition of "Anesthesia": Dr. Gwathmey
In his 1914 Edition of "Anesthesia," Dr. James Tayloe Gwathmey made some quite illuminating comments about the so-called Status
Lymphaticus deaths which occurred in relation to anesthetic administration (p.331):
"Status Lymphaticus. Definition. Status lymphaticus or thymicus, or lymphatism, is a condition of infancy and childhood, marked by
hyperplasia of the lymphatic structures, spleen and bone marrow, and persistence of the thymus gland (Stedman). It has also been defined as a condition of unstable equilibrium, coma, convulsions
and vomiting accompanying hyperplasia of the persisting thymus (Gould); and as a morbid state due to excessive production or growth of lymphoid tissues, such as the thymus and thyroid glands,
resulting in impaired development, lowered vitality, and sometimes death (Dorland)." And:
"History. As early as 1614 attention was called by Felix Plater to the fact that the thymus was enlarged in three cases of sudden death
from dyspnea in one family. In 1823, and again in 1829, Kopp mentioned the association of the enlargement of the thymus gland with sudden death. Paltauf, in 1889 and 1890, collected, for the first
time, a large number of cases of sudden death in adults, in which there was enlargement of the tonsils, lymphatic gland system, the follicles at the base of the tongue, the spleen, and the thymus gland,
with narrowing of the aorta. Kundrat, in 1895, published ten cases of death immediately after anesthesia by chloroform or some mixture containing it, also one case in which ether was the anesthetic.
Sudden deaths were noted after this time in many cases in which no anesthetics had been administered. Lymphatic hyperplasia had been found to occur in every chloroform fatality for the past twenty years
in the children's clinic at Gratz. The first case recorded in England was reported by Wolff in 1905." And, in commenting on some features of such patients (p.332):
"Pasty complexion, a large amount of subcutaneous fat, and, in adults, a scant amount of axillary or pubic hair are usual; also the
hair of the head has a peculiar dry brittle character ..." And (p.332):
"Most patients dying during or immediately after anesthesia have been young people or children, of flabby type, with enlarged
adenoids, tonsils, thyroid (usually), and thymus; with narrow, high-arched palate, small mouth and throat, and weak heart sounds. During anesthesia a grayness of complexion or pallor is witnessed,
with weak heart action and shallow breathing. Enlargement of the thyroid is said to exist in more than 50% of cases. Enlargement of the tongue is an important factor in diagnosis. The spleen has been
found to be greatly enlarged in many cases, also the mesenteric, popliteal, axillary, and inguinal glands. Exophthalmic goiter may also be present, in which event heart failure under the anesthetic is
probable. Congenital defects such as cleft palate and cleft kidney are sometimes associated with status lymphaticus. All patients have a pale, thin skin, pasty complexion, and usually subcutaneous fat. The
glands of the neck are also sometimes enlarged. The above complex symptoms are noted when, given chloroform for any length of time, much of the anesthetic is absorbed and less secreted than is usual,
with a consequent continual poisoning of the system until death occurs several days after the anesthetic. Sometimes delayed chloroform poisoning is mistaken for status lymphaticus. In status
lymphaticus, especially in children, patients seem to dread the anesthetic more than is usually the case ..."
And Dr. Gwathmey offers a strong warning against using chloroform (p.333):
"From the study of a large number of statistics, the fact that chloroform is contraindicated cannot be questioned. Roberts
concludes that ether is the safest anesthetic for all of these cases. Unquestionably, chloroform should be avoided in all suspected cases."
An Alternative Hypothesis about Deaths during Anesthesia
Dr. Gwathmey appeared skeptical about some of the cases alleged to be deaths due to status lymphaticus. At p.336, he cites Yandell
Henderson (in Surgery, Obstetrics, and Gynecology, August 1911), who felt that unskillful anesthesia is more often the cause of death, and especially in adenoid and tonsil cases, than the status
lymphaticus or heart disease. According to Dr. Gwathmey, Dr. Henderson wrote in 1911:
"Writers assume that status lymphaticus was the cause of death, although there may have been no autopsy. Even in those cases in
which an autopsy was performed, the pathologist's report sometimes indicates that if he had not been told what to find, he would scarcely have found it."
And Dr. Henderson predicted as follows (according to Gwathmey):
"In many of the very best text books of pharmacology ... the practice of occasionally interrupting the administration of ether, and of
allowing the patient to come for a few moments pretty well out of anesthesia, is expressly recommended. If anesthetists will only realize that this is a procedure which, above all others, should be
shunned, the number of cases of so-called status lymphaticus fatalities, under anesthesia will, I believe, show a sudden and marked decrease."
We do not know how many anesthetists looked at Dr. Henderson's advice. But we do know that concern about sudden death in
childhood, especially during anesthesia, caused decades of radiation screening and treatment for "Status Lymphaticus" and "enlarged thymus."
Differentiation of Thymus Disorders from Others ... with "Happy Results"
A number of writers (Dr. Henry Pancoast, 1930, in particular) have recorded their opinions that a variety of disorders in the thorax need
differentiation from a possible enlarged thymus. Especially has this been true of bronchitis, bronchopneumonia, tuberculous adenitis, sinusitis with associated bronchitis, non-tuberculous lymphadenitis,
and possibly other disorders.
Dr. C. Winfield Perkins is another who alluded to possible mis-identifications (1925, p.219): "Many sudden deaths of children
FORMERLY SUPPOSED TO BE DUE TO BRONCHOPNEUMONIA [emphasis in original], congenital anomaly of the heart or acute intestinal indigestion, in which autopsies have given little information
as to the cause of death, may have been due to unrecognized thymic hypertrophy. Such types of cases have recently been examined, considering the possibility of thymic enlargement, in spite of possible
negative roentgen findings, [and have been] treated as such with the roentgen ray with happy results and the disappearance of the cyanosis and dyspnea."
Part 4. The Belief That the Radiation Did No Harm
In Part 2, we featured two pertinent questions of Dr. O'Brien. The second question concerned prophylactic use of radiation therapy for
"enlarged thymus." In closing the discussion at the 1929 presentation, Dr. O'Brien made a very strong statement about the safety of thymus irradiation (p.280):
"As to the danger connected with treating the thymus, Hammar has studied the thymus for twenty years and should know something
about it. He says there is absolutely no danger from roentgen treatment. The cases he has examined show an emigration of lymphocytes which return rather promptly after the treatment has
ceased. That emigration of lymphocytes accounts for the decrease in the shadow" [when it does occur, of course].
This is not the first time we have reported assurances that such roentgen treatments appeared to be harmless (see Index: Safety
assurances). And in an earlier paper than O'Brien's, Dr. Roy M. Greenthal was arguing as follows (1922, p.438):
"On the other hand, it seems reasonable to give these patients the benefit of a treatment which we know will reduce the size of the
thymus gland. We are aware of the marked reduction in the size of the thymus that can be secured when patients with thymic symptoms are exposed to therapeutic roentgen rays or to radium emanations.
We know of no reports of harmful effects following this form of treatment of the thymus and we have never observed any in this clinic."
Possible long latency in development of radiation-induced CANCER simply was not part of the discourse on the presumed harmlessness
of roentgen-ray exposure in 1922. Nor did radiation-induction of cancer receive widespread attention for several additional decades.
Prophylactic Irradiation: "Not Only Desirable, but Requisite"
How did Dr. O'Brien answer his second question about screening for enlarged thymus and about prophylactic radiation therapy in
symptom-free infants, children, and young adults?
"Since our second query concerns the enlarged thymus without symptoms in children, it is not necessary to consider here
tracheobronchial adenitis or lymphosarcoma or thymoma except to say that any of these conditions sufficiently advanced to give a broadened mediastinal shadow would carry with them a very definite
clinical as well as roentgenological picture." And Dr. O'Brien continued (p.276):
"I am therefore presuming that the 6 to 7 percent of cases of `broadened mediastinal shadow' seen in children without symptoms
represent at least relatively enlarged thymus glands. No one who is informed thinks for a moment that all of this group represent pathological glands. This group comprises, undoubtedly, those which
have not undergone accidental involution from disease, those in whom the rate of chest growth has not kept pace with the thymus, as well as those glands considered potentially a menace."
Dr. O'Brien's emphatic recommendation, about thymic irradiation prior to anesthesia, was tied to the presumed harmlessness of such irradiation (p.276):
"Since there is no evidence that the thymus is not an integral causative factor in the type of death under discussion, and since it is
known that involution of the thymus takes place rapidly and without harm (Hammar) following roentgen or radium treatment, it would appear not only desirable but requisite, until such time as more exact
knowledge or experience shall warrant a contrary opinion, to prescribe radiation therapy for those children presenting roentgen evidence of `broadened mediastinal shadow' without symptoms in
whom general anesthesia or surgery is contemplated."
Part 5.
Quantitative Analysis of the Massachusetts Eye and Ear Infirmary Data
Here, we shall evaluate the breast-dose received by children of ages about 1 to 9 years old, from thymic irradiation administered due to
the fear of sudden death when such children had a variety of chest problems. This will become the entry for Column M of our Master Table. While some of the children had surgical procedures, we shall
treat the cases of tonsillectomy and adenoidectomy separately in the next chapter.
We begin with the 1971 study by Janower and Miettenen entitled "Neoplasms after Childhood Irradiation of the Thymus Gland." The
average age of the children in their study was 4.7 years old at the time of irradiation, as mentioned already in Part 1. Thus, these children were considerably older than the children evaluated in the
previous chapter, about 90 percent of whom were under 6 months of age. The children in the Janower/Miettenen Study represent children with a variety of chest problems plus some head and neck problems,
including bronchitis, lymphadenitis, and other disorders which brought them into the Massachusetts Eye and Ear Infirmary.
We shall use almost the same checklist of "items" used in the previous chapter.
Item 1: What was the place of study? The Massachusetts Eye and Ear Infirmary in Boston, Massachusetts which is SuffolkCounty. This
is a single well-defined facility in a stable location in which essential population information will be available.
Item 2: Can we regard the study's participants as representative of Suffolk County for the relevant period? Unfortunately, we have no
basis whatever for assuming that all the hospitals and private practitioners referred their patients to this one Infirmary. Nonetheless, we shall make our dose-estimate as if ONLY the
children in the Janower/Miettenen Study received such treatment in Suffolk County. For any children of this age-bracket who were treated in other institutions of Suffolk County, we assign ZERO dose.
This means that we shall definitely be underestimating the person-rads of breast-dose for Column M of our Master Table. But
our intention is for doses in the Master Table to represent a credible LOWER limit of annual average breast-dose.
Item 3: How many persons were treated? Over the 22 year period (1924-1946), there were 1,131 children treated for thymic enlargement.
Item 4: What ages were represented in the treated group? Only the mean age was given in the report, a value of 4.7 years. We shall
assume that the age-range of those irradiated was from 1 through 9 years of age. We shall assign equal numbers of children to each age-year of the 1-9 year age-range.
Item 5: What was the period over which the treatments continued? The total period was about 22 years, starting in 1924 and ending in 1946.
Females of Each Age-Year Irradiated per Calendar-Year, Suffolk County.
Item 6: We need to know how many children were present in each age-year for each year of the study. Since 1,131 children were
irradiated in the course of 22 years, the number of children treated per year was (1,131 / 22), or 51.4 children per year. We shall make the approximation that one-half of the children were female, so there
were 25.7 female children treated per year of the study.
If we divide this number equally into nine age-years, we arrive at (25.7 / 9), or 2.86 female children in each age-year who received
therapeutic radiation at this Infirmary, in a calendar-year.
Total Females Ages 1-9, per Year, USA and Suffolk County
Item 7: We need to know the total population of female children in each age-year (1-9) in SuffolkCounty for the average year in the
period 1920-1960. We do this as we did it in Chapter 8 (Item 6).
In 1960, Suffolk County had 791,329 persons.
In 1960, the U.S. population was 179,333,000 persons.
The ratio, Suffolk / USA = (791,329 / 179,333,000).
In the Master Table, Column A, we have the number of females (age-year 1): (892,820 national) x (the ratio of 791,329 / 179,333,000) = 3,940 age-1 females.
And in this way, the full nine-year tabulation is built.
Age-Year Females, National: Females, Suffolk Cy.:
Number in Age-Year Number in Age-Year
1 892,820 3,940
2 892,097 3,936
3 891,518 3,934
4 890,657 3,930
5 890,332 3,929
6 890,051 3,927
7 889,806 3,926
8 889,589 3,925
9 889,390 3,925
Breast-Dose per Treated Child
Item 8: We need to know the radiation dose absorbed in this "enlarged thymus" therapy. The treated children generally had a
cumulative air dosage of 400 Roentgens (4 doses of 100 R each), but we cannot be sure what the distribution was to the breasts. A phantom study, as done by Dr. Rosenstein for the Hildreth Study in
Rochester, would have been desirable. Absent that, we shall assume the same irradiation techniques were used in Boston as in Rochester, and that the absorbed breast-dose was the same: About 32.62 rads
per child, after adjusting for supra-linear bending of the dose-response curve (see Chapter 8, Item 8). We will use 32.6 rads, below. If most of the Boston children received 400 R (air dosage),
our use of 32.6 breast-rads may underestimate the true dose, but this is not provable within the data.
Conversion of Individual Dose to Population-Dose
Item 9: We need the average population-dose from this irradiation, rather than the raw individual doses per treatment. We calculated in
Item 6 that there were 2.86 female children in each age-year who received therapeutic radiation in SuffolkCounty, in a calendar-year. We use the same two-step process shown in Chapter 8, Item 9. First,
we obtain "person-rads." So for each age-year:
(2.86 persons) x (32.6 rads) = 93.2 person-rads.
The second step is to distribute these person-rads, received by only 2.86 persons, into all the children of the same age-year in Suffolk
County. We illustrate with the age-1 group:
93.2 person-rads
Population Exposure, rads = --------------------- = 0.02365 medical rads
3,940 females per breast-pair.
And we must do this calculation for all nine age-groups.
Age- Females in Person- Mean Population Dose,
Year Suffolk County Rads medical rads per breast-pair
1 3,940 93.2 0.02365
2 3,936 93.2 0.02368
3 3,934 93.2 0.02369
4 3,930 93.2 0.02372
5 3,929 93.2 0.02372
6 3,927 93.2 0.02373
7 3,926 93.2 0.02374
8 3,925 93.2 0.02375
9 3,925 93.2 0.02375
Item 10: We have considered, so far, only the dose received by those children chosen to get radiation therapy to the thymus gland.
This does not tell us what dose was received for those who were roentgenographed, but who did not qualify for radiation therapy. The Janower paper indicates that the criterion used was a certain
width of thymic shadow in an antero-posterior roentgenogram. If the Infirmary took just one film and never used diagnostic fluoroscopy, the diagnostic radiation dose to breasts distributed over the whole
population of those ages could have been quite low.
We shall assign a ZERO dose for the "entrance exam" for this series. Of course, this underestimates the doses received, but we prefer an
underestimate where there are no usable data.
Item 11: Duration. Janower and Miettenen say explicitly that such treatments were given for the years 1924-1946. They do not
explicitly say that no such therapy was given in any of the other years of 1920-1960. We are consistently trying to develop a credible LOWER limit of dose, so we will not assume treatments in all forty
years. For the period before 1924, we will assume 2 years without activity. And for the period beyond 1924-1946, we will assume no activity during 7 years. So, we will approximate that treatment
occurred for 31 years, and no treatment occurred at all for 9 years. Therefore, we adjust the average annual dose downwards, as follows:
((31 x 0.02368) + (9 x 0))/40 = 0.01835 medical rads for age-years 1 through 3, and
((31 x 0.02374) + (9 x 0))/40 = 0.01840 medical rads for age-years 4 through 9.
This completes the analytical work for this group, and we make nine entries for nine age-years into Column M in the Master Table.
Use of These Data As Typical for Nationwide Practice
There are sometimes regional differences in medical practice. In our study of the literature, we have looked for evidence of such
differences with respect to all chapters of this work. So far, we have not found any reason to think that the Boston data used above were atypical. But if we just suppose that treatment for "enlarged thymus"
was more popular in Boston than elsewhere, for age-years 1-9, we should still not worry about any OVERestimate of national breast-dose in Column M. Why not? Because of the undeniable UNDERestimate discussed in Item 2, above.
1922: No Surgery Planned? Reduce The Thymus Anyway.
In the debate as to whether infants and children with evidence of enlarged thymus should be irradiated, we have the following (at p. 438):
"Because some patients with thymic hyperplasia go through operations or severe illnesses without trouble, does not mean that all
will do so. We have no means of knowing beforehand who will be the fortunate ones. It would seem, therefore, that the reduction of an enlarged thymus is indicated in all patients before operation."
As for those not being considered for surgery, Dr. Greenthal concluded that the following should occur:
"How shall we treat nonoperative cases which show thymic enlargement? We have given all these patients roentgen-ray
treatments in order to reduce the size of the gland. It is our belief that this, too, is a beneficial procedure.
Why, we ask, did Dr. Greenthal think it was beneficial? The answer centered on one statement:
"It has long been known that some patients with enlargement thymus react to illnesses in a violent manner."
Roy M. Greenthal, "The Incidence of Thymic Enlargement Without Symptoms in
Infants and Children," American Journal of Diseases of Children Vol.24: 433-440. 1922.
CHAPTER 12 Reaching into the Womb: Pre-Birth Breast Irradiation
Part 1. Cancer Production by Prenatal Exposure to Ionizing Radiation
In an important communication in Lancet, 1988, Yoshimoto, Kato, and Schull reported as follows (p.665):
"This study examines the risk of cancer (incidence) over 40 years among the in-utero exposed survivors of the atomic bombing of
Hiroshima and Nagasaki, and adds eight years of follow-up to a previous report confined to mortality. Only two cases of childhood cancer were observed among these survivors in the first 14 years of
life; both had been heavily exposed. Subsequent cancers have all been of the adult type. Not only did the observed cancers occur earlier in the 0.30+Gy [30+ rads] dose group than in the 0 Gy dose
group but also the incidence continues to increase, and the crude cumulative incidence rate, 40 years after the A-bombing, is 3.9-fold greater in the 0.30+ Gy group."
This finding of a significant elevation in cancer rate in those irradiated in-utero is important. However, the total incidence of
cancers is numerically small, 18 cases in all, with 16 of the 18 occurring in adults. This suggests, according to the authors, that:
"These results, when viewed in the perspective of fetus doses, suggest that susceptibility to radiation-induced cancers is higher in
prenatally than in postnatally exposed survivors (at least those exposed as adults). However, definitive conclusions must await further follow-up studies" (p.665).
It is very early in this study. By 1984 (which was the closing date of the Yoshimoto study), those exposed in-utero were just about forty
years old. The cancers are largely yet to come. There were three breast cancers in the series of 18 cancers in toto, and all three of them were in the ostensibly unexposed category. In view of the
random fluctuations of small numbers (and three cases make a severe "small numbers problem"), and in view of what is already known about age-years 0-9 from larger parts of the same study (see
Chapter 3, for example; also Gofman 1990), the distribution of the three breast cancer cases in Yoshimoto 1988 is almost certainly due to pure chance, with no biological meaning. We consider it highly
reasonable to assume that breast cancer sensitivity is about the same for irradiation in utero as it is for irradiation at 0-9 years of age. Of course, we will continue to observe the on-going follow-up, of the
in-utero cohort of A-bomb survivors, to ascertain whether the assumption is strenghthened or weakened by continued observation.
Part 2. Proportion of Infants Receiving X-Ray Doses in-Utero (USA)
The most common reason that pregnant women receive x-ray examinations which expose their infants, is to determine whether or
not the women will be able to deliver the infants vaginally. The x-ray examinations sometimes take place during labor itself. According to Kevin Kelly and co-workers (1975):
"Roentgenographic evaluation of the relative sizes of the fetal head and maternal pelvis has been used clinically almost since the advent
of medical radiography. The technique was considerably refined by Colcher and Sussman in 1944. Further refinements and variations have been instituted since that time."
Pelvimetry was a routine topic in medical textbooks of the 1930s and 1940s. For example, from Christopher's Textbook of Surgery, Third
Edition (1942), we quote Dr. James T. Case, Professor of Radiology at NorthwesternUniversityMedicalSchool (p.1635):
"Roentgen measurements of the pelvic diameters can be taken without any special apparatus; the ordinary x-ray equipment of a
hospital should be satisfactory. Space here does not permit description of the technic of pelvic and fetal mensuration (see the author's description in Curtis: Obstetrics and Gynecology, Phila.,
W.B. Saunders Co, 1932, vol.3, p.762)."
(a) Frequency of In-Utero Irradiation: MacMahon's Study
Dr. Brian MacMahon (1962) published a paper entitled "Prenatal X-Ray Exposure and Childhood Cancer." Our major interest here is in
his evaluation of the frequency of prenatal exposure to x-rays.
The study-population consisted of 734,243 children born in, and discharged alive from, any of 37 large maternity hospitals in the
northeast United States in the years 1947-1954. These hospitals were located in the nine states comprising the Northeast Region of the United States as defined by the U.S. Bureau of the Census. All
but three of the hospitals were situated in Massachusetts, Rhode Island, Connecticut, or New York City. The frequency of intrauterine x-ray exposure in the population was estimated in MacMahon 1962
by review of the records of a 1 percent systematic sample.
MacMahon acknowledged that births in these hospitals were not representative of the general population of births in the area, since
the included hospitals were not rigorously representative. For example, a special effort was made to obtain the collaboration of three hospitals in which the use of x-ray pelvimetry was believed to
have been high, and in general, large hospitals were approached. We shall deal with the bias of this selection-process in a moment.
The MacMahon study concerns x-ray examinations of the maternal abdomen and pelvis in which the fetus received essentially direct
whole-body exposure. The majority of such exams are pelvimetry examinations, but flat-plate examinations for twins, placentography and series-studies of the intestinal tract or urinary tract are also included.
The systematic sample comprised 7,346 live births, in which 104 occurred in multiple births and 7,242 in single pregnancies. X-ray of
the maternal abdomen or pelvis was recorded in 32 (30.8%) of the multiple and 770 (10.6%) of the single pregnancies. In his Table 2, MacMahon lists 9.9% of all the female children as x-rayed, out of
3,570 cases observed. This is the percentage of special interest to us. For personal reasons, some readers may be interested in MacMahon's finding that first births showed a much higher rate of x-raying than
did second and later births. Moreover, this finding has important implications for arranging proper control groups in health studies of in-utero radiation.
MacMahon obtained no estimates of in-utero doses in this series of cases. For doses, we must search elsewhere (Part 3).
(b) Frequency of In-Utero Irradiation: Kelly's Study
Kevin Kelly and colleagues (1975) addressed the question of "The Utilization and Efficacy of Pelvimetry." They reported the following (p.66):
"This study analyzed clinical information from 67,078 single deliveries of 1,000 grams or greater from 16 hospitals [in the years
1969 and 1970]. Pelvimetries were performed during 6.9 percent (4,599) of these deliveries ..." Later (p.68), they reported that pelvimetry accounted for 72% of the pelvic and abdominal x-ray
procedures in their study. Thus, the rate of prenatal irradiation was (6.9% / 0.72), or 9.6% in remarkably close agreement with the MacMahon findings for a period some 20 years earlier. Like
MacMahon, Kelly et al noted that their study-population was not a perfectly random sample, due to some geographic, economic, and racial factors. Also, all of the hospitals providing data were training institutions.
Our Adjustment Downward in the Frequency of X-Raying
For Dr. MacMahon's purposes (comparing frequency of prenatal X-raying in children having a malignancy, versus frequency in
children having no malignancy), seeking out a few hospitals with a high frequency of pelvimetry is not a serious matter. For our purposes, such bias is undesirable. In order to avoid overestimating
the frequency of prenatal irradiation, we shall simply reduce the total frequency of x-raying to 75% of the total observed by Dr. MacMahon. This should take care of the possible consequence of MacMahon's selection-process. So:
(9.9%) x (0.75) = 7.4 % of live births had pelvimetry or abdominal radiation.
Part 3. The Question of Radiation Dose to the Fetus in Such Studies
Robert Berman and Benjamin Sonnenblick (1957) have addressed the issue of doses received by the fetus and female pelvis (1957, p. 4):
"The purpose of this communication is to record actual measurements in roentgens of radiation dosage directed to the
depths of the female pelvis during the exposure of films for x-ray pelvimetry and hysterosalpingography." Measurements were provided for a total of 28 women, 13 of whom had pelvimetry films
taken at or near 38 weeks of gestation.
The total intrapelvic dose of x-ray radiation, as measured in the posterior vaginal fornix in 10 patients who were exposed for the full
exam (4 pelvic views), had an average value of 2.9 R, with 6 patients receiving less than 3 R and only one receiving more than 4 R. The total range of doses was 2.1 to 4.4 R.
We shall use the Berman-Sonnenblick estimates for dose, and the MacMahon estimates (adjusted downward by us) for frequency of the examination.
Part 4. Preparation of the Dose Estimate for the Master Table
Item 1: In the Master Table we have an entry (in Column A) of 905,213 female infants in the 0-1 age-year group, nationwide. This
number is approximately the number of female live-births in the average year of 1920-1960.
Item 2: We shall use the reduced value from the MacMahon studies as the frequency of examinations irradiating the fetus (pelvimetries
plus abdominal examinations). That value is 7.4 % of live-births per year.
Item 3: Number of infants who received the radiation in the 905,213 live-births = (905,213 births) x (0.074) = 67,000, rounded off, per year.
Item 4: Person-rads per year = (67,000 persons) x (Radiation Dose). For dose, we shall evaluate the two extremes of Berman and
Sonnenblick: 2.1 and 4.4 Roentgens. Since this is medical x-radiation, and since these are depth doses measured in Roentgens, we use the approximation here that person-Roentgens are equivalent to person-rads.
Person-rads = 67,000 persons x 2.1 rads = 140,700 person-rads. Person-rads = 67,000 persons x 4.4 rads = 294,800 person-rads.
The other approximation we make here is that the smaller component in the MacMahon frequency (the abdominal radiation)
delivers about the same fetal dose as the dose delivered by pelvimetry.
Item 5: We wish never to overestimate radiation dose, so we shall accept the lowest of the person-rad values obtained in Item 4, namely 140,700 person-rads.
Item 6: For the Population Exposure in the Master Table, we need to distribute the person-rads into the entire 905,213 persons:
Thus, Population Exposure (in-utero) = 140,700 person-rads / 905,213 persons
= 0.16 rad per fetus.
This conservative value, reduced in Item 2 and reduced again in Item 5, is entered into Column K of the Master Table. For this singular
entry, we can use the table's first row, because (as noted in Part 1) we will use the same conversion-factor, from dose to breast cancer, as we use for the year after birth until the first birthday.
In view of Kelly's comment (Part 2), we can assume pelvimetry was in common use for the entire 1920-1960 period.
CHAPTER 25 Weapons-Test Fallout, Pre-1960, and Breast Dose
For our considerations of the 1920-1960 breast-irradiation-doses, we wish to include only doses up to 1960 from weapons testing. For
1960 and beyond, such irradiation will be considered in further research on this topic. While we shall see in this discussion that weapons-test fallout contributes very little to the 1920-1960
breast-doses, the much larger fraction of the fallout in the years beyond 1960 implies that a larger contribution from weapons-test fallout can be anticipated in the post-1960 period.
Since there were no doses of any consequence before 1945, we have 62% of the 1920-1960 period without ANY contribution of fallout to
dose. The period 1945-1960, or 38% of the total years, needs an estimate of dose contribution. Whatever that total dose-contribution is, it will be divided by 40 for the total years, 1920-1960.
Two Major Classes of Radionuclides
There are two major classes of radionuclides, those of very short half-lives, and those of relatively long half-lives. For those of
relatively long half-lives (such as strontium-90 and cesium-137), the radiation dose PER YEAR is a small fraction of the ultimate dose-commitment. Since we are dealing with YEARLY radiation
doses in this analysis of breast cancer, we need to consider nuclear test fallout doses on a per-year basis. For those radionuclides of very short half-lives, material injected into the stratosphere largely decays
before returning to earth, and hence much of the potential dose does not occur.
The Time-Distribution of Fallout Deposition
UNSCEAR 1977 (Annex C) Table 2 (at p.122) provides some of the requisite information. We have there the annual deposition and
cumulative deposition of strontium-90 up through January 1976. We shall, of course, use the data for the Northern Hemisphere, since pre-1960 fallout was largely there.
Strontium-90 Deposition
|
Year
|
Deposition in Mega-Curies
|
Pre-1958 |
1.80 |
1958 |
0.63 |
1959 |
1.05 |
1960 to Jan. 1976. |
8.65 |
Grand total |
12.13 |
|
Therefore, we have the approximation that before 1960, 3.48 mega-Curies out of a total of 12.13 mega-Curies, or about 28.7 % of
the total, fell out. As a good approximation, we shall state that the cesium-137, the other prominent long-lived radionuclide, fell out quantitatively, before and after 1960, as did strontium-90.
The Short-Lived Radionuclides
The combination of Ce-144, Ru-106, Zr-95, Ru-103, Ce-141, and Ba-140 (plus their short-lived daughters) provide the major share of
worldwide exposure in the very early years post-test.
At Table 26, p.153 of UNSCEAR 1977, external radiation from short-lived nuclides is given as 48 milli-rads. As a reasonable
approximation for the pre-1960 period, we multiply this value by the same fraction, 0.287, as used for strontium-90. External dose from short-lived nuclides before 1960 is (0.287 x 48), or 13.8 milli-rads.
While we believe UNSCEAR has overestimated the correction for body shielding of the breast, we shall, as part of our conservative
approach, utilize their values for organ doses directly, and we shall accept 13.8 milli-rads as dose to the breasts for the short-lived gamma-emitters during the 1945-1960 period.
The Long-Lived Radionuclides: Cesium-137 and Strontium-90
At Table 26, the dose contribution from external Cs-137 is given as 62 milli-rads (lifetime commitment). Using our 0.287 factor, we have
0.287 x 62, or 17.8 milli-rads. Gofman (1990, Ch.36, p.29) provides the datum that cesium-137 external dose during first 10 years is 20% of the all-time total. And since the pre-1960 period means less
than 10 years since deposition, on the average, we can say external Cs-137 dose is less than 20% of total, or less than 20% of 17.8 milli-rads, or 3.6 milli-rads. Let us assign one-half of this value, or
1.8 milli-rads, for the shortness of the exposure period.
Total dose in the early period (before 1960) = 13.8 + 1.8, or 15.6 milli-rads delivered to breast from all external gamma-emitting sources.
For internal dose from Cs-137, it is estimated that 95% of the total effect is attained in a few years after deposition. The general rule is
that internal / external dose, for Cs-137, is 3 / 7. But since the internal commitment is nearly over a few years after deposition, we must use the total external committed Cs-137 dose, which is 17.8
milli-rads, to be multiplied by (3/7), and this gives a value of 7.6 milli-rads for internal breast dose from Cs-137.
So, for the early period, total external dose to breast = 15.6 milli-rads. And for the same period, total internal dose to breast =
7.6 milli-rads. Combined total, internal plus external = 23.2 milli-rads to breast.
What about dose from strontium-90? Up to 1960, we can neglect it. This nuclide, having no gamma ray, delivers no breast-dose when it
is external to the body. And the internally deposited strontium would add very little to the breast-dose during this short period of time (pre-1960). However, by also ignoring the external and internal dose
from cesium-134 (radiological half-life of 2.06 years), we do underestimate dose here.
The Total Breast-Dose up to 1960
The 23.2 milli-rads must be divided by 40 to obtain the AVERAGE year's contribution to dose in the 1920 to 1960 period.
Therefore, final entry, for all ages, in the Master Table, for fallout from weapons testing is (23.2 / 40), or 0.58 milli-rads per year of
high-energy radiation. And since all our entries in the Master Table are in MEDICAL RADS, we first convert to rads, and then divide by 2 to correct to medical rads. The final result in medical rads to transfer
to the Master Table, Column "O," is 0.00029 medical rads per year for the average year of 1920-1960 period.
Also refer to On Mammography & Mammograms, Thermograms: superior painless alternative to mammograms for women desirous of having their breasts screened, On Health Effects (Cancer Risk) of Small Doses of Ionizing Radiation, Geopathic Stress Solutions, Bras, Lymph Node Constriction & Breast Cancer Link and Combatting radiation poisoning tips: chelating (detoxifying) excess ionizing radiation
& destructive radioactivity from your body and treating radiation burns naturally.
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