Effects on Populations of Exposure to Low Levels of Ionizing Radiation (1972) / Chapter Skim
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CHAPTER VII SOMATIC EFFECTS OF IONIZING RADIATION Summary and Conclusions I: Introduction 85 II. Some Principles Underlying Induction of Somatic Effects 85 III.
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III. Analysis of Viewpoints on Record 181 IV.
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CHAPTER VII SOMATIC EFFECTS OF IONIZING RADIATION Summary and Conclusions I Introduction Consideration has been given in this portion of the report to those effects of ionizing radiation that are manifested in exposed individuals themselves (i.e., somatic effects)
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little or no risk of inducing such effects at doses and dose rates approaching natural background radiation levels. For induction of some tumors, on the other hand, a linear non-threshold dose-effect relationship cannot be excluded from existing data, nor can the possibility that such effects might result from sublethal injury in only one or a few cells of the body.5 Moreover, evidence available at this time indicates that the most important effect of radiation on the mortality of human populations results from carcinogenesis, including leukemogenesis.6 Whether in human populations there are radiation effects on mortality from causes other than cancer is still uncertain.1?
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The slope of the fitted straight-line corresponds to a risk of about 1 case of leukemia per 106 exposed persons, per year, per rem.io The excess in incidence, which was evident within 34 years after irradiation, declined within 15 years but still persists at a diminished level in atomic bomb survivors, now 25 years after exposure. Data for other irradiated populations are less quantitative but imply, for high doses, a comparable excess of leukemia per unit of average dose to the bone marrow, despite wide differences in the conditions of exposure.
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to estimate the probability of cancer in other populations exposed at lower doses and lower dose rates if it is assumed that the relationship between mortality and dose remains the same irrespective of changes in dose, dose rate, and population at risk. There are cogent radiobiological reasons for doubting that the dose-incidence relationship for cancer induction in man does, in fact, remain constant in the face of such changes, one of which is the widespread occurrence of repair of most other types of radiation injury at low doses and low dose rates, particularly in the case of low-LET radiations, i?
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data available on human populations exposed to alpha emitters (underground miners, thorotrast-or radium-treated patients, and radium dial painters) indicate that for cancer production alpha particles delivered at relatively low dose rates are 5-10 times more effective per rad average tissue dose than x rays or gamma rays delivered at high dose rates.
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duration of the effect; and calculations should be made on the basis of the actual age distribution of the population and the presently-observed age-specific mortality from leukemia and other forms of cancer. Since virtually all human data derive from much higher doses and dose rates than those of present interest, and do not extend beyond 25 years of systematic follow-up, the Subcommittee has considered it advisable to illustrate the uncertainty that must necessarily, at this time, characterize estimates of the effect of a particular level of chronic low-dose irradiation on the entire population by choosing, for both leukemia and all other cancers combined, a range of values for each parameter entering into such estimates.
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fit analysis. It is essential, however, that these problems remain under constant review, to observe, record, and evaluate all relevant new data, in order to insure that the estimation of risk from radiation in exposed populations be as precise as possible.
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APPENDICES TO CHAPTER VII Appendix I Review of Scientific Bases of Evaluation of Risks of Low-Level Radiation A
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situation. In this process of assembly and integration of data there may come a point at which it becomes - for the purpose of making decisions or taking actions of practical import - more prudent to act as though the association were causal, than to continue to regard it as non-causal.
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and hampers evaluation of the exposure history of individuals in retrospective studies; (3) because of the long duration of the latent period and the limited follow-up of irradiated populations to date, it is not yet possible to estimate the risks of radiation-induced cancer for the entire life span; (4)
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to high doses and high dose rates, and to utilize these data in developing guidelines for human exposure at low doses and low-dose rates requires interpolation between the region of high dose and zero dose. The significance of the threshold-dose concept enters at the point where one asks: How is the interpolation to be done?
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When only parts or combined fragments of the total dose-incidence curve are observed and used to extrapolate to the low-dose range for which there are no adequate, concrete data, as the basis for estimating the risk of low-level irradiation for man, assumptions must be made concerning the shape of the curve in the lowdose region. In concept, this will depend on the particular carcinogenic mechanisms, the influence of dose rate, the distribution of individual thresholds within the population, and the latent periods for carcinogenic effects as influenced by dose and dose rate.
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Dose -- •Fig.
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trapolation to low dose levels is obtained by interpolation between effects observed at zero dose and those observed in the most rapidly rising: segment of the curve, the estimated risk per unit dose at the low dose levels is likely to overestimate the real risk at low doses. However, if the slope for linear extrapolation is obtained by interpolation between effects observed at zero dose and those observed within the high dose range of the dose-effect curve, where the doses exceed the maximum effective induction dose, the risk per unit dose at low dose levels may be underestimated.
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underestimation of the lifetime risk for cancers with a longer modal latent period, or may give an overestimation of lifetime risk for cancers with a short modal latent period. One of the most serious problems is the fact that existing knowledge of cancer induction in man is based on a limited number of years after exposure, and information is lacking about risk during later years when the natural cancer incidence increases greatlyREFERENCES (1)
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Commission (ABCC) in Japan, provide the first truly dose-specific analysis of the leukemia experience of the A-bomb survivors.
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Table a-1 Incidence of Leukemia in A-bomb Survivors, by T-65 Dose and by City 1950-1966. ABCC Master Sample (from Ref.
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different dose-response curves for the two cities, but the curve for Hiroshima now appears steeper than that for Nagasaki (Figure a-1)
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Rate 140 120 100 80 8 Of u •z.
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Table a-2 Incidence of Leukemia in A-bomb Survivors by T-65 Dose, City, and Type of Leukemia, 1950-1966, ABCC Master Sample (from Ref.
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The excess rate of leukemia for Nagasaki remains about 1.0/106/year/rem under either assumption concerning RBE, since neutrons did not contribute significantly to the dose in that city. These estimated excesses can be factored into acute and chronic cases and when this is done (Table a-3)
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Table a-3 Approximate Factors for Estimating Excess Cases of Leukemia, Based on the Experience of the A-bomb Survivors, 1950-1966 (From Ref.
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Table a-4 Mortality from Leukemia in A-bomb Survivors, by T-65 Dose and by City, 1950-1970, JN1H-ABCC Mortality Sample (Extended)
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Table a-5 Calculation of Excess Deaths from Leukemia.
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Table a-6 Observed and Expected Deaths from Leukemia, 1935-1960 Among 14.554 Patients with Ankylosing Spondylitis Treated by X ray, 1935-1955 Leukemia deaths Followup Of observation Observed (0) Expected (E)
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dose to the entire marrow, given a spinal marrow dose ranging from 525 to 894 R (14) , is estimated (see p.
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The Seltser-Sartwell data on U.S. radiologists are also of interest for their possible relevance to the question of a dose-rate effect for x radiation in man.
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with an expected number of 0.24 determined from general population incidence data on cancer registration. Waggoner (35)
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5CH 300 500 DOSE (iods) 700 Figure a-3.
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an increase of the chronic lymphocytic form in irradiated populations imply that pathogenetic mechanisms may vary appreciably from one form of leukemia to another. The presence of the Philadelphia chromosome in the great majority of patients with chronic granulocytic leukemia and the high susceptibility of leukemia associated with congenitial diseases involving chromosomal abnormalities (e.g., Down,s syndrome, Bloom,s syndrome, and Fanconi,s syndrome)
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2 J - 1 10 8a30H300J /sa8B3 JO i 33a3 SJ 1ad ui asn.uDui ju .3,i,,C, 3SH (3/0)
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SUUimooo JO /SOSEO JO Uf O-,-C..JDii ' ji.".-J • (3/0)
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REFERENCES (1) United Nations Scientific Committee on the Effects of Atomic Radiation.
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(39) de Silva Horta, J., Abbat, J.D., Cayolla da Motta, L.A.R.C., and Roriz, M.L.: Malignancy and Other Late Effects Following Administration of Thorotrast, Lancet 2:201,1965.
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5.040o t o I 1.0Lfe100 200 300 400 500 THYROID DOSE (RADS-l 600 Figure b-1 -- Incidence of thyroid neoplasms versus thyroid dose (rads) : O refers to tumor incidence in the AP-treated individuals of the oldest cohort (born before 1940)
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gland, there is some circumstantial evidence that beta rays from a mixture of internally deposited radioiodine isotopes are as effective as x rays in initiating tumor formation in children (5)
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Mechanisms In animals and in human beings, there is evidence that the pathogenesis of thyroid cancer is a multistage process, involving a primary event causing lasting damage (possibly chromosomal) to thyroid cells, followed by secondary events which promote cell division, thereby allowing the neoplastic potential of the altered cells to be expressed (19)
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OnatnDOt) loq3o Jo 8d30l13004 § Morbidity; se footnote (b)
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(11) Klassovskii, IuA.: Dependency of Irradiation Effects on the Determination of Dose in Thyroid Histological Structures.
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Another important group of subjects in which the relationship between cancer incidence and radiation exposure has been investigated includes about 770 exposed individuals, mainly dial painters, observed in studies at M.I.T.
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irradiated from radioactivity deposited in mineral volume. On the basis of this model, the apparent discrepancy between the results obtained with radium-224 and those with radium226 and radium-228 is clarified.
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also had pre-existing bone disease, Spiess and Mays (11) attempted to determine whether their cancers were more likely to appear in the areas of bone affected by the disease, and they concluded that there was no predilection for cancer to develop in regions with active tuberculosis or spondylitis.
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B T ^ go S £t O """ C n a 4)
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RISK OF BONE CANCER T RADIUM 224 EXPOSED 1 GERMAN PATIENTS FOLLOWUP THROUGH 1969 I/ /I 30,000 • / \ / of / \ 1 / \ / r / 4 \ | \ # 1 _i 2 20,000 I 'fcV i UJ i /^ 1 i \ /
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There is not close agreement among the three studies, particularly the two groups exposed to the radium isotopes. If, however, a quality factor of 7 is applied for radium-226 and a quality factor of 50 is applied for radium-224 (to take into account differences in surface dose as well as in LETT)
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basal-cell carcinomas have been noted, the latter more commonly on the head and neck. Sarcomas of subcutaneous tissues, which are infrequent, have been found most often in association with long-standing and severe radiodermatitis.
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Table d-1-Reiative Risks for Skin Cancer at Various Exposure Levels After Therapeutic Radiation (External Sources)
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Host Factors The frequency of skin cancers appears to be related to the severity of pre-existing radiodermatitis, in that it is far more common (of the order of 10-28%) in severe cases and relatively uncommon (about 1%)
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(4) Sulzberger, M
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Corroborative evidence that the increase in the number of breast cancers seen in human populations was induced by radiation comes from the demonstration of a carcinogenic effect of radiation on breast tissue in laboratory animals (4)
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Figure e-1: Incidence of breast cancer per 103PYR (1966 data) against the number of fluoroscopies received.
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I I CO te 00 c u 5 4)
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30 25 15 20 Q: i 15 10 Ageat Birth 0-9 10-19 Age at Death(Years} 30 -44 20-34 40-54 35-49 55-74 Figure e-2: Mortality ratios and 80% confidence intervals for deaths from breast cancer during 1965-70 in A-bomb survivors exposed to 50+ rads (from Ref.
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risk (since the spontaneous cancer incidence rises by a factor of approximately 4 in the United States from 30-44 to 55-74)
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risk estimate and so have been used, even though they would tend to produce a slight: underestimate of this risk. The relative risk of developing breast cancer in the fluoroscoped group compared with the controls is 6.73 or 6.79 depending on whether the 1966 or 1971 PYR are used.
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C) Breast Cancer Following Treatment for Postpartum Mastitis: Mettler et al.
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(17) Preliminary Report of the Third National Cancer Survey, Biometry Branch National Cancer Institute, 1971.
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There has been considerable discussion of the comparability of the different types of tumors associated with environmental agents. The epidemiology and histologic types of these tumors have been reviewed by Berg (9)
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subcommittee of the Advisory Committee to the Federal Radiation Council by Lundin, Wagoner and Archer (20)
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Absent or infrequent sampling of air of some of the mines, especially in the early exposure prior to 1950, makes estimates of cumulative dose only approximate at best, but it is unlikely that these estimates can greatly be improved at this time, and it is probable that in the aggregate the estimates of exposure are adequate to determine trends in the data. It should be emphasized that among these miners the dose rate was quite high in comparison to that in some of the other mining groups (about 10 Working Levels on the average, see below)
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There has been observed in the U.S. Colorado Plateau workers an inverse relationship between cumulative radiation dose and the latent period for cancer after initial exposure in the mines, but this effect is not very striking at the present time.
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analyses have concluded that the issue is basically a probabilistic one, in that a more widespread exposure is likely to subject more cells to the carcinomatous transformation. Also at issue is the critical number of cells which must be affected within a single region, and various theoretical models have been applied to this, such as that of Bevan and Haque (35)
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j £ on s See footnote (b) S See footnote (b)
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300 O CO cc LU D
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There is fairly good agreement among these four studies in the absolute risk calculated, when the RBE corrections are applied. On the other hand, the relative risk estimates for the fluorspar miners are somewhat divergent.
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(26) Miller, R
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s es O x 09 I s JC e go * 4 9 n BiujumoD jaqjo 10 •a^otUOOj 4)
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h. All Cancers Other Than Leukemia Tables h-1 and h-2 show the data for all cancer excluding leukemia, the sources again being the A-bomb survivors and the patients treated with x rays for ankylosing spondylitis.
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b o a t. e es M "s (B 1 gquaraooa Jsqjo V 4*
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e w u. b i -- , s r I e I S S (a JO ••30113004 N se footnote (b)
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CN See footnote (b) Value of E estimated from 1950-52 vital statistiys for Japan maa/JBaX/ QT S S C a a o 9 3 ^ "s o /sasCo JO 8l43BaP E C _ J 00 ^3 CT*
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to 10 years of age) in the study of Stewart et al.
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(in press) finds that the relative risk of leukemia induction from previous diagnostic x rays to the mother during pregnancy is higher among children prone to allergy and some other diseases than among children whose immune and repair mechanisms, apparently, are in better order (22)
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3. Total Cancer Risk In view of variations among the different types of cancer in their relative rate of induction by irradiation (see Table 2., Appendix III)
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In patients treated with fractionated x-ray exposures for ankylosing spondylitis (5) , the excess mortality corresponds to a cumulative total of 92 to 1652 deaths from cancer per 106 persons per rem during the 27 years immediately following irradiation.
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Table 3-1 Estimated numbers of deaths per year in the U
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a lifetime plateau (b) when applied to all cancers other than leukemia.
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Table 3-2 Assumed values used in calculating estimates of risk shown in Table 3-1. Risk Estimate Duration Duration Absolute of Latent of Plateau Riskb Age at Ir- Type of Period Region (deaths/106/ radiation Cancer (years)
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ce s.
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REFERENCES (1) Jablon, S., and H
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British radiologists initially resident in Britain or Eire or belonging to the Colonial or Armed Services, over the period 1897-1956. With 463 deaths observed and expectation variously estimated on the basis of the general population, men in Social Class I, and physicans generally, they were unable to find evidence of non-specific life-shortening, but did observe a significant excess of mortality from cancer among men entering the practice of radiology before 1921, when serious attention seems first to have been paid to protective measures.
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association between the working environment and morbidity, and fewer deaths than expected from the mortality rates of the general population of the same age and sex (18)
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suggestion of a radiation effect ever having been seen. It should be n< ted, however, that some of the specific diseases included in the cardiovascular-renal complex have very different mortality rates in Japan in comparison with the U
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radiation injury, and (c) 133 "controls" whose mothers were between 4000 and 5000 meters distant from the hypocenter.
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In short, there is at the present time no convincing evidence that the low levels of radiation in question are associated with increased risk of mortality in infancy. Hence, for the purposes of this report, no estimate of risks are considered to be applicable.
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are relatively resistant to killing. Spermatogonia are drastically depleted by small amounts of radiation; i.e., a dose of 50 rem delivered in a single brief exposure may result in cessation of sperm formation.
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Appendix III. Analysis of Viewpoints on Record A
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conclusion was based on data from Court Brown and Doll (5) on the spondylitics.
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F. Reports by Gofman and Tamplin Estimates have been made that if the current FRC guidelines for the maximum "allowable" dose from all nonmedical sources of 0.17 rem per year to the general population is reached, some 32,000 extra deaths per year from all malignancies in the U
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O Age specific rate Mean for all ages Age at Birth O-9 Age at Death 2O-34 1O-19 30-44 20-34 40-59 35-49 55-74 Figure Ill-l. The relative risk of induction of all malignancies (except leukemia)
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critical part of the evidence used in support of generalizations I and II. Basically, these two rules would predict that in a population receiving whole-body irradiation the ratio of the excess number of cancers to excess number of leukemias should be the same as the ratio of spontaneous rates experienced by a non-irradiated population.
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Table 111-2: A comparison of relative and absolute risk estimates of the major types of malignancies induced among the A-bomb survivors (all ages) -- continued Type of Neoplasm Period of Observations Spontaneous Incidence1 Absolute Risk Est.2 Doubling Dose2 All GI less Stomach Cancer Leukemia 1960-70 1950-70 61.8 4.5 0.76 1.71 813 26 Calculated from the rate in the 0-9 rads group and expressed in deaths/105/year.
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O Age specific absolute risk A Age specific cancer death rate Age at birth O-9 1O-19 Age at Death 2O-34 3O-44 2O-34 4O-59 35-49 55-74 Figure 111-2. The absolute risk of induction of all malignancies (except leukemia)
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(ii) Irradiation at all subsequent times: a latency period of 2-3 years followed by a plateau length of 20-30 years for leukemia development, and for all other malignancies a latency period of 10 to 15 years (depending on the type of cancer)
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(23) Court Brown, W
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We impose the condition that x + y be constant and, summing the corresponding probabilities, obtain: Appendix V Radiation Dosimetry of HeavilyIrradiated Sites in Patients Treated for Ankylosing Spondylitis x + y exp(-X - Y)
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On radiographic and fluoroscopic examination in which a barium meal is used, a pressure filling defect is observed. The variation in the anteroposterior thickness of the abdomen between the erect and prone positions may be great; the change in diameter is usually 3 to 5 cm in patients with average build, less in thin patients, and considerably more in obese patients.
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Liver Stomach Transverse Section of Cadaver at Thoracic -12 Figure V-2. Transverse section of cadaver at thoracic-12 vertebra «»-79T O - 72 - l4 193
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report, the mean dose to the stomach in this series has been taken as 250-500 rads.
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Hiroshima (H) and Nagasaki (N)
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dose in rads multiplied by the RBE factor. The latter is obtained for a specified form of radiation as the ratio of the dose (in rads)
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group, and calendar period by the corresponding U
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19-20. Absolute Risk, Deaths or Cases/I0 |
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