Radiation and mental retardation.
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Biomedical subjects
Publications and source records attributed to E E Pochin.
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The risks of occupational exposure to radiation need fuller and more explicit characterization. They also need a more developed quantitative comparison with more familiar occupational hazards. To achieve this, some criterion is needed for establishing the amount of detriment one should attribute to different harmful effects, e.g., from accidents at work which cause death, temporary or permanent disability; from fatal and nonfatal cancers; from developmental abnormalities and any likely nonstochastic effects; and from a range of genetic defects. No such criterion for comparing incommensurable kinds of harm can be scientifically defined, but one is essential if occupational exposure standards are to be put into perspective. A comparison of the frequency of fatal cancers and "severe" genetic defects with that of accidental deaths at work is admittedly incomplete. One possible starting point is from a review of the average length of healthy life and activity lost as a result of nonfatal industrial accidents and some curable cancers, or of gross impairment during the course of an active disease or as a result of many types of genetic defect, or of life expectancy lost absolutely owing to fatal accidents and diseases. Estimates are discussed to emphasize the areas in which opinion is most needed to translate measures of risk based simply on total time lost into acceptable criteria of perceived detriment. Standards of industrial safety are reviewed on this basis, both for risk from accidents at work and from radiation exposure, with evidence on the rate at which both types of risk are being reduced.
The main difficulty in presenting radiation risks in their proper perspective is that they must, in most cases, be estimated predictively. This contrasts with most other occupational and public risks, of which the magnitude and severity are known from past records and experience. The problem is greater at the low effective dose rates now observed in the majority of all forms of exposure, usually of less than 3 mSv per year from natural causes, from occupational exposure, and from exposure of "critical groups" of the general public. For most of these populations there are particular problems also in epidemiological studies at low dose, in addition to those due to the very large numbers of person-years that need to be studied and the long latencies of most radiation effects. Adequate estimates can, however, now be made of the carcinogenic risk of exposure at higher dose of various organs selectively and of the whole body uniformly, and of modes of inference to the risk at lower dose. Estimates can also be made of the risks of inducing major types of inheritable and developmental abnormality. An essential step in viewing the sum of all such radiation risks in the perspective of other occupational and public risks must now be to develop an informed consensus on the relative weight that is regarded as attaching to hazards of different kind and severity.
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The development of sound methods of radiation protection depended upon reliable dosimetry, both for internal and for external radiation. The proper safety of practices involving radiation exposures can only be adequately reviewed in light of the doses to which tissues are exposed by these practices, and of the types and magnitudes of the risks associated with these doses. Evaluation of risk is an essential step in the pursuit of safety.
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In an increasing number of situations, it is becoming possible to obtain and compare numerical estimates of the biological risks involved in different alternative sources of action. In some cases these risks are similar in kind, as for example when the risk of inducing fatal cancer of the breast or stomach by x-ray screening of a population at risk, is compared with the risk of such cancers proving fatal if not detected by a screening programme. In other cases in which it is important to attempt a comparison, the risks are dissimilar in type, as when the safety of occupations involving exposure to radiation or chemical carcinogens is compared with that of occupations in which the major risks are from lung disease or from accidental injury and death. Similar problems of assessing the relative severity of unlike effects occur in any attempt to compare the total biological harm associated with a given output of electricity derived from different primary fuel sources, with its contributions both of occupational and of public harm. In none of these instances is the numerical frequency of harmful effects alone an adequate measure of total biological detriment, nor is such detriment the only factor which should influence decisions. Estimations of risk appear important however, since otherwise public health decisions are likely to be made on more arbitrary grounds, and public opinion will continue to be affected predominantly by the type rather than also by the size of risk.
In defining criteria for good protection against ionizing radiation, it is important to assess quantitatively the likely risk of any radiation exposure. The 'somatic' risks to the individual result mainly from induction of cancer in the organs irradiated, and these risks can now be estimated on the basis of numerous detailed epidemiological surveys of exposed human populations. Estimates of the risk of hereditary effects, from genetic changes induced in germ cells, are based largely on the frequency with which such effects are induced in other species. In both cases the risk at very low dose can be inferred using knowledge of the way in which radiation damage is caused in tissues. Coherent systems of radiation protection are based on a restriction of doses to the whole body and to individual organs, such that the induction of cancer and genetic harm is infrequent, and the threshold dose for causing other, 'non-stochastic', effects is not exceeded.
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As a basis for establishing radiation protection standards, a substantial amount of quantitative information is now available on the frequency with which malignant diseases are induced in man by moderately high doses of radiation. Such estimates can now be made not only for irradiation of the whole body but also for exposure of a number of body organs individually. The frequency with which cancers might follow the much lower doses involved in occupational or environmental exposure to radiation, however, cannot be derived from any available epidemiological surveys. It can at present only be inferred by the (probably pessimistic) assumption that the frequency of such effects is linearly proportional to the size of dose received, even down to the lowest doses. Increasing information as to the probable form of the actual dose--effect relationship for radiation is indicating the extent to which the use of this "linear hypothesis" may overestimate the risk of low doses as inferred from the observed risk of higher doses. A linear hypothesis has been used in the same way for estimating the likely frequency of harm from low doses of chemical substances which have defined harmful effects at high dose. The appropriateness of this procedure depends critically upon the way in which chemical pollutants, or the relevant products of their metabolism in the body, are likely to become distributed through body tissues and cause the relevant harmful effects on cells.
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Estimates have been made of the rate of uptake, metabolism and excretion of radioiodine given in treatments of patients with hyperthyroidism or thyroid carcinoma. Average values for the exposures to be expected at a given distance from such patients, and the variability of such exposures, are derived from these data. The mean exposure of a patient in an adjacent bed, at 2.5 m bed spacing, following typical therapeutic doses of 131-I in the treatment of hyperthyroidism or thyroid carcinoma, is estimated to be about 0.02 or 0.08 R respectively. Variations in the metabolic parameters would increase these exposures to about 0.03 and 0.14 R, at the 90 percentile values. Exposures following treatments with 100 mCi of 198-Au, or of 300 mg days of -226Ra would be about 0.2 and 0.6 R.
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