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flrahh Ph,estcs Vol. 55, No. 2(August). pp. 351-356, 1988 po17-9Q78/88 S3A0 +.00 ,,,n,,d n the U.S.A. (D 1988 Health P6ysies Society Pexppmon Pras plc o Socioeconomic Perceptions of the Future INDUSTRIAL RISK PERCEPTIONS E. E. Pochin National Radiological Protection Board, Chilton, Didcot, Oxfordshire, OX I 1 ORQ, United Kingdom AbstrracP-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 andl nonfatal cancers; from developmental abnormalities and any likely nonstochastic effects; and from a range of geneti'c defects. 1\io such criterion ffor comparing incommensurable kinds of harm can be scientifically defined, but one is essentiaL if occupztional exposure standards are to be put into perspective. A comparison of the frequency of fatal cancers aand usevere" genetic defects with that of accidental deaths at work is admittedly incomplete. dtn e possible startieeg 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 diseimes. 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. Sitaadards 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. INTItODUMON STANDARDS o'fsafety at work need to be better expressed and understoo3, particularly in their quantitative ranking in different indu stries. No industry is completely safe- some are very safe, and some are much less safe. This obvious statem,e)at may be adequate for a general view of occupational risk. It is quite inadequate when reviewing safety criteria in,occupations involving exposure to aggnts such as ionizing radiation, asbestos, and probably many chemicals, for which no threshold for the induction of harmful effects can be assumed, for which the occupa- tional risks must ordinarily be predictive rather than based securely on past records, and when the predictions for exposure at low <3oses must often be derived by inference from the frequen cy of effects observed at higher doses. In such cases, the efficacy of protection criteria must be judged by comparing the total of all risks of exposure at given dose rates in relation to the total of all risks in other occupations. How do the risks of occupational ex- posure at a dos~ irate of 3 mSv y' compare with those in an industry with an annual fatal accident rate at work of 3 per 100,000; and, more pertinently, how can qualita- ' tively dissimilar risks be compared quantitatively? If any such comparisons are to be convincing, they must fulfill three conditions: (1) All significant types of harmful effects should be taken into account, not only the fatal effects of occupa- tional injuries and diseases. (2) Some factor which is common to all these types of harmful effect should be identified and its importance estimated in different occupations. One such factor is the total amount of time lost, both from normal health and activity and from the normal life expectancy, as a result of occupational accidents and diseases of different sev- erities. (3) A simple numerical estimate of the total amount of time lost in this way as a result of these accidents or diseases is, however, obviously inadequate as a measure of the safety or risk of an industry. Very different weight should, and would, be attached to equal periods of time lost in different circumstances. A third step is therefore essential-to evaluate the weight that should properly be applied to different forms of harm, as assessed according to this criterion. No estimate of harm could be regarded as valid unless the perceived risk of different detriments was considered in some such way; although, the detriment attributed to different kinds of risk ought to be related to the magnitude of the risk, as well as to the type of harm involved. Therefore, in comparing the safety of different in- dustries, a first step could be to assess the length of time 351

352 Health Physics lost, from periods of good health and from average life span, because of the industries' characteristic occupational injuries and diseases, so,that at least the magnitudes of these hazards can be compared. INDUSTRIAL ACCIDENTS For most types of occupational injuries, this is rel- atively simple. In many countries, records have been maintained for several decades of the annual frequencies, for example, per 100,000 workers at risk, of fatal and nonfatal accidents at work, the latter commonly including all those involving days off work. Fatal accidents In the case of fatal accidents, the annual loss of life expectancy can often be assessed directly, e.g., in years per 1000 worker-y, from the frequency of such accidents, the distribution of ages at which they occur, and the nor- mal expectation of life at these ages among men and women in the countries concerned. The mean age'at which fatal occupational accidents occur among males varies somewhat in different indus- tries, but A usually ranges within a few years of mean age of male workers in the industry (ICRP 1985, Table 9). In heavily ird dustrialized countries, with a male life expec- tancy of longer than 70 y at birth, the mean loss of life expectancy per fatal accident at work is typically about 35 y (ICRP 1985, paragraph 41). In female workers, with a much lower frequency of accidental deaths, with a longer mean life expectancy, and often with a younger workforce, the value is probably somewhat higher, but it cannot usu- ally be assessed reliably. For ,an industry with an annual fatal accident rate of 3 per I OD,000, and with a predominantly male work- force, fatal accidents would therefore contribute a total amount of time lost, by loss of life expectancy, in the region of I y per 1000 worker-y. Accidents causing temporary disability The total time lost due to nonfatal accidents can also often be reliably assessed in the case of accidents causing temporary disability. From the annual frequency of such accidents and from the mean resulting number of days off work, which may range in different countries and in- dustries from about 15-30 working days (ICRP 1985, Ta- ble 11), the average annual (calendar) period of time lost (as assess+ d. in terms of disability for work) can be deter- mined. In general, it is found that the total time lost per year in an industry-with many short periods of impaired health and activity-is broadly similar in amount to the annual loss of life' expectancy due to fatal accidents in that indusiry. There is not, however, a simple propor- tionality bctween these two contributions to time loss in industries cf different safety or risk. In the more hazardous industries, with fatal accident rates of more than about August 1988, Volume 55, Number 2 20 per 105 worker-y, the time losses due to fatal accidents are usually somewhat greater than those from accidents causing temporary disability, by a factor of up to 3 or 4. Conversely, in the safest industries, time losses from tem- porary disabilities are up to three times greater than those from fatal accidents, simply because a much smaller pro- portion of all accidents are fatal in the safer industries. Overall, however, it would probably be thought that the detriment due to the nonfatal accidents, with more numerous short periods off work, was less or much less than that of the comparable total period of lost life from fatal accidents. One would also expect that, whatever rel- ative weighting was given to being away from work or to being dead, the fatal accidents would make the dominant contribution to perceived risk. Accidents causing permanent disability With accidents causing some degree of permanent disability, the position is less clear. It is easy to assess the total period of disability caused annually in an industry, given the frequency of new cases per year, the ages at which they occur, and given evidence on how frequently people so classed do remain permanently disabled. The main difficulty in any quantitative assessment, however, lies in the very wide range in severity of the disabilities which are recorded in different industries and countries, ranging perhaps from stiffness of a finger joint to loss of two limbs. It is evident that the detriment per year of a very severe disability, both to the worker and to his family, may be considered to approach that of a year's loss of life expectancy or perhaps, sometimes, even to exceed it. At the same time, most ofthe permanent disabilities recorded are much less severe, at least as judged by the average level of pension or compensation awarded, in comparison with the maximum level available for award. In some national records, the annual numbers of new cases of dis- ability are expressed as an equivalent number of total dis- abilities, either in terms of some fractional assessment at the time of initial medical evaluation, or as an estimated number of days of complete disability. In consequence, estimates of time loss due to per- manent disabilities, either in terms of actual risk or per- ceived risk, depend very much on national or industrial policies in compensation and classification. Even when risks can be expressed in some more or less arbitrary equivalent to cases of maximum disability, or even when-as in several countries-the equivalence is based on the same anatomical criteria of injury in all industries, the relationship in detriment between a year of maximal disability and a year of lost life depends on the criteria of maximal detriment adopted nationally or in the industry. Given the rather sparse available data on the annual fre- quencies and rated severities of new cases of permanent disability, it seems likely that accidents causing such dis- ability might be thought to involve a detriment of between half, and up to twice, that of fatal accidents in the samr industry, but this question needs more attention.

Industrial risk perceptions 0 E. E. PocxiN Detriment from all accidental injuries Meanwhile, however, if permanent disabilities were judged to add a detriment about equal to that of fatal accidents in a rather safe industry (having an annual fatal accident frequency of 3 per 100,000 workers) and if the detriment from the temporary disabilities was considered to be small when compared to that from fatal accidents, the total detriment from accidents at work in this industry would be equivalent to about 2 y of substantial disability per 1000 worker-y, if equal weight were given to the total of all nonfatal accidents, as compared to that given to fatal accidents. OCCUPATIONAL DISEASES-OTHER THAN RADIATI®N-INDUCED In most industries, the total periods of health im- pairment and of life expectancy lost resulting from oc- cupational diseas-~s are small compared to periods of time lost owing to accidental injuries at work (ICRP 1985, Ta- ble 17A). The frequencies of disease are higher, however, in many forms of mining and tunneling, and in some chemical industries. In manufacturing industries also, the low time losses due to accidents may be significantly in- creased by those due to recognized occupational diseases; and in various occupations, the mortality from certain forms of cancer has been increased (ICRP 1985, Ta- ble 16). In principle, the detriment due to occupational dis- ease in any indusmy could be expressed in terms of health or life lost, as in the case of occupational injuries, although p'resumably with a need for differing weights attached to y'ears of mild or severe disease or of loss of life. In practice, however, the severity of symptoms and limitation of ac- tivity are as difficult to assess in any quantitative way as are those in cases of petmanent disability from accidents, and the durations of such symptoms of active disease or of life-shortening due to fatal conditions are not com- monly reported. There is, in any case, no constant component of dis- eases of varying s.-verity in different industries, in the way that appears to hold for accidental injuries. For most in- dustries, the contribution of industrial diseases to an index of occupational harm, based on years of substantial dis- ability per 1000 worker-y, would be small compared to that from accidental injuries (ICRP 1985, Tables 17A and B). RADIATIONV-INDUCED CONDITIONS In most resp", the harmful effects of radiation ex- posure at low dos.- rates can be evaluated in terms of periods of life lost or impaired, as readily as can those of accidental injuries. Forms of impairment are more varied and complex than the simpler alternatives of lost life ex- Pectancy and short temporary disabilities due to accidental injunes, since they involve periods of active disease or detriment in the exposed or in their progeny, and periods of stress, disability and subsequent anxiety in the effective 353 treatment of those induced cancers which prove to be curable, as well as the losses of life expectancy resulting from fatal cancers and inherited diseases which cause pre- mature death. The need to form a considered opinion on the weight that should be attached to these is, however, in itself a reason for reviewing the estimated periods of impairment or lost life that may result from occupational exposure at any given dose rate and mode of exposure. It is necessary, therefore, to consider the induction of fatal and of curable cancers, and of genetic effects of exposures received before conception of children. Non- stochastic effects are most unlikely to be caused by ex- posure under conditions in which both nonstochastic and stochastic dose limits to all organs are respected, with the possible exception of mental retardation in children if this effect is inducible without threshold by exposure of the mother during certain stages of her pregnancy. Induction of cancers that cause death The loss of healthy life due to the induction of fatal cancers involves periods of illness, commonly with severe disability before death and a variable amount of subse- quent life-shortening. The former period is likely to av- erage about 1 y, as indicated by medical evidence on the average length of survival from first diagnosis of the types of cancer, including leukemia, that are induced by radia- tion. The average amount of life-shortening in the exposed population can be assessed from estimates of the fatal cancer induction rate, the ages at which occupational ex- posures are found to occur, and the mean latencies from exposure to death that are assumed for radiation-induced fatal cancers. ~ The periods of illness from diagnosis to death, and of life-shortening due to the premature death, might be regarded as involving about equally severe detriment per year. The average periods of health or life lost for each fatal cancer induced can be estimated as about 1 y of severe illness and 14 y of lost life expectancy, if exposure was occurring throughout a working life from age 20 to 65. At a mean effective dose equivalent rate of 3 mSv y', fatal cancer induction would then contribute a life-loss detriment of about 0.6 y per 1000 worker-y, taking 15 y of severe detriment for each fatal cancer induced, and an induction rate of 1.25 • 10-5 mSv ' as an average for males and females. This estimate depends on the assumption of an "ab- solute risk" hypothesis, with a working population com- posed of both sexes equally and an average age of 40. It also assumes a slightly older mean age of exposure, as typically observed, and a mean latency to diagnosis of 13 y for leukemia and of 25 y for other cancers induced, which represent some 80% of all fatal cancers. On a "rel- ative risk" hypothesis, the number of fatal cancers induced by exposure between ages 20 and 65 would be somewhat greater, probably by about 70% (NAS/NRC 1980, Table V.22) but with a greater proportion developing at older ages, so that the mean life-shortening for all fatal cancers

354 Health Physics appears likely to be similar to that estimated on the basis of an absolute risk hypothesis (ICRP 1985). Induction of cancers that prove to be curable For most forms of cancer, it is much more difficult to estimate total rates of induction by clinical records or cancer registry d.ata than to estimate mortality rates of the relevant cancers from epidemiological studies of death certifications. The number of curable cancers induced by radiation can probably be more reliably estimated on the conventional assumption that the cancers induced by ra- diation appear to resemble "naturally occurring" cancers of the same typ-s in their clinical and pathological be- havior. On this basis, the number of induced but curable cancers could be: inferred from the recorded numbers of fatal induced cancers by conventional knowledge of the cure rate (or the l5-y recurrence-free survival rate) of can- cers of the types, and in the proportions, found to be induced by radiation. . On this basis, the number of curable cancers esti- mated to be induced by (whole-body) radiation appears likely to be about twice the number of fatal cancers. This imbalance in numbers is due largely to the inclusion of skin cancers, for which the cure rate (of the types induced by radiation) is very high, and the cure is ordinarily very simple, the detriment involved in occurrence and cure of the cancer bei:ng correspondingly small. Of the forms of ; thyroid cancer found to be induced by radiation, the cure rate is relatively high-probably in the region of 90%. The detriment i nvolved in cure in terms of symptoms, operative trauma and any subsequent treatment is ordi- narily less than for cure: of most other cancers. For curable induced cancers as a whole, the detriment appears likely to be judged as substantial but as consid- erably less than that from induced fatal cancers, taking account of the rdlatively minor detriment involved in the cure of the majority of such cancers and the absence of a component of liife-shortening in the group as a whole. A measure of detriment of 0.6 y per 1000 worker-y from fatal cancers alone could be regarded as increased to 0.75 y when including all cancer induction; or of 0.6 y or 0.9 y per 1000 worker-y in male and female sections of the workforce, respectively, taking account of the difference in both fatal ar, d curable breast cancers and, to a lesser extent, thyroid cancers. Induction of inherited abnormalities Impairment of the whole life or of much of the life of descendants of those exposed to radiation involves quite different considerations from those associated with detri- ment in workeis who are themselves occupationally ex- posed. In tenms of the amount of harm resulting from any level of occupational exposure, however, and its as- sessment in terms of years of detriment and disability, it is obviously relevant to include whatever evaluation is possible for the genetic.effects of exposure in these terms. In this respect, the more recent reports of the United Nations Scientific Committee on the Effects of Atomic Radiation (UNSCEAR 1977, 1982) include estimates not August 1988, Volume 55, Number 2 only of the frequencies with which different kinds of in- herited abnormality are likely to be induced by radiation but also of the average lengths of life that are likely to be unimpaired, substantially impaired, or lost through pre- mature death as a result of each type or group of inherited abnormalities. Given the amounts of genetically significant occu- pational exposure received at ages before the conception of children, therefore, some estimate can be made of the total subsequent years of impaired health and loss of life expectancy due to inherited diseases in all progeny of those exposed. The "weighting" that would be given to such an estimate of the years of time loss in descendants, per 1000 worker-y of exposure, will not necessarily be the same as the weight that is thought to apply to years of disease, or of life loss, in those who are themselves exposed. It is, however, important to take account of any such inherited consequence of occupational exposure and to assess it in the light of its magnitude. The genetic significance of any dose varies contin- uously with age as the probability of subsequent concep- tion of children decreases with age. As an adequate ap- proximation, it is sufficient to take as fully effective all gonad doses delivered before the mean age at conception of children, and as ineffective all such doses received sub- sequently. The mean ages at conception of children differ in different countries and differ substantially in men and women. Mean values in 41 countries are 30.6 (standard deviation [SD], 2.9) y in men and 25.9 (SD, 1.7) y in women (UN 1983, ICRP 1985, Table 21). The genetically significant proportion of any collective dose of occupa- tional exposure therefore varies strongly with the sex and age distribution of workers and with the age of initial ex- posure, particularly in women. This proportion varies from 0.15 to 0.35 in groups of occupations in the United States (ICRP 1985, Table 22). The detriment due to genetic defects induced in all generations subsequent to exposure was estimated by UNSCEAR as equivalent to 3.4 • 10-` y of life impaired, and 2.9 • 10-4 of life expectancy lost, mSv ' of genetically significant irradiation of a parent. In a wholly male work- force of 1000, therefore, with equal numbers from age 20 to 65, with a mean age at conception of children of 30.6 y, and with a uniform mean dose rate of 3 mSv y' from age 20, the annual genetically significant dose to workers would be that to the (240) workers younger than the mean age of conceptions, or 720 mSv. With a severe detriment, totaling 6.3 • 10-4 y mSv ', the inherited harm, as assessed on this basis, would contribute about 0.45 y of severe detriment per 1000 worker-y. For a female workforce, with a mean age at conceptions of about 26 years and with exposures equally from ages 20 to 65, the contri- bution would be about 0.25 y per 1000 worker-y. These examples are, of course, expressed with an ac- curacy which is ridiculous as compared with the precision of the risk estimates on which they are based, let alone with the variability in age structure of different industrial groups. They can, however, offer some comparison be- tween the carcinogenic risks to the individuals exposed

Industrial risk perceptions! E. E. POCHIN (of0.6 and 0.9 y oer 1000 worker-y in males and females) and the genetic risks to their descendants (of 0.45 and 0.25 y in males and females per 1000 worker-y); and could stimulate the necessary consideration of the relative weight that might be piu't on detriments to health and life in the exposed individual or in his and her progeny. Detriment due to exposure during pregnancies The detriment incurred as a result of exposures dur- ing pregnancies obviously depends on policies adopted with regard to restriction or continuation of radiation ex- posures at work during different stages of pregnancies, as well as on the age and sex structure of a workforce and on the frequency with which pregnancies are undertaken by full- or part-time workers in radiation-related indus- tries. An upper limit to detriment can, however, be given if it is assumed that a worker does not restrict her preg- nancies and thw, :in a non-expanding population, she will have, on average, two pregnancies during a period of em- ployment starting at age 20; and that she works at constant dose rate throughout the whole of these pregnancies. On this basis, one in 30 of all female workers would ' be pregnant at any one time, if there were equal numbers of women at all aF;es. However, as based on an actual age distribution of all women at work in England and Wales (U.K. Department of Health and Social Services 1970)- with 50% of the employed population younger than 30- this chance of a pregnancy being present in a member of the female work:force whether currently at work or not would be greater, with a probability of about 0.065 (ICRP ' 1977). The likelihoc d that any form of harm might result from exposure of the developing child to low doses will depend upon the length of exposure time during preg- nancy, and hence the size of dose received while the con- ceptus is sensitive to induction of that form of damage, and the probability per unit dose of inducing such damage during that tim e. For the induction of cancers which would occur during childhood or of harmful mutations in the developing gonads, which would be expressed in later generations,lhe period at risk corresponds to all or most of the preEmancy, although the risk per unit dose delivered during tltis period is likely to low, on the order of 1 or 2• 10-5 miSv ' in each case. For pre-implantation death of the concdptus, the risk per unit dose may be higher, as judged by findings in rodents, but the period of sensitivity, and hence the likely dose, is considerably shorter. For the one form of developmental defect which may be induced by low doses without threshold (namely, severe mental retardation), the induction risk has been estimated to be about 4• 10-4 mSv ' during an 8-wk pe- riod in pregnancy (Otake and Schull 1984). Each of these forms of harm that may be caused by exposures of the conceptus has serious and, effectively, lifelong effects in the child or prolonged effects in genet- ically affected desoendants. The total detriment, expressed in terms of lengths of life lost or of life seriously impaired, would amount to about 1.5 y per 1000 female worker-y Cxposed throughout all pregnancies at 3 mSv y'' (and 355 with a potential probability of a pregnancy of 0.065). Of this value, about 60% would be attributable to the devel- opmental damage resulting in serious mental retardation, if this effect is in fact induced without threshold, although the epidemiological evidence does not exclude a threshold of some tens of millisieverts. Pre-implantation deaths and induced fatal cancers would each account for about 20% of the total estimate. CONCLUSIONS It should be emphasized that no simple catalogue of the frequency of different kinds of occupational injuries or diseases is sufficient in itself to define the relative levels of safety or risk of different industries, or the safety that they are judged to have by workers, by the public or by governments. Still less can any summation of years of detriment to health or loss of life give such a comparison, unless an appropriate weight is attached to years of dif- ferent kinds or severities of detriment and probably to other factors such as the ages at which the years of detri- ment occur, and their occurrence in the exposed worker or in his immediate or remote descendants. A merit of any attempt to formulate a unified index of total harm, however, is that it should provoke just such an evaluation of the importance that is attached to the different disabilities that contribute to occupational risks. And it will be a more considered evaluation than is ob- tainable if comparisons are based only on the kinds of effect which may be caused, regardless of the frequency with which they occur. Certainly the future evaluation of radiation protection criteria should take account of all the various forms of harm that may be caused by exposure to low doses, their relative frequencies, and the importance that is attached to their occurrences. The same need for some unified estimate of the im- pact of different kinds of harm will be increasingly needed in work that necessarily involves some exposure to other potentially carcinogenic and mutagenic agents for which no entirely safe threshold can be assumed, as may apply in the case of asbestos and various chemical substances. A similar informed perspective on the relative risks of different agents and environmental conditions is equally or more urgently needed in regard to different sources and circumstances of public exposure. Meanwhile, however, the present analysis, although obviously crude and capable of much improvement, does suggest the possibility of developing useful intercompar- isons between dis>'ar industrial risks. For example, the detriment associated with an occupational exposure rate of 3 mSv y' might appropriately be regarded as com- parable in safety, as judged by periods of health and life lost, with conditions in an industry with a fatal accident rate of 3 per 100,000 workers at risk. In the case of male workers, the detriment is even less, as illustrated in the index of harm given below for an industry with a fatal accident rate of 3• 10-s y', and at a radiation dose rate of3 mSvy':

356 Health Physics Years of health impaired or life lost per 103 worker-y From injuries 2.2 Males Females From radiation By canocr induction 0.6 0.9 By genetic effects 0.45 0.3 During pregnancy - <1.0 Currently, in the majority ofall occupations recorded in the Un.1tcd States and the United Kingdom (Kumazawa et al. 1984, Hughes and Roberts 1984) and in 14 occu- pational groups reported by UNSCEAR (1982), dose rates are less than 3 mSv y', although those in some forms of mining may reach about 10 times this rate. The mean rate for all potentially exposed workers in the United States was 1.1 mSv y'(ICRP 1985). Similarly, the annual ac- cidental death rate at work varies very widely in different industries (and countries) from less than 1 to over 100 per 100,000 at risk (ICRP 1985, Table 2). Manufacturing industries ih<<d an annual accidental death rate per 100,000 workers of 1;2.5 during the 1970s (ILO 1980) as the median value from 51 countries. More recently, 7.6 was the me- dian (or 2.9 as the lower 25-percentile) of different man- ufacturing industries in eight highly industrialized coun- tries (ICRP 1985, Table 7). August 1988, Volume 55, Number 2 Any intercomparisons of risk should also take into account the rate at which the various risks are being re. duced. In 40 occupational groups for which rates an available over a number of years (ICRP 1985, Tables 28A_ C), the recorded dose rates have been decreasing by a mean of 6.4% y'(SE, 1.1). This rate of decrease in annual dose (and, therefore, of effective radiation risk) is some_ what faster than that of fatal accident rates at work, as recorded in 20 industrial groups in North America, Eu. rope and Japan, for which the mean percentage rate of fall was 3.3% y'(SE, 0.4) (ICRP 1985, Table 8A). Any purely numerical comparison or summation of dissimilar kinds of risk must necessarily be artificial to a great extent. Certainly, however, a sound perception of industrial risks must depend upon an adequate quanti•- tative assessment of the size of all major components of these risks, whether oftrauma, disease or hereditary efffects, as well as on the more subjective assessment of their rd. ative importance, not only to the worker, but also to the family and to the community. It should be a proper func- tion of radiation protection to provide a realistic and comprehensive assessment of all significant aspects of the safety or risk of different occupations, and of different circumstances of routine or accidental exposure, and to present these assessments explicitly and quantitatively in the general context of the more familiar hazards of all other industrial activities. REFERENCES Hughes, J. S.; Roberts, G. C. The radiation exposure of the UK population-1984 review. Chilton: National Radiological Protection Board; Report NRPB-R173; 1984. International Commission on Radiological Protection. Problems involved in developing an index of harm. ICRP Publication 27. Ann. ;ICRP 1 Publication 27. Ann ICRP 1(4)1-24; 1977. International Commission on Radiological Protection. Quan- titative bases for developing a unified index of harm, ICRP Publication 45. Ann. ICRP 15 Publication 45. Ann ICRID 15(3)1-64; 1985. International Labour Organization. ILO year book of labour statistics. (:n.neva: ILO; 1980. Kumazawa, S.; Nelson, D.R.; Richardson, A. C. B. Occupational exposure to ionizing radiation in the United States: A com- prehensive, nrview for.the year 1980 and a summary oftrends for the ye:am 1960-1985. Washington, DC: U.S. Environ- mental Protection Agency; 1984. National Academy of Sciences/National Research Council. The effects on populations of exposure to low levels of ionizing radiation. Washington, DC: National Academy Press; BEIR III Report; 1980. Otake, M.; Schull, W. J. In utero exposure to A-bomb radiatioa and mental retardation: A reassessment. Br. J. Radiol. 57: 409-414;1984. U.K. Department of Health and Social Services. Digest of sw tistics analyzing certificates of incapacity (U.K.). London: Her Majesty's Stationery Office; 1972. United Nations Scientific Committee on the Effects of Atomic Radiation. Sources and effects of ionWng radiation: 1977 report to the General Assembly. New York, NY: UN;1977. United Nations Scientific Committee on Effects of Atomic Ra- diation. Ionizing radiation. Sources and biological effatz 1982 report to the General Assembly. New York, NY: tlN; 1982. United Nations. UN demographic yearbook 1981. New Yodc, NY: UN; 1983.