Principles and Application of Collective Dose in Radiation Protection (N C R P Report)

NCRP REPORT No. 121

PRINCIPLES AND APPLICATION OF COLLECTIVE DOSE IN RADIATION PROTECTION Reconimendations of the NATIONAL COUNCIL O N RADIATION PROTECTION AND MEASUREMENTS

Issued November 30, 1995

National Council on Radiation Protection and Measurements / Bethesda, MD 20814-3095 791 0 Woodmont Avenue

LEG& NOTICE This report was prepared by the National Council on Radiation Protection and Measurements (NCRP). The Council strives to provide accurate, complete and useful information in its reports. However, neither the NCRP, the members of NCRP, other persons contributing to or assisting in the preparation of this Report, nor any person acting on the behalf of any of these parties: (a) makes any warranty or representation, express or implied, with-resped to the accuracy, completeness or usefulness of the information contained in this Report, or that the use of any information, method or process disclosed i n this Report may not infringe on privately owned rights; or (b) assumes any liability with respect to the use of, or for damages resulting from the use of any information, method or process disclosed in this Report, under the Civil Rights Act of 1964, Section 701 et seq, as amended 42 U.S.C. Section 2000e et seq. (Title VZZ) or any other statutory or common law theory governing liability.

Library of Congress Cataloging-in-PublicationData Principles and application of collective dose in radiation protection. p. cm.-(NCRP report ; no. 121) Includes bibliographical references and index. ISBN 0-929600-46-0 1. Radiation-Dosage. 2. Radiation-Safety measures. I. National Council on Radiation Protection and Measurements. 11. Series. RA569.P6713 1995 616.9'897-dc20

95-26030 CIP

Copyright Q National Council on Radiation Protection and Measurements 1995 All rights reserved. This publication is protected by copyright. No part of this publication may be reproduced in any form or by any means, including photocopying, or utilized by any information storage and retrieval system without written permission from the copyright owner, except for brief quotation in critical articles or reviews

Preface The Committee on Interagency Radiation Research and Policy Coordination asked the National Council on Radiation Protection and Measurements (NCRP) to provide advice on the use of collective dose in radiation protection, particularly as it should pertain to radiation exposures of the United States public. In response to this request, NCRP Scientific Committee 1-3,Collective Dose, was established. Serving on Scientific Committee 1-3 were:

Ronald L. Kathren, Chairman Washington State University Richland, Washington Members

John R. Johnson Battelle, Pacific Northwest Laboratories Richland, Washington

Barbara J. McNeil Harvard Medical School Boston, Massachusetts

Dade W. Moeller Dade Moeller & Associates, Inc. New Bern, North Carolina

Keith J. Schiager University of Utah Salt Lake City, Utah

Roy E. Shore New York University Medical Center New York, New York

Robert Ullrich University of Texas Galveston, Texas

David A. Waite Ebasco Environmental Bellevue,Washington Scientific Committee 1 Liaison

Eric J. Hall Columbia University New York, New York

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PREFACE

NCRP Secretariat William M. Beckner, Senior Staff Scientist Cindy L. O'Brien, Editorial Assistant The Council wishes t o express its appreciation to the Committee members for the time and effort devoted to the preparation of this Report. Charles B. Meinhold President

Contents Preface ........................................................................................ 1 Introduction ......................................................................... 2 Historical Development ........................,... ....................... 2.1 Introduction ..................................................................... 2.2 Applications ..................................................................... 2.3 Concept Evaluations ....................................................... 3 Scientific Bases for Collective Dose ............................. 3.1 Introduction ..................................................................... 3.2 Mutagenesis ..................................................................... 3.2.1 Cellular Studies .................................................... 3.2.1.1 Cytogenetics .......................................... 3.2.1.2 Somatic Cell Mutations .......................... 3.2.2 Animal Studies ...................................................... 3.2.2.1 Chromosome Aberrations ........................ 3.2.2.2 Germ Cell Mutations ............................... 3.3 Transformation and Carcinogenesis .............................. 3.3.1 Tumor Induction ................................................... 3.3.1.1 Leukemia .................................................. 3.3.1.2 Solid Tumors ............................................ 3.3.2 Life Shortening ................................................... 3.3.3 I n Vitro Transformation ....................................... 3.4 Human Studies ............................................................... 3.4.1 Human Studies of Cancer Risks from Low Radiation Doses ................................................. 3.4.1.1 Thyroid Cancer ........................................ 3.4.1.2 Breast Cancer .......................................... 3.4.1.3 Leukemia .................................................. 3.4.1.4 Multiple Myeloma ................................... 3.4.1.5 In Utero Irradiation ................................. 3.4.1.6 Lung Cancer ............................................ 3.4.1.7 Other Cancers .......................................... 3.4.2 Genetic Risks ......................................................... 3.5 Summary .......................................................................... 4 Limitations ........................................................................... 4.1 Conceptual Limitations ................................................. 4.2 Practical Limitations ......................................................

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CONTENTS

4.2.1 Tissue Weighting Factors .................................... 4.2.2 Population Characteristics .................................. 4.2.2.1 Uncertainties in Future Population

................................. .................................................

Size and Location

4.2.2.2 Uncertainties in Future Population

Fertility

4.2.2.3 Uncertainties in Future Medical

Technology

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............................................

4.2.3 Environmental Exposure Pathways .................... 4.2.3.1 Agriculture ............................................... 4.2.3.2 Resource Conservation ............................

5 Risk Assessment and Management ................................ 5.1 Collective Dose as a Surrogate for Societal Risk .......... 5.2 Collective Dose Distributions ......................................... 5.3 Risk Assessment in Specific Applications ..................... 5.3.1 Medical Procedures ............................................... 5.3.2 Radiation Workers ............................................... 5.3.3 Special Occupational Groups ............................... 5.3.4 Current Exposures to Members of the Public

from Localized Environmental Sources

...........

5.3.5 Indoor Radon ......................................................... 5.3.6 Consumer Products and Other Miscellaneous

Sources

...............................................................

5.3.7 Future Exposures from Long-Lived

Environmental Contaminants

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5.4 Risk Management ........................................................... 5.4.1 Acceptability of Risk ............................................. 5.4.2 Categorizing Levels of Risk .................................. 5.4.3 Optimization of Protection (ALARA) ................... 5.4.4 Valuation of Collective Dose Avoided ..................

6 Conclusions and Recommendations .............................. Glossary ...................................................................................... References ................................................................................. The NCRP .................................................................................. NCRP Publications .................................................................. Index ...........................................................................................

1. Introduction Conceptually, collective dose is the summation of all doses received by all members of a population a t risk, and may thus be expressed mathematically as: where S refers to the collective dose to the population a t risk, and

Hiis the per capita dose in subgroup i, and Pi is a subgroup i of population P (ICRP, 1977). Any dose quantity can be used, provided usage is consistent. Collective dose is expressed in units of persondose, using the appropriate dose units for the quantity selected. Typically, collective dose to a population is expressed in units of person-sievert. Collective dose is applicable only to stochastic risks. Implicit in the concept of collective dose is the assumption that the effect or risk of a given dose is identical whether the collectivedose is administered to a single individual or distributed over a population of individuals. Application of collective dose in this manner assumes linearity of dose response, and lack of any dose-rate effect. While these assumptions may or may not be valid, they are considered to be conservative and have been generally accepted by the scientific community concerned with radiation protection (ICRP, 1977; 1991; NASI NRC, 1990; NCRP, 1987a; 1993). In recent years, collective dose has been applied ever increasingly to prospective radiation protection problems, particularly relating to long-term effects of environmental radiation. Such applications lead to questions regarding the applicability of the collective dose concept to large populations with very small individual doses and to populations that will exist several generations hence. This Report seeks to address these and other questions regarding collective dose and its applicability for radiation protection purposes, and to provide practical guidance for the employment of this potentially useful concept in consonance with current National Council on Radiation Protection and Measurements (NCRP) philosophy and recommendations on exposure limitation a s described i n NCRP Report No. 116 (NCRP, 1993). This Report provides a review of the historical development and current applications of the collective dose concept, and attempts to

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1. INTRODUCTION

identify and examine the scientific and other bases that underlie it. It examines the meaning and utility of the concept ofcollective dose in radiation protection and risk assessment for workers and members of the general public. Finally, it provides recommendations for applying collective dose based on current scientific knowledge of the health effects and potential risks of radiation. Underlying the consideration of the collective dose concept and the recorrfmendations provided herein is the continuous evolution of radiation protection standards towards a system based on risk. For such a risk based system to be practical, it must take account of the uncertainties in the risk estimates which form its basis. Additionally, consideration should be given to societal factors, including the willingness of society to incur certain risks in view of the perceived overall benefit to be derived.

2. Historical Development 2.1 Introduction The collective dose concept is widely used within the radiological protection community in the estimation of radiological risk, in the optimization or decision making processes, and in the development of regulations. Some authors trace the origin of the concept back to the term "genetically significant dose," or "population dose" which was proposed to limit radiation induced genetic risk of populations as early as the late 1950s and early 1960s [see NCRP (1957); ICRPI ICRU (1957) and ICRPACRU (1961)l. An early usage was the 1965 annual collective dose limitation of 100 person-Sv y-' for each nuclear power station imposed by the Canadian Atomic Energy Control Board (Hurst and Boyd, 1972). The concept does appear in the International Commission on Radiological Protection's (ICRP) Publication 22 (ICRP, 1973), where it was first called "population dose," and evolved to "collective dose" by the time of ICRP Publication 26 (ICRP, 1977). Modern usage of the collective dose concept originated in the early 1970s within the United Nations Scientific Committee on the Effects ofAtomic Radiation (UNSCEAR)and the ICRP. The 1969 UNSCEAR report did not mention collective dose, but by 1977, the use of collective dose by UNSCEAR was prevalent (LTNSCEAR, 1977). The transition seems t o have occurred i n the 1972 UNSCEAR report (UNSCEAR, 1972), in which the unit man-rad was introduced. Population doses in units of person-rem were also used in the initial report of the Committee on the Biological Effects of Ionizing Radiation [BEIR (NASINRC, 1972)l. A discussion of topics similar to collective dose in NCRP Report No. 39 (NCRP, 1971) did not mention the conceptper se. But, NCRP (1957) talked of "The maximum permissible dose to the gonads for the population of the United States as a whole from all sources of radiation, including medical and other manmade sources, and background, shall not exceed 14 million rems per million of population over the period from conception up to age 30, and one-third of that amount in each decade thereafter." The first specific reference to the collective dose concept in an NCRP report occurred in NCRP Report No. 43, entitled Review of the Current State of Radiation

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Protection Philosophy (NCRP, 1975), and the concept has been discussed, refined and applied in subsequent NCRP reports and recommendations. 2.2

Applications

The use of the collective dose concept has permeated into many aspects of radiation protection policy making and program implementation worldwide. The scientific and technical literature contains numerous examples of collective dose-based estimates of the collective risk for a wide variety of radiation-related activities. In its series of reports assessing the ionizing radiation exposure to the population of the United States (NCRP, 1987b; 1987c; 1987d; 1987e), the NCRP has made extensive use of the collective dose concept. NCRP Report No. 93 (NCRP, 1987b) summarizes radiation exposures from all sources that were individually reviewed in the other assessment reports, and includes collective dose estimates. Other NCRP reports, notably Reports No. 105, 107 and 116 (NCRP, 1989; 1990a; 1993) consider collective dose in their discussion of radiation protection recommendations. Other examples of considerations of collective dose for radiation protection purposes in other countries include a study by Iyengar and Soman (1987) which examines in detail the collective occupational and public doses from all components of the Indian nuclear fuel cycle. Similarly, Hyvonen (1990) evaluates the effectiveness of the Finnish radiation protection programs vis-a-vis exposures in medicine, industry, research and nuclear power. Early United States examples include the final environmental statements for Pilgrim Nuclear Power Station (AEC, 1972) and for Hanford Waste Management Operations (ERDA, 1975), both of which discuss impacts and comparative population or overall risks in terms of collective doses, and a more generic study of light-water reactor effluents (AEC, 1973). Relevant guidance documents incorporating collective dose have been prepared by others including the ICRP (19731, and the Organization for Economic Cooperation and Development/Nuclear Energy Agency (OECDLVEA, 1988). In the mid-1950s the principle of maintainingradiation exposures to the lowest practicable limit was introduced into its recommendations by the NCRP (1954) and the concept of optimization, also known as ALARA (as low as reasonably achievable), began to evolve (ICRP, 1955; 1959). This concept is now central to radiation protection practice and is based on a balancing of risks and benefits. The ALARA concept was formally introduced as a recommendation for radiation protection by the ICRP in 1977 (ICRP,

2.3 CONCEPTEVALUATIONS

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1977), although its origins in radiation protection practice go back a t least to the early 1950s (Kathren et al.,1980). Regulatory bodies have integrated the collective dose concept into United States radiation protection regulations in various ways. In the mid-1970s, the Nuclear Regulatory Commission (NRC) adopted the use of the collective dose concept with a spatial cutoff of 50 miles, see Appendix I to 10 CFR 50 (NRC, 1975). Amplification of the regulation was provided two years later in NRC Regulatory Guide 1.109, Appendix D, which stated that "These doses should be evaluated for the population within a 50-mile radius of the site.. . For the purpose of calculating the annual population-integrated dose, the 50-mile region should be subdivided into a number of subregions consistent with the nature of the region" (NRC, 1977). This type of spatial truncation has been widely accepted and utilized in the past, particularly in documents such as environmental impact statements prepared for regulatory purposes. Such acceptance has not been the case when dose-related and other truncation rationales have been attempted in other aspects of the regulatory framework such as the NRC proposed adoption of "below regulatory concern" for determining when individual radiation exposures are or will be so low that they do not warrant further regulatory control (NRC, 1988). In addition to an individual dose criterion, the NRC proposed a collective dose limit as well, stating in its 1988 policy statement that "The Commission specifically seeks comments on the need for establishing a collective dose limit in addition to a n individual dose criterion" (NRC, 1988). These proposals have not been adopted.

2.3 Concept Evaluations In recent years at least two studies have examined the fundamental validity and utility of the collective dose concept. The first was a study by Lindell(1984) who was commissioned by the OECDINEA to prepare a report describing the various situations in which ICRP recommendations would require a n assessment of collective dose, the objectives of such assessments, the related methods, and the limits and difficulties of these collective dose assessments. Regulatory aspects were not addressed in this study. In the Lindell report (Lindell, 1984), the following applications of the collective dose concept are identified as the most commonly used in radiation protection:

1. in the assessment of the highest per capita dose in the future from a continued practice which exposes some members of the population to radiation, 2. in the limitation of present use of radioactive material, if it is believed that additional sources in the future may add to the per capita dose in a population so that it might reach unacceptable levels unless all sources are controlled a t a n early stage, 3. as a n input to justification assessments, indicating the total detriment from a certain practice, and 4. as an input to optimization assessments as the basis for costing detriment in differential cost-benefit analysis of protection arrangements. His primary conclusion is that while it is often said that for the collective dose to be useful, an assumption of a nonthreshold, linear dose-response relation is needed, in truth, this assumption is not always necessary. Applications (1)and (2) are possible without any assumptions on the dose-response relationship at low doses. Only applications (3) and (4) require a strictly defined dose-response relationship. Lindell also acknowledges that there is some hesitation in using the collective dose, not only due to distrust of the biological assumptions implied by uses (3) and (4), but also in lack of confidence in the predictiveness of collective doses that have been derived by adding contributions over very long time periods. However, none of the four applications is by necessity related to extreme time scales. The second was a study commissioned by the German Radiological Protection Commission in 1985 (SSK, 1985). The objective of this investigation was to determine whether collective dose is suitable as (1)a measure of the radiation-related detriment and (2) a tool for the optimization of radiological protection and for the comparison of safeguards, and thus a meaningful measure of radiation exposures. The study considered both the scientific state-of-the-art and the legal situation that existed in Germany in 1985, and reached the following conclusions relative to detriment, optimization and regulation: "1. The collective dose is only suited to be a measure of detriment if there i s a sufficient knowledge of t h e risk coefficients required for the calculation of detriment in the dose range of interest. As far as the relevant dose ranges in practical radiological protection are concerned, it must be recognized that the required risk coefficients are derived from estimates and not from quantitative determinations. This applies in particular to dose ranges t h a t a r e of importance for t h e populations.

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"2. With respect to protection implementation, the Radiological

Protection Commission considers the optimization of the radiological protection of personnel by means of a minimization of the collective dose and the comparison of safeguards suitable, using the collective dose a s a measure of comparison. "3. Although there is a binding obligation for the optimization of radiological protection, there is no obligation to consider the collective dose as a suitable tool for reaching this objective. The Radiological Protection Commission recommends that collective dose not be included in legal regulations." The following sections of this Report extend the considerations made in these earlier studies and reviews these issues in the context of present circumstances in the United States.

3. Scientific Bases for Collective Dose 3.1 Introduction The utility of collective dose rests on the assumption that the biological response at low dose and dose rates is both linear and time independent, and that the response of any individual to a given dose is more or less uniform. This logically leads to the prediction that at low doses the response will be the same whether the dose is delivered as a single acute exposure, as multiple small fractions, or as a protracted low-dose rate exposure. The assumption of time independence also implies that the time between each fraction and the time over which the total dose is delivered are not important. Whether these assumptions are appropriate have not been determined from human epidemiologic data. Some animal studies have shown that both the time between fractions and the time over which the total dose is delivered are important. The following sections will review cellular, animal and human studies on the mutagenic and carcinogenic effects of radiation which have bearing on these assumptions of linearity and time independence a t low doses.

3.2 Mutagenesis 3.2.1

Cellular Studies

3.2.1.1 Cytogenetics. The effects of dose, radiation quality, and dose rate or fractionation on the yield of chromosome aberrations have been extensively studied using cultured lymphocytes from a variety of species including humans. Data indicate that similar results are obtained whether cells are irradiated in vivo or in vitro (Brewen and Gengozian, 1971; Schmid et al., 1974). Pertinent reviews can be found in NCRP (1980; 1990b) and UNSCEAR (1988; 1993). A large body of data examining the induction of chromosome

3.2 MUTAGENESIS

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aberrations following in vitro exposure of human lymphocytes has shown, for low-LET radiation, that over a 0.05 to 8 Gy dose range, two-break chromosome aberrations, such as dicentric aberrations, increase with dose according to the linear quadratic function:

where I is the incidence of radiation induced chromosome aberrations, D is the dose and a and p are numerical constants with the linear term predominating a t low doses. A reduction in the doserate results in a reduction in the PD2 term with no apparent effect on the aD term of the response equation (NASNRC, 1990).The data imply that the response a t low doses is linear and time independent. At very low doses induced by internally deposited radioactive materials, the yield of aberrations was found to be described by the function (I = d). A linear dose-response function was found regardless of the LET of the radiation (NCRP, 19870. The a coefficient is similar a t low radiation doses whether protracted or delivered as an acute exposure. For high-LET radiation, the yield of aberrations increases as a linear function of dose over a wide range and is dose-rate independent. This point is discussed in greater detail below.

3.2.1.2 Somatic Cell Mutations. The induction of gene mutations in cultured cells by irradiation has been studied by a number of investigators using several different cell lines including those derived from mice, hamsters and humans. In addition, specially engineered hybrid hamster cells containing the bacterial gene gpt or containing human chromosome number 11have also been used to study radiation mutagenesis (Evans et al., 1990; NCRP, 1990b). Because of the limited sensitivity of these model systems, most studies have not directly examined the dose response at doses below about 0.5 Gy. Although data a t low doses are limited, inferences can be drawn about the shape of the dose-response curve in the low-dose range based on the effects of dose rate on the response and based on molecular analyses of the induced lesions. The data indicate that the dose-rate dependence of radiation induced mutations depends upon the type of mutation induced (NASNRC, 1990). In general, lesions that can be hypothesized to involve the interaction of damaged DNA, such as intragenic deletions, rearrangements and other multilocus mutations, have been found to be dose-rate dependent. Because of the apparent involvement of the interaction of sublesions, the prediction of a linear-quadratic dose-response function and doserate dependence for such lesions seems reasonable over the range of doses used. In other instances, such as point mutations (i.e., base substitutions), the data suggest no dose-rate effect and also strongly

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suggest a more linear dose-response relationship over a wide range of doses. In either case, the response a t low doses is expected to be linear and independent of the time course over which the dose is delivered: For high-LET radiation, the association is somewhat less certain although the data indicate an approximately linear dose response following acute exposures. Studies examining effects of dose rate and fractionation, however, suggest that reducing the dose-rate results in an increase in the induced mutation frequency over the 0.10 to 1Gy dose range (NCRP, 1990b).

3.2.2

Animal Studies

The principal focus when considering genetic effects in animals is on the germ cells, for which information comes primarily from experiments examining chromosome aberrations in these cells and from studies of specific locus mutations in the mouse. These studies have been reviewed extensively and most recently in ICRP (19911, NAS/NRC (1990) and UNSCEAR (1988). With respect to low-LET effects at low doses and dose rates, the most comprehensive reviews can be found in NCRP (1980) and Searle (1974). A comprehensive review of high-LET effects from external exposure is presented in NCRP Report No. 104 (NCRP, 1990b) and for internally deposited radionuclides in NCRP Report No. 89 (NCRP, 1987~). 3.2.2.1 Chromosome Aberrations. The induction of reciprocal translocations in spermatogonia has been studied over the dose range 0.5 to 12 Gy of low-LET radiation and can be described by a linear-quadratic equation followed by a downturn a t higher doses (UNSCEAR, 1986). Reducing the dose rate or the size of the dose fractions reduces the response principally by reducing the beta term (see Equation 3.1). This suggests a more nearly linear response at dose rates below about 0.1 mGy min-l. Further reduction in the dose rate below 0.1 mGy min-I does not significantly affect the slope of this response. Information on chromosomal changes in oocytes is available from studies of Brewen and coworkers (Brewen and Payne, 1977; 1979; Brewen et al., 1976). In these studies, the yield of chromosome aberrations following acute exposures increased as a linear quadratic function of dose. Chronic gamma irradiation resulted in a linear response function with a slope similar to the linear portion of the linear quadratic responses obtained following high-dose rate exposures.

3.2 MUTAGENESIS

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3.2.2.2 Germ Cell Mutations. Evaluations of specific locus mutations in mice have emphasized the studies of spermatogonia and the resting oocyte. Because of the extreme sensitivity of the oocyte, which results in killing and early onset of sterility a t intermediate to high doses of low-LET radiation, studies first concentrated on responses in spermatogonia. While dose-response data for spermatogonia are limited, i t is clear that lowering the dose-rate results in a progressive decrease in mutation incidence down to a dose rate of approximately 10 mGy min-' (UNSCEAR, 1986). Importantly, lowering the dose rate below 10 mGy min-l results in no additional decrease in mutation incidence. Although fractionation studies are more difficult to interpret, it is important to point out the studies of Lyon et al. (1972) that compared the effects of a single 6 Gy dose with fractions divided into 60 daily doses delivered as acute fractions or split into weekly doses of 0.5 Gy delivered as acute fractions. The daily fractionation regimen resulted in mutation frequencies similar to those obtained at lowdose rates while the higher weekly fractions resulted in mutation frequencies similar to those after acute exposures. These results, as well as the dose-rate data described above, are consistent with additivity of effects a t low doses and dose rates. In the female mouse, few if any mutations are observed a t doses up to several Gy when delivered at low-dose rates (NCRP, 1980; 1990b;Searle, 1974). Because of the extreme sensitivity of the mouse oocyte to killing by x rays, this test system has been called into question as far as its applicability to humans is concerned. The dose-response relationship for mutation induction following exposure of spermatogonia to neutron irradiation appears to be linear over the 0.5 to 0.9 Gy dose range, but the mutation frequency is markedly lower a t a dose of 2 Gy (NCRP, 1990b).Dose rate appears to have little influence on the mutation yield obtained in the 0.5 to 0.9 Gy dose range. At higher dose rates and dose, a reduction in yield is observed for many endpoints. This is most often explained on the basis of cell killing. More significant for radiation protection considerations is the apparent lack of any influence of dose rate a t lower doses. Considering the small amount of data available in the low-dose range and the associated complicating factors, particularly with respect to the female mouse, it appears that most of the data on mutations a r e consistent with a linear and time-independent response to radiation in the low-dose region following exposure to low-LET radiation. Data for spermatogonia irradiated with highLET radiations are also consistent with a linear, dose-rate independent response.

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3.3 Transformation and Carcinogenesis 3.3.1

Tumor Induction

Studies of dose-response, time-dose relationships and influence of radiation quality for tumor development in laboratory studies of animals have been reviewed extensively in NCRP (1980)and NCRP (1990b).Despite the large body of data, there are only a few instances in which the dose response is sufficiently well defined and for which time-dose relationships have been studied.

3.3.1.1 Leukemia. A large body of data is available on the induction of myeloid leukemia in two strains of mice. It has generally been concluded from these data that the dose response is linear quadratic, although a linear response cannot be excluded (Barendsen, 1978)and the data for one of the strains has been described to fit a quadratic with a cell killing term (Mole et al., 1983).Lowering the dose rate has been shown to result in a reduced response per unit dose. From analysis of data for myeloid leukemia, Barendsen (1978) concluded that the linear component of the linear quadratic model fitted to the high-dose rate data adequately predicted the data obtained for continuous low-dose rate and fractionated doses. These data support the conclusion of a linear, time independent, additive response a t low doses. For thymic lymphoma induction, the dose response and the effect of low-dose rate are complex and the response a t low doses has not been sufficiently well characterized to allow any conclusions to be reached. 3.3.1.2 Solid Tumors. Ullrich (1983)and Ullrichet al. (1987)have reported studies on mammary and lung adenocarcinoma development as a function of dose, dose rate and fractionation. Following high-dose rate exposures, the data indicate linear quadratic doseresponse functions for both tumor types although the dose range over which the linear response predominated differed markedly. For low-dose rate exposures the data were best described by linear functions with slopes similar to the linear portions of the linear quadratic equations obtained following high-dose rate exposures. On the basis of these results, the effects of low-dose rate exposures and of high-dose rate low-dose fractions were compared in a direct test of the prediction of dose-rate independence a t low doses, i.e., doses where the linear response predominates. The data demonstrate that the effects of fractionation were predicted by the linear quadratic regression equations derived from the high-dose rate data. When the dose per fraction was on the predominantly linear portion of the

3.3 TRANSFORMATION A I D CARCINOGENESIS

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dose-response relationship, the effect was similar to that after lowdose rate exposures. These conclusions are also supported by results of studies on the induction of pituitary and Harderian gland tumors, although the data are not as extensive (NCRP, 1980; Ullrich and Storer, 1979). For these tumor types in RFM mice, linear quadratic dose responses have also been reported. Further, linear responses a t low doses with slope coefficients similar to those derived from the high-dose rate linear quadratic response were observed. Such results are not obtained when ovarian tumor induction has been examined. Rather, the reported data from several studies of ovarian tumor induction are more consistent with a threshold model. However, the apparent extreme sensitivity of the oocyte to killing effects, and the possible role of indirect mechanisms in ovarian tumor development, suggest that this may be a response unique to ovarian tumors in the mouse. Data for induction of other tumors are not sufficient to contribute to resolution of the question. Taken as a whole the above data are consistent with t h e concept of a n additive, time independent response for tumor induction a t low doses. All available data for tumor induction following high-LET radiation support a linear dose response a t doses below 0.1 Gy (NCRP, 1990b). Further, with the exception of mammary tumor induction, it appears that the response following fractionated or protracted exposures to low total doses is also linear. For mammary tumors the incidence is two- to threefold higher following low-dose rate exposure than after high-dose rates, even after a dose as low as 0.025 Gy. The reason for this effect is not known.

3.3.2 Life Shortening Life shortening is one of the most extensively studied late effects of exposure to ionizing radiation. Since it has been shown that virtually all the excess life-shortening effects that occur after an exposure a t low dose or low-dose rates is due to excess tumor mortality, this endpoint is a useful quantitative tool for the study of the neoplastic effects of radiation a t low doses and dose rates. The quantitative nature of this endpoint and the ease of measurement have allowed investigators to examine dose-response relationships and to rigorously examine effects of dose rate, protraction and radiation quality. A review of these data is available in NCRP Reports 64 and 104 (NCRP, 1980; 1990b). Several concepts have emerged from these studies which are of direct relevance to this Report. Results obtained with a number of

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different strains of mice, have led to the general conclusion that at low doses and low-dose rates a linear relationship exists between the degree of life shortening and the magnitude of low-LET radiation exposure. Data from other species also tend to support these conclusions. While there is some evidence of apparent life lengthening a t low radiation doses (Congdon, 1987; Lorenz et al., 1955; Mine et ak., 1990), the mechanisms of this effect may be related more to the low grade stress of the radiation exposure rather than to a true radiogenic effect that could be extrapolated to human risk estimates. A discussion of these observations and their biologic mechanisms can be found in NCRP (1980), Sacher and Trucco (1962) and Sagan (1989). Investigators have concluded that the dose response for high-LET irradiation is linear at low doses. At doses above about 0.2 to 0.4 Gy, there is a bending or deviation from linearity in the dose-response curve. While enhanced life shortening effects have been observed following low-dose rate exposures a t total doses greater than 0.2 Gy, fractionation and dose-rate studies strongly support the conclusion that the response is in fact linear and additive a t low doses (NASI NRC, 1990; UNSCEAR, 1986).

3.3.3 In Vitro Transformation Since the first published report of radiation induced transformation in uitro, these model systems have served as useful tools with which to explore many questions (Borek and Sachs, 1966). Particularly relevant to this Report are studies of dose-rate and fractionation effects. The repairability of low-LET radiation induced transformational damage was one of the first observations made with the C3H 10T1/2 cell system. Subsequently, it has been demonstrated that reduction of the dose rate of low-LET radiation results in a reduction in the transformation frequency in most systems studied. Results following fractionation are more complex and depend on total dose, fraction size and time between fractions. The most complete data set for studies of dose-rate and fractionation effects for low-LET radiation for in uivo transformation studies comes from the work of Elkind and Han (Elkind et al., 1985; Han et al., 1984). These investigators reported a reduced transformation frequency after lowdose rate exposures. Daily fractions of high-dose rate exposures of 0.5 Gy also resulted in a lower transformation frequency than that from a single acute dose. In contrast to the results with photons, studies of dose-rate effects in C3H 10T112 cells with neutron irradiation suggest an enhanced effect a t doses above 0.1 mGy when the dose rate is less than

3.4 HUMAN STUDIES

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5 mGy min-' (Elkind et al., 1985;Hill et al., 1982; 1984).While these results were initially somewhat controversial, similar results have now been reported by some other, but not all, investigators using different in vitro cell systems (see Hall et al., 1991). This so called inverse dose-rate effect appears to be a complex function of LET, dose and dose rate. The reason for this effect is not known. Recently, Brenner and Hall (1990)have proposed a model involving a sensitive stage in the cell cycle for transformation which is consistent with the experimental data.

3.4 Human Studies

Two interrelated questions pertinent to the issue of collective dose can be examined in the human epidemiologic database. The first is whether projections of risks from high doses to low doses are correct using a dose-response relationship that is a linear function of dose. Alternatively, the question may be whether a linear-quadratic (convex upward) model, for which both components have been estimated, projects the risk with reasonable accuracy. If the doseresponse curve is truly linear quadratic, but is estimated with a simple linear function, then low-dose effects and the estimated risk from collective low-level doses will be overestimated. The second question is whether the effects of many small dose fractions or highly protracted doses are additive. If so, then the application of collective dose is appropriate, but if not, then collective dose based on many small doses could overestimate the risk. The current risk estimates are largely based on epidemiologic studies involving acute exposures up to a few Gy, such as the Japanese atomic-bomb survivors and people receiving x-ray treatments for a variety of medical conditions. A number of studies have documented the nature of risks in these populations, and there is reasonable agreement among the studies as to the magnitude of risk per unit dose. There is less certainty about the magnitude of risks resulting from exposures at low doses andlor doses at low-dose rates. It is intrinsically difficult to assess risk accurately and precisely when doses are below 50 mSv or when they are delivered at rates of a few mSv per year. Even among the survivors of the atomic bombings in Japan, a risk from doses below approximately 200 mSv has not yet been precisely demonstrated. Lowdose studies tend to be limited for at least two reasons. First, with a lowdose study the magnitude of confounding effects may be as large or larger than the exposure-caused effects and

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hence may give "false positive" or "false negative" results. Typically, most of the potential confounding variables are either unknown, or data are not available to control their influence. Second, there is a signal-to-noise ratio (SNR) problem in low-dose studies: the smaller incidence of radiation-induced cancers may be drowned out by the much larger spontaneous incidence. This means that for low-dose studies, a large sample size will improve the SNR and permit detection of smaller differences between the spontaneous or background rate and the observed rate. In particular, the required sample size is a nonlinear function of the expected size of the effect. To give a hypothetical example; if there is a linear relationship between radiation dose and lung cancer risk, and 1,000 subjects need to be studied to detect an excess risk when the dose they receive is 1 Sv, then over 70,000 subjects with doses of 0.1 Sv would need to be studied to detect the same excess risk, and nearly seven million if the dose was 0.01 Sv. In short, the necessary sample size becomes prohibitively large when doses are small. In the sections that follow, the available human data for several of the most radiosensitive cancer types have been surveyed to determine whether the data support additivity of effects when the doses are relatively low, fractionated or protracted. In particular, the data for multiple myeloma are discussed below. This cancer, which has been noted in a few occupational studies, is examined across the range of doses to determine whether its induction is more likely to appear a t low doses or dose rates. It should be noted when comparing human studies that differences in dose and dose rate are not the only confounders, other factors such as the "healthy-worker effect" should also be considered.

3.4.1 Human Studies of Cancer Risks porn Low Radiation Doses Thyroid Cancer. There are a number of epidemiologic studies of thyroid cancer following radiation exposures. In most of these studies, acute thyroid doses of 0.5 Gy up to 10 Gy or more were involved. The available evidence indicates that radiation exposure a t younger ages (less than 20 y) confers more risk than a comparable exposure at older ages (Hanford et al., 1962; Ron et al., 1995). The focus of this review of epidemiological studies is on populations who received exposure before 20 y of age. These risk estimates are shown in Table 3.1.

3.4.1.1

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The cohort studies provide the most reliable estimates of risk because of their essentially complete ascertainment of thyroid cancer over time. The screening studies should be used with some caution because of possible subject selection biases and incomplete ascertainment over time. In addition, only two screening studies (Maxonet al., 1980; Pottern et al., 1990)nhadscreened comparison groups for use as a baseline. For most screening studies there is, therefore, additional uncertainty in the expected number of cancers, since the estimates are from populations that did not have the screening. It should be noted that when the expected numbers are small, as in the screening studies in Table 3.1, the uncertainty in the expected numbers makes the estimates of excess relative risk especially unreliable, more so than the estimates of absolute risk. A few studies have evaluated the effect of thyroid doses on the order of 0.1 Gy. These include two studies of children epilated with x rays during treatment of ringworm of the scalp (Ron et al., 1989; Shore, 1991') (see Table 3.1). The risk estimates in the larger study were a t least three times higher than those from other cohort studies of thyroid cancer. Whether this is due to unusual susceptibility within this population or to other factors is unknown. The smaller study showed a n absolute excess risk about six times lower, but the difference in risk estimates between the two studies was only marginally significant (p < 0.10). The thymus irradiation study reported by Shore (1989) included about 1,500 persons who received <0.5 Gy (mean dose of 0.18 Gy). There was a significant dose-response relationship, although it was based on small numbers (five irradiated cases versus five cases among the 4,800 unirradiated subjects). When the analysis was restricted to less than 0.3 Gy, however, the dose trend was still positive, but no longer statistically significant. The widespread use of 1311for diagnostic purposes has provided several opportunities to examine thyroid cancer risk following exposure to protracted, low-dose rate radiation. In the first, Holm et al. (1988) studied 35,000 persons to whom 13'1 was administered, of whom about 1,800 were under the age of 20 at the time of exarnination. The average thyroid dose was 0.5 Gy among adults and 1.6 Gy among children. Among those whose initial diagnostic examination was not because of a suspected thyroid tumor, there was a deficit of thyroid cancers (Table 3.1). For those under age 20 a t 1311 exposure, two thyroid cancers were observed with 1.1expected (not statistically lunpublished data (Shore,R.E., Department of Environmental Medicine,New York University Medical Center, 1991).

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significant). A second study, conducted by the Center for Devices and Radiological Health (Hamilton et al., 1989), examined thyroid morbidity in 3,500 children to whom 1311was administered for diagnostic purposes. Thyroid doses ranged from less than 0.1 to 20 Gy. No significant excess of thyroid cancer was observed. Finally, a German study (Globel et al., 1984) also failed to find a significant doseresponse slope for thyroid cancer following diagnostic I3lI exposure in nearly 14,000 patients. As part of the studies of the effects of fallout in Nevada and Utah fiom atmospheric nuclear weapons tests during 1951to 1958, Rallison et al. (1974; 1990) conducted screening examinations for thyroid disease in 2,600 children located downwind from the nuclear weapons test site in Nevada and another 2,100 from relatively unexposed children in Arizona. With about 32 y of follow-up after the testing, only eight thyroid cancers were found, and the dose-response trend was not statistically significant. Thyroid doses were estimated on the basis of residential history and milk-drinking status. Table 3.1 shows relative and absolute risk estimates for thyroid cancer from the major studies of external x-ray and internal 13'1 irradiation in juveniles. The external x-ray and internal 1311studies are different in dose rate and in the microdosimetric distribution of dose. The absolute risk estimates for the external radiation studies are about 10 times greater than those for the 1311studies. If dose rate, and not microdosimetric considerations, is the main difference between 1311and external thyroid radiation, then at face value lowering of the dose rate appears to substantially reduce carcinogenic potency. However, the data available for 1311administered to juveniles are very limited and caution should be exercised in drawing conclusions f?om them. In particular, the I3lIresults for those under age 20 are drawn from only six cases from the diagnostic series and 12 cases from the fallout series. Furthermore, the fallout series are of limited utility since only a small fraction of the Marshall Island dose was from 13'1and dose-response analyses for the Utah fallout study have been statistically significant (p 5 0.05) only for neoplasms (Brillinger, 1992). The Utah fallout study was limited by the small number of subjects in the highest exposure group and the relatively short follow-up time in comparison to the long latency period for thyroid carcinoma. A few studies of thyroid cancer are available in relation to occupational radiation exposures. Wang et al. (1990) conducted long-term studies of 27,000 diagnostic x-ray workers in China. The observed RR of 1.7 among the x-ray workers was not considered to be significantly elevated. The doses to this population are not well characterized,

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but before about 1960 the doses were sufficiently high to depress white cell counts; the mean dose has been estimated to be about 1Gy (Wang et al., 1988). Preliminary results of another occupational study have been reported by Boice et al. (1990). The study includes about 105,000 United States x-ray technologists who were queried by mail questionnaire with subsequent medical documentation and radiation exposure estimates. Preliminary analyses suggest that thyroid cancer incidence is significantly elevated (208 observed, RR = 2.31, but the dosimetry and full analyses have not yet been completed. Finally, Polednak (1986) reported a small, nonsignificant excess of thyroid cancer among United States radium dial workers. For this group, the radiation exposure to the thyroid was from a combination of photon and alpha radiation and is estimated to have averaged about 0.7 Sv. In conclusion, several studies have indicated a risk of thyroid cancer among children exposed to low-to-moderate doses of acute radiation. This risk appears comparable per unit dose to that incurred following higher doses. The limited evidence for thyroid cancer following acute doses in adulthood suggests that thyroid irradiation has several times less effect in adults than in children (Table 3.1). The 1311data suggest that protracted irradiation may be less carcinogenic than acute exposures, but this conclusion is based largely on acute x-ray irradiation to children and low-dose rate 1311 irradiation to adults. Attempts to compare effects within the same age group are confounded by the fact that the number of children treated with 1311 is small while few adults have received thyroid doses from external x-ray exposure. The consistency among the occupational studies in showing suggestive elevations in risk reinforces the idea that the thyroid gland has a high relative risk for radiation induced cancer. From the data available at this time, additivity of effects can prudently be assumed and, therefore, is not in conflict with an assumption that collective dose calculations are appropriate. 3.4.1.2 Breast Cancer. Analyses of the incidence of breast cancer among Japanese atomic-bomb survivors have indicated that the dose-response curve is essentially linear (Tokunaga et al., 1987) (Table 3.2). The low-dose portion of the data set has also been examined. In the irradiated group with <0.5 Gy, 179 breast cancers were observed as compared with 163 expected. A statistically significant dose-response trend was seen over the range 0.2 to 0.5 Gy, and the trend was suggestive, but not statistically significant for the dose range up to 0.2 Gy. In a study of infants irradiated for purported enlarged thymus glands, breast cancer risk was assessed among

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1,200 females (Hildreth et al., 1989). There was a significant doseresponse relationship which was consistent with linearity. There was also a significant elevation of risk in the subgroup who received less than 0.5 Gy. Breast cancer incidence has been studied among women who received multiple chest fluoroscopic examinations during artificial pneumothorax therapy for tuberculosis (Boice et al., 1991b; Hrubec et al., 1989). The 2,500 women in this cohort received an average breast dose of 0.8 Gy from an average of 88 fluoroscopic examinations. The risk estimate for this highly fractionated exposure protocol was comparable in magnitude to those from studies with unfractionated exposures (Table 3.21, and the dose-response relationship was well approximated by a simple linear model. Similar results were found in a large multiple fluoroscopy study of 31,700 women in Canada (Miller et al., 1989)where it was reported that a linear dose-response provided agood fit with a risk estimate comparable with other breastirradiation studies. An excess was evident over the entire dose range, including doses below 0.4 Gy. Women who received multiple diagnostic x rays for scoliosis early in life have been followed to determine breast cancer risk (Hoffman et al., 1989).This cohort totaled 970 women who received an average of 41 examinations, and a total dose to the breast estimated to average 0.13 Gy. Eleven breast cancers were obsemed (RR = 1.81, and a suggestive, but not statistically significant, dose-response trend was seen. The relatively small size of this study limited its statistical power. In the group of Chinese diagnostic x-ray workers mentioned previously, 20 breast cancers were observed (RR = 1.5) (Wang et al., 1990).The excess tended to be greater among those employed in the earlier years when the exposures were thought to be higher. Breast cancer risk is also evaluated among 1,400 women who were treated with 1311for hyperthyroidism (Goldman et al., 1988). The doses to the breast were not calculated, but probably averaged about 0.1 Gy. The relative risk for breast cancer in the 1311-treatedgroup was 1.2(not statistically significant),based on 51 breast cancer cases. Two other studies (Hoffman and McConahey, 1983; Holm et al., 1991) of breast cancer in women receiving similar doses of 1311for hyperthyroidism were also negative (23 cancers, RR = 0.8; and 134 cancers, RR = 1.0;respectively). In a study of I3lItreatment for thyroid cancer by Edmonds and Smith (1986), 258 patients received a mean breast dose of 1.0 Gy. Six breast cancers were observed (RR = 2.4), which was a significant excess. In summary, there have been a number of studies of women who received breast irradiation from fractionated exposures, protracted

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exposures andlor relatively low doses. These results are summarized in Table 3.2. Most of the studies have either shown, or are consistent with, a significant increase in the risk of breast cancer resulting from irradiation of the breast. The data are supportive of an interpretation that low doses or fractionated doses have a substantial degree of additivity of their effects upon breast cancer risk, although this seems less clear with exposures to 1311.The data for breast cancer from x-ray irradiation, perhaps more than any other human cancer, supports the notion of a dose-response relationship that is a linear function of dose and largely independent of dose rate or fractionation, thus supporting the concept of collective dose. Animal data on mammary cancer (see Section 3.3.1) have shown a linear-quadratic doseresponse function and a compatibility between the linear slope and the results with fractionated exposures. 3.4.1.3 Leukemia. The BEIR V Report (NAS/NRC, 1990) evaluated the Japanese atomic-bomb data, and to a lesser extent the ankylosing spondylitis data, for leukemia and concluded that the dose-response curve was best fit by a linear-quadratic model. Since the quadratic component becomes negligible at low doses, the magnitude of the linear component is critical in defining risks a t the low-dose levels used in calculation of collective dose. The linear component as estimated by the BEIR V analysis is dominant over a small range for those with radiation exposure at ages 20 or older. For example, if a group of workers all received a 0.1 Gy whole-body dose and were followed for 25 y, their estimated leukemia risk would be increased to 0.27 percent from the spontaneous or "background" rate of 0.21 percent. For a 0.01 Gy dose, the estimated risk would increase to only 0.215 percent. Particularly in the latter case, it would bevery difficult to detect an increased risk in an epidemiologic study. A number of studies of leukemia have been reviewed to determine if fractionated exposures or low-dose rate exposures appear to show significant leukemia risks (Table 3.3). Studies with a high, acute dose to the irradiated volume (e.g., cancer radiotherapy studies) were excluded from consideration. Five case-control studies have been reported of (mostly) adult leukemia in relation to diagnostic radiation or fallout from atmospheric weapons tests (Table 3.3) (Gibson et al., 1972; Gunz and Atkinson, 1964; Stewart et al., 1962; Linos et al., 1980; Preston-Martin et al., 1989).Three were marginally positive and the other two were negative. These studies should be interpreted cautiously because of the inherent potential for various biases (e.g., reporting bias). A casecontrol study of leukemia in relation to fallout radiation showed a

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suggestive trend (Stevens et al., 1990),while a comparison of leukemia in high- and low-background radiation areas in China (Wei, 1980)showed no differences. Caution should be exercised in interpreting these studies because of differences in the two populations. The three studies of 1311treatment for hyperthyroidism summarized in Table 3.3 (Hoffman et al., 1982; Holm et al., 1991; Saenger et al., 1968) showed no association with leukemia. A smaller study of 1311treatment for thyroid cancer (Edmonds and Smith, 1986)had a much higher bone-marrow dose and was suggestively positive. A large study of persons administered diagnostic 1311(Holmet al., 1989) was also positive although the dose to the bone marrow was relatively low. Other medical irradiation studies with low dose or protracted exposures tend to show a positive association (Davis et al., 1987; Inskip et al., 1990a; Spengler et al., 1983). Studies of patients administered the radiologic contrast medium Thorotrast reveal a definite leukemogenic effect, which is not surprising since the protracted bone-marrow irradiation is mainly by highLET alpha particles (da Silva Horta et al., 1978; Kathren and Hill, 1992; Mori et al., 1983; Olsen et al., 1989; van Kaick et al., 1989). On the other hand, radium dial painters have not shown an excess of leukemia (Baverstockand Papworth, 1989; Stebbings et al., 1983), even though the marrow doses are believed to have been appreciable and a substantial fraction of the dose was attributable to alpha radiation. Several studies of radiologists or x-ray workers with relatively high doses showed excess leukemia (Aoyama, 1989;Matanoski et al., 1975;Smith and Doll, 1981;Wanget al., 1990).The studies ofpersons with lower doses did not show a significant excess, although they were not incompatible with such an effect (Boice et al., 1990; Jablon and Miller, 1978). The final 18 citations in Table 3.3 are studies in the nuclear power or nuclear weapons industries. By and large, the bone-marrow doses in these studies are low as well as highly fractionated. Some of the occupational cohorts were exposed to internal radionuclides as well as external radiation, as noted in Table 3.3. Although only one of the 18 nuclear industry studies shows a significant overall excess of leukemia mortality among the radiation workers, the healthy worker effect makes such overall comparisons difficult to interpret. Also, in most of these studies, only a small fraction of the workers were regularly exposed to doses substantially above background, and thus such overall comparisons are greatly diluted. A more meaningful approach to investigating radiation-induced disease in these populations is to conduct dose-response analyses. Ten of the studies had individual dosimetry data, and conducted

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such analyses. Of the individual studies, only the study of Sellafield workers showed evidence of a statistically significant correlation of leukemia with external radiation exposure. However, as indicated by confidence limits and trend test results, the possibility of positive risks could not be excluded. The most informative assessment of radiation risks based on nuclear worker studies is that obtained from analyses of combined data from several studies. International analyses including data from the United States, the United Kingdom and Canada were recently conducted to evaluate the risk for leukemia, total solid cancers, and a number of specific cancer sites (Cardis et al., 1995). I t included some 95,000 workers with a collective dose of 3,843 person-Sv. The study included detailed consideration of the comparability of dosimetry across studies and over time. For leukemia the estimate of excess relative risk was 218 percent Sv-' (95 percent CI = 130 to 570). For comparison, UNSCEAR (1988) presents a linear excess relative risk estimate for leukemia of 370 percent Sv-' for males exposed in adulthood. The risk estimate from this pooled analysis was thus positive, but somewhat lower than the linear estimate based on the atomic-bomb survivors. It is also notable that the upper bound on the confidence interval excludes a risk more than twice as great as the atomic-bomb estimate, which indicates that high-risk estimates for low dose and low-dose rate irradiation are not plausible. 3.4.1.4 Multiple Myeloma. I t has been suggested that multiple myeloma is more likely to appear following low dose or low-dose rate exposures than following high dose and high-dose rate exposures. This concept arose originally Gom the excess seen at Hanford (Gilbert et al., 1989a), which yielded a central estimate of risk greater than that among the Japanese atomic-bomb survivors. Table 3.4 summarizes the available data on radiation and multiple myeloma. An examination of the studies shows that while there are several low-dose studies (with primarily low-LET radiation) with suggestively elevated multiple myeloma rates (e.g., United States radiologists, Hanford workers and Sellafield workers), there are a number of others which show no excess. Several of the high-dose studies (e.g., the Japanese atomic-bomb survivors, and patients irradiated for uterine bleeding or ankylosing spondylitis) also show suggestive excesses as do several of the studies with high-LET internally deposited alpha emitters (radium dial painters and Thorotrast patients). Hence, there is no clear pattern of greater or lesser risk per unit dose from acute versus protracted, or high-dose versus low-dose, radiation. While the data for myeloma do not argue against the

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concept of collective dose, neither can the evidence be construed as providing strong support. 3.4.1.5 In Utero Irradiation. Radiation exposure to the fetus appears to confer a larger carcinogenic risk per unit dose than postnatal irradiation (Stewart et al., 1958). Until recently, this belief was qualified by the fact that no excess ofchildhood malignancies was seen among the atomic-bomb survivors who were exposed in utero. However, the recent report of a dose-response relationship for early adult cancers among those in Hiroshima and Nagasaki with fetal exposures (Yoshimotoet al., 1988)has now demonstrated the carcinogenic risk of in utero irradiation, although this effect is clearly different from that discussed by Stewart, involving, as it does, a different age group and different cancer types. A summary of the available literature on intrauterine exposure and hematopoietic or solid cancers is given in Table 3.5. The studies reported there vary with regard to several characteristics, such as the type of study design (case-control or cohort study), the age range of the population that was studied, the type and size of comparison groups, and very importantly, the sources of information. Among the numerous case-control studies (Table 3.5, first 10 studies), those which utilized medical records to determine intrauterine exposures are generally the most reliable, and those which used only maternal recall are the least reliable. Although the cohort studies were based on a reasonably good assessment of intrauterine radiation exposure, they vary in the quality of their documentation of cancer incidence. A question about whether the observed increase in risk is real has been generated by the concern that pelvimetric irradiation has usually been administered for certain maternal or uterine indications which might themselves be unsuspected risk factors for leukemia. Mole (1974; 1979) suggested that observation of cancer risk among intrauterine irradiated twins would help settle the issue, because their irradiation was, for the most part, due to the twin conception. He reanalyzed the twin data from the large study by Stewart et al. (1958)and found an elevated risk among twins. Since that time, two other studies of twins have been performed (Harvey et al., 1985; Rodvall et al., 1990),and both show elevated risks compatible with the other intrauterine radiation studies. Although the risk from intrauterine exposure in the Japanese atomic-bomb study (Yoshimoto et al., 1988) is probably smaller per unit dose than the risks shown in the pelvimetry studies, it is qualitatively similar to risk estimates based on other data. The consistency of the risk estimates in Table 3.5, except for a few studies involving a small number of people, is remarkable and lends credence to the

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relationship. Taken as a whole, the information on risks from intrauterine radiation exposure appears to fit the concept of collectivedose additivity well.

3.4.1.6 Lung Cancer. Follow-up studies of more than a dozen groups of miners have consistently shown that exposure to highLET alpha particles from radon progeny is associated with lung cancer (Samet, 1989). Similarly, several relatively high-dose studies of low-LET radiation, such as the studies of Japanese atomic-bomb survivors (Shimizu et al., 1990; Thompson et al., 1994), ankylosing spondylitis patients (Darby et al., 1987) and peptic ulcer patients (Griem et al., 1994), have shown an elevated risk for lung cancer. Land et al. (1993) recently showed that both low- and high-LET radiation predominantly increase small-cell lung cancers. For low-LET radiation the dose-response relationship is approximately linear, while for radon progeny it is linear only if an inverse dose rate is factored in (otherwise it is concave downward). The miner data lack sufficient statistical power and precision to determine whether the inverse dose-rate effect extends down to the levels characteristic of residential radon exposures. One study suggests that a t exposures rates below about 10 WL, the excess relative risk increased linearly with time weighted cumulative exposure and did not depend on exposure rate or duration of exposure (Tomasek, 1994). Other features of the miner data indicate that the excess relative risk decreased with time following exposure and with attained age (i.e., years-at-risk rather than age-at-irradiation). Both the Japanese atomic-bomb data and the miner data indicate that the joint effects of smoking and radiation on lung cancer risk are somewhere between additive and multiplicative (Lubin et al., 1994a; Prentice et al., 19831, although it is unclear to what degree inaccuracies and limitations in the available smoking data may affect the statistical modeling. The most important unresolved questions pertain to the magnitude of risk from low-exposure levels or from fractionated or protracted exposures. It is notable that the two studies of tuberculosis patients with appreciable, but highly fractionated, doses from multiple fluoroscopic examinations have shown no excess lung cancer risk (Davis et al., 1987; Howe, 1992). Although a few studies of radiation workers or other groups with relatively low exposures to low-LET radiation showed statistically significant (Hohryakov and Romanov, 1994; Holm et al., 1991; Wing et al., 1991) or suggestive associations (Aoyarna, 1989; Checkoway et al., 1988;Rinskyet al., 1981;Stebbings et al., 1983), most have not shown statistically significant elevations in lung cancer risk (Carpenter et al., 1994; Charpentier et al., 1993; Checkoway et al., 1988; Cookfair et al., 1983; Cragle et al., 1988;

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Dupree et al., 1987; Gilbert et al., 1993a; 1993b; Gribbin et al., 1993; Jablon and Miller, 1978;Kendall et al., 1992;Kossenko and Degteva, 1994; Matanoski, 1991; Smith and Doll, 1981; Wang et al., 1990; Wiggs et al., 1991). These results should be treated cautiously, however, since information on smoking, which may have been a confounder, was generally not available. Given the wide CIS on the risk estimates in these studies, they are compatible with, although not strongly supportive of, linearity and, hence, the use of collective dose as a means to estimate population risk. The studies of lung cancer and residential radon exposure have produced mixed results. Of the major residential studies with reasonably adequate radon measurements and information on smoking, one can be classified as positive (Pershagen et al., 19941, one showed no association (Blot et al., 1990), and four others were mixed or weakly positive (Axelson et al., 1988; Lubin et al., 1994b;Schoenberg et al., 1990; Svensson et al., 1989). In the aggregate, the studies are roughly consistent with risks extrapolated from higher-dose studies, but the results are too imprecise to define the appropriate mathematical form of the extrapolation. The problems and limitations of residential radon studies have also been examined by Lubin et al. (1990). 3.4.1.7 Other Cancers. Several other sites at which cancers are known to be caused by radiation have not been examined above, including bladder, esophagus, liver, stomach and colon. The last two, in particular, have been assigned major weights in the assessment of radiation risk (ICRP, 1991; NCRP, 1993). The risk estimates for colon and stomach cancer have been based primarily on the Japanese atomic-bomb data (Shimizu et al., 1990; Thompson et al., 19941, which poses a major question of how to "transport" these risk estimates to the United States population, i.e., whether to use an excess relative risk (ERR) model or an absolute excess risk (AER) model, since United States colon cancer rates are much higher and stomach cancer rates much lower than the corresponding rates in Japan. Using the Japanese ERR estimate for colon cancer would, therefore, give a much greater absolute risk in the United States population than would using the AER estimate, whereas the opposite would be true for stomach cancer. Unfortunately, there are insufficient data to resolve the issue of how best to "transport" the risk estimates to other populations. For colon cancer, studies of 226Ratherapy for uterine bleeding (Inskip et al., 1990b; Ryberg et al., 1990), x-ray treatment for peptic ulcer (Griem et al., 1994) and the use of 1311 for hyperthyroidism (de Vathaire et al., 1989; Hoffman et al., 1982) are consistent with a radiation-related increase in risk, as are occupational studies of United States radium dial painters (Stebbings et al., 1983), early

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United States radiologists (Matanoski, 1982) and Japanese medical radiation workers (Aoyama, 1989). On the other hand, a series of other occupational radiation studies showed no excess colon cancer risk: early United Kingdom radiologists (Smith and Doll, 1981), Chinese medical x-ray workers (Wang et al., 1990), United States nuclear shipyard workers (Matanoski, 1991), the combined DOE studies a t Hanford, Oak Ridge and Rocky Flats (Gilbert et al., 1993a; 1993b), Savannah River workers (Cragle et al., 19881, Oak Ridge Y-12 workers (Checkoway et al., 1988; Polednak and Frome, 19811, the United Kingdom combined registry of nuclear workers (Kendall et al., 1992) and Canadian nuclear workers (Gribbin et al., 1993). A few radiation studies besides the Japanese atomic-bomb survivor study have shown statistically significant or suggestive excesses of stomach cancer, e.g., cervical cancer patients (Boice et al., 19881, peptic ulcer patients (Griem et al., 1994), 1311-treatedthyroid cancer patients (Hall et al., 1991), United States radiologists before 1929 (Matanoski, 19821, and United States radium dial painters (Stebbings et al., 1984). However, several other studies with radiation doses to the stomach less than 0.5 Gy did not show an excess, e.g., ankylosingspondylitis patients (Darby et al., 1987), early United Kingdom radiologists (Smith and Doll, 1981),United States radiologists registered 1920 to 1939 (Matanoski, 1982), Chinese medical x-ray workers (Wang et al., 1990) and Japanese medical radiation workers (Aoyama, 1989). Stomach cancer was not elevated in a number of studies with lower doses: patients with uterine bleeding (Inskip et al., 1990b),tuberculosis patients with multiple fluoroscopic examinations (Davis et al., 1987),patients given 1311for hyperthyroidism (Holmet al., 1991),residents near the Techa River (Kossenko and Degteva, 1994), United States nuclear shipyard workers (Matanoski, 1991), the combined DOE studies a t Hanford, Oak Ridge and Rocky Flats (Gilbert et al., 1993a; 1993b), Savannah River workers (Cragle et al., 1988),Oak Ridge Y-12 workers (Checkowayet al., 1988;Polednak and Frome, 1981), the United Kingdom combined registry of nuclear workers (Kendall et al., 1992) and Canadian nuclear workers (Gribbin et al., 1993). In the aggregate, for colon and stomach cancer there is no evidence t h a t risk estimation based on the collective dose would underestimate the cancer risk, and the confidence limits on risk in most studies are broadly compatible with a linear function; hence, from this point of view the use of collective dose to estimate population risk is reasonable and prudent. 3.4.2 Genetic Risks The primary source of human data on the genetic risks of ionizing radiation has been the Japanese study of about 31,000 offspring

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conceived subsequent to the exposure of their parents in the atomic bombings of Hiroshima or Nagasaki (greater than 0.01 Gy) and 41,000 control offspring (less than 0.01 Gy). This study evaluated various genetic endpoints in the F1generation2,including untoward pregnancy outcomes, sex ratio, neonatal deaths, disturbances of normal growth and development, cancer incidence, cytogenetic abnormalities (balanced chromosomal rearrangements and sexchromosome aneuploidy) and alterations of serum or erythrocyte protein phenotypes. For none of these endpoints has a significant dose-dependent excess risk been seen. From a combination of these endpoints the doubling dose has been estimated as 1.7 to 2.2 Gy for acute doses, i.e., the excess RR is about 0.4 to 0.6 per Gy (Nee1et al., 1989; 1990). No substantial human data are available which would permit a determination of whether there is a diminution in the riskcoefficient with low or protracted exposures. The report of an apparent association between fathers' preconception radiation exposure at the Sellafield (United Kingdom) nuclear waste reprocessing plant and leukemia in their offspring (Gardner et al., 1990) suggested a radiation-induced germinal mutation that produced a carcinogenic effect. However, the study was based on only four leukemia cases from fathers in the highest exposure group. The study of the other United Kingdom waste reprocessing facility at Dounreay, which also showed an excess of childhood leukemia among residents in the vicinity, does not confirm the findings of Gardener et al. (1990) regarding paternal radiation exposure, but because of its low power, is not necessarily inconsistent with those findings (Urquhart et al., 1991).Other epidemiologic studies of paternal preconception radiation have been of variable methodologic quality, e-g., whether the purported preconception exposures were documented or merely based on retrospective interviews and have been mixed in their findings. One study has suggested a paternal preconception effect (Shu et al., 1988), while the large study by Kneale and Stewart (1980), the Japanese atomic-bomb study (Yoshimoto, 1990) and others (Graham et al., 1966; Hicks et al., 1984)have not shown such an effect. Important evidence against the hypothesis comes from two studies. No excess of childhood leukemia was seen in the larger region around Sellafield, although the risk estimate from Seascale would have predicted over 50 excess cases among the offspring of the workers (Draper et al., 1993).A case-control study of childhood leukemia among children born near five Canadian nuclear facilities found no =TheF1generation is the pregnancy or offspringof the parents who were irradiated.

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evidence of an association with paternal preconception irradiation (McLaughlin et al., 1993). In short, based on the human data alone, there is no clear evidence of genetic effects to which collective dose concepts should be applied. The existence of human genetic effects is primarily inferred from animal experiments, as discussed in Section 3.2.2.

3.5

Summary

Taken as a whole, the body of evidence from both laboratory animals and human studies allows a presumption of a linear no threshold response a t low doses and low-dose rates, for both mutations and carcinogenesis. Therefore, from the point of view of the scientific bases of collective doses for radiation protection purposes, it is prudent to assume the effect per unit dbse in the low-dose region following single acute exposures or low-dose fractions is a linear response. There are exceptions to this general rule of no threshold, including the induction of bone tumors in both laboratory animals and in some human studies due to incorporated radionuclides, where there is clearly evidence for an apparent threshold. However, few experimental studies, and essentially no human data, can be said to prove or even to provide direct support for the concept of collective dose with its implicit uncertainties of nonthreshold, linearity and dose-rate independence with respect to risk. The best that can be said is that most studies do not provide quantitative data that, with statistical significance, contradict the concept of collective dose. Ultimately, confidence in the linear no threshold dose-response relationship at low doses is based on our understanding of the basic mechanisms involved. Genetic effects may result from a gene mutation, or a chromosome aberration. The activation of a dominant acting oncogene is frequently associated with leukemias and lymphomas, while the loss of suppressor genes appears to be more frequently associated with solid tumors. I t is conceptually possible, but with a vanishingly small probability, that any of these effects could result from the passage of a single charged particle, causing damage to DNA that could be expressed as a mutation or small deletion. I t is a result of this type of reasoning that a linear nonthreshold doseresponse relationship cannot be excluded. It is this presumption, based on biophysical concepts, which provides a basis for the use of collective dose in radiation protection activities. The limitations of the concept of collective dose are discussed in Section 4.

4. Limitations

4.1 Conceptual Limitations The paradox of the use of collective dose in radiation protection is that, at high doses and high-dose rates where the risk coefficients are reasonably well known, the concept of collective dose may not be applicable since the dose-response curve for many effects is clearly nonlinear and dose-rate dependtnt, and the major concern is likely to be on individual risk and protection of the individual. By contrast, at low-dose rates where linearity between dose and effect is presumed, the risk coefficients are much less certain. Collective dose is a rigorous concept only if the following three conditions are met: 1. the risk of the biological effect of interest must be proportional to dose over the range of interest: 2. the biological response to a given dose must be independent of the temporal pattern over which the dose is delivered, i.e., independent of dose rate or fractionation, and 3. the doses involved must not be so high that cell killing and/or deterministic effects complicate the outcome.

Almost all risk coefficients for stochastic effects have been derived from individuals who received doses in excess of 0.1 Gy. However, for most practices forwhich risks to populations need to be evaluated, the additional doses, i.e., above natural background, to individuals are considerably lower and may be only in the order of pGy y-l, or less than 0.01 Gy lifetime. It is not readily apparent that the risk coefficients derived from rather large doses should apply to such small incremental doses. However, because even the most trivial of T h e requirement of proportionality can be met most simply by a dose-response relationship that is linear without threshold down to zero dose. However, since background radiation is ubiquitous, there is in fact no need to make any assumption concerning the shape of the dose-response relationship for doses below background; it may be linear, exhibit a dose threshold, or show evidence of an adaptive response or even supra-linearity. Provided proportionality with dose holds for all doses above background in the range of concern for radiation protection, collective dose is a meaningful concept.

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dose increments is always added to the dose from natural background, the individual doses to which the risk coefficients are extrapolated generally exceed 1mGy y-l or 50 to 100 mGy lifetime. By their very nature, deterministic effects apply only to specific exposed individuals and should be described in terms of severity of effects as well as incidence. It may be appropriate to include individual doses exceedingthresholds for deterministic effects in calculating the collective dose to ensure that it is truly representative of the potential risk for stochastic effects. In such cases, the stochastic and deterministic components of the risk must be evaluated separately. If a given number of individuals in a population received a given dose of ionizing radiation, the projected number of excess cancers or deleterious genetic effects will vary considerably with the nature of the population involved. The principal factors that will influence the biological consequences are the age and sex distributions of the exposed population, but other factors such as the genetic make-up of the population and the presence of potentiating or competing processes may also play a role. Consequently, the risk associated with a given collective dose will not have a unique value, but will vary with the population exposed. When very low doses are spread out over a long period of time, as would be the case for a radiation worker during an average career, differences in radiosensitivity as a function of age become less critical as an averaging effect occurs. A special situation may include effects on the developing embryo and fetus. This would be of importance to pregnant or potentially pregnant radiation workers. The concept of a negligible individual dose (NID) (NCRP, 1993) implies that there is a point beyond which further efforts to reduce radiation exposure are unwarranted. The basic premise is that at or below the NID level, the assumed risk to the individual is trivial compared with ordinary societal activities and can therefore be dismissed from consideration. A concept of this kind is necessary to avoid wasteful expenditures ofhealth protection resources that could be employed more effectively elsewhere. Since it is generally accepted that a dose of ionizing radiation, however small, has associated with it a risk of eliciting a deleterious biological response, there is no conceptual basis to exclude even the individuals receiving the lowest dose from a calculation of collective dose. However, such small doses may have such large uncertainty associated with them that their usefulness in assessing risk may be of questionable value. This is examined further in connection with the guidance provided in Sections 4.2 and 5.2. In summary, the NID should not be used to limit the calculation of collective dose, but it is an important concept in allocation of

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resources associated with dose reduction for individuals, a use which the Council continues to recommend. A concept, such as the NID, provides a legitimate lower limit below which action to further reduce individual.dose is unwarranted, but it is not necessarily a legitimate cut-off dose level for the calculation of collective dose. Collective dose addresses societal risk while the NID and related concepts address individual risk.

4.2 Practical Limitations Although there are some situations in which collective dose may be used with reasonable confidence a s the primary variable for describing societal risk from radiation exposure, there are other situations in which a calculated collective dose contains such large inherent uncertainties that it is an extremely poor indicator of risk and, therefore, should not be considered valid as a basis for decisions on radiation protection. This Section discusses how the limitations to the concept of collective dose relate to specific applications in risk assessment and risk management. A collective dose is often the only quantity available for deriving a n estimate of the collective or total health detriment from radiation exposure. However, the legitimate application of collectivedose must include clearly defined boundary conditions for the time, locations and pathways of exposure, as well as characteristics of the exposed populations. The uncertainties must not only be stated, but should be used to determine the extent to which the collective dose can be used as a surrogate for risk. When the combined uncertainties in the exposed population, e.g., size, those related to characteristics, exposure pathways and individual doses, result in a collective dose with a relative uncertainty of more than an order of magnitude, neither estimates of collective dose nor estimates of collective risk are adequate for making decisions. Inherently, calculation of collective dose includes consideration of: (1)the exposed population and (2) the radiation doses toits members. Collective dose should be used for risk assessment only if both of these components are very well characterized, i.e., only then can the uncertainties in the calculated collective dose be small enough to make the calculation of value. Uncertainties and limitations in various elements involved in collective dose calculations are discussed below. 1. the exposed population needs to be defined and characterized with respect to size, age and sex distributions,

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2. the exposure pathways must be characterized for the population at risk, and 3. individual contributions to collective dose must include only doses to the whole body or to specific organs or tissues for which stochastic risk coefficients have been adopted.

4.2.1

Tissue Weighting Factors

A collective risk may be represented by a collective organ dose, obtained by summing the equivalent doses to a given organ of all individuals in the population at risk. Calculation of a collective effective dose from radionuclidestaken into the body is based on summing the doses to individual organs, each weighted according to its contribution to the total risk. The ICRP (1991) and NCRP (1993) give tissue weighting factors (wTs)for 12 specific tissues that account for 93 percent of the serious health effects, or detriment, from radiation exposures, i.e., bladder, bone marrow, bone surface, breast, colon, esophagus, gonads, liver, lung, skin, stomach and thyroid. Doses from internally deposited radionuclides or from partial-body external irradiation may be summed to obtain a collective dose only ifproperly weighted for the radionuclides involved and the specific tissues or organs exposed. It must be remembered that the WTS are averages for both sexes. In cases where one sex predominates, appropriate W T S , e.g., for breast, should be applied. Similarly, age adjusted WTS may be appropriate rather than averages. For radionuclides within the body that have long effective half-lives, it is recommended that the collective committed effective dose be used in the calculation of collective dose in estimating societal risk.

4.2.2

Population Characteristics

A collective dose can be valid for representing collective risk only if the population that is exposed can be described and quantified. Although the number of individuals in the exposed population is the most important factor, the age and sex distribution may also greatly affect the calculated risk. Two examples will illustrate the extremes of quantification of exposed populations: (1)radiation workers and (2) those exposed to environmental contamination at times far in the future. Workers in a particular industry can be characterized with respect to age and sex, work assignments, length of employment, and many other factors. If all exposed workers are monitored, the collective

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doses can be estimated with reasonable accuracy by summing the individual contributions. Separate estimates of collective organ doses for each sex can also be obtained to h r t h e r refine the estimates of risk. Even if a large fraction of the workers is not monitored, a reasonable estimate of collective dose can usually be obtained by including the estimated average dose for the unmonitored workers. In marked contrast with a current worker population, no reliable estimate of collective dose can be made for populations exposed to long-lived environmental contamination thousands or even hundreds of years in the future. There will simply be too many unknowns with respect to demography and ecology to allow meaningful calculations. 4.2.2.1 Uncertainties in Future Population Size and Location. Geographic distributions of populations tend to change dramatically over relatively short time periods as environmental conditions and resource values change. In general, the fastest-growing cities in the United States during recent decades either did not exist or were inconsequential a century ago. As recently as a generation ago, few people would have foreseen the dynamic changes in the population distribution across the United States, particularly in cities such a s Phoenix, Arizona or Las Vegas, Nevada. Demographers typically will not make projections of population distributions more than a quarter of a century into the future, much less a century or more (Bogue, 1969;Krueckeberg and Silvers, 1974; Murdock and Leistritz, 1983). Thus, predictions of collective dose based on demographic projections of more than a few decades into the future are inherently accompanied by uncertainties of sufficient magnitude as to render them unreliable. 4.2.2.2 Uncertainties in Future Population Fertility. Assessment of the genetic component of risk from radiation requires that the population be characterized with respect to fertility. UNSCEAR (1988) defines the "genetically significant dose (GSD)" as "the dose which, if received by every member of the population, would be expected to produce the same total genetic injury to the population as do the actual doses received by the various individuals." In this case, the GSD is a n age- and sex-weighted average dose that results in a particular collective risk. For a given average whole-body or gonadal dose, the GSD would be different in populations with different birth control practices. For large, unselected populations, the w ~ include s considerations for genetic effects. In populations that are heavily weighted toward one sex or a narrow age range, collective organ (gonad) doses for subgroups in the population may be more

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PRACTICAL LIMITATIONS

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appropriate than the collective effective dose for expressing genetic risk. Uncertainties in Future Medical Technology. One of the most important factors likely to affect the significance of radiation dose in the centuries and millennia to come is the effect of progress in medical technology. Medical progress achieved during the past several decades has reduced the risk of premature death and increased the average age of the population, leading to a relative increase in diseases prevalent in the elderly, e.g., cancer. The success of medical science has also been felt in the increased numbers of people in the procreative age group who have survived hereditary defects that would once have been fatal and who are now capable of passing that hereditary defect on to their offspring. At some future time, it is possible that a greater proportion of somatic diseases caused by radiation will be treated successfully. If, in fact, an increased proportion of the adverse health effects of radiation prove to be either preventable or curable by advances in medical science, the estimate of long-term detriments may need to be revised as the consequences (risks) of doses to future populations could be very different. 4.2.2.3

4.2.3

Environmental Exposure Pathways

Exposures to large populations are typically calculated rather than measured. Environmental transport models not only utilize such geophysical parameters as atmospheric and hydrologic dispersion, but also ecological and agricultural characteristics that are highly dependent on human endeavors. Radiation doses calculated by these models are only as good as the input data, which become highly uncertain for centuries, or even decades, in the future. Agriculture. The geographic distribution of agriculture in the United States has changed significantly during the nation's history. Mechanization, automation, improved plant stocks, fertilizers and insecticides have greatly enhanced crop yields and, in addition, have had a direct impact on the demographic shift from the farm to the urban environment. I t is entirely plausible that within a few decades significant changes in the present-day patterns of transport of contaminants through agricultural products will have occurred and the agricultural environment may be more closely controlled to maximize quantity and quality of yield with reduced interaction with the uncontrolled 4.2.3.1

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environment. Large-scale irrigation projects and long-range, refrigerated transportation have radically changed the relationship between population and food production and distribution. Food supplies are increasingly becoming global rather than localized within agricultural communities.

4.2.3.2 Resource Conservation. As natural resources are depleted and become more expensive to obtain, increasing emphasis is being placed on consel-vation and recycling of mineral resources, organic materials and water. Given intensive recycling of resources, future exposure pathways for contaminants may be quite different from those recognized today, with concomitant differences in collective doses and dose distributions.

5. Risk Assessment and Management 5.1 Collective Dose as a Surrogate for Societal Risk

Informal or nonrigorous risk assessments are performed daily by every individual; they are simply the evaluations of the actual or potential consequences of anticipated or ongoing actions. UNSCEAR (1982) uses the term "risk assessment" to mean the calculation of average individual risk of induced fatality within a n exposed population. Although a collective dose is implied, it is not expressly stated; only the average organ or whole-body doses are used and the size of the population is thus normalized. I n many situations, this approach to risk assessment is preferable to expressing risk as the total detriment to a n entire population, regardless of size or the distribution of the doses. A composite risk to a defined population may include risk from sources that expose only part of the population, e.g., the risk to the United States population, from occupational doses. Similarly, comparison of risks from defined sources may involve populations of very different sizes, resulting in distortion in the potential harm of the sources themselves. For example, comparison of the number of fatal cancers presumed to be caused by radon released from uranium mines and mill tailings with those presumed to be caused by UF6 released from uranium conversion facilities may not reveal the fact that the impacts of radon are distributed over the entire northern hemisphere and many generations, whereas those from UF6 may be limited to a small region during the active life of the facility. In developing standards for disposal of spent nuclear fuel and high-level and transuranic radioactive wastes, the Environmental Protection Agency (EPA) has evaluated the capabilities of mined geologic repositories to isolate the wastes from the environment (EPA, 1988).The EPA's analysis of needed containment over a period of 10,000 y indicated that the small residual risks allowed by the disposal standards would be comparable to the risks to which future populations would have been exposed if the uranium ore used to produce the high-level wastes had not been mined. On this basis,

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AND MANAGEMENT

the primary standards being promulgated are containment requirements that limit projected releases of radioactive materials to the accessible environment. The release limits, which are risk related, thus serve as a surrogate for collective dose limits. The EPA (1988) approach assumes that the total release approach is more appropriate in view of the very long time periods and uncertainties involved.

5.2 Collective Dose Distributions To the extent that collective dose is a measure of societal risk, a single value of collective dose may be useful and meaningful provided that no individual dose or risk is predominant. However, if the range of doses to individuals covers several orders of magnitude, the distribution of doses is also necessary for characterizing the risk adequately, if for no other reason than to assure that a few cases at either extreme of the dose distribution range do not drive or disproportionately affect the characterization of risk. The distribution might best be characterized by dividing it into several ranges of individual doses, each covering two or three orders of magnitude, with the population size, average individual dose, collective dose, and uncertainty given for each range. Therefore, whenever the collective dose is smaller than the reciprocal of the relevant risk coefficient, e.g., less than 10 percent, the risk assessment should note that the most likely number of cancer deaths is zero. This does not imply that a population should be divided into smaller and smaller groups to obtain this result.

5.3 Risk Assessment i n Specific Applications 5.3.1 Medical Procedures Risk assessment in medicine is dominated by the consideration of individual patients, where the potential for benefit is expected to justify any concomitant risk. Screening procedures involving radiation exposure to a group of individuals present a somewhat different situation, since neither the benefit nor the risk is to an identified individual, but is distributed statistically over the screened population. Because screening is often performed on population subgroups of a single sex, or with a narrow age distribution, risk coefficients need to be selected with care for use with collective organ doses.

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For determining risks from medical procedures, care should be taken in applying the risk estimates derived for an average over the whole population to patients with short life expectancies, e.g., significantly shorter than the latency period for stochastic effects. Such exposures might reasonably be excluded from the consideration of risk, even though these may account for a major portion of the total collective dose to a given population. Some procedures produce dose rates and partial-body doses that are quite high compared with natural background or typical occupational doses, and may approximate those doses from which risk coefficients are derived. However, such exposures are typically to specific organs (or portions of organs) or tissues, or are nonuniform distributions. Thus, appropriate care must be taken to ensure that this fact is reflected in the calculation of the collective effective dose, and that the conditions of Section 4.1 are met.

5.3.2 Radiation Workers

Although more effort has been devoted to describing dose distributions for workers than for the general public, single values for collective doses may be more appropriate for occupational exposures than for most other sources. This is because most of the individual dose contributions may be measured or estimated with reasonable accuracy and all of the doses and risks are to current populations that are relatively small and comparatively homogeneous and wellcharacterized. Many occupational exposures to external irradiation involve only partial-body doses. For example, when a worker's body is shielded, the head and hands may receive most of the exposure. For exposure situations of this type, calculations of collective doses and risks may be inappropriate if the risk coefficients for the exposed tissues have not been established. In such cases, it may be appropriate to use some measure or indicator of risk other than collective dose, or, if collective dose is to be used, to recognize and attempt to account for the limitations inherent in its use for the specific situation.

5.3.3 Special Occupational Groups

Several occupational groups can be identified that traditionally have not been considered to be radiation workers, because their duties are not specified in terms of deliberate use of radiation sources, but nonetheless involve enhanced exposures to radiation. Among

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these are airline flight crews, business travelers who fly frequently, those who work underground in mines, caves or in masonry vaults with above-normal exposures to natural radiation. The criteria for categorizing and calculating collective doses to members of these special occupational groups are essentially the same as those for radiation workers in medicine or other industries. The exposure conditions are often sufficiently stable and predictable that individual doses need not be monitored. Rather, collective dose may be computed from measurements in the work environment and from work schedules. All relevant dose should be included, even that only incidentally arising out of and in the course of employment. For airline crews, this may include additional exposure incurred dead-heading to and from duty stations, since it is an integral part of the occupation. Another category that warrants special attention in any calculation of collective dose is those who receive less than normal exposures from natural radiation sources, such as ship crew members and, especially, submariners. The long periods spent shielded from significant components of terrestrial radiation, and also cosmic radiation in the case of submariners, is a unique characteristic of this group. 5.3.4

Current Exposures to Members of the Public from Localized Environmental Sources

Source-related environmental risk assessments provide some of the most common, but also the most misleading, uses of collective dose. The doses are usually distributed in a population with characteristics similar to the national population or the hypothetical population used in other risk assessments. However, only a small portion of the collective dose comes from the very small number of real or hypothetical individuals in close proximity to the source, while most of the collective dose comes from large numbers of individuals who receive negligible doses. That is not to say that calculations of collective doses in such situations are not useful or valid; they simply should not be expressed as a single value that includes contributions from individual doses that differ by several orders of magnitude, i.e., all doses included in the collective dose calculations should be in the low dose, low-dose rate range where linearity of response with dose may be assumed. 5.3.5 Indoor Radon For the general public, exposures to indoor radon produce an average annual risk to an individual of death from lung cancer of less

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than y-l, although smokers and some occupants of houses with unusually high radon concentrations have higher annual risks. Because conversions from potential alpha energy exposures to effective doses have a high degree of uncertainty, and risk estimates are based on exposure in terms of potential alpha energy, expressing collective exposures in collective units of potential alpha energy is preferable in that it eliminates the uncertainties and possible biases associatedwith such conversions. Furthermore, since the interaction of smoking and radon exposure is considered to be important (NAS/ NRC, 1991),although still uncertain, distributions of collective exposures should be subdivided into smoking and nonsmoking categories to facilitate risk estimates.

5.3.6 Consumer Products and Other Miscellaneous Sources In essentially all cases, with the notable exception of the radiation dose from 210Poto cigarette smokers and users of chewing tobacco, the individual contributions to collective dose from consumer products and other generally-distributed miscellaneous sources produce annual individual risks in the order of 10-I or less (NCRP, 1987e). Exposure pathways and individual doses may be known sufficiently well to justify calculation of the collective dose, but the average individual risk should always be determined.

5.3.7 Future Exposures from Long-Lived Environmental Contaminants Neither population size and characteristics nor environmental exposure pathways for most radioactive elements are predictable with any degree of confidence for more than a few generations into the future (see Section 4). Consequently, there can be no meaningful calculation of collective or individual doses for populations far in the future. For this reason, collective dose projected more than a few generations into the future should not be used as a basis for estimating societal risk or for limitation of practices, although such pmjections may have some utility for other purposes. The most reasonable risk assessment that can be made for such situations is to calculate potential individual doses for a range of scenarios in order to: (1)evaluate protective measures and (2) to try to place some boundaries on estimates of future individual risks. For the few very long-lived radionuclidesthat are metabolically regulated in the body and more or less uniformly distributed within the

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biosphere (e.g., 14C and lZ9I), future average individual doses may be estimated from total quantities in the environment even though there could be no valid estimate of collective dose because of the lack of knowledge regarding future populations and their demographics.

5.4 Risk Management It is possible to use objective criteria and methods in risk management, and guidance for the application of such criteria and methods to risk management is provided below. Risk management should be based on clearly stated objectives, e.g., health protection, environmental, financial, aesthetic and other considerations.

5.4.1 Acceptability of Risk

Use of a single value for collective dose, as has been common in the practice of radiation protection, has in many instances led to a lack of acceptance of any avoidable risk from radiation exposure, regardless of the offsetting benefits or costs of avoidance. This is true primarily because all individual contributions to collective dose from a given source have usually been consolidated into a single value from which a risk estimate was calculated. The summation of trivial average risks over very large populations or time periods into a single value in this manner has produced a distorted image of risk, completely out of perspective with risks accepted every day, both voluntarily and involuntarily. In many instances, the collective dose increases with the increasing size of the exposed population, but the benefits and risks to individuals remain nearly constant.

5.4.2

Categorizing Levels of Risk

A decision to limit the individual lifetime risk of cancer from any specific source category to a predetermined or arbitrary value ignores the questions of competing risks and costs of avoidance, and is difficult to justify on scientific or technical grounds. The criteria recommended in Section 4.2 for categorizing collective dose by individual risk levels for performing risk assessments applies equally to risk management. The presentation of collective doses and risks in broad categories of individual risk would clarify risk management decisions and make them more readily understood.

5.4 RISKMANAGEMENT

5.4.3

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Optimization of Protection (ALARA)

The concept of ALARA, viz., that all radiation doses shall be kept as low a s reasonably achievable, taking into account social and economic factors, has been a fundamental principle in radiation protection for several decades. The concept is considered to be identical to the optimization requirement included in the ICRP system of dose limitation in that both connote qualitative, as well as quantitative, evaluations. The concept of ALARA presumes that any increment of radiation dose may produce a proportionate incremental risk. Risks from exposures to ionizing radiation are often expressed as a number of deaths or serious health effects per unit collective dose. Costs of radiation protection (dose reduction) are usually expressed in monetary units. The term "excess deaths" is used in epidemiology to describe the number of observations beyond the expected deaths within particular population groups over prescribed time intervals. Premature death from cancer causes loss of a portion of a human life span, about 15 y on the average (ICRP, 1991). This is quite different from the loss of life resulting from the accidental death of a child. 'Years of life lost or impaired" may provide a better basis for comparison of risks and should be considered for assessment of risks and for making risk management decisions. The loss of life expectancy has another advantage over number of deaths in that it is not very sensitive to the risk projection model used, i.e., additive versus multiplicative. The use of collective dose to calculate risk for purposes of optimization of protection is acceptable and desirable whenever the basic limitations and boundary conditions described in this Report are observed.

5.4.4

Valuation of Collective Dose Avoided

The valuation of collective dose avoided is defined by the ICRP as consisting of two distinct elements: alpha is the valuation of the "objective health detriment" and beta is the valuation of the "nonobjective health detriment" (ICRP, 1989). Alpha is the sum of the somatic and genetic stochastic risks, which may be expressed as the number of years of life lost or seriously impaired per unit collective dose. Beta may not be a health detriment at all, but may depend on political, administrative and public relations issues, and as such is beyond the scope of this Report. Since only alpha is uniquely a function of collective dose, it is the only valuation that is discussed here.

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The application of the conversion factor, alpha, requires that the loss of future human resources (life expectancy) per unit collective dose be quantified. The ICRP and NCRP (ICRP, 1991;NCRP, 1993) provides nominal probability coefficients for stochastic effects, weighted for the detriment from nonfatal cancers and severe hereditary effects, of 5.6 percent Sv-l for adult workers and 7.3 percent Sv-' for the general population. For the multiplicative model, the loss of life per fatal cancer is 13 to 15 y (ICRP, 1991). As a first approximation for the purpose of illustration, the amount of life lost or impaired may be taken as the total detriment multiplied by the amount of life lost per fatal cancer. The estimated loss of life is then calculated to be approximately 0.8 y Sv-l for workers and 1.0y Sv-I for the general population. One method for calculation of years of life lost per unit dose, which also considers age a t the time of irradiation and organs irradiated, has been published (Maillie et al., 1993). An important question then is: "How much of current human resources (time and effort) are we willing and able to trade for future human resources?" As a society, we appear to be willing to spend extraordinary sums to save or prolong the life of identified individuals and we are willing to spend large sums as long as the number of individuals a t risk is small. The amount we are willing to spend to improve life expectancy or quality of life for people we do not know and cannot identifjr is less clear, but the available funds are clearly limited. The principles and problems associated with evaluation of dose have been discussed in ICRP Publication 37 (ICRP, 1983).

6. Conclusions and Recommendations It is clear that the concept of collective dose has, over the years, found increasing application in radiation protection, both as an operational tool for controlling radiation exposures to radiation workers and to the general public, and as a means of estimating the prospective risks to populations from real or potential radiation exposures. The application of the concept of collective dose for these purposes, however, is subject to certain limitations and qualifications, and the Council therefore cautions against inappropriate usage of this potentially valuable but limited tool. Implicit in the concept of collective dose is the assumption of a direct proportionality between the risk incurred and the radiation dose, over the range of doses and dose rates of concern, i.e., the response to radiation is both linear and time independent, and that any incremental dose above background, no matter how small, carries with it a proportionate risk of a specific stochastic effect or group of effects. The absence of a threshold is not essential to the use of collective dose, provided its magnitude is smaller than the natural background. The assumption of linearly without threshold isjustified for radiation protection purposes. It should be recognized, however, that a t low levels of individual exposure the risk estimates are uncertain by a factor of two or more in either direction and a threshold in the dose response can not be excluded, nor can the possibility that the risks are underestimated a t low doses be excluded. Modern radiation protection practice is based on three tenets: Justification of a practice to ensure that it, in fact, provides a net positive benefit; ALARA, taking into account social and economic factors; and dose limits which are established to ensure that the procedures for justification and ALARA do not result in excessive risk to individuals or to groups of individuals. The first two of these tenets-justification and ALARA-imply consideration of the total practice, and therefore collective dose may be the only reasonable quantity on which a suitable evaluation may be based. Dose limits normally apply to the individual, but constraints on the collective dose may also be applicable, albeit with important restrictions.

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6. CONCLUSIONS AND RECOMMENDATIONS

Given the foregoing discussion of the underlying bases and limitations of collective dose, the Council recommends the following:

1. The concept of collective dose should be considered as one of the means for assessing the acceptability of a facility or practice. However, because collective dose depends upon demographic variables as well as radiation doses, it is recommended that regulatory limits not be set in terms of collective dose. 2. Collective dose is most useful when applied to populations with known characteristics such as size, age, sex, etc. Where population characteristics are poorly defined or highly uncertain or subject to significant temporal change, collective dose should be applied with appropriate caution. 3. When the uncertainty in the number of individuals summed in the population component of collective dose is large (e.g., one or more orders of magnitude), collective dose should not be used as a surrogate for risk even a t relatively highlevels of individual radiation doses. 4. Application of collective dose should be limited to stochastic effects (deterministic effects are not included) and to the dose range in which risk is assumed to be proportional to dose and independent of dose rate. 5. Assessing risk from collective exposures in medicine must reflect the great uncertainty in applying population based risk estimates to patients due to specific age distributions, health status and, possibly, shorter life expectancy. 6. All doses should be included in calculations of collective dose; there is no conceptual basis for excluding any individual doses, however small, from the collective dose calculation. There may, however, be practical limitations [see recommendations (2), (3) and (4)l. 7. When the range of individual doses spans several orders of magnitude, the distribution should be characterized by dividing it into several ranges of individual doses, each coveringno more than two to three orders of magnitude, with the population size, mean individual dose, collective dose and uncertainty being considered separately for each range. 8. Projection of collective committed doses to future populations and situations should be done with care and situations must recognize the large uncertainties introduced by unpredictable changes in relevant parameters, e.g., less than about 10 percent. 9. When the collective dose is smaller than the reciprocal of the relevant risk coefficient, the risk assessment should note that the most likely number of excess cancer deaths is zero.

6. CONCLUSIONS AND RECOMMENDATIONS

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In the future, broader application of collective dose may be appropriate, but extension will necessitate a greater knowledge and understanding of the parameters used in the determinationand calculation of collective dose and its attendant risks.

Glossary absolute risk: excess risk that adds to the existing or baseline risk already present by an increment that depends upon the dose, but is independent of the level of existing risk. ALARA: an acronym for as low as reasonably achievable, a radiation protection philosophy or practice that specifies reduction of radiation exposures to as low as reasonably achievable, with economic and social factors being taken into account. collective dose: the sum total of all individual radiation doses to a specified group or population. committeddose: the time integration of dose rate, usually for a 50 y period for adults and 70 y for children. The committed dose may be expressed in terms of the collective dose or the dose to an individual and may be expressed in terms of the various dose quantities such as absorbed dose and effective dose. deterministic effect: a n effect that has a clinical threshold, i.e., exposures below the threshold do not result in the clinical effect of concern, whereas at exposures above the threshold the effect will occur in a greater number of persons so exposed and the severity increases with dose. Formerly, deterministic effects were termed "nonstochastic" effects. dose: a s used in the general sense, refers to deposition of energy by ionizing radiation. dose-response curve: a graphical characterization of the relationship between a defined biological endpoint and the dose received. effective dose (E):is the sum of the weighted equivalent doses in all the tissues and organs of the body given by the expression: E = 2wTH T , ~ where W T is the weighting factor for organ or tissue, T; and HT,X is the equivalent dose in tissue or organ T due to a given radiation, R. equivalent dose (H): is the absorbed dose averaged over a tissue or organ, DT (rather than a point) and weighted for the radiation quality, w~ (radiation weighting factor) of the irradiating radiation, i.e., H T , = ~ DT wg. negligible individual dose (NID):a level of effective dose to an individual that may be dismissed. The NID is 0.01 mSv y-l. radiation weighting factor (wR): a factor selected to account for the biological effectiveness of the radiation incident on the body or, in the case of sources within the body, emitted by the source. It ranges from 1 to 20 depending on the radiation type and energy of the radiations. relative risk: risk relative to the existing or baseline risk typically expressed as a multiple of the existing or baseline risk.

GLOSSARY

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risk coefficient:the probability or chance that a particular stochasticeffect will occur per unit dose. sievert (Sv):the special name for the unit of effective dose and equivalent dose, 1 Sv = 1 J kg-'. stochastic effect: an all-or-nothing effect, the severity of which does not vary with dose, although the probability of occurrences does. (More generally, stochastic means probabilistic or' random in nature.) tissue weighting factor (wT):a factor that indicates the ratio of the risk of effects attributable to irradiation of a given organ or tissue, T, to the total risk when the whole body is uniformly irradiated.

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SAENGER, E.L., THOMA, G.E. and TOMPKINS, E.A. (1968). "Incidence of leukemia following treatment of hyperthyroidism. Preliminary report of the Cooperative Thyrotoxicosis Therapy Follow-Up Study," J. Am. Med. Assoc. 205, 855-862. SAGAN, L.A. (1989). "On radiation, paradigms and hormesis," Science 245, 574, 621. SALONEN, T. (1976). "Prenatal and perinatal factors in childhood cancer," Ann. Clin. Res. 8, 27-42. SAMET, J.M. (1989). "Radon and lung cancer," J. Natl. Cancer Inst. 81, 745-757. SCHMID, E., BAUCHINGER, M., BUNDE, E., FERBERT, H.F. and VON LIEVEN, H. (1974). "Comparison of the chromosome damage and its dose response aRer medical whole-body exposure to =OCogamma-rays and irradiation of blood in vitro," Int. J. Radiat. Biol. Relat. Stud. Phys. Chem. Med. 26,31-37. SCHNEIDER, A.B., SHORE-FREEDMAN, E., RYO, U.Y., BEKERMAN, C., FAVUS, M. and PINSKY, S. (1985). "Radiation-induced tumors of the head and neck following childhood irradiation. Prospective studies," Medicine 64, 1-15. SCHOENBERG, J.B., KLOTZ, J.B., WILCOX, H.B., NICHOLLS, G.P., GIL-DEL-REAL,M.T., STEMHAGEN, A. and MASON, T.J. (1990). "Casecontrol study of residential radon and lung cancer among New Jersey women," Cancer Res. 50,6520-6524. SEARLE, A.G. (1974). "Mutation induction in mice," Adv. Radiat. Biol. 4, 151. SHIMIZU,Y., KATO, H. and SCHULL, W.J. (1990)."Studies of the mortality of A-bomb survivors. 9. Mortality, 1950-1985: Part 2. Cancer mortality based on the recently revised doses (D586),"Radiat. Res. 121, 120-141. SHIONO, P.H., CHUNG, C.S. and MYRIANTHOPOULOS, N.C. (1980). "Preconception radiation, intrauterine diagnostic radiation, and childhood neoplasia," J. Natl. Cancer Inst. 65, 681-686. SHORE, R.E. (1989). "Radiation epidemiology: Old and new challenges," Environ. Health Perspect. 81, 153-156. SHORE, R.E., HILDRETH, N., DVORETSKY, P., ANDRESEN, E., MOSESON, M. and PASTERNACK, B. (1993). 'Thyroid cancer among persons given x-ray treatment in infancy for a n enlarged thymus gland," Am. J. Epidemiol. 137, 1068-1080. SHU, X.O., GAO, Y.T., BRINTON, L.A., LINET, MS., TU,J.T., ZHENG, W. and FRAUMENI, J.F., JR. (1988). "A population-based case-control study of childhood leukemia in Shanghai," Cancer 62, 635-644. SMITH, P.G. and DOLL, R. (1981). "Mortality from cancer and all causes among British radiologists," Br. J. Radiol. 54, 187-194. SPENGLER, R.F., COOK, D.H., CLARKE, E.A., OLLEY, P.M. a n d NEWMAN, A.M. (1983). "Cancer mortality following cardiac catheterization: A preliminary follow-up study on 4,891 irradiated children," Pediatrics 71,235-239. SPIESS, H., MAYS, C. and CHMELEVSKY, D. (1989). "Malignancies in patients injected with radium-224," Br. Inst. Radiol. 21, 7-11.

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The NCRP The National Council on Radiation Protection and Measurements is a nonprofit corporation chartered by Congress in 1964 to: 1. Collect, analyze, develop and disseminate in the public interest information and recommendations about (a) protection against radiation and (b)radiation measurements, quantities and units, particularly those concerned with radiation protection. 2. Provide a means by which organizations concerned with the scientific and related aspects of radiation protection and of radiation quantities, units and measurements may cooperate for effective utilization of their combined resources, and to stimulate the work of such organizations. 3. Develop basic concepts about radiation quantities, units and measurements, about the application of these concepts, and about radiation protection. 4. Cooperate with the International Commission on Radiological Protection, the International Commission on Radiation Units and Measurements, and other national and international organizations, governmental and private, concerned with radiation quantities, units and measurements and with radiation protection.

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President Vice President Secretary and Treasurer Assistant Secretary Assistant Treasurer

S. JAMES ADELSTEIN

W. ROGERNN CARLD. HOBELMAN JAMES F. BERG Members

KEITH F. ECKERMAN THOMASF. GESELL ETHELS. GILBERT JOEL E. GRAY ARTHUR W. GUY ERIC J. HALL NAOMIH. LEY WILLIAM R. HENDEE DAVIDG. HOEL F. OWENHOFFMAN DONALD G. JACOBS A. EVEREWE JAMES, JR JOHN R. JOHNSON BERNDKAHN KENNETHR. KASE AMY KRONENBERG HAROLD L. KUNDEL CHARLESE. LAND JOHN B. LITTLE RICHARD A. LUBEN ROGER0.MCCLELLAN J. MCNEIL BARBARA CHARLESB. MEINHOLD FREDA. M E T ~ E R W. MILLER CHARLES Honorary Members

L A U R I ~S.N TAYLOR, Honorary President WARREN K. SINCLAIR,President Emeritus ROBLEY D. EVANS RICHARD F. FOSTER HYMERL. FRIEDELL R.J. MICHAEL FRY ROBERT 0 . GORSON JOHN W. HEALY PAULC. HODGES GEORGE V. LEROY WILFRIDB, MANN A. ALAN MOGHISSI KARLZ. MORGAN ROBERTJ. NELSEN WESLEYL. NYBORG CHESTERR. RICHMOND

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Currently, the following subgroups are actively engaged in formulating recommendations: Basic Radiation Protection Criteria SC 1-4 Extrapolation of Risk from Non-Human Experimental Systems to Man SC 1-5 Uncertainty in Risk Estimates SC 1-6 Basis for the Linearity Assumption Structural Shielding Design and Evaluation for Medical Use of X Rays and Gamma Rays of Energies Up to 10 MeV Operational Radiation Safety SC 46-8 Radiation Protection Design Guidelines for Particle Accelerator Facilities SC 46-10 Assessment of Occupational Doses from Internal Emitters SC 46-11 Radiation Protection During Special Medical Procedures SC 46-12 Determination of the Effective Dose Equivalent (and Effective Dose) to Workers for External Exposure to Low-LET Radiation SC 46-13 Design of Facilities for Medical Radiation Therapy Dosimetry and Metabolism of Radionuclides SC 57-2 Respiratory Tract Model SC 57-9 Lung Cancer Risk SC 57-10 Liver Cancer Risk SC 57-14 Placental Transfer SC 57-15 Uranium SC 57-16 Uncertainties in the Application of Metabolic Models Radiation Exposure Control in a Nuclear Emergency Radionuclides in the Environment SC 64-6 Screening Models SC 64-17 Uncertainty in Environmental Transport in the Absence of Site Specific Data SC 64-18 Plutonium SC 64-19 Historical Dose Evaluation SC 64-20 Contaminated Soil SC 64-21 Decontamination and Decommissioning of Facilities Biological Effects and Exposure Criteria for Ultrasound Efficacy of Radiographic Procedures Radiation Protection in Mammography Guidance on Radiation Received in Space Activities Guidance on Occupational and Public Exposure Resulting from Diagnostic Nuclear Medicine Procedures Risk of Lung Cancer from Radon Hot Particles in the Eye, Ear or Lung Radioactive and Mixed Waste SC 87-1 Waste Avoidance and Volume Reduction SC 87-2 Waste Classification Based on Risk SC 87-3 Performance Assessment Fluence as the Basis for a Radiation Protection System for Astronauts Nonionizing Electromagnetic Fields SC 89-1 Biological Effects of Magnetic Fields

SC 91

SC 92 SC 93

SC 89-3 Extremely Low-Frequency Electric and Magnetic Fields SC 89-4 Modulated Radiofrequency Fields SC 89-5 Biological Effects and Exposure Criteria for Radiofrequency Electromagnetic Fields Radiation Protection in Medicine SC 91-1 fiecautions in the Management of Patients Who Have Received Therapeutic Amounts of Radionuclides SC 91-2 Dentistry Policy Analysis and Decision Making Radiation Measurement

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American Podiatric Medical Association American Public Health Association American Radium Society American Roentgen Ray Society American Society of Health-System Pharmacists American Society of Radiologic Technologists American Society for Therapeutic Radiology and Oncology Association of University Radiologists Bioelectromagnetics Society Campus Radiation Safety Officers College of American Pathologists Conference of Radiation Control Program Directors Council on Radionuclides and Radiopharmaceuticals Electric Power Research Institute Electromagnetic Energy Association Federal Communications Commission Federal Emergency Management Agency Genetics Society of America Health Physics Society Institute of Nuclear Power Operations International Brotherhood of Electrical Workers National Aeronautics and Space Administration National Association of Environmental Professionals National Electrical Manufacturers Association National Institute of Standards and Technology Nuclear Energy Institute Oil, Chemical and Atomic Workers Union Radiation Research Society Radiological Society of North America Society of Nuclear Medicine United States Air Force United States Army United States Coast Guard United States Department of Energy United States Department of Housing and Urban Development United States Department of Labor United States Department of Transportation United States Environmental Protection Agency United States Navy United States Nuclear Regulatory Commission United States Public Health Services Utility Workers Union of America

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liaison between the organization and the NCRP; (2) that the individual designated will receive copies of draft NCRP reports (at the time that these are submitted to the members of the Council) with an invitation to comment, but not vote; and (3) that new NCRP efforts might be discussed with liaison individuals as appropriate, so that they might have an opportunity to make suggestions on new studies and related matters. The following organizations participate in the Special Liaison Program: Australian Radiation Laboratory Commissariat a I'Energie Atomique (France) Commission of the European Communities Defense Nuclear Agency Health Council of the Netherlands International Commission on Non-Ionizing Radiation Protection Japan Radiation Council National Radiological Protection Board, (United Kingdom) National Research Council (Canada) Office of Science and Technology Policy South African Forum for Radiation Protection Ultrasonics Institute (Australia) United States Air Force United States Nuclear Regulatory Commission

The NCRP values highly the participation of these organizations in the Special Liaison Program. The Council also benefits significantly from the relationships established pursuant to the Corporate Sponsor's Program. The program facilitates the interchange of information and ideas and corpor a t e sponsors provide valuable fiscal support for the Council's program. This developing program currently includes the following Corporate Sponsors: Amersham Corporation Commonwealth Edison Consolidated Edison Duke Power Company Eastman Kodak Company Florida Power Corporation Landauer, Inc. 3M New York Power Authority Public Service Electric and Gas Company Westinghouse Electric Corporation

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Agfa Corporation Alfred P. Sloan Foundation Alliance of American Insurers American Academy of Dermatology American Academy of Oral and Maxillofacial Radiology American Association of Physicists in Medicine American Cancer Society American College of Medical Physics American College of Nuclear Physicians American College of Occupational and Environmental Medicine American College of Radiology American College of Radiology Foundation American Dental Association American Healthcare Radiology Administrators American Industrial Hygiene Association American Insurance Services Group American Medical Association American Nuclear Society American Osteopathic College of Radiology American Podiatric Medical Association American Public Health Association American Radium Society American Roentgen Ray Society American Society of Radiologic Technologists American Society for Therapeutic Radiology and Oncology American Veterinary Medical Association American Veterinary Radiology Society Association of University Radiologists Battelle Memorial Institute, Canberra Industries, Inc. Chem Nuclear Systems Center for Devices and Radiological Health College of American Pathologists Committee on Interagency Radiation Research and Policy Coordination Commonwealth of Pemsylvania Consumers Power Company Council on Radionuclides and Radiopharmaceuticals Defense Nuclear Agency Duke Power Company Edison Electric Institute Edward Mallinckrodt, Jr. Foundation EG&G Idaho, Inc. Electric Power Research Institute Federal Emergency Management Agency Florida Institute of Phosphate Research ' Fuji Medical Systems, U.S.A., Inc. Genetics Society of America Health Effects Research Foundation (Japan) Health Physics Society Institute of Nuclear Power Operations James Picker Foundation Martin Marietta Corporation

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Motorola Foundation National Aeronautics and Space Administration National Association of Photographic Manufacturers National Cancer Institute National Electrical Manufacturers Association National Institute of Standards and Technology Nuclear Energy Institute Picker International Radiation Research Society Radiological Society of North America Richard Lounsbery Foundation Sandia National Laboratory Siemens Medical Systems, Inc. Society of Nuclear Medicine Society of Pediatric Radiology United States Department of Energy United States Department of Labor United States Environmental Protection Agency United States Navy United States Nuclear Regulatory Commission Victoreen, Inc.

Initial funds for publication of NCRP reports were provided by a grant from the James Picker Foundation. The NCRP seeks to promulgate information and recommendations based on leading scientific judgment on matters of radiation protection and measurement and to foster cooperation among organizations concerned with these matters. These efforts are intended to serve the public interest and the Council welcomes comments and suggestions on its reports or activities from those interested in its work.

NCRP Publications NCRP publications are distributed by the NCRP Publications Office. Information on prices and how to order may be obtained by directing an inquiry to: NCRP Publications 7910 Woodmont Avenue Suite 800 Bethesda, MD 20814-3095 The currently available publications are listed below.

NCRP Reports No.

Title Control and Removal ofRadioactive Contamination i n Laboratories (1951) Maximum Permissible Body Burdens and Maximum Permissible Concentrations of Radionuclides i n Air and in Water for Occupational Exposure (1959)[IncludesAddendum 1 issued in August 19631 Measurement of Neutron Flux and Spectra for Physical and Biological Applications (1960) Measurement ofAbsorbed Dose of Neutrons, and of Mixtures of Neutrons and Gamma Rays (1961) Stopping Powers for Use with Cavity Chambers (1961) Safe Handling of Radioactive Materials (1964) Radiation Protection i n Educational Institutions (1966) Dental X-Ray Protection (1970) Radiation Protection i n Veterinary Medicine (1970) Precautions i n the Management o f Patients Who Have Received Therapeutic Amounts of Radionuclides (1970) Protection Against Neutron Radiation (1971) Protection Against Radiation from Brachyt herapy Sources (1972) Specification of Gamma-Ray Brachytherapy Sources (1974) Radiological Factors AffectingDecision-Makingin a Nuclear Attack (1974)

NCRP PUBLICATIONS

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Krypton-85 i n the Atmosphere-Accumulation, Biological Significance, and Control Technology (1975) Alpha-Emitting Particles in Lungs (1975) Tritium Measurement Techniques (1976) Structural Shielding Design and Evaluation for Medical Use of X Rays and Gamma Rays of Energies Up to 10 MeV (1976) Environmental Radiation Measurements (1976) Radiation Protection Design Guidelines for 0.1-100 MeV Particle Accelerator Facilities (1977) Cesium-137fromthe Environment to Man: Metabolism and Dose (1977) Medical Radiation Exposure of Pregnant and Potentially Pregnant Women (1977) Protection of the Thyroid Gland i n the Event of Releases of Radioiodine (1977) Instrumentation and Monitoring Methods for Radiation Protection (1978) A Handbook ofRadioactivity Measurements Procedures, 2nd ed. (1985) Operational Radiation Safety Program (1978) Physical, Chemical, and Biological Properties of Radiocerium Relevant to Radiation Protection Guidelines (1978) Radiation Safety Training Criteria for Industrial Radiography (1978) Tritium i n the Environment (1979) Tritium and Other Radionuclide Labeled Organic Compounds Incorporated in Genetic Material (1979) Influence of Dose and Its Distribution i n Time on DoseResponse Relationships for Low-LET Radiations (1980) Management of Persons Accidentally Contaminated with Radionuclides (1980) Radiofrequency Electromagnetic Fields-Properties, Quantities and Units, Biophysical Interaction, and Measurements (1981) Radiation Protection i n Pediatric Radiology (1981) Dosimetry of X-Ray and Gamma-Ray Beams for Radiation Therapy i n the Energy Range 10 keV to 50 MeV (1981) Nuclear Medicine-Factors Influencing the Choice and Use of Radionuclides in Diagnosis and Therapy (1982) Operational Radiation Safety-Training (1983) Radiation Protection and Measurement for Low-Voltage Neutron Generators (1983)

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NCRP PUBLICATIONS

Protection in Nuclear Medicine and Ultrasound Diagnostic Procedures i n Children (1983) Biological Effects of Ultrasound: Mechanisms and Clinical Implications (1983) Iodine-129: Evaluation of Releases from Nuclear Power Generation (1983) Radiological Assessment: Predicting the Transport, Bioaccumulation, and Uptake by Man of Radionuclides Released to the Environment (1984) Exposures from the Uranium Series with Emphasis on Radon and Its Daughters (1984) Evaluation of Occupational and Environmental Exposures to Radon and Radon Daughters i n the United States (1984) Neutron Contamination from Medical Electron Accelerators (1984) Induction of Thyroid Cancer by Ionizing Radiation (1985) Carbon-14 i n the Environment (1985) SI Units in Radiation Protection and Measurements (1985) The Experimental Basis for Absorbed-Dose Calculations in Medical Uses of Radionuclides (1985) General Concepts for the Dosimetry of Internally Deposited Radionuclides (1985) Mammography-A User's Guide (1986) Biological Effects and Exposure Criteria for Radiofrequency Electromagnetic Fields (1986) Use of Bioassay Procedures forAssessment of Internal Radionuclide Deposition (1987) Radiation Alarms and Access Control Systems (1986) Genetic Effects from Internally Deposited Radionuclides (1987) Neptunium: Radiation Protection Guidelines (1988) Public Radiation Exposure from Nuclear Power Generation i n the United States (1987) Ionizing Radiation Exposure of the Population of the United States (1987) Exposure of the Population i n the United States and Canada from Natural Background Radiation (1987) Radiation Exposure of the U.S. Population from Consumer Products and Miscellaneous Sources (1987) Comparative Carcinogenicity of Ionizing Radiation and Chemicals (1989) Measurement of Radon and Radon Daughters i n Air (1988) Guidance on Radiation Received i n Space Activities (1989) Quality Assurance for Diagnostic Imaging (1988)

NCRP PUBLICATIONS

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Exposure of the U.S. Population from Diagnostic Medical Radiation (1989) Exposure of the U.S. Population from Occupational Radiation (1989) Medical X-Ray, Electron Beam and Gamma-Ray Protection for Energies Up to 50 MeV (Equipment Design, Performance and Use) (1989) Control of Radon i n Houses (1989) The Relative Biological Effectiveness of Radiations of Different Quality (1990) Radiation Protection for Medical and Allied Health Personnel (1989) Limit for Exposure to "Hot Particles" on the Skin (1989) Implementation of the Principle of As Low As Reasonably Achievable ~AI;IIRA)for Medical and Dental Personnel (1990)

Conceptual Basis for Calculations of Absorbed-Dose Distributions (1991) Effects of Ionizing Radiation on Aquatic Organisms (1991) Some Aspects of Strontium Radiobiology (1991) Developing Radiation Emergency Plans for Academic, Medical or Industrial Facilities (1991) Calibration of Survey Instruments Used in Radiation Protection for the Assessment of Ionizing Radiation Fields and Radioactive Surface Contamination (1991) Exposure Criteria for Medical Diagnostic Ultrasound:I. Criteria Based on Thermal Mechanisms (1992) Maintaining Radiation Protection Records (1992) Risk Estimates for Radiation Protection (1993) Limitation of Exposure to Ionizing Radiation (1993) Research Needs for Radiation Protection (1993) Radiation Protection i n the Mineral Extraction Industry (1993)

A Practical Guide to the Determination of Human Exposure to Radiofrequency Fields (1993) Dose Control at Nuclear Power Plants (1994) Principles and Application of Collective Dose in Radiation Protection (1995) Binders for NCRP reports are available. 'Ibvo sizes make it possible to collect into small binders the "old series" of reports (NCRP Reports Nos. 8-30) and into large binders the more recent publications (NCRP Reports Nos. 32-121). Each binder will accommodate from five to seven reports. The binders carry the identification "NCRP Reports"

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NCRP PUBLICATIONS

and come with label holders which permit the user to attach labels showing the reports contained in each binder. The following bound sets of NCRP reports are also available: Volume I. NCRP Reports Nos. 8, 22 Volume 11. NCRP Reports Nos. 23, 25, 27, 30 Volume 111. NCRP Reports Nos. 32, 35, 36, 37 Volume IV. NCRP Reports Nos. 38, 40, 41 Volume V. NCRP Reports Nos. 42,44,46 Volume VI. NCRP Reports Nos. 47, 49, 50,51 Volume VII. NCRP Reports Nos. 52,53,54,55,57 Volume VIII. NCRP Report No. 58 Volume IX.NCRP Reports Nos. 59,60,61,62,63 Volume X. NCRP Reports Nos. 64, 65, 66, 67 Volume XI. NCRP Reports Nos. 68,69, 70, 71,72 Volume XII. NCRP Reports Nos. 73, 74,75, 76 Volume XIII. NCRP Reports Nos. 77, 78, 79,80 Volume XIV.NCRP Reports Nos. 81, 82, 83, 84, 85 Volume XV. NCRP Reports Nos. 86, 87,88, 89 Volume XVI. NCRP Reports Nos. 90, 91, 92, 93 Volume XVII. NCRP Reports Nos. 94, 95,96, 97 Volume XVIII. NCRP Reports Nos. 98, 99, 100 Volume XM. NCRP Reports Nos. 101, 102, 103, 104 Volume XX.NCRP Reports Nos. 105,106, 107, 108 Volume XXI. NCRP Reports Nos. 109,110, 111 Volume XXII. NCRP Reports Nos. 112, 113, 114 Volume XXIII. NCRP Reports Nos. 115, 116, 117,118 (Titles of the individual reports contained in each volume are given above.)

NCRP Commentaries No. 1 3 4

Title

Krypton-85 in the Atmosphere-With Specific Reference to the Public Health Significance of the Proposed Controlled Release at Three Mile Island (1980) Screening Techniques for Determining Compliance with Environmental Standards-Releases of Radionuclides to the Atmosphere (1986), Revised (1989) Guidelines for the Release of Waste Water from Nuclear Facilities with Special Reference to the Public Health Significance of the Proposed Release of Treated Waste Waters at Three Mile Island (1987)

NCRP PUBLICATIONS

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Review of the Publication, Living Without Landfills (1989) Radon Exposure of the U.S. Population-Status of the Problem (1991) Misadministration of Radioactive Material i n MedicineScientific Background (1991) Uncertainty i n NCRP Screening Models Relating to Atmospheric Transport, Deposition and Uptake by Humans (1993) Considerations Regarding the Unintended Radiation Exposure of the Embryo, Fetus or Nursing Child (1994) Advising the Public about Radiation Emergencies: A Document for Public Comment (1994) Dose Limits for Individuals Who Receive Exposure Pom Radionuclide Therapy Patients (1995) Radiation Exposure and High-Altitude Flight (1995)

Proceedings of the Annual Meeting No.

Title

1

Perceptions of Risk, Proceedings of the Fifteenth Annual Meeting held on March 14-15,1979(includingTaylor Lecture No. 3) (1980) Critical Issues i n Setting Radiation Dose Limits, Proceedings of the Seventeenth Annual Meeting held on April 89, 1981 (including Taylor Lecture No. 5) (1982) R a d i a t i o n Protection a n d N e w Medical Diagnostic Approaches, Proceedings of the Eighteenth Annual Meeting held on April 6-7,1982 (including Taylor Lecture No. 6) (1983) Environmental Radioactivity, Proceedings of the Nineteenth Annual Meeting held on April 6-7,1983 (including Taylor Lecture No. 7) (1983) Some Issues Important i n Developing Basic Radiation Protection Recommendations, Proceedings of the Twentieth Annual Meeting held on April 4-5,1984 (includingTaylor Lecture No. 8) (1985) Radioactive Waste, Proceedings of the Twenty-first Annual Meeting held on April 3-4,1985 (includingTaylor Lecture No. 9)(1986) Nonionizing Electromagnetic Radiations and Ultrasound, Proceedings of the Twenty-second Annual Meeting held on April 2-3,1986 (includingTaylor Lecture No. 10)(1988)

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NCRP PUBLICATIONS

New Dosimetry at Hiroshima and Nagasaki and Its Implications for Risk Estimates, Proceedings of the Twenty-third Annual Meeting held on April 8-9,1987 (including Taylor Lecture No. 11)(1988) Radon, Proceedings of the Twenty-fourth Annual Meeting held on March 30-31, 1988 (including Taylor Lecture No. 12) (1989) Radiation Protection Today-The NCRPat Sixty Years, Proceedings of the Twenty-fifth Annual Meeting held on April 5-6, 1989 (including Taylor Lecture No. 13)(1990) Health and Ecological Implications of Radioactively Contaminated Environments, Proceedings of the Twentysixth Annual Meeting held on April 4-5, 1990 (including Taylor Lecture No. 14) (1991) Genes, Cancer and Radiation Protection, Proceedings of the Twenty-seventh Annual Meeting held on April 3-4,1991 (including Taylor Lecture No. 15) (1992) Radiation Protection i n Medicine, Proceedings of the Twenty-eighth Annual Meeting held on April 1-2, 1992 (including Taylor Lecture No. 16) (1993) Radiation Science and Societal Decision Making, Proceedings of the Twenty-ninth Annual Meeting held on April 7-8, 1993 (including Taylor Lecture No. 17) (1994) Lauriston S. Taylor Lectures No.

Title

1

The Squares of the Natural Numbers in Radiation Protection by Herbert M. Parker (1977) Why be Quantitative about Radiation Risk Estimates? by Sir Edward Pochin (1978) Radiation Protection-Concepts and Trade Offs by Hymer L. Friedell (1979) [Available also in Perceptions of Risk, see above] From "Quantity of Radiation" and "Dose" to "Exposure" and 'Xbsorbed Dose7'-An Historical Review by Harold 0. Wyckoff (1980) How Well Can We Assess Genetic Risk? Not Very by James F. Crow (1981) [Available also in Critical Issues in Setting Radiation Dose Limits, see abovel Ethics, Trade-offs and Medical Radiation by Eugene L. Saenger (1982) [Available also in Radiation Protection and New Medical Diagnostic Approaches, see abovel

NCRP PUBLICATIONS

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99

The Human Environment-Past, Present and Future by Merril Eisenbud (1983) [Available also in Environmental Radioactivity, see above] Limitation and Assessment i n Radiation Protection by Harald H. Rossi (1984) [Available also in Some Issues Import a n t i n Developing Basic R a d i a t i o n Protection Recommendations, see abovel Truth (and Beauty) i n Radiation Measurement by John H. Harley (1985) [Available also in Radioactive Waste, see abovel Biological Effects of Non-ionizing Radiations: Cellular Properties and Interactions by Herman P. Schwan (1987) [Available also in Nonionizing Electromagnetic Radiations and Ultrasound, see abovel How to be Quantitative about Radiation Risk Estimates by Seymour Jablon (1988) [Available also in New Dosimetry at Hiroshima and Nagasaki and its Implications for Risk Estimates, see abovel How Safe is Safe Enough? by Bo Lindell (1988) [Available also in Radon, see abovel Radiobiology and Radiation Protection: The Past Century and Prospects for the Future by Arthur C. Upton (1989) [Available also in Radiation Protection Today, see abovel Radiation Protection and the Internal Emitter Saga by J. Newel1 Stannard (1990) [Available also in Health and Ecological Implications of Radioactively Contaminated Environments, see abovel When is a Dose Not a Dose? by Victor P. Bond (1992) [Available also i n Genes, Cancer and Radiation Protection, see abovel Dose and Risk in Diagnostic Radiology: How Big? How Little? by Edward W. Webster (1992)[Availablealso in Radiation Protection in Medicine, see above] Science, Radiation Protection and the NCRP by Warren K. Sinclair (1993)[Available also in Radiation Science and Societal Decision Making, see abovel Mice, Myths and Men by R.J. Michael Fry (1995) Symposium Proceedings No. 1

Title The Control of Exposure of the Public to Ionizing Radiation in the Event ofAccident orAttack, Proceedings of a Symposium held April 27-29, 1981 (1982)

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NCRP PUBLICATIONS

Radioactive and Mixed Waste-Risk as a Basis for Waste Classification, Proceedings of a Symposium held November 9,1994 (1995)

NCRP Statements No.

Title

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"Blood Counts, Statement of the National Committee on Radiation Protection," Radiology 63, 428 (1954) "Statements on Maximum Permissible Dose from Television Receivers and Maximum Permissible Dose to the Skin of the Whole Body," Am. J. Roentgenol., Radium Ther. and Nucl. Med. 84, 152 (1960) and Radiology 75, 122 (1960) X-Ray Protection Standards for Home Television Receivers, Interim Statement of the National Council on Radiation Protection and Measurements (1968) Specification of Units ofNatura1 Uranium and Natural Thorium, Statement of the National Council on Radiation Protection and Measurements (1973) NCRP Statement on Dose Limit for Neutrons (1980) Control of Air Emissions of Radionuclides (1984) The Probability That a Particular Malignancy May Have Been Caused by a Specified Irradiation (1992)

2

3 4 5 6 7

Other Documents The following documents of the NCRP were published outside of the NCRP report, commentary and statement series: Somatic Radiation Dose for the General Population, Report of the Ad Hoc Committee of the National Council on Radiation Protection and Measurements, 6 May 1959, Science, February 19, 1960, Vol. 131, No. 3399, pages 482-486 Dose Effect Modifying Factors In Radiation Protection, Report of Subcommittee M-4 (Relative Biological Effectiveness) of the National Council on Radiation Protection and Measurements, Report BNL 50073 (T-471) (1967) Brookhaven National Laboratory (National Technical Information Service Springfield, Virginia) The following documents are now superseded and/or out of print:

NCRP PUBLICATIONS

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101

NCRP Reports No. 1 2

Title X-Ray Protection (1931)[Superseded by NCRP Report No. 31 Radium Protection (1934)[Superseded by NCRP Report No. 41 X-Ray Protection (1936)[Superseded by NCRP Report No. 61 Radium Protection (1938)[Superseded by NCRP Report No. 131 Safe Handling of Radioactive Luminous Compound (1941) [Out of Printl Medical X-Ray Protection Up to Two Million Volts (1949) [Superseded by NCRP Report No. 181 Safe Handling of Radioactive Isotopes (1949)[Superseded by NCRP Report No. 301 Recommendations for Waste Disposal of Phosphorus-32 and Iodine-131 for Medical Users (1951)[Out of Printl Radiological Monitoring Methods and Instruments (1952) [Superseded by NCRP Report No. 571 Maximum Permissible Amounts of Radioisotopes i n the Human Body and Maximum Permissible Concentrations in Air and Water (1953)[Superseded by NCRP Report No. 221 Recommendations for the Disposal of Carbon-14 Wastes (1953)[Superseded by NCRP Report No. 811 Protection Against Radiations from Radium, Cobalt-60 and Cesium-137 (1954)[Superseded by NCRP Report No. 241 Protection Against Betatron-Synchrotron Radiations Up to 100 Million Electron Volts (1954)[Superseded by NCRP Report No. 511 Safe Handling of Cadavers Containing Radioactive Isotopes (1953)[Superseded by NCRP Report No. 211 Radioactive-Waste Disposal in the Ocean (1954)[Out of Printl Permissible Dose from External Sources of Ionizing Radiation (1954)including Maximum Permissible Exposures to Man, Addendum to National Bureau of Standards Handbook 59 (1958)[Superseded by NCRP Report No. 391 X-Ray Protection (1955)[Superseded by NCRP Report No. 261 Regulation o f Radiation Exposure by Legislative Means (1955)[Out of Print] Protection Against Neutron Radiation Up to 30 Million Electron Volts (1957)[Superseded by NCRP Report No. 381

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Safe Handling of Bodies Containing Radioactive Isotopes (1958) [Superseded by NCRP Report No. 371 Protection Against Radiations from Sealed Gamma Sources (1960) [Superseded by NCRP Reports No. 33,34 and 401 Medical X-Ray Protection Up to Three Million Volts (1961) [Superseded by NCRP Reports No. 33, 34, 35 and 361 A Manual of Radioactivity Procedures (1961) [Superseded by NCRP Report No. 581 Exposure to Radiation in an Emergency (1962) [Superseded by NCRP Report No. 421 Shielding for High-Energy Electron Accelerator Installations (1964) [Superseded by NCRP Report No. 511 Medical X-Ray and Gamma-Ray Protection for Energies up to 10 MeV-Equipment Design and Use (1968) [Superseded by NCRP Report No. 1021 Medical X-Ray and Gamma-Ray Protection for Energies Up to 10 MeV-Structural Shielding Design and Evaluation Handbook (1970) [Superseded by NCRP Report No. 491 Basic Radiation Protection Criteria (1971) [Superseded by NCRP Report No. 911 Review of the Current State of Radiation Protection Philosophy (1975) [Superseded by NCRP Report No. 911 Natural Background Radiation in the United States (1975) [Superseded by NCRP Report No. 941 Radiation Protection for Medical and Allied Health Personnel (1976) [Superseded by NCRP Report No. 1051 Review ofNCRP Radiation Dose Limit for Embryo and Fetus in Occupationally-Exposed Women (1977) [Out of Printl Radiation Exposure from Consumer Products and Miscellaneous Sources (1977) [Superseded by NCRP Report No. 951 A Handbook of Radioactivity Measurements Procedures, 1st ed. (1978) [Superseded by NCRP Report No. 58, 2nd ed.1 Mammography (1980) [Out of Print] Recommendations on Limits for Exposure to Ionizing Radiation (1987) [Superseded by NCRP Report No. 1161

NCRP Commentaries

No. 2

Title Preliminary Evaluation of Criteria for the Disposal of Transuranic Contaminated Waste (1982) [Out of Printl

NCRP PUBLICATIONS

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NCRP Proceedings No. 2

Title Quantitative Risk in Standards Setting, Proceedings of the Sixteenth Annual Meeting held on April 2-3, 1980 [Out of Print]

Index Absolute risk 64 Acceptability of risk 58 Agriculture 51 ALARA 59,61,64 Below regulatory concern 5 Breast cancer risks 22-24 fluroscopic examinations 24 Cancer risks 16-18,38 cohort studies 17 fractionatedlprotracted irradiation 18 from low radiation doses 16 in utero irradiation 38 thymus irradiation 17 thyroid cancer 16, 18 Carcinogenesis 12 leukemia 12 solid tumors 12 Cellular studies 8 Chromosome aberrations 9-10 in spermatogonia 10 Cohort studies-external radiation 18 thyroid cancer risks 18 Collective dose 1, 3-6,46, 53-54, 64 annual limitation 3 applications 4-5 as a comparison of safeguards 6 as a.measure of the radiationrelated detriment 6 as a tool for the optimization of radiological protection 6 concept evaluations 5 conceptual limitations 46 distributions 54 in radiation protection regualtions 5 surrogate for societal risk 53 validity and utility 5 Collective dose avoided 59 valuation of 59

Collective dose concept 3 Committed dose 64 Consumer products 57 risk assessment 57 Cytogenetics 8 Deterministic effect 47,64 Diagnostic x-ray workers 24 breast cancer risks 24 Dicentric aberrations 9 Dose 64 Dose limits 61 Dose protraction 15 additivity of dose 15 Dose-rate effects 14 with neutron irradiation 14 Dose-rate independent response 11 with high-LET radiations 11 Dose-response 15 linear function of dose 15 linear-quadratic function of dose 15 Dose-response curve 64 Effective dose ( E ) 64 Environmental risks 56 from localized environmental sources 56 Equivalent dose (H) 64 Exposure pathways 51 Fractionation studies 11 Future exposures 57 risk assessment 57 Future population fertility 50 uncertainties 50 Genetic risks 43 Hanford workers 34 Healthy worker effect 33 In utero irradiation 37-38 cancer risks 38

INDEX

In vitro transformation 14 Iodine-131 studies 19 thyroid cancer risks 19

.

Justification 61 Leukemia 12 Leukemia risks 25-26,33 ankylosing spondylitis data 25 atomic-bomb data 25 fractionated exposures 25 1311 treatment for hyperthyroidism 33 radiologists or x-ray workers 33 Thorotrast administration 33 Levels of risk 58 categorizing 58 Life shortening 13-14 dose-rate effects 14 Low-dose studies 16 signal-to-noise ratio 16 Lung adenocarcinoma 12 Lung cancer risks 41 for low-LET radiation 41 for radon progeny 41 Mammary adenocarcinoma 12 Mammary tumors 13 dose-rate effects 13 Multiple myeloma 34 Multiple myeloma risks 35 Mutagenesis 8 cellular studies 8 Mutation induction 11 spermatogonia 11 Mutations 9, 11 germ cell 11 in spermatogonia 11 point mutations 9 somatic cell 9 Negligible individual dose (NID) 47,64 Neutron irradiation 11 mutations in spermatogonia 11 Nuclear worker studies 34 Occupational radiation studies 21 thyroid cancer risks 21

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Occupational studies 19 thyroid cancer risks 19 Oocyte.13 extreme sensitivity 13 Optimization of protection 59 Other cancer risks 42 Other cancers 42 Population characteristics 49 Population dose 3 Preconception radiation exposure 44 carcinogenic risks 44 Radiation protection practice 61 ALARA 61 dose limits 61 justification 61 Radiation weighting factor (wR) 64 Radiation workers 55 risk assessment 55 Radium dial workers 22 thyroid cancer risks 22 Radon 56 risk assessment 56 Relative risk 64 Risk assessment 53-57 consumer products 57 future exposures 57 in specific applications 54 medical procedures 54 miscellaneous sources 57 radiation workers 55 radon 56 special occupational groups 55 Risk coefficient 65 Risk management 53, 58 Scoliosis 24 Screening studies-external radiation 18 thyroid cancer risks 18 Sellafield workers 34 Sievert (Sv) 65 Solid tumors 12-13 Harderian gland 13 pituitary 13

Special occupational groups 55 risk assessment 55 Spermatogonia 11 mutations 11 Stochastic effect 65

Transformation 12, 14-15 cell cycle effects 15 in 'vitro 14 Tumor induction 12

Thymus irradiation 17 Thyroid cancer 16-17, 22 1311 exposure 17 Thyroid cancer risk 18, 22 radium dial workers 22 Tissue weighting factor (wT)49, 65

Uncertainties 50-51 future medical technology 51 future population fertility 50 future population size 50 location 50 Utah fallout study 21 thyroid cancer risks 21