ML20202F995
| ML20202F995 | |
| Person / Time | |
|---|---|
| Issue date: | 05/10/1979 |
| From: | Minogue R NRC OFFICE OF STANDARDS DEVELOPMENT |
| To: | |
| References | |
| SECY-79-322, SECY-79-322-R, NUDOCS 9902040229 | |
| Download: ML20202F995 (50) | |
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v y 10,1979 a
uwco surts SECY-79-322 NUCLEAR REGULATORY COMMISSION
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INEORMATION REPORT.
For:
b ine wuno a a wn= > a y
From:
Robert B. Minogue, Director h.p.
Office of Standards Development g,g.C.,
Ir,#
j Thru:
Lee V. Gossick Executive Director for Operations i
Subject:
THE BCIR III REPORT puroose:
To transmit to the Comissioners advance copies of the new National Academy of Sciences Report on the Biological Effects of Ionizing Radiation (BEIR III_ Report). _
j Discussion:
Enclosed for your informationi is an advance copy of the updated NAS Report on the Biological Effects of Ionizing Radiation. The National Academy of Sciences is expected to have the report printed in the near future.
We are initiating a staff r*! view of the report to deter-mine what effect, if any, this updated report will have on our regulatory strategies for radiation protection.
This will be a rather extensive effort due to the volume and complexity of the document.
We will provid. the Comission with the results of this
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review when it is completed.
A preliminary analysis of the report, to highlight significant changes since the earlier BEIR report (1972) and to tentatively identify potential impacts on NRC radiation protection policies, will~ be' forwarded by July 1,1979.
- LQ40 Y p 9902040229 790510 PDR SECY abert B. Minogue, Director 79-322 R PDR ffice of Standards Development
Enclosure:
BEIR III REPORT - Comissioners & SECY only
Contact:
DISTRIBUTION Steve Whitfield Comissioners 443-5860 g ;s g L Comission Staff Offices Exec Dir for Operations W
onal Offices 3 MD' N " M Secretariat
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A6c/plc.
neds rom the NATIONAL RESEARCH COUNCll; The National Research Council u as organi:rd by the National Academy of Sciences in 1926 in order to provide for a broader participation by American scientists and engineers in the reork of the Academy, The Academy was chartered by the U.S. Congress in
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1863 as a private organi:ation uith a responsibility for examining questions of science and technology at the request of the
- Federal Government. The National Academy of Engineering u as organi:ed in 1961 under the original NAS charter. The National Research Council now serces as the agent of both Academies in the conduct of studies and investigations in the public interest.
2l01 CONSTITUTION AV EN U E, N.W..
D.C.
2011H AREA CODE 20c EX 3-8100 For further information call Howard J. Lewis, (202) 389-6518, Md44
}9-N2 or Jim Lindler, (202) 389-6511 MH 3 lot 7. T&&)6k3 BEIR COM.iITTEE gg j
l ISSUES NEW ESTIMATES gog s4 AGA/pRC.
OF RAD 1ATION RISES l
FOR IMCIATE RELEASE (Mailed 3/2/79)
WASHINGTON--After painstaking examination of several proposals that have been mace as a basis for estimating the effects on human populations of low levels of ionizing radiation, a committee of the National Research Council has selected one that extrapolates a straight line from known high-level exposure data down to background levels and assumes that there is no threshold below which radiation ceases to have adverse effects on humans.'
Using the linear model, the committee's estimate of possible risk from ionizing radiation is in the range of 70 to 353 excess cases of fatal cancer per million persons exposed per rad per year for single exposure, and 68 to 293 per million persons exposed per rad per year for continuous cumulative exposure, f
Although the amount of radiation any single individual receives can vary l
t considerably depending on place and type of residence and occupation, the national average j
approximates one-quarter of a rad per year, almost all of the radiation coming from natural sources and medical and dental X rays. Workers in certain occupations may, however, l
receive almost a full rad in the course of a year.
In addition, some individuals may be i
more vulnerable to radiation effects than others because of age and constitutional susceptibility.
The complete report
- of the Committee :a the Biological Effects of Ionizing i
I Radiations (the so-called BEIR Committee) will not he available for several weeks, but a completed final draft report has been submitted to the Office of Radiation Programs of i
l the Environmental Protection Agency, which supported the study.
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- Abridged copies of the final draft report, The Effects on Populations of Exposure to Low l
l Levels of Ionizing Radiations, are available to the working press only from the Office of 7
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Information at the letterhead address. Copies are limited to one per publication.
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s The committee, eperating trithin the Division of Medical Sciences cf the Research Council's Asse tly cf 1.ife Sciences, was charged with tringire up to date a study ty the same eccr.ittee in 1972. The repcrt does not make recoccendations fer the purpose cf standard-settir.g, but rather presents seientific judg ents based on the evaluation cf a. ilable animal and human data.
Edward P. hadford of the University of Pittsburgh chaired the full comittee and also the Subcomittee on Somatie Effects. A Subcomittee on Genetic Effects was chaired ty pean R. Parker, retired geneties prcresser cf the University er Califernia at Riverside.
In estimatire genetic effects of low levels of ionizir# radiation, the comittee predicted by linear extrapolatien froc. e tical data that one res of human parental exposure in the general population would result in an increase cf 5 to 7's serious genetic disorders per million live births in the first generation. The natural incidence of genetie discrders is apprcximately 107,000 per million live tirths. The natural background exposure is approximately 1/10 re per year.
Less clear were the possitle effects of Icw levels of ionizire radiation on human develcpment--e.g., estaracts, aging, and Infer *.ility.
In this regard, it was concluded stat adverse effects depended strergly upon the stage at which the e=tryo or fetus was exposed and whether the exposure was sir #1e er cultiple.
The comittee tock note cf the fact that it is not yet known whether the l
natural background dese rate cf 100 tillirads (1/10 rad) per year is detrirental to hu=ans; effects at this level would be masked by cther facters that produce the same discrders.
Ner have there been ar,y otservations cf human effects from low-level incremental exposures slightly ateve tackground level Furtherm:re, the exa-ination of socatie effects other i
1 than cancer and devel prental dis:rders does nct s qEest arv increased risk from low-dose s
exposure of hume pcpulation:.
Nevertheless, a majority cf the co=ittee judged the most prudent assumption l
l tc te cne that derived a ra ge cf pessitie human effects at low levels from linear extrap:1stien cf data derived free ctservations of high-level effects on both humans and experimental animals.
l Five cf the 16 centers cf the Subco=ittee en Somatic Effe:ts, however, disagreed j
with the cor 'itee's cethodology fer estimatire health risks cf low-level exposures and issued a dissentir.g view. Essentially, this sincrity view held that cancer risk estimates derived frc: high doses cf radiatien should not be extrapoleted using a linear non-threshold hypothesis tc low dose rates
- fer which no epidemiological evidence exists. There is at this time, this sincrity view states, "far too little theeretical information to serve er
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i a re116tle guide for extrapelaticn.'
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The cincrity repcrt, which was prepared by Harald H. Rossi and Edward W.
netster, and endorsed by Charles W. Ways, Henry N. wellman, and Marylou Ir.gra=, was i
appended to the report cuttitted to the Office cf Radiation Programs. It was ncted that althcuit the fortal reviewers cf the study were provided copies of the minority repcrt, it was not itself the subject of review.
A list of all comittee siembers is attached. Albert W. Hilberg was the principal staff cfficer fer the report.
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COT:ITTEE ON THE BIOLOGICAL EFFECTS OT IONIZING RADIATIONS Edward P. Radford Jacob I. Fabrikant Department of Epide=1 ology Donner Laboratory University of Pittsburgh University of California Craduate School of Public Health Berkeley, California Pittsburgh, Pennsylvania, Chairman
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Marylou Ingra=
l Seymour Abrahaesen Institute for Cell Analysis Department of Zoology University of Miaci School i
University of Wisconsin of Medicine Madison, Wisconsin Miami, Florida Gilbert W.
Beebe Charles E. Land Clinical Epiderfology Branch Environmental Epidemiology National Cancer Institute Branch i
Bethesda, Maryland National Cancer Institute i
Bethesda, Maryland Michael A. Bender Medical Department Charles W. Mays Brookhaven National Laboratory Radiobiology Laboratory Upton, Long Island, New York University of Utah Medical Cent er A. Be r t r a r,.i Brill Salt Lake City, Utah Division
- Nuclear Pedicine and Bic
. sics Dade W. Moeller Vanderbilt 1versity Harvard University 1
School of h+ aicine School of Public Health
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Nashville, Tennessee Boston, Massachuset t s Reynold T. Brown Dean R. Parker Offies of Environmental Austin, Texas Health University of California Harald H. Rossi l
San Francisco, Calif ornia Radiological Research Laboratory Columbia University College of Stephen F. Cleary Physicians and Surgeons Departcent of Biophysics New York, New York Virginia Commonwealth University Richmond, Virginia Liane B. Russell Biology Division Cyril L. Cocar Oak Ridge National Laboratory Electric Power Research Institute Oak Ridge, Tennessee Palo Alto, Calif ornia i
William L. Russell
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Carter Denniston Biology Division Laboratory of Genetics Oak Ridge National Laboratory l
University of Wisconsin Oak Ridge, Tennessee Madison, Wisconsin 1
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4 Committee on the Biological Effects of lonizing Radiations continued i
Paul B. Selby Biology Division Oak Ridge. National. Labora t ory.
Oak Ridge, Tennessee i
l Margaret H.-Sloan L
Division of Cancer Control I
and Rehabilitation l
National Cancer Institute Silver Spring, Maryland J
Edward W. Webster
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l Division of Radiological Sciences Massachusetts General Mospital
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Boston, Massachusetts i
Henry N. Welican Nuclear Medicine Division
- Indiana University School of
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Medicine In(lanapolis, Indiana 4
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SUBC0911TTEE ON SOMATIC ETTECTS Edward P. Radford Charles E. Land Department of Epidemiology Environmental Epidemiology University of Pittsburgh Branch Graduate School of Public Health National Cancer Institute Pittsburgh, Pennsylvania, Chairman Bethesda, Maryland Gilbert W.
Beebe Charles W. Mays Clinical Epidemiology Branch Radiobiology Laboratory
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National Cancer Institute University of Utah Medical Bethesda, Maryland Cent er i
Salt Lake City, Utah A. Bertrand Brill Division cf Nuclear Medicine and Dade W. Moeller Biophysics Harvard University Vanderbilt University School of School of Public Health Medicine Boston, Massachusetts Nashville, Tennessee Herald H. Rossi l
Reynold T. Brown Radiological Research Laboratory Office of Enviro nental Health Columbia University College of l
University of California Physicians and Surgeons i
San Trancisco, California New York, New York Stephen F. Cleary Liane B. Russell Department of Biophysics Biology Division i
Virginia Commonwealth University Oak Ridge National Laboratory Richmond, Virginia Oak Ridge, Tennessee Cyril L. Comar Margaret H. Sloan Electric Power Research Institute Division of Cancer Control and Palo Alto, Calif ornia Rehabilitation National Cancer Institute Jacob 1. Fabrikant Silver Spring, Maryland Donner Laboratory University of California Edward W. Webster Berkeley, California Division of Radiological Sciences Marylou Ingram Massachusetts General Hospital Institute for Cell Analysis Boston, Massachusetts University of Miami School of Medicine Henry N. Wellman Miami, Florida Nuclear Medicine Division Indiana University School of Medicine Indianapolis, Indiana j
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.Subcomeittee on Somatic Effects continued 1.-
t CONSULTANTS i
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Robert L. Brent Roy E. Shore
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Department of Pediatrics Department of Environmental i
Jef ferson Medical College of Medicine Thomas Jefferson University
- New York University Medical Pennsylvania Center New York, New York Bernard E. Oppenheim Nuclear Medicine Division
'l Indiana University School of Medicine Indianapolis, Indiana l
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SUBCOMf1TTEE ON GENETIC EFFECTS Dean R. Parker Liane B. Russell l
Austin, Texas, Chairman Biology Division Oak Ridge National Laboratory Seymour Abrahamson Oak Ridge, Tennessee Department of Zoology University of Wisconsin William L. Russell l
Madison, Wiscondin Biology Division Oak Ridge National Laboratory Michael A. Bender Oak Ridge, Tennessee l
Medical Department Brookhaven National Laboratory Paul B. Selby I
l Upton, Long Island, New York Biology Division Oak Ridge National Laboratory Carter Denniston Oak Ridge, Tennessee Laboratory of Genetics University of Wisconsin Fbdison, Wisconsin Albert W. Hilberg, Principal Staff Officer Division of Medical Sciences Assembly of Life Sciences National Research Council David A. McConnaughey, Senior Staff Officer Division of Medical Sciences Assembly of Life Sciences National Research Council Norman Grossblatt, Editor l
Assembly of Life Sciences National Research Council i
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TOR RELEASE ON MAY 2, 1979 i
The health effects of low doses of ionizing radiation are a matter of considerable public concern and a subject of basic significance to National i
energy policy.
It is therefore unfortunate that the BEIR Committee of the National Academy of Sciences has not produced a report that is endorsed by all of its members.
Although there appears to be agreement with regard to genetic effects, the Subcommittee dealing with somatic effects is clearly i
divided on some major issues.
Since this development may well increase pb11: confusion on the hazards of radiation, it is of crucial importance to stress those aspects of the subject on which the Committee is in agreement.
Restricting the following remarks to thosa radiations that are of primary practical importance (the so-called low LLO radiations such as X rays, gamma rays, and beta rays), it may be said that the Committee believes that the
" hypothesis of linearity" is likely to lec.s to an overestimation of the risk of cancer from low doses of radiation. The Committee also has provided risk estimates for leukemia indicating that the risk decreases more rapidly than proportionally with dose.
The Committee has determined that it is impossible at this time to provide valid risk estimates for single doses of less than j
10 rad.
It also states that while it is unknown whether doses of the order of 100 mrad (per year) are detrimental to exposed people, it is unlikely that any effects are demonstrable at this level. The Committee furthermore has discounted studies that purport to demonstrate somatic effects at such levels.
The above are highly significant conclusions on which the entire Committee is in agreement.
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The principal objectione raised in the Dissenting Report are twofold.
One is that a great body of radiobiological evidence and theory, as well as important epidemiological data, which indicate that the linear hypothesis leads to sub-stantial overestimates of radiation risks, has been discounted in the report on somatic effects. Therefore it is recommended that instead of identifying the risk with an upper limit based on linearity, a lower limit of equal validity should also be recognized.
It should then be stated that the true risk is between these limits and very likely near the lower limit. The other objection is that the available data relating to cancer incidence rather than cancer mortality are either misleading or mreliable.
Such data are derived either from observa-l tions on diseased individuals who received massive doses of radiation or from l
surveys that have not been critically scrutinized.
l We believe that, because of these failings, the BEIR III report will contribute j
to excessive, and potentially detrimental, apprehension over radiation hazards.
l The above statement was prepared by Harald H. Rossi and' Edward W. Webster of the BEIR Committee.
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1 CONTAINS ONLY SUMM RY AND CONCLUSIONS CHAPTER;
SUMMARY
AND CONCLUSIONS SECTIONS OF CHAPTERS 3, 4, and 5; AND DISSENTING REPORT OF THE SOMAIIC SUBCOMMITTEE.
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THE EFFECTS ON POPULATIONS OF EXPOSURE TO LOW LEVELS OF IONIZING RADIATIONS 19 79 i
Report of the Committee on the Biological Effects of Ionizing Radiations Division of Medical Sciences Assembly of Life Sciences National Research Council National Academy of Sciences 19 79 1
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i ICTICE i
F The project that is the subject of this report was approved by the Governing Board of the 1:adonal Research Comcil, whose nebers are dram f
i of Engineering, and the Institute of Medicine.from the Counc i
The nrhers of the Ccemittee responsible for the report were chosen for their special cecpetences and with regard for appropriate balance.
Tnis report has been reviewed by a grorp other than the authors i
according to procedres approved by a Report Review Cctrdttee co.sisti:q Engineering, and the Institute of Medicine.or nrbers of the 1 ationa l
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. The work presented in this report was supported by the Office of Ra Hation Programs, Faviro.etal Protection Agency, under Contract No, 68-01-4301.
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'Proftce in the f all of 1976, the Office of Radiation Programs, Environmental Protection Agency, asked the National Academy of Sciences for current in-formation relevant to an evaluation of ef fects of human exposure to low levels of ionizing radiation.
This report, prepared by the Committee on Biological Ef f ects of lonizing Radiations (BEIR Committee) and its subcom-mittees, in the Division of Medical Sciences of the National Research 1
Council's Assembly of Life Sciences, is in response to that request.
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it deals with the scientific basis of low-level eff ects of radiation 1
and encompasses a review and evaluation of scientific knowledge developed since the first BEIR report (published in 1972) concerning radiation ex-posure of human populations.
The BEIR Committee endeavored to ensure that no sources of relevant knowledge or expertise were overlooked in its study.
To this end, it established liaison with appropriate national and international organiza-tions and solicited the opinions and counsel of individual scientists.
We hope that the information contained herein will serve not only as a summary o.' present knowledge on the ef f ects of ionizing radiation on human populations, but also as a scientific basis for the development of suitable radiation protection standards.
It should be noted that the members of the Committee and its subcommittees acted as individuals, not as representatives of their organizations.
We extend our gratitude to the consultants who contributed to the development of this report, many of whom gave unstinting1y of their time and thought.
We want to make special note of t'ie contributions of Dr. Arthur C.
Upton, who served as chairman of the C.ammittee from November 1976 to 1
July 1977 and resigned when he became.he director of the National l
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l Cancer' Institute, and Dr. Ben Trimble, of British Columbia, who served on the Subcommittee on Genetic Effects until his untimely death in November 1977.
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The BEIR Committee especially wishes to thank the scientists t
who have aided it in its work, particularly Drs. Robert L. Brent,
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John -T. Lyman, Bernard E. Oppenheim, and Roy Shore, who not only l
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contributed their time, but also gave considerable assistance in the l
i preparation of some sections of the report.
A special note of appreciation is extended to Mr. Norman Crossblatt, of the Assembly of Life Sciences, who edited this report.
The prepara-tion of this report required information from several scientific disci-i plines, and most sections were prepared by members who had particular expertise.
Chapter IV was prepared by the Subcommittee on Genetic Ef f ects, and Chapter V, by the Subcommittee on Somatic Ef f ects.
The other chapters were prepared by various members of the Committee with I
direction and advice f rom the entire Committee.
i There were unresolvable differences among the members of the l
l Subcommittee on Somatic Effects concerning the methods of interpretation of human data to arrive at an estimate of health risks of low-dose, low-LET whole-body radiation exposure. As a result of these differences in the interpretation of human data, a dissenting minority view has been prepared; it is presented as an addendum to Section 3 of Chapter V,
- Estimating the Total Cancer Risk of Low-Dose, Low-LET Whole-body-l Radiation."
l Dissenting st&tements prepared by individual members of a National Research Council Committee are not subject to the normal review processes
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of the National Academy of Sciences; nor are they subject to commictee or i
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staff editing or review.
They appear exactly as the dissenting committee
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members prepare them.
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C0rNITTEE ON THE BIOLOGICAL EFFECTS OF IONIZING RADIATIONS l
Edward P. Radford Jacob I. Fabrikant Department of Epideciology Donner Laboratory University of Pittsburgh University of California Graduate School of Public Health Berkeley, California Pittsburgh, Pennsylvania, Chairman Marylou Ingram Seymour Abrahaeson Institute for Cell Analysis Department of Zoology University of Mia=1 School University of Wisconsin of Medicine Madison, Wisconsin Miami, Florida Gilbert W.
Beebe Charles E. Land Clinical Epiderfology Branch Environmental Epidemiology National Cancer Institute Branch Bethesda, Maryland National Cancer Institute Bethesda, Maryland Michael A.
Bender Medical Departcent Charles W. Mays Brookhaven National Laboratory Radiobiology Laboratory Upton, Long Island, New York University of Utah Medical Center A. Bertrand Brill Sal t Lake City, Utah Division of Nuclear Skdicine and Biophysics Dade W. Moeller Vanderbilt University Harvard University School of Medicine School of Public Health Nashville, Tennessee Boston, Massachusetts Reynold T. Brown Dean R. Parker Of fice of Environmental Austin, Texas Health University of California Harald H. Rossi San Trancisco, Calif ornia Radiological Research Laboratory Colu=bia University College of Stephen F. Cleary Physicians and Surgeons Department of Biophysics New York, New York Virginia Commonwealth University Richmond, Virginia Liane B. Russell Biology Division Cyril L. Cocar Oak Ridge National Laboratory Electric Power Research Institute Oak Ridge, Tennessee Palo Alto, Calif ornia William L. Russell Carter Denniston Biology Division j
Laboratory of Genetics Oak Ridge National Laboratory i
University of Wisconsin Oak Ridge, Tennessee Madison, Wisconsin iv
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Comeittee. on the Biological Effects of Ionizing Radiations continued
. Paul;B. Selby Biology Division Oak Ridge National Laboratory Oak Ridge,. Tennessee Margaret H. Sloan i
- Division of Cancer Control-j and Rehabilitation
. National Cancer Institute Silver Spring,_ Maryland Edvard W. Webster Division of Radiological Sciences Massachusetts General Hospital
.l Boston, Massachusetts
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Henry N. Wellman Nuclear Medicine Division Indiana University School of Medicine Indianapolis, Indiana 1
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e-SUBCOMMITTEE ON SOHATIC ETTECTS Edward P. Radford Charles E. Land Department of Epidemiology Environmental Epidemiology University of Pittsburgh Branch l
Graduate School of Public Health National Cancer Institute Pittsburgh, Pennsylvania, Chaircan Bethesda, Maryland Gilbert W.
Beebe Charles W. Hays Clinical Epide=iology Branch Radiobiology Laboratory National Cancer Institute University of Utah Medical Bethesda, Maryland Ce nt e r Salt Lake City, Utah A. Bertrand Brill Division of Nuclear Medicine had Dade W. Moeller Biophysics Harvard University Vanderbilt University School of School of Public Health Medicine Boston, Massachusetts Nashville, Tennessee Harald H. Rossi Reynold F. Brown Radiological Research Laboratory Office of Environeental Health Columbia Ur.tversity College of University of Calif ornia Physicians and Surgeons San Francisco, California New York, New York Stephen T. Cleary Liane B. Russell Department of Biophysics Biology Division Virginia Cocoonwealth University Oak Ridge National Laboratory Richmond, Virginia Oak Ridge, Tennessee Cyril '.. Comar Margaret H. Sloan Electric Power Research Institute Division of Cancer Control and Palo Alto, Calif ornia Rehabilitation National Cancer Institute Jacob 1. Fabrikant Silver Spring, Maryland Donner Laboratory University of California Edward W. Webster Berkeley, Calif ornia Division of Radiological Sciences Marylou Ingram Massachusetts General Hospital Institute for Cell Analysis Boston, Massachusetts University of Miami School of Medicine Henry N. Wellman Mi ami, Florida Nuclear Medicine Division Indiana University School of Medicine Indianapolis, Indiana l
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i L-l Subcommittee on Somatic Effects - continued CONSULTANTS Robert L. Brent Roy E. Shore Department of Pediatrics Department of Environmental Jef ferson Medical College of -
Medicine
' thomas Jefferson University New York University. Medical Pennsylvania Center New York, New York
.' Bernard E. Oppenheim l
Nuclear Medicine Division Indiana University School of
- Medicine Indianapolis, Indiana 1
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SUBCOMMITTEE ON GENETIC EFFECTS
-Liane B. Russell Dean R. Parker Austin, Texas, Chairman Biology Division Oak Ridge National Laboratory Oak Ridge, Tennessee Seymour Abrahamson Department of Zoology William L. Russell University of Wisconsin Madison, L'iscondin Biology Division Oak Ridge National Laboratory H1ct.sel A. Bender Oak Ridge. Tennessee Medical Department Brookhaven National Laboratory Paul B. Selby Ur >n, Long Island, New York Biology Division Oak Ridge National Laboratory Carter Denniston Oak Ridge, Tennessee Laboratory of Genetics Universit; of Wisconsin Madison, Wisconsin Albert W. Hilberg, Principal Staff Officer Division of Medical Sciences Assembly of Life Scie.nces National Research Council David A. McConnaughey, Senior. Staff Officer Division of Medical Sciences Assembly of Life Sciences National Research Council Norman Grossblatt, Editor Assembly of Life Sciences National Research Council Q
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Table of Contents Preface.
i Committee Membership.
iv Summary and Conclusions.
1 Chapter I.
Introduction.
9 Chapter II.
Scientific Principles in Analysis of Radiation Effects.
15 Chapter III.
Sources and Rates of Radiation Exposure in the United States.
57 Chapter IV.
Genetic Effects 107 Chapter V.
Somatic Effects - Cancer.
234 Chapter VI.
Somatic Effects - Other Than Cancer.
752 Glossary.
822 Lis ting of Meetings.
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,BEIR Keport 1979 SU!CiARY AND C0?;C1,l'510NS l
This report is intended to bring up to date the report of the l
Committee on' the Biological Effects of Ionizing Radiations issued
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in 1972.
In carrying out this intent, we have concentrated primarily-on the long-term somatic and genetic risks to people' exposed to radia-tion at low doses--the condition of principal concern with respect to risks to large population grou;s.
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l The eajor contributors of. the ionizing radiation to which the I
general population is exposed continue.to be natural background I
(with a whole-body dose of about 100 crees /yr) and medical applications of radiation (which contribute sicilar doses to various tissues of the body).
For a given person, the dose from natural background f
varies with altitude and. geographic location, as well as with living i
habits. L'orkers in nuclear and other industrial facilities in which j
radioactive caterial or x-ray equipment is used are occupationally.
i exposed to radiation that may exceed background severalfold', and the nu ber of such workers is increasing.
The Coc:ittee cautions that the risk estimates presented here should in no way be interpreted as precise numerical expectations.
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They are based on incomplete data and involve a large degree of t
uncertainty, especially when applied to interpretation of health effects of low doses.. These estimates may well change as new informa-
. k'hatever the magnitude of these risks to
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society end to the individuals exposed, thay cust be kept in per-r spective if society is to derive benefits from the use of ionizing radiation.
The Comeittee has no ras,ponsibility to recommend regulatory i
limits nor does it address issues of cost-benefit involving the use of i
ionizing radiation.
These issues are beyond the scope of the task or expertise of this ~ Committee.
i Risk of Somatic Effects from Radiction s
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Evidence indicates that cancers arising in a variety of oceans and gissues are the principal late somatic effects of radiation Organs and tissues differ greatly in their susceptibility exposure.
to cancer induction by radiation.
Induction of leukemia by radiation stands out i
l because of the natural rarity of the disease, the relative ease of its induction by radiation, and its short latent period.
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the total risk of radiation-induced malignancies is considered, however, i
t l-it is clear that solid tumors such as breast, thyroid and lung cancers rather than leukemia are'the dominant forms of cancer risk.
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The Committee recognizes that information from human data I
is highly uncertain with regard to the shapes of dose-response curves i
for cancer' induction by radiation, especially at low doses.
Estimates of risk at low doses may depend more on what is assumed about the mathe-I
-matical form of the dose-response function than on the data themselves.
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For most calculations of estimated cancer risk at low doses, the i
i Committee has used.the If near no-threshold hypothesis (ef fect propor-j i
tional to dose).
The ' Committee recognizes that some experimental t
and human data, as well as. theoretical considerations, suggest that, for exposure to low-LET* radiation at low doses, most cancer risk l
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- LET is fully defined in the Clossary. Low-LET is. radiation characteristic i
of X-rays and gamma rays. Righ-LET is radiation characteristic of' fast i
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protons and. neutrons, e.g., alpha particles.
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estimates based on the linear hypothesis are high and should not i
be regarded as more than upper limits of risk.
For' exposure to
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.high-LET radiation, the risk estimates derived for low doses are less likely to be overestimates of risk and may, in fact, be
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underestimates.
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There is now considerable evidence from human studies that age, both at exposure to radiation and at appearance of cancer, can be a major determinant of radiation-induced cancer risk.
For this reason, the Comeittee recommendt that risk be expressed in age-specific terms wherever possible.
4.
The Committee's most difficult task has been to reach a consensus on how to estimate the carcinogenic risk of low dose, low-LET radiation.* It was recognized early that there is no truly adequate or generally acceptable scientific basis for such estimation, but that policy or regulatory decisions require a position on the estimation of risk.
In resolving the differing positions taken by I
I Committee members, the Committee came to the judgment. that emphasis should be placed, not only on specific numerical estimates, but also on the assumptions, procedures--and uncertainties--involved in the quantitative risk estimation.
For the lifetime risk of cancer incidence induced by low LET radiation for a single whole-body exposure to 10 I
rad the range of increased risk is estimated to be 1.2 to 4.5% above i
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- There were unresolvable differences among the members of the l
L Subcommittee on Somatic Effects concerning the methods of interpretation of human' data to arrive at an estimate of health i
risks of low-dose, low-LET whole-body radiation exposure. As a result of these differences in the interpretation of human data, i
1 a dissenting minority view has been prepared; it is presented as an addendum to Section 3 of Chapter V, " Estimating the Total Cancer Risk of. Low-Dose, Low-LET Whole-body-Radiation."
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4 l
- the naturally occurring rate for females and 0.8% to 3.2% for males.
The correspo'nding estimated increase in mortality from a single 10 rad exposure is 0.5% to 2.7% for f emales and 0.4% to 2.0% for males.
The risk of cancer incidence induced from continuous lifetime exposure to I rad per year ranges from an 8.4% to 32.6% increase for females and 5.2% to 17.90 for males.
The corresponding mortality estimates are 16.9% for females and 2.7% for males.
'Ihese ranges of risk estimates reflect various factors of uncertuinty which are described in detail.
5.
We do not know whether case rates of gamma or x rays of about 100 crad!yr ~are detrimental to exposed people. Any detrimental somatic i
I
-f fects will be masked by enviromental or other factors that produce the-same types of effects on the nealth of exposed people as does ionizing radiation.
It is unlikely that carcinogenic tnd teratogenic l
l effects of doses of low-LET radiation ad=inistered at this dose rate will be demonstrated in the foreseeable future.
For larger doses, as from high-dose lifetice occupational exposure, a discernable carcinogenic effect could be manifest.
6.
A Juctions in dose rate may decrease the observed radiation eff ect per unit dose, particularly for low-LET radiation.
There appear to be. mechanisms, however, especially pertaining to exposure to high-LET radiation, that' increase the observed effect per unit dose when the dose rate is reduced.
The Com=f ttee recognizes that dose-rate effects may be a source of uncertainty in risk estimates for cancer induction, but believes that available information f rom human data is insufficient to permit appropriate corrections.
i
)
L.-
r "6
l-7.
A notable development since the 1972 BEIR report is the l
increasing recognition that there are human genotypes that confer both increased cancer risk and increased susceptibility to DNA damage after exposure to carcinogenic agents, incleding ionizing radiation.
i l
The role of constitutional susceptibility to cancer induction is not vell enough. understood to be used as a factor for modifying risk l
estimates for radiation carcinogenesis.
Inasmuch as the risk estimates developed for this report are averages for large populations that pre-J 1.
su. ably include many genotypes, it is unlikely that these risk esti-tates would be notably altered if data representing very seall subsets l
of abnorr. ally radiosensitive persons could be recognized and excluded l
l fror the~ calculations.
Howest, where there are large subsets of this I-type--for exar.ple, in the case of breast ' cancer, with f emales highly sensitive in co:parison with cales--the risk is calculated separately for the sensitive group.
If other substantial population subsets can
{
be identified in the future as being at substantia 11y' greater risk i
of radiatior. carcincgenesis, their risk will also require separate consideration.
B.
The developmental effects of radiation on the embryo and fetus are strongly related to the stage at which exposure occurs.
Most inforeation on such effects is derived from laboratory anical studies, but the human data are sufficient to indicate qualitative l
. correspondence f or developeentally equivalent stages.
In laboratory animals, some developmental abnorcalities have been observed at doses below 10 rads.
Atomic-bomb data for Hiroshima indicate that micro-cephaly was induced by acute air doses in the range of 1-9 kerma 4
i 4-
- ~.- - - -
t l
L*'
I f
(average. fetal dose, gamma rays at 1.3 rads and neutron rays at 0.1 i'
rad) received during the sensitive period.
Because a given gross i
malformation or functional impairment probably results from damage i
to more than a single target, the existence of a threshold radiation i
dose below which that effect is r.ot observed may be predicted.
i There c
is evidence of such threshc'is, but they vary widely, depending on the abnormality.
Observed dose-rate effects may.also be the result of the multitarget causation of these abnormalities.
Further= ore, exposure protraction can reduce dose effectiveness by decreasing to below the threshold the portian of'the dose received during a particular sensitive f
period. k'here s developmental ef fect is ceasured in terms of damage to i
individual cells, as in occyte-killing, a threshold for this effect cay be absent.
9.
For somatic effects other than cancer and developmental effects (e.g., cataracts, aging, and infertility) considered in this report, the available data do not suggest an increased risk with low-dose exposure of human populations.
j Risk of Genetic Effects fro: Radiation 1.
Because of the almost cocplete absence of human data on radiation-induced transeitted genetic effects and because of the likelihood that.such data vill not soon be' forthcoming, estimation of genetic risks must be based on laboratory animal data.
This entails the uncertainty of extrapolation from the laboratory mouse to man.
~
However, there is information on the nature of the basic lesions, which are believed to be similar in all organisms; and several physical and biologie variables of radiation mutagenesis have been 1
l t
m.___ _.._._. _
experimentally explored.
For these reasons, some of the uncertainties 1
encountered in the evaluation of somatic effects are absent in the estimation of genetic risk.
Human data have been used for estination of genetic effects resulting from gross chromosomal aberrations.
2.
In evaluating genetic risks, the Committee has considered new data on the incidence of genetic disease in human populations.
In addition, recent theories of curvilinear dose-response functions and information on dose-rate effects for radiation of different qualities have beer, reviewed.
For low doses and dose rates, a linear extrapolation from fractionated-dose and low-dose-rate laboratory nouse data continues to constitute the basis for estimating genetic risk to the general population.
The Committee's genetic-risk estimates are expressed as ef fects per generation per rem, with appropriate cor-rections for special situations, such as exposures of small groups to high-LET radiation.
3.
Although the Cocnittee used a new method of estimating genetic effects expressed in the first generation, the present estinates of gent'ic effects are not notably different from those of the 1972 BEIR report.
In the first generation, it is estimated that I rem of parental
-exposure throughout the general population will result in an increase of 5-75 additional serious genetic disorders per million liveborn offspring.
l Such an exposure of I rem received in each generation is estimated to result, at genetic equilibrium, in an increase of 60-1,100 serious genetic disorders per million liveborn offspring.
4 The ranges of the risk estimates given in the preceding
]
paragraph emphasize the limitations of current understanding of genetic i
i i
i
m.._
_ _ _.. - ~
___m..
L I
l ef f ects of radiation on human populations.
Within this range of un-l i
certainty, however, the risk is nevertheless small in relation to i
l current estimates of the incidence of serious human disorders of genetic origin--about 107,000 per million liveborn offspring.
5 General Conclusions I
i Genetic. risk estimates have been restricted to persons with induced disorders judged to cause a serious handicap at some time during life.
Even in that category,-so=e disorders are obvious 1v core i=portant than others.
In contrast with induced somatic effects, which occur only in the persons exposed, induced genetic disorders occur in descendants of exposed persons and can often be u ansmitted to many i
future generations.
Socatic-risk esticates are concerned with induced cancers.
Although cost of these are fatal, some, such as thyroid cancer, are usually curable, but entail the risk and costs of medical followup care.
Sonatic ef fects also include developmental abnormalities of varied severity caused by fetal or embryonic exposure.
It is important to realize that evaluation of co:parisons of genetic and so=atic effects cust take into account ethical or socioeconomic i
judgments that t
are beyond the scope of the Committee's responsibility.
-As an example of the probles, it is extremely difficult to compare the i
societal impact of a cancer with that of a serious genetic disorder.
L These conclusions concerning genetic risks have been strengthened l
by new methods and data obtained since the 1972 BEIR report, but the i
resulting risk estimates are nearly the same as those presented in that i
(
. report.
The conclusions concerning somatic risks have added to and i
extended the earlier estimates, but in general the present Commi t t ee 's conclusions are not in fundamental disagreement with those presented in f-the 1972 report.:
c.
i p* CHAPTER 11I SOURCES A;w RATES OF RADIATION EXPOSURE IN THE UNITED STATES I
NATURA1. BACKCROUND RADIATIO" Although mankind has produced many sources of radiation, natural background remains the greatest contributor to the radiation exposure of the U. S. population today.
Background radiation has three coc-ponents:
terrestrial radiation (external), resulting from the presence of naturally occurring radionuclides in the soil and earth; cosmic radiation (external), arising fro outer space; and naturally occurring radionuclides (internal), deposited in the human body.
Terrestrial Radiaticn The rate at which a person receives radiation from natural back-ground is a function of the person's Eeographic location and living habits. For exa ple, the dose equivalent (DE) rate from terrestrial sources varies with the type of soil in a given area and its content of naturally occurring radionuclides.
The penetrating gam =a radia-tion from these radionuclides produces whole-body exposure.
In general, the conterminous United States can be divided into three broad areas, from the standpoint of terrestrial whole-body DE rates (see Figure 111-1):
the Atlantic and gulf coastal plain, where terrestrial DE rates range f rom 15 to 35 mrem /yr; the north-eastern, central, and far western portions, with DE rates ranging i
l from 35 to 75 mre=/yr; and the Colorado plateau area, in which I
terrestrial DE rates range from 75 to l'*0 mrem /yr.
l I
.m b
P I
i
\\
~
h 4
l Northeastern Eastern. Central and Far Western Areas RANGE: 35 to 75 mrems/yr AVERAGE: 46 mrems/yr p
b I
a e:.
y
\\
\\ MMH
"\\
/
Colorado Plateau Aree
/
\\
6 RANGE: 75 to 140 mrems/yr 6
\\
[h AVERAGE: 90 mrems/yr
/ Atfantic and Gulf Coastal Pfein N
/
[ RANGE: 15 to 35 mrems/yr AVEFt AGE. 23 mrems/y r
/
i
,/
i e
Fir,ure III-1.
Terrestrial dose-equivalent rates in the enntermlnntis tinited States l
fin <llfleil from Oaktsv
1 4-e e
-102-SU.91ARY This review shows that the major contributor to exposure of the l
general population to ionizing radiation continues to be natural back-ground, which results in an average whole-body dose rate of about 100 f
mrem /yr.
For a given person, the dose rate from this source varies with altitude and geographic location, as well as his or her living habits.
The greatest man-=ade contributor to population exposure l
is the medical application of x rays, which results in a comparable average dose rate (about 100 mrad /yr) to the mean active bone marrow of the adult U.S. population.
The administration of radiopharmaceuticals for medical diagnosis results in an average population dose rate about 20% of that fro: x rrys.
It is estimated that the approximately 200,000
]
people who are occupationally exposed in the operation of medical x-ray equipment receive an average whole-body dose rate of 300-350 mrem /yr; an approximately equal number of people who are occupationally exposed in the operation of dental x-ray equipment receive an average whole-body dose rate of 50-125 mrem /yr; and approximately 100,000 additional medical personnel who are involved in handling radionuclides receive an average whole-body dose rate of 260-540 mrem /yr.
Average whole-body dose rates to the 30,000 people who are occupationally exposed in the civilian nulcear-power industry range from 600 to 800 mrem /yr; average whole-body dose rates to the approximately 35,000 people who I
are occupationally exposed in the operation and maintenance of naval nuclear-propulsion plants range from 130 to 330 mree/yr; and average l
whole-body dose rates to the approximately 100,000 people who are occupationally involved in research and development work conducted in the national laboratories of, and by contractors to, the Department o -:
Energy are comparable.
I
F i
h,
-107-l CHAPTER IV I
('
GENETIC EFFECTS l
l A.
INTRODUCTION AND BRIEF HISTORY This chapter considers the health consequences of genetic damage that result when human populations are exposed to low levels of l
fonizing radiation in addition to natural background radiation. As l
in the 1972 review, The Effects ea Populations of Exposure to Low Levels of Ionizing Radiation (BEIR I),I the main text is intended for l
the inforced, nontechnical reader; further details are given in notes at the end of the chapter. This chapter constitutes an updating of l
Chapter V of BEIR I; our task would have been vastly more difficult had we not had that work to build on.
(Indeed, where it is feasible, I
material from BEIR I is merely repeated here.) The recently completed review prepared by the United Nations Scientific Committee on the Effects of Atomic Radiation (UNSCEAR)2 has also been extremely helpful.*
f Since the publication of BEIR I seven years ago, new data he.c been obtained, and perspectives have been modified to an extent that e des a new review desirable.
The methods of BEIR I remain valid; however, new numbers have caused some changes in the estimates and some new methods
.of. estimation have been added.
~
1
-i
- UNSCEAR has issued a series of reports that collectively constit.te a wealth of information on this subject.2-7 In general, throughout this report,.we shall-not further document conclusions that are in the UNSCEAR reports, but instead simply refer to these reports. The i
bibliographies therein are very extensive, and the reader is referred i
to them for more detailed information.
I l
i t
t -
s l
l
~~
b i -*-
-122-i TABLE IV-1 Estimated Annual Average Genetically Significant Dose Equivalents
- Dose Equivalent Rate Source-
' (arem/ year) l Natural Radiation Cosmic' radiation 28 Radionuclides in the b' dy 28 o
External gamma radiation from' terrestrial sources 26 Subtotal 82 Man-made - Ra diation Medical and dental x-rays Patients 2"
Occupatior.a1 0.4 l
Radiopharmaceuticals Patients 2-4 Occupational 0.15 Commercial Nuclear Power l
Environmental 1
Occupational 0.15 National Laboratories j
and. Contractors Occupational 0.2 l
Industrial applications Occupational
- 0. 01 l
Military applications Occupational 0.04 l
Weapons testing fallout 4-5 i
I k
l Consumer products 4-5 Air travel 0.5 Subtotal 30 - 40 i
2 0
-147-H.
SUMMARY
The genetic disorders that can result from radiation exposure are (1) those which depend on changes in individual genes (gene mutations or small deletions) and (2) those which depend on changes in chromosomes, either in total number or in gene arrangement (chromosomal aberrations). The former are expected to have greater consequences than the latter.
At low levels of exposure, the effects of radiation in producing either kind of genetic change will be proportional to dose, in that highs.-order interactions (those involving more than one ionizing event) are extremely unlikely to occur.
For reasons of prudence, and to the extent possible, estimates are based either on experimental findings at the lowest doses and dose rates for which reliable data have been obtained or on adjustment of the observed data obtained at high doses and dose rates by a dose-rate reduction factor deemed appropriate by the committee.
Two methods are used to estimate the changes in incidence of disorders caused by gene mutations.
One method estimates the inci-dence of such disorders expected after the continuous exposure of the population over a large number of generations.
The other method esti-mates the incidencc of disorders expected to be seen in a single generation after the exposure of the parents.
By the first method, it is estimated that only about 1-6% of all l
5 spontaneous mutations that occur in humans can be ascribed to the effects of background radiation.
Therefore, a small increase in I
s'
-148-radiation exposure above background will lead only to a correspondingly small relative increase in the rate of mutation.
The numerical re-lationship of rates of induced and spontaneous mutation.is shown as a relative-mutation-risk factor, which is the ratio of the rate of mutations induced per rem to the spontaneous rate.
(The reciprocal of this is the " doubling dose," the amount of radiation required to produce as many more mutations as are already occurring spontaneously.)
The estimated relative mutation risk for humans is 0.02-0.004 per rem (or a doubling dose of 50-250 rem).
Af ter many generations of increased exposure to radiation, it is expected that human hereditary disorders that are maintained in the population by. recurrent gene mutation would show a similar increase in incidence.
However, not all such human disorders have this simple relationship to mutation.
It is estimated that the increase will be 60-1,100 per million liveborn
- offspring per rem of parental exposure received in each generation before conception.
The current incidence (resulting frcm causes i
other than the added radiation) of human genetic disorder is approxi-mately 107,000 cases per million liveborn.
These expected incidences are reached only af ter a large number of generations of exposure, because, in any given generation, the disorders experienced result both from newly induced mutations and from mutations transmitted from an earlier generation.
The number of generations required to reach an equilibrium between the induction of mutations and their elimination from the population depenas on how long the induced damage persists before being eliminated.
l l
I l
1 i
)
-149-In applying the second method of risk estimation, the incidence
)
of induced, transmissible damage to one organ system (skeleton of the nouse) has been used to calculate the effects expected for all human organ s ystems. This estimate is for the effects in a single t
generation after exposure of the parents to radiation; it takes into l
account the proportion of all known human hereditary defects that affect the one system, and this is used to estimate the range of effects that is expected for all systems. An average parental exposure of I rem before conception is expected to produce 5-65 additional disorders per million liveborn offspring.
The estimates arrived at by the two different methods are in good agreement.
One is for single generation effects, and the other is for effects seen at equilibrium, af ter long-continued exposure of the population.
Although no assumptions have been made in this report as to rates of elimination, the use of the i
estimates of persistence assumed in BEIR I (five generations for autosomal dominants and 10 generations for irregularly inherited diseases) results in an agreement between the two sets of estimates that is quite good.
Disorders due to chromosomal aberrations, estimated from the aberration incidence seen in a late developmental stage of the germ
- cells (primary spermatocytes) af ter exposure of the immature germ cells (stem cell spermatogenia) to radiation, and assuming that the i
risk for oocytes is of equal size, will amount to less than 10 anomalies per million liveborn, and most Subcommittee members felt that the true 1 -
value may be near zero.
3 4
1 m --
o'-
I
-236-l CHAPTER V j
i SOMATIC EFFECTS - CANCER
-l
SUMMARY
AND CONCLUSIONS L
This chapter has considered the effects of ionizing radiation-that are manifested in exposed' people themselves (i.e..' somatic effects -
. cance r), in contrast.with' effects that are manifested in later generations (i.e., genetic, or inherited, effects).
The Subcom=ittee has not. considered acute ef fects of radiation, 1
.because these occur only at doses well above~those of interest in the' setting of protection standards. k'ith few exceptions, the somatic effects considered nanifest'themselves only years or decades after irradiation and are indistinguishable from lesions that occur naturally in nonirradi-ated populations.
The Subcommittee considers cancer induction to be the most important of these effects.
At low doses the radiation induction-of cancer is detectable only in a statistical sense; that is, in any given individual a particular effect cannot be attributed-exclusively to radiation, as opposed to some other cause.
In general, the smaller the dose of radiati.a, the less the likelihood that radiation was the principal cause.
L there are observational data relative to cancer induction in man over a range of higher doses, but little evidence presently available at l
doses of a few rads. Estimation of the risks of effects at these low doses involves extrapolation from observations at higher doses on the basis of assumptions about the nature of t he dose-response relationship.
1 I
1.
Cancer Incidence In regard to evaluating radiation carcinogenesis, the following i
i observations are pertinent:
~.
i
- _ = - - _._. _ _ _. _. _ _ _. _.
_.._.--..m
-235-l
.o i
i 4
e Cancers induced by radiation are indistinguishable from l
l
.those occurring naturally; hence, their existence can be l
l inferred only on the basis of an excess above the natural t
incidence.
j l
I e The natural incidence of cancer varies over several orders j
of magnitude, depending on the type and site of the neo-plastic growth, age, sex, and other factors.
e The time elapsing between irradiation and the appearance of a clinically detectable neoplasm is characteristically
- long, i.e., years or even decades.
This long induction time must be taken into consideration e
in the prospective followup of irradiated populations for observation of possible cancer development and in the j
retrospective evaluation of cancer patients with a history j
of relevant radiation exposure.
l Some of the existing human and animal data on radiation-e in'duced cancers come-from populations expoced to internally l
deposited radionuclides, with the dose-incidence relation-ship influenced by marked nonuniformities in the temporal and spatial distribution of radiation.
j i
e Some of the human data concern cancer mortality, whereas l
other
.ta concern incidence; it is appropriate to l
)
distinguish radiation-induced malignancies that may not l.
t l
greatly alter the death rate (e.g., skin and thyroid i
cancer) from others that are generally fatal (e.g., leukemia i
and lung cancer).
f i
..~
l
-236-Despite the dif ficulties mentioned, a clear-cut increase in incidence with increasing radiation dose has been documented for many types of cancer in human populations, as well as for several types of neoplasms in experimental animals. At the time of the 1972 BEIR report, most of the observed dose-incidence data pertained i
to relatively high doses (above 50 rems) and high dose rates. New evidence has added some further dose-incidence data at lower doses (e.g., 10-50 re=s).
Moreover, most of the additional information includes results that are reasonably consistent from one irradiated human populwtion to another; this sugEests applicability to the general population for purposes of risk evaluation.
Further followup of irradiated populations that were reviewed for the 1972 BEIR report and new studies carried out since then have suggested a number of principles that have modified our view of radiation-induced cancer in man.
First, the tissues in which cancer may be induced include nearly all the types present in the body.
Furthermore, it is apparent that the relative sensitivity of the various tissues to cancer induction by radiation is widely divergent, some tissuec being relatively resistant and others quite sensitive.
Second, solid tumors now are known to be of greater significance than leukemia, with respect to excess risk of cancer from whole-body exposure to radiation.
Major sites are the breast in women, the lung, the thyroid, and the digestive system.
Quantitatively, cancers at I
these sites now dominate the total cancer risk. These cancers have long latent periods and continue to appear 30 yr or more af ter radiation exposure.
In contrast, excess risk of leukemia, including acute and P
~
I J
-237-t.
I chronic myelogenous leukemia and acute lymphatic leukemia, appears l
very soon after radiation exposure and largely disappears within 25 yr'after exposure.
Third, the incidence of radiation-induced breast and thyroid cancer indicates that the total cancer risk is greater for women than for men.
Breast cancer occurs a3most exclusively in women, anc risk est'icates for thyroid-cancer induction by radiation are higher for women than for men (as is the case with the natural incidence). With respect to other cancers, the radiation risk in the twc sexes is approximately equal, according to available evidence.
For these reasons, estimates of total cancer risk should be expressed 1
separately for the two sexes.
Tourth, there is now considerable evidence from human studies that age is a major factor in cancer risk related to radiation exposure.
Both age at exposure and age at cancer diagnosis appear l
to be important for proper interpretation of human data.
If risks i
are given as absolute risks--i.e., numbers of cancer induced per unit of population and per unit of radiation exposure--then a single L
value independent of age may be inappropriate.
The 1972 BEIK report concluded that the risk of some kinds of cancer was greater for children and for fetuses irradiated jijl utero.. It is now apparent I
i l-that other age groups may also have risks above those of the general population, e.g., for breast cancer in women exposed during the second i
decade of life.
Where possible in this report, we have attempted to 1
indicate how age-specific rates can be applied to risk estimates for t
a total population.
i l
I-
i
-238-J l
Fifth, various host or environmental factors may interact with carcinogenic agents, such as radiation, to affect cancer incidence in different tissues in man.
These may include hormonal effects, immunologic status, and nonspecific stimuli to cell renewal in tissues sensitive to cancer induction by radiation exposure.
These are some of the reasons that it is not yet possible to derive precise' dose-response relationships for cancer induction by radiation.
The variety of possible biologic mechanisms of human cancer development suggests that the radiation dose-incidence relation-ship might not be the same for all types of cancer irmuced by radiation.
however, the fact that epidemiologic studies of widely differing human populations exposed to radiation have given reasonably concordant re-sults for some cancer sites ~and over a substantial range of radiation doses adds considerable strength to the dose-response information that was available in the 1972 BEIR report.
II.
Probability of Cancer Induction at Low Doses and Low Dose Rates Thgre are two questions of major interest:
(1) Will the effects,
{
as calculated with the use of the risk factors,' occur in a general popu-lation exposed to tent or a few hundreds of millirads per year of low-
-LET radiation in addition to the natural background of about 100 arems/yr I
already.being received?
(2) Will the effects occur in an occupational population exposed to about 0.5-5 rems /yr in addition to the natural l
background and medical exposure?
l t
4 4
4
,e
+
v
+
v.
y
i
-239-i l
Vith respect to question (1) the 1972 BEIR report stated that l
"... expectations based on linear extrapolation f rom the i
known effects in man of larger doses delivered at high dose rates in the range of a rising dose-incidence i
i relationship may well overestimate the risks of low-LET radiation at low dose rates and may, therefore, be re-garded as upper Ilmits of risk for low-level low-LET t
irradiation. The lower limit, depending on the shape of l
the dose-incidence curve for low-LET radiation and the i
efficiency of repair processes in counteracting carcino-genic effects, could be appreciably smaller (the possibility of zero is not excluded by the data). On the other hand, z
because there is greater killing of susceptible cells at i
high doses and high dose rates, extrapolation based on effects observed under these exposure conditions may be postulated to underestimate the risks of irrr.t.iatian at low doses and low dose rates."
The present Committee endorses this view.
It is not known whether i
dose rates of gamma or x radiation of around 100 mrads/yr are detrimental to exposed people; somatic effects would be masked by environmental or l
other factors that produce the same types of effects on the health of l
i those exposed as does ionizing radiation.
It is unlikely that carcino-(
genic and teratogenic effects of low-1.ET radiation administered at this t
dose rate will be demonstrated in the foreseeable future. Notwithstand-t ing these licitations, the Committee recognizes the need to estimate l
b l
the effects on human populations exposed to radiation at very low i
doses and in particular to assess the validity of the nonthreshold model.
For most radiation-induced cancers, the possibility of a linear non-l threshold dose-effect relationship cannot be excluded.
i Although dose-effect relations for somatic effects are unknown l
for doses of a few hundred millirads, it appears possible that they j
differ for different types of cancer.
In most cases, the linear j
~
l i.
hyp".hesis, as the 1972 BEIR report indicated, probably overestimates, j
J i
I
g
!(>.
j 5
-240-rather than underestimates, the risk from low-LET radiation.
For high-LET radiation, such as from internally deposited alpha-emitting radio-nuclides, the application of the linear hypothesis is less likely to lead to overestimates of risk and may, in fact, lead to underestimates.
For low doses, the linear hypothesis is consistent with plausible carcinotenic mechanisms at the level of a single cell.
In studies of anirtal or human populations, the shape of a dose-effect relationship at low doses may be practically impossible to ascertain statistically.
{
I This is because the population sample sizes required to estimate or t
te" a small absolute cancer excess are extremely large; specifically, the required sample sizes are approximately inversely proportional to the square of the excess.
For example, if the excess is truly pro-
.portional to dose and if 1,000 exposed and 1,000 control subjects are required to test the cancer excess adequately at 100 rads, then about j
f 100,000 in each group are required at 10 rads, and about 10,000,000 1
in each group are required at I rad.
I In regard to question (2), the Committee believes that, for the larger doses, as froci high-dose lifetime occupational exposure, a discernible carcinogenic effect could be manifest.
i 111. Relative Biologic __ Effectiveness I
[
There is substantial evidence, from both animal and human data, l
l of a wide variation in relative biologic effectiveness (RBE) among different types of ionizing radiation. This variation, which is related to differences in the microdistribution of radiation energy deposited 1 the tissues and of linear energy transfer (LET), say cause a given total absorbed dose to differ in its biologic effect by a factor of I
l l
D o
-241-10 or more, depending on the type of radiation.
The RBE is defined as the ratio between the doses of low-LET and high-LET radiation for equal effects. The wide variations in RBE pertain directly to the interpretation of epidemiologie date fro: several of the important available sources--
atomic-bomb survivors of Hiroshica, underground miners exposed to radio-active decay products of radon gas, and a number of populations with high body burdens of alpha-emitting radionuclides.
Many radiobiologic data indicate that the risk per rad for low-LET radiation, such as x rays and gasca rays, decreases to a greater degree with decrease in the dose and dose rate than does the risk for high-LET radiation.
Hence, the RBE of high-LET radiation can be expected to in-crease with decrease in the dose and dose rate. The data available on human populations exposed to alpha-emitters (underground niners, Thorotrast-or radf un-treated patients, and radium-dial-painters) indicate i
that, for cancer production, alpha particles are many times more ef fective per rad of average tissue dose than are x rays or gamma rays delivered at high dose r.tes.
Furthermore, epidemiologic data indicate that the effect per dose of alpha radiation at low dose rates (i.e., because of protraction ot fractionation) is greater than that of high dose-rates.
IV.
The Linear Nonthreshold Model The cancer-risk estimates presented in the 1972 BEIR report were obtained as average excess risks per rad at doses generally of a hundred or more rads. These estimates have been criticized on the grounds that the increment in cancer risk per rad may depend on dose and that the true risk at low doses may therefore be lower or higher than estimated.
i t
l-1 i
co
?
i I
-342-l 4
i Radiation carcinogenesis is a highly complex process, and an attempt i
to express risk as.a mathematical function of dose may be aisleading l
in situations where direct observation of excess risk is not possible.
i Unfortunately, the sampling requirements for precise estimates based l
on direct observations of risk at low doses are so formidable that no l
t present data come close to satisfying them,'and it is unlikely that i
1 they can be met in the foreseeable future.
If the cancer risk from low doses of radiation is to be estimated, it must be done by extrap-t o1 sting or curve-fitting from data that represent populations exposed
}
to doses high enough to give adequate risk esticates.
I In anical experiments, it has been shown, often with considerable i
statistical precision, that the dose-effect curve for radiogenic cancer can have a variety of shapes (sometimes including even a negative
{
initial slope).
As a rule, the dose-ef fect curve has a positive curvature for low doses of low-LET radiation, i.e.,
the slope of the i
curve increases with increasing dose. However, at higher doses (around i
i
. 100 rads or more),
the slope often decreases and may even becoce 4
negative.
Dose-effect curves may also vary with the kind of cancer, with spocies, and with dose rate.
J Human populations are genetically more diverse than the inbred 1
animal strains used in most experimental studies.
The existence J
of subsets of high or low susceptibility to radiation carcinogenesis
~
l 1s a factor that could modify the dose-effect curve.
The most likely l
l effect of such diversity is probably a tendency toward greater j
linearity, although the existence of e>quisitely sensitive subgroups l
of suitable size conceivably would produce a dose-effect curve that B
i
5
- A sg.
i
-243-i showed a greater effect per rad at very low doses.
The sensitive-subgroup
}
t hypothesis does not itself suggest a particular shape for the dose-effect These considerations and the diveraf ty of dose-effect relationship curves.
l' obtained from animal studies argue against the adoption of a universally applicable nonlinear dose-response curve of fixed shape.
I Epidemiologic data for humans exposed to a range of doses of low-L LET radiation have resulted in dose-effect curves'that often seem to l
conform with the general conclusions reached on the basis of animal data.
3r example, the dose-effect curves for cancers of the skin and leukemia l
appear to have positive curvature, and it is likely that this is also the i
l i
case f or the curves for some other cancers.
However, the incidence of l
breast cancer is perhaps adequately described by a linear (or, more j
accurately, proportional) relation between dose and excess incidence.
It seens probable that, for most types of radiogenic cancer, linear l
. extrapolation from incidence at high doses results in an overestimate i
j l
of risk associated with doses of a few rads of low-LET radiation.
l Nevertheless, in most cases the linear hypothesis emerges by default I
j; as the simple model whose use appears to be least objectionable in the absence of clear evidence as to the shape of the dose-effect curve.
V.'
Risk Estiestion*
In the absenc'e of a comprehensive theory of radiation carcino-genesis and of adequate direct observation of low-dose risks in man,
- There were unresolvable differences among the members of the j.
Subcommittee on Somatic Effects concerning the methods of interpretation of human data to arrive at an estimate of health risks of low-dose, low-LET whole-body radistion exposure.
}
AE.a result of these differences in the interpretation of human data, a dissenting minority view has been prepared; it is pre-sented as an a/dendum to Section 3 of Chapter V, " Estimating i
the Total Cancer Risk of Low-Dose, Low-LET Whole-body Radiation."
e.
i 5
"Y o
-244-quantitative estimation of risk is subject to numerous uncertainties, the greatest of which concerns the shr e of the dose-response curve e
f or low-LET radiation.
tbreover, the uncertainties, unlike sampling variation, cannot be sue:arized merely in probabilistic ter=s.
In rejecting a single cancer risk estimate in favor of a range, the Com=f ttee elected to review critically the data and methods available for any such estimation and to illustrate the uncertainty that they introduce into final estimates.
For example, the model used for pro-jecting risk coefficients beyond the period of actual observation cay codify the lifetime esticates by a f actor of up to 4, higher values being obtained with the relative-risk model than with the absolute-risk model.
In addition, very different results may be obtained from data from different sources.
The chibf sources of data used in this report are:
the populations exposed to whole-body irradiation in Hiroshica and Nagasaki; patients with ankylosing spondylitis exposed to partial-body irradiation therapeutically; various other series of people exposed occupationally such as uranf un miners and radio-dial-painters and a variety of patients exposed to partial-body irradiation therapeutically.
Moreover, if data from the combined Hiroshima and Nagasaki survivors are used, the P.BE for neutrons that cust be assumed adds to the uncertainty.
Because most human data do not systematically cover the range of low to moderate doses where the Japanese data appear 'o be fairly strong, we have relied particularly on the Nagasaki observations that are little influenced by neutrons.
Both incidence data f rom the Nagasaki tumor registry and the Nagasaki Hortality Study from death certificates have been presented as a basis of risk assessment.
l
c t
j V
- 5
- n j
-245-'
)
In addition to the foregoing major sources of uncertainty in esti-mating the carcinogenic effect of whole-body exposure to low-dose, low-I LET radiation, there are other, generally smaller, sources: length of followup, length of latent period, length of the period to which the excess risk applies, age at irradiation, dose rate or dose fractionation,
-and the possible influence of the disease treated by radiation on any estimate of carcinogenic effect.
For its illustrative computations of lifetime risk, the Comnittee chose three situations quite arbitrarily and these are higher by a factor of 10 to 100 frot the er*icates cade in the BEIR 1972 report.
An occupational exposure to 1 rad /yr.
e A continuous exposure of the general population of all ages e
to I rad /yr.
A single exposure of the general population of all ages to e
10 rads.
l.
These'three exposure situations do not reflect circumstances t
l that would norcally occur but embrace the areas of concern: occupa-tional and general population exposure, and single and continuous exposure.
The U.S. 1969-1973 life table was used as the basis for the calculations, and all results were expressed in terms of excess cancers per tillion persons of lifetite exposure.
The r.stimates differ by as 1
i l
much as an order of magnitude, depending on the precise combination of data sources, assueptions, and procedures.
For.the lifetime excess of cancer incidence induced by low-LET radiation, the range is 268 to 103) excess cancer cases per million 1
persons. exposed per rad for single exposure, and 254 to 946 per L
i
- 4 l
i=
. w l
l
-266-1 l
1 l
i I
million' persons per rad for continuous exposure.
In terms of the j
If fetime excess f atal cancer induced by low-dose, low-LET radiation, the risk estimate is in1the range of 70-to 353 excess cases per aillion 1
L persons exposed per rad for. single exposure,' and 68 to 293 per million I
l per rad'for continuous exposure.
Expressed in terms of the percentage increase in the natural lifetime occurrence of cancer..the estimate of j
~
i excess cancer'from a single dose of 10 rad ranges from 0.81 percent for.
l 1
males under the absolute risk projection model to 4.5 percent for females 1
l under th'. relative risk model.
For cancer mortality, the corresponding.
percentages are 0.40 percent and 2.7 percent over the r-mal lifetite
- occurrence.
The estimated lifetime cancer excess above the natural I
l incidence due to continuous exposure of I rad per year beginning at
)
birth, ranges from 5.1 percent for males under the absolute risk projection model to 32.6 percent for females under the relative risk projection model for cancer incidence, and 2.7 percent to 16.9 percent
+
for cancer mortalilty.
I
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1 I
d e
a 5
4 e-
.m--
y'
{
-342-
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Table 5:
Comparative Lifetime Cancer Risk Estimates for the General Population from Exposures to Low-Dose, Low-LET Radiation, Single Exposure
- and Continuous
. Exposure **, Both Sexes Combined J
s Source of Continuous Estimates Single Exposure exposure (per million population exposed per rad)
J
.)
)
BEIR 1979 i
. Incidence
' Relative Risk 636-1031 592-946 l
Absolute Risk 268-399 254-373 Mortality Relativa Risk 177-353 150-293 J
Absolute Risk 70-124
~68-119 i
j BEIR 1972 Factors **
)
Mortality Relative Risk 621 568 l*
Absolute Risk 117 115 i
1
-UNSCEAR 1977 l
Mortality 100 100' L
J l
- The BEIR 1979 single-exposure estimate was based on a 10-tad dose and was divided by 10 for comparison with the other values; the estimate for con-l
-tinuous exposure is based on a lifetime exposure of 1 rad / year.
t BEIR 1972 post-natal, age-specific risk fsetors used with 1969-1971 life-tables,-vith plateau extending throughout the years of life remaining
.after irradiation, estimate (b) in the 1972 BEIR Report.
The average age of the 1969-1971 life-tables is older than that of the 1967 U.S. population used in the 1972 BEIR report.
For this reason, the numbers obtained here for continuous exposure are larger, on a per rad l
basis, than those obtainable from Tables 3-3 and 3-4 of the 1972 BEIR report.
i 3-j i
i i
J 0'
ADDENDUM j
DISSENTING REPORT OF THE SOMATIC SUBCOMMITTEE OF BEIR III*-
B.)
Concl usions We conclude that data on the mortality of A-bomb survivors from all malignant neoplasms are in concordance with the general findings of radiobiology and that the biological effectiveness of high LET relative to low LET radiations increases with decreasing level of effect.
We furthermore conclude that for high LET radiation the total carcinocenic effect of doses between a few and about 100 rad is essentially proportional to dose.
In cont ast the dose-effect relation for low LET radiation is very unlikely to be linear in this dose range.
We conclude furthermore that risk estimates for whole body irradiation that are based on individual organ risk estimation in BEIR III l
are overestimates of incidence at low doses. We do not believe that there 4
is adequate infomation to determine accurately the magnitude of the error.
It seems likely however that it is as much as an order of magnitude and possibly more.
It follows that, collectively, the risk estimates given in BEIR III i
for specific oroans are excessive. They might therefore be used to justify radiation exposu.e but not to interdict it.
It is to be noted however that l
the shapes of the dose-effect relations derived here for mortality from all l
cancers may not apply to cancers induced in individual organs.
i i
- This " Dissenting Report" was prepared by Ors. Harald H. Rossi and Edward W. Webster.
It has been endorsed by Drs. Charles W. Mays, Henry N. Wellman, Marylou Ingram
r
(,
,, 4
- l 9
Le t
It i's a consequence of these conclusions that low dose exposure to high LET radiations represents a substantially larger hazard relative _to. low L
LET radiation than is implied by the currently adopted value of about 10 for the quality factor (Q) for neutrons.
In order to relate the free-in-air excess cancer indidence to absorbed
' dose rather than to kerma it is necessary to evaluate the ratio-of these quantities for the gama and neutron radiations emitted by the A-bombs at Hiroshima and Nagasaki. As indicated in BEIR III such data are available
'for the marrow and other tissues and organs.
However, the selection of a representative ratio for total cancer induction involves uncertainties.
Conversely the concept of a cancer risk conferred by one rad of "whole body dose" is of little practical value since it is very likely that in any exposure to ionizing radiation the absorbed dose in the human (adult) body will vary by at least a factor of two and usually more.
l in order to obtain an approximate estimate of cancer risk that is independent of exposure conditions it is in the following assumed that the ratios of absorbed dose and kema for atomic-bomb radiations, which are l-applicable to the bone marrow are representative for all induced cancers.
These ratios (D /K, = 0.5 and D /K.= 0.25) evidently apply to leukemia but 3 g would not seem to differ by more than about 30% for most other organs.
With these assumptions and on the basis of the data in Figures 1 and 2 herewith, the excess annual mortality of all malignant neoplasms for the
' period from 1950-1974 is given by:
y = 1.3 x 10~4 D / rad P
g l
for the fission neutrons emitted by the Hiroshima weapon; and t
My = 1.7 x 10-8 (D / rad)2 i
i
r 1 O. vi i
- n'
_3_
l i
for gamma -radiation. emitted at Nagasaki.
This calculation is based on the l
conclusion that gamma radiation had a negligible effect at low doses in l
Hiroshina and that in Nagasaki neutron effects are negligible at all doses.
As stated above the existence of an additional term that is linear in dose is not ruled out for gamma radiation but this must be far less than that derived from the sum of organ estimates in BEIR I11.
The non-linear characteris. tics of the dose-mortality curve for gamma j
radiation indicates that the concept of a " risk per rad" is misleading.
A risk estimate in these terms should in any case not be provided without stating the dose at which it applies.
A further and even core fundanental problem arises when any of the cancer risk estimates given here or in BEIR III which are primarily based on observations for high or moderately high doses of low LET radiation are extrapolated to doses that are less than a few rad.
It cannot be assumed that any relation that agrees with epidemiological data in e given range i
l of doses is even approxicately valid for doses that are substantially different and,at this tine there is far too little theoretical informat ion to serve l
as a reliable guide for extrapolation. As stated in BEIR 11? it is unknc a whether low LET radiation administered at a dose rate of 10D m rad / year has i
any effect except that this is very likely to be undetectable.
l l
l
~
..h
.j0 752-CHAPTER VI SOMATIC EFFECTS OF RADIATION OTHER THAN CANCER SLMMARY Among the somatic effects of radiation other than cancer, de-velopmental effects on the unborn child are of greatest concern.
Exposure of an embryo or fetus to relatively high doses of radiation can cause death, malformation, growth retardation, and functional impairment.
Recent information, most of it published since the 1972 BEIR report, indicates that measurable damage can be produced by doses of I-9 rads.
The effects of radiation are related to the developmental stage at which exposure occurs, and correspondence has been demonstrated in this respect between man and other man =als.
The laboratory data can therefore be used with some confidence to fill in gaps in human experience.
k'here developmental ef fects of radiation can be measured at the l
cellular level, as in the case of oocyte-killing during fetal or
(
early postnatal stages, thresholds may not be demonstrable. However, most of the perceived abnormalities produced by radiation probably I
result from damage to more than a single cell.
It is therefore un-1 l
likely that such effects bear a linear relationship to dose.
Threshold I
\\
1 doses for some effects have, in f act, already been demonstrated, but
[
these thresholds vary for different abnormalities. For a given total i
j dose, decreases in dose rate generally lead to decreases in developmental effects.
Because sensitive stages for many specific abnormalities are l
relatively short, dose protraction may result in lowering to below the threshold the portion of the total dose that is received during a par-j ticular critical period.
i i
)
i