B. ,
Printed on Recycled Paper
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40 61 520/1-S9-005
national Emission Standards
for Hazardous Air Pollutants
Risk Assessment Methodology
Environmental Impact Statement
for NESHAPS Radionuclid.es
VOLUME I
BACKGROUND INFORMATION DOCUMENT
September 1989
U.S. Environmental Protection Agency
Office of Radiation Programs
Washington, D.C. 20460
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Preface
The Environmental Protection Agency is promulgating National
Emission Standards for Hazardous Air Pollutants (NESHAPs) for
Radlonuclides. An Environmental Impact statement (EIS) been
prepared in support of the rulemaking. The EIS consists of the
following three volumes:
VOLUME I ~ Risk Assessment Methodology
This document contains chapters on hazard
identification, movement of radionuclides through
environmental pathways, radiation dosimetry,
estimating the risk of health effects resulting from
expose to low levels of ionizing radiation, and a
summary of the uncertainties in calculations of dose
and risks.
VOLUME II - Risk Assessments
This document contains a chapter on each radioniaclide
source category studied. The chapters include an
introduction, category description, process
description, control technology, health impact
assessment, supplemental control technology, and cost.
It has an appendix which contains the inputs to all
the computer runs used to generate the risk
assessment,
VOLUME III - Economic Assessment
This document has chapters on each radionuclide source
category studied. Each chapter includes an
introduction, industry profile, summary of emissions,
risk levels, the benefits and costs of emission
controlsr and economic impact evaluations.
Copies of the EIS in whole or in part are available to all
interested persons; an announcement of the availability appears in
the Federal Register. For additional information, contact James
Hardin at (202) 475-9610 or write to:
Director, Criteria and Standards Division
Office of Radiation Programs (ANJR-460)
Environmental Protection Agency
401 M Street, SW
Washington, DC 20460
111
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Various staff members from EPA's Office of Radiation Programs
contributed In the development, and preparation of the EIS.
Terrence HcLaughlin
James Karelin
Byron Hunger
Fran Cohen
Albert Colli
Larry Gray
W. Daniel Hendricks
Paul Magno
Christopher B, Nelson
Dr. Neal s. Nelson
Barry Parks
Dr. Jerome Pushkin
Jack L. Russell
Dr, James T. Walker
Larry Weinstock
Chief, Environmental
Standards Branch
Health Physicist
Economist
Attorney Advisor
Environmental
Scientist
Environmental
Scientist
Environmental
Scientist
Environmental
Scientist
Environmental
Scientist
Radiobiologist
Health Physicist
Chief Bioeffects
Analysis Branch
Engineer
Radiation
Biophysiclst
Attorney Advisor
Project Officer
Author/Reviewer
Reviewer
Author/Reviewer
Author/Reviewer
Reviewer
Author/Reviewer
Author
Author
Reviewer
Author/Reviewer
Author/Reviewer
Author
Reviewer
An EPA contractor? S. Cohen and Associates, Inc., McLean, VA,
provided significant technical support In the preparation of the
EIS.
IV
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LIST OF ..................... vli
LIST OF ..................... x
1, INTRODUCTION ...................... 1-1
1,1 OF ......... 1-1
1.2 OF THE FINAL BACKGROUND
INFORMATION ............... 1-3
1.3 ................ 1-4
2. CURRENT STRATEGIES ............ 2-1
2.1 INTRODUCTION ................... 2-1
2.2 THE INTERNATIONAL COMMISSION ON RADIOLOGICAL
PROTECTION AND THE NATIONAL COUNCIL ON
RADIATIOM PROTECTION AND ....... 2-2
2.3 FEDERAL GUIDANCE ................. 2-8
2.4 THE ENVIRONMENTAL PROTECTION AGENCY ....... 2-10
2.5 NUCLEAR REGULATORY COMMISSION .......... 2-12
2.6 DEPARTMENT OF .............. 2-14
2.7 AGENCIES ............. 2-15
2.8 STATE AGENCIES ................. 2-16
2.9 ................... 2-17
3. HAZARD IDENTIFICATION ................. 3-1
3.1 IS CARCINOGENIC ...... 3-1
3.2 IS MUTAGENIC ....... 3-6
3,3 EVIDENCE RADIATION IS TERATOGENIC ...... 3-8
3.4 ................... 3-8
3.5 OF RADIATION IS A
........ 3-9
3.6 ................... 3-11
4. OF
........................ 4-1
4.1 INTRODUCTION ................... 4-1
4.2 OP THROUGH
THE AIR ...................... 4-1
4.3 DEPOSITION OF ATMOSPHERIC RADIONBCLIDES ...... 4-8
4.4 THE FOOD CHAIN ........ 4-11
4.5 CALCULATING THE ENVIRONMENTAL CONCENTRATION
OF RADIONUCL1DES: THE AIRDOS-EPA CODE ..... 4-14
4.6 ................... 4-21
5. RADIATION
5.1 INTRODUCTION ................... 5-1
5.2 BASIC CONCEPTS .................. 5-1
5.3 EPA ............... 5-8
5.4 ................... 5-36
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THE OF
TO LOW OF
6,1 ................... 6-1
6.-2 FOR .... 6-3
6.3
RADIATION .................... 6-33
6.4 THE
RADON-22 ......... 6-3?
6.5 OTHER RADIATIOW-INDUCED ..... 6-54
6.6 OF EPA'S RADIATION -
A PERSPECTIVE .................. 6-7?
6.7 REFERENCES ................... 6-81
7-. AN ANALYSIS OF UNCERTAINTIES IN FOR
SELECTED SITES ..................... 7-1
7.1 INTRODUCTION ................... 7-1
7.2 GENERAL APPROACH ................. 7-2
7.3 UNCERTAINTY IN ............. 7-9
7.4 RESULTS ..................... 7-21
7.5 REFRENCES .................... 7-30
APPENDIX A ASSESSMENT METHODOLOGY ............. A-l
A.I INTRODUCTION ................ A-l
A. 2 ENVIRONMENTAL PATHWAY ....... A-l
A.3 REFERENCES ................ A-14
APPENDIX B MECHANICS OF LIFE IMPLEMENTATION OF THE
ESTIMATES .................... B-l
B.I INTRODUCTION ................ B-l
B.2 LIFE TABLE ANALYSIS TO THE
OF EXCESS .............. B-l
B.3 ................. B~5
APPENDIX C OVERVIEW OF TECHNIQUES TO QUANTIFY IN
ENVIRONMENTAL ............... C-l
C.I INTRODUCTION ................ C-l
C.2 ASSESSMENTS ................ C-2
C.3 LEVELS OF ANALYSIS ............. C-4
C.4 UNCERTAINTY ANALYSIS DUE TO
UNCERTAINTY ................ C-5
C.5 TECHNIQUES FOR . . C-7
C.6 DISTRIBUTIONS .......... C-8
C.7 ................ C-10
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OF
Table 5-1
Table 5-2,
Table 5-3.
Table 5-4.
Table 6-1.
Table 6-2.
Table 6-3.
Table 6-4.
Table 6-5.
Table 6-6.
Table 6-7.
Table 6-8.
Table 6-9.
Quality factor for various types
of radiation ................ 5-5
Weighting factors recommended by
the ICRP for stochastic risks ........ 5-6
Comparison of customary and SI
special units for radiation quantities .... 5-8
Target organs and tissues used for
calculating the ICRP effective dose
equivalent and the EPA cancer risk 5-10
Site specific incidence risk
coefficients (106 per rad rad-y) 6-15
Site-specific mortality to incidence
risk ratios ................ 6-16
BEIR III L-L model for excess
fatal cancers other than leukemia
and bone cancer .............. 6-17
Mortality risk coefficients
(10' per rad} for the constrained
relative risk model ............ 6-18
BEIR III L-L model for excess
incidence of (and mortality from)
leukemia and bone cancer
(absolute risk model) ........... 6-19
Site-specific mortality risk
per unit dose (l.OE-6 per rad)
for combined leukemia-bone
and constrained relative risk model . . .
6-21
Site-specific incidence risk
per unit dose (10E-6 per rad)
for combined leukemia-bone
and constrained relative risk model
Comparison of general population
risk estimates for fatal cancer
due to low level, whole-body
low-LET radiation ........
6-22
6-26
Site-specific mortality risk per
million person-rad from low level,
low-LET radiation exposure of the
general population ........
6-27
Vll
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Table 6-12,
Table 6-13,
Table 6-14,
Table 6-15,
Table 6-16,
Table 6-17,
Table 6-18,
Table 6-19.
Table 6-20,
Table 6-21,
BEIR IV committee estimate of lung
cancer risk coefficient for age-
constant, relative-risk model . .
BEIR IV risk model - lifetime
exposure and. lifetime risk . . . .
Estimated lung cancer risk coefficients
from radon progeny exposure for
three miner cohorts ..........
Lifetime risk from radon daughter
exposure of lung cancer death
(per 106 win) ..........
Lifetime risk from excess radon
daughter exposure {adjusted for
a background exposure of 0.25 WLM/yr)
Lifetime risk for varying age at
first exposure and duration of
exposure (Background = 0.25 WLM/yr)
Lifetime risk for varying age at
first exposure and duration of
exposure (Background = 0,25 WLM/yr)
UNSCEAR 1988 risks of genetic
disease per 1 million live-births
in a population exposed to a
genetically significant dose of
1 rad per generation of low-dose
rate, low-dose, low-LBT irradiation
BEIR III estimates of genetic effects
of an average population exposure of
1 rem per 30-yr generation (chronic
x-ray or gamma radiation exposure) « .
6-43
6-45
6-45
6-49
6-51
6-52
6-53
6-57
6-59
Summary of genetic risk estimates per 10
liveborn of low-dose rate, low-LET radiation
in a 30-yr generation ........... 6-60
Genetic risk estimates per 10 live-born
for an average population exposure of 1
rad of high-LET radiation in a 30 year
generation .,.«.....
6-61
Table 6-22
Radiation-induced reciprocal translocation
in several species ............. 6-62
¥111
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6-23.
Table 6-24,
Table 6-25.
Table 6-26.
Table 6-27,
Table 7-1.
Table 7-2.
Table 7-3.
Table 7-4.
Table 7-5.
Table 7-6.
Table A-l.
Table A-2.
Table A-3.
Table A-4.
Table A-5.
of
in a birth, cohort to of
parents to 1 per generation . . , . .
Increase in background or level of genetic
effects after 30 generations or more . . .
6-67
Causes of uncertainty in the genetic
risk estimatel ............... 6-68
Possible effects of iajLiterQ radiation
exposure ............. 6-76
Summary of BPA's radiation risk factors . . 6-78
Environmental transport factors ...... 7-14
Distribution of ingestion pathway parameters 7-15
Distribution of miscellaneous pathway factors 7-18
Probability distributions for risk factors . 7-22
Comparison of Monte-Carlo individual risk estimates
to those in Volume II ........... 7-26
Contributions of various pathways to risk . 7-28
Presumed sources of food for urban and
rural sites ................. A-l
AIRDOS-EPA parameters used for generic site
assessments ................. A~5
Default values used for element dependent
factors ................... A-7
Cattle densities and vegetable crop
distribution for use with
AIRDOS-SPA .................. &™9
Risk factors for selected radionuclides
(see Table A-3 for default inhalation class
and ingestion f, values) .......... A-ll
IX
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OF
Figure 4-1.
Figure 4-2.
Figure 4-3.
Figure 5-1.
Figure 5-2.
Pathways of airborne radionuclides into the
environment ................
4-2
Vertical concentration profiles for plume vs
downwind distance from release ........ 4-6
Circular grid system used by AIRDGS-EPA . , 4-16
A schematic representation of radioactivity
movement among respiratory tract,
gastrointestinal tract, and blood ..... 5-11
The ICRP TasJc Group lung model for
particulates ................ 5-16
Figure 7-1.
Figure 7-2.
Figure C-l
Example of the output of a risk assessment
using quantitative uncertainty analysis
7-3
Cumulative probability distributions for risk 7-24
Example of the output of a risk assessment
using quantitative uncertainty analysis
. C-3
X
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1.I HISTORY OF
In 1977, Congress amended the Clean Air Act, (the Act) to
address emissions of radioactive materials. Before 1977, these
emissions were either regulated under the Atomic Energy Act or
unregulated. Section 122 of the Act required the Administrator
of the U.S. Environmental Protection Agency (EPA), after
providing public notice and opportunity for public hearings (.44
FR 217G4, April 11, 1979), to determine whether emissions of
radioactive pollutants cause or contribute to air pollution that
may reasonably be expected to endanger public health. On
December 27, 1979, EPA published a notice in the Federal Register
listing radionuclides as hazardous air pollutants under Section
112 of the Act (44 FR 76738, December 27, 1979). To support this
determination, EPA published a report entitled "Radiological
Impact Caused by Emissions of Radionuclides into Air in the
United States, Preliminary Report" (EPA 520/7-79-006, Office-of
Radiation Programs, U.S. EPA, Washington, D.C., August 1979).
On June 16, 1981, the Sierra Club filed suit in the U.S.
District Court for the Northern District of California pursuant
to the citizens' suit provision of the Act (Sierra Club v
Gorsuch, No. 81-2436 WTS). The suit alleged that EPA had a
nondiscretionary duty to propose standards for radionuclides
under Section 112 of the Act within 180 days after listing 'them.
On September 30, 1982, the Court ordered EPA to publish proposed
regulations establishing emissions standards for radionuclides,
with a notice of hearing within 180 days of the date of that
order.
On April 6f 1983, EPA published a notice in the Federal
Register proposing standards for radionuclide emission sources in
four categories: (1) DOE facilities, (2) Nuclear Regulatory
Commission facilities, (3) underground uranium minesf and (4)
elemental phosphorus plants. Several additional categories of
sources that emit radionuclides were identified, but It was
determined that there were good reasons for not proposing
standards for them. These source categories were (1) coal-fired
boilers? (2) the phosphate industry; (3) other mineral extraction
industries," (4) uranium fuel cycle facilities, uranium tailings,
and high-level waste management; and (5) low energy accelerators
(48 FR 15077, April 6, 1983). To EPA's knowledge, these comprise
the source categories that release potentially regulative amounts
of radionuclides to the air.
To support these proposed standards and determinations, EPA
published a draft report entitled "Background Information
Document, Proposed Standards for Radionuclides" (EPA 520/1-83-
001, Office of Radiation Programs, U.S. EPA, Washington, D.C.,
March 1983).
l-l
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Following publication of the proposed standards, EPA held an
informal public hearing in Washington, D.C., on April 28 and 29,
1983. The comment period held open an additional 30 to
receive written comments. Subsequently,, EPA received a number of
requests to extend the time for submission of public continents and
to accommodate persons who were unable to attend the first public
hearing. In response to these requests, EPA published a notice
in the Federal Register that extended the comment period by an
additional 45 days and held an additional informal public hearing
in Denver, Colorado, on June 14, 1983 (48 FR 23655, May 26,
1983} .
On February 17, 1984, the Sierra Club again filed suit in
the U.S. District Court for the Northern District of California
pursuant to the citizens' suit provision of the Act (Sierra Club
v Ruckelshaus, No. 34-0656 WHO) .. The suit alleged that EPA had a
nondiscretionary duty to issue final emissions standards for
radionuclides or to find that they do not constitute a hazardous
air pollutant (i.e., "de-list" the pollutant). In August 1984,
the Court granted the Sierra Club motion and ordered 1PA to take
final actions on radionuclides by October 23, 1934.
On October 22, 1984, the Agency issued its Background
Information Document in support of the Agency's final action on
radionuclides. The report contains an integrated risk assessment
that provides the scientific basis for these actions (EPA 520/1-
84-022-1) .
On February 6, 1985, National Emission Standards for
Hazardous Air Pollutants (NBSHAPS) were promulgated for
radionuclide emissions from DOE facilities, NEC-licensed and non-
DOE Federal facilities, and elemental phosphorus plants (50 FR
5190). Two additional radionuclide NESHAPS^ covering radon-222
emissions from underground uranium mines and licensed uranium
mill tailings, were promulgated on April 17, 1985 (50 FR 15386}
and September 24, 1986 (51 FR 34056)', respectively.
The ER&'s basis for the radionuclide NESHAPS was challenged
in lawsuits filed by the Sierra Club and the National Resources
Defense Council (NRDC). While these suits were under
adjudication, the U.S. Court of Appeals for the District of
Columbia issued a decision finding that the EPAss NESHAP for
vinyl chloride was defective in that costs had been improperly
considered in setting the standard. Following the Court's order
to review the potential effects of the vinyl chloride decision on
other standards, the EPA determined that costs had been
considered in many rulexsakings on radionuclide emissions. On
December 9, 1987, the Court accepted the EPA's proposal to leave
the existing radionuclide NESHAPS in place while the Agency
reconsidered the standards. In the interimf the suits filed by
the Sierra Club and the NRDC have been placed in abeyance.
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1.2 OF THE FINAL
Volume I contains background Information on, radiation
protection programs and a detailed description of the Agency's
procedures and. methods for estimating radiation dose and risk due
to radioraiclide emissions to the air. This material Is arranged
as shown in the following descriptions of the chapters:
o Chapter 2 - A summary of regulatory programs for
radiation protection and the current positions of the
various national and international advisory bodies and
state and Federal agencies in regard to radiation.
o Chapter 3 - A description of what makes radiation
hazardous,, the evidence that proves the hazard, and the
evidence that relates the amount of radiation exposure
to the amount of risk.
o Chapter 4 - An explanation of how radionuclid.es, once
released into the air, move through the environment and.
eventually cause radiation exposure of people. This
chapter also contains a description of how EPA
estimates the amounts of radionuclides in the
environment,, i.e., in the air, on surfaces, in the food
chain, and in exposed humans.
o Chapter 5 - A description of how radionuclides, once
inhaled and ingested, move through the body to organs
and expose these organs. This chapter also contains a
description of how EPA estimates the amounts of
radiation dose due to this radiation exposure of
organs. It also describes how the amount of radiation
dose is estimated when the source of radiation is gamma
rays from a source outside of the body.
o Chapter 6 - A description of how the risk of fatal
cancers and genetic effects is estimated once the
amount of radiation dose is known,
o Chapter 7 - A summary of the uncertainties in the dose
and risk estimates of source categories emitting
significant amounts of radionuclides, which were
by using the procedures and information in the previous
chapters. Associated uncertainties are discussed in
the appropriate chapter, but overall uncertainties are
discussed In this chapter,
Volume I also contains three appendices. Appendix A
describes the environmental transfer factors used In the dose
assessment models. Appendix B describes the mechanics of the
life table analysis used to estimate risk. Appendix C presents
an overview of the quantitative uncertainty analysis techniques
currently under review for use as a method for expanding the
semiquantitative uncertainty analysis provided in Volume I.
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luiae II contains detailed risk estimates for source
of emissions,, which were performed according to procedures
given in Volume I. Each chapter in Volume II four
topics: (1) the source category, the processes that result in
releases of radionuclides to the environment, and existing
controls, (2) the bases for the risk assessment, including
reported emissions^ source terms used, and other site parameters
relevant to the dose assessment, (3) the results of the dose and
risk calculation,, along with an extrapolation to the entire
category, and (4) a description of supplementary emissions
controls and their cost and effectiveness in reducing dose and
risk.
Two appendices are also provided in Volume II. Appendix A
presents the detailed AIRDOS input sheets used to calculate
individual and population doses and risks associated with each
category. Appendix B presents the methodology used to evaluate
the costs and effectiveness of earthen covers to control radon
emissions from area sources of radon.
1.3 UPDATE METHODOLOGY
The categories of emissions addressed in this document are
similar to those addressed in the 1984 Background Information
Document. DOE NRC-licensed facilities, elemental phosphorus
plants, underground uranium mines, and licensed uranium mills are
addressed because they are covered by NESHAPS. Uranium fuel
cycle facilities, high-level waste disposal facilities, coal-
fired boilers, and inactive uranium mill tailings sites are
addressed because of challenges to previous determinations that
they were adequately covered by other laws. Surface uranium
mines, DOE radon, and phosphogypsum stacks are addressed because
of challenges to the BPA's lack of risk assessment for these
facilities. In sum, this Background Information Document
addresses the following categories of radiological emissions to
air:
o DOE Facilities
o NRC-Licensed and Non-DOE Federal Facilities
o Uranium Fuel Cycle Facilities
o High-Level Waste
o Elemental Phosphorus Plants
o Coal-fired Boilers
o Inactive Uranium Mill Tailings
o Licensed Uraniura Mill Tailings
o DOE Radon
o Underground Uranium Mines
o Surface Uranium Mines
o Phosphogypsum Stacks
For each category, Volume II presents updated information on
the number of facilities, radionuclide emissions to air, and
control technologies. Depending on the number of facilities in a
category, risks are provided for individual facilities, or a set
1-4
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of reference facilities Is defined that conservatively
the category. Risks to the critical population group the
population within 80 "km are presented for each category.
EPA recognizes that when it performed a risk assessment to
determine the need for regulation of uranium mill tailings under
the Uranium Mill Tailings Radiation Control Act (UMTRCA), the
Agency considered the national health impact from the radon
released from the tailings. In this assessment, EPA is
considering only the health effects within 80 km of the source.
EPA is using 80 km as the limit in order to be consistent with
the other NESHAP rulemakings. This risk assessment in no way
disputes the validity of the approach or the results used in the
UMTRCA rulemaking.
1-5
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2.
. 1
of radiation radioactivity only to
of the last century—to the discovery of x-rays in 1895
discovery of radioactivity in 1896. discoveries
beginning of radiation, science the deliberate of
radiation radionuclides in science, medicine, industry,
The findings of radiation science rapidly led to
development of medical industrial radiology, nuclear physics,
and nuclear medicine. By the 1920's, the of x-rays in
diagnostic medicine and industrial applications widespread,
and radium was being used by industry for luminescent dials
by doctors in therapeutic procedures, By 1930's, biomedical
and genetic researchers were studying the effects of .radiation on
living organisms, and physicists were beginning to understand the
mechanisms of spontaneous fission radioactive decay. By the
1940's, a self-sustaining fission reaction was demonstrated,
which led directly to the construction of the first nuclear
reactors and atomic weapons.
Developments since the of World War II have been rapid.
Today the of x-rays radioactive materials is widespread
and includes",
Q Nuclear reactors (and their supporting fuel-cycle
facilities) generate electricity, power ships and
submarines,, produce ractioisotopes for research, space,
defense, medical applications. They also
as research tools for nuclear engineers physicists.
o Particle accelerators produce radioisotopes
as research tools for studying structure of
materials atoms,
o The radiopharmaceutical industry provides
radioisotopes needed for biomedical research and
nuclear medicine.
o Nuclear medicine has developed as a recognized medical
specialty in which radioisotopes are in
diagnosis and treatment of numerous diseases.
o X-rays widely as a. 'diagnostic tool in medicine
and in such diverse industrial fields as oil
exploration and nondestructive testing.
o Radionuclides used in such common consumer pro-ducts
as luminous-dial wristwatch.es and detectors.
The following sections of this chapter provide a brief
history of the evolution of radiation protection philosophy and
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an outline of the current regulatory programs and strategies of
the government agencies responsible for ensuring that radiation
and radionuclides safely.
2,2 THE ON
AND THE COUNCIL ON AND
MEASUREMEMTS
Initially, the dangers and risks by x-rays
radioactivity were little understood. By 1896, however, "x-ray
burns" were being reported in the medical literature, by
1910, it was understood that such "burns" could also be caused by
radioactive materials. By the 1920§s, sufficient direct evidence
(from experiences of radium dial painters, medical radiologists/
and miners) and indirect evidence (from biomedical genetic
experiments with animals) had been accumulated to persuade the
scientific community that an official body should be established
to make recommendations concerning human protection against
exposure to x-rays and radium.
At the Second International Congress of Radiology meeting in
Stockholm^ Sweden, in 1928, the first radiation protection
commission was created. Reflecting the use of radiation and
radioactive materials at the time, the body was named the
International X-ray and Radium Protection Commission and was
charged with developing recommendations concerning protection
from radiation. In 1950, to reflect better its role in a
changing world, the Commission was reconstituted and renamed the
International Commission on Radiological Protection (ICRP).
During the Second International Congress of Radiology, the
newly created Commission suggested to the nations represented at
the Congress that they appoint national advisory committees to
represent their viewpoints before the ICRP, to in concert
with the Commission in developing and disseminating
recommendations on radiation protection. This suggestion led to
the formation, in 1929, of the Advisory Group, After a of
reorganizations and changes, this committee emerged in 1964
in its present form as the congressionally chartered National
Council on Radiation Protection and Measurements (NCRP). The
congressional charter provides for the NCRP to:
o Collect, analyze, develop, and disseminate in the
public interest information and recommendations about
radiation protection and radiation quantities, units,
and measurements.
o Develop basic concepts about radiation protection
radiation quantities, units, and measurements, the
application of these concepts.
o Provide a means by which organizations concerned with
radiation protection and radiation quantities, units,
and measurements may cooperate to use their combined
-------
resources effectively to stimulate the work of such
organizations,
o Cooperate with the ICRP and other national
International organizations concerned with radiation
protection radiation quantities, units,
measurements.
Throughout their existence, the ICRP the HCRP have
woriced together closely to develop radiation protection
recommendations that reflect the current understanding of the
dangers associated with exposure to ionizing radiation. The ICRP
and the HCRP function as non-government advisory bodies. Their
recommendations are not binding on any government or user of
radiation or radioactive materials.
The first exposure limits adopted by the ICRP the
(ICRP34, ICRP38, and HCRP36) established 0.2 roentgen/day1 as the
"tolerance dose11 for occupational exposure to x-rays and
radiation from radium. This limit, equivalent to an absorbed
dose of approximately 25 rads/y as measured in air, was
established to guard against the known effects of ionizing
radiation on superficial tissue, changes In the blood, and
"derangement" of internal organs, especially the reproductive
organs. At the time the recommendations were made, high doses of
radiation were known to cause observable effects, but the
epidemiological evidence at the time was inadequate even to imply
the carcinogenic Induction effects of moderate or low doses.
Therefore, the aim of radiation protection was to guard against
known effects, and the "tolerance dose'1 limits that were adopted
were believed to represent the level of radiation that a person
in normal health could tolerate without, suffering observable
effects. The concept of a tolerance and
occupational exposure limit of 0,2 R/day for x
radiation remained in effect until the end of the 1940's,
recommendations of the ICRP and the KCRP made no mention of
exposure of the general populace.
By the end of World War II, the widespread use of
radioactive materials and scientific evidence of genetic and
somatic effects at lower doses and dose rates suggested that the
radiation protection recommendations of the NCRP and ICRP
would have to be revised downward.
By 1948, the HCRP had formulated Its position on appropriate
new limits. These limits were largely accepted by the ICRP in
its recommendations of 1950 and formally issued by the NCRP in
1954 (ICRP51, NCRP54). Whereas the immediate effect was to lower
1 The NCRP's recommendation was 0.1 roentgen/day measured in
air. This limit is roughly equivalent to the ICRP limit, which was
conventionally measured at the point of exposure and included
backscatter.
-------
basic whole body occupational limit to equivalent of
0.3 rad/weelc (approximately 15 rads/y) p the revised
recommendations also embodied several new and important: concepts
in formulation of radiation protection criteria.
First; the recommendations recognized the difference in
effects of various types and energies of radiation; both, 1CRP and
NCRP include discussions of the weighting factors
that should be applied to radiations of differing
energies, The HCRP advocated the of the "rem" to the
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types energy. Although the ICRP rioted the shift toward the
acceptance of the rein, it continued to its
recommendations in terms of the radf with the caveat that
limit for the absorbed dose due to neutron radiation should be
one-tenth the limit for x; gamma, or beta radiation.
Second,, the recommendations of both organizations introduced
the concept of critical organs tissues. This concept was
intended, to ensure that no tissue or organ, with exception of
the skin, would receive a dose in excess of that allowed for the
whole body. At the time, scientific evidence was lacking on
tissues organs. Thus, all blood-forming organs were
considered critical and were limited to the exposure as the
Third, the NCRP recommendations included the suggestion that
individuals under the age of 18 receive no than one-tenth
exposure allowed for adults. The reasoning behind
particular recommendation is interesting, as it reflects clearly
the limited knowledge of the times. The scientific evidence
indicated a clear relationship between accumulated
genetic effect. However, this evidence obtained exclusively
from animal studies that had been conducted with ranging
2 Defining the exact relationship between exposure, absorbed
dose, and do-se equivalent is beyond the scope of this document,
In simple terms, the exposure is a. measure of the charge induced
by x and radiation in air. Absorbed dose is a measure of
the energy per unit mass imparted to matter by radiation. Dose
equivalent is an indicator of the effect on an organ or tissue by
weighting the absorbed dose with a quality factor, Q, dependent
on the radiation type and energy. The customary units for
exposure, absorbed dose, and dose equivalent are the roentgen,
rad and rent, respectively. Over the range of energies typically
encountered, the exposure, dose and dose equivalent from x and
radiation have essentially the values in these units.
For beta radiation, the absorbed dose and dose equivalent are
generally equal also. At the time of these recommendations, a
quality factor of 10 was recommended for alpha radiation. Since
1977, a quality factor of 20 has primarily been used, i.e., for
alpha radiation, the dose equivalent is 20 times the absorbed
2-4
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25 to thousands of rads. no evidence, from
than 25 accumulated dose, the
interpretation of animal data the implications for
unclear did not a specific permissible close*
The did that genetic on
accumulated than previously believed,
that exposure for periods to permissible
limit (1.0 R/week) did in
effects, MCRP it not to
the occupational limit to provide additional protection
that provided by reduction in permissible limit
of 0*3 R/week, At time, it Halting
exposure of individuals under of 18 to that they
did not accumulate a genetic that would later preclude their
employment as radiation workers. The factor of ten rather
arbitrary but was believed to be sufficient to protect the future
employability of all individuals (NCRP54)»
Fourth, the concept of a tolerance dose replaced by
concept of a maximum permissible dose. The in terminology
reflected the increasing awareness that any radiation exposure
might involve some risk that repair mechanisms might be less
effective than previously believed. Therefore, concept of a
maximum permissible dose (expressed, as dose per unit of time)
adopted because it better reflected, the uncertainty in our
knowledge than did the concept of tolerance dose. The
permissible defined as the level of exposure
entailed a small risk compared with those posed by other hazards
in life (ICRPSl),
Finally, in explicit recognition of the inadequacy of our
knowledge regarding effects of radiation of
possibility that any might have potential for ham,
the recommendations included an admonition that every effort
should be to reduce exposure to all kinds of ionising
radiation, to the lowest possible level. This concept,
originally as ALAP (as low as practicable) later as ALARA (as
low as reasonably achievable), would become a cornerstone of
radiation protection philosophy.
During the 1950*s, a great deal of scientific evidence on
the effects of radiation available from studies of radium
dial painters, radiologists, survivors of
dropped on Japan. This evidence suggested that genetic effects
and long-term somatic effects were more important at low doses
than previously considered. Thus, by the late 1950SS; ICRP
and recommendations were again revised (ICRP59, .
These revisions include the following major changes: the maximum
permissible occupational dose for whole body exposure and the
roost critical organs (blood forming organs, gonads,
larger lens of the eye) lowered to 5 rems/y, with a quarterly
limit of 3 rents; the .limit for exposure of other organs
at 30 rems/y»• internal exposures controlled by a
comprehensive of permissible concentrations of
2-5
-------
radionuclides in air and water on roost restrictive
of a young worker; recommendations Included for
nonoccupationai for the general population (for
first time).
The lowering of the maximum permissible whole-body from
0.3 rad/week to 5 rems/fr with a quarterly limit of 3 rams,
reflects both the new evidence, the uncertainties of time.
Although no adverse effects had been observed
had received the maximum permissible of 0.3 rad/weeK, there
was concern that the lifetime accumulation of as much as 750
(15 rads/y times 50 years) too much. Lowering maximum
permissible dose by a factor of three believed to provide a
greater margin of safety. At the time, operational
experience showed that a limit of 5 rems/y could be met in most
instances, particularly with the additional operational
flexibility provided by expressing the limit on an annual
quarterly basis,
The recommendations given for nonoccupational were
based on concerns about genetic effects. The evidence available
suggested that genetic effects were primarily on the
total accumulated dose. Thus, having sought the opinions of
respected geneticists, the ICRP and the NCRP adopted the
recommendation that accumulated gonadal to 30 be limited
to 5 rents from sources other than natural background medical
exposure. As an operational guide, the NCRP that the
maximum dose to any individual be limited to 0,5 rem/y, with
maximum permissible body burdens of radionuclides (to control
internal exposures) set at one-tenth that allowed for radiation
workers. These values were derived from consideration of
genetically significant to the population
established "primarily for the purpose of keeping
'to whole population as low as reasonably
not because of the likelihood of specific injury to the
individual" (NCRP59).
In the late 1950!s and early 1960!s, the and again
lowered the maximum permissible dose limits (ICRP65, NCRP71).
The considerable scientific data on the effects of to
ionizing radiation were still inconclusive with to
dose response relationship at low exposure levels; thus, both
organizations continued to stress the need to all
to the lowest possible level,
The NCRP ICRP the following similar
recommendations:
o Limit the dose to the whole-body,, red bone marrow, and
gonads to 5 in any year, with a retrospective
limit of 10 to 15 rems In any given year as long as
total accumulated dose did not exceed 5X(N~18), where N
is the age in years.
2-6
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o Limit to the skin, hands,
75, snd 30 rents psir year, respectively.
o Limit the to any other organ or tissue to 15
per year.
o Limit the average dose to the population to 0,1?
per year.
The scientific the protection philosophy on
which the above recommendations were based forth, in
detail in NCRP71. In the case of occupational exposure limits,
the goal of protection was to ensure that the risks of genetic
somatic effects were small enough to be comparable to the
risks experienced by workers in other safe industries. The
numerical limits recommended were based on the linear, no-
threshold, dose-response model and were believed to represent a
level of risk that was readily acceptable to an average
individual. For nonoccupational exposures, the goal of
protection was to ensure that the risks of genetic or somatic
effects were small compared with other risks encountered in
everyday life. The derivation of specific limits was complicated
by the unknown dose-response relationship at low exposure levels
and the fact that the risks of radiation exposure did not
necessarily accrue to the individuals who benefited from the
activity responsible for the exposure. Therefore,, it was
necessary to derive limits that adequately protected member
of the public and to the gene pool of the population as a whole,
while still allowing the development of beneficial uses of
radiation and radionuclides.
In 197?, the ICRP made a fundamental change in its
recommendations it abandoned the critical organ concept in
favor of whole-body effective equivalent
concept for limiting occupational exposure (ICRP77). The change,
to reflect an increased understanding of the differing
radiosensitivity of the various organs and tissues, did not
affect overall limit of 5 rents per year for workers, but
included a recommendation that chronic exposures of the general
public from all controllable sources be limited to no more than
0.5 rem/y to critical groups, which should result in average
exposures to the public of less than 0.1 rem/y.
Also significant, ICRP's 1977 recommendations the
first explicit attempt to relate and justify permissible
radiation exposures with quantitative levels of acceptable risk,
Thus? average occupational exposures (approximately 0.5 rem/y)
equated with risks in safe industries, given as 1.0 £-4
annually. At the maximum limit of 5 rems/y, the risk is equated
with that experienced by workers in recognised hazardous
occupations. Similarly, the risks implied by the nonoccupational
limit of 0.5 rem/y are equated to levels of risk of less than 1.0
£-2 in a lifetime; the general populace's average exposure is
equivalent to a lifetime risk on the order of 1.0 B-4 to 1.0 E-3,
-------
The ICRP believed these levels of risk were in the range that
most individuals find acceptable.
In June 1987, the NCRP revised its recommendations to be
comparable with those of ICRP (NCRP8?). The adopted the
effective dose equivalent concept and its related recommendations
regarding occupational and nonoccupational exposures to
acceptable levels of risk. However^ the NCRP did not a
fully risk-based system because of the uncertainty in risk
estimates because the details of such a system have yet to be
The NCRP recommendations in (KCRP87) for occupational
exposures correspond to the ICRP recommendations, In addition,
the relevant nonoccupational exposure guidelines, which the NCRP
first recommended in 1984 (NCRP84a), are:
o 0.5 rem/y effective whole-body dose equivalent, not
including background or medical radiation, for
individuals in the population when the exposure is not
continuous.
o 0.1 rem/y effective whole-body dose equivalent, not
including background or medical radiation, for
individuals in the population when the exposure is
continuous.
o Continuous use of a total dose limitation system based
on justification of every exposure and application of
the "as low as reasonably achievable" philosophy.
The NCRP equates continuous exposure at a level of 0.1 rem/y
to a lifetime risk of developing cancer of about one in a
thousand. The NCRP not formulated exposure limits for
specific organs, but it notes that the permissible limits will
necessarily be higher than the whole-body limit in inverse ratio
for a particular organ to the total risk for whole-body exposure.
In response to EPA's proposed national emission
for radionuclides, the NCRP suggested that since the 0.1 rem/y
limit is the limit for all exposures from all sources (excluding
natural background and medical radiation), the operator of any
site responsible for more than 25 percent of the annual limit be
required to assure that the exposure of the maximally exposed
individual is less than 0.1 rem/y from all sources (NCRP84bf
NCRP87).
2.3
The wealth of new scientific information on the effects of
radiation that available in the 1950!s prompted the
President to establish an official government entity with
responsibility for formulating radiation protection criteria and
coordinating radiation protection activities. Executive Order
-------
10831 Radiation Council (FRC) In 1959.
Council included representatives all of Federal
agencies concerned with radiation protection as a
coordinating body for all of the radiation activities conducted
by the Federal government. In addition to its coordinating
function, the Council's major responsibility to w..»advise
the President with respect to radiation matters, directly or
indirectly affecting health, including guidance for all Federal
Agencies in the formulation of radiation standards in the
establishment and execution of programs of cooperation with
States..." (FRC60).
The Council's first recommendations concerning radiation
protection standards for Federal agencies were approved by the
President in 1960. Based largely on the work; and recommendations
of the ICRP and the NCRP, the guidance established the following
limits for occupational, exposures:
o Whole-body head and trunk, active blood-forming organs,
gonads, or lens of eye—not to exceed 3 rems in 13
weeks and total accumulated dose limited to 5 times the
number of years beyond age 18.
o Skin of whole body and thyroid—not to exceed 10 rems
in 13 weeks or 30 reins per year.
o Hands, forearms, feet, and ankles---not to exceed 25
rems in 13 weeks or 75 rems per year.
o Bone—not to exceed 0.1 microgram of Ra~226 or its
biological equivalent,
o Any other organ—not to exceed 5 rents per 13 or
15 per year,
Although these levels differ slightly
by NCRP and ICRP at the time, the differences did not
any greater or lesser protection. In fact, the FRC only
accepted the levels recommended by the NCRP for oceugational,
exposure, it adopted • the NCRP's philosophy of acceptable risk for
determining occupational exposure limits. Although quantitative
measures of risk were not given in the guidance, the prescribed
levels were not expected to cause appreciable bodily injury to an
individual during his or her lifetime. Thus, while the
possibility of some injury was not zero? it was expected to be so
low as to be acceptable if there was any significant benefit
derived from the exposure.
The guidance also established dose equivalent limits for
membersofthepublic. These were set at 0.5 per year (whole
body) for an individual and an average of 5 in 30 years
(gonadal) per capita. The guidance also provided for developing
a suitable sample of the population as a basis for determining
compliance with the limit when doses to all individuals
2-9
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unknown, of this population i» - - -eeed
0.1? capita year. population litu „ -. C >• ~ to
any Individual per year considei n - i-jo ...?
background exposure. Natural radiation by a
factor of two to four from location to location.
In addition to the formal exposure limits, also
established as Federal policy that there should be no radiation
exposure without an expectation of benefit, that "every effort
should be made to encourage the maintenance of radiation as
far below this guide as practicable," The to
consider benefits and keep all exposure to a
on the possibility that there is no threshold for radiation.
The linear non-threshold, dose response was to place an
upper limit on the estimate of radiation risk. However, FRC
explicitly recognized that it might also represent level
of risk. If so, then any radiation exposure carried risk,
and it was necessary to avoid all unproductive to
keep all productive exposures as "far below- this guide as
practicable."
In 1967, the Federal Radiation Council issued guidance for
the control of radiation hazards in uranium mining (FRC67). The
need for such guidance was clearly indicated by the
epidemiological evidence that showed a higher incidence of lung
cancer in adult males who worked in uranium with
the incidence in adult males from the locations not
worked in the mines. The guidance established specific exposure
limits and recommended that all exposures be kept as far below
the guide limits as possible. The limits chosen a
tradeoff between the risks incurred at, various exposure levels,
the technical feasibility of reducing the exposurej
benefits of the activity responsible for the exposure.
2,4 THE ENVIRONMENTAL PROTECTION
In 1970, "the functions of the Federal Radiation Council
transferred to the Administrator of the U.S. Environmental
Protection Agency. In 1971, the EPA revised the Federal guidance
for the control of radiation hazards in uranium mining (EPA71).
Based on the risk levels associated with the exposure limits
established in 1967, the upper limit of exposure reduced by a
factor of three. The EPA also provided guidance to Federal
agencies in the diagnostic use of x-rays (EPA78). This guidance
establishes maximum skin entrance doses for various types of
routine x-ray examinations. It also establishes the
that all x-ray exposures be based on clinical indication
diagnostic need,, and that all exposure of patients should be
as low as reasonably achievable consistent with diagnos
need.
In 1981, the EPA proposed new Federal guidance fox
occupational exposures to supersede the i960 guidance {
2-10
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The 1981 guidance follows, upon, the
principles forth by ICRP in 1977. This
adopted as policy In 198? (EPA87).
The Environmental Protection Agency various statutory
authorities and responsibilities regarding regulation of
to radiation In addition to the statutory responsibility to
provide Federal guidance on radiation protection. EPAss
standards and regulations for controlling radiation exposures are
summarized here.
Reorganization Plan No. 3 transferred to the EPA the
authority under the U.S. Atomic Energy Act of 1954, as amended,
to establish generally applicable environmental standards for
exposure to radionuclides. Pursuant to this authority, in 197?
the EPA issued standards limiting exposure from operations of the
light-water reactor nuclear fuel cycle (EPA??). These standards
cover normal operations of the uranium fuel cycle, excluding
aiining and spent fuel disposal. The standards limit the annual
dose equivalent to any member of the public from all phases of
the uranium fuel cycle (excluding radon and its daughters) to 25
mrents to the whole body, 75 mrems to the thyroid, and 25 mrems to
any other organ. To protect against the buildup of long-lived
radionuclides in the environment, the standard also sets
normalized emission limits for Kr-85f 1-129, and Pu-239 combined
with other transuranics with a half-life exceeding one year. The
dose limits imposed by the standard cover all exposures resulting
from releases to air and water from operations of fuel cycle
facilities. The development of this standard took into account
both the maximum risk to an individual and the overall effect of
releases from fuel cycle operations on the population and
balanced these risks against the costs of effluent control.
Under the authority of the Uranium Mill Tailings Radiation
Control Act, the EPA has promulgated standards limiting public
exposure to radiation from uraniun tailings piles (EPA83af
(EPA83b)* Whereas the standards for inactive and active tailings
piles differ, a consistent basis is used for these standards.
Again, the Agency sought to balance the radiation risks imposed
on individuals and the population in the vicinity of the pile
against the feasibility and costs of control.
Under the authority of the U.S. Atomic Energy Act of 1954,
as amended, the EPA has promulgated 40 CFR 191, which establishes
standards for disposal of spent fuel, high-level wastes, and
transuranic elements (EPA82). The standard establishes two
different limits: (1) during the active waste disposal phase,
operations must be conducted so that no member of the public
receives a dose greater than that allowed for other phases of the
uranium fuel cycle? and (2) once the i-epository is closed,
exposure Is to be controlled by limiting releases. The release
limits were derived by summing, over long time periods, the
estimated risks to all persons exposed to radioactive materials
released into the environment. The uncertainties involved in
2-11
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estimating the performance of a theoretical repository led to
this unusual approach, the proposed standard the
agencies responsible for constructing and operating
repositories to to reduce releases below the upper
bounds given in the standard to the extent reasonably achievable.
Under the authority of Atomic Energy Act of 1954, as
amended, and the Toxic Substance Control Act, the EPA is
developing proposed environmental standards for land disposal
of low-level radioactive and certain naturally occurring
and accelerator-produced radioactive wastes. The proposed
standards will establish (1) exposure limits for pre-disposal
management and storage options, (2) criteria for other agencies
to follow in specifying wastes that are Below Regulatory Concern
(BRC), (3) post-disposal exposure limits, and (4) groundwater
protection requirements. The proposed regulations are scheduled
to be published in the Federal Register in late 1988 (GrSS).
Under the authority of the Safe Drinking Water Act, the 1PA
has issued interim regulations covering the permissible levels of
radium, gross alpha and man-made beta, and photon-emitting
contaminants in community water systems (EPA76). The limits are
expressed in picocuries/liter. The limits chosen for man-made
beta and photon emitters equate to approximately 4 mrems/y whole-
body or organ dose to the most exposed individual.
Section 122 of the Clean Air Act amendments of 197? (Public
Law 95-95) directed the Administrator of the EPA to review all
relevant information determine if emissions of hazardous
pollutants into air will or contribute to air pollution
that may reasonably be expected to endanger public health. In
December 1979, EPA designated radionuclides as hazardous air
pollutants under Section 112 of the Act, On April 6, 1983,
published proposed National Emission Standards for radionuclides
for selected sources in the Federal Register (48 CFR 15076} .
Three National Emission Standards for Hazardous Air Pollutants
(NESHAPS), promulgated on February 6, 1985, regulated emissions
from Department of Energy (DOE) and non-DDE Federal facilities,
Nuclear Regulatory Commission (NRC) licensed facilities,
elemental phosphorus plants (FR85a). Two additional NESHAPS,
covering radon emission from underground uranium
licensed uranium mill tailings, were promulgated on April 17,
1985 and September 24, 1936, respectively (FR85b, „
2,5 NUCLEAR REGULATORY
Under the authority of the Atomic Energy Act of 1954, as
amended, the NRC is' responsible for licensing regulating the
use of byproduct, source, special nuclear material, and for
ensuring that all licensed activities are conducted in a manner
that protects public health and. safety. Federal guidance on
radiation protection applies to the NRC? therefore, the NRC must
assure that none of the operations of its licensees a
member of the public to more than 0,5 rem/y. The limits
•12
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by EPAfs standard for uranium fuel cycle facilities
also apply to fuel cycle facilities licensed by MRC,
These facilities prohibited from releasing radioactive
effluents in that would result in greater than the
25 mrems/y limit by that standard.
The NEC its statutory authority by imposing a
combination of design criteriar operating parameters; and license
conditions at of construction licensing. It assures
that the license conditions fulfilled through inspection•and
enforcement. The licenses than 7,000 of
radioactivity. The regulation of fuel cycle licensees is
discussed separately from regulation of byproduct material
licensees.
2.5.1 F-UjilCycle Licenses
The NRC does not the term "fuel cycle facilities" to
define its classes of licensees. The term is used here to
coincide with EPA's of the term in its standard for uranium
fuel cycle facilities. As a practical matter, this term includes
the NEC's large source and special nuclear material and
production and utilization facilities. The NRC's regulations
require an analysis of probable radioactive effluents and their
effects on the population near fuel cycle facilities. The NRC
also ensures that all exposures are as low as reasonably
achievable by imposing design criteria and specific equipment
requirements on licensees. After a license been issued,
fuel cycle licensees monitor their emissions and take
environmental to ensure that they the design
criteria and license conditions. For practical purposes, the NRC
adopted the maximum permissible concentrations developed by the
NCRP to relate effluent concentrations to exposure.
'In the 1970's, the NEC formalized the implementation of as
low as reasonably achievable exposure levels by issuing a
regulatory guide for as low as reasonably achievable design
criteria. This coincided with a decision to adopt, as a design
criterion, a permissible dose of S-mrems/y from a single
nuclear electric generating station. The 5 limit applies to
the most individual actually living in vicinity of
the reactor refers to whole-body from external
radiation by air pathway (NRC77).
2.5.2 BroroductJSaterial Licenses
MRCfs licensing and, inspection procedure for byproduct
material is less uniform than that imposed on major fuel
cycle licensees for two reasons: (1) the much larger number of
byproduct material licensees, and (2) their much smaller
potential for releasing significant quantities of radioactive
materials into the environment. The prelicensing assurance
procedures of imposing design reviews, operating practices, and
license conditions prior to construction, and operation are
similar.
2-13
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The protection afforded public of
radioactive materials from facilities vary considerably
because of factors. First, the requirements that NEC
imposes for monitoring effluents environmental radioactivity
are much less stringent for these licensees. If the quantity of
materials handled is small enough, the NRC might not impose any
monitoring requirements. Second, and more important, the level
of protection can vary considerably because the exact point where
the licensee must the effluent concentrations for an area of
unrestricted access is not consistently defined. Depending on
the particular licensee, this area has been defined as the
nearest inhabited structure, as the boundary of the user's
property line, as the roof of the building where the effluents
are vented, or as the mouth of the stack of vent. Finally, not
all users are allowed to reach 100 percent of the maximum
permissible concentration in their effluents. In fact, the NFC
has placed as low as reasonably achievable requirements on many
of their licensees by limiting them to 10 percent of the maximum
permissible concentration in their effluents.
2.6 DEPARTMENT OF ENERGY
The DOE operates a complex of national laboratories and
weapons facilities. These facilities are not licensed by the
NRC. The DOE is responsible, under the U.S. Atomic Energy Act of
1954, as amended^ for ensuring that these facilities are operated
in a manner that does not jeopardize public health and safety.
The DOE is subject to the Federal guidance on radiation
protection issued by EPA and its predecessor, the FRC. For
practical purposes, the DOE has adopted the NCRP's maximum
permissible concentrations in air and water as a workable way to
ensure that the dose limits of 0.5 rem/y whole-body and 1.5
rems/y to any organ being observed. The DOE also a
requirement that all doses be kept as low as is reasonably
achievable, but the contractors who operate the various DOE sites
have a great deal of latitude in implementing policies and
procedures to ensure that ail doses are kept to the lowest
possible level.
The DOE ensures that its operations are within its operating
guidelines by requiring its contractors to maintain radiation
Monitoring systems around each of its sites and to report the
results in an annual summary report. New facilities and
modifications to existing facilities are subject to extensive
design criteria reviews (similar to those used by the NRC}.
During the mid-1970!s, the DOE initiated a systematic effluent
reduction program that resulted in the upgrading of many
facilities and effected a corresponding reduction in the
effluents (including airborne and liquid radioactive materials)
released to the environment.
As a continuation of this program,, DOE has issued proposed
Order 5400,3 "Draft Radiation Protection of the Public and the
2-14
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Environment" several Internal
including procedures for the calculation of internal
to the public guidance on environmental surveillance.
2.7,1
The of Defense operates several nuclear
installations, including a fleet of nuclear-powered submarines
and. their support facilities. The DOD, like other Federal
agencies, comply with Federal radiation protection guidance.
The DOD has not formally adopted any more stringent exposure
limits for members of the public than the 0.5 rem/y allowed by
the Federal guidance.
2»?,2 Center for_Medi_cal^_Dejf_lcgg and Radiological Health
Under the Radiation Control Act of 1968, the major
responsibility of the Center for Medical Devices and Radiological
Health in the area of radiation protection is the specification
of performance criteria for electronic products, including x-ray
equipment and other medical devices. This group also performs
environmental sampling in support of other agencies, but no
regulatory authority is involved.
2.7.3 Mine Safety and Health Administration
The Mine Safety Health Administration (MSHA) has the
regulatory authority to standards for exposures of miners to
radon its decay products and other (nonradiological)
pollutants in mines. The adopted the Federal guidance
for exposure of uranium miners (EPA71). It no authority or
responsibility for protecting members of the general public from
the hazards associated with radiation,
2.7,4 Occupational Safety, and Health Administration
The Occupational Safety arid Health Administration (OSHA) is
responsible for assuring a safe workplace for all workers. This
authority, however, does not apply to radiation workers at
government-owned or NRC-licensed facilities. This group
have the authority to set exposure limits for workers at
unlicensed facilities, such as particle accelerators, but it does
not have any authority to regulate public exposure to radiation.
OSHA adopted the occupational exposure limits of NRG,
except it not imposed the requirement to keep all doses as
low as is reasonably achievable.
2.7.5 Departaent Qj_T.r_ang..p_or^ta,!ti_Qn
The Department of Transportation (DOT) has statutory
responsibility for regulating the shipment and transportation of
2-15
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radioactive, materials. This authority includes the
responsibility to protect public to radioactive
materials while they are in transit, For practical purposesf the
DOT implemented Its authority through the specification of
performance standards for shipment containers and by setting
maximum rates at the surface of any package containing
radioactive materials. These limits were set to assure
.iance with the Federal guidance for occupational exposure,
they are believed to be sufficient to protect the public from
exposure. The DOT also controls potential public exposure by
managing the routing of radioactive shipments to avoid densely
populated areas.
2.8
States have important authority for protecting the public
from the hazards associated with ionizing radiation. In 26
states, the states have assumed NRC's inspection, enforcement,
and licensing responsibilities for users of source and byproduct
materials and users of small quantities of special nuclear
material. These "NRC Agreement States," which license and
regulate more than 11,500 users of radiation and radioactive
materialsf bound by formal agreements to adopt requirements
consistent with those imposed by the NRC. The NRC continues to
perform this function for all licensable uses of the source,
byproduct, and special nuclear material in the 24 states that are
Monagreement states, as well as NRC Agreement States,
regulate the exposures to workers from electronic sources of
radiation. Also, all states retain the authority to regulate the
of naturally occurring (i.e., radium) and accelerator-
produced radioactive materials.
2-16
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EPA77
EPA78
EPA81
EPAS3J3
EPA87
FRSSa
FR85b
FRC60
U.S. Environmental Protection Agency, "Radiation
Protection Guidance for Federal Agencies: Underground
of Ore," Federal .......... Eegister 36(132), July
9, 1971.
U.S. Environmental Protection Agency, lla/tj;^!!^],,,,^!!^^!®
EPA~570/9-76~003(,
1976.
U.S. Environmental Protection Agency , "Environmental
Radiation Protection Standards for Nuclear Power
Operations,11 40 CFR 190, Federal,^egister 42(9),
January 13, 1977.
U.S. Environmental Protection Agency, "Radiation
Protection Guidance to Federal Agencies for Diagnostic
X-Rays,88 Federal Register 43(22), February 1, 1978,
U.S. Environmental Protection Agency, "Federal
Radiation Protection Guidance for Occupational
Exposure," Federal__Regl_ster 46(15), January 23, 1981.
U.S. Environmental Protection Agency, "Environmental
Standards for the Management and Disposal of Spent
Nuclear Fuel, High-Level and Transuranic Radioactive
Wastes/8 40 CFR 191, Federal__J|egister 47(250), December
29, 1982=
U.S. Environmental Protection Agency , "Standards for
Remedial Actions at Inactive Uranium Processing Sites,"
48(590), January 5, 1983.
U.S. Environmental Protection Agency, "Environmental
Standards for Uranium Mill Tailings at Licensed
Commercial Processing Sites; Final Rule," Federal
Register 48(196), October 7, 1983.
U.S. BPA? "Radiation Protection Guidance to Federal
Agencies for Occupational Exposure/' Fed^ral__Register
52 (2822), January 27, 1987,
Federal Register 50, 5190-5200, February 6, 1985.
Federal Register 50 , 15386-15394, April 17, 1985.
51, 34056-34067, September 24, 1986.
Federal Radiation Council, "Radiation Protection
Guidance for Federal Agencies,"
44(02) , May 18, I960.
2-17
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Gr88
1967
,f Report No. 8f
Gruhlke, J.M., Galpin, F.L., and Holcomb, W.F.,
"Overview of EPA's Environmental Standards for the Land
Disposal of LLW and Waste~1988,'» QRP/EPA, for
presentation, at DOEss 10th Annual LLW Management
Conference, Denver, Colorado, August 30 - September 1,
ICRP34 International X~Ray Radium Protection Commission,
"International Recommendations for X-Ray and Radium
Protection/* British j our na l_o£_Rad i pi gg v 1, 695-699,
1934.
ICRP38
ICRP51
ICRP59
1CRP65
ICRP??
NCRP36
HCRP54
NCRP59
NCRP71
International X-Ray and Radium Protection Commission,
"International Recommendations for X-Ray and Radium
Protection," &|iier,.,,.,._J,.,.._.o_f__._£oent ....... and ...... Radium 40, 134-138,
1938.
International Commission on Radiological Protection,
"International Recommendations on Radiological
Protection 1950," Briti^sh^Joiirnal of ............ Radiology; 24 , 46-
53, 1951,
International Commission on Radiological Protection,
RecommenAatiQns^Qf^t^ie. ....... ICRP 1958, ICRP Publication 1,
Pergaition Press, Oxford, 1958,
International Commission on Radiological Protection,
Re^gjamengS^tion.g.---of the ICRP 1965, ICRP Publication 9,
Pergamon Press/ Oxford, 1965.
International Commission on Radiological Protect ion ,
, ICRP Publication 26,
Pergamon Press, Oxford, 1977.
Advisory Committee on X-Ray and Radium Protection, X~
NCRP Report No, 3f 1936.
National Commi-ttee on Radiation Protection, Permissible
Pg_g_e. ........... From ....... External. Sour ces Q f „ I on 1.2. ing Rad i at ion ,
National Bureau of Standards Handbook 59, 1954,
National Committee on Radiation Protection, Maximuia
£erniis,si_b.l e_Boci¥__.__.Biird_ensT and M^x_iinun!i..Perin_i_s_sibl_e
Concent r a t Lons _of ...... Rad.ionucl ides in ...... ...... Air and in Water for
Qccupat ijonal__Ejcp.osur.e , National Bureau of Standards
69, 1959.
National Council on Radiation Protection and
Measurements, Basic Radiation JPrptection Criteria. NCRP
Report No, 39, 1971.
2-18
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HCRP84a Rational Council on Radiation Protection
JMBfellJlilLJ^^^ NCRP 77,
15, 1984,
NCRP84b National Council on Radiation Protection and
Measurements, OOTtyro]LJ2J^^
Radlonuclides, September 18, 1934.
NCRP87 National Council on Radiation Protection
Measurements, Recommendations on ..Limits..::._fo.riJExp.Qsure to
Xonj=zlng__M4iatJ:onf NCRP Report 91, June 1, 1987.
NRC77 U.S. Nuclear Regulatory Commission^ 1977, Appendix I:
10 CFR 50, Federal Register 44, September 28, 1979.
2-19
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3.
The adverse biological reactions associated with ionizing
radiations, and hence with, radioactive materials,
carcinogenlcity, mutagenicity, and teratogenicity,
Carcinogenicity is the ability to produce cancer. Mutagenicity
is the property of being able to induce genetic mutation, which
may be in the nucleus of either somatic (body) or germ
(reproductive) cells. Teratogenicitf refers to the ability of an
agent to induce or increase the incidence of congenital
malformations as a result of permanent structural or functional
deviations produced during the growth and development of an
embryo (these are more commonly referred to as birth defects).
Ionizing radiation causes injury by breaking constituent
body molecules into electrically charged fragments called "ions"
and thereby producing chemical rearrangements that may lead to
permanent cellular damage. The degree of biological damage
caused by various types of radiation varies according to how
close together the ionizations occur. Some ionizing radiations
(e.g., alpha particles) produce intense regions of ionization.
For this reason, they are called high-LET (linear energy
transfer) particles. Other types of radiation (such as
high-energy photons [x~rays]) that release electrons that cause
ionization and beta particles are called low-LET radiations
because of the sparse pattern of ionization they produce. In
equal doses, the carcinogenicity and mutagenicity of high-LET
radiations are generally an order of magnitude or more greater
than those of low-LET radiations,
Radium, radon, radon daughters, and several other naturally
occurring radioactive materials emit alpha particles,• thus, when
these materials are ingested or inhaled, they are a source of
high-LET particles within the body. Man-made radionuclides are
usually beta and photon emitters of low-LET radiations. Notable
exceptions to this generalization are plutonium and other
transuranic radionuclides, most of which emit alpha radiation.
3.1 EVIDENCE THAT RADIATION IS CARCINOGENIC
The production and properties of x-rays were demonstrated
within one month of the public reporting of Roentgen's discovery
of x-rays. The first report of acute skin injury was made in
1896 (Mo67). The first human cancer attributed to this radiation
was reported in 1902 (Vo02). By 1911, 94 cases of
radiation-related skin cancer and 5 cases of leukemia in man had
been reported in the literature (Up75). Efforts to study this
phenomenon through the use of experimental animals produced the
first reported radiation-related cancers in experimental animals
in 1910 and 1912 (MalQ, Mal2). Since that time, an extensive
body of literature has evolved on radiation carcinogenesis in man
and animals. This literature has been reviewed most recently by
the United Nations Scientific Committee on the Effects of Atomic
Radiation (UNSCEAR) and by the National Academy of Sciences
3-1
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Advisory on Biological Effects of ionizing
(NAS-BE1R
Identification of carcinogenicity of radioactive
emissions followed a parallel course. In 1921, Uhlig first
associated inhaled radioactive -material and carcinogenesis in man
in a study of lung cancer in underground miners in the Erz
Mountains {Uh21J. This association reaffirmed by Ludewig and
Lorenser in 1924 (Lu24). Ingestion of radioactive materials_was
also demonstrated to be a pathway for carcinogenesis in man. As
early as 1925, ingested radium was known to cause bone necrosis
(Ho25), and in 1929, the first report was published on the
association of radium ingestion and osteogenic sarcoma (Ma29)«
The expected levels of exposure to radioactive pollutants in
the environment are too low to produce an acute (immediate)
response. Their effect is more likely to be a delayed response,
in the form of an increased incidence of cancer long after
exposure. An increase in cancer incidence or mortality with
increasing radiation dose has been demonstrated for many types of
cancer in both human populations and, laboratory animals
(UNSCEAR77, 82). Studies of humans exposed to internal or
external sources of ionizing radiation have shown that the
incidence of cancer increases with increased radiation exposure.
This increased incidence, however, is usually associated with
appreciably greater doses and exposure frequencies than those
encountered in the environment. Malignant tumors most often
appear long after the radiation exposure, usually 10 to 35 years
later (NAS80, UMSCEAR82). The tumors appear in various organs.
In the case of internal sources of radiation due to radioactive
materials, the metabolism of the materials generally leads to
their deposition in specific organs, which results in a radiation
dose and higher-than-normal risk of cancer in organs.
Whereas many, if not most, chemical carcinogens appear to be
organ- or tissue-specific, ionizing radiation be considered
pancarcinogenic. According to storer (St75): "Ionizing
radiation in sufficiently high dosage acts as a complete
carcinogen in that it serves as both initiator promoter.
Further,, cancers can be induced in nearly any tissue or organ of
man or experimental animals by the proper choice of radiation
dose and exposure schedule," Radiation-induced cancers in humans
have been reported in the following tissues: thyroid, female
breast, lung, bone marrow (leukemia), stomach, liver, large
intestine, brain, salivary glands, bone, esophagus, small
intestine, urinary bladder, pancreas, rectum, lymphatic tissues,
skin, pharynx, uterus, ovary, mucosa of cranial sinuses, and
kidney (UNSCEAH77, 82; NAS72, 80? Be77, Ka82, Wa83).
Studies of populations exposed to high levels of radiation
have identified the organs at greatest risk following radiation
exposure. Brief discussions of these findings follow.
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1. Atomic Survivors - The survivors of
explosions at Hiroshima Nagasaki, Japan, to
whole-body external radiation, of 0 to 200
rads.1 An international
population since 1950. The recent by
this group (Ka82, WaS3) indicate that an. in cancer
mortality has been shown for many cancers, including
leukemia; thyroid, breast, lung cancer? and
stomach cancer; colon cancer? cancer of urinary organs;
multiple myeloma.
2. Ankyloslng Spondylitics - A large group of patients
given x-ray therapy for ankylosing spondylitis of spine
during the years 1934 to 1954. X-ray usually
100 rad. British investigators have following
group since about 1957. The most recent review of
shows excess cancers in irradiated organs, including
leukemia, lymphoma, lung and bone cancer, and cancer of the
pharynx, esophagus, stomach, pancreas, large
intestine (UNSCEAR88, NAS80).
3. Mammary Exposure - Several groups of
exposed to x-rays during diagnostic radiation of thorax
or during radio-therapy for conditions Involving the breast
have been studied. Although of
followed only a relatively short time (about 15 , a
significant increase in the incidence of cancer
been observed (UNSCEAR88). The dose produced
effects averaged about 100 rads.
4. Medical Treatment of Benign Conditions - several groups
of persons who were medically treated with x-rays to
alleviate some benign conditions have studied.
cancer has developed in many of the organs irradiated (e.g.,
breast, brain, thyroid, probably salivary glands, skin,
bone, and pelvic organs) following ranging
than 10 to more than 100 (UN'SCBARSS) «
has also occurred in some groups. The. followup period for
most groups has been short, often less than 20 years.
5, Underground Miners - Studies of excess cancer mortality
In U.S. underground miners exposed to elevated levels of
radon started in the 1950»s and 1960's. Groups that
worked in various types of mines, including uranium
fluorospar, are being studied in the United States, Canada,
Great Britain, Sweden, China, Czechoslovakia. of
the miners studied have been subjected to high of
exposure; however, a recent review indicates that increased
incidence of lung cancer has been observed in
exposed at cumulative levels approximating those that can
' The rad is the unit of absorbed dose in common use; 1 rad
equals 100 ergs of absorbed energy per gram of material.
3 — 3
-------
high environmental concentrations of
6. Ingested or Inj ected Radium - Workers who
Ra~226 while painting watch clock dials
studied for 35 to 45 years, and patients who received
injections of Ra~226 or Ra~224 for medical
been studied for 20 to 30 years (NAS72, 80).
incidence of leukemia and, osteosarcoma related to Ra-224
exposure has been observed. Calculated cumulative average
doses for these study groups ranged from 200 to 1,700 rads,
A study now underway that deals with exposure levels under
90 rads should provide additional data (NAS80).
7. Injected Thorotrast - Medical use of Thorotrast
(colloidal thorium dioxide) as an x-ray contrast medium
introduced radioactive thorium and its daughters into a
number of patients. Research studies have followed patients
in Denmark, Portugal, Japan, and Germany for about 40 years
and patients in the United States for about 10 years
(UNSCEARSSj NAS8G). An increased incidence of liver, bone,
and lung cancer has been reported in addition to increased
anemia, leukemia, and multiple myeloma (In79). Calculated
cumulative doses range from tens to hundreds of rads.
8. Diagnostic X-ray Exposure During Pregnancy - Effects of
x-ray exposure on the fetus during pregnancy have been
studied in Great Britain since 1954, and several
retrospective studies have been made in the United States
since that time (NAS80, UNSCEAR88). Increased incidence of
leukemia and other childhood cancers have been observed in
populations exposed to absorbed doses of 0,2 to 20 rads in
Utero (NAS80, UNSCEAR88).
all of the cancers induced by radiation fatal. The
fraction of fatal cancers is different for each, type of cancer.
The BE1R III committee estimated the fraction of fatal cancers by
site and (NASSO). Estimates of cancers by site ranged from
about 10 percent fatal in the of thyroid cancer to 100
percent fatal in the case of liver cancer. They concluded that,
on the average, females have 2 times as many total cancers as
fatal cancers following radiation exposure, and males have 1.5
times as many (NASSO)« Although many of the radiation-induced
cancers are not fatal, they still are costly and adversely affect
the person's lifestyle for the remainder of his or her life,,
Just how these costs and years of impaired life should be
weighed in evaluating the hazards of radiation exposure is not
certain. This assessment addresses only the risk of fatal
carcinogenesis.
In addition to the evidence that radiation is a
pancarcinogen, and as such can induce cancers in nearly any
-------
or organ, It also that It can induce cancer by any
of (dermal, inhalation, ingestion, and injection).
Inhalation Is likely to be major route of environmental
exposure to airborne radioactive pollutants, the principal
at risk is likely to be lung, radiation,
to airborne pollutants by the ingestion route is possible,
however, as pollutants arc deposited on soil, on plants, or
in. sources of water, Ingestion of inhaled participates also
occurs. radionuclides may rij.co cause whole-body
radiation exposure while airborne or after their deposition on
the ground.
Estimates of cancer risk on absorbed of .
radiation in an organ or tissue. Given the type of
radiation, the risk for a particular dosage would be the same,
regardless of the source of the radiation. Numerical estimates
of the. cancer risk posed by a unit close of radiation, in various
organs and tissues are presented in Chapter 6. The models used
to calculate radiation doses from a specific source described.
in Chapters 4 and 5.
The overwhelming body of human epidemiological data makes it
unnecessary to major conclusions concerning the risk of
radiation-induced cancers on evidence provided by animal tests;
however, data are relevant to the interpretation of human
(NASSG) contribute additional evidence to
epidemiological database for "humans. Radiation-induced cancers
have demonstrated, in several animal species, including rats,
mice, hamsters, guinea pigsf cats, dogs, sheep, cattle, pigsf
monkeys. Induced through multiple routes of administration and
at multiple dose levels, these cancers have occurred IB several
organs or tissues. These animal studies have provided
information on the significance of dose rate compared with the
of the animals at exposure, the of animals,
genetic characteristics of the test strain, They have shown that
radiation-induced cancers become detectable after varying latent
periods, several years after exposure. The studies
further show that the total number of cancers that eventually
develop varies consistently vith the dose animal receives.
Experimental studies in animals have also established that
carcinogenic effect of high-LET radiation (alpha radiations or
neutrons) is greater than that of low-LET radiation (x-rays or
rays).
A. number of researchers have induced transformations in
mammalian tissue culture, Including embryonic cells of mice and
(Bo84, Ke84r Ha84, Gu84). Chromosome aberrations in
cultured human peripheral lymphocytes have been deiaonstrated at
Rn-222 alpha of about 43 mrads/y with an external gamma
of about 100 mrads/y (Po7?), Another major finding of
recent research (Gu84) is that BNA from radiation-induced
tumors contains an activated oncogene that can transform specific
types of cultured cells when introduced into these cells. The
-------
also found that a difference in only
as for the transformation,
only a small in occurs
as a result of irradiation.
3.2 IS
structure, number; or genetic
content of in a cell nucleus, genetic
radiation effects classified as either mutations or
aberrations. Gene mutations refer to alterations of
of heredity, genes, aberrations
to in normal or structure of
mutation chromosomal aberrations
heritable; therefore, considered together as genetic
effects. Mutations chromosomal aberrations can occur in
(body) or (reproductive) cells. In the. case of germ
cells, mutagenic eiffr i cj radiation is not in those
to ra • .1 j u, but in their descendents.
itions often result in miscarriages or produce such
undesirable changes in a population as congenital malformations
that result in mental or physical defects. Mutations occur in
many types of cells; no tendency toward any specific locus or
identified. .For this reason, they can affect
any chatractenstiLC of a species* A relatively wide array of
aberrations occurs in both humans and animals.
Early experimental studies showed that x-radiation is
c. In 1927, H.J. Muller reported radiation-induced
ancres in animals and in 1928 L«J« Stadlsr reported
in plants (Ki62) , Although, genetic
carried out in the 1930's, mostly in plants fruit flies
(Drosophila), the bulk of the studies on
the of nuclear weapons in World War II
Yery few quantitative data are available on radiogenic
mutations in humans, particularly from low-dose exposures, for
following these mutations are Interspersed over
many generations, so mild they not noticeable, and
that do occur similar to nonmutagenic
effects therefore not necessarily recorded as mutations.
The bulk of data supporting the mutagenic character of ionizing
radiation from extensive studies of experimental animals,
mostly mice (UNSCEAR77, 32; NAS72, 80). These studies have
demonstrated all forms of radiation mutagenesis—lethal
mutations, translocations, inversions,, nondisjunction, point
mutations, etc. Mutation rates calculated from these studies are
extrapolated to (because the basic mechanisms of mutations
believed to be the in all cells) basis for
genetic impact of ionizing radiation on humans
(NAS80, UNSCEAR82). The vast majority of demonstrated
mutations in human germ cells contribute to both increased
mortality illness (NAS8G, HNSGEARS2). Moreover,
-------
radiation protection community is generally in
probability of inducing genetic linearly with.
dose and that no "threshold" is required to initiate
heritable damage to germ cells.
Considerable evidence has been documented concerning the
production of mutations in cultured cells exposed to radiation,
Such mutations have been produced in Chinese hamster ovary cells,
mouse lymphoma cells/ human diploid fibroblasts, and human blood
lymphocytes. Many of the radiation-induced specific types of
mutations produced in human and Chinese hamster cultured ceils
are associated with structural changes in the X chromosome.
Evidence suggests that these mutations my be largely due to
deletions in the chromosomes,
Mutagenicity in human somatic cells has been demonstrated on
the basis of chromosome aberrations detected in cultured
lymphocytes. Chromosome aberrations in humans have been
demonstrated in lymphocytes cultured from persons exposed to
ingested Sr~90 and Ra~226 (Tu63); inhaled/ingested Rn-222,
natural uranium, or Pu-239 (Br77) »* or inhaled Rn-222 (Po78) ; and
in atomic bomb survivors (Aw78). Although no direct evidence of
health impact currently exists, these chromosome aberrations
demonstrate that mutagenesis is occurring in somatic cells of
humans exposed to ionizing radiation.
Evidence of mutagenesis in human germ cells (cells of the
ovary or testis) is less conclusive. Studies have been made of
several populations exposed to medical radiation? atomic bomb
survivors, and a population in an area of high background
radiation in India (UNSCEAR7?), Although these studies suggest
an increased incidence of chromosomal aberrations in germ cells
following exposure to ionizing radiation, the data not
convincing (UNSCEAR7?). Investigators who analyzed the data on
children born to survivors of the atomic bombings of Hiroshima
and Nagasaki found no statistically significant genetic effects
due to parental exposure (Ne88, ScSl, Sc84). They did find,
however, that the observed effects are in the direction of
genetic damage from the bomb radiation exposure.
The incidence of serious genetic disease due to mutations
and chromosome aberrations induced by radiation is referred to as
genetic detriment. Serious genetic disease includes inherited
ill health, handicaps, or disabilities. Genetic disease may be
manifest at birth or may not become evident until some time in
adulthood. Radiation-induced genetic detriment includes
impairment of life, shortened life span, and increased
hospitalization. Estimates of the frequency of radiation™induced
genetic impairment are presented in Chapter 6 of this document.
Although the numbers represent rough approximations, they are
relatively small in comparison with the magnitude of detriment
associated with spontaneously arising genetic diseases
(UNSCEAR82).
3-7
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3.3 IS
Teratogenicity Is the malformation of tissues or of a
fetus resulting physiologic biochemical
Radiation is a well-known teratogenic agent. Case reports of
radiation-induced teratology were made as early as 1921 (St21).
By 1929, an extensive review of a series of pregnancies yielded
data indicating that 18 of the children born to 76 irradiated.
mothers had abnormally small heads (microcephaly) (Mu30).
Although the radiation dose in these cases is not known, it
high.
Early experimental studies (primarily in the 1940's and
1950!s) demonstrated the teratogenic properties of x-rays in
fish, amphibia, chick, mouse, and rat embryos (Ru53). These
experiments showed that the developing fetus is much more
sensitive to radiation than the mother and provided data on
periods of special sensitivity and dose-response. The
malformations produced in the embryo depend on which cells,
tissues, or organs in the fetus are most actively differentiating
at the time of radiation. Embryos are relatively resistant to
radiation-induced teratogenic effects during the earliest stages
of their development and are most sensitive during development of
the neuroblast (these cells eventually become the nerve cells)„
These experiments showed that different malformations could be
elicited by irradiating the fetus at specific times during its
development.
Substantial evidence points to the ability of radiation to
induce teratogenic effects in human embryos as well. In a study
of mental retardation in children exposed in utero to atomic bomb
radiation in Hiroshima and Nagasaki, researchers found that
damage to the child appears to be related linearly to the
radiation dose that the fetus receives (GtB4, Du88),
greatest risk of damage occurs at 8 to 15 weeks, which Is
time the nervous system is undergoing the most rapid
differentiation and proliferation of cells. They concluded that
the age of the fetus at the time of exposure is the most
important factor in deter- mining the extent and type of damage
from radiation. A numerical estimate of mental retardation risk
due to radiation is given in Chapter 6.
3.4 UNCERTAINTIES
Although much is known about radiation dose-effect
relationships at high-level doses, uncertainty exists when
dose-effect relationships based on direct observations are
extrapolated to lower doses, particularly when the dose rates are
low. As described in Chapter 6, the range of extrapolation
varies depending on the sensitivity of the organ system. For
breast cancer, this may be as small as a factor of four.
Uncertainties in the dose-effect relationships are recognized to
relate to such factors as differer.css in quality and type of
radiation, total dose, dose distribution, dose rate,
3-8
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radlosensitivlty (including repair mechanisms, sex, variations in
ager organ, and of health.) . The range of uncertainty in
of radiation risk is examined in detail in
Chapters 5, 6 7.
The uncertainties in the details of the mechanisms of
carcinogenesisf mutagenesis, and teratogenesis make it necessary
to rely on considered judgments of experts on the biological
effects of ionizing radiation. These findings, which are well
documented in publications by the National Academy of Sciences
and the United Nations Scientific Committee on the Effects of
Atomic Radiation, are used by advisory bodies such as the
International Commission on Radiological protection (ICRP) in
developing their recommendations. The EPA has considered all
such findings in formulating its estimate of the relationship
between radiation dose and response,
Estimates of the risk from ionizing radiation are often
limited to fatal cancers and genetic effects. Quantitative data
on the incidence of nonfatal radiogenic cancers are sparse, and
the current practice is to assume that the total cancer incidence
resulting from whole-body exposure is 1.5 to 2,0 times the
mortality. In 1980, the NAS-BEIR Committee estimated the effects
of ionizing radiation directly from epidemiology studies on the
basis of both cancer incidence and the number of fatal cancers
induced per unit dose (NAS80)* The lifetime risk from chronic
exposure can be estimated from these data, either on the basis of
(1) relative risk (i.e., the percentage of increase in-fatal
cancer)r or (2) absolute risk (i.e., the number of excess cancers
per year at risk following exposure). The latter method results
in numerically smaller estimated risks for common cancers, but a
larger estimated risk for rare cancers.
3,5 OF RADIATION IS A
Radiation has been shown to be a carcinogen, a mutagen, and
a teratogen. At sufficiently high doses, radiation acts as a
complete carcinogen, serving as both initiator and promoter.
With proper choice of radiation dose and exposure schedule/
cancers can be induced in nearly any tissue or organ in both
humans and animals. At lower doses, radiation produces a delayed
response in the form of increased incidence of cancer long after
the exposure period. This has been documented extensively in
both humans and animals. Human data are extensive and include
atomic bomb survivors, many types of radiation-treated patients,
underground miners, and radium dial workers. Animal data include
demonstrations in many mammalian species and in mammalian tissue
cultures.
Evidence of mutagenic properties of radiation comes mostly
from animal data, in which all forms of radiation-induced
mutations have been demonstrated, mostly in mice* Tissue
cultures of human lymphocytes have also shown radiation-induced
3-9
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mutations, Limited that not, more sensitive
from studies of the A-bomb survivors in Japan.
Evidence that radiation is a teratogen has been demonstrated
in animals in humans. A fetus is most sensitive to radiation
during the early stages of organ development (between 8 and 15
weeks for the human fetus). The radiation-induced malformations
produced depend on which cells are most actively differentiating.
In conclusion, evidence of the mutagenic and teratogenic
properties of radiation in man is strong, and for carcinogenesis,
the evidence is overwhelming and well quantified at moderate
doses.
3-10
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JjI_At^y1c_^Boj^__SMI3!livor:aA.
TR 12-77, Radiation
Effects Research Foundation, Japan, 1978,
G.W., Kato, H,, and Land, C.E.,
tic* Boittb Survivors. 1950~1974 Life
Span Study Report. 8, TR 1-77", Rad'iation~Ef fects'
Research Foundation, Japan,- 1977,
Bo84 Borek; c., et al., "Inhibition of X~ray Ultraviolet
Light-Induced Transformation in Vitro
Modifiers Poly (ADP-ribose) Synthesis,
Research 99:219-227,
Br77 Brandoffl, W.F., et al., "Somatic Cell Chromosome Changes
in Humans Exposed to 2j9Pl.utGii.ium and 222Radon,"
Contract No. 1(29-2)-3639, Progress Report, July 1,
1976, through September 30, 1977, Department of Energy,
Washington, D.C., 1977.
Ca80 Carter, C.O., "Some Rough Estimates of the Load From
Spontaneously Arising Genetic Disorders ^!l
submitted to the U.N. Scientific Committee on the
Effects of Atomic Radiation, September 1980.
Du88 Dunn, K., H. Yoshimaru, M, Otakef J.F. Annegersf
W. J. Schu 11, PjEenjM^aJLJSSSOjsr^^
and_Jub^^gMMIJL_5sz^ljJEiie^ ( Technica 1
Report TR 13-83, Radiation Effects
Foundation, Hiroshima, 1988.
Gu84 Guerrero, I., "Villasante,- A., Corces, V., Pellicer
A., "Activation of a c-K-ras Oncogene by Somatic
Mutation in Mouse Lymphomas Induced by
Radiation," Science. 225, 1159-1162, 14,
HaS4 Han, A., Hill, C.K., and Elkind, M.M., "Repair
Processes and Radiation Quality in Neoplastic
Transformation of Mammalian Cells,
99, 249-261,
Ho25 Hoffman, F.L., "Radium
J.A.M«.A. 85, 961-965, 1925.
In79 International Meeting on the Toxicity of Thorotrast
Other Alpha-Emitting Heavy Elements, Lisbon, June 1977,
EjiyLirQjnmejDjbal_Research 18, 1-255, 1979.
3-11
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Kato, H., and Schull, W.J., "Studies of the Mortality
of A-Bomb Survivors," Report 7 Part l, "Cancer
Mortality Atomic Survivors, 1950-78,"
90, 395-432, 1982.
Kennedy, A.R., Little, J.B., "Evidence a
Second Event in X-ray Induced Oncogenic Transformation
in Vitro Occurs During Cellular Proliferation,11
Ki62 King,. R.C., Genetj-Cjs, Oxfox'd University Press f
Lu24 Ludewlg, P., and Lorenser, E., "Untersuchung der
Gruhertiuft in dan Schneeberger Gruben auf den Gebait an
Radiumemanation," Zschr._£,_._Pli^s,«, 22, 178-185, 1924.
MalO Marie, P., Clunet, J. , Raulot-Lapointe, G.,
"Contribution a L* etude du Developpement Tumeurs
Malignes sur les Ulceres de "Roentgen," Bulli^Ajisoc^
E ±ude_Ca: nc e^r , 3f 404, 1910^" cited in
Mal2 Marie, P., Clunet, J., Raulot-Lapointe, G. „
"Nouveau de Tumeur Maligne Provoquee par
Radiodermite Experimentale Chez let Rat Blanc,"
Asscsc,. _ Fraiic_.__^tude_Cancer 5, 125, 1912, cited in
UNSCEAR77.
Mart land, H.S., and Hu.rriphri.es,, E.E»f "Osteogenic
Sarcoma in Dial Painters Using Luminous Paint,"
7, 406-417, 1929,
Morgan, K.Z., and Turner, J.E., Pjtin£jjg].es_j2i^
EEOtection, John Wiley and Sons,. Inc., fork, 1967,
Mu30 Murphy , D.P., and DeRenyi, M.; "Post-Conception Pelvic
irradiation of the Albino Rat (Mus norvegicus) : Its
Effect on the Offspring," Sujr5^ryJ_Gyjne^oJ;p^y_and
50, 861-863, 1930.
National Academy of Sciences - National Research
Council , TJXe_J3JLf^c^^
,&ev^s_,^J_lOTij^jig,^i4il.M-OIlf Report of Committee
on the Biological Effects of Ionizing Radiations (BEIR
Report), Washington, D.C., 1972,
National Academy of Sciences ~ National Research
Counc i 1 , Thejg fjecjts_joji_Popu31
Committee on the
Biological Effects of Ionizing Radiation, Washington,
D.C., 1980.
3-12
-------
National of - national
Council , Health ........... Rigks ........... of JRacjorL ..... anci ........ Other; ......... Internally
DeBOsited_^lEhajrlaitters, iv, national
Press , Washington ? D.C., 1988.
Neel, J.V., Schull, W.J., Awa, A.A. , Satoh, c., Otakef
M. r Kato, H. r Yoshiraato, Y., iBplications. ...... o,f .jthe
Hiroshima. -,
_
of ._..the,.,Htima:Q=,__>'poiibl.lpg ..... Dose," ...... Qf_Ra.djajbiQng
Presentation at XVI the International Congress of
Genetics , Toronto, 1988.
Ot84 Gtake, M. , and Schull W. , Mental ....... Retardation.,.. in
Children Exposed in. ...... Utero_,.,to .the Atomic .Bombs; ......... _ ..... A
Reassessment , Technical Report RERF TR 1-83, Radiation
Effects Research Foundation, Japan, April 1984.
Po77 Pohl-Ruling, J., Fischer, P., and Pohl, E., "Einfluss
Erhohter Umweltradio-Aktivitat and Beruflicher
Strahlen-Belastung auf die Chromosomen-Aberrationen in
den Lymphocyten des Peripheren Blutes," Tagungsaber ,
Osterr . -Ungar , Tagung uber biomedizin, Forschung,
Seibersdorf, September 1977.
Po78 Pohl -Ruling, J,, Fischer, P., and Pohl, E., "The
Low-Level Shape of Dose Response for Chromosome
Aberrations," IAEA-SM-224/403, presented at
Internatinal symposium on the Latent Biological Effects
of Ionizing Radiation^ IAEA, Vienna, 1978,
Ru53 Rugh, R. , "Vertebrate Radiobiology: Embryology," Ann.
Rev. Mud. Sci. 3, 271-302, 1953.
ScSl Schiall, W.J., Otake, M. , and Neel, J.V. , "Genetic
Effects of the Atomic Bombs : A Reappraisal," Science
213, 1220-1227, September 1981.
Sc84 Schull, W.J, and J.K. Bailey, "Critical Assessment of
Genetic Effects of Ionizing Radiation on Pre- and
Postnatal Development," pp. 325-398, im Issues and
Reviews in Teratology , Volume 2, H, Kalter, editor.
Plenum Press, New Yorlc? 1984.
St21 Stettner^ E., "Bin Weiterer Fall einer Schadingung
einer Menschichen Frucht durch Roentgen Bestrahlung,
Jb. Kinderheitk, " Phys. Erzieh.... 95, 43-51, 1921.
St75 Storerf J.B., "Radiation Carcinogenesis , " Cancer 1,
pp. 453-483= F.F. Becker, editor, Plenum Press, New
York, 1975.
3-13
-------
Tr?7 Trimbi'j, B.K., Smith, M.E., Incidence of
Iv,, Disease the Impact on of an Altered,
Mutation Rate,11 CmiadiMLjIou£nal_o£_GenetJ^ CyJ:olocgf
19, 375-385, 1977.
Tuscany, R., and Klener, ¥., "Pokles Euploidie v
Kostni Drene osob s Vnitrni Kontamlnaci
Nekterymi Radioisotopy," Cisk. Fysio_l_._ 12, 3911 1963.
Uhlig, M., "Uber den Schneeberger Lungenkrefas,
ws,M Arch. Pathol. Anat. 230, 76-98, 1921,
UNSCEAR58 United Nations Scientific Committee Report on the
Effects of Atomic Radiation, Official Records:
Thirteenth Session, Supplement No. 17(A/3838), United
Nations, New York, 1958.
0NSCEAR77 United Nations Scientific Committee on the Effects of
Atomic Radiation, Sources and E.ffect;s___o£=3IiOni-Z-..lng
Radiation. United Nations, New York, 1977.
United.Nations Scientific Committee on the Effects of
Atomic Radiation, Ionizing Radiation;Sources and
Bio1ogica1 Eff&cts, United Nations, New York, 1982.
UNSCE&R88 United Nations Scientific Committee on the Effects of
Atomic Radiation, Sources, E f f ect s and Risks,..., o.f
Ion iz at ioo__RM Ja t ion _, 1988 Report to the genera 1
Sales No. #. 88. IX, 7, United National, New
York, 1988,
Up75 Upton, A.C., "Physical Carcinogenesis: Radiation--
History and Sources," Cancer 1, 387-403, F.F. Becker,
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Vo02 Von Frieben, A,, "Demonstration Linas Cancroids des
Rechten Handruckens, das sich nach Langdauernder
Einwirkung von Rontgen-strahlen Entwickelt Hatte,"
jte^.chr;..j.j_Gel3>_._..iRojitgenstr,j 6, 106, 1902, cited in Up75,
Wakabayashi, T., et al., "Studies of the Mortality of
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Nagasaki," RaJla^_Res., 93, 112-146, 1983.
3-14
-------
c
When radloniaclides are released to the air, they a
number- of pathways leading to human exposure.
environmental pathways are shown in Figure 4-1.
Radionuclldes, released in the of particulates or
gases, form a plume that disperses down wind (Section 4.2),
These radibnuclides in the air can directly affect people in
ways: through, external dose caused by photon
plume, or through internal dose resulting from radionuclide
inhalation. As the airborne radionuclides move from the point of
release, they (especially those in particulate form) deposit on
ground surfaces and vegetation as a result of dry deposition and
precipitation scavenging (Section 4.3). Photon radiation from
the radionuclides deposited on the ground contributes to
external doses. Finally, small fractions of the radionuclides
deposited on plant surfaces and agricultural land enter the food
chains, concentrating in produce and in animal products such, as
milk "and meat (Section 4,4), Consumption of contaminated
foodstuff then contributes to the internal doses of radiation to
individuals.
The concentrations of radionuclides in air, on soil
surfaces, and in food products are calculated using the computer
code AIRDOS-EPA. A description of the code and examples of
its applications, with an overview of the uncertainties,
provided in Section 4.5. (See references Ha82, Ti83? and HCRPS4
for a more detailed description of the processes, modeling
techniques, and uncertainty estimates.)
4.2 DISPERSION OF RADIONUCLIDES THROUGH THE
4.2.1 Introduction
Radionuclides entering the atmosphere are transported away
from their point of release and are diluted by atmospheric
processes. To perform a radiological assessment, it is necessary
to model the long-term average dispersion resulting from these
processes. This is because the sources under consideration
release radionuclides at rates that are substantially uniform
when considered over long periods of time, and because the
somatic and genetic effects on human health are generally treated
as being the result of chronic exposure over long periods of
time.
As large-scale winds move over the earth.'s surface, a
turbulent boundary layer, or mixed layer, is created that
controls the dispersion of the released radionuclides. The depth
and dispersion properties of the mixed layer, which are highly
variable over short periods of time, are controlled by two
l-l
-------
Figure 4-1,
Pathways of airborne radiomiclides
environment.
-------
of turbulent effects; mechanical of
transfer Into or from boundary layer. The
of surface on a
that significant mechanical mixing. The
mixing Is stronger the wind is stronger the
(water, grains of dirt, grass, crops, shrubs
trees, buildings, etc,} larger. The vertical scale
(dimension or thickness) of the mechanical mixing zone Is related
to of roughness elements. Heat transfer into or
layer, second source of turbulent effects,,
strongly layer's turbulent structure and
thickness. Solar heating creates rising bubbles or thermals
near the ground. These large bubbles produce turbulent eddies of
a than those from the mechanical drag of the
surface. With strong solar heating on a clear day, the
mixing layer may be a few thousand meters deep. On a clear, calm
night, the boundary layer virtually disappears, so that
radionuclides {and other pollutants) are dispersed with very
little turbulent diffusion.
The objective of atraospfaeric transport models used by
EPA, is to incorporate the essential physical data necessary to
characterize an extremely complex turbulent flow process into a
simplified Is adequate to predict the long-term
dispersion of radionuclide releases. In general, the data
necessary to Implement a detailed theoretical model of
atmospheric dispersion are not available and would be impractical
to obtain. the data problem, mathematical
complexities difficulties of a direct solution to the
turbulent dispersion problem are profound and beyond the
practical scope of routine EPA regulatory assessments. The
widely accepted alternative has to incorporate experimental
observations into a semi-empirical model, such as outlined below,
that Is practicable to implement.
Three basic meteorological quantities govern dispersion:
direction, wind speed, and stability. Wind direction
determines which way a plume will be carried by the wind; a wind
front northwest moves the plume toward the southeast.
Although wind direction is a continuous variable, wind directions
commonly divided into 16 sectors, each centered on one of the
cardinal directions (e.g., north, north-northeast,
northeast, etc.)- Since there are 16 sectors, each one covers a
22™l/2~degree angle. Wind speed directly influences the dilution'
of radionuclides in the atmosphere. If other properties are
equal, concentration is inversely proportional to wind speed,
Customary wind categories Include 0 to 3 knots (lowest
speed) to greater than 21 knots (highest speed).
Atmospheric stability, the third meteorological quantity,
categorizes the behavior of a parcel of air when it is
adiabatically (without heat transfer) displaced in a vertical
direction. If the displaced parcel would be expected to return
toward its original position; the category is stable; if it would
4-3
-------
to original position? is
conditions of neutral stability, the
be to at its elevation without moving
or from its old one,
Typically, unstable classes are associated with
conditions of very little cloud .cover, low wind speeds^ and a sun
high in sky. The atmosphere is neutral on a windy, cloudy
day or night is stable at the surface at night when sky
is clear and wind are low. Dilution due to vertical
mixing occurs more rapidly with increasing distance under
unstable conditions than tinder stable ones. Stability categories
range from A (very unstable) to D (neutral) to G (very stable) .
A table of joint frequencies (fractions of time) for each
combination of stability, wind direction, and wind speed is the
starting point for any assessment of long-term atmospheric
dispersion. These data are usually obtained by the analysis of
long-term observations from weather stations or from site-
specific meteorological facilities.
4.2.2 Air Pi sper s i cm,,, Mode 1 s
EPA uses an empirical Gaussian model for most radionuclide
dispersion calculations. The model also considers such processes
as plume rise, depletion due to deposition, and radionuclide
ingrowth decay.
Model
The basic workhorse of EPA dispersion calculations is the
Gaussian model. Several reasons why the Gaussian model is of
the most commonly used are quoted below (Ha82) :
M (1) It produces results that agree with experimental data
as well as any model.
(2) It is fairly easy to perform mathematical operations
on this equation.
(3) It is appealing conceptually.
(4) It is consistent with the random nature of
turbulence.
(5) It is a solution to the Fickian diffusion equation
for constants K and u.
(6) Other so-called theoretical formulas contain large
amounts of empiricism in their final stages,
(7) As a result of the above, it has found its way into
most government guidebooks,, thus acquiring a
^blessed1 (sic) status."
4-4
-------
long-term plume
for vertical concentration distribution.
a ground level source, concentration is at
level and decreases with elevation like half of a or
Gaussian distribution. For an elevated releasef
concentration is symmetrically distributed
height of the plume, characteristic of a full Gaussian
distribution. Actually, the vertical dispersion is limited by
the ground surface below and any inversion lid
(see Figure 4-2). An inversion lid is defined by altitude in
the atmosphere where the potential temperature begins to
with increasing height, thus limiting the volume of air available
for diluting releases.
At large distances from the point of the release,
radiomiclide concentration becomes uniformly distributed
the ground and the lid. Within each of the 16 direction sectors,
the concentration is considered to be uniform at any given
distance from the release. For a ground-level release, the
ground-level concentration decreases monotonically with distance
from the release point. For an elevated release, the
ground-level concentration increases, reaches a maximum value,
and then decreases with increasing distance from the release
point.
Mathematically, the long-term average dispersion calculation
used by EPA can be expressed as
X/Q = 2.03
x a, (4-1)
z
where X/Q (s/m ) is the concentration for a unit at
a distance x(ai) from the release point, he(m) is the effective
height of the release, «Jz{m) is the vertical dispersion
appropriate to the stability category and distance x, /i(m/s)
is the wind speed. At distances where the release is uniformly
mixed between the ground and lid, the expression
X/Q = 2V55.. (4-2)
p x ht
where ht(m) is the lid height (meters), and the other quantities
are the same as before.
Plume Ri_se Model
Vertical momentum or buoyancy can cause a plume to rise to
an effective height that is several times the physical of
-------
(HALf OAOCTIA» MA^f
out TO a%oy*ioi
MlXmfl UO ALS
-------
release. The flux of a release is proportional
totfae product of volume flow rate and vertical exit
velocity, while buoyancy flux Is proportional to product
of flow difference
temperatures of the release gases and the ambient air,
rise Is Initially dominant for most plumes, though buoyant
rise important process at larger distances.
In any case, plume rise increases with distance from
point? the effective height of the plume may not reach a limiting
value until the plume is several kiloiaeters from point of
release.
As radionuclides in the plume are dispersed , their activity
is depleted by dry deposition and precipitation scavenging. The
rate of plume depletion clue to dry deposition and precipitation
scavenging is proportional to the deposition rate (see Section
4.3). EPA's Office of Radiation Programs "uses a source depletion
model which considers the shape of the vertical concentration
profile to be unchanged by depletion. Depletion due to
deposition generally does not cause more than half of
released activity to be removed at a distance of 80 km.
Depletion by precipitation scavenging occurs only during periods
of precipitation.
Had I ol og leal. Decay and I ngr owth
Radiological decay can also reduce the radionuclide
concentration in the plume. A typical elapsed time for traverse
between the point of release and a receptor located 80 JOB is
about 5 hours. Thus, only nuclMes with short half -lives would
be appreciably depleted by radiological decay. For example,
argon~41f which has a 1.8 hour half-life, decays to about 15
percent of Its original activity in 5 hours. When a released
radionuclide is a parent for other radionuclides in a chain,
those decay products will become part of the plume's activity
even though they were not released by the source. For example,
cesium-137 is the parent of barium- 13 7m, which, has a half-life of
about 2.6 minutes. The barlum-137m activity would 90
percent of that of the cesium-137 in about 8.5 minutes, time
required at a typical wind speed of 5 m/s for the release to
travel about 2.5 km. For many nuclides, the radiological effects
associated with exposure to decay products are at least as
important as those from exposure to the parent. For example,
external photon dose from a release of cesium-13? Is entirely
to photons from its decay product bariua-137m.
4.2.3 UnjgjgrjL^iiitU^s^_n^.^A^inQ^BLh^ri,g Dispersion ............ ModejLing
EPA must deal with several uncertainties in its modeling of
atmospheric dispersion. Two basic considerations contribute to
these uncertainties. The first involves the parameters that
enter into the model and how well they are known or can be
4-7
-------
a particular situation. is
which the model
uncertainty of predicted concentrations
primarily on uncertainty of the in
calculations* The consideration involves of a
conditions that do not satisfy
the model developed. Such be
only alternative available for
dispersion, but the principal uncertainties
related, to evaluating the significance of these effects that
in model. An example of would be
of Gaussian plume model, which was developed for short
over an open, flat terrain, to assess dispersion over
or in a complex terrain dominated by hills
valleys.
In regard to the first consideration, the authors of HCRP84
concluded that the appropriate basic parameters, such as wind
speed and direction, can be determined accurately enough so that
they not major contributors to model uncertainty. However,
uncertainties associated with derived parameters (such as
stability class) or lumped parameters (such as those used to
characterize deposition, resuspensionf or building wake effects)
can dominate the model uncertainties.
The effect of the uncertainty of an input variable can
strongly or weakly influence the model output depending upon
circumstances. For example^ the effective:height of a release,
he/ be estimated using a plume rise model to within a factor
of 1.4 (NCRP84). From equations 4-1 and 4-2, it is clear
that. ffz is much smaller than he the effect of this
uncertainty on equation 4-1 is strong; whereas at large distances
where equation 4-2 is appropriate, the value of he little
effect on calculated concentration.
Little Miller (Li?9 and Mis2) have surveyed a of
.validation studies of atmospheric dispersion models. Although
studies provide limited data, they indicate an uncertainty
of approximately a factor of 2 for annual average concentrations
for locations within 10 km of the release and approximately a
factor of 4 (77 percent of their samples) to 10 (92 percent of
for locations between 30 and 140 km of the
release. The validation studies were for fairly complex terrain,
i.e., substantial hills and valleys, but not extreme conditions
of either terrain or meteorology.
4.3 OF ATMOSPHERIC RADIONUCLIDES
4.3.1 Introdystion
Atmospheric deposition includes a complex of
that result in the transfer of radionuclides from the plume to
surface vegetation. Processes categorized as
-------
"dry" result in direct transfer
the surfaces in contact with it and "wet" transfer
first from the plume to precipitation
precipitation to the ground or vegetation surfaces,
4.3,2 Dr^LDe-positi._Qn Model
Dry deposition models generally relate the surface
deposition flux to the air concentration at some reference
height, typically 1 meter above the ground. The resulting
equation is
W = Vd X0 (4-3)
where W is the deposition flux to the surface (Ci/m2s), % is the
reference height air concentration (Ci/m3), and vd is the
deposition velocity (m/s). Although vd has the units of a
velocity (hence its name), it is a luaped variable relating the
deposition flux to the air concentration. The value of the
deposition, velocity depends on a complex interaction of
effects—atmospheric, aerosol, and surface (canopy). Thus, while
the deposition velocity is often assigned a simple fixed value,
it actually represents the result of a diverse combination of
effects,
4.3.3 Wet Deposition Model
Wet deposition models relate the flux due to precipitation
scavenging to the concentration in the plume. Since the activity
scavenged from the plume by an element of precipitation is
presumed! to remain with the precipitation element until reaching
the ground surface, the deposition flux is proportional to
total wetted activity in a vertical segment of the plume (Ci/m2) .
The resulting equation can be expressed as
W = Asc jf L (4-4)
where W is the surface flux (Ci/m2s) , x is the average wetted
air concentration (Ci/m3), L is the depth of the wetted layer
(m) , and A is the scavenging rate (s ) . ASC is a variable that
lumps together the complex interactions between precipitation and
the plume. Because the deposition flux is proportional to the
vertically integrated concentration (i.e., the total activity in
a column of unit ground surface area), it is independent of the
effective height of the release. Raising the effective height of
a release may lower the dry deposition flux but leaves the flux
resulting from precipitation scavenging unchanged.
4-9
-------
radionuclides accumulate In soil
until they are removed either by radiological decay or by
processes such as leaching. The"areal concentration can be
expressed as
[i-exp(-Xg tb)]
X (4-5)
,
where Ca is the areal concentration (Ci/m2) , W is the
radionuclide flux to the ground surface (Ci/m2s) , tb (s) is the
time for radionuclide buildup in soils, and AB is the effective
removal rate from soil (s ). When the deposited radionuclide is
the parent of other radionuclides, their soil concentrations at
time tb due to ingrowth from the parent must also be calculated.
For calculating root transfer to crops, the radionuclide
concentration in the surface soil layer can be expressed as
Cs = Ca/P (4-6)
where Cs is the soil concentration (Ci/kg) and P is the areal
density of dry soil (Icg/m2) for the plowed or mixed soil layer.
The value of tb, the deposition accumulation time, is
typically in the range of 20 to 100 years. For nearby individual
assessments, tb is chosen to correspond to the expected
operational life of the facility. If EPA considers it likely
that facility would be replaced by another.sinilar at
that time, then tb is increased accordingly up to a maximum value
of 100 years. Of course, only those environmental concentrations
that depend on soil deposition are affected by the choice of tu.
For collective (population) assessments, a value of 100 years is
used for tb. This value corresponds to establishing a 100-year
cutoff for the time following a release when any significant
intake or external exposure associated with deposition on soil
might take place. Since radionuclide inhalation is generally the
dominant risk pathway, total risk is not sensitive to the choice
of tb.
The value of AB is the sum of the radiological decay
constant, \, and an environmental removal rate for deposited
radionuclides from soil, Ag» Hoffman and Baes (Ho79) considered
a simplified leaching-loss model appropriate to agricultural soil
for calculating Xs. Their range of values for the parameter Kp
(the equilibrium distribution coefficient relating the ratio of
the radionuclide concentration in soil water to that on soil
particles) for cesium is from 36.5 to 30,000 ml/g. The
4-10
-------
ratio of A3 is 820:1. The uncertainty in Ag is
significantly affected by uncertainty in
Although their model is a reasonable one,
its validation do not exist. Since the choice of
values for Ag is so uncertain, EPA has used. 0,2 y"1 as
a nominal value (the geometric mean of Xs for Pu*, I",
Cs , Sr * ions is 1.2X10"2 y"1 using Hoffman and Baes median
data values) a value of 0.1 y"1 for urban settings where
runoff would be expected to increase the effective
4.3.5 Uncertainties
Uncertainties in vd and Xse are substantial? NCRP84 lists
measured values of vd which vary over three orders of magnitude.
Hanna et al. note that "The use of scavenging coefficient for wet
removal modeling is probably best regarded as an order of
Magnitude estimation procedure" (Ha82). Actually, much of the
wide range of values reflects measurement uncertainties as well
as actual variations. Furthermore, most field deposition
measurements reflect short-term or episodic studies rather than
long-term observations. Miller and Little (Mi82) concluded that
the data necessary to quantify the accuracy of calculated ground
concentrations are not currently available,
4=4 TRANSPORT THROUGH THE FOOD CHAIN
4.4.1 introduction
Deposited radionuclides may become associated with
vegetation by two principal routes; (1) direct interception of a
fraction of the deposited activity by plant surfaces, and (2)
transfer of deposited activity from the soil through the plant's
system. Radionuclides in animal feed crops such as pasture
grass or stored feeds can be transferred to foods such as milk
and meat.
4.4.2 Conc6ntratlOTi_JjiJ7e^eiailon
The radionuclide concentrations in plants due to
interception of the deposition flux can be calculated as (Ba?6)
Cv = W [ fr Tv (l-exp(-XE te)]
Yv XE
(4-7)
d
where Cv is the crop concentration (Ci/kg) at harvest, W is the
deposition flux (Ci/m2s) , fr is the fraction of the deposition
flux which the vegetation intercepts, Y is the vegetation yield
4-11
-------
, Ty Is a translocatlon, factor, AE is effective removal
of radionuclide from the vegetation (s~1),
tft Is time of the vegetation to the radionuclide
flux (s) . Miller (Mi79) has observed that data for fr and ¥y are
well by the expression
f= 1 ~ ovn, (~*yY \ /J.~Q\
r — -JL exp | F±VJ (%""&}
where t was found to range between 2,3 and 3.3 vf/'k.g when Yv-is
expressed in kg/m2, dry. Since the product -yYv is generally less
than 1.0, for many practical purposes equation 4-8 can be
approximated as
fp = j Yv (4-9)
In this case, the quantity fr/Yy {4-7} can be replaced by t
which shows much less environmental variation than fr and Yv do
separately. Note that Yy is the total vegetative yield which can
be several times the edible portion yield for a crop. T , the
translocation factor, relates the radionuclide concentration in
the edible portion to that in the entire plant. Baker et al.
(Ba76) suggest a value of 1.0 for leafy vegetables and fresh
forage^ and 0.1 for all other produce. (A value of 1.0 is used
for all crops in AIRDOS-EPA.)
The value for XE is the sum of X , the radionuclide decay
constant and AH, the weathering rate factor. For a typical
weathering half-life of 14 days, AM has a value of 5»7xlG"7 s"1»
In general, the product AE te >1 and equation 4-9 can be
simplified to
(4-10)
Radionuclides also transfer directly from the soil to
vegetation through the plant's root system. The plant
concentration doe to this process can be calculated as
i¥
(4-11)
4-12
-------
Cy is plant concentration at (ci/kg), C is
soil concentration (Ci/kg}, B|V is the element-specific
to factor. The total
is
C,™» /"* „£_ ff^ /A 1 **% \
v - Cv, + Cv (4-12)
Generally, contribution of c^ to C¥ is greater of
C* for atmospherically dispersed radionuclides.
4,4.3 Coflceilti^^
For a concentration Cv (Ci/kg) in animal feed,
concentration in meat Cf (Ci/kg) can be calculated as
Cf = Qf Ff Cv
where Qf is the animal's feed consumption (kg/d) and Ff is
feed to meat transfer factor (d/kg). Fi is element dependent and
represents the average mean concentration at slaughter for a unit
ingestion rate over the animal's lifetime. Most systematic
studies of Ff have been made for cattle or other ruminants,
although a few measurements for other species also
(NCRP84) . In practice, even the Ff values for beef often
based on collateral data (Ba84).
Similarly for milk, the concentration Cm (Ci/L) can be
calculated as
'4-14;
where Fm (d/L) is the equilibrium transfer factor to milk
other parameters are as for equation 4-13, Although
statistical data are available for Fm than for Ff, the estimation
of transfer coefficients to animal pro-ducts is a subject needing
both integration and better documentation (NCRP84)„
4.4.4 Summary
Radionuclide intake through the food chain upon both
the concentration in food and human usage. The concentration in
food upon the food source use of foods grown in proximity
to the release location, the fraction of an individual's food
that Is produced and other factors that can strongly
influence the significance of the food pathway. Unfortunately,
generally useful validation studies to quantify the substantial
uncertainties in the food chain have not been made. References
such as NCRP84, Ti83, Mi82, and Li79 cite ranges for some
4-13
-------
limited model uncertainty & ,t do
quantitative evaluations of for
ingestion pathway as a whole,
«# A, wi
a factor of 10 as a
for the uncertainty in both the deposition model
calculated intake from eating food containing deposited
radionuclides. Assuming that the two factors are independent,
uncorrelated, correspond to the 2 sigma values for a log
distribution, the combined uncertainty for the pathway
{deposition intake of radionuclides from food) is a factor of
26. EPA this value to 30 as an estimate of the
overall food pathway uncertainty factor.
4.5 THE ENVIRONMENTAL CONCENTRATION OF
THE AIRDQS-EPA CODE
4.5,1 Introduction
Environmental concentrations of radionuclides calculated by
EPA may be site specific, meaning that available data relevant to
the site incorporated into the assessment. Or an assessment
may be generic? that is, an assessment of a hypothetical facility
at a location considered an appropriate possibility for such a
facility class. Frequently, EPA performs site-specific
for existing facilities, e.g., a national laboratory.
In addition, EPA often employs generic assessments in evaluating
alternative sitings for a proposed facility or assessing a
class of facilities, e.g., industrial coal-burning
boilers*
In any case, EPA makes both individual collective
(population) assessments. The purpose of the individual
is to doses and lifetime risk to individuals
living a facility. EPA"s assumption is that
individuals reside at the same location much of their lives
that their extend from infancy on through, adulthood*
The risks calculated are expectation values, i.e., the
estimates are intended to -be typical for a person living a long
period of time under the assessed conditions. EPA's collective
(or population) assessments evaluate doses and risks to a
population that may be regional (typically up to 80 Jem distant) ,
long-range (e.g., the coterminous United States), or worldwide as
appropriate. The risk is usually expressed as the expected
of premature deaths in the population per year of facility
operation.
4.5,2 AJRDOS-EPA
the AIRDOS-EPA code (Mo79) to calculate
environmental concentrations resulting from radionuclide
1 exp[2 In2 (10) ]1/2 = 26
4-14
-------
air. The results of this analysis
of air ground surface radionuclide concentrations!
via Inhalation of air; ingestion of radioactivity via
meat, milk, vegetables. The atmospheric
terrestrial transport models used in the code, their
implementation, the applicability of the to different
types of emissions are described in detail in Mo?9. Input to
AIRDGS-EP& is extensive, but Its preparation can be facilitated
by using the preprocessor PREPAR (SjS4), Appendix A of this
document summarizes many of the default values assumptions
used in EPA's assessments,
AIRDGS-1PA calculates atmospheric dispersion
radionuclides released from one to six stacks or sources.
Radlonuclide concentrations in meat, milk; and fresh produce are
estimated by coupling the deposition rate output of the
atmospheric dispersion models with the Regulatory Guide 1,109
(NRC77) terrestrial food chain models. Radionuclide
concentrations for specified distances and directions are
calculated for the following exposure pathways: (1) immersion in
air containing radionuclides, (2) exposure to ground surfaces
contaminated by deposited radionuclides, (3) inhalation of
radionuclides in air, and (4) ingestion of food in the area. The
code may be used to calculate either annual individual exposures
or annual population exposures at each grid location. For either
option, AIRDOS-EPA output tables summarize air concentrations and
surface deposition rates as well as the intakes exposures for
each location. In addition, working level exposures
calculated and tabulated for evaluating the Inhalation of
short-lived progeny of radon-222.
Assessment Grid
provision for either a rectangular or a
circular calculational grid. The customarily circular grid
(see Figure 4-3) has 16 directions proceeding counterclockwise
from north to north-northeast. The user chooses grid
distances. Generally, successive distances with
increasing spacing. It is important to realize that the
calculational grid distances and the set of distances associated
with, population and food production data are and the same.
Hence, the concentration calculated for each grid distance must
be the appropriate average value for the corresponding range of
distances covered by the population arid agricultural data,
Choosing a suitable set of grid distances may require different
compromises of convenience for different assessments be
different for individual and collective assessments of same
facility,
EnvirQnmgnta_l_ Accumula11on Time
An AIRDOS-EPA assessment is based on what can be viewed as a
snapshot of environmental concentrations after the assessed
facility has been operating for some period of time. The choice
-------
X - Assessment grid locations at up to 20 distances
(2 shown) and 16 directions (5 shown)
Figure 4-3. Circular grid system used by AIRDOS-EPA.
t-16
-------
of an accumulation time affects only
on terrestrial concentrations, i.e.,
intakes. Usually, the accumulation for an
individual is chosen to be consistent with
life of facility (or 100 years a similar
facility might be expected to replace the present at the
of its useful life). For collective assessments, 100 is
customarily used*
Point sources are characterized by their physical height
andf when desired., the parameters to calculate buoyant or
momentum plume rise using Brigg's (Br69) or Rupp's (Ru48)
formulations respectively. Alternatively, a fixed plume rise
be specified for each Pasquill-Gifford atmospheric stability
class A through G.
The area source model is similar to that of Cuikowski
Patterson (Cu76) and transforms the original source into an
annular segment with the same area. At large distances,
transformed source approaches a point source at the origin, while
at distances close to the origin, it approaches a circle with the
receptor at its center.
Building wake effects and downwash are not included in
&IRDQS-EPA models. The same type of rise calculation (buoyant,
momentum, or fixed) is used for all sources. As many as six
sources may be assessed, but for calculational purposes, they are
all considered to be co-located at the origin of the assessment
grid.
Releases for up to 36 radionuciides may be specified for
JklRDQS-EPA. Each release is characterized by the radionuclide
name, effective decay constant during dispersion, precipitation
scavenging coefficient^ deposition velocity,, and settling
velocity, as well as the annual activity release for each source.
Decay products that are significant for the assessment of a
radionuclide must be included in the list of releases. There is
no explicit method for calculating radionuclide ingrowth during
atmospheric dispersion in AIRDOS-EPA.
Parameters such as particle size, respiratory clearance
class, and gastrointestinal absorption factor (ft) on
for in the DARTAB (BeBl) dose and risk assessments as
described in Chapters 5 and 6.
The approach ORP has used for calculating a precipitation
scavenging coefficient is based on Slinn's (S177) equation 32j
4-17
-------
where Agc Is the scavenging coefficient, c is a (Si inn
uses 0.5), J0 is the rainfall rate, and E is the collection
efficiency for a particle of radius a by drops of characteristic
radius R^. Slinn (S177, p. 23} considers the effects- of dry
deposition interprets Dana and Wolf fs (Da68f W069, Da?Q) data
as supporting a value for E of 0.2, essentially of
particle size. Adopting Slinn's typical value of R^ for a
frontal rain (0.3 mm) and selecting a long-term average value of
1,000 itm/yr (3.16xlO~5 mm/s) for J0, we obtains
0.3
= 1.05X10"5 S~1
This value has been rounded to 1Q~5 s"1 as a working value
for the precipitation scavenging coefficient and then scaled
according to the annual precipitation at the assessment location
for use in AIRDOS-EP&. There is substantial uncertainty in
interpreting environmental scavenging data, and this estimate is
accurate to within an o-rder of magnitude. The EPA scaling
procedure reflects the premise that the variation of rainfall
from one location to another depends more on rain frequency than
•fe Jt *&
on intensity during rainfall episodes,
Dispersion
Wind and stability class frequencies for each direction are
the primary data for calculating atmospheric dispersion. The
required data for AIRDOS-EPA are calculated from a joint
frequency distribution of wind speed and atmospheric stability
class for each direction. Inasmuch as the assessments require
long-term average dispersion values, the sector-averaged Gaussian
plume option is used. The vertical dispersion parameter (®z) is
calculated using Brigg's formulas (Gi76) « Vertical dispersion is
limited to the region between the ground and a mixing depth lid.
The harmonic mean of Holzworth's (Ho72) morning and afternoon
mixing depths is customarily employed for this value? that is,
4-18
-------
lg I respectively the morning
h£ is their harmonic mean. At large
concentration is uniform between the ground lid.
AIRDOS-EFA models both dry and wet deposition processes.
Resuspension, relntroduction of deposited material Into the
atmosphere, is not modeled in AXRDGS-EPA.. The dry deposition
rate is product of the deposition velocity and the near
ground-level air concentration, while the wet deposition rate is
the product of the precipitation scavenging coefficient and the
vertically integrated air concentration. Wet deposition
decreases monotonically with distance and is independent of the
effective release height of the source , while the effect of
source height can be significant for dry deposition. For
locations close to an elevated source, wet deposition can provide
the principal source of radionuclide exposure. Concentrations
are adjusted for depletion due to deposition at each downwind
distance.
Ground . Jjur f_ace .Cpnpentr a t i on
AIRDOS-EPA calculates the ground surface concentration from
the total (dry plus wet) deposition rate. The soil concentration
is calculated by dividing this value by the effective
agricultural soil surface density (kg/in ) , Both concentrations
are calculated for the end of the environmental accumulation time
tb and can include the ingrowth from deposited parent
radionuclides as well as removal due to radiological decay and
environmental processes such as leaching.
Ingrowth from a parent radionuclide Is calculated using a
decay product ingrowth factor. The ingrowth factor Is the
equivalent deposition rate for a unit deposition rate of the
radionuclide. For example, the ingrowth factor for
lead-210 as a parent of polonium-210 would be calculated by
determining the concentration of poloriiura--210 at time tb due to a
unit deposition rate of lead-210 and dividing it by the
corresponding concentration for a unit deposition rate of
polonium-210. These ingrowth factors must be calculated, in
advance of running AIRDOS-EPA and are dependent on both the
accumulation time tfe and the soil removal constants for the
nuclides in the radionuclide chain (lead-210r bisiauth-210, and
polonium-210 in this case) .
iix.JFo.Qd,
Radionuclide concentrations in food are calculated using
essentially the model as in NRC Regulatory Guide 1.109
(NRC7?) . Changes from that model include consideration of
environmental removal from the root zone, and separate values for
food and pasture crops of the interception fraction, areal yield,
and soil-to-plant transfer values. Concentration calculations
for meat and milk use the same models as the Regulatory Guide
model. There are numerous parameters in the terrestrial pathways
-------
A of this volume of the BID contains of
in assessments.
For a collective (population) assessment, population
agricultural data for each grid location must be provided, 1PA
1970 enumeration district data to calculate
population distributions, AIRDOS-EPA calculates collective
for agricultural products based on consumption by the
area population. The assessment can be on
agricultural production by choosing utilization factors large-
enough to ensure that all items produced are consumed.
Food iiJt..il_i_z_afelQ.n....JFac.t;Q.gs
In addition to the consumption rate for different food
categories (leafy vegetables, other produce, meat, and milk), the
user may specify the fraction of vegetables, meat, and milk that
are (1) home grown, (2) produced in the assessment area, or (3)
imported from outside the assessment area. Those in the third
category are considered to contain no radionuclides. Those from
the second category have the average concentration for that
category produced within the assessment area, while
concentrations for the first category are those that would occur
at each grid location. Appendix A of this volume provides
typical food source fractions for urban and rural assessment
areas. Note that if the assessment considers food to be only
home grown or imported from outside the assessment area, then the
actual quantity of food produced at each location is not relevant
to Experience has shown that the ingestion doses
risks for the nearby individual are usually dominated by the
radio-raidide intake from home-grown food, and hence there is
generally no significant difference between assuming that food
that is not grown is obtained from the assessment or is
outside the assessment area.
Special consideration is given to the radionuclides
tritium, carbon-14, and radon-222. The specific activity of
tritium in air (pCi/g of H20) is calculated for an absolute
humidity of 8 mg/m (NRC77). Etnier (EtSO) has calculated
absolute humidities for over 200 U.S. locations. The
8 mg/m value would be within a factor of 2 for most of then.
The specific activity of atmospheric carbon-14 (pCi/g of carbon)
is calculated for a C02 concentration of 330 ppm by volume
(Ki78). Concentrations of these nuclides in vegetation are
calculated on the assumption that the water and carbon content in
vegetation from the atmosphere anci have the same specific
activity as in the atmosphere. The radon-222 concentration in
air is replaced by its short-lived decay product concentration in
working level units using a fixed equilibrium fraction (typically
0,5 for calculating population health risks).
4-20
-------
Ba76 Baker, D.A. , Hoenes, G.R., Soldat, J.K
interactive code to calculate internal radiation
from contaminated food products , " in
Con f erence, ..... on ...... ,E nvi r onmeat a 1 ,,Mode 1 .ing ...and ... S iajilatio|j .
Ott, W.R., editor, 600/9~76-016f p, 204, of
Research Development and Office of Planning
Management, U.S. Environmental Protection Agency f
Washington, D.C. , July 1976.
Ba84 Baes, C.F. Ill, Sharp, R.D., Sjoreen, A.L.,
R.W., A Review and, ,Ana.lysis _o£ Parameters_,^for
Transport of Environmentally... Released .Radionuclides
throjigh Agriculture, ORNL-5786, Oak Ridge National
Laboratory, Oak Ridge, Tenn,, September 1984.
Be81 Begovich, C.L., Eckerman, K.F., Schlatter, E.G., Ohr,
S.Y., and Chester, R.O., DAR'TAB; A prograTO^to. s.Qmbine
airborne radionuclide environmental. ..ejtposur^_data_wi^h
dosiBietric and health effect_s data to. generate
tabulation of predicted impacts, ORNL/5692f
National Laboratory, Oak Ridge, Tenn., August 1981,
Br69 Briggs, G.A., Plume Rise, TID-25075, U.S. Atomic Energy
Commission Critical Review Series, National Technical
Information Service, Springfield, Va., 1969.
Cu76 Culkowski, W.M. and Patterson, M.R.,
Atmospheric Transport and. Diffusion Model,
ORNL/NSF/1ATC-17, National Oceanic and Atmospheric
Administration, Atmospheric Turbulence Diffusion
Laboratory, Oak Ridge, Tenn.f 1976.
Da68 Dana, M.T. and Wolf, M.A., "Experimental in
Precipitation Scavenging," in P3£ific__Northwgst
Laboratory Annual Report for 1967 t^th^iZgAEC^Divlsioji
of Biology andMedicine, Vol. II, Physical Sciencesf
Part 3, Atmospheric Sciences, Simpson C.L. et al.,
US.AEC Report BNWL-715-3, pp. 128-140, Pacific
Northwest Laboratories, Richland, Wa., October 1968.
'Da70 Dana, M.T., Wolf, M.A., and duPlessis, L.A., "Field
Experiments in Precipitation Scavengingf 8! in Eagi£ic
Northwest Laboratory Annua 1, Re.B.ort_f^,r_JL9.69 to
USAEC Division of Biology and Medicine, Vol. II,
Physical Sciences, Part 1, Atmospheric Sciences,
Simpson, C.L. et al., USAEC Report BNWL-1307 (Pt. 1),
pp. 77-81, Battelle Pacific Northwest Laboratories,
June 1970.
4-21
-------
Gi?6
Has 2
H072
H079
Ki78
Li79
"Regional site-specific
for use in tritium calculations/w
39, 318-320, 1980.
Gifford, F.S. Jr., "Turbulent Diffusion-Typing
Nucl. Sa.f. 17(1), 68-86, 1976.
, Briggs, G.A. , and HosJcer, R.P. Jr.,
Handbook on Atmospheric Diffusion, DOE/TIC-11223,
Technical Information Center, U.S. Department of
D.C., January 1982.
Holzworth, G.C., jflxj±ng,jJiejg|its^.__Wiiid Speeds .......... an
Potent.! a. 1 for: ..... Urban Air__. Pol_lution___Throug;hQut the
Cs^tigiKas,ai|Jnited ............... States, Publication No. AP-101, U.S.
Environmental Protection Agency, Office of Air
Programs, Research Triangle ParJcf N.C., 1972.
Hoffman, P.O. and Baes? C.F. Ill, A .Statistical
..^
and Ip;tgriial__J}ose_Qf Radionucl.idesf
NUREG/CR-1004f Oak Ridge National Laboratory, Oak
Ridge, Term. , 1979.
Killough, G.C. and Rohwer, P.S., "A new look at the
dosimetry of 14C released into the atmosphere as carbon
dioxide,"
34, 141-159, 1978.
Little, C.A. and Miller, C.W, , The ..Uncertainty
Associated with Selected
Models, ORNL-5528f Oak Ridge National Laboratory, Oak
Ridge^ Tenn., November 1979,
Miller, C.W, Little, C.A., A_JRej£iew__fil_
E_stiffiates...Associated with Models, fojr_.AsjSiessring_iigthe
Im^a^_^_BKQ^SK_E3^ioactj^j^_Ms^&Mses^ ORNL-5832,
Oak Ridge national Laboratory, Oak Ridge, Tenn., August
Mo79
NCRP84
Moore, R.E., Baes? C.F. Ill, McDowell-Boyer, L.M.,
Watsons, A.P., Hoffman, P.O., Pleasant, J.C., and
Miller, C.W. , AIRDQS-EPA..; A Cgmpaterlzed..Methodology
for Estimating EnvironmentalConcentrationsandDoseto
Maji_frOBL_Ai.rborne Releases of:i.JRadioPMC 1 ides, EPA
520/1-79-009 (reprint of ORNL-5532), U.S. Environmental
Protection Agency, Office of Radiation Programs,
Washington, D.C., December 1979.
National Council on Radiation Protection and
Measurements, Radiological.,,Assessment;. P.redi_c.tinq the
Transportx... Bioaccumulation, and Uptake by Man of
Radiortuclides Released to the Enyi_ronm_ent f NCRP Report
No. 76, national Council on Radiation Protection and
Measurement, Bethesda, Md,, March 1984.
-22
-------
NRC77
RU48
U.S. Unclear Regulatory Commission, "Calculation of
Annual to from Routine of Reactor
Effluents the Purpose of Evaluating Compliance with
10 50 Appendix I (Revision 1),"
Guide 1.109, Office of Standards Development,
Washington, D.C., October 1977.
JRupp, A.F., Beall, S.E., Bornwasser,, L.P., Johnson,
D.H., Dilut._ion._pf._StacK..._Gaseg in...Cross^Winds, USA1C
Report AECD-1S11 (CE-1620), Clinton Laboratories, 1948.
S177
SJ84
Ti83
W069
Slinn, W.G.N., "Precipitation Scavenging: Some
Problems, Approximate Solution, and Suggestions for
Future Research," in Precipitation Scavenging (1974),
CONF-7410Q3, Technical Information Center, Energy
Research and Development Administration, Washington,
D.C., June 1977.
Sjoreen, A.L., and Miller, C.W., PREJPAR-A Us_er Friendly
Preprocessor to Create....AIRPQS-EPA Input Data Sheets,
ORNL-5952, August 1984,
Till, J.E. and Meyer, H.R./ Radlglpglcal Assessment,
NUREG/CR-3332, ORNL-5968, Division of Systems
Integration, Office of Nuclear Reactor Regulation, U.S.
Nuclear Regulatory Commission, Washington, D.C.,
September 1983,
Wolf, M.A. and Dana, M.T., "Experimental Studies in
Precipitation Scavenging," in Pacific, Northwest
Laboratory Annual .....Report, for 1968 to the USAEC Division
of Biology and Medicine.
4-23
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5.1
The setting of standards for radionuclldes requires an
assessment of the received by individuals
by coming into contact with radiation sources. Two of
potential radiation exposures can occur from sources —-
internal and external. Internal exposures can result from the
inhalation of contaminated air or the ingestion of contaminated
food or water. External exposures can occur when individuals are
immersed in contaminated air or water or are standing on
contaminated ground surfaces. Internal or external doses can
result from either direct contact with the radiation from
radionuclides at the site area or from radionuclid.es that have
been transported from these sites to other locations in the
environment. The quantification of the doses received by
individuals from these radiation- exposures is called radiation
dosimetry. This chapter highlights the internal and external
dosimetric models used by EPA to assess the dose to individuals
exposed to radionuclides,
The models for internal dosimetry consider the quantity of
radionuclides entering the body, the factors affecting their
movement or transport through the body, and the energy deposited
in organs and tissues from the radiation that is emitted during
spontaneous decay processes. The-models for external dosimetry
consider only the photon doses to organs of individuals who are
immersed in air or are exposed to a contaminated surface.
In addition, the uncertainties associated with each model will be
discussed.
5.2 BASIC CONCEPTS
Radioactive materials produce radiation, as their constituent
radioactive nudities undergo spontaneous radioactive decay. The
forms of emitted energy are characteristic of the decay process
and include energetic charged particles (alpha beta
particles) and photons (gamma rays and x-rays), Alpha particles
are nuclei of helium- atoms and carry a positive charge two times
that of an electron. These particles can produce ionization
tracks in the biological material that they traverse.
particles are electrons or positrons emitted in radioactive
decay. Their penetration power in material is greater than that
of alpha particles. Gamma and x-rays are electromagnetic
radiation and are distinguishable from alpha and beta particles
by their greater penetrating power in material,
This section introduces some terminology used in Chapters
5 and 6 to describe internal and external dosimetry. For a more
detailed explanation, the reader is referred to reports published
in this area by the International Commission on Radiation Units
and Measurements (ICRU80), International Commission on
5-1
-------
Radiological Protection (ICRP34), and-national Council on
Radiation Protection (NCRP71),
5.2.1 Activity
The activity of a sample of any radionuclide of species, i,
is the rate at which the unstable nuclei spontaneously decay. If
N is the number of unstable nuclei present at a certain time, t,
its activity, A, (t), is given by
A. (t) = -dM/dt = X* N , (5-1)
R
where Xt is the radioactive decay constant. The customary unit
of activity is the curie (Ci); its submultiples, the millicurie
(raCi) , the microcurie (jiCi) , and the picocurie (pCi), are also
often used. The curie, which is defined as 3.7x10
disintegrations per second, is the approximate activity of 1 gin
of radium-226.
The time variation of the activity can be expressed in the
form:
A,(t) = A0, exp(» Aj t). (5-2)
A • is the activity of nuclide i at time t=0. For a sample
of radioactive material containing more than one. radionuclide,
the.total activity is determined by summing the activities for
each radionuclide:
A(-t) = 2? A,(t) (5-3)
5.2.2 Radioactive Half-Life
From the above equations, it is apparent that the activity
exponentially decays with time. The time when the activity of a
sample of radioactive material containing species i becomes one-
half its original value {i.e., the time t that A. (t) = Aoi/2) is
called its radioactive half-life, T*, and is defined as:
T? - (In 2)/ A* (5-4)
The unit for the radioactive half-life is any suitable unit
of time such as seconds, days, or years. The specific activity
of a radionuclide (the activity per unit mass) is inversely
5-2
-------
proportional to half-life vary of
magnitude.
5.2.3
Radionuclides decay either to stable atoms or to other
radioactive species called daughters. For some species, a decay
chain of daughter products may be produced until stable atoms are
formed. For example, strontium~90 decays by emitting, a beta-
particle, producing the daughter yttrium~90, which also decays by
beta emission to form the stable atom zirconium-90;
9EW,oQ 6 yrj f 90y(64,0 h) * 9QZr(stable) (5-5)
5.2.4 Biological Half-Life
The biological half-life of radionuclides is the time
required for biological tissues to eliminate one-half of the
activity by elimination processes. This time is the same for
both stable and radioactive isotopes of any given element,
5.2,5 Internal_ and ..External Exposures to Radionuclides
The term "exposure", in the context of this report, denotes
physical interaction of the radiation emitted from the
radioactive material with cells and tissues of the human body.
An exposure can be "acute" or "chronic" depending on how long an
individual or organ is exposed to the radiation. Internal
exposures occur when radionuclides, which have entered the body
through inhalation or ingestion pathway, deposit energy to
organ tissues from the emitted gamma, beta, and alpha radiation.
External exposures occur when radiation enters the body directly
from sources located outside the body, such as radiation from
material on ground surfaces, dissolved in water, or dispersed in
the air.
In general, for sources of concern in this report, external
exposures are from material emitting gamma radiation. Gamma rays
are the most penetrating of the emitted radiations, and external
gamma ray exposure may contribute heavily to radiation doses to
the internal organs. Beta and alpha particles are far less
penetrating and deposit their energy primarily on the skin's
outer layer. Consequently, their contribution to the absorbed
dose to the total body, compared to that deposited by gamma rays,
is negligible and will not be considered in this report.
5-3
-------
5.2.6
radiological quantity absorbed dose, Dr
A if, by ionizing radiation to a small finite
of with a massf Am, and is expressed as
D = d?/dm = lint (Af/Am) . (rad) (5-6)
Internal external exposures from radiation sources are
not usually instantaneous but are distributed over extended
periods of time. The resulting time rate of change of the
absorbed dose to a small volume of mass is referred to as the
absorbed dose rate, D;
D = dD/dt = lim (AD/At). (rarad/y) (5-7)
At--*o
The customary unit of absorbed dose rate is any quotient, of
the rad (or its multiple or submultiple) and a suitable unit of
time* In this report, absorbed dose rates are generally given in
mrad/yr.
5.2.7 Linear Energy^JTransfer ..(LET)
The linear energy transfer, Lm, is a quantity that
represents the energy lost, by collision,, per unit length by
charged particles in an absorbing medium. It represents the
increment of the energy lost, AE/ to tissue by a charged
particle of specified energy in traversing a distance, AX:
It. = = lim (AE/AX) (ke¥ 0m"1) (5-8)
Ax-^Q
For photons, L0 represents the energy imparted by the
secondary electrons (electrons that are knocked out of their
orbitals by primary radiation) resulting from secondary
interactions between the photons and tissue material. High-LET
radiation (alpha particles) imparts more energy per unit length
of organ tissue than does low-LET radiation (x-rays, gamma rays,
and beta particles), Consequently, the former are more effective
per unit dose in causing biological damage.
5.2.8 DoseJEguivalent and Dose Equivalent Rate
Dose equivalent is a special radiation protection quantity
that is used to express the absorbed dose in a manner that
-------
difference in biological effectiveness of
of Ionizing radiation. The ICRU has defined
equivalent, H, as the product of the absorbed dose, D, the
quality factor, Q, and all other modifying factors, ft, at the
point of interest in biological tissue (ICRU80). This
relationship can be expressed in the following manner:
H = D Q N. (rem) (5-9)
The quality factor is a dintensionless quantity that depends
on the collision stopping power for charged particles, and it
accounts for the differences in biological effectiveness found
among varying types of radiation. By definition, it is
independent of tissue and biological endpoint. The generally
accepted values for quality factors for high- and low-LET
radiation, which are used by EPA, are given in Table 5-1. The
product of all other modifying factors, N, such as dose rate,
fractionation, etc., is taken as 1.
Table 5-1. Quality factor for various types of radiation
(ICRP77).
Radiation Type Quality Factors (Q)
x-rays, gamma rays, and electrons 1
alpha particles ' 20
The dose equivalent rate, H, is the time rate of change of
the dose equivalent to organs and tissues and is expressed as;
»
H = dH/dt = lira (AH/At). (mrem/yr) (5-10)
At-*o
5,2,9 Effective Dose Equivalent and Ll|.£ectiye_ Pose Equivalent
Rate
The ICRP has defined the effective dose equivalent, HE, as:
He - 2T WT HT, (rem) (5-11)
where HT is the dose equivalent in tissue and WT is the weighting
factor, which represents the estimated proportion of the
stochastic risk resulting from tissue, T, to the stochastic risk
5-5
-------
quantities Is in Table 5-3. While SI radiological
units almost universally In other countries for
radiation protection regulation, United not yet
officially their for such, purposes,
Table 5-3, Comparison, of customary
radiation quantities,
SI special units for
_SBecial_S.LJJnit..
SI Unit
Definition
Activity (A) curie (CI)
(D) rad
3,7x10™ s'1
10"2 J kg"1
Dose
equivalent (H)
Linear energy
"2
10" J kg
"1
becquerel (Bq) 1.0 s"
gray (Gy) 1.0 J kg'1
slevert (Sv) 1.0 J kg"1
klloelectron 1. 602x10" w J nf1
inicroaeter
(ke¥ pi"1)
5.3
The EPA dosimetric models, to be discussed in the following
sections, have been described in detail in previous publications
(DuSOf Su81) . Information on the elements treated in these
sections taken directly from those documents or reports. In
most cases, the EPA models are similar or identical to those
recommended by the ICRP (ICRP79, ICRP80, ICRP81) . However,
differences in model parameters do exist for radionuclides
(Su81) . The basic physiological metabolic data used by EPA
in calculating radiation doses taken from ICRP reports
5.3.1
EPA implements contemporary models to estimate absorbed dose
rates as a function of time to specified organs In the body,
Estimates of the doses resulting from the deposition and
retention of inhaled particulates In the lung and their
subsequent absorption into the blood and clearance into the
gastrointestinal (Gl) tract are made using the ICRP Task Group
Lung Model (ICRP66) .
5-8
-------
5.3.1.1 for Estimating Organ
Rates
5,3.1.1.1 Distribu£4onoJLActlvitv_of Radionuclides in
behavior of radionuclides is simplified
conceptually by considering the body as a of A
compartment be anatomical, physiological/ or physical
subdivision of throughout which the concentration of a
radionuclide is to be uniform at any given time,
terms "compartment" and "organ" are often used interchangeably,
although of the compartments considered in this report may
represent only portions of a structure usually considered to be
an organ, while some compartments may represent portions of the
body usually not associated with organs. Examples of
compartments used in this report are the stomach, the pulmonary
region of the lung, the blood, or the bone. Within a
compartment, there may be more than one "pool" of activity, A
pool is defined to be any fraction of the activity within a
compartment that has a biological half-life which is
distinguishable from the half-time(s) of the remainder of
activity within the compartment,
Activity entering the body by ingestion is to
originate in stomach compartment; activity entering through
inhalation is assumed to originate in a compartment within the
lung (the tracheo-bronchial, pulmonary, or naso-pharyngeal
region), From the stomach, the activity is viewed as passing in
series through the snail intestine, the upper large intestine,
and the lower large intestine, from which it may be excreted.
Also, activity reaching the snail intestine be
through the wall into the bloodstream, which it be
in parallel into any of several compartments within skeleton,
liver, kidney, thyroid, and other organs and tissues.
list of organs or regions for which
calculated is found in Table 5-4, Activity in the lung
the bloodstream either directly or indirectly through
or lymphatic system. The respiratory system and gastrointestinal
tract models are discussed further in later sections. Figure 5-1
illustrates the EPA model used to represent the of
radioactivity in the body,
EPA models separately consider the intake
behavior of radionuclide in the body. The also allow
for the formation of radioactive decay products within body,
and it is assumed that the movement of internally
radioactive daughters is governed by their own metabolic
properties rather than those of the parent. This is in,
to the ICRP assumption that daughters behave exactly as
parent.
5-9
-------
Target tissues for calculating
ICRP effective equivalent
risk.
equivalent
Ovaries
Testes
Breast8
Red marrow
Lungsb
Thyroid
Bone surface
Stomach wall
Small intestine wall
Upper large intestine wall
Lower large intestine wall
Kidneys
Liver
Pancreas
Brain
Spleen
Thyums
Uterus
Breast
Red narrow
Pulmonary lung6
Thyroid
Bone surface (endosteum)
Stomach wall
Intestined
Kidneys
Liver
Pancreas8
Bladder wall
a) Dose to breast is assumed to equal dose to muscle.
b) The ICRP considers the lungs to be a composite of
trachiobronchial region, pulmonary region, the pulmonary
lymph with a combined mass of 1,000 g (ICRP79).
c) The EPA calculates lung cancer risk on the of
to pulmonary lung. The mass of this region; which
not include venous or arterial blood, is considered to be
d) The EPA averages the values for the small, upper large,
and lower large intestine using weights of 0.2, 0.4, and
0.4 respectively for calculating the rislc of bowel cancer.
e) The pancreas is also used as a surrogate organ for
calculating the cancer risk for all other organs tissues,
5-10
-------
Figure 5-1.
A schematic representation of radioactivity
movement among respiratory tract, gastrointestinal
tract, and blood.
- stomach
= small intestine
= upper large intestine
= lower large intestine
= elimination rate constant
LLI
X
5-11
-------
activity of ith of
in k if that activity is divided
-» *£ WW^WW.-™-*-™™-*™. -««.*™s
"pools* or "compartments" indexed by subscript 1, time
of of activity can be modeled by a of
differential of the following form;
i-1 L!f,
'+ Pfk)
(5-14)
,lk( 2 B5j 2 A+ pfk>
"
where compartment 1 is assumed to have Lik separate pools of
activity, where;
Aflk = the activity of species i in compartment 1 of
organ k;
A* = (In 2) / T*, where T1? = radioactive half of
species ij
8 , .1
AUk = rate coefficient (time ) for biological removal
of species i from compartment 1 of organ k;
Lfk = number of exponential terms in the retention
function for species i in organ k;
Bj, = branching ratio of nuclide j to species i?
pik = inflow rate of the 1th species onto the organ k?
and
c{(c — the fractional coefficient for nuclide i in the
1th compartment of organ k.
The described by these Lik equations be
interpreted as a biological compartment in which the fractional
retention of radioactive species is governed by exponential
decay. Radioactivity that enters an organ may be lost by both
radioactive decay and biological removal processes. For each
source organ, the fraction of the initial activity remaining at
any time after uptake at time t = 0 is described by a retention
function consisting of one or more exponentially decaying terms:
-<*1 + A!ik)t3 (5-15)
The subscript 1 in the above equation represents the 1th
of the retention function, and the coefficients ciik can be
considered as "pathway fractions,"
5-12
-------
activity of a radionuclide in a compartment Is a
of of being emitted in that at any
time, t, be related to the dose to a specific
at that time. This requires estimating the fraction of
energy emitted by decay of the radionucli.de in
compartment that is absorbed by the specific organ,
The absorbed dose rate, D|(X;t) to target organ X at time t
to radionuclide species I in source organs Yiry2/....» YM is
estimated by the following equation:
D,(X;t) - |Df(X*-Yk;t) (5-16)
(£""6
where; D.(X*-Yk>'t) = S,(X*-Yk) Afk(t) ? and Aik(t) is the
activity, at time t of species I in source organ Yfc.
S| (X+-Yk) , called the S-factor, represents the average dose
rate to target organ X from one unit of activity of the
radionuclide uniformly distributed In source organ or compartment
Yk. It Is expressed in the following manners
S,(X-Yk) = C I fm Em 0,(X-Yk}' ' (5-17)
where t
c -a constant that depends on the units of
dose/ energy, and time being used?
fm = Intensity of decay (nuiaber
disintegration);
la| = average energy of decay event (Mev) ;
#m(X*"Yk) = specific absorbed fraction, i.e.,
fraction emitted energy from source organ Yk
absorbed by target organ X per of X,
where the summation is taken over all events of type HI. The
units for S~factors depend on the units used for activity and
time,* thus, the S-factor units may be rad/Ci-day, The S-factor
is similar in concept to the SEE factor (specific effective
energy) by the ICRP Committee 2 in Publication 30. However,
the SEE factor includes a quality factor for the type of
radiation emitted during the transformation.
The above equations are combined to produce the following
expressions for the absorbed, dose rates to target organs at any
5-13
-------
time to unit of activity of radionuclide species? i,
uniformly distributed in source organs Y1 ... Ykt
It m ik im k
The corresponding dose equivalent rate, H? (X;t), can be
by inclusion of the quality factor, Qm, the modifying factor,
Nm(¥k) :
Implicit in the above equations is the assumption that the
absorbed dose rate to an organ is determined by averaging
absorbed dose distributions over its entire mass.
Alpha and beta particles are usually not sufficiently
energetic to contribute a significant cross-irradiation dose to
targets separate from the source organ. Thus, the absorbed
fraction for these radiations is generally assumed to be just the
inverse of the mass of organ X, or if the source and target
separated, then $m(X*-Y) = 0, Exceptions occur when the source
and target are in very close proximity, as is the case with
various skeletal tissues. Absorbed fractions for cross-
irradiations by beta particles among skeletal tissues taken
from ICRP Publication 3 (ICRP80). The energy of alpha particles
and their associated recoil nuclei is generally to be
absorbed in the source organ. Therefore, $m(X^X) is taken to be
the inverse of the organ mass, and $m(X*-Y) = 0 if X Y
separated. Special calculations are performed for active marrow
and endosteal cells in bone, based on the method of Thome
(Th77).
5.3.1.1.3 MonteCarlo Methodology.to Estimate Photon.Poses
to_0rga_ns
The Monte Carlo method uses a computerized approach to
estimate the probability of photons interacting within target
organ X after emission from source organ Y. The method is
carried out for all combinations of source and target organs
for several photon energies. The body is represented by an
idealized phantom in which the internal organs are assigned
masses, shapes, positions, and attenuation coefficients based
on their chemical composition. A mass attenuation coefficient,,
HQ is chosen, where JJ,Q is greater than or equal to the
a€tenuation coefficients for any region of the body. Photon
courses are simulated in randomly chosen directions,
potential sites of interactions are selected by taking distances
traversed by them as -In r//i , where r is a random number
distributed between 0 and 1, The process is terminated when
•14
-------
either total energy of photons has been or
the body. The energy deposition an
Interaction is determined according to standard
.
5.3.1.1.4
In calculating from internal and external
in-growth of radioactive decay products (or
be considered for some radionuclides. When an
radioactive decay, the new atom created in the process, which
also be radioactive, can contribute to the radiation to
organs or tissues in the body. Although these decay products nay
be treated as independent radionuclides in external
decay products of each parent must be followed through
in internal exposure situations. The decay product contributions
to the absorbed dose rates, which are included in EPA
calculations, based on the metabolic properties of
individual daughters and the organ in which they occur,
5,3.1.2 Inhalation Dosimetry - ICRP Respiratory Tract
As stated earlier, individuals immersed in contaminated air
will breathe radioactive aerosols or particulates, which lead
to to the lung and other organs in the body. The total
internal dose caused by inhalation of these aerosols
on a variety of factors, such as breathing rates, particle sizes,
physical activity. Estimating the total to individuals
over a specific time period requires specifying distribution
of particle depositions in the respiratory tract and the
mathematical characteristics of the clearance
currently assumptions established by ICRP
ori Lung Dynamics (TGLM) (ICRP66) , This section will
essential of that model. For a more
treatment, the is referred to the actual report.
The basic features of the ICRP lung compartmental model
shown in Figure 5-2. According to this model, the respiratory
tract is divided into four regions: naso-pharyngeal (N-P),
trachea-bronchial (T-B), pulmonary (P), and lymphatic tissues.
In model, regions N-P, T-B, P to
receive fractions D3, D4, and D5 of the inhaled particulates,
where the of these is less than 1 (some particles
by prompt exhalation) « The values D3, D4, and D5 on
activity aerodynamic diameter {AMAD} of the inspired
particles. For purposes of risk calculations,, EPA of
1 micron. The lung model employs three clearance classes, Dr W,
Y, corresponding to rapid, intermediate, and low clearance,
respectively, of material deposited in the respiratory
clearance class depends on chemical properties of inhaled
particles.
5-15
-------
4,
r , Is-'* \
s jv-
t$ I
The columns labeled D, W, Y correspond, respectively, to rapid, intermediate?
clearance of inspired material (in days, weeksf or years). The T and F
biological half-time (days) coefficient, ively, of a in
function. values D3r D4, DR to activity
= l pt? fraction of
depositing in lung regions.
Figure 5-2. The ICRP Task Group lung model for particulates.
-------
ICRP, that absorbed to
N-P be neglected. Unlike ICRP, however, EPA
over the pulmonary region of lung
e through h), to which is assigned a of 570 g,
including capillary blood {ICRP75J, In addition, it is
total of air breathed in one by a typical
of population is 22,000 liters. This value
by averaging the 23 ICRP adult male
on 8 hours of working "light activity," 8 of
nonoccxipational activity, 8 hours of resting.
5,3.1,3 Dosimetry - ICRP GI Tract
According to the ICRP 30 GI tract model, the
gastrointestinal tract consists of four compartments? the stomach
(S), intestine (SI), upper large intestine (ULI), and lower
large intestine (LLI). The fundamental features of the model are
in Figure 5-1, It is assumed that absorption into the
only from the small intestine (SI).
Tills postulates that radioactive material entering the
compartments of GI tract Is exponentially removed by both
radioactive decay biological removal processes, that
is no feedback. Absorption of a particular nuclide from
GI tract Is characterized by ft, which represents that
fraction of nuclide ingested which is absorbed into body
fluids if no radiological decay occurs:
f = i»fc> /( lab 4- \ \ (5 — 70)
J*1 Asi ' ^ si Asi' l /
A* = absorption coefficient (s )
XS! = transfer coefficient fron the small intestine
to the large intestine (s"1)
5-1 graphically presents the role of these coefficients in
gastrointestinal model. The kinetic model, as formulated by
ICRP, not permit total absorption of a nuclide (f1 = 1} „
5.3.1.4 Conversion Factors
computer code RADR1SK (Du80) for calculating
radiation and risks to individuals resulting from a unit
Intake of a radionuclide, at a constant rate, for a lifetime
(50-yr commitment}» These calculations
for inhalation and ingestion pathways to individuals who are
by immersion in contaminated air or by contaminated
ground surfaces,
5-17
-------
s for both chronic
Following an intake, it is activity in
monotonically, particularly for radionuclides with
rapid radiological decay rates or rapid biological clearance. In
the of chronic exposure, the activity in of
body monotonically until a steady is achieved, at
which time activity remains constant.
rates at various times after the start of chronic
provide a reasonably accnr^ e (aiid conservative) of
total annual for chroii^ exposure conditions. However,,
instantaneous rates s-:/ et" substantially in the
of annual from an acucr e^p jsuref particularly if
activity levels i,jf ! ; t
-------
5.3.1,5.2
Retention of noble gases in the lungs is
to described by Dunning et al. (Du79). inhaled
gas'is to remain in the lungs until lost by radiological
decay or respiratory exchange, Translocation of noble to
is not considered, but doses to translocated
decay products produced in the lungs are calculated. The
inhalation of short-lived decay products of radon is
using a potential alpha energy exposure model (see Chapter 6}
by calculating the doses to lung
radionuclid.es.
5.3.1,5.3 Urji»iiujtt_stnd^
The metabolic models for transuranics elements (polonium,
neptunium, plutonium, aroericium, and curium) consistent with
those for the EPA transuranic guidance (EPA?7}. A 61 tract
to blood absorption factor of 10"3 is used for the short-lived
nuciides of plutonium (plutonium-239,-240, and -242}, while a
value of 10" is used for other transuranics. For soluble forms
of uranium, a GI tract to blood absorption factor of 0.2 is
in accordance with, the high levels of absorption observed for
low-level environmental exposures (Hu73, Sp?3).
5.3,1.6 Uncertainties in Internal Dose Estimates
Estimates of radiation dose in risk assessment studies have
traditionally been based on dosimetric models derived in the
context of radiation protection for adult workers. Despite
obvious differences between risk assessment and radiation
protection, the dosimetric formulations of the latter
generally adopted, often with no modifications, in risk
activities. This approach permits of a substantial
body of information assembled by international
occupational setting and provides models that avoid the complex
encountered in biokinetic modeling of radionuclides for
general public in an age-dependent sense. However,
continued in risk assessment of dosimetric data derived for
workers, which neglects organ-specific biokinetics and
dependence, is becoming increasingly difficult to justify.
major limitation of the current aj| hoc dosimetric formulations is
the great difficulty in making informed estimates of the
uncertainties in the estimated dose.
All dosimetry models are inherently uncertain. At best,
models can only approximate real situations in organs and
tissues in humans. Consequently, without extensive human data,
the uncertainties associated with their use for risk
is extremely difficult, and in impossible,
to quantify. However, consideration of their limitations in
estimating to an average member of the general population
is essential.
5-19
-------
In applying doslmetric models in current use, as
in the previous sections, the primary sources of
attributed to ICRP model formulation
"variability produced by measurement error or* natural
variation. purpose of this section is to provide a general
limited discussion of these sources and to introduce an
uncertainty scheme for classifying radioiiuclides. The
gratefully acknowledge Dr. Keith Eckerman of Oak Ridge Laboratory
for discussions with respect to implementation of ICRP models
for guidance regarding the magnitude of uncertainties, ,
the conclusions presented here are those of the Agency.
5.3.1.6.1 UncertiaJJQM^^
Uncertainty in calculations based on ICRP models
primarily front five sources: (1) the uncertainty in the Reference
Man datai (2) the uncertainty in the lung and Gl-tract model
describing the translocation and absorption of inhaled or
ingested activity into the blood? (3) the uncertainty associated
with the formulation of the ICRP Publication 30 biokinetic models
describing the distribution and retention of the activity among
the various organs in the body; (4) the uncertainty in the
models to calculate the absorbed dose to organs from that
activity? (5) the uncertainty in the model parameters,
5.3.1,6.2 aa_£oncept
To establish a degree of consistency in occupational
dosimetry calculations, the ICRP developed concept of
Reference (ICRP75). Reference Man is a conceptual individual
who the anatomical and physiological characteristics of a
healthy 20 to 30 year old male with a total body of 70-kg.
The anatomical and physiological data of Reference have
in many computational models for estimating organ
applied in radiation protection and in some calculations for
medicine.
Although these data have been extensively applied in
calculating doses, the approach in which Reference is
to represent average individuals in a specific population
introduces bias from the outset. The uncertainties in this
approach are primarily due to age- and sex- specific differences
in the anatomical and physiologic parameters. Biological and
ethnic variability also contribute. In addition, the Reference
Man do not always represent data for a 70-kg man. Many of
the data found in ICRP Publication 23 were from adults who had
anatomical or physiological characteristics significantly
different from those of a 70-kg man.
to the many parameters involved and the quality of
data available to define the numerical values, it is very
difficult to establish the level of uncertainty in using
Reference data to estimate doses to the average individual in
the U.S. population. Furthermore, the Reference concept
5-20
-------
.ted, so as to facilitate a quantitative analysis of
uncertainty in estimates. Finally, Reference Is
to be representative of the 11,5* population.
individuals inhale radioactive aerosols, the to
other organs in the body depends primarily on
aerosols deposited in and cleared from of
the respiratory tract. Mechanisms involved in deposition of
inhaled aerosols and gases are affected by physical chemical
properties, including aerosol size distribution, density, shape,
area, electrostatic charge, chemical composition
diffusivity solubility. Deposition is also affected by
respiratory physiology, morphometrics and pathology.
The ICRP modeling system assumes that deposition rates for
aerosols in the respiratory tract are controlled primarily by
mechanismss sedimentation, impaction and Brownian
diffusion. The major uncertainties associated with ICRP
deposition models for .the lungs are. (1) the uncertainty in the
anatomical model of the respiratory tract, (2) the uncertainty in
effective aerodynamic diameter of the inhaled particles, (3)
the uncertainty in the breathing patterns and rates, (4) the
questionable validity of the fluid dynamic models for all
exposure situations.
in the lung
on physiologic, morpheme trie and anatomical properties,,
such as airway dimensions and numbers, branching
gravitational angles of airways, and distances to the alveolar
walls. The ICRP respiratory tract model (ICRP66) uses the
anatomical model devised by Findeisen (Fi,35) in its dosimetric
calculations. This model that lung airways rigid
with symmetric dichotomous branching patterns
their morphometric properties those of an adult male* In
reality, however, the airways have circular ridges or
longitudinal grooves (FRC6?), and many airways, like the trachea,
irregular in shape (Br§2), In addition, airways in
diameter and length during inspiration and expiration (Ho75,
Hu72, Th78), which affects gravitational and branching angles
(PhS5). Since many of these properties depend on sex,
using the anatomic and morphometric lung properties of an adult
male for estimating doses to other members of the population is
likely to introduce considerable bias.
Clearance of particles from the respiratory tract on
many factors, such as site of deposition, chemical composition,
physical properties of the deposited material, ssucociliary
transport rates. The uncertainties associated with
values provided by the ICRP are due primarily to the
of data on lung clearance mechanisms, in general, and secondarily
to age, activity levels and general health status, of
individual at the time of exposure. Furthermore, as si
•21
-------
earlier, of the lung deposition data and models
cf healthy adults. Studies shown,
children's differ from adults' with to
anatomical, physiological, and morphological properties» As a
particle deposition in the respiratory tract is
to be higher in children than in adults,
5.3.1.6.4 ICRJLjGI> . .act_Model
The ICRF Gl-tract model assumes that ingested material
(rad.ionuclid.es) in sequence through the stomach, small
intestine, upper large intestine, and lower large intestine
model depicts an exponential removal from each compartment,
characterized by a single removal rate that depends only on
compartment. The model has no provision for addressing
endogenous secretion. In addition, it is assumed that
radionuclides absorbed into the blood from the small
intestine (SI).
Uncertainties arise when applying these assumptions to
estimation of doses to average individuals. Although
radionuclides transported through the GI tract are primarily
absorbed into the blood stream from the SI, fractions be
absorbed from the other compartments. Furthermore, the
ratesj which are model parameters, vary among different
individuals in the population. Considerable differences can
exist depending on the type of radionuclide ingested, its
&T «•? •£ •£. _j F
chemical fora, the amount and composition of food in
at the time of intake and other factors which vary of
nutritional status, age, and the sex of the individual. The ft
factor, which represents the fraction of material
the SI, generally contributes the largest uncertainty in the GI
tract model, This parameter will be discussed in a later section
5.3.1.6.5 ICRP 30 Biokinetic Models
The ICRP biokinetic models were chosen to represent adult
male members of population. Uncertainties associated
with the approach because they do not account for differences in
the metabolic behavior of radionuclides, which vary depending on
age, sex, dietary intakes of an individual at the time of
exposure. In addition, many of the models chosen for dosimetry
calculations are based on very limited observational data that
cannot be reliably applied across the population.
Below is a list of additional uncertainties associated with
the ICRP biokinetic models:
(a) The models have been constructed largely from animal
data in such a way that extrapolation to humans no
strong logical or scientific support.
(b) Doses to heterogeneously distributed radiosensitive
tissues of an organ (e.g., skeletal and lung tissues)
-------
cannot be estimated accurately, since
movement of radionuclides in the body is not accurately
(c) radionuclides are assigned of an
apparently related nuclide (e.g., americium, curium,
neptunium are assigned the plutonium
differences in metabolism are known.
(d) The growth of radioactive daughters is
handled realistically, and the format of
it difficult to supply alternative assumptions.
models often yield inaccurate of
:retion even for the average adult.
5.3.1,6 = 6 ICJRP__Oo^e_J|gdels
1CSP models estimate doses to organs of the body by
considering the distribution of the radioactivity
interaction of radiation with cells and. tissues in organs.
Estimates of the, absorbed dose in a region (referred to as
target region) depend upon the spatial relationships of that
region to regions containing the radionuclide (referred to as
regions) bow the activity is distributed in
region, For other than bonef it is assumed that
>.,-.* -^r-Y"~ffii\r distributed tit ths soiurcs rsciions anci
-i-c cells of interest, are uniformly
*-->"ret region. However, this nay
LI > because of the nonuniformity of
activity that j~,..< ,.,~i-u^ly found in human organs.
5.3.1.6.7 IM£Jl.r te ij^^
Most discussions concerning the. uncertainties in
estimates focus on the uncertainty associated with
$rs. These discussions assume that the ICRP
els correct. The most important of
concern, for assessment calculations are: radionuclide intake
rates, organ masses, blood transfer factors, organ uptake rates,
biological, half-times of radionuclides. Although
variability can be attributed to measurement and samp"
natural biological variation, in "many cases, is
source of variability.
Depending on the type of radionuclide ingested, the
dependency in the metabolic and physiological processes
how the dose, to target organs varies with For
example, strontium tends to follow the calcium in
body to a large extent in the skeleton. In fact,
fraction of ingested strontium eventually reaching
skeleton at a given depends largely on the skeletal for
calcium at that age, even though the body is able to discriminate
-------
strontium in favor of calcium after
Given Importance of age as a contributor to
variability In estimates, the possible in
thyroid for chronic ingestion of a fixed iodine~13I
concentration In milk is examined in more detail below.
other of parameter variability will also be noted.
A simple model that can be used to relate the
rate to a target organ due to radioactivity located In that organ
can be expressed as follows :
D(t> = c 1 £t fg B [l-exp(-Xt)]/m> (5-21)
where:
D(t) = absorbed dose rate (rad/day);
I = radionuclide intake rate (Ci/day)j
f1 = fraction of ingested activity transferred to
the blood;
f> — fraction of blood activity transferred to the organ;
IB = target organ mass (g) ?
A = elimination constant (day"1} — 0.693/T1/2 T1/2 is
the effective half-time, including the effects of
both biological removal and radioactive decay.
E = energy absorbed by the target organ for each
radioactive transformation,
c = proportionality constant
(51.2 x 106g rad Ci°1 MeV'V) ,
For simplicity, we will consider the case where t is very
large compared to the biological half-life of the incorporated
radionuclide, so that the term in the bracket is approximately 1:
D(t) = c 1 f1 f'2 E/ffiA (5-22)
In addition, it is assumed that the parameters remain
constant throughout the period of investigation and are
t of each other.
5-24
-------
5-22 Is a simplified form of by x.
to the dose rates to target organs resulting
ingestion of radioactive material. It
to a target organ from particulate radiation
to radioactivity that is uniformly distributed in that organ.
For illustration, the chronic intake of iodine~131 is
that it behaves metabolically the as
iodine. It is further assumed that iodine is rapidly
almost completely absorbed into the bloodstream following
inhalation or ingestion. Proa the blood, iodine the
extracellular fluid quickly becomes concentrated in
salivary, gastric, and thyroid glands. It is rapidly secreted
from salivary and gastric glands but is retained in the
thyroid for relatively long periods.
The intake metabolism of iodine have been reviewed
extensively in the literature. Two papers have used published
data to model the absorbed dose from radioiodine. In the first
(Du81), the authors compiled and evaluated the variability in
three of principal biological parameters contained in
Equation 5-22; m, A, and f{, In the second (Br69), the author
provided age-specific values for most of the same model
parameters. Differences in these data illustrate how parameter
variability, when used in the same model, can affect absorbed
dose rate estimates for members of the general population.
Intake
of radioactive material taken into the body over
a specified period of time by ingestion or inhalation is expected
to be proportional to the rate of intake of food, water, or air
containing material, which, in turn, would depend on
factors as age, sexf diet, and geographical location. Therefore,
understanding the patterns of food intake for individuals in the
population is important in assessing the possible range of intake
rates for radionuclides.
EPA analyses were done to assess the daily intake
rates of food and water for individuals in the general
population. These studies showed that age and sex played an
important role (Ne84). Age significantly affects food intake
for all of the major, food classes and,, with exception,
subclasses. The relationships between food intake and age are,
in most cases, similar to growth curves; there is a rapid
increase in intake at an early stage of physical development,
then a plateau is reached in adulthood, followed by an occasional
decrease after age 60,
differences were significant, males, without
exception, consumed more than females. The study also showed
that relative consumption rates for children and adults on
the type of food consumed. The amount of radioactivity taken into
the body per unit intake of food, air, and watex depends on its
5-25
-------
tty (amount of radioactivity contained In
anit volume), The most likely pathway to
of radioactive
According to the abov- , -I/sis, daily
3y children {under 1 yr) r< ' ice an
The Intake . r f. Ik in
0.5 L/day for the c1 ?': nd adult.
While uncertainty in f1 Is not an important consideration
for Iodine, It be very significant for
Experimental studies suggest that ,ft value for
jrpitiloTOicIidss may toe orders of magnitude higher in risw'tsorTii
in adult mammals, with the largest relative with age
occurring for nuclides with small adult f1 (Cr83) .
For radionuclides, the f1 value appears to rapidly
year of life. This can be related to
this time period, which could affect both
rate from the small intestine to the upper large intestine
absorption rate from the small intestine to the bloodstream.
Studies indicated that the wall of the small intestine is a
selective tissue that absorption of nutrients is to a
controlled by body's (Cr83). In particular,
fraction of calcium or iron on bodyss
for elements, so the f1 value for
related elements such as strontium, radium, (in
of calcium) plutonium (in the of iron) m
as for calcium or iron changes during various of
1 i f e.
For essential elements, such as po*' >>•„>-,<>
chemically similar radioelements, such as rui < , u
eiibsGrptlGR in-co the bloodstream is nearly coii1 \ < * • ~ •> <„ /!*"r.,
so that with age possible hoxaeos1 ~ '" ~t - •» i
absorption are not discernible. The fr? ' < / ' : j - • ! ~t*< •r
that is transferred to the blood depends » »< •> uLsfcitixucii, .Lu,i.Ta,-
and wide of values are found in t i. < !:>»rature for
individuals who Ingest the material undt- -' > a.rent conditions.
For example, ft values for uranium were found to 0.005
to 0.05 for industrial workers, but a higher average value of 0,2
(0.12 to 0.31} Is indicated by dietary data from persons not
occupationally (ICRP79), EPA used the 0,2 value
uranium ingest ion by the general population,,
It sppsairs that all iodine enterinc* the small intestine is
into the blood? hence the f, value is taken as 1 for all
-------
of target organs listed in Table 5-2,
during childhood continues to increase until adulthood, at
which time the net growth of the organ ceases; there may be a
gradual decrease in (for some organs) in later years.
Based on data reviewed by Dunning and Schwarz (Du81), the
mass of an adult thyroid ranges from 2 to 62 g. It is expected
that this parameter variability would be reflected in large
dosimetric variability among adults. Children in the age group
from .5 to 2 yr were found to have a mean thyroid mass of 2.1 g,
while the adult group had a mean mass of 18.3 g. For this
illustration, the same values are used as employed by the ICRP
(20 g for the adult thyroid mass and 1.8 g for that of a
6-month-old child), which are also consistent with the
recommendation of Bryant (Br69)»
Organ Uptake Fraction, f2'
The fraction of a radionuclide taken up from the blood in an
organ is strongly correlated with the size of the organ, its
metabolic activity, and the amount of material ingested. Iodine
introduced into the bloodstream is rapidly deposited in the
thyroid, usually reaching a peak slightly after 24 hours. The
uptake of iodine-131 by the thyroid is similar to that of stable
iodine in the diet and can be influenced by sex and dietary
differences. There can be considerable variation among
populations.
Dunning and Schwarz (Du81) found a mean f2' value of 0.4?
for newborns, 0.39 for infants, 0.47 for adolescents, and 0,19
for adults. This analysis uses f,1 values of .35 and .15
for a child and adult, respectively.
Effective Half-Life, T1/2
Some data suggest a strong correlation between biological
half-lives of radionuclides in organs in the body and- the age of
the individual. Children are expected to exhibit faster
elimination rates and greater uptakes (Ro58). For iodine, a
range of biological half-lives of 21 to 200 days for adults has
been observed, and a similarly wide range would be expected for
other age groups (Du81). Rosenberg (Ro58) found a significant
correlation between the biological half-life and the age of the
individual and an inverse relationship between uptake and age in
subjects from 22 to 50 yr of age. Dunning and Schwarz (Du81)
concluded that for adults the observed range was from 21 to 372
days; for children in the age group from ,5 to 2 yr, the range
was 4 to 39 days.
In light of the possible inverse relation between the
biological half-life and the f, value, this analysis uses
biological half-lives of 24 ana 129 days, respectively, for
children and adults, based on the paper by Bryant (Br69).
Including the effect of radioactive decay, these values imply an
effective half-life of 6 days in adults and 8 days in children.
5-2?
-------
effective energy per disintegration (MeV/dis) of a
radlonuclide within an organ depends on the decay energy of the
radionuclide the effective radius of the organ containing the
(ICRP59), It is expected, therefore, that E is an
age-dependent parameter which could vary as the size of the organ
While very little work has been done in determining E
for radionuclides, some information has been published for
iodine-131 cesium-is?. Considering the differences between
child the adult thyroid, Bryant (Br69) estimates E to be
0.18 MeV/dis for the child and 0.19 MeV/dis for the adult. The
above values correspond to a 6-month-old child with a mass of
1.8 g an £2 value of 0,35, The corresponding E value for the
adult calculated for a 20-g thyroid with an f2 value of 0.3.
Taking into account all the age-dependent factors discussed
above, this analysis indicates that, for a given concentration of
1-131 in milk, the estimated dose rate to the thyroid of a
6-month-old child would be approximately 13 times that to an
adult thyroid. In other words, use of adult parameters would
underestimate the thyroid dose to the child by about a factor of
13,
5.3.1.6.8 Significance ofParameter Variabililty toEPA
Dose and Risk Assessments
In its radiological risk assessments, EPA is generally
interested in estimating the risk to an average individual due to
chronic lifetime exposures, variation in dosimetric parameters
between people between age groups is of reduced importance in
this context because such variation gets averaged over a
population and/or over a lifetime. Nevertheless, it should be
Jcept in that some individuals in a population going to
be at higher risk from a -given exposure. Furthermore, despite
such averagingf parameter variability can contribute
substantially to the uncertainty in the dose and risk estimates.
Parameter variation among individuals contributes
uncertainty to the models by causing random errors in any
human data upon which the dosimetric models are based.
To extent that the subjects from whom such data are collected
atypical of the U.S. population (e.g., with respect to health
status), parameter variation may also be a source of bias. In
this respect, since the parameters contained in the dosimetric
models were estimated for adult males/ primarily, they may not
provide an adequate basis for calculating the average dose or
risk in where age- and sex-related variations in these
parameters are large. This problem becomes more significant, in
light of the generally higher risks associated with a given dose
for childhood exposures (see Chapter 6); if doses are also higher
in childhood, the enhanced effect on risk will be compounded.
5-28
-------
3 . 1 . 6 . 9
.Organ.J3o.se .........
As In any predictive exercise, it is useful to question the
reliability of the predictions. Variations in environmental
levels, dietary and life style preferences , and the variability
of controlling physiological and metabolic processes contribute
to the distribution of dose among members of the
population. Superimposed on this variability is a component of
uncertainty arising from limitations in the predictive ability of
the dosimetric models themselves. Various approaches have been
taken to understand and quantify these uncertainties.
It has recently become popular to estimate the uncertainty
by computing the distribution of- dose among exposed individuals.
This approach consists of repeated solution of the dosimetric
model using parameter values selected at random from a frequency
distribution of potential values suggested in the literature. It
is assumed that the dosimetric model has been properly
formulated^ although 'these models were developed to yield point
estimates. Despite these and other difficulties, propagation of
parameter uncertainty through the dosimetric equation can provide
a measure of the model uncertainty. Application of these methods
to the estimation of dose from iodine-131 and cesium-13?
ingest ion can be found in the literature (Du8l, Sc82) .
An alternative approach to assessing the potential
variability is to consider that the observed frequency
distribution of a measurable quantity is closely related to dose.
Cuddihy and co-workers (Cu79) have investigated the variability
of selected target organ deposition among test animals and some
individuals exposed. However , they did not address differences
in age, gender, magnitude or duration of exposure.
5.3.1,6.10 Uncertainty Cl ass i flea t ion of Radigniicl
In this section, radionuclides of interest are classified in
terms of the uncertainties in estimated dose per unit intake.
Nuclides are placed in broad groups, largely reflecting the
general status of information on their biokinetic behavior in
body* It is assumed that the uncertainty associated with the
calculation of the energy, deposition in the target tissues is a
minor contributor to the overall uncertainty.
Classif ication vof Uncertainty _i_n Radionuclide Pose
Establishing numerical values of uncertainty for model
estimates of each of the many radionuclides, for each route of
exposure, is- a formidable task. Even if there is agreement on
the definition of uncertainty, any quantification will be
arbitrary to a degree. No model has been verified in for any
long-term exposure scenario; some of the models may be
fundamentally wrong in their formulation. In addition, the data
selected to establish the parameters used in the model may not be
5-29
-------
of the population being evaluated.
informed scientific judgment in
level of uncertainty In a model.
A broad categorization of radionuciides reflecting
estimated magnitude of the dosimetric uncertainties is presented.
Because of the problems cited above with respect to the
development of models and model parameters, it is quite possible
that the error in model estimates may be larger than indicated in
some cases. Nevertheless, this exercise is useful since it
provides some perspective on the magnitude of the uncertainties
in light of current evidence and focuses attention on the largest
gaps in knowledge. Ultimately, however, better quantification of
dose estimates and their associated uncertainties can be obtained
only through the development and verification of improved
dosimetric models,
Radioisotopes behave biologically like their stable
elements. The elements, in turn, can be broadly grouped as: (1)
essential elements and their analogs, (2) inert gases, (3) well-
studied toxic metals and (4) others. Uncertainties for each of
these categories will be expressed as multiplicative factors,
which roughly estimate the 95% upper and lower confidence
interval limits. [Since the interval is based on judgment, a
preferable term would be "credibility interval" (NIH85).]
Group I - Essential Elements and Their Analogs
Essential elements are controlled by homeostatic mechanisms
to within narrow tolerances. Usually, analogs of essential
elements have distribution and deposition patterns similar to
those of the essential element. The uncertainty expected in
calculated dose for essential elements is a factor of two or less
in major critical organs, perhaps 3 or less in other significant
tissues organs. The expected dose uncertainty for analogs of
essential elements is perhaps a little greater, a factor of 3 or
less in major organs and up to 5 or more in less significant
tissues. Important radionuciides of essential elements include
hydrogen-3, carbon-14, phosphorus-32, potassiurti-4Q, calsium-45,
cobalt-60, iodine-129, and iodine~131»* important analogs include
strontium™89, strontium-90, cesium-134, cesium-137? radium-226,
and radium-228.
Group II - Inert Gases
Uptake and retention of inhaled inert gases has been fairly
well studied. The uncertainty in dose, particularly average
whole body dose, is not expected to be large. However, the gases
do not distribute uniformly in body tissues, and the effect of
distribution on organ dose estimates has not been carefully
addressed. The uncertainty in the calculated dose is expected to
be about a factor of 2. This group includes, but is not limited
to argon-41, krypton-85, xenon-133, and radon-222.
5-30
-------
Ill - Well-Studied Toxic
A number of elements have been extensively In
animals with limited information available for
here include toxic elements encountered in industrial activities,
e.g., mercury, cadmium, lead, and uranium, for which.
carried out to help establish safe working conditions.
available information is not sufficiently complete to identify
the dominant processes governing the biokinetic behavior or is
simply fragmentary. For example, while much information
on the biokinetics of uranium, considerable uncertainty
associated with the absorption to blood from the small intestine.
Uncertainties for dose estimates in this group of elements would
be variable, ranging from 2 or less for lead up to about 5 or
more for polonium, thorium, uranium, and the transuranics.
Nuclides in this group include, but are not limited to lead-210,
polonium-210, uranium-235f uranium~238, thorium-230, thorium-232,
plutonium-239, plutonium-241, and aiaericiuro-241.
Group IV - Other Elements
For a number of radionuclides information is largely limited
to data from animal studies. While animal studies often are the
major source of detailed information on the processes governing
the biokinetics, the lack of a general framework for
extrapolations to man and the limited information upon which to
judge the reasonableness of the extrapolations suggest that
estimates must be considered to be potentially in error by at
least an order of magnitude. Nuclides in this group include, but
are not limited to cerium-144 and other rare earth elements,
technetium-99f curium~244, californium-252, etc,
The groupings listed above represent the Agency's best
judgment on the uncertainty of internal radionuclide
estimates. The primary source of uncertainty is in the
biokinetic modeling with little uncertainty in physics.
magnitudes of the uncertainties posited for each group of
radionuclides should be regarded as only rough estimates;
however, the qualitative breakdown between groups is fairly
reliable.
SpecificProblems
Certain radioisotopes and aspects of dosimetry unique
problems. While the effect of these problems may be to increase
the uncertainty in dose estimates, the extent of such an
has yet to be evaluated,
Long-Lived Bone Seekers
Radioisotopes with effective half-lives that short
compared to the average life span are expected to be in dynamic
equilibrium. However, some bone seekers have long effective
half-lives; therefore, they do not reach dynamic equilibrium
5-31
-------
during a life span. Since relevant human biokinetic
limited, for such radionuclldes
Nonuniformity of Distribution
The distribution of' an element within an organ may not be
uniform; In particular, the distribution may be nonunifona with
respect to biological targets of interest. This can be a serious
problem with respect to the estimation of relevant doses from
internally deposited alpha emitters, given the short range of
alpha particles in matter. For example,, where an alpha emitter
is distributed nonuniformly in bone, the calculation of doses "to
sensitive cells In the bone and the bone marrow will be
difficult:. Another example is the uncertainty in estimating
doses to cells lining the GI tract from ingested alpha emitters
passing through the tract. In some cases, the mucus lining may
effectively shield the target cells from irradiation.
5.3.2 ExternalDose Models
This section Is concerned with the calculation of dose rates
for external exposure to photons from radionuclides dispersed in
the environment. Two exposure models are discussed? (1)
immersion in contaminated air and (2) irradiation from material
deposited on the ground surface. The immersion source is
considered to be a uniform semi-infinite radionuclide
concentration in air, while the ground surface irradiation source
is viewed as a uniform radionuclide concentration on an infinite
plane. In both exposure modes, the dose rates to organs are
calculated from the dose rate in air.
Dose rates are calculated as the product of a dose rate
factor, which Is specific for*each radionuclide, tissue,
exposure mode, and the corresponding air or surface
concentration. The dose rate factors used were calculated with
the DOSFACTOR code (Ko8la,b). Note that the dose rate factors
for each radionuclide do not include any contribution for decay
products. For example, the ground surface dose factors for
cesima-137 are all zero, since no photons are emitted in its
decay. To assess surface deposition of cesium™137, the ingrowth
of its decay product, metastable barium-137, which is a photon
emitter, must first be calculated.
5.3.2.1 Immersion
For immersion exposure to the photons from radionuclides in
air, EPA assumes that an individual is standing at the base of a
semi-infinite cloud of uniform radionuclide concentration.
Firstf the dose rate factor (the dose rate for a unit
concentration) in air is calculated for a source of photons with
energy EL. At all points In an infinite uniform source,
conservation of energy considerations require that the rates of
absorbed and emitted energy per unit mass be equal. The absorbed
5-32
-------
unit at boundary of a semi-infinite
cloud is just half value. Hence
DRFyfEy) - 1/2K Ey//» {5-23}
where :
DRF.S ™ the immersion dose rate per unit air
concentration (rad v?/Ci s) ;
Ey = emitted photon energy (MeY) ;
k = units conversion factor
« 1.62E-13 (J/MeV) x 3.7B4-1G (dis/s-ci) x
l.OE+3 (g/kg) x 100 (rad kg/J)
= 5.93E4-2 (g rad/MeV Ci s) ; and
/> = density of air (g/m ) .
The above equation presumes that for each nuclide
transformation, one photon with energy Ey is emitted.
rate factor for a nuclide is obtained by adding together the
contributions from each photon associated with the transformation
process for that radionuclide.
5.3.2.2 Ground Surface Irradiation
In the case of air immersion, the radiation field
same throughout the source region. This allows the dose rate
factor to be calculated on the basis of energy conservation
without having to consider explicitly scattering
taking place. For ground surface irradiation, the radiation
field depends on the height of the receptor above the surface,
and the dose rate factor calculation is more complicated.
radiation flux per unit solid angle is strongly on
angle of incidence. It increases from the value for photons
incident from immediately below the receptor to a close
to the horizon. Attenuation and buildup due to scattering
be considered to calculate the dose rate factor, secondary
scattering provides a distribution of photon energies at the
receptor, which increases the radiation flux above that
calculated on the basis of attenuation. Trubey (Tr66)
provided a useful and reasonably accurate expression to
approximate this buildup:
B(M.r) = 1 + C HB r exp(D^ar)
where B^ is the buildup factor (i.e., the quotient of total
energy flux and that calculated for attenuation) only for
5-33
-------
in air? jia is attenuation coefficient at the of
released photon (if1) »• r is the distance between the
source the receptor; and the Berger buildup coefficients c
and Da are dependent on energy and the scattering medium. The
buildup factor is ctimensionless and always has a value greater
than unity. The resulting expression for the dose rate factor at
a height z (m) above a uniform plane is
DRF^Z^Ey) » l/2k(Ey//>)(Mef/P)a{E1(/iaz) + (5-25)
Ca/(l-Da)exp[-(l-Da)/iaz3}
where (uen/p)a is the mass energy-absorption coefficient (
for air at photon energy Ely (MeV) ; E1 is the first order
exponential integral function, i.e.,
Et(x) = J exp (~u)__du
X U (5-26)
Cg and Dg are the buildup coefficients in air at energy E~; and
k=5.93x!0z (g rad/MeV Ci s) as for the immersion calculation.
As for immersion, the dose rate factor for a nuclide
combines the contribution from each photon energy released in the
transformation process.
5.3.2.3 Organ Doses
The dose rate factors in the preceding two sections for
the absorbed dose in air. For a radiological assessment,
absorbed doses in specific tissues and organs are needed. For
this purpose, Kerr and Eckerman (KeSO, KeSOa) have calculated
organ dose factors for immersion in contaminated air. Their
calculations are based on Monte Carlo simulations of the absorbed
dose in each tissue or organ for the spectrum of scattered
photons in air resulting from a uniform concentration of
monoenergetic photon sources. Kocher (Ko81) has used these data
to calculate values of the ratio of the organ dose factor to the
air dose factor, Gk(EL) , for 24 organs and tissues at 15 values
of Ey ranging from 0.01 to 10.0 MeV.
The resulting organ-specific dose rate factor for immersion
is
(5-27)
5-34
-------
specific- mielide, the dose rate factor is
of the contributions from each photon
with the radionuclide
Ideally, a separate set of Gk(EL) values would be
angular and spectral distributions of -incident ph,otons from a
uniform plane source. Since these data are not available, Kocher
of Gk(EL) values for calculating
factors for both types of exposure (Ko81).
5.3,2.4 Uncertainty Considerations in External Factors
In computing the immersion dose rate factor in
factor of 1/2 in Equation 5-27, which accounts for
infinite geometry of the source region, not provide a
rigorously correct representation of the air/ground interface.
However, Dillman (Di74) has concluded that this result is within
the accuracy of available calculations. The radiation field
between the feet and the head of a person standing on
contaminated ground is not uniform, but for source photon
energies greater than about 10 keV, the variation value
at l meter becomes minimal, A more significant source of
is the assumption of a uniform concentration, Kocher (Ko81)
shown that sources would have to be approximately uniform
distances of as much as a few hundred meters from the receptor
for the rate factors to be accurate for either
surface or immersion exposures. Penetration of deposited
materials into the ground surface, surface roughness, terrain
irregulari'i€3f as well as the shielding provided by buildings to
their inborn v,ants, all serve to reduce doses.
The effect of using the same factors to relate
to dose a,:i air for ground surface as for immersion
ii";k. not been studied, The assumptions that radiation,
field the ground surface source is isotropic
energy distribution as for immersion clearly do not bold true,
precise estimates of these distributions likely
to change the organ dose rate factors substantially,
Kocher (Ko81) has noted that the idealized photon
factors "likely to be used quite extensively even for
exposure conditions for which they are not strictly applicable...
because realistic estimates are considerably difficult
expensive [to make]."
5-35
-------
5.4
Cr83
Cu79
D174
DU79
Du81
Fi35
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Bryant, P.M. , "Data for Assessments Concerning
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, R.G., McClellari, R.O., and Griffith, W.C.,
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ICRP59
ICRP66
XCRP75
ICRP77
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ICRU8Q International Commission on Radiation
Measurements„ ICR0 Report No 33, B.C.,
1980.
KeSO Kerr, G.D., and Eckerman, K.F., Oak Ridge National
Laboratory, private communication; see also Abstract
P/192 presented at the Annual Meeting of the Health
Physics Society, Seattle, Washington, July 20-25, 1980.
KeSOa Kerr., G.D., "A Review of Organ Doses from Isotropic
Fields of X-Rays", Health Phvs. , J3_9(l):3f 1980.
Ki78a Killough, G.C., Dunning, D.E Jr., Bernard, S.R, and
Pleasant, J.C., Estimates, of Internal Dose Equivalent
to 22 Target Organsfor Radionuclides Occurringin
Routine Re lea, s e s f r. om Nu c 1 e ar _ Fuel Cy c 1 e Fa c i lit ies,
Vol. l, Report No. ORNL/NUREG/TM-19Q, Oak Ridge
National Laboratory, Tennessee, June 1978.
Ki78b Killough, G.C., and Rohwer, P.S., "A New Look at the
Dosimetry of 1 C Released to the Atmosphere as Carbon
Dioxide", Health Phvs.. 34(2):141, 1978.
KoSla Kocher, D.C., and Eckerman, K.F., "'Electron Dose-Rate
Conversion Factors for External Exposure of the Skin",
Health Phvs.. 40(1)-67t 1981.
KoSlb Kocher, D.C., "Dose-Rate 'Conversion Factors for
External Exposure to Photon and Electron Radiation from
Radionuclides Occurring in Routine Releases from
Nuclear Fuel-Cycle Facilities", HealthPhvs.,
38(4)J543-621, 1981.
NAS80 National Academy of Sciences - National Research
Council, The Effects on Populations,..jgf^JSxjposar^ to Low
Levels of Ionizing, Radiation,. Report of the Committee
onthe_JBi..Q.l.Qgica_l..Effects o,f___Ioni,zing RadiatioiL-XBEIE
III1, Washington, D.C., 1980.
NCRP71 National Council on Radiation Protection and
Measurements, Ba.sig Radiation Protection Criterlaf NCRP
Report No. 39, Washington, D.C., 1971.
Ne84 Nelson, C.B., and Yang, ¥,, An Estimation of the Daily
Average Food Intake by Age and Sex for Use in Assessing
the Radionuclide Intake of Individuals in the General
Population, EPA 520/1-84-015, 1984.
NIH85 National Institutes of Health, Report of the National
Institutes of Health Ad Hoc Working Group to Develop
Radioepidemiological Tables, NIH Publication No.
85-2748, U.S. Government Printing Office, Washington,
DC 20402, p 92, 1985.
5-38
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ORNL85
Ph85
Ro58
SC82
Sn74
Sp73
SuSl
Th77
Th?8
Tr66
Oak Bidge national Laboratory,, of
from Exposure to Radioactive Pollutants, ORNL/SM-7745,
Ridge, Term,, 1981.
Oak Ridge National Laboratory, "Report of Current Work
of the Metabolism and Dosimetry Research Group",
ORNL/TM-9690, Oak Ridge, Tennessee, 1985.
Phalen, R.F., Oldham, M.J. , Beaucage, C.B.,
Crocker, T.T., and Mortensen, J.D., Postnatal
Enlargement of Human Tracheobronchial Airways and
Implications for Particle Deposition, Aitat. Rec. 21J2;
368, 1985.
Rosenberg, G., "Biologic Half-life of 151I in the
Thyroid of Healthy Males" , J..._.CJJLn. Endocrinol. Metab.,
It, 516-521, 1958.
Schwarz, G., and Dunning, Jr., D.E., Imprecision in
Estimates of Dose from Ingested Cs-137 due to
Variability in Human Biological Characteristics, Health
Phys. 11, 631-645, 1982,
Snyder W.S., Ford, M.R., Warner, G.G. , and
Watson, S.B., A Tabulation of Dose Equivalent per
Microcurie-Day for Source and Target Organs of an Adult
for ¥arious Radionuclides, Oak Ridge National
Laboratory, QRNL-SOOO, 1974,
Spoor, N.L., and Hursh, J.B., "Protection Criteria",
Chapter 5 in Uraiuum, Plutoniuro and the, Transplutonic
Elements, Springer, New York, 1973.
Sullivan, R.E., Nelson, M.S., Ellett, W,H«,
Dunning, D.E. Jr., Leggett, R.W., Yalcintas, M.G. and
Eckerman, K.F., Estimates of Health Risk frop Exposure
.tp_Rad,loi.Stive Pol 1 utant.s, Report No. ORNL/TM-7745, Oak
Ridge National Laboratory, Oak Ridge, Tennessee, 1981.
Thorne, M.D., "Aspects of the Dosimetry of Alpha-
Emitting Radionuclides in Bone with Particular Emphasis
on 2 Ra and 239Pu», Phys. Med. Biol. , 22,! 36-46, 1977.
Thurlbeck, W.M. "Miscellany", 287-315 in The Luna;
Structure Functionand Disease, Thurlbeck, W.M. and
Abell, M.R,, editors, The Williams and Wilkins Co.,
Baltimore, Maryland, 1978.
Trubey, O.K., A Survey of Empirical Functions Used to
Fit Gamma-Ray Buildup Factors, Oak Ridge National
Laboratory Rep., ORNL-RSIC-10, 1966.
5-39
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OF
TO LOW OF
This describes how EPA estimates the risk of fatal
cancer, serious genetic effects, other detrimental
effects caused by to low levels of Ionizing radiation.
Ionizing radiation refers to radiation
from atoms in a through which it passes. The highly
reactive electrons ions created by this process in a living
cell can produce, through a series of chemical reactions,
permanent (mutations) in the cell's genetic material,
DMA. These may result in cell death or in an abnormally
functioning cell. A mutation in a germ cell (sperm or ovum)
be transmitted to an offspring and be expressed as a genetic
defect in that offspring or in an individual of a subsequent
generation; such a defect is commonly referred to as a
effect. There is also strong evidence that the induction of a
mutation by ionizing radiation in a non-germ (somatic) cell
serve as a step in the development of a cancer. Finally,
mutational or other events, including possible cell killing,
produced by ionizing radiation in rapidly growing
differentiating tissues of an embryo or fetus can give rise to
birth defects; these are referred to as teratologleal, effects.
At. acute doses above about 25 radsf radiation induces other
deleterious effects in man; however, for the low doses
rates of interest in this document, only those three kinds of
effects referred to above are thought to be significant.
Most important from the standpoint of the total societal
risk, from exposures to low-level ionizing radiation risks
of cancer genetic mutations. Consistent with our current
understanding of their origins in terms of DNA damage,
believed to be stochastic effects; i.e., the probability (risk)
of these effects increases with the absorbed of radiation,
but the severity of the effects is independent of dose. For
neither induction of cancer nor genetic effects, moreover, is
there any convincing evidence for a "threshold,," i.e., dose
level below which the risk is zero. Hence, so far as is known^
any dose of ionizing radiation, no matter how small, might give
rise to a cancer or to a genetic effect in future generations.
Conversely, there is no way to be certain that a given of
radiation, no matter how large, has caused an observed cancer in
an individual or will cause one in the future,
Beginning nearly with the discovery of x-rays in 1895 but
especially since World War II, an enormous amount of research has
been conducted into the biological effects of ionizing radiation.
This research continues at the level of the molecule, cell,
the tissue, the whole laboratory animal, and man. There two
fundamental aspects to most of this work:
-------
radiation to a (cell
etc.), This (dosimetry), which
involve consideration of physiological, metabolic,,
factors, is fully In 5.
2, of effects of a
with a certain (or ,
For of risk to
to ionizing radiation!. important information
epideraiological in which of
in an Irradiated population is to
in an control population. epideiiiological
radiation-induced extensive, &s a
result, risk be estimated to within an order of magnitude
with a of confidence. Perhaps for only
carcinogen - tobacco - is it possible to risks
reliably.
Nevertheless, in the on radiation
risks. Ho clear-cut evidence of excess genetic effects
in Irradiated populations, for probably
to limited in exposed cohort providing
to a close-response, .Likewise, no statistically
significant of cancers has been demonstrated below about 5
of interest frora the of
exposures. Since epideiniological
In respects/ risk rely on
to estimate the risk from exposures to low-
level ionizing radiation. The choice of models, of necessity,
Involves subjective judgments but should be on all relevant
of collected by both laboratory scientists
.epidemiologists* Thus, radiation risk Is a
to evolve as scientific information
of cancer
largely on the results of a National of
(IAS) as given in the BEIR III report (NAS8Q). The
radiation risks at low exposure levels. As by
of the Academyf "We believe that report will be
helpful to EPA other agencies as they radiation
protection It provides the scientific
which be decided after nonscientific social values
taken into account."
In this discussion, the various assumptions in
calculating risks on 1980
outlined, risk estimates are with
by scientific groups, such as 1972 BEIR
(NJk572) , United Nations Scientific on
of Atomic Radiation. (UNSCEAR77, 82, 86, 88), and the
national Radiological Protection Board of the United Kingdom
(St88), information on radiation risks is incomplete,
6-2
-------
of risk on various not be highly
accurate * This discussion Identifies of deficiencies in
available data points out possible sources of
in current risk estimates. Nevertheless, the risk estimates
by believed to be reasonable in light of
evidence ,
Sections 6.2 to 6.2.6 consider the cancer risk resulting
from whole-body exposure to low-LET (see Chapter 5} radiation,
i.e., sparsely ionizing radiation like the energetic electrons
produced fay x-rays or gamma rays. Environmental contamination by
radioactive materials also leads to the ingestion or Inhalation
of the material and subsequent concentration of the radioactivity
in selected body organs. Therefore, the cancer risk resulting
from low-LET irradiation of specific organs is examined in
Sections 6,2.7 to 6.2,9. Sections 6.2.10 to 6.2.12 summarize
recent developments in radiation risk estimation and discuss the
uncertainties in the estimates.
Organ doses can also result from high-LET radiation, such as
that associated with alpha particles. The cancer risks when
high-LET radiation is distributed more or less uniformly within a
body organ is the third situation considered (Section 6.3).
Because densely Ionizing alpha particles have a very short range
in tissue, there are exposure situations where the dose
distribution to particular organs is extremely nonuniform. An
example is the case of inhaled radon progeny, Po-218, Pb-214, and
Po-214. For these radionuclides, cancer risk estimates are based
on the of radon progeny inhaled rather than the estimated
dose, which is highly nonuniform and cannot be well quantified.
Therefore, risk estimates of radon exposure are examined
separately (Section 6,4).
Section 6.* 5 reviews and quantifies risk of deleterious
genetic effects from, radiation and the effects of exposure in
utefo on the developing fetus. Finally, in Section 6,6, cancer
genetic risks from background radiation calculated using
the models described in this chapter.
6.2 ESTIMATES FOR LOW-LET RADIATION
6 = 2.1
There are extensive human epidemiological data upon which to
base risk estimates for radiation-induced cancers. Most of the
observations of radiation-induced carcinogenesis In humans are of
groups exposed to low- LET radiations. These groups include the
Japanese A-bomb survivors and medical patients treated with
diagnostic or therapeutic radiation, most notably for ankylosing
spondylitis in England from 1935 to 1954 (Sm78) . Comprehensive
reviews of these and other data on the carcinogenic effects of
human available (UNSCEAR??f NAS80) .
6-3
-------
The Important source of epidemlological on
radiogenic cancer Is the population of Japanese
survivors have been studied for more 38
of then (the Life Span Study Sample) followed
since 1950-in a carefully planned and monitored epidemiologicai
survey (Ka82, Wa83), They are the largest group that
studied, and they provide the most detailed information on
response pattern for organs, fay age and sex, over a wide of
of low-LET radiation. Unfortunately, the 1980 BEIR
Committee's analysis of the A-bomb survivor data collected up to
1974 was prepared before bias in the dose estimates for the
survivors (the tentative 1965 dose estimates, T65) became widely
recognized (Lo81). It is now clear that the T65 dose equivalents
to organs tended, on average, to be overestimated (Bo82,
RERF83,84) so that the BEIR Committee's estimates of the risk per
unit dose are likely to be too low. A new dosimetry system,
termed the Dosimetry System 1986 (DS86), is now nearly complete,
and preliminary analyses of the risk based on DS86 have been
published (Pr87,88; Sh87)„
At present, the "BEIR V Committee" of the National Academy
of Sciences is preparing a report on radiation risks in light of
DS86 and other new information. A detailed reevaluation of EPA's
current risk estimates is indicated when this report is issued.
h brief discussion of the new dosimetry and its likely effect on
risk estimates is included.
To derive risk estimates for environmental exposures of the
general U.S. population from epidemiologicai studies of
irradiated populations requires some extrapolation. First, much
of the useful epidemiologicai data pertain to acute of
50 rad or higher, whereas we are concerned with small chronic
incremental to the natural background level of about 100
mrad/year. Second, epidemiologicai follow-up of
study cohorts is incomplete,' hence, obtaining lifetime risk
estimates involves some projection of risk beyond the period of
follow-up. Third, an extrapolation must be made from a study
population to the U.S. population. In general, these populations
will differ in various respects, for example, with respect to
organ-specific, base-line cancer rates.
Data pertaining to each of these three extrapolations exist;
but in no case are they definitive. Hence, uncertainty in our
risk estimates is associated with each of them. These
uncertainties are in addition to statistical uncertainties in the
epidemiologicai data (sampling variations) and errors in
determinations. Generally speaking, it is the former, modeling
uncertainties, which are more important.
6.2.2 pose_Response Functions
Radiogenic cancers in humans have been observed, for the
most part, only following doses of ionizing radiation that are
6-4
-------
-------
-------
-------
Preliiiinary on DS86 dosiiaetry
quadratic generally provides a fit to
do (ShB8), laboratory
risk in nay increase linearly with
at low (Gr85)-. Thus, though a quadratic at
low (or even a threshold) cannot now be definitively
out, EPA not consider such models suitable for radiation
risk assessment.
Finally, "supralinear models/1 in which the risk coefficient
decreases with increasing close (downward bending, or convexf
response curve) should be mentioned. Such models imply that
risk at low doses would actually be greater than predicted by
linear interpolation from higher doses. The evidence
radiation biology investigations, at the cellular as well as the
whole animal level, indicates that the dose response curve for
induction of mutations or cancer by low-LET radiation is either
linear or concave upward for doses to mammalian systems below
about 250 rads (NCRP80). Somewhere above this pointf the dose
response curve often begins to bend overs this is commonly
attributed to "cell-killing." The A-bomb survivor data, upon
which most of these risk estimates depend, is dominated by
individuals receiving about 250 rads or less. Consequently, the
cell-killing phenomenon should not produce a substantial
underestimate of the risk at low doses.
Noting that human beings, in contrast to pure strains of
laboratory animals, may be highly heterogeneous with respect to
radiation sensitivity, Baum (Ba73) proposed an alternative
mechanism by which a convex dose response relationship could
arise. He pointed out that sensitive subgroups may exist in the
population who are at very high risk from radiation. The result
could be a steep upward slope in the response at low
predominantly reflecting the elevated risk to of
subgroups, but a decreasing slope at higher doses as the risk to
these highly sensitive individuals approaches unity.
Based on current evidence, however, it seems unlikely that
the effect postulated by Baum would lead to substantial
overestimation of the risk at low doses. While there may
be small subgroups at very high risk, it is difficult to
reconcile the A-bomb survivor data with a strongly convex dose
response relationship. For example, if most of the leukemias
found among the cohort receiving about 200 rads or more in fact
arose from subgroups whose risk saturated below 200 rads, then
many more leukemias ought to have occurred in lower dose cohorts
than were actually observed. The U.S. population, it could be
argued, may be more heterogeneous with respect to radiation
sensitivity than the Japanese. The risk of radiation-induced
breast cancer appears, however, to be similar in the two
populations, so it is difficult to see how the size of
hypothetical sensitive group could be large enough in former
to alter the conclusion reached above. The linear dose-response
-------
-------
a in
6.2,4
of the exposed populations have been
enough to the full effects of their exposures if, as
currently "thought, most radiogenic cancers occur throughout an
exposed person's lifetime (NAS80) . Therefore, another major
choice that must be made in assessing the lifetime risk
due to radiation is to select a risk projection model to
the risk for a longer period of time than currently available
observational data will allow.
To estimate the risk of radiation exposure that is
the years of observation, either a relative risk or an absolute
risk projection model (or suitable variations) may be used.
These models are described at length in Chapter 4 of 1980
report (NAS80). The relative risk projection model projects the
currently observed percentage increase in annual cancer risk per
unit dose into future' years, i.e., the increase is proportional
to the underlying (baseline) risk. An absolute risk model
projects the average annual nurober of excess cancers unit
dose Into future years at risk, independent of the risk.
Because the underlying risk of most types of cancer
increases rapidly with age, the relative risk model predicts a
larger probability of excess cancer toward the end of a person's
lifetime. In contrast, the absolute risk model predicts a
constant incidence of excess cancer across time. Therefore,
given the incomplete data and less than lifetime follow-up, a
relative risk model projects a somewhat greater total lifetime
cancer risk than that estimated using an absolute risk model.
Neither HAS BEIR Committee -nor other scientific
(e.g., UNSCEAR) have concluded which projection, model is
appropriate choice for most radiogenic cancers. However, recent'
evidence favors the relative risk projection model for solid
cancers. As pointed out by the 1980 HAS BEIR Committee:
If the relative-risk model applies, then the of
exposed groups, both at the time of exposure as
they move through life, becomes very important.
is now considerable evidence in nearly all the adult
human populations studied that persons irradiated at
higher ages have, in general, a greater excess risk of
cancer than those irradiated at lower ages, or at
they develop cancer sooner. Furthermore, if they
irradiated at a particular age, the excess risk
to rise'pari gassu [at equal pace] with the risk of
population at large. In other words, the relative-risk
model with respect to cancer susceptibility at
as a function of age, evidently applies to kinds
6-10
-------
Of C3HC61T tticit llS'VS ]366B, ObS
-------
However, it is important to that calculated
lifetime risk of developing a fatal cancer from a of
varies with the age of the recipient at the of
.
6.2,5 EPA As§mnptiQ.ss ..about Cancer JjjgksL-jte suiting from
Low™LET Radiation
estimates of radiation risks, presented in Section
6*2*6,, based on a presumed linear dose response function.
Except for leukemia and bone cancer, where a 25-year expression
period for radiogenic cancer is used, a lifetime expression
period is used, as in the NAS report (NAS80). Because the most
recent Life Span Study Report (Ka82) indicates that absolute
risks for solid cancers are continuing to increase 33 years after
exposure, the 1980 NAS Committee choice of a lifetime expression
period appears to be well founded.
To project the number of fatalities resulting from leukemia
bone cancer, EPA uses an absolute risk model, a minimum
induction period of 2 years, and a 25-year expression period. To
estimate the number of fatalities resulting from other cancers,
EPA has used a relative risk projection model (EPA84), a 10-year
minimum induction period, and the remaining balance of an exposed
person*s lifetime as the expression period.
6.2.6 Methodology for Assessing the Risk of Radiogenic__C_ancer
uses a life table analysis to estimate the number of
fatal radiogenic cancers in an exposed population of 100,000
persons. This analysis considers not only death due to
radiogenic cancer, but also the probabilities of other competing
causes of death which are, of course, much, larger vary
considerably with age (BuSl, Co78). Basically, it calculates for
0 to 110 the risk of death due to all causes by applying the
1970 mortality data from the National Center for Health
Statistics (NCHS75) to a cohort of 100,000 persons. Additional
details of the life table analysis are provided in Appendix B.
It should be noted that a life table analysis is required to use
the age-dependent risk coefficients in the BEIR III report. For
relative risk estimates, EPA has used age-specific cancer
mortality data also provided by NCHS (NCHS73). The EPA computer
program used for the life table analysis was furnished to the NAS
III Committee by EPA and used by the Committee to prepare
its risk estimates. Therefore, the population base and
calculations should be essentially the same in both the NAS and
EPA analyses.
Both absolute and relative risk models have been considered
to project the observed risks of most solid radiogenic cancers
beyond the period of current observation. The range of estimated
fatal cancers resulting from the choice of a particular
projection model and its internal assumptions is about a factor
of 3. Although the relative risk model has been tested in some
J-12
-------
only for lung breast cancer (La?8), on current
it to be the better projection for solid
Therefore^ It been adopted for risk in
this report. Previously, EPA an of
by absolute and relative risk projection
To cancer risk from low-LET, whole-body,
lifetime exposure^ the analysis uses relative risk projections
(the III L-L model) for solid cancers risk
projection for leukemia bone cancer (the BEIR 111 L-L ,
Since expression period for leukemia bone cancer is less
follow-up period, the risk values would be
calculated for cancers using either projection method, For
a to whole body, this procedure yields about 400
fatalities million person-rad (for BEIR III linear-
quadratic model, a low-LET whole-body dose would yield an
estimated lifetime risk of about 160 fatalities million
person-rad),
III also presented estimates of soft tissue
cancer incidence risk coefficients for specific sites, as a
function of at exposure, in its Table ¥-14. By summing
site-specific risks, it then arrived at an estimate for
whole-body risk of cancer incidence {other than leukemia
cancer) as given in Table V-3Q. Finally, by using
incidence/mortality ratios given in Table V-15 of
(NAS80), the results in Table ¥-30 can be in of
mortality to yield (for lifetime exposure) a risk of
about 242 776 cancer fatalities per 106 person-rad,
on an absolute or a relative risk projection
respectively^, is to estimate lifetime risk.
1.7 and 2,1 times their counterparts for BEIR III
,
2 5.2 times the LQ-L values,
all a uniform dose to all tissues at risk in
In practice, such uniform whole-body exposures seldom occur
particularly for ingested or inhaled radioactivity. The next
section describes how this risk estimate is apportioned for
whole-body when considering the risks following
of specific organs,
6.2.7
For most sources of environmental contamination, inhalation
and ingestion of radioactivity are more common than external
exposure. In many cases, depending on the chemical physical
characteristics of the radioactive material, inhalation
ingestion result in a rtonuniform distribution of radioactive
materials within the body so that organ systems receive
higher than others. For example, since iodine isotopes
concentrate preferentially in the thyroid gland, the to this
organ be orders of magnitude larger than the. average to
i-13
-------
To probability that fatal cancer at a
particular site, EPA performed life tabie analyses
cancer type using the information on cancer incidence
mortality in N&S8G, NAS80 published incidence risk coefficients
(NAS80 Table V-14) and mortality to incidence ratios (NASSQ Table
V-15). The data in Tables 6-1 and 6-2 are from these tables with
the exception of the mortality to incidence ratios for thyroid
and lung cancer. Since not all forms of thyroid cancer be
induced by radiation and since, for those that arep a more
reasonable mortality to incidence ratio would be 0.1 (NRC85), EPA
has used that value in its calculations. Lung cancer incidence
and mortality have both shown an Increasing trend between 1970
and 1980. Since incidence leads mortality, an uncorrected
mortality to incidence ratio gives a low estimate of the fraction
of those persons who, having been diagnosed with lung cancer,
will die of that disease. Therefore, a mortality to incidence
ratio of 0.94, based on long-term survival studies by the
National Cancer Institute for lung cancer (J. Horn, private
communication), has been used.
Risk coefficients for a site-specific relative risk model
were calculated as follows:
1. Mortality risk coefficients for an absolute risk model
were calculated using the data in Tables 6-1 and 6-2.
2. Following the procedure used in NAS80, absolute risks
at an absorbed dose rate of 1 mrad/y were calculated
for each site for males and females in each age group.
A 10-year minimum latency and a 20-year plateau - i.e.,
a 30-year follow up - was used for these calculations.
3. The relative risk coefficients (1/rad) for each
group providing the 30-year projected risk
then calculated. Following the NAS80 convention, the
values calculated for ages 10-19 were used for ages 0~
9. For consistency, this report uses this convention
for all cancers including lung and.breast, for which
the NAS80 absolute risk coefficients are zero in the
first decade. For calculating thyroid risks, the
relevant age-specific mortality rate was considered to
be one-tenth of the corresponding incidence rate.
4, Male and female risks for lifetime expression of risk
at 1 mrad/y were then calculated and combined to obtain
estimates for the general population,
EPA used the NCHS 1970 life table and mortality data for all
these calculations. Male and female cohort results were combined
presuming a male:female sex ratio at birth of 1.0511, consistent
with the expected lifetimes at birth for the 1970 male, female,
and general cohort life tables.
6-14
-------
Table 6-1. Site-specific incidence risk coefficients
(ID"6 rad-y) .
Age,, at Exposure
Site
Males
Thyroid
Breast
Lung
Esophagus
Stomach
Intestine
Liver
Pancreas
Urinary
Lymphoma
Other
All Sites
Females
Thyroid
Breast
Lung
Esophagus
Stomach
Intestine
Liver
Pancreas
Urinary
Lymphoma
Other
All Sites
Source: NAS80f
0-9
2.20
0.00
0.00
0,07
0.40
0.26
0.70
0.24
0.04
0,27
0.62
4.80
5.80
0.00
0.00
0.07
0.40
0.26
0.70
0.24
0.04
0.27
0,62
8,40
Table
10-19
2.20
0.00
0.54
0.07
0.40
0.26
0.70
0.24
0.23
0.27
0.38
5.29
5.80
7.30
0.54
0.07
0.40
0.26
0.70
0.24
0.23
0.27
0.38
16.19
V-14
20-34
2.20
0.00
2.45
0.13
0.77
0.52
0.70
0.45
0.50
0.27
1.12
9.11
5.80
6.60
2.45
0.13
0.77
0.52
0.70
0.45 -
0.50
0.27
1.12
19.31
35-49
2,20
0.00
5.10
0.21
1.27
0.84
0.70
0.75
0.92
0.27
1.40
13.66
5.80
6.60
5.10
0,21
1.27
0.84
0,70
0.75
0.92
0.27
1.40
23.86
504-
2.20
0.00
6.79
0.56
3.35
2.23
0.70
1.97
1.62
0.27
2.90
22.59
5.80
6,60
6.79
0.56
3.35
2.23
0.70
1.97
1.62
0.27
2.90
32.79
6-15
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_Table 6-2. Site-specific mortality to
Site Male
0.10 0.10
—— 0.39
0.94 0,94
1,00 1.00
0.75 . 0.78
0=52 0.55
Liver 1,00 1.00
Urinary 0.3? 0=46
0.73 0.75
0.65 0,50
Source: NASSQ, Table V-15, except thyroid and lung text)
The average risk for a uniform dose to all tissues
calculated to be 542 x 1C)'6, 806 x 10"6, and 678 x 10"6 for
males, females, and the general population, respectively.
It is generally accepted that the risk estimates for the
individual, sites less certain than are the risk for
all sites combined. Table 6-3 jsumxnarizes the relative risk
calculations for III L-"L model. The calculations!
procedure was the as that, outlined above.
risks tabulated in Table 6-3 are slightly different
in NAS80. These differences reflect a correction in
interval for each age group of final
rather than preliminary 1970 mortality data. NAS80
male and female risk estimates presuming a ratio at birth of
1:1, which is not consistent with natality data,
Since total risk for all sites is considered
certain the risk forjeach site individually, the lifetime
risks calculated for the L-L model have been as a constraint
for the of the individual site estimates. The relative risk
coefficient for each site shown in Table 6-4 calculated
by multiplying the coefficient for the unconstrained for
sexjby *^e quotient of the average risk for all
for L-L unconstrained site-specific model. The
risk coefficients are about one-half of the unconstrained values.
The L-L absolute risk model coefficients for
are shown in Table 6-5. The risk coefficient for
obtained by dividing the value for alpha particles
(high-LET) in Table A-2? by an RBE of 8 to obtain a
value of 1.25 x 10"7 per rad~year. The risk coefficients for
leukemia obtained by subtracting the risk coefficients for
-16
-------
Table 6~3 • BEIR III L™Li model for excess fatal cancers othsir
leukemia cancer.
Group 0-9
Risk Coefficients
Male 1.920
Female 2.56?
Risk Coefficients
Male 4.458
Female 4.748
General 4.586
Cohort Deaths at
Male .612
Female .689
General .649
10-19
(10"6 per
1.457
1.955
(1Q"3 per
4.458
4.748
4.586
10"3 rad/y
.609
.686
,647
Risk Unit {10"6
Male 62?
Female 702
General 664
Source: NAS80,
20-34
35-49 50+ All
rad~y) for Absolute Risk Model*
4.327
5.80?
rad) for
2.793
3.875
3.322
5.291 8.808
7,102 11.823
Relative Risk Model
1.007 0,861
1.902 1.586
1.447 1.257
for Relative Risk Model
.563
.824
.690
rad) for
629 39?
703 568
665 481
Table V-2G
.181 .112 2,076
.357 .268 2.823
.26? .188 2.440
Relative Risk Model
134 56 310
252 101 378
193 81 345
6-17
-------
Table 6-4, Mortality risk coefficients (10"' per rad) for
relative risk .
..Age ..at Exposure^
Site
Thyroid
Brssst
Lung
'Esophagus
Stonach
Intestine
Liver
Pancreas
Urinary
Lymphoma
Other
Thyroid.
BlTSclSt
Lung
Esophagus
Stomach
Intestine
Liver
Pancreas
Urinary
Lymphoma
Other
General
Thyroid
Breast
Lung
Esophagus
Stomach
Intestine
Liver
Pancreas
Urinary
Lymphoma
Other
0-9
52,74
0.00
2,99
6.15
11.71
3.35
*$ *"fc f& *"S ""?
120. J /
7,81
4.14
4.41
X » Jl «£*
35.30
10.52
6.36
13.31
14 , 15
2,63
142.77
11.81
8,10
6.28
0.53
40.01
10.57
3.61
8.01
12.63
2,95
126.87
9,66
5.48
5.28
0.76
10-19
52.74
0.00
2,99
6.15
11.71
3.35
120. 37
7.81
4,14
4.41
1.12
35.30
10.52
6.36
13.30
14.15
2.63
142.77
11.81
8.10
6,28
0.53
40.18
10.57
3.61
8.01
12.63
2.95
126.84
9.66
5.48
5.28
0.76
20-34
38.00
0.00
2 . 15
1.44
^.ZO
1.28
25.19
2 4a
1,28
1
-------
Ill L-L
(and mortality from)
(absolute risk model).
Site
0-9
Risk Coefficients (10
Male
Leukemia
Bone
Female
Leukemia
Bone
General
Leukemia
Bone
Cohort Deaths
Male
Leukemia
Bone
Total
Female
Leukemia
Bone
Total
General
Leukemia
Bone
Total
RisJc per Unit
Male
Leukemia
Bone
Total
Female
Leukemia
Bone
Total
3.852
0.125
2.417
0,125
3.147
0.125
at 10"3
.0923
.0030
.0953
.0588
,0030
.0618
,0760
,0030
.0790
10-19 20-34
"6 per rad-y)
1.724 2
0,125 0
1.067 1
0.125 0
1.399 2
0*125 0
rad/y
.0405
.0029
.0435
.0257
.0030
.0287
.0333
.0030
,0363
*
.471
.125
.541
.125
.005
.125
0829
0042
0871
0543
0044
0587
0689
0043
0732
35-49
1.796
0,125
1.112
0.125
1.439
0.125
.0508
.0035
.0543
.0357
.0040
.0398
.0435
.0038
.0472
50+
4,194
0.125
2.635
0,125
3.277
0.125
,0968
,0029
.0997
.0932
• .0044
.0976
.0950
.0036
.0987
Dose (10"6 per rad)
94.7
3.1
97.8
59.9
3.1
63.0
41.9 58
3.0 3
44.9 61
26.3 37
3.1 3
29.4 40
.5
.0
.4
.4
.0
,4
37.5
2.6
40.1
25.3
2.8
28,1
48,6
1.4
50.1
35,3
1.7
36,9
* Source; NAS80, Table V-17.
3634
0165
3799
2677
0189
2866
.3167
.0177
,3344
54.2
2,5
56.7
35.9
2.5
38.4
6-19
-------
Table 6-5. BE1P I'I i > for incidence of
(absolute risk model'
(Continued),
10-19 20-34 35-49 504- All
Risk per Unit (10"' per
General
Leukemia
Bone
Total
77,7
3,1
80.8
34.3
3,1
37.4
48.1 31.4 41.2 44.8
3.0 2.7 1.6 2.5
51.1 34.1 42,8 47.3
bone fro® the risk coefficients for leukemia and bone from NAS3Q
Table V-17. has followed the III Committee's practice of
using the absolute risk model projections for leukemia and bone
cancer with the relative risk projection for all other cancers.
Since expression period for leukemia and bone cancer is 27
years, there is no difference between the number of cancers
projected for a 30-year and a lifetime follow-up period.
Table 6-6 the average mortality risks per unit absorbed
dose for the combined leukemia/bone constrained relative
riskmodels. The risk, in general, decreases with increasing
at exposure. For a constant, uniform absorbed dose rate to all
organs tissues, about 60 percent of the risk is conferred by
the exposures in the first 20 years of life.
The mortality to incidence ratios in Table 6-2 to
convert the mortality risk estimates in Table 6-6 to incidence risk
estimates. For leukemia bone cancer, incidence risks
considered to be equal as in N&SSG. The resultant incidence risks
in Table 6-7,
Iodine-131 has been reported to be only one-tenth as effective
as x-rays or gamma rays in inducing thyroid cancer (NAS72, NCRP77,
NCRP85), BEIR III reported estimates of factors of 10-80 times
reduction for iodine-131 compared to x-rays noted estimates
derived primarily from animal experiments (NAS80). However,
one study in reported that iodine-131 was just as effective
as x-rays in inducing thyroid cancer, leading an NRC review group
to select one-third as the minimum ratio of iodine-131 to x-ray
effects that is compatible with both old and new data (NRC85).
6-20
-------
Table 6-6. Site-specific mortality risk per unit dose (l.QE-6 per rad) foi
combined leukemia-bone and constrained relative risk model.
..Age, at Exposure
Site
0-9
10"-19
20-34
35-49
50+
All
Male
Leukemia
Bone
Thyroid
Breast
Lung
Esophagus
Stomach
Intestine
Liver
Pancreas
Urinary
Lymphoma
Other
Total
Female
Leukemia
Bone
Thyroid
Breast
Lung
Esophagus
Stomach
Intestine
Liver
Pancreas
Urinary
Lymphoma
Other
Total
General
Leukemia
Bone
Thyroid
Breast
Lung
Esophagus
Stomach
Intestine
Liver
Pancreas
Ur inary
Lymphoma
Other
Total
94.68
3.07
8.76
0.00
145.90
25.57
110.95
53.49
168.01
74.36
40.73
33.43
37.48
796.43
59.93
3.10
15.85
309.33
78.57
21.47
102.64
57.15
115.94
103.00
46.40
45.71
27,69
986.78
77.69
3.09
12.22
151.24
112.98
23.56
106.89
55.28
142.55
88.36
43.50
39.44
32.69
889.49
41.86
3.04
8.25
0.00
146.95
25.76
111.72
53.83
168.24
74.90
40.99
33.28
37.23
746.05
26.35
3.09
14.54
310.52
78.89
21.57
103.05
57.38
115.25
103.48
46.54
45.66
27.65
953.96
34.26
3.06
11.33
152.03
113.63
23.71
107.48
55.57
142.30
88.89
43,71
39.34
32.54
847.84
58.46
2,96
5.08
0.00
107.22
6.13
40.63
20.89
35.40
24.21
13.85
9,62
33.72
358.15
37.39
3.03
11.46
81.01
77.09
6.32
51.49
23.07
36.97
31.71
19.64
11.54
24.48
415.21
48.06
2.99
8.23
39,95
92.34
6.22
45.98
21.96
36.17
27.90
16.70
10.56
29.16
386.21
37.52
2.61
2.69
0.00
61.40
2.82
16.4
7.60
9.48
10.34
5.79
2.88
13.09
172.65
25.27
2.84
7.46
36.93
64.70
3.46
22.38
9.57
11.95
12.70
9.08
3.35
11.27
220.95
31.39
2.72
5.07
18.40
63.00
3.14
19.37
8.58
10.71
11.51
7.43
3.11
12.18
196.60
48.64
1.45
0.80
0.00
22,55
2.03
9,36
4,30
2,50
6.55
2.22
0.71
6.93
108.06
35.27
1.67
2.24
10.30
24.96
2.26
10.73
5.01
2.80
7.11
3.06
0.79
5.80
112.01
41.20
1.58
1.61
5.75
23.91
2.16
10.13
4.70
2.67
6.87
2,69
0.76
6.30
110.32
54,19
2.47
4.32
0.00
84.21
9.91
46.95
22.78
58.87
30.78
16.60
12.49
22.66
366.25
35.86
2.53
8.42
107.63
56.72
8.33
45.00
23.08
40.74
38.15
18.80
15.13
16.20
416.59
44.76
2.50
6.43
55.36
70.07
9.09
45.95
22.94
49.55
34.57
17.73
13.85
19.34
392.14
6-21
-------
Table 6-7. Site-specific incidence risk per unit dose (1.01
combined leukemia-bone and constrained relative
-6 per rad) for
risk model.
Site
10-19
20-34
35-49
50+
All.
Male
Leukemia
Bone
Thyroid
Breast
Lung
Esophagus
StoHtsch
Intestine
Liver
Pancreas
Urinary
Lymphoma
Other
Total
Female,
Leukemia
Bone
Thyroid
Breast
Lung
Esophagus
Stomach
Intestine
Liver
Pancreas
Urinary
LymphoHia
Other
Total
General
Leukemia
Borte
Thyroid
Breast-
Lung
Esophagus
Stomach
Intestine
Liver
Pancreas
Urinary
Lymphoma
Other
Total
94.68
3.07
87.59
0.00
155.21
25.57
14? . 94
102.8?
168.01
81.71
110.08
45,80
57.66
1080,20
59,93
3.10
158.45
793.16
83.59
21.47
131.59
103.90
115.94
114.44
100.88
60.95
55.38
1802.80
77.69
3.09
122.24
387.78
120.19
23.56
139.95
103.38
142.55
97.71
105.58
53.21
56,55
1433.50
41.86
3.04
82.52
0.00
156.33
25.76
148.97
103,52
168.24
82.31
110.79
45.58
57,27
1026.20
26,35
3.09
145.42
796,20
83.93
21.57
132.11
104.34
115.25
114.98
101.16
60.88
55.30
1760.60
34.26
3.06
113.32
389.82
120.88
23.71
140.71
103.92
142.30
98.30
106.08
53.07
56.31
1385.70
58.46
2.96
50,84
0,00
114.07
6.13
54.18
40.17
35.40
26.60
37,44
13,17
51.88
491.27
37.39
3.03
114.59
207.73
82.01
6.32
66.01
41.94
36.97
35.23
42.70
15.38
48.97
738.28
48.06
2.99
82.26
102 ..42
98,24
6.22
60.00
41.03
36.17
30.85
40.02
14.26
50,43
612.96
37
2
26
0
65
2
21
14
9
11
15
3
20
232
,52
.61
.92
,00
.31
.82
.87
.63
.48
,37
.65
.94
.15
.28
48
1
8
0
23
2
12
8
2
7
6
0
10
132
,64
.45
,04
.00
.99
.03
.48
.28
,50
.20
.01
.98
.65
,25
54.19
2.4?
43.23
0,00
89.58
9.91
62.61
43,81
58.87
33,83
44.87
17.12
34,86
495.35
25.2?
2.84
74.60
94,69
68.83
3.46
28.69
17,40
11,95
14.11
19,74
4,47
22,54
388.58
31,39
2,72
50.66
47,18
67,02
3.14
25.25
16.00
10.71
12.73
17.68
4.20
21.33
310.01
35.2?
1.67
22.38
26.40
26.56
2.26
13.75
9.11
2.80
7.91
6.66
1.06
11.61
167.42
41.20
1.58
16,05
14.74
25.44
2.16
13.20
8,74
2.67
7.60
6.37
1.02
11.19
151.96
35.86
2.53
84.16
275.9?
60.34
8.33
57,70
41.96
40.74
42.39
40.88
20.18
32.40
743,44
44,76
2.50
64.28
141,95
74.54
9.09
60.08
42.86
49.55
38,23
42.82
18.69
33.60
622.96
-------
-------
-------
18} and the British
similar Japanese U.K.
It that either a linear or linear-quadratic
is consistent with the survivor data, analyzed
to DS86 (Pr87)« HoweverP as noted above, linear linear-
quadratic best fits to the data differ only slightly in their
predictions at low doses. It would also
in risk per unit dose between Hiroshima
is no longer statistically significant under DS86 dosimetry
(Sh87).
6.2.11 CgmparisQii^of EJsk Estimates .for Low^ET Radiation
Table 6-8 summarizes various estimates of risk from low
levelr low-LET exposures of the general population. As
above, the highest risk estimates are obtained by assuming a
linear response (for purposes here, equivalent to a
DREF=1.0) a relative risk projection model. EPA's current
risk estimate of 392 x 10"6/rad corresponds to that obtained by
the BUS III committee (N&SSO) using these "conservative"
assumptions. However, this estimate was not derived from
most recent Japanese data, recent calculations based on similar
assumptions but revised data yield about three tines higher risk
Pr88 in Table 6-8), Thus, as illustrated by a comparison
with and entries in Table 6-8, the
is in good agreement with the new data if
projected from a linear fit to epidestiological
data should be reduced by a factor of about
extrapolating to chronic low dose conditions, an
is in view of supportive laboratory
effectiveness of iodine-131 in causing thyroid
cancer in relative to X-rays (NCRP7?). However, it
be noted that while the current estimate 392 x lQ"6/rao! is
reasonable, well within the range of uncertainty, it no
longer be regarded as conservative, in the of providing an
extra margin of public health protection. The EPA plans to
reevaluate Its risk: models, including the choice of DREF? in
light of the and V reports.
It is that this review will also lead to
in the distribution of fatal cancer risk among organs. To assign
organ risks, evidence on the Japanese A-bomb survivors to be
integrated with that from other epidemiological studies. As an
indicator of the possible impact that the new Japanese may
have on EPAss organ-specific risk estimates, Table 6-9
EPA's current organ risk estimates with those recently published
by NRPB for the general U.K. population (St88), which
into account recent changes in the Japanese data. Two
estimates presented from the NRPB publication: (a)
on a linear extrapolation of high dose epidemiological
(b) on an assumed DREF of two for breast
induction three for all other sites. Both of model
6-25
-------
fatal
population risk for
to low level, whole-body, low-LET
UNSC1&R77
Pr88f
UNSCEAR88f
St88f
Fatalities per Risk projection
10*> person-rad model
75-175
1200
110-550
450
Relative6
Relative0
Relative0
DREF
115
568
158
403
67
169
280
392
Absolute
Relative
Absolute
Relative0
Absolute
Relative0
Ave. (Rel.S Abs.)
Relative0
1.0
1.0
1.0
1.0
2^48d
1.0
1.0
2,5
1.0
2-10
3.09
Factor by which risk estimate is reduced from that
obtained by linear extrapolation of high 'dose
epidemiological results.
As revised in HAS80.
For all cancers other than leukemia and bone cancer.
on comparison of linear coefficients for linear
linear-quadratic models used to calculate
radiogenic cancers other than leukemia and bone cancer;
corresponding DREF is 2.26 for these two sites.
Refers to this document.
From analyses of A-bomb survivor data using DS86
dosiEietry.
Except breast - a DREF of 2 is assumed for that site.
6-26
-------
6-9. Site-specific mortality risk million
from low level, low-LET radiation of
general population.
cancer
Leukemia 44.8 84 28
Bone 2.5 15 5
Thyroid 6.4 (2.1)c 7,5 2,5
Breast 55,4 110 55
Lung 70»l 350 120
Stomach 46,0 73 24
Intestine 22.9 110 37
Liver 49.6 45 15
Pancreas 34.6 —— -—
Urinary 17»7 —~ ——
other 42.3 500
Total 392 1290 450
Relative risk model recommended by authors for only
at high dose rates. Use at low dose rates would be
equivalent to adopting a DREF of 1. (St88).
Preferred relative risk model projection for at low
dose rates; assumes DREF=2 for breast and DR1F=3 for
all other sites.
Value in parentheses represents estimate for important
case of iodine-131 (or iodine-129) exposure.
estimates assume a relative risk protection for
than bone cancer and leukemia. Thus the model assumptions
underlying the first NRPB set of organ risk estimates closely
parallel those employed by EPA. The difference in risk
estimates largely reflect changes in the Japanese data.
second, set of NRPB risk estimates, which the authors preferred to
use at low environmental doses and dose rates, are, for the
part, in reasonable agreement with EPA's current model
(to within about a factor of two),
6.2.12 Sour cejs^gf^JJn c er tain t y in Low - LET R i sk JS st ijaates
The most important uncertainties in estimating risk
whole body, low-LET radiation appear to relate to; (1) the
extrapolation of risks observed in populations exposed to
relatively high doses, delivered acutely, to populations
receiving relatively low dose chronic exposures and (2)
projection of risk over a full lifespan ~ most critically, the
extent to which high relative risks seen over a limited follow-up
6-27
-------
as children
jj- ^ •*.$, ~ -™ •*- jjf ""<•• "
of life baseline cancer
significant uncertainty relates to
of risk estimates from one population to another {e.g.,
Japanese A-bomb survivors to the U.S. general population). This
of uncertainty is regarded as important for
risk of radiogenic cancer in specific organs for which
baseline incidence rates differ markedly in the two populations.
In addition to the model uncertainties alluded to ,
in doslmetry and random statistical variations will
contribute to the uncertainty in the risk estimates. The errors
In T65 dosimetry were discussed Section 6,2.10. The residual
error of DS86 dosimetry Is estimated to be a relatively
contributor to the overall uncertainty (see below). Statistical
variability will be most important where relatively
cancers have so far been observed: e.g., with, respect to specific
cancer sites or with respect to childhood irradiation in A--
bomb survivors,
6.2.12.1 Low Dose Extrapolation
Results from animal and cellular studies often show
decreasing effects (e.g., cancers, mutations,, or transformations)
per rad of low-LET radiation at low doses dose rates.
on a review of this literature, the National Council on Radiation
Projection (NCRP80) has concluded that "linear interpolation
high (150 to 350 rads) and dose rates (>§ min"1) may
overestimate the effects of either low doses (0-20 or
or of any dose delivered at dose rates of 5 rad y"1 or less by a
factor of two to ten," Judged solely from laboratory
therefore, about a factor of ten reduction
linear prediction would seem to constitute a plausible lower
limit on the effectiveness of low-LET radiation under chronic low
dose conditions.
Epidemic-logical evidence would seem to argue against a
large DREF from human cancer introduction, however. Data on
&-boifib survivors and patients irradiated for medical
indicate that excess breast cancer incidence Is proportional to
dose and independent of dose fractionation (NAS80, NIH85).
evidence on thyroid cancer induction Is equivocal: medical x-ray
data suggest a linear dose response (NAS80, NIH85); on other
hand, iodine~131 radiation appears to be at least 3 times
effective than an equal dose of x-rays in inducing human thyroid
cancer, one plausible explanation for which is a
effectiveness at low dose rates (NCRP7?),
The III Committee's analysis of the A-bomb survivor
on T65-dosimetry, suggested a quadratic component to
the response function. After removing the estimated
neutron™induced leukemia, the Committee's linear-quadratic fit to
6-28
-------
a linear coefficient a factor of 2,3
the coefficient obtained a linear
fit (E&S80). Thus, analysis a 2.3
at (and rates) than estimated by
extrapolation of high dose data. Results of
fitting for solid tumors were too unstable to a
for the dose response? for simplicity, the Committee that
of the linear-quadratic fit for solid
identical to that derived for leukemia. At low
linear-quadratic model predicts about 2.5 times solid
tumors than the corresponding linear model. However,, the DS86
data appear to be more consistent with a simple linear
response for both leukemia and solid tumors. Reflecting this
finding, low dose extrapolations of the linear and linear-
quadratic fits to the DS86 data apparently differ from
another by less than a factor of 2 (Sh88, Pi89). Thus, if
posits a linear-quadratic dose response model, the available
human data would suggest that linear extrapolation from high
doses and dose rates overestimates risks at low doses
rates by about a factor of 2 or less.
6.2.12,2 Time and Age Dependent Factors
Because epidemiological follow-up of exposed population is
generally incomplete, a risk projection model must be in
estimating lifetime risks due to a given exposure. For leukemia
bone cancer, where the expression time is limited to 25
years, absolute and relative risk projection models yield the
number of radiogenic cancers. For other cancers, BEIR
III Committee assumed that radiogenic cancers would occur
throughout the estimated lifetime. This makes of
projection model more critical because the relative risk
projection yields estimated lifetime risks 2-3
an absolute risk projection. Recent follow-up of
survivor population strongly suggests that the relative risk
projection model better describes the variation risk of solid
tumors over time (HIH85). However, there may be
apart from leukemia and bone cancers, for which
projection model is a better approximation. For other cancers,
the relative risk may have been roughly constant for current
period of follow-up but may eventually decrease over time.
uncertainty relating to risk projection will naturally
with further follow-up of irradiated study cohorts, but in view
of continuing increase in attributable risk with. in
A-bomb survivors, it would appear that the relative risk
projection model does not overestimate the lifetime in
general population by more than about a factor of 2.
Similarly, there is yet insufficient information on
radiosensitivity as a function of the age at exposure,
particularly on the ultimate effects of exposure during
childhood. As the A-bomb survivor population ages,
information will become available on the cancer mortality of
irradiated when they were young. Recent follow-up
6-29
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view that relative in
on a major contributor to in
analysis on
6,2.12,3 Extrapolation of Risk Estimates to U.S. Population
is also an uncertainty associated with
of an epideniiological study on a population to
having different demographic characteristics. A
typical is application of the A-
survivors to Western people, Seymour Jablon this
"transportation problem," a helpful designation it is
confused with, the risk projection problem described above.
However, is than a geographic aspect to
"transportation problem." Risk estimates for
be on data for the other. In transporting risk
from group to another, one may have to
habits influencing health status, such as differences
nonsmoJcers, as described in Section 6.4 for
of risk for radon progeny.
The 8SIR 111 Committee addressed this problem in its
concluded, largely on the breast
evidence, that appropriate way to transport risk
to U.S. population was to assume that the absolute over
s given observation period was transferrsible but tfist icsls'fci'vs
risk not. Therefore, the Committee calculated
relative risk would be if the number of
in a U.S. population having
characteristics as the A-bomb survivors. A constant absolute
risk model? as postulated by the Committee, would imply that,
whatever factors are that cause Japanese U.S. ba
to differ, they have no effect on incidence
radiation-induced cancers? i.e./ the effects of radiation
An alternative approach to the "transportation problem11
by the 1972 NA>S BE1R-I Committee. This committee
relative risks would be the same in the United States
transferred observed percentage increase directly to
U.S. population. Since the U.S. D'apanese baseline
differ drastically with respect to mortality from specific
implies large differences in
predicted of specific cancers resulting a
of in the two countries. The most important
differences relate to cancers of the breast, lung, stomach.
of lung cancers higher in
by factors of about 4 and 2, respectively, while
of cancer is about 8 times higher in
(Gi85) . As noted, above, it appears that the absolute risk should
be transported for breast cancer. Evidence is lacking
sites, however. If lung risk to be
6-30
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with a relative risk model; retaining
cancers, risk a
would by 20 percent; on
applying the relative risk model to
lower whole-body risk by about 8 percent. on
considerations, including the tendency for in specific
to cancel another, EPA believes that
risk "transportation model" is unliJceiy to
errors in total risk estimate, Thusf in the of
the amount of uncertainty introduced by
transporting cancer risks observed in Japan to the U.S.
population appears to be small compared to other of
uncertainty in this risk assessment.
6.2.12.4 Dosimetry and Sampling Errors
As discussed in Section 6,2.10, there were systematic
in the T65 ctosimetry system for the Japanese A-bomb survivors,
leading to a significant downward bias in the of risJc
to low-LET radiation. Under DS86 dosiraetry, systematic
errors believed to be no more than about 15% (1 SD) (K-a89),
Random errors in the individual dose estimates are estimated to
be 28% (1 SD) , with art overall uncertainty in individual
of about • 32% (Ka89). The random errors in dosimetry will
to cancel, but they are expected to bias the slope of
curve downward, reducing the estimate of risk (Ma§9,
Gi84), The magnitude of this bias has to be
precision of risk estimates, are also limited by
statistical fluctuations due to finite sample size. The
uncertainty in low-LET risk coefficient for leukemia or all
to this is about . 20% (90% confidence
interval) (Sh89) . Uncertainties due to sampling error larger
sparse, e.g. with respect to risks for specific
or specific cancer sites (Sh88), Finally, will
be error in ascertaining cancer cases, most often an. under-
reporting of or mislabeling of cancer type,
type of would not be expected to greatly affect
of whole-body risk from ionizing radiation, The former
would to bias risk estimates downward. somewhatf but it would
be difficult to quantify this effect.
6-31
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6.2.12.5 Conclusions Regarding Uncertainties in
Low-LET Cancer Risk Estimates
Uncertainties in low-LET risk estimates
pertaining to ascertainment of
from uncertainties in the proper choice of
assumptions. The data uncertainties include both systematic
(biases) and random errors. Generally speaking,
modeling uncertainties are larger, but random sampling
be a very important contributor to the uncertainty in for
of radiogenic cancers or for certain irradiated
subpopulations.
EPA central estimate of average lifetime risk,
approximately 400 fatal cancers per 10 person-rad, is taken
HAS BEIR III Committee report (NAS80), incorporating the
conservative model assumptions utilized by the Committee, i.e., a
linear dose response and age-specific relative risks projected
over a lifetime for solid tumors (L-RR model). For
discussed above, it would now appear that estimates of average
lifetime risk based on the L-RR model assumptions must be revised
- to roughly 1,200 fatal cancers/10 person-rad.
Although further analysis of the A-bomb survivor data
increase this estimate, the conservatism inherent in the model's
assumptions supports the view that the 1,200/106 value is an
upper bound, pending release of the MAS BEIR V report now in
preparation.
Animal would suggest that the linear
overestimate risk by roughly a factor of 3. Likewise, while
epideittiological data clearly indicate an increase in risk with
at expression, the (age-specific) constant relative risk
projection may overstate lifetime risk by about a factor of 2.
Allowing for the additional sources of uncertainty
above, it would appear that the upper bound (L-RR) model
may be high by a factor of 5 to 10. Therefore, as a lower
estimate of the average lifetime risk, a value which is DIM
upper bound, or 120 fatal cancers/106 person~rad,
adopted.
L-BR model estimate from BEIR III, about 400 fatal
cancers/106 person-rad, falls near the geometric of
tentatively appears to be a reasonable range for the estimate of
risk; on current information, EPA has chosen BSIR III,
L-RR model value as its "central estimate." It should be
emphasized that this estimate cannot be regarded as
"conservative" in the sense of providing any significant
of safety with respect to public health protection. The decision
by EPA to employ the central estimate of 400 fatalities/106
person-rad a range of 120-1,200 fatalities/10* person-rad
reviewed and approved by a special panel set up by the Agency's
outside Radiation Advisory Committee and by the Committee itself,
as an interim measure for this proposed ruleraaking.
6-32
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uncertainty in for specific
substantially the uncertainty in the whole-body risk.
is that epidemiological pertaining to
may be very sparse. In addition, the uncertainty in
projecting risk from one population to another (e.g., to
U.S.) is important at sites for which incidence rates differ
markedly between populations,
6.3 RESULTING HIGH-LET
This section explains how EPA estimates the risk of fatal
cancer resulting from exposure to high-LET radiations. Unlike
exposures to x-rays and gamma rays where the resultant
particle flux results in linear energy transfers (LET) of
order of 0.2 to 2 ke¥ per Jim in tissue, S~Me¥ alpha particles
result in energy deposition of more than 100 ke¥ per |im. High-
LET radiations have a larger biological effect per unit
(rad) than low-LET radiations. How much greater on
particular biological endpoint being considered. For cell
killing and other readily observed endpoints, the relative
biological effectiveness (RBE) of high-LET alpha radiations is
often 10 or store times greater than low-LET radiations.
may also depend on the dose level; for example^ if linear
linear-quadratic dose response functions are appropriate for
high- and low-LET irradiations, respectively, then the RBE will
decrease with increasing dose.
6.3.1 QualitY FactQ.rs=anca_RBE to^ Mphaparticles
For purposes of calculating dose equivalent, each type of
biologically important ionizing radiation has been assigned a
quality factor, Q, to account for its relative efficiency in
producing biological damage. Unlike an RBE value, which is for a
specific tissue and well-defined endpoint, a quality factor is
based on an overall assessment by radiation protection experts of
potential of a given radiation relative to x or
radiation. In 1977, the 1CRP assigned a quality factor of 20 to
alpha particle irradiation from radionuclides (ICRP7?), However,
the appropriateness of this numerical factor for estimating fatal
radiogenic cancers is still unclear, particularly for individual
The dose equivalent (in rem) is the absorbed dose (in rad)
times the appropriate quality factor for a specified kind of
radiation. For the case of internally deposited alpha-particle
emitters, the dose equivalent from a one-rad dose is 20 rem.
Prior to IGRP Report 26 (ICRP79), the quality factor assigned to
alpha particle irradiation was 10. That is, the biological
effect from a given dose of alpha particles was estimated to be
10 times that from an acute dose of low-LET x-rays or gamma rays
of the magnitude in rad. The ICRP decision to increase this
quality factor to 20 followed from its decision to estimate
risk of low-LET radiations, in occupational situations, on
-------
is that the risks high-LET
radiation linear with Independent of (for
low to . Implicit in lCEP8s rislc
rate radiation is a dose rate reduction
of 2.5. The (linear) risk model for low-LET
radiation not employ a DREF? therefore, in order to avoid an
artifactual inflation in high-LET risk estimates, EPA
an of 8 (20/2,5) for calculating the risks from alpha
particles Section 6,3.3).
In 1980, the 1CRP published the task group report
'•Biological Effects of Inhaled Radionuclides," which compared the
results of animal experiments on radiocarcinogenesls following
the inhalation of alpha-particle and. beta-particle emitters
(ICRP80). The task group concluded that: "...the experimental
animal data tend to support the decision by the ICRP to change
the recommended quality factor from 10 to 20 for alpha
radiation."
6.3,2 Dose_Respojise Fun_cti_Q.n
In the case of high-LET radiation, a linear dose response is
commonly observed in both human and animal studies. This
is not reduced at low dose rates (NCRP80). Some data on
lung cancer indicate that the carcinogenic response per
unit, dose of alpha radiation is maximal at low doses (ArSl, HoSl,
Wh.83) ; in addition, some studies with animals show the
(ChSl, U182). EPA agrees with the HAS III
Committee that: "For high-LET radiation, such as from Internally
deposited alpha-emitting radionuelides, the linear hypothesis is
likely to lead to overestimates of the risk and may, in
fact, lead to underestimates" (HAS80). However, at low doses,
from linearity small compared to the uncertainty
in human epidemiological data, and IPA believes a linear
provides an adequate model for evaluating risks in the
general environment,
A possible exception to a linear response is provided by the
data for bone sarcoma (but not sinus carcinoma) among U.S. dial
ingested alpha-emitting Ra-226 (NAS80). These data
consistent with a dose-squared response (Ro78).
Consequently,, the NAS BEIR III Committee estimated bone cancer
risk on the basis of both linear and quadratic dose response
functions. However, as pointed out in NAS6Q, the number of U.S.
dial painters at risk who received less than 1,000 rads was so
small that the absence of excess bone cancer at low doses is not
.inconsistent with the linear response model. Therefore, the
consistency of these data with a quadratic (or threshold)
response is not remarkable and, perhaps, not relevant to
evaluating risks at low doses. In contrast to the dial painter
data, the incidence of bone cancer following short-lived radium-
224 irradiation, observed in spondylitics by Mays and Spiess
(Ma83, NAS80) in a larger sample at much lower doses, is
6-34
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with a linear response. Therefore,
radiations, EPA has a linear function to
the risk of cancer.
Closely related to the choice of a is
what effect the rate at which a dose of high-LET radiation is
delivered on its carcinogenic potential. This is an of
active current research. There is good empirical evidence, from
both human and animal studies, that repeated to radiuin-
224 alpha particles are 5 times more effective in
sarcomas than a single exposure that delivers the
{MESS, NASSQ). The 1980 NAS BEIR Committee took this
account in its estimates of bone cancer fatalities, is
using.
6.3.3 Assumptions Made by EPA for Evaluating the Bisk. friom
Alpha-Particle..Emitters
EPA has evaluated the risk to specific body by
applying an RBE of 8 for alpha radiations to the risk
for low dose rate, low-LET radiations as described above. As in
the case of low-LET radiations, EPA risk estimates for faigfa-t»BT
radiations are based on a linear dose response function. For
bone cancer and leukemia, EPA uses the absolute risk projection
model described in the previous section. For other cancers, the
Agency uses relative risk projections.
Lifetime risk estimates for alpha doses, as a function of
age, sex, and cancer site, are easily obtained by multiplying
appropriate entry in Table 6-6 or 6-7 by a factor of 8=
whole-body risks from lifetime exposure of the general population
are then calculated to be 3,1 X "iQ'^/r&A (mortality)
5.0 X 10"3/rad (incidence).
As outlined above, the risk estimate for in
BUR III report is based directly on data for high-LET (alpha)
radiation. Some readers may note that the EPA high-LlT risk
estimate, 20 bone cancer fatalities per 106 person-rad, is
than the 27 fatalities listed in Table A-27 of NASSG for alpha
particles. This is because the analysis in Appendix A of NAS80
(but not Chapter ¥ of that report) assumes that in addition to a
2-year minimum induction period, 25 years are available for
cancer expression. This is usually not the case for
received beyond about age 50. Hence, the estimated lifetime risk
is smaller when it is based on a life table analysis that
considers lifetime exposure in conjunction with competing causes
of death,
6.3,4 Uncerta.int.ies..._ln Riskg
The uncertainties in risk associated with internally
deposited alpha emitters are often greater than for low-LET
radiation. Human epidemiological data on the risks from alpha
emitter are largely confined to: (1) lung cancer induced by radon
5-35
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products below); (2) cancer by radium?
.(3) liver induced by injected thorotrast (thorium).
of risk estimates presented for irradiation
an of a, as determined from high on
animals. available evidence on cells, animals,
points to a linear dose response relationship
{NAS88}. The extrapolation to low is
considered to t>e less important as a source'of
uncertainty for alpha irradiation than for low-LET irradiation,
is, however, considerable variability in
studies? the extrapolation of to
Is also problematic.
For alpha-emitting radionuclides, the
source of uncertainty in the risk estimate is in
the to target cells, Contributing to this uncertainty
uncertainty in the location of these cells, ignorance
the metabolisffi of the radionuclidef nonuniforaity of radionuclide
deposition In an organ, and the short range of alpha particles in
tissue (see Chapter 5}.
In the of alpha irradiation of the lung by
products, there are human epidemiologlcal data that allow direct
estimation of the risk per unit exposure. Knowledge of
the actual to target cells is therefore not important
as the per unit exposure night differ between ralne
indoor environments. As a consequence, the estimated uncertainty
in radon risk estimates is similar to that low-LET
radiation. [As discussed in Section 6.4.5, the EPA Is employing
a central risk estimate for excess radon exposure of 360 fatal
cancers/106 WLM an uncertainty range of 140-720
lung cancers/106 WLM.)
As in Section 6-2, recent of
A-bomb survivor data indicate that risk estimates whole-body,
low-LET radiation predicated on the linear, relative
will to be increased approximately three-fold, although
individual organ risks will generally change by differing
factors. Since the organ specific, high-LET risk
8 times those calculated for low-LET radiation,
would expect a corresponding 3-fold increase in tiigla-LET risk
Moreover,, application of a DREP to the calculation of
low-LET risks would, not affect this conclusion, since, as
abovej this would imply a compensating in
RBI. Consequently, it might be argued that current
of risk due to alpha irradiation are too low.
While EPA intends to conduct a comprehensive review of
its low- high-LET risk estimates after BEIR ¥
available, we do not believe, that current high-LET risk
estimates are biased low in a serious way. It should be
in this connection, that the doses from internally deposited
alpha emitters are usually concentrated in certain -
especially bone, bone marrow, and lung. Risks of
6-36
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by inhaled radon decay products Section 6.4}
derived directly from epicjemiological on hIgh-LIT
radiation,* consequently, these risk estimates will not be
affected by changes In the Japanese data. Epidemiological
evidence Indicates that the risk of radiogenic
by alpha emitters deposited in the bone is lower than would be
estimated from the gamma ray risk after adjusting for
(NAS88); possibly this discrepancy relates to difficulty in
estimating dose to target cells in the bone marrow t.o alpha
particles originating in the mineral phase of the bone. EPA*s
estimates of risk from alpha emitters deposited in the lung in
the form of insoluble particles are also conservative. Alpha
radiation emitted from such particles, for the most part,
irradiate the pulmonary region of the lung (the alveoli). The
risk of lung cancer is calculated, in this case, by multiplying
the pulmonary region' dose by the risk factor for the whole lung.
Using the pulmonary dose as an effective lung dose will bias the
risk estimate high by an unknown but possibly large factor,
especially since the great majority of human lung cancers to
originate in the tracheobronchial region of the lung.
The next section describes how EPA estimates the risk to
inhalation of alpha-emitting radon progeny, a situation where the
organ dose is highly nonuniform.
6.4 ESTIMATING THE RISK FROM LIFETIME POPULATION
RADQN-222 PROGENY
The Agency's estimates of the risk of lung cancer to
inhaled radon progeny do not use a dosimetric approach, but
rather are based on what is sometimes called an epidemic-logical
approach: that is, on the excess human lung cancer in
known to have been exposed to radon progeny.
When radon-222, a radioactive noble gas, decays, a of
short half-life radionuclides (principally polonium~218, lead-
214, bismuth~214, and polonium-214) are formed. These decay
products, commonly referred to as "progeny" or "daughters,s>
readily attach to inhalable aerosol particles in air. When
inhaled, the radon progeny are deposited on the surfaces of the
larger bronchi of the lung- Since two of these radionuclides
decay by alpha-particle emission, the bronchial epithelium is
irradiated by high-LET radiation. A wealth of data indicate that
a range of exposures-to the bronchial epithelium of underground
miners causes an increase in bronchial lung cancer, both in
smoking and in nonsmoking miners, and in some members of the
general public. Recently the National Academy of Sciences, BSIR
IV Committee, and the International Commission on Radiological
Protection reviewed the question of radon risks and reported
their conclusions (NAS88, 1CRP87).
Although considerable progress has been made in modeling the
deposition of radon daughters in the lung, it is not yet possible
6-37
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to bronchial delivered by
rsdon-222 progeny (NAS88). is in
to uncertainty concerning of cells in
is initiated of
in epithelium.
from uncertainties in the calculations, a
purely dosimetric approach to radon risk
untenable. an approach relates risk a
to lung resulting
to or x-ray exposure. This'approach
extensive epidemiological. data on radon
risk estimates indirectly on epidemiological of
populations to low-LET radiation. It also,
therefore, of an RBE for alpha particles
animal studies. Given the uncertainties in the latter
epidemiological studies in the RBE, there would to be no
advantage to this approach. Consequently, EPA
BEIR IV Committee conclusion that radon decay product
in the lung is only useful for extrapolating radon risk
from exposure situation to another
6.4.1 Cjmracterl.2±ngL_Expoaai^^
J^
Exposures to radon progeny under working conditions
cosoaonly reported in a special unit called the working level
(WL) . working level is any combination of half-life
radon~222 having 1.3 x 105 MeV liter of potential
alpha (FRC67) . This value it is
alpha energy released from the total decay of the short-lived
progeny at radioactive equilibrium with 100 pCi/L of
radon-222. The WL unit was developed
of specific on ventilation
factors. A working level month (WLM) is unit to
characterize a miner's exposure to one working level of
progeny for a working month of about 170 hours,
results of epidemiological studies are expressed in of WL
and WLM, the following outlines how they can be
of the general population exposed to radon progeny,
There are age- sex-specific respiratory
differences, as well as differences in duration of in a
general population as compared to a mining population. In
earlier reports, EPA used an "exposure equivalent^ " a Modified
WLM in which adjustments were made for age-specific differences
in airway dimensions and surface area, respiratory frequency,
tidal volume. These factors were expected to influence
deposition and, therefore, radiation dose from radon
This approach to quantifying exposure , correcting for differences
in these factors, recommended by Evans (Ev69) is
consistent with the original derivation of the working level
(Ho5?) .
6-38
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BE1R IV Committee, however, concluded that
bronchial "dose WLM In homes,, as compared to in
differs by than a factor of 2, " advised
risk WLM exposure in residences IB be
to be identical until better doslmetric
. will follow the lead of the IV
In this regard will not the
equivalent" correction employed to compensate for age-
specific tracheo-bronchlal deposition in earlier EPA In
this report, exposure of any* individual to 1 WL for 170 is
1 for 1 year Is 51.56 WLM. This change BPH,
in standard units generally used for this
still without requiring dose calculations.
For indoor exposure, an occupancy factor of 0.75 is still
employed. Discussion of the support for this estimate be
found in SPAS6,
6.4,2 The__EPA_iIodel
The initial EPA method for calculating radon risks
described in detail (EPA79f E179). As new data were reported,
EPA revised Its model to reflect changes, as contained In
consecutive reports (EPA79, EPA82, EPA83a? EPA83b, EP&84,
EPA85,and EPA86). The Agency initially projected radon lung
cancer for both absolute and relative risk models, but,
since 1978, EPA has based risk estimates due to inhaled radon-222
progeny on a linear dose response function, a relative rislc
projection Model, and a minimum Induction period of 10 years- A
life table analysis has been used to project this rislc over a
full life span. Lifetime risks were initially projected on
an effective exposure of l WLM increased
specific risk of lung cancer by 3 percent over the age-specific
in U.S. population as a whole (EPA79), In
recent documents, lifetime risks were calculated for a of
risk coefficients from 1 percent to 4 percent per
Although occupational exposures to pollutants other than
radon-222 progeny are probably not important factors in
lung cancer risk for underground miners (E179, Th82t
Mu83, Ra84, Se88), the use of occupational risk data to
risk of a general population is far from optimal, as it
provides no information on the effect of radon progeny
for children and women. While for most estimates, it is
that the risk per unit dose received by children is no higher
than that received by adults, this assumption may not be correct.
The A-bomb survivor data indicate that, in general, the risk
from childhood exposure to low-LET radiation Is greater than
adult exposure and continues for at least 33 years, the time over
which A-boiab survivors have been observed (Ka82), There not,
as yet, adequate age-specific data on occurrence of lung cancer
in under 10 years of age at the time of exposure (Ka.82) .
Another limitation of the underground miner data is
6-39
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-------
6-10. for to
Fatalities per
10 person-WLM
ICRP
Dec. Jibs,
760 (460}
730 (440)
600 (300}
150-450
200-450
130
Lifetime
Lifetime
Lifetime
Working
Lifetime
Expression
Lifetime
Lifetime
Lifetime
30 years
40 years
Lifetime
III
AECB based their estimates of risk for
population on an exposure equivalent, corrected for breathing
rate (and other factors). For comparison purposes, the values in
parentheses express the risk in more customary units, in which a
continuous annual exposure to 1 WL corresponds to 51.6
Adjusted for U.S. General Population: text.
Table 10.2; assumes risk diminishes exponentially with a
20-year halftime, and no lung cancer risk is before
Sources5 EPAS3b? NAS80; Th82; ICRP81; EPA36;
Rel. - Relative Risk Projection
A-S Abs. - Age-Specific Absolute Risk Projection
Dec. Jibs., - Decaying Absolute Risk Projection
-41
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-------
of a relative-risk 5 ,t _
analysis with a
generalization of methods. parallel
analyses carried to establish a single
for each parameter.
The mathematical form of the Committee's
for the radon related age-specific mortality rate at a is
r(a) = r0(a)[l + 0,025 T(a) (W, + 0.5W2)] (6-1)
where
r0(a) = age-specific lung cancer mortality rate
7 (a) = l«2r if a is less than 55 years
1.0, if a is between 55 and 64 years
0.4, if a is greater than 64 years
Wj = WLM incurred between 5 and. 15 years prior to a
W2 = WIM incurred more than 15 years prior to age a
The Committee model is, therefore, an age-specific, relative-risk
projection model with a 5-year latent period prior to expression
of risk.
The BEIR IV Committee also estiaated what the lung cancer
risk coefficient would be for an age-constant, relative-risk
model. The results of this analysis are summarized in
Table 6-11.
Table 6-11. BEIM IV committee estimate of lung cancer risk
coefficient for age-constant, relative-risk model,
Cohort Excess Risk 95% Confidence
per WIM Limits
U.S.
Ontario
Eldorado
Malmberget
Combined
0,6
1.4
2.6
1.4
1.34
0.3
0.6
1.3
0.3
0,8
- 1.3
- 3.3
- 6.0
- 8.9
- 2,3
In its analysis, the BEIR IV Committee identified two major
areas of uncertainty affecting its conclusions: (1) uncertainty-
related to the Committee's analysis of cohort data and
6-43
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uncertainty related to projection of irie-ji o
groups. Committee's TSE model risk coefficients
from analysis of from four miner cohorts. or
systematic errors, particularly systematic errors, could
conclusions. Sources of error in addition to
variation include: (1) errors in exposure estimates, particularly
since the magnitude of error may differ among the studiesi
(2) of misclassification of cause of death? (3.) in
status of individual miners, and (4) modeling
uncertainty—i.e., does the model properly address all
determinants of risk?
Having developed the TS1 model for miners, the
anticipated the following sources of uncertainty in projecting
model across other groups: (1) effect of gender
all for males); (2) effect of age (miner data contain no
information on exposures before about age 20); (3) effect of
smoking (miner data contain poor information on smoking status);
{4} temporal expression of risk (not enough miners have died to
establish, accurately the pattern of lifetime risk from radon
exposure), and (5) extrapolation from mining to indoor
environments (what are significant differences in the air in
mines compared to air indoors?). After reviewing the various
sources of uncertainty, the BEIR IV committee concluded [p42]?fl
...The imprecision that results from sampling variation be
readily quantified, but other sources of variation cannot be
estimated in a quantitative fashion." Therefore, the Committee
chose not to combine the various uncertainties into a single
numerical value" {N&S88).
The question of errors in exposure estimates is particularly
interesting since the modeling is strongly influenced by U.S.
uranium miner data. In fact, the model risk estimates would be
33 percent higher if the U.S. cohort was removed. in
U.S. cohort is poorly known: cumulative WLM (CWIM)
calculated from measured radon levels for only 10.3 percent of
miners, varying amounts of estimation required for
36.1 percent, of the miners, and guesswork is used for
53,6 percent of the miners (NAS33, Lu71). Only 26.1 of
U.S. uranium miner exposure data are based on
The Ontario cohort exposure estimates also are not well
founded. Upper and lower estimates were developed; lower
from measured values, the upper based on engineering judgment
(KAS88). Eldorado cohort estimates of CWLM were based almost
entirely on measured values, while Malmberget cohort estimates
were based on a reconstruction of past ventilation conditions
(NAS88). Of the four cohorts, the United States of
poorest for CWIM estimates. One serious problem is
potential error due to large excursions in radon daughter
concentrations (NTOSH87). The uncertainties in exposure
estimates are particularly significant in view of the rather
large impact the U.S. cohort has on the form of the
6-44
-------
I? Is
vital at an level of 0.001 year,
risk be calculated Table 6-12).
Table 6-12. BUR IV - Lifetime Lifetime
Risk.
Group (10'VwiM)
Male 530
Female 185
Combined 350
6.4.4.2 ICRP 50
The International Commission on Radiological Protection, in
its Publication 50, addressed the question of lung cancer risk
from indoor radon daughter exposures. The ICRP Task Group took a
direction quite different from the BEIR Committee. The Task
Group reviewed published data on three miner cohorts: UcS,f
Ontario, and Czech uranium miners. The estimated risk
coefficients by cohort are presented in Table 6-13.
Table 6-13. Estimated lung cancer risk coefficients from radon
progeny exposure for three miner cohorts.
Cohort Follow-up Relative model Absolute
U.S. 1950-1977
Czech 1948-1975
Ontario 1958-1981
Average
Source: ICRP87.
0"> %• "1 A *£•
& o*oX* U*S
1.0%-2.0%
0.5%-1.3%
1%
2-8
10-25
3-7
10
cases/ 106
cases/106
cases/106
cases/106
The relative risk model then developed for a constant
rate is:
t-T
= X0(t)[l + J r(te) E(tt) dte] (6-2)
0
= the mortality rate at age t
6-45
-------
f = lag (minimal latency) = 10
In of a constant exposure or annual
equation collapses to;
X0(t)[l + r E(t - T)] (6-
= averaged relative risk coefficient
') = E [t - T]
= cumulative exposure to radon daughters to
t-r
ICRP the of the relative risk model,
ICRP 50 absolute risk model will not be further in
To relative risk derived of
for general population, ICRP
adjustments. first to correct
for co-carcinogenic influences in mines. To account for
unidentified, carcinogens that might be in mine
but not elsewhere, only 80 of risk
to radon. adjustment for dosimetric
corrections. to bronchial epithelium. by
Group for indoors estimated to be only 80 percent as
as for persons in mines; therefore, risk to
public radon was considered to be 80 percent of risk of
miners.
Adjusting average relative risk coefficient of
1 by factors gives a risk coefficient
of 0.64
1,0% X 0,8 X Q.i
-------
ret adjustiftsnt made by trie Taslc Group is 3t'~ i?i • to
Since reports of Japanese A~boinb survivors re «
radiation-exposed groups support an elevated • • t t«*k in
children to adults, the Task Group tu* »isk
coefficient of between birth 20 by a „«. t*- of 3.
final relative risk coefficients in 1CRP 50
ares 1.9 WLM if the age at time of is
birth 20 years, and 0,64 percent
of exceeds 20 years.
ICSP 50 relative risk model is run with ]
lifetable vital statistics at an exposure level of
year, reference risk calculated is:
Female
Combined
6.4.5 ^ele.at4orvjEtf_.Ri!sK ^efficients
To estimate the range of reasonable risks to
radon-222 progeny for use in the Background Information
for Underground Oranium Mines (EPA85), EPA averaged
of BEIR III, the SPA model, and the AECB to establish an
bound of range. The lower bound of the
by averaging the UNSCEAR and ICRP estimates. The Agency
to include NCRP estimate in its determination of
this estimate believed to be
bound. With this procedure, the EPA arrived at
risk coefficients of 1.2 percent to 2.8 percent
equivalent (300 to 700 fatalities per million
equivalent) as estimates of the possible range of effects
inhaling radon-222 progeny for a full lifetime. Although.
rislc did not encompass the full range of uncertainty,
they to illustrate the breadth of much of current
scientific opinion.
The lower limit of the range of 1985 EPA relative
ficients, 1.2 percent per effective WLM, was similar to
derived by the Ad Hoc Working Group to Develop Radioepidemio-
logical Tables, which also used 1.2 percent per WLM (NIH85)»
However, other estimates based only on U.S. and Czech M:
averaged 1 percent per WLM (JaSS) or 1.1 percent per WLM
(St85). On the other handf three studies - two on (KaS4,
BoSS) one on residential exposure (Ed83, EdS4) - indicated a
relative risk coefficient greater than 3 percent per WLM,
as large as 3.6 percent,
The therefore increased the upper limit of
of relative risk coefficients. To estimate rislc to
6-47
-------
radon~222 progeny, the EPA of relative
coefficients of 1 to 4 percent per WLM. (See 1PA86 for a
detailed discussion.) Based on 1980 vital statistics,
yielded, for members of the general public, a of lifetime
380 to 1,520 fatal cases per 10 WLM In
equivalents). In standard exposure units,
rate and age, this corresponds to 230 to 920
per 106 WLH. Coincidentally, the geometric mean estimate
obtained in this way with 1980 vital statistics, 4.6x10 /WLM in
units of exposure, is numerically the sane as that
obtained using a 3 percent relative risk coefficient 1970
vital statistics (see Table 6-7) .
However, in light -of the two recently published consensus-
based reports, BEIR IV and ICRP 50, and a recent report on
Czech miner groups (Se88), the Agency has reviewed its basis for
radon risk estimation. Comparable relative risk coefficients for
miners {age-constant relative risk) yield a coefficient of around
1 percent in ICRP 50, 1.34 percent in BEIR IV, and 1.5 percent in
the Czechs. This suggests that the range, 1 percent to
4 percent, used by EPA may be too wide. Nevertheless, note that
only 5 of the 20 or so studies for which there are
Included in these estimates.
The BEIR IV Committee noted and modeled a drop in relative
risk with increasing time of exposure and a decreasing relative
risk with increasing age after exposure (NAS88) , The Czech.
miners show a similar response pattern (Se88). Though the
Committee did note a dose rate effect in the U.S. uranium miner
cohort, i.e., a decrease in risk per unit exposure at high
rates, It not included in the model (NAS86). The possibility
of a similar dose-rate effect was found recently in a study on
Port Radium uranium miners (Ho87).
ICRP 50 Task Group worked from a different
developed a simpler model with fewer age- and time-dependent
parameters. The Task Group provided a 3 times higher risk for
between birth and 20 years of age than after 20 of
(ICRP87). The finding in the recent Czech report that
prior to 30 Is 2 to 2,5 times greater than after 30
support, to- the ICRP conclusions (SeSS) ,
Both BEIR IV and ICRP 50 models treat radon smoking
as multiplicative. This conclusion is based primarily on
from the U.S. uranium miner cohort. Although apparently
on weaker evidence, the report on Malmberget miners
report on Czech miners both concluded that the interaction
of smoking and radon exposure is small (Ra84, Se88). The
attributable risk per unit exposure in smokers and. non-smokers
essentially the same (Se88), The true interaction of
cigarette smoking is controversial. Both antagonistic (Ax78,
Lu79, AxSO) and multiplicative (Lu69, Wh83) interactions
reported in man, and animal studies can be found to justify
any position (Ch81, Ch85, Cr78). In prior calculations,
6-48
-------
interaction between
as multiplicative. EPA will continue to
daughter-smoke Interaction as multiplicative at
time.
Important unresolved issues pertaining to the risks from
progeny remain. At the advice of
of EPA's Science Advisory EPA will
continue to relative risk models but shall include BEIR
IV ICSP 50 calculations to illustrate in
two models. The ICRP 50 model will be slightly
modified. risk reduction factor of 0.8 to
in doslstetry will be removed to place 1CR? 50
BEIR IV model on a comparative basis. Calculations in
ICRP 50 model will be made using risk coefficients of 2.4
percent WLM from birth to age 20 and 0,8 percent for
greater than 20 years, yielding estimates listed in Table
6-14.
Table 6-14 summarizes risk estimates based on BEIR IV
ICRP 50 model, modified as described above. For
calculations in this document, both models were adjusted
effect of background radon exposure (see section below).
Table 6-14. Lifetime risk from radon daughter exposure of lung
cancer death (per 106 WLM) .
Model
IV 50
530
185 255
350 500
The ICRP Task Group concluded that, all things considered^
of variation of the mean relative risk coefficient Is
0.3 up to 2 times the value stated (1CRP8?).
of cited in Table 6-14 for the ICRP model
uncertainty in the risk coefficient, since the BEIR IV
did not provide a numerical range of uncertainty, no
is given for that model.
6-49
-------
A relative risk for radon-Induced lung cancer
generally risk, Ap, from a given exposure^ is
proportional to the observed baseline risk of lung cancer in the
population, AO, Thus, for a constant exposure rate, w, the
at age, a, attributable to previous exposure can be
writtent
(w,a) (6-5)
For example, in the case of an age-constant relative risk model
with a 10-yr minimum latency:
0(a) = j? = constant (6-6)
f(w,a) - (a-10)w (6-7)
Although Ar is commonly assumed to be proportional to \0, a
isore consistent (and biologically plausible) way to formulate a
relative risk model is to assume 'that the radon risKf Ap, is
proportional to X0', the lung cancer rate that would prevail in
of any radon exposure (Pu88) :
(6-8)
the risJc model can' be to relate A0(a) to
X,' (a) f then
= A (a) [1 + 0(a)f(w,a)]
w is average exposure rate in the population. It
follows from the previous equation that
+ |(a)f(w,a)3 (6-10)
inferred baseline rate without radon exposure depends,
of course, on both the risk model and the presumed average
background exposure rate. The excess risk associated- with an
arbitrary exposure situation can be calculated using standard
life table methodology.
6-50
-------
ICRP 50 did correct in
In calculating lifetime population risks^ an
of 0*2 WLM/yr. The IV
incorporate correction, noting that it would be
NAS88, p« 53). In arriving at a final estimate on ICRP
50 and BEIR IV models (see Table 6-15}, incorporated a
model-specific baseline correction, calculated on the assumption
of a 0.25 WLM/yr average radon exposure rate (Pu88). As
from Tables 6-14 and 6-15, this correction results in roughly a
15 percent reduction in each, of the estimates of lifetime risk
for the general population.
Table 6-15, Lifetime risk from excess radon daughter exposure
(adjusted for a background exposure of 0.25 WLM/yr)
Risk of Excess LungCancer Deaths
BEIR IV
ICRP 50
Men
Women
Population
Combined
(Range)
460
160
305
640
215
420
(140-720)
550
190
360
(140-720)
Summary of Baseline Corrected Radon Risk. Estimates
Consistent with the recommendations of the Agency's Radiation
Advisory Committee, SPA here averaged risk
derived from the BUR IV and ICRP 50 models. These estimates
based on 1980 U.S. vital statistics and are adjusted for an
assumed background exposure of 0.25 WLM/yr. Thus, as shown in
Table 6-15; the excess lifetime risk in the general population
due to a constant, low-level, lifetime exposure is estimated to
be 360 excess lung cancer deaths per 106 WLM, with a range of 140
to 720 excess lung cancer deaths per 106 WLM. (At lifetime
exposures above about 100 WLM, numerical estimates would be
reduced because of "competing risk" considerations.)
The BEIR IV and ICRP models differ substantially with respect to
their dependence on age and time since exposure. Hence, in
evaluating exposures at different ages or time periods it is
instructive to consider the predictions made by each model.
Illustrative examples of such calculations are given in Tables
6-16 and 6-17.
6-51
-------
Table 6-16. Lifetime risk for varying at first
duration of exposure (Background ~ 0.25 WLlf/yr} .
Lifetime Risk of Lung Cancer per 10 WIM
Male
Age(yr)
Birth
10
20
30
40
50
60
70
80
90
100
Exposure
Duration(yr)
1
10
Lifetime
1
10
1
10
1
10
1
10
1
10
1
10
1
10
1
10
1
10
1
10
BEIR IV
476
480
459
481
483
486
495
509
535
572
592
602
516
378
331
251
182
88
55
12
8
2
1
ICRP 50
1382
1394
638
1398
1402
470
474
477
472
461
435
392
335
253
182
96
57
15
8
1
1
«,
**.
Female
I¥
184
185
159
186
186
188
190
195
205
217
217
208
170
114
95
69
52
32
21
7
4
1
«BB
ICRP50
511
515
213
516
517
173
173
172
168
161
148
130
109
79
58
34
22
8
4
MM,
—
,~,
6-52
-------
Lifetime risk for varying
duration of (Baa
at first
=0.25 WlM/yr).
Excess Lung Cancer Deaths per 10
Persons Exposed at 1 WLM/yr
Male
Age(yr)
Birth
10
20
30
40
50
60
70
80
90
100
Exposure
Duration (yr)
1
10
Lifetime
1
10
1
10
1
10
1
10
1
10
1
10
1
10
1
10
1
10
1
10
BEIR IV
472
4723
32171
481
4814
486
4902
508
5299
571
5804
600
4909
374
2949
246
1406
84
323
11
30
2
2
ICRP 50
1372
13725
44859
1398
13984
470
4691
476
4678
461
4267
391
3187
251
1623
94
439
14
45
1
2
M
KW
Female
IV
183
1828
12352
186
1857
187
1891
195
2041
217
2142
208
1652
114
895
68
456
31
146
7
19
«»
2
1CRP50
508
5085
16545
516
5159
172
1721
172
1676
161
1468
129
1051
79
546
34
192
8
30
«.
1
-,
*™
6-53
-------
earliest report of radiation-Induced health
In 1896 (M0S7) , it dealt with acute In generally
by very large x-ray exposures. Within six-year
following, 170 radiation-related skin damage
reported. Such injury, like many other effects, is
result of to hundreds or thousands of rads. Under
normal situations, environmental exposure does not
large , so possible acute effects will not to be
considered in assessing the risk to the general population from
routine radionuclide emissions,
Radiation™ induced carcinogenesis was the first ^elax®d
health effect described: the first case was reported In 1902
(Vo02), and 94 cases of skin cancer and 5 of leukemia were
reported by 1911 (Up? 5) . Radiation-induced genetic changes
noted soon afterward. In 1927, H.J. Muller described x-ray-
induced mutations in animals (in the insect, Drosophila) , in
1928, L.J. Stactler reported a similar finding In plants (Ki62) .
At about the same time, radiation effects on the developing human
embryo were observed1. Case reports in 1929 showed a high rate of
microcephaly (small head size) and central nervous system
disturbance and one case of skeletal defects in children
irradiated .In utero (UNSCEAR69) , These effects, at unrecorded
but high exposures and at generally unrecorded gestatlonal ages,
appeared to produce central nervous system and eye
similar to those reported In rats as early as 1922 (Ru5G) .
For purposes of assessing the risks of environmental
exposure to radionuclide emissions , the genetic effects in,
utero developmental effects are the only health hazards other
than cancer that are addressed in this Background Information
(BID) .
6.5.1 35fl2*iyiLJ2JLJl^^
Genetic (or genetic effects) of radiation
is defined as stable, heritable changes induced in cells
(eggs or sperm) of exposed individuals, which are transmitted to
and only in their progeny and in future generations.
Of the possible consequences of radiation exposure,
genetic risk is more subtle than the somatic risk, since It
affects not the persons exposed, but relates only to
progeny. Hence, the time scales for expression of the risk
very different. Somatic effects are expressed over a period on
the order of a lifetime, while about 30 subsequent generations
(nearly'lf000 years) are needed for near complete expression of
genetic effects. Genetic risk is incurred by fertile people when
radiation the nucleus of the cells which become their
eggs or sperm. The damage, In the form of a mutation or a -
chromosomal aberration^ is transmitted to, and may be
in, a child conceived after the radiation exposure. However,
6-54
-------
be in subsequent or only
Alternatively/ It be
of failure to reproduce or failure of to
EPA genetic risk as independent of
though somatic risk may be caused by mutations in cells
because, sosiatlc risk is expressed in
genetic risk is expressed only In progeny and, in general,
subsequent generations. Moreover, the types of
Incurred often differ in kind from cancer and cancer death.
Historically, research on genetic effects and development'of risk
estimates have proceeded independently of the research on
carcinogenesis. Neither the dose response models nor the risk
estimates of genetic harm are derived from data on studies of
carcinogenesis,
Although genetic effects may vary greatly in severity, the
genetic risks considered by the Agency in evaluating the hazard
of radiation exposure include only those "disorders traits
that a serious handicap at some time during lifetime"
(NA.S8G) . Genetic risk may result from one of several types of
damage that ionizing radiation can cause in the DMA within eggs
and sperm. The types of damage usually considered are: dominant
recessive mutations in autosonial chromosomes, mutations in
sex-linked (x-linked) chromosomes, chromosome aberrations
(physical rearrangement or removal of part of the genetic
on the chromosome or abnormal numbers of chromosomes),
irregularly inherited disorders (genetic conditions with complex
causes, constitutional and degenerative diseases, etc.).
Estimates of the genetic risk per generation
conventionally based on a 30~yr reproductive generation. That
is, the median parental for production of children Is defined
as 30 (one-half the children are produced by
30, the other half by persons over age 30). Thus,
radiation accumulated up to age 30 is used to
genetic risks, EPA assessment of risks of genetic effects
includes both first generation estimates and total genetic
estimates.
In the EPA Background Information Document for ionucl
(EPA34J, direct and indirect methods for obtaining genetic risk
coefficients described, and some recent estimates on
these methods are tabulated. Briefly, the direct method takes
the frequency of nutation or occurrence of a heritable defect per
unit expcsure observed in animal studies and extrapolates to what,
is expected for humans. Direct estimates are usually used for
first generation effects estimates. The indirect method, on the
other hand, uses animal data in a different way. The
human spontaneous mutation rate per gene site Is divided by
average radiation-Induced mutation rate per gene observed in
studies, to obtain the relative radiation mutation risk in
humans. The Inverse of this relative radiation mutation is
6-55
-------
expected "doubling dose" for radiation-induced in
man. The doubling dose Is the exposure in which, will
the.current genetic malformation level In and usually is
to estimate equilibrium effects or all future generation effects.
A doubling dose estimate assumes that the total population
of both sexes is equally irradiated, as occurs from background
radiation, and that the population exposed is large enough so
that all genetic damage can be expressed in future offspring.
Although it is basically an estimate of the total genetic burden
across all future generations, it can also provide an estimate of
effects that occur in the first generation. Usually a fraction
of the total genetic burden for each type of damage is assigned
to the first generation using population genetics data as a basis
to determine the fraction. For example, the BEIR III Committee
geneticists estimated that one-sixth of the total genetic burden
of x-1inked mutations would be expressed in the first generation
and five~sixths across all subsequent generations. EPA
assessment of risks of genetic effects includes both first
generation estimates and total genetic burden estimates.
The 1986 UNSCEAR report (UNSCEAR86) reviewed data on genetic
effects. While there was much new information, changes in direct
estimates of first generation risk were minimal, reflecting
primarily changes in estimates of survival of reciprocal
translocations. There was however, an appreciable change in the
doubling dose estimate of genetic risk. Because of Hungarian
studies the birth prevalences of isolated and multiple congenital
anomalies of in man was estimated to be 597.4 per 104 live births
(UNSCEAR86). The UNSCEAR Committee also estimated congenital
anomalies and other multifactorial disorders to have a
spontaneous prevalence of 600,000 per 106 live births. The
UNSCEAJR Committee however, made no estimate of the genetic
radiation risk coefficients for these types of conditions
(UNSCIAR86). The 1988 UNSCEAR Committee also reviewed genetic
risks (UNSCEAR88) and confirmed the conclusions of the 1986
UNSCEAR committee (Table 6-18).
The Agency concluded that the "spontaneous prevalence" of
multifactorial disorders described by the UNSCEAR Committees were
not all "disorders and traits that cause a serious handicap at
sometime during lifetime." Since the multifactorial disorders
compose a large fraction of the genetic risk in the BEIR III
report, the BEIR III risk estimates will be used until the
relevance of the Hungarian studies can be evaluated. The Agency
also has concluded estimates of detrement (years of life lost or
impaired) as made by several UNSCEAR Committees (UNSCEAR82, 86,
88) should not be used to evaluate genetic risk at this time. As
these changes in genetic risk assessment mature, the Agency will
review their applicability.
6-56
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Table 6-18. 1988 Risks of genetic disease per 1 million
live-births in a population exposed to a genetically
significant dose of 1 rad per generation of
low-dose-rate, low-dose, low-LET irradiation.
Type of genetic
disorder
(100 rad doubling dose)
Current incidence
per 106 liveborn
Effects, of ._1 Tad per generation
First Generation Equilibrium
Autosomal dominant
and x-linked 10,000
Autosomal recessive 25,000
diseases
-Homozygous effects
-Partnership effects
Chromosomal diseases
due to structural
anomalies 400
Sub-total (rounded) 13,000
Early acting dominants unknown
Congenital anomalies 60,000
Other multifactorial
diseases* 600,000
Heritable tumors unknown
Chromosomal diseases
due to numerical
anomalies 3,400
15
no increase
negligible
2,4
18
not estimated
not estimated
not estimated
not estimated
not estimated
100
11
4
4
115
* prevelance up to age 70
Source: UNSCEAR88
6-57
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from Low-LET
A of committees have addressed question of
coefficient (NAS72, 80, 88; 62, 66, 72,
77, 82, 86, 881 OfSO). The detailed estimates of III
Committee listed in Table 6-19, those of
(0NSC1AR88) listed in Table 6-18, a of
of the various committees is listed in Table 6-20.
Although, all of the reports cited above used
different sources of information, there is reasonable agreement
in the estimates. However, all these estimates have a a
considerable margin of error, both inherent in the original
observations and in the extrapolations from experimental species
to man. Some of the committee reports assessing the situation
have attempted to indicate the range of uncertainty? others have
simply used a central estimate (see Table 6-20) . The same
uncertainties exist for the latter (central estimates) as for the
former.
Most of the difference is caused by the newer information
used in each report. Note that all of these estimates are based
on the extrapolation of animal data to humans. Groups differ in
their interpretation of how genetic experiments in animals might
be expressed in humans. While there are no comparable human data
at present, information on hereditary defects among the children
of A-bomb survivors provides a degree of confidence that the
animal data do not lead to underestimates of the genetic risk
following exposure to humans. (See "Observations on Human
Populations," which follows.)
It should be noted that the genetic risk estimates
summarised in Table 6-20 for low-LET, low-dose, low-dose-
rate irradiation. Much of the data was obtained from high
rate studies, and roost authors have used a sex-avera0ed factor of
0.3 to correct for the change from high-dose rate, low-LET to low
dose rate, low-LET exposure (NAS72, 80, UNSCEAR72, 7?). However,
factors of 0,5 to 0.1 have also been used in estimates of
specific types of genetic damage (ONSCEAR72, 77, 82).
Studies with the beta-particle-emitting isotopes carbon™14
and tritium yielded of 1.0 and 0,7 to about 2.0,
respectively, in comparison to high-dose rate, high-dose exposure
to x-rays (UNSCEAR82). At present^ the RBE for genetic endpoints
due to beta particles is taken as 1 (UNSCEAR77, 82).
6.5.3 Est_imates_pf Genetic Harm _friM.,Mah~LETiu Radiations
Although genetic risk estimates -are made for low-LET
radiation, some radioactive elements, deposited in the ovary or
testis, can irradiate the germ cells with alpha particles. - The
relative biological effectiveness (RBE) of high-LET radiation,
such as alpha particles, is defined as the ratio of the
6-58
-------
Table 8-19, BEIR III estimates of genetic effects of an average
population exposure of 1 rein per 30-yr generation
(chronic x-ray or gamma radiation exposure).
Type of genetic
disorder
Current incidence
per 106 llveborn
Effect per 106 liveborn
First Generation* Equilibritu
Autosomal dominant
and x- linked 10,000
Irregularly inherited 90,000
Recessive 1,000
Chromosomal aberrations 6,000
5-65 40-200
(not estimated) 20-900
Very few Very slow
increases
Fewer than 10 Increases
only
slightly
Total
107,000
5-75
60-1100
First-generation effects estimates are reduced from acute fractionated
exposure estimates by a factor of 3 for dose rate effects and 1,9 for
fractionation effects
(NAS80, p. 117)
Equilibrium effects estimates are based on low dose rate studies in
mice (NAS80, pp. 109-110).
Source:
HASSO,
6-59
-------
Table 8-20. Summary of genetic risk estimates per 10 liveborn
of low-dose ratef low-LET radiation in a 30-yr
generation.
Source
BEAR, 1956 (NAS72)
BEIR I, 1972 (NAS72)
UNSCEAR, 1972 (UNSCEAR72)
UNSCEAR, 1977 (UNSCEAR77)
ICRP, 1980 (Of80)
BEIR III, 1980 (NAS8Q)
UNSCEAR, 1982 (UNSCEAR82)
UNSCEAR, 1986 (ONSCEAR86)
BNSCSAR, 1988 (UNSCEAR88)
First
_
49
9
63
89
19
22
17
18
Serious hereditary effects
generation Equilibrium
(all generations)
500
a (12~200}b 300a (60-1500)
8 (6-15) 300
185
320
a (5-75) 260s (60-1100)
149
104
115
Geometric mean of the lower and upper bounds of the
estimates. The geometric mean of two numbers is the square
root of their product.
Numbers in parentheses are the range of estimates.
6-60
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(irad) of low—LET radiation to the dose of high—LET radiation
producing specific patho-physiological endpoint.
In the Background Information Document for Radionuclides
(EPA84), an RBE of 20 was assigned to high-LET radiation
estimating genetic effects. It was noted that studies
cytogenetic endpoints after chronic low-dose-rate radiation
exposure, or incorporation of plutonium-239 in the testis,
have yielded RBEs of 23 to 50 for the type of genetic Injury
(reciprocal translocations) that might be transmitted to livehorn
'offspring (NAS80, UNSCE&R77, 82). Neutron RBE,
cytogenetic studies in mice, also ranged from about 4 to 50
(UNSCEAR82, Gr83a, Ga82). However, an RBE of 4 for plutonium-239
compared to chronic gamma radiation was reported for specific
locus mutations observed in neonate mice (NAS80),
Most recently, the MAS BEIR IV Committee reviewed the
effects of alpha-emitting radionuclides and estimated the genetic
effects (See Table 6-21). The BEIR IV genetic risk estimates for
alpha-emitters were based on the low-LET estimates given in Table
IV-2 in the 1980 BEIR III report, applying an RBE of 15 for
chromosome aberrations and 2,5 for all other effects*
Table 6-21. -Genetic risk estimates per 106 live-born for an
average population exposure of l rad of high-LET
radiation in a 30-year generation.
Serious HereditaryEffects
First Generation Equilibrium
(all generations)
28 -
Geometric Mean 91 690
Source;
These risk estimates, to a first approximation, give an
average of about 2.7 relative to the III low-LET
estimates. This is numerically similar to the dose
effectiveness factor for high dose rate. Therefore, for
simplicity, it would be possible to use the genetic risk
coefficients per rad of high dose-rate, low-LET and per of
high-LET radiation,
6.5.4 URcertaJjity Jin Estim.a^s_pj_J,ad_io..geiiic Harm
Chromosomal damage and mutations have been demonstrated in
cells in culture, in plants, in-insects, and in mammals
(UNSCEAR?2,77f82), and in peripheral blood lymphocytes of
6-61
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Ev79, Po?S}» However,
be for predicting genetic risk in of
believe such to be a direct of
to induced by radiation in cells, At
least, in peripheral lymphocytes radiation-
can occur in vivo in
Since are so sparse, they be only to
upper bounds of some classes of genetic risks following
radiation exposure. numerical genetic risk
OB extrapolations from animal data.
(Table 6-22), collected by ¥an (YaSO), on
induction of reciprocal -translocations in spermatogonia in
various species, indicate that animal-based estimates this
of genetic effect nay be within a factor of 4 of
value. Committee (UNSCEAR86) did report on
radiation induction of reciprocal translocations in other
primates, but the range of responses and conclusions
However, if there were no human data on this genetic
injury, in the majority of cases, assuming that animal results
and human results would be similar would underestimate risk
in
6-22, Radiation-induced reciprocal translocations in
several species
Translocations
(1Q"4 per
0.86 + 0.04
1.29 ± 0,02 to 2.90 + 0,
1.48 ± 0.13
0.91 ± 0,10
7.44 + 0,95
3,40 + 0.72
A basic assumption in the doubling-dose method of estimation
is that there is a proportionality between radiation-induced
mutation rates. Some of the uncertainty
in the 1982 UNSC1AR report.with the observation that in two-test
(fruit flies and bacteria), there is a proportionality
spontaneous and. induced mutation rates at a number of
individual sites. There is still some question as to
or not the sites that have been examined are
representative of all sites and all gene loci, with developing
that mouse ?~locus system is sensitive to
radiation other members of the mouse genome (NeSS). Current
is focused on transposable genetic elements
relevance of "mobile-genetic-element-mediated spontaneous
6-62
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mutations11 to in doubling
. The will review as
There is uncertainty as to which hereditary
would be doubled by a doubling dose; future studies on genetic
conditions diseases can apparently, only increase total
of conditions. Every report, from 1972 BEIS
0NSCEAR reports to the most recent, listed an
number of conditions and diseases that have a genetic
be increased by exposure to ionizing radiations.
6.5.4.1 Observations on Human Populations
A of birth cohort consisting of children of
Japanese A-bomb survivors was initiated in mid-1946. In a
detailed monograph, Neel and Schull (Ne56) outlined
background of this first study and made a detailed analysis of
the findings to January 1954 when the study terminated.* The
study designed to determine: (1) if during the first of
life, any differences could be observed in children born to
exposed parents when compared to children born to suitable
control parents, and (2) if differences existed,
be interpreted (Ne56).
This study addressed a number of endpoints, including
ratio, malformations, perinatal data, and anthropometric data;
subsequent studies have addressed other endpoints. Recent
on this birth cohort of 70,082 persons
on six endpoints. Frequency of stillbirths, major congenital
defects, prenatal death, and frequency of death prior to 17
have been examined in the entire cohort. Frequency of
cytogenetic aberrations (sex chromosome aneuploidy)
of biochemical variants (a variant enzyme or protein
electrophoresis pattern) have been measured on large of
There were small but statistically insignificant
the number of effects in the children of the proxiaally
and distally exposed with respect to these various indicators.
differences are in the direction of the hypothesis
mutations were produced by the parental exposure. Taking
differences then as the point of departure for an of
human doubling doser an estimated doubling dose for low-LET
radiation at high doses and dose rates for human genetic effects
of about 156 (ScSl) or 250 rent (Sa82) was obtained as an
unweighted average. When each individual estimate
by the inverse of its variance, an average of 139
(Sc84). of the assumptions necessary for
calculations, as well as the inherent statistical errors,
errors associated with these estimates are rather large. As a
result, a reasonable lower bound to the human estimate overlaps
much of the range based on extrapolation from data.
-------
report evaluated following possible
effects^ (1) untoward pregnancy outcomes,, (2) ill
of early mortality, (3) balanced chromosomal exchangesf |4) sex-
aneuplolds, (5) early onset cancer, (6) protein
mutations. On the basis of the findings of the study,
concluded that the garnetic doubling dose In
humans for acute penetrating radiation exposure from atomic
is 150 rent to 190 rem (Ne88).
is using the geometric' mean of the BEIR III range of
doubling doses; about no rads, EPA believes this estimate of
doubling dose probably overstates the risk? however, it Is
compatible with both human and mouse data and should not be
changed at this time. EPA estimates of genetic risks will be
reviewed and revised, if necessary, when more complete reports on
the Japanese JV~bomb survivors are published.
6.5.4.2 Ranges of Estimates Provided by Various Models
Following recommendations of the 1980 BEIR III and earlier
committees, EPA has continued to use a linear nonthreshold model
for estimating genetic effects, although some data on specific
genetic endpolnts obtained with acute low-LET exposures are
equally well described by a linear-quadratic function. Moreover,
in of these cases, it has been found that a reduction in
dose rate (or fractionation of dose) produced a reduction in the •
quadratic term seen at high doses with little or no effect on the
linear component. Such observations can be qualitatively
explained, as previously discussed in reference to somatic
effects (Section 6.2.2), in terms of the dual radiation action
theory of Kellerer and Rossi (Ke72), as well as alternative
theories, e.g., one involving enzyme saturation (Go80, Ru58).
Even though genetic risk estimates made by different
committees based on the linear non-threshold model vary, the
agreement is reasonably good. Some of the committees made
estimates In terms of a range. These ranges are expressed as a
single value by taking the geometric mean of the range. This
method was recommended and first used by UHSCEAR (UNSCEAR58) for
purposes of expressing genetic risk estimates. While the authors
of the reports used different animal models, interpreted them in
different ways, and had different estimates of the level of human
genetic conditions In the population, the range of risk
coefficients is about an order of magnitude (see Table 6-20).
For the most recent, more comparable estimates, the range is a
factor of 2 to 4 (see ICRP, BEIR III, and UNSCEA-R 1982 in Table
6-17}.
6.5.5 The EPA Genetic Risk Estimates
has used the estimates from BEIR III (NAS80) based on a
"doubling dose" range with a lower bound of 50 rem and an upper
bound of 250 rem. The reasons are as follows: mutation rates
for all gene loci affected by ionizing radiation are not known
6-64
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ail loci associated with "serious" genetic conditions
identified, the risk estimated by
Is Incomplete;, even for subject animal speciesf not
Include the types of damage estimated bj doubling doses,, EPA
not consider It further. Moreover, the BEIR III
risk estimates provide a better estimate of uncertainty the
UNSCEAR 1982 and ICRP estimates because the BEIR III Committee
assigned a range of uncertainty for multifactorial
(> 5 percent to < 50 percent) that reflects the uncertainty in
the numbers better than the other estimates (5 percent
10 percent, respectively).
The BEIR III estimates for low-LET radiations give a
considerable range. To express the range as a single estimatef
the geometric mean of the range is used, a method first
recommended by UHSCEAR (UHSCEAR58) for purposes of calculating
genetic risk. The factor of 3 increase in risk for high-dose
rate, low-LET radiation, noted earlier, is also used. The
weighted RBI for high-LET radiation as estimated in BEIR IV Is
about 3, which is numerically the same as the dose rate factor
noted above.
Genetic risk estimates used by EPA for high- and low-LET
radiations are listed in Table 6-23. As noted above
(Section 6.5.1), EPA uses the dose received before age 30 In
assessing genetic risks.
The EPA estimates in Table 6-23 are limited, like all other
human genetic risk estimates, by the lack of confirming evidence
of genetic effects in humans. These estimates depend on a
presumed resemblance of radiation effects in animals to those In
humans. The largest human source of data, the Japanese A-bomb
Table 6-23. Estimated frequency of genetic disorders in a
birth cohort due to exposure of the parents to
1 rad per generation.
Serious heritable disorders
, ._ r____ _ (Cases per 1.Q6 1 iveborn)^ , m
Radiation First generation All generations
Low Dose Rate,
LOW-LIT 20 260
High Dose Rate,
Lo¥-I»ET 60 780
High-LET 90 690
6-65
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survivorsf at to provide an of
calculating the genetic risk In which Is not
statistically significant (Ne88).
In developing average mutation rate for the
in the calculation of the relative mutation risk, the BSIR
III Committee postulated that the induced mutation rate in
about 40 percent of-that in males (NAS80), Studies
by Dobson', et al., show that the basis for the assumption
invalid that human oocytes should have a risk equivalent to
that of human speraiatogonia. This would increase the risk
estimate obtained from doubling-dose methods by a factor of 1.43
(Do83, Do84, DoSS). Recently Dobson et al, (DoSS) have shown
mouse oocytes are very sensitive to radiation, doses of 4 to
12 racts killing 50 percent of the immature mouse oocytes.
Immature oocytes in women are not so easily killed. Dobson et
al, (DoSS) have also shown the existence of a special,
hypersensitive, non-DNA lethality target (apparently the plasma
membrane) in immature mouse oocytes. Irradiation with low energy
neutrons, whose recoil protons have track lengths less than a
cell diameter, induces genetic effects in immature mouse oocytes
yields effects similar to those observed in other cells
(Do88). Immature human oocytes do not have the same
hypersensitive target as mouse oocytes and so should be as
susceptible as spermatogonia to genetic effects of radiation.
Unfortunately^, BEIR III and/ since it is based on BEIR III,
BEIR IV have embedded sex-sensitivity differences in their risk
estimates. In BEIR III; (1) autosomal dominants and X-linked
effects based on a lower estimate where the oocyte has zero
sensitivity and an upper estimate where the oocyte is 44 percent
as sensitive as spermatogonia (p. 118) ,* (2) Irregularly inherited
effects based on an estimate where the oocyte is 44 percent
as sensitive as spermatogonia (pp. 114 and 110}; (3) '
chromosomal aberrations estimates >are based on oocytes and
spermatogonia of equal sensitivity (p. 123, NAS80).
Since the sex-specific differences are in both BUR III and
BEIK IV, no attempt is made at this time to correct them. After
BEIR V is published, EPA's genetic risk estimates will be
reviewed may then be revised.
The combined uncertainties in doubling-dose estimates
the magnitude of genetic contributions to various disorders
probably introduce an overall uncertainty of about an order of
magnitude in the risk estimates. Moreover, the BEIR Committee,
in deriving its estimate, has assumed that almost all of the risk
due to irregularly inherited mutations which would be
eliminated slowly. They may include mild mutations which are but
slightly detrimental in their heterozygous state. However, they
may be sustained by advances in medical science, thus persisting
and accumulating for generations. To what extent this occurs
will depend on medical practices in the future.
6-66
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6.5.6 Effects of, _Mu 11 lg.ep.erafei.pia _E j
As earlier, while the somatic (cancer)
In to Ionizing radiation, genetic
occur in progeny, perhaps generations later. The of
effects appearing in the first generation is on direct
estimates of the mutations induced by irradiation not
change appreciably regardless of the background, or "spontaneous"
mutation rate in the exposed population. The estimate for total
genetic effectsf or the equilibrium estimate, is on
doubling-dose concept. For these estimates, the background
mutation rate is important: it is the background rate that is
being "doubled."
If there is long-lived environmental contamination, such
that 30 generations or more are exposed (>1000 years), the
background mutation rate will change and come into equilibrium
with the new level of radiation background. There will be an
accumulation of new radiation-induced mutations until the
background Mutation rate has reached equilibrium with, this
continued insult.
While predicting 1,000 years in the future is chancy at
best, if it is assumed that there are no medical advances, and no
changes in man or his environment, then an estimate can be made.
In Table 6-23, it is estimated that exposure to 1 rad per
generation of low-dose-rate, low-LET radiation will induce 260
cases of serious heritable disorders per 106 live births in all
generations. This is for a background mutation rate leading to
29,120 cases of serious heritable disorders per ID6 live births.
The "all generations" estimate in Table 6-23 is equal to the
III "equilibrium" estimate in Table 6-20. The "all
generations" estimate is used for exposures to a single
generationi the same number is employed as the "equilibrium"
estimate for multigeneration exposures (see NAS80f p. 126,
note 16). Thus, the risk estimate can be re-expressed as an
estimate of the effects expected for a given change in the level
of background radiation (Table 6-24}. Since these calculations
are based both on the background level mutations doubling
dose, changes in either must be reflected in new calculations.
Table 6-24.
Increase in background or level of genetic effects
after 30 generations or more.
Increase in background
radiation (mrad/y)
Increase in serious heritable
._di sord_ers per 10 . .Live birtjis
Low-dose rate, High-LET
low-LET radiation radiation
0.1
1.0
.0.0
80
2.1
21.2
212
6»67
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I TF? r1* ^ T"ih PI i
w Jl J, *™
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Although teratogenesis (congenital abnormalities or
defects) associated with x-ray exposure has a long history, the
early literature deals mostly with case reports. (St.21, nn29t
Go29). However, the irradiation exposures were high.
In 1930, Murphy exposed rats to x-rays at doses of 200 R to
1,600 R. Of 120 exposed females, 34 had litters, and five of the
litters had animals with developmental defects {Mu30}. He felt
that this study confirmed his clinical observations and earlier
reports of animal studies. Although there were additional
studies of radiation-induced mammalian teratogenesis before 1950,
the majority of the studies were done after that time (see Ru53
for a review), perhaps reflecting concerns about radiation
hazards caused by the explosion of nuclear weapons in 1945
(Ja?0).
Much of the work done after World War II used mice (Bu50,
Ru54, Ru56) or rats (Wi54, Hi54). Early studies, at relatively
high radiation exposures, 25 R and above, established some dose~
response relationships. More important, they established the
timetable of sensitivity of the developing rodent embryo and
fetus to radiation•effects (Ru54, Hi53, Se69, Hi66).
Rugh, in his review of radiation teratogenesis (Ru70),
listed the reported mammalian anomalies and the exposures causing
them* The lowest reported exposure was 12.5 R for structural
defects and 1 R for functional defects. He also suggested human
exposure between ovulation and about 7 weeks gestational age
could lead to structural defects, and exposures from about 6
weeks gestational age. until birth could lead to functional
defects. In a later review (Ru71), Hugh suggested structural
defects in skeleton might be induced as late as 10th week
of gestation and functional defects as early as the 4th week. It
should be noted that the gestation period in mice is much shorter
than that in humans and that weeks of gestation referred to above
in terms of equivalent stages of mouse-human development.
However, estimates of equivalent gestational age are not very
accurate.
Rugfa (Ru71) suggested there may be no threshold for
radiation-induced congenital effects in.the early human fetus.
In the case of human microcephaly (small head size) and mental
retardation, at least, some data support this theory (Ot83,
Ot84)•
However, for most teratogenic effects, the dose response at
low doses is not known. In 1978, Michel and Fritz-Niggli (Mi78)
reported induction of a significant increase in growth
retardation, eye and nervous system abnormalities, and post-
implantation losses in mice exposed to 1 R. The increase was
still greater if there was concurrent exposure to
radiosensitizing chemicals such'as iodoacetimide or tetracyeline
(H178).
6-69
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In of animal studies, it as if
teratologic effects, other than growth retardation,
Induction of effects (Ru54, Ru53, Wi§4).
Ohzu (Oh65) that doses as low as 5 R to preisplantation
increased resorption of Implanted
structural abnormalities in survivors. Then in 1970,
(Ja70) reported a study In which mice to 5,
20, or 100 R on eighth of pregnancy. He
function for Induction of skeletal
linear, or nearly linear, with no observable threshold. This
consistent with a report by Russell (Ru57),
a threshold for effects whereas others to
be linearly proportional to dose.
of the problems with the teratologic studies In animals
is the difficulty of determining how dose response data should be
interpreted. Russell (Ru54) pointed out some aspects of the
problem; (1) although radiation is absorbed throughout the
embryo, it causes selective damage that is consistently
on of embryonic development at the time of irradiation,
and (2) the damaged parts respond, in a consistent manner, within
a narrow time range. However, while low-dose irradiation at a
certain of development produces changes only in those
systems that are most sensitive at that time, higher
may induce additional abnormalities in components that
most sensitive at other stages of development, and may further
modify expression of the changes induced in parts of
at maximum sensitivity during the time of irradiation. In the
first, case, damage may be to primordial cells themselves, while
In second, the damage may lead indirectly to or
different endpoints.
embryo/fetus starts .as a single, fertilized
divides differentiates to produce the normal Infant at
term* (The embryonic period, when organs develop, Is
conception through 7 weeks gestational age. fetal
period, a time of in utero growth, is the period from 8
gestational age to birth,} The different organ and tissue
primordla develop Independently and at different rates. However,
they in contact, through chemical Induction or evocation
(ArS4). These chemical messages between cells are important in
bringing about orderly development and the correct timing
fitting together of parts of organs or organisms. While
radiation can disrupt this pattern, interpretation of
may be difficult. Since the cells in the embryo/fetus
differentiate, divide, and proliferate at different during
gestation at different rates, gestational times cells of
specific organs or tissues reach maximum sensitivity to radiation
different. Each embryo/fetus has a different timetable. In
fact, each half (left/right) of an embryo/fetus may a
slightly different timetable.
In addition, there is a continuum of variation from the
hypothetical normal to the extreme deviant which is obviously
-------
recognizable. is no logical place to a line of
normal abnormal.
variations of frank malformation, is
an arbitrary onse^ investigator establish. or
criteria apply to spontaneous
abnormalities alike (HWC73),
The limitations of human data available of
in descriptive and experimental inevitable,
, rise to speculation about
relevance of studies to man. There
in development attributable partly to the differing of
adult organs, but especially to differences in growth
timing of birth in relation to the developmental For
example, histological structure of the brain is, in
surprisingly'similar, both in composition and in function,
one mammalian species to another, and the sequence of is '
also similar (Do?3). However, the processes of brain
that occur from conception to about the second year of life in
man are qualitatively similar to those seen in rat during
first six weeks after conception (Do79f DoSl).
For example, a aajor landmark, the transition from
principal phase of multiplication of the neuronal to
that of glial multiplication, occurs shortly before mid-gestation
in man, but at about the time of birth in the rat (Do73). In
this respect, thenf the rat is much less neurologically at
birth than the newborn human infant. Many other
mature at birth; the spectrum ranges from the late-maturing
-and rat to the early-maturing guinea pig, with non-human
much closer to guinea pig than to man (Do?9, DoSl}. As a
consequence, it is unreasonable to compare a newborn ratfs brain,
which not to rayelinate, with that of a
which has, or with that, of a newborn guinea pig in which
myelination completed (Do79, DoSl}.
Nevertheless, in the study of teratogenic of
to ionizing radiation, in which timing of
in relation to the program of developmental
dictates the consequences of that insult, it is only to
aPPly "the experimental exposure at the appropriate (rather
than at a similar age) of embryonic or fetal development in
species to produce similar results in all (Do?9f DoSl). The
duration of exposure must, however, match the different
scales in different species. Unless these elementary
of cross-species adjustments are followed, extrapolation of
qualitative estimates of effects will be of dubious relevance
worth.
of the problems in interpretation listed above, a
pragmatic approach to evaluation of studies is useful,
response should be given as the simplest function that fits
(often linear or linear with a threshold). No attempt
6~7l
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be to develop complex
is unequivocal.
6,5,8.1 Teratologic Effects; Mental Retardation in
The first report of congenital abnormalities in children
in utero to radiation from atomic of
Plununer (P152) . Twelve children with microcephaly, of which
also had mental retardation, had been identified in Hiroshima in
a small set of the in utero. exposed survivors. They
as part of a program started in 1950 to study children in
the first trimester of gestation. However, not all of the in
iiterp exposed survivors were examined. In 1955, the program was
expanded to include all survivors exposed in utero.
Studies initiated during the program have shown radiation-
related (1) growth retardation,' (2) increased microcephaly;
(3) increased mortality, especially infant mortality;
(4) temporary suppression of antibody production against
influenza? and (5) increased frequency of chromosomal aberrations
in peripheral lymphocytes (Ka73).
Although there have been a number of studies of Japanese
A-bomb survivors, including one showing a dose- and gestational
age-related increase in postnatal mortality (Ka73), only the
incidences of microcephaly and mental retardation have been
investigated to any great extent. In the most recent report,
Qtake and Schull (Ot83, 84) showed that mental retardation
particularly associated with exposure between 8 and 15 weeks of
gestation (10 to 17 weeks of gestation if counted from the last
menstrual period). They further found the data suggested little,
if any, non-linearity and were consistent with a linear dose-
response relationship for induction of mental retardation that
yielded, a probability of occurrence of severe mental retardation
of 4.16+0.4 cases per 1,000 live births per rad of exposure
(Ot84). A child was classified as severely mentally retarded if
he or she was "unable to perform simple calculations, to make
simple conversation, to care for himself or herself, or if he or
she was completely unmanageable or had been institutionalized"
(Ot83, 84). There was, however, no evidence of an effect in
those exposed at 0 to 7 weeks of gestation (Ot83). Exposure at
16 weeks or more of gestation was about a factor of 4 less
effective, with only a weak relationship between exposure and
risk, and with few cases below 50 rads exposure (Ot84).
Mental retardation can be classified as mild (IQ 50-70),
moderate (IQ 35-49}, severe (IQ 20-34), and profound (IQ < 20)
(WHO75). However, some investigators use only mild mental
retardation (IQ 50-70) and severe mental retardation (IQ < 50) as
classes (Gu77b, HaSla, St84). Mental retardation is not usually
diagnosed at birth but at some later time, often at school age,
Since the mental retardation may have been caused before or
during gestation, at the time of birth, or at some time after
birth, that fraction caused before or during gestation be
6-72
-------
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circumference for
, in a population of live-born children,
2.275 will a head circumference 2
deviations or smaller than mean, 0.621 will
a head circumference 2.5 standard deviations or
the mean, 0.135 percent will have a head circumference 3
standard deviations or smaller than the (statistical
estimates on a normal distribution).
For of the studies of the Japanese A-bomb survivors
exposed in utero, if the head circumference was two or aore
standard deviations smaller than the mean for the appropriate
controls in the unexposed population, the case was classified as
having reduced head circumference even if the data had not been
adjusted for differences in stature (Ta67, Mi72; Wo65). While a
definitive relationship between reduced head circumference and
mental retardation not been established, there is evidence
that they related.
Studies of the Japanese survivors show a relationship
between reduced head size and mental retardation, but all these
studies are based on subsets of the total jjn utero population.
The fraction of mentally retarded with reduced head circumference
has been reported as 50 percent (RERF7S) to 70 percent (Wo66),
while the fraction of those selected for reduced head
circumference who had mental retardation has been reported as
11 percent (Wo66) to 22 percent (Mi72), Thus, while
relationship appears to exist, it has not been quantified.
majority of the cases of reduced head size
in those exposed in the first trimester of gestation,
particularly 6th or 7th to 15th weeks of gestation (Mi59,
Wo66r Mi?2, Wo65, Ta67). Most recently, it
reduction in circumference was a linear function of
(Is84) . However,, authors noted that the analysis
on T65 dosimetry, and the data should be reanalyzed after
completion of dosimetry reassessment currently in progress,
findings of reduction in head circumference, with a
window of effect IB the same time period of gestation as mental
retardation, help support the observations on mental retardation.
Although the exact dose response functions are still uncertain,
data on both types of effects have so far been consistent with a
linear, no-threshold response during the critical period.
6.5.8.3 Other Teratologic Effects
Effects other than mental retardation and microcephaly
been noted in the Japanes A-bomb survivors. Schull et al (Sc99)
reported that in individuals exposed prenatally between 8
and 25 of gestation there is a progressive shift downward in IQ
score with increasing exposure and that the most sensitive group
6-74
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Is 8 15 gestational at of
Much, the pattern reported for average
performance, expecially in the earliest of schooling
(Ot88) . Finally, a, JLJUiejirrllo^^
exposure incidence of unprovoked seizures in later life
been demonstrated to be consistent with the data for Individuals
exposed between 8 and 15 weeks gestational
Japanese A-bomb survivors exposed in utero also a
number of structural abnormalities and, particularly in
were microcephalic, retarded growth (Wo65). No estimate
made of the radiation-related incidence or dose-response
relationships for these abnormalities. However, 0KSCIAR
(UHSCEAR77) made a very tentative estimate based on animal
studies that the increased incidence of structural abnormalities
in animals may be 0,005 cases per R per live born^ but
that projection, to humans was unwarranted. In 1986, UNSCEAR
assumed the risk of an absolute increase of malformed fetuses of
the order of 5E-3 per rad seen in animals might apply to the
human species as well, for exposure over the period from 2 to 8
weeks post-conception (UNSCEAR86). In any event, the available
human data cannot show whether the risk estimates derived from
high-dose animal data overestimate the risk in humans or if a
threshold can be excluded.
It should be noted that all of the above estimates
based on high-dose-rate, low-LET exposure. In 19??, UNSCEAR also
Investigated the dose rate question and stated:
"In conclusion! the majority of the data available
for most species indicate a decrease of the cellular
and malformature effects by lowering the dose or
by fractionating the dose. However, deviations from
this trend have been well documented in a
instances and are not inconsistent with the knowledge
about mechanisms of the teratogenic effects. It Is
therefore Impossible to assume that dose rate
fractionation factors have the Influence on all
teratological effects." (UNSCEAR7?).
6*5.9 NQngtochastic .Effects
Nonstochastic effects, those effects that increase In
severity with increasing dose and have a threshold, have been
reviewed in the 1982 UNSCEAR report (UMSCEAR82). Nonstochastic
effects following in^utero exposure were reviewed in the 1986
UNSCEAR report (UNSCEAR86). In general, acute doses of 10 rads
low-LET radiation and higher are required to induce these effects
In animals. It is possible that some of the observed effects of
in utero exposure are nonstochastic: e.g., the risk of embryonic
lossr estimated to be 10"2 per R (UNSCEAR??) or per rad
(UNSCEAR86) following radiation exposure soon after
fertilization. However, there are no data to address
question of similar effects in humans. Usually, nonstochastic
6-75
-------
at environmental levels of
In 1986, United Nations Scientific Committee on
Effects of Atomic Radiation also reviewed the question of
retardation as a part of the overall review of biological
of prenatal radiation exposure (UNSCEAR86).
like ICRP, concluded there a risk of
retardation of 4 x 10"3 per rad over the period of 8 to 15
conception and of 1 x 10"S per rad over the period 16-25
after conception (UNSCEAR86). UNSCEAR also (1) a
pre-implantation loss of 1 x 10"2 per rad during the first
after conception, (2) a malformation risk of 5 x 10"5
rad during weeks 2 to 8 after conception, and (3) a risk of
leukemia and solid tumors expressed during the first 10 of
life of 2 x 10"4 per rad (UNSCEAR86) .
The British National Radiation Protection Board (NRPB)
reviewed available Information including the 1988 UMSCEAR report
to develop new health effects models (St88). The NRPB estimated
a mental retardation risk of 4.5 X 10 cases per rad of exposure
during weeks 8 to 15 of gestation. The NRPB also estimated a
cancer risk of 2.5 X 10" cases of leukemia and 3.5 X 10"4
of solid tumors per rad of in utero exposure (St88) .
EPA has adopted similar risk coefficients for estimating
prenatal carcinogenic, teratologic, and nonstochastic effects In
man (see Table 6-26).
Table 6-26, Possible effects of in_jitero radiation exposure.
Type of Risk Risk per Rad Risk per in a
100
Background
Fatal Cancer 6.0 x 10"4 4.5 x 10"5
Mental Retardation 4 x 10"3 6.0 x 10"5
(exposure at 8 - 15 weeks)
Mental Retardation
(exposure at 16 ~ 25 weeks)
Malformation
(exposure at 2 - 8 weeks)
Mental Retardation 1 x 10"3 1.5 x 10"5
Malformation 5 x 10"3 5.8 x 10"5
Pre~Implantation 1 x 10"2 3.8 x 10"5
Loss (exposure at
0-2 weeks)
6-76
-------
6»6 .SuiiiaiX^-^£.^-EPA^.g.--Adi.atio.p Risk Factors ~ A _P,ejrg|jec:tige
6-27 summarizes EPA's estimate of risk lifetime
whole-body to high- and low-LET radiation to
decay products. The nominal risk factors reflect EPA8s
judgment as to the relationship between and risk on
review of all relevant information available to the .
Likewise the cited ranges reflect, EPA's current best judgment as
to the uncertainties in these risk factors,
To provide a perspective on the risk of fatal radiogenic
cancers and the hereditary damage due to radiation,
calculated the risk from background radiation to the U.S.
.population using the risk factors summarized in Table 6-23, The
risk from background radiation provides a useful perspective for
the risks caused by emissions of radionuclides. Unlike cigarette
smoking, auto accidents, and other measures of common risks,
risks resulting from background radiation are neither voluntary
nor the result of self-induced damage. The risk caused by
background radiation is largely unavoidable? therefore, It is a
good benchmark for judging the estimated risks from radionnclide
emissions. Moreover, to the degree that the estimated risk of
radionuclides Is biased, the same bias is present in the risk-
estimates for background radiation.
The absorbed dose rate from low-LET background radiation
has three major components: cosmic radiation, which averages
about 28 mrad/yr in the United States; terrestrial sources,
as radium In'soil, which contribute an average of 28 mrad/yr
(NCRP87); and the low-LET dose resulting from internal emitters.
The last differs among organs, to some extent, but for soft
tissues it Is about 24 mrad/yr (NCRP8?). Other minor radiation
sources such as fallout from nuclear weapons tests, cosmogenic
radionuclides, naturally occurring radioactive materials In
buildings, airline travel, and consumer products, contribute
about another 7 mrad for a total low-LET whole-body of about
87 mrad/yr. The lung and bone receive somewhat larger
included in the 87 mrad/yr estimate, due to high-LET radiations
(see below). Although extremes do occur, the distribution of
this background annual dose to the U.S. population Is relatively
narrow. A population-weighted analysis Indicates that 80
of the U.S. population would receive annual doses that are
between 75 mrad/yr and 115 arad/yr (EPA81),
.As outlined In Section 6,2, the BEIR III linear, relative
risk models yield, for lifetime exposure to low-LET radiation, an
average lifetime risk of fatal radiogenic cancer of 3.9x10" per
rad. Note that this average is for a group having the age-
sex-specific mortality rates of the 1970 U.S. population. This
risk estimate can be used to calculate the average lifetime risk
due to low-LET background radiation as follows, The average
duration of exposure in this group is 70.7 yr, and at 90 mrad/yr,
the average lifetime dose Is 6.4 rads. The risk of fatal cancer
per person in this group is:
6-77
-------
6-27. of SPA's factors,
_RlsJc ...... Factor..
rad )
retardation
Genetic;
Severe hereditary
defects, all
Somatic-.
Fatal cancers
All cancers
Fatal cancers
High LET (10"6 rad"1)
Genetic:
Severe hereditary
defects, all
Somatic:
Fatal
Period
8 to 15
of gestation
30 year
reproductive
generation
Lifetime
Lifetime
In utero
30 year
reproduct ive
generation
Lifetime
Lifetime
»-6
Nominal
260
390
620
600
690
3,100
5,000
4,000 2,500 - 5,500
60 - 1,100
120 - 1,200
190 - 1,900
180 - 1,800
160 - 2,900
960 - 9,600
1,500 - 15,000
Fatal lung cancer Lifetime
360
140 - 720
assumes a linear, non-threshold response.
However, it is plausible that a threshold may exist for this
effect.
6-78
-------
) (S.7xlO~3 rad/y} (70,7 y) = 2.4 x 10*3 (6-11)
or 0,24 percent of all deaths. The vital
In EPA's radiation risk analyses indicate that the probability of
dying from cancer in the United States from all is
0.16, i.e., 16 percent. Thus, the 0.24 percent result
BEIR III linear dose response model indicates that about 1.5
percent of all U.S. cancer is due to low-LET background
radiation. The BEIR III linear-quadratic model
about 0.1 percent of all deaths are due to low-LET background
radiation or about 0.6 percent of all cancer deaths.
Table 6-11 indicates a risk of 5.6x10"4 rad"1 for alpha
emitters in lung tissue. UNSCEAR estimated that in "normal11
areas the annual absorbed dose in the lungs from alpha emitters
other than radon decay products would be about 0,51
(UNSCEAR77). The individual lifetime cancer risk
exposure is:
(6-12)
(5.6 x 10"4 rad"1) (5.1 x 10"4 rad/y) (70.7y) = 2.0 x 10"5P
which is about 1/100 of the risk due to low-LET background
radiation calculated by means of the BEIR III linear model.
The 1982 UNSCEAR report indicates that the annual
absorbed dose to the endosteal surfaces of bone due to naturally
occurring, high--LET alpha radiation is about 6 mrad/yr, on
a quality factor of 20 and an absorbed dose equivalent of
120 mrem/yr (UNSCEAR82). Table 6-11 indicates the
individual lifetime risk of fatal bone cancer to this
of the naturally occurring radiation background is:
{2.0 x 10"5 rad"1) (6 x 10"3 rad/y) (70.7/y) = 8.5 x 10"6.
The exposure due to naturally occurring background radon-222
progeny in the indoor environment is not well known. The 1982
UNSCEAR report lists, for the United States an indoor
concentration of about. 0,004 working levels (15 Bq/m3}
(UNSCEAR82). This estimate is not based on a national
is known to be exceeded by as much as a factor of 10 or in
houses. However, as pointed out in UNSCEAR32, the national
collective exposure may not be too dependent on exceptions to
mean concentration. The UNSCEAR estimate for the United
now appears low (NeS6); the average residential exposure is
probably 0,2-0.3 WLM/yr (in standard exposure units).
6-79
-------
0.25 WLM/yr Is a reasonable
to radon-222 progeny In this country,
indoors, is about 18 WLM. on
lifetime risk coefficient from Section 6.4.5f 360 cases/106 WIM,
a lifetime risk of 0.64 percent is estimated. For
roughly 5 percent of all deaths in 1980 were to lung
on these assumptions, therefore, about one of eight
cancer deaths may be attributable to background radon exposure.
This would correspond to about 4 percent of all cancer
This is 2.5 times the 1.61 percent of all cancer fatalities
estimated above for lowLET background radiation. The is
cautioned, however, that this risk estimate applies only to
United States population taken as a whole, i.e., men women,
smokers and nonsmokers. Since the vast majority of the 1980 lung
cancer mortality occurred in male smokers, this risk estimate
cannot be applied indiscriminately to women or nonsmokers (see
Section 6.4).
The spontaneous incidence of serious congenital and genetic
abnormalities has been estimated to be about 105,000 per 106 live
births, about 10,5 percent of live births (NAS80, UNSCEAR82).
The low-LET background radiation dose of about 87 mrad/year in
soft tissue results in a genetically significant dose of 2.6
during the 30-year reproductive generation. Since this
would have occurred in a large number of generations, the genetic
effects of the radiation exposure are thought to be at an
equilibrium level of expression. Since genetic risk
vary by a factor of 20 or more, EPA uses a log mean of this
to obtain an average value for estimating genetic risk. on
this average value, the background radiation causes 690
genetic effects per 10* live births (see Section 6.5). This
result indicates that about 0.6 percent of the current
spontaneous incidence of serious congenital and genetic
abnormalities may be to the low-LET background
6-80
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6-97
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7. AN OF IN FOR
7.1
Volume II of this Background Information Document (BID)
presents estimates of the risks attributable to radionuclides
released to air from various facilities categories of
facilities. The risks using data characterizing
airborne emissions and the models and assumptions described in
Chapters 4, 5, 6. The results of analyses provided in.
Volume II fatal cancer risks, in of the
additional lifetime risk to individuals and the number of
additional cancer fatalities in the exposed populations.
Rather than using mathematical models to assess impacts, one
would prefer to measure the actual impacts directly? .i.e.,
radionuclide'concentrations and radiation fields in the
environment and radionuclide concentrations in the various organs
of the exposed populations. However, this is seldom possible
because the radionuclide releases do not generally result in
detectable levels of radionuclides in the environment or in the
exposed members of the population. In addition, any additional
theoretical cancers that may be attributable to radionuclide
exposures cannot be detected in the presence of the large numbers
of cancers endemic in any population. Accordingly, the actual or
potential impacts of the emissions must be estimated using
mathematical models.
risk estimates for category provided in Volume II
presented as discrete values. Each of these calculated
values is an expression of impact on an individual or small group
of individuals or on a population as a whole. values are
intended to be reasonable best of risk,* that is, to not
significantly or be of
sufficient accuracy to support decisionmalcing. However, because
each facility is unique, the models used to calculate risk are
generalizations and simplifications of the processes which result
in exposure risk. In addition, ability to model the
processes is also limited by availability of data
characterizing each site and the understanding of the processes.
As a result, the estimates of risk have a considerable
degree of uncertainty.
Because of these uncertainties, values presented are of
more use to decisionmakers when there is some characterization of
their uncertainty. For example, a calculated risk may be small,
e.g., 10" lifetime risk of cancer for an individual. If the
uncertainty in this number is several -orders of magnitude, the
real risk of this source of emission may in fact be higher than
another source of emission which a calculated risk of 10'5
lifetime risk of cancer but a small of uncertainty.
Alternatively, a risk of 10" calculated using upper bound
techniques may appear to represent an unacceptable risk.
7-1
-------
a of be of
This situation occur when, to limited in format: ion
uncertainty in calculational parameters, conservative
throughout calculation in to
that the risks are not underestimated. This result in
a risk that is limit of what is plausible
it is on a very unlikely combination of
conservative assumptions. Quantitative uncertainty analysis
provide results that indicate likelihood of realizing
different risk levels across of uncertainty. This type
of information is very useful for incorporating acceptable and.
reasonable confidence levels into decisions.
The Office of Radiation Programs has initiated a program to
analyze the uncertainty in the risk estimates. This chapter
summarizes the quantitative uncertainty analysis performed in
support of selected risk provided in Volume II.
An assessment is provided of the uncertainty in estimating the
best estimate of the lifetime fatal cancer risk to members of the
general population that reside at locations which tend to
maximize risk. These Individuals referred to as "maximum
individuals.11 A detailed description of the mathematical models
and calculational assumptions used in the uncertainty analysis is
provided in SCA89.
7,2
7.2.1 Ap^l..lca_t.ion o£...JIiicj5rt^^^
RiskAssessment
of quantitative uncertainty analysis to
environmental following Reactor
Safety Study (NRC75), In 1984 by
In support of environmental risk (EPA84),
technique results in a of values of a
single discrete value by using a range of values for the
calculational Input parameters. In this wayf the iitpacts of a
given technological activity can be bounded different
technologies can be intercoropared. In where probability
distributions be to of calculational model
model results be as
probability distributions. Figure 7-1 is an of
output of an analysis. The as a
cumulative probability distribution. Inspection of
distribution reveals that, in this case, there is a high level of
confidence that technological activity will result in a
lifetime fatal risk of cancer of lo"4, that median risk
estimate (i.e., the 50th percentile value) is about 5x10 .
-------
1,000
t 0.750
-j
so
tt
O
fiC
*: 0.500
u
0.2SO
10
10*
10
"4
10
*3
10"
Figure 7-1.
Example of the output of a risk assessment using
quantitative uncertainty analysis.
7-3
-------
It is important to distributions of
calculated risks no"*" rigorously on
objective observations^ an ro include
of so as to reasonably
their uncertainties. As a result, the probability of a given
risk as calculated using these techniques should not be
considered rigorous estimates of the actual values, but rather
the results of using the calculational for of
parameters with the prescribed uncertainties.
Selected uncertainty analyses,, which are especially
relevant, include work performed by Hoffman (HO79f BOS2, HOS3,
HOSSa, HO88), Rish (RI83, RI88), and Crick (CR88),
7.2.2 Design, of the . .Uncertainty. Ana lysis
A review was performed of previous uncertainty analyses and
guidance documents (HO83, BOSS, RI88, and CR88) to identify the
approach that most appropriately applies to the analyses
presented in Volume II. The review addressed the extent of the
analysis required and the alternative analytical techniques
available to support the analyses. In addition, an evaluation
was performed to determine if all 12 source categories required
an uncertainty analysis, or whether a limited number of selected
categories could be used to characterize the overall uncertainty.
7.2.2.1 Extent of the Analysis
Uncertainty in the results of any risk assessment are the
result of the following (Cr88):
(1) Modeling uncertainties
(2) Completeness uncertainties
(3) Parameter uncertainties
7.2.2.1.1 Modeling Uncertainties
Modeling uncertainties pertain to the formulation of
mathematical models used to predict risk the degree to which
they accurately represent reality. One way to address this
source of uncertainty is to perform the analysis using a set of
feasible alternative model structures.
In general, modeling uncertainty is the most difficult
component to assess since it is often impossible to justify a set
of plausible alternative models in light of the available data
and to assign probabilities to these alternatives. To an extent,
modeling uncertainty is incorporated into the estimates of
uncertainty. For example, the uncertainty in the risk factors
includes a consideration of the uncertainty in the form of the
dose-response and risk projection models. On the other hand, as
noted in Chapter 5, uncertainty in the formulation of metabolic
models is a serious problem in estimating dose conversion factors
for many radionuclides. Modeling uncertainty for dispersion and
7-4
-------
As a resultf
of in radiological do fully
reflect of uncertainty.
be to validate models,
therefore reduce this of uncertainty, is to field
of the conditions of interest. However,
this is rarely to other limitations.
Alternatively, additional uncertain could be included
in the or of the values assigned to uncertain
parameters could be to account for this.source of
uncertainty.
7.2.2.1,2 Completeness Uncertainties
Completeness uncertainties are applicable to all risk
assessments. The issue has to do with whether all significant
radionuclides and pathways of exposure have been addressed. For
most facilities addressed in Volume II, the source terms are well
characterized there is little likelihood that, a significant
undetected radionuclide release is occurring. With regard to
pathways of exposure, the analyses assume that all the major
pathways of exposure (ingestion of milk, meat and vegetables,
inhalation, immersion in contaminated air, and exposure to
contaminated ground) are present at all sites (except those
emitting only radon^ where inhalation is the only pathway of
significance).
However, even -though a pathway is included; it may itself be
incomplete. For example, the analyses do not explicitly address
the direct ingestion of contaminated soil and the use of goat's
milk (vs. cow's milk) in the ingestion pathway. In addition,
changes in land living habits could introduce pathways
here, that treated
generically {such as hospitals} may-include sites which
unique pathways. types of completeness uncertainties were
not explicitly in the uncertainty analysis because,
though pathways could contribute to risk over any given
year, they unusual, and it is unlikely that they would
persist over the life of an individual. Hence, they would not
contribute significantly to- risk or the uncertainty in the
lifetime risk to an average individual.
One method that is sometimes to account for this type
of completeness uncertainty is to add an additional term to the
pathway model to represent unknown pathways and assign to it a
distribution based on judgement. This approach was not used
because it is considered unlikely that unusual pathways, such as
goat's milk .and soil ingestion, would be present at the critical
locations for prolonged periods of time.
-------
7.2.2.1.3
Uncertainties In of calculational input
parameters are the major sources of uncertainty in risk
assessments when modelling or completeness uncertainties are
small. In addition, model and completeness uncertainties are not
readily amenable to explicit analysis. Accordingly, the
quantitative uncertainty analysis focuses on parameter
uncertainties.
The assessment of parameter uncertainty involves the
development of quantitative characterizations of the
uncertainties associated with key model parameters. These
characterizations can be probability distributions or a set of
discrete values. Once key uncertain parameters are
characterized, their uncertainties are propagated through the
models using a simulation technique producing a probability
distribution representing uncertainty about the risk assessment
model results.
In order to perform an uncertainty analysis, It is necessary
to clearly define the risk that is being estimated. Is the risk
for a real or hypothetical person, is it the maximum or the
average risk, and is it the current or possible future risk that
is of concern? The individuals constructing the distributions
must clearly understand the objectives of the analysis or the
resulting distributions will be incompatible.
The results of the risk assessments provided in each of the
chapters of Volume II are expressed in terms of the risk to the
maximum individual and the total incidence of fatal cancer in an
exposed population. Because population risks represent the sum
of Individual risks, uncertainties in the individual risks tend
to cancel each other out during the summing process. As a
result, the uncertainty in estimates of population risk are
smaller than the uncertainty in the estimates of the risks
associated with the individual members of the population.
Because of this, the uncertainty analysis is limited to the
uncertainty in risks to an individual.
The concept of the individual risk must also be clearly
defined in order to develop the appropriate distributions for use
in the uncertainty analysis. In this BID, the individual risk is
defined as the lifetime risk from a lifetime exposure to a
typical member of the population currently residing either at the
location with the maximum potential for exposure, or, where
actual demographic data are known, at the inhabited location of
greatest exposure. It is assumed that the individual resides at
the same location for a lifetime. Since the risk being estimated
is the lifetime risk, year to year variabilities average out.
This is an important consideration since, over any given short
period of time, a particular person could have highly unusual
living habits. But over a prolonged period of time, living
habits tend to resemble the population average, thereby reducing
7-6
-------
in
their
lifetime rlslc. distributions for
Individual uncertainties In do not
represent variations Individuals.
A of calculations to
individual risk, Is an
exposure variable, with a distribution that follows
times for of U.S. population.
assumptions, Individuals belonging to specific
assumed to be for randomly selected time periods. As a
result, to to for
differences In risk factors as'a function of of
A final consideration important to development of
meaningful uncertainty distributions is Individual differences in
metabolism and radiosensltivity. The risks provided in BID
are for "typical" members of the population, and, as a result,
the uncertainties in these rislcs are, in part, on
uncertainty in our understanding of these as they
apply to a typical of the population, A Is
known about the biological behavior of radionuclides into
the body the potential adverse effects of exposure radiation.
As a result, the uncertainty in Is relatively
small. Conversely, any one individual .in the population could
have biological characteristics that differ markedly
"typical.11 The uncertainty distributions for biological
parameters for atypical individuals is not In
uncertainty analysis.
In summary, for of the uncertainty analysis,
distributions were developed for of
of as they pertain to calculation of
lifetime fatal cancer risks to typical of population
residing for a lifetime at currently-occupied locations that
the potential for exposure.
7.2.2.2 Techniques for Propagating Uncertainties
After each of calculational
assigned probability distributions, distributions
as input to models that propagate uncertainties, Two widely
used analytical and numerical approac3h.es for propagating
uncertainties of techniques Carlo
techniques, of is
propagating error described In fundamental on statistics.
This propagates errors by calculating a linear combination
of the first for model factor. This is
the simplest of for propagating
that the distributions of values of uncertain
can be approximated by their first two moments. In addition,
since the coefficients which quantify uncertainty about
parameter depend on the values of" the parameters, the Is
-------
only uncertainty in is
it will significantly coefficients,
The alternative to the of is the of
numerical techniques, primarily Carlo analysis. Numerical
techniques advantage that they do require
parameters to follow normal or lognormal distributions or a
small of uncertainty relative to the mean. However,
approaches can consume considerable computer resources.
Monte Carlo techniques calculate risk in the as
described in Chapters 4, 5 and 6, except they perform
•calculation many times, each time randomly selecting an input
value from each of the probability distributions representing
uncertainty about each parameter. The output is a risk
distribution. The number of repetitions determines the precision
of the output distribution. The more repetitions and the larger
the number of calculational parameters treated as distributions
in the model, the greater the computer resource requirements.
By controlling how the values are sampled from each
distribution, parameters that are directly or indirectly
correlated can also be modeled. In addition, by a linear
regression analysis of individual parameters, the parameters that
are important contributors to uncertainty can be identified,
A Monte_Carlo technique for propagating uncertainty
chosen for use in this analysis. The computer code selected is
called MOUSE (KLEE86). To use MOUSE, a subroutine is written
that defines the risk equations the distributions for each
parameter. MOUSE then uses these distributions and equations to
choose a random value for each parameter and calculate the risk.
It does this over and over (typically 1000 to 5000 times), and
stores the results of each trial. At the it computes
tabulates statistics for of calculated values,
result is an estimate of the distribution of risk.
7.2.2,3 Choice of Source Categories
Of the 12 source categories, four site-specific analyses
were selected for this uncertainty analysis. The choice made
on the basis of those having either a high risk or a high
uncertainty and therefore to be representative of the 12 source
categories in terms of the overall uncertainty in the risk
assessments provided in the BID.
The scenarios and facilities considered in this study are as
follows;
1. Elemental Phosphorous Plants--FMC, Idaho
2. DOE Facilities-Reactive Metals, Inc., Ohio.
3. Phosphogypsum*Stack~IMC, Inc., Florida
4. Uranium Mill Tailings Pile-Sherwood, Western Nuclear,
Washington
7-8
-------
o
o
Environmental
following a discussion
of basis for of the distributions to character!**1
uncertainty about values of in of *'
To mitigate possibility of absurdly small or large
values for the parametersf the normal lognormal distri
truncated by imposing limits of deviations
That, is/ if MOUSE a value
deviations away it
to go back try again until value
the limits. In of normal distributions,
distributions restricted so .that they could be j
(this is a dognormal distributions). For
uncertainty of
magnitude, a logarithmic distribution (i.e.,
log-uniform,, lognormai, or log-triangular). This to give
to of distribution
sanpling representative,,
7.3.1
as of
rates, in Ci/yr* ' values on
to
uncertainty In in year. However,
of this Is to uncertainty in
the uncertainty in
a of time. a*1
have a of uncertainty than uncertainty in,
for period. From-
this perspective, distributions to
overestimate uncertainty.
In many cases, the on a limited
of which with a relatively
small analytical error, a of
uncertainty regarding of '"V- - -1 ,
for of time. In general, v^i * > < ' < ,
individual as indicati J' > < ' t •
variability of long » - - <
Y.
7-9
-------
7.3,1,1 FMC Elemental Plant
Metals, Inc. Fuel Fabrication Plant
from these facilities are measured by of
monitors. The uncertainty in the source term for FMC
plant is on EPA88.
for 7 rate measurements for poloniuis-210 6 for
lead-210. The measurements were represented by lognormal
distributions. The results are as follows:
Nuclide Geometric Mean Geometric Standard Deviation
(Ci/yr) (dimensionless multiplier)
Po-210
Pb~210
9.7
0.11
1.2
2.6
The uranium, thorium and radium source terms were not
explicitly addressed because collectively they were found to
contribute only about 0.2 percent to the dose.
source term for the Reactive :Metals fuel fabrication
facility is based on effluent measurements. The uncertainty in
these values was assumed to be only measurement error, having a
normal distribution with a standard deviation of 30 percent of
the value. The release rates used in the analysis
Nuclide Arithmetic Mean Arithmetic Standard Deviation
(Ci/yr) (Ci/yr)
U-234
U **• 2 3 5
U-238
2.2E-4
4,41-5
5.5E-3
6.6E-5
1.3E-5
1.7E-3
7.3.1.2 IMC Phosphogypsum Stack
There has been a fairly extensive program to measure radon
emissions from phosphogypsum stacks. From this program, it has
been determined that the radon flux is different for different
regions of the stack. The results are as follow:
7-10
-------
Region of Stack Flux (pCi/m2~sec)
Beach 0,33
Dry areas 13.1
Roads 8.54
Pond. 0,
Sides 5.91
The geometric standard deviation of the measurements is
considered to be about 2.5.
The release from a gypsum stack depends not only upon the
flux from these regions, but also upon the fraction of the top or
side area that they represent. Note that these areas and
fractions are for operating or idle stacks. When a stack is
closed, there are no beaches or ponds. The fractions are as
follows for the IMC gypsum stack (which is operating):
Region of Stack Fraction of Top or Side Area
Beach
Dry Areas
Roads
Pond
Sides
0.1 to 0.2
0.2
0.05
0.55 to 0.65
1.0
(top)
(top)
(top)
(top)
(side)
The fraction of beach was assumed to vary uniformly between
the limits given above (representing the rise and fall of the
water level in the pond) and the pond fraction varied
accordingly,
7.3.1.3 Sherwood Uranium Mill Tailings Pile
The source term used in the BID, 210 Ci/yr» is a predicted
value based on measured concentrations of radium-226 in the pile
and assumptions regarding the long term conditions of the pile,
This estimated value was used as the median of a lognormal
distribution with a geometric standard deviation of 4, This is
slightly greater than that for gypsum stacks (i.e., 2,5} in order
to account for the additional uncertainty because of varying
release rates over the 70-year period.
7.3.2 Atstospherjic Disper s ion
The product of the average annual source tena (Cl/sec) and
the location specific average annual atmospheric dispersion
7-11
-------
(Chi/Q, sec/ia)1, yields annual airborne
concentration of radionuclides at specific locations {Cl/m3} .
4 (Section 4.2} a discussion of
factors Indicates that uncertainty in the
Chi/Q for any given location can from about
a factor of 2 to 10, depending on distance from the release point
complexity of the terrain.
In this section, uncertainty distributions for
Chi/Q values are developed. A distinction is
uncertainty distribution for the Chi/Q values at the
locations of the maximum individuals and the locations of locally
grown food.
7.3.2.1 Atmospheric Dispersion for the Location of the
Individual
For all cases, the median value of Chi/Q was taken to be the
value front the AIRDOS runs used to estimate the risks for the
BID. The geometric standard deviation for an annual average
Chi/Q within 10 km of the release point was based on Miller
Hively (Mi87). They are as follows:
Conditions Geometric Standard Deviation
Simple"terrain 1.5
and meteorology
Complex terrain 3.8
meteorology
7.3,2.2 Atmospheric Dispersion Factors for the Locations of
Gardens and Farms
For food grown at home, the Chi/Q distribution associated
with the maximum individual's location was used. A substantial
portion of the maximum individual's diet/ however, is to
be grown within an 80™ltilometer radius of release
point. AIRDOS estimates the risk from eating contaminated food
grown within this region by distributing food production over the
area. Such detail was not feasible in this
uncertainty analysis. Instead, the distance to the locations of
the regional food sources was assumed to vary randomly. For
urban sites, it was assumed that the distance varies uniformly
1 The atmospheric dispersion factor is often referred to as
Chi/Q, where Chi is radionuclide concentration at a particular
location Q is the source term. When the units cancelled,
Chi/Q is expressed in units of sec/m3.
-------
69,000 to 80,000 25
of site. For rural sitesf it
that distance varied 200 to 80,000 meters,
effectively whole region. A uniform distribution for
distance to the locations of the and used, even
though of distances more than two decades. Use
of a uniform distribution gives more weight to distant
locations which have more area in proportion to their distance
and agricultural production. The resulting Chi/Q
distributions for food obtained from other than local
gardens as follows:
Geometric Geometric
Facility Mean, sec/m3 Standard Deviation
FMC Elemental
Phosphorous 7.4x10-9 5.8
Reactive Metals 8.7x10-9 3.8
7 » 3 . 3
Once the airborne radionuclide concentration is determined
by product of the source term and Chi/Q, the concentrations
of radioroiclides in various components of the environment , such
as in on the ground, are determined through use of
pathway factors. In addition, for the purpose of this analysis,
intake of radionuclides via inhalation and ingestion
are treated as factors representative of the average
individual. Accordingly, to calculate
radionuclide concentrations in the environment and in foods
the intake rates of these radionuclides through 'ingestion- and
inhalation calculated with the usage factors.
Table 7-1 gives the definitions of the parameters used In
the risk for the maximally exposed individuals.
Chapter 4 presents a description of the parameters how they
to model the behavior of radionuclides In the
environment. The uncertainty analysis includes one additional
parameter to account for the differences between the indoor
outdoor airborne radionuclide concentrations (i.e., Fc!-n} •
Tables 7-2 and 7-3 present the distributions for the pathway
parameters in this uncertainty analysis. A comparison of
values of parameters used In Volume II with the
distributions for those parameters provides Insight into
uncertainty in BID risk estimates and the degree to which the
BID risks representative of actual risks,
7-13
-------
•1. Environmental
B = breathing rate (n3/y
-------
BID Mia
Fr/Y psstured
Fr/Y
vegetables
TM
Q^ (dry wt . )
Qf (dry wt.)
T (itilk)
T (neat)
T (veg)
texp <™*>
tejtp (pasture.
F dry soil
Yj Particles
¥d Iodine
V
1.4
.1
14.
16.
12.
2.
20.
14.
60.
) 30.
215.
160.
3000.
0.01
2.7e-5
B2/kg LS
M2/kg IH
days IS
kg/d N
kg/d 1
day T
day T
day T
day f
day T
kg/m2 U
e/d M
m/d LS
*1 Y If
./ «
d"1
1.8
.1
12
16
12
2
17
11
60
30
-
250
500
.
1.6
1.8
1,7
11
8.3
"" JL
1
1
30
15
190
3.8
3,5
7.3e
8 Probability dlstrilititions, where U9 — lognomai, N — nonsal,
T — triangular, 0 - uniform, HC — log-triangular,
IB — log-uniform.
For normal distributions, PAB.1 is the arithmetic mesa.; for
lognomai distributions, it is the geometric raean; for
triangular distributions, it is the mode.
c For normal distributioas, PAR2 is the arithmetic
deviation; for lognomai distributions it is the geometric
standard deviation.
values are based on dry weight for aninal feed (which is
about 25% of fresh weight and range from .2 to ,35
-------
able 7-2 Distributions of ingestion {continued).
1 (vegetables,, Cl/kg plant Ci/kg soil--average values)**
PG 4E-4 LU - - 1E-4 3E-4
Pb 3E-4 LU - - 2E-6 5K-4
U 61-4 LU 7.31-5 - 1E-5 IE-3
Probability distributions, where JUS ~ lognormal, I
I =» triangular-, U -- uniform, LT = log-triangular,
Hi •=• log-i
"S'Q IE-3 LIJ - 21-6 7E-3
Pb IE-2 III - - 5E-4 4E-2
U 2E-3 1U - 1.4E-3 .2
Pb 9E-2
U 11-2
B, (forage, Cl/kg plant per Ci/kg soil)d
F (milk, day/1 or day/kg)
btitloris, PAR1 Is the arithmetic mean; for
lognormal distributions, It is the geometric mean; for
triangular distributions, It is the mode.
e For normal distributions, PAR2 is the arithmetic standard
deviation; for lognormal distributions it is the geometric
standard deviation.
d The Bv values on fresh weight of vegetables dry
weight of animal, feed. Soil is dry weight for both.
e The "walu.es in 1G82 for drj weght. The values for fresh weight
obtained by Multiplying the values for dry weight by four,
7-16
-------
Table 7-2 Distributions of ingestion pathway factors (continued)
Mean/
Parameter BIO Distr* SDC Min Max
Ff (neat, day/kg)
-d _«•
21-4 2E-3 MC80
d d
Po
Pb
U
SE-3
81-4
IE- 2
UJ
IB
I»
a Probability distributions, where IS - lognormal, N - normal,
T - triangular, U - wniform, LT « log-triangular,
III — log-uniform.
b For normal distributions, PAR! is the arithmetic mean; for
lognomal distributions, it is the geometric mean; for
triangular distributions, it is the mode,
c For normal distributions, PAR2 is the arithmetic standard
deviation; for lognotmal distributions it is the geometric
standard deviation.
^ No values available; used 0.1 and 10 times BID value.
7-17
-------
Table 7-3 Distributions of
BID Distr8 Parlb Par2c Min
B 8000 m3/yr
Fcff)
Fin (urban)
FIn (rural)
site
Fhomc (rural)
Vegetables
Milk
Meat
Fh«ne (urban)
Vegetables
Milk
Meat
Fregn (rural)
Vegetables
Milk
Meat
Fregn (urban)
Vegetables
Milk
Meat
_
_
0,7
0.4
0.6
0.076
0.
0.008
0.3
0.6
0.558
0.924
1.0
0.992
N 8000
U
u
u
u
0
u
u
u
u
u
u
u
u
0
o
u
1.2
0.5
0.96
0.92
0.6
0.
0.
0.
0.
0.
0.
0.2
0.8
0.4
0.1
0.2
0.1
«,
1.0
1.0
1.0
0.8
0.6
0.2
0.2
0,2
0.02
0.02
0.8
1.0
0.8
0.4
0.4
0.2
SCA89
SCA89
SCA89
SCA89
SCA89
SCA89
SCA89
SCA89
SCA89
' wash
0.5
U
0.1
0.9 SCA89
8 Probability distributions, where N = normal, U
T = triangular.
b
uniform,
For normal distributions, PAR1 is the arithmetic mean; for
triangular distributions, PAR1 is the mode.
c For normal distributions, PAJR2 is the arithmetic standard
deviation.
7-18
-------
uncertainty distributions primarily on
following
o NUREG/CR-2612, "Variability in Estimates
Associated with the Food Chain Transport and Ingestion
of Selected Radionuclides". Prepared by P.O. Hoffman,
et al of the ORNL for the NEC, June 1982, -(HO82).
o HUREG/CR-1004, "A Statistical Analysis of Selected
Parameters for Predicting Food Chain Transport and
Internal Dose to Radionuclides". Prepared by P.O.
Hoffman and C.F. Baes, III, of the ORNL for NRG.
November 1979. (H079).
o Ng, Y.c. A Review of Transfer Factors for Assessing the
Dose from Radionuclides in Agricultural Products,
Nuclear Safety, 23(1), 57, 1982. (NG82).
o NRPB-R184 A Report by the National Radiological
Protection Board entitled "Uncertainty Analysis of the
Food Chain and Atmospheric Dispersion Modules of MARC
by M.J. Crick et al.r May 1988. (CR88).
In addition, a review of the Health Physics Journal was
performed to supplement the above review articles. A detailed
description of the bases for the distributions is provided in
"Analysis of the Uncertainties in the Risk Assessment Performed
in Support of the Proposed NESHAPS for Radionuclides" (EPA89).
The distributions presented in Tables 7-2 and 7-3 are based
primarily upon distributions reported in the literature. They
provide an indication of the range of possible values; however,
for a specific site, the range may be narrowed by selecting only
closely to site. a
level of refinement was not possible for this' study, and thus the
degree of dispersion of risk about the mean for specific sites
may be an overestimate. On the other hand, the generic hospitals
represent sites located all over the United States. For them,
the range of values probably does not encompass all of the
possibilities, and hence, the degree of dispersion in the risk
may be underestimated.
7.3.4 Risk Factors
Risk factors are expressions of the lifetime risk of fatal
cancer per unit exposure or intake of individual radionuclides,
A detailed discussion of the sources and magnitudes of
uncertainties associated with the calculation of risk is provided
in Chapters 5 and 6,
Except for exposure to radon, the calculation of risk is a
two step process. First, dose rate is calculated as a function
of age for individual organs from each radionuclide and exposure
pathway. Then the risk attributable to the organ doses is
7-19
-------
calculated. For radon, a deal of epideatialogical
which a direct relationship
to progeny risk of lung cancer.
Accordingly, to the lung Is not to lung
cancer risk associated with exposure to a given concentration, of
radon progeny (see Section 6.4). Because of these differences,
fundamentally different approaches were for developing
uncertainty distributions in the risk factors for to
radon and radionuclides other than radon,
For exposures to radon, risk factors ranging from 140 to 720
deaths per 106 working level months were used. The basis for
this distribution is described in Chapter 6 (Section 6,4). The
risk factors were assumed to be log-uniform between these limits.
In order to account for the additional uncertainty when
exposure duration was varied, an additional GSD of 1.5 was
incorporated into the uncertainty distribution for the radon
exposure risk factor (see Section 6.5),
For radionuclides other than radon, the risk distributions
were calculated from the following expression:
Risk = F S E-. R.. (7-1)
ij
where:
Risk is the lifetime risk of fatal cancer from
exposure to all radionuclides via all pathways,
Ef - is the intake or nuclide I via pathway j,
Ry is the risk factor for nuclide i via pathway j, and
F is a factor to account for the overall uncertainty in the
risk model.
Each parameter in the equation is assigned a distribution.
However, the distribution assigned to the risk factor (Ry) only
accounts for the portion of the uncertainty associated with
estimating dose from a given intake of radionuclides. The
contribution to overall uncertainty in going from dose to risk is
accounted for through the use of F, which is a unitless
multiplier. This approach allows the uncertainty in the risk
model, which is common to all radionuclides, to be treated
separately from the uncertainty in the dose estimates, which is
radionuclide specific.
-------
F is to be lognormally distributed with a
of 1.0 a deviation of 1.3 (l=84f or a
factor of 10, would 95 of the risk),
choice of l.S as geometric deviation is on
discussion of uncertainty provided in Section 6.2.12.
In order to account for the additional uncertainty
introduced by the dependence of the risk factors when
exposure duration varied, the GSD was increased from l.S to
2,4, based on the following. Assuming that the distribution of
ages in the U.S. population is roughly uniform, and the ratio of
the highest to lowest age-dependent risk factor is 9:1 and is
distributed log-uniformly, then the geometric standard deviation
is:
In(GSD) = {[In3 - ln(0.33)]2 / 12}V2 = 0.63 (7-2)
GSD =1.9
Combining this with the geometric standard deviation for the
model uncertainty (i.e.,1.8):
In(GSD) = {[ln(1.8)]2 + [ln(1.9)J2 }1/2 = 1.25 (7-3)
GSD =2.4
For the case where it is assumed that the maximum individual
resides in one location for a lifetime, the distribution of F was
assumed to have a GSD of 1.8= For the case when moving is
accounted for, a GSD of 2.4 was used. In both the geometric mean
was 1.0.
Table 7-4 presents the distributions used to characterize
Rr. The values are based on Chapter 5 (Section 5.3). In all
cases, for internal exposures, it is that probability
distributions are lognormal having a geometric mean equal to the
values of the risk factors in Table A-5. For example, in the
category ''Essential Element", it is suggested that a factor of
two or less for critical organs is the 95 percent confidence
interval or two standard deviations from the mean, so the
geometric standard deviation is the square root of 2, or 1.4.
For external exposures, it is assumed that the 95 percent
confidence interval is a factor of 2, giving a geometric standard
deviation of 1.4.
7,4
7.4.1 Cumulative Frjsgiiimcy..D.istribu.fcioas_
Figure 7-2 presents the cumulative frequency distributions
from the MOUSE runs for the four cases. While it is not obvious
from Figure 7-2, the distributions are, for all practical
purposes, lognormal. The risks were plotted on a log-probability
graph and are very close to a straight line, indicating that the
7-21
-------
7-4. Probability distributions factors6.
Geometric
Pathway Meanb Std, Dev.
1-125
Groundfa 0.63 1.4
Immersion 14.0 1=4
Ingestion 2.7 1.4
Inhalation 1.8 1.4
Ground 14.0 1.4
Immersion 67.0 1.4
Ingestion 3.7 1.4
Inhalation 2.6 1.4
Pb-210
Ground 0,085 1.4
Immersion 1.8 1.4
Ingestion6 55.0 1.4
Inhalation0 3.6E+4 l.4
Po-210
Ground 2,91-4 l.4
Immersion 0.015 1.4
Ingestion6 140,0 2.2
Inhalation6 1.1E4 2.2
a Note that this distribution only accounts for the
uncertainty associated with the calculation of dose from
intake. The uncertainty associated with the calculation of
risk from dose is taken care of by F.
b The units are m2/Ci~year (ground), m3/Ci-ye-ar (immersion) ,
Ci"1 (ingestion and inhalation) .
c These values differ from the values in Table A-5 because,
in the risk assessment provided in Volume II, actual particle
sizes and solubility classes specific to these facilities were
used. The values in Table A-5 were not used for these
facilities.
7-22
-------
Table. 7-4. Probability distributions
Pathway
Geometric
Meanb
Geometric
Std. Dev.
Ground
Immersion
Ingestionc
Inhalation6
0.024
0,23
75.0
2.51+4
1.4
1.4
2,2
2.2
Ground
Immersion
Ingestionc
Inhalation0
5.5
250.0
73.0
2.3E+4
1.4
1.4
2.2
2,2
U-238
Ground
Immersion
Ingestionc
Inhalationc
0.019
0.15
74.0
2.2E+4
1.4
1.4
2.2
2.2
8 Note that this distribution only accounts for the
uncertainty associated with the calculation of dose from
intake. The uncertainty associated with the calculation of
risk from dose is taken care of by P.
b The units are m2/Ci~year (ground) , si3/ Ci~year (immersion) ,
Ci"1 (ingestion and inhalation) .
c These values differ from the values in Table A-5 because,
in the risk assessment provided in Volume II, actual particle
sizes and solubility classes specific to these facilities were
used. The values in Table A-5 were not used for these
facilities.
7-23
-------
100
50
ELBfHTflL PLfW
emulative Percent
G.Q01 0.01 0.1
— Hove uith
U.S. -(w
—• One place
•lor ?0 yrs
10 100
Risk Kama! ized to Geometric Nean
Risk for ?0-¥ear Residence line
10D
emulative Percent
^ _ - j<">;»jps«««*"~""— — *
_„./ J
001 0.01 0.1 1 10 1C
— - {fc¥6 With
U.8. -freq
— One place
for ?D yrs
»
Risk Noraalized to Qeo&etric Mean
Risk tor K5-Year Residence Tise
IKRNIUN REL IfMFflCTUffiR
. Cumulative Percent
S3
0
0.
I .-7 1
; ^ /
— - teve usth
U.S.' -freq
— One place
for 7Q yrs
301 0.01 0.1 1 10 100
Risk Horaalized to Geowtric Iteai
Bisk for 70-fear Residence Tise
HILL TfflLINGS PILE
.Cusulative Percent
yith
U.S,
ftw place
•for 70 yrs
0.00! 0.01
10 JOO
Risk NorsalizeeS to Geometric Wean
Risk for ?0-Veir lesidsret lirte
Figure 7-2 Cumulative probability distributions for risk.
7-24
-------
(50th percentlies) differ by only about
10 or less, while arithmetic differ
by factors of 2 to 20. If a distribution Is lognormai,
median is equal to geometric If it is median
is equal to arithmetic Thus, the distributions for
risks to be lognormally distributed,
characterized by geometric
deviations.
7.4 = 2 ComBarisoB..-..-..^!, the. ..Results of _ the .Uncertainty. Analysis
Table 7-5 presents the geometric of
_»™~-~- «*» ™ ^~ ™-~.~ ~- ^ ™ ~~ -~ ^
results of the uncertainty analysis. The of values
derived by dividing and multiplying the geometric by
square of the standard deviation. This is believed to be
interval-within the'true risks are likely to fall.
Table 7-5 also includes the values of risk provided in
Volume II of the BID. For the case where individual
Is assumed to reside at the location for 70 years, the
results in Volume II lie approximately in the center of the range
of values. This provides a high level of confidence that
values in ¥olume II represent a reasonable realistic estimate
of risk.
In response to several requests, agency an
uncertainty analysis, which Included the effects of distributing
the exposure period according to- U.S. residency duration data.
The effect of doing this is large, as by Table 7-5
Figure 7-2. the central values overall
uncertainties are strongly affected. The geometric
lower by a factor of limits by a factor
of two five. However,
which deserve consideration in evaluating effects.
The principal the Agency to
individual risk the lifetime risk a lifetime
exposure. The lifetime exposure is not intended as a
conservative overestimate of the duration, It
does allow consistent comparisons to be which can
unambiguously take Into account effects of at exposure.
Clearly, one can scale such an estimate for other periods of
exposure, e.g., the average lifetime risk a
exposure. But such a scaling only redefines individual risk?
it should not affect any decision making process.
It is important to note that the'distribution for
the residency period is based on population distribution of
exposure duration due to moving, rather than on uncertainty
in the mean exposure duration. In contrast, the parameters
as breathing rate are distributed according to
uncertainty in their values. There would be little
7-25
-------
-------
risk. Furthermore, application of a
easily lead to conclusions regarding in
risk
results also reveal that there is substantial
uncertainty associated with risk estimates. In all cases,
the range of uncertainty several orders of magnitude. This
means that It is possible that the true risks could be
times higher or lower than the values reported in Volume II.
7.4.3
For the facilities analyzed, the major pathway is
inhalation. The significance of this finding is that the risk is
not affected by the very complicated food pathway or the somewhat
less complicated ground exposure pathway. Thus uncertainties in
hard-to-determine parameters, like the deposition velocity and
environmental removal constant, are not significant for these
facilities.
A multiple linear regression analysis was performed to
identify the parameters that are important contributors to the
uncertainty in the risk estimates. In this analysis, the
dependent and independent regression variables were the
logarithms of the parameters. It was determined that the log
transformation gave a much better fit to the data than the
untransformed data. In all cases, the correlation coefficient is
95 percent or more, indicating a good fit.
The results of the regression analysis are presented in
Table 7-6. Of the approximately 40-60 parameters addressed in
this analysis, only about 5 or 6 are important contributors to
the uncertainty in the risk estimates. In all ,
dispersion factor is an important contributor to
uncertainty in risk, and, for the case where•the resident is
assumed to move, uncertainty in the residence time is an
important contributor to uncertainty in the risk estimates. For
the individual facilities, uncertainties in the source terms
risk factors consistently are important contributors to
overall uncertainty in risk*
7-27
-------
7-6. of to risk8
Facility
JEragtion of Piiggrtain.t.Ym_diie to Earameter
Based on Not Moving on Residence
During a Lifetime Time of Distributions
(70 Years) of the U.S. Population
Elem. Phos.
Fuel. Fab.
Phospho-
gypsum Stack
8 See Table 7-1
Atm Disp
Inh Risk
Factor for
Po-210
F
B
Inh Risk
Factor for
U-238
F
Atm Disp
Release Rate
for 0-238
B
Rn Risk
Factor
Top Dry
Rn Flux
Atm Disp
Side Rn Flux
.64
.18
.13
.01
.29
.28
.13
.10
.02
.28
.26
.20
.15
Indoor Rn
Equi Fraction .05
for the definition of
Atm Disp
Res Time
F
Inh Risk
Factor for
Po-210
Res Time
F
Inh Risk
Factor for
U-238
Atm Disp
Release for
U-238
Res . Time
Rn Risk Factor
Top Dry Rn Flux
Atm Disp
Age Component
of F
terms.
.36
.33
.16
.11
.50
.22
.12
.05
.03
.62
.09
.08
.06
.06
7-28
-------
Table 7-6. Contributions of various to risk8
(continued).
Fraction of Uncertaintydueto Parameter
Based on Not Moving Based on Residence
During a Lifetime Time of Distributions
Facility (70 Years) of the U.S. Population
Uranium Tailing
Pile
Atm Disp
Rn Release
Rn Risk
Factor
.46
.46
.06
Rn Release
Atm Disp
Res Time
Rn Risk Factor
.32
.31
,27
.04
See Table 7-1 for the definition of terms.
7-29
-------
? . 5
BOC88
CRP87
CR88
EPA84
EPA88
H079
MI87
MC80
NG77
Bureau of Census, "American Housing Survey for the
United States in 1985." H-150-85, 1988.
Council of Radiation Program Directors, Inc.,
"Compilation of State-by-State Low-Level Radioactive
Waste Information", U.S. Department of Energy,
DOE/ID/12377, Frankfort, KY,
Crick, M.J. et al, "Uncertainty Analysis of the
Foodchain and Atmospheric Dispersion Modules of MARC11,
NRPB-R184, National Radiological Protection Board. May
1988.
U.S. Environmental Protection Agency, Proposed
Guidelines for Exposure Assessment, Request for
Comments, 49 FR 46304, November 23, 1984.
U.S. Environmental Protection Agency, "Elemental
Phosphorus Production - Calciner Offgases. EMB Report
No. 88-EPP-Q2, Volume 1, January 1989.
Hoffman, P.O. and Baes III, C.F., "A Statistical
Analysis of Selected Parameters for Predicting Food
Chain Transport and Internal Dose of Radionuclides'1,
MJREG/CR-1GQ4. Prepared by Oak Ridge National
Laboratory for the NRC. November 1979.
Hoffman, H.O. et al, "Variability in Dose Estimates
Associated with the Food Chain Transport and Ingestion
of Selected Radionuclides", MJREG/CR-2612, Prepared by
Ridge National Laboratory for the NRC, June 1982.
Ibrahim, S.A. and Whicker, F.W., "Comparative Uptake of
U and Th by Native Plants at a U Production Site8*,
Health Physics, 54, 413, April 1988. KLEE86, Albert J.
Klee, "The MOUSE Manual", U.S. Environmental Protection
Agency, Cincinnati, Ohio, May 23, 1986.
Miller, c.W. and L.M, Hively. "A Review of Validation
Studies for the Gaussian Plume Atmospheric Dispersion
Model." Nuclear Safety, 28(4), Oct - Dec 1987.
McDowell-Boyer L.M. et al. A Review of Parameters
Describing Terrestrial Transport of Lead-210 and
Radium-226. Nuclear Safety, 21, 486, August 1980.
Ng, Y.C. et al., "Transfer Coefficients for the
Prediction of the Doses to Man via the Forage-Cow-Milk
Pathway from Radionuclides Released to the Biosphere1*,
UCRL-51939. Prepared by Lawrence Livermore laboratory
for DOE, July 1977,
7-30
-------
Ng, Y.C., "A of
from Radlonuclides in Agricultural Products",
Nuclear Safety, 23, 57, January 1982.
NRC75 U.S. Nuclear Regulatory Commission, "Reactor S&fiAj1
Study: An Assessment of Accident Risks in United *
Commercial Nuclear Power Plants", WASH-1400,
1975.
RI83 Rish, W.R,, Maura, J.M., and Schaffer, S.A.,
of Uncertainties in the EPA Ore Body River
Mode Exposure Pathway Models Used as the for
Proposed Geologic Repository Release Limits11, Final
Report to Battelle Project Manager Division for
the Department of Energy, June 10, 1983.
SCA89 U.S. Environmental Protection Agency, "Analysis of
Uncertainties in the Risk Assessment Performed in
Support of the Proposed MESHAPS for Radionuclides.
7-31
-------
-------
A
This to Volume I provides a brief overview of
of calculational assumptions used by the Environmental
Protection Agency (SPA) to the doses health risk iron
radiation
.2.1
The nearby individuals were assessed on the following basis;
(1) The nearby individuals for each source, category are
intended to represent an average of individuals living
near each facility within the source category. The
location of or more persons on the grid
which provides the greatest lifetime risk (all pathways
considered) was chosen for the nearby individuals.
(2) The organ dose-equivalent rates in the tables
on calculated environmental concentrations by
AIRDOS-EPA (Mo?9). For inhaled or ingested
radionuclides, the conversion factors are 50-year
committed dose equivalents,
(3) The individual is assumed to home-grow a portion of his
or her diet consistent with the type of site.
Individuals living in urban areas were to
much less home-produced food than an individual
living in a rural area. It was that in an
agriculturally unproductive location, people would
home-produce a portion of their food comparable to
residents of an urban area, and so the urban fraction
is used for such nonurban locations. The fractions of
home- produced food consumed by individuals for the
generic sites are shown in Table A-l.
A-l. Presumed sources of food for urban and rural sites.
Fl F2
¥egetables .076 .924 0. .700 .300 0
,008 ,992 0. .442 .558 0
Milk 0. 1. 0. .399 .601 0
-------
Fl F2 home-produced fractions at
individuals' location within the 80 km area,.
respectively. of diet, F3, is to be
imported from assessment areaf with negligible
radionuclide concentrations to the source. If
is insufficient production of a food category within the
to provide house-produced fraction for
population, F2 is F3 is increased accordingly.
Fractions on an analysis of household data from the
1965-1966 Consumption Survey (USDA72).
A.2,2
The collective assessment to the population within an 80 km
radius of the facility under consideration was performed as
follows:
(I) The population distribution around the generic site was
on the 1980 census. The population was assumed
to remain stationary in time.
(2) Average agricultural production data for the state in
which the generic site is located were assumed for all
distances greater than 500 meters from the source. For
distance less than 500 meters, no agricultural
production is calculated.
(3) The population in the assessment area consumes food
from the assessment area to the extent that the
calculated production allows. Any additional food
required is assumed to be imported without
contamination by the assessment source. Any surplus is
not considered in the assessment,
(4) The collective organ dose-equivalent rates are based on
calculated environmental concentrations. Fifty-
year commitment factors (as for the individual
case) are used for ingestion inhalation. The
collective equivalent rates in the tables can be
considered to be either the dose commitment rates after
100 years of plant operation, or equivalently, the
incurred that will be for up to 100 years from
the time of release. Tables A-2 and A-3 summarizes
AIRDOS-EPA parameters used for the (SJ84).
Table A-2 summarizes agricultural model parameters,, usage
factors, and other AIRDGS-EPA parameters which independent of
the released radionuclides. Table A~3 tabulates element
dependent data. These include the default inhalation clearance
class and, fraction of the stable element reacting body
fluids after ingestion. Inhaled clearance classes D, W and -y
correspond- to those materials which clear from the lung over
periods of days, weeks, and years respectively. Class * is for
gases. Biv1 and Biv2 are the soil to pasture and soil to produce
-------
concentration factors respectively. Both factors for soil
concentration on a dry weight basis. The pasture
concentrations on dry and fresh weight respectively.
Fm and Ff relate the stable element intake rate to the
concentration in milk and meat, respectively. The values for the
factors in this table are maintained in the PREPAR file A.CCRAD
(SJ84).
A.2.3 Dairy and Beef Cattle
Dairy and beef cattle distributions are part of the AIRDOS-
EPA input. A constant cattle density is assumed except for the
area closest to the source or stack in the case of a point
source, i.e., no cattle within 500 m of the source. These
densities were derived from data developed by NEC (NRC75). Milk
production density in units of liters/day-square mile was
converted to number of dairy cattle/square kilometer by assuming
a milk production rate of 11.0 liters/day per dairy cow. Meat
production density in units of kilograms/day-square mile was
changed to an equivalent number of beef cattle/square kilometer
by assuming a slaughter rate of .00381 day-1 and 200 kilograms of
beef/animal slaughtered. A 180-day grazing period was assumed
for dairy and beef cattle.
A.2.4 ¥eget ab 1 e._ Crop.. _Area
a certain fraction of the land within 80 km of the source is
used for vegetable crop production and is assumed to be uniformly
distributed throughout the entire assessment area with the
exception of the first 500 meters from the source. Information
on the vegetable production density in terms of kilograms (fresh
weight)/day-square mile was obtained from NRC data (NRC75)„ The
vegetable crop fractions by state were
production densities by assuming a production rate of 2 kilograms
(fresh weight)/year-square meter (NRC77),
A.2.5 Population
The population data for each generic site were generated by
a computer program, SECPOP (At74), which utilizes an edited and
compressed version of the 1980 United States Census Bureau's MAHF
data containing housing and population counts for each census
enumeration district (CED) and the geographic coordinates of the
population centroid for the district. In the Standard
Metropolitan Statistical Areas (SMSA), the CED is usually a
"block group" which consists of a physical city block. Outside
the SMSAs, the CED is an "enumeration district," which may cover
several square miles or more in a rural area.
There are over 250,000 CEDs in the United States with a<
typical population of about 800 persons.' The position of the
population centroid for each CED was marked on the district maps
by the individual census official responsible for each district
A-3
-------
Is only on personal judgment inspection of
population distribution on a map. The CED entries is
ascending order by longitude on the final data tape.
The resolution of a calculated population distribution
cannot be better than the distribution of the CEDs. Hence, in a
metropolitan area the resolution is often as small as- one block,
but in rural areas it may be on the order of a mile or more,,
A-2.6 Risk Conversion Factors
Table A-5 summarizes the average lifetime fatal cancer risk
per unit intake or exposure for most of the radionuclides
considered in the assessments. Note that the external exposure
factors do not include the contribution from any decay products,
For example, the external risk factors for cesium-137 have values
of 0, since there is no photon released in its decay. Hence, the
exposure due to the cesium-137 decay product barium-137m must be
considered in assessing cesium-137. The clearance class and
gut-to-blood transfer factor, f,, values are shown in Table A~3.
A-4
-------
-EP.A parameters for generic
.
Symbolic
variable
BRTHRT
T
DDI
TSUBHI
TSUBH2
TSUBH3
IAMW
TSUBI1
TSUBE2
Description
Breathing Rate (cm3/h)
Surface buildup time (days)
Activity fraction after washing
Time delay-pasture grass (h)
Time delay-stored food (h)
Time delay-leafy vegetables (h)
Weathering^ removal rate
factor (h )
Exposure period-pasture (h)
Exposure period-crops or leafy
Value
9.17E+5
3.65E+4
0.5
0.0
2.16E+3
336,
2.10E-3
720.
1.44E+3
YSUBV1
¥SUB¥2
FSUBP
FSUBS
QSUBF
TSUBF
uv
UM
UF
UL
TSUBS
vegetables (h)
Productivity-pasture (dry 0,280
weight) (kg/m )
Productivity-crops and leafy 0,716
vegetables (kg/m )
Time fraction-pasture grazing 0,40
Pasture feed fraction-while 0,43
pasture grazing
Feed or forage consumption 15.6
rate (Jcg-dry/day)
Consumption delay time-milk (d) 2.0
Vegetable utilization rate (kg/y) 176.0
Milk utilization rate (kg/y) 112.0
Meat utilization rate (kg/y) 85.0
Leafy vegetable utilization 18,0
rate (kg/y)
Consumption time delay-meat (days) 20.0
A-5
-------
AIRDOS-EPA
(continued).
Symbolic
variable
FS0BG
FStJBL
TSOBB
P
Description
Produce fraction (garden of
interest)
Leafy veg fraction (garden of
interest)
Soil buildup time (y)
Effective surface density of
¥alue
1.0
1.0
100.
215.
TA0BEF
MSUBB
VSUBM
Rl
E2
soil (kg/m2)
Meat herd-slaughter rate
factor {d"1)
Mass of meat of slaughter (kg)
Milk production rate of cow (L/d)
Deposition interception fraction-
pasture
Deposition interception fraction-
leafy vegetables
3.18E-3
200.
11.0
0.5?
0.20
A-6
-------
Ele-
ment
Ac
Ag
Am
Ar
As
At
Ba
Be
Bi
Br
C
Ca
Cd
Ce
Cf
Cm
Co
Cr
Cs
CU
Eu
F
Fe
Fr
Ga
Gd
H
Hf
Hg
Ho
I
In
ir
K
Kr
la
Mn
Mo
N
Ma
A-3 . Default values for
Inh. Ing, Biv1
Class f,
Y
Y
W
*
W
D
D
Y
W
D
*
W
Y
Y
Y
W
Y
Y
D
Y
W
D
W
D
W
W
*
W
W
W
D
W
Y
D
*
W
W
Y
*
n
1.
5.
1.
0.
5.
9.
1.
5,
5.
9,
9.
3.
5.
3.
1.
1.
3,
1.
9.
5.
1.
9.
1.
9.
1.
3.
9.
2.
2,
3,
9.
2.
1 .
9.
0.
1.
1 .
8.
9.
9.
OE-3
01-2
OE-3
0
OE-1
5E-1
OE-1
OE-3
OE-2
5E-1
5E-1
OE-1
OE-2
01-4
OE-3
OE-3
OE-1
OE-1
5E-1
OE-1
OE-3
5E-1
OE-1
5E-1
OE-3
OE-4
5E-1
OE-3
OE-2
OE-4
5E-1
OE~2
OE-2
5B-1
0
OE-3
01-1
OE-1
5E-1
5E-1
3.
4.
5,
0.
4.
1.
1.
1.
3.
1.
0.
3.
5.
1.
0.
8.
2.
7,
8,
4.
1.
6.
4.
3 .
4.
1.
0.
3 .
9.
1.
1.
4.
5.
1.
0.
1.
2.
2,
3,
7,
5E-3
OE-1
51-3
0
OE-2
0
51-1
OE-2
5E-2
5
0
5
5E-1
OE-2
0
5E-4
OE-2
SE-3
OE-2
OE-1
OE-2
OE™2
OE-3
OE-2
OE-3
OE-2
0
SE-3
OE~1
OE-2
0
OE-3
5E-2 '
0
0
OE-2
5E-1
51-1
OE+1
5E-2
d
Blv2
1.
4.
1.
0.
2,
6.
6.
6.
2.
6.
0.
1.
6.
1.
0.
6.
3.
1,
1.
1.
1.
2.
4.
3,
1.
1.
0,
3.
8.
1.
4.
1.
6.
2.
0.
1.
2.
2.
1.
2,
SE-4
31-2
1E-4
0
61-3
4E-2
41-3
4E-4
1E-3
4E-1
0
5E-1
4E-2
7E-3
0
4E-6
OE-3
9E-3
31-2
1E-1
71-3
6E-3
3E-4
4E-3
7E-4
7E-3
0
6E-4
6E-2
*7 "JC* 't
/JCi — J
3E-1
7E-4
4E-3
4E-1
0
7E-3
1E-2
6E-2
•3E+1
4E-2
.
Fn Ff
(d/L)
2,
I „
4.
0.
6.
1.
3 .
9,
5 .
2.
0.
1.
1.
2.
0.
2.
2,
1.
7.
1.
2.
1.
2.
2.
5.
2 .
0,
5.
4.
2,
1 .
1,
2,
7 .
0,
2,
3 ,
1.
2.
3 «
OE-5
r«E-2
OS-7
0
OE-5
OE-2
5E-4
OE-7
OE-4
01-2
0
OE-2
OE-3
01-5
0
GE-5
OE-3
5E-3
OS-3
5E-3
OE-5
OE-3
51-4
OE-2
OE-5
OE-5
0
OE-6
5E-4
OE-5
OE-2
OE-4
OE-6
OE-3
0
OE-5
5E-4
5S-3
5E-2
5E-2
2 .
3.
3.
0.
2.
1.
1.
1.
4.
2.
0.
7.
5.
7,
0.
3.
2.
5.
2.
1.
5,
1.
2.
2.
5 .
3,
0.
1.
2,
4.
7.
8.
1 .
2.
0.
3.
4.
6,
7 .
5,
5E-5
OE-3
5E-6
0
OE-3
OE-2
5E-4
OE-3
OE-4
5E-2
0
OE-4
5E-4
SE-4
0
5E-6
OE-2
5E-3
OE-2
OE-2
OE-3
5E-1
OE-2
51-3
OE-4
SE-3
0
OE-3
5E-1
5E-3
OE-3
QE-3
5E-3
OE»2
0
01-4
OE-4
OE-3
5E-2
5E-2
-------
Table A-3, Default values for element factors
(continued),
Ele-
ment
Nb
Nd
Mi
Np
O
P
Pa
Pb
Pd
Pm
Po
Pr
Pu
Ra
Rb
Re
Rh
Rn
Ru
S
Sb
Sc
Se
SHI
SB
Sr
Tb
Tc
Te
Th
Tl
U
W
Xe
¥
Zn
Zr
Inh.
Class
?
Y
W
W
*
D
¥
D
Y
Y
W
Y
Y
W
D
W
I
*
¥
D
W
Y
W
W
W
D
W
W
W
Y
D
¥
D
*
Y
¥
W
ft " '^ (
1.
3.
5.
1.
9 .
3.
1 .
2,
5,
3.
1.
3.
1.
2.
9 .
8.
5,
0.
5 .
8,
1,
1 .
8 .
3.
2.
3,
3 .
8.
2.
2.
9,
2.
1
0,
1 «
5,
2.
OE-2
OE-4
OE-2
OE-3
§E~1
OE-1
OE-3
OE-1
OE-3
OE-4
OE-1
OE-4
QB~3Cfl)
OE-1
51- 1
OE-1
01-2
0
OE-2
OE-1
OE-1
OE-4
OE-1
OE-4
01-2
QE— 1
OE-4
OE-1
OE-1
OE-4
51 -1
OE-1
OE-2
0
QB-4
OE-1
OE-3
2.
1.
6.
1.
0.
3,
2.
4.
1.
1.
2.
1.
4,
1.
1.
1.
1.
0.
7 ,
1.
2.
6.
2,
1.
3 .
2.
1.
9.
2.
8,
4.
8,
4.
0.
1.
1.
2.
OE-2
OE-2
01-2
OE-1
0
5
5E-3
5E-2
5E-1
OE-2
51-2
OE-2
5E-4
5E~2
5E-1
5
5E-1
0
5E-2
5
OE-1
OE-3
5E-2
OE-2
OH-2
5
w /bj /&
5
SB-2
5E-4
OE-3
5E-3
5E-2
0
5E-2
5
OE-3
2.
1,
2,
4.
0,
1.
1.
3.
1 .
1.
1 .
1.
1 .
6.
3 .
1.
1.
0.
8.
6.
1.
4.
1.
1 .
2.
1.
1 .
6,
1,
3*
1.
1.
4.
0.
2,
3 ,
2.
IE- 3
7E-3
61-2
31-3
0
5
1E-4
9E-3
7E-2
7E-3
*"l *£? *!S
/ IS J
7E-3
SS-5
4E-4
OE-2
5E-1
7E-2
0
6E-3
4E-1
3E-2
3E-4
1E-2
7E-!-3
6S-3
1E-1
7E-3
4E-1
7E-3
61- 5
7E-4
7E-3
32- 3
0
6E-3
91-1
11-4
2
2
1
5
0
1
5
2
1
2
3
2
1
4
1
1
1
0
6
1
1
5
4
2
1
1
2
1
2
5
2
6
3
0
2
1
3
F,
d/L)
,
,01-5
»OE~3
,OE~6
.0
.51-2
.OE-6
»5E-4
»OE-2
,01-5
,5E™4
. OE-5
.OE-7
,5E™4
.OE-2
.51-3
. OE-2
.0
.OE-7
. 5E-2
.OE-4
.OE-6
. OE-3
, OE-5
, 01-3
>5E-3
.OE-5
. OE-2
.OE-4
.01-6
.01-3
.OE-4
.OE-4
.0
,OE~5
. OE-2
.
Ff
2.
3,
6.
5 .
0.
5.
1.
3.
4,
5.
3,
3.
5.
2.
1.
8.
2,
0.
2.
1.
1.
1.
1 .
5.
8.
3 .
4 .
8.
1.
6.
4,
2.
4.
0,
3.
1.
5.
5S-1
OE-4
01-3
5E-5
0
5E-2
OE-5
0E-4
OE-3
OE-3
OE-4
OE-4
OE-7
5E-4
5E-2
OE~3
OE-3
0
OS™ 3
OE-1
OE-3
5E-2
5E-2
OS-3
OE-2
01-4
5B-3
5E~3
5E-2
OE-6
OE-2
OE-4
5E-2
0
OE-4
OE-1
5E-3
(a) For PU239f Pu240. and Pu242, F ~ l.OE-4
-------
Alabama
Arizona
Arkansas
California
Colorado
Cattle
for with
Dairy cattle
density
#/km2
7.021-1
2.80E-1
5.90E-1
2,85
3.5GE-1
crop
density
1.5E+1
3.73
1.27E+1
8.81
1.13E+1
crop,fraction
km2/Jem2
Connecticut
Delaware
Florida
Georgia
Idaho
2.50E-1
2.72
1.37
8.63E-1
8.56E-1
3.60
6.48
1.23E+1
1 .431+1
7.19
5.85E-2
6,921-3
2,171-3
7.15E-2
Illinois
Indiana
Iowa
Kansas
Kentucky
Louisiana
Maryland
Massachusetts
Michigan
Mississippi
Missouri
2.16
2.80
3.14
2.57
9.62E-1
8.07E-1
6.11
3.13
3.51
4.88
Nebraska
1.89
9.27E-2
8.78E-1
3.33E+1
3.34E+1
7.4014-1
2.9GE+1
2.65E-+1
1.08E+1
7.65E-1
1.09E+1
2,90
7.90
1.751+1
3.431+1
7,29
2.80E-2
2.72E-2
2.43E-2
5.97E-2
3.98E-3
4.35E-2
5.97E-2
1.11E-2
4.96E-3
1.70E-2
3 , 05E-2
1.07E-3
3.78E-3
2.39B]~2
New Hampshire
Mew Jersey
New Mexico
New York
North Carolina
Horth Dakota
Ohio
Oklahoma
Oregon
5.65E-2
1.58
3.29
1.14E-1
8.56
1.26
6.25E-1
4,56
7.13E-1
4.53E-1
1.40
4,25
4,13
5.83
1.02E+1
1.18E+1
2.03E+1
2.68E+1
4.56
A-9
-------
use
Dakota
Texas
Utah
Vermont
Virginia
Washington
West ¥irginia
Wisconsin
Wyoming
vegetable
(continued).
cattle
density
#/!on2
Dairy cattle
density
crop fraction
6.46
2.30
7.02E-1
8.85E-1
2.00E-1
5.30E-1
4.46E-1
8.88
1.84
1.50
6.00E-1
1.43E+1
5.79E-2
9,63
2,50
8.87
2.32E+1
2.11E+1
1.90E+1
2.84
4.71
1.31E+1
5.62
6,23
1.811+1
5.12
1.32E-2
4.54E-2
1.84E-3
1,201-2
2.72E-3
5.77E-3
1.83E-3
1.08E-3
8.70E-3
5.20E-2
1.16E-3
1.78E-2
1.59E-3
iL-10
-------
Table A-5. Fatal risk
(see Table A™ 3 for default inhalation
ingestion ft values) .
Nuclide
Ac-227
AC-228
Ag-lio
Ag-llOm
Am-241
Ar-4l
Au-198
Ba-137m
Ba-140
Bi-210
Bi-211
Bi-212
Bi-214
C-14
Ce-144
cm-244
Co-60
Cr-51
Cs-134
CS-137
Eu-154
Fe-59
Fr-223
Ga-67
Gd-152
H™3
Hf-181
Hg-197
Hg-203
1-123
1-125
1-129
1-131
1-133
In-113m
Ir-192
K-40
Kr-83m
Inhal .
(per1)
7.9E-02
2.5E-05
7.6E-10
6.0E-05
3.9E-02
4.9E-10
1.8E-06
5.1E-10
1.6E-06
7.5E-05
1.8E-07
6.2E-06
2.0E-06
4.1E-09
3.2E-04
2.6E-02
1.3E-04
2.7E-07
1.7E-05
1.2E-05
1.3E-04
8.0E-06
4.11-07
3.0E-07
O.OE+00
4.9E-08
8.6E-06
3.8E-07
4.3E-06
8.7E-08
1.8E-06
1.3E-05
2.6E-06
1.5E-06
2.6E-08
2.5E-05
5.0E-06
4.8S-11
Ingest .
3.5E-G4
3.2E-07
2.3E-09
3.5E-06
3.0E-04
6.9E-07
1.8E-09
1.5E-06
l.OE-06
9.4E-09
2.3E-07
l.OE-07
5.9E-07
3.4E-06
1.9E-04
9.7E-06
2.5E-08
2.5E-05
1.7E-05
2.GE-06
1.7E-06
1.6E-07
1.2E-07
O.OE+00
3.4E-08
7.2E-07
1.5E-07
3.8E-07
1.2E-07
2.7E-06
1.9E-Q5
3.7E-06
2.2E-06
3.4E-08
9.8E-07
6.7E-06
Iismer.
(itt3/pCi yr)
2.01-07
1.61-03
5.3E-05
4.8E-03
2.7E-05
2.3E-03
6.7E-04
l.OE-03
3.1E-04
7.8E-05
3.2E-04
2.8E-03
O.OE+00
2.8E-05
1.2E-07
4.4E-03
5.2E-05
2.7E-03
O.OE+00
2.2E-03
2.1E-03
7.1E-05
2,41-04
O.OE+00
9.0E-04
9.3E-05
3.8E-04
2.6E-04
1.4E-05
1.1E-05
6.7E-04
l.OE-03
4.2E-04
1.4E-03
2.8E-04
Surface
(m /fjkCi. yr)
6.5E-09
3.1E-05
l.OE-06
9.1E-05
8.5E-07
3.9E-05
1.4E-05
2.0E-G5
6.6E-06
1.7E-06
6.0E-06
4.8E-05
O.OE+00
6.6E-07
2.4E-08
7.7E-05
1.1E-06
5.3E-05
O.OE+00
4.1E-05
3.7E-05
1.8E-06
5.3E-06
O.OE+00
1.9E-05
2.4E-06
8.2E-06
5.8E-06
6.3E-07
5.7E-07
1.4E-05
2.1E-05
9.0E-06
2.9E-05
4.7E-06
3.4E-08
A-ll
-------
?able A-5
Nuclide
Fatal risk
A- 3 for default
Ingestiott f, values) (continued) .
Inhal .
Ingest .
Immer
Surface
Kr-85
Kr~85lft
Kr-87
Kr-88
La~140
Mn-54
Na~24
Nb-95
Ni-63
P-32
Pa™231
Pa-234m
Pb-210
Pb-2ll
Pfo-212
Pb-214
Po-210
Po-212
Po-214
Po-215
Po-216
Po-218
Pu-238
Pu-239
Pu-240
Pu-241
Pu-242
Ra-223
Ra-224
Ra~226
Ra™228
Rh-I03m
Rh-106
Rn-220
Sn-222
Ru-103
Ru~106
S-35
3
3
1
3
2
4
7
4
1
2
3
1
1
2
4
2
2
5
2
5
4
5
4
3
3
2
3
2
1
2
5
3
1
1
4
7
4
1
.51-10
.7B-10
.7E-09
.5E-09
.5E-06
.3E-Q6
.7E-07
.4E-06
.5E-06
.5E-06
.8E-02
.5E-09
.4E-Q3
.6E-06
.IE-OS
.7E-06
.4E-03
.7E-16
.7E-13
.3E-12
.5E-10
.4E-07
.01-02
.9E-02
.9E-02
.8E-04
.7E-02
.9E-03
. 11-03
.8E-03
.8E-04
.6E-09
.1E-09
.OE-07
.7E-07
.51-06
.1E-04
•4E-07
1
7
6
3
1
2
1
4
5
1
5
1
1
1
8
2
2
2
2
3
3
4
2
6
3
9
7
5
3
5
5
1
awa
_
-
_
.3E-06
.31-07
,91-07
.81-07
.41-07
.6E-06
.9E-04
.4E-G9
.5E-04
.3E-Q7
.01-06
.31-07
,41-04
.7E-17
.OE-15
.1E-13
.6E-11
.01-08
.71-04
.OE-05
,01-05
.71-06
.8E-05
.OE-05
.5E-G5
.4E-05
.OE-05
.OE-09
.3E-09
_
_
.1E-07
.5E-06
.4E-07
3.
2.
1.
3.
4.
1.
8.
1.
0.
0.
4.
2.
8.
2.
4.
1.
0.
1.
2.
2.
0,
1.
1.
1.
0.
1.
2.
1.
1.
1.
2.
3.
8.
6.
8.
0,
0.
7E-06
6E-04
5E-03
9E-03
2E-03
5E-03
2E-03
3E-03
OE+00
OE+00
91-05
OE-05
_
8E-05
4E-04
1E-04
5E-08
OE+00
5E-07
5E-07
5E-08
01+00
31-07
3E-07
2E-07
OE+00
1E-07
11-04
7E-05
IE-OS
OE-13
5E-07
5E-04
8E-07
5E-07
1E-04
OE+00
OE+00
7.
5.
2.
6.
7.
2,
1.
2.
0.
0.
1.
3.
1.
5.
8,
2.
0.
2.
5,
4.
0.
2.
1,
2.
0.
2.
4.
3.
2.
2,
2.
7 .
1.
1.
1.
0,
0,
7E-08
8E-06
SE-Q5
11-05
3E-0S
81-05
21-04
6E-05
OE+00
OE+00
2E-06
8E-Q7
_
8E-06
3E-06
8E-06
9E-10
OE+00
8E-09
2E-09
91-10
OE+00
51-08
11-08
4E-08
OE+00
OE-08
8E-06
6E-G7
4E-07
2E-14
8B-08
OE-06
8E-08
3E-GS
7E-05
OE+00
OE+00
k-12
-------
•5, Fatal risk factors for radionuclides
(see Table h-3 for default inhalation
ingestlon f1 values) (continued).
Mud Ids
Sb-124
Sc-46
Se™75
Sn-113
Sr-BS
Sr-89
Sr-90
Tc-95
Tc-95lfl
Tc-99
Tc-99m
Th-227
Th-228
Th™230
Th-231
Th-232
Th-234
Tl-207
Tl-208
U-234
U-235
U-23S
U-238
W-187
Xe~131m
Xe~133
Xe~133m
Xe-135
¥-90
Zn-65
zr»95t.
Inhal.
2.0E-05
2.4E-05
4.8E-06
8.5E-06
6.8E-07
2.4E-06
5.41-05
1.7E-08
3.0E-06
7.4E-06
1.9E-08
4.61-03
7.21-02
2.9E-02
4.1E-07
2.9E-02
2.9E-05
4.1E-09
4.4E-09
2 . 5E-02
2.3E-02
2.4E-02
2. 21-02
3,21-07
3. 11-10
3.01-10
3.9E-1Q
5.81-10
4.7E-06
1.3E-05
8.9E-06
Ingest.
1.71-06
9.3E-07
4.2E-06
5.0E-07
4.9E-07
1.9E-06
3,11-05
3.3E-Q8
6.9E-07
7.4E-07
2.4E-08
2.9E-06
1.3E-05
2.3E-05
2.21-07
2. 11-05
2.2E-06
l.OE-08
1,41-08
7.5E-05
7.3E-05
7.11-05
7,41-05
3.6E-07
—
~
_
_
1.7E-06
5.2E-06
5.6E-07
.
(ia /|iCi yr)
3.4E-03
3.6E-G3
6.4E-04
1.21-05
8.6E-04
2.4E-07
0.01+00
1.41-03
1.1E-03
8.0E-10
2.1E-04
1.7E-04
3.1E-06
5.91-07
1.71-05
2.8E-07
1.21-05
3.8E-06
6.81-03
2.3E-07
2=51-04
1,81-07
1.5E-07
8.01-04
1.21-05
5.1E-05
4.7E-05
4.1E-04
0,01+00
l.OE-03
1.31-03
Surface
(ii2/>Ci yr)
6,01-05
6,61-05
1.4E-05
4.2E-07
1,81-05
4.6E-09
O.OE+00
2.7E-05
2.3E-05
1.9E-11
4.71-06
3.8E-06
8.6E-08
2. 71-08
5.61-07
2.01-08
3. 01-07
7.3E-08
1,01-04
2.41-08
5.5E-06
2.2E-08
1. 91-08
1.6E-05
4.7E-07
1.4E-06
1.2E-06
8.91-06
0,01+00
1.91-05
2.5E-05
A-13
-------
NRC75
NRC77
SJ84
USDA72
T.W., R.A. Tell, and D.E. Janes, 1974, of
an Automated Data Base In Population Exposure
Calculations, from Population Exposures, Health Physics
Society, CONF-74018, October 1974.
Moore R.E., C.F. ~Ba.es, III, L.M. McDowell-Boyer, A.P.
Watson, F.O. Hoffman, J.C. Pleasant, C.W. Miller, 1979,
AIRDOS-EPA: A Computerized Methodology for Estimating
Environmental Concentrations and Dose to Man from
Airborne Releases of Radionuclides, EPA 520/1-79-009,
1PA Office of Radiation Programs, Washington, D.C.
20460, December 1979.
Memo from K. Eckerman, N. Dayem, R. Emch, Radiological
Assessment Branch, Division of Technical Review,
Nuclear Regulatory Commission, Code Input Data for
Man-Rent Estimates (Washington, DC, October 15, 1975).
U.S. Nuclear Regulatory Commission, Calculation of
Annual Doses to Man from Routine Releases of Reactor
Effluents for the Purpose of Evaluating Compliance with
10 CFR Part 50 Appendix I (Revision 1}, Regulatory
Guide 1.109, Office of'Standards Development,
Washington, D.C., October 1977.
Sjoreen, A.L., and Miller, C.W,, PRERPAR - A User
Friendly Preprocessor to Create AIRDOS-EPA Input Data
Sets, ORNL-5952, August 1984.
United States Department of Agriculture, 1972, Food
Consumption of Households in the United States (Seasons
and Year 1965-1966}, Household Food Consumption Survey
1965-1966, Report No. 12,. Agricultural Reseach Service,
USDA, Washington, DC (March 1972).
A-14
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B
OP THE
OF THE
B.I
This appendix describes the mechanics of life
implementation of the risk estimates derived in Chapter 6.
B.2 TABLE ANALYSIS TO ESTIMATE OF
Radiation effects can be classified as stochastic or
nonstochastic (NAS8Q, ICRP7?). For stochastic effects,
probability of occurrence of the effect, as opposed to
severity, is a function of dose; induction of cancer, for
example, is considered a stochastic effect. Nonstocliastic
effects are those health effects for which the severity of
effect is a function of dose; examples of nonstochastic
include cell killing, suppression of cell division, cataracts,
and nonmalignant skin damage. At the low levels of radiation
exposure attributed to radionuclides in the environment,
principal health detriment is the induction of (solid
tumors and leukemia) and the expression, in later generations, of
genetic effects. In order to estimate these effects?
instantaneous dose rates for each organ at specified
sent to a subroutine adaptation of CAIRD (Co78) in
RADRXSK code. This subroutine uses annual doses derived
transmitted dose rates to estimate the number of
fatalities in the cohort due to radiation induced in
reference organ. The calculation of incremental fatalities is
on annual incremental risks,
doses to the organ, together with radiation risk factors, as
those given in tha 1980 MAS report BEIR-3 (NAS80). of
the risk factors in current use is discussed in Chapter 6,
An important feature of this methodology is the of
actuarial life tables to account for the time of
radiation insult and to allow for competing of in
estimation of risk due to radiation exposure. A life
consists of data describing age-specific mortality all
causes of death for a given population. This information is
derived from data obtained on actual mortality in a real
population. Mortality data for the U.S..population during
years 1969-1971 (HEW75) are used throughout this study.
The of life: tables in studies of risk to low-level
radiation exposure is important because of the time delay
inherent in radiation risk. After a radiation dose is received,
there is a minimum induction period of several years (latency
period) before a cancer is clinically observed. Following
latency period, the probability of occurrence of a
B-l
-------
plateau periods upon type of cancer. During or after
radiation exposure, a potential cancer victim may experience
years of life in which he is continually to risk of death
from causes other than incremental radiation Hence,
individuals will be lost from the population due to
competing
-------
PR is to be relative to PN, an
which is only for low-level (Bu81), such as
those considered here. The total number of Incremental deaths for
cohort is then obtained by summing Q(m) over all organs for
110 years.
In addition to providing an estimate of the incremental
number of deaths, the life table methodology can be used to
estimate the total number of years of life lost to those dying of
radiation-induced cancer, the average number of years of life
lost per incremental mortality, the in the
population's life expectancy. The total number of years of life
lost to those dying of radiation-induced cancer is computed as
the difference between the total number of years of life lived by
the cohort assuming no incremental radiation risk^ and the total
number of years of life lived by the same cohort assuming the
incremental risk from radiation. The decrease in the
population's life expectancy can be calculated as the total years
of life lost divided by tha original cohort size
(N(0) = 100,000).
Either absolute or relative risk factors can be used.
Absolute risk factors, given in terms of deaths per unit dose,
are based on the assumption that there is some absolute number of
deaths in a population exposed at a given age per unit of dose,
Relative risk factors, the percentage increase in the ambient
cancer death rate per unit dose, are based on the assumption that
tha annual rate of radiation-induced excess cancer deaths,, due to
a specific type of cancer, is proportional to the ambient rate of
occurrence of fatal cancers of that type. Either the absolute or
the relative risk factor is assumed to apply uniformly during a
plateau period, beginning at the end of the latent period.
The estimates of incremental deaths In cohort from
chronic exposure are identical to those obtained if a
corresponding stationary population (i.e., a population in which
equal numbers of persons are born and die In each year) Is
subjected to an acute radiation dose of the magnitude.
Since the total person-years lived by the cohort in this study is
approximately 7.07 million, the estimates of incremental
mortality in the cohort from chronic irradiation also apply to a
one-year dose of the same magnitude to a population of this size,
age distribution, and age-specific mortality rates. More precise
life table estimates for a specific population can be obtained by
altering the structure of the cohort to reflect the age
distribution of a particular population at risk.
In addition, since the stationary population is formed by
superposition of all age groups in the cohort, each age group
corresponds to a segment of the stationary population with the
total population equal to the sum of all the age groups.
Therefore, the number of excess fatal cancers calculated for
lifetime exposure of the cohort at a constant dose rate would be
numerically equal to that calculated for the stationary
1-3
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to an annual of
Thus, risk may be reported as a lifetime (the
cohort interpretation) or as the risk ensuing from an annual
exposure to the stationary population. This equivalence is
particularly useful in analyzing acute population exposures. For
example, estimates for a stationary population, exposed to annual
doses that vary from year to year may be obtained by summing the
results of a series of cohort calculations at various annual dose
rates.
B-4
-------
Bu81
Bunger, B.M. , Cook, J.R. , Barrick, M.K.,ttLife Table
Methodology for Evaluating Radiation Risk; An
Application on Occupational Exposures , »f HeaJLJHi
Phs. 40 439-455,
C078
HEW75
Cook, J.R
Cojde__for
Bunger, B.
and Barrick? M.K.,
ICRP77
HAS 80
(CAIRO) , EPA 520/4-78-012, 1978.
U.S. Department of Health Education Welfare, "U.S.
Decennial Life Tables for 1969-1971," Vol. 1., No. 1.,
DHEW Publication No. (ERA) 75-1150, Public Health &
Service , Health Resources Administration, National
Center for Health Statistics, Rockville, Maryland,
1975.
International Commission on Radiological Protection,
"Recommendations of the International Commission on
Radiological Protect ion ," Ann. ICRP, Vol. l, No. 1,
Pergamon Press, 1977,
National Academy of Sciences - National Research
Council , The Effects on Population of Exposure to Low
Levels of Ionizing Radia/tion, Committee on the
Biological Effects of Ionizing Radiation, Washington,
D.C., 1980,
5-5
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OF TO
IN
C.I
The doses and risks attributable to airborne emissions from
the various facilities and categories of facilities in
Volume II have been estimated using the models and assumptions
described in this volume. The calculational methods use
monitored data characterizing airborne emissions and then apply
mathematical models to estimate the radionuclide concentrations
and radiation fields in the environment. These calculated values
are then used to derive radiation doses to individuals exposed to
these radionuclides. The final products of this exercise are the
doses to individuals and populations, expressed in units of
mrem/yr and person-rem/yr, respectively. In addition, cancer
risks, expressed in terms of the additional lifetime risk to
individuals and the number of additional cancer fatalities in the
exposed populations, are also estimated.
Rather than using mathematical models to assess impacts, it
would be preferable to measure the actual impacts directly; i.e.,
radionuclide concentrations and radiation fields in the
environment, radionuclide concentrations in the various organs of
the exposed populations, and the increased'incidence of cancer,
if any, due to the exposures. However, this is not possible
because the radionuclide releases do not generally result in
detectable levels in the environment or in the exposed members of
the population. Accordingly, the actual or potential impacts of
the emissions must be predicted using calculational models.
The dose and risk estimates provided 'in "this BID for
facility or release category should be considered a reasonable
assessment which does not significantly underestimate or grossly
overestimate impacts and is of sufficient accuracy to support
decisionmaking. Since each facility is unique, the models used
to calculate doses and risks are generalizations and
simplifications of the processes which result in exposure and
risk. In addition, our ability to model the processes is also
limited to a degree by the availability of data characterizing
each site and our understanding of the processes,
In Volume II, doses and risks for each category are
presented as discrete values? i.e., mrem/yr? person™rem/yry
individual probability of a fatal cancer, and number of cancer
fatalities per year in a population. Each of these calculated
values is an expression of impact on an individual or small group
of individuals or on a population as a whole. The values
presented, however, are of more use to decision-makers when there
is some characterization of their uncertainty. For example!, a
C-l
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be calculated; i.e.; l.OE-6 lifetime of
cancer for an individual. However, if uncertainty In this
Is of magnitude, real risk of
source of emission may in fact be higher than another source of
emission which a calculated risk of l.OE-5 lifetime risk of
cancer but a small degree of uncertainty. Alternatively, an
upper bound risk of l.OE-2 lifetime risk may be calculated
appear to represent an unacceptable risk. However, the actual
risk may be an order of magnitude smaller. This situation often
occurs when, due to limited information and uncertainty in the
caleulational parameters, conservative assumptions are used
throughout the calculation in order to ensure that the risks are
not underestimated.
The Office of Radiation Programs has initiated a
quantitative uncertainty analysis to supplement the
semiquantitative analysis provided in Volume I of the BID.
This appendix summarizes the quantitative uncertainty analysis
techniques currently under review by the Office.
C.2 QUANTITATIVE UNCERTAINTY ANALYSIS
The use of quantitative uncertainty analysis to address
environmental risks became widespread following the Reactor
Safety Study (NRC75), and was recommended by the Agency in
support of environmental risk assessments in 1984 (EPA84). The
technique results in a range of values of Impact rather than a
discrete value by using a range of values for the caleulational
input parameters. In this way, the impacts of a given
technological activity can be bounded and different technologies
can be Intercompared. In cases where probability distributions
can be assigned to the value of a given set of caleulational
parameters, the results are expressed as probability
distributions. Risks can thereby be expressed as "best estimate"
values, 90 percentile values or 99 percentile values, etc,
Figure C-l presents an example of the output of such an analysis.
The results are expressed as a cumulative probability
distribution. Inspection of the distribution reveals that, in
this case, there is about a 90 percent level of confidence that
the technological activity will result in less than 1 mortality
per 10,000 years, and that the best estimate (i.e., the 50
percentile value) is less than 0,1 fatality per 10,000 years.
Though the concept Is simple, the implementation and
interpretation of uncertainty analyses performed in support of
environmental risk assessment has evolved into an area of
specialization founded in work performed at Carnegie Mellon
University (Mo78). The use of quantitative uncertainty analyses
In support of environmental radiological risk assessment has been
steadily increasing since its use in the Reactor Safety Study
(NRC75). Selected uncertainty analyses, which are especially
relevant to this Background Information Document, include work
performed by Hoffman (NUREG79, NUREG81), Rish (Ri83), and Crick
(Cr88).
C-2
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1.000
o
EC
a.
u
<
«J
3
U
0.500
0.2SO
*
*
JL
.001 .01 ,1 1
MORTALITY EFFECTS/10,000 YEARS
Figure Ol. Example of the output of a risk assessment using
y quantitative uncertainty analyses (from Ra.83)..
C-3
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applications of uncertainty analysis
undergoing review to Identify the approach appropriately
applied to analyses presented In Volume II of this BID,
application a somewhat different calculational
set of Input data. The appropriateness of the
on types of risks being calculated and on the level of analysis
required to support rulemaking. The following describes
different approaches being considered and the
C.3 OF ANALYSIS
The results of any risk assessment are uncertain to the
following three sources of uncertainty (Cr88);
(1) Modeling uncertainties
(2) Completeness uncertainties
(3) Parameter uncertainties
Modeling uncertainties pertain to the formulation of
mathematical models used to predict risk and the degree to which
they accurately represent reality. One way to address this
source of uncertainty is to perform the analysis using a set of
feasible alternative model structures,
In general, modeling uncertainty is the most difficult
component to assess since It is often impossible to justify a set
of plausible alternative models in light of the available data
and to assign probabilities to these alternatives. To an extent,
modeling uncertainty is Incorporated into the estimates of
uncertainty, e.g., the uncertainty in risk factors for low-LET
radiation includes a consideration of the uncertainty in the
of the dose-response and risk projection models. On the other
hand, as noted in Chapter 5, the uncertainty in formulation of
metabolic models is a serious problem in estimating
conversion factors for many radionuclides. Modeling uncertainty
for dispersion and pathway calculations pose similar problems.
As a result, the Agency's estimates of uncertainty in
radiological risk do not fully reflect the contribution of
modeling uncertainty.
Completeness uncertainties are applicable to this BID, as
they are to all risk assessments. The issue has to do with
whether all significant radionuclides and pathways of exposure
have been addressed. For most facilities addressed in this BID,
the source terms are well characterized and there is little
likelihood that a significant undetected, radionuclide release Is
occurring. With regard to pathways of exposure, the analyses
assume that all the major pathways of exposure are present at all
sites, and it is more likely that a pathway has been assumed to
be present which in fact is not. Accordingly, except for
specific categories of emissions, such as C-14 and H-3 emissions
from research hospitals, this source of uncertainty is not
expected to be an important contributor to overall uncertainty.
C-4
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Uncertainties in values of calculational
believed to be major of uncertainty in
risk provided in the BID. Accordingly,
quantitative uncertainty analysis being is focusing on
appropriate methods for quantifying this of uncertainty,
The uncertainty in input parameters, as dose and risk
factors, reflects consideration of both parameter modeling
uncertainties. For purposes of a quantitative uncertainty
analysis,, those considerations are combined and will be treated
in subsequent calculations as an equivalent parameter
uncertainty.
C.4 UNCERTAINTY ANALYSIS DUE TO UMCERTAINTY
The assessment of this source of uncertainty involves the
development of quantitative characterizations of the
uncertainties associated with key model parameters. These
characterizations can be probability distributions,, bounding
ranges or a set of discrete values. Once key uncertain
parameters are characterized, their uncertainties are propagated
through the models using a simulation technique producing a
probability distribution representing uncertainty about the risk
assessment model results. To describe how such an analysis is
performed, it is convenient to use a specific example.
Table 13-10 of Volume II reveals that the highest calculated
lifetime risk to the maximum individual residing in the vicinity
of phosphogypsum stacks is 2.0E-4 for an individual located 800
meters downwind of the Royster Phosphate stack in Palmetto,
Florida. The question that an uncertainty analysis needs to
answer is what is the possible range of values of this risk
estimate for a real person currently residing in the vicinity of
that stack. It would be desirable to construct a probability
distribution of the risk, similar to the example provided in
Figure C-l. It would also be desirable to construct a similar
distribution for a hypothetical individual who may reside in the
vicinity of the stack at some future date. Accordingly, two
analyses may be needed, one for the actual residents and one for
a possible future resident.
The risk from this source of exposure is from the radon gas
emanating from the phosphogypsum stacks. The calculation of
risk involves the multiplication of five values:
(1) the radon source term from the stack, expressed in
terms of Ci/yr,
(2) the atmospheric dispersion factor, which is used to
calculate the average annual airborne radon
concentration at the receptor location,
C~5
-------
(3) daughter conversion factor,
calculated airborne radon concentration to
daughter concentration in working levels (WL), which
is the parameter that is directly related to risk,
(4) exposure duration in hours per year,
(5) the risk conversion factor, which converts risk
expressed in WL to probability of cancer.
The product of each of these parameters, along with
appropriate unit conversions, results in an estimate of lifetime
cancer risk due to exposure. Each of the five parameters has
some degree of uncertainty, which contributes to the uncertainty
in the calculated risk.
The source term (Ci/yr) is itself an estimated value which
varies as a function of time. However, since this is a lifetime
risk, it is necessary to estimate the uncertainty in the average
annual release rate over many years. This distinction is
important because it virtually eliminates the need to explicitly
consider uncertainties associated with the time-varying nature of
the source term. If the concern was with the maximum risk to an
individual in any one year, the time-varying nature of the source
term would need to be explicitly addressed.
Ideally, ~based on extensive measurements made over the area
of the stack over prolonged periods of time, the source term
could be accurately defined. However, the source term has been
approximated using a limited number of samples and a conservative
set of assumptions which provides assurance that the real source
term has not been underestimated. In a quantitative uncertainty
analysis, a source term probability distribution would be
constructed based on a -close inspection of the measurements
assumptions used in the analysis.
The second calculational parameter is the atmospheric
dispersion factor, which is used to derive the average annual
radon concentration at the receptor location. The dispersion
factor is expressed in units of sec/in3, so that when it is
multiplied, by the release rate in Ci/yr, along with the
appropriate unit conversion, the result is the average annual
radon concentration at the receptor location. Uncertainty in the
actual location of the nearest resident is an important source of
uncertainty.
A second important, and less obvious source of uncertainty,
is the method used to estimate dispersion. The accuracy of this
method is provided in Chapter 4. As applied to this particular
problem, the uncertainties increase due to the non-uniformity of
the area source term. This could either increase or decrease the
risk estimate, depending on the location of the receptor relative
to areas of the pile that are the major contributors to
source term. Note that the magnitude of this source of
C-6
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since j, as distance from the receptor to the pile
the behaves more more as a point relative
Considering all of these factors, an uncertainty
distribution Is developed for the atmospheric dispersion factor.
Sote that distribution of the atmospheric dispersion factors
for the individual the population risk
will differ.
The third parameter converts radon concentration to radon.
daughter concentration, which is the parameter of interest. The
uncertainty in this value is well characterized, and constructing
a reasonable probability distribution for this parameter will be
a relatively straight forward exercise.
The fourth parameter, occupancy time, is the fraction of the
time the individual is located at the receptor location. For
purposes of this BID, the individual at maximum risk is presumed
to be a lifetime resident at the presently occupied location that
results In the greatest lifetime risk. Hence the value of this
factor is the average fraction of each day that a resident is
expected to be within his or her home. The presumption of
lifetime residence does not have any uncertainty,* It is a given
condition for the assessment.
The last parameter, the risk factor, relates exposure to
risk. As discussed in Chapter 6, values for this parameter are
based on epidemiologlcal data and only apply to large
populations. It Is assumed that the maximum Individual the
average radiosensitivityf and a risk factor probability
distribution Is developed based on uncertainty in the average
factor.
It is apparent frora this discussion that in order to
an uncertainty analysis, it is necessary to clearly define the
risk that is being estimated. Is the risk for a real or
hypothetical person, is it the maximum or the average risk,
is it the current or possible future risk that is of concern?
individuals constructing the distributions must clearly
understand the objectives of the analysis or the resulting
distributions will be incompatible.
Upon completion of this exercise, each of the calculatlonal
parameters will have been assigned probability distributions.
These distributions are used as input to models that propagate
the uncertainties.
C.5 FOR PROPAGATING UNCERTAINTIES
The basic approaches used to propagate uncertainties are
method of moments techniques, or Monte Carlo techniques. Method
of moments is the standard method for propagating error described
C-7
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in on statistics. This
by calculating a linear combination of
each, model factor. Since these coefficients on
of the parameters, the method is only useful of
each parameter is small enough that it will not significantly
perturb the coefficients. Even if these conditions net,
it is possible to establish reasonable estimates of uncertainty
using this technique.
The alternative to the method of is of a
Monte Carlo, or Monte Carlo type, analysis. This
consume considerable computer resources but has potential to
yield more satisfying results. The technique calculates in
the same mariner as described above, except it performs
calculation many times, each time randomly selecting an input
value from each of the probability distributions representing
each parameter. The output is a risk distribution. The
times the calculation is performed, the more complete the
results. The number of repetitions will determine the precision
of the output. The more repetitions and the larger the of
calculational parameters treated as distributions in the model,
the greater the computer resource requirements.
By controlling how the values are sampled from each
distribution, parameters that are directly or indirectly
correlated can also be modeled. In addition, by selectively
fixing the value of individual parameters, the parameters
are important contributors to uncertainty can be identified.
A number of computerized techniques are available to perform
quantitative uncertainty analysis. Descriptions of
methods, provided by Crick (Cr88) and Hofer (Ho85),
reviewed in order to determine which methods appropriate
for quantifying the uncertainty in the risk estimates provided in
BID* In addition, a comprehensive guide on
analysis is scheduled for publication in the spring of 1989
(Mo89). The publication will be the first comprehensive
treatment of this subject.
C.6 DISTRIBUTIONS
The final and by far the most important issue pertinent to
the implementation of a quantitative uncertainty analysis is the
completeness and reliability of the data characterizing
distributions of each of the calculational parameters. The
number of radionuclides, pathways and parameters used in risk
assessments (see the AIRDOS input sheets in the Appendix to
Volume II) is very large. However, through a screening processf
the number of radionuclides and pathways that require explicit
analysis can be sharply reduced.
Once the parameters of interest are identified, it is
necessary to evaluate how each parameter is used in the risk
calculations,- that is, is it used to calculate risks to a
-------
population or an individual; is it to calculate
or lifetime risk?
Once this is determined, probability distributions for
parameter, as it is used in the risk calculations,
constructed. A number of such distributions have been
constructed in the past which will facilitate this process
(NUREG79, Ri83). In addition, it will likely be
necessary to elicit subjective probability distributions for
specific by interviewing researchers specializing in
each parameter. In order to obtain unbiased distributions,
formal elicitation techniques, as described by Hogarth (Ho75),
may be required.
C-9
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et al
Ho75
Ho85
M078
M089
NRC75
NUREG79
NUREG81
R183
___^i
FgodGhain and Atmogph,_er ic _Pi.spersJLoii JModules of .......... M&RC ,
NRPB-R184, May 1988
U.S. Environmental Protection Agency, Proposed
Guidelines for Exposure Assessment, Request for
Comments, 49 FR 46304, November 23 , 1984.
Hogarth, R.M. , "Cognitive Processes and the Assessment
of Subjective Probability Distributions", J ..... , .......... &f_the
Aa,.__Statlgtical Assoc. . 70(350), 271, June 1975.
Hofer, E., and Krzykacz, B, , CE€_^tudv__Contracti
Uncertainty analysis of the ..... jgoinputat.ional assessment of
the radiological consecrnences of. nuclear accidents^
Final Report to Part I (October 1984) and to Part II
(July 1985) ,
Morgan, M.G., et al., "Sulfur control in coal-fired
power plants; A probabilistic approach' to policy
analysis," APCA Journal. 28(10) 993, 1978,
Morgan, M.G., and Henrion, M. , Unce r t ajLnty ; & ........... Gu ide _fc o
Dealing with Uncertainty in Quantitative Risk and
Policy Analysis. Cambridge University Press (scheduled
for publication in the summer of 1989) .
U.S. Nuclear Regulatory Commission, Reactgr__Sa.fety
Study ; . ..An.__Assessment of Accident Risks in United
States CQamercial^ucleaj^P^we^^Plants, WASH-1400,
October 1975.
U.S. Nuclear Regulatory Commission, A__ltatistical
analysis of selected... parameters for predictin.a_fQOd
.chain transport ........ and interna !„ dose of . .. radionucl ides „.
Hoffman, P.O., and Baes, C.F., III (eds.)/
NUREG/CR-1004, 1979,
U.S. Nuclear Regulatory Commission, Yari ab i l.i ty_. Jji
dose estimate associated with food cha in_jt ran sport
and ingesjfcion of selected ...... radionuc,! jdes, , by F.O.
Hoffman, R.H. Gardner, and K.F. Eckersian,
NUREG/CR-2612, 1981.
Rish, W.R. , Mauro, J.M,, and Schaffer, S.A., "Analyses
of Uncertainties in the EPA Ore Body Release and River
Mode Exposure Pathway Models Used as the Bases for
Proposed Geologic Repository Release Limits", Final
Report to Battelle Project Manager Division (BPMD) for
the Department of Energy, June 10, 1983.
C~10
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