OHico ol          / EPA 520/5-85-02C
                            Rndinlion Protinirns      \May 1986
                            W;i;;liiiii|U'H. IXC. 204GO
&EPA         Environmental Pathway
               Models for Estimating
               Population Health Effects
               from Disposal of High-Level
               Radioactive  Waste in
               Geologic Repositories
                                     RecycledyRecyclable
                                     Printed with Soy/Canola In!
                                     contains at least 50% recycled liber
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                                      EPA  520/5-85-026
      ENVIRONMENTAL  PATHWAY  MODELS  FOR
 ESTIMATING POPULATION HEALTH EFFECTS FROM
DISPOSAL OF HIGH-LEVEL RADIOACTIVE WASTE IN
           GEOLOGIC REPOSITORIES


              J.  Michael  Smith
               Ted W. Fowler
             Abraham S. Go!din
                Final  Report
                August 1985
    U.S.  ENVIRONMENTAL  PROTECTION  AGENCY
       Office  of Radiation  Programs
  Eastern Environmental  Radiation  Facility
             1890 Federal  Drive
         Montgomery, Alabama 36109

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                                 FOREWORD

    The Agency published environmental standards addressing disposal of
high-level radioactive wastes  (40 CFR 191} for public review and comment
in December 1982  (47 FR 58196).  The comments received have been considered
and the Agency has promulgated the final rule on August 15, 1985.  An
important part of the rulemaking was the evaluation of how effective mined
geologic repositories are for isolating high-level  wastes from the
environment for many thousands of years.  EPA's assessments indicate that
carefully designed repositories at good sites can keep long-term risks
below those that would exist if (on a generic basis) the uranium ore used
to create the wastes had not been mined to begin with.  Accordingly, the
Agency has promulgated environmental  standards that would restrict
projected releases from high-level waste disposal systems—for 10,000
yearsr after disposal --to levels that should keep the risks to future
generations less than the risks they would have been exposed to. from the
unmined ore if these wastes had not been created..

    This technical report presents the methodology  used to assess the
long-term population risks from projected releases  of waste from a
geologic repository.  It describes the models that  the Agency developed
specifically for this project and reviews the various assumptions made.
The Agency expects that population distributions, food chains, and living
habits may change dramatically over 10,000 years.  Rather than attempt to
predict such changes, this methodology uses very general models of
environmental  pathways that consider present values for the various
parameters used in the models.

    Because much of this methodology is new, and because these risk
assessments are a key part of our rulemaking, the Agency published a draft
of this report.  Comments were received from the public and from EPA's
Science Advisory Board High-level  Radioactive Waste Disposal Subcommittee.
This Subcommittee conducted an independent technical review of the EPA
risk assessments during 1983, and its suggested changes have been
incorporated in the methodology which is described  in this final  report.
    I encourage users of this report to submit a nr comments or suggestions
they might have.  Such comments should be sent to:  Central Docket Section
(A-130); Environmental Protection Agency; Attn:  Docket No. R-82-3;
Washington, D.C.  20460.  For additional  information,, please contact
Mike Smith at (205) 272-3402; Office of Radiation Programs; Eastern
Environmental Radiation Facility; Environmental Protection Agency;
1890 Federal Drive, Montgomery, Alabama  36109.
                                 Sheldon Meyers,  Acting Director
                              Office of Radiation Programs (ANR-458)

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                             TABLE  OF  CONTENTS

                                                                      Page^

Acknowledgements  	   xi

SUMMARY	s_  i

    •S.I  The Methodology	S-  2

          S.I.I  Releases to a River (Surface Water)   	   S-  3
          S.I.2  Releases to an Ocean	S-  5
          S.I.3  Releases Directly to Land Surface	S-  6
          S.I.4  Releases Due to a Volcanic Eruption or Meteorite
                   Impact	S-  7

    S.2  Results	S-  7

1.  INTRODUCTION	1_  !

    1.1  Background Information 	   1.  1
    1.2  Pathways Considered  	   1_  3
    1.3  Approach to Calculations	1_  5

2.  SOURCE TERMS	2.  j

    2.1  River Source Terms 	   2-1
    2.2  Ocean Source Terms 	   2-6
    2.3  Land Surface Source Terms	2-7
    2.4  Volcano/Meteorite Interaction Source. Terms  	   2-7

3.  ENVIRONMENTAL TRANSPORT AND RISK MODELS 	   3-1

    3.1  Releases to a River	3.  3

          3.1.1  General Considerations 	   3-  3
          3.1.2  Drinking Water Ingestion 	   3.  4
          3.1.3  Fresh Water Fish Ingestion	3-6
          3.1.4  Food Ingestion	3.  8
          3.1.5  Inhalation of Resuspended Material  	   3-10
          3.1.6  External Risk Commitment - Ground Contamination  .   3-15
          3.1.7  External Risk Commitment - Air Submersion  ....   3-17

    3.2  Releases to an Ocean	3-18

          3.2.1  General Considerations 	  3-18
          3.2.2  Ocean Two - Compartment Model  	  3-21
          3.2.3  Seafood Ingestion  	  3-23
                                    11

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                   TABLE  OF  CONTENTS  (continued)
                                                                 Page
3.3  Releases to the Land Surface	3-24

      3.3.1  General Considerations 	  3-24
      3.3.2  Food Ingestion	3-26
      3.3.3  Inhalation of Resuspended Material 	  3-29
      3.3.4  External Risk Commitment - Ground Contamination   .  3-33
      3.3.5  External Risk Commitment - Air Submersion  ....  3-34


3.4  Releases Due to Volcano/Meteorite Interaction  	  3-34

      3.4.1  General Considerations 	  3-34
      3.4.2  Releases Directly to Land Surface	3-35

           3.4.2.1  General Considerations  	  3-35
           3.4.2.2  Food Ingestion	-.  .  3-36
           3.4.2.3   Inhalation of Resuspended Material  ....  3-36
           3.4.2.4  External Risk Commitment-Ground
                      Contamination 	  3-36
           3.4.2.5  External Risk Commitment-Air Submersion .  .  3-37

      3.4.3  Releases to Air Over Land	3-37

           3.4.3.1  General Considerations  	  . .  .  3-37
           3.4.3.2  Air-Above-Land Two Compartment Model   . .  .  3-39
           3.4.3.3  Food Ingestion  	  3-41
           3.4.3.4   Inhalation of Dispersed and
                       Resuspended Material 	  3-44
           3.4.3.5   External Risk Commitment -
                       Ground Contamination 	  3-44
           3.4.3.6   External Risk Commitment -
                       Air Submersion	3-45

      3.4.4  Releases to Air Over Oceans   	  3-45

           3.4.4.1   General Considerations  	  3-45
           3.4.4.2  Air-Above-Water:   Three Compartment Model  .  3-48
           3.4.4.3   Seafood Ingestion  	  3-50

3.5  Special Calculations  for C-14 Environmental Risk
         Commitment	3-50
                                iii

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                       TABLE OF CONTENTS (continued)

                                                                     Page

4.  METHODS FOR DERIVATION OF FATAL CANCER RISK CONVERSION FACTORS   4- 1

    4.1  Fatal Cancer Risk Conversion Factors 	  4-1
    4.2  Analytical Treatment of Daughter Product Buildup During
           Environmental Transport  	 .  	  4-9
    4.3  Application of Risk Factors for Environmental Pathway
           Calculations 	  4-11
    4.4  Risk Conversion Factors for Np-237	4-15

5.  DISCUSSION OF VALUES FOR PARAMETERS 	  5-1

6.  HEALTH EFFECTS PER CURIE RELEASE RESULTS  	  6-1
    6.1  Fatal Cancers per Curie Release to the Accessible
            Environment	6-1
    6.2  Comparison of Fatal Cancers and Serious Genetic Effects
            (All Generations) per Curie Release to the Accessible
            Environment	6-7

7.  UNCERTAINTY ANALYSIS	7-1

    REFERENCES	R- 1

    NOMENCLATURE   	  N- 1

    APPENDIX A:  Method for Consideration of Daughter
                   Product  Ingrowth	A -1

    APPENDIX B:  Fatal Cancer Risk Factors   ............  B- 1

    APPENDIX C:  Computational  Details   	  C- 1
       C.I  Curie Intake per Unit Area Deposition  (RInp)	C- 1
       C.2  Persons Fed per  Unit Area  (CPp)	C-13
       C.3  Fraction of River Flow Used  for  Irrigation  (fR)   ....  C-17
       C.4  Population Density  (PDp)  	  C-18
       C.5  Correction Factor for the  Ground  Surface Risk, Factors
              (GCpp)	  C-19
       C.6  Leaching Removal Rate Constant for  Soil  (x$n)	C-23
       C.7  Ratio of Persons Drinking  Water and  Eating  Fish to
             River Flow	  C-26
       C.8  Total Fraction of Initial  River  Inventory  Deposited  to
             Cropland for Radionuclides Rapidly Transferred  Through
              Soil  (Radionuclide Recycle)	C-26
       C.9  Tabulation of Estimated Range  of  Parameter Values  .  .  .  C-30
       C.10 Determination of Values for  the  Parameters  yj,
              Y2» SF^n and SF2n  Used  for the  Ocean Release
             Mode	C-42
                                     1v

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                  TABLE OF CONTENTS  (continued)
                                                                 Page
APPENDIX D:  Sample Derivation of an Environmental Pathway
               Equation and Calculation of Population
               Fatal  Cancers	D- 1

APPENDIX E:  FORTRAN Listing of Computer Program  	  E- 1

Notes Pertinent to Appendices F, G and H  	

APPENDIX F:  Radiation Dosimetry  	  F- 1
  F.I  Introduction	F- 1
  F.2  Definitions	F- 1
  F.3  Dosimetric Models	F- 3
  F.4  EPA Dose Calculations	F- 9
  F.5  Uncertainty Analysis	F-10
  F.6  Distribution of Doses in the General Population   ....  F-26
  F.7  Summary	F-27

APPENDIX G:  Estimating the Risk of Health Effects Resulting
               from Radionuclide Releases 	  G- 1
  G.I  Introduction	G- 1
  G.2  Cancer Risk Estimates for Low-LET Radiations  	  G- 2
  G.3  Fatal Cancer Risk Resulting from High-LET  Radiations  .  .  G-20
  G.4  Uncertainties in Risk Estimates for Radiogenic Cancer   .  G-23
  G.5  Other Radiation-Induced  Health Effects  	  G-32
  G.6  Radiation Risk - A Perspective	G-54

APPENDIX H:  A Description of the RADRISK and  CAIRO
               Computer Codes Used by EPA in Assessing  Doses
               and Risks from Radiation Exposure	  H- 1
  H.I   Introduction	H- 1
  H.2  Overview of the EPA Analysis	H- 1
  H.3  Dose Rates  from Internal  Exposure	H- 1
  H.4  Dose Rates  from External  Exposure	H- 5
  H.5  Life Table  Analysis to Estimate the Risk of Excess
         Cancer	H- 8
  H.6  Risk Analysis Methodology	H-ll

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                          LIST OF TABLES
S-l   Fatal  cancers per curie released for different release
                                                                 Page

1-1
4-1

4-2
5-1
5-2
5-3
5-4
5-5
5-6

6-1

6-2

6-3

6-4

6-5


B-l

C-l
modes 	
Release modes and environmental pathways 	
Summary table from RADRISK computer code for Ra-226
inhalation 	
Fatal cancer risk conversion factors 	
Radionuclide decay constants 	
Bioaccumulation factors for freshwater fish and seafood
Radionuclide intake factors 	
Leaching coefficients for radionuclides in soil 	
Ground surface radionuclide correction factors (GCnp) . .
Values for ocean sedimentation coefficients {SFin

Fatal cancers per curie released for different
release modes 	
Fatal cancers per curie released for releases to
a river 	
Fatal cancers per curie released for releases to an
ocean 	
Fatal cancers per curie released for releases to a
land surface 	 	
Comparison of fatal cancers and genetic effects per
curie release to the accessible environment for
different release modes 	
Fatal cancer risk conversion factors for parent and
significant daughters 	
Radionuclide specific data used to compute RInD 	
S- 9
1- 4

4- 6
4-13
5- 3
5- 6
5- 7
5-11
5-13

5-15

6- 3

6- 4

6- 5

6- 6


6- 9

B- 3
C-ll
                                 vi

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                    LIST OF TABLES (continued)
C-2   Productivity and relative importance of vegetative
                                                                 Page
C-3
C-4
C-5
C-6
C-7
C-8
C-9
c-in
c-n
F-1
F-2
F-3
G-l
G-2
G-3
G-4
G-5
Area! yield and fraction of diet for cattle feed crops .
Values for persons fed per unit area of land (CPp) . . .
Fraction of river flow used for irrigation (f^) by
U.S. regional values for population density (PDp) ....
Ground surface radionuclide correction factors (GCnp) . .
Oil
Ratio of persons drinking water and eating fish to river

Distribution coefficients for radionuclides on sediment .
Age-dependent parameters for iodine metabolism in the
Distributions or organ doses from inhalation and ingestion
Range of cancer fatalities induced by 10-rad low-LET
radiation (average value per rad per million persons
A comparison of estimates of the risk of fatal cancer from
a lifetime exposure at 1 rad/year (low-LET radiation) .
Proportion of the total risk of fatal radiogenic cancer
UNSCEAR estimates of cancer risks at specific sites . . .
Comparison of proportion of the total risk of radiogenic
cancer fatalities by body organ 	
^-.10
C-14
C-16
C-17
C-18
C-22
C-25
C-27
C-31
C-45
F- 9
F-17
F-28
G-10
G-12
G-16
G-17
G-lfi
                                Vll

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                    LIST  OF  TABLES  (continued)
G-6   Estimated number of cancer fatalities from a lifetime
        exposure to internally deposited ALPHA particle
        emitters	G~24

G-7   A ranking of causes of uncertainty in estimates of   •
        the risk of cancer	G~31

G-8   ICRP task group estimate of number of cases of serious
        genetic ill health in liveborn from parents irradiated
        with 106 man-rem in a population of constant size  . .  .   G-37

G-9   BEIR-3 estimates of genetic effects of an average population
        exposure of 1 rem per 30-year generation  .......   G-38

G-10  UNSCEAR 1982 estimated effect of 1 rad per generation of
        low dose or low dose rate, low-LET radiation on a
        population of 10° liveborn according to the doubling
        dose method	G-39

G-ll  Summary of genetic risk estimates per 106 liveborn
        for an  average population exposure of  1 rad of low dose
        or low  dose rate, low-LET radiation in a  30-year
        generation	G-40

G-12  Estimated frequency of  genetic  disorders 1n a birth
        cohort  due to exposure  of the parents  to  1  rad per
        generation	G-47

H-l   Small  Intestine to blood  transfer fractions,  fi, for
        transuranlc elements   	  H-  6
                                viii

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                         LIST OF FIGURES
2-1


2-2


3-1

3-2


3-3


3-4


7-1



C-l



D-l

F-l



F-2

F-3


F-4


F-5
                                                           Page

Schematic diagram for transport of radionuclides
  from repository to river	2-3

Release rate to river as a function of time after
  placement of radioactive waste in repository  	  2-5

Compartment model for the ocean release mode  	  3-19

Activity (mass) balance for soil element away
  from source	3-30

Compartment model for air over land-volcano/
  meteorite release mode  	  3-38

Compartment model for air over ocean-volcano/
  meteorite release mode	3-47

Cumulative probability distribution showing uncertainty
  about fatal cancer risk estimate for 1 curie of Am-243
  released to a river	7-7

Dose rates in air at 1 meter above ground for an infinite
  uniform plane source and an infinite uniform slab
  source	  C-21

Radionucllde travel from repository to river  	  D- 4

Typical pattern of  decline of activity of a radionuclide
  in an organ, assuming an initial activity in the organ
  and  no additional uptake of radionuclide by the organ  .  F- 4

The ICRP Task Group lung model  for particulates	F- 6

Schematic representation of radionuclide movement among
  repository tract, gastrointestinal tract, and blood  .
F- 7
 Dose  rate  from chronic ingestion of iodine-131 in water at
  a concentration of  1 nCi/1   	F-15

 Dose  rate  from chronic inhalation of iodine-131  in  air at a
  concentration  of  1  nCi/nr	F-16
                                 IX

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                   LIST OF FIGURES (continued)
F-6   Compartments and pathways 1n  model  for  strontium
        1n skelton	F-18

F-7   Dose rate from chronic Ingestion  of strontium-90  in water
        at a concentration of 1 uCi/1	F-19

F-8   Dose rate from chronic inhalation of strontium-90 in air
        at a concentration of 1 pd/m3	F-20

F-9   Dose rate from chronic inhalation of plutonium-239 in  air
        at a concentration of 1 pCi/m3	F-22

F-10  Compartments and pathways in  model  for  plutonium  in
        skeleton	  F-23

F-ll  Dose rate from chronic ingestion  of plutonium-239 in water
        at a concentration of 1 iid/1	F-24

F-12  Dose rate from chronic inhalation of plutonium-239 in  air
        at a concentration of 1 pd/m3	F-25

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                             Acknowledgements
    The authors gratefully acknowledge the contributions of C.B. Nelson,
W.H. Ellett, A.C.B. Richardson, U.S. Nelson, R.E. Sullivan, and D.J. Egan.
A.C.B. Richardson and W.H. Ellett participated in the development of the
conceptual approach of this report, particularly that for the river
pathv/ay models.  C.B. Nelson provided substantial assistance in developing
many of the ideas and basic equations contained in the manuscript.
W.H. Ellett, M.S. Nelson and R.E. Sullivan were primarily responsible for
the development of EPA's dosimetry and risk methodology which is applied
in this report and which they have described in Appendices F, G, and H.
D.O. Egctn made many helpful suggestions regarding the format and technical
content of the manuscript.

    Two of the authors of this report are no longer with EPA.  Ted W. Fowler
is currently employed by the National  Institutes of Health.  His mailing
address is National  Institutes of Health, 9000 Rockville Pike,  Bldg. 21,
Room 116,  Bethesda,  MD  20205.   Abraham S. Goldin is retired from EPA.
His mailing address  is 1505 Columbia Avenue,  Rockville,  MD  20850.
                                    XI

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                                 SUMMARY
     As part of its program to develop environmental  standards for
disposal  of high-level  radioactive  wastes,  the Environmental  Protection
Agency estimated population health  risks for 10,000 years after disposal
in mined geologic repositories (EPA85a).  This report describes the
mathematical models we formulated to calculate the environmental  risk
commitments (ERC's—fatal  cancers and serious genetic effects to all
generations) that could occur as a  result of releases from such
repositories.  The report also identifies the data we chose to use in
these models and presents our estimates of the premature fatal cancers
caused per unit of radionuclide released to the accessible environment.
These estimates will be used in selecting the containment requirements in
the Agency's final disposal standards (40CFR191).

      In performing these long-term assessments of population health
effects, we recognize that it is pointless to try to make precise
projections of the actual risks from repositories.  Population
distributions, food chains, living habits, and technological capabilities
will  undoubtedly change in major ways over 10,000 years.  Unlike
geological  processes, they can be realistically predicted'only for
relatively  short times.  Accordingly, we formulated very general models
of environmental pathways, and we assumed population sizes and
characteristics  similar to those of today.   In particular, we usually
avoided the detailed analytical techniques that would be appropriate
for  near-term environmental assessments of specific facilities.
                                    S-l

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     The models described 1n this report consider risks to populations, as
opposed to risks to individuals.  Therefore, individual risks caused by
potential releases from a repository cannot be determined from these
analyses.  However, a companion report (EPA85a) describes analyses that
assess individual risks from several types of releases.

S.I  The Methodology

     The Agency's risk assessment report  (EPA85a) identified four ways
that radionuclides might be released to environmental pathways: to surface
water  (e.g.,  a  river) through groundwater; to an ocean through surface
water; to a  land  surface directly;  or to multiple pathways after the very
unlikely possibility of disruption  by a volcano or a meteorite.  For each
of these four release modes, we modeled the ways that radionuclides can
move through the  geosphere and the  biosphere to the population, and we
estimated the intake by or exposure to the population through each of
these  environmental pathways.  We then applied risk conversion factors per
 unit  intake  or per  unit external exposure to estimate  fatal cancers and
                    i
 serious  genetic effects to all  generations per curie released to the
'accessible  environment.

      Following procedures  similar to those  used  for computing
 environmental dose  commitments,  we  calculated the total  health effects
 for the  entire population  exposed to the  releases from a repository,
 rather than terminate  the  calculation at  some  arbitrary distance  from the
 repository.   A time integration was performed  to sum the health effects
                                     S-2

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from the time  the  repository  is  sealed  ("disposal")  until a  specified  time
in the future  (usually  10,000 years  after  disposal).  The following
sections summarize the  procedures  we used  to  calculate the population
intake of radioactivity for the  internal pathways  or integrated  population
exposure for the external  pathways for  each of the four  release  modes.
The population intakes  of  and exposures to radioactivity are converted to
population ERC's by multiplying  by the  appropriate risk  conversion factor.

S.I.I  Releases to a River (Surface  Water)

     In the surface water  release  model, the  repository  containment  is
breached—after some initial  period—and groundwater circulates  through
the repository into the surrounding  geologic  media and eventually to an
aquifer.  The  aquifer then flows underground  until it intersects a river.
To determine the total  release  to  the river,  we developed and  integrated
an equation describing the release rate.  The integrated form  of the
release equation was then  used  to  compute  integrated river water
concentrations for use in  the following environmental pathway  models:

     Drinking Water.  We assumed that the  population of  interest receives
drinking water from the river with no reduction in radionuclide
concentrations due to water treatment.   The intake rate  for  surface  water
by an  individual is combined with the ratio of the population  drinking
water  to the river flow rate to obtain an  estimate of the total  intake of
the radionuclide by the population per curie of the radionuclide released
to the river.
                                    S-3

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     Ingestion of Fish.  We  assume  that  fish  caught  1n  the  river  take  up
radioactivity from the water.   By calculating the  concentration of
radlonuclldes 1n the  fish  and  by multiplying  by estimated fish  Ingestion
rates by the population, we  determined the total population intake,  due to
consumption of fish,  of the  radionuclides released from the repository.

     Ingestion of Food Raised  on  Irrigated Land.   We assume that  river
water containing radionuclides from the  repository is used  to spray
irrigate farm land by direct deposition  onto  the crops  and  the  land
surface below the crops.   Furthermore, we assume that irrigated plants
that have incorporated radionuclides through  their leaves and root  systems
are consumed by humans as  food—or  are consumed by either dairy or  beef
cattle that transfer  radionuclides  to milk and meat.  Ingestion rates  of
these various food products are used to  estimate the total  radionuclide
Intake by the population  due to using river water  for Irrigation.

     Inhalation of Resuspended Material.  Some of  the radionuclides
deposited on the soil by  irrigation are  resuspended  into the air.  Using  a
resuspension factor and  the integrated soil surface  concentration,  we
estimated the resulting  integrated  concentration of  radionuclides.   We
calculated the population intake of radionuclides  using a  standard
inhalation rate and the  size of the population.

     External Exposure  from Air Submersion.  The radionuclides resuspended
into the air can cause  submersion exposures to the population.  These
exposures are analogous  to the Integrated air concentration to which the
                                    S-4

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population Is exposed and are calculated from the integrated air
concentration, the population density,  and a shielding and occupancy
factor.

     External Exposure from Ground Contamination.  The radioactive
material deposited on the ground during irrigation can also cause external
exposures to persons in the area.  Throughout the irrigation period,
radionuclides continue to build up on the ground until either irrigation
stops or equilibrium with losses through the soil is reached.  The methods
for estimating these exposures are similar to those applied for air
submersion.

S.I.2  Releases to an Ocean

     We assume that releases to a river system subsequently discharge into
the ocean.  Since we do not consider radidnuclide decay during travel in
the river or depletion of the radionuclide inventory due to river water
use or  sedimentation, the radionuclide releases to the ocean are identical
to the  releases to a river.  Our model  of the ocean pathway has two
compartments: a shallow upper layer in which it is assumed that all edible
seafood is grown and a lower layer that includes the remainder of the
ocean.  We developed coupled differential equations whose solutions
express the  quantities of radionuclides in these two compartments.  The
equation  for the upper compartment inventory was divided by the volume of
                                    S-5

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the compartment to determine the time-dependent concentatlon  of  radlonucHdes
1n the upper layer.  This concentration was  then  used  to  estimate the  amount
of radioactivity taken up by the ocean fish  and  shellfish consumed by  the
population.

S.I.3  Releases Directly to Land Surface

     For the land surface pathway models, we assume that  some of the
radioactive waste from the  repository is brought to the surface after an
event such as  inadvertant intrusion while drilling for resources.  Such
releases to the surface are assumed to be over a small area and a short
period of  time—so that they can be modeled as instantaneous point
sources.   The  mechanisms distributing the material to humans are
resuspension and  subsequent dispersion 1n the atmosphere.  When the initial
release to the land  surface is  determined, a time-dependent release rate
to the air is  estimated using a simple exponential model  that depletes the
land  surface source  to account  for resuspension and radioactive decay.
This  release rate is applied in conjunction with an atmospheric  dispersion
equation to  predict  air  concentrations as a function  of  time and  distance
from  the source;  these air  concentrations are then used  to estimate ground
 surface concentrations as a function  of  time and distance.   Once  ground
 surface concentrations are  determined, the  techniques used to calculate
 population Intake are similar  to those described for  the river  release
mode.  The pathways  considered for  releases to land surface  are:   (1)
 ingestion  of food raised on land contaminated with radionuclides,
                                     S-6

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Including food crops, milk, and meat;  (2)  inhalation of resuspended
radionuclides; (3)  external exposure  due to air  submersion;  and
(4) external  exposure due  to  ground contamination.

S.I.4  Releases Due to  a Volcanic  Eruption or Meteorite  Impact

     Releases caused by the extremely unlikely events  of  disruption  by
volcanoes or meteorites can be to  the land surface  and directly  to the
air.  For the material  released to the land surface, we  used the
methodology described for  the land surface release  mode.   For the material
released to the air, we assume that  the radioactivity  would be  quickly
dispersed in such a manner that  it would eventually be distributed
uniformly within the troposphere.  The airborne  material  is divided  into
the fraction over land  and the fraction over water—using the ratio  of
earth land surface and  earth  water surface.  We  then used compartment
models, with their systems of coupled differential  equations, to estimate
the quantity of radionuclides reaching the land surface  or ocean.
Finally, we estimated the  amount of  radioactivity or radiation exposure
reaching people through the  same pathways described for  the land surface
or the ocean,  respectively.

S.2  Results

     The specific equations used for each of the steps in the methodology
discussed above, and the parameters used  in our current application of
this methodology, are presented in the body of this report.  Chapter 6 of
                                    S-7

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the report describes the detailed  results of our assessment, indicating
the population health effects estimated—per curie released to the
accessible environment—for each of the  environmental pathways considered
under each release mode (a total of 30 pathways).  Chapter 7 discusses the
consideration of parameter uncertainty that EPA took  into account in
obtaining the results discussed In Chapter 6.  The following table
displays the total fatal cancers per curie release values calculated for
each of the four release modes. The most  stringent of  these sets of
values—that for surface water—was used in calculating the release limits
for the containment requirements of the  Agency's  proposed disposal
standards  (EPA85b).
                                    S-8

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TABLE S-l:
Fatal cancers per curie released for different release  modes
Nuclide
C - 14
NI- 59
SR- 90
ZR- 93
TC- 99
SN-126
I -129
CS-135
CS-137
SM-151
PB-210
RA-226
RA-228
AC-227
TH-229
TH-230
TH-232
PA-231
U -233
U -234
U -235
U -236
U -238
NP-237
PU-238
PU-239
PU-240
PU-241
PU-242
AM-241
AM-243
CM-245
Cm-246
Releases to
a River
5.83E-02
4.61E-05
2.25E-02
1.51E-04
3.65E-04
1.05E-02
8.07E-02
7.73E-03
1.07E-02
9.38E-06
1.18E-01
1.63E-01
2.41E-02
6.67E-02
3.49E-02
5.38E-01
3.40E-01
1.48E-01
2.15E-02
1.96E-02
2.17E-02
1.85E-02
2.06E-02
7.95E-02
4.23E-02
4.97E-02
4.84E-02
2.17E-03
4.79E-02
5.42E-02
5.72E-02
1.01E-01
4.99E-02
Releases to
an Ocean
5.83E-02
1.70E-06
6.14E-06
8.59E-06
3.17E-06
2.07E-03
1.43E-04
2.61E-05
2.28E-05
4.01E-07
6.91E-03
5.40E-03
1.07E-04
1.94E-03
2.71E-02
1.87E-01
4.32E-02
1.70E-03
1.90E-04
1.73E-04
1.89E-04
1.64E-04
1.83E-04
7.03E-03
4.06E-04
2.19E-03
1.91E-03
9.24E-06
2.18E-03
3.74E-03
1.09E-02
2.29E-02
1.01E-02
Releases to
Land Surface
5.83E-02
6.79E-07
3.76E-05
2.26E-05
5.65E-08
1.38E-03
3.96E-03
5.75E-04
2.19E-05
6.71E-08
1.52E-04
5.62E-03
1.57E-05
1.24E-04
1.90E-02
3.86E-01
3.76E-01
2.36E-02
7.51E-04
6.54E-04
8.42E-04
6.18E-04
6.90E-04
1.21E-04
3.10E-04
6.23E-03
5.22E-03
2.50E-06
6.34E-03
1.05E-03
2.45E-03
8.08E-03
3.54E-03
Releases due
to Violent
Interactions*
5.83E-02
2.89E-05
1.16E-03
1.22E-04
1.99E-04
2.73E-02
5.57E-02
4.91E-03
3.39E-03
4.72E-06
4.31E-02
7.20E-02
2.78E-02
3.82E-02
5.06E-02
1.26E-t-00
3.73E-01
1.28E-01
7.75E-03
5.94E-03
8.27E-03
5.62E-03
5.67E-03
2.83E-02
2.07E-02
1.20E-02
1.15E-02
9.36E-04
1.09E-02
2.54E-02
3.40E-02
6.09E-02
2.89E-02
     *For example,  interactions  of  a metorite or a  volcanic eruption with a
 repository.
                                    S-9

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                         Chapter 1:   INTRODUCTION

1.1  Background Information

     This report describes the methodology used by  EPA to estimate future
cancer fatalities to populations due to radionuclides -that escape to the
environment from a high-level  waste repository.* Mathematical  models for
estimating these cancer fatalities are presented.   An estimate of the
fatal cancers per curie release to the accessible environment for several
radionuclides is needed for use in setting curie release limits in EPA's
high-level waste standard and these estimates are  given in Chapter 6.

     We obtained population cancer fatality estimates in a manner consjstent
with methods used by others to calculate population environmental dose**
commitments.  The difference is that in our calculations we used risk
conversion factors in place of dose conversion factors.  Hence, the equations
given in Chapter 3 are used to determine population "environmental risk
commitments" rather than environmental dose commitments.  The nomenclature
used to specify environmental risk commitment is FHEn *** where the
    *Unless we state otherwise, we are estimating "excess" cancer
 fatalities, i.e., those caused by elevating radiation levels and in
 addition to those from other causes.
    **For  simplicity, the term "dose" will be used to denote "dose
 equivalent."
    ***The variables used in the equations in this report are defined in
 the nomenclature, p. N-l ff.
                                    1-1

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subscripts n refer to radionuclide and p to pathway.   However,  since the
concept of environmental  dose commitment will  be  most  familiar  to the
reader, the basis for its calculation 1s reviewed below.

     The environmental dose commitment is identical  to collective dose
commitment, S, as used in ICRP Publication 26, "Recommendations of the
International Commission on Radiological Protection" (ICRP77) and the
report entitled "Sources and Effects of Ionizing  Radiation" (UN77).
Mathematically, the environmental dose commitment is expressed as
        =  f   r  D1 N(D',t) dD'dt
          o   o
                                                (1.1-1)
where D' is the dose commitment rate and N(D',t) dD1 is the number of
people  receiving a dose commitment rate between D1 and D'+dD' at time t.
The  incomplete collective dose commitment, S(t), is defined as follows:
                    oo
      S(t)  =
f/D1 N(D',t") dD'dt" .
o  o
(1.1-2)
 The  term  "dose commitment rate" as used here means the 50-year dose
 commitment  rate to  individuals due to  Intake 1n the case of internal
 emitters, or, in the case of external  exposure, simply the annual dose rate
      In this  assessment, the  population of  interest is the world population,
 which is assumed  to  be constant  over  the time period, t.  Specifically, we
 assume that
        oo
                               10
         N(D',t)dD'  = N(t)  = 10±u  persons  (UN77).
                                               (1.1-3)
                                    1-2

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     Other EPA reports,  besides  this  one,  discuss dosimetry and health
risk analysis for the EPA high-level  waste standard (EPA85a, EPA85b).   In
these reports, individual  and population risk assessments for various
scenarios which release  radionuclides from a repository, are discussed.
The risk assessment report (EPA85a)  discusses risk assessments used to
determine repository release limits  for inclusion in the EPA standard.

1.2  Pathways Considered

     These analyses consider four general  modes of radionuclide releases
from a waste repository:  releases to a river, to an ocean, to a land
surface, and from a volcanic or meteorite interaction with a waste
repository.  The releases to a river, an ocean, or a land surface can  be
caused by any number of events.   For example, drilling a mining borehole
through a repository could allow groundwater to leach radionuclides from
the radioactive waste.  The radionuclides could be transported to a river
and subsequently to an ocean.  A variation of this scenario would be
radionuclide releases directly to the land surface by a drilling event.
Volcanic eruption or meteorite impact have a lower probability of
occurrence than those events discussed above.  This class of events
generally results in violent release of radioactive material directly to
the land surface and to the air.  These four release modes are subdivided
into a total of 30 pathways, as listed in Table 1-1'.
                                    1-3

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TABLE 1-1:
Release modes and environmental pathways
Release Mode
Releases to River
 Pathways Included In this Release Mode    Pathway
                                           Number
Releases to Ocean
Releases Directly
 to Land Surface
 Drinking Water Ingestion
 Freshwater Fish Ingestlon
 Food Crops Ingestion
 Milk Ingestlon
 Beef Ingestlon
 Inhalation of Resuspended Material
 External Dose-Ground Contamination
 External Dose-Air Submersion

 .Ocean F1sh Ingestion
 Ocean Shellfish Ingestlon

 Food Crops Ingestlon
 Milk Ingestlon
 Beef Ingestlon
 Inhalation of Resuspended Material
 External Dose-Ground Contamination
 External Dose-Air Submersion
 Releases Due to Volcano/
 Meteorite  Interaction

  Releases
  Directly to  Land
   Releases  to  Air
   Over  Land
   Releases to Air
   Over Ocean
  Food Crops Ingestion
  Milk Ingestlon
  Beef Ingestion
  Inhalation of Resuspended  Material
  External  Dose-Ground  Contamination
  External  Dose-Air Submersion

~Tood Crops Ingestion
  M1U Ingestlon
  Beef Ingestlon
  Inhalation of Dispersed and
    Resuspended Material
  External  Dose-Ground  Contamination
  External  Dose-Air Submersion

  Ocean Fish Ingestlon
  Ocean Shellfish Ingestlon
 1
 2
 3
 4
 5
 6
 7
 8

 9
10

13
14
15
12
16
11
25
26
27
24
28
23

19
20
21

17
22
18

29
30
                                     1-4

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1.3  Approach  to  Calculations

     The goal  of  the  analysis  for each specific  pathway  Is to estimate the
population cancer fatalities committed to time t per unit nuclide release
to the accessible environment*.  After the normalized values are
determined as  a function of nuclide and pathway, a summation over pathways
may be performed.  The result  is a normalized set of ERCs, for a release
mode, which are a function only of nuclide.  With this approach, these
normalized ERCs can be used to predict the total ERC for various scenarios
which lead to  releases to the  biosphere from a repository, without a
"reanalysis" for each new event.

     Developing pathway computation models involves applying the
mechanisms for leakage of radionuclides from a repository and predicting
the processes that cause these radionuclides to disperse in the
environment.  These models and methods are discussed in more detail in
Chapters 2 and 3.  In general, the pathway equations integrate the risks
over all persons exposed from the time the material is placed in the
repository until time, t, in the future, to yield the incomplete
     *According to our terminology in section 1.1, these population cancer
 fatalities are the normalized, incomplete environmental risk commitments.
 For ease of reference, the acronym used throughout the report to refer to
 these  quantities will be ERC.
                                    1-5

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environmental risk commitment.  Conceptually, the incomplete environmental
risk commitment, ERC(t), can be defined in a manner analogous to equation
1.1-2, i.e.,
                                                               (1.3-1)
ERC(t) =    /    I  R1 N(R',t) dR'dt .
            o  o
where R" is the risk commitment rate and N(R',t)dR' Is the number of
people receiving a risk commmitment rate between R1 and R'+dR' at time t
                                    1-6

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                         Chapter  2:   SOURCE  TERMS

     We use simple transport  models  to estimate the  movement of
radionuclides from the repository into the accessible environment.
Different scenarios are applied in developing the  source term models for
the four release modes.  For  some of the release modes,  several different
mathematical models for determining  releases to the  environment are
possible.  In this report,  only one  release model  has been addressed for
each release mode.  The environmental pathway calculations for other
release models would be treated 1n a manner similar  to the methods
discussed in this report.  A more complete discussion of source terms is
included in the risk assessment report (EPA85a).

2.1  River Source Terms
     For the river pathway, we assume the radionuclides remain 1n the
repository for the initial delay period, t  t following placement.*
After this time, we assume that the repository is breached and that
radionuclides can be removed from the repository and eventually be
transported to a river.  There are several different mechanisms that
determine the rate of removal of radionuclides from a repository, such as
their susceptibility to leaching, water flow through the repository,
solubility of the chemical compound containing the radionuclides, waste
heat from the buried waste, and type of event causing the release.  The
      *The  variables  used  in this  report  are  defined in the  nomenclature,
 p.  N-l  ff.
                                    2-1

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methods for obtaining the specific releases for a release scenario are
discussed in the risk assessment report (EPA85a).  In this report, we use
a radionuclide removal model limited by the rate of leaching to illustrate
typical river environmental transport equations.  Several other release
models are plausible, but this "leaching-limited11 model has been chosen
because it is reasonably simple and leads to closed-form environmental
pathway equations.
     The total human intake for each river pathway is taken to be
proportional to the total quantity  (i.e., the integrated concentration) of
the radionuclide in the river.  Therefore, the time-dependent rate of
entry of radionuclides to the river must be developed so that it can be
integrated.  We assume that the repository is breached and groundwater
circulates through the repository and leaches radionuclides into the
surrounding area and eventually to  an aquifer after passage of additional
time, t    .  The radionuclide-specific source term equation that
describes the time-dependent  rate of entry of each radionuclide (n) into
the aquifer, QlanDf't)» *s expressed as (see Fig. 2-1)
        anp
      and
      ''anP(t)=°
L von ~K t"xDnt " xLn (t"ter"tran:
                                                           an
                        for t
                                             (2.1-1)
 The aquifer flows  underground for a  representative  distance  until  it
 intersects  a river system.   Radionuclides  entering  the  aquifer are assumed
 to reach the river after a  delay  time,  t_«_.   The equation for
                                         am
                                     2-2

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           REPOSITORY
                                          Travel time from
                                          repository to
                                          aquifer = tran
Initial  Inventory  =  Qon
   Time between repository sealing
   and entry of groundwater = ter
   Leaching coefficient =
                                    Travel time in aquifer
                                    to river = tarn
(Note:   tRn = ter * tran + tarn = time between sealing of
repository and entry of radionuclides into the river.)
        Fig. 2-1.  Schematic diagram for transport of radionuclides
                   from repository to river
                                    2-3

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radionucllde release rate to a river 1s simply the previously presented
source term for radioactivity entering the aquifer (equation 2.1-1)
corrected to account for the additional time (t,-r,) required to
                                               arn    ^
transport each radionucllde from the point of entry into the aquifer to
the river.  Thus, the river source term Q1  (t) is the rate of entry to
the river of radionucllde n, in curies per year, as a function of time.
The equation for Q'nD(t) for the Teaching-limited case is as follows:
                   fL "on
                                                                  (2.1-2)
and
     Q'np-o
                                        for t>t   + t    + t
                                             *cer   Lran    tirn
                                        for  ttRn    (2.1-4)
                                                + tarn)
                                                          t
-------
ro
i
01
         S-
         QJ
o
-M

QJ
•M
(O
S-

OJ
(/)
ra

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Once the source term to the river 1s determined, we can calculate
radionuclide concentrations 1n the river.  These calculations are
discussed in Section 3.1.

2.2  Ocean Source Terms

     For the ocean pathway models, we assume that radionuclides from a
waste disposal facility reach the ocean only by transport through a river
system.  We also assume that

     travel time 1n the river to the ocean is so small that radionuclide
     decay may be neglected; and

     It is acceptable to neglect depletion of radionuclides in the river
     due to removal by irrigation and sedimentation.  (This assumption
     leads to a conservative estimate of the quantity of radionuclides
     reaching the ocean, since irrigation and sedimentation will remove a
     portion of the radionuclides In the river.)

     In light of these assumptions, the  source  terms for the ocean and
river releases are the same.  The release rate  and total integrated
release for the ocean release mode  for the Teaching-limited case are given
by  equations 2.1-2 and 2.1-4, respectively.  The computation of
radionuclide concentrations  in the  ocean is  discussed in Section 3.2.
                                    2-6

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2.3  land Surface Source Terms

     For the river and ocean release mode,  the  source term model  employed
predicts a continuous long-term release of  radionuclides to the biosphere
after leakage begins at a waste repository.  The events hypothesized for
the land surface release mode are those which could cause radionuclides
from the repository to be brought directly  to the earth's surface in a
short time period — such as drilling a well  into or through a waste
repository.  We assume that these events result in an instantaneous
release of some fraction, f,s, of the contents  of the repository to the
land surface at a time, t. , after emplacement of waste in a repository.
The release is assumed to be to a small area of land, which can be
considered as a point source for calculation of the resuspension from
ground to air and the subsequent redistribution in the environs.  The ERC
pathway analyses for the  land  surface release mode are discussed in
Section 3.3.

2.4  Volcano/Meteorite  Interaction  Source  Terms

     We assume that a violent  volcanic eruption or a meteorite impact
liberates materials from  the  repository in a short time.  A fraction,
f,,, of this material goes  directly to the land surface  and the rest is
released  directly to the  air.  That released to the  land surface is
conservatively  assumed  to be  distributed in a  small  area, and the
methodology  for  treating  the  redistribution of this  material in the
environment  is  the  same as  that  used  for the land  surface release.  We
                                    2-7

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assume that the material released to the air 1s dispersed 1n such a manner
that 1t Is, eventually, distributed uniformly 1n the troposphere.  The
airborne material 1s divided Into the fraction over land, fAL> and the
fraction over water, f.,,, using the ratio of earth land surface area to
total earth area and earth water surface area to total earth area.

     The methodology used to predict distribution of radionuclides in the
environment and to analyze the ERC pathways for the volcano/meteorite
release mode is discussed in Section 3.4.
                                    2-8

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           Chapter 3:  ENVIRONMENTAL TRANSPORT AND RISK MODELS

     This section contains  the  specific mathematical  models used to
calculate environmental  risk  commitment (ERC)  for each pathway and a
discussion of the rationale for each model.*  The sources  of the data used
in applying the models are  discussed in Chapters 4 and 5.

     The models used in these analyses are simple, but we  believe they are
appropriate for setting generally applicable environmental standards.
There is a large amount of  uncertainty in some of the parameters (see
Chapter 7 for a discussion  of uncertainty).  For this reason, it would not
be appropriate to apply more sophisticated models.  When possible, the end
results of existing, more detailed model evaluations are used.

     We have used to the greatest extent possible what we consider to be
realistic assumptions in developing these environmental pathway models.
When we use conservative assumptions, we note them in the discussion of
the affected pathway models.   In this  regard, one potentially conservative
assumption affects all the environmental pathway models:  the computation
of the environmental risk commitment using the linear, non-threshold
assumptions to estimate risks to the exposed population.**  The procedure
      *The  variables used in the equations in this report are defined in
 the nomenclature, p. N-l ff.
      **The environmental risk commitment and the linear, non-threshold
 theory  are discussed more fully in  Chapters 1 and 4 and Appendices F and G,
                                    3-1

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for performing these calculations involves computation of risks to the
entire exposed population, some of whom will  experience very low dose
equivalent rates. To the extent that there may be a threshold below which
the dose equivalent does not result in a fatal cancer risk, these
calculations are conservative.  However, application of the linear,
non-threshold theory is a prudent assumption since the existence of a
threshold has not been proved.  It is applied by essentially all
regulatory agencies in the radiation protection field.

      Terms used  in the equations in the following  sections  are defined in
the "Nomenclature", except where a term is used only  locally in a
section.   In those  instances, the terms may be defined  in the  sections
where they are used.

      In  the  following  sections,  the equations that are  discussed  are
for the  normalized  population environmental risk  commitment (ERC)  per
unit  of  radionuclide  release  to  the accessible environment for the
30 pathways,  i.e.,  for all  pathways,  we calculate the possible fatal
cancers  per  unit of radioactivity  release (or the "normalized" fatal
cancers).   This  is  done by  multiplying normalized radionuclide Intake by
the  appropriate  Internal  fatal  cancer risk factor for the internal
 pathways {inhalation or ingestion)  and by multiplying normalized
 radionuclide exposure by the appropriate  external fatal cancer risk factor
 for the external pathways (exposure from  ground surface Irradiation or
 from air submersion).   In this report, the internal and external  fatal
                                     3-2

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cancer risk factors are denoted as FCF.  (fatal  cancer factor for
radionuclide n and pathway p).
     The cancer fatalities for the various pathways within a release mode
may be summed to obtain total fatal  cancers per unit release to the
accessible environment for each specific radionuclide.  The mathematical
formulation for this process can be written as
     FHE.
        n
     u—
     y
VRIEnn
-TC*
£.,
(3.1-1)
where the summation over pathways (p) extends over the number of pathways
Included in a release mode.

3.1  Releases to a River

3.1.1  General Considerations

     The methods for determining the release of radionuclides from the
repository to the river are discussed in Section 2.1.  Using these
releases, the radionuclide concentrations In the river are computed by
dividing the average yearly radionuclide source terms by the average river
flow rate.  Radionuclides from the river expose the local population
through drinking water, ingestion of freshwater fish, Irrigation pathways
(including ingestion of food crops, milk, and beef), inhalation of
resuspended radioactivity, and direct radiation dose from ground surfaces
and from air.  These specific pathways are discussed below.
                                    3-3

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     In estimating the ERC for these pathways,  we  did  not  consider removal
of radlonuclides from the river water by sedimentation.     There 1s no
question that certain radionuclides deposit into sediments in slowly
flowing rivers and lakes, and, during the short-term,  sedimentation lowers
river water concentrations.  However, over the long time period considered
in these calculations, massive floods (100 and 1000 year floods, etc.),
may occur so that much of the deposited activity may be resuspended from
the sediment and distributed on farm land.  For this reason and because of
the difficulty involved  in modeling sedimentation and subsequent
resuspension during floods, we chose what we consider to be a conservative
position and did not  model radionuclide  loss from river water due  to
 sedimentation.  Also, we conservatively  assumed that the entire river is
contaminated so that  all persons  in the  vicinity of the river are
 subjected to the  radiation risk.

 3.1.2  Drinking Water Ingestion [pathway number (p) =  1]

      The drinking water supply for a population can be taken from rivers,
 lakes, or groundwater sources.  While selected aquifers may  be
 contaminated by leaching of radionuclides from a high-level  waste
 repository, we believe that repositories will  be sited far enough away
 from potable groundwater supplies to preclude the contamination of potable
 groundwater for significant populations.  Thus we have assumed that
                                     3-4

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contaminated drinking water would come only  from rivers or lakes.   For the
long periods chosen for this analysis, lake  and river water concentrations
should become equal.  Thus, we have restricted our analysis to
consideration of consumption of river water  by the population.

     The annual risk commitment to an individual is given by the product
of the amount of river water drunk (Iu.feu)» the radionuclide
                                     W  5>W
concentration in drinking water (Q'n n-
                                   np
factor (FCF  ) in the equation:
                                            . and the risk conversion
     RIV
                 np  w    np   sw   wt
         np
                                                               (3.1.2-1)
 The annual population risk commitment can be expressed as the annual
 individual risk commitment multiplied by the number of persons drinking
 the water, or
                             nn
      FHE'np  -  RIV'np  PR -    P
                                         f    f
                                         T<;w  Twt
                                                               (3.1.2-2)
              ynp  *w  ' w np  fsw fwt  PR
            ^             R
 By integrating  the  above expression over time we obtain
 where
 and
r
                  FHE-   (f)  dt»  .  FHEnp
                  lip'*''  dt"  •  Qnp
                                                               (3.1.2-3)

                                                               (3.1.2-4)

                                                               (3.1.2-5)
      *In this equation,  the only time  dependent term is Q
                                                         np'
                                    3-5

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     Upon dividing  both sides of equation  3.1.2-3  by the  integrated
release to the river,  Q  »  we obtain
    FHEnp   PR *W FCFnp  fsw  fwt
     'np
                                                               (3.1.2-6)
     After obtaining values for the parameters,  equation  3.1.2-6  can  be
used to calculate the normalized ERC to the  population  from the  ingestion
of river water.  Parameter values are discussed  in Chapters 4  and 5.
While provisions were Included in the model  to allow for  removal  of
nuclides by water treatment plants, the modifying factor, fwt, was not
used in these analyses.  This is a conservative  assumption.

3.1.3  Freshwater Fish Ingestion (p=2)

     The annual risk commitment to an Individual is given by the amount  of
fish eaten (If), the radionuclide concentration  in the  river water
   i
(Qnp/R)» a concentration factor expressing the concentration of
radlonuclides in fish compared to the concentration in  water (CF  ),  and
the risk conversion factor (FCFnD):
     RIV
                           raF
                              np
         np
(3.1.3-1)
     For some radlonuclides, the fish concentration factors may be based
on total radioactivity in the fish rather than only radioactivity in the
fish muscle (the tissues used for food).  In cases where this occurs and
                                    3-6

-------
where the radionuclide tends to concentrate in the parts of the fish which
are not eaten, the CF factors will  be conservatively high.

     The annual population risk commitment can be expressed as the annual
individual risk commitment multiplied by the number of persons eating fish
     FHE'
np
                       FF
                    CF   I, FCF    Pcc
                 np   np  f    np   FF
                          R
                                                      (3.1.3-2)
By integrating this expression over time, using the same procedures as for
the drinking water pathway, we obtain
         CF
     FHE
           np
                          FCFnp  PFF
         np
                                                      (3.1.3-3)
where the method  for obtaining FHE   and Q   is given in equations
3.1.2-4  and  3.1.2-5.  Upon dividing both sides of equation 3.1.3-3 by the
integrated release to the river, Q  , we obtain
    FHE.
CFnp PFF
              FCF
                           np
                                                      (3.1.3-4)
     (np
      This equation  is  for  freshwater  fish  from  rivers,  since we assume
 that all  freshwater fish eaten  by the population come from  rivers.
 Similar to the drinking water pathway,  this  assumption  allows  us to  ignore
 additional pathways for fish consumption associated  with  lakes.  Using the
 data discussed in Chapters 4 and 5, equation 3.1.3-4 can  be used to
 calculate the ERC to the  population from ingestion of freshwater fish.
                                    3-7

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3.1.4  Food Ingestion
                Food  crops  (p=3)
                Milk  (p=4)
                Beef  (p=5)
     The annual  risk  commitment  to  an  individual  from  consuming  foods
raised on irrigated land is  a  product  of the  concentration  of
radionuclides in the  river water (Q'np/R)»  the  irrigation rate  (W),  a
conversion factor to  express the radionuclide intake by  an  individual  per
unit deposition  to the ground  surface  (RInD)» and the  risk  conversion
factor (FCFnp):
     RIV,
        np *
Q'
  nP
                          FCF
                             nP
                                                 (3.1.4-1)
The annual population risk commitment can be expressed as the annual
individual risk commitment multiplied by the number of persons being  fed a
particular food crop raised on irrigated land.  The size of the population
eating irrigated food crops can be determined by multiplying the number of
persons who can be fed by raising the food crop on a unit area of land
(CP ), the area of the irrigated land (A), and a weighting factor that
expresses the fraction of irrigated land used for a particular crop
     PFP - CPP A fp
Then the annual population risk commitment is
     FHE'np=RIVnp  PFP
                                 W RInp FCFnp CPp A fp
By integrating this expression over time we obtain
                                                                      -
                                                 (3.1.4-2)
                                                 (3.1.4-3)
    W RI
     FHE
        np
                      np
                               CP
                                                 (3.1.4-4)
                                    3-8

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     The ratio (W/R)  1s  needed  for  each  food  pathway.  We can write  the
relationship
     WA = fRR
                                        •j
where A is the area of land irrigated (m ).
Rearranging,  we have
     W   fR
     IT = 7T  '
which can be substituted into equation 3.1.4-4,
(3.1.4-5)
(3.1.4-6)
     As mentioned previously, RI   is the intake of radionuclide n by
standard man for crop p for an acute deposition to the surface (Ci intake
        2
per Ci/m  deposited on the soil surface).  Values for RI   are listed
in Chapter 5 (Table 5-3) and the methods and data used to determine values
for RI   for food products are discussed in detail in Appendix C.
     The mathematical models used to determine values for RI   are
 similar to those used by the U.S. Nuclear Regulatory Commission (NRC77)
 and those used by EPA in the AIRDOS-EPA computer program (Mo79).  One
 significant change was made to the EPA models, which is included in
 determining the values for RInD-  The loss of radionuclides from the
 soil root zone was taken into account in computing uptake of radionuclides
 into plants through plant root systems*.  This loss mechanism from the
 soil can be important for long-lived radionuclides.
      *This change was made to the AIRDOS-EPA computer code after the
 program manual  (Mo79) was prepared.  The loss mechanism is not described
 in the program  manual.
                                    3-9

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     The values of RI   Include a  component  for^direct  deposition to
plant foliage and a component for  uptake from the soil  via the plant root
systems.  Therefore, the results are representative of  spray Irrigation.
Risks associated with ditch Irrigation will  be conservatively high since
direct deposition to crop surfaces is included.  The only transfer
mechanism for ditch-Irrigation 1s  uptake by  the crops from the soil.

     Substituting (fR/A) for (W/R) In equation 3.1.4-4, the Irrigation
area, A, cancels out and we obtain the following expression for the ERC to
the local population due to the ingestion of crops:
     FHE
      'np
cp
        np
(3.1.4-7)
We make the conservative assumption that all Irrigated land is used to
produce edible food crops; 1n fact, some would probably be used to raise
non-food crops.  Conversely, there will be some food crops whose  roots
extend below the assumed 15 cm soil root zone such that they can  take up
radioactivity from the  soil below this depth.  For these cases, our use of
a  xs  based on a 15 cm  soil root zone 1s not conservative.

3,1.5  Inhalation of  Resuspended Material   (p=6)

     The annual  risk  commitment to an Individual  from  inhalation  occurs
due to material  being deposited on the ground surface  by irrigation and
subsequently  resuspending  from the ground  surface into the air.   This
                                    3-10

-------
annual risk commitment 1s  the product  of  the  a I/  concentration  (XR_),
the Inhalation rate of an  individual  Ug)»  and  the  risk  conversion  factor
(FCFnp>:
     RIV  = XD  ID FCF
        np    Rn  B    np
(3.1.5-1)
The annual population risk commitment is  the  annual  individual  risk
commitment multiplied by the number of persons  inhaling air containing
radionuclides:
     FHE'np=  RIVlnpPAP.
(3.1.5-2)
The number of persons subject to inhalation can be determined by
multiplying the population density for the irrigation area by the size of
the area:
     PAn " PDP
(3.1.5-3)
Since the exposed population was confined to persons within the irrigation
area, the implicit assumption for equation 3.1.5-3 is that the radioactive
material deposited during irrigation remains on the ground or in the air
above the irrigated ground.  Although, in practice, radioactive material
resuspended into air would be diluted and distributed over a wider area,
our approach should yield approximately the same numerical population risk
commitment as the more exact and more complicated method of accounting for
dispersion of radionuclides in the air beyond the irrigation area.
Combining equations 3.1.5-1, 3.1.5-2 and 3.1.5-3 yields
                                   3-11

-------
     PHEV xRn !B FCFnp PDp
                                                          (3.1.5-4)
     The air concentration,  XRn(t),  at the center  of  a  uniformly
contaminated area having a surface concentration,  *L(t)»  due to
resuspenslon of radionuclldes from the ground surface 1s  shown by Nelson
(Ne78) to be
     XRn(t) . RF
where
     RF = XRn(t)/*n(t) . *R/v   ^
                                                          (3.1.5-5)

                                                          (3.1.5-6)
RF Is the ratio of air concentration to soil  surface concentration.
     Equation 3.1.5-6 holds 1f the radius of the ground surface source
term 1s large compared to the depletion distance for material  resuspended
to the air (I.e., this approximation 1s only valid for large,  uniformly
contaminated areas).  We assume that redistribution of materials by
resuspenslon in the contaminated area Is inconsequential, which is
equivalent to saying that the resuspended air concentration at a point in
the contaminated area only depends on the soil surface concentration at
the point of interest.

     Substituting equation 3.1.5-5 Into equation 3.1.5-4 yields
FHE'np - RF
                       JB FCFnp PDp A
By Integrating equation 3.1.5-7 over time, we obtain the following
expression for the Inhalation pathway environmental dose commitment
                                   3-12

-------
FHE =
np
RF
7-
.0
Jn(f)
dt"
I FCF
*B hthnp
PDP
                                                               (3.1.5-8)
     Our procedures for developing the algorithm to describe soil surface
concentration as a function of time must be explained.   Since these
high-level  waste computations are for long time periods and for Irrigated
soil, which would be frequently tilled, we have assumed that radionuclides
initially deposited on the ground surface are rapidly mixed into the plant
root zone,  which is assumed to be 15 cm deep.  Bennett (Be76) has
suggested that radioactive material resuspended into air generally comes
from the top 1 cm of soil so that soil surface concentrations (the
material subject to resuspension) should represent the inventory of
radioactive material within the top 1 cm of soil.  We have developed an
algorithm to predict the inventory of radionuclides within the 15 cm soil
root zone per unit surface area of soil, ^jn(t),* and have assumed that
one-fifteenth of this  inventory represents the radioactive material
subject  to resuspension  (the  ground surface concentration),  i.e., **n(t)
=  0r  (t)/15.  The  soil root zone  inventory per unit  surface  area of
soil, as a function of time,  **in(t),  is calculated by solving the
differential equation
                                    w
                                                                (3.1.5-9)
     *  For simplicity,
inventory.
                                will  be  referred  to  as  the root zone
                                    3-13

-------
where 0'jn(t) 1s the rate of change with time of the soil  root zone
inventory for radionuclide n; x.  1s the removal constant  from the  soil
root zone to the soil  sink; and the other terms have been  previously
defined.
The term -(*Dn * xs )
                                  represents the rate of removal  of
radionuclide n from the root zone, and the term (W/R)  Q1   (t) represents
the rate of deposition of radionuclide n to the root zone by irrigation.
     The basic assumption in the expression 0'jn{t) is that removal of
radionuclides from the ground surface by resuspension, An $•< {t)/15, is
offset by deposition to the ground surface of the resuspended material,
XRn(t) v  .  Thus these terms do not appear in equation 3.1.5-9.  This
assumption should be adequate for a large distributed source.  Substituting
fR/A for W/R as before, we can solve the differential equation 3.1.5-9 to
obtain the expression for the soil root zone Inventory, which is
                 exp
                                  ' (xDnnSn)t]
                                   - (xDnnLn)t]
                                                 for t > t
and
*In(t) = o
where, again: tRn = t
                                                          Rn
                                                          (3.1.5-10)
er
                      pan
                                  flrn>
As discussed in Section 2.1, this equation Is based on a leach-rate
limited release model, which is only one of several release models
considered by EPA.  The method used to address resuspension is based on
                                   3-14

-------
Nelson's (Ne78) assumptions;  however,  resuspension is addressed in a
direct manner rather than using Nelson's method.   The results of both
methods should be identical.   Substituting equation 3.1.5-10 into
equation 3.1.5-8 {recognizing that tf (t) = s$In(t)/15) and integrating,
the resulting equation can be used to calculate the ERC to the local
population due to inhalation of resuspended material from the ground
surface.  If one factors out the integrated source term to the accessible
environment, Q  , expressed in equation 2.1-4, the resulting equation
for ERC per unit release to the river for inhalation of resuspended
material becomes
FHE
   np
 cnp
and
RF
15
                 FCF
                    np  R
(x
                              Dn
-e
                                          for t > t
                                                   Rn
                                                       (3.1.5-11)
      np
                                          for * 1  *Rn .
                                                -1
 Note that the irrigation area cancels out of equation 3.1.5-11.

 3.1.6   External Risk Commitment  - Ground Contamination   (p=7)

     The derivation of  an expression for environmental risk commitment
 from external radiation for material deposited on the ground is  similar  to
 the derivation  for the  inhalation pathway.  As with the  inhalation  pathway,
                                    3-15

-------
1t 1s assumed that the deposited radlonuclldes ^are  rapidly  mixed  Into  the
15 cm root zone.  The equation 1s
     FHE   = [PD
        np      p
                 . A]f
                     J n
" .  [FCFnp .  GCnp .  SOF]    (3.1.6-1)
where FCF   1s the external  risk conversion factor for ground surface
                                                   2
contamination In fatal cancers committed per Ci-y/m  Integrated soil
surface concentration and SOF 1s a shielding factor that accounts for the
reduction In external dose due to household shielding and occupancy.
Since the external risk conversion factors are derived assuming that  all
radioactive material 1s deposited on the soil surface, the correction
factor {GC  ) 1s included in the algorithm to account for reduction 1n
the external risk commitment due to soil shielding.  The method of
derivation of this correction factor 1s discussed more fully in Appendix C
(Section C.5).  The other terms have been previously defined or appear in
the "Nomenclature" section.  Using equation 3.1.5-10, the Integrated root
zone Inventory 1s given by
        (t")dt"= xLnfLQonfR
                                               xDn   xSn
                                              - (xDnnLn)t]  "
                                               Dn
                                                             (3.1.6-2)
                                        for  t  > tRn  .
     Substituting the above equation Into  equation 3.1.6-1,  and
normalizing by the integrated source term  to the  accessible  environment,
using equation 2.1-4, one obtains the following expression for the  ERC  to
                                    3-16

-------
a local  population due to direct exposure from radionuclide n deposited in
the soil:
   np   fR PDP FCFnP SOF GCnp
    ^
and
     FHE
                              L(WX:
                                        for t > tRn
                                        for t < t
                                                 Rn
                                                                            -1
                                                          (3.1.6-3)
3.1.7  External Risk Commitment - Air Submersion  (p=8)
     The procedure for developing an equation to predict ERC from external
exposure due to air submersion follows a rationale very similar to that
for the ERC for external exposure due to ground contamination.  The
variation from the procedure described in Section 3.1.6 is that the
material subject to resuspension is in the top 1 cm of soil, a
resuspension factor (RF) is added to equation 3.1.6-1 to predict
integrated air concentration due to resuspension and the risk factor has
units of fatal cancers committed per Ci-y/m  integrated air
concentration , i.e.:
FHEnp = [RF PDp A]
            15
                              dt"
.   SOF] .
(3.1.7-1)
                                   3-17

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After substituting equation 3.1.6-2 for the Integral  In  equation 3.1.7-1
and normalizing by the Integrated source term,  one  obtains  the following
expression for the ERC to a local population due to direct  exposure from
radionucllde n in the air:
FHE
Vpp FCFnp SOF
*xLn"  xSn'
[e ""V,
^SnVW^n'13]
                                t6""0" R" -e ^ '
                                                                         -1
and
     FHE
      (np
           =  0
                                        for t > tRn
                            for t £ tRn.
                                                 (3.1.7-2)
3.2  Releases to an Ocean*

3.2.1  General Considerations

     This section describes the calculation of partial environmental risk
commitments as the result of exposure to high-level waste radionuclldes 1n
the ocean, specifically for the case of a leaching-rate-limited source
term where radionuclldes from a geological repository reach the ocean
through rivers.  The model employed for these ocean pathway calculations
is Illustrated in Fig. 3-1.  The model Includes two compartments.
    *The variables used in the equations in this section are defined in
 the "Nomenclature" section, p. N-l ff.
                                   3-18

-------
            Input from River
Radiological
Decay
Transfer to
lower level
                     
-------
Compartment 1 1s the  upper mixed  layer  of the ocean and compartment 2 1s
the lower layer (the  remainder) of  the  ocean.   Rad1onucl1de n enters the
upper layer from the  river and leaves this  layer  by transport to the lower
layer (TJ), by radioactive decay  (xDr))  and  by sedimentation (SFln),
Radlonuclide n Is returned to the upper layer by  back-transport from the
lower layer d2).  Radionucllde n enters the lower layer  by transport
from the upper layer (YJ) and by  sediment passing from the upper to
lower layer (SFln) and 1s removed by decay  (*n,J' by  Dack-transP°rt to
the upper layer (Y2)» a"d by sedimentation  (SF2n).

     Several basic assumptions are made 1n deriving  this  model. First,  the
Input to the ocean is taken to be of the form A^xpl^t), which is
assumed to  equal the input  into the river  (equation 2.1-2) from a
repository  with no reductions of input by decay during river travel,  by
Irrigation,  or  by sedimentation.  These are conservative assumptions and
were made  to allow releases directly to an ocean to be evaluated without
considering the effects  of  various  removal mechanisms in a river system.
 Second,  the two compartment model  is a  simplification since the actual
 transport  from the upper mixed layer to the lower layer  is diffusion
controlled.  In this model, we assume  that  both  layers are fully mixed.
 This will  lead to a  discontinuity  in concentration at the boundary between
 the two layers.  Third,  fish and shellfish ingestion  are considered to be
 the only non-negligible  routes of  radiation uptake and exposure to humans
 via the ocean pathway.   Fourth,  all edible fish  and  shellfish are assumed
 to be taken from the upper compartment.
                                    3-20

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     The steps involved in computing  the  environmental  risk  commitment
from each nuclide are outlined below:

     (a)  Calculate the quantity  of radionuclide  n  in the  upper  (mixed)
layer of the ocean, qln, as a function of time, and the concentration  in
ocean water as a function of time.

     (b)  Calculate the concentration of  radionuclide n in the edible  fish
and shellfish in the upper layer  as a function of time.

     (c)  Apply the appropriate ingestion rates by  the  population  for  fish
and shellfish to obtain the total  ingestion radionuclide intake  rate.

     (d)  Apply the appropriate ingestion fatal cancer  risk  factors  to
determine the risk commitment rate to the population  from  fish and
shellfish consumption.

     (e)  Integrate the population risk commitment  rate from time  of
arrival of radionuclides in the ocean to  the desired  time, t, to get the
environmental risk commitment.

3.2.2  Ocean Two-Compartment Model

     To calculate the concentration of radionuclide n in the upper
compartment, the quantity of n in the upper compartment, q-  » must be
predicted as a function of time and divided by the  volume, V,, of  the
                                   3-21

-------
upper compartment.  To obtain qln, we must write a system of two coupled
differential  equations based on the nucllde balance In each compartment as
depicted 1n Fig.  3.2.1-1.  These equations are
TT-  Aie
«2n - (x
                          Dn
                                                 qln
                                                       (3.2.2-1)
and
     = (SF
               ln
                             -(SF
                         2n
                                                       (3.2.2-2)
with the associated Initial  conditions  of
         • q2n=°  at  t=tRn-
     After transforming variables,  these coupled  differential equations
 may  be  solved by methods such as successive elimination to yield qln and
 q2n.  Since q2n, the radioactivity in the lower compartment,  is not
 used in the analysis for the ocean pathway, the analytical expression 1s
 not  presented.  Then
 "in

A2n
l%- V '
' (aln-V .V'-W ''in-V
«V "in' (un - M2n'
+ ,'n ln. . n 	 .. . e
                         •n   -'2nf  lwn " rlln
 where
                                                        (3.2.2-3)
       2n
ln
                    SF
                      ln
                                    3-22

-------
     2n
                  SF
                    2n
        = -{X
             Dn
B3n ' -
                  b2n>
      (aln-b2n)  '
      3n
     Mln - '  -  B3n  +VB3n  ' 4C3n
                                  SFln]
and
                          -  4C
                              3n   .
     Equation 3.2.2-3 can  be  used  to  predict  the  quantity  of  a
radionuclide, n,  which is  uniformly mixed within  the  upper compartment  of
the ocean at any  time, t,  after placement of  radionuclides in a  waste
repository.  If equation 3.2.2-3 is divided by  V,,  an equation to
express the average concentration  of  nuclide  n  in the upper compartment of
the ocean is obtained.
                              Ocean Fish (p=9)
                              Ocean Shellfish (p=10)
3.2.3  Seafood Ingestion

     The equation used to calculate  ERC  for  these pathways  is
           CF
             np
                      FCF
                         np
                                    ln
                                                         (3.2.3-1)
where q,  is described in equation 3.2.2-3.  Equation 3.2.3-1 is
integrated between the limits of tRn and t since no dose is incurred
prior to time t=tR .  After integration and normalization by the
                                   3-23

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Integrated source term (equation 2.1-4),  the following  expression for the
ERC to an exposed population due to consumption of seafood 1s obtained:
    FHE
       nP =
    ^np
FCFnP CFnp 'p PP
Vl

. 1
xDn <
- e
h *Ln
kDn+ W'^R
                                                             (COMn)
                                                               (3.2.3-2)
where
COM. =
                              (aln- M2n>
                                         "V
                                  - V
                              (M2n" MlnJ
                                                               (3.2.3-3)
3.3  Releases to the Land Surface*

3.3.1  General Considerations

     As discussed in Chapter 2, we assume that radioactive material 1s
placed 1n a repository at time t=0 and that the material is brought to the
surface of the earth at t=ti  by some event such as exploratory drilling
for resources.  The release to the surface of the earth 1s assumed to be
over a small area and over a short period of time so that the source to
the land surface can be modeled as an Instantaneous point source.  The
    *The variables used in the equations In this section are defined in
the "Nomenclature" section, p. N-l ff.
                                   3-24

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released material is assumed to be uniformly distributed,  vertically,
within the top 15 cm of soil rather than concentrated on the soil
surface.  The philosophy behind this assumption is based on an article by
Cline (C184) where it is shown that, in the absence of tillage, phenomenon
such as biological transport, contraction and expansion cycles, mass flow,
and diffusion can significantly .flatten expected vertical  radionuclide
profiles, for measurements taken 25 years following soil surface
contamination.  The choice of a 15 cm vertical  mixing depth is arbitrary
and probably conservative.  Cline's data indicate that enhanced mixing,
due to the phenomenon listed above, might occur to soil depths of  30 to
100 cm.  The 15 cm depth was chosen partly for the sake of conservatism
and partly for the convenience of remaining consistent with the soil
distribution assumptions chosen for the river release mode.  The
distribution of source material within the top 15 cm of soil is not nearly
as conservative as assuming all material remains indefinitely on the
earth's surface.

     Once the initial source deposition to the soil is determined,
calculations can be made to estimate the resuspension of radioactive
material at this source and to predict how this material disperses in the
environment.  As for the river release mode, it is assumed that
resuspension occurs for the radioactive material in the top 1 cm of soil.
The resuspended material results in exposure to the population due to
consumption of contaminated food crops, inhalation of the resuspended
material, and external exposure due to ground contamination and air
submersion.
                                   3-25

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                              Food crops  (p=13)
                              Milk (p=14)
                              Beef (p=15)
     For the land surface  release mode, predicting uptake of  radionuclides
into foods and the subsequent  ingestion of  radioactivity by human
receptors involves modelling resuspension from the ground source to  air,
air dispersion, and deposition to the land  surface.   When land surface
deposition has been determined, the  RInp  factors discussed  in section
3.1.4* can be applied to quantify  ingestion of radionuclides  by man. The
additional steps involved in determining  the environmental  risk commitment
for food ingestion are similar to  those discussed in section  3.1.4.
     In calculating air concentration as a function of distance and time,
we assume Nelson's (Ne 78) isotropic dispersion, which was based on
annual -average atmospheric dispersion factor data for ground-level
releases at  17 nuclear power reactor sites as presented in Appendix I to
10 CFR 50 (AEC73).  The equation is
     X.n(r,f)  .
Q'(t')   4-
                                     - z
(3.3.2-1)
 where
      X.Jr,t')  =  air concentration  at  point  r  and time t'
       in               q
                   (Ci/nT),
      (X/Q1)    =  atmospheric dispersion  factor at the known  point  rn
            r"     (sec/m3),
      *The derivation of these RInp factors is discussed in more detail
 in Appendix C, section C.I.
                                    3-26

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     Q'(t')    =  source term from ground to a I/ at time t1 (C1/yr)
       2       =  "fitting" exponent to adjust shape of X(r,t') curve to
                  agree with empirical  data, and
       t1      =  time after material 1n repository reaches ground
                  surface (yr).
     An equation that describes Q'(t')  in terms of the material initially
present at the ground surface is
Q'(t') = xR(Qnp/15) exp [ - (XR +
                  t'  ]
                                                               (3.3.3-2)
But this equation is not corrected for plume depletion during travel.  A
correction factor which makes a downward adjustment of the source term,
Q'(t'), to correct for plume depletion can be expressed as
where
                  c -
                   (2-z)
                         (2-2)
                              n J
                               (3.3.2-3)
                                                               (3.3.2-4)
Combining equations 3.3.2-2 and 3.3.2-3, we have
     Qn(t') = xD(Qnn/15) exp[-(x,nn +xcJt'3 exp[-
                       (2-2)
R
                                       Sn
                            ] ;(3.3.2-5)
and the equation for air concentration at a point r and at time t1  due to
dispersion of material resuspended from the point source is (substituting
QD(t') for Q'(t') in equation 3.3.2-1)
                                   3-27

-------
    Xin(r,t') .
               \   I  r  V   ill      I  ui    \.                   w|
                                                               (3.3.2-6)
    We next estimate  the deposition  to the ground surface  at  distances
away from the resuspension point by  multiplying  equation 3.3.2-6  by  the
dry deposition velocity.  An equation that expresses the total  deposition
to the ground surface over all  area  and to time  t' is obtained  from
equation 3.3.2-6 as follows:
    DEP(oo,t')=
X.n(r,t")v   dt" (rdedr)
                                                               (3.3.2-7)
                r=o  e=o
    Performing these integrations yields  an  expression  for  the total
deposition to the ground surface to  time  t1:
                              X(Q/15)  r                         1
                                          i  - exp[-(xRnD nSn)t']   .
                                         L            K   un   in
     DEP(oo.t')  = DEP(t')
                               x
                                Dn  Sn
                                                               (3.3.2-8)
     To  obtain  the  ERC  for any one of the food pathways, we use a method
 similar to that  described in section 3.1.4.  The equation is
     FHE
        np
              DEP(t')
                      fp RInp (CPP V FCFnp
                              (3.3.2-9)
 where Ar Is land area  on which  resuspended material  is deposited, and
 the other terms have been previously  defined  or  are  listed  1n the
 "Nomenclature" section.
     Upon cancelling the area terms,  substituting equation 3.3.2-8  for
 DEP(t'), normalizing by the quantity of radionuclides initially  released
                                    3-28

-------
to the ground surface, Qn_» and redefining t'=t-t, ,  equation 3.3.2-9
becomes
F% _ fp RInp CPp FCFnp XR I1"  e
            LSn
                                                             tL)l
     (np
                          1R   ADn
lSn
                                                               (3.3.2-10)
    We make the conservative assumption that all-farm land is used to
produce edible food crops; in fact, some would be used to raise non-food
crops.  Conversely, there will  be some food crops whose roots extend below
the assumed 15 cm soil  root zone such that they can take up radioactivity
from the soil  below this depth.  For these cases, our use of a x-  based
on a 15 cm soil root zone is not conservative.

3.3.3  Inhalation of Resuspended Material (p=12)

    The calculation of the ERC  due to inhalation of radioactive nuclides
for the land surface release mode must consider the initial resuspension
at the point source.  In addition, deposition to the ground surface and
resuspension from the ground surface away from the source must be
modeled.  For the reasons discussed in section 3.1.1, it is assumed that
radionuclides deposited to the  land surface after dispersion away from the
source are uniformly mixed within the 15 cm soil root zone and that
resuspension occurs for the radionuclides within the top 1 cm of soil.
These assumptions maintain consistency with the methods used for treating
source resuspension for the land surface release mode (see section 3.3.1)
                                   3-29

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and for treating resuspension from Irrigated land  for the river release
mode (see section 3.1.5).  These assumptions are more realistic than
assuming that all material remains on the ground surface indefinitely.   An
activity (mass) balance around a segment of ground away from the source
can be depicted as shown in Fig. 3-2.

    The  soil surface concentration as a function of time and location is
estimated so that a resuspension factor can be applied to obtain the air
concentration  as a function of time and location.
      Resuspension
 15 cm
 root zone    f
        Deposition
      (initial  plume)
          X1nvgn
I  I  I  I  I  I
            Deposition
       (resuspended material)
             *Rnvgn
i  i  /  i  i
77 Ground
          Radioactive
            decay
             Loss to soil subsurface
                    layers
    F1g. 3-2.  Activity (mass) balance for soil  element away from source
 A differential equation which addresses the activity balance depicted in
 Fig. 3-2 Is
            Xinvgn + XRnvgn
                                                (3.3.3-1)
                                     3-30

-------
where $  • 4Tn/15» *in ^s ^e a^r concentra't''01] of radionuclide n
due to resuspension from the initial  point source and subsequent  .
dispersion and XR  is the air concentration of radionuclide n due to
resuspension from the ground surface  at the location of interest.  The
other terms have been previously defined.   If the assumption is made that
there is no redistribution of radioactive  material  due to continual
deposition to and resuspension from the ground surface after equilibrium
is reached, we may equate the terms   XR v   an^ An0jn/15 in
equation 3.3.3-1 and write
          = Xin vgn ' (xDn
                               (3.3.3-2)
    An expression for X.  was discussed in Section 3.3,2
(equation 3.3.2-6).  If this expression for X^  is applied in
equation 3.3.3-2 and the integration factor exP(xnn+xsn^t' 1S used»
the equation is solved to yield an expression for the total  soil  root
zone inventory as a function of distance and time:
•z  -(r/rd)
  e
                                           (2-z)
                                                               -e
                                                               (3.3.3-3)
Assuming, as discussed in Section 3.1.5, that the air concentration due to
resuspension can be calculated by applying a resuspension factor to the
soil surface concentration (0 ,  which is fJjn/15), we have
        = RF
                               (3.3.3-4)
                                   3-31

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Then the total  air concentration at a particular location and time 1s
    Xn(r,t')=X1n(r,t'MXRn(r,f)
                                            (3.3.3-5)
and using equations 3.3.2-6,  3.3.3-3,  and 3.3.3-4 we have
                                       (2-z)
               -z  [-(p/rd)
                                '"' [«•
                                                       0622 + 0.0044 e
                                                                      ARf
where
xTn = XR
                                               (3.3.3-6)
     Equation 3.3.3-6 yields an expression for air concentration to use 1n
 computing the ERC due to Inhalation of resuspended material.   The
 relationship to apply for calculating ERC Is
     FHE
        np
/*'   /
                 Xn(r,t")  IB  FCFnp  PDp  dAr  dt"  .    (3.3.3-7)
     This equation 1s  similar to the one derived for the Inhalation pathway
 1n Section 3.1.5.  Using  the expression for Xn(r,t') from equation
 3.3.3-6, the relationship dAr=rdedr, performing the area integration
 from r=0 to r=ooand  e*0  to 6=2*  (integrating over all area where people
 are exposed), and normalizing  the  result by the quantity of radlonuclldes
 released to the ground surface,  Qnp, we have
     FHE
      'np
        St. (PDp)(RF)(IB)(FCFnp)
                      0.0622
                           [l - e-^Tn*']
                                   +   °-0044    r,  _
                                      i   +  i    i
                                 ^    ADn   ASn  L
                                                                (3.3.3-8)
                                    3-32

-------
    Redefining t1 as t-t, the equation for ERC can be written
FHE
 'np
                                 0.0622
                                           l-e
                                                        t, h
                                                         L]
                                 ,0,0044
                                   xDn   xSn
                                                  - e-(xDn +  'SnXt'V]

                                                              (3.3.3-9)
3.3.4  External  Risk Commitment-Ground Contamination (p=16)
    The equation  to apply  in calculating ERC is
               t'     r A
    FHE
       np
                               ,t") FCF   SOF GC   PD  dA dt".  (3.3.4-1)
    Using the expression  for ^tn^»t') developed in Section 3.3.3
(equation 3.3.3-3),  the relationship dA =rdedr with the integration
limits 0
-------
3.3.5  External  Risk Commitment-Air Submersion  (p=ll)
    The equation for calculating ERC  is
                 t1   r A
    FHE
       np
J      f    Xn(r,t") FCF   SOF PD  dA dt"  .       (3.3.5-1)
              o     o
    Using the.expression for X (r,t*) developed in Section 3.3.3
(equation 3.-3.3-6), the relationship dA=rdedr with the integration limits
0
-------
Interactions are violent,  we  assume  that the material  released  Into  air
would be distributed uniformly  throughout  the  troposphere.   Radionuclldes
released to air will affect people  differently depending  on  whether  the
nuclides are in the inhalation  zone  over land  or  in  the air  over  the ocean
and on whether they deposit on  land  or in  the  ocean.   We  account  for this
by splitting the inventory released  to the air into  two parts:  that over
oceans and that over land, using the respective^surface areas of  the
oceans and the land surface of  the  earth.   This division  of  the airborne
material is for calculational convenience  in  developing the  mathematical
equations for the environmental dose commitment analyses.  Each curie of
radionuclide which is released  is divided  between that quantity released
directly to the land surface  (f|_L)»  that released to air  above land
(fAL), and that released to air above oceans  (fAW)«   We assume that
airborne material above land remains over  land and that airborne  material
above water remains over water.

3.4.2  Releases Directly to Land Surface

3.4.2.1  General Considerations

     The  radionuclides released directly to the land surface  are
conservatively  assumed to be distributed  in a  small area around the
release  point.  The methods  used to  determine  vertical distribution  and
resuspension  at the source,  dispersion in the  environment,  and resulting
ERC  to  the  affected population are  the same as those  devised for the land
                                    3-35

-------
surface pathway (Section 3.3).   The equations used for releases directly
to the land surface will be listed, for the sake of completeness, in the
following sections.
3.4.2.2  Food Ingestion
                             Food Crops (p=25)
                             Milk (p=26)
                             Beef (p=27)
FHE.
                                        - >Tn(t-tv)
      • '
                           LL
                                                               (3.4.2,2-1)
where f.,  is the fraction of the radionuclides released to the
environment which go directly to land and ty is the time after placement
of radioactive material in the repository that material is released to the
environment.
3.4.2.3  Inhalation of Resuspended Material (p=24)
                                      0.0622
     np
          =PDp  RF  IB
                                LL
                                                1 - e
                                                      ^Tn(t-ty)
                                        xDn   xSn
                                                               + XSn)(t-tv)]
                                                               (3.4.2.3-1)
3.4.2.4  External Risk Commitment-Ground Contamination (p=28)
  FHE.
np   PDp FCFnp SQF fll GCnp
    1 —•     15
                                        ' {x
                                   .
                                   1 - e
                                            Dn
                                            xDn * xSn
                                                                            ,
                                                                           -1
                                                                (3.4.2.4-1)
                                   3-36

-------
3.4,2.5  External  Risk  Commitment-Air  Submersion  (p=23)
  FHE.
   (np
        = SOF  FCF   PD   RF  f
                              LL
0.0622
 *Tn
[l-
                                       Dn     Sn
                                                    -  e
                                                          (3.4.2.5-1)
3.4.3  Releases to Air-Over-Land

3.4.3.1  General Considerations

    The radionuclides released to the air over land surfaces are assumed
to be distributed uniformly In a volume determined by multiplying the
land surface area of the earth by the average height of the troposphere.
With the material distributed in this manner a two compartment model  is
established, as depicted in Fig. 3-3, to predict radionuclide movement
between the air and the soil for use in computing the ERC for the various
pathways.  The upper compartment in Fig. 3-3 is the tropospheric volume
above the earth's land surface and the lower compartment is the available
land layer, i.e., the layer of land containing the soil surface as an
upper boundary and including the root zone or plow layer of soil.  It is
assumed that radionuclides enter the upper compartment at the instant a
volcano or meteorite Interaction releases radioactivity from the
repository.  No further radionuclides are introduced into the system
after the initial input at t'= 0.

    Radionuclides leave the upper compartment by radioactive decay (*Qn)
and by transfer  from air to soil  (vgn.AL/V,_) and they reenter the
                                     3-37

-------
                         Initial  Input
                         To Air
                                 (Initial  Condition)
Radioactive
Decay
Radioactive
Decay
                         Trope-spheric
                         Air Over Land

                         (Volume VL)
                              1) » quantity of material
                                   in upper compartment, Ci
                    Transfer to soil
resuspenslon
to air
                              Available Land Layer
                                    ) = quantity of material
                                        in lower compartment, Ci
                       nn
                    Removal from
                    available soil
              F1g. 3-3.  Compartment model for air over land,
                         volcano/meteorite release mode
                                   3-38

-------
upper compartment due to resuspension  (XR).   The  assumptions controlling
our resuspension calculations are  the  same  as discussed  In  sections  3.1
and 3.3.  When radionuclides are deposited  to the ground surface, we
assume that they quickly mix in the  soil  root zone (15 cm vertical depth)
and that only the radionuclides in the top  1  cm of soil  are subject  to
resuspension.  Radionuclides enter the lower  compartment by deposition
from air (Van-Ai/V| ) and are removed from the lower compartment  by
transfer to the unavailable soil layer USn), radioactive decay  (xDn).
and resuspension from the top 1 cm of  soil  layer  to air  (XR).  The.
radionuclide balance equations which can  be written for  this two
compartment system are discussed in  the next  section.

3.4.3.2  Air-Above-Land:  Two Compartment Model
     To obtain the concentration of radionuclide n in the upper (air)
compartment, the quantity of n in the upper compartment,  Pin^')*  must
be predicted as a function of time and divided by the volume,  V^,  of the
upper air compartment.  Similarly, to obtain the soil root zone inventory
of radionuclide n for the lower compartment, ^Tn^'^* tne 1uant'i'ty of n
in the lower compartment, Qcr/t'K must &e predicted as a function of
time and divided by the surface area, A. , for the lower compartment.  To
obtain Qin(t') and Qcn(t')» a system of two coupled differential
equations, based on the nuclide balance shown in Fig. 3-3, is written and
solved.  These equations are:
        'Ln
       dt
lDn vLn
«Sn'15
(3.4.3.2-1)
                                   3-39

-------
and
      dQ-    vnn A.
                                                              (3.4.3.2-2)
and the Initial  conditions  for  our model are
and
            = fAL 'np
            = 0
              at t1 = 0  .
After a transformation of variables,  these coupled differential equations

may be solved to yield QLn and QSn  as follows:


    ^^-'-^'   +<>-»"M6nt     ^.4.3.2-3)
15 f
    AL
where
           I5n
U6n =  '

B4n -  - (a
                                   - a5n)
                                XR/15)
           •4n
                     5n
          I5n
                              vinxR
          M5n=  -!*L
                                 4C
                         4n
M
           6n
                               -  4C
                                    4n
i        6n   1
    -e      J
                                                               (3.4.3.2-4)
                                   3-40

-------
Now, using equations  3.4.3.2-3  and  3.4.3.2-4, the air and  ground
concentrations of  radionuclides as  a  function of time can  be calculated.

     To compute the air concentration in  the upper compartment  as  a
function of time,  equation  3.4.3.2-3  is divided by the  volume of the upper
compartment, which is V.  =  A. .h., to  yield
          AL .  Qn
         _
         V
                                       e °n   +   e
                                                               (3.4.3.2-5)
     The soil  root zone inventory for the  lower compartment as a  function
of time is obtained by dividing equation 3.4.3.2-4  by  the surface area,
A,, of the lower compartment to yield
              .   np   5n    5n    6n   5n
              ^R(M6n - M5n'  AL
i        6n   1
    -e      J
                                                               (3.4.3.2-6)
   '  The equations generated above are used for the ERC pathway models
discussed below.
3.4.3.3.   Food Ingestion
                              Food crops (p=19)
                              Milk (p=20)
                              Beef (p=21)
     Methods similar to those discussed in sections 3.1 and 3.3 are
employed in calculating the ERC due to food ingestlon.  The derivation of
the values for RI   for food crops is discussed in detail in Appendix
C.  The deposition to the ground surface due to the radioactive material
originally distributed in the air above the land surface (neglecting
                                   3-41

-------
resuspension)  1s  calculated and  applied 1n conjunction with the values of
RI  .   Since the  RI   values were  determined without considering
resuspension,  we  must  compute the  radfonucllde flux to ground as a
function of time  for the radionuclides originally dispersed into the air
at t'=0.  Referring to Fig. 3-3, the  flux of nuclide n to ground as a
function of time, F1 (t1),  can be  calculated as
     rn(t')-
gn
                                    (3.4.3.3-1)
where, for these three pathways,  QLn(t')  is  determined  using
equation 3.4.3.2-3 with XR set equal  to 0.   Setting  xR=0 will yield
QLn(t') based only on material originally dispersed  in  the  air and
neglects resuspension altogether.  To obtain Fn(t'),  the quantity of
radlonuclide n deposited per unit area from  the time  material was
originally dispersed into the air (t'=0)  to  time  t1,  we integrate as
follows:
         /•            t>
          F"(t")dt"=/
                    "en*"             '
            .- a,J e bn  +(ar - MCJ e
          I6n  U5n
I5n  "5n
After Integrating, the result is
        f.i  • Q   • v
F ftM- ,AL    "P.   9"
 n      tM- MJ '
    I5n
                                                        '6n
                                                               (3.4.3.3-2)
                                       "
                                        6"
                                                               (3.4.3.3-3)
                                     3-42

-------
which has units of Ci deposited per m .  The ERC for these pathways is
derived in a manner similar to the methods applied 1n Section 3.1.4 and may be
computed using the following equation:
                     fp  RInp  FCFnp CPp  AL
                                                           (3.4.3.3-4)
After substituting equation 3.4.3.3-3 for F"n{t'), normalizing by the
original total release, Q  , substituting V,=A. .h., and making the
substitution t'=t-ty, we have
FHEnp_ fAL "gn FCFnp RInp fp CPp
"V          ^
                                     (M6n-a5n
                                 TWW "5n

                                 :a5n- V
                                   ^/CI    %/lI
                                 I  (M- - Mr )
                                  on  on   5n
 )    r M, (t-t )   i
***    1  **C**V»w.»i   I
n     i   *^n    w    i
"      p 3tl    v   11
^RTjlc      .     l\
                                                               (3.4.3.3-5)
or, defining COML  as:
COML  =
          (Mc -a- )
            6n  5n
n   M5n(M6n-'
                                         M6n6n-5n
FHE.
          AL
             FCFnp RInp fp CPp COMLn
  'np

                  (3.4.3.3-6)

                  (3.4.3.3-7)
     We make the conservative assumption that all farm land is used to
produce edible food crops; in fact, some would be used to raise non-food
crops.  Conversely, there will be some food crops whose roots extend below
the assumed 15 cm root zone such that they can take up radioactivity from
the soil below this depth.  For these cases, our use of a xSn based on a
15 cm soil root zone is not conservative.
                                   3-43

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3.4.3.4  Inhalation of Dispersed and Resuspended Material  (p=17)
     In considering the ERC due to Inhalation of dispersed and resuspended
material an equation similar to the one derived In Section 3,1.5 was used,
which is
FHE.
np
     t1
=[/  Vf
                               >BFCFnpPDpAL
                                                       (3.4.3.4-1)
      Since the equation for Xn(t') has already been described in
 equation  3.4.3.2-5,  it can be substituted into equation 3.4.3.4-1.  After
 performing the  indicated  integration, normalizing by the  release of
 radionuclide n  at  t'=0 and replacing t1  by t-ty, we have
                           PD
                                                    (3.4.3;4-2)

 3.4.3.5  External  Risk Commitment-Ground Contamination  (p=22j

      The equation to use in deriving an expression for the ERC for
 contaminated ground is
                   t1
      FHE
         np
            'in'*"1  dt"]  FCFnp PDp  AL SOF   GCnP  .
       Equation  3.4.3.2-6 is used to express *In(t').  After the equation for
  FHE    1s  Integrated and normalized by the Initial release from the
    np       9
  repository,  Q   .  and  t1 is redefined as t-ty, the ERC equation becomes
                                       3-44

-------
FHE
                                                  [e
                                                                      -1]
                                                               (3.4.3.5-2)
3.4.3.6  External  Risk Commitment-Air Submersion (p=18)
     For air submersion external risk commitments,  the ERC equation is
written as
     FHE
        'np
              x ft") dt"
FCFnp PDp AL SOF
(3,4.3.6-1)
     Equation 3.4.3.2-5 can be substituted for X (t1).  After the
equation for FHE   is integrated and normalized by the initial release
from the repository, Q  , and t1 is redefined as t-ty, the ERC
equation becomes
FHEnp   fAL FCFnp PDp SOF  COMLn
                  F£
                                                               (3.4.3.6-2)
 3.4.4   Releases to Air-Over-Oceans

 3.4.4.1  General Considerations

     The radionuclides  released to the air over the oceans are assumed to
 be  distributed uniformly  in  a  volume determined by multiplying the earth's
 ocean  area  by the average height  of the troposphere.  With the material
 distributed in this  manner a three compartment model  is established, as
                                    3-45

-------
shown in Fig.  3-4,  to describe radionuclide movement between the air and
the two ocean  compartments.   Using  this model, concentrations  of
radionuclldes  can be determined as  a  function of time  in the air and in
each of the two ocean compartments.  These concentrations  can  be used  in
estimating the ERC  for the pathways considered in this section.

     The upper compartment (Compartment  1) in Fig.  3-4 is  the  tropospheric
volume above the earth's oceans.  The middle compartment  (Compartment  2)
is the top compartment of the ocean and  the lower compartment  (Compartment
3) is the bottom compartment of the ocean.
     We assume that radionuclides enter the air (Compartment 1)  at the
instant a volcano or meteorite interaction releases radioactivity from the
repository and that no additional radioactivity is injected into the
system after that.  Radionuclides leave the air compartment by radioactive
decay (XD ) and by deposition into the ocean (v  Ay/V^).  Radionuclides
enter Compartment 2 by deposition from the air (Vg^/V^) and by transfer
from Compartment 3 (TO)-  Radionuclides leave Compartment 2 by radioactive
decay (XD ) and by diffusion transfer (YJ) and sedimentation transfer
(SF, ) to Compartment 3.  Radionuclides enter Compartment 3 by diffusion
transfer  (YI) and sedimentation transfer (SFln) from the upper ocean
compartment and leave this compartment by radioactive decay (*n,n).
sedimentation to the ocean floor  (SF2n), and transfer to the upper ocean
compartment  (Y2K  The differential equations which can be solved for
radionuclide  inventory in this three compartment system are discussed in
the next  section.
                                    3-46

-------
                             Initial  Input
                             to Air
                                      (Initial  Conditions)
Radioactive
Decay
                        quantity of radionuclides
                        in Compartment 1 (Ci)
                             Transfer to Ocean
Radioactive
Decay
                                             Compartment 1
                                             Air

                                             Volume =
                                                      Surface Area
                                            Compartment 2
                                             Ocean
                                             (Upper compartment)
                                             Volume = \
   Qln(t') = quantity of radionuclide
             in Compartment 2 {Ci)

Transfer to
Lower Layer
                                                      Sedimentation
                                                      from upper layer
                                                      SFln.Qln(t'>
                    Transfer to upper
                    layer
                                                      Compartment  3
                                                      Ocean
                                                      (Lower  compartment)
                                                      Volume  =  \
Radioactive Decay
                        = quantity of radionuclides
                          In Compartment 3 (Ci)
                                        ,
                   Sedimentation  from lower  layer
                Fig.  3-4.   Compartment  model  for  air-over-ocean,
                           volcano/meteorite  release mode
                                     3-47

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3.4.4.2  Air-Above-Water:   Three Compartment  Model

     The ERC pathways considered for air-over-oceans are consumption of
ocean fish and shellfish.   Since the assumption is made that all  edible
fish and shellfish are harvested in the upper ocean layer, it will  be
necessary to obtain the quantity of each nuclide, Qln(t'K In the middle
compartment (upper ocean layer).  This quantity can be divided by the
volume of the middle compartment, Vj, to yield the concentration in the
zone where edible fish and shellfish are produced.  The differential
equations which describe the transfer of radionuclldes between
compartments  In Fig. 3-4 and which  are used  to obtain the quantities of
radionuclides In the three compartments are
                  LDn
                         v   A
                          wn  Wx
                         ~~
                                    (3.4.4.2-1)
       dt
 and
ln
                                       SF
                                         2n
                                    (3.4.4.2-3)
 The initial conditions for this model are
      QAn = fAW V
 and
                             at t1 = 0
  The  procedure used to solve these differential equations Is to integrate
  equation 3.4.4.2-1 directly and then use the resulting equation for QAn '
                                     3-48

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the solution of  equations 3.4.4.2-2 and 3.4.4.2-3,  which are coupled
differential equations.  The resulting equations for QAn and Qln are
            2n
Qln(t>)z (M, -M,J
           2n "In
                                                              (3.4.4.2-4)

'vV'v'V
         (3.4.4.2-5)
where
            v   f    n
             wn  AW  vnp
      '2n
and aln, b2n, B3n,  C3n,  Mln  and M2f) are as defined in Section
3.2.2.  Qonft') is  not needed  in  this analysis, .so the equation for
Q2 (t1) is not presented.

     The concentration of  radionuclides in the upper compartment of the
ocean as a function of time  can be computed by dividing equation 3.4.4.2-5
by V,, the volume of the upper ocean compartment, which yields
V   ft')-
xln(t >-
                      (a
                        ln
                                                              (3.4.4.2-6)
                                      3-49

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3.4.4.3  Seafood Ingestion    Ocean Fish (p=29)
                              Ocean Shellfish fp=30)
     The equation used to calculate ERC for these pathways is:
                                   f
^^M

                                f
                                          (3.4.4.3-1)
where Q^n is described by equation 3.4.4.2-5.  After performing the
integration, normalizing by the total  release, Q  ,  and making the
substitution t'=t-t , we have
FHEnp _ CFnp
 %P
where
                     Pp FCFnp vwn fAW
                    hAVl
                  COMO.
(3.4.4.3-2)
     COMO =
         n
     (aln-M2n)[ e
                                                -1]
                                ("sn-Mln)Mln
                                      M(t-tJ
                              (usn-M2n)twsn-Mln)usn
                                          (3.4.4.3-3)
3.5  Special Calculations for C-14 Environmental Risk Commitment

     The pathway models described in Sections 3.1 through 3.4 are used for
all pathway ERC calculations for all nuclides except carbon-14.  Unlike
the other radionuclides considered in these analyses, stable carbon
constitutes a significant fraction of the elemental composition of the
human body and man's diet.  Transport processes through the different
                                   3-50

-------
environmental  pathways and within plants,  animals,  and man,  that  apply  to
trace quantities of radionuclides do not necessarily  apply to
radionuclides, such as C-14,  where the corresponding  stable  elements are
present in such quantities that saturation effects  are significant
(Mo79).  Atmospheric releases of C-14 as carbon dioxide can  be evaluated
using a diffusion-type model  of the carbon cycle developed by  Killough
(Ki77).  It seems clear that  this model is the correct calculational
procedure to use for releases for the volcano/meteorite release mode where
it is assumed that high-temperatures would cause carbon releases  to be
oxidized to carbon dioxide.  To our knowledge, models are not  available to
explicitly treat the ERC calculations for C-14 released to water, land
surfaces, or air in a chemical form other than carbon dioxide. We
performed some preliminary calculations using various plausible models  and
assumptions.  Our literature review indicated that the chemical form of
C-14 released in the water and land surface release modes was  not well
known.  Also, the rate of oxidation to carbon dioxide of other chemical
forms of C-14 over the extensive integration period is not known  for these
release modes.  Considering all these uncertainties,  we concluded that the
most prudent course was to use the Killough carbon dioxide model  for all
four release modes, realizing that this probably leads to conservative
estimates of the ERC for the water and land release modes.

     The environmental risk commitment for C-14 is obtained by calculating
the total body environmental  dose commitment  (EDC) and multiplying  by a
fatal cancer risk conversion factor.   Values of the total bocty environmental
dose commitment per curie of C-14 released to the atmosphere  have been
                                    3-51

-------
calculated by Fowler (Fo79) using the K11lough model  (K177).   It Is
estimated that the Ingestlon pathway contributes  99  percent of the carbon-14
environmental dose commitment (Fo76); however, we assume that the Ingestlon
pathways contribute 100 percent for purposes of computational convenience.
For estimating the environmental dose commitment, a  cubic spline was fit to
Fowler's curve of worldwide EDC to the total bocjy per curie release versus
time after release.  This cubic spline procedure  yields the following
equations for worldwide total body EDC vs time after C-14 placement 1n a
repository:
for  10
-------
for 10,000_ 100,000 yr:

DTB14 = 537.0
                                                               (3.5-10)
                                                  (3.5-11)
     The environmental risk commitment is obtained by multiplying the

total bocty environmental dose commitment, as obtained from equations 3.5-5

through 3.5-11, by the fatal cancer risk factor of 1.46E-4 fatal cancers

per total bocty man-rem* as given by Fowler (Fo79).  The equation is
     FHE
        np  =  CARCAN  •
                                                  (3.5-12)
      'np
This equation expresses the total environmental risk commitment for all

pathways within a release mode and is not applied separately for each

pathway.  Equation 3.5-12 can be multiplied by fLL, fAL, and fAW to

estimate the C-14 ERC for the volcano/meteorite release mode for releases

directly to land, releases to air over land, and releases to air over

water.
     *This C-14 fatal cancer risk factor is less than would be used for
most other radionuclides because a significant percentage of the total
body dose from C-14  is to adipose tissue and is not effective in producing
cancer  (Fo79).
                                   3-53

-------
     The C-14 dosimetry and risk Information upon which our analysis is
based (Fo79), estimates C-14-fatal  cancer risks using total body
environmental dose-equivalent  commitment and a fatal  cancer risk per unit
total body dose-equivalent conversion factor.  If we  were to revise
Fowler's analysis, we would use our latest RADRJSK data (not available
when Fowler performed his analysis) and compute an effective-environmental
dose-equivalent commitment and apply a fatal cancer risk per unit
effective dose-equivalent conversion factor.  We estimate that if our
newer data had been applied, the fatal cancer risk per curie of C-14
released to the accessible environment would have increased by a factor of
approximately 1.5.  However, due to the rounding of the calculated
radionuclide release limits in preparing Table 1 of 40 CFR 191 (EPA85c),
the Table 1, C-14 release limit would not change.
                                    3-54

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Chapter 4:  METHODS FOR DERIVATION OF FATAL CANCER RISK CONVERSION FACTORS*

     Fatal  cancer risk conversion factors  are  applied  in  each  of  the
pathway equations discussed in Chapter 3.   In  some  cases,  risk conversion
factors for daughter products are added to those  for the  parent** as  an
approximate method to account for ingrowth of  daughter products during
environmental-transport.  The methods used to  obtain the  risk  conversion
factors and to account for daughter ingrowth during environmental
transport are discussed in this section.

4.1  Fatal Cancers Risk Conversion Factors
     For each of the 30 pathways, either internal  doses occur due to
inhalation or ingestion of radionuclides or external doses are delivered
due to ground contamination or air submersion and fatal cancer risk
conversion factors are needed to use with the equations developed in
Chapter 3.  The computer code used by EPA to calculate dose and risk
conversion factors is RADRISK (Du84, Su81, Du80).  RADRISK calculates the
radiation dose and risk resulting from an annual unit intake of a given
radionuclide or the risk resulting from external exposure to a unit
concentration of radionuclide in air or on the ground surface.  Since both
dose and risk models are linear, the unit dose and risk results can then
be  scaled to reflect the exposure associated with a specific source.
      *The variables  used in  this chapter are defined in the  "Nomenclature"
 section,  p.  N-l  ff.
      **In these  instances, the sum of  the  risk factors is  reported  for the
 parent.
                                    4-1

-------
     Internal exposures occur when radioact1ve.mater1al  1s Inhaled or
Ingested.  The RADRISK code Implements contemporary  dosimetric  models to
estimate the dose rates at various times to specified reference organs in
the body from inhaled or ingested radionuclides.   The dosimetric methods
in RADRISK are adapted from those of the INREM II  code (Ki78b), based
primarily on models recommended by the International  Commission on
Radiological Protection (ICRP79) and the National  Radiation Protection
Board (Ad78).  In some instances, input parameter  values have been
adjusted to be more representative of the U.S. population as a  whole
rather than an occupationally exposed group (Su81).   The principal
qualitative difference is that RADRISK computes dose rates to specified
organs separately for high and low linear energy transfer (LET)
radiations, whereas INREM II calculated the committed dose equivalent to
specified organs.

     Dose rates to organs of an Individual Immersed in contaminated air or
standing on a contaminated ground surface are computed by the DOSFACTER
computer code of Kocher (KoSlc).  These calculations assume that the
radionuclide concentration 1s uniform throughout an infinite volume of air
or area of ground surface, and that the exposed individual is standing on
the ground surface.  Since only photons penetrate  the bo
-------
3 (NAS80).  The dose response functions  applied in  this  report  are  linear
for both low and high-LET risk estimates*.   To  project the  number of
fatalities due to leukemia and bone  cancer  the  Agency uses  an absolute
risk model, a minimum induction period of two years, and a  25 year
expression period.  To estimate the  number  of fatalities due to other
cancers, the Agency uses the arithmetic  average of  absolute and relative
risk projection models.  For these cancers, we  assume a  10-year minimum
induction period and lifetime expression of radiation  induced cancer.  For
high-LET risk estimates, we consider the risk from  high-LET (alpha
particle) radiation to be eight times that  for low-LET  radiation to the
same tissue except for bone cancer,  where the high-LET  risk coefficient is
twenty times the low-LET value.  A fuller discussion is  included in
Appendix G, Section G.3.

     An important feature of our methodology is the use of actuarial  life
tables to account for the time dependence of the radiation insult and to
allow for competing risks of death in the estimation of risk due to
radiation exposure.  A life table consists of data describing age-specific
mortality rates  from all causes of death for a given population.  This
information is  derived from data obtained on actual mortality rates  in a
real population; mortality data for the  U.S. population during the years
1969-1971 are  used throughout this study.
      *We  have applied the BEIR-III  (NAS80) linear dose response function
 in  computing the  risk factors listed in Table 4-2 and in computing the
 fatal  cancers per curie release to  the accessible environment listed in
 Chapter 6.   However, in Appendix G, we have included discussions of both
 the BEIR-III linear and the  linear  quadratic dose response functions for
 cancer induction  from low-LET radiation.  This  has been done to show a
 comparison  between the results obtained using the two models.
                                    4-3

-------
     The use of life tables 1n studies of risk.due  to  low-level  radiation
exposure 1s Important because of the time delay  Inherent 1n radiation
risk.  After a radiation dose 1s received, there Is a  minimum induction
period (latency period) of several  years before  a cancer is clinically
observed.  Following the latency period, the probability of occurrence of
a cancer during a given ye-ar 1s assumed to be constant for a specified
period, called a plateau period.  The length of  both the latency and
plateau periods depends upon the type of cancer.

     During or after radiation exposure, a potential cancer victim may
experience years of life In which he or she Is continually exposed to risk
of death from causes other than incremental radiation  exposure.   Hence,
some individuals will be lost from the population due  to competing causes
of death, and are not victims of Incremental radiation-induced cancer.

     We assume that each member of the hypothetical cohort 1s exposed to a
specified activity of a given radionucllde.  In  the analysis, each member
of the cohort annually Inhales or Ingests 1 pC1  of  the nucllde,  or 1s
exposed to a constant external concentration of  1 pCi/cc 1n air or
        2
1 pCi/cm  on ground surfaces.  Since the models  used in RADRISK are
linear, these results may be scaled to evaluate  other  exposure
conditions.  The cohort consists of an initial population of 100,000
persons, all of whom are simultaneously liveborn.  In  the scenario
employed, the radiation exposure 1s assumed to begin at birth and continue
throughout the entire lifetime of each Individual.
                                    4-4

-------
     No member of the cohort  lives  more  than  110 years.  The  span  from 0
to 110 years 1s divided Into  nine age  Intervals, and  dose  rates  to
specified organs at the midpoints of the age  Intervals  are used  as
estimates of the annual dose  during the  age  interval.   For a  given organ,
the Incremental probability of death due to  radiation-induced cancer is
estimated for each year using radiation  risk  factors  and the  estimated
doses during that year and relevant preceding years.  The  incremental
probabilities of death are used in  conjunction  with the actuarial  life
tables to estimate the incremental  number of radiation-induced deaths each
year for each organ.  The number of incremental  deaths  for the cohort for
each organ is obtained by summing the  deaths each  year  over 110 years.
The total number of incremental deaths for the  cohort is then obtained by
summing the total deaths for each organ over all  organs.

     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, and
the decrease  in the population's life expectancy.   An example summary
table of output from the RADRISK computer code, for inhalation of Ra-226,
Is shown in Table 4-1.

     Risk estimates for chronic  irradiation of the cohort may also be
applied to a  stationary population  having the same age-specific mortality
rates as the  1970 U.S. population.  That is, since the stationary
population  is formed by superposition of all age  groups in the. cohort,
                                    4-5

-------
TABLE 4-1:
Summary table from RADRISK computer code for Ra-226 Inhalation
                             TOTAL COHORT (l.OE+5 PERSONS)  CANCER FATALITIES FROM LIFETIME RA-226
                                           AMAD = 1.00, RESP CLEARANCE CLASS =U, Fl = 0.200E+00
                                                           FOR 1.0 PCI/YR INTAKE
                                                                                        INHALATION
                                                                                                                            [12-28-83]


CANCER

LEUKEMIA

BONE

THYROID

BREAST

LUNG

STOMACH

BOWEL

LIVER

PANCREAS

URINARY

OTHER

ADULT
LATENCY
PERIOD
(YEARS)
2

5

2

15

10

15

15

15

15

15

15

ADULT
PLATEAU
PERIOD
(YEARS)
25

30

45

110

110

110

110

no

110

110

no



RISK

ABS

ABS

ABS

ABS

ABS

ABS

ABS

ABS

ABS

ABS

ABS



LET

LOW
HIGH
LOU
HIGH
LOU
HIGH
LOU
HIGH
LOW
HIGH
LOU
HIGH
LOU
HIGH
LOU
HIGH
LOU
HIGH
LOU
HIGH
LOU
HIGH
ADULT
DEATH
RATE (DTHS/
1E6/MRAD/YR)
2.17E+00
1.74E+OI
4.47E-02
8.94E-01
9.25E-01
7.40E+00
1.49E+00
1.19E+01
2.03E+00
1.63E+01
9.61E-01
7.69E+00
4.47E-01
3.57E+00
9.77E-01
7.81E+00
6.72E-01
5.16E+00
2.84E-01
2.27E+00
1.30E+00
1.04E+01
SUMMARY TABLE
NUMBER OF
70- YEAR
DOSE RATE
(MRAD/YR)
6.83E-05
1.34E-04
9.75E-05
1.52E-03
2.68E-06
3.03E-05
3.41E-06
3.03E-05
7.01E-06
4.80E-03
2.14E-06
3.03E-05
1.29E-05
3.41E-05
2.40E-06
2.13E-05
3.33E-06
3.03E-05
4.63E-06
3.94E-05
3.33E-06
3.03E-05
PREMATURE
DEATHS
IN COHORT
1.47E-05
2.44E-04
4.48E-07
1.41E-04
4.14E-07
4.57E-05
6.16E-07
5.90E-05
2.53E-06
1.58E-02
2.68E-07
3.81E-05
9.38E-07
2.01E-05
2.90E-07
2.67E-05
2.74E-07
2.56E-05
1.82E-07
1.48E-05
5.31E-07
5.18E-05
AVERAGE
YEARS OF
LIFE LOST
(YEARS)
2.64E+01
2.72E+01
2.44E+01
2.45E+01
2.59E+01
2.75E+01
1.99E+01
2.10E+01
•2.24E+01
2.30E+01
2.02E+01
2.10E+01
2.12E+01
2.11E+01
1.99E+01
2.09E+01
1.99E+01
2.10E+01
2.05E+01
2.11E+01
1.99E+01
2.10E+01
TOTAL
YEARS OF
LIFE LOST
(YEARS)
3.88E-04
6.64E-03
1.10E-05
3.46E-03
1.07E-05
1.26E-03
1.22E-05
1.24E-03
5.66E-05
3.64E-01
5.42E-06
8.02E-04
1.99E-05
4.24E-04
5.79E-06
5.57E-04
5.44E-06
5.39E-04
3.74E-06
3.13E-04
1.06E-05
1.09E-03
DECREASE
IN LIFE
EXPECTANCY
(YEARS)
3.88E-09
6.64E.08
1.10E-10
3.46E-08
1.07E-10
1;26E-08
1.22E-10
1.24E-08
5.66E-10
3.64E-06
5.42E-11
8.02E-09
1.99E-10
4.24E-09
5.79E-11
5.57E-09
5.44E-11
5.39E-09
3.74E-11
3.13E-09
1.06E-10
1.09E-08
70-YEAR
DOSE EQUIV-
ALENT RATE
(MREM/YR)
2.75E-03

3.06E-02

6.09E-04

6.10E-04

9.59E-02

6.08E-04

. 6.95E-04

4.28E-04

6.09E-04

7.94E-04

6.09E-04

RISK
EQUIVALENT
FACTOR

8.39E-04

2.06E-02

2.35E-04

2.31E-04

3.84E-02

2.30E-04

2.71E-04

1.59E-04

2.23E-04

3.05E-04

2.32E-04

TOTAL (SOMATIC)

30-YEAR GENETIC  DOSE COMMITMENTS (MRAD):
                                                       1.65E-02    2.31E+01    3.80E-01   3.80E-06
                                                                                        2.08E-02
   LET
   LOW
   HIGH
 TESTES
5.59E-05
8.52E-04
 OVARIES
7.44E-05
8.52E-04
 AVERAGE
6.51E-05
8.52E-04
                                                                                        8.31E-03

-------
each age group corresponds to a segment of the-stationary population with
the total population equal to the sum of all the age groups.  Thus, 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 population receiving a population dose of
the same magnitude.  This equivalence was used in deriving the risk
.factors for the environmental pathways analysis described in this report.
More detailed discussions of the methodology used by EPA to compute fatal
cancer risk estimates are included in Appendices F through H, and in
several of the references (Du84, Du80, Su81) for those readers who desire
more details than are presented in this section.

     In our high-level waste environmental pathway calculations, we have
calculated fatal cancer risk commitment factors using the RADRISK data to
convert from lifetime radionuclide intake for the inhalation and ingestion
pathways and from lifetime external exposure for the air submersion and
ground surface pathways directly to fatal cancer risk without calculating
dose commitments or dose rates*.  As an example, the derivation of an
inhalation risk commitment factor will be described in the following
paragraphs.

     Using the summary tables from the RADRISK computer code output
(example in Table 4-1), column 8, total (somatic), gives the total number
of premature fatal cancers in a cohort of 100,000 persons born
                                    4-7

-------
simultaneously and Inhaling 1 pCi/y  continuously throughout  their
lifetime.  The average lifetime for  the persons comprising the  cohort  is
70.756 years.  Thus, the deaths tabulated in  column  8  are the result of
the collective lifetime intake by the cohort  of
      (1E+5 personsMl  pCi     H70.756 yr)(!E-12 Ci  )  = 7.076E-6  Ci
                       yr-person                  pCT

Then, for a constant lifetime rate of intake', a fatal  cancer risk
commitment factor can be calculated  using the equation
     FCF
        np
deaths committed
   Ci inhaled
     premature deaths in cohort
(col.  8,  Total Somatic, Table 4-1)
         7.076E-6 Ci inhaled
(4.1-1)
This equation is applicable to a stable population (i.e., a population in
which equal numbers of persons are born and die in each year) which has
the same age distribution and age specific mortality ratio as used for the
cohort.  The factors derived using this equation are not applicable for
computation of fatal cancer risks to an individual for an acute intake of
radioactivity.

     For Ra-226 particulates having AMAD s 1.0 micron and respiratory
clearance  class W, the total number of premature fatal cancers in a cohort
of 100,000 persons is 1.65E-2 (Table 4-1, column 8, total (somatic)).
Then, applying equation  4.1-1, the fatal cancer risk conversion factor
is calculated to be 2,332  deaths committed .
                              Ci inhaled
                                    4-8

-------
     This illustration shows the methodology for deriving the fatal  cancer
risk conversion factors for inhalation pathways.  The procedures used to
obtain the factors for the ingestion,  air submersion, and ground surface
exposure pathways are very similar to  those presented above*.

4.2  Analytical Treatment of Daughter  Product Buildup During
     Environmental Transport

     Daughter product buildup during environmental transport was not
addressed rigorously in the 30 pathway equations discussed in Section 3.
An examination of the decay schemes for the nuclides revealed that,  in
general, the nuclides either (a) had stable daughters, (b) had daughters
that were very short-lived compared to the,parent, or (c) had moderately
to very long-lived first or second daughters.  The following techniques
were applied as an approximate method  of handling daughter product
ingrowth during environmental transport.

     For case (a), no action to account for daughter product buildup was
required.
     In case (b), we assumed that the daughter was in secular equilibrium
with the parent, i.e., that the activity of the daughter was equal  to that
of the parent, at all  locations of the parent in the environment.
     *Those wishing to compare their fatal  cancer risk assessment
methodology to that used by EPA should multiply their dosimetry and fatal
cancer risk factors for each organ at risk, sum these products, and
compare their sums to the EPA risk factors listed in Table 4-2.
                                   4-9

-------
Obviously this is a simplifying assumption,  since  daughter  products  may
behave differently than the parents in the environment.   The  risk  factors
for daughters were added to the risk factors for the  parent in cases where
the daughters were dosimetrically significant.   An example  of case (b)  is
Zr-93.  Zr-93 has a half life of 1.53E+6yr and  an  ingestion fatal  cancer
risk factor of 8.46E-2 fatal cancers per curie  intake.   The only
radioactive daughter of Zr-93 is Nb-93m, which  has a  half life of  14.6yr
and an ingestion fatal cancer risk factor of 4.21E-2.  This is clearly  a
case where Nb-93m is in secular equilibrium  with the  Zr-93 parent  in the
environment and we have added the risk factors  to obtain the reported risk
factor for Zr-93 of 1.27E-1 fatal cancers/Ci ingested (see Appendix B,
Table B-l).  The rationale  is that for each curie of Zr-93 ingested a
curie of Nb-93m  is present  and 1s also ingested.

      In  case  (c), we  performed simple calculations to determine whether  a
 significant  buildup of  the  long-lived daughters would occur  during the
 residence  time of  the parent 1n  the accessible environment.   The
 accessible environment  1s  that portion  of the environment  where the
 material would be  available to man.   For example,  radionuclides present
 within  the root  zone  of the soil  would  be 1n the  accessible  environment,
 but radionuclides  that have moved below the root  zone would  have  left the
 accessible environment.  Since we believe that  the soil  root zone is an
 environmental medium  which will  have  one of the longest  retention times
 for radionuclides  1n  the accessible environment,  we  calculated the  mean
 lifetime in  soil of  radionuclides 1n  category  (c).   The  mean lifetime was
                                    4-10

-------
taken as the reciprocal  of the leaching removal  rate  constant,  xs ,  for
the 15 cm soil  root zone.  Using standard Bateman equations  (Ev55)t  we
evaluated the maximum activity of the significant daughter products  which
could build up during the mean lifetime of the parent and compared this
activity to the original activity of the parent.  For daughters where the
maximum activity exceeded 1 percent of the original  parent activity, we
added the product of the ingrowth fraction and the daughter  risk factor to
the parent risk factor.   We neglected the contribution of those daughters
which built up to less than 1 percent of the original parent activity.
Any short-lived daughters in the decay chain between the parent and  the
first moderate to long-lived daughter are assumed to be in secular
equilibrium as described for case (b) above.  The specific treatment of
daughter products, for each parent nuclide in this analysis is specified in
Appendix A.

4.3  Application of Risk Factors for Environmental Pathway Calculations

     For the inhalation and ingestion pathways two categories of fatal
cancer risk factors were calculated which were designated Inhalation 1,
Inhalation 2, Ingestion 1 and Ingestion 2.  The category 1 factors were
used when we believed radionuclides will be present in the accessible
environment in a reasonably insoluble chemical form.  The category 2
factors were used when we believed the nuclides are in a more soluble
chemical form.  Class Y risk factors were used for the Inhalation 1
category for all nuclides where they were available and Class W risk
                                   4-11

-------
factors were used for the Inhalation 2  category-where  they  were
available.  However, for some radionuclides,  only  Class  D or Class D and
Class W inhalation risk factors were available.   In  these cases,  the
factors for the least soluble clearance class available  were applied.  For
example, if inhalation risk factors were available for Class D and Class W
but not for Class Y, the Class W factors were listed 1n  both the
Inhalation 1 and Inhalation 2 categories.  For the Ingestion 1 and
Ingestion 2 categories, risk factors were used which were derived using
the same absorption fraction from gut-to-blood, (f«),  as was used for
the Inhalation 1 and Inhalation 2 categories, respectively.

     For the volcano/meteorite release mode, the Inhalation 1 and
Ingestion 1 risk factors were used and for the other three release modes
(releases to rivers, releases to oceans, and releases to land surfaces)
the Inhalation 2 and Ingestion 2 risk factors were used.  This procedure
was followed because we believe that the radionuclides released in the
volcano/meteorite release mode will be 1n a less soluble chemical form
than the  radionuclides released in the other three release modes.

     The  risk factors used  in our analysis are tabulated 1n Table 4-2.
Included  1n Appendix B is a  tabulation of the risk factors  for the parent
radionuclides, and  the daughter radionuclides where the  risk  factor  was of
sufficient magnitude to be  added to the  risk factors  for the  parent.
                                    4-12

-------
i-atai uancer KISK conversion razors-
/fatal cancers committed
Nuclide
C-14
Ni-59
Sr-90
Zr-93
Tc-99
Sn-126
1-129
Cs-135
Cs-137
Sm-151
Pb-210
Ra-226
Ra-228
Ac -227
Th-229
Th-230
(fatal
Inhalation 1
3.05E-3
4.76E-1
4.52E+2
2.72E+1
6.12E+0
5.72E+1
1.61E+1
1.27E+0
8.49E+0
5.27E+0
2.27E+4
4.38E+4
7.98E+4
6.97E+4
6.45E+4
6.89E+4
cancers committed per Ci intake)
Inhalation 2 Ingestion 1 Ingestion 2
3.05E-3
4.76E-1
5.19E+1
6.60E+0
6.12E+0
5.72E+1
1.61E+1
1.27E+0
8.49E+0
5.27E+0
2.99E+3
5.33E*3
1.58E+4
3.74E+4
2.82E+4
2.05E+4
4.32E-1
3.76E-2
2.29E+0
1.27E-1
5.37E-1
2.04E+0
2.41E+1
1.82E+0
1.24E+1
3.46E-2
4.13E+2
4.91E*2
9.71E+1
2.85E+2
8.55E+1
5.13E+2
4.32E-1
3.76E-2
2.85E+1
1.27E-1
5.37E-1
2.04E+0
2.41E+1
1.82E+0
1.24E+1
3.46E-2
4.13E+2
4.91E*2
9.71E+1
2.85E+2
8.55E+1
5.13E+2
Ci-y/m3
Air Submersion
0
4.10E-2
0
1.23E-1
5.97E-4
2.54E+3
7.57E+0
0
7.18E+2
8.15E-4
1.34E+0
2.35E*3
3.43E*3
4.81E+2
3.30E*2
2.35E+3
H fatal cancers committed \
CiW '
Ground Contamination
0
8.87E-3
0
1.89E-2
1.41E-5
5.11E+1
3.98E-1
0
1.43E+1
9.43E-5
6.09E-2
4.20E+1
5.88E+1
1.05E+1
7.46E+0
4.20E*1
     *The fatal  cancer risk  conversion  factors  in this table  are the sum of the risk factors for the listed
nuclide plus any significant daughter products  which can  grow in during the residence time of the nuclide in
the accessible environment.   For  a  more complete discussion,  see section 4.2 and Appendices A and B.

-------
TABLE 4-2 Continued:
Fatal Cancer Risk Conversion Factors
/fatal cancers committed^ /fatal cancers committed \
Nucllde
Th-232
Pa-231
U-233
U-234
U-235
U-236
U-238
Np-237
Pu-238
Pu-239
Pu-240
Pu-241
Pu-242
Am-241
Am-243
Cm-245
Cm-246
(fatal
Inhalation 1
1.05E+5
1.03E+5
2.42E+4
2.07E+4
2.03E+4
1.96E+4
1.86E+4
2.89E+4
V
3.13E+4
3.09E+4
3.09E+4
1.19E+3
2.94E+4
3.27EH
3.19E+4
6.54E+4
3.26E+4
cancers comnltted per C1 Intake)
Inhalation 2 Ingestlon 1 Ingestion 2
2.94E+4
6.19E+4
3.70E+3
2.26E+3
2.72E*3
2.14E+3
2.04E+3
2.46E+4
2.49E+4
2.65E+4
2.65E+4
1.23E+3
2.52E+4
2.75E+4
2.73E+4
5.58E+4
2.78E+4
1.17E+2
4.67E+2
5.21E+0
9.38E-1
5.8.6E+0
8.86E-1
1.99E+0
1.86E+2
1.86E+2
2.04E+1
2.04E+1
9.57E+0
1.94E+1
2.07E*2
2.06E+2
4.21E+2
2.10E+2
1.17E+2
4.67E+2
5.07E+1
4.61E+1
5.02E+1
4.35E+1
4.84E+1
1.86E+2
1.86E+2
2.00E+2
1.99E+2
9.57E*0
1.90E+2
2.07E+2
2.06E+2
4.21E+2
2.10E+2
ClW 'l
Air Submersion
3.43E+3
5.17E+2
1.68E+1
1.63E-1
2.01+2
1.27E-1
2.36E+1
2.83E+2
8.80E-2
9.06E-2
8.63E-2
5.98E-1
7.36E-2
1.99E+1
2.55E+2
1.02E+2
6.81E-2
Cl-y/m*2 '
Ground Contamination
5.88E*1
1.14E+1
3.84E-1
1.63E-2
4.60E+0
1.48E-2
5.17E-1
6.39E+0
1.68E-2
7.64E-3
1.61E-2
1.87E-2
1.34E-2
6.24E-1
5.95E+0
2.58E>0
1.41E-2

-------
4.4  Risk Conversion Factors for Np-237
     Neptunium-237 deserves special  mention  in this document.   In ICRP
Report 30 (ICRP80) the value for absorption  through the gut (f.)  is
   n                                                             A
10" .  This is a 100-fold increase over the  previous value of  10
recommended 1n ICRP Report 2 (ICRP60).   According to Cohen, this  increase
in fj plus the high cancer risk factor  for the liver quoted in BEIR III
have caused Np-237 to become a principal  nuclide of concern in various
assessments of the health effects from  disposing of high-level radioactive
waste (Co82).  In ICRP30, it is mentioned that a value for f,  of  10
may be more appropriate for trace quantities of the element or for
neptunium incorporated in food.  Information published subsequent to the
publication of ICRP30 (Th82a, Th82b) suggests that 10   is probably the
most appropriate value for f, for neptunium  for low environmental
levels.  The internal dose conversion factors for Np-237 utilized by EPA
                                       -3
in this report are based on an f, of 10  ; EPA believes, based on
current information, that this is the best value to use 1n these
calculations.  EPA is aware that ICRP Committee 2 has a task group to
recommend the most appropriate values of f,  for actinides and that the
NCRP has established a task group on neptunium.  EPA will consider the
recommendations, when they become available, of both of these committees
in future analyses concerning the disposal of high-level radioactive waste,
                                   4-15

-------

-------
             Chapter 5:   DISCUSSION  OF  VALUES F0R  PARAMETERS*

     Some of the parameters  used  in  these  calculations  appear  in  several
of the 30 pathway equations.   For this  reason,  we  decided  to discuss
parameter values in a separate chapter  rather than in the  chapters
describing the pathway ERC equations.   For many parameters, a  range of
values will be found in the literature. A list of the  estimated  range of
possible values for these parameters is in Appendix C,  Section C.9, Table
C-10.  The parameter values listed in this chapter are  used  for the fatal
cancer risk calculations summarized in  Chapter  6 and discussed in more
detail in EPA's analysis of the population risks from geologic
repositories (EPA85a).

     The parameter *Ln is the rate at which radionuclides  are  leached
from the waste into the groundwater in the repository and  is assumed  to be
the same for all nuclides.  A range of values from 1.0 E-2 yr   to
1.0 E-6 yr"  was examined in the EPA analysis (EPA85a)  based on
information furnished by the Arthur D.  Little Company (L177b).  The value
applied  in computing fatal cancers per Ci  release is 1.0 E-4 yr"  .

     The parameter t   is the time after placement in a repository that
leaching from the repository begins and usually corresponds  to failure of
the waste  canister.  Canister lifetimes ranging between 100 and 5000 years
were considered  in EPA's analysis of geologic repositories (EPA85a).   We
assume t_ is the same for all radionuclides.
         er
     *The  variables used in this chapter are defined in the "Nomenclature"
 section,  p.  N-l ff.
                                    5-1

-------
     The parameter tran 1s the time required foj radlonuclldes to travel
from the repository to an aquifer.   This time varies  depending upon the
situation being addressed 1n EPA's  analysis of geologic  repositories,  but
the time Is usually on the order of a few years.

     The parameter tfirn 1s the time required for material  to travel from
the aquifer to the river.  The value chosen for t    1s  760 R  yr
                                                 arn          n
where R  1s the retardation factor  for the nuclide being considered.
Rp varies between 1 and 10,000 depending on the radionuclide and the
situation being considered.  Values for R  are discussed in the A. D.
Little report (Li77c) and in EPA's  risk assessment report (EPA85a).

     The parameter tR  is the time  after placement in a  repository that
radionuclide-n enters the river or ocean and is the sum  of t  , t
                                                            er   ran
and tarn-  For these calculations,  tRn is set equal to zero.  This 1s
permissible since we are computing  the health effects per curie released
to the environment.  Appropriate non-zero values for t^w, t^aw and
                                                      er*  ran
tarn must be selected when computing the total release quantity of
radionuclides from a repository.

     The parameter QQn Is the initial activity of nuclide n in the
repository at time t=0.  The value for QQn remains constant for various
scenarios and is discussed in the risk assessment report (EPA85a).

     The parameter xQn is the radioactive decay constant for nuclide n.
The values for >Dn are calculated using half-life information from
Lederer  (Le67) and Kocher  (KoSla)  (see Table 5-1).
                                    5-2

-------
TABLE 5-1:
Radionuclide decay constants
Nucllde
C-14
Ni-59
Sr-90
Zr-93
Tc-99
Sn-126
1-129
Cs-135
Cs-137
Sro-151
Pb-210
Ra-226
Ra-228
Ac-227
Th-229
Th-230
Th-232
Pa-231
U-233
U-234
U-235
U-236
U-238
Np-237
Pu-238
Pu-239
Pu-240
Pu-241
Pu-242
Am-241
Am-243
Cm-245
Cm-246
n
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
^Dnb"""1)
1.21 E-4
8.66 E-6
2.47 E-2
4.62 E-7
3.27 E-6
6.93 E-6
4.08 E-8
2.31 E-7
2.31 E-2
7.97 E-3
3.11 E-2
4.33 E-4
1.21 E-l
3.18 E-2
9.44 E-5
9.00 E-6
4.93 E-ll
2.12 E-5
4.35 E-6
2.81 E-6
9.85 E-10
2.96 E-8
1.55 E-10
3.24 E-7
8.06 E-3
2.84 E-5
1.05 E-4
4.81 E-2
1.83 E-6
1.51 E-3
8.72 E-5
8.15 E-5
1.46 E-4
                                    5-3

-------
     The parameters f,. ,  f., ,  and fAW are  the  fractions  of  the  total
release for a volcano/meteorite event which  are released to the land
surface, the air-above-land,  and the air-above-water,  respectively.   The
values used for these parameters are f,, = 0.500,  f.,  =  0.150,  and
f... = 0.350.
 AW

     The parameter PR 1s the number of people  who  drink  water from the
river and R is the river flow rate.  The ratio PR/R is needed in several
equations, and it can be determined for the purpose of this generic
evaluation without obtaining site specific data.  Utilizing data from
Annex D of the 1977 UNSCEAR Report (UN77), the annual  flow rate of the
rivers of the world is 3 E+16 liters/yr.  If one assumes a constant world
                10         *
population of 10   persons,  the ratio PR/R is 3.3 E-7
person-yr/liter.  This value for-the ratio PR/R 1s within the range of
values found for various river basins In the United States.  These values
ranged from a high for PR/R of 5.73 E-7 for the Lower Colorado WRC**
region to a low of 2.39 E-8 for the Pacific Northwest WRC  region based on
1975  river  flow and population estimates  (see  Appendix C,  Section C.7).
     The  parameter  I   Is the per capita annual consumption of drinking
                    W
water and water-based  drinks.  The reference adult man drinking rate of
water and water-based  drinks 1s 1.65 liters/d  (ICRP75), which yields a
      *The  current world  population  1s about  3.8  E9.   However, an estimate
 of  average world population  during  the time  period involved 1n this
 calculation  1s  10*0  people  (UN77).
      **WRC - Water Resources Council.
                                    5-4

-------
value of Iw of 603 liters/yr.   Note  that  the  fraction  of the  global
flowing water drunk by the world population 1s approximately  2  E-4.

     The parameter Ppp is the  population  eating freshwater fish from the
river and 1^ is the per capita annual  freshwater fish  consumption rate.
The ratio of the population fish consumption  rate (Pr-F If) to the
river flow rate (R) is needed  for the  calculation.   The UNSCEAR freshwater
fish consumption rate for the  world  is 3.8 E9 man-kg/yr (UN77).  We  assume
that fish consumption will increase  proportionately as the population
increases from the present level of  3.8 E9 people.   For an eventual  world
population of 10   people, this yields an annual freshwater fish
consumption rate of 10   man-kg/yr.   Considering the average  flow rate
of the rivers of the world, the ratio  of the  population freshwater fish
consumption rate to the river  flow rate is 10  /3 E16 = 3.3 E-7
man-kg/liter.
     The parameter CF   is the bioaccumulation factor for fish or
shaJIflsh for nuclide n and pathway p.  The primary reference used for
CF   for freshwater fish, ocean fish, and ocean shellfish is UCRL-50564,
Rev.l (Th72).  The values of the bioaccumulation factors are listed in
Table 5-2.  The references for the bioacculumation factors not taken from
UCRL-50564, Rev. 1 are noted in Table 5-2.
     The parameter RI   is the symbol for the terrestrial food pathway
factors discussed in Chapter 3.  The values used for these factors are
listed in Table 5-3.  The methodology used to derive these factors is
similar to that applied in the AIRDOS-EPA computer code (Mo79) and is
                                    5-5

-------
TABLE 5-2:
Bioaccumulation factors for freshwater fish and seafood
Nuclide
C-14
Ni-59
Sr-90
Zr-93
Tc-99
Sn-126
1-129
Cs-135
Cs-137
Sm-151
Pb-210
Ra-226
Ra-228
Ac-227
Th-229
Th-230
Th-232
Pa-231
U-233
U-234
U-235
U-236
U-238
Np-237
Pu-238
Pu-239
Pu-240
Pu-241
Pu-242
Am-241
Am-243
Cm-245
Cm-246
n
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18 '
19
20
21
22
23
24
25
26
27
28
29 .
30
31
32
33
CFnp (Ci/kg per d/liter)
Freshwater Ocean Ocean
Fish Fish Shellfish
NA
l.OOE+2
1.10E+1 (Ho79)
3.33E+0
4.30E+1 (B182a)
3.00E+3
3.30E+1 (Ho79)
1.30E+3 (Ho79)
1.30E+3 (Ho79)
2.50E+1
l.OOE+2
5.00E+1
5.00E+1
2.50E+1
3.00E+1
3.00E+1
3.00E+1
1.10E+1
l.OOE+1
l.OOE+1
l.OOE+1
l.OOE+1
l.OOE+1
5.00E+2 (Sc83)
8.00E+0 (Ri83)
8.00E+0 (R183)
8.00E+0 (R183)
8.00E+0 (Ri83)
8.00E+0 (R183)
8.10E+1 (R183)
8.10E+1 (R183)
2.50E+1
2.50E+1
NA
l.OOE+2
2.00E+0
2.00E+2
l.OOE+1
3.00E+3
l.OOE+1
4.00E+1
4.00E+1
2.50E+1
3.00E+2
5.00E+1
5.00E+1
2.50E+1
l.OOE+3 (Ng84)
l.OOE+3 (Ng84)
l.OOE+3 (Ng84)
l.OOE+1
l.OOE+1
l.OOE+1
l.OOE+1
l.OOE+1
l.OOE+1
l.OOE+2 (Sc83)
3.00E+0
3.00E+0
3.00E+0
3.00E+0
3.00E+0
2.50E+1
2.50E+1
2.50E+1
2.50E+1
NA
2.50E+2
2.00E+1
8.00E+1
5.00E+1
l.OOE+3
5.00E+1
2.50E+1
2.50E+1
l.OOE+3
l.OOE+3
l.OOE+2
l.OOE+2
l.OOE+3
2.00E+3
2.00E+3
2.00E+3
l.OOE+1
l.OOE+1
l.OOE+1
l.OOE+1
l.OOE+1
l.OOE+1
l.OOE+2 (Sc83)
2.00E+2
2.00E+2
2.00E+2
2.00E+2
2.00E+2
l.OOE+3
l.OOE+3
l.OOE+3
l.OOE+3 .
 NA -  Not  Applicable,
                                    5-6

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TABLE 5-3:
Radionuclide intake factors
Nuclide
                                              RI
                                                np
  (Ci intake per Ci/m^ deposited)

Food Crops           Milk
Meat
C-14
Ni-59
Sr-90
Zr-93
Tc-99
Sn-126
1-129
Cs-135
Cs-137
Sin- 151
Pb-210
Ra-226
Ra-228
Ac-227
Th-229
Th-230
Th-232
Pa-231
U-233
U-234
U-235
U-236
U-238
Np-237
Pu-238
Pu-239
Pu-240
Pu-241
Pu-242
Aro-241
Am-243
Cm-245
Cm-246
NA
4.38E+0
2.57E+0.
4.21E+0
1.57E+0
1.10E+0
1.17E+1
1.40E+1
8.51E-1
5.47E-1
4.98E-1
6.62E-1
3.95E-1
3.95E-1
7.33E-1
2.77E+0
6.73E+0
6.92E-1
1.19E+0
1.19E+0
1.19E+0
1.19E+0
1.19E+0
5.42E-1
3.92E-1
4.77E-1
4.53E-1
3.90E-1
4.89E-1
4.35E-1
4.87E-1
4.10E-1
4.08E-1
NA
3.22E-1
1.07E+0
8.18E-2
4.00E+0
3.04E-1
1.03E+1
8.04E+0
1.74E+0
4.54E-3
5.75E-2
1.26E-1
9.81E-2
4.36E-3
1.49E-3
3.87E-3
8.51E-3
1.43E-3
1.57E-1
1.57E-1
1.57E-1
1.57E-1
1.57E-1
2.52E-3
2.17E-5
2.37E-5
2.32E-5
2.17E-5
2.40E-5
9.45E-5
1.03E-4
4.67E-3
4.63E-3
NA
2.48E-1
8.20E-2
2.10E+1
1.31E+0
9.36E+0
2.78E+0
8.84E+0
1.91E+0
4.37E-1
2.66E-2
6.26E-2
4.53E-2
2.10E-3
6.87E-4
1.79E-3
3.93E-3
1.10E-3
2.01E-2
2.01E-2
2.01E-2
2.01E-2
2.01E-2
1.94E-2
1.67E-4
1.83E-4
1.79E-4
1.67E-4
1.85E-4
3.18E-4
3.48E-4
3.14E-4
3.12E-4
NA - Not Applicable,
                                    5-7

-------
discussed,  along with input parameter values,  mpre  fully  in  Appendix  C.
Those readers Interested in the details of the derivation of these  RI
factors should refer to Appendix C,  Section C.I.
np
     The fraction of land used for various food crops is f .   For the
river pathway, irrigation water provides the source of radionuclides to
land, so irrigated farmland is the only land of concern.  We assume that
50 percent of the irrigated land is used for growing food crops; 25
percent for grazing milk cows; and 25 percent for grazing beef cov/s.  For
the  non-river release modes, radionuclides reach the land surface via
dispersion in air so that the values for the fraction, f_, must include
the  portion of U.S. land surface used for farming.   It was found that 45
percent of the U.S. land surface was used for farming in 1974 (Wo79).  To
obtain a value for f  for the non-river release modes, 45 percent of the   .
value of f  applied for the river release mode was used.  Thus, for the
non-river release mode, 1t was assumed that 23 percent of the land 1s used
for  growing food crops; 11 percent for grazing milk  cows; and 11 percent
for  grazing beef cows.  The values selected for f  are  upper limits
since for all release modes part  of the agricultural  land will  be used for
non-food crops  (e.g., cotton, etc.).
      The fraction of the river flow used for Irrigation,  fR, was  set
 equal to 0.1.   This number represents the average  fraction  of  total
 surface water  flow used for irrigation for the  U.S.  and  1s  taken  from USGS
 Circular 765 (Mu77).  Data from other publications generally  support  the
 choice of 0.1  for a U.S. average (WRC78, WIC70).   The value for fR
                                    5-8

-------
varies for various regions of the U.S.  from  a  Toy  of  zero  for  the  Ohio  and
Tennessee regions to a value of almost  one for the Lower Colorado  region,
as shown In Appendix C, Section C.3.
     The parameter CP  Is the population  that  can  be  fed  by  raising
crop p on a unit area of land.   The quantity is  obtained  by  dividing the
                               2
agricultural  productivity (kg/m -y) of land on which  crops are raised by
the annual consumption rate of an individual consuming  the crop
(kg/y-person).  Values for CP  were obtained from  information in two
references (Sh82, Ba84) and were derived  taking  into  consideration the
types of crops consumed by humans and by  milk  and  beef  producing animals,
In this analysis, the value of CP  for food crops  is  4.79E-3 persons
     2                                 2
fed/nr; for milk, 1.56E-3 persons fed/m ; and  for  beef, 7.85E-5
             2
persons fed/m .  The details of the derivation of  these numbers are
discussed in Appendix C, Section C.2.
     The parameter PD  is the population density for pathway p.   The
                                       2
value used for PD  is 6.67 E-5 person/m , which is the world average
population density and was obtained by dividing the assumed world
population of 10   persons  by the land surface area of the earth of 1.5
     o
E14 m  (Wo79).  This value is within the range of population densities
for various regions of the U.S. (Wo79), as shown in Appendix C,  Section
C.4.
     The parameter RF is the resuspension factor for material resuspending
from the ground surface to the air.  It is defined as the ratio of air
concentration to ground concentration, X ft' )/jzf (t1), which is equal
                                    5-9

-------
to *D/vQn where XR 1s a rate constant for resuspension  of
radlonuclides from ground to air and vQn 1s the deposition velocity  from
air to land surface.  The value of XR chosen for this analysis 1s
10"   sec" , which should be representative of weathered material
                                        -2
(Ne78); and the value used for v   is 10   m/sec.  The  resulting value
           -9  «1
of RF is 10   m   and this value agrees well with the long-term
average value suggested by Bennett (Be76).  Actually, XR and RF are
functions of time, but the time dependent relationships were not known and
constant values were used to represent the average values  over the
calculation interval.  The value selected for XR is appropriate to dry
land  resuspension, so the dose due to resuspension from wet irrigated land
(the  river release mode) may be conservatively high.
     The parameter  !„ is the standard man breathing rate.  Based
on
 Information contained In  ICRP Report 23 (ICRP75), a value of 8400 m /yr
 has  been chosen for this  parameter.

      The parameter SOF  1s a factor that accounts for the reduction in
 external dose  due to household  shielding and occupancy.  A conservative
 value of 1.0 has been chosen for this analysis for all release modes
 except the  river release  mode.  For the river release mode, the area where
 external dose  could be  received is irrigated farm land.  After considering
 the  fraction of time a  person might spend  around irrigated land, we
 decided to  assign a value of 0.33 to SOF for the river release mode.
                                    5-10

-------
     The rate constant for transfer of nuclides.from available

to unavailable soil  is xs .  The value for x-  is nuclide dependent

and is determined using a method (Ba79a)  and data (Ba84)  described by

Baes.  The values used for xs  in this analysis are given in Table 5-4.

Baes models the loss of radionuclides from the soil root  zone due to water
TABLE 5-4:
Leaching coefficients for radionuclides in soil
          Element
Leaching Coefficient U$n)

        (yr-1)
          C
          N1
          Sr
          Zr
          Tc
          Sn
          I
          Cs
          Sm (Rare Earth)
          Pb
          Ra
          Ac
          Th
          Pa
          U
          Np
          Pu
          Am
          Cm
         NA
      5.40E-3
      2.31E-2
      2.70E-4
      4.90E-1
      3.24E-3
      1.57E-3
      8.10E-4
      1.25E-3
      9.00E-4
      1.80E-3
      5.40E-4
      5.40E-6
      3.24E-4
      1.80E-3
      2.69E-2
      1.80E-4
      1.16E-3
      4.05E-4
 NA  -  Not Applicable.
                                    5-11

-------
leaching but does not consider erosion of soil  Jand radionuclides)  as a
removal mechanism.  For long time periods, erosion may be a significant
removal mechanism which would make the Baes model  conservative for  this
application.

     The risk conversion factors used for radionuclides deposited to the
ground were derived using the assumption that the material remains  on the
surface.  Over the long time periods involved in these calculations, the
radionuclides will move vertically downward into the soil.  The gamma
radiation emitted from these nuclides is partially shielded by the  soil
such that the dose equivalent per unit deposition is less than given by
the surface dose conversion factors.  We derived correction factors for
each nuclide by assuming that the radioactivity was uniformly distributed
vertically within the soil root zone  {see the discussion in Section
3.1.6).  These correction factors are listed in Table 5-5 and were derived
using the methodology discussed in Appendix C, Section C.5.

     The parameter fw- is the fraction of a radionuclide which passes
through a drinking water treatment plant and remains in potable water.  We
conservatively assumed a value of 1.0 for all radionuclides.  However,
values  In the literature will range from 0.2 to 1.0 for the radionuclides
considered  in this analysis  (F171, De75, NRC78).
                                   5-12

-------
TABLE 5-5:

Ground surface radionuclide correction factors (GCnp)
          Nuclide
     GCnp
(Dimensionless)
C-14
Ni-59
Sr-90
Zr-93
Tc-99
Sn-126
1-129
Cs-135
Cs-137
Sm-151
Pb-210
Ra-226
Ra-228
Ac-227
Tn-229
Th-230
Th-232
Pa-231
U-233
U-234
U-235
U-236
U-238
Np-237
Pu-238
Pu-239
Pu-240
Pu-241
Pu-242
Am-241
Am-243
Cm-245
Cm-246
Beta emitter
8.8E-5
Beta emitter
1.3E-3
Beta emitter
2.2E-1
l.OE-2
Beta emitter
2.4E-1
Beta emitter
2.3E-2
2.4E-1
1.8E-1
1.5E-1
9.7E-2
2.4E-1
1.8E-1
1.3E-1
7.5E-2
2.9E-2
7.3E-2
2.5E-4
4.3E-2
9.2E-2
3.8E-4
4.1E-4
4.0E-4
1.2E-2
4.0E-4
1.2E-2
6.9E-2
3.3E-2
4.0E-4
                                   5-13

-------
     The parameter f  'Is  the  fraction of drinking water which 1s
                    sw                        "
supplied by surface water.   State  average values varied from a high of
0.90 for Maryland to a low of  0.08 for  Idaho with the U.S. average being
~ 0.65 (Mu77).  We used the U.S. average value in these calculations.
     The transfer rate coefficients used in the ocean  model  are  y^ and
Y2.  That for movement of water from the lower to the  upper  ocean
compartment is Y2 and the value of it used for this  analysis is  6.25  E-4
yr  (Ma73).  For movement of water from the upper to the lower ocean
compartment, the transfer rate coefficient 1s Yl, and the value  applied
for this analysis is 3.3 E-2 yr" , which is derived using the
methodology discussed in Appendix C, Section (MO.
     The parameters SFln and SF2n are the sedimentation coefficients
 from the upper layer and the lower layer of the ocean, respectively, for
 nuclide n.  The treatment of sedimentation 1s taken from a report of the
 working group of  the International Nuclear Fuel Cycle Evaluation
 (INFCE78),  and the methodology used to derive nuclide specific values for
 SF.  and SF2n Is  discussed  in Appendix C, Section C.10.  The values we
 used for these two parameters are listed 1n Table 5-6.
      The ratio of the population  seafood consumption  rate  (P   I  ) to
the ocean upper compartment volume
                                         1s  needed  In these
 calculations.  P  is the population eating seafood  and  I   1s the per
                                    5-14

-------

TABLE 5-6:
Values for ocean sedimentation
Element
C
N1
Sr
Zr
Tc
Sn
I
Cs
Sm (Rare Earth)
Pb
Ra
Ac
Th
Pa
U
Np
Pu
Am
Cm
coefficients
Sedimentation
SFm
0
5.33E-6
2.671-7
2.67E-4
0
0
0
2.67E-6
4.00E-5
2.67E-4
1.33E-6
6.67E-5
2.00E-3
2.67E-4
4.00E-5
1.33E-7
2.67E-4
1.33E-4
4.00E-5
(SFin and SF2n)
Coefficients (yr'M
SF2n
0
1.02E-7
5.10E-9
5.10E-6
0
0
0
5.10E-8
7.64E-7
5.10E-6
2.55E-8
1.27E-6
3.82E-5
5.10E-6
7.64E-7
2.55E-9
5.10E-6
2.55E-6
7.64E-7
5-15

-------
capita seafood annual  consumplon  rate  for  pathway p (p = 9 for fish
ingestion and p « 10 for shellfish  Ingestion).  Vj Is the volume of the
upper compartment of the ocean  where 1t  is assumed that the edible fish
are harvested.  For this generic  analysis, average values for the world
are used.  For ocean fish,  the  projected average population consumption
rate 1s 6 kg/yr'1010 persons =  6  ElO kg-persons/yr and for ocean
shellfish it is 1 kg/yr*1010 persons = 1 ElO kg-persons/yr  (UN77).
The volume of the upper compartment of the ocean is obtained  by
                                                     2
multiplying the world ocean surface area of  3.6 E14 m  (CRC75) by the
assumed depth of the upper compartment of  the ocean of  75 m.  The
resulting volume is 2.7 E16 m3 or 2.7  E19  liters.  Thus the  ratio
P  .1 /V, is 2.2 E-9 kg-people/liter-yr for ocean fish and
 p  p  1
3.7 E-10 kg-people/liter-yr for ocean shellfish.

     The terms t. and ty represent the times after placement in  a
repository that  radioactive material  is transmitted to the land  surface or
into  air for  the land surface  and the volcano/meteorite pathways,
 respectively.  The  values  for  tL and  ty change with various scenarios
and discussion of the values chosen for these parameters for various
 scenarios  is  Included in the risk assessment report (EPA85a).  However,
 for this analysis,  where we are  calculating the fatal cancers per C1
 released to  the  available  environment,  we have set tL and ty equal to
 zero.
                                    5-16

-------
     The average height of the troposphere 1s h_A.   Tropospheric height
ranges from 25000 ft (7600 m) to 60,000 ft (18,000 m)  (Wo79).   An average
value of 13,000 m was selected for these calculations.

     The deposition velocity from air to oceans is v.,n.   In this
                                                    wn
analysis, a value of 2 cm/sec was used for all  nuclides,  which was derived
from general deposition velocity information contained in Meteorology and
Atomic Energy, 1968 (AEC68).
     The rate constant for deposition from air to ocean is x  ,  which is
                                                            wn
equal  to vwn/h..  Thus, the value calculated for this analysis is
48.7 yr"1.
                                   5-17

-------
          Chapter 6:  HEALTH EFFECTS PER CURIE "RELEASE RESULTS*
6.1  Fatal  Cancers per Curie Release to  the  Accessible  Environment
     In this section, we list the fatal  cancers  in  the  first  10,000 years
per curie release to the accessible environment  for all  nuclides
considered in the EPA environmental transport  pathway analysis.   These
fatal cancer estimates have been computed using  the methodology  and
algorithms presented in Chapters 2 and 3 and the parameter values
discussed and listed in Chapters 4 and 5.  These fatal  cancer estimates
have been used to develop the radionuclide release limits in Table 1 of
EPA's  environmental  standards for  high-level and transuranic radioactive
waste  disposal 40CFR191 (EPA85c).  Fatal cancer estimates for each of the
four release modes,  for each radionuclide, are shown in Table 6-1.
Tables 6-2, 6-3, and 6-4  show the  contributions of the various
environmental pathways to the fatal  cancers per curie values for the
river, ocean, and  land  surface  release modes.  As mentioned previously, a
period of 10,000 years  was used for  the  integration time.  A value of  .
 10"4 parts per year was  used for the waste  leach rate  ULn). although
 these  fatal  cancers per curie  parameters have only  a very  slight
 dependence on the  value chosen  for xLn.

      For the fatal cancer estimates listed in Tables 6-1  through  6-5, the
 dose response functions applied are linear for  both low and  high-LET
      *The variables used in this chapter are defined in the "Nomenclature"
  section, p. N-l ff.
                                     6-1

-------
radiation.  For low-LET radiation,  EPA considers plausible two of the dose
response functions discussed in the BEIR-III report (NAS80).  They are the
linear model and the linear-quadratic model; with the linear model being
more conservative.  In Appendix G,  where we have discussed the methodology
employed in estimating the risk of  fatal cancers resulting from
radionuclide releases, we have presented information on both the linear
and the linear-quadratic model for  low-LET radiation so that the reader
can compare the magnitude of the risk estimates obtained for given doses
using both models.  The use of the  linear model for both low and high-LET
radiation in our calculation has been thoroughly reviewed and accepted by
the High-level Radioactive Waste Disposal Subcommittee of the EPA Science
Advisory Board (EPA84a).
                                   6-2

-------
TABLE 6-1:
Fatal cancers per curie released to the accessible environment for
different release modes
Nuclide
C - 14
Ni- 59
Sr- 90
Zr- 93
Tc- 99
Sn-126
I -129
Cs-135
Cs-137
Sm-151
Pb-210
Ra-226
Ra-228
Ac-227
Th-229
Th-230
Th-232
Pa-231
U -233
U -234
U -235
U -236
U -238
Np-237
Pu-238
Pu-239
Pu-240
Pu-241
Pu-242
Am-241
Am-243
Cm-245
Cm-246
Releases to
a River
5.83E-02
' 4.61E-05
2.25E-02
1.51E-04
3.65E-04
1.05E-02
8.07E-02
7.73E-03
1.07E-02
9.38E-06
1.18E-01
1.63E-01
2.41E-02
6.67E-02
3.49E-02
5.38E-01
3.40E-01
1.48E-01
2.15E-02
1.96E-02
2.17E-02
1.85E-02
2.06E-02
7.95E-02
4.23E-02
4.97E-02
4.84E-02
2.17E-03
4.79E-02
5.42E-02
5.72E-02
1.01E-01
4.99E-02
Releases due
Releases to Releases to to Violent
an Ocean Land Surface Interactions*
5.83E-02
1.70E-06
6.14E-06
8.59E-06
3.17E-06
2.07E-03
1.43E-04
2.61E-05
2.28E-05
4.01E-07
6.80E-03
5.40E-03
1.07E-04
1.94E-03
2.71E-02
1.87E-01
4.32E-02
1.67E-03
1.90E-04
1.73E-04
1.89E-04
1.64E-04
1.83E-04
7.03E-03
4.06E-04
2.19E-03
1.91E-03
9.24E-06
2.18E-03
3.74E-03
1.09E-02
2.29E-02
1.01E-02
5.83E-02
6.79E-07
3.76E-05
2.26E-05
5.65E-08
1.38E-03
3.96E-03
5.75E-04
2.19E-05
6.71E-08
1.52E-04
5.62E-03
1.57E-05
1.24E-04
1.90E-02
3.86E-01
3.76E-01
2.36E-02
7.51E-04
6.54E-04
8.42E-04
6.18E-04
6.90E-04
1.21E-04
3.10E-04
6.23E-03
5.22E-03
2.50E-06
6.34E-03
1.05E-03
2.45E-03
8.08E-03
3.54E-03
5.83E-02
2.89E-05
1.16E-03
1.22E-04
1.99E-04
2.73E-02
5.57E-02
4.91E-03
3.39E-03
4.72E-06
4.31E-02
7.20E-02
2.78E-02
3.82E-02
5.06E-02
1.26E+00
3.73E-01
1.28E-01
7.75E-03
5.94E-03
8.27E-03
5.62E-03
5.67E-03
2.83E-02
2.07E-02
1.20E-02
1.15E-02
9.36E-04
1.09E-02
2.54E-02
3.40E-02
6.09E-02
2.89E-02
      *For  example,  interactions  of a metorite or a volcanic eruption with a
  repository.
                                     6-3

-------
en
Fatal cancers per curie



Nuclide

C - 14
Ni- 59
Sr- 90
Zr- 93
Tc- 99
Sn-126
I -129
Cs-135
Cs-137
Sm-151
Pb-210
Ra-226
Ra-228
Ac-227
Th-229
Th-230
Th-232
Pa-231
U -233
U -234
U -235
U -236
U -238
Np-237
Pu-238
Pu-239
Pu-240
Pu-241
Pu-242
Am-241
Am-243
Cm-245
Cm-246
^


TOTAL

5.83E-02
4.61E-05
2.25E-02
1.51E-04
3.65E-04
1.05E-02
8.07E-02
7.73E-03
1.07E-02
9.38E-06
1.18E-01
1.63E-01
2.41E-02
6.67E-02
3.49E-02
5.38E-01
3.40E-01
1.48E-01
2.15E-02
1.96E-02
2.17E-02
1.85E-02
2.06E-02
7.95E-02
4.23E-02
4.97E-02
4.84E-02
2.17E-03
4.79E-02
5.42E-02
5.72E-02
1.01E-01
4.99E-02
released to

Drinking
Water
Ingestion
(p = 1)
N/A
4.91E-06
3.72E-03
1.66E-05
7.02E-05
2.67E-04
3.15E-03
2.38E-04
1.62E-03
4.52E-06
5.40E-02
6.41E-02
1.27E-02
3.72E-02
1.12E-02
6.70E-02
1.53E-02
6.10E-02
6.62E-03
6.02E-03
6.56E-03
5.68E-03
6.32E-03
2.43E-02
2.43E-02
2.61E-02
2.60E-02
U25E-03
2.48E-02
2.70E-02
2.69E-02
5.50E-02
2.74E-02
the accessible environment for releases to a river

Freshwater
Fish
Ingestion
(p = 2)
N/A
1.25E-06
1.04E-04
1.41E-07
7.70E-06
2.04E-03
2.65E-04
7.89E-04
5.37E-03
2.88E-07
1.38E-02
8.18E-03
1.62E-03
2.37E-03
8.55E-04
5.13E-03
1.17E-03
1.71E-03
1.69E-04
1.54E-04
1.67E-04
1.45E-04
1.61E-04
3.10E-02
4.96E-04
5.33E-04
5.31E-04
2.55E-05
5.07E-04
5.59E-03
5.56E-03
3.51E-03
I.75E-03
Above
Surface
Crops
Ingestion
(p = 3)
N/A
3.94E-05
1.75E-02
1.28E-04
2.02E-04
5.37E-04
6.75E-02
6.10E-03
2.53E-03
4.53E-06
4.93E-02
7.78E-02
9.19E-03
2.70E-02
1.50E-02
3.40E-01
1.89E-01
7.74E-02
1.44E-02
1.31E-02
1.43E-02
1.24E-02
1.38E-02
2.41E-02
1.75E-02
2.28E-02
2.16E-02
8.94E-04
2.23E-02
2.16E-02
2.40E-02
4.13E-02
2.05E-02


Milk
Ingestion
(p = 4)
N/A
4.72E-07
1.19E-03
4.05E-07
8.38E-05
2.42E-05
9.68E-03
'5.71E-04
8.42E-04
6.13E-09
9.26E-04
2.41E-03
3.71E-04
4.85E-05
4.97E-06
7.74E-05
3.88E-05
2.60E-05
3.10E-04
2.82E-04
3.07E-04
2.66E-04
2.96E-04
1.83E-05
1.57E-07
1.85E-07
1.80E-07
8.10E-09
1.78E-07
7.63E-07
8.28E-07
7.67E-05
3.79E-05


Beef
Ingestion
(p = 5)
N/A
1.83E-08
4.59E-06
5.23E-06
1.38E-06
3.75E-05
1.31E-04
3.1J5E-05
4.65E-05
2.97E-08
2.16E-05
6.03E-05
8.63E-06
1.17E-06
1.15E-07
1.80E-06
9.02E-07
1.01E-06
2.00E-06
1.82E-06
1.98E-06
1.72E-06
1.91E-06
7.08E-06
6.10E-08
7.18E-08
6.99E-08
3.14E-09
6.90E-08
1.29E-07
1.41E-07
2.59E-07
1.29E-07
Inhalation
of
Resuspended
Material
(p = 6)
N/A
3.25E-10
4.05E-09
6.58E-08
4.67E-11
6.47E-08
3.68E-08
5.38E-09
1.33E-09
2.14E-09
3.45E-07
8.91E-06
5.61E-07
4.29E-06
4.85E-04
4.29E-04
6.27E-04
5.33E-04
7.41E-06
4.53E-06
5.46E-06
4.29E-06
4.09E-06
3.40E-06
1.14E-05
3.14E-04
2.75E-04
8.73E-08
3.13E-04
3.85E-05
7.92E-05
3.85E-04
1.75E-04
External
Dose -
Ground
Contam.
(p = 7)
N/A
3.17E-10
O.OOE+00
1.45E-07
O.OOE+00
7.55E-03
5.41E-06
O.OOE+00
3.19E-04
O.OOE+00
9.60E-08
l.OOE-02
2.23E-04
1.07E-04
7.39E-03
1.25E-01
1.34E-01
7.58E-03
3.43E-05
5.63E-07
4.00E-04
4.41E-09
2.65E-05
4.83E-05
1.74E-09
2.21E-08
3.97E-08
9.46E-09
3.95E-08
6.22E-06
7.08E-04
3.49E-04
2.11E-08
External
Dose -
Air
Submersion
(p = 8}
N/A
1.11E-15
O.OOE+00
4.86E-14
1.80E-19
1.14E-10
6.86E-13
O.OOE+00
4.45E-12
1.31E-17
6.13E-15
1.56E-10
4.83E-12
2.18E-12
2.25E-10
1.95E-09
2.90^-09
1.76E-10
1.33E-12
1.29E-14
1.60E-11
1.01E-14
1.88E-12
1.55E,-12
1.60E-15
4.26E-14
3.55E-14
1.68E-15
3.62E-14
1.10E-12
2.93E-11
2.79E-11
1.70E-14

-------
TABLE 6-3:
Fatal cancers per curie released to the accessible environment for
releases to an ocean
Nuclide
C - 14
141- 59
Sr- 90
Zr- 93
Tc- 99
Sn-126
I -129
Cs-135
Cs-137
Sm-151
Pb-210
Ra-226
Ra-228
Ac-227
Th-229
Th-230
Th-232
Pa-231
U -233
U -234
U -235
U -236
U -238
Np-237
Pu-238
Pu-239
Pu-240
Pu-241
Pu-242
Am-241
Am-243
Cm-245
Cm-246
TOTAL
5.83E-02
1.70E-06
6.14E-06
8.59E-06
3.17E-06
2.07E-03
1.43E-04
2.61E-05
2.28Er05
4.01E-07
6.80E-03
5.40E-03
1.07E-04
1.94E-03
2.71E-02
1.87E-01
4.32E-02
1.67E-03
1.90E-04
1.73E-04
1.89E-04
1.64E-04
1.83E-04
7.03E-03
4.06E-04
2.19E-03
1.91E-03
9.24E-06
2.18E-03
3.74E-03
1.09E-02
2.29E-02
1.01E-02
Ocean
Fish
Ingesti on
(p = 9)
N/A
1.20E-06
2.30E-06
8.05E-06
1.73E-06
1.96E-03
7.82E-05
2.36E-05
2.07E-05
5.23E-08
4.42E-03
4.05E-03
8.02E-05
2.53E-04
2.03E-02
1.40E-01
3.24E-02
1.43E-03
1.63E-04
1.48E-04
1.62E-04
1.41E-04
1.57E-04
6.03E-03
3.35E-05
1.81E-04
1.57E-04
7.63E-07
1.80E-04
4.88E-04
1.42E-03
2.98E-03
1.31E-03
Ocean
Shellfish
Ingestion
(p = 10)
N/A
5.00E-07
3.84E-06
5.37E-07
1.44E-06
1.09E-04
6.51E-05
2.46E-06
2.15E-06
3.49E-07
2.46E-03
1.35E-03
2.67E-05
1.69E-03
6.76E-03
4.67E-02
1.08E-02
2.38E-04
2.71E-05
2.47E-05
2.70E-05
2.34E-05
2.61E-05
l.OOE-03
3.73E-04
2.01E-03
1.75E-03
8.48E-06
2.00E-03
3.25E-03
9.44E-03
1.99E-02
8.75E-03
                                     6-5

-------
en
 t




Nuclide

C - 14
Ni- 59
Sr- 90
Zr~ 93
Tc- 99
Sn-126
I -129
Cs-135
Cs-137
Sm-151
Pb-210
Ra-226
Ra-228
Ac -227
Th-229
Th-230
Th-232
Pa-231
U -233
U -234
U -235
U -236
U -238
Np-237
Pu-238
Pu-239
Pu-240
Pu-241
Pu-242
Am-241
Am-243
Cm-245
Cm-246
srb per iune



TOTAL

5.83E-02
6.79E-07
3.76E-05
V2.26E-05
5.65E-08
1.38E-03
3.96E-03
5.75E-04
2.19E-05
6.71E-08
1.52E-04
5.62E-03
1.57E-05
1.24E-04
1.90E-02
3.86E-01
3.76E-01
2.36E-02
7.51E-04
6.54E-04
8.42E-04
6.18E-04
6.90E-04
1.21E-04
3.10E-04
6.23E-03
5.22E-03
2.50E-06
6.34E-03
1.05E-03
2.45E-03
8.08E-03
3.54E-03

Above
Surface
Crops
Ingestion
(p = 13)
N/A
6.68E-07
3.53E-05
2.11E-05
3.99E-08
1.46E-05
3.47E-03
5.25E-04
1.01E-05
4.61E-08
1.46E-04
2.96E-03
8.44E-06
7.94E-05
3.44E-03
9.63E-02
5.46E-02
1.13E-02 [
6.61E-04 ]
6.01E-04
6.56E-04
5.68E-04
6.32E-04
8.57E-05
2.00E-04
4.20E-03
3.47E-03
1.64E-06
4.30E-03
7.00E-04
1.49E-03
5.04E-03
2.29E-03


Milk
Ingestion
(p = 14)
N/A
7.65E-09
2.29E-06
6.39E-08
1.58E-08
6.30E-07
4.76E-04
4.70E-05
3.22E-06
5.96E-11
2.63E-06
8.78E-05
3.26E-07
1.36E-07
1.09E-06
2.10E-05
1.08E-05
3.65E-06
1.36E-05
1.24E-05
1.35E-05
1.17E-05
1.30E-05
6.21E-08
1.73E-09
3.25E-08
2.77E-08
1.42E-11
3.29E-08
2.37E-08
4.91E-08
8.93E-06
4.06E-06


Beef
Ingestion
(p = 15)
• N/A
2.96E-10
8.83E-09
8.25E-07
2.61E-10
9.76E-07
6.47E-06
2.60E-06
1.78E-07
2.89E-10
6.11E-08
2.19E-06
7.58E-09
3.31E-09
2.53E-08
4.88E-07
2.50E-07
1.41E-07
8.75E-08
7.96E-08
8.68E-08
7.52E-08
8.37E-08
2.40E-08
6.68E-10
1.26E-08
1.08E-08
5.49E-12
1.28E-08
4.01E-09
8.35E-09
3.02E-08
1.38E-08
Inhalation
of
Resuspended
Material
(p = 12)
N/A
3.11E-09
4.02E-08
4.47E-07
4.66E-10
6.03E-07
3.23E-07
4.32E-08
1.31E-08
2.07E-08
3.41E-06
7.88E-05
5.59E-06
4.24E-05
2.77E-03
2.56E-03
3.76E-03
3.69E-03
6.59E-05 '
4.03E-05
4.85E-05
3.82E-05
3.64E-05
3.36E-05
1.10E-04
2.03E-03
1.75E-03
8.66E-07
2.04E-03
3.46E-04
6.63E-04
2.73E-03
1.24E-03
External
Dose -
Ground
• Contam.
(p - 16)
N/A
3.54E-11
O.OOE+00
1.91E-07
O.OOE+00
1.37E-03
1.89E-06
O.OOE+00
8.33E-06
O.OOE+00
1.86E-09
2.49E-03
1.34E-06
2.06E-06
1.27E-02
2.87E-01
3.18E-01
8.53E-03
1.06E-05
1.74E-07
1.24E-04
1.37E-09
8.21E-06
1.12E-06
1.30E-10
3.21E-08
4.71E-08
1.13E-10
6.23E-08
1.32E-06
2.96E-04
3.07E-04
1.64E-08
External
Dose -
Air
Submersion
(p = 11)
N/A
3.19E-14
O.OOE+00
9.92E-13
5.41E-18
3.19E-09
1.81E-11
O.OOE+00
1.32E-10
3.81E-16
1.82E-13
4.13E-09
1.44E-10
6.49E-11
3.85E-09
3.49E-08
5.23E-08
3.66E-09
3.56E-11
3.46E-13
4.27E-10
2.70E-13
5.01E-11
4.61E-11
4.63E-14
8.25E-13
6.78E-13
5.01E-14
7.09E-13
2.98E-11
7.37E-10
5.94E-10
3.62E-13

-------
6.2  Comparison of Fatal  Cancers  and Serious Genetic  Effects (All
Generations) per Curie Release to the Accessible Environment

     The curie release limits for 40CFR191 are based on fatal cancer
risks.  The estimated fatal cancers per curie of various radionuclides
released to the accessible environment are summarized, for the four
release modes we considered, in Table 6-1.

     We also computed estimates of the serious genetic, effects to all
future  generations  per curie release to the accessible environment.  The
mechanics  of computing the estimates of serious genetic effects is the
 same as is described  in  this  report  for fatal cancer  risks  except that
 genetic effects  risk  factors  are  applied  in place  of  the  fatal cancer  risk
 factors (FCF   ).   The genetic  effects  risk  factors are derived using the
 genetic risk  estimates  from  BEIR-3  (NAS80)  and  using  the  dose received
 before age 30.  The BEIR-3 estimates are  "indirect"  estimates and are
 calculated using the normal  prevalence of genetic  defects and the  dose
 that is considered to double this risk.   The MAS  estimates used  by  EPA are
 based on a doubling dose range,  with a lower bound of 50 rem and an upper
 bound-of 250 rem.  To express the range as a single estimate, the
 geometric mean of the range 1s used, a method first recommended by UHSCEAR
 (UN58) for purposes of calculating genetic risk.   A factor of three
 increase  in risk for high dose rate, low-LET radiation is also used.  We
 apply an  RBE of 20 to estimate the genetic risks for all high-LET
 radiations.
                                     6-7

-------
     In developing the average mutation rate for the two sexes used in the
calculation of the relative mutation risk, the BEIR-3 committee postulated
that the induced nutation rate in females was about 40 percent of that in
males (NAS30).  Recent studies by Dobson et al. (Do83a, Do83b, Do84a,
Do84b) suggest that the assumption was invalid and that human oocytes
should have a risk equivalent to that of human spermatogonia.  Use of the
results of the Dobson studies in place of the BEIR-3 postulation would
increase our genetic risk estimates by a factor of 1.43.

     A discussion of radiation-induced health effects other than fatal
cancer is  included in section G.5 of Appendix G.  Specifically a more
detailed discussion of the basis for the EPA genetic risk estimates is
incorporated in section G.5.5.

      In Table 6-5, we have listed our estimates for both the fatal cancers
and the serious genetic effects to all generations so that the reader can
compare the relative magnitude of these two health effects.   In  reviewing
Table 6-5, we note that the genetic effects are about 50 percent of the
fatal cancers for 126Sn, 135Cs, 137Cs, 228Ra, and 232Th and 25 to 50 percent
for 59Ni,  226Ra, 227Ac, 229Th, 230Th, and 231Pa.  The genetic effectsr
                                                       210    237
are between 15  and 25 percent of the  fatal cancers for    Pb,    Np
and all Pu, Am, and Cm  isotopes.  For the other radionuclides, the genetic
effects are less than 15 percent of the fatal cancer estimates.  Our curie
release limits  for 40 CFR  191 were based  only on consideration of fatal
cancers because we believe that the consideration of genetic  and other
effects, along  with the fatal cancers, would  not significantly effect the
results.
                                    6-8

-------
curfe
                                                              to
                                                                                envtron.ent for
Nuclide
~ • i ••
C - 14
Ni- 59
Sr- 90
Zr- 93
Tc- 99
Sn-126
I -129
Cs-135
Cs-137
Sm-151
Pb-210
Ra-226
Ra-228
Ac-227
Th-229
Th-230
Th-232
Pa-231
U -233
U -234
U -235
U -236
U -238
Np-237
Pu-238
Pu-239
Pu-240
Pu-241
Pu-242
Am-241
Am-243
Cm-245
Cm-246
•••
Release to a River
Fatal . A .
Cancers Genetic
— — 	 : 	 — . — _ 	
5.83E-02
4.61E-05
2.25E-02
1.51E-04
3.65E-04
1.05E-02
8.07E-02
7.73E-03
1.07E-02
9.38E-06
1.18E-01
1.63E-01
2.41E-02
6.67E-02
3.49E-02
5.38E-01
3.40E-01
1.48E-01
2.15E-02
1.96E-02
2.17E-02
1.85E-02
2.06E-02
7.95E-02
4.23E-02
4.97E-02
4.84E-02
2.17E-03
4.79E-02
5.42E-U2
5.72E-02
1.01E-01
4.99E-02
3.03E-02
1.55E-05
4.40E-04
9.36E-06
1.74E-05
4.22E-03
1.82E-04
3.19E-03
4.13E-03
1.24E-09 i
1.91E-02
3.54E-02
1.11E-02
1.57E-02
8.31E-03
1.35E-01
1.36E-01
2.33E-02
2.03E-03
1.66E-03
2.06E-03
1.57E-03
1.50E-03
1.29E-02
7.23E-03
8.05E-03
7.85E-03
3.20E-04
7.71E-03
8.89E-03
9.45E-03
1.64E-02
8.08E-03
	 — _ ...
Release to an Ocean
Fatal _ _
Cancers Genetic
5.83E-02
1.70E-06
6.14E-06
8.59E-06
3.17E-06
2.07E-03
1.43E-04
2.61E-05
2.28E-05
4.01E-07
6.80E-03
5.40E-03
1.07E-04
1.94E-03
2.71E-02
1.87E-01
4.32E-Q2
1.67E-03
1.90E-04
1.73E-04
1.89E-04
1.64E-04
1.83E-04
7.03E-03
4.06E-04
2.19E-03
1.91E-03
9.24E-06
2.18E-03
3.74E-03
1.09E-02
2.29E-02
1.01E-02
3.03E-02
5.74E-07
1.20E-07
5.31E-07
1.51E-07
6.57E-04
3.19E-07
1.07E-05
8.77E-06.
5.28E-11
1.11E-03
1.10E-03
4.91E-05
4.53E-04
5.09E-03
3.64E-02
1.65E-02
2.38E-04
1.77E-05
1.46E-05
1.68E-05
1.39E-05
1.32E-05
1.14E-03
6.94E-05
3.54E-04
3.10E-04
1.36E-06
3.52E-04
6.13E-04
1.75E-03
3.69E-03
1.63E-03
Dft, . . J ^ ^ Releases due to Violent
Release to Land Surface Interactions*
/atal Genetic Fata1 r +-
Cancers tenenc Cancers Genet7c
5.83E-02
6.79E-07
3.76E-05
2.26E-05
5.65E-08
1.38E-03
3.96E-03
5.75E-04
2.19E-05
6.71E-08
1.52E-04
5.62E-03
1.57E-05
1.24E-04
1.90E-02
3.86E-01
3.76E-01
2.36E-02
7.51E-04
6.54E-04
8.42E-04
6.18E-04
6.90E-04
1.21E-04
3.10E-04
6.23E-03
5.22E-03
2.50E-06
6.34E-03
1.05E-03
2.45E-03
8.08E-03
3.54E-03
—
3.03E-02
2.29E-07
7.34E-07
1.44E-06
2.66E-09
6.01E-04
9.79E-06
2.37E-04
8.83E-06
' 6.45E-12
2.42E-05
1.69E-03
4.70E-06
2.61E-05
6.13E-03
1.42E-01
1.57E-01
5.57E-03
6.79E-05
5.19E-05
1.11E-04
4.91E-05
5.02E-05
1.93E-05
5.12E-05
9.76E-04
8.21E-04
3.61E-07
9.92E-04
1.67E-04
4.62E-04
1.35E-03
5.55E-04
5.83E-02
2.89E-05
1.16E-03
1.22E-04
1.99E-04
2.73E-02
5.57E-02
4.91E-03
3.39E-03
4.72E-06
4.31E-02
7.20E-02
2.78E-02
3.82E-02
5.06E-02
1.26E+00
3.73E-01
1.28E-01
7.75E-03
8.*27E-03
5.67E-03
2.83E-02
2.07E-02
1.20E-02
1.15E-02
9.36E-04
1.09E-02
2.54E-02
3.40E-02
6.09E-02
2.89E-02
3.03E-02
9.73E-06
8.40E-06
7.23E-06
9.37E-06
1.17E-02
1.34E-04
2.02E-03
1.36E-03
4.59E-10
6.01E-03
1.26E-02
3.08E-03
5.13E-03
7.26E-03
4.32E-01
1.37E-01
2.38E-02
1.81E-04
9.10E-06
7.47E-04
8.08E-06
4.98E-05
3.63E-03
2.42E-03
7.08E-04
6.73E-04
1.06E-04
6.50E-04
3.06E-03
5.04E-03
7.56E-03
3.54E-03
*For example, interactions of a metorite or a volcanic eruption with a repository.

-------
                    Chapter  7:  UNCERTAINTY ANALYSIS*

     Environmental  pathway dosimetry and risk  models  generally employ
environmental  transport methodology consisting of  multiplicative chain
algorithms incorporating several variables.   In performing  regulatory
analyses, there is  a tendency to choose conservative  values for these
variables due to the inherent uncertainty in the parameters.   The
multiplicative nature of the models means that conservatisms  in chosen
values for individual  parameters can lead to larger conservatism in the
result.  This becomes an issue of contention between  the regulators and
those being regulated in virtually every rulemaking action  where
regulatory decisions will be made based on the results of the application
of multiplicative chain models.  Since the protection of public health is
at stake, regulators believe that they must choose conservative values to
"insure" that the public is protected.  The problem with this approach is
that multiple conservatisms can lead to extremely  conservative and
sometimes unrealistic results.  Those being regulated generally experience
escalating project costs as regulatory requirements become  more stringent
so that there is strong  incentive to encourage the use of less
conservative parameter values.
     *In addition to the discussions of uncertainty included in this
chapter, uncertainty 1s discussed in Appendices F and G.  In Section F.5
of Appendix F, uncertainty analysis related to radiation dosimetry
calculations is addressed.  The uncertainties 1n risk estimates for
radiogenic cancer are discussed in Section G.4 of Appendix G.
                                    7-1

-------
     The consideration of uncertainty  1n  Individual  parameter values  used
1n environmental  pathway models has been  a  subject  of  discussion  in the
technical community for more than a decade  (Ba79a,  Ba79b,  Ho79, M179,
Ru79, Sh79).  However, the comprehensive  consideration of  overall
uncertainty in environmental pathway,  dosimetry and health impact analyses
has begun to be addressed only recently (R183,  Ru83).

     When considering the uncertainty  in  the input  parameters associated
with environmental pathway calculations,  the most common procedure has
been to qualitatively consider the range  of reported parameter values and
to use judgement to select the "best"  value to use for a particular
application.  More recently, there has been a tendency to statistically
analyze the distribution of data for individual parameters and to choose a
mean or median as the "best" value.

     It  appears that the most  systematic mechanism for considering
uncertainty in multiplicative  chain models would be to include a
probability distribution  representing  current  uncertainty about parameter
values  in  the input data and to  run a  sufficient number of cases  (with
parameter  values  for each case chosen  by a suitable sampling  procedure)
such that  the distribution  of  results  can be evaluated. The  results  of
this type  of analysis could be considered in choosing an  appropriate set
of single-valued  parameters to apply  for regulatory calculations.
Alternately, a decision might  be made  to perform the  regulatory
calculations probabilistically,  then  choose limits  for a  standard
                                    7-2

-------
(or to perform calculations to see if a limit is met)  at a specified
confidence level.  We believe the subject needs additional study to
determine the most appropriate use of uncertainty analysis for standards
setting applications;'however, it is clear to us that  a quantitative
analysis of the uncertainties is most useful  for focusing on important
uncertainties for more intensive consideration.

     EPA is presently involved in a re-evaluation of the methodology we
apply in risk assessment calculations.   In a  speech at Princeton
University on February 18, 1984, EPA Administrator William Ruckelshaus
stated (Ru84), in proposing some principles for more reasonable
discussions about risk, "First, we must insist on risk calculations being
expressed as distributions of estimates and not as magic numbers that can
be manipulated without regard to what they really mean.  We must try to
display more realistic estimates of risk to show a range of
probabilities.  To help do this we need new tools for  quantifying and
ordering sources of uncertainty and for putting them in perspective."
Thus, at the highest level, EPA management is calling  for an upgrading
of our risk assessment methodology so that risk estimates can be more
realistically expressed and the range of uncertainty in risk estimates
more thoroughly quantified.

     Most of the technical analyses discussed in this  report were
performed prior to the increase in emphasis on uncertainty in risk
assessment calculations.  The results presented in Chapter 6 were
                                   7-3

-------
determined using point values  for each parameter.   In  most  cases,  these
point values were chosen after review of the range  of  values  reported 1n
the literature and were chosen to be near the mean  or  median  value to
avoid obtaining unrealistically conservative results.   There  are certain
cases where conservative assumptions have been made, and these are
discussed in the sections of the report describing  the algorithms used in
the computations (Chapter 3).   Baes (Ba84) has published a  very complete
review and analysis of parameters used to predict the  transport of
radionuclides through agricultural pathways.  For most radionuclides we
considered, the  river release mode was dominant and the agricultural
pathways  either  dominated or were major pathways in determining the fatal
cancers calculated for the  river release mode.  Default values  from Baes
report were used for many critical  food pathway parameters and  Baes states
that these  default values were chosen to be  realistic rather  than  highly
conservative.   Since  we  were  able to  use  default values based on  Baes
 recent  and  extensive  review of the. literature, we  believe  that  this
 significantly  strengthens the analysis  and  causes  it  to be more realistic
 than would  be  the  case if other  sources of  data were  used.

      The Envirosphere Company,  a Division of Ebasco Services  Incorporated,
 has recently  completed a significant project (Ri83, ENV85) where they
 performed an  uncertainty analysis for the input  parameters of the river
 release mode algorithms.  These are the algorithms used to derive the
 radionuclide release limits for Table 1 of 40CFR191  (EPA85c).  Envirosphere
                                     7-4

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reviewed the EPA river pathway models and identified the key uncertain
input parameters for each river pathway.  The key uncertain parameters
were:
          soil-to-plant bioaccumulation factor (B. . and B, „'
          soil sink removal rate constant (\~)
                                            5n
          fish reconcentration factor (CF  )
          resuspension factor (RF)
          sedimentation removal fraction*
          irrigation fraction (fR)
          water-treatment removal fraction
          cow-to-milk transfer factor (F	)
                                        mn
   (a)
   (a)
r
          cow-to-beef transfer factor
          effective decay constant from vegetation
          dose conversion factors**
          risk conversion factors**
                (a)
The uncertainties in these parameters were characterized by probability
distributions which were propagated through the pathway models using a
simulation technique which produced uncertainty distributions in the
estimates of fatal cancers per unit radionuclide release to a river.  The
      *These  factors were  set equal to 1.0  in the EPA calculations  but were
 assigned a range of values for the Envirosphere calculations.
      **These factors were combined in the  EPA analysis  into the fatal
 cancer  risk  factor (FCFnp).
               factors are  used  in calculating  the term  RInp  in the  EPA
 algorithms.   They  are defined and their application  in  the calculation  of
 RInp  values  is discussed in  Section C.I of Appendix  C.
                                    7-5

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purpose of this work was to estimate  the uncertainty  associated  with  the  EPA
river release mode pathways to first-order and to identify  the important
uncertain parameters so that the values  chosen for these  parameters could be
carefully re-evaluated.  Preliminary  Envirosphere analyses  were  presented to
expert reviewers (Ri83) whose comments were used to improve some of the
model input parameter uncertainty distributions for the final analysis, to
better reflect the current state of knowledge about those factors.

     An example of the results of the Envirosphere uncertainty analysis is
shown in Figure 7-1, which shows uncertainty distributions  for the fatal
cancers risk for Am-243 releases to a river*.  Figure 7-1 shows  a probability
plot of the fatal cancers per 10,000 years per curie of Am-243 released to a
river.  The plots are generated by propagating the uncertainty distributions
for the parameters listed above through  the eight river pathway  algorithms
using stochastic simulation and a Latin  Hypercube sampling  technique. The
details of the analysis are presented in the Envirosphere reports (R183,
ENV85).  Figure 7-1 indicates a 70 percent probability, considering parameter
uncertainties, that the fatal cancers over 10,000 years per curie of  Am-243
released to a river will be 5.72E-2, as  calculated by EPA (Table 6-2), or
less.

     Similar calculations were performed for several other  radionuclides
listed in Table 1 of 40CFR191 and these  calculations and  the results  are
discussed in detail in the Envirosphere  reports  (R183, ENV85).   The  results
     *The 40CFR191 release limit for Am-243 1s 100 C1/10,000 yr/1000 MTHM.
                                    7-6

-------

-------
indicated,  for all  radionuclides  analyzed except Np-237,  a  probability of
50 percent  or more  that  the  fatal  cancers over  10,000 years per curie
released to a river will  be  the number  calculated by EPA  or less.  The
exception was Np-237,  which  showed a  10 percent probability in the
Envirosphere calculations.   However,  we believe there are equally
supportable differences  of expert opinion as to the appropriate shape of
the parameter uncertainty distributions for the plant uptake factor
(Biy) and the fish  concentration  factor (CF   ).  We requested that
Envirosphere provide us  an additional analysis  for Np-237,  using the
alternate parameter uncertainty  distributions for B.  and CF^.  This
                              *                    iv        np
analysis yielded a  probability of about 50  percent for  the  EPA  Np-237
fatal cancers per curie  released  to the accessible environment.

     The Envirosphere project also included a number of model sensitivity
analyses which are not discussed  here but which are discussed in  detail  in
their report.  In addition,  the Envirosphere  reports discuss the  following.
subject areas:

     a. quantitative comparisons  of important differences in expert
      1  opinion regarding how to characterize key  uncertainties,
     b. an examination of the sensitivity  of dose  and  risk  uncertainty
        results to the simulation technique used to  propagate uncertainties,
        type of parameter uncertainty distributions  used (e.g., uniform vs.
        log  normal) and possible parameters correlation effects,
     c. the  relative importance of model parameter uncertainties with
        respect to the overall uncertainties in dose  and risk estimates.
                                    7-8

-------
We used these results, along with suggestions by the EPA Science Advisory
Board (SAB) Subcommittee (EPA84a), to identify those radionuclide release
limits that warranted further consideration regarding the selection of
appropriate values for important uncertain model parameters.  Based upon
this re-evaluation, some revisions were made to our input parameters in
order to better reflect the current state of understanding regarding these
parameters.

     The Envirosphere report summarized a number of findings and
conclusions which are quoted below.  In some cases, we have added
explanatory notes.  We gave careful consideration to these findings and
conclusions in the final analysis used as a basis for the 40CFR191
(Table 1) release limits.

Envirosphere Findings (Ri83)
     1.  "Uncertainty about the EPA model  dose and risk outputs can span
        over nine orders of magnitude, depending on the radionuclide being
        analyzed."
     2.  "Most of the model's dose output  uncertainty is attributable to
        uncertainties about the ingestion dose conversion factor, the
        soil-to-plant concentration factor (B1yl and B1v2), the soil
        root zone removal rate constant (x$ ) and the fraction of river
        flow used for irrigation.  These  pathway factors are all
        associated with the crop ingestion pathway, which is the  largest
        dose contributing pathway of the  eight included."
                                   7-9

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3. "Environmental  pathway factor uncertainties  are  at  least as
   significant as  dose conversion factor uncertainty and risk
   coefficient uncertainty.  In fact,  many pathway  factor
   uncertainties are larger contributors to effects uncertainty than
   are risk coefficient uncertainties  in the EPA model, especially
   for high LET alpha emitters."
4. "Uncertainties about external dose conversion factors, transfer
   coefficients for forage to milk and forage to meat  (Fmn and
   Ffn), the plant surface removal coefficient UEn) and the
   fraction of radionuclide removed by municipal water treatment are
   not  important  contributors to EPA model output  uncertainty  for
   this  application."
 5. "Soil  resuspension  factor uncertainty  is only important  for
   Plutonium  in this  application of the  EPA model,  because  plutonium
    is the only  radionuclide  specified  in 40CFR191  which has a
    significant  inhalation pathway  dose contribution."   (EPA Note:  the
    air resuspension model has  been modified,  based on suggestions by
    the SAB subcommittee, and does not  now contribute in a major way
    to the total  dose and risk  values  for plutonium.)
 6. "Several expert reviewers expressed dissatisfaction with the
    manner in which the EPA treated the removal of radioactivity from
    the soil root zone and resuspension of radioactive soil.   In
    addition, removal of  radionuclides by sedimentation processes in
    the river was considered to be important, especially for
    radionuclides with high binding coefficients, yet the EPA  did not
    include sedimentation in their model.  The treatment of these
                                7-10

-------
   processes  in the EPA river pathways modeling warrants further
   consideration."  (EPA Note: EPA is not aware of expert reviewer
   dissatisfaction with the model used to remove radioactivity
   from  the soil  root zone.  Calculations were performed (see
   Appendix C, Section C.8) to show that recycling from the soil
   below the  root zone into the river and back to the soil root zone
   was not significant for fR values in the range applied by EPA
   (fR = 0.1).  Also, distribution coefficients (K^'s) have
   been  revised to generally agree with those suggested by Baes
   (Ba84).  As mentioned above, the resuspension model used by EPA
   has been revised in accordance with suggestions provided by the
   Science Advisory Board subcommittee.  Several reviewers did
   suggest that EPA add sedimentation removal to our  river model.
   There is no question that certain radionuclides deposit into
   sediments  in slowly flowing rivers and lakes and,  during the
   short-term, sedimentation lowers river water concentrations.
   However, in the long time period considered in these calculations,
   massive floods (100 and  1000 year floods, etc.), may occur so  that
   much  of the deposited activity may be resuspended  from the
   sediment and distributed on farm land.   For this reason and
   because of the difficulty involved in modelling sedimentation  and
   subsequent resuspension  during floods, we chose what we consider
   to be a conservation position and did not model radionuclide loss
   from  river water  due to  sedimentation.)
7. "Possible  correlations among model parameters can  have a
   significant effect on uncertainty analysis  results.  Correlation
                              7-11

-------
       effects can increase or reduce model output uncertainties
       depending on the extent of correlation and the structure of the
       model.  A lack of  sufficient understanding about the processes
       which might result  in parameters being correlated permits only a
       limited treatment  of correlation effects."
     8. "Identifying a specific repository  site would considerably reduce
       model dose and effects output uncertainties since many key
       uncertainties are  for site-related  pathway factors; however, there
       would still be significant uncertainty contributions from dose
       conversion factors  and the risk coefficient.  Much of the overall
       uncertainty in dose estimation  is contributed by site related
       pathway  parameters, and,  assuming time can be "frozen" in the
       assessment, once a specific  site is identified measurements and
       data can  be collected for these parameters.  The time invarient
       assumption is necessary because to  do otherwise eliminates the
       ability  to make  reasonably based quantitative judgments  about
       model uncertainties.  Also,  the uncertainty characterization
       developed provides a structure  for  updating the analysis as the
        state of knowledge evolves and  as changes  occur."

Envirosphere Conclusions (R183)
     Envlrosphere stated the following  conclusions concerning the  use  of
probabilistic techniques for examining  uncertainties  In risk assessments:

     1, "It 1s  important to assure  high quality  1n the  Input parameter
        uncertainty  distributions used  in  an uncertainty analysis.   The
                                   7-12

-------
   validity  of  the  results depends directly on the quality of the
   input  uncertainty characterizations and the results are quite
   sensitive to the type  of  distribution  assumed.  Careful
   consideration must  be  given to the implications of using a
   particular probability distribution to represent a state of
   •knowledge.  Where valid differences of opinion exist, the
   sensitivity  of model  results  to those  alternative formulations
   should be tested."
2. "The type of analysis  presented in this  (Envirosphere)  report
   focuses on important  technical issues  of the  problem, provides  a
   structure for updating the assessment  as new  information and
   understanding evolves and provides  a  basis for  defensible  and
   consistent standard-setting."
3. "The value of performing  an analysis  of  uncertainties  depends  on
   the costs associated with being wrong about a risk  management
   decision.  These costs might include:  (1)  unexpected or unforeseen
   negative consequences; (2) misplaced or practically irreversible
   commitments of time,  funds, manpower and capital; (3)  adopting
   policies which are difficult to alter at a later date when new
   information becomes available, or (4) licensing, regulatory or
   legal complications and  delays.   For  risk management applications
   an  analysis of  risk assessment uncertainties is, in effect, an
   analysis  of  investment uncertainties, and as such the uncertainty
   analysis  should be coupled with a cost-benefit analysis.  For the
   application  examined  in-this stu
-------
        limits and the degree of certainty  that-those  limits  will  achieve
        an acceptable level  of population protection."

     In summary,  EPA is placing new emphasis  on  analyzing  and discussing
the uncertainty in our risk  assessments.   The basic  calculations  presented
in this report were completed before the  new  emphasis  was  Implemented.  We
have used point parameter values to calculate fatal  cancers per unit
radionuclide release and have generally used  what  we believe  are  realistic
parameter values  in the calculations, refined by the insights gained  from
the Envirosphere  analysis and by suggestions  by  the  SAB  subcommittee.
Taking into account the uncertainty analysis  performed by  Envirosphere
helps to provide  reasonable  assurances that the  EPA  goal  of  10 deaths  in
10,000 years per  1000 MTHM is reflected by the release limits in  Table  1
of 40CFR191.
                                   7-14

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Ad78
AEC68
AEC73
Ba79a
Ba79b
Ba83a
Ba83b
Ba84
Be 76
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                                    R-4

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          1978, "Estimates of Internal Dose Equivalent to 22 Target Organs
          for Radionuclides Occurring in Routine Releases from Nuclear
          Fuel-Cycle Facilities", USNRC Rep. NUREG/CR-0150,
          ORNL/NUREG/TM-190, (Springfield, VA:  NTIS).
                                    R-5

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Ki78b     Killough G.G., Dunning D.E.. Jr.  and Pleasant J.C., 1978, "INREH
          II:  A Computer Implementation of Recent Models for Estimating
          the Dose Equivalent to Organs of Man from an Inhaled or Ingested
          Radionuclide", USNRC Rep. ORNL/NUREG/TM-84, Oak Ridge National
          Laboratory, (Springfield, VA: NTIS).

KoSla     Kocher D.C.,  1981, "Radioactive Decay Data Tables -- A Handbook
          of Decay Data for Application to Radiation Dosimetry and
          Radiological  Assessments", USDOE Rep. DOE/TIC-11026, Technical
          Information Center, U.S. Department of Energy, (Springfield,
          VA:  NTIS).

KoSlb     Kocher D.C.,  1981, "A Dynamic Model of the Global  Iodine Cycle
          and Estimation of Dose to the World Population from Releases of
          Iodine-129 to the Environment", Environment  International, Vol.
          5, 1981, pp.  15-31.

KoSlc     Kocher D.C.,  1980, "Dose-Rate Conversion Factors for External
          Exposure to Photon and Electron Radiation  from Radionuclides
          Occurring  in  Routine Releases from  Nuclear Fuel-Cycle
          Facilities",  Health Physics, Vol. 38, No.  4, April  1980,
          pp. 543-621.

Ko83a     Personal Communication,  D.C. Kocher - Oak  Ridge  National
          Laboratory to J.M. Smith -  U.S. Eavironmental Protection Agency,
          March 9, 1983.

Ko83b     Personal Communication,  D.C, Kocher - Oak  Ridge  National
          Laboratory to J.M. Smith -  U.S. Environmental Protection Agency,
          April 20,  1983.

Ko85     Kocher  D.C. and  Sjoreen  A.L.,  1985, "Dose-Rate Conversion
          Factors  for External  Exposure to  Photon Emitters in Soil",
          Health  Physics,  Vol.  48, No,  2, February  1985, pp.  193-205.

 Le67     Lederer C.M., Hollander  J.M.  and  Perlman  I., 1967,  Table of
           Isotopes,  (New York,  NY: John  Wiley and  Sons,  Inc.T

 L177a     Little  A.D.  Inc.,  1977,  "Technical  Support of Standards  for
          High-Level  Radioactive Waste Management:   Volume A-Source  Term
          Characterization",  USEPA Rep.  EPA 520/4-79-007A, (Washington,
          DC:   USEPA).

 Li77b     Little  A.D.  Inc.,  1977,  "Technical  Support of Standards  for
           High-Level  Radioactive Waste Management:   Volume B-Engineering
          Controls", USEPA Rep. EPA 520/4-79-007B,  (Washington,  DC:
           USEPA).

 Li77c      Little  A.D.   Inc.,  1977,  "Technical Support of Standards  for
           High-Level Radioactive Waste Management:   Volume C-Migration
           Pathways", USEPA Rep. EPA 520/4-79-007C, {Washington,  DC:
           USEPA).
                                     R-6

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L180      Little A.D. Inc., 1980, "Technical Support of Standards for
          High-Level Radioactive Waste Management:  Volume D-Release
          Mechanisms", USEPA Rep. EPA 520/4-79-007D, (Washington, DC:
          USEPA).

Ma73      Machta L., 1973, "Prediction of C02 in the Atmosphere", in
          Carbon and the Biosphere (Edited by G.M. Woodwell and E.V.
          Pecan) Upton, NY, 16-18 May 1972, USAEC Rep. CONF-720510, pp.
          21-31, (Springfield, VA:  NTIS).

Ml79      Miller C.W., 1979, "The Interception Fraction", in: A
          Statistical Analysis of Selected Parameters for Predicting Food
          Chain Transport and Internal Doses of Radlonuclides Udlted by
          F.O. Hoffman and C.F.  Baes 111) USNRC Rep. ORNL/NUREG/TM-282,
          pp. 31-42, USNRC (Springfield, VA:  NTIS).

Mo79      Moore R.E., Baes C.F.  Ill, McDowell-Boyer L.M., Watson A.P.,
          Hoffman F.O., Pleasant J.C. and Miller C.W., 1979, "AIRDOS -
          EPA:  A Computerized Methodology for Estimating Environmental
          Concentrations and Dose to Man from Airborne Releases of
          Radionuclides", USEPA Rep. EPA 520/1-79-009, Oak Ridge National
          Laboratory, (Washington, DC:  USEPA).

Mu77      Murray C.R. and Reeves E.B., 1977, "Estimated Use of Water in
          the United States in 1975", USGS Rep. Circular 765, USDOI,
          (Arlington, VA:  USGS).

NAS80     The Effects on Populations of Exposure to Low Levels of Ionizing
          Radiation:  1980, Committee on the Biological Effects of
          Ionizing Radiations, Division of Medical Sciences, Assembly of
          Life Sciences, National Research Council, National Academy of
          Sciences,  (Washington, DC: National Academy Press).

Ne78      Nelson C.B., Davis R.  and Fowler T.W., 1978, "A Model to Assess
          Population Inhalation Exposure from a Transuranium Element
          Contaminated Land Area", in:  Selected Topics:  Transuranium
          Elements in the General Environment", USEPA Technical Note
          ORP/CSD-78-1, pp. 213-280, (Washington, DC:  USEPA).

Ne84      Personal Communication, C.B. Nelson -- U.S. Environmental
          Protection Agency to J.M. Smith -- U.S. Environmental Protection
          Agency, December 19, 1984.

Ng77      Ng Y.C., Colsher C.S., Quinn D.J. and Thompson S.E., 1977,
          "Transfer Coefficients for the Prediction of the Dose to Man Via
          the Forage - Cow - Milk Pathway from Radionuclides Released to
          the Biosphere", USDOE Rep. UCRL-51939, Lawrence Livermore
          Laboratory, (Springfield, VA:  NTIS).
                                    R-7

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Ng82a     Ng Y.C., Colsher C.S. and Thompson S.E., 1982, "Transfer
          Coefficients for Assessing the Dose from Radionuclides 1n Meat
          and Eggs", USNRC Rep. NUREG/CR-2976, Lawrence Livermore National
          Laboratory, (Springfield, VA:  NTIS).

Ng82b     Ng Y.C., Colsher C.S. and Thompson S.E., 1982, "Soil - to -
          Plant Concentration Factors for Radiological Assessments", USNRC
          Rep. NUREG/CR-2975, Lawrence Livermore National Laboratory,
          (Springfield, VA:  NTIS).

Ng82c     Ng Y.C., 1982, "A Review of Transfer Factors for Assessing the
          Dose from Radionuclides in Agricultural Products", Nuclear
          Safety, Vol. 23, No. 1, January-February 1982, pp. 57-71.

Ng84      Personal Communication, Y.C. Ng - Lawrence Livermore National
          Laboratory to J.M. Smith -- U.S. Environmental Protection
          Agency, January 9, 1984.

NRC77     U.S. Nuclear Regulatory Commission, 1977, "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", USNRC Regulatory Guide 1.109, revision 1, (Washington, DC:
          USNRC).

NRC78     U.S. Nuclear Regulatory Commission, 1978, "Liquid Pathway
          Generic Stutfy", USNRC Rep. NUREG-0440,  (Springfield, VA:  NTIS).

ORNL78    Personal Communication, G.G. Killough - Oak Ridge National
          Laboratory to C.B. Nelson - U.S. Environmental Protection
          Agency, November  1978.

Pe83      Peterson, H.T., 1983, "Terrestrial and  Aquatic Food Chain
          Pathways", in: Radiological Assessment:  A Textbook on
          Environmental Dose Analysis  (Edited by  J.E. Tin  and H.R. Meyer)
          USNRC Rep. NUREG/CR-3332, pp. 5-1 through 5-156,  (Springfield,
          VA:  NTIS).

Ri83 i     Rish W.R., Schaffer  S.A. and Mauro J.J., 1983, "Uncertainty and
          Sensitivity Analysis of the  Exposure Pathways Model Used as the
          Basis for Draft 40 CFR191",  November 1983, Supplementary Report
          to National Waste Terminal Storage Technical  Support Team  -
          USDOE,  (New York, NY:  Envirosphere Company,  A Division of
          Ebasco  Services  Incorporated).

Ru79      Rupp E.M., 1979,'  "Annual Dietary  Intake and Respiration Rates,
          Uap", in: A Statistical Analysis of Selected  Parameters for
          Predicting Food Chain Transport and  Internal  Doses  of
          Radlonuclldes  (Edited by P.O. Hoffman  and C.F. Baes  III)  USNRC
          Rep. ORNL/NUREG/TM-282,  pp.  109-132, USNRC  (Springfield,  VA:
          NTIS).
                                    R-8

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Ru83
Ru84


Sc83



Sh79
Sh82
Sm82
Su81
Th72
Th82a
Th82b
Runkle G.E.,  1983,  "Calculation of Health Effects per Curie
Release for Comparison with the EPA Standard", in: Technical
Assistance for Regulatory Development:  Review and Evaluation of
    Draft EPA Standard 40CFR191 for Disposal of High-Level
          the
          Waste,
          7CTTST.
       USNRC Rep. NUREG/CR-3235, Vol. 6 USNRC (Springfield, VA:
Ruckelshaus W.D., 1984, "Risk in a Free Society", EPA Journal,
Vol. 10, No. 3, April 1984, pp. 12-15.

Personal Communication, S.A. Schaffer, Envirosphere Company - A
Division of Ebasco Services Incorporated to J.M. Smith - U.S.
Environmental Protection Agency, September 21, 1983.

Shor R.W. and Fields D.E., 1979, "Animal Feed Consumption Rate,
Qp", in: A Statistical Analysis of Selected Parameters for
Predicting Food Chain Transport and Internal  Doses oT
Radionuclides (Edited by F.O. Hoffman and C.F. Baes III) USNRC
Rep. ORNL/NUREG/TM-282, pp. 51-58, USNRC (Springfield, VA:
NTIS).

Shor R.W., Baes C.F. Ill and Sharp R.D., 1982, "Agricultural
Production in the United States by County:  A Compilation of
Information from the 1974 Census of Agriculture for Use in
Terrestrial Food - Chain Transport and Assessment Models", USDOE
Rep. ORNL-5768, Oak Ridge National Laboratory, (Springfield,
VA:  NTIS).

Smith C.B., Egan D.J., Williams W.A., Gruhlke J.M., Hung C.Y.
and Serini B.L., 1982, "Population Risks from Disposal of
High-Level Radioactive Wastes in Geologic Repositories', USEPA
Rep. EPA 520/3-80-006, (Washington, DC:  USEPA).

Sullivan R.E., Nelson N.S., Ellett W.H., Dunning D.E., Jr.,
Leggett R.W., Yalcintas M.G. and Eckerman K.F., 1981,  "Estimates
of Health Risk from Exposure to Radioactive Pollutants", USDOE
Rep. ORNL/TM-7745, Oak Ridge National Laboratory, (Springfield,
VA:  NTIS).

Thompson S.E., Burton C.A., Quinn D.J. and  Ng Y.C., 1972,
"Concentration Factors of Chemical Elements in Edible  Aquatic
Organisms", USAEC Rep. UCRL-50564/Rev. 1, Lawrence Livermore
Laboratory, (Springfield,  VA:  NTIS).

Thompson R.C., 1982, "Neptunium - The Neglected Actinide:  A
Review of the Biological and Environmental  Literature",
Radiation Research,  Vol. 90, No. 1, April 1982, pp. 1-32.

Thompson R.C., 1982, "Neptunium - The Neglected Actinide:
Corrections and Extensions," Radiation Research, Vol.  92,
December 1982, pp. 620-621.
                                    R-9

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 UN58       United  Nations,  1958,  Report of the United Nations Scientific
           Committee  on  the  Effects of Atomic Radiation, Official Records:
           Thirteenth Session, Supplement No. II  (A/3838),  (New York, NY:
           United  Nations).

 UN77       United  Nations,  1977,  Sources and Effects of Ionizing
           Radiation:  UNSCEAR 1977 Report, United Nations  Publlcation
           Sales No.  E.77.IX.1, United Nations Scientific Committee on the
           Effects of Atomic Radiation, (New York, NY:  United Nations).

 USDA82     U.S. Department of Agriculture, 1982, Agricultural Statistics:
           1982, (Washington, D.C.: USGPO).        	

 USDC70     U.S. Department of Commerce, 1970, Statistical  Abstract of the
           United States:  1970,  91st. edition, Bureau of the Census,
           (wasnington,  u.u.: uSGPO).

 USDC83     U.S. Department of Commerce, 1983, Statistical  Abstract of the
           United States:  1984,  104th. edition, Bureau of the Census,
           (Washington,  D.C.: USGPO).

We73       Wetzel R.G. and Rich P.H., 1973, "Carbon in Freshwater Systems",
           in:  Carbon and the Biosphere (Edited by G.M. Woodwell and E.V.
           Pecan) Upton, NY, 16-18 May 1972, USAEC Rep. CONF - 720510, pp.
           241-263, (Springfield, VA:  NTIS).

WIC70      Water Information Center, 1970, The Water Encyclopedia (Edited
           by O.K. Todd),  (Port Washington,~RY:WIC).

Wo79       Newspaper  Enterprise Association, Inc., 1978, The World Almanac
           and Book of Facts 1979, (New York, NY).      "

WRC78      U.S. Water Resources Council,  1978, The Nation's Water
           Resources: 1975-2000,  Volume 1: Summary, (Springfield, VA:
           NTIS).
                                   R-10

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                               NOMENCLATURE
SUBSCRIPTS.:
     Unless specifically stated otherwise,  these subscripts refer to the
following:
  a                            aquifer
                               aquifer-to-river
                               air
                               air-over-land
                               air-over-water
                               breathing
                               radionuclide  C-14
                               radioactive  decay
                               repository breaching event
                               freshwater fish
                               air to  ground
                               leaching  (except refers to  land  surface
                               pathway when  used with variable  t)
                               directly to  land
                               land  surface
                               nuclide
                               organ
                               pathway
                               repository-to-aquifer
                               river (except refers to resuspension when
                               used with variable  x)
                               soil
                               surface water
ar
A
AL
AW
B
c, 14, and C-14
D
er
f and FF
9
L

LL
LS
n
o
P
ra
R

s
sw
                                   N-l

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SUBSCRIPTS (continued):
  v
  w
  VI
  0
  1
  2
SYMBOLS:
  A
  AL
  CARCAN
  CF
    np
  CP
   D'(t)
                               volcano/meteorite event
                               water  or  ocean
                               water
                               initial condition
                               upper  ocean  compartment
                               lower  ocean  compartment
                 area of land irrigated (m2)
                 land surface area for earth (m2)
                 land area on which resuspended material is
                 deposited (m2)
                 ocean  surface area for earth  (m2)
                 Initial release  rate of radionuclides  Into  the ocean  from
                 the  river (C1/y)
                 risk factor to convert total  bocty environmental  dose
                 commitment  to environmental risk commitment for  C-14
                  (fatal  cancers/total bod|y  man rem)
                 bloaccumulatlon  factor for fish or  shellfish for
                 nuclide n and pathway p  (C1/kg per  Ci/liter)
                 the  number  of persons who  can be fed  from the quantity  of
                 crops  (pathway p)  raised annually on  a unit area of land
                  (man fed/m2)
                  dose commitment  rate as  a  function  of time  (rem/yr)
                  total  bo^y  EDC as  a function  of  Integration time for C-14
                  releases  (man rem/C1 released)
                  fraction  of total  release  for the volcano/meteorite
                  release mode which goes  into  air (dimensionless)
                                    N-2

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SYMBOLS (continued):

  fAL
  fAW


  fL
  fwt
  Fn(f>
  FHE,
fraction of total  release  which  goes  to  air  over  land
(dimensionless)

fraction of total  release  which  goes  to  air  over  water
(dimensionless)

fraction of repository which  is  being leached
(dimensionless)

fraction of total  release  which  goes  directly onto land
(dimensionless)

fraction of the  repository contents which is released to
the land surface (dimensionless)

fraction of land used for  various food crops for
pathway p (dimensionless)

fraction of river flow used for  irrigation (dimensionless)

fraction of drinking water which is  supplied from surface
water sources (dimensionless)

fraction of nuclide which  passes through a water
treatment plant  and remains in potable water
(dimensionless)

quantity of radionuclide n deposited to  ground per unit
area integrated to time t' (Ci/mz)

flux of nuclide  n to ground as a function of time
(Ci/mz-yr)

fatal cancer risk factor for nuclide n and pathway p: for
inhalation and ingestion (fatal  cancers  committed/Ci
intake); for external air submersion (fatal  cancers
committed per Ci-y/m3 integrated air concentration);
for external ground contamination (fatal cancers
committed per Ci-y/m2 integrated ground concentration)

environmental risk commitment to the population for
nuclide n, integrated to time t, for the release  mode
under consideration (fatal cancers committed)
                                    N-3

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SYMBOLS (continued):
  FHE
     np
  FHE
      np
  GC
    np
  hA
   If
  N(D',t)
   PFF
   PFP
   PP
   PR
   PD
environmental  risk commitment to the population for
nuclide n and  pathway P»  integrated to time t (fatal
cancers committed)
risk commitment rate to the population for nuclide n  and
pathway p (fatal  cancers  committed/yr)
radionuclide specific factor used to correct ground
surface fatal  cancer risk factors to account for uniform
distribution of radionuclides within the 15 cm soil root
zone (dimensionless).
height of troposphere (m)
standard man breathing rate (nrVyr)
freshwater fish annual consumption rate (kg/yr-person)
seafood annual consumption rate for pathway p (kg/yr)
annual individual water ingestion rate Oiters/yr-person)
size of the population exposed to dose commitment rate
D'(t) at time t (persons)
population subjected to inhalation of radionuclides for
pathway p (persons)
population eating freshwater fish from the river  (persons)
population eating food included in pathway p  (persons)
population eating seafood for pathway p (persons)
population drinking water from river  (persons)
                                                  i
population density for pathway p  (man/m^)
quantity of radionuclide n In the upper compartment of
the ocean for  releases to ocean from  rivers  (Ci)
quantity of radionuclide n in the lower compartment of
the ocean for  releases to ocean from  rivers  (Ci)
source term from  ground  to air  at time t1  (Ci/yr)
                                    N-4

-------
SYMBOLS (continued):
  Q'anp(t)


  Q'D
   np
  Qn
  Q'np(t)


  Qon
  R

  RF
quantity of radionuclide n 1n the  air-over-ocean
compartment (Ci)

rate of entry of radionuclide n to an aquifer for
pathway p (Ci/yr)

source term from ground to air at  time t1  corrected for
depletion (Ci/yr)

quantity of radionuclide n in the  air-over-land
compartment (Ci)

total release of radionuclide n to the accessible
environment into pathway p (Ci).  For the  land surface
and air release mode, the release  is instantaneous; for
the river and ocean release mode,  the release is
integrated from time of placement  in the repository out
to time t.

total release of radionuclide n to the accessible
environment for the release mode under consideration (Ci)
Note:  Qn = Qpp since the releases considered for the
different pathways within a release mode are all equal.

rate of entry of radionuclide n into the river or ocean
(Ci/y)

initial inventory of radionuclide n in the repository (Ci)

quantity of radionuclide n in the soil root zone (Ci)

quantity of radionuclide n in the upper compartment of
the ocean for releases to ocean from air (Ci)

quantity of radionuclide n in the lower compartment of
the ocean for releases to ocean from air (Ci)

radial distance from source of radionuclide to point of
Interest (m)

an empirical expression which is given in equation 3.3.2-4

river flow rate  (liters/yr)

resuspension factor  (nr*)
                                    N-5

-------
SYMBOLS (continued):

  RI
    np
  RIE
     np
  RIV
      np
   SOF

   t


   t1


   t"
     an
Intake of nucllde n by an individual  for the crop
represented by pathway p and for a unit acute deposition
to the surface (C1 intake per C1/m2 deposited on soil
surface)

radionuclide intake or exposure for pathway p: for
inhalation and ingestion (Ci intake); for external air
submersion (Ci-y/m^ exposure); for external ground
contamination (C1-y/m2 exposure)

annual risk commitment to an individual for nuclide n and
pathway p (fatal cancers committed/yr)

sedimentation coefficient from upper layer of ocean for
radionuclide n  (yr~*)

sedimentation coefficient from lower layer of ocean for
radionuclide n  (yr"M

shielding and occupancy  factor (dimensionless)

time  after placement  1n  repository at which ERC  is
calculated  (yr)

time  after release of radionuclides to  the environment at
which ERC is calculated  (yr)

dummy variable  used for  integration  {yr)

time  for  radionuclide n  to  travel  from  aquifer  to river
 (yr)

time  after  placement  in  repository that radioactive
material  leaves the repository  (yr)

 time  after  placement  in  repository that the  material
. comes to  the surface  for the land surface release mode
 (yr)

 time  for  radionuclide n  to  travel  from repository to
 aquifer (yr)
                                    N-6

-------
SYMBOLS (continued):

  tRn
  tv



  Tl/2

  VAW

  vgn

  VL

  vwn

  vl


  W

  xln
  (X/Q1



  xRn
time after placement in repository that radionuclide n
enters the river or ocean (yr)

time after placement in the repository that the material
enters into the land and air environment as the result of
a volcano or meteorite {yr)

radiological half life (yr)

volume of tropospheric air-over-water (m3)

deposition velocity from air to land surface (m/yr)

volume of tropospheric air over land (m3)

deposition velocity from air to ocean (m/yr)

volume of compartment 1 (upper compartment) of ocean
(liters)

irrigation rate (Iiters/m2-yr)

concentration of radionuclide n in the upper compartment
of the ocean for releases to the ocean from air (Ci/liter)

air concentration at point r and time t1 due to
resuspension at initial source (Ci/m3)

air concentration of radionuclide n due to resuspension
from the ground surface at the location of interest and
due to resuspension at the initial source and subsequent
dispersion to the location of interest (Ci/m3)

atmospheric dispersion factor at the reference
distance rn (sec/m3)

air concentration of radionuclide n at the center of a
uniformly contaminated area having a surface
concentration *5n(t) due to resuspension of
radionuclides from the ground surface (Ci/m3)

"fitting" exponent in empirical equation for Xfn (r,t')

transfer rate coefficient  from upper to lower ocean
(yr-1)

transfer rate coefficient  from lower to upper ocean
(yr-1)
                                    N-7

-------
SYMBOLS (continued):

                 radioactive decay constant for nuclide  n (yr"1)

                 rate constant for deposition from air to ground  (yr"1)

                 leaching rate constant from repository  (yr"1)

                 rate constant for resuspension of nuclides from  soil  to
                 air (yr"1)

                 rate constant for transfer of nuclides  from available to
                 unavailable soil for nuclide n (yr*1)
  O'n
rate constant for deposition from air to ocean (yr"1)

rate of change with time of inventory of radionuclide n
within the 15 cm root zone, expressed per unit surface
area of soil (Ci/m2-y).

inventory of radionuclide n within the 15 cm root zone,
expressed per unit surface area of soil  (Ci/m2)

rate of change with time of ground surface concentration
(material within top 1 cm) for radionuclide n (Ci/mz-y)

ground surface concentration (material within top 1 cm)
of radionuclide n as a function of time (C1/m2)
                                    N-8

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    APPENDIX  A:  METHODS FOR CONSIDERATION OF DAUGHTER PRODUCT INGROWTH

  For each parent  radionuclide discussed in  this  report,  the  method  for
considering daughter product  ingrowth is given  in this Appendix  (also  see
the discussion in  section  4.2).
Radionuclide
              Method  for Consideration  of Daughter Product  Ingrowth
  C-14                 stable daughter - no action  required
  (T1/2 = 5730 yr)
  Ni-59
  (T1/2 = 8 E4 yr)
               stable daughter - no  action  required
  Sr-90
               assume Y-90 (Tj/2 =  64  hr)  is  in  secular
= 28.1 yr)     equilibrium and add  Y-90 risk  factors to those  for
               Sr-90.
  Zr-93                assume Nb-93m (Tj/2 - ^.6 yr)  is  in  secular
  (Ti/2= 1.5 E6 yr)    equilibrium and add Nb-93m  risk factors  to  those
                       for Zr-93.
  Tc-99
  (T1/2 = 2.1 E5 yr)
               stable daughter - no action  required.
  Sn-126
  (Ti/2 = 1 E5 yr)
               use the decay scheme given  by  Kocher  (Ko81a)  for
               Sn-126.  Assume Sb-126m and Sb-126  are  in  secular
               equilibrium with Sn-126.  Then,  using Kocher's
               decay scheme, add Sb-126m risk factors  and
               0.14-Sb-126 risk factors  to those for Sn-126.
  1-129
  (T1/2 = 1.7 E7 yr)
               stable daughter - no action required.
  Cs-135
  (T1/2 = 3 E6 yr)
               stable daughter - no action required.
                                    A-l

-------
Radlonuclide
Methods for Consideration of Daughter Product  Ingrowth
  Cs-137
  (Tj/2 = 30 yr)
  decays to Ba-137m 94.6 percent  of the time.   Assume
  that Ba-137m (Ti/2 = 2.55 nin)  is in secular
  equilibrium with Cs-137 and add 94.6 percent of
  dose factors for Ba-137m to the dose factors for
  Cs-137.
  Sm-151
  (Ti/2 = 87
  stable daughter - no action required.
  Pb-210
  (Ti/2 = 22.3 yr)
  assume Bi-210 (Ti/2 = 5.01 d)  and Po-210
  (Ti/2 = 138.4 d) are in secular equilibrium and
  add the risk factors for these two nuclides to
  those for Pb-210.
  Ra-226
  (Ti/2 - 1602 yr)
  assume that all daughters of Ra-226 are in
  secular equilibrium and add their risk factors to
  the factors for Ra-226.  The daughters assumed
  to be in secular equilibrium are Rn-222
                       (Tw2 = 3.82 d), Po-218 (T1/2 = 3.05 m),
                       Pb-214 (Ti/2 = 26.8 m), Bi-2I4 (T1/2 = 19.9 m),
                       Po-214 (Ti/2 = 163.7 Ms),  Pb-210 (Ti/2 =  22.26 y),
                       Bi-210 (T1/2 = 5.01 d)( and Po-210 (Ti/2  = 138.4 d).
  Ra-228
  (Ti/2 = 5.75 yr)
  assume that all daughters of Ra-228 are in secular
  equilibrium and add their risk factors to the factors
  for Ra-228.  The daughters assumed to be in secular
  equilibrium are Ac-228 (Ti/2 = 6.13 hr),
  Th-228 (Ti/2 = 1.91 yr), Ra-224 (T1/2 = 3.62 d),
  Rn-220 (Ti/2 = 55.6 s), Po-216 (Ti/2 = 0.15 s),
  Pb-212 (T1/2 = 10.64 hr), Bi-212 (Ti/2 = 60.6 m),
  0.64 Po-212  (Ti/2 = 0.298 Ms), 0.36 Tl-208
  (T1/2 = 3.05m).
  Ac-227
  (Ti/2 - 21.77 yr)
  assume that all daughters of Ac-227 are in secular
  equilibrium and add their risk factors to the factors
  for Ac-227.  The daughters assumed to be in secular
  equilibrium are Th-227 (Ti/2 = 18.7 d),
  Ra-223 (T1/2 = 11.4 d), Rn-219 m/2 = 3.96 s),
  Po-215 (Ti/2 = 1.78 ms), Pb-211 (Ti/2 = 36.1 m),
  Bi-211 (Ti/2 = 2.13 m), and Tl-207 ft1/2 = 4.77 m).
                                      A-2

-------
Radionuclide
Methods for Consideration of Daughter Product Ingrowth
  Th-229
  (T1/2 = 7.34E3 yr)
  assume that all daughters of Th-229 are In secular
  equilibrium and add their risk factors to the
  factors for Th-229.  The daughters assumed to be in
  secular equilibrium are Ra-225 (Tj/g = 14-8 d),
  Ac-225 (T1/2 = 10.Od), Fr-221 (T1/2 = 4.8m),
  At-217 (Ti/2 = 32.3ms), Bi-213 (T1/2 = 45.65m),
  Po-213 (Tj/g =. 4.2Ms), and Pb-209 (T1/2 = 3.25h).
  Th-230
  (T1/2 = 7.7E4 yr)
  the mean residence time of Th-230 in the soil  root
  zone (l/xs), based on removal  by leaching, is
  185,200 yr.  The first daughter is Ra-226
  (Ti/2 = 1600 yr).  We calculated that the Ra-226
  concentration would peak at 0.92 of the initial
  Th-230 concentration so we assumed that all
  daughters of Th-230 are in secular equilibrium and
  add their risk factors to the factors for Th-230.
  The daughters assumed to be in secular equilibrium
  are Ra-226  {Ti/2 = 1600 yr), Rn-222
  (Ti/2 = 3.82 d), Po-218 (T1/2 = 3.05 m), Pb-214
  (T1/2 = 26.8 m), Bi-214 (Ti/2 = 19.9 m), Po-214
  (T1/2 = 163.7 us), Pb-210 lT1/2 =22.26 yr),
  Bi-210  (Ti/2 = 5.01 d), and Po-210
  (Ti/2 = 138.4 d).
  Th-232               assume that all daughters of Th-232 are in secular
  (Ti/2 = 1.405E10 yr) equilibrium and add their risk factors to the
                       factors for Th-232.  The daughters assumed to be in
                       secular equilibrium are Ra-228 (T]y2 = 5.75yr),
                       Ac-228 (T1/2 = 6.13 h), Th-228
                       (T1/2 = 1.91 yr), Ra-224 {T1/2 = 3.62 d),
                       Rn-220 (T1/2 = 55.61 s), Po-216
                       (T1/2 = 0.146 s), Pb-212 (T1/2 = 10.64 hr),
                       Bi-212 (T1/2 = 60.55 m), 0.64 Po-212
                       (T1/2 = 0.298 us), and 0.36 Tl-208
                       (Ti/2 = 3.05 m).
   Pa-231               assume that all daughters of Pa-231 are in secular
   (Ti/2 * 3.276E4 yr)  equilibrium and add their risk factors to the
                       factors for Pa-231.  The daughters assumed to be in
                       secular equilibrium are Ac-227 (Ti/2 = 21.Syr),
                       Th-227 (T1/2 = 18.7 d), Ra-223 (T1/2 = 11.4 d),
                       Rn-219 (Ti/2 = 3.96 s), Po-215
                       (Tl/2 = 1.78 ms), Pb-211 (Ti/2 = 36.1 m),
                       Bi-211 (Ti/2 = 2.13 m), and Tl-207
                       (Ti/2 = 4.77 m).
                                    A-3

-------
Radionuclide
            Methods for Consideration of Daughter Product Ingrowth
  U-233                the mean residence  time of  U-233 in the  soil  root
  (Ti/2 = 1.592E5 yr)  zone (l/xs),  based  on removal  by Teaching,  is
                       556 yr.  The  first  daughter is Th-229
                       (Tj/2 = 7.34E3 yr).  We calculated that  the
                       Th-229 concentration would  peak at 0.05  of  the
                       initial U-233 concentration so we assume that all
                       daughters of  U-233  attain 5 percent of secular
                       equilibrium and add 0.05 times their risk factors
                       to the factors for  U-233.  The daughters assumed to
                       reach 5 percent of  secular  equilibrium are  Th-229
                       (Ti/2 = 7.34E3 yr), Ra-225  (T1/2 = 14.8 d),
                       Ac-225 (T1/2  = 10.0 d), Fr-221 (Ti/2 = 4.8  m),
                       At-217 (T1/2  = 32.3 ms), Bi-213
                       (Ti/2 = 45.65 m), Po-213 (Ti/2 = 4.2 Ms), and
                       Pb-209 (T1/2  = 3.25 h).
  U-234                the mean residence time of U-234 in the soil  root
  (Ti/2 = 2.5E5 yr)    zone (l/xs), based on removal by leaching, is
                       555 yr.  The first daughter is Th-230
                       (Jl/2 = 8E 4 yr'-  We calculated that no
                       significant levels of Th-230 would build up within
                       the mean lifetime of U-234 in the soil root zone.
                       Thus, there were ££ additions to the U-234 risk
                       factors.
  U-235
  (Tl/2
= 7.038E8 yr)
assume Th-231 (Tw2 = 25.52 hr)  is in secular
equilibrium with 0-235.   The mean residence time
of U-235 in the soil  root zone (l/xs)» based on
removal by leaching,  is  556 yr.   The second
daughter is Pa-231 (T1/2 = 3.276E4 yr).  We
calculated that the Pa-231 concentration would peak
at 0.01 of the initial U-235 concentration so we
assumed that Pa-231 and  the remaining daughters
attain 1 percent of secular equilibrium.  Thus,
we added 100 percent of  the Th-231 risk factors
and 1 percent of the remaining daughter risk
factors to the factors for U-235.  The daughters
for which the additions  were made are
1.0 Th-231 (Ti/2 = 25.5  h), 0.01 Pa-231
      * 3.276 E4yr), 0.01 Ac-227
                                     = 18.7 d),
                                     •219
(T1/2 = 3.96 sV.'O.Ol Po-215 (T^ * 1.78 ms),
0.01 Pb-211  (Ti/2 = 36.1 m), 0.01 Bi-211
(Tl/2 = 2'-13 m), and 0.01 Tl-207 (4.77 m).
                        (Ti/2  *  3.276 E4 yr), 0.01 Ac-227
                        (Ti/o  =  21.77 yr), 0.01 Th-227  (Ti/2 =
                        O.Ol Ra-223  (T1/2 = 11.4 d), 0.01 Rn-21
                        (Ti/o  =  3.96 s), 0.01 Po-215 (T1/2 = 1.
                                    A-4

-------
Radionuclide
                   Methods for Consideration  of  Daughter  Product Ingrowth
U-236
                       the mean residence time  of U-236  in  the  soil  root
        = 2.3415E7 yr) zone (l/xs),  based on  removal  by  leaching,  is
                       556 yr.   The  first daughter is Th-232
                       (T!/? =  l-405E10yr).  We  calculated that  no
                       significant levels of  Th-232 would build up within
                       the mean lifetime of U-236 in  the soil  root zone.
                       There were no additions  to the risk  factors.
  U-238
        = 4.468E9 yr)
                     the mean residence time  of U-238  in  the soil  root
                     zone UAc), based on removal  by  leaching,  is
                     556 yr.  The first and second  daughters are Th-234
                     (Tj/2 = 24.1 d),  and Pa-234m (Tj/2 = 1.17 m)
                     which are assumed to be  in secular equilibrium with
                     U-238.   The third daughter is  U-234
                     (TI/£ = 2.445E5yr).  We calculated  that no
                     significant levels of U-234 would build up within
                     the mean lifetime of U-238 in  the soil  root zone.
                     Thus, only the risk factors for Th-234  and Pa-234m
                     were added to those for  U-238.
  Np-237
  (Ti/2= 2.14 E6 yr)
                     assume Pa-233 (Tjy? = 27d) is in secular
                     equilibrium and ada Pa-233 dose factors to those
                     for Np-237.  The mean residence time of Np-237 in
                     the soil root zone (l/xs), based on removal by
                     leaching, is 37 yr.  The first long-lived daughter
                     is U-233 (T1/2 = 1.62E5 yr).  We calculated that
                     no significant levels of U-233 (and the daughters
                     beyond) would build up within the mean lifetime of
                     Np-237 in the soil root zone.  Thus, there were no
                     additions to Np-237 risk factors for U-233 and th"e
                     daughters beyond U-233.
  Pu-238
  (T1/2 = 86 y)
                     the mean residence time of Pu-238 in the soil root
                     zone (l/xs), based on physical removal by
                     leaching, is 5560 yr.  The first daughter is U-234
                     (Tjy2 = 2.5E5yr).  We calculated that no
                     significant levels of U-234 (and the daughters
                     beyond) would build up in the soil root zone due to
                     the decay of Pu-238.  There were no_ additions to
                     the Pu-238 risk factors.
                                    A-5

-------
Radionuclide
Methods for Consideration of Daughter Product Ingrowth
  Pu-239
  (T1/2 = 2.4 E4 yr)
  The mean residence time of Pu-239 in the soil  root
  zone (1/>S), based on removal  by leaching,  is
  5560 yr.  The first daughter is U-235
  (fl/? = 7.1E8yr).  We calculated that no
  significant levels of U-235 would build up  within
  the mean lifetime of Pu-239 in the soil root zone.
  There were no additions to the Pu-239 risk  factors
  Pu-240
  (T1/2 = 6580 yr)
  The mean residence time of Pu-240 in the soil  root
  zone (l/xs), based on removal  by leaching, is
  5560 yr.  The first daughter is U-236
  (TI/£ = 2.4E7yr).  We calculated that no
  significant levels of U-236 would build up within
  the mean lifetime of Pu-240 in the soil root zone.
  There were no additions to the Pu-240 risk factors
  Pu-241
  (1*1/2 «
  The mean residence time of Pu in the soil root
  zone  (l/xs), based on removal by leaching, is
  5556 yr.  This is far longer than it would take the
  Pu-241 to disappear due to radioactive decay.  The
  first daughter is Am-241 (Ti/2 = 432.2 yr).  We
  calculated that the Am-241 concentration would peak
  at 0.03 of the initial Pu-241 concentration.
  Np-237  (Ti/g - 2.14E6 yr) is the second daughter
  and there would be no significant buildup in the
  soil  root zone.  The Pu-241 risk factors were
  augmented by the addition of 0.03 times the risk
  factors for Am-241.
  Pu-242
  (T1/2 = 3,8 E5 yr)
  The mean residence time of Pu-242 in the soil root
  zone  (l/xs), based on removal by leaching, is
  5560 yr.  The first daughter is U-238
  (Tj/2  • 4.5E9yr).  We calculated that no
  significant levels of U-238 would build up within
  the mean lifetime of Pu-242 in the soil root zone.
  There  were no additions to the Pu-242 risk factors.
  Am-241
  (T1/2 = 458 yr)
  The mean residence time of Am-241 in the soil root
  zone  (1/Xe), based on removal by leaching, is
  862 yr.  The first daughter is Np-237
  (Tj/g = 2.1E6yr).  We calculated that no
  significant levels of Np-237 would build up within
  the mean lifetime .of Am-241 .in'.the soil root zone.
  There were no additions to the Am-241 risk factors.
                                    A-6

-------
Radionuclide
Methods for Consideration  of  Daughter Product Ingrowth
  Am-243
  (Ti/2 = 7950 yr)
  Assume Np-239 (Tj/g = 2.3  d)  is in secular
  equilibrium and add Np-239 risk factors to those
  for Am-243,  The mean residence time of Am-243 in
  the soil root zone (l/xs), based on removal by
  leaching, is 862 yr.  The  first long-lived daughter
  is Pu-239 (Tj/2 = 2-4E4 *r)-   We calculated that
  no significant levels of Pu-239 would build up
  within the mean lifetime of Am-243 in the soil root
  zone.  There were n£ additions to the Am-243 risk
  factors for Pu-239 and the daughters beyond Pu-239.
  Cm-245
  (T1/2 = 8.5E3 yr)
  The mean residence time of Cm-245 in the soil  root
  zone (l/xs), based on removal  by leaching, is
  2470 yr.  The first and second daughters are Pu-241
  (Ti/2 = 14.4 yr) and Am-241 (Tj/e = 432.2 yr)
  whicn are assumed to be in secular equilibrium with
  Cm-245.  The third daughter is Np-237
  (Ti/2 = 2.14E6 yr).  We calculated that no
  significant levels of Np-237 would build up within
  the mean lifetime of Cm-245 in the soil root zone.
  Thus, only the risk factors for Pu-24i and Am-241
  were added to those for Cm-245.
  Cm-246
  (Ti/2 = 4.75E3 yr)
  The mean residence time of Cm-246 in the soil root
  zone  (l/xs), based on removal by leaching, is
  2470 yr.  The first daughter is Pu-242
  (Ti/2 = 3.758E5 yr).  We calculated that no
  significant levels of Pu-242 would build up within
  the mean lifetime of Cm-246 in the soil root zone.
  There were no additions to the Cm-246 risk factors,
                                    A-7

-------

-------
                  APPENDIX  B:   FATAL  CANCER  RISK FACTORS

     The fatal  cancer risk  factors  which  were  applied  in  these  analyses
are listed in Table B-l.  Table B-l lists the  risk  factors  for  the  parent
radionuclide and for daughter  radionuclides  which can  grow  in  (and  be
inhaled, ingested, or cause external  exposure  in addition to the  parent)
during the mean lifetime  of the parent in the  soil  root zone.   For
inhalation and ingestion, all  risk  factors listed in Table  B-l  incorporate
the ingrowth and ctynamics of daughters in the  body  after  intake of  a
radionuclide.

     The radionuclides shown in Table B-l have risk factors whose
magnitude exceeds 1 percent of the  maximum risk factor for  any  nuclide in
the decay chain which could grow in during the mean lifetime of the parent
in the soil root zone.  Included in Table B-l  is the clearance  class and
value for the gut-to-blood transfer fraction,  fj, as applicable.   The
source of these risk factors is a run of the EPA RADRISK  computer code
using the V8401BD version of the input data file (Ne84).
     An explanation of the methodology used to derive these risk factors
is given in Chapter 4*.  For the inhalation and ingestion pathways two
categories of fatal cancer risk factors were calculated which were
designated Inhalation 1, Inhalation 2, Ingestion 1, and Ingestion 2.
Class Y risk factors were used for the Inhalation 1 category for all
     *The technical basis for the EPA RADRISK computer code and data base
 in  discussed in detail in Appendices F, G and H.
                                    B-l

-------
nuclides where they were available and Class W risk  factors were used for
the Inhalation 2 category where they were available.   However,  for some
radionuclides, only Class D or Class D and Class W Inhalation risk factors
were available.  In these cases, the factors for the least soluble
clearance class available were applied.  For example, if inhalation risk
factors were available for Class D and Class W but not for Class Y, the
Class W factors were listed In both the Inhalation 1 and Inhalation 2
categories.  For the Ingestion 1 and Ingestion 2 categories, risk .factors
were used which were derived using the same absorption fraction from
gut-to-blood (f,) as was used for the Inhalation 1 and Inhalation 2
categories, respectively.
                                    B-2

-------
TABLE B-l
Inhalation 1: Fatal  cancer risk conversion factors for parent  and significant*  daughters
********************************* Daughters *******************************
Nuclide, Clearance Class, fj**
Parent R*sk factor
C-14, -, -,
3.053E-3
N1-59, W, 5E-2
4.761E-1
Sr-90, Y, 1E-2
4.479E2
Zr-93, Y, 2E-3 Nb-93m, Y, 1E-2
1.269E1 1.449E1
Tc-99, W, 8E-1
6.120EO
Sn-126, W, 2E-2 (.14)Sb-126, W, 1E-2
5.637E1 8.310E-1
1-129, D, 9.5E-1
1.605E+1
Cs-135, D, 9.5E-1
1.266EO
Parent *
Daughters
3.05E-3
. 4.76E-1
4.52E2
2.72E1
6.12EO
5.72E1
1.61E1
1.27EO
*  Daughters for which the risk factor exceeds 1 percent of the maximum risk factor for any nuclide in the decay chain
   which can grow in while the parent exists in the accessible environment.
** For each nuclide listed for inhalation pathways, the first line includes  the nuclide symbol  and the clearance class and
   value for f  used to derive the risk factor.  The second line lists the risk factor.

-------

TABLE B-l (Continued) .
Inhalation 1: Fatal cancer risk conversion factors for parent and significant* daughters
{fatal cancers committed per Ci intake)
********************************* Daughters *******************************
Parent
Cs-137, D, 9.5E-1
8.486EO
Sm-151, W, 3E-4
5.271EO
Pb-210, Y, 2E-1
1.715E4
Ra-226, Y, 2E-1
2.116E4
Ra-228, Y, 2E-1
1.841E4
Ac-227, Y, 1E-3
6.339E4
Th-229, Y, 2E-4
6.138E4
Th-230, Y, 2E-4
2.510E4



B1-210, Y, 5E-2
1.910E2
Pb-210, Y, 2E-1
1.715E4
Th-228, Y, 2E-4
6.030E4
Th-227, Y, 2E-4
3.826E3
Ra-225, W, 2E-1
1.211E3
Ra-226, Y, 2E-1
2.116E4
Nuclide, Clearance Class, fj
Risk Factor


Po-210, Y, 1E-1
5.311E3
Po-210, Y, 1E-1
5.311E3
Ra-224, Y, 2E-1
9.901E2
Ra-223, W, 2E-1
2.443E3
Ac-225, Y, 1E-3
1.883E3
Pb-210, Y, 2E-1 Po-210, Y, 1E-1
1.715E4 5.311E3
Parent +
Daughters
.8.49EO
5.27EO
2.27E4
4.38E4
7.98E4
6.97E4
6.45E4
6.89E4
*  Daughters for which the risk factor exceeds 1  percent of the  maximum risk  factor for  any  nuclide  in  the  decay  chain
   which can grow in while the parent exists in the accessible environment.

-------

TABLE B-l
Inhalation

Parent
Th-232, Y,
2.475E4
Pa-231, Y,
3.287E4
U-233, Y,
2.095E4
U-234, Y,
2.070E4
U-235, Y,
1.922E4
U-236, Y,
1.959E4
U-238, Y,
1.854E4
Np-237, Y,
2.888E4
(Continued)
1: Fatal cancer risk conversion factors for parent and significant* daughters
(fatal cancers committed per Ci intake)


2E-4
1E-3
2E-3
2E-3
2E-3
2E-3
2E-3
1E-3
********************************* Daughters *******************************
Nuclide, Clearance Class, fi
Risk Factor
Ra-228, Y, 2E-1 Th-228, Y, 2E-4 Ra-224, Y, 2E-1
1.841E4 6.030E4 9.901E2
Ac-227, Y, 1E-3 Th-227, Y, 2E-4 Ra-223, W, 2E-1
6.399E4 3.826E3 2.443E3
(.05)Th-229, Y, 2E-4
3.069E3

{.01)Pa-231, Y, 1E-3 (.Ol)Ac-227, Y, 1E-3
3.287E2 6.339E2




Parent +
Daughters
1.05E5
1.03E5
2.42E4
2.07E4
2.03E4
1.96E4
1.85E4
2.89E4
*  Daughters for which the risk factor exceeds 1  percent of the maximum risk  factor for any  nuclide  in  the decay  chain
   which can grow in while the parent exists in the accessible environment.

-------

TABLE B-l (Continued)
Inhalation 1: Fatal cancer risk conversion factors for parent and significant* daughters
(fatal cancers committed per Ci intake)
********************************* Daughters *******************************
Nuclide, Clearance Class, fi
Parent Risk Factor
Pu-238, Y, 1E-3
3.134E4
Pu-239, Y, 1E-4
3.093E4
Pu-240, Y, 1E-4
3.092E4
Pu-241, Y, 1E-3 (.03)Am-241, Y, 1E-3
2.073E2 9.798E2
Pu-242, Y, 1E-4
2.936E4
Am-241, Y, 1E-3
3.266E4
Am-243, Y, 1E-3
3.193E4
Cm-245, Y, 1E-3 Am-241, Y, 1E-3
3.249E4 3.266E4
Cm-246, Y, 1E-3
3.263E4

Parent *
Daughters
3.13E4
3.09E4
3.09E4
1.19E3
2.94E4
3.27E4
3.19E4
6.54E4
3.26E4
*  Daughters for which the risk  factor exceeds  1  percent  of  the maximum  risk  factor for any nuclide  in the decay chain
   which can grow in while the parent  exists  in the  accessible environment.

-------
TABLE B-l (Continued)
Inhalation 2: Fatal cancer risk conversion factors for parent and significant* daughters
(fatal cancers committed per Ci intake)
********************************* Daughters *******************************
Nucllde, Clearance Class, fi
Parent Risk Factor
C-14, -, -
3.053E-3
Ni-59, W, 5E-2
4.761E-1
Sr-90, D, 3E-1 Y-90, W, 1E-4
4.833E1 3.556EO
Zr-93, W, 2E-3 Nb-93m, W, 1E-2
4.819EO 1.776EO

Parent +
Daughters
3.05E-3
4.76E-1
5.19E1
6.60EO
Tc-99, W, 8E-1
6.120EO

Sn-126, W, 2E-2
5.637E1

1-129, D, 9.5E-1
1.605E1

Cs-135, D, 9.5E-1
1.266EO
                     (0.14)Sb-126,  W, 1E-2
                     8.310E-1
5.72E1


1.61E1


1.27EO
*  Daughters for which the risk factor exceeds 1  percent of the maximum risk factor for any nuclide in the decay chain
   which can grow in while the parent exists in the accessible environment.

-------

TABLE B-l (Continued)
Inhalation 2: Fatal cancer risk conversion factors for parent and significant* daughters
(fatal cancers committed per Ci intake)
Parent
Cs-137, D, 9.5E-1
8.486EO
Sm-151, W, 3E-4
5.271EO
Pb-210, W, 2E-1
' 9.961E2
Ra-226, W, 2E-1
2.331E3
Ra-228, W, 2E-1
4.754E2
Ac-227, W, 1E-3
3.232E4
Th-229, W, 2E-4
2.528E4
Th-230, W, 2E-4
1.514E4
********************************* Daughters *******************************
Nuclide, Clearance Class, fj Parent *
•Risk Factor , Daughters


Bi-210, W, 5E-2
6.182E1
Pb-210, W, 2E-1
9.961E2
Th-228, W, 2E-4
1.434E4
Th-227, W, 2E-4
2.667E3
Ra-225, W, 2E-1
1.2UE3
Ra-226, W, 2E-1
2.331E3


Po-210, W, 1E-1
1.930E3
Bi-210, W, 5E-2 Po-210, W, 1E-1
6.182E1 1.930E3
Ra-224, W, 2E-1
9.443E2
Ra-223, W, 2E-1
2.443E3
Ac-225, W, 1E-3
1.715E3
Pb-210, W, 2E-1 Po-210, W, 1E-1
9.961E2 1.930E3
8.49EO
5.27EO
2.99E3
5.33E3
1.58E4
3.74E4
2.82E4
2.05E4
*  Daughters for which the risk factor exceeds 1  percent of the maximum risk  factor for any  nuclide in the decay chain
   which can grow in while the parent exists  in the accessible  environment.

-------
TABLE B-l (Continued)
Inhalation 2: Fatal  cancer risk conversion factors for parent and significant* daughters
                                 (fatal  cancers committed per Ci  intake)
********************************* Daughters *******************************

Parent
Th-232, W, 2E-4
1.358E4
Pa-231, W, 1E-3
2.442E4
U-233, W, 2E-1
O 9Q1 C"*


Ra-228, W, 2E-1
4.754E2
Ac-227, W, 1E-3
3.232E4
(.05)Th-229, W, 2E-4
i 9fiAr*
Nuclide, Clearance Class, f^
Risk Factor
Th-228, W, 2E-4 Ra-224, W, 2E-1
1.434E4 9.443E2
Th-227, W, 2E-4 Ra-223, W, 2E-1
2.667E3 2.443E3
(,05)Ra-225, W, 2E-1 (.05)Ac-225, W, 1E-3
fi.fWBFl 8.575F1
Parent +
Daughters

2.94E4

6.19E4

3.70E3
U-234, W, 2E-1
2.263E3

U-235, W, 2E-1
2.104E3

U-236, W, 2E-1
2.141E3

U-238, W, 2E-1
2.026E3

Np-237, W, 1E-3
2.464E4
(.01}Pa-231. W, 1E-3    (.01)Ac-227, W, 1E-3  (,01)Th-227, W, 2E-4   (,01)Ra-223, W, 2E-1
2.442E2                 3.232E2               2.667E1                2.443E1
                                                                                              2.26E3
•2.72E3
                                                                                              2.14E3
                                                                                              2.04E3
                                                                                              2.46E4
   Daughters for which the risk factor exceeds 1 percent of the maximum risk factor for any nuclide in the decay chain
   which can grow in while the parent exists in the accessible environment.

-------

TABLE B-l (Continued) _
Inhalation 2: Fatal cancer risk conversion factors for parent and significant* daughters
(fatal cancers committed per Ci intake)
********************************* Daughters *******************************
Nuclide, Clearance Class, fi
Parent R*sk Factor
Pu-238, W, 1E-3
2.491E4
Pu-239, W, 1E-3
2.648E4
Pu-240, W, 1E-3
2.645E4
Pu-241. W, 1E-3 (,03)Am-241, W, 1E-3
4.071E2 8.247E2
Pu-242, W, 1E-3
2.515E4
Am-241, W, 1E-3
2.749E4
Am-243, W, 1E-3
2.727E4
Cm-245, W, 1E-3 Pu-241, W, 1E-3 Am-241, W, 1E-3
2.794E4 4.071E2 2.749E4
Cm-246, W, 1E-3
2.782E4

Parent +
Daughters
2.49E4
2.65E4
2.65E4
1.23E3
'2.52E4
2.75E4
2.73E4
5.58E4
2.78E4
*  Daughters for which the risk factor exceeds 1  percent of the maximum risk factor for any nuclfde in the decay chain
   which can grow in while the parent exists in the accessible environment.

-------

TABLE B-l (Continued) ^ j
Ingestlon 1: Fatal cancer risk conversion factors for parent and significant* daughters.
(fatal cancers committed per Ci intake)
******************************** Daughters *******************************
Nuclide, fj**
Parent R*sk Factor
C-14, -
4.321E-1
Ni-59, 5E-2
3.761E-2
Sr-90, 1E-2 Y-90, 1E-4
w 1.452EO 8.391E-1
- Zr-93, 2E-3 Nb-93m, 1E-2
8.459E-2 4.213E-2
Tc-99, 8E-1
5.374E-1
Sn-126, 2E-2 Sb-126m, 1E-2 (.14)Sb-126, 1E-2
1.895EO 2.859E-2 1.182E-1
1-129, 9.5E-1
2.407E1
Cs-135, 9.5E-1
1.819EO


Parent +
Daughters
4.32E-1
3.76E-2
2.29EO
1.27E-1
, 5.37E-1
2.04EO
2.41E1
1.82EO
*  Daughters for which the risk factor exceeds  1  percent of the maximum  risk factor for any nuclide in the decay chain
   which can grow in while the parent  exists  in the  accessible environment.
** For each nuclide listed for ingestion  pathways, the  first  line  includes the  nuclide symbol and the value for fx used
   to derive the risk factor.   The second line  lists the risk factor.

-------

TABLE B-l (Continued)
Ingestion 1: Fatal cancer ri
sk conversion factors for parent and significant* daughters
(fatal cancers committed per Ci intake)

********************************* Daughters *******************************
Parent
Cs-137, 9.5E-1
1.241E+1
Sm-151, 3E-4
3.461E-2
Pb-210, 2E-1
3.409E2
Ra-226, 2E-1
7.783E1
Ra-228, 2E-1
5.474E1
Ac-227, 1E-3
2.335E2
Th-229, 2E-4
3.526E1
Th-230, 2E-4
2.198E1



Po-210,
7.181E1
Pb-210,
3.409E2
Th-228,
1.053E1
Ra-223,
4.938E1
Ra-225,
4.419E1
Ra-226,
7.783E1
Nuclide, fj
Risk Factor


1E-1
2E-1 Po-210, 1E-1
7.181E1
2E-4 Ra-224, 2E-1 Pb-212, 2E-1
2.828E1 3.265EO
2E-1
2E-1 Ac-225, 1E-3
5.883EO
2E-1 Pb-210, 2E-1 Po-210, 1E-1
3.409E2 7.181E1
Parent *
Daughters
1.24E1
3.46E-2
4.13E2
4.91E2
•9.71E1
2.85E2
8.55E1
5.13E2
*  Daughters for which the risk factor exceeds 1  percent  of  the  maximum  risk  factor  for  any  nuclide  in  the  decay chain
   which can grow in while the parent exists  in the accessible environment.

-------

TABLE B-l (Continued)
Ingestion 1: Fatal cancer risk conversion factors for parent and significant* daughters
(fatal cancers committed per Ci intake)
********************************* Daughters *******************************
Parent
Th-232, 2E-4
1.985E1
Pa-231, 1E-3
1.827E2
U-233, 2E-3
3 9.387E-1
U-234, 2E-3
9.382E-1
U-235, 2E-3
1.081EO
U-236, 2E-3
8.864E-1
U-238, 2E-3
9.361E-1
Np-237, 1E-3
1.860E2

Ra-228, 2E-1
5.474E1
Ac-227, 1E-3
2.335E2
(.05)Th-229, 2E-4
1.763EO

Th-231, 2E-4
1.083E-1

Th-234, 2E-4
1.049EO

Nuclide, fi Parent +
Risk Factor Daughters
Th-228, 2E-4 Ra-224, 2E-1 Pb-212, 2E-1
1.053E1 2.828E1 3.265EO 1.17E2
Ra-223, 2E-1
4.938E1 4.67E2
(.05)Ra-225, 2E-1 (,05)Ac-225,lE-3
2.210EO 2.942E-1 5.21EO
9.38E-1
(.01)Pa-231, 1E-3 (.Ol)Ac-227, 1E-3 (0.01)Ra-223, 2E-1
1.827EO 2.335EO 4.938E-1 '5.86EO
8.86E-1
1.99EO
1.86E2
*  Daughters for which the risk factor exceeds  1  percent  of the  maximum  risk  factor  for  any  nuclide  in the  decay chain
   which can grow in while the parent exists  in the accessible environment.

-------

TABLE B-l (Continued)
Ingestion 1: Fatal cancer risk conversion factors for parent and significant* daughters
(fatal cancers committed per Ci intake)
********************************* Daughters *******************************
Muclide, fi
Parent Risk Factor
Pu-238, 1E-3
1.856E2
Pu-239, 1E-4
2.043E1
Pu-240, 1E-4
2.041E1
Pu-241, 1E-3 (,03)Am-241, 1E-3
3.361EO 6.207EO
Pu-242, 1E-4
1.941E1
Am-241, 1E-3
2.069E2
Am-243, 1E-3
2.059E2
Cm-245, 1E-3 Pu-241, 1E-3 Am-241, 1E-3
2.111E2 3.361EO 2.069E2
Cm-246, 1E-3
2.098E2

Parent *
Daughters
1.86E2
2.04E1
2.04E1
9.57EO
1.94E1
2.07E2
2.06E2
4.21E2
2.10E2
*  Daughters for which the risk  factor exceeds  1  percent of the maximum risk factor for any nuclide in the decay chain
   which can grow in while the parent  exists  in the  accessible environment.

-------

TABLE B-l (Continued)
Ingestion 2: Fatal cancer risk conversion factors for parent and significant* daughters
(fatal cancers committed per Ci intake)
********************************* Daughters *******************************
Nuclide, fj
parent Rl*sk Factor
C-14, -
4.321E-1
Ni-59, 5E-2
3.761E-2
Sr-90, 3E-1 Y-90, 1E-4
2.762E1 8.391E-1
Zr-93, 2E-3 Nb-93m, 1E-2
8.459E-2 4.213E-2
Tc-99, 8E-1
5.374E-1
Sn-126, 2E-2 Sb-126m, 1E-2 (.14)Sb-126, 1E-2
1.895EO 2.859E-2 1.182E-1
1-129, 9.5E-1
2.407E+1
Cs-135, 9.5E-1
1.819EO

Parent *
Daughters
4.32E-1
3.76E-2
2.85E1
1.27E-1
S.37E-1
2.04EO
2.41E*1
1.82EO
*  Daughters for which the risk  factor exceeds  1 percent of the maximum risk factor for any nuclide in the decay chain
   which can grow in while the parent  exists  in the accessible environment.

-------

TABLE B-l (Continued)
Ingestion 2: Fatal cancer risk conversion factors for parent and significant* daughters
(fatal cancers committed per Ci intake)
********************************* Daughters *******************************
Parent
Cs-137, 9.5E-1
1.241E1
Sm-151, 3E-4
3.461E-2
Pb-210, 2E-1
3.409E2
Ra-226, 2E-1
7.783E1
Ra-228, 2E-1
5.474E1
Ac-227, 1E-3
2.335E2
Th-229, 2E-4
3.526E1
Th-230, 2E-4
2.198E1
Nuclide, fi
Risk Factor


Po-210, 1E-1
7.181E1
Pb-210, 2E-1 Po-210, 1E-1
3.409E2 7.181E1
Th-228, 2E-4 Ra-224, 2E-1 Pb-212, 2E-1
1.053E1 2.828E1 3.265EO
Ra-223, 2E-1
4.938E1
Ra-225, 2E-1 Ac-225, 1E-3
4.419E1 5.883EO
Ra-226, 2E-1 Pb-210, 2E-1 Po-210, 1E-1
7.783E1 3.409E2 7.181E1
Parent *
Daughters
1.24E1
3.46E-2
4.13E2
4.91E2
9.71E1
2.85E2
8.55E1
5.13E2
*  Daughters for which the  risk  factor exceeds 1 percent of the maximum risk factor for any nuclide in the decay chain
   which can grow in while  the parent exists  in the accessible environment.

-------

TABLE B-l (Continued)
Ingestion 2: Fatal cancer risk conversion factors for parent and significant* daughters
(fatal cancers committed per Ci intake)

Parent
Th-232, 2E-4
1.985E1
Pa-231, 1E-3
1.827E2
U-233, 2E-1
4.646E1
U-234, 2E-1
4.605E1
U-235, 2E-1
4.546E1
U-236, 2E-1
4.353E1
U-238, 2E-1
4.735E1
Np-237, 1E-3
1.860E2
********************************* Daughters *******************************
Nuclide, fi
Risk Factor
Ra-228, 2E-1 Th-228, 2E-4 Ra-224, 2E-1 Pb-212, 2E-1
5.474E1 1.053E1 2.828E1 3.265EO
Ac-227, 1E-3 Ra-223, 2E-1
2.335E2 4.938E1
(.05)Th-229, 2E-4 (.05)Ra-225, 2E-1
1.763EO 2.210EO

(.01)Pa-231, 1E-3 (.Ol)Ac-227, 1E-3 (.01)Ra-223, 2E-1
1.827EO 2.335EO 4.938E-1

Th-234, 2E-4
1.049EO


Parent *
Daughters
1.17E2
4.67E2
5.07E1
4.61E1
5.02E1
4.35E1
4.84E1
1.86E2
*  Daughters for which the  risk  factor exceeds 1 percent of the maximum risk factor for any nuclide in the decay chain
   which can grow in while  the parent exists  in the accessible environment.

-------

TABLE B-l (Continued)
Ingestion 2: Fatal cancer risk conversion factors for parent and significant* daughters
(fatal cancers committed per Ci intake)
********************************* Daughters *******************************
Nucllde, fi
Parent Risk Factor
Pu-238, 1E-3
1.856E2
Pu-239, 1E-3
1.997E2
Pu-240, 1E-3
1.994E2
Pu-241, 1E-3 (.03)Am-241, 1E-3
3.361EO 6.207EO
Pu-242, 1E-3
1.897E2
Am-241, 1E-3
2.069E2
Am-243, 1E-3
2.059E2
Cm-245, 1E-3 Pu-241, 1E-3 Am-241, 1E-3
2.111E2 3.361EO 2.069E2
Cm-246, 1E-3
2.098E2

Parent *
Daughters
1.86E2
2.00E2
1.99E2
9.57EO
1.90E2
2.07E2
2.06E2
4.21E2
2.10E2
*  Daughters for which the  risk  factor exceeds  1 percent of the maximum risk factor for any nuclide in the decay chain
   which can grow in while  the parent exists  in the accessible environment.

-------
TABLE B-l (Continued)
Air Submersion: Fatal cancer risk conversion factors for parent and significant* daughters
                                                                3
	(fatal cancers committed per Ci-y/m  exposure)	.

                       ******************************* Daughters *********************************

                                                        Nuclide**
  Parent                                               Risk Factor
                                                                                                Parent
                                                                                              Daughters
C-14
0

Ni-59
4.100E-2

Sr-90
0

Zr-93
0

Tc-99
5.974E-4

Sn-126
5.395E1

1-129
7.572EO

Cs-135
0
Nb-93m
1.232E-1
Sb-126m
1.993E3
M4)Sb-126
4.913E2
   0


   4.10E-2


   0


   1.23E-I


'   5.97E-4


   2.54E3


   7.57EO


   0
 *   Daughters  for which the risk factor exceeds 1 percent of the maximum risk factor for any nuclide in the decay chain
    which can  grow  in while the parent exists in the accessible environment.
 **  For  each nuclide listed for air submersion and for ground deposition, the first line includes the nuclide symbol and the
    second  line lists the risk factor.

-------

TABLE B-l (Continued)
Air Submersion: Fatal cancer risk conversion factors for parent and significant* daughters
3
(fatal cancers committed per Ci-y/ra exposure)
******************************* Daughters *********************************
Parent
Cs-137
0
Sm-151
8.148E-4
Pb-210
1.332EO
Ra-226
8.183EO
Ra-228
6.814E-9
Ac-227
1.445E-1
Th-229
9.923E1
Th-230
4.350E-1

(.946)Ba-137m
7.179E2


Pb-214
3.033E2
Ac-228
1.202E3
Th-227
1.258E2
Ra-225
6.457EO
Pb-214
3.033E2
Nuclide
Risk Factor



Bi-214
2.032E3
Pb-212 Bi-212
1.763E2 2.392E2
Ra-223 Rn-219
1.589E2 7.019E1
Ac-225 Fr-221
1.574E1 3.748E1
Bi-214
2.032E3
Parent *
Daughters
7.18E2
8.15E-4
1.33EO
2.35E3
(.36)11-208
1.793E3 ' 3.43E3
Pb-211 Bi-211
6.464E1 5.786E1 4.81E2
Bi-213
1.711E2 3.30E2
2.35E3
*  Daughters for which the  risk  factor exceeds 1 percent of the maximum risk factor for any nuclide in the decay chain
   which can grow in while  the parent exists  in the accessible environment.

-------

TABLE B-l (Continued)
Air Submersion: Fatal cancer risk conversion factors for parent and significant* daughters •
3
(fatal cancers committed per Ci-y/m exposure)
******************************* Daughters *********************************
Parent
Th-232
2.019E-1
Pa-231
3.629E1
U-233
2.734E-1
U-234
1.631E-1
U-235
1.833E2
U-236
1.269E-1
U-238
1.085E-1
Np-237
2.581E1

AC-228
1.202E3
Th-227
1.258E2
(.05)Th-229
4.962EO

Th-231
1.285E1

Th-234
8.635EO
Pa-233
2.575E2
Nuclide Parent +
Risk Factor Daughters
Pb-212 Bi-212 (.36)11-208
1.763E2 2.392E2 1.793E3 3.43E3
Ra-223 Rn-219 Pb-211 Bi-211
1.589E2 7.019E1 6.464E1 5.786E1 5.17E2
(.05)Ra-225 (.05)Ac-225 (.05)Fr-221 (.05)Bi-213 .
3.229E-1 7.870E-1 1.874EO 8.555EO 1.68E1
1.63E-1
2.01E2
1.27E-1
Pa-234m
1.485E1 2.36E1
2.83E2
*  Daughters for which the  risk  factor  exceeds  1 percent of the maximum risk factor for any nuclide in the decay chain
   which can grow in while  the parent exists  in the accessible environment.

-------

TABLE B-l (Continued)
Air Submersion: Fatal cancer risk conversion factors for parent and significant* daughters
(fatal cancers committed per Ci-y/m3 exposure)
******************************* Daughters *********************************
Nuclide
Parent Risk Factor
Pu-238
8.802E-2
Pu-239
9.058E-2
Pu-240
8.634E-2
Pu-241 (.03)Am-241
0 5.982E-1
Pu-242
7.362E-2
Am-241
1.994E1
Am-243 Np-239
5.592E1 1.986E2
Cm-245 Am-241
8.242E1 1.994E1
Cm-246
6.805E-2

Parent +
Daughters
8.80E-2
9.06E-2
8.63E-2
5.98E-1
7.36E-2
1.99E1
2.55E2
1.02E2
6.81E-2
*  Daughters for which the risk  factor exceeds 1 percent of the maximum risk factor for any nuclide in the decay chain
   which can grow in while the parent exists  in the accessible environment.

-------

TABLE B-l (Continued)
Ground Deposition: Fatal cancer risk conversion factors for parent and significant* daughters
(fatal cancers committed per Ci-y/m exposure)
********************************* Daughters *******************************
Nuclide
Parent Risk Factor
C-14
0
Ni-59
8.871E-3
Sr-90
0
Zr-93 Nb-93m
0 1.885E-2
Tc-99
1.409E-5
Sn-126 Sb-126m (.14)Sb-126
1.354EO 4.001E1 9.769EO
1-129
3.977E-1
Cs-135
0

Parent +
Daughters
0
8.87E-3
0
1.89E-2
1.41E-5
5.11E1
3.98E-1
0
*  Daughters for which the risk factor exceeds  1  percent of the maximum risk factor for any nuclide in the decay chain
   which can grow in while the parent  exists  in the  accessible environment.

-------
TABLE B-l (Continued)
Ground Deposition: Fatal  cancer risk conversion factors  for  parent and  significant* daughters

                                (fatal  cancers  committed per Ci-y/m  exposure)
Parent
Cs-137
0
Sm-151
9.425E-5
Pb-210
6.067E-2
Ra-226
1.811E-1
Ra-228
1.427E-8
Ac-227
4.661E-3
Th-229
2.390EO
Th-230
1.928E-2
********************************* Daughters *******************************
Nuclide Parent +
Risk Factor Daughters
(,946)Ba-137m
1.432E1


Pb-214
6.528EO
Ac-228
2.264E1
Th-227
2.825EO
Ra-225
2.873E-1
Pb-214
6.528EO



Bi-214
3.521E1
Ra-224
2.670E-1
Ra-223
3.583EO
Ac-225
3.806E-1
Bi-214
3.521E1
1.43E1
9.43E-5
6.09E-2
4.20E1
Pb-212 Bi-212 (.36)T1-208 .
3.927EO 4.436EO 2.745E1 5.88E1
Rn-219 Pb-211 Bi-211
1.509EO 1.293EO 1.242EO 1.05E1
Fr-221 Bi-213
8.267E-1 3.577EO 7.46EO
4.20E1
*  Daughters for which the risk factor exceeds 1 percent of the maximum risk  factor  for any nuclide in the decay chain
   which can grow in while the parent exists in the accessible environment.

-------

TABLE B-l (Continued)
Ground Deposition: Fatal cancer risk conversion factors for parent and significant* daughters
(fatal cancers committed per Ci-y/m exposure)
********************************* Dau g hte r s *******************************
Parent
Th-232
1.383E-2
Pa-231
8.488E-1
U-233
1.076E-2
U-234
1.634E-2
U-235
4.080EO
U-236
1.476E-2
U-238
1.300E-2
Np-237
7.105E-1

Ac-228
2.264E1
Th-227
2.825EO
(.05)Th-229
1.195E-1

Th-231
4.089E-1

Th-234
2.225E-1
Pa-233
5.681EO
Nuclide
Risk Factor
Ra-224 Pb-212
2.670E-1 3.927EO
Ra-223 Rn-219
3.583EO 1.509EO
{.05)Ra-225 (.05)Ac-225
1.437E-2 1.903E-2

(.01)Ra-223
3.583E-2

Pa-234m
2.815E-1

Parent *
Daughters
Bi-212 (.36)11-208
4.436EO 2.745E1 5.88E1
Pb-211 Bi-211
1.293EO 1.242EO 1.14E1
(,05)Fr-221 (,05)Bi-213
4.134E-2 1.789E-1 3.84E-1
1.63E-2
4.60EO
1.48E-2
5.17E-1
6.39EO
*  Daughters for which the  risk  factor exceeds 1 percent of the maximum risk factor for any nuclide in the decay  chain
   which can grow in while  the parent exists in the accessible environment.

-------

TABLE B-l (Continued) . ^^ J u^ •
Ground Deposition: Fatal cancer risk conversion factors for parent and significant* daughters
(fatal cancers committed per Ci-y/m exposure)
********************************* Daughters *******************************
Nuclide
Parent R*sk Factor
Pu-238
1.681E-2
Pu-239
7.642E-3
Pu-240
1.610E-2
Pu-241 (,03)Am-241
0 1.871E-2
Pu-242
1.337E-2
Am-241
6.236E-1
Am-243 Np-239
1.437EO 4.511EO
Cm-245 Ara-241
1.959EO 6.236E-1
Cm-246
1.411E-2

Parent *
Daughters
1.68E-2
7.64E-3
1.61E-2
1.87E-2
1.34E-2
6.24E-1
5.95EO
2.58EO
1.41E-2
*  Daughters for which  the  risk  factor exceeds 1 percent of the maximum risk factor for any nuclide In the decay chain
   which can grow In while  the parent exists in the accessible environment.

-------
                    APPENDIX  C:  COMPUTATIONAL .DETAILS

     In this appendix, we will  provide  the  details  of the  derivation  of
the values used for several parameters  which were discussed  in Chapter 5.
A subsection of this appendix has  been  set  aside for each  parameter to be
discussed.
C.I  Curie Intake per Unit Area  Deposition  (RInp)
     The parameter, RInD»  expresses  the  individual  intake  of  a
radionuclide (n) per unit  acute  deposition  to the  soil  surface  for a  food
crop (p).  The associated  units  attached to this parameter are  Ci intake
        o
per Ci/m  deposited to the soil.   The  algorithms used to compute values
for RI   were similar to those given in  the AIRDOS-EPA"computer code
      np
manual (Mo79) and those applied  by NRC in Regulatory Guide 1.109(NRC77).
The computational techniques can be  traced  back to the  HERMES computer
code (F171) which was prepared by the  Pacific Northwest Laboratories  in
the early 1970's.
     For food crops consumed directly  by humans, we can express RI
using the rate of consumption of vegetation by a human  (Up and  U  ),
the concentration of radionuclides in  the vegetation  (Cp and
CL), and the deposition rate of  radionuclides to the  ground (dn) as
     RI
       np

               n
                                                               (C-l)
where
     Up and UL =
quantity of vegetation consumed by a human
receptor per unit time for produce (kg wet/yr)
and leafy vegetables (kg dry/yr),  respectively,
                                   C-l

-------
            CLn-
concentration of nuclide n  1n and on  vegetation
for produce (Ci/kg wet)  and leafy vegetables
(C1/kg dry), respectively,

the deposition rate of nuclide n onto the
            2
ground (Ci/m -yr).
     Note that the dimensions for RI    from equation C-l are
                               2
C1 intake/yr per Ci  deposited/m -yr whereas the  dimensions we desire are
                                                 2
Ci Intake over all time per Ci deposited (total)/m  .   It can be shown
that the ratio of the equilibrium intake rate to a  continuous deposition
                                     2
rate (C1 intake/yr per Ci deposited/m -yr) is numerically equal to the
ratio of the total integrated intake  to the acute surface deposition
                             2 •
(C1 intake per Ci deposited/m ).  Thus, if we apply equation C-l  for
equilibrium conditions (long buildup  times), 1t  Is  appropriate to use the
equation to compute values of RI   for our analysis.   The expressions
for C^ and Cj: are basically the same  as given in equation 49,
page 40, of AIRDOS-EPA (Mo79) modified to account for  removal of
radlonuclides from the plant root zone to a soil sink  Usn)«  The
equations are
r«>ifcp[i-. *•>] ,
B1 v2 E l - e ^ ] "
vpxEn *xDn x$ir
e"XDnthp
 and
                                     (C-2)
          DDI fcL [ 1 - e' En eL ]     B.vl [ 1 - e'
                                                        +XcJt,
                   V^T
                                          .^DnV
                                                               (C-3)
                                    C-2

-------
where
     DDI =
fraction of nuclide retained on plant foliage
which remains after washing (dimensionless),
     f   and f ,
      cp      cL
fraction of deposited nuclide retained on
edible portions of produce and leafy
vegetables, respectively (dimensionless),
      lEn
the effective removal rate constant for nuclide
n from crops (yr~ ),
     t   and t .
      ep      eL
      Yvp and V
time period that crops are exposed to
contamination during growing season for produce
and leafy vegetables, respectively (yr),

agricultural productivity (yield) of the edible
                            2
portion of produce (kg wet/m ) and leafy
                    2
vegetables (kg dry/m },
     Biv2 and Bivl
the concentration factor for uptake of
radionuclide n from soil by edible parts of
crops for produce (Ci/kg wet plant per Ci/kg
dry soil) and leafy vegetables (Ci/kg dry plant
per Ci/kg dry soil), respectively,
      lDn
 radioactive decay constant for nuclide n
 (yr'1),
                            removal rate constant for transfer of nuclide n
                            from the root zone to the soil below the root
                            zone {yr   ),
                                    C-3

-------
      t.  =               period  of  long-term buildup of activity 1n soil
                         (yr).
      P =                effective  density of the root zone (top 15 cm of
                         soil)  (kg  dry  soil/square meter), and
                         a holdup  time  that represents the time interval
                         between harvest  and consumption of produce- and
                         leafy vegetables (yr).
An implicit assumption in equations C-2  and  C-3  is that  irrigation water
deposits radionuclides on the ground surface continuously.  This 1s a
conservative assumption since Irrigation would actually  take place for
less than the full year in many locations within the  U.S.

     As mentioned above, a significant change was made in equations C-2
and C-3 that is not included in the models 1n the AIRDOS-EPA program
manual.  The loss of radionuclides from  the  soil root zone  due  to leaching
of radionuclides to the soil below the root  zone was  accounted  for by
adding the x-  term to the equation.  This loss  mechanism can be
important for long-lived radionuclides and this  is the reason for
including the modification 1n the equations. The addition  of this loss
mechanism causes the majority of the total intake of  radionuclides from
deposition on crop land to occur over a  shorter  time  period after
deposition of radioactivity in the environment than would  be the case  if
radioactive decay were the only mechanism for removal from the  soil  root
zone.  Substituting equations C-2 and C-3 Into C-l yields
                                    C-4

-------
                                                    -(x*x)t
RI
  np
"DDI f

, [ 1 - e '
Yvp xEn
•n ep ] B.
•*• ,

f . '"On "Sn'-b 1 -
V2 ~ ' J
p (xDn + xsn' J
e'*Dnthp
       DDI  fcL  [  1  -
                                   ]      Biyl[.l-e'(XDn+Xsn)tb]
                      vL  En
."XDnthL
                                                               (C-4)
     The methods used to derive algorithms  for.Rl    for milk and  beef
are similar to those used to derive equation  C-l.  For milk, we may write
where
                           quantity of milk consumed by  a  human  receptor
                           per unit time (liters/yr).
rm
Ln =
                           concentration of nuclide  n  in milk (Ci/liters),
                           and d  is as defined previously.   The
                           algorithm for cJJ is  obtained using the
                           methodology discussed on  pages 42  and  43  of
                           AIRDOS-EPA (Mo79) and can be written as
-X t
n = m ^m
<



rf r_e -Wen]
Yvf xEn

_ f 1 + \ ^ t .
r ™\"r^«* **^>*J*'l* •
. n I i Dn Sn D I
^ivll1-6 J
P(X + X« ) J
\ l Dn Sn' '
                                                                    -X
                                                                  )e
                                                                Dnthff]d
                                                               (C-6)
                                    C-5

-------
where
      •fm a
      cf =
      'em
       vf =
      'hsf
average fraction of a cow's daily intake of
radionuclide n which appears in each liter of
milk (Ci/liter per Ci/day intake),

amount of feed consumed by the cow (kg dry/day),

average transport time of the activity from the
feed into the milk and to the receptor (yr),

fraction of the deposited radionuclides
retained on edible portions of animal feed
crops (dimensionless),

time period that milk cow feed crops are
exposed to contamination during the growing
season (yr),
agricultural productivity (yield) of the edible
                                      2
portion of animal feed crops (kg dry/m ),
 fraction of year that animals graze on pasture
 {dimenslonless),

 fraction of feed that Is pasture grass when the
 animals graze on pasture (dimensionless),

 the  time interval between harvest and
 consumption for stored animal feed (yr),
 and the  other  terms  are as defined previously.  Substituting equation C-6
 Into equation  C-5 yields
                                    C-6

-------
                                "
                        „
                                    E"H
                               Yvf  xEn
     For  beef, RInp is determined by
     RI
       np
                                                                   )  e
"xDnthsf
                                                              (C-7)
                                                            (C-8)
where
     \y  =                 quantity of meat consumed by a human  receptor
                          per unit time (kg/yr)

     C  =                 concentration of radionuclide n in meat (Ci/kg)

and d  is as defined  previously.  The algorithm used to determine
values for C^ is obtained as  described on pages 43 and 44 of
AIRDOS-EPA (Mo79) and is
- , Ff Qf e
                   f      F     -A   t  rl
                      
-------
where
     Q* =
     t. =
     'ef
average fraction  of a cow's daily intake of
radionuclide  n which appears in each kilogram
of meat (Ci/kg per Ci/day Intake),

amount of feed consumed by the cow (kg dry/day),

average time  from slaughter to consumption (yr),

time period that  meat animal feed crops are
exposed to contamination during the growing.
season (yr),
and the other terms  are  as defined previously.   Substituting  equation C-9
into equation C-8 yields
RIlip-UFf«f
                                    tnVl
      vf
                         B1vlll-e
                                 x
                                  Dn
                                                                         Dnthsfl
                                                              (C-10)
     The parameter  values chosen for this analysis  are  discussed below and
the references  used to derive these values are listed.


     For Vegetative Food Crops


     Up = 176 kg wet vegetation/yr  (Mo79)
                                   C-8

-------
    DD1 = 1.0  (conservative assumption)
     f   = 0.052  (Ba84)
     cp
     XE  =  18.4 yr""1  (all  nuclides except I)  (Mo79)
     This  is  based  on  a weathering half time of 13.75 d,
     x£n  =  31.6 yr'1  (I  isotopes)   (Ba84)
     This is based on  a  weathering  half time of 8 d.
     t   = te|_ = 100 d =  0.274 yr  (Ba83a)
     Y   = 1.6 kg wet/m*  (Ba84)
     The parameters xDn and \Sn are  discussed  in Chapter 5  and  values


for various radionuclides are given  in  Tables  5-1 and 5-4.  Values  for


x,.  are also repeated in Table C-l of this  appendix.  As discussed
 Sn

earlier, equation C-4, C-7, and C-10 must be evaluated  at equilibrium so


the term e~*xDn + xSn'tb must drop out  of the  equation  and  a  value


for tt. is not needed.
     P = 215 kg dry soil/m2  (Mo79)
th  = *hL = 336 hr
                                 (produce and leafy vegetables)
                                    C-9

-------
For all radionuclldes considered, the half I1fe.s are long enough such that
e"xDnthp and e"xDnthl are -1.0 so that these terms can be set
equal to 1 for our analysis.
     UL = 1.2 kg dry veg./yr  (Mo79, Ba83a)
     fcL = 0.15  (Ba84)
     Yv|_ = 0.12 kg dry veg./rrf  (Ba84)
     The values for B^vl and Bjv2 are radionuclide specific and are
listed in Table C-l.  The values are based on information provided by Baes
(Ba84) except where'noted in the table.

     For Milk
      ,m
      IT =  112  liters milk/yr   (Mo79)
      F  values are specific  to  each  radionuclide and are listed in
       m             r
 Table C-l.   The values are based  on  information provided by Baes  (Ba84)
 except where noted otherwise In the  table.
      Qm = 18.1 kg dry  veg./day   (Sh82)
      tfm = 4 days = 0.011 yr  (Mo79)
                                    C-10

-------
Nucl i de
C
Ni
Sr
Zr
Tc
Sn
1
Cs
Sm
Pb
Ra
Ac
Th
Pa
U
Np
Pu
Am
Cm
* Value
** Val ue
*** Value
a Value
aa Value
+ See S«
B1vl
pCi/kg dry plant
pCi'Ag dry soil
NA
6.00 E-2
2.50 EO
7.20 E-2**
9.50 EO
3.00 E-2
1.50 E-l
8.00 E-2
1.00 E-2
4.50 E-2
1.50 E-2
3.50 E-3
8.50 E-4
2.50 E-3
8.50 E-3
1.00 E-l
4.50 E-4
5.50 E-3
8.50 E-4
B1v2
pCi/kg wet plant x$n
pCi/kg dry sol I (yr-1)
NA NA
2.60 E-2 5.40 E-3
1.10 E-l 2.31 E-2
7.70 E-4** 2.70 E-4
6.40 E-l 4.90 E-l
2.60 E-3 3.24 E-3
2.10 E-2 1.57 E-3
1.30 E-2 8.10 E-4
1.70 E-3 1.25 E-3
3.90 E-3 9,00 E-4
6.40 E-4 1.80 E-3
1.50 E-4 5.40 E-4
3.60 E-5 5.40 E-6
1.10 E-4 3.24 E-4
1.70 E-3 1.80 E-3
4.30 E-3 2.69 E-2
1.90 E-5 1.80 E-4
1.10 E-4 1.16 E-3
6.40 E-6 4.05 E-4
Fm
pCi/1
pCi /day Intake
NA
1.00 E-3
1.50 E-3
3.00 E-5
1.00 E-2
1.00 E-3
1.00 E-2
7.00 E-3
2.00 E-5
2.50 E-4
4.50 E-4
2.00 E-5
5.00 E-6
5.00 E-6
6.00 E-4
1.00 E-5°
1.00 E-7
4.00 E-7
2.00 E-5
is arithmetic average of values given by Baes (Ba84) and Ng (Ng82a).
is based on data suggested by Ng (Ng82b).
is based on data suggested by Ng (Ng82a).
based on data suggested by Schaffer (Sc83).
based on judgement after reviewing data from Baes (Ba84), Ng (Ng82a)
jction C.6 of this appendix for explanation of methodology used to co
Ff
pCi/kg
pCi/day intake
NA
2.00 E-3***
3.00 E-4
2.00 E-2***
8.50 E-3
8.00 E-2
7.00 E-3
2.00 E-2
5.00 E-3
3.00 E-4
5.80 E-4*
2.50 E-5
6.00 E-6
1.00 E-5
2.00 E-4
2.00 E-400
2.00 E-6***
3.50 E-6
3.50 E-6
, and Schaffer
impute xcn.
mT/g
NA
150
35
3,000
1.5
250
10
1,000
650
900
450
1,500
150,000 '
2,500
450
30
4,500
700
2,000
(Sc83).

-------
     fcf =  0.57   (Mo79,  Ba83a)
     tem =  65  days  =  0.178 yr   {Ba83a, Sh82)
     Yyf = 0.28 kg  dry  veg./m'
          = 90 days = 0.246 yr  (Mo79)  (stored feed)
For the radionuclides in this analysis,  the  half llfes are long enough
such that e~ Dn hsf are "1.   This makes  1t unnecessary to select
values for f  and f  since they drop  out of  the equation.  Values  for
the other parameters in equation C-7  are the same as those used for the
vegetative food crops.
     For Meat

     UF = 94 kg meat/yr  (Mo79)

     Ff values are specific to each radionuclide and  are  listed in Table
C-l.  The values are based on information provided by Baes (Ba84)  except
where noted.

     Qf = 8.3 kg dry veg./day  (Sh82)
     ts = 20 days = 0.055 yr  (Mo79)
     t f = 65 days = 0.178 yr  (Ba83a, Sh82)
                                   C-12

-------
Values for the other parameters  1n equation C-10 are the  same as those
used for the milk pathway.

     Using the algorithms and  parameter  values  discussed  in this section,
the values for RI   for vegetative food  crops,  milk and meat can be
derived.  These values are listed in  Table 5-3.
C.2  Persons Fed per Unit Area (CPp)
     The parameter CP_ expresses the  number of  persons who can  be  fed
per unit area of land for the vegetative  food crops,  milk and meat
pathways.  The deviation of this parameter for  the  various foods will  be
discussed in this section.
     Vegetative Food Crops

     Shor (Sh82) gives agricultural  productivity for four different
categories of vegetative food crops.  In a recent report, Baes (Ba84)
lists estimates of the relative importance of these categories in the
human diet.  This data is recorded in Table C-2.
TABLE C-2:  Productivity and relative importance of vegetative human
              food crops
Crop Category
Leafy vegetables
Exposed produce
Protected produce
Grains
Productivity
kg wet/m^
2.44
1.65
0.91
0.23
Percent of Vegetative
Human Food
5.8
20.0
42.2
32.0
                                   C-13

-------
We have assumed that one food crop per year is .raised  and  that each person
consumes 194 kg wet of vegetative  food crops per year  (Mo79)  so that CP
(veg) may be calculated as
CPp (veg) =
                                                 kg wet
2.44(.Q58)  + 1.65(.2Q)  +  0.91(.422)  +  0.23(.32)   m2-yr

                                     Kg wet
                                    yr-person
CP  (veg) = 4.79 E-3 persons fed/m*
     Milk
     Shor (Sh82) gives agricultural productivity and area!  yield data for
four categories of cattle feed crops.  She also discussed the fraction of
total cattle diet furnished by each feed crop.  This data is listed in
Table C-3.
TABLE C-3: Area!
Crop Category
Pasture
Grain
Hay
Silage
yield and fraction of diet for cattle
Areal Yield
(kg dry/m^-yr)
0.09
0.31*
0.46
0.66*
feed crops
Fraction of
Cattle Feed
0.55
0.17
0.21
0.07
 *   Productivity  (kg dry/m2); assume 1 crop/yr to obtain area! yield.
                                   C-14

-------
     Shor  (Sh82) also provides the following data:
     Milk
     Cow
     Feed
     Rate
= Qm = 18.1  kg dry  veg./day  consumed  by  milk  cows
     Milk Production = 12.9  liters
                           day-cow
     From the  AIRDOS-EPA computer code manual  (Mo79)
     Milk consumption  by man =  112 liters
                                  yr-man

     Then, using  the data  from  Table C-3 and the above listed values,
CP (milk) = L.09(.55)+.31(.17)+{
kg dry veg]
.46)(.21)+.66(.07) yr-m2 J
«9 p liters milk 1
day cow j
                 18.1
kg dry veg

  day-cow
                          112
liters milk

   y-man
                      roan
*n i  JIL\   i  cc r- o
CPn(milk) = 1.56 E-3 - «
  P                     m
     Meat
     The data on area!  yield and percentage of cattle  feed listed in Table

C-3 were utilized 1n deriving CPp for the meat pathway.   Other data

listed by Shor (Sh82) which were used are:
Q- = 8.3 kg dry feed
 T           ff^y

     Slaughter factor = 0.34/yr

     Live weight at slaughter = 477  kg
                                   animal
                                   C-15

-------
     dressed weight  =  0.56
      live weignt
Therefore,
     Neat production =  [477  kg  live
                            arnma
                       0.56 kg meat
                            kg 1i ve
               0.34
                     =   90.8 kg  meat    =  0.25 kg meat
                 ,
               animal -yr
                                                ,
                                             animal -day
From the AIRDOS-EPA computer program manual,  human annual meat consumption

is 94 kg meat/yr.   Using this data,  we  can  derive the CP  for meat as
CPp(meat) =
.09(.55) + .
              kg dry yeg
                 yr-m   .
                                                                 n ?5
                                                                         meat
                                                                      am ma i -day
                   8.3
         kg  dry  veg
          day-cow
94
kg meat \
y-personj
CPJmeat) = 7.85 E-5
                        m
In summary, the values used for CP_ in our analysis are  listed  in Table

C-4.
TABLE C-4:  Values for persons fed per unit area  of  land  (CPp)
                    Food
                                                   CP,
                                 person fed/m2
            Vegetative Food Crops
                    M1lk
                    Meat
                                   4.79 E-3
                                   1.56 E-3
                                   7.85 E-5
                                   C-16

-------
C.3  Fraction of River Flow Used for Irrigation.(fR)

     The fraction of the river flow used for irrigation,  fR,  was set
equal to 0.1 in this analysis.  This number is  representative of the
average fraction of total  surface water flow used for irrigation for the
U.S.  The reader may obtain a feel for the variation  in fR for various
regions of the U.S. by referring to the data in Table C-5.
TABLE C-5:  Fraction of river flow used for irrigation (fp) by Water
            Resources Council region for 1975 (Mu77)
          Water Resources
          Council Region
         New England
         Mid-Atlantic
         South Atlantic-Gulf
         Great Lakes
         Ohio
         Tennessee
         Upper Mississippi
         Lower Mississippi
         Souris-Red-Rainy
         Missouri Basin
         Arkansas-Whitened
         Texas-Gulf
         Rio Grande
         Upper Colorado
         Lower Colorado
         Great Basin
         Pacific Northwest
         California
         U.S. (conterminous)
0.001
0.001
0.009
0.001
  0
  0
0.001
0.020
0.003
0.370
0.029
0.031
0.580
0.285
0.969
0.667
0.114
0.307
0.070
                                   C-17

-------
     For the conterminous U.S.,  the fR values  was  rounded from 0.07 to

0.1.  The data for the conterminous U.S.  from  the  above table have been

compared to data from other references which generally support the fR

value of 0.1 (WIC70, WRC78).

C.4  Population Density (PD )

                                                                o
     The value used for population density is  6.67 E-5 persons/m .  This

value is the world average population density  and  was obtained by dividing

the assumed population of 10   persons* by the land surface area of the

earth of 1.5 E14 m2 (Wo79).  A review of the data  listed in Table C-6

will show that the PD  used is within the range of current values for

various regions of the U.S.  As the world population increases, the U.S.

population would also increase.
TABLE C-6:  U.S. regional values for population density (PDp) ( USDC83)
   Region
 Population Density
for 1982 (persons/m2)
U.S. Average
New England
Middle Atlantic
East North Central
West North Central
South Atlantic
East South Central
West South Central
Mountain
Pacific
       2.51 E-5
       7.65 E-5
       1.43 E-4
       6.57 E-5
       1.31 E-5
       5.52 E-5
       3.21 E-5
       2.28 E-5
       5.41 E-6
       1.43 E-5
      *The  current world population Is about 3.8 E9.  However, an estimate
 of  average world population during the time period Involved in this
 calculation is  1010  people (UN77K
                                    C-18

-------
C.5  Correction Factor for the Ground Surface Risk Factors (GC  )
     The risk conversion factors used for radionuclides deposited on the
ground were derived using the assumption that the material remains on the
surface.  Over the long time periods involved in these calculations, the
radionuclides will move vertically downward into the soil.  The gamma
radiation emitted from these nuclides is partially shielded by the soil
such that the dose equivalent per unit deposition is less than given by
the surface dose conversion factors.  We derived correction factors for
each nuclide by assuming that the radioactivity was uniformly distributed
vertically within the soil root zone (see the discussion in Section
3.1.6).  The algorithm used for calculating the correction factor is
     GC.
       np
     where
                        [15 DiplW]
                                                (C-ll)
     GC
        np
      Dis1(r)
= radionuclide specific factor used to correct ground
  surface fatal cancer risk factors to account for uniform
  distribution of radionuclides within the 15 cm soil root
  zone (dimensionless),
                           4i~tc—
= gamma intensity for the i— gamma (gammas
  emitted/disintegration),
= dose rate in air due to 1 Bq/cm  ground volume
  concentration within the 15 cm soil root zone for gamma
  energy 1  (Sv/y),
                                 2
= dose rate in air due to 1 Bq/cm  ground surface
/
  concentration for gamma energy i (Sv/y).
                                    C-19

-------
The summations are for all gammas emitted by the parent radionuclide and
the daughter radionuclides which were Included 1n deriving the risk
conversion factors.  The multiplier, 15,  in the denominator of the
equation is to adjust the radionuclide content of the soil surface to
equal that of the 15 cm slab representing the soil root zone.  Values for
D^sl(r) and D^ -J(Y), as a function of gamma energy, were furnished by
Kocher (Ko83b).  D- -J(T) and 15 0^ -|{Y) are plotted as a function of   '.
gamma energy in Figure C-l.  Using the algorithm given above, the gamma
energy intensity information for the parents and significant daughters
given by Kocher (KoSla) and the data plotted in Figure C-l, the
radionuclide specific correction factors listed in Table C-7 were
computed.  These factors were multiplied by the RADRISK risk conversion
factors  (derived assuming surface deposition) to obtain risk conversion
•factors  for uniform distribution of radionuclides within the 15 cm soil
root zone.
                                    C-20

-------
            ours
                       L'ose  t'6 i^'b  'i n a "• r -3i i  \\^\.i:r s L'Gvo yround  1 or
                       infinite uniform plane  source and an  infinite
                       uniform slab source
> ID
uo
o>
res
i-
V)
o
-o

t-

03

QJ
 QJ
 C
 ro

 O.
i—i
ID
                                             The infinite plane source is
                                             located at ground level and
                                             has an area concentration of
                                             15 Bq/cm2.              _
                                             The infinite slab source has
                                             the top surface at ground level
                                             and the bottom surface at a
                                             depth of 15 cm and has a volume
                                             concentration of 1 Bq/cm3.
                                                                                  QJ
                                                                                  •M
                                                                                  (O
                                                                                  s-

                                                                                  QJ
                                                                                  trt
                                                                                  O
     o

    ID
     10
       -7
           0.01
                               0.10                    1.0
                                  gamma energy,  (MeV)
10.0

-------
TABLE C-7:
Ground surface radionucllde correction factors  (GCnp)
          Nuclide
     GCnp
(Dimensionless)
C-14
Ni-59
Sr-90
Zr-93
Tc-99
Sn-126
1-129
Cs-135
Cs-137
Sm-151
Pb-210
Ra-226
Ra-228
Ac-227
Th-229
Th-230
Th-232
Pa-231
U-233
U-234
U-235
U-236
U-238
Np-237
Pu-238
Pu-239
Pu-240
Pu-241
Pu-242
Am-241
Am-243
Cm-245
Cm-246
Beta emitter
8.8E-5
Beta emitter
1.3E-3
Beta emitter
2.2E-1
l.OE-2
Beta emitter
2.4E-1
Beta emitter
2.3E-2
2.4E-1
1.8E-1
1.5E-1
9.7E-2
2.4E-1
1.8E-1
1.3E-1
7.5E-2
2.9E-2
7.3E-2
2.5E-4
4.3E-2
9.2E-2
3.8E-4
4.1E-4
4.0E-4
1.2E-2
4.0E-4
1.2E-2
6.9E-2
3.3E-2
4.0E-4
                                    C-22

-------
C.6  Leaching Removal  Rate Constant for Soil (x$n)

     The leaching  rate constant  for transfer of nuclides from available to
unavailable soil  is  x- .  The  value for x.  is nuclide dependent and
is determined by  a method described by Baes (Ba79a).  The algorithm is
              w
where
              I1*
                                            (C-12)
                   leaching  removal  rate constant from soil root zone
                   (yr'1),
      w
velocity of vertical  water percolation  (cm/yr),

depth of soil  root zone (cm),   -

                       3
soil bulk density (g/cm )

                         3
soil water content (ml/cm )

equilibrium distribution coefficient of the  nuclide
species between soil  and water (ml/g)
                                   C-23

-------
     Parameter values for these generic  calculations were chosen after
discussion with C.F.  Baes III  of Oak  Ridge National Laboratory.  The
parameter values and  references are listed below:
     Vw and p -    used median value  from  Table  3.19,  NUREG/CR-1004  (Ba79a)
      W
     Vw    = 74 cm/yr
     p     e 1.4 g/cnT
     d     = 15 cm (assumed soil root zone depth)
     o -  used average of median field capacity volumetric  water content
          and median wilting point volumetric water content for all  soils
          from Table 2 of Baes and Sharp 1983 article In the Journal  of
       •   Environmental Quality (Ba83b)

     e = 0.23   ml
               cm

     K. -   values used are the default values recommended by Baes in
            ORNL-5786  (Ba84)

     Kd values are nucllde specific and are listed in Table C-l.
                                   C-24

-------
     Using the above listed  parameter  values,  the  values  for  ASn  listed
in Table C-l were computed,  except  for 1-129.   For 1-129,  data  from
Kocher's dynamic model  of  the  global iodine  cycle  {KoSlb,  Ko83b)  were
applied to determine AS .  Kocher has  a  surface soil  region with  a depth
of 100 cm in his model. Dr. Kocher recommended that  we consider  transfer
from his surface soil  region to  the ocean mixed layer, the shallow land
subsurface region and the  deep land subsurface region in  determining a
value for A- .  The rate constants  listed by Kocher for transfer  from
his 100 cm deep surface soil region to the other three regions-are listed
in Table C-8.  We linearly scaled these  rate constants to obtain  rate
constants for our 15 cm soil root zone (Table C-8),  The  summation of
these three rate constants gives a  value for ASP for 1-129 of
1.57 E-3 yr-1.
TABLE C-8:
Determination of A$n for 1-129
Transfer from Surface
Soil Region to
    Rate Constant,
        (yr-1)
                                         100 cm depth
               15 cm depth
Ocean Mixed Layer
Shallow Subsurface Region
Deep Subsurface Region
2.0 E-4
3.5 E-5
7.0 E-7
   1.3 E-3
   2.3 E-4
   4.7 E-6
=  1.57 E-3 yr-1
                                   C-25

-------
C.7  Ratio of Persons Drinking Water  and Eating F1sh to River Flow Rate

     PR 1s the number of people who drink water and/or eat  fish  from a
river and R is the river flow rate.   The ratio PR/R is needed in several
equations, and it can be determined for the  purpose of this generic
evaluation without obtaining site specific data.  Utilizing data from
Annex D of the 1977 UNSCEAR Report (UN77), the annual flow  rate  of the
rivers of the world is 3E+16 liters/yr.   If  one assumes a constant world
population of 10   persons*, the ratio PR/R  is 3.3E-7 person-yr/liter.
This value for the ratio PR/R 1s midrange of values found for various
river basins in the United States. These values  ranged from a  high  of
5.73E-7 for the Lower Colorado Water  Resources Council region to a low  of
2.39E-8 for the Pacific Northwest Water  Resources Council region, based on
1975 river flow and population estimates.  Table  C-9  lists  these ratios
for the various Water Resources Council  regions.

C.8  Total Fraction of Initial River Inventory  Deposited  to Cropland for
     Radionuclides Rapidly Transferred Through  Soil  (Radionuclide Recycle)

     The  algorithms used to compute environmental risk  commitment from
Irrigated food crop consumption do not Include  the  consideration of
recycle of radionuclides deposited on the cropland  back  to  the river and a
     *The current world population is about 3.8E9.  However, an estimate
 of  average world population during the time, period Involved in this
 calculation 1s 10*0 people (UN77).
                                   C-26

-------
TABLE C-9:  Ratio of persons drinking water and eating fish to river
            flow rate by Water Resources Council  region (Mu77, USDC83)
          Water Resources
          Council  Region
(Person-yr/liter)
         New England
         Mid-Atlantic
         South Atlantic-Gulf
         Great Lakes
         Ohio
         Tennessee
         Upper Mississippi
         Lower Mississippi
         Souris-Red-Rainy
         Missouri Basin
         Arkansas-White-Red
         Texas-Gulf
         Rio Grande
         Upper Colorado
         Lower Colorado
         Great Basin
         Pacific Northwest
         California
      1.32E-7
      2.88E-7
      1.03E-7
      2.02E-7
      1.50E-7
      5.62E-8
      2.00E-7
      6.27E-8
      1.78E-7
      1.19E-7
      9.24E-8
      1.90E-7
      4.40E-7
      8.76E-8
      5.73E-7
      1.09E-7
      2.39E-8
      2.52E-7
         U.S. (conterminous)
      1.30E-7
                                   C-27

-------
redeposltlon of this material  back  to the  cropland  via  Irrigation.   We
assume that when the radionuclides  are removed  from the  soil  root zone  (by
leaching) they are no longer available for uptake by foodcrops.  For
radionuclides which leach rapidly through  the soil, 1t  1s  of  interest to
consider the effects of recycling.   Of the radionuclides we consider, the
one most subject to this phenomenon Is Tc-99.

     Dr. Kocher (Ko83a) has suggested a bounding calculation  to  determine
the Importance of recycle 1n making material available  for plant uptake
from soil.  The computation 1s shown below.
     River
                              Irrigated
                              Cropland
                    0.85 returns
                    to river
                                                 0.15 Is not available
                                                 for recycle.
Assumptions:
          Neglect radioactive decay as a removal mechanism.
          85 percent of radionucllde deposited on cropland Immediately
          recycles back to the river (Xcn 1s very large).
          15 percent of radionuclide deposited on cropland Is permanently
          fixed within the soil below the plant-root-zone and Is no longer
          available for uptake or recycle.
                                   C-28

-------
     Then let
               fraction of river flow used for  irrigation.
               initial  inventory in river (Ci).
     I,
  final  inventory  on  cropland  (Ci}.
     We may write
        = fR To * (0'85fRIo>fR + (0.85f*I0)(0.85)(fR)
                                             3
            [(0.85)   fj  I0](0.85)(fRK{0.85)   f  IQ](0.85)(fR)+
     Then
     If   » fR + (0.85fR)fR + (0.85fR)2fR + (0.85fR)3fR + (0.85fR)4fR+ .  .
     "£
The above series is a geometric progression where the square of the common
ratio (0.85fR) Is less than one.  For this case,  the value of If/^0
for an infinite summation is
     If
     I.
                 (6u48)
(C-14)
1-0.85f
                    R
The ratio If/IQ represents the total fraction of the initial inventory
in the river which is deposited on cropland' due to infinite recycling of
radionuclides.  For our chosen value of fR of 0.10, we have
                0.10
                          = 0.11.
     I0     1-0.85(0.10)
                                   C-29

-------
Since this ratio is very close to our  chosen vajlue of fR of 0.10, the
effects of recycling are not significant  in our calculations.

C.9  Tabulation of Estimated Range of  Parameter Values

     A specific request of the Science Advisory Board High-level
Radioactive Waste Disposal Subcommittee was that we  include,  In the  final
pathways report, a listing of parameter values used  in  the analysis  and an
estimate, where possible, of the range of values for the parameters.   This
information is included in Table C-10.  In addition  to  listing the
estimated range of parameter values, the  values used for our  analyses,
which are also listed in other sections of this report, are  restated in
the table.  The parameters which are essentially invarient  (such  as  earth
land area) are not listed 1n the table.

     For some parameters, a range of values was not  given  in  the
references we consulted and only the default  value which we  used  is
given.  For others, intuition dictates that the range  given  appears  to be
too narrow (for example, the  range of Kd for  Sm, 600-650 ml/g).   If  more
data were available, 1t is probable that the  range would  be  larger.   In
some cases, we applied  a parameter value for  our  analysis  which was  near
an extreme of the  range rather than one near  the midpoint.   This  1s  ah
indication that the bulk of the  data had values near this  extreme and/or
that we  had more confidence 1n the data near this  extreme.
                                   C-30

-------
     TABLE C-10:
     Listing of parameter value  ranges
Parameter
PD/R and Prjr/R
Estimated Range
of Values
10'6 to ID'2 per yr
2.4E-8 to 5.7E-7
Value
Used
10-4/yr
3.3E-7
Notes
Estimated range

for USA based on 1975
o
I
OJ
                          (Pacific  Northwest)(Lower Colorado)
                          320 to 712
603 1/y
(Ref. man value)
data (Mu77, USOC83).  Value used is
world average number for a stable
world population which is about 2.6
times the current population (UN77).

Range is measured data.  Ref. man
value is set higher than most
measured values.  See pages 358 and
360 of ICRP No. 23 (ICRP75).
                          4.4 to 13.9 (Supplies of fish)
1.0 kg/y            Range is per caput.   Data  from page
(fresh water fish)  349,  ICRP No. 23 (ICRP75).   Values
                    used  from UNSCEAR (UN77).

6.0 kg/y
(Ocean fish)
                                                             1.0 kg/y
                                                             (Ocean shellfish)
                          Values could vary from 0 to  1.0     0.50
                                                             (food crops)
                                                             0.25
                                                             (Milk)
                    Value used column  lists  the  fraction
                    of crop land used  for the various
                    food crops.
                          0 to 0.97
0.25
(Meat)

0.10
Value used is U.S. average (See
Table C-5).

-------
o
UJ
ro
TABLE C-10 (Continued):
Parameter
CPp

PDP
RF
-
IB
Estimated Range
of Values
5.1E-5 to 9.3E-2
2.1E-5 to 1.4E-1
1.1E-6 to l.OE-2
5.4E-6 to 1.4E-4
(Mountain) (Hid- Atlantic)
1E-10 to 1E-8
See Note
750 to 14,600
Value
Used
d.79F_3 man fed
(Food crops) m*
l.SfiF.3 ««" fed
(Milk) m*
7.85F-5 man fed
(Meat) m^
6.67E-5 Persons
m2
lE-ftlT1
lE-llsec-1
3
8400 m
y
Notes
(Ba79b, Ho82b, USDA82, Ba84)

Estimated range for USA based on 1982
data (USDC83). Value used is world
average number for a stable world
population which is about 2.6 times
the current population (UN77, Wo79).
Weathered material. (Ri83, Be76).
Calculated from range of RF using the
equation RF=Xp/vg with vg=0.0l
m/sec .
(ICRP75) Minimum is for 1 yr old rest
24 hr/day. Maximum is for adult man
     fwt
0.2 to 1.0
                                                             1.0
doing heavy work 10 hr/day, light
activity 6 hr/day and resting 8 hr/
day.  Value used is for Reference Man
(Adult man).

Estimated range is for various
nuclides.  Data from (NRC78, F171,
De75).

-------
      TABLE C-10 (Continued):
      Parameter
 Estimated Range
    of Values
 Value
 Used
                                                                                 Notes
o
I
to
      HA

      vgn
0.10 to 0.90



7,600m to 18,000m


0.0004 to 0.09



0.009 to 0.057
0.65



13,000m


0.01



0.02
                                                             48.7y
                                                                  -1
Value used Is U.S. average.   Range
represents variation within  U.S.
(Mu77).

Value used is mean of estimated
range.  Estimated range from (Wo79).

Estimated range is from data in
Meteorology and Atomic Energy, 1968
(AEC68).

Estimated range is from data in
Meteorology and Atomic Energy, 1968
(AEC68).  There is not nearly so much
data for vwn as for Vgn*  The
available data suggests that vwn is
at least twice vgn.

Value calculated from vwn and fy*

-------
     TABLE C-10 (Continued):
     Parameter
                      Estimated Range
                         of Values
                                                             Value
                                                             Used
                                                       Notes
o
I
(A)
CFnp*
(Freshwater Fish)

C
Ni
Sr
Zr
Tc
Sn
I
Cs
Sm
Pb
Ra
Ac
Th
Pa
U
Np
     Pu
4550-5000
100
7.0E-1 to 2,
3.3
11 to 75
100-10,000
10-132
40-14,000
25
100-300
3-750
25
30-80
11
2-20
10-10,000
                     0.1-50,000
                                      OE2
4550
 100
  11
   3.3
  43
3000
  33
1300
  25
 100
  50
  25
  30
  11
  10
 500
                                                                8
(Th72)
(Th72)
(B1825,  R183)
(Th72)
(B182a)
(Ri83,  Th72)
(Ho79)
(Pe83,  Bl82b,  Ho79)
(Th72)
(Th72)
(B182b,  Pe83,  Th72)
(Th72)
(Th72,  Pe83, Th72)
(Th72)
(Th72,  B182b,  Th72)
(Th72,  Ri83)  Value of 10,000 was
top of range used by Envlrosphere Co.
This was not a measured value.
(B182b, Ri83)  Value of 50,000 appears
to be an outlier.  Most reported
values are between 3.5 and 50.
Am
Cm
15 to 452
25
81
25
(R183)
(Th72)
     *CFnp data for ocean fish and ocean shellfish not Included In this tabulation because of minor significance
     of these pathways.

-------
o
I
to
on

TABLE C-10 (Continued):

Parameter
Parameters used in
vw
if
p
0

K(j values (ml/g)
C
Ni
Sr
Zr
Tc
Sn
I
Cs
Sm
Pb
Ra
Ac
Th
Pa
U
Np
Pu
Am
Cm
Estimated Range
of Values
calculating \$n (See equation C-12).
36.5-376
0.93-1.84
0.03-0.40


NA
80-150
0.15-3,300*
2000-3000
0.0029-1.5*
250
0-10
10-52,000*
600-650
4.5-7640*
100-450
1000-1500
2000-510,000*
2500-4000
10.5.4400*
0.16-929*
11-300,000*
1.0-47,230*
99.3-51,900*
Value
Used Notes

74 cm/y (Ba79a)
1.4 g/cm3 (Ba79a)
0.23 ml/cm3 (Ba79a)
15 cm (Ba79a)

NA
150
35
3000
1.5
250
10
1000
650
900
450
1500
150,000
2500
450
30
4500
700
2000
     *Range as listed in Table 2.13  (Ba84).   Range estimates without * are based on default value in (Ba84) and

     value listed in Table C-3 of  (Li77c).  Values used are the default values In (Ba84).

-------
o
 I
to
en
TABLE C-10 (Continued):
Parameter

UP
DD1
fcp
xw
tep
Yyp
P
UL
DD1
fcL
teL
YVL
*hL
Estimated Range
of Values

0 to 540
0-1.0
0.027 to 0.073
1.7-128.0
60-180d
l.OE-2 to 5.6
100-300
84-336
0 to 3.7
0-1.0
0.06-1.0
40-120d
0.024 to 0.35
84-336
Value
Used
Parameters used in calculating RInp
i?fi Kg wet
y
1.0
0.052
18.4/y
lOOd
1 Tfi kg wet
?15 kg dry
336 hr
1.2 kg dry/yr
1.0
0.15
lOOd
n.1? kg dry
336 hr
Notes

(Ho82b,

(Ba84)
(Ho82b,
(Ho82b,
(Ba79b,
(Ho82b,
(B177,
(Ho82b,

(Mi79f
(Ho82b,
(Ba79b,
(B177,


Mo79)

Ho79)
Ba84)
Ba84)
Ho79)
Mo79)
Ba84)

Ba84)
Ba84)
Ba84)
Mo79)

-------
 I
CO

TABLE C-10 (Continued):
Parameter
um
Qm
tfm
fcf
fcem
Yvf
thsf
uf
Qf
ts
W
Estimated Range
of Values
0 to 600
4 to 25
3-4d
0.02 to 0.82
15-200d
0.03 to 1.7
0 to 300
1.6-18
12-20d
15-200d
Value
Used
112 1/yr
ift.l kg dry
d
4d
0.57
65d
n_?8 kg dry
90d
94 kg/yr
8.3 kg dry/d
20d
65d
Notes
(Ho82b, Ho79)
(Ho82b, Sh82)
(8177, Mo79)
(M179, Mo79)
(Ho82b, Ba84)
(Ba79b, Mo79)
(Mo79)
(Ho82b, Ho79)
(Ho82b, Sh82)
(B177, Mo79)
(Ho82b, Ba84)

-------
to
oo
TABLE
C-10 (Continued):
Estimated Range
Parameter of Values
Blvl
Ni
Sr
Zr
Tc
Sn
I
Cs
Sm
Pb
Ra
Ac
Th
Pa
U
Np
Pu
Am
Cm
(pCl/kg dry crop per pCI/kg dry soil)
5.7E-3 to 5.5E-1
4.3E-2 to 2.3E1
7.2E-3 to 2.5E-1
1.4 to 4.4E+1
1.3E-2 to 3.0E-2
1.5E-2 to 2.0
3.8E-3 to 5.7E-1
l.OE-2
1.3E-2 to 9.0E-1
2.4E-3 to 7.1E-1
3.5E-3 to l.OE-2
8.5E-4 to 2.7E-3
2.5E-3 to l.OE-2
8.5E-3
4.8E-3 to 3,5
10-6 to ID'2
1.7E-3 to 5.5E-3
3.0E-5 to 8.5E-4

Value
Used*

6.0E-2
2.5
7.0E-2
9.5
3.0E-2
1.5E-1
8.0E-2
l.OE-2
4.5E-2
1.5E-2
3.5E-3 *
8.5E-4
2.5E-3
8.5E-3
l.OE-1
4.5E-4
5.5E-3
8.5E-4

Notes**

(Ng82b)
(Ba84, Ng82b)
(Pe83, Ba84)
(Ho80)
(Ba84)
(Ng82b, Ba84)
(Ng82b)
(Ba84)
(Ba84)
(Ba84)
(Ba84, Mo79)
(Ba84, Mo79)
(Ba84, Mo79)
(Ba84)
(Pe83, Ng82b)
(Ba84)
(Pe83, Ba84)
(Pe83, Ba84)
     *Va1ues used are default values given by Baest  et.  al  (Ba84)  except for Zr which was taken from Ng,  et.  al

     (Ng82b).
     **Notes indicate references used to estimate range  of  values.

-------
 I
CO
TABLE
C-10 (Continued): x
Estimated Range
Parameter of Values
Biv2
Ni
Sr
Zr
Tc
Sn
I
Cs
Sm
Pb
Ra
Ac
Th
Pa
U
Np
Pu
Am
Cm
(pCi/kg wet crop per pCI/kg dry soil)
3.0E-4 to 1.5E-1
8.6E-5 to 1.1E-1
3.4E-6 to 1.8E-2
9.6E-2 to 3.00***
l.OE-3 to 1.0E2
2.0E-4 to 1.5
1.5E-5 to 6.8E-1
1.7E-3 to 7.0E-3
3.0E-4 to 7.3E-2
7.0E-5 to 7.5E-1
1.5E-4 to 2.5E-3
. 3.0E-5 to 8.6E-3
1.1E-4 to 2.5E-3
3.0E-5 to 8.6E-3
5.7E-6 to 1.3E-1
3.8E-8 to 4.0E-2
2.3E-7 to 5.0E-3
1.1E-6 to 1.2E-5

Value
Used*

2.6E-2
1.1E-1
7.7E-4
6.4E-1
2.6E-3
2.1E-2
1.3E-2
1.7E-3
3.9E-3
6.4E-4
1.5E-4
3.6E-5
1.1E-4
1.7E-3
4.3E-3
1.9E-5
1.1E-4
6.4E-6

Notes**

(Ba84, Ng82b)
(Ba84)
(Ng82b)
(Ba84)
(Ri83)
(Ng82b, Ng82c)
(Ng82b, Ng82c)
(Ba84)
(Ng82c)
(Ng82c)
(Ba84, Mo79)
(Pe83, Ba84)
(Ba84, Mo79)
(Pe83, Ba84)
(Pe83, Ng82b)
(Ng82c)
(Ng82c)
(Pe83)
     *Values used are default values given by Baes, et. al (Ba84) except for Zr which was taken from Ng, et. al
     (Ng82b).
     **Notes indicate references used to estimate range of values.
     ***Range estimated from Bfvl range in Ho80 and BfV2/BiVl ratio given in Ba84.

-------
o
i
TABLE C-10 (Continued):
Parameter 	
Fm (day/liter)
Mi
Sr
Zr
Tc
Sn
I
Cs
Sm
Pb
Ra
Ac
rl\*
Th
Pa
u
Np
•r
Pu
Am
Cm
Estimated Range
of Values

l.OE-3 to l.OE-2
3.5E-4 to 3.8E-3
3.0E-5 to 8.0E-2
2.0E-3 to 4.3E-2
l.OE-4 to l.OE-1
1.4E-3 to 5.4E-2
1.3E-3 to 3.7E-2
2.0E-5
9.1E-6 to 7.7E-4
9.0E-5 to 7.0E-4
2.0E-5
3.0E-6 to 5.0E-6
5.0E-6
7.3E-5 to 6.1E-4
l.OE-7 to l.OE-3
2.7E-9 to l.OE-7
4.0E-7 to 2.0E-5
2.0E-5
Value
Used*

l.OE-3
1.5E-3
3.0E-5
l.OE-2
l.OE-3
l.OE-2
7.0E-3
2.0E-5
2.5E-4
4.5E-4
2.0E-5
5.0E-6
5.0E-6
6.0E-4
l.OE-5
l.OE-7
4.0E-7
2.0E-5
Notes**

(Ba84, Pe83)
(Ng82c)
(Ba84, Pe83)
(Ri83)
(Ri83)
(Ng82c, Ng77)
(R183)
(Ba84)
(Ng77)
(Ng77)
(Ba84)
(Ng77, Ba84)
(Ba84)
(Ng77)
(R183)
(Ng77)
(Ba84, Ng77)
(Ba84)
      *Values  used  are  default  values given by Baes, et. al  (Ba84) except for Np which was taken from Rish, et. al

      (R183).
      **Notes  indicate  references used to estimate range of  values.

-------
     TABLE C-10 (Continued):
     Parameter
Estimated Range
 of Values ***
Value
Used*
Notes**
o
I
     Ff  (day/kg)
N1
Sr
Zr
Tc
Sn
I
Cs
Sm
Pb
Ra
Ac
Th
Pa
U
Np
Pu
Am
Cm
3.4E-4 to 1.1E-2
2.0E-6 to 8.0E-2
5.5E-3 to 2.0E-2
l.OE-3 to 2.0E-1
l.OE-4 to l.OE-1
1.8E-4 to 2.0E-1
2.9E-3 to 4.5
5.0E-3
l.OE-4 to 2.0E-3
2.5E-4 to 2.0E-3
1.6E-6 to 2.5E-5
1.6E-6 to 2.0E-4
1.6E-6 to l.OE-5
1.6E-6 to 1.2
l.OE-6 to 5.0E-3
5.0E-9 to 1.6E-4
3.5E-6 to 1.8E-4
3.5E-6
2.0E-3
3.0E-4
2.0E-2
8.5E-3
8.0E-2
7.0E-3
2.0E-2
5.0E-3
3.0E-4
5.8E-4
2.5E-5
6.0E-6
l.OE-5
2.0E-4
2.0E-4
2.0E-6
3.5E-6
3.5E-6
(Ng82e)
(R183, Ng82c)
(Ba84, Ng82a)
(R183, Ng82a)
(R183)
(Ng82a, Ng82c)
(R183, Mg82c)
(Ba84)
(Ng82a, Ng82c)
(Ba84, Ng82c)
(Mo79, Ba84)
(Mo79, Pe83)
(Mo79, Ba84) '
(Mo79, Ng82a)
(R183)
(Ng82c, Ng82a)
(Ba84, Ng82a)
(Ba84)
     *Va1ues used are default values given by  Baes,  et.  al  (Ba84)  except  for HI, Zr, Ra, Np, and Pu.  Values of Ff
     for these five elements were discussed with  C.F.  Baes,  III  (ORNL) and S.A. Schaffer (Envlrosphere) and the
     concensus was:
          N1, Zr, and Pu - use values given by Ng, et. al  (Ng82a);
          Ra - average the values given by Baes,  et. al  (Ba84) and Ng, et. al  (Ng82a);
          Np - values given by Baes, et.  al  (Ba84) and Ng, et. al  (Ng82a) are  based on an Injection study where gut
          uptake was not considered.  The value should be  Increased to account for gut uptake.
     **Notes Indicate references used to estimate range  of values.
     ***For several elements, values of Ff given  by  Ng,  et.  al (Ng82a, Ng82c)  Include data for chicken.  Ff for
     chicken Is generally substantially higher than  for  beef and pork.  The "values used" are more representative of
     beef values.  However, for several elements, the  upper  limit  of the  "estimated range of values" 1s for chicken.
     This Is the reason that the "value used"  1s  nearer  the  lower  limit for several elements (see U; for example).

-------
C.10  Determination of Values for the Parameters   YI, -^g,  SFjn and
           Used for the Ocean Release Mode
     In this section, we will  show the methodology  used  to determine
parameter values which are applied in the algorithms  for the  ocean release
mode.  These algorithms are discussed in Chapter 3, sections  3.2 and  3.4.4,

     The transfer rate coefficients used in the ocean model are -y^ and
Yg (see Figures 3-1 and 3-4).   That for movement of water from the lower
to the upper ocean compartment is -^ an(* tne value  of it used for this
analysis is 6.25 E-4 yr" (Ma73).  For movement of water from  the upper
to the lower ocean compartment, the transfer rate coefficient is Yl,  and
the  value applied for this analysis 1s 3.3 E-2 yr"  , which 1s derived
from the expression TI « Y2 (3925/75) where 3925 m is the assumed
depth of the ocean lower compartment and 75 m is the assumed depth of the
ocean upper compartment.
      The  relationship between Y^ and -^ 1s derived by assuming that
 interchange of water between the upper and lower layers of the ocean
 results 1n no net transfer  from one layer to the other, I.e., the mass of
 each  layer remains the  same.  If we further assume that the density of
 water In  the upper and  lower layer is equal close to the boundary between
 the layers, we can derive a value for YI using the value for Yg and
 using conservation of mass.*  The volume of water transport upward per
      *For equal  densities  close  to the  boundaries of the two ocean layers,
 conservation of  mass  will  also result in  conservation of volume.
                                    C-42

-------
year 1s equal to 
-------
     The Kn_ values that  we used are  more conservative than those 1n
INFCE78 to allow for expected competition for  adsorption  sites by the sea
water ions, especially Mg and Ca.   In the absence of  detailed experimental
work on sorption, anionic ions were assigned KDn values of zero; major
sea water ions were given KD  values  of 1;  and neptunium  was also given
a KD  of 1.  The effect of the sea water ions  on divalent ions and  on
cesium was approximated by reducing the desert soil KDn values given by
Arthur D. Little (L177c)  by a factor of 10.  Since  the monovalent and
divalent sea water cations would be expected  to have  a  smaller effect on
the adsorption of polyvalent cations, the Arthur D. Little KQn values
were reduced by a factor of 2 for trivalent ions and  unchanged for
tetravalent ions.  The values of KDn used in  this  report  are  listed in
Table C-ll.  Using these values and equations C-16  and  C-17,  the values
for SF,  and SF0« listed In Table 5-6 were  computed.
      in       in
                                    C-44

-------
TABLE C-li:
Distribution coefficients for radionuclides on  sediment
Element KQnCnvMI iliters/g)
C
Ni
Sr
Zr
Tc
Sn
I
Cs
Sm (Rare Earth)
Pb
Ra
AC
Th
Pa
U
Np
Pu
Am
Cm
0
40
2
2000
0
0
0
20
300
2000
10
500
15,000
2000
300
1
2000
1000
300
                                   C-45

-------

-------
  APPENDIX  D:   SAMPLE DERIVATION  OF  AN ENVIRONMENTAL PATHWAY EQUATION AND
                  CALCULATION OF  POPULATION FATAL CANCERS
     A derivation of an environmental  risk commitment equation and the
application of representative data in  the equation to compute population
health effects for an environmental  pathway will  serve to illustrate the
application of the methodology described in this  report.   The
environmental  pathway chosen for demonstration is ingestion of food crops
for radionuclide releases to a river (pathway number 3).   Terms that are
explained in the "Nomenclature" section are not defined again in this
Appendix.
     An expression for environmental risk commitment must be derived and
is the same as is described in section 3.1.4.  The starting point is the
annual risk commitment to an individual.
     The annual risk commitment is given by the concentration of
radionuclides in the river water (Q'nD/R)» the irrigation rate (W), a
conversion factor to .express the radionuclide intake by an individual per
unit deposition to the ground surface  (RInD), and the risk conversion
factor (FCF  ) as
     RIV
                      RInp FCFnP
         np
(D-l)
     The annual population risk commitment can be expressed as the
individual risk commitment multiplied by the number of persons being fed a
particular food crop raised on irrigated land.  The number of persons fed
can be determined using an estimate of the number of persons who can be
fed by raising the food crop on a unit area of land (CP ), the area of
                                    D-l

-------
land irrigated (A),  and a weighting  factor to express  the  fraction  of
irrigated land used  for a particular crop (f  ) as
      FP
               A f
               A f
                                                              (D-2)
Then the annual population risk commitment is
                          Q'   W RIM FCFnn CPn A f,
     FHEnp - RIV'np PFp
                            np
                                   np     np ' p    p
                                     R
                                                         (D-3)
By integrating this expression over time, we obtain an equation for
environmental risk commitment as
     FHE
             Qnp W RInp FCFnp CPp A fp
         np
                                                               (D-4)
     Some  rearrangement of terms is desirable in equation D-4 since it is
to  be  used for generic rather than site specific analyses.  We can write
the  relationship
     W A = f R R
which yields
     W   fR
     * = -R  .
If equation D-6 is substituted into equation D-4, we obtain
                                                               (D-5)
                                                               (D-6)
FHE
   np
                 fR fp
                            CPp FCFnp
      Implicit in equation  D-7  is  the  assumption that all river water used
 for irrigation contains  radlonuclides and, consequently, that all land
 irrigated by river water receives radlonuclides released from the waste
 repository.
                                    D-2

-------
     Our food pathway calculation will  be performed for Tc-99.   Parameter
values from Chapters 4 and 5 will be used in the sample calculation.

     A leaching-rate-limited.source-term equation will  be used  for this
Illustrative calculation.  Figure D-l shows the predicted travel of
radionuclides from the waste repository to the river.   An expression  for
the rate of entry of radionuclide n to the river can be developed after
examination of Figure D-l.  The inventory of material  at time,  ter, when
leaching begins Is
W'er' = Qon e
                                                               (D-8)
where
     Q   (ter) = inventory of radionuclide n in the repository at the
                 time leaching begins (C1) .
     At any time t, (t,xt  ) the rate of exit of radionuclide n from
the repository Is
     it }
  rnp(tlj
                  Ln
                                                               (D-9)
where
     Q'
        -.
       rnp
            rate of exit of radionuclide n from the repository at
            time t. (where t1 _> t  ) (Ci/yr) .
     Now, assuming that radioactive decay is the only mechanism of loss of
radionuclide n during travel from the repository to the aquifer
                                                                  ,^,
                                                                  ran
                                    D-3

-------
REPOSITORY;

Initial Inventory=Qon

Time between placement
of nuclides and initi-
ation of 1eaching=ter

t=o at time radioactive
material 1s placed 1n
repository
Travel time from
repository to
aquifer=tran
    * leaching coeff.
      from repository
AQUIFER

Travel time in
aquifer to
river = tarn
                     RIVER
       F1g.  D-l.   Radionucllde travel  from repository  to  river
                                 D-4

-------
and travel  from the aquifer to the river  (tarn)*  the  equation  for

release rate to the river at any time t is
                          -W'ran'tarn'
                                for  t  >  t    +  t     *  t
                                         er     ran    arn
and
             =0                for t £ ter +  t_  + t

The relationship between t and t,  is
or
                   an
         1 =      ran "  arn .
                                                                D-10)
(D-ll)

(D-12)
Substituting equations D-8 and D-9 into equation D-10 yields
     Q'n (t) - xLf| Oon
                                                               (D-13)
or
and substituting equation D-12 into D-14 gives
                                                               (D-14)
     n-  /tl   ,   n   /XDn(ter+trannarn)
     Q np(t) = xLnQone                     e
                                                               (D-15)
     *0ther removal mechanisms will be operative during groundwater
transport of radionuclides from the respository to a river.  However,
since our objective is to determine the fatal cancers per Ci released
to a river, this simplified transport model is acceptable for these
calculations.
                                    D-5

-------
or

                                                            (0-16)
     Now,  assuming that only  a  fraction, f, ,  of  the contents of the
repository are subject to leaching, we can write the final expression  for
the release rate of radlonuclide n to the river  as
                  fL Qon
and
     Q-  (t)  .  0
                                 for t > t  + t   +  t
                                         er   ran  arn
                           for t < t  +  t   + t
                                 —  er  ran   arn .
                                                           (D-17)
     To obtain the total (Integrated) amount of radionuclide n that has
 entered the river up to time t, we Integrate equation D-17  and get
Vtl-   /  Q1np(t">dt"
           0
 Using equation D-17  and the relationship
      Rn =  er    ran    arn
                                                             (D-18)
                                                       (D-19)
 we obtain
               °ww"   r  DnRn-eLnl
                                          for t > t
                                                  Rn .
 and
            = 0
                                    for t < t
                                                  Rn .
                                                            (D-20)
                                   D-6

-------
     To determine  the total release of Tc-99 we will  use the following
data:
     Q    = 1000  curies  of Tc-99
                       -1
                       -1
      fL   = 0.01

     xLn   " ^^ E"4 yr
     \Dn   = 3.27 E-6 yr
     ter   = 100 yrs  ,
      ran
     ;arn = 76°  Rn yrs' where Rn
          = 760  (1)  =  760 yrs.
                                 =  1  (Li77c), therefore
Now, from equation  C-23

     *Rn  - ler + Van  +  'arn
                                         76° - 861
Let the tine, t, for computation  of the health effects commitment be
t = 10,000 yrs.  Then, using equation  D-20 we have
and
              \n fl Qon  f ^Dn^   „  \n\n /'WW
              —i^	r—.     ie        -  e        e
                                      -  (3.27E-6)(861)
                                                          1
                                      [(1.00E-4)(861)-(3.27E-6+1.00E-4)(10,000)]
                                  - e
      Q(IO.OOO) =  (9.683) (0.997 - 0.388)
      Q(10,000) =  5.90 curies of Tc-99 released over 10,000 yrs.

      To compute a value for RI  , we have the following equation  (from
 Appendix C,  Equation C-4).
                                       D-7

-------
% = ""  I  DDI '^P11-6
                              *r_ t.
                       vp
     + u'
                 •  f    1 - e
                                              P
                                                                                 hL
The parameter values used in this equation are given 1n Appendix  C  (with

the references).  They are listed again here for completeness.
      IT  = 176 kg wet/yr

      f_ = 0.052
                                    DDI  = i.O
     'En
"1
                                               "1
                                                            '1
                + *w = 3.26 E-6 yr"  + 18.41 yr"   = 18.41 yr',  where
      x   = time constant for loss from vegatation due to weathering, yr"1
     'ep
      'ivl
teL = 0.274 yrs


q s  Ci/kg dry crop
    Ci/kg dry soil
                                    Yyp  . 1.6 kg wet/m'
          = 3.26 E-6 y
                      -1
                                    B     -  0  64  C1/kg  wet crop
                                    B1v2  '  °'M  Ci/kg  dry soil


                                    xsn = 0.49 yr'
                /kg dry

               -1
      hp
          = 1 E15 yrs*
            *hL = 3'83 E'
                                     P   .  215  kg  dry  soll/m1
     UL   = 1.2 kg dry/yr
     YyL  = 0*12 kg dry/m'
                                    fcL  =  0.15
     *The large value of
for RInp 1s computed.
                            is used to assure that an equilibrium value
                                   D-8

-------
     Using these  values,  the  value of RI   can be computed as
RI
  np
  176
(1M.052)
[l-e-18'41(-274>]  M.64)[l]
                     U.6M18.4T)
                   M2HT8.W
                                       215(3.26E-6 + .49)

                                       9.5E1]	
                                       215(3.26E-6 +
                                                                  -(3.26E-6M.0383
                                                                  -{3.26E-6)(.C383
     RI   = 176 [1.754  E-3  +  6.075  E-3] 1.0 + 1.2[6.746 E-2 + 9.018 E-2]1.0

     RI.1.57    Ci  intake	  ^    ^
       np         Ci/m   deposited
     The remaining parameter  values for use in equation D-7 to compute
environmental  dose commitment are
     fR = o.:*
                 f  =  0.5
                                              2*
                           CP   =  4.8  E-3 man/m  .
     FCFnp = 5.4E-1 fatal  cancers/CI  Intake  (Appendix B)
     The expression for computation of  environmental dose commitment Is
equation D-7, i.e.
FHE
   np
                 fR fp RInp CPP FCFnp
                                                   (D-7)
Substituting the parameter values discussed above  into  equation D-7 yields
     FHE   = (5.90)(0.1)(0.5)(1.57)(0.0048) (0.54)  =  1.19E-3  fatal cancers

     Thus, for 5.90 Ci of Tc-99 released to the  river,  the  number of fatal
cancers in 10,000 yrs to the affected population from consumption of food
crops irrigated by contaminated river water is estimated to be 0.00119.
     *See more detailed discussion in Appendix C.
                                    D-9

-------
The fatal  cancers per curie released to the accessible environment for
this sample calculation are 0.0012/5.90 « 2.02 E-4.   The fatal  cancers per
curie release to the accessible environment for the  other nuclldes and
pathways discussed 1n this report are determined in  a similar manner and
are presented in Chapter 6.
                                    D-10

-------
          APPENDIX E:  FORTRAN SOURCE LISTING OF PROGRAM WESPDOSE2:
             WESP POPULATION ENVIRONMENTAL RISK COMMITMENT CODE
  J.  M. SMITH
  EPA/EERF
  P.  0. BOX 3009
  MONTGOMERY,AL 36193
  INCLUDE COMMON FILE
INCLUDE 'DRO:WESPCOM2.FTN/LIST'

  BYTE DIMENSION FOR FILE
     BYTE FILE(30)

 'DIMENSION STATEMENT FOR  DUMMY  VARIABLES  FOR  PRINTING ALL PATHWAY
  HEALTH EFFECTS INFORMATION
     DIMENSION PRINTF(MAXP),PRINTG{MAXP)

  DATA WHICH RARELY OR NEVER CHANGES IS  CONTAINED  IN BLOCK DATA
  SUBPROGRAM.  READ IN OTHER DATA.

  PROMPT AND TERMINAL READ

   ' WRITE(5,900)
     READ(5,903)IPRINT,(XLABEL{J),J=1,30KLTH,FILE

  ASSIGN 30TH BYTE  IN FILE TO BE ZERO

     FILE(LTH+1)=0

  OPEN FILE AND READ MISC. INPUT DATA AND  CLOSE  FILE

     OPEN(UNIT=lfNAME=FILE,TYPE='OLD',SHARED,READONLY,ERR=2)

     READ(1,906)NN,NCARB,FRASUR,{WATER(P),POP(P),
    1USEFR(P),GENVAR(P),PD(P),SOF(P),P=1,MAXP)
     CLOSE(UNIT=1)

  OPEN ALL OUTPUT FILES

     OPEN(UNIT=1,NAME='DRO:POPDOSE.SUMI,TYPE=:INEW1}
     OPEN(UNIT=2,NAME='DRO:POPHEF.SUM1JYPE-'NEW1)
     OPEN(UNIT=3,NW^E='DRO:POPHEG.SUMI,TYPE=1NEW1)
     OPEN(UNIT^4,NAME='DRO:DILHEF.SUM',TYPE=INEW)
     OPEN(UNIT=6,NAME=IDRO:DILHEG.SUMI,TYPE=INEW)
     OPEN(UNIT=7,NAME='DRO:INOUT1.DATI,TYPE='NEWI)
     OPEN{UNI%8,NAME='DRO:INOUT2.DATIJYPE='NEWI)
     OPEN{UNIT=11,NAME=IDRO:EGANHEF.SUB',TYPE=INEW')
     OPEN(UNIT=12,NAME='DRO:EGANHEG.SUBIJYPE=1NEW')
     IF(IPRINT.EQ.2)OPEN(UNIT=9,NAME=IDRO:POPHE.SUBIJYPE='NEW')
  WRITE OUT APPROPRIATE INPUT DATA AND HEADINGS.
                                    E-l

-------
  MRITElT^OgjIPRINT.FILE.IW.IB.NN.MAXO.MAXP.MAXSUM.NWLBOD,
 INCARB.OVARIE.TESTES.FRASUR.CARCAN.CARGEN,-
 2(P,WATER(P),POP(P),USEFR(P),GENVAR(P),PD(P),
 3INTAKE(P).F(P),CP(P),FRCARB(P},SOF(PMP1(P),IP2(P),IP3(P),P,
 4IM.MAXP)
         .
  WR1TE(8,915)(JDUM,ODUM=1>MAXP2),(JDUM>JDUM=1IMAXP3)
  WRITE(1,918)((HEAD1(IDUM,0),IDUM=1,2),0=1,MAXO)
  WRITE(2,921)
  WRITE(2,927)((HEAD2(IDUM,PDUM),IDUM=1,2),PDUM=1,MAXSUM)
  WRITE(3,924)
  WRITE(3l927)((HEAD2(IDUMtPDUM),IDUMsl,2),PDUM=l,MAXSUM)
  WR!TE(4,928)(XLABEL(J),J=1,19)
  WRITE(6,928)(XLABEL(0),J=1,19)
  WRITE(11,970)
  WRITE(ll,928)(XLABEL(J),J«lf19)
  WRITE(12,975)
  WRITE(12,928)(XLABEL(J),J.1,19)
   IF(IPRINT.EQ.2)WRITE(9,930)

  OPEN(UNlT=10,NAME=lDRO:WESP2NUC.DAT',TYPE='OLDl,SHARED,READONLYf
  1ERR=2)
INITIATE  LOOP  TO  CYCLE  THROUGH  NUCLIDES
  DO 100 N-l.NN
   PDUM=1
   READ(10,940)(HEAD3(IDUM)>IDUM=1I2),DIALNU,(CF(J)>J=1,MAXP2),
  KRI(J),J»l1MAXP3)tVGiVW,WTRTREtGNDCOR,
  2((D(J,0)(0=lfMAXO),CHEFAC(J),GHEFAC{0),J=l,f-WXPl)

   WRITE(7,942)(HEAD3(IDUM),IDUM=1,2)(((HEAD4(IDUM)J),IDUM=1>2),
  1{D(J,0),0=1,MAXO),CHEFAC(J),GHEFAC(J),J=1,MAXP1)

   WRITE(8>944)(HEAD3(IDUM),IDUM=1,2),DIALNU,N,(CF{J),J=1,MAXP2),
  KRI(J),J=1(MAXP3),VG,VW,WTRTRE.GNDCOR

INITIATE LOOP TO CYCLE THROUGH PATHWAYS

   DO 70 P.l.MAXP

INITIATE LOOP TO CYCLE THROUGH ORGANS

   DO 50 0=1,MAXO

   DOS=DOSN(N,P,0)
   IF(O.EQ.OVARIE.OR.O.EQ.TESTES)DOS=DOS/2.
                                   E-2

-------
      DOSSUM(0)=DOSSUM(0)+DOS
50    CONTINUE
C    .
C  CALCULATE FATAL CANCER INFORMATION
C
      HEFN=HEF(N,P)
   .   HEFSUM(PDUM)*HEFSUM(PDUM)+HEFN
60

63
70
C
CALCULATE SERIOUS GENETIC EFFECTS INFORMATION

   HEGN=HEG(N,P)
   HEGSUM(PDUM)*HEGSUM(PDUM)+HEGN

   PRINTF(P)*HEFN
   PRINTG(P)=HEGN

   IF(IPRINT.EQ.2)WRITE(9,950)(HEAD3{IDUMKIDUM=1,2),P,
  1HEFN.HEGN

   IF(P.NE.5.AND.P.NE.8.AND.P.NE.10.AND.P.NE.12.AND.P.NE.15.AND.P
  1.NE.16.AND.P.NE.21.AND.P.NE.22.AND.P.NE.24.AND.P.NE.27.AND.P.NE.
  228.AND.P.NE.30)GO TO 63

   WRITE(1,953)(HEAD3('IDUM),IDUM=1>2),(HEAD2(IDUM,PDUM),IDUM=1,2),
  1(DOSSUM(0),Q=1,MAXO)
   DO 60 0*1,MAXO
   DOSSUM{0)=0.
   PDUM=PDUM+1
   CONTINUE
   CONTINUE

   WRITE(2,956){HEAD3(IDUM},IDUM=l,2),{HEFSUM(PDUM},PDUH=lfHAXSUM)
   WRITE{4,959)DIALNU,(HEFSUM(PDUM)>PDUM=i,MAXSUM)
   WRITE(3,956)(HEAD3(IDUM),IDUM=1,2),(HEGSUM(PDUM),PDUM=1,MAXSUM)
   WRITE(6,959)DIALNU,(HEGSUM(PDUM),PDUM=1,MAXSUM)
90
C
100
C
   WRITE{12,977)DIALNU,(PRINTG(P)>P=1,MAXP)
   WRITE(1,963)
   IF(IPRINT.EQ,2)WRITE(9,963)

   DO 90 PDUM=1,MAXSUM
   HEFSUM(PDUM)=0.
   HEGSUH(PDUM)=0.

   CONTINUE
                                      E-3

-------
900
903
906
909
912
915
918
921

924
927
 928
      FORMATr   HEY: HEY: HEY:  LET us GET STARTED: :VIH ,
     TON  FIRST  LINE TYPE  IN  IPRINT AND THE LA&EL',
     2'  TO BE PUT ON EGANS FILES.'/1H  'ON SECOND LINE',
     3'  TYPE  IN  INPUT DATA FILE NAME.')
      FORMAT(I3,30A4/Q,30A1)
      FORMAT(I3,2X,I3,2X,E10.3/(6E10.3))
      FORMAT(36X,'WESP  ENVIRONMENTAL DOSE COMMITMENT ESTIMATES'///
     155X,'INPUT DATAV//2X,'CALCULATION OPTIONtIPRINT) = ',I2.7X,'GENE',
     2'RAL INPUT DATA FILE NAME IS  '.30A1//2X,'IW=',
     31PE10.3,1  L/Y      IB-MPE10.3,1 M**3/Y     NN=',I3,4X,'MAXO*1,
     4I3,3X,'MAXP='.I3,3X,'MAXSUM=',I3//2X/NWLBOD=',I3,5X,'NCARB=',
     4I3,5X,'OVARIE=',I3I5XJ'TESTES=',I3,5X,'FRASUR=t,lPE10.3/
     42X,'CARCAfJ=',lPE10.3,t  FATAL CANCERS/T.B. MAN-REM',5X,
     4'CARGEN=',1PE10.3/  SERIOUS GENETIC EFFECTS/T.B. MAN-REM'///
     552X,'PATHWAY DEPENDENT  INPUT DATA'//2X,'P WATER(P)    POP(P)',
     63X,  'USEFR(P) GENVAR(P)    PD(P)    INTAKE(P)    F(P)      CP(P)',
     73X,'FRCARB(P)   SOF(P)    IP1   IP2   IPS    P1/
     776X,'PERSONS'/4X,'L/Y  OR L',4X,
      '                   MAN/M**2    KG/Y',14X,'FED/M**2'/(X>I2,
      FORIlAT(52Xf'NUCLIDE DEPENDENT INPUT DATAV/41X, 'DOSE EQUIVALENT
     1' FACTORS AND RISK CONVERSION FACTORS ' //4X, ' (DOSE UNITS: INHAL.
     2' AND  INGEST. =REM/CI  INTAKE, AIR SUBMER.=REM PER CI-Y/M**3  ',
     3'GROUND CONTAM.=REM PER CI-Y/M**2) '/4X, ' (RISK UNITS: INHAL. AND
     4' INGEST. =EFFECTS/CI  INTAKE, AIR SUBMER.=EFFECTS PER CI-Y/M**3,
     5' GROUND CONTAM. ^EFFECTS PER CI-Y/M**2) V/124X, 'SERIOUS'/
     6115X, 'FATAL   GENETICV2X, 'NUCLIDE   PATHWAY *****' ,38X, 'ORGAN1
     739X, ******    CANCER  EFFECTSl/20X,A5,A4,2A5,5(A5,A4) ,2A5,
     82(A5,A4) ,5X, 'RISK     RISKV116X, 'FACTOR   FACTOR' )
      FORMAT(//27X,'**********CF(N,IP2)**********  *********RI(N,IP3)
     1'**********'/34Xi'CI/KG PER CI/L        CI INTAKE  PER CI/M**2',
     21 DEPOSITED   VG(N)    VW(N)   WTRTRE(N) GNDCOR(N)1/
     329X,IIP2=I,I2,4X,'IP2=',I2,4X,
     3'IP2=l,I2,4X(IIP3=l,I2,4X,lIP3=1,I2,4X,IIP3=',I2,6XflM/Y',6X,
     4'M/Y'/2X,INUCLIDE  DIALNU(N)  N1//}
      FORMAT (/26X,1 SMITH FACTORS FOR POPULATION  DOSE AS  A FUNCTION OF
     1' NUCLIDE AND ORGAN'//14X, 'SUB1 ,46X, 'ORGANV2X, 'NUCLIDE1 ,2X,
     2'PATHWAYS'/12X, 'SUMMED', (X,2A5),3X,2(X,2A5)/)
      FORMAT(/33X,' SMITH FACTORS FOR POPULATION  FATAL  CANCERS1,
     1' AS A FUNCTION OF NUCLIDE1/)
      FORMATC22X,1 SMITH FACTORS  FOR POPULATION GENETIC EFFECTS TO ',
     1'FIRST GENERATION AS  A  FUNCTION  OF NUCLIDE'/)
      FORMAT(/2X, 'NUCLIDE   ********************',
     1 ' *********************************SUBPATHWAYS  SUMMED********** '
     2 ' *************************************** ' /9X ,  ( 4X , 2A3 ) )
       FORMATUH  ,30A4)
                                       E-4

-------
930   FORMATU7X, 'SMITH FACTORS FOR POPULATION HEALTH EFFECTS AS A1,
     I1 FUNCTION OF NUCLIDE AND SUBPATHWAY'//13X,'SUB1,23X,
     2'SERIOUS'/2X,1NUCLIDE  PATHWAY  FATAL',
     3' CANCERS  GENETIC EFFECTS1//)
940   FORMAT(A4,A3,2X,F8.3,3X,(E10.3)/
     1(E10.3-))
942   FORMAT(/2X,A4,A3f2X,2A4fX,lPE9.2,lPE10.2,lP5E9.2,lPE10.2,
     11P2E9.2,2X,1P2E9.2/(11X,2A4,X,1PE9.2J1PE10.2,1P5E9.2,1PE10.2>
     21P2E9.2.2X.1P2E9.2))
944   FORMAT(2X,A4,A3,3X,F8.3,2X,I2,2X>(1PE10.3))
950   FORMAT(2X,A4,A3,4X,I3,2(6X,1PE10.3))
953   FORMAT{2X,A4,A3,2X,2A3,X,(X,1PE10.3),3X,2(X,1PE-10.3))
956   FORMAT(2X,A4,A3,2X,(1PE10.3))
959   FORMATUH .F8.3.1P6E10.3/1H ,1P6E10.3)
963   FORMAT(/)
970   FORMAT(IX,'FATAL CANCER SMITH FACTORS FOR EACH PATHWAY1)
975   FORMAT(1X,'GENETIC EFFECTS-ALL GENERATIONS SMITH FACTORS',
     1' FOR EACH PATHWAY')
977   FORMATdH ,F8.3,1P6E10.3/(1H .1P6E10.3))
      CLOSE(UNIT=1,DISP=ISAVE1)
      CLOSE(UNIT=2,DISP='SAVE')
      CLOSE(UNIT=3,DISP='SAVE')
      CLOSE(UNIT=4,DISP='SAVEI)
      CLOSE(UNIT=6,DISP='SAVEl)
      CLOSE(UNIT=7,DISP='SAVE')
      CLOSE(UNIT=8,DISP='SAVE')
      IF (IPRINT.EQ.2)CLOSE(UNIT=9,DISP='SAVE')
      CLOSEtUNIT^lO.DISPx'SAVE1)
      CLOSE(UNIT=11,DISP='SAVE')
      CLOSE(UNIT=12,DISP='SAVE')
      STOP
      END
C
      BLOCK DATA
C  THIS SUBPROGRAM CONTAINS ALL DATA STATEMENTS
C
C  INCLUDE COMMON FILE
 INCLUDE 'DRO:WESPCOM2.FTN/NOLIST'
C
C  DATA STATEMENTS
      DATA HEAD1/1   BO' ,'NE1, 'RED M','ARROW','   LU'.'NG1,'   LIVVER1,
     1'  GI^/LLI1,1  THY'.'ROIDV  KID1,'NEY','OTHER1,'ORGAN1,
     2' OVAR'.'IES1,'  TES'/TES'/
      DATA HEAD2/1  I'.'-S1,1   6','-8','  9-l,'IO',' 11','-12','  13',
     l'-15','   I'.'e1,1 l?1,1^!',1  2','21,' 23','-241/  25','-27',

      DATA HEAD4/' INH'/ALl1,1 INH1,'AL21,' INGE','ST1', UNGE1,'ST2',
     1'EXT ','AIR','EXT ','GND'/
                                      E-5

-------
      DATA DOSSUM/MAXO*0./
      DATA HEFSUM/MAXSUM*0./
      DATA HEGSUM/MAXSUM*0./
      DATA IPl/4,4.4,4,4,2,6,5,4,4,5,2,4,4,4,6,1,5,3,3,3,6,5,1,3,3,3,
     16,3,37
      DATA IP2/0,1,0,0,0,0,0,0,2,3,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,
     10,2,3/
      DATA IP3/0,0,1,2,3,0,0,0,0,0,0,0,1,2,3,0,0,0,1,2,3,0,0,0,1,2,3,
     10,0,0/
      DATA FRCARB/0.,0.,1.,0.,0.,0.,0.,0.,1.,0.,0.,0.,1.,0.,0.,0.,
     10.,0.,1.,0.,0.,0.,0.,0.,1.,0.,0.,0.,1.,0./
      DATA NWLBOD,OVARIE,TESTES/8,9,10/
      DATA IW,IB/603.,8401./
      DATA F/0.,0.,.50,.25,.25,0.,0.,0.,0.,0.,0.,0.,.23,.11,.11,0.,0.,
     10,,.23,.11,.-11,0.,0.,0.,.23,,11,.11,0.,0.,0./
      DATA CP/0.,0.,.00479,.00156,.0000785,0.,0.,0.,0.,0.,0.,0.,.00479,
     1.00156,.0000785,0.,0.,0...00479,.00156,.0000785,0.,0.,0.,.00479,
     2.00156,.0000785,O.,0.,0./
      DATA INTAKE/0.,1.,0.,0.,0.,0.,0.,0.,6.,1.,0.,0.,0.,0.,0.,0.,0.,
     10.,0.,0.,0.,0.,0.,0.,0.,0.,0.,0.,6.,1./
      DATA CARCAN,CARGEN/1.46E-04,7.60E-05/

      END

      FUNCTION DOSN(N,P,0)
C  THIS FUNCTION SUBPROGRAM SELECTS THE PROPER FUNCTION FOR CALCULATING
C  DOSE MULTIPLIER FOR SUBPATHWAY P AND COMPUTES THE DOSE
C  QUANTITY.
C
C  INCLUDE COMMON FILE
 INCLUDE  'DRO:WESPCOM2.FTN/NOLIST'
      IF(N.EQ.NCARB)GO TO 9
      GO TO (1,2,3,3,3,4,5,6,2,2,6,4,3,3,3,5,4,6,7,7,7,5,6,4,3,
     13,3,5,8,8}P
30

C
      DOSN=DOSNA(P)*D(IP1{P),0)
      GO TO 40
2     DOSN=DOSNB(P)*D{IP1(P),0)
      GO TO 40
3     DOSN=DOSNC(P)*D(IP1(P),0)
      GO TO 40
4     DOSN=DOSND(P)*D(IP1(P),0)
      GO TO 40
5     DOSN=DOSNE(P)*D(IP1(P),0)
      GO TO 40
6     DOSN=DOSNF(P)*D(IP1(P),0)
      GO TO 40
7     DOSN=DOSNG(P)*D(IP1(P),0)
                                      E-6

-------
8

9
40

C
C

C
C
C
C
C
C
      GO TO 40
      DOSN=DOSNH{P)*D(IP1(P),0)
      GO TO 40
      DOSN=DOSNI(P,0)
      RETURN
      END
   *************************

      FUNCTION HEF(N.P)

   THIS FUNCTION SUBPROGRAM SELECTS THE PROPER FUNCTION FOR CALCULATING
   FATAL CANCER HEALTH EFFECTS MULTIPLIER FOR SUBPATHWAY P AND
   COMPUTES THE FATAL  CANCERS QUANTITY FOR EGAN'S CODE.
   INCLUDE COMMON FILE
 INCLUDE 'DROiWESPCOMZ.FTN/NOLIST1
      IF(N.EQ.NCARB)GO TO 9
30    GO TO (1,2,3,3,3,4,5,6,2,2,6,4,3,3,3,5,4,6,7,7,7,5,6,4,3,
     13,3,5,8,8)P
35
C
40
      HEF=DOSNA(P)*CHEFAC(IP1(P))
      GO TO 40
      HEF=DOSNB(P)*CHEFAC(IP1(P))
      GO TO 40
      HEF=DOSNC(P)*CHEFAC(IP1(P))
      GO TO 40
      HEF=DOSND(P)*CHEFAC(IP1(P})
      GO TO 40
      HEF=DOSNE(P)*CHEFAC(IP1(P))
      GO TO 40
      HEF=DOSNF(P)*CHEFAC(IP1(P))
      GO TO 40
      HEF=DOSNG(P)*CHEFAC(IP1(P))
      GO TO 40
      HEF=DOSNH(P)*CHEFAC(IP1(P))
      GO TO 40
   EQUATION 9 HANDLES FATAL CANCER RISK CALCULATIONS FOR C-14 FOR
   PATHWAYS 1 THROUGH 30.

      CONTINUE
      IF(P.NE.3.AND.P.NE.9.AND.P.NE.13.AND.P.NE.19.
     1AND.P.NE.25.AND.P.NE.29)GO TO 35
      HEF=CARCAN
      GO TO 40
      HEF=0.

      RETURN
      END
                                      E-7

-------
      FUNCTION HEG(N,P)
C                                             -       '
C  THIS FUNCTION SUBPROGRAM SELECTS THE PROPER FUNCTION FOR CALCULATING
C  SERIOUS GENETIC EFFECTS TO ALL GENERATIONS MULTIPLIER FOR
C  SUBPATHWAY P AND COMPUTES THE SERIOUS GENETIC EFFECTS QUANTITY
C  FOR EGAN'S CODE.
C
C  INCLUDE COMMON FILE
 INCLUDE  'DRO:WESPCOM2.FTN/NOLISr
      IF(N.EQ.NCARB)GO TO 9
30    GO. TO {1,2,3,3,3,4,5,6,2,2,6,4,3,3,3,5,4,6,7,7,7,5,6,4,3,
   '  13,3,5,8,8)P
C
1     HEG=DOSNA(P)*GHEFAC{IP1(P))
      GO TO 40
2     HEG=DOSNB(P)*GHEFAC(IP1(P)}
      GO TO 40
3     HEG=DOSNC(P)*GHEFAC(IP1(P))
      GO TO 40
4     HEG=DOSND(P)*GHEFAC(IP1(P))
      GO TO 40
5     HEG=DOSNE(P)*GHEFAC(IP1(P)}
      GO TO 40
6     HEG=DOSNF(P)*GHEFAC{IP1(P))
      GO TO 40
7     HEG=DOSNG(P)*GHEFAC(IP1(P))
      GO  TO 40
8     HEG=DOSNH(P)*GHEFAC(IP1{P))
      GO  TO 40
C  EQUATION 9 HANDLES  SERIOUS  GENETIC  RISK  CALCULATIONS FOR C-14 FOR
C  .P=l  THROUGH  30.
C
9     CONTINUE
      IF(P.NE.3.AND.P.NE.9.AND.P.NE.13.AND.P.NE.19.
      1AND.P.NE.25.AND.P.NE.29)GO TO  35
      HEG=CARGEN
      GO  TO 40
      HEG=0.

      RETURN
      END
   *************************

      FUNCTION  DOSNA(P)
    DRINKING  WATER SUBPATHWAY.   P=l

    INCLUDE COMMON FILE
  INCLUDE  IDRO:WESPCOM2.FTN/NOLIST1
35
C
40

C
C

C
C
C
                                       E-8

-------
      DOSNA=POP(P)*IW*WTRTRE*FRASUR/WATER(P)

      RETURN
      END
   ********************
      FUNCTION DOSNB(P)
C  FISH AND SHELLFISH INGESTIOM.   P=2>9,10
C
C  INCLUDE COMMON FILE
 INCLUDE 'DRO:WESPCOM2.FTN/NOLI$r
C
      DOSNB=CF(IP2(P))*POP(P)*INTAKE(P)/WATER(P)
C .
      RETURN
      END
Q  ********************
C
      FUNCTION DOSNC(P)
C  ABOVE SURFACE CROPS, MILK, BEEF INGESTION.  P=3, 4, 5, 13, 14, 15, 25, 26, 27
C
C
  INCLUDE COMMON FILE
INCLUDE 1DRO:WESPCOM2.FTN/NOLIST1

     DOSNC=USEFR(P)*F(P)*RI(IP3(P))*CP(P)

     RETURN
     END
  ********************
      FUNCTION DOSND(P)
C  INHALATION OF RESUSPENDED MATERIAL.  P=6,12,17,24
C
C  INCLUDE COMMON FILE
 INCLUDE  'DRO:WESPCOM2.FTN/NOLIST'
C
      DOSND=GENVAR(P)*PD(P)*IB*USEFR(P)
C
      RETURN
      END
£  ********************
C
      FUNCTION DOSNE(P)
C  EXTERNAL DOSE—GROUND CONTAMINATION.  P=7,16,22,28
C
C  INCLUDE COMMON FILE
 INCLUDE  'DRO:WESPCOM2.FTN/NOLIST'
                                      E-9

-------
      DOSNE=US£FR(P)*PD(P)*GNDCOR*SOF(P)
      RETURN
      END
Q  ********************
c
      FUNCTION DOSNF(P)
C  EXTERNAL DOSE-AIR SUBMERSION.  P=8,ll, 18,23
C
C

c

c
  INCLUDE COMMON FILE
INCLUDE 'DRO:WESPCOM2.FTN/NOLIST'

     DOSNF=GENVAR(P)*PD(P)*USEFR{P)*SOF(P)
      RETURN
      END
Q  ********************

C
      FUNCTION DOSNG(P)
C  ABOVE SURFACE CROPS,MILK,BEEF  INGESTION.  P=19,20,21
    INCLUDE COMMON FILE
  INCLUDE  'DRO:WESPCOM2.FTN/NOLIST'

       DOSNG=VG*RI(IP3(P))*F(P)*CP(P)*GENVAR(P)

       RETURN
       END
    ********************
       FUNCTION DOSNH(P).
 C  OCEAN FISH AND SHELLFISH INGESTION.   P=29,30
    INCLUDE COMMON FILE
  INCLUDE 'DRO:WESPCOM2.FTN/NOLIST'

       DOSNH=CF(IP2(P))*INTAKE(P)*POP(P)*VW*
      1GENVAR(P)/WATER(P)

       RETURN
       END
    ********************
       FUNCTION DOSNI(P,0)
 C  HANDLES ALL DOSE CALCULATIONS FOR C-14.
    INCLUDE COMMON FILE
  INCLUDE 'DRO:WESPCOM2.FTN/NOLIST'
                                       E-10

-------
20
40
965
C
60
   IF(D(IP1(P),NWLBOD).EQ.O..AND.D(IP1(P),0).NE.O.)GO TO 20
   IF(D(IP1{P),NWLBOD).EQ.O..AND.D(IP1(P),OKEQ.O,)GO TO 40
   DOSNI=FRCARB(P)*D{IP1(P),0)/D(IP1(P),NWLBOD)
   GO TO 60
   WRITE(7,965)
   DOSNI=0.
   FORMAT(/2X,'YOU IDIOT—YOU HAVE SET WHOLE BODY DOSE1,
  1'  FACTOR FOR  CARBON TO ZERO WITHOUT SETTING'/2X,'OTHER ',
  2'  DOSF. FACTORS TO ZERO'/)

   RETURN
   END
********************
INFORMATION COMMON TO MAIN CODE AND ALL SUBPROGRAMS
C
C
C  SET VALUES FOR PARAMETERS
C
      PARAMETER MAXP=30>MAXN=19,MAXO=10,MAXSUM=12,MAXP1=6,MAXP2=3,
     1MAXP3=3
   DEFINE REAL AND INTEGER VARIABLES AND THEIR LENGTHS

      INTEGER*2 PtO,PDUM,OVARIE,TESTES
      REAL*4 IW.INTAKE.IB
      REAL*8 HEAD1

   COMMON STATEMENTS

      COMMON/BLK1/HEAD1{2,MAXO),HEAD2(2,MAXSUM),HEAD3(2),HEAD4(2,MAXP1),
     1DIALNU,NN,NWLBOD,NCARB,IPRINT,OVARIE,TESTES,XLABEL(30)

      COMMON/BLK2/D(MAXP1>MAXO)IRI(MAXP3),CF(MAXP2),WATER(MAXP),
     1POP(MAXP),USEFR(MAXP),GENVAR(MAXP),PD(MAXP),INTAKE(MAXP),
     2F{MAXP),CP(MAXP)>FRCARB{MAXP),DOSSUM(MAXO),HEFSUM(MAXSUM),
     3HEGSUM(MAXSUM),IPl{MAXP)fIP2(MAXP),IP3(MAXP),
     4VG,VW,SOF(MAXP),IW,IB,CARCAN,CARGEN,CHEFAC(MAXP1),GHEFAC{MAXP15,
     SWTRTRE^FRASUR.GNDCOR
                                     E-ll

-------
NOTES PERTINENT TO APPENDICES F, G, AND H.
     The Information contained 1n Appendices F,  G,  and H 1s adapted from
Chapters 7 and 8 and Addendums A and B of the EPA report entitled
"Radionuclides: Background Information Document, for Final Rules",
Volume 1 (EPA84b).  These appendices contain their own list of references
and definition of symbols and do not utilize, the "REFERENCES" and
"NOMENCLATURE" sections, of the main report.

      In our high-level waste environmental pathway calculations, we have
used  the RADRISK data to convert from  radionuclide intake for the
inhalation and ingestion pathways  and  from external exposure for the air
submersion and ground surface pathways directly to fatal cancer  risk,
without calculating dose commitments or  dose rates.  The methodology
applied to compute  our fatal cancer risk factors is described in
Section 4.1 of Chapter 4.  Since the RADRISK computer code  utilizes
computed  dose rates in calculating fatal cancer risks, we  have  included
Appendix  F, which  describes  the radiation  dosimetry techniques  applied  by
 EPA in these  RADRISK  calculations.

-------
                     APPENDIX F:   RADIATION  DOSIMETRY
F.I  Introduction
     Radlonuclides transported through  the  environment  may  eventually
reach people.  This contact occurs  through  either  external  exposure to
radioactive air,  water,  and ground  surfaces or  internal  exposure  from
inhaling or ingesting radioactive air,  water, or food.   Individuals in the
population may absorb energy emitted by the decaying  radionuclides.
The quantification of this absorbed energy  is termed  dosimetry.   This
appendix describes the dosimetric models for Internal and external
exposures, the EPA procedure for implementing the  dosimetric  equations
associated with the models, and the uncertainties  in  dosimetric
calculations.

     Mathematical models are used to calculate  doses  to specific  human
body organs.  The models account for the amount of radionuclides  entering
the body, the movement of radionuclides through the body, and the energy
deposited in organs or tissues resulting from irradiation by  the
radionuclides that reach the tissue.  These models provide  the basis for
the computer codes, RADRISK and DARTAB, which EPA  uses  to calculate doses
and dose rates.  (See Appendix H.)  .

     Uncertainties in dosimetric calculations arise from assumptions of
uniform distribution of activity in external sources  and source organs and
assumptions concerning the movement of the radionuclides 1n the body.   The
uncertainties associated with dosimetric calculations are difficult to
quantify because the data available for determining distribution  for the
parameters used in the models are usually insufficient.  The  major source
of uncertainty in dosimetry is the  real variation  in  parameter values
among individuals in the general population while  doses and dose  rates are
calculated for a "typical" member of the general  population.   The three
sources of dosimetric uncertainty assessed by  EPA are:   individual
variation, age, and measurement errors.  The effects  of uncertainty are
discussed in greater detail in Section F.6 of  this appendix and in
Chapter 7.

F.2  Definitions

F.2.1  Activity

     Radioactive decay is a process whereby the nucleus of  an atom emits
excess energy.  The emission of this energy is  referred to  as radioactivity.
The "activity" of a radioactive material is characterized by the number of
atoms that emit energy, or disintegrate, in a given period  of time.  The
unit of activity used in this report is the picocurie (pCi),  which equals
2.22 disintegrations per minute.  The excess energy is normally emitted as
charged particles moving at high velocities and photons.  Although there are
many types of emitted radiations, or particles, only  three  are commonly
encountered  in radioactive material found  in the general environment:   alpha
radiation  (nuclei of helium atoms), beta radiation (electrons), and gamma
radiation  (photons).
                                     F-l

-------
     The primary mechanism for radiation  damage  1s  the  transfer  of
kinetic energy from the moving alpha and  beta  particles and  photons  to
living tissue.  This transfer leads to the rupture  of cellular
constituents resulting 1n electrically charged fragments (ionlzatlon).
Although the amount of energy transferred is  small  in absolute terms,  it
Is enough to disrupt the molecular structure  of  living  tissue, and,
depending on the amount and location of the energy  release,  leads to the
risk of radiation damage.

F.2.2  Exposure and Dose

     The term "exposure" denotes physical contact with  the radioactive
material.  The term "dose" refers to the amount  of  energy absorbed per
gram of absorbing tissue as a result of the exposure.   An exposure,  for
example, may be acute, I.e., occur over a.short  period  of time,  while the
dose, for some internally deposited materials, may  extend over a long
period of time.

     The dose is a measure of the amount of energy  deposited by  the alpha
and beta particles or photons and their secondary radiations 1n  the
organ.  The only units of dose used in this chapter are the rad--defined
as 100 erg  (energy units) per gram  (mass unit)--and the millirad (mrad),
which Is one one-thousandth of a rad.  The rad represents the amount, on
average, of potentially  disruptive energy transferred by ionizing
radiation to each gram of tissue.  Because 1t is necessary to know the
yearly variation In dose for the calculations described in this  report,
the quantity used will be the average annual  dose (or dose rate) 1n rad
or millirad (per year).

F.2.3  External and Internal Exposures

     Radiation doses may be caused  by either external  or internal
exposures.  External exposures are  those caused by radioactive materials
located outside the bocty, such as Irradiation of the body by  radioactive
material lying on the ground or suspended  In the air.   Internal  exposures
are caused  by radioactive material  that  has entered the bocjy  through the
Inhalation  or consumption of radioactive material.  Having once entered
the body, the contaminant may be transmitted to other  Internal organs and
tissues.

     The external exposures considered In  this  report  are those resulting
from irradiation of the  bocjy by gamma rays only.  Gamma rays  (high  energy
photons) are the most penetrating of  those radiations  considered and
external gammas may normally contribute  to the  radiation dose affecting
all organs  1n the bocjy.  Beta particles  (electrons), which are far  less
penetrating,  normally deliver their dose to,  or slightly below, the
unshielded  surface of the skin and  are not considered  because their
Impact  is small, particularly on clothed individuals.   Alpha  particles
(helium  nuclei), which are  of major Importance  internally, will  not
penetrate unbroken  skin  and so are  also  excluded from  the external  dose
calculations.   The  Internal  exposures considered in this  report  originate
from all three  types  of  radiation.
                                    F-2

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F.2.4  Dose Equivalent

     Different types of charged particles differ in  the  rate  at  which
their energy is transferred per unit of length traveled  in  tissue,  a
parameter called the linear energy transfer (LET)  of the particle.  Beta
particles generally have a much lower LET than alpha particles.   Alpha
particles are more damaging biologically, per rad, than  gamma rays  and
beta particles.  In radiation protection, this difference is  accounted
for by multiplying the  absorbed dose by a modifying  factor, Q, the
quality factor, to obtain a dose equivalent.  The  quality factor is
intended to correct for the difference in LET of the various  particles.
At present, the International Commission on Radiological Protection
(ICRP77) recommends the values Q=l for gamma rays  and beta  particles  and
Q=20 for alpha particles.  The units for the dose  equivalent, corre-
sponding to the rad and millirad, are rem and millirem.   Thus, dose
equivalents for gamma rays and beta particles are  numerically equal to
the dose since the dose equivalent (mrem) = (Q=l)  x  dose (mrad)  while
alpha dose equivalents  are twenty times as large,  dose equivalent (mrem)
= (Q=20) x dose (mrad).

F.3  Dosimetric Models

     The radiation dose has been defined, in Section F.2.2, as the  amount
of energy absorbed per  unit mass of tissue.  Calculation of the  dose
requires the use of mathematical models such as that shown  later in
Equation (F-2).  In this equation, the amount of activity ingested, I, is
multiplied by the fraction, fj, going to the blood,  and the fraction,
f*2» going to a specific tissue.  E is the amount of energy absorbed  by
the tissue for each unit of activity so that the product of all  these
factors divided by the  mass of the tissue is, by definition,  the
radiation dose per unit activity.  The remaining term, [l-e"^]/x,
indicates how the activity deposited in the tissue changes  with  time.
All these factors together yield the dose rate.  A more comprehensive
description of the equations used is given in Appendix H.

F.3.1   Internal Doses

     Any effort at calculating dose and risk must, of necessity, involve
the use of models.  In its simplest form, a model  is a mathematical
representation of a physical or biological system.  If, for example,  the
amount of radioactive material in an organ is measured periodically,
a graph of the activity in the organ, such as that in Figure F-l, is
obtained.  In the simplest case, analysis of these data may indicate that
the fraction of the initial activity, R, retained in the organ at any
time, t, is given by an equation of the form
                              R = e-
(F-l)
                                   F-3

-------
o;
o
o
•a:
                                   TIME
  Figure F-l.  Typical pattern of decline of activity of a
               radionuclide in an organ, assuming an initial activity

               1n the organ and no additional uptake of radionuclide

               by the organ (ORNL81)
                                  F-4

-------
where x 1s the elimination rate constant.   (More  generally,  It  may
require the sum of two or more exponential  functions  to  properly
approximate the decrease of radioactivity  in  the  organ.   This may be
interpreted physically as indicating the existence  of two or more
"compartments" in the organ from which the  radionuclide  leaves  at
different rates.)

     The elimination rate constant,  x, is  the sum of  two terms, which may
be measured experimentally, one proportional  to the biological  clearance
half-life and the other proportional to the radioactive  half-life.  The
effective half-life, twg, for these processes is the time required for
one-half of the material originally  present to be removed by biological
clearance and radioactive decay.

     If radionuclides are generally  found  to follow this behavior,  then
this equation may be used as a general model  for  the  activity  in  an organ
following deposition of any initial  activity.  In general, the  models
used by EPA are those recommended by the  International Commission on
Radiological Protection (ICRP79) and are  documented in detail  in  the
cited reference.  A brief description of  each model is given below  as an
aid to understanding the material presented in the  balance of  this
chapter.

     As mentioned earlier, all radiations—gamma, beta,  and alpha—are
considered in assessing the doses resulting from  internal exposure, that
is, exposure resulting from the inhalation or ingestion of contaminated
material.  Portions of the material  inhaled or ingested may not leave the
body for a considerable period of time (up to decades);  therefore,  dose
rates are calculated over a corresponding time interval.

     The calculation of internal doses requires the use of several
models.  The most important are the ICRP lung model,  depicted in
Figure F-2, and the gastrointestinal  (GI) tract model shown in Figure
F-3.  The lung model is comprised of three regions, the nasopharyngial
(N-P), the tracheobronchial (T-B),  and the pulmonary   (P) regions.  A
certain portion of the  radioactive material inhaled is deposited in each
of the three lung regions  (N-P, T-B, and P) indicated 1n Figure F-2.   The
material is then cleared  (removed)  from the lung to the blood and
gastrointestinal tract, as indicated  by the arrows, according to the
specified clearance parameters  for  the clearance class of the inhaled
material.

     Deposition and clearance of inhaled materials in the lung are
controlled  by the particle size and clearance class of the material.
The particle size distribution  of the airborne material is specified by
giving its  Activity Median Aerodynamic Diameter  (AMAD) in microns  (one
micron equals 10"" meters).  Where  no AMAD is known,  a value of 1.0
micron is assumed.  Clearance classes are  stated in terms of the time
required for the material  to leave  the lung, that  is, Class D  (days),
Class W  (weeks), and Class Y  (years).
                                   F-5

-------
Compartment
N-P
(D3 = 0
T-B
(D4 = 0

P
(D5 = 0

L

.30)

.08)


.25)


a
b
c
d
e
f
9
h
1
Class
D
T
0.01
0.01
0.01
0.2
0.5
n.a.
n.a.
0.5
0.5
F
0.5
0.5
0.95
0.05
0.8
n.a.
n.a.
0.2
1.0
W
T
0.01
0.4
0.01
0.2
50
1.0
50
50
50
F
0.1
0.9
0.5
0.5
0.15
0.4
0.4
0.05
1.0
Y
T
0.01
0.4
0.01
0.2
500
1.0
500
500
1000
F
0.01
0.99
0.01
0.99
0.05
0.4
0.4
0.15
0.9
cr»



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                           Figure F-2.  The ICRP Task Group lung model for particulates

             The columns labeled D, W, and Y correspond, respectively, to rapid, intermediate, and slow
        clearance of the inspired material (in days, weeks, or years).  The symbols T and F denote the
        biological half-time (d^ys) and coefficient, respectively, of a term in the appropriate retention
        function.  The values shown for 03, 04, and 05 correspond to activity median aerodynamic
        diameter AMAD = 1 Mm and represent the fraction of the inspired material depositing in the lung
        regions.

-------
                                    INGESTION
     RESPIRATORY

        TRACT
                           xab
                           ASI
                                              Xs = 24 day'
SI
                            ab
                                                  = 6 day'
                                        ULI
                            ab
                            Ul
                                              XULI = 1>85 day
                                                             -1
                                        LLI
                                               LLI
                                                       day'
Figure F-3.  Schematic representation of radionuclide  movement among
             respiratory tract, gastrointestinal  tract, and blood

               S      = stomach
               SI     = small  Intestine
               ULI    = upper large intestine
               LLI    m lower large Intestine
               x      = elimination rate constant
                              F-7

-------
     The gastrointestinal  tract model  consists ^of  four compartments,  the
stomach (S), small  Intestine (SI),  upper  large "Intestine (ULI),  and lower
large Intestine (LLI).   However, It 1s only  from the small  Intestine  (SI)
that absorption Into the blood Is considered to  occur.  The fraction  of
material that 1s transferred Into blood 1s  denoted by the symbol  fj.

     Radionuclides  may  be  absorbed by  the blood  from either the  lungs or
the GI tract.  After absorption by the blood, the  radlonuclide is
distributed among botty  organs according to  fractional uptake coefficients,
denoted by the symbol f£.   Since the radioactive material may be
transported through the bocjy, dose rates  are calculated for each organ or
tissue affected by  using a model of the organ that mathematically
simulates the biological processes Involved. The  ^general form of the
model for each organ Is relatively simple.   It  postulates that the
radioactive material which enters the  organ 1s  removed by both
radioactive decay and biological removal  processes.

F.3.2  External Doses

     The example just described for modeling the activity of a
radionuclide in an organ pertains to estimating doses from Internal
exposure.   In contrast, the external immersion  and surface doses are
calculated as follows.   First, the number of photons reaching the body is
determined.  The model  used here is a set of equations governing the
travel of photons (gamma radiation) 1n air.  The simplifying assumptions
used in these calculations are that the medium (air) Is an Infinite
half-space and is the only material present.  This makes the calculation
relatively straightforward.  In the second portion of the calculation,
the photons reaching the body are followed through the body using a
"Monte Carlo*1 method.  The "phantoms," I.e., the models of the body, are
those used by the Medical Internal Radiation Dose Committee  (MIRD69).
The Monte Carlo method is a procedure 1n which the known properties of
the radiation and tissues are employed to trace (simulate) the paths of  a
large number of photons In the bocly.  The amount of energy released at
each Interaction of the radiation with boc|y tissues  Is recorded  and,
thus, the dose to each organ or tissue 1s estimated  by evaluating a large
number of photon paths.

F.3.3  Effects of Decay Products

      In calculating doses from  Internal and external exposures,  the
occurrence  of radioactive decay products (or daughters) must  be
considered  for some radionuclldes.  When an atom  undergoes radioactive
decay, the  new atom created  1n the process may also  be radioactive and
may contribute to the radiation dose.  Although these decay  products may
be treated  as Independent radionuclldes 1n external  exposures, the decay
products of each parent must be followed through  the  bodly  1n  Internal
exposures.  The decay product contributions to the dose  rate  are included
In the dose calculations, based on the metabolic  properties  of the
element and the organ In which they occur.
                                   F-8

-------
F.3.4  Dose Rate Estimates

     For each external  and internal  exposure,  dose rates to each of the
organs listed in Table' F-l are calculated for  each radioisotope.  These
organ dose rates serve as input to the life table calculations described
in Appendix G.
TABLE F-l:
Organs for which dose rates are calculated
             Red bone marrow
             Bone
             Lung
             Breast
             Stomach
             Pancreas
Intestine
Thyroid
Liver
Urinary tract
     (^Esophagus, lymphatic system, pharynx, larynx, salivary gland,
brain.
F.4  EPA Dose Calculation

F.4.1  Dose Rates

     The models described in Section F.2 are used by EPA to calculate
radiation dose rates resulting from internal and external exposures to
radioactive materials.  A more complete description of the methodology,
equations, and parameters used is given in Du84, ORNL80, and ORNL81.  EPA
has adopted two refinements to the ICRP-recommended protocol for these
calculations.  The first is to track the movement of internally produced
radioactive daughters by assuming that their movement is governed by
their own metabolic properties rather than those of the parent.  Although
not enough information is available to allow a rigorously defensible
choice, this appears to be more accurate for most organs and
radionuclides than the ICRP assumption that daughters behave exactly as
the parent.  In the second departure from ICRP recommenda-
tions, age-dependent values of the parameters governing the uptake of
transuranic radionuclides have been taken from two sources, deemed
appropriate to the .general population, the National Radiological
Protection Board (NRPB82) and the EPA transuranic guidance document
(EPA77).

     The internal dose equations given by ICRP may be used to calculate.
either radiation doses (rad), i.e., the total dose over a given time
period, or radiation dose rates (rad/yr), i.e., the way in which the dose
                                   F-9

-------
changes with time after intake.  The integral  of the  dose rates 1s,  of
course, the total dose.  EPA calculates dose rates rather than doses,
because EPA considers age when assessing the effects  of radiation on the
population.

     External irradiation does not result in any residual internal
material.  Therefore, external dose rates to a g'iven  organ are constant
as long as the external radionuclide is present.  That is, the dose  rate
caused by a given amount of radionuclide present in air or on a ground
surface becomes zero when the radionuclide is removed.

     The calculation of dose rates, rather than integrated doses, allows
the use of age-dependent metabolic parameters more appropriate to the
general population to be taken into account.  In the  vast majority of
cases, however, there is not now sufficient Information available to make
such calculations.  The effect of using age-dependent metabolic
parameters 1s discussed in Section F.5.2 for some radionuclides for which
sufficient information 1s available.

F.4.2  Exposure and Usage

     The ICRP dosimetrlc equations used by EPA are linear, i.e., an
intake of 10 picocuries will result in dose rates ten times as large as
those from an intake of 1 picocurie.   In similar fashion, exposure to 10
times as large an air or ground surface concentration will increase the
external doses by a factor of 10.  EPA uses this linearity to avoid
having to calculate radiation dose rates for a range of concentrations.
The standard EPA procedure Is to use unit Intakes of 1 pCi/yr and air and
ground surface concentrations of 1 pCTTcm3 and 1 pd/cmS respectively.
The doses for other intakes and concentrations may then be scaled up or
down as  required.

     In  most cases, it is necessary to make certain assumptions regarding
the exposure conditions in order to perform an assessment.  EPA calculates
dose rates for lifetime exposure to the unit Intakes and concentrations.
Appendix G describes the different ways 1n which these rates can  be
applied.   In addition, the exposure assessment will usually depend on
other  usage  conditions.assumed for the exposures.

F.5  Uncertainty Analysis

     Uncertainty, in the dose, refers  to the manner in which the
calculated dose  changes when  the parameters used in the calculation
(intakes, metabolic factors,  organ  sizes, etc.) are changed.   The
uncertainty  associated with the dosimetric calculations  Is extremely
difficult to .quantify  because  the term "uncertainty analysis"  implies a
knowledge of parameter distributions that is  usually  lacking.   Internal
doses, for example, depend on  the parameters  used to characterize the
physiological and metabolic properties of an  Individual, while external
doses  must consider parameters such as organ  size and  geometry for  a
particular individual.  The data available  for  most of these parameters  is
not  sufficient to define the  form of the parameter distribution.
                                    F-10

-------
The major source of uncertainty in calculating the dose to a distinct
individual, however, in most Instances, does not result from errors in
measuring the parameters but from the real variation in parameter values
among individuals in the general population.  Thus,  a calculated dose is
thought to be representative of a "typical" member of the general
population and is probably reasonably precise for some large segment of
that population.

     The basic physiological and metabolic data used by EPA in calcu-
lating radiation doses are taken from the ICRP Report of the Task Group
on Reference Han (ICRP75) and from the ICRP Limits for Intakes for '.
RadTonuclTdes by Workers (ICRP79).  The "Reference Han" report is the
most comprehensive compilation of data available on the intake,
metabolism, internal distribution, and retention of radioisotopes in the
human body.  Its major purpose, however,  is to "define Reference Man, in
the first instance, as a typical occupational individual," although
differences with respect to age and sex are indicated in some instances.

     The limitations inherent in defining Reference Man, and 1n
estimating uncertainties due to variations in individuals in the general
population, are recognized by the Task Group (ICRP75):

          "The Task Group agreed that it was not feasible to
     define Reference Man as an "average1 or a 'median1
     individual of a specified population group and that it was
     not necessary that he be defined in any such precise
     statistical sense.  The available data certainly do not
     represent a random sample of any specified population.
     Whether the sample is truly representative of a particular
     population group remains largely a matter of judgement which
     cannot be supported on the basis of statistical tests of the
     data since the sampling procedure is suspect.  Thus the Task
     Group has not always selected the 'average1, or the
     'median', of the available measurements in making its
     selection, nor has it attempted to limit the sample to some
     national or regional group and then seek an average or
     median value.  However, the fact that Reference Man is not
     closely related to an existing population is not believed to
     be of any great importance.  If one did have Reference Man
     defined precisely as having for each attribute the median
     value of a precisely defined age group in precisely limited
     locality (e.g., males 18-20 years of age in Paris, France,
     on June 1, 1964), these median values may be expected to
     change somewhat with time, and in a few years may no longer
     be the median values for the specified population.
     Moreover, the Reference Man so defined would not have this
     relation to any other population group unless by
     coincidence.  To meet the needs for which Reference Man is
     defined, this precise statistical relationship to a
     particular population is not necessary.  Only a very few
     individuals of any population will have characteristics
     which approximate closely those of Reference Man, however he
                               F-ll

-------
     1s defined.   The Importance of the  Reference Man concept  1s
     that his characteristics are defined  rather precisely, and
     thus If adjustments for individual  differences are to be
     made, there  Is a known basis for the  dose  estimation
     procedure and for the estimation of the  adjustment factor
     needed for a specified type of individual."

     With  respect to the dosimetric calculations performed by EPA to
assess the impact of radioactive pollutants on  a general population,
three sources of  uncertainty should be considered:

     (1)  that due to the variation In Individual parameters  among
          adults  1n the general population

     (2)  that due to the variation in individual parameters  with age

     (3)  that due to experimental error 1n the determination of
          specific parameters

     Each of these sources of uncertainty  Is  discussed  1n  this section.
As noted above, the data required to perform  a  rigorous uncertainty
analysis are lacking, and a form of uncertainty analysis called
sensitivity analysis is employed.  The sensitivity  analysis  consists of
substituting known ranges 1n the parameters  for the recommended value  and
observing the resulting change  in the calculated dose rate.

F.5.1  Dose Uncertainty Resulting from Individual  Variation

     This section discusses the uncertainty  1n calculated  radiation
doses occasioned by differences In physical  size and metabolism among
Individuals in the general population.  In order to investigate the
effects  of  Individual differences in  Intake,  size,  and metabolism, It Is
necessary to consider the form  of the equation used to calculate
radiation dose rates.   Equation F-2  1s a simplified form of the one used
by EPA to represent the 1ngest1on of  radioactive materials.
* c
f  f
Tl T2
                                        Tl-
                                  m   x  L1
                                            .-xt-
(F-2)
      where  D       is  the  dose  rate  (mrem/yr)
            I       is  the  intake  rate of radioactivity  (pC1/yr)
            fj      1s  the  fraction of I transferred to  blood after Ingestion
             i
            f2   [   1s  the  fraction'transferred to an organ from the blood
            m       is  the  mass  of the organ  (g)
            x       1s  the  elimination constant, which denotes how rapidly
                   the activity 1s removed from the organ  (yr-1)
            E       is  the  energy  absorbed by the organ  for each radioactive
                   disintegration (ergs)
            c       1s  a proportionality constant.
                                   F-12

-------
For simplicity, we will  assume that  dose rates _at  large times,  t,  are  to
be studied so that the term in the bracket is approximately unity.

     Although the actual  equations used are considerably more complicated
because they must describe the lung  model  and the  GI  tract, and also
treat all radioactive progeny, the essential  features of the uncertainty
in dose calculation are reflected in the terms of  Equation (F-2).   The
sensitivity of the dose to each of the terms in the equation may be
studied by substituting observed ranges of the quantities for the  single
value recommended by Reference Man.   For some of these quantities,  as
noted below, no range 1s cited because of insufficient data.

     Intake, I

     As an example, postulate that the ingestion mode to be calculated is
for fluid intakes.  The average fluid intake is about 1900 ml,  with an
adult range of 1000 to 2400 for "normal" conditions.   Under higher
environmental temperatures, this range may be increased to 2840 to
3410 ml.  Thus, a dose calculated as 1.9,  for example, could range from
1.0 to 2.4.

     Transfer Fraction, fj
     The value of the transfer fraction to blood depends on the chemical
form of the element under stucly.  One of the most common naturally
occurring radionuclides is uranium,  which is used here as an example.
ICRP79 cites values of fj ranging from 0.005 to 0.05 for industrial
workers, but notes that a higher value of 0.2 is indicated by dietary
data from persons not occupationally exposed.  EPA has used the 0.2 value
for the general population but, based on the ICRP range above, a
calculated dose determination could vary by a factor of 10.

     Organ Mass, m

     The range of organ masses depends primarily on the organ under
investigation.  For example, reported values for the bloodless lungs
range from 461 to 676 grams.  Liver weights ranged from 1400 to 2300
grams for adult males and 1200 to 1820 grams for females.  Thus, because
the organ mass appears in the denominator, calculated lung doses might be
expected to vary by a factor of 1.5 and liver doses by a factor of
about 2.
Remaining Terms,
                          x, E
     There are few reported data on the ranges in values to be expected
for the remaining variables.  They are all quantities which are less
directly observable than I, fj, and m and their influence on the dose
calculation can only be estimated.  The discussion In Section F.6 Is
intended to augment the uncertainty analysis by introducing the results
of some direct observations on segments of the general population.
                                  F-13

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F.5.2  Dose Uncertainty Resulting from Age

     The dose rates calculated by EPA are normally  based  on  the  metabo-
lism and physical characteristics of Reference Man  (ICRP75).   These
properties may obviously be expected to depend on the  age of an
Individual.  Most particularly, for Infants and children  such factors as
breathing rates, liquid and solid intakes, organ size  and growth rates,
and boc(y geometry are known to vary considerably from  adult  values.  The
effect of such changes on the radiation dose also depends on the
chemistry of the radioactive element under stu(Jy.   For example,  rapid
bone growth in children is of more Importance when  a  "bone seeker"  such
as strontium 1s considered.  Although the data available  for most age and
chemical element combinations are insufficient to allow estimation  of the
uncertainty 1n dose, some organ/element combinations,  for which  more
information Is available, are discussed below.

     Iodine and the Thyroid

     Iodine 1s rapidly and virtually completely absorbed  into the blood-
stream following Inhalation or ingestlon.  From the blood, Iodine enters
the extracellular fluid and quickly becomes concentrated  in the  salivary,
gastric, and thyroid glands.   It 1s rapidly secreted from the salivary
and gastric glands, but it 1s retained in the thyroid for relatively long
periods.

     The Intake and metabolism of Iodine have been  reviewed extensively
(ORNL84a) to develop an age-dependent-model for Iodine.  In the  model
used here, ingested iodine is assumed to be almost  completely absorbed by
the blood.  The remaining parameters are age dependent and are shown In
Table F-2.  The fluid intake varies from 0.72 liters per day for a
newborn to about 2.0 liters per day for an adult.

     These age-dependent parameters may then be used in Equation (F-2) to
calculate the dose rate resulting from a constant concentration of iodine
1n water and air.  The resulting curves for the dose rate as a function
of age are shown in Figures F-4 and F-5.  These may be compared to the
dose rates obtained using Reference Man parameters at all ages,  Indicated
by the dotted lines 1n the same figures.  Thus, for this particular
combination of organ and Isotope, the total (70-year) dose Is seen to
increase by about 30 percent for Ingestlon and 35 percent for Inhalation
when dependence on age is considered.

     Strontium and Bone

     Because of the chemical similarities of  strontium and calcium,
strontium tends to follow the  calcium pathways in the,body and deposits
to a large extent in the skeleton.   In fact, the fraction of Ingested
strontium eventually reaching  the skeleton at a given age depends  largely
on the  skeletal needs for calcium at that age, although the bocjy Is  able
to discriminate  somewhat against strontium In favor of calcium after the
first few weeks of life.
                                   F-14

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             Age-dependent model
                    Adult model
   0.0    10.0  20.0  30.0
40.0   50.0  60.0
 AGE (YEARS)
70.0  80.0   90.0  100.0
Figure F-4.   Dose  rate  from chronic ingesUon of iodine-131 in
             water at a concentration of 1 pCi/1
                             F-15

-------
                  Age-dependent mddel
                        Adult model
        10.0   20.0  30.0
40.0  50.0   60.0  70.0

 AGE (YEARS)
89.0   90.0   100.0
Figure F-5.  Dose rate from chronic inhalation of ^ocline-131 in
             air at a concentration of 1  yCi/m3
                              F-16

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TABLE F-2:
Age-dependent parameters for Iodine metabolism In the thyroid
    Age     Fractional  uptake
                            i
   (days)      to thyroid,  f«
Thyroid mass
     (g)
Biological half-time
  1n the thyroid
      (days)
Newborn
100
365
1825
3650
5475
7300
0.5
0.40
0.3
0.3
0.3
0.3
0.3

-
1.78
3.45
7.93
12.40
20.00
15
20
30
40
50
65
80
     The ICRP model for bone is more complicated than that for the
thyroid because It consists of more than one compartment.   For purposes
of modeling the transport of strontium by the skeleton, it suffices to
view the mineralized skeleton as consisting of two main compartments:
trabecular (cancellous, porous, spongy) and cortical  (compact) bone.
Two subcompartments, surface and volume, are considered within each of
these main compartments.  The four subcompartments of mineralized
skeleton and the movement of strontium among these compartments are shown
schematically in Figure F-6.  The equations governing the  age dependence
of the parameters are given in (ORNL84a).  Dose rate  curves for the
inhalation and ingestion of constant concentrations of strontium-90 are
given in Figures F-7 and F-8  The comparable curves for Reference Man  are
again indicated by dashed lines.  Thus, for this element and organ
combination, the dose rate resulting from ingestion is somewhat higher,
while the dose rate resulting from inhalation exhibits only minor
perturbations, when the age dependence of the parameters is considered.
The lifetime (70-year) dose resulting from ingestion  is about 7 percent
greater and the inhalation dose less than 1 percent different when age
dependence is considered.

     Plutonium and Lung and Red Bone Marrow

     Apparently plutonium and iron bear sufficient chemical resemblance
that plutonium Is able to penetrate some iron transport and storage
systems.  It has been shown that plutonium in blood serum  complexes with
transferrin, the iron-transport protein.  Thus, plutonium  will partially
                                  F-17

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Figure F-6.   Compartments  and  pathways in model for
             strontium in  skeleton
        TRABECULAR
          SURFACE
        TRABECULAR
         VOLUME
                              BLOOD
  CORTICAL
  SURFACE
  CORTICAL
-  VOLUME
                                                   1
                           F-18

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   o  n
               Age-dependent model
                             Adult model
                  —i	1—
                  20.0   30.0
40.0   50.0  60.0
 AGE (YEARS)
70.0   80.0  90.0   100.0
Figure F-7.   Dose rate from chron-ic. Ingestlon of^strontlum-90
             in water at a concentration of 1  vCi/1
                              F-19

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                       Age-dependent model
       Age-dependent model
    10.0   20.0
30.0  40.0   50.0  60.0  70.0
      AGE (YEARS)
                                                 80.0  90.0   100.0
Figure F-8.  Dose rate from chronic"Inhalation--of strontium-90
             in air at a concentration of 1 pC1/m3
                             F-20

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trace the Iron pathway, with the result that a .substantial  fraction of
systemic plutonium is carried to the bone marrow and to the liver.   In
the skeleton, plutonium may be released mainly at sites of  developing red
cells.  Plutonium that has reached the skeleton behaves very differently
from iron; its movement is governed by fairly complicated processes of
bone resorption and addition.  Because the total  metabolic  behavior of
plutonium is not closely related to that of any  essential element,  any
retention model for plutonium as a function of age will involve much
larger uncertainties than the analogous model  for strontium.  Still,
there is enough information concerning the metabolism of plutonium  by
mammals to justify an examination of potential differences  with age in
doses to radiosensitive tissues following intake of this radioelement.

     The effect of age-dependent parameters on dose rate calculations is
most evident for the lung when the inhalation pathway is considered.
Figure F-9 exhibits the variation in dose rate to the total  and pulmonary
portions of the lung both for the adult and age-dependent cases. The
increased dose rate from age 0 to about 20 is typically caused by
variations in the breathing rate-lung mass ratio for infants and
juveniles.  For this model, the age-dependent pulmonary lung 70-year dose
is about 9 percent greater than for the adult model.

     To describe retention of plutonium in the skeleton, it is convenient
to view the skeleton as consisting of a cortical  compartment and
trabecular compartment.  Each of these is further divided into three
subcompartments:  bone surface, bone volume, and a transfer compartment.
The transfer compartment, which includes the bone marrow, may receive
plutonium that Is removed from bone surface or volume; plutonium may
reside in this compartment temporarily before being returned either to
the bloodstream or to bone surfaces (Figure F-10),  Because of the  large
amount of recycling of plutonium among the skeletal compartments, blood,
and other organs, recycling is considered explicitly in the model.   The
age-dependent features of the model are described in detail  in (ORNL84a).

     Red bone marrow dose rates for the age-dependent model  are shown in
Figure F-ll, for ingestion, and in Figure F-12,  for inhalation.  The
dashed curves are the dose rates using non-age-dependent parameters.  As
in the corresponding curves for strontium, the difference is more
pronounced for the ingestion pathway.  Because of the long  physical and
biological half-lives of plutonium in the skeleton, the dose rate,  for a
chronic intake, does not reach equilibrium within the one hundred year
time period of the figures.  The total lifetime  (70-year) dose to the red
marrow 1s about 25 percent greater for ingestion, and nearly unchanged
for inhalation when the age-dependent parameters are used.

     In summary, it is difficult to make generalizations concerning
the uncertainty Involved in neglecting age dependence in the dose
calculations.  Although the examples given indicate higher  dose rates
for the ingestion pathway, with smaller changes  for inhalation, when
using age-dependent parameters, this results from the complex interaction
between parameters in the dose equation and depends on the  element/organ
combination under consideration.
                                  F-21

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                                       dose
                                         rates
                                               and
                                                          rates
                                                            rates
                     Adult dose rates and,intake rate (pulmonary lung)

                 Adult dose rates and intake rate (total lung)
         Q.O  10.0   20.0  30.0   40.0   50.0   60.0   70.0
                                 AGE  (YEARS)
80.0  90.0  100.0
Figure F-9.  Dose rate from chronic Inhalation of plutonium-239
             in air at a concentration of 1  pCi/m3
                              F-22

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Figure F-10.   Compartments and pathways in model
              for plutonium in skeleton
                TRABECULAR
                  SURFACE
                TRABECULAR
                  VOLUME
                TRABECULAR
                  MARROW
                                  BLOOD
CORTICAL
 SURFACE
CORTICAL
 VOLUME
 CORTICAL
  MARROW
                               F-23

-------
   o

   o .,
O O


E UD -,
UJ r-
o: •^
o:
<: o
              Age-dependent model
                       30.0  40.0  50.0

                             AGE (YEARS)
60.0
 T	1	1	1

70.0  80.0  90.0  100.0
 Figure F-ll.  Dose rate from chronic ingestion of pluton$um-239

               1n water at a concentration of 1 yd/1
                               F-24

-------
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   o
   o
   ID
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ca:
a o
^ o
E o
UJ IT)
or
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 o
 CtL O
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F.5.3  Dose Uncertainty Caused by Measurement  Errors

     The last potential source of uncertainty  in  the  dose  calculations  1s
the error Involved In making measurements  of fixed quantities.   The
radioactive half-life of an Isotope,  for example,  may be measured
independently of any biological system,  but the measurement is  subject  to
some error.  The organ mass of a given organ may  also be measured  with
only a small error.  Repeated determinations of these quantities,  in
addition, can reduce the error.  Although  this source of uncertainty may
be of importance in other aspects of  an environmental assessment,  it is
of little consequence in the dosimetry,  because 1t 1s overwhelmed  by the
magnitude of the uncertainties resulting from  individual variations.

     Although consideration of the factors described  above implies large
uncertainties in calculated doses, the actual  variation is expected to  be
considerably smaller.  The reason for this, and  some  supporting studies
on real populations, are presented in Section  F.6.

F.6  Distribution of Doses in the General  Population

     Although the use of extreme parameter values in  a sensitivity
analysis indicates that large uncertainties in calculated  doses are
possible, this uncertainty is not usually reflected in the general
population.  There are several reasons for this:   the parameter values
chosen are  intended to be typical of an individual in the  population; it
is Improbable that the "worst case" parameters would be chosen for all
terms in the equation; and not all of the terms are mutually Independent,
e.g., an increased intake may be offset by more rapid excretion.

     This  smaller  range of uncertainty in real populations Is demon-
strated  by  studies performed on various human and animal populations.  It
should be  noted that there is always  some variability In observed doses
that results primarily from differences 1n the characteristics of
individuals.  The  usual way of specifying the dose,  or activity,
variability in an  organ 1s in terms of the deviation from the average,  or
mean, value.   In the following studies, it should also be noted that, in
addition to the variability resulting from individual characteristics,
the exposure levels  of Individuals may also have  varied .appreciably  - .
another  factor tending to  Increase the dose uncertainty.'  The following
studies  are representative of  those carried out on real populations:

      (1)   An analysis  of the thyroid  from 133 jackrabblts  1n a nuclear
fallout  area  (Tu65)  found  that  in only  2  did  the  iodine-131 content
exceed  three times the same mean.

      (2)   Measurements of  the  strontium-90 content of  adult whole
skeletons  (Ku62)  showed that  only about 5 percent of the  population would
exceed  twice the  average activity, with only  about 0.1 percent exceeding
four times the  average.
                                   F-26

-------
     (3)  In another study,  the cesium-137 consent  of  878  skeletal  muscle
samples (E164a, E164b) was measured.   This radioisotope  1s also the
result of nuclear tests so that the muscle content  depends not  only on
the variation In individual  parameters but also on  the pathways leading
to ingestion or inhalation of the isotope.  Nevertheless,  analyses  of
these samples indicated that only 0.2 percent exceeded three  times  the
mean activity at a 95 percent confidence level.

     (4)  A stucty of the variability  in organ deposition among  individuals
exposed under relatively similar conditions to toxic substances has also
been performed (Cu79).  In eleven exposure situations  (Table  F-3),  the
geometric standard deviation of the apparently lognormal organ  doses
ranged from 1.3 to 3.4.  This means that 68 percent of the bone doses
resulting from ingestion of strontium-90 would lie  between 0.56 and
1.8 times the average.

     In all  but two of the situations examined, there  is the  complicating
factor that there was probably a great deal of variation in the exposure
levels experienced by members of the  population. The  magnitude of
geometric standard deviations of the  studies listed in Table  F-3 may be
the evidence of this variation since, except for the two beagle studies,
the exposure was not uniform.  Despite these nonuniform  exposures,
however, the organ dose is not greatly affected probably because of
differences in metabolic processes.  For example, there  is probably some
"self-adjustment" in the amount of strontium-90 absorbed from the small
intestine to blood of different persons, since strontium-90 tends to vary
with calcium in food; if a person has a low calcium intake, then he may
absorb a higher fraction of the calcium and strontium-90 than a person
with a high calcium intake.

     In the beagle studies,  the geometric standard  deviation  is 1.8 for
inhaled metals in bone or liver, but  is only 1.3 for ingested
strontium-90 in bone.  An important difference is that all dogs ingesting
strontium-90 at a given level were administered the same amount, whereas,
in the inhalation studies, the exposure air concentrations were controlled
but the dogs inhaled variable amounts depending upon their individual
characteristic breathing patterns.

     Thus, in real situations, the overall uncertainty in  dose  is seen to
be considerably smaller than would be expected solely  on a basis of the
"worst case" sensitivity analyses.

F.7  Summary

     This appendix presents an overview of the methods used by  EPA to
estimate radiation doses.  The appendix defines the basic  quantities
reported by EPA and describes briefly the models employed. The appendix
also points out departures from the occupational parameters and
assumptions employed in the basic ICRP methodology  and gives  the reasons
for the deviations outlined.
                                  F-27

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TABLE F-3;
Distributions of organ doses'8'  from Inhalation and  1ngest1on of metals
Population
Beagle
Humans
Humans
Humans
Humans
Beagles
Humans
Humans
(smokers)
Humans
(nonsmokers)
Humans
Humans
Exposure
Metals
Plutonium
(fallout)
Titanium
(soil)
Aluminum
(soil)
Vanadium
(fuel com-
bustion)
Strontium-90
Strontium-90
(fallout)
Cadmium
Cadmi urn
Lead
Lead
Principal
exposure mode
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Ingestion
Ingestion
Inhalation and
Ingestion
Inhalation and
Ingestion
Inhalation and
Ingestion
Inhalation
Geometric standard
Target deviation of
organ organ doses*8'
Bone or liver 1.8
Lung 3
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     Many of the physiological  and metabolic  parameters  recommended 1n
methods for calculating radiation doses are based  on  a limited number of
observations, often on atypical humans or on  other species.   EPA has
attempted to bound the uncertainty associated with the ranges observed
for some of the more important parameters used.   In fact,  some empirical
data on population doses mentioned here indicate that actual  dose
uncertainties are much less than is implied by this "worst case" analysis.
For the sources of uncertainty discussed, the large dose range$ possible
because of variation in individual characteristics must  be modified by
consideration of the narrower ranges indicated by  studies  of  real
populations; the dose range resulting from age dependence  appears to be
small for lifetime exposures, and the range resulting from experimental
error 1s negligible by comparison.  Based on  these observations, 1t is
reasonable to estimate that EPA's calculated  doses should  b,e  accurate
within a factor of 3 or 4.  It should be emphasized that much of the
"uncertainty" in the dose calculation is not  caused by parameter error
but reflects real differences in individual characteristics within the
general population.  Therefore, the uncertainty  in the dose estimates
cannot be dissociated from specification of the  segment  of the population
to be protected.

     More complete derivations and explanations  for the  EPA methodology
are given in the references cited in the text, and a  technical descrip-
tion of the dose rate equations and their use 1n conjunction  with the
life table risk evaluation is given in Appendix  H.
                                   F-29

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                               REFERENCES
Cu79      Cuddihy R. G., McClellan R. D., and Griffith W. C., Variability
          in Target Organ Deposition among Individuals Exposed to Toxic
          Substances, Toxicology and Applied Pharmacology 49, 179-187,
          1979.                                           ~~

Du84      Dunning D. E. Jr., Leggett R. W., and Sullivan R. E., An
          Assessment of Health Risk from Radiation Exposures, 1n Health
          Physics 46 (5), 1035-1051, May 1984.

E164a     Ellett W. H. and Brownell G. L., Caesium-137 Fall-Out Body
          Burdens, Time Variation and Frequency Distributions, Nature 203
          (4940), 53-55, July 1964.

E164b     Ellett W. H. and Brownell G. L., The Time Analysis and
          Frequency Distribution of Caesium-137 Fall-Out in Muscle
          Samples,  IAEA Proceedings Series, STI/PUB/84, Assessment of
          Radioactivity in Man, Vol.  II, 155-166, 1964.

EPA77     U.S.  Environmental Protection Agency, Proposed Guidance on Dose
          Limits for Persons Exposed to Transuranium Elements in the
          General Environment, EPA 520/4-77-016, 1977.

ICRP75    International Commission on Radiological Protection, Report of
          the  Task  Group on Reference Man,  ICRP Publication  No. 23,
          Pergamon  Press, Oxford,  1975.

ICRP77    International Commission on Radiological Protection,
          Recommendations of the  International Commission  on Radiological
          Protection,  ICRP  Publication No.  26, Pergamon  Press, Oxford,
          1977.

ICRP79    International Commission on Radiological Protection, Limits for
          Intakes of  Radionuclides by Workers, ICRP  Publication No. 30,
          Pergamon  Press, Oxford,  1979.

Ku62     Kulp J.  L.  and Schulert  A.  R.,  Stront1um-90  in Man V, Science
          136  (3516),  May 1962.

MIRD69    Medical  Internal  Radiation Dose Committee,  Estimates of
          Absorbed  Fractions  for  Monoenergenetic  Photon  Sources  Uniformly
          Distributed in Various  Organs  of a Heterogeneous Photon,  MIRD
          Supplement  No. 3, Pamphlet 5,  1969.

NRPB82    National  Radiological  Protection Board,  Gut Uptake Factors  for
          Plutonium,  Amerldum,  and Curium, NRPB-R129, Her Majesty's
           Stationery  Office,  1982.
                                   F-30

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ORNL80    Oak Ridge National Laboratory, A Combined Methodology for
          Estimating Dose Rates and Health Effects for Exposure to
          Radioactive Pollutants, ORNL/RM-7105, Oak Ridge, Tennessee,
          1980.

ORNL81    Oak Ridge National Laboratory, Estimates of Health Risk from
          Exposure to Radioactive Pollutants, ORNL/RM-7745, Oak Ridge,
          Tennessee, 1981.

ORNL84a   Oak Ridge National Laboratory, Age Dependent Estimation of
          Radiation Dose, to be published,.

ORNL84b   Oak Ridge National Laboratory, Reliability of the Internal
          Dosimetric Models of ICRP-30 and Prospects for Improved Models,
          to be publ-ished.

Tu65      Turner F. B., Uptake of Fallout Radionuclides by Mammals and a
          Stochastic Simulation of the Process, in Radioactive Fallout
          from Nuclear Weapons Tests, U.S. AEC, Division of Technical
          Information, November 1965.
                                  F-31

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          APPENDIX G:  ESTIMATING THE RISK OF HEALTH EFFECTS
                 RESULTING FROM RADIONUCLIDE RELEASES

G.I  Introduction

     This appendix  describes how EPA estimates  the probability of fatal
cancer, serious genetic effects, and other detrimental  health effects
caused by exposure  to ionizing radiation.   Such risk estimates are
complex and uncertain, even though much  scientific effort has been
expended to increase the understanding of  radiation effects.

     Because the effects of radiation on human  health are known more
quantitatively than for most other environmental  pollutants,  it is
possible to make numerical estimates of  the risk  from a particular
source of radioactivity.   Such numbers may give an unwarranted aura of
certainty to estimated radiation risks.  Compared to the baseline
incidence of cancer and genetic defects, radiogenic cancer and
radiation-induced genetic defects do not occur  very frequently.  Even
among heavily irradiated populations, the  number of cancers and genetic
defects resulting from radiation is not  known with either accuracy or
precision simply because of sampling variability.  In addition, exposed
populations have not been followed for their full lifetime, so that
information on ultimate effects is limited.  Moreover,  when considered
in light of Information gained from experiments with animals and from
various theories of carcinogenesis and mutagenesis, the observational
data on the effects of human exposure are  subject to a number of
interpretations.  This in turn leads to  differing estimates of
radiation risks by  both individual radiation scientists and expert
groups.  Readers should bear 1n mind that  estimating radiation risks is
not a mature science and that the evaluation of radiation hazards will
change as additional information becomes available.  In this appendix,
a number of simple  mathematical models are presented that may describe
the main features of the human response  to radiation.  However, most
scientists would agree that the underlying reality is quite complicated
and largely unknown, so that such models should not be taken too
literally but rather as useful approximations that will someday be
obsolete.

     EPA's estimates of cancer and genetic risks in this report are
based on the 1980 National Academy of Sciences  BEIR-3 report (NAS80).
This report was prepared for the purpose of assessing radiation risks
at the low exposure levels of interest in  standard setting.  As phrased
by the President of the Academy, "We believe that the report will be
helpful to the EPA  and other agencies as they reassess radiation
protection standards.  It provides the scientific bases upon which
standards may be decided after non- scientific  social values have been
taken into account."

     In the sections below, we outline the various assumptions made in
calculating radiation risks based on the 1980 MAS report and compare
these risk estimates with those prepared by other scientific groups,
                                  G-l

-------
such as the 1972 NAS BEIR  Committee  (NAS72).  the United  Nations
Scientific Committee on the  Effects  of Atomic Radiation  (UNSCEAR),  and
the International  Commission on Radiation Protection (ICRP).   We
recognize that information on radiation risks is incomplete and do  not
argue that the estimates made by the 1980 NAS BEIR Committee  are  highly
accurate.  Rather, we discuss some of the deficiencies 1n the available
data base and point out possible sources of bias in current risk
estimates.  Nevertheless,  we believe the risk estimates  made  by EPA are
"state-of-the-art."

     In the sections below,  we first consider the cancer risk resulting
from whole-body exposure to  low-LET* radiation, i.e.,  lightly ionizing
radiation like the energetic electrons produced by 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 1n selected bocty organs.   Therefore,
the cancer risk resulting  from low-LET Irradiation of specific organs
is examined next.  Organ doses can also result from high-LET  radiation,
such as that associated with alpha particles.  The estimation of  cancer
risks for situations where high-LET  radiation is distributed  more or
less uniformly within a body organ  Is the third situation considered,
Section G.3.  In Section G.4, we review the causes of uncertainty in
the cancer risk estimates  and the magnitude of this uncertainty so that
the public as well as EPA  decision makers have a proper  understanding
of the degree of confidence  to place in them.  In Section G.5, we
review and quantify the hazard of deleterious genetic effects from
radiation and the effects  of exposure 1n utero on the developing
fetus.  Finally, 1n Section  G.6, we  calculate cancer and genetic  risks
from background radiation  using the  models described in  this  appendix.

G.2  Cancer Risk Estimates for Low-LET Radiations

     Most of the observations of radiation-induced carcinogenesls in
humans are on groups exposed to low-LET radiations.  These groups
Include the Japanese A-bomb  survivors and medical patients treated with
X-rays for ankylosing sponcjylitis 1n England from 1935 to 1954 (Sm78).
The UNSCEAR (UNSCEAR77) and  NAS Committee on the Biological  Effects of
Ionizing Radiations (BEIR) (NAS80)  have provided knowledgeable reviews
of these and other data on the carcinogenic effects of human  exposures.

     The most Important epidemiological data base on radiogenic cancer
1s the A-bomb survivors.  The Japanese A-bomb survivors  have  been
studied for more than 38 years and  most of them, the Life Span Stucty
Sample, have been followed in a carefully planned and monitored
epidemiological survey since 1950 (Ka82, Wa83).  They were exposed to a
wide range of doses and are  the largest group that has been studied.
     *Linear Energy Transfer (LET) — the energy deposited per unit of
distance along the path of a charged particle.
                                  G-2

-------
Therefore, they are virtually the only group providing  information on
the response pattern at various levels of expos'ure to low-LET
radiation.  Unfortunately, the doses received by various individuals In
the Life Span Study Sample are not yet known accurately.  The 1980 BEIR
Committee's analysis of the A-bomb survivor data was prepared before
bias in the dose estimates for the A-bomb survivors (the tentative 1965
dose estimates, T65) became widely recognized (Lo81).  It is now clear
that the T65 doses tended 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 detailed reevaluation of current risk estimates is
indicated when the A-bomb survivor data have been reanalyzed on  the
basis of new and better estimates of the dose to individual  survivors.

     Uncertainties in radiation risk estimates do not result just from
the uncertainties in the Japanese data base and in other epidemio-
logical studies.  Analyses of these data bases require  a number  of
assumptions that have a considerable effect on the estimated risk.
These assumptions are discussed below.  The degree of uncertainty
introduced by choosing among these assumptions is probably greater than
the uncertainty of the estimated risk per unit dose among the A-bomb
survivors or other sources of risk estimates for radiogenic cancer in
humans.

G.2.1  Assumptions Needed to Make Risk Estimates

     A number of assumptions must be made about how observations at
high doses should be applied at low doses and low dose rates for
radiation of a given type (LET).  These assumptions include the shape
of the dose response function and possible dose rate effects.  A dose
response function expresses the relationship between dose and the
probability that a radiogenic cancer is induced.  Observed excess
cancers have occurred, for the most part, following relatively high
doses of ionizing radiation compared to those likely to occur as a
result of the combination of background radiation and environmental
contamination from controllable sources of radiation.  Therefore, a
dose response model provides a method of interpolating between the
number of radiogenic cancers observed at high doses and the number of
cancers resulting from all causes including background radiation.

     The range of interpolation is not the same for all kinds of cancer
because it depends upon the radiosensitivity of a given tissue.   For
example, the most probable radiogenic cancer for women is breast
cancer.  As described below, with appropriate references, breast cancer
appears not to be reduced when the dose is delivered over a long period
of time.  For example, the number of excess cancers per unit dose among
Japanese women, who received acute doses, is about the same per unit
dose as women exposed to small periodic doses of X-rays over many
years.  If this is actually the case, background radiation is as
carcinogenic for breast tissue as the acute exposures from A-bomb gamma
radiation.  Moreover, the female A-bomb survivors show an excess of
breast cancer at doses below 20 rad which is linearly proportional to
                                  G-3

-------
that observed at several hundred rad (To84).  Women In their 40's, the
youngest age group 1n which breast cancer 1s common, have received
about 4 rad of whole-body low-LET background radiation and usually some
additional dose Incurred for' diagnostic medical purposes.  Therefore,
for this cancer, the difference between observed radiogenic cancer,
less than 20 rad, and the dose resulting from background radiation 1s
less than a factor of 5, not several orders of magnitude as 1s
sometimes claimed.  However, it should be noted that breast tissue is a
comparatively sensitive tissue for cancer Induction and that for most
cancers, a statistically significant excess has not been observed at
doses below 100 rad, low-LET.  Therefore, the range of. dose
Interpolation between observed and calculated risk 1s often large.

G.2.2  Dose Response Functions

     The 1980 NAS report (NAS80) examined three dose response functions
in detail:  (1) linear, in which effects are directly proportional to
dose at all doses; (2)  linear quadratic, in which effects are very
nearly proportional to  dose at very low doses and proportional to the
square of the dose at high doses; and  (3) a quadratic dose response
function, where the risk varies as the square of the dose at all dose
levels.

     We believe the first two of these functions are compatible with
most of the data on human cancer.   Information which became available
only after the BEIR-3 report was published  indicates that a quadratic
response  function is Inconsistent with the  observed excess risk of
solid cancers at Nagasaki, where the estimated gamma-ray doses are not
seriously confounded by an assumed  neutron  dose component.  The chance
that a quadratic response function  underlies the excess cancer observed
In the Nagasaki  incidence data has  been reported as only 1 in 10,000
(Wa83).  Although a quadratic response function 1s  not  incompatible
with the  Life Span Stu<(y Sample data on leukemia incidence at Nagasaki,
Beebe and others  (Be78, E177) have  pointed  out how  unrepresentative
these data are of the total observed dose response  for  leukemia in that
city.  There is  no evidence that a  quadratic response function provides
a better  fit to  the observed leukemia  excess among  all  A-bomb survivors
in the Life Span Study  Sample than  a simple linear  model  (NAS80).
Based on these considerations, we do not believe a  quadratic response
can be used in a serious effort to  estimate cancer  risks due to
Ionizing  radiation.  EPA notes that neither the NCRP, the  ICRP, nor
other authoritative scientific groups, e.g., NRPB and UNSCEAR, have
used a quadratic response function  to  estimate the  risks due to
ionizing  radiation.

     The  1980 NAS BEIR  Committee considered only the Japanese mortality
data in their analysis  of possible  dose  response functions  (NAS80).
Based on  the T65 dose estimates, this  Committee showed  that the excess
Incidence of solid cancer and leukemia among the A-bomb -survivors Is
compatible with  either  a linear or  linear  quadratic dose response to
                                   G-4

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the low-LET radiation component and a linear response to the high-LET
neutron component (NAS80K  Although the 1980 8EIR report indicated
low-LET risk estimates based on a linear quadratic response were
"preferred" by most of the scientists who prepared that report,  opinion
was not unanimous,  and we believe the subsequent reassessment of the
A-bomb dose seriously weakens the Committee's conclusion.  The
Committee's analysis of dose response functions was based on the
assumption that most of the observed excess leukemia and solid cancers
among A-bomb survivors resulted from neutrons (NAS80).   Current
evidence, however,  is conclusive that neutrons were only a minor
component of the dose in both Hiroshima and Nagasaki (Bo82, RERF83.84).
Therefore, it is likely that the linear response attributed to neutrons
was caused by the gamma dose, not the dose from neutrons.  This point
is discussed further in Section G.3.

     Reanalysis of the Japanese experience after completion of the dose
reassessment may provide more definitive information on the dose
response of the A-bomb survivors, but it is unlikely to provide a
consensus on the dose response at environmental levels, I.e., about 100
mrad per year.  This is because at low enough doses there will always
be sampling variations in the observed risks so that observations are
compatible, in a statistical sense, with a variety of dose response
functions.  In the absence of empirical evidence or a strong
theoretical basis,  a choice between dose response functions must be
based on other considerations.

     Although there is evidence for a nonlinear response to low-LET
radiations in some, but not all, studies of animal radiocarcinogenesis
(see below), we are not aware of any data on human cancers that are
incompatible with a simple linear model.  In such a case, 1t may be
preferable to adopt the simplest hypothesis that adequately models the
observed radiation effect.  Occams's razor is still a viable scientific
rule for separating necessary from ad hoc assumptions.   Moreover, EPA
believes that risk estimates, for tfie" purpose of assessing radiation
impacts on public health, should be based on scientifically creditable
risk models that are unlikely to understate the risk.  The linear model
fulfills this criteria.  Given the current bias in the doses assigned
to A-bomb survivors (see Section 7.5.1 below), such an approach seems
reasonable, as well as prudent.  Therefore, in this appendix, EPA has
used the BEIR-3 linear dose response model as one of two dose response
models for discussing the risk of radiogenic cancer due to low-LET
radiations.

     For low-LET radiations, we have also Included in the appendix,
discussions of risk that are based on the BEIR-3 linear quadratic dose
response model.  While In the dose range of interest (environmental
levels) the dose squared term in this model Is Insignificant, the
linear term is about 2.5 times smaller than that In the BEIR-3 linear
response model, NAS80.  That Is, for the same dose, risk estimates
based on the BEIR-3 linear quadratic dose response model are only 40
percent of those based on the BEIR-3 linear model.
                                  G-5

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     Many of the risk estimates needed to evaluate the effect of
radlonucllde emission must be made on an organ "specific basis.  The
BEIR-3 report provides risk coefficients for Individual solid cancers
only for the linear model, Tables V-14 and V-15  1'n NAS80.  We have
therefore divided BEIR-3 organ risk estimates for a linear response by
a factor of 2.5 to obtain organ specific linear  quadratic risk
coefficients.

     The underlying basis for a linear quadratic response is thought to
be that repair of radiation damage mitigates the effect of small doses
of radiation or those which occur over a long time period, the reduced
linear term being Indicative of this repair.  Use of a linear quadratic
dose response function, as formulated by the BEIR-3 Committee, 1s
equivalent to the use of a dose rate effectiveness factor (DREF) of 2.5
(see below).

     The discussions of both the linear and the  linear-quadratic dose
response models for low-LET radiations are Included in this appendix to
compare the risk estimates obtained for given doses using both models.
The more conservative of these two models is the linear model.  We have
used this model for the calculation of the fatal cancers per curie
release to the accessible environment which are listed 1n Chapter 6.
This policy was thoroughly reviewed and accepted by the High-level
Radioactive Waste Disposal Subcommittee of the EPA Science Advisory
Board  (EPA84).

G.2.3  The Possible Effects of Dose Rate on Radiocarcinogenesis

     The BEIR-3 Committee limited its risk estimates to a minimum dose
rate of 1 rem per year and stated that it "does not know 1f dose rates
of gamma rays and X-rays of about 100 mrad/y are detrimental to man."
At dose rates comparable to the annual dose that everyone receives for
naturally-occurring radioactive materials, a considerable boc|y of
scientific opinion holds that the effects of radiation are reduced.
NCRP Committee 40 has suggested that carcinogenic effects of  low-LET
radiations may be a factor of from 2 to  10 times less  for small doses
and dose rates than have been observed at high doses  (NCRP80).

     The low dose and low dose rate effectiveness factors developed  by
NCRP Committee 40 are based on their analysis of a large bocjy of plant
and animal data that  showed reduced effects at low doses for  a  number
of biological endpoints, Including radiogenic cancer  In  animals,
chiefly  rodents.  However, no  data for cancer in humans  confirm these
findings as yet.  A few human  studies contradict them.   Highly
fractionated small doses to human breast tissue are apparently  as
carcinogenic as large acute doses  (NAS80, La80).  Furthermore,  small
acute  (less  than  10  rad)  doses to the thyroid are as  effective  per rad
as much  larger  doses  1n Initiating thyroid cancer  (UNSCEAR77, NAS80).
Moreover, the  Increased breast cancer resulting from  chronic  low dose
occupational gamma ray  exposures  among  British  dial painters  is
comparable  to,  or larger,  than that  expected  on the basis of acute high
dose  exposures  (Ba81).
                                   G-6

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     While none of these examples is persuasive by itself,  collectively
they indicate that it may not be prudent to assume that all  kinds of
cancer are reduced at low dose rates and/or Tow doses.   However,  it may
be overly conservative to estimate the risk of all cancers  on the basis
of the linearity observed for breast and thyroid cancer.  The
International Commission on Radiation Protection and the United Nations
Scientific Committee on Atomic Radiations have used a dose  rate
effectiveness factor of about 2.5 to estimate the risks from
occupational  (ICRP-263 and environmental exposures (UNSCEAR77).  Their
choice of a DREF is fully consistent with and equivalent to the
reduction of risk at low doses obtained by substituting the BEIR-3
linear-quadratic response model for their linear model.  Use of both a
DREF and a linear quadratic model for risk estimation is inappropriate
(NCRP80).

     The difference between risk estimates obtained with the BEIR-3
linear and linear-quadratic dose response models is by no means the
full measure of the uncertainty in the estimates of the cancer risk
resulting from ionizing radiation (Section G.4 below summarizes
information on uncertainty).  Using two models serves as a  reminder
that there is more than one creditable dose response model  for
estimating radiation risks and that it is not known if all  radiogenic
cancers have the same dose response.

G.2.4  Risk Projection Models

     None of the exposed groups have been observed long enough to
assess the full effects of their exposures, if, as currently thought,
most radiogenic cancers occur throughout an exposed person's lifetime
(NAS80).  Therefore, another major decision that must be made 1n
assessing the lifetime cancer risk due to radiation is to select a risk
projection model to estimate the risk for a longer period of time than
currently available observation data will allow.

     To estimate the risk of radiation exposure that is beyond 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 the 1980 WAS report (NAS80).  A
relative risk projection model projects the currently observed
percentage increase in cancer risk per unit dose into future years.  An
absolute risk model projects the average observed number of excess
cancers per unit dose Into future years at risk.

     Because the underlying risk 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 we have now, less than lifetime
follow-up, a relative risk model projects somewhat greater risk than
that projected using an absolute risk model.
                                  G-7

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     The National Acaderny of Sciences BEIR Committee  and other
scientific groups, e.g., UNSCEAR, have not concluded  which projection
model is the appropriate choice for most radiogenic cancers.   However,.
evidence is accumulating which favors the relative risk projection
model for most solid cancers.  As pointed out by the  1980 MAS BEIR
Committee,

         "If the relative-risk model applies, then the age of the
         exposed groups, both at the time of exposure and as  they
         move through life, becomes very important.   There 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 least they
         develop cancer sooner.  Furthermore, if they are
         Irradiated at a particular age, the excess risk tends to
         rise pan' passu (at equal pace) with the risk of the
         population at large.  In other words, the relative-risk
         model with respect to cancer susceptibility  at least as
         a function of age, evidently applies to some kinds of
         cancer  that have been observed to result from radiation
         exposure." (NAS80, p.33)

     This observation is confirmed by the Ninth A-bomb Survivor Life
Span Study, published two years after the 1980 Academy report.  This
latest  report indicates that, for solid cancers, relative risks have
continued to remain constant in recent years while absolute risks have
increased substantially  (Ka82).  Smith and Doll (Sm78) have reached
similar conclusions on the trend in excess cancer with time among the
irradiated spondylitic patients.

     Although we believe considerable weight  should be given to the
relative  risk model for most solid cancers  (see below), the model does
not  necessarily  give an accurate projection  of lifetime risk.  The mix
of tumor  types  varies with age so that the  relative frequency of  some
common  radiogenic  tumors,  such as thyroid cancer, decreases for older
ages.   Land has  pointed out  that this may result 1n overestimates of
the  lifetime risk  when they  are  based on a  projection' model using
summed  sites, relative  risks (La83).  While  this may turn out to  be
true for  estimates of cancer Incidence that  Include cancers less  likely
to be fatal, e.g., thyroid,  1t may  not be too Important in estimating
the  lifetime risk  of fatal cancers  since the incidence of most of the
common  fatal cancers, e.g.,  breast  and lung  cancers,  increases with age.

     Leukemia and  bone cancer are exceptions to the general validity of
a lifetime expression period for  radiogenic  cancers.  Most, if not all,
of the  leukemia  risk has apparently  alreac(y  been expressed in both the
A-bomb  survivors and the sponctylitlcs  (Ka82,  Sm78).   Similarly,  bone
sarcoma from acute exposure  appears  to  have  a limited  expression  period
 (NAS80, Ma83).   For these  diseases,  the  BEIR-3  Committee  believed that
an absolute  risk projection  model with  a  limited  expression period is
appropriate  for estimating lifetime risk  (NAS80).
                                   G-8

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     Note that, unlike the MAS BEIR-1  report (NAS72),  the BEIR-3
Committee's relative and absolute risk models are age  dependent.  That
is, the risk coefficient changes, depending on the age of the exposed
persons.  Observation data on how cancer risk resulting from radiation
changes with age is sparse, particularly so in the case of childhood
exposures.  Nevertheless, the explicit consideration of the variation
in radiosensitivity with age at exposure is a significant improvement
in methodology.  It is important to differentiate between age
sensitivity at exposure and the age dependence of cancer expression.
In general, people are most sensitive  to radiation when they are
young.  In contrast most radiogenic cancers occur late in life,  much
like cancers resulting from other causes.  In this appendix we present
risk estimates for a lifetime exposure of equal annual doses.  The
cancer risk estimated is lifetime risk from this exposure pattern.
However, age-dependent analyses using  BEIR-3 r;sk coefficients indicate
that the risk from one year of exposure varies by a factor of at least
5, depending on the age of the recipient.

G.2.5  Effect of Various Assumptions on the Numerical  Risk Estimates

     Differences between risk estimates made by using  various
combinations of the assumptions described above were examined in the
1980 WAS report.  Table G-l below, taken from Table V-25 (NAS80), shows
the range of cancer fatalities that are induced by a single 10-rad dose
as estimated using linear, linear quadratic, and quadratic dose
response functions and two risk projection models, relative and
absolute (NAS80).

     As illustrated in Table G-l, estimating the cancer risk for a
given risk projection model on the basis of a quadratic as compared to
a linear dose response reduces the estimated risk of fatal cancer by a
factor of nearly 20.  Between the more credible linear and linear
quadratic response functions, the difference is less,  a factor of about
2.5.  For a given dose response model, results obtained with the two
projection models, for solid cancers,  differ by about a factor of 3.

     Even though the 1980 NAS analysis estimated lower risks for a
linear quadratic response, it should not be concluded that this
response function always provides smaller risk estimates.  In contrast
to the 1980 NAS analysis where the proportion of risk due to the dose
squared term (e.g., Cj in equation c of Table G-l) was constrained to
positive values, the linear quadratic  function (which agrees best with
Nagasaki cancer incidence data) has a  negative coefficient for the
dose-squared term (Wa83).  Although this negative coefficient is small
and indeed may not be significant, the computational result is a larger
linear term which leads to higher risk estimates at low doses than
would be estimated using a simple linear model (Wa83).  Preliminarily,
the BEIR-3 analyses of the mortality,  which were not restricted to
positive coefficients of the dose squared terms, yielded similar
results.
                                  G-9

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     Differences in the estimated cancer risk  introduced by  the choice
of the risk projection model  are also appreciable.   As pointed out
above, the 1980 NAS analysis  indicates that relative risk estimates
exceed absolute risk estimates by about a factor of 3, Table G-l.
However, relative risk estimates are quite sensitive to how  the risk
resulting from exposure during childhood persists throughout life.
This question is addressed in the next section,  where we compare risk
estimates made by the 1972 and 1980 NAS BEIR Committees with those of
the ICRP and UNSCEAR.
TABLE G-l:
Range of cancer fatalities induced by 10-rad low-LET radiation
(Average value per rad per million persons exposed)
    Dose response

     functions
                                 Lifetime risk projection model

                                  Relative*3*         Absolute
Linear(b)
(c)
Linear Quadratic
id]
Quadratic10'
501
226

28
167
77

10
      (a)Relative risk projection for all solid cancers except
 leukemia and bone cancer fatalities, which are projected by means of
 the absolute risk model (NAS80).
^'Response R varies  as  a  constant  times  the  dose,  I.e.,  R=
                                                                CiD
 Source:   NAS80, Table V-25.
 G-2.6   Comparison  of Cancer Risk  Estimates for Low-LET Radiation

     A number  of estimates of the risk  of fatal cancer following
 lifetime exposure  are  compared  in Table G-2.  Although all  of these
 risk estimates assume  a  linear  response function, they differ
 considerably  because of  other assumptions.   In contrast with absolute
 risk estimates, which  have increased  since the first  NAS  report
 (BEIR-1) was  prepared  in 1972-(NAS72),  the 1980 NAS BEIR-3  Committee's
 estimates of  the relative risk,  as shown in  Table G-2, have decreased
 relative to those  in the BEIR-1 report.  This illustrates the
                                  G-10

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sensitivity of risk projections to changes in modeling assumptions.
For the NAS80 report, the relative risk observed  for ages  10  to  19 was
substituted for the considerably higher relative  risk observed for
those exposed during childhood, ages 0 to 9.   In  addition, the relative
risk coefficients used in the BEIR-3 analysis are based on excess
cancer in the Japanese A-bomb survivors compared  to U.S. population
cancer mortality rates.  In the 1972 MAS report this excess was
compared to cancer mortality in Japan.  Moreover, the difference
introduced by these two changes, particularly the former,  is  somewhat
greater than indicated in the 1980 MAS report.  'The relative  risk
estimate attributed to the BEIR-1 Committee in the NAS 1980 report is
incorrect.  Therefore, two BEIR-1 relative risk estimates  are listed in
Table G-2: the risk estimate^ in NAS80 attributed  to the BEIR-1
Committee and an estimate which is based on the risk coefficients  in
NAS72.  The NAS 1980 estimate did not use the  relative risk coefficient
for childhood exposure given in the BEIR-1 report, which for  solid
cancers is a factor of 10 larger than adult values (p. 171 in NAS72),
but rather used the adult risk for all ages including children.   The
estimate in Table G-2 labeled NAS72 uses the relative  risk coefficients
actually given in the BEIR-1 report.

     By comparing the three  relative  risk estimates  in Table  G-2,  it is
apparent that the relative risk estimates are fairly  sensitive to the
assumptions made as to what  extent the observed high  relative risk of
cancer from childhood exposure continues throughout  adult  life.   The
Life Span Study  (Ka82) indicates that the high-risk  adult  cancer caused
by childhood exposures is continuing, although,  perhaps,  not  to the
extent predicted by the NAS  BEIR-1 Committee in 1972.

     The major reason the risk estimates in Table G-2 differ  is
because of the underlying assumption  in each set of risk estimates.
The NAS BEIR estimates are for  lifetime exposure and lifetime
expression of induced cancers  (NAS72, 80).  Neither the  age
distribution of  the  population  at  risk nor the projection models  (if
any) have  been specified by  either the UNSCEAR (UNSCEAR77) or the ICRP
(ICRP77).  UNSCEAR apparently  presumes the same  age distributions as
occurred  in the  epidemiological  studies they cited,  mainly the  A-bomb
survivors, and a 40-year period of cancer expression.  The ICRP risk
estimates  are for adult workers,  presumably exposed between  ages  18
and 65, and a similar  expression  period.  These  are essentially
age-independent  absolute risk  models  with less than lifetime expression
of  induced cancer mortality.  For these  reasons  alone, risks estimated
by  ICRP and UNSCEAR  are expected to  be  smaller than those made  on the
basis  of  the BEIR-3  report.

     The  last entry  in Table G-2  (Ch83)  is of interest because  it
specifically excludes  the  A-bomb survivor data based on T65  dose
estimates.  The  authors  reanalyzed the  information on radiogenic  cancer
in  UNSCEAR77  so  as to  exclude  all  data  based on  the Japanese
experience.  Their estimate  of fatalities ranges from 100 to 440  per
                                  G-ll

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TABLE G-2:
A comparison of estimates of the risk of fatal  cancer from a lifetime
exposure at 1 rad/year (low-LET radiation)
Source of
estimate
BEIR-1 (NAS72)(a)
BEIR-1 (NAS80) b , ,
BEIR-3 (NASSOjtbMc)
BEIR-3 (NAS80)td)
BEIR-3 (NAS80)(b)
BEIR-1 (NAS80)(b)
BEIR-3 (NAS80)(d)
UNSCEAR (UNSCEAR77)(e)
UNSCEAR (UNSCEAR77)(e)
ICRP (ICRP77)

CLM (Ch83)

Cases per 106
person rad
667
568
403
169
158
115
67
200-300
75-175
125

100-440

Projection model
Relative Risk
Relative Risk
Relative Risk
Relative Risk
Absolute Risk
Absolute Risk
Absolute Risk
None-high dose > 100 rad
None-low dose/dose rate
None-occupational -
Tow dose/dose rate
UNSCEAR77 without A-bomb
data
            -l relative risk model.

              V-4 1n NAS80, linear dose response.

     lc'L-L absolute risk model  for bone cancer and leukemia;  UT relative
     risk model for all other cancer.
              V-4 in NAS80 linear-quadratic dose response.

         Paragraphs 317 and 318 in UNSCEAR77.
106 person rad for high doses and dose rates.  As indicated 1n Table
G-2, this is somewhat greater but comparable to the UNSCEAR estimate,
which includes the A-bomb survivor data.  The mean number of fatalities
given 1n Ch83 is 270 per 10° person-rem, which is nearly identical  to
the value EPA has used for a linear dose response model —280 fatalities
per 10° person rad (see below).

G.2.7  EPA Assumptions About Cancer Risks Resulting from Low-LET
       Radiation?

     EPA's discussion of radiation risks in this appendix are based on
presumed linear and linear quadratic dose response functions.  We believe
these are the most credible dose response functions for  estimating risks
to exposed populations.  Using the BEIR-3 linear quadratic model Is
equivalent, at low dose, to using a dose rate effectiveness factor of
                                   G-12

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2.5.  As discussed in section  G.2.2,  we  have  used a  linear  dose
response function for low-LET  radiation  in competing the  fatal cancers
per curie released to the  accessible  environment which  are  listed  in
Tables 6-1 through 6-4.

     Except for leukemia and bone  cancer,  where we use  a  25-year
expression period for radiogenic cancer, we use a lifetime  expression
period, as was done in the NAS report (NAS80).   Because the most recent
Life Span Stuc(y Report (Ka82)  indicates  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'.  We do not believe limiting  cancer expression  to 40 years {as
has been done by the ICRP  and  UNSCEAR) is  compatible with the
continuing increase in solid cancers  that  has occurred  among irradiated
populations (Ka82).  Analyses  of the  spondylitic data have  led others
to similar conclusions (Sm78).

     To project the number of  fatalities resulting from leukemia and
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  uses the
arithmetic average of absolute and relative risk projection models.
For these cancers, we assume a 10-year minimum induction  period and
expression of radiation-induced cancer for the balance  of an exposed
person's lifetime after the minimum induction period.

G.2.8  Methodology for Assessing the  Risk  of Radiogenic Cancer

     EPA 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 and vary considerably  with age (Bu81, Co78).
Basically, it calculates for ages  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
information on the details of  the  life table analysis is  provided  in
Appendix H.  It should be  noted that  a life table analysis  is required
to use the age-dependent risk  coefficients in the BEIR-3  report.   For
relative risk estimates, we use age-specific cancer  mortality data also
provided by NCHS (NCHS73). The EPA computer program we use for the
life table analysis was furnished  to  the NAS BEIR-3  Committee by EPA
and used by the Committee  to prepare  its risk estimates.  Therefore, we
believe that the population base and  calculational approach are similar
in both the NAS and EPA analyses.

     To project the observed risks of most solid radiogenic cancers
beyond the period of current observation,  we use both absolute and
relative risk models, but  usually  present  an arithmetic average based
on these projections.  Using a single estimate, instead of  a range of
values, does not mean that our estimate  is precise.   As indicated  in
                                 G-13
                                                                            /

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Table G-2, the range of estimated fatal  cancers  resulting  from the
choice of a particular projection model  and Its" internal assumptions 1s
about a factor of 3.  Although we think  it is likely  that  the  relative
risk model 1s the best projection model  for most solid  cancers, 1t has
been tested rigorously only for lung and breast  cancer  (La78).   Until
it has more empirical support, we prefer to use  an average risk based
on both projection models.  A second reason for  this  choice is to avoid
overly conservative risk estimates caused by the compounding of
multiplicative conservative assumptions.

     To estimate the cancer risk from low-LET, whole-bo
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G.2.9  Organ Risks

     For most sources of environmental  contamination,  Inhalation and
1ngest1on of radioactivity are more common than direct exposure.  In
many cases, depending on the chemical  and physical  characteristics of
the radioactive material, inhalation and Ingestion  result in a
nonuniform distribution 'of radioactive materials within the body so
that some organ systems receive much higher doses than others.  For
example, iodine isotopes concentrate in the thyroid gland, and the dose
to this organ can be orders of magnitude larger than the average dose
to the bocly.

     Fatal Cancer at Specific Sites

     To determine the probability that fatal  cancer occurs at a
particular site, we have performed life table analyses for each cancer
type using the Information on cancer incidence and  mortality in NAS80.
For cancer other than leukemia and bone cancer, we  used NAS80 Table V-14
(Age Weighted Cancer Incidence by Site Excluding Leukemia and Bone
Cancer) and NAS80 Table V-15, which lists the BEIR  Committee's
estimates of the ratio of cancer fatality to cancer incidence for these
various organs.  The proportions of leukemia and fatal bone cancer
caused by low-LET radiation were estimated using the results given in
Tables V-17 and V-20 of NAS80.  Normalized results, which give the
proportion of fatal cancer caused by radiogenic cancer at a particular
site, are listed in Table G-3.  As noted above, these proportions are
assumed to be the same for the BEIR-3 linear quadratic dose response
model.

     Information on the proportion of fatal cancers resulting from
cancer at a particular organ is not precise.  One reason is that the
data In NAS80  (and Table 6-3} are based on whole-boc(y exposures, and it
is possible that the incidence of radiogenic cancer varies depending on
the number of exposed organs.  Except for breast and thyroid cancer,
very little information is available on radiogenic  cancer resulting
from exposure of only one region in the body.  Another reason is that
most epidemiology studies use mortality data from death certificates,
which often provide questionable information on the site of the primary
cancer.  Moreover, when the existing data are subdivided Into specific
cancer sites, the number of cases becomes small, and sampling
variability 1s  increased.  The net result of these factors is that
numerical estimates of the total cancer risk are more reliable than
those for most  single sites.

     The  1977  UNSCEAR Committee's estimated  risks  (UNSCEAR77) to
different organs are shown in Table G-4.  For all of the organs, except
the breast, a  high and low estimate was made.  This range varies by a
factor of 2 or  more for most organs, Table G-4.  Other site-specific
estimates show  a similar degree of uncertainty  (Ka82), and it is
clear that  any  system for allocating the  risk of fatal cancer on an
                                  G-15

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TABLE G-3:
Proportion of the total  risk of fatal  radiogenic cancer resulting from
cancer at a particular site
       Site
Proportion of
 total ri
Lung lh\
Breasttb)
Red bone marrow^0'
Thyroid
Bone
Liver
Stomach
Intestines
Pancreas
Kidneys and urinary tract
Other^J
0.21
0.13
0.16
0.099
0.009
0,085
0.084
0.039
0.058
0.025
0.11
   ia'NAS80--L1fetime exposure and cancer expression; results are
rounded to two figures.

   ^'Average for both sexes.

   lc'Leukem1a.
            risk for all other organs, Including the esophagus,
 lymphatic  system, pharynx, larynx, salivary gland, and brain.
organ-specific basis is Inexact.  Table G-5 compares proportional risks
by  the  MAS  BEIR-3 Committee, UNSCEAR, and the  ICRP.  ICRP Report 26
provides  organ-specific weights for assessing  combined genetic and
cancer  risks  from occupational exposure (ICRP77K   In Table G-5, we
have  renormalized ICRP risks so that they pertain to cancer alone.

      Considering that the cancer  risk for a particular site is usually
uncertain by  a factor of 2 or more, as indicated by the range of
UNSCEAR estimates in Table G-4, we would not expect perfect agreement
in  apportionment of total body risks.  Table G-5, however, does
indicate  reasonable agreement among the three  sets  of estimates
considered  here.
                                  G-16

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TABLE G-4:
UNSCEAR estimates of cancer risks  at specified sites
Site
      Fatalities               Average
(per 106  person rad)    (per  106  organ  rad)
  Proportion

of total risk
Lung
Breast*3'
Red bone marrow'0'
Thyroid
Bone
liver
Stomach
Intestines
Pancreas
Kidneys and urinary
tract
Otheric)
25-50
25
15-25
5-15
2-5
10-15
10-15
14-23
2-5

2-5
4-10
37.5
25.0
20.0
10.0
3.5
12.5
12.5
18.5
3.5

3.5
7.0
0.24
0.16
0.13
0.065
0.23
0.081
0.081
0.12
0.023

0.023
0.046
     laJAverage for both sexes.
     }b|Leukemia,
     '^Includes esophagus and lymphatic tissues.
Source:  UNSCEAR77.
     The differences between the proportions of the total  risk of fatal
cancer shown in Table G-5 are, for the most part,  small  in comparison to
their uncertainty.  We have used the BEIR-3 organ  risks  in preference to
those made by other groups such as UNSCEAR or the  ICRP for several
reasons.  BEIR estimates of organ risk are based on a projection of
lifetime risk using age-specific risk coefficients, rather than just
observations to date.  Moreover, the 1980 BEIR Committee considered cancer
incidence data as well as mortality data.  This gives added confidence that
the diagnostic basis for their estimates is correct.  And, finally, because
we apply these proportional organ risk estimates to the  NAS80 cancer risk
estimates for whole-body exposures, we believe it  is consistent to use a
single set of related risk estimates.  The way we  have used NAS80 to
estimate mortality resulting from cancer at a particular site is outlined
in the next section.
                                   G-17

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TABLE G-5:
Comparison  of proportion of the total  risk  of  radiogenic  cancer  fatalities
by bocty organ
Site
                        (a)
NAS80
UNSCEAR77
1CRP77
                                          (b)
Lung
Breast
Red Marrow
Thyroid
Bone
Liver
Stomach
Intestine
Pancreas
Kidneys and
urinary tract
Other
.21
.13
.16
.099
.009
.085
.084
.039
.058

.025 %
.11(0)
.24
.16
.13
.065
.023
.081
.081
.12
.023

.023
.046
.16
.20
.16
.04
.04
( ,08)*c'
(.08)
(.08)
(.08)

(.08)
      (^Lifetime exposure and cancer expression.
      {^Normalized for risk of fatal cancer (see text).
      (c'Five additional organs which have the highest dose are assigned
        0.08 for a total of 0.4.
             s include esophagus, lymphatic system, pharynx, larynx,
        salivary gland, and brain.
 G.2.10  Methodology  for  Calculating the Proportion of Mortality
        Resulting  from Leukemia

      Application of  NAS80  to  particular problems is straightforward but
 requires  some  familiarity  with the details of that report.  In this section
 we  provide  sample  calculations based on the BEIR-3 linear dose response
 model for the  case of fatal leukemia resulting from irradiation of the bone
 marrow  throughout  an average  person's lifetime.  We then compared this
 number  to the  average number  of  all fatal radiogenic cancers to obtain the
 proportion  due to  leukemia (Table G-3).

      The  NAS80 estimates in Table G-3 differ from the others in that they
 include both a consideration  of  age at exposure and a full expression of
 radiogenic  cancer  resulting from lifetime exposure.  For example, Table
 V-17 in (NAS80) gives explicit age- and sex-dependent mortality
 coefficients for leukemia and bone cancer together.
                                    G-18

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     The ratio of leukemia to bone  cancer  fatalities  is given by  the
coefficient in the dose response relationship  listed  in Table V-17, i.e.,
2.24/0.05.  For lifetime exposure at  a  dose  rate  of one rad per year,  Table
V-17 lists 3,568 leukemia (and bone)  deaths  per 106 males and 2,709
deaths per 106 females (NAS80).   Using  a male-female  birth ratio  of 1.05
to 1.0,' this averages to 3,149 fatal  cancers per  million persons  in the
general  population.  The total  person rads causing  these excess fatalities
is the product of one rad per year,  10^ persons,  and  70,7 years (the
average age of this population at death).  Dividing the total number  of
fatalities by this product yields 44.5  fatalities per 106 person  rad  of
which about 43.5 are due to leukemia.  As  noted above,  for total  body-
exposure, the average of the absolute and  relative  risk projection models
yielded 280 premature cancer deaths per 10°  person  rad.

Therefore, P, the proportion of the whole-body risk caused by the lifetime
risk of a leukemia death due to lifetime exposure of  the red bone marrow,
is:
P = 43.5 = .16  (cf.  with  Table  G-3)
                                                               (G-l)
To obtain the proportional mortality for other-cancers, we have used
the site-specific, age-dependent risk coefficients in Table V-14
(NAS80) and the mortality ratios in Table V-15 to calculate the risk of
fatal cancer from lifetime exposure at one rad per year (for each sex)
and proceeded as in the example for leukemia outlined above.

     To apply the data shown in Table G-3 to a particular organ, we
multiply the average of the relative and absolute lifetime risk
estimates for whole body lifetime exposure for a linear dose response,
280 fatalities per 106 person rad and 112 fatalities per 106 person
rad for a linear quadratic response by the proportional mortality for
that cancer.  For example, using the linear model, a one rad dose
Oow-LET) to the kidney (urinary tract) resulting from lifetime
exposure is estimated to cause a lifetime probability of death caused
by radiogenic cancer that is equal to (.025) x (280xl06) or 7xlQ'6,
i.e., 7 chances in a million.

     Iodine-131 has been reported to be only 1/10 as effective as
X-rays or gamma rays in inducing thyroid cancer (NAS72, NCRP77).  For
this cancer a linear dose response and a DREF of 10 is used in
calculating lifetime probability of death.  For example, the risk from
a one rad dose to the thyroid from exposure to iodine-131 or iodine-129
is calculated as follows:  (0,099) x (0.10) x (280xlO~6) or
2.8xl(H>f about 3 chances in a million.
                                 G-19
                                                                                 \

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G.2.11  Cancer Risks Due to Age-Dependent  Doses

     As noted 1n Appendix F, almost  all  of the dose models  we  have  used
are based on ICRP "Reference Man."   ICRP dosimetric models  are
appropriate for adult workers and do not take into account  differences
resulting from the changes 1n physiological  parameters  between children
and adults, e.g., intake rates,  metabolism,  and  organ  size.  Although
it is difficult to generalize for all  radionuclides, in some cases
these differences tend to counterbalance each other.  For example,  the
ratio of minute volume to lung mass  is relatively constant  with age,
i.e., within a factor of two, so that the  ICRP adult model  for
Insoluble materials provides a reasonably  good estimate of  the average
annual dose throughout life.

     An exception is the thyroid where the very  young  have  a relatively
high uptake of radloiodine into a gland which is much  smaller  than  the
adult thyroid, as noted in Table F-l.  This results in a larger
childhood dose and an increased risk which persists throughout life.
Since this is a worst case situation, we have examined it with some
care, using the age-specific risk coefficients for thyroid  cancer in
Table V-14 of the BEIR-3 report (NAS80) and the  age-dependent  dose
model in ORNL84.  For iodine-131 ingestlon, the  estimated lifetime  risk
is increased by a factor of 1.56 due to the 30 percent increase in
lifetime dose over that obtained with the  ORNL adult model, c.f.
Appendix F.  Results are about the same for inhalation of iodine-131—
the estimated lifetime risk of fatal thyroid cancer is increased by a
factor of 1.63 for ORNL's age-dependent dose estimate.

     As noted in Appendix F, use of an age-dependent dosimetry for
other radionuclides has yielded much smaller increased doses relative
to adult models and therefore has little effect  on estimates of
lifetime risk.  In particular, the lung dose and risk resulting from
the inhalation of insoluble alpha particle emitters is nearly
unchanged.  The lifetime dose for an age-dependent dose model  is only
1.09 times greater than that calculated using an adult model
(Appendix F); the lifetime risk of lung cancer for this age-dependent
model is a factor of 1.16 greater than we calculate for life exposure
with the adult only model.

G.3  Fatal Cancer Risk Resulting from High-LET Radiations

      In this section we explain how EPA estimates the risk  of fatal
cancer resulting from exposure to high-LET radiations.   In  some cases,
ingestion and inhalation of alpha particle emitting radionuclides can
result in a relatively uniform exposure of specific body organs by
high-LET radiations.  Unlike exposures to X-rays and gamma  rays where the
resultant charged particle  flux results In linear energy transfers (LET)
of the order of 0.2 to 2 keV per micron In tissue,  5 MeV alpha particles
                                   G-20

-------
result in energy deposition at a track average rate  of  more  than 100 keV
per micron.  High-LET radiations have a larger Biological  effect per unit
dose (rad) than low-LET radiations.  How much greater depends on the
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 more  times greater than
low-LET radiations.

G.3.1  Quality Factors for Alpha Particles

     Charged particles have been assigned quality factors, Q, to account
for their efficiency in producing biological  damage. Unlike an RBE
value, which is for a specific and well-defined endpoint,  a  quality
factor is based on an average overall assessment by  radiation protection
experts of potential harm of a given radiation relative to X or gamma
radiation.  In 1977, the ICRP assigned a quality factor of 20 to alpha
particle irradiation from radionuclides (ICRP77). The  reasonableness of
this numerical factor for fatal radiogenic cancers at a particular site
is not well known, but it is probably conservative for  all sites and
highly conservative for some.

     The dose equivalent (in rem) is the 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 equal to 20 rem.  It should be noted  that prior to
ICRP Report 26 (ICRP79), the quality factor for alpha particle
irradiation was 10.  That is, the biological  effect  from a given dose of
alpha particle radiation was estimated to be 10 times that from an acute
dose of low-LET X-rays or gamma rays of the same magnitude in rad.  The
ICRP decision to increase this quality factor to 20  followed from their
decision to estimate the risk of low-LET radiations, in occupational
situations, on the assumption that biological effects were reduced at low
dose rates for low-LET radiation.  There is general  agreement that dose
rate effects do not occur for high-LET (alpha) radiations.  The new ICRP
quality factor for alpha particles of 20 largely compensates for the fact
that their low-LET risks are now based on an assumed dose rate reduction
factor of 2.5.  This DREF has been addressed in preparing EPA estimates
of the risk per rad for alpha particle doses described  below, in Section
G.3*3*

     In 1980 the ICRP published a task group report  "Biological Effects
of Inhaled Radionuclides" which compared the results of animal
experiments on radiocarcinogenesis 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."
                                   G-21

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G.3.2  Dose Response Function

     In the case of high-LET radiation,  a  linear dose response 1s
commonly observed 1n both human and animal  studies and the response £$
not reduced at low dose rates (NCRP80).   Some data on human lung cancer
ThUicate that the carcinogenic response  per unit dose of alpha
radiation is higher at low doses than higher ones (Ar81, Ho81, Wh83);
1n addition, some studies with animals show the same response pattern
(Ch81, U182).  We agree with the MAS BEIR-3 Committee that, "For
high-LET radiation, such as from Internally deposited alpha-emitting
radionuclides, the linear hypothesis 1s  less likely to lead to
overestimates of the risk and may, 1n fact, lead to underestimates"
(NAS80).  However, at low doses, departures from linearity are small
compared to the uncertainty 1n the human epidemiological data, and we
believe a linear response 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 painters who
have ingested alpha-emitting radium-226 (NAS80).  These data are
consistent with a dose-squared response (Ro78).  Consequently, the MAS
BEIR-3 Committee estimated bone cancer risk on the basis of both linear
and quadratic dose response functions.  However, as pointed out 1n
NAS80, the number of U.S. dial painters at risk who received less than
1000 rad was so small that the absence of excess bone cancer at low
doses 1s not statistically significant.  Therefore, the consistency of
this 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 radium-224 irradiation, observed In  sponctyHtics by Mays and
Spiess  (Ma83» NAS80), 1n a larger sample at much lower  doses,  is
consistent with a linear response.  Therefore, for high-LET radiations
EPA has used a linear response function to evaluate the risk of bone
cancer.

     Closely related to the choice of a dose  response function  is what
effect  the  rate at which a dose of h1gh-LET radiation is  delivered has
on its  carcinogenic potential.  This  Is a  very active area of  current
research.   There  Is good empirical evidence,  from both  human  and animal
studies, that repeated exposures to  radium-224 alpha  particles  is  5
times more  effective in Inducing bone sarcomas than  a single  exposure
which delivers the  same dose  (Ma83,  NAS80).   The  1980 MAS BEIR
Committee took this Into account In  their  estimates  of  bone cancer
fatalities  which  EPA is using.  We do not  know to what  extent,  if  any,
a similar enhancement of carclnogenicity may  occur  for  other  cancers
resulting  from  internally  deposited  alpha  particle  emitters.
Nevertheless, we  believe the  ICRP  quality  factor of 20  1s conservative,
even  at low dose  rates.
                                  G-22

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G.3.3  Assumptions Made by EPA for Evaluating  the  Dose from Alpha
       Particle Emitters:
     We have evaluated the risk to  specific  body  organs by applying  the
ICRP quality factor of 20 for alpha radiations  to the risk estimates .
for low dose rate low-LET radiations as  described above.  For some
organs this quality factor may be too conservative.   Several  authors
have noted that estimates of leukemia based  on  a  quality factor of 20
for bone marrow irradiation overpredicts the observed Incidence of
leukemia in persons receiving thorotrast (thorium oxides) (Mo79)  and in
the U.S. radium dial painters (Sp83). Nevertheless,  in view of the
paucity of applicable human data and the uncertainties discussed above,
the ICRP quality factor provides a  reasonable and prudent way of
evaluating the risk due to alpha emitters deposited within body organs.

     All of EPA risk estimates for  high-LET  radiations are based on  a
linear dose response function.  For bone cancer and  leukemia we use  the
absolute risk projection model described in  the previous section.  For
other cancers we use the arithmetic average  of  relative and absolute
risk projections.

     Table G-6 indicates the Agency's estimates of the risk of fatal
cancer due to a uniform organ dose  in various organs  from internally
deposited alpha particles.  These estimates  are for  lifetime doses at a
constant dose rate.  It was prepared by  multiplying  the average risk
(based on the linear model for a uniformly distributed whole-body dose
of low-LET radiation and a dose rate effectiveness factor of 2.5) by a
quality factor of 20 and then apportioning this risk  by organ, as
indicated in Table G-6.

     This procedure was not followed for bone cancer.  As outlined
above, the risk estimate for this cancer in  the BEIR-3 report 1s based
on data for high-LET (alpha) radiation and a direct  estimation of the
effect of the alpha radiation per high-LET rad.  Some readers may note
that the risk estimate in Table G-6, about 20 bone cancer fatalities
per 106 person rad, is less than the 27  fatalities listed in Table
A-27 of (NAS80) for alpha particles.  This is because the analysis in
Appendix A of NAS80, but not Chapter V of that  report, assumes that in
addition to a 2-year minimum induction period,  27 years are available
for cancer expression.  This is usually  not  the case for doses received
beyond middle age.  Hence, the estimated lifetime risk Is smaller when
it is based on a life table analysis that considers  lifetime exposure
in conjunction with death from all  causes.

G.4  Uncertainties in Risk Estimates for Radiogenic  Cancer

     As pointed out in the introduction  of this appendix, numerical
estimates of risks due to radiation are  neither extremely accurate nor
precise.  A numerical evaluation of radiogenic  cancer risks depends
both on epidemiological observations and a number of ad hoc assumptions
which are largely external to the observed data set.  "These assumptions
                                 G-23

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TABLE G-6:
Estimated number of cancer fatalities from a lifetime exposure  to
Internally  deposited ALPHA particle emitters
 Site
Proportional risk'3'
Fatalities per
106 person
Lung
Breast*0'
Red marrow(d)
Thyroid -
Bonefe)
Liver
Stomach
Intestine
Pancreas
Kidneys and
urinary tract
Other-Sum (total)
.21
.13
.16
.099
.009
.085
.084
.039
.058

.025
.11
460
290
350
220
20
190
190
90
130

55
250
     {^Proportion of whole body risk from Table G-3.
     JbJRounded to two figures.
     }cjAverage for both sexes.
      d Leukemia.
     
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G.4.1' Uncertainty of the Dose Response  Models  Due  to  Bias  In the
       A-bomb Dosimetry

     Although the BEIR-3 Committee's choice  of  a  linear-quadratic
response has gained considerable attention,  it  may  not be generally
appreciated that the BEIR-3 Committee's  numerical evaluations of dose
response functions for cancer due to low-LET radiation were based
exclusively on the cancer mortality of the A-bomb survivors.
Unfortunately, the dosimetry for A-bomb  survivors,  on  which the BEIR-3
Committee relied, has since been shown to have  large systematic errors
which serve to undermine the analyses made by the Committee.   As
outlined below, the mathematical analyses made  by the  Committee were
"constrained" to meet certain a priori assumptions. These  assumptions
have since been shown to be dotlbtful.

     A careful state-of-the-art evaluation of the dose to A-bomb
survivors was carried out by investigators from Oak Ridge National
Laboratory in the early 1960's (Au67, Au77). The results of these
studies resulted in a "T65" dose being assigned to  the dose (kerma)  in
free air at the location of each survivor for both  gamma rays and
neutrons.  A major conclusion of the ORNL study was that the mix of
gamma ray and neutron radiations was quite different in the two cities
where A-bombing occurred.  These results indicated  that at  Hiroshima,
the neutron dose was more important than the gamma  dose when the
greater biological efficiency of the high-LET radiations produced by
neutrons was taken into account.  Conversely, the neutron dose at
Nagasaki was shown to be negligible compared to the gamma dose for that
range of doses where there were a significant number of survivors.
Therefore, the 1980 BEIR Committee evaluated the cancer risks to the
survivors at Hiroshima on the assumption that the combined  effects of
gamma rays and particularly neutrons caused  the observed cancer
response.

     Since the BEIR-3 report was published,  it  has  become evident that
the organ doses due to neutrons at Hiroshima were overestimated by
about an order of magnitude, at distances where most of the irradiated
persons survived bomb blast and yet received significant doses,
1000-1500 meters.  In fact, the neutron  doses at Hiroshima  are quite
comparable to those previously assigned, at  similar distances, to
Nagasaki survivors (KeSla, KeBlb, RERF83, RERF84).   Moreover, there is
now grounds to believe the T65 estimates of gamma ray  doses in both
cities are also incorrect .(RERF83, RERF84).   While  several  factors need
further evaluation, reduction of the gamma  dose to  individual survivors
due to the local shielding provided by surrounding  structures, is
significant.  The important point, however,  is  that the overestimate of
the neutron dose to the Hiroshima survivors  led to the BEIR-3 Committee
attributing most of the risk to neutrons rather than gamma-rays.
Hence, they underestimated the risk for low-LET radiations by, as yet,
an unknown amount.
                                  G-25

-------
     For their analysis of the  A-bomb  survivor data, the BEIR-3.
Committee expanded the equations  for low-LET ra'dlations listed  1n
Section G.2,  Table G-l, to Include  a linear dose  response  function  for
neutrons:
1)  P(d.D) = cid +

2)  P(d,D) = c2d2

3)  P(d.D) = c3d +
                             k2D
                                   k3D
(G-2)

(G-3)

(G-4)
where d is the gamma dose and D.is that part  of dose  due  to  high-LET
radiations from neutron Interactions.   Note that in equation G-4 the
linear-quadratic (LQ) response, has two linear terms,  one for neutrons  and
one for gamma radiation.  In analyzing approximately  linear  data In terms
of equation G-4, the decision as to how much  of the observed linearity
should be assigned to the neutron or the gamma component, i.e, k3 and
c3, respectively, is crucial.  As shown below, the BEIR-3 Committee
attributed most of the observed radiogenic cancer to  a linear response  from
neutron doses which did not occur.

     The BEIR-3 Committee's general plan was  to examine the  dose response
for leukemia and for solid cancer separately  to find  statistically valid
estimates of the coefficients cj	04 and kj	k3 by means of
regression analyses.  The regressions were made after the data were
weighted in proportion to their statistical reliability; thus, Hiroshima
results dominate the analysis.  The T65 neutron and gamma doses to
individual survivors are highly correlated since both are strongly
decreasing functions of distance.  This makes accurate determination of the
coefficients in equation G-4 by means of a regression analysis extremely
difficult.   In addition, there is considerable sampling variation in the
A-bomb survivor data due to small sample size which exacerbates the
regression problem.  Herbert gives a  rigorous discussion of these problems
for the case of the A-bomb survivors  (He83).   Because of these and other
problems, agreement  between the observed response  for solid cancers and
that predicted by any of the dose response functions examined by the BEIR-3
Committee is not impressive.   For example, goodness of fit,  based on Chi
square, ranges from 0.20 for equation G-3 to 0.23  for equation G-4, to 0.30
for equation G-2 (Table V-ll in NA.S80).  For leukemia, the goodness of fit
between the  observed data and  that predicted by the regression analysis  is
better, e.g., 0.49 for  equations G-2  and G-3  (Table V8 in NAS80).

     The  Committee analyzed the A-bomb  survivor data in two separate sets,
I.e.,  first  leukemia and then  all cancer excluding leukemia  (solid
cancers).  Their treatment of  these two cases was  not equivalent.   Unlike
the analysis of  solid cancers, the Committee's  analysis  of  leukemia
considered the Nagasaki  and  Hiroshima data separately.   Their approach
                                    G-26

-------
(p. 342 in NAS80) appears to be  based  on  an  unpublished paper by
Charles Land and a published report  by Ishimaru  et  al. on estimating the
RBE of neutrons by comparing leukemia  mortality  TW  "Hiroshima to that in
Nagasaki (Is79).  Unlike the case for  solid  cancers,  (see below), the
Committee's regression analysis  of the leukemia  mortality data did  provide
stable values for all  of the coefficients in equation G-4,  and therefore  an
RBE for neutrons as a  function of dose, as *ell  as  the ratio of the linear
to the dose-squared terms for leukemia induction due to gamma rays,
     Estimating the linear-quadratic  response  coefficients for  solid
cancers proved to be less straightforward.   When the BEIR-3 analysis
attempted to fit the A-bomb survivor  data on sol id .cancers to a  .
linear-quadratic dose response function, they  found that the linear
response coefficient, 03 in equation  G-4, varied from  zero to 5.6
depending on the dose range considered.  Moreover, their best estimate  of
the coefficient for the dose-squared  term in equation  G-4, I.e., 04, was
zero, i.e., the best fit yielded a linear response.  Therefore, it was
decided that the observations on solid cancers were "not strong enough  to
provide stable estimates of low dose, low-LET  cancer risk when  analyzed in
this fashion," (NAS80, p. 186).

     As outlined in the BEIR-3 Report, the  Committee decided to use a
constrained regression analysis, that is, substitute some of the parameters
for equation G-4 found in their analysis of leukemia deaths to  the
regression analysis of the dose response for solid cancers.  That is, both
the neutron RBE at low dose (the ratio of the  coefficient ks to 03) and
the ratio of cj to 04, as estimated from the leukemia  data, were
assumed to apply to the induction of  fatal  solid cancers.  Regression
analyses that are constrained in this manner can yield much higher
estimates of precision than is warranted by the data,  as discussed by Land
and Pierce (La83).  They can also be  very misleading.  Herbert  has
discussed this point in detail as it  applies to the BEIR-3 regression
analysis (He83).  The BEIR-3 Committee's substitution  of the results of the
leukemia regression for the data on solid cancers allowed them  to make
stable estimates of C3, C4, and k3.  These  estimates became the basis
for the "preferred" linear quadratic  risk estimates for solid cancers
presented 1n NAS80, I.e., the LQ-L model, page 187.  (The response models
for solid cancers that are based on the Committee's constrained regression
analysis are designated with a bar In their 1980 report,  e.g., UPU and
L~L* )

     Given the Information discussed above, 1t Is possible  to see,  at  least
qualitatively, how the high bias 1n the estimated T65  neutron dose  to  the
Japanese survivors affects the 1980 BEIR Committee's  "preferred"  LQ
estimates of the risk coefficients for leukemia.  The  Committee's
age-adjusted risk coefficients for leukemia are listed In Table V-8 (NAS80,
page 184).  For the linear-quadratic response, k3, the neutron risk
coefficient 1s 27.5.  Tables A-ll (NAS80, page 341) and V-6 (NAS80, page
152) provide the estimates of neutron and gamma doses  to  the bone marrow of
                                   G-27

-------
Hiroshima survivors that  were used by  the  Committee.  Substituting these
doses In their risk equations (Table V-8)  Indicates that about 70 percent
of the leukemia deaths were ascribed to the  neutron dose component then
thought to be present at  Hiroshima.  As noted  above, subsequent research
indicates that the high-LET dose due to neutrons was actually much smaller

     It is not possible to accurately  quantify what effect the Committee's
use of these same coefficients had on  their  analysis of the  dose response
for solid cancers.  Equation V-10 for  solid  cancers, p. 187  1n NAS80,
indicates about 60 percent of the solid tumor  response was attributed  to
the T65 neutron dose; but this Is a minimum  estimate that Ignores the
effect of the assumed neutron doses on the value of k$ and the ratio of
€  to €.
     The BEIR-3 Committee's LQ-L model  assumes an  RBE  of  27.8 at  low
doses.  In the Committee's L-L linear response model,  the assumed RBE 1s
11.3.  Therefore, this linear model  is  considerably  less  sensitive to the
neutron dose component, assumed by the  Committee,  than their LQ-L model.
For either model, most of the A-bomb survivors'  radiogenic cancer was
ascribed to the T65 neutron doses at Hiroshima.

     There 1s no simple way of adjusting the 1980  BEIR risk estimates to
account for the risk they attributed to neutrons.  Adjustment of  neutron
doses alone is clearly Inappropriate, since there  is good reason  to believe
that T65 estimates of the dose due to gamma rays are also subject to
considerable change.  Moreover, not all of the individuals In a given T65
dose category will, necessarily, remain grouped together  after new
estimates of neutron and gamma doses are obtained.  Both  the numerator and
denominator 1n the ratio of observed to expected cases are subject to
change and indeed could change 1n opposite directions, a  fact not
considered In some preliminary (and premature) analyses (St81).
Nevertheless, it 1s reasonable to conclude that bias in the estimated
neutron doses at Hiroshima has led to considerable uncertainty in the
BEIR-3 risk estimates and also to a systematic underestimation of the risk
due to low-LET radiations.  For this reason we believe that estimates based
on the more conservative linear dose response should be given considerable
weight ^ll £ Xli tnose ma(*e using the BEIR-3 linear  quadratic models.

G.4.2  Sampling Variation

     In addition to the systematic bias 1n the BEIR-3 risk estimates for
low-LET radiation outlined above, the precision of the estimated linear and
quadratic risk coefficients in the BEIR-3 report is  poor  due to statistical
fluctuations due to sample size.  Recently, Land and Pierce have
reevaluated the precision of the BEIR-3 linear quadratic  risk estimates to
take Into account, at least partially, the Committee's use of a constrained
regression analysis (La83).  This new analysis indicates  that for the
BEIR-3 LQ-L model for leukemia, the standard deviation of the linear term
Is nearly as large as the risk coefficient Itself (jK).9 compared to a risk
coefficient of 1).  For the HPT model , solid cancer, the standard
deviation is +1.S compared to a risk coefficient of 1.6.
                                    G-28

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     It Is likely that at least part  of  the uncertainty attributed to
sampling variation in the BE3R-3 risk estimates'ls not due to  sample size
and other random factors but rather due  to the use of Incorrect dose
estimate for the A-bomb survivors.  The  correlation of neutron and
gamma-ray doses has been a major underlying cause of the uncertainty in
regression analysis using the T-65  doses.  Analyses of revised data with
much smaller neutron doses may result in better precision.  At present, we
have concluded that the BEIR-3 risk coefficients are uncertain by at least
a factor of 2, see below, as well as  being biased low by an additional
factor of 2 or more.

G.4.3  Uncertainties Arising from Model  Selection

     In addition to a dose response model, a  "transportation model" is
needed to apply the risks from an observed irradiated group to another
population having different demographic  characteristics.  A typical example
is the application of the Japanese  data  for A-bomb survivors to western
people.  Seymore Jablon, (Director  of the Medical Follow-up Agency of the
National Research Council, NAS) has called this the "transportation
problem," a helpful designation because  it is often confused with the-risk
projection problem described below.  However, there is more than a
geographic aspect to demographic characteristics.  The  "transportation
problem" includes estimating the risks for one sex based on data for
another and a consideration of habits influencing health status  such as
differences between smokers and nonsmokers.

     The BEIR-3 Committee addressed this problem in their  1980 report and
concluded, based largely on the breast cancer evidence, that the
appropriate way to transport the Japanese risk to the U.S. population was
to assume that the absolute risk over a  given observation  period was
transferable but that relative risk was  not.  Therefore, the Committee
calculated what the relative risk would be if the same  number  of excess
cancer deaths were observed in a U.S. population having the  same age
characteristics as the A-bomb survivors. The base line cancer rates  in  the
U.S. and Japan are quite different  for some  specific cancers so this  is  a
reasonable approach.  However, it contains the assumption  that while the
cancer initiation process Is the same in the  two countries,  the actual
number of radiogenic cancers that actually occur 1s the result of cancer
promotion, the Tatter being a culturally dependent variable.

     An alternative approach to solving the  "transportation  problem"  is
that of the 1972 NAS BEIR-1 Committee.  This  Committee  assumed relative
risks would be the same In the United States  and Japan  and transferred the
observed percentage increase directly to the  U.S. population.   We  have
compared estimates of the lifetime  risk for  these two treatments of the
"transportation problem" in order to  find out how sensitive  the BEIR-3
Committee risk estimates are to their assumptions.  To  do  this, we
calculated new relative risk estimates for solid cancers based on  the
age-specific cancer mortality of the  Japanese population rather than the
U.S. data used by the BEIR-3 Committee.  We  found that  this  alternative
                                   G-29

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approach did not have much effect on the  estimated  lifetime  risk  of  solid
radiogenic cancer, I.e., a change of 3 percent Tor  males,  and  17  percent
for females.  We have concluded that the  amount  of  uncertainty Introduced
by transporting cancer risks observed 1n  Japan to the  U.S. population  1s
small compared to other sources of uncertainty 1n this risk  assessment.
Base-line leukemia rates are about the same in the  countries,  so  we  believe
these risks are also "transportable."

     The last of the models needed to estimate risk 1s a  risk  projection
model.  As outlined in Section G.2, such  models  are used  to  project  what
future risks will be as an exposed population ages.  For  leukemia and  bone
cancer, where the expression time is not  for a full lifetime but  rather 25
years, absolute and relative risk projection models yield the  same number
of radiogenic cancers, but would distribute them somewhat differently  by
age.  For solid cancers, other than bone, the BEIR-3 Committee assumed -that
radiogenic cancers would occur throughout the lifetime.  This  makes  the
choice of projection model more critical, because  the relative risk
projection yields estimated risks about three times larger than that
obtained with an absolute risk projection, as shown in Table G-2.  Because
we have used the average of these two projections for solid cancers, we
believe this reduces the uncertainty from the choice of model  to about a
factor of 2 or perhaps less, depending on the age distribution of fatal
radiogenic cancer, as outlined in Section G.2 above.

     Similarly, there 1s as yet insufficient Information on radiosensltivity
as a function of the age at exposure.  The age-dependent risk coefficients
we have used are those presented In the BEIR-3  report.  As yet, there is
little Information on the ultimate effects of exposure during childhood.
As the A-bomb survivors' population ages, more  information will become
available on the cancer mortality of persons irradiated when they were
young.  Table G-2 Indicates that the more conservative BEIR-1 estimates for
the  effect  of childhood exposures would Increase BEIR-3 risk estimates by
about 40 percent.  As this is probably an upper limit, the lack of more
precise Information  Is  not a major source of uncertainty 1n estimates of
the  risk caused  by lifetime exposure.  Similarly, the BEIR-3 Committee did
not  calculate population risks for radiogenic cancer that Included in utero
radiation because they  felt the available data were unreliable.  We have
deferred to their judgment in this regard.  The BEIR-1 report did Include
in utero.cancer  risk.   These had little effect, 1 to  10 percent, on the
TTfetime  risk of cancer from lifetime exposure.  An effect this small is
not  significant  relative to other  sources of uncertainty 1n the risk
assessment.

Summary

     We can only  semi-quantitatively  estimate the  overall uncertainty in
the  risk  per  rad for low-LET radiations.  We expect that more quantitative
estimates of the  uncertainty will  be  possible only  after the  A-bomb dose
reassessment  is  completed  and the  A-bomb  survivor  data reanalyzed on  the
basis  of  the  new dose estimates.   It  should  be  noted,  however, that even  if
                                    G-30

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all systematic bias is removed from the new dos* estimates, there will
still be considerable random error in the dose estimate for each survivor.
This random error biases the estimated slope of the dose response curve so
that it is smaller than the true dose response (Da72,  Ma59).  The amount of
bias introduced depends on the size of the random error in the dose
estimates and their distribution which are unknown quantities at this stage
of the dose reassessment.

     The source of uncertainty in risk estimates for low-LET radiations can
be ranked as shown in Table G-7.
TABLE G-7:
A ranking of causes of uncertainty in estimates of the risk of cancer
         Source of uncertainty
Degree of uncertainty
     Choice of dose response model

     Slope of dose response resulting
      from sampling variation

     Choice of an average risk
      projection model

     Choice of transportation model

     A-bomb T-65 dosimetry
       ±250 percent^

       ^200 percent^)


       +100 percent(c>
        ^20 percent
(d)
       Plus only,
       amount unknown
     (a)For choices limited to BEIR-3 linear and linear quadratic
        models, see G.2.
     ^Estimate of 2 standard deviations for the BEIR-3 OJ" model (La83).
     jcjAverage of relative and absolute projection as described above.
     *dJFor the total of  all  cancers, not specific cancers.
    The estimates of uncertainty in Table G-7 are not wholly comparable and
must be interpreted carefully.   However,  they do have some illustrative
value, particularly when ordered in this  way.  The uncertainty listed for
the slope of dose response is a nominal value for the BEIR-3 linear
quadratic UJ" formulation (La83) 1n that it is only valid Insofar as the
Committee's assumptions are true.   It is  based on a two standard deviation
error so that the expectation that the error is less than indicated is 95
percent.  We do not believe the uncertainty in the BEIR-3 linear estimate,
     is'significantly smaller,  c.f. Tables V-9 and V-ll in NAS80.
                                   G-31

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     The other uncertainties listed 1n Table G-7 are quite different, being
more 1n the nature of Informed judgments  than the  result of a  statistical
analysis.  It 1s doubtful  that all  radiogenic cancers have the  same  type  of
response functions.  However, 1f they were  all  linear, as breast cancer and
thyroid appear to be, the  BEIR-3 linear quadratic  response model would
underestimate the response by 250 percent.   If  most cancers have a linear
quadratic response, or equivalently, a dose rate reduction factor equal to
the difference in slope at low doses between the BEIR-3  linear and linear
quadratic models, the use  of a linear model would  overestimate the response
by a factor of 2.5.  We believe that a factor of 250 percent  is a
conservative estimate of the uncertainty  introduced by the lack of data at
low dose rates.

     As discussed above, the uncertainty  due to the choice of an absolute
or a relative risk model is about a factor of 3.   The  use of  the average
risk for these two models reduces the uncertainty  in risk projection by
more than a factor of 2, since 1t 1s known that a  relative risk projection
is high for some kinds of cancer and that an absolute  risk projection 1s
low for others.

     The uncertainties listed in Table G-7 are  largely independent  of each
other and therefore unlikely to be correlated  in  sign.   Their root mean
square sum is about 300 percent, indicating the expectation  that calculated
risks would be within a factor of 3 or so of the  true  value.   This  result
is overly optimistic because it does not Include  consideration of  the
uncertainty introduced by the bias  in the A-bomb  dosimetry  or by the
constrained regression analysis used by the BEIR-3 Committee.

G.5  Other Radiation-Induced Health Effects

     The earliest  report of  radiation-induced  health  effects was in 1896
(Mo67), and It dealt with acute effects In skin caused by x-ray exposures.
Within the six-year period  following,  170  radiation-related skin damage
cases had been reported.  Such  Injury, like many  other acute effects, Is
the result of exposure to hundreds  or  thousands of rad.  Under normal
environmental exposure situations,  however, such exposure conditions are
not possible and therefore  will not be considered 1n assessing the risk to
the general population from radionuclide releases.

     Although  radiation-induced cardnogenesis was the first delayed health
effect  reported, radiation-Induced  genetic changes were reported early
ToolIn  1927,  H.J.  Muller  reported on x-ray Induced mutations In animals
and 1n  1928,  L.J.  Stadler reported  a  similar finding In plants (K162).   At
about the  same time,  radiation  effects on  the  developing embryo were
reported.  Case  reports In  1929 showed a high  rate of microcephaly  (small
head  size) and central  nervous  system disturbance and one case of skeletal
defects  1n children  Irradiated  In  utero  (UNSCEAR69).   These effects, at
unrecorded but  high  exposures,  appeared  to produce central nervous  system
and eye  defects  similar to  those  reported  In rats as early as  1922 _(Ru50).
                                    G-32

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    For purposes of assessing the risks of environmental exposure from
 radionuclide releases, the genetic effects and in utero developmental
 effects are the only health hazards other than cancer that are addressed in
 this  appendix.

 G*5-l  Types of Genetic Harm and Duration of Expression

    Genetic harm or the genetic effects of radiation exposure are those
 effects induced in the germ cells (eggs or sperm) of exposed individuals,
 which  are transmitted to and expressed only in their progeny and future
 generations.

    Of the possible consequences of radiation exposure, the genetic  risk is
 more  subtle than the somatic risk.  Genetic risk is incurred by fertile
 people when radiation damages the nucleus of the cells which become  their
 eggs  or sperm.  The damage, in the form of a mutation or a chromosome
 aberration, is transmitted to, and may be expressed in, a child conceived
 after the radiation exposure and in subsequent generations.  However, the
 damage may be expressed only after many generations, may.be lost by  chance,
 or, alternately, it may never be expressed because of failure to reproduce.

    EPA treats genetic risk as independent of somatic risk because,
 although  somatic risk is expressed in the person exposed, genetic risk is
 expressed only in progeny and, in general, over many subsequent generations.
.Moreover, the types of damage incurred often differ in kind from cancer and
 cancer death.  Historically, research on genetic effects and development of
 risk  estimates has 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 evaluating the hazard of radiation exposure
 include only those "disorders and traits that cause a serious handicap at
 some  time during lifetime"  (NAS80).  Genetic risk may result from one of
 several types of damage that ionizing radiation can cause in the DNA within
 eggs  and  sperm.  The types of damage usually considered are:  dominant and
 recessive mutations in autosomal chromosomes, mutations in sex-linked
 (x-linked) chromosomes, chromosome aberrations  (physical_rearrangement or
 removal of part of the genetic message on the chromosome or abnormal
 numbers of chromosomes), and irregularly inherited disorders (genetic
 conditions with complex causes, constitutional and degenerative diseases,
 etc.).

     Estimates of the genetic risk per generation are based on a 30-year
 reproductive generation.  That is, the median parental  age for production
 of children is age 30  (one-half the children are produced by persons less
 than  age  30, the other half by persons over age 30).  Thus, the radiation
 dose  accumulated up to age 30 is used to estimate the genetic risks. Using
 this  accumulated dose and the number of live births in  the population along
                                    G-33

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with the estimated genetic risk per unit dose,  1t 1s  possible to estimate
the total number of genetic effects per year,  tfiose 1n the first generation
and the total across all time.  Most genetic risk analyses have provided
such data.  EPA assessment of risks of genetic  effects Includes both first
generation estimates and total genetic burden estimates.

Direct and Indirect Methods of Obtaining Risk Coefficients for Genetic
Effects

    Genetic effects, as noted above, may occur in the offspring of the
exposed Individuals or they may be spread across all  succeeding
generations.  Two methods have been used to estimate the frequency of
mutations in the offspring of exposed persons,  direct and indirect.  In
either case, the starting point is data from animal studies, not data
obtained from studies of human populations.

    For a direct estimate, the starting point is the frequency of a
mutation per unit exposure in some experimental animal study.  The 1982
IMSCEAR  (UNSCEAR82) report gave an example of the direct method for
estimating induction of balanced reciprocal translocatlons  (a type of
chromosomal aberration) in males per  rad of low level, low-LET radiation.
      1)   Rate of induction in rhesus monkey
          Spermatogonia:  cytogenetic data

      2)   Rate of induction that relates to
          recoverable translocations in the FI
          (1st filial generation) progeny [divide
      .    (1) by 4]

      3)   Rate after low  dose rate X-rays:
          based on mouse  cytogenetic observations
          [divide (2) by  2]
      4)
      5)
      6)
Rate after chronic gamma-irradiation:
based on mouse cytogenetic observations
[divide (2) by 10]

Expected rate of unbalanced products:
[multiply (3) and (4) by 2]     for (3)
                                for (4)
                                                    Induction rate/rad
                                           0.86  x lO'4
                                           0.215 x 10-4
                                           0.1075 x 10-4
                                                    0,022 x  ID'4
                                                    0.215 x  10-4
                                                    0.043 x  ID'4
Expected frequency of congenital ly
malformed children in the Fjf assuming
that about 6 percent of unbalanced products
[item (5) above] contribute to this
          for low dose rate X-rays         1.3 x 10-6
          for chronic gamma radiation      "0.3 x 10~6
                                  G-34

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     For humans, UNSCEAR estimates  that  as  a  consequence of Induction
of balanced reciprocal translations  in exposed fathers, an estimated
0.3 to 1.3 congenital!,/ malformed children  would occur in each 10°
live births for every rad of parental  radiation exposure.

     A complete direct estimate of  genetic  effects would include
estimates, derived in a manner similar to that shown above for each
type of genetic damage.  These direct  estimates can be used to
calculate the risk of genetic effects  in the  first generation (Fi)
children of exposed parents.

     The indirect (or doubling dose) method of estimating genetic risk
also uses animal data but in a different way.  The 1980 BEIR-3 report
(NAS80) demonstrates how such estimates  are obtained.
     1)  Average radiation induced-mutation per
         gene for both sexes in mice [based on
         12 locus data in male mice]:   induction
         rate per rad

     2)  Estimated human spontaneous mutation
         rate per gene
     3)  Relative mutation risk in humans
         [divide (1) by (2)]

     4)  Doubling dose:  the exposure needed
         to double the human mutation rate
   0.25 x 10-7
   0.5 x 10~6 to
   0.5 x 10-5
   0.005 to 0.05
   200 to 20 rad
     The doubling dose can then be used to- estimate the equilibrium
genetic effects or the genetic burden in all  future generations caused
by the exposure of parents.  Since the genetic component of congenital
defects occurring in the population can be estimated by epidemiological
surveys, and this component is considered to be maintained at an
equilibrium level by mutations, a doubling dose of ionizing radiation
would double these genetic effects.  Dividing the number of the various
genetic effects in 106 live-births by the doubling dose yields the
estimate of genetic effects per rad.  For example:
    1)   Autosomal dominant and x-1inked
         diseases, current incidence

    2)   Estimated doubling dose

    3)   Estimate of induced autosomal
         dominant and x-1inked diseases
10,000 per 106
live births

20 to 200 rad

50 to 500 per 106
live births per rad of
parental exposure.
                                 G-35
                                                                                  r

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     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 1s large enough so that all  genetic  damage
can be expressed in future offspring.  Although 1t is basically  an
estimate of the total  genetic  burden across all future generations,  1t
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-3 committee geneticists estimated that one-sixth of the total
genetic burden of x-Hnked mutations would be expressed 1n the first
generation, five-sixths across all future generations.  EPA  assessment
of risks of genetic effects includes both first generation estimates
and total genetic burden estimates.

G.5.2  Estimates of Genetic Harm Resulting from Low-LET Radiations

     One of the first estimates  of genetic risk was made In  1956 by the
NAS Committee on the Biological  Effects of Atomic Radiation  (BEAR
Committee).  Based on Drosophila (fruit fly) data and other
considerations, the BEAR Genetics Committee estimated that 10 Roentgens
(10 R*) per generation continued indefinitely would lead to  about 5,000
new Instances of "tangible inherited defects" per 106 births, and
about one-tenth of them would  occur in the first generation  after the
irradiation began (NAS72).  The UNSCEAR addressed genetic risk in their
1958, 1962, and 1966 reports  (UNSCEAR58, 62, 66).  During this period,
they estimated one rad of low-LET radiation would cause a 1  percent to
10 percent increase in the spontaneous incidence of genetic  effects.

     In 1972, both the NAS BEIR Committee (NAS72) and UNSCEAR
(UNSCEAR72) reexamlned the question of genetic risks.  Although  there
were no definitive human data, additional Information was available on
the genetic effects of radiation on mammals and Insects.  In 1977,
UNSCEAR Devaluated the 1972  genetics estimates (UNSCEAR77).  Their new
estimates used recent Information on the current incidence of various
genetic conditions, along with additional data on radiation  exposure of
mice and marmosets and other considerations.

     In 1980, an ICRP Task Group (ICRPTG) summarized recommendations
that formed the basis for the genetic risk estimates published in ICRP
Report 26 (Of80).  These risk  estimates are based on data similar to
that used by the BEIR and UNSCEAR Committees, but with slightly
different assumptions and effect categories, Table G-8.
*R is the symbol for Roentgen, a unit of measurement of x-radiation,
equivalent to an absorbed dose in tissue of approximately 0.9 rad.
                                 G-36

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          Table  G-8.   ICRP  task  group estimate of number of cases
                      of  serious genetic  ill health in  liveborn  from
                      parents  Irradiated  with 10° man-rem  in  a
                      population of  constant size9
                      (Assumed doubling dose = 100 rad)
      Category  of
     genetic  effect
First generation
Equilibrium
 Unbalanced translocations:
 risk  of malformed liveborn          23

 Trisomics and XO                   30

 Simple dominants and sex-
 linked mutations                   20

 Dominants of incomplete
 penetrance and multifactorial
 disease maintained by mutation     16

 Multifactorial disease not
  maintained by mutation             0

 Recessive disease

     Total                          89
                              30

                              30


                             100



                             160


                              0



                             320
aThis 1s equivalent to effects per 10^ liveborn following an average
     parental  population exposure of 1 rem per 30-year generation,  as used
     by BEIR and UNSCEAR.
Source:  Of80.
    The 1980 MAS BEIR Committee revised genetic risk estimates BEIR-3
(NAS80).  The revision considered much of the same material  that was in
BEIR-1 (NAS72), the newer material considered by UNSCEAR in  1977
(UNSCEAR77), and some additional  data.  Estimates for the first generation
are about a factor of 2 smaller than reported in the BEIR-1  report.   For
all generations, the new estimates are essentially the same, Table G-9.

    The most recent genetic risk estimate, in the 1982 UNSCEAR Report
(UN82), Includes some new data on cells in culture and the results of
genetic experiments using primates rather than rodents, Table G-10.

    Although all of the reports described above used somewhat different
sources of information, there is reasonable agreement in the estimates
(Table G-ll).  Most of the difference is caused by the newer information
                                   G-37

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used In each report.   Note that all  estimates listed above are based on
the extrapolation of  animal data to  humans.  Groups differ In their
Interpretation of how genetic experiments  In animals might be expressed  1n
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.)
      Table G-9.  BEIR-3 estimates of genetic  effects  of  an  average
                  population exposure of 1  rem per 30-year generation
  Type of genetic
      disorder
Current Incidence
per 106 Hveborn
Effects per 106 Hveborn
 per rem per generation
Autosomal dominant
and x-1 Inked
Irregularly Inherited
Recessive
Chromosomal aberrations
10,000
90,000
1,100
6,000
First Generation
5-65
(not estimated)
Very few
Fewer than 10
Equilibrium
40-200
20-900
Very slow
Increase
Increases
only
slightly
      Total
  107,100
 5-75
60-1100
  Source:   NAS80.
                                    G-38
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        Table G-10.  UNSCEAR 1982 estimated effect of 1 rad per
                     generation of low dose or low dose rate,  low-LET
                     radiation on a population of 10° liveborn
                     according to the doubling dose method
                     (Assumed doubling dose = 100 rad)
 Disease classification   Current incidence
          Effect of 1 rad
          per generation
Autosomal dominant and
 x-linked diseases             10,000

Recessive diseases              2,500

Chromosomal diseases
   Structural                     400
   Numerical                    3,000
Congenital anomalies,
anomalies expressed later,
constitutional and
degenerative diseases          90,000

    Total                     105,900
First Generation  Equilibrium

      15              100

    Slight         slow increase
       2.4
    Probably very
    small
       4.5

      22
 45

149
Source:  (UNSCEAR82).
                                   G-39

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     Table  G-ll.   Summary of genetic risk estimates per 106 Hveborn for
                  an average population exposure of 1 rad of low dose or
                  low  dose  rate, low-LET radiation 1n a 30-year generation
      Source
                                  Serious  hereditary effects
                           First generation
                      Equilibrium
                   (all  generations)
 BEAR,  1956  (NAS72)

 BEIR-I,  1972  (NAS72)

 UNSCEAR,  1972 (UNSCEAR72)

 UNSCEAR,  1977 (UNSCEAR77)

 ICRPTG,  1980  (Of80)

 BEIR-3,  1980  (NAS80)

 UNSCEAR,  1982 (UNSCEAR82)
49a (12-200)

 9a (6-15)

63

89

19a (5-75)

22
500

300a (60-1500)

300

185

320

257a (60-1100)

149
  Numbers In parentheses are the range of estimates.

aGeometr1c Mean 1s calculated by taking the square root of the product
 of two numbers for which the mean is to be calculated.  The cube root
 of three numbers, etc.  In general,  It Is the Ntn root of the product
 of N numbers for which the mean is to be calculated.
                                   G-40

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     It should be noted that the genetic risk estimates summarized in
Table G-ll are for low-LET, low dose, and low dose rate Irradiation.
Much of the data were obtained from high dose rate studies,  and most
authors have used a sex-averaged 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, 77).  However, factors of 0.5 to 0.1 have also been used
in estimates of specific types of genetic damage (UNSCEAR72,77,82).

G.5.3  Estimates of Genetic Harm for High-LET 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 ratio of the dose (rad) of low-LET
radiation to the dose of high-LET radiation producing the same endpofnt
is called RBE and is a measure of the effectiveness of high-LET compared
to low-LET radiation in causing the same specific endpoint.

     Studies with the beta particle emitting isotopes carbon-14 and
tritium yielded RBEs of 1.0 and 0.7 to about 2.0, respectively
{UNSCEAR82).  At the present time, the RBE for genetic endpoints due to
beta particles is taken as one (UNSCEAR77.82).

     Studies of the RBE for alpha-emitting elements in germinal tissue
have used only plutonium-239.  Studies comparing cytogenetic endpoints
after chronic low dose rate gammma radiation exposure, or incorporation
of plutonium-239 in the mouse testis, have yielded RBEs of 23 to 50 for
the type of genetic injury  (reciprocal translocations) that might be
transmitted to liveborn offspring  (NAS80, UNSCEAR77,82).  However, an RBE
of 4 for plutonium-239 compared to chronic low-LET radiation was reported
for specific locus mutations observed in neonate mice  (NAS80).  Neutron
RBE, determined from cytogenetic studies in mice, also ranges from about
4 to 50  (UNSCEAR82, Gr83a, Ga82).  Most reports use an RBE of 20 to
convert  risk estimates for low dose  rate, low-LET  radiation to  risk
estimates  for high-LET radiation.

G.5.4  Uncertainty  in Estimates of Radiogenetic Harm

     Chromosomal damage and mutations have been demonstrated  in cells  In
culture,  in plants,  in insects, and  1n mammals  (UNSCEAR72,77,82).
Chromosome  studies  in peripheral blood  lymphocytes of  persons exposed to
 radiation  have  shown a dose-related  increase  in chromosome aberrations
 (structural damage  to chromosome)  (UNSCEAR82).   In a stucly of nuclear
dockyard workers exposed  to  external x-radiation at rates of  less than  5
rad per year, Evans, et al.  (Ev79)  found a significant increase in the
 Incidence  of  chromosome aberrations.  The increase appeared to  have  a
linear dependence  on cumulative  dose.   In a  stucjy  of people working  and
 living in  a high natural  background  area where  there was  both external
gamma-radiation  and internal  alpha-radiation,  Pohl-Ruling et  al.  (Po78)
                                   G-41

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reported a complex dose response curve.   For majnly  gamma-radiation
exposure (less than 10 percent alpha radiation)",  they  reported that  the
increase in chromosome aberrations Increased linearly  from 100 to 200
mrad per year then plateaued from 300 mrad to 2 rad  per year.   They
concluded:

         "From these data,  and data in the literature,  it  can  be
         concluded that the initial part of the dose-effect curve
         for chromosome aberrations is not linear or sigmoid with
         a threshold at the lowest dose, but rises sharply and
         passes into a complex upward form with a kind  of  plateau
         until it meets the linear curve of the high dose.

     Although chromosomal  damage in peripheral  blood lymphocytes  cannot
be used for predicting genetic risk in progeny of exposed  persons,  it
is believed by some to be  a direct expression of the damage, analogous
to that Induced In germ cells, resulting from the radiation exposure.
It is at least evidence that chromosome damage can occur  in vivo  in
humans.

     Although evidence from the genetic studies in Japan  falls short of
providing statistically significant conclusions,  all indicators support
the hypothesis that genetic damage resulted from the radiation exposure
(ScSJb, Sa82).  While these data give rise to estimates of the doubling
dose (see below) and probabilities of mutation per locus  per rad  that
have large errors, there Is no reason to believe that  they are biased,
and they are adequate to recommend the elimination of  some previously
conjectured values.  However, In the sources of numerical  risk
estimates used in this document, human genetic risks following
radiation exposure are based on extrapolations from animal data.   As
genetic studies proceeded,  emphasis has shifted from Drosophlla (fruit
flies) to mammalian species in attempts to find an experimental system
which would reasonably project what might happen in humans.

     For example, Van Buul  (Va80) reported the slope (b)  of the linear
regression, Y = a + bD, for Induction of reciprocal  translations 1n
spermatogonia (one of the  stages of sperm development)  In various
species as follows:

     ~~~~:       b x 104 + sd x  104
Rhesus monkey
Mouse
Rabbit
Guinea Pig
Marmoset
Human
0.86 + U.U4
1.29 + 0.02
1.48 ^0. 13
0.91 7 0.10
7.44 + 0.95
3.40 + 0.72

to 2.90 + 0.34
^~



These data indicate that animal-based estimates for this type of genetic
effect would be within a factor of 4 of the true human value.  In this
case most of the animal results would underestimate the risk in humans.
                                   G-42

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     However,  when risk estimates such  as  this  are  used  in  direct
estimation of  risk for the first generation,  the  total uncertainty in the
estimate becomes indeterminate.   Even  if studies  have  been  made  in a
species which  can predict the dose response and risk coefficient for  a
specific-radiation induced genetic damage, there  is no certainty that it
predicts the response for all genetic  damage  of that type.   In addition,
as shown in the example from the 1982  UNSCEAR report  (UNSCEAR82) in
Section G.5.1, additional assumptions  based on observations,  usually  in
other animal species, are used to adjust the  risk coefficient to what is
expected for humans.  The uncertainty  in these extrapolations has not been
quantified.

     A rough estimate of the uncertainty can  be obtained by comparing
direct estimates of risk for the first generation with doubling-dose
estimates in the 1977 UNSCEAR report (UNSCEAR77).  The estimates differ by
a factor between 2 and 6 with the direct estimate usually smaller than the
doubling dose estimate.

     A basic assumption in the doubling-dose  method of estimation is  that
there is a proportionality between radiation  induced  and spontaneous
mutation rates.  Some of the uncertainty was  removed  in  the 1982 UNSCEAR
report with the observation that in two test  systems  (fruit flies and
bacteria), there is a proportionality  between spontaneous and induced
mutation rates at a number of individual gene sites.   There is still  some
question as to whether the sites that  have been examined are representa-
tive of all sites and all gene loci or not.   The  doubling dose estimate
dose, however, seems better supported  than the direct estimate.

     While there is still some uncertainty as to  what should be doubled,
future studies on genetic conditions and diseases can only increase the
total number of such conditions.  Every report, from  the 1972 BEIR and
1958 UNSCEAR reports to the most recent, has  listed an increased number of
conditions and diseases which have a genetic  component.

     Observations on Human Populations

     As noted earlier, the genetic risk estimates are based on interpreta-
tion of animal experiments as applied to data on  naturally-occurring  .
hereditary diseases and defects  in man.  A study  of birth cohorts was
initiated in the Japanese A-bomb survivors in mid-1946.   This resulted  in
a detailed monograph by Neel and Schull (Ne56) which  outlined the
background of the first study and made a detailed analysis of the findings
to January 1954 when the  study terminated.  The authors concluded "•   •  •
under circumstances where, on the basis of what is known concerning the
radiation genetics of mammals,  it appears unlikely that conspicuous
genetic effects of the atomic bombs could be demonstrated, such effects
have in fact not been demonstrated.  The  present stucjy can in no way  be
interpreted to mean that  there were no mutations induced in the survivors
of the atomic blasts.  Neither,  on the other hand, is the reverse
interpretation - that of  mutation production - permissible from this
series of observations •  •  •.   We are left with inconclusive findings,
albeit findings which permit us  to set confidence  limits." (Ne56).
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Further, 1t appeared that 1t was improbable that human genes were so
sensitive that exposures as low as 3 R, or even 10 R,  would double the
mutation rate.  While this first stuc(y addressed a number of endpoints
such as :  sex ratio, malformations, pre- and perinatal  mortality and
anthropometric data, subsequent studies have addressed these and other
endpoints.  The most recent reports on this birth cohort of 70,082 persons
have attempted to estimate the minimum doubling dose for genetic effects
in humans (ScSla, Sa82).

     Data on four endpoints have been reviewed for this birth cohort.
Frequency of stillbirths, major congenital defects, prenata-1 death, and
frequency of death prior to age 17 have been examined in the entire
cohort.  Frequency of cytogenetic aberrations (sex chromosome aneuploidy)
and frequency of biochemical variants (a variant enzyme or protein
electrophoresls pattern) have been measured on large subsets of this
cohort.

     Although the updated data reported appear to suggest radiation
effects have occurred, the numbers are small and not statistically
significant.  Overall, the estimated doubling dose for low-LET radiation
at high doses and dose rates for human genetic effects is about 156 rem
(ScSla) or 250 rem  (Sa82).  As noted above, animal studies indicate that
chronic exposures to low-LET radiation would be less hazardous by a factor
of 3 (NAS72, 80).   This would increase the estimated doubling dose to 468
rem to 750 rem, respectively.  These recent reports suggest the minimum
doubling dose for humans may be 4 to 7 times higher than those in Table
G-ll (based on animal data).  It would be premature to reach a firm
decision on the exact amount since these reports are based on the T65D
dosimetry in Japan  (see Section G.2) which Is being revised.  However, we
believe EPA estimates of genetic risks will prove to be very conservative
even when the dosimetry of A-bomb survivors Is revised.

     EPA is using the geometric mean of the BE1R-3 range of doubling
doses, about  110 rad.  The minimum doubling dose reported above 1s 4 to 7
times greater.   It  Is unlikely that dose estimates for Japanese survivors
will change by this much  (RERF83, 84).  Therefore, EPA believes the
estimate of a doubling of about 100 rad will continue to be a conservative
estimate.

     Ranges of Estimates Provided by Various Models

     EPA has continued to follow the recommendations of the 1980  BEIR-3
committee and use a linear  nonthreshold model for estimating genetic
effects.  Although,  as pointed out by the  1982 UNSCEAR committee, there
are a number  of models other than linear  (Y = c  + ad), e.g., linear
quadratic  (Y  = c +  bD + eDz), quadratic  (Y = k + fD2), even power
function  (Y = k  + gDn)*.  However, there are strong data to support  the
     *Y  1s yield  of  genetic  effects;  D  is  radiation dose; c, C,  k, and  K
 are  spontaneous incidence  constants for genetic effects; and a,  b, e, f,
 g, and h are  the  rate  constants  for radiation  induced genetic effects,

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hypothesis that mutations themselves are  single, track  events.   That  is,
the mutations follow a linear dose response function while the observed
mutation rate shows the influence of other factors,  and may be nonlinear
(UNSCEAR82).

     Most of the arguments for a nonlinear dose response have  been based
on target theory (Le62) or microdosimetric site theory (Ke72).  However,
other theories based on biology [e.g.,  enzyme induction-saturation
(Go80,82), repair-misrepair (To80)] could also provide models  that fit the
observed data.  There is still much disagreement on  which dose response
model is appropriate for estimating genetic effects  in humans.  Until
there is more consensus, the linear nonthreshold model appears to be a
prudent approach that will not underestimate the risks.

     The agreement in estimates made on a linear nonthreshold  model  in
various reports is reasonably good.  Even though 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 G-ll).  For the most recent, more comparable
estimates, the range is a factor of 2 to  4 (see ICRPTG, BEIR-3 and
UNSCEAR 1982 in Table G-ll).

G.5.5  The EPA Genetic Risk Estimate

     There is no compelling evidence for  preferring  any one set of the
genetic risk estimates listed in Table G-ll.  EPA has  used the estimates
from BEIR-3 (NAS80).  These "indirect"  estimates are calculated using the
normal prevalence of genetic defects and  the dose that is considered to
double this risk.  The WAS estimates which EPA uses  are based  on a
"doubling dose" range with a lower bound  of 50 rem and an upper bound of
250 rem.  We prefer these risk estimates  to those made by the  ICRP task
group (Of80), which used a "direct" estimate because the ICRPTG tabulation
combines "direct" estimates for some types of genetic  damage with doubling
dose estimates for others.  We also prefer the BEIR-3  risk estimates to
the "direct" estimates of UNSCEAR 1982 which tabulates genetic risk
separately by the direct method and by the doubling  dose method.  The risk
estimated by the direct method does not include the  same types of damage
estimated by doubling doses and was not considered further. Moreover, the
BEIR-3 genetic risk estimates provide a better estimate of uncertainty
than the UNSCEAR 1982 and ICRPTG estimates because the BEIR-3  Committee
assigned a range of uncertainty for multifactorial diseases (>5 percent  to
<50 percent) which reflects the uncertainty in the numbers better than the
other estimates do (5 percent and 10 percent, respectively).

     In developing the average mutation rate for the two sexes used in the
calculation of the relative mutation risk, the BEIR-3  Committee postulated
that the induced mutation rate 1n females was about  40 percent of that in
males (NAS80).  Recent studies by Dobson  et al. suggest that the
assumption was invalid and that human oocytes should have a risk
equivalent to that of human spermatogonia.  This would increase the risk
estimate obtained from doubling-dose methods by a factor of 1.43 (Do83a,
Do83b, Do84a, Do84b).

                                   G-45

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     We recognize, however,  that the  use  of the doubling-dose  concept  does
assume that radiation-Induced genetic damage' 1s 1n  some  way  proportional
to "spontaneous" damage.  As noted earlier,  the recent evidence obtained
1n Insects (prosophila) and bacteria  (E.  coll)  supports  the  hypothesis
that, with the exception of "hot spots'nr"for mutation, the radiation-
induced mutation rate is proportional to  the spontaneous rate  (UNSCEAR82).
No proof that this is also true in mammals is available  yet.

     The BEIR-3 estimates give a considerable range.   To express the  range
as a single estimate, the geometric mean  of the range  is used, a method
first recommended by UNSCEAR (UNSCEAR58)  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 question of RBE for high-LET radiation 1s more  difficult.  As
noted above, estimated RBEs for plutonlum-239 alphas versus chronic  gamma
radiation for reciprocal translocations as determined by cytogenetic
analyses are between 23 and 50 (NAS80, UNSCEAR82).  However, the observed
RBE for single locus mutations in developing offspring of male mice  given
pluton1um-239 compared to those given X-ray irradiation  is 4 (NAS80).  The
average of RBEs for these reciprocal translocations for specific locus
mutations is 20.25.  Since  reported neutron RBEs are similar to those
listed above for  plutonium-239 alpha radiation, we use an RBE of 20 to
estimate genetic  risks for  all high-LET radiations.  This- is consistent
with the RBE for  high-LET particles recommended for estimated genetic
risks associated  with  space flight (Gr83b).

     Genetic risk estimates used by EPA for high- and low-LET radiations
are  listed 1n Table G-12.   As noted earlier, EPA uses the dose received
before age 30 in  assessing  genetic risks.

     The EPA estimates  in Table G-12 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 magnitude of the
possible error  is indeterminable.  The study with the largest data base,
the  Japanese A-bomb survivors,  appears, at best, to provide only an
estimate of the minimum doubling  dose which calculates the  maximum
estimate of genetic risk  In man.   However, doubling-dose  estimates are
also uncertain  because the  number  of human disorders having a recognized
genetic component is constantly  Increasing,  and the type  of genetic damage
implicated 1n a specific  disorder  may  change.   The combined uncertainties
in  doubling dose  estimates  and  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  was due to
recessive  mutations which would eventually be  eliminated.  To  what extent
this occurs will  depend on medical practices 1n the future.  It 1s
possible,  as  our  knowledge of medicine Improves,  that recessive hereditary
 defects will  be carried on for many  more generations than assumed by  the
BEIR Committee.
                                    G-46

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   Table G-12.  Estimated frequency of genetic.disorders in a birth cohort
                due to exposure of the parents to 1 rad per generation
     Radiation
                                      Serious Heritable Disorders
                                       (Cases per 106 liveborn)
                             First Generation
                             low3        highb
All Generations
lowa      high6
Low Dose Rate, Low-LET
High Dose Rate, Low-LET
High-LET
20
60
400
30
90
600
260
780
5200
370
1110
7400
aFemale sensitivity to induction of genetic effects is 40 percent as
 great as that of males.
^Female sensitivity to induction of genetic effects is equal  to that of
 males.
     The relative risk of high-LET radiation compared to low-dose-rate,
low-LET radiation (RBE) is also uncertain.   The data are sparse,  and
different studies often used different endpoints.   In addition,  the
microscopic dosimetry, i.e., the actual  absorbed dose in the cells at
risk, is poorly known.  However, the RBE estimate used by EPA should be
within a factor of 5 of the true RBE for high-LET radiation.

G.5.6  Teratogenic Effects

     Although human teratogenesis (congenital  abnormalities or defects)
associated with x-ray exposure has a long history, the early literature
deals mostly with case reports.  Stettner reported a case in 1921 (St21)
and  Murphy and Goldstein studied a series  of pregnancies in which 18 of
the children born to 76 irradiated mothers  were microcephalic {Mu29,
Go29).  However, the irradiation exposures  were high.

     In 1930, Murphy exposed some rats to X-rays at doses of 200 R to
1600 R.  Thirty-four of 120 exposed females had litters, and 5 of the
litters had animals with developmental  defects (Mu30).  He felt that this
stucly 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 interest
in radiation hazards caused by the explosion of nuclear weapons  in 1945
(Ja70).
                                  G-47

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     Much of the work  done after World War II  was  done  1n mice  (Ru50,
Ru54, Ru56) and rats (W154, H154).   Early studfes,  at relatively  high
radiation exposures, 25 R and above, established  sone dose  response
relationships.   More importantly, they established the  time table of
sensitivity of  the developing rodent embryo and fetus to radiation
effects (Ru54,  Hi53, Se69, Hi66).

     Rugh, in his review of radiation teratogenesls (Ru70)  listed the
reported mammalian anomalies and the exposure  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
from about 6 weeks gestational age until  birth could lead to functional
defects.  In a  later review (Ru71), he suggested  structural defects  in
the skeleton might be  Induced as late as  the 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 are In terms of equivalent stages of
mouse-human development.  Estimates of equivalent gestational age are  not
very accurate.

     In the reports of animal studies it appeared as if teratologic
effects, other than perhaps growth retardation, had a  threshold for
induction of effects (Ru54, Ru53, W154).   However, Ohzu (Oh65)  showed
that doses as low as 5 R to preimplantation mouse embryos caused
Increased resorption of implanted embryos and structural  abnormalities 1n
survivors.  Then 1n 1970, Jacobsen (Ja70) reported a stucly  In which  mice
were exposed to 5, 20 or 100 R on the 8th day of  pregnancy.  He concluded
that the dose-response function for Induction of  skeletal effects was
linear, or nearly linear, with no observable threshold.  This appears
consistent with a report by Russell (Ru57), which suggested a threshold
for some effects whereas others appeared linear.

     Rugh (Ru71) suggested there may be no threshold for  radiation-
Induced congenital effects 1n the early human fetus.  In  the case of
microcephaly (small head size) and mental retardation,  at least this may
be the case.  For other teratogenic effects, the  dose  response 1n humans
1s unknown.  In 1978,  .Michel and Fritz-N1ggl1 (M178) 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 1f there was concurrent exposure to
radlosensitizing chemicals such as lodoacetlmide or tetracycllne  (M178).

     One of the problems with the teratologic studies 1n animals 1s 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
which 1s consistently dependent on the stage of embryonic  development at
                                   G-48

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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 stage of development  produces changes only  in  components  at
their peak sensitivity, higher doses may  induce  additional  abnormalities
which have peak sensitivity at other stages  of development, and may
further modify expression of the changes  induced in  parts of the  embryo
at peak sensitivity during the time  of irradiation.   In  the first case,
damage may be to primordial cells  themselves, while  in the  second, the
damage may lead indirectly to the  same or different  endpoints.

     The embry'o/fetus starts as  a  single  fertilized  egg  and divides  and
differentiates to produce the normal infant  at term.   (The  embryonic
period, when organs develop, is  the  period from  conception  through 7
weeks gestational age.   The fetal  period, a  time of  in utero growth, is
the period from 8 weeks gestational  age to birth.) THe  different organ
and tissue primordia develop independently and at  different rates.
However, they are in contact through chemical induction  or  evaporation
(Ar54).  These chemical messages between  cells are important in bringing
about orderly development and the  correct timing and fitting together of
parts of organs or organisms.  While radiation can disrupt  this pattern,
interpretation of the response may be difficult.  Since  the cells in the
embryo/fetus differentiate, divide,  and proliferate  at different  times
during gestation and at different  rates,  gestational  times  when cells of
specific organs or tissues reach maximum  sensitivity  to  radiation are
different.  Each embryo/fetus has  a  different timetable.  In fact, each
half (left/right) of an embryo/fetus may  have a  slightly different
timetable.

     In addition, there is a continuum of variation  from the hypothetical
normal to the extreme deviant, which is obviously  recognizable.   There is
no logical place to draw a line  of separation between normal and
abnormal.  The distinction between minor  variations  of normal  and frank
malformation, therefore,  is an arbitrary  one, and  each investigator  must
establish his own criteria and apply them to spontaneous and induced
abnormalities alike (HWC73).  For  example, some  classify mental
retardation as IQ 80 or lower, some  classify on  ability  to  converse  or
hold a job, some on the basis of the need to be  institutionalized.

     Because of the problems in interpretation listed above, it appears a
pragmatic approach is useful.  The dose response should  be  given  as  the
simplest function that fits the data, often  linear or linear with a
threshold.  No attempt should be made to  develop complex dose-response
models unless the evidence is unequivocal.

     The first report of congenital  abnormalities  in children  exposed
in utero to radiation from atomic  bombs was  that of  Plummer (P152).   In
tFis selected group, twelve children with microcephaly of which  10 also
had mental retardation had been identified in  Hiroshima  in  the in utero
exposed survivors.  They  were found  as part  of a program started  in  1950
to stucjy children exposed in the first trimester of  gestation.  In 1955
the program was expanded to include  all survivors  exposed in utero.
                                  G-49

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     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 incidence of microcephaly
and mental retardation have been investigated to any  great extent.   In
the most recent report, Otake and Schull  (Ot83) showed that mental
retardation was 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 a linear dose-response relationship for
induction of mental retardation  that had a slope yielding a tentative
estimate of doubling dose for mental retardation of about 2 rad, fetal-
absorbed dose (Ot83).   Classification as mentally  retarded was based on
"unable to perform simple calculations, to care for himself or herself,
or 1f he or she was completely unmanageable or  had been
institutionalized" (Ot83).

     Estimates of the risk of mental retardation for a rad of
embryo/fetus exposure in the U.S. population can be derived by three
methods.  The first and easiest method is to use the absolute risk
calculated by Otake and Schull for the Japanese survivors  (Ot84).  A
second method 1s to use the doubling dose calculated by Otake and Schull
(Ot83) times the incidence of mental retardation per 103 live births.
Unfortunately, a number of assumptions must be  made to establish the
incidence of mental retardation per 103 live births.  Mental
retardation may be classified as mild  (IQ 50-70),  moderate (IQ 35-49),
severe  (IQ 20-34) and profound (IQ  <20) (WH075).  However, some
investigators use only mild mental  retardation  (IQ 50-70)  and severe
mental  retardation (IQ <50) as classes (Ha81, St84).  Mental retardation
1s 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 must be estimated.   In like
manner  since mental retardation caused before birth may be due to genetic
conditions, Infections, physiologic conditions, etc., the  fraction
related to unknown causes during gestation must be estimated.  This Is
the fraction that might possibly be doubled by  radiation exposure.

     A  third method to estimate the risk Is Indirectly using the
relationship of microcephaly and mental retardation  reported  in the
Japanese  survivors (Wo65, Ot83).   If head size  is assumed  to be normally
                                   G-50

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distributed, then the fraction of the population with a head size 2 or 3
standard deviations smaller than average can be "obtained from statistical
tables.  The fraction of 103 liveborn with microcephaly multiplied by
the proportion of mental retardation associated with that head size
yields an estimate of the incidence of mental retardation per 10^ live
births, which can then be used with the doubling dose to estimate the
risk as described above.

     Risk estimates for mental retardation are derived below for
comparison purposes using each of the three methods described above.
A.
Estimate of Incidence Per Rad Based on Direct Application of the
Slope of the Japanese Data       "                    '•	
     Otake and Schull (Ot84) gave an estimate of 'The Relationship of
Mental Retardation to Absorbed Fetal Exposure in the "Sensitive" Period
When All "Controls" are Combined.1  The estimate of 0.416 cases of mental
retardation per 100 rad could be directly applicable to a U.S.
population.  In this case the risk estimate would be about:

     4 cases of mental retardation per rad per 1000 live births.

B-  Estimate of Incidence Per Rad Based on the Doubling Dose

     The Otake and Schull report (Ot83) suggested the doubling dose for
mental retardation was about 2 rad fetal  absorbed dose or about a 50
percent increase in mental retardation per rad.  It would seem reasonable
that this doubling dose would apply only  to ideopathic cases of mental
retardation caused during gestation.  That is, those which have no known
genetic, viral, bacterial, etc., cause.

     Data from studies of the prevalence  of mental  retardation in school
age populations in developed countries suggest a prevalence of
2.8 cases/1000 (Uppsala County, Sweden) to 7.4 cases/1000 (Amsterdam,
Holland) of severe mental retardation, with a mean of about 4.3 + 1.3
cases/1000 (St84).  Where data are available for males and females
separately, the male rate is about 30 percent higher than the female rate
(St84).  Historically, the prevalence of  mild mental retardation has been
6 to 10 times greater than that of severe mental retardation.  But in
recent Swedish studies, the rates of prevalence of mild and severe mental
retardation have been similar (St84).  This was suggested to be due to  a
decline in the "cultural-familial syndrome."  That is, improved
nutrition, decline in infection and diseases of childhood, increased
social and intellectual stimulation, etc., combined to reduce the
proportion of• nonorganic mental retardation and, therefore, the
prevalence of mild mental retardation (St84).
                                               i
     In studies of the causes of mental retardation, 23 percent to 42
percent of the mental retardation has no  identified cause (Gu77, Ha81,
St84).  It is this portion of the mental  retardation which may be
                                  6-51

-------
susceptible to Increase from radiation exposure of the embryo/fetus.
In that case,  the prevalence of Ideopathic mental retardation would.be
0.6 to 3.1 cases per 1000 of severe mental retardation and perhaps  an
equal number of cases of mild mental  retardation.

     For purposes of estimating the effects  of radiation  exposure of the
embryo/fetus,  a risk of spontaneous idoopathic mental retardation of 1  to
6 per 1000 will be used.  If this spontaneous  ideopathic  mental
retardation can be increased by radiation the  estimate would  be:

        (1 to 6 cases per 1000 live births){0.5  Increase  per  rad)

or about 0.5 to 3 cases of mental retardation  per rad per 1000  live
births.

     This estimate may be biased low because mental  retardation induced
during gestation is often associated with high childhood  death  rate
(St84).   If this is generally true for ideopathic causes  of  mental
retardation, It would cause an underestimation of the risk.

C.   Estimate of  Incidence Per Rad Based on Incidence of Microcephaly

     1)  Of live born children, 2.275 percent  will  have  a head
circumference  2  standard deviations or more smaller than  average,  0.621
percent will have a head circumference 2.5 standard deviations  or more
smaller than average, and 0.135 percent will have a head  circumference 3
standard  deviations or more smaller than average (statistical estimate
based on  a normal distribution).

     2)   There is evidence  1n a nonselected group of 9,379 children that
mental retardation can be estimated using incidence of microcephaly,  even
though head circumference In the absence of other supporting data, e.g.,
height or proportion,  Is an uncertain indicator of mental retardation.
Based on  a  study of  9,379 children, Nelson and Deutschberger (Ne70)
concluded that about  half of the children with a head circumference 2.5
standard  deviations  or more smaller than average had IQs of 79 or  lower.
Since 0.67  percent of those studied were in this group, the observed
number is about what  would  be  expected based on the normal distribution
of head  size  in a population,  0.62 percent.  The estimated incidence of
mental retardation  per live birth  in  a population would be:

            (6.7 cases of microcephaly per 1000 live births) x
            0.5
                 cases  of mental  retardation
                     case  of microcephaly

 or about 3.4 cases of mental  retardation  per  1000  live  births.
                                    G-52

-------
     3)  A first approximation of risk of mental retardation might then be

           (3.4 cases of mental retardation per 1000 live births)

                          (0.5 increase per rad)

or about 2 cases of mental retardation per 1000 live births per rad.

     Both microcephaly and mental retardation were increased in Japanese
survivors (Wo65, Wo66).  However, the relationship of mental retardation
to microcephaly in Japanese A-bomb survivor data is not1 clear.   Estimates
range from about half of those with head sizes 2 or more standard
deviations smaller than average having mental retardation (RERF78), a
result similar to that observed by Nelson and Deutschberger (Ne70), to
about ten percent of those with small head size having mental  retardation
(Wo66).  Therefore, the above estimate based on the incidence of
microcephaly in a population should be a reasonable estimate of the risk
from radiation.

Summary of the Calculated Risk of Mental Retardation

     The risk of increased mental retardation per rad of embryo/fetus
exposure during the 8- to 15-week gestational period estimated above
ranges from about 5 x 10~4 to 4 x 10~3 cases per live birth, the
largest being a direct estimate.  The geometric mean of these estimates^is
1.4 x 10~3; the arithmetic mean is 2.4 x 10"3 cases per live birth.

     All the estimates derived above by any of the three methods are in
the same range as an earlier UNSCEAR (UNSCEAR77) estimate of an increase
of 1 x 10'3 cases of mental retardation per rad per live birth.  The
UNSCEAR estimate, however, did not consider gestational age at the time of
exposure.  The Otake and Schull report (Ot83) did address gestational age
and estimated a higher risk, but a narrower window of susceptibility.

     If the estimates are applicable, the 15 mrad of low-LET background
radiation delivered during the 8- to 15-week gestational age-sensitive
period could, induce a risk of 6 x 10'5 to 7.5 x 10'° cases of mental
retardation per live birth.  This can be compared to an estimate of a
spontaneous occurrence of 1.5 x 10"z to 3.4 x 10~3 cases of mental
retardation per live birth.

     Japanese A-bomb survivors exposed in utero also showed a number of
structural abnormalities and, particularly in those who were
microcephalic, retarded growth (Wo65).  No estimate has been made of the
radiation-related incidence or dose-response relationships for these
abnormalities.  However, UNSCEAR (UNSCEAR77) made a very tentative
estimate based on animal studies that the increased Incidence of  ;
structural abnormalities in animals may be 5 x 10~3 cases per R per live
born, but stated that projection to humans was unwarranted.  In any event,
the available human data cannot show whether the risk estimates derived
from high dose animal data overestimates the risk in humans.
                                   G-53

-------
     It should be noted that  all  of  the  above  estimates  are  based on  high
dose rate low-LET exposure.   UNSCEAR 1n  1977 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 rate  or by
         fractionating the dose.   However, deviations from this
         trend have been well documented in a  few instances  and
         are not inconsistent with the knowledge about
         mechanisms of the teratogenic effects.   It is therefore
         Impossible to assume that dose rate  and fractlonatlon
         factors have the same Influence on all  teratological
         effects." (UNSCEAR77).

     From this analysis, EPA has  concluded that a range of risk is
4 x 10-3 to 5 x 10"* cases of mental retardation per live birth per
rad of low-LET radiation delivered between weeks 8 and 15 of gestation
with no threshold Identified at this time.

     No attempt can be made now to estimate total teratogenic effects.
However, It should be noted that the 1977 UNSCEAR estimate from animals
was 5 x 10~3 cases of structural  abnormalities per R per live birth
(about the  same number  per rad of low-LET).  This estimate must be viewed
as a minimum one  since  it Is based, to a large extent, on observation of
grossly visible malformations.  Differences 1n criteria for  identifying
malformations have compounded the problem, and questions of  threshold and
species differences  have made risk  projection to humans unwarranted.

G.5.7  Nonstochastic  Effects

     Nonstochastlc effects,  those effects that Increase 1n  severity with
increasing  dose  and  may have a threshold, have been  reviewed in the 1982
UNSCEAR report  (UNSCEAR82).  In general,  acute doses of 10  rad low-LET
radiation and  higher are  required to  Induce these  effects.   It 1s
possible that  some of the observed  effects of ^ utero exposure are
nonstochastlc,  e.g.,  the  risk of  embryonic loss,  estimated  to be  10'z
per R  (UNSCEAR77), following radiation  exposure  soon after  fertilization.
However, there  are no data to address the question.   Usually, no
non-stochastic  effects  of radiation are expected at  environmental  levels
of  radiation  exposure.

G.6  Radiation  Risk  - A Perspective

     To  provide a perspective  on  the risk of  fatal  radiogenic cancers  and
the hereditary damage due to radiation, we have calculated  the risk  from
background  radiation to the  U.S.  population using the risk  coefficients
presented  In  this chapter and the computer codes described  In Appendix H.
                                   G-54

-------
The risk resulting from background radiation  is
the risks caused by releases of radionuclides.
auto accidents,  and other measures of common  ri
from background  radiation are neither voluntary
abuse.   The risk caused by background radiation
unavoidable; therefore, it is a good benchmark
risks from radionuclide releases.   Moreover,  to
estimated risk of radionuclides is biased,  the
risk estimates for background radiation.
           a useful perspective  for
           "Unlike cigarette  smoking,
           sks, the  risks  resulting
           nor the  result of alcohol
           is very  largely
           for judging  the estimated
           the degree  that the
           same bias is present  in the
    Low-LET background radiation has three major components:   cosmic
radiation, which averages to about 28 mrad per year in the U.S.:
terrestrial sources, such as radium in soil,  which contributes an average
of 26 mrad per year (NCRP75); and the low-LET dose resulting  from internal
emitters.  The last differs between organs, to some extent, but for soft
tissues is about 24 mrad per year (NCRP75).  Fallout from nuclear weapons
tests, naturally occurring radioactive materials in buildings, etc.,
contributes about another 10 mrem for a total low-LET whole-body dose of
about 90 mrad per year.  The lung and bone receive somewhat larger doses
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
percent of the U.S. population would receive annual doses that are between
75 mrad per year and 115 millrad per year (EPA81).

    As outlined in Section G.2, the BEIR-3 linear models yield, for
lifetime exposure to low-LET radiation, an average lifetime risk of fatal
radiogenic cancer of 280 per 106 person rad.  Note that this average is
for a group having the age- and sex-specific mortality rates of the 1970
U.S. population.  We can use this datum 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 years and at 9 x 10~2 rad per year, the
average lifetime dose is 6.36 rad.
this group is:
The risk of fatal  cancer per person in
                 280 fatalities x 6.36 rem = 1.78 x 10-3

                 106 person rad  ,
or about 0.18 percent of all deaths.  The vital statistics we use in our
radiation risk analyses indicate that the probability of trying from
cancer in the United States from all causes is about 0.16, i.e.,
16 percent.  Thus, the 0.18 percent result for the BEIR-3 linear dose
response model indicates that about 1 percent of all U.S. cancer is due
to low-LET background radiation.  The BEIR-3 linear quadratic model
indicates that about 0.07 percent of all deaths are due to low-LET
background radiation or about 0.4 percent of all cancer deaths.
                                   G-55

-------
    Table G-6 Indicates a risk of 460 fatalities  per 106  organ rad for
alpha emitters 1n lung tissue.  The lifetime cancer from  this  exposure is:
460 fatalities v 0,03 rad
— £ - x      - x
10° organ rad
                                             ,         _  no   1A
                                            .7years *  0.98 x 10
                                                               -3
This is twice the risk due to low-LET background radiation calculated by
means of the BEIR-3 linear quadratic model  and more than half of the risk
calculated by means of the BEIR-3 linear model.

     The 1982 UNSCEAR report Indicates that the average annual  dose to the
endosteal  surfaces of bone due to naturally-occurring high-LET alpha
radiation is about 6 mrad per year or, for  a quality factor 20, 120 mrem
per year (UNSCEAR82).  Table G-6 indicates  that the lifetime risk of fatal
bone cancer due to this portion of the naturally occurring radiation
background is:
               20 cases   „ .0.006 rad
           105 person rad     *ear
                                      x 70.7 years = 8.5 x 10
                                               -6
     The spontaneous incidence of serious congenital  and genetic
abnormalities has been estimated to be about 105,000 per 10° live
births, about 10.5 percent of live births {NAS80,  UNSCEAR82).  The low-LET
background radiation dose of about 90 mrad/year in soft tissue results 1n
a genetically significant dose of 2.7 rad during the 30-year reproductive
generation.  Since this dose would have occurred 1n a large number of
generations, the genetic effects of the radiation exposure are thought to
be an equilibrium level of expression.  Since genetic risk estimates vary
by a factor of 20 or more, EPA uses a log mean of this range to obtain an
average value for estimating genetic risk.  Based on this average value,
the background radiation causes 700 to 1000 genetic effects per 106 live
births, depending on whether or not the oocyte is as sensitive to
radiation as the spermatogonla (see Section G.5).   This result Indicates
that about 0.67 percent to 0.95 percent of the current spontaneous
incidence of serious congenital and genetic abnormalities may be due to
the low-LET background radiation.
                                   G-56

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           to Pelvic Radium or Roentgen Irradiation, Amer. 0. Obstet.
           Gyn., _18, 179-187, 1929.

Mu30       Murphy D. P. and DeRenyi M., Postconception Pelvic Irradiation
           of the Albino Rat (Mus Norvegieus):  Its Effects Upon the
           Offspring, Surg. Qynecol. Obstet., J50, 861-863, 1930.

NAS72      National Academy of Sciences - National Research Council, The
           Effects of Populations of Exposures to Low Levels of Ionizing
           Radiation, Report of the Cormrittee on the Biological Effects
           of Ionizing Radiations (BEIR Report), Washington, D.C., 1972.

NAS80      National Academy of Sciences - National Research Council, The
           Effects of Populations of Exposure to Low Levels of  Ionizing
           Radiation, Committee on the Biological Effects of Ionizing
           Radiation, Washington, D.C., 1980.

NCHS73     National Center  for Health Statistics, Public  Use Tape, Vital
           Statistics - Mortality Cause of  Death Summary  - 1970,
           PB80-133333, NTIS, Washington, D.C.. 1973.

NCHS75     National Center  for Health Statistics, U.S. Decennial Life
           Tables  for  1969-71, 1(1), DHEW Publication  No.  (HRA) 75-1150,
           U.S.  Public  Health Services, NCHS, Rockville,  Maryland, 1975.

NCRP75     National Council  on Radiation Protection and Measurement,
           Natural  Background Radiation 1n  the United  States,  NCRP Report
           No.  45,  NCRPM, Washington, D.C., 1975.

NCRP77     National Council  on Radiation Protection and Measurements,
           Protection  of  the Thyroid Gland  1n the  Event of Releases  of
           Radioiodine,  NCRP Report  No. 55, NCRPM,  Washington,  D.C.,  1977.

NCRP80     National Council  on Radiation Protection and Measurements,
            Influence  of Dose and  Its Distribution  in Time on
           Dose-Response  Relationships  for  Low-LET Radiation,  NCRP Report
           No.  64,  NCRPM, Washington, D.C., 1980.

Ne56      Neel  J.  V.  and Schull  W.  J., The Effect of  Exposure to  the
           Atomic Bombs on  Pregnancy Termination  1n Hiroshima  and
           Nagasaki,  National  Academy of Sciences,  Publ.  461,  Washington,
          r D.C., 1956.

Ne70      Nelson K.  B.  and Deutschberger 0.,  Head Size  at One Year  as a
            Predictor  of Four-Year I.Q.,  Develop.  Med.  Child  Neurol., 12,
            487-495, 1970.                                            ~
                                   G-62

-------
ORNL84     Oak Ridge National Laboratory, Age Dependent Estimation of
           Radiation Dose, [1n press], 1984.

OfSO       Oftedal  P. and Searle A. G.,  An Overall  Genetic Risk
           Assessment for Radiological Protection Purposes, J. Had.
           Genetics, j7. 15-20, 1980.

Oh65       Ohzu E., Effects of Low-Dose  X-Irradiation on Early Mouse
           Embryos, Rad. Res. 26, 107-113, 1965.

Ot83       Otake M. and Schull W. H., Mental Retardation 1n Children
           Exposed In Utero to the Atomic Bombs:  A Reassessment,
           Technical Report RERFTR 1-83, Radiation Effects Research
           Foundation, Hiroshima, 1983.

Ot84       Otake M. and Schull W. J., In Utero Exposure to A-bomb
           Radiation and Mental Retardation:  A Reassessment, Brit. J.
           Radio!., 57, 409-414, 1984.

P152       Plumrner G. W., Anomalies Occurring in Children Exposed  in
           Utero to the Atomic Bomb in Hiroshima, Pediat., J£, 687-692,
           1952.

Po78       Pohl-Ruling J., Fischer P., and Pohl E., The Low-Level  Shape
           of Dose Response for Chromosome Aberration, pp. 315-326 in
           Late Biological Effects of Ionizing Radiation, Volume  II,
           International Atomic Energy Agency, Vienna, 1978.

RERF78     Radiation Effects  Research Foundation, 1 April 1975 -  31 March
           1978.   RERF Report 75-78,  Radiation Effects Research
           Foundation, Hiroshima,  1978.

RERF83     Radiation Effects  Research Foundation, Reassessment of Atomic
           Bomb Radiation  Dosimetry  in Hiroshima and  Nagasaki, Proc. of
           the U.S.-Japan  Joint Workshop, Nagasaki, Japan, Feb.  16-17,
           1982, Radiation Effects Research  Foundation, Hiroshima, 730,
           Japan,  1983.
                                        i
RERF84     Radiation  Effects  Research Foundation, Second  U.S.-Japan Joint
           Workshop  for  Reassessment  of  Atomic  Bomb  Radiation  Dosimetry
           in  Hiroshima  and  Nagasaki, Radiation  Effects Research
           Foundation,  Hiroshima,  730, Japan,  1984.

Ro78       Rowland R.  E.,  Stehney  A.  F., and Lucas  H. F.,  Dose Response
           Relationships for Female  Radium  Dial  Workers,  Rad^  Res. 76,
           368-383,  1978.

Ru50       Russell L.  B.,  X-ray Induced  Developmental Abnormalities in
           the Mouse and Their Use in the Analysis  of Embryo!ogical
           Patterns,  I.   External  and Gross Visceral  Changes,  J.  Exper.
           Zool.,  114,  545-602,  1950.
                                   G-63

-------
Ru53


Ru54



Ru56
Ru57
Ru70
Ru71


Sa82



ScSla


ScSlb
Se69


Sm78
Sp83
St21
Rugh R., Vertebrate Radiobiology:  Embryology, Ann. Rev. Nucl.
Sci., ;3, 271-302,  1953.

Russell L. B. and  Russell W. L., An Analysis of the Changing
Radiation Response of the Developing Mouse Embryo, J. Cell.
Comp. Physiol., 43 (Suppl.  1).  103-149, 1954.

Russell L. B., X-Ray Induced Developmental Abnormalities in
the Mouse and Their Use  in  the  Analysis of Embryological
Patterns, II.  Abnormalities of the Veretebral Column and
Thorax, J. Exper.  Zool., 131, 329-390, 1956.

Russell L. B., Effects of Low Doses of X-rays on Embryonic
Development 1n the Mous, Proc.  Soc. Exptl. Bibl. Med., 95,
174-178, 1957.                                         —

Rugh R., The Effects of  Ionizing Radiation on the Developing
Embryo and Fetus,  Seminar Paper No. 007, Bureau of
Radiological Health Seminar Program, Public Health Service,
Washington, D.C.,  1970.

Rugh, R., X-ray Induced  Teratogenesis in the Mouse and Its
Possible Significance to Man, Radiol., j)9, 433-443, 1971.

Satoh C., et al.,  Genetic Effects of Atomic Bombs, in:  Human
Genetics, Part A:  The Unfolding Genome, A. R. Liss, Inc., New
York, 267-276, 1982. '

Schull W. J., Otake M,,  and Neel J. V., Genetic Effects of the
Atomic Bombs:  A Reappraisal, Science, 213, 1220-1227, 1981.

Schull W.J., Otake M., and  Neel J.Y., A Reappraisal of the
Genetic Effects of the Atomic Bombs, Summary of a 34-Year
Study, RERF PR7-81, Radiation Effects Research Foundation,
Hiroshima, 1981.

Senyszyn J. J. and  Rugh R., H/drocephaly Following Fetal
X-Irradiat1on, Radiol^.93, 625-634, 1969.

Smith P. G. and Doll R., Radiation-Induced Cancers 1n Patients
with Ankyloslng Spondylitls Following a Single Course of X-ray
Treatment, In:  Proc. of the IAEA Symposium, Late Biological
Effects of Ionizing Radiation,  U 205-214, IAEA, Vienna, March
1978.

Spiers F. W., Lucas H.  F.,  Rundo J., and Anast G. A., Leukemia
Incidence 1n the U.S. Dial Workers, In:  Conference Proc. on
Radloblology of Radium and  the  Actlnldes 1n Man,
October 11-16, 1981, Health Phys., 44 Suppl. j.. 65-72, 1983.

Stettner E., E1n weiterer Fall  einer Schadingung einer
menschichen Frucht durch Roentgen Bestrahlung., Jb.
Kinderheilk.  Phys. Erzleh., 95, 43-51, 1921.
                                  G-64

-------
St81
St84
To80


To84
U182
UNSCEAR58
UNSCEAR62
UNSCEAR66
UNSCEAR69
UNSCEAR72
UNSCEAR77
Straume T. and R. L. Dobson,  Implications of New Hiroshima and
Nagasaki Dose Estimates:  Cancer Risks  and Neutron RBE, Health
Phys. 4U 666-671, 1981.

Stein Z. A. and Susser M. W.,  The Epidemiology of Mental
Retardation, in Epidemiology  of Pediatric Neurology, B.
Schoenberg, editor, Marcel  Dekker,  Inc.,  New York, [in press],
1984.

Tobias C. A., et al., The Repair-Misrepair Model, pp. 195-230,
In R. E. Meyn and H. R. Withers, eds.,  Raven, New York, 1980.

Tokunaga M., Land C. E., Yamamoto T.,  Asano M., Takioka S.,
Ezaki E., and Nishimari I., Incidences of Female Breast Cancer
Among Atomic Bomb Survivors,  Hiroshima and Nagasaki,
1950-1980, RERF TR 15-84, Radiation Effects Research
Foundation, Hiroshima, 1984.

Ullrich R. L., Lung Tumor Induction in Mice:  Neutron RBE at
Low Doses, DE 82009642.  National Technical Information
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United Nations, New York, 1958.

United Nations, Report of the United Nations Scientific
Committee on the Effects of Atomic Radiation, Official
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United Nations, Report of the United Nations Scientific
Committee on the Effects of Atomic Radiation, Official
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United Nations, Report of the United Nations Scientific
Committee on the Effects of Atomic Radiation, Supplement
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United Nations Scientific Committee on the Effects of  Atomic
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Volume  II:  Effects, Report to the General Assembly.   Sales
No.  E. 72.  IX.18., United Nations, New York, 1972.

United Nations Scientific Committee on the Effects of  Atomic
Radiation,  Sources and Effects of  Ionizing Radiation,  Report
to the-General Assembly, with Annexes, Sales No.  E.77  IX.1.,
United Nations, New York, 1977.
                                   G-65

-------
UNSCEAR82  United Nations Scientific Committee .on the Effects of Atomic
           Radiation, Ionizing Radiation:   Sources and Biological
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           IX.8, United Nations, New York, 1982.
Ya80
Wa83
Wh83
WH075
W154
Wo65
Wo66
Van Buul  P.  P.  W.,  Dose-response Relationship for X-ray
Induced Reciprocal  Translocations in Stem Cell  Spermatogonia
of the Rhesus Monkey (Macaca mulatta), Mutat. Res., 73,
363-375,  1980.   (Cited in UNSCEAR82.)

Wakabayashl  T., Kato H., Ikeda T., and Schull W. J., Studies
of the Mortality of A-bomb Survivors, Report 7, Part III,
Incidence of Cancer In 1959-78 Based on the Tumor Registry
Nagasaki, Radiat. Res.. 93, 112-142, 1983.

Whittemore A. S. and McMillan A., A Lung Cancer Mortality
Among U.S. Uranium Miners:  A Reappraisal, Technical Report
No. 68, SIAM Inst.  Math. Soc., Stanford University, Stanford,
1983.

World Health Organization, International Statistical
Classification of Diseases, Injuries, and Causes of Death, 9th
Revision, WHO, Geneva, 1975.

Wilson J. G.f Differentiation and the Reaction of Rat Embryos
to Radiation, J. Cell. Comp. Physio!., 43 (Suppl. 1), 11-37,
1954.

Wood J. W., Johnson K. G., and Omarl Y.,  In  Utero Exposure to
the Hiroshima Atomic Bomb:  Follow-up at Twenty Years,
Technical Report 9-65, Atomic Bomb Casualty  Commission,
Hiroshima, 1965.

Wood J. W., Johnson K. G., Omarl  Y., Kawamoto S., and Keehn
R. J., Mental Retardation  In Children Exposed In Utero to the
Atomic Bomb—Hiroshima and Nagasaki, Technical Report 10-66,
Atomic Bomb Casualty Commission,  Hiroshima,  1966.
                                   G-66
                                                                                 .f

-------
  APPENDIX H:  A DESCRIPTION OF THE RADRISK AND CAIRO COMPUTER CODES
    USED BY EPA IN ASSESSING DOSES AND RISKS FROM RADIATION EXPOSURE

H.I  Introduction

     This appendix  provides a  brief overview of the RADRISK (Du80) and
CAIRD (Co78)  computer codes used by the  Environmental  Protection Agency
to assess the health risk from radiation exposures.  It  describes how
the basic dose calculations are performed and describes  the mechanics
of the life table implementation of the  risk estimates derived 1n
Appendix G.

H.2  Overview of  the EPA Analysis

     RADRISK, the computer code used to  calculate dose and risk (Du84,
Su81, Du80),  calculates the radiation dose and risk resulting from an
annual unit intake  of a given  radionuclide or the risk resulting from
external exposure to a unit concentration of radionuclide 1n air or on
ground surface.  Since both dose and risk models are linear, the unit
dose and risk results can then be scaled to reflect the exposure
associated with a specific source.

     As outlined  in Appendix F, estimates of the annual  dose rate to
organs and tissues  ,of interest are calculated by using,  primarily,
models recommended  by the International  Commission on Radiological
Protection (ICRP79, ICRP80).  Because EPA usually considers lifetime
exposures to a general population, these dose rates are used in
conjunction with  a  life table  analysis of the increased risk of cancer
resulting from radiation (Co78).  This analysis, described below, takes
account of competing risks and the age of the population at risk.

H.3  Dose Rates from Internal  Exposures

     Internal exposures occur  when radioactive material  1s Inhaled or
Ingested.  The RADRISK code Implements contemporary dosimetric models
to estimate the dose rates at  various times to specified reference
organs in the botty  from inhaled or Ingested radionuclides.  The
dosimetric methods  in RADRISK  are adapted from those of the INREM-II
code (K178) which is based on  models recommended by the International
Commission on Radiological Protection UCRP79).  The principal
qualitative difference is that RADRISK computes dose rates to specified
organs separately for high and low linear energy transfer (LET)
radiations, while INREM-II calculates the committed dose equivalent to
specified organs.  The time-dependent dose rates are used in the life
table calculations  of RADRISK.
                                  H-l

-------
     In RADRISK,  the direct Intake of each radionuclide 1s treated
separately.  For  decay chains, the Ingrowth an3 ctynamics of decay
products (daughters) 1n the bccty after Intake of a parent radtonucllde
are considered explicitly 1n the calculation of dose rate.  The decay
product contributions to the dose rate are Included In the dose
calculations, based on the metabolic properties of the element and the
organ in which they occur.


     The dose rate Df(X,t) to target organ X at time t due to
radionuclide 1 (l
-------
experts.  In almost all  cases, doses to soft tissues calculated on this
basis differ only slightly, if at all,  from ICRP80 dose estimates, but
the difference is large for some radlonuclides when the parent is
Incorporated into bone, as In lead-210.  For this radionuclide the
ICRP80 model has been used without any  modifications.

     A schematic representation of radioactivity movement in the boc[y
is shown in Appendix F.  Except for radon daughters, which are
considered separately, inhaled activity is assumed to be originally
deposited in the lungs (distributed among the nasopharyngeal,
tracheobronchial, and pulmonary regions), and ingested activity is
originally deposited in the stomach.  From the lungs, activity may be
absorbed by the bloodstream or migrate to the stomach.  Activity in the
stomach may proceed through the small intestine, upper large intestine,
and lower large intestine; activity may be absorbed by the bloodstream
from any of these four segments, although only absorption from the
small intestine is considered in this stuoV-

     The activity, A^ft), of radionuclide i in organ k may be divided
among several  "pools  or "compartments," denoted here by the subscript p,
Each differential equation describing the rate of change of activity
within a compartment is a  special case of the equation:
 A,
  ipk
                      1-1
                      £  Bu
pal,..., p^


       (H-3)
 where
      xipk
      cipk
      Pik
= activity of radionuclide i  in compartment p of organ k,

= number of exponential  terms in the retention function for
  radionuclide i in organ k,

s branching ratio of radionuclide j to nuclide i,

« rate coefficient (time'M for radiological decay of
  radionuclide i,

= rate coefficient (time'*) for biological removal of
  radionuclide i from compartment p of organ k,

= fractional coefficient for radionuclide 1 in the p-th
  compartment of organ k,

= inflow rate of radionuclide i into organ k.
                                    H-3

-------
     If the Inflow rate P^ remains constant,  the equations  may  be
solved explicitly for Aik(t) as described by Kfllough,  Dunning,  and
Pleasant (Ki78).  In many cases the Inflow into a compartment  will  not
be a constant rate over a long period of time.  To handle  this problem,
the time interval over which solution of the activity  equation 1s
desired (e.g., 110 years) is divided into 1-year subintervals.  The
inflow rate on each subintorval is then taken  to be that constant  value
which would yield the total activity flowing out of the preceding
compartment(s) during the same subinterval.

     The model used in RADRISK for particulate deposition  and  retention
in the respiratory tract is the ICRP task group lung model (Mo66,
ICRP72).  In this model, shown in Appendix F,  there are four major
regions:  the naso-pharyngeal, tracheobronchial, pulmonary,  and
lymphatic tissues.  A fraction of the inhaled activity is  Initially
deposited in each of the naso-pharyngeal, tracheobronchial,  and
pulmonary regions.  The material  is then cleared (removed) from  the
lung to the blood and the gastrointestinal tract, also as  shown  in
Appendix F.  Deposition and clearance of inspired partlculates in  the
lung are controlled by the particle size and solubility classification.

     The size distribution of the particles is specified by  the  activity
median aerocjynamic diameter (AMAD); where no AMAD is known,  a  value of
1.0 micron is assumed.  The model employs three solubility classes,
based on the chemical properties of the radionuclide;  classes  D, W, and
Y correspond to rapid (days), intermediate (weeks), and slow (years)
clearance, respectively, of material deposited in the respiratory
passages.  Inhaled nonreactive, I.e., noble, gases are handled as  a
special case.

     Movement of activity through the gastrointestinal (GI)  tract  is
simulated with a catenary model, consisting of four segments:   stomach,
small intestine, upper large intestine, and lower large intestine.
Exponential outflow of activity from each segment into the next  or out
of the system Is assumed.  Outflow rate constants are calculated from
the transit times of Eve (Ev66).  Although absorption may  occur  from
any combination of the four segments, only activity absorbed into  the
blood.from the small Intestine is normally considered; the fractional
absorption from the small intestine into the blood is traditionally
denoted fj.

     Activity absorbed by the blood from the GI or respiratory tract is
assumed to be distributed immediately to systemic organs.   The
distribution of activity to these organs is specified by fractional
uptake coefficients.  The list of organs 1n which activity 1s  explicitly
                                  H-4

-------
distributed (termed source organs)  is element-dependent, and may
include such organs as bone or liver where sufficient metabolic data
are available.   This 11st is complemented by an additional  source
region denoted  as OTHER,  which accounts for that systemic activity not
distributed among the explicit source organs; uniform distribution of
this remaining  activity within OTHER is assumed.

     Radioactive material that enters an organ may be removed by both
radioactive decay and biological  removal processes.  For each source
organ, the fraction of the initial  activity remaining at any time after
intake is described by a  retention  function consisting of one or more
exponentially decaying terms.

     The metabolic models and parameters employed in the present stucty
have been described by Sullivan et  al. (Su81).  In most cases, the
models are similar or identical to  those recently recommended by the
ICRP (ICRP79, ICRP80, 1CRP81).  However, some differences in model
parameters do exist for some radionuclides (Su81).  In particular,
parameter values that are thought to be more representative of
metabolism following low-level environmental exposures, rather than
occupational exposures, have been used In this analysis [e.g., fi=0.2
for uranium In the environment (ICRP79, NAS83)].  For transuranic
isotopes, metabolic parameters from EPA77, related comments from EPA78
and from the National Radiological  Protection Board (Ha82),.have been
used rather than those from  ICRP80.  These parameters are listed In
Table H-l.

     The EPA values were recommended by U.S. experts on transuranic
element metabolism at Battelle Pacific Northwest Laboratory (EPA78).
The recently-adopted National Radiation Protection Board fj values
for transuranics in the general environment are closer to the values
proposed by EPA In 1977 than those currently advocated by ICRP for
occupational exposures.  The larger f$ values will increase the
estimated dose and risk from ingestion of transuranic materials but
have little effect on doses following  inhalation.

H.4  Dose Rates from External Exposures

     Because of the penetrating nature of photons, radioactivity need
not be taken Into the body to deliver a dose to bocjy organs.  Energy
absorbed from photons emitted by radionuclides  in  the air or  on the
ground surface may also contribute to the overall  risk.  Natural
background radiation 1s an example of  an important external exposure,
ordinarily contributing the  largest component of dose to people.
                                   H-5

-------
TABLE H-l:
Small intestine to blood
elements
Element
Isotope
Plutonium-238 and 241
Oxide form
Nonoxide form
Bio. inc.*3)
Plutonium-239 and 240
Oxide form
Nonoxide form
Bio. inc.
Americium
Oxide form
Nonoxide form
Bio. inc.
Curium
Oxide form
Nonoxide form
Bio. inc.
Neptunium


transfer
EPA
Child
0-12 mo
10-2
10-2
5x10-2
10-3
10-2
5x10-2
10-2
10-2
5x10-2
10-2
5x10-2
-

fractions,

Adult
>12 mo
lO-3
10-3
5xlO-3
10-4
10-3
5x10-3
lO-3
ID'3
5x10-3
10-3
ID'3
5x10-3
ID'3

fit for

Adult
5x10-4
5x10-4
!0-5
5x10-4
5x10-4
5x10-4
5x10-4
5x10-4
5x10-4
5x10-4
5x10-4
10-3

transuranic
NRPB
Chil
0-12 mo
5x10-4
5x10-3
5x10-3
5x10-4
5x10-3
5x10-3
5x10-3
5x10-3
5x10-3
5x10-3
5x10-3
5x10-3
5x10-3



d
0-3 mo
10-2
10-2
10-3(b)
10-2
lO-2
10-2
10-2
10-2
10-2
10-2
10-2
10-2
 aBioiogically Incorporated form.
           e form.
Source:  EPA77, EPA78, Ha82.
NRPB:  National Radiological Protection Board,
                               H-6

-------
     Organ dose rates to an individual  immersed in  contaminated air or
standing 'on a contaminated ground surface are computed by Kocher's
DOSFACTER computer code (Ko81).  These  calculations assume that the
radionuclide concentration 1s uniform throughout an infinite volume of
air or area of ground surface, and that the exposed individual  Is
standing on the ground surface.  Only photons penetrate the body
sufficiently to deliver a significant dose to internal  organs,  and only
doses from photon radiation are considered in this  analysis.  Beta
radiation is far less penetrating and delivers a dose only to the bo
-------
     The photon dose rate factor Djz (X)  to organ X of an Individual  at
a distance z above a unit concentration contaminated ground surface may be
computed as:
                  0}z (X) = O.ScK   £  fj Ej[(M/p)t]n
                           exp(-uanr) dr-[Can/(6an-l)]
                                                               (H-5)
where
     K
       pm

      Man

      z
           = 1.0 s particle-material  correction  factor,

           s mass attenuation coefficient  for the  ntn  discrete  proton,

           = height of reference position  above  ground surface  (taken
             to be 1 meter 1n this study).

     c     = unit conversion proportionality constant.

     The coefficients Can and Dan are functions  of the photon energy.
For detailed discussion of the derivation  of these equations and a
tabulation of dose rate factors for various radionuclides, see Kocher
(Ko79, Ko81).

     In the analysis here, the dose rate factors described by these
equations are scaled to achieve a continuous exposure of 1 pC1/cm3 for
air immersion and 1 pCi/cm* for ground surface exposure.  Risk estimates
for these exposure pathways are based on continuous lifetime exposure  to
these levels.

H.5  Life Table Analysis to Estimate the Risk of Excess Cancer

     Radiation effects can be classified as stochastic or nonstochastic
(NAS80,  ICRP77).  For stochastic effects, the probability of occurrence
of the effect, as opposed to the severity, is a function of dose;
induction of cancer, for example, is considered a stochastic effect.
Nonstochastic effects are those health effects for which the severity
of the effect is  a  function of dose; examples of nonstochastic effects
Include cell killing, suppression of cell division, cataracts, and
nonmalignant skin damage.
                                     H-8

-------
     At the low levels of  radiation  exposure  attributed  to
radionuclldes 1n the  environment,  the  principal  health detriment  1s the
Induction of cancers  (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  times are
sent to a subroutine  adaptation of CAIRD (Co78)  contained in the
RADRISK code.  This  subroutine uses  annual  doses derived from  the
transmitted dose rates to  estimate the number of incremental fatalities
in the cohort due to  radiation-induced cancer in the reference organ.
The calculation of Incremental fatalities  is  based on estimated annual
incremental risks, computed  from annual  doses to the organ, together
with radiation risk  factors  such as  those  given  in the 1980 MAS report
BEIR-3 (NAS80).  Derivation  of the risk  factors  in current use is
discussed in Appendix G.

     An important feature  of this  methodology is the use of actuarial
life tables to account  for the time  dependence of the radiation insult
and to allow for competing risks of  death  in  the estimation of risk  due
to radiation exposure.  A  life table consists of data describing
age-specific mortality  rates from  all  causes  of death for a  given
population.  This information is  derived from data obtained on actual
mortality rates in a real  population;  mortality  data for the  U.S.
population during the years  1969-1971 (HEW75) are used throughout this
study.

     The use of life tables  in studies of risk due 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  the  latency period,  the  probability of
occurrence of a cancer  during a  given year 1s assumed to be  constant
for a  specified period,  called a plateau period.  The length of both
the latency and plateau periods  depends upon the type of cancer.

     During or after radiation exposure, a potential cancer victim may
experience years of life in which he is continually exposed to risk of
death  from causes other than incremental radiation exposure.   Hence,
some individuals  in the population will die  from competing causes of
death,  and are not potential victims of incremental  radiation-induced
cancer.

     Each member of the hypothetical cohort  is  assumed to be exposed
to a specified activity of a given radionuclide.  In this analysis
each member  of the cohort annually inhales or ingests 1 pCi  of the
radionuclide, or  Is exposed to a constant external concentration of
           in air or 1 pd/cm* on  ground surfaces.  Since the models
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used 1n RADRISK are linear, these results  may  be  scaled to  evaluate
other exposure conditions.  The cohort consists" of  an  Initial
population of 100,000 persons, all  of whom are simultaneously
llveborn.  In the scenario employed here,  the  radiation exposure  1s
assumed to begin at birth and continue throughout the  entire lifetime
of each Individual.

     No member of the cohort lives  more than 110  years.   The span from
0 to 110 years is divided into nine age intervals,  and dose rates to
specified organs at the midpoints of the age intervals are  used as
estimates of the annual dose during the age Interval,  For  a given
organ, the incremental probability  of death due to  radiation-induced
cancer is estimated for each year using radiation risk factors and the
calculated doses during that year and relevant preceding  years.   The
incremental probabilities of death  are used in conjunction  with the
actuarial life tables to estimate the incremental number  of radiation-
induced deaths each year.

     The estimation of the number of premature deaths  proceeds in the
following manner.  At the beginning of each year, m, there  is a
probability PN of dying during that year from  nonradiological causes,
as calculated from the life table data, and an estimated  incremental
probability PK of dying during that year due to radiation-induced
cancer of the given organ.  In general, for the m-th year,  the
calculations are:
= total  number of deaths in cohort  during year m,
= CPN(m) + pR(m)] x N(m)
= incremental number of deaths during year m due to
  radiation-induced cancer of a given organ,
= PR(m) x
     M(m)


     Q(m)
     N(m+l) = number of survivors at the beginning of year m + 1
            = N(m) - M(m)
              (NtlMOO.OOO).

PR Is assumed to be small relative to PN, an assumption which is
reasonable only for low-level exposures (Bu81),  such as those
considered here.  The total number of incremental  deaths for the  cohort
Is then obtained by summing Q(nO 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 (tying of radiation-induced
cancer, the average number of years of life lost per Incremental
mortality, and the decrease In the population's  life expectancy.   The
total number of years of life lost to those (tying of radiation-Induced
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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
the original cohort size  (N(l)=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  the annual rate of radiation-induced
excess  cancer  deaths, due to  a spec.ific 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 the cohort from chronic
exposure are identically  those which are 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 same magnitude.  Since the total persons years
lived by the cohort in this  stucty  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.

 H.6  Risk  Analysis  Methodology

      Risk  estimates  in current use at EPA are  based on  the  1980  report
 (BEIR-3) of  the National  Academy of Sciences Advisory  Committee  on  the
 Biological  Effects  of Ionizing Radiation  (NAS80).   The  form of  these
 risk estimates is,  to some extent, dictated by  practical considerations,
 e.g., a desire to  limit  the  number of cases which  must  be  processed for
 each environmental  analysis  and a need to conform to  limitations  of the
 computer codes in  use.   For  example,  rather than analyze male and
 female populations separately, the risk  estimates  have  been merged for
 use with the general  population;  rather  than perform both  an absolute
 and a relative risk calculation,  average values have  been  used.

      The derivation of  the risk estimates  from the BEIR-3  report  is
 presented in Appendix G.   A brief outline  of the general  procedure is
 summarized below.   Tables referenced from  Chapter V of NAS80 are
 designated by a V prefix.
                                   H-ll

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     (1)  The total  number of premature  cancer fatalities from lifetime
exposure to 1 rad per year of low-LET radiation 1s constrained to be
equal to the arithmetic average (280 per million person rad)  of the
absolute and relative risk values  (158 and 403) given in Table V-25 of
the BEIR-3 report (NAS80) for the  L-L and FT models for leukemia and
solid cancers, respectively.

     (2)  For cancers other than leukemia and bone cancer,  the age and
sex-specific Incidence estimates given 1n Table V-14 were multiplied  by
the mortality/incidence ratios of  Table  V-15  and processed through the
life table code at constant,  lifetime dose rates of 1 rad per year.
The resulting deaths are averaged,  using the  male/female birth ratio,
and proportioned for deaths due to  cancer 1n  a specific organ as
described in Appendix G.  These proportional  risks are then used to
allocate the organ risks among the  (235.5) deaths per million person
rad remaining after the 44.5  leukemia and bone cancer fatalities
(Table V-17) are subtracted from the arithmetic average of 280 given
in Table V-25.

     (3)  The RADRISK code calculates dose rates for high- and low-LET
radiations independently.  A quality factor of 20 has been applied to
all alpha doses (ICRP77) to obtain the organ dose equivalent rates in
rem per year.  The derivation of the proportional organ risks and
mortality coefficients for alpha particles are, however, based on the
dose in rad as described in Appendix G,  Table G-6.

     A typical environmental  analysis requires that a large number of
radionuclides and multiple exposure modes be considered.  The RADRISK
code has been used to obtain  estimates of cancer risk for intakes of
approximately 200 radionuclides and external  exposures by approximately
500 radionuclides.  For each  radionucllde and exposure mode,  we assume
that each member of a cohort  of 100,000  persons 1s exposed to a
constant radionuclide Intake  of 1  pCI/year, or a concentration of
1 pC1/cc-year for air Immersion, or of 1 pC1/cm2-year from the ground
surface, until they die or are 110 years old, the maximum cohort.  The
mean life span of the cohort  population  is 70.7 years, a result
obtained from 1970 age-specific mortality rates.  The calculated dose
rates and mortality coefficients described in the preceding sections
are then processed through the life table subroutine of the RADRISK
code to obtain lifetime risk  estimates.   At the low levels of
contamination normally encountered in the environment, the life table
population 1s not appreciably perturbed  by the excess radiation deaths
calculated and, since both the dose and  risk models are linear, these
unit exposure results may be scaled to reflect excess cancers due to
the radionucllde concentrations predicted in the analysis of a specific
source.
                                 H-12

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     As noted in the discussion of the life table analysis,  risk
estimates for chronic irradiation of the cohort" may also be  applied to'
a stationary population having the same age-specific mortality rates as
the 1970 U.S. population.  That is, 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 population exposed to an annual dose of
the same magnitude, -Thus, the risk estimates may be reported as a
lifetime risk (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
which vary from year to year may be obtained by summing the results of
a series of cohort calculations at various annual dose rates.
                                  H-13

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Bu81
Co78
DuSO
Du84
EPA77
EPA78
Ev66
Ka82
HEW75
ICRP72
ICRP77
                      REFERENCES

Bunger B. M., Cook J.R., and M.K. Barrlck, Life Table
Methodology for Evaluating Radiation Risk:  An Application
Based on Occupational Exposures, Health Phys. 40, 439-455.

Cook J.R., Bunger B., and M.K. Barrlck, A Computer Code for
Cohort Analysis of Increased Risks of Death (CAIRO), EPA
520/4-78-012, 1978.

Dunning, D.E. Jr., Leggett R.W., and M.G. Yaldntas, A
Combined Methodology for Estimating Dose Rates and Health
Effects from Exposure to Radioactive Pollutants, ORNL/TM-7105,
1980.

Dunning D.E. Jr., Leggett R.W., and R.E. Sullivan, An
Assessment of Health Risk from Radiation Exposures, Health
Physics, 46 (5), May 1984.

U.S. Environmental Protection Agency, Proposed Guidance on
Dose Limits for Persons Exposed to Transuranium Elements in
the General Environment, EPA 520/4-77-016, 1977.

U.S. Environmental Protection Agency, Response to Comments:
Guidance on Dose Limits for Persons Exposed to Transuranium
Elements in the General Environment, EPA 520/4-78-010, 1978.

Eve I.S., A Review of the Physiology of the Gastrointestinal
Tract in Relation to Radiation Doses from Radioactive
Materials, Health Physics, 1£, 131-162, 1966.

Harrison J.D., Gut Uptake Factors for Plutonium, Americium
and Curium, NRPB-R129, National Radiological Protection Board,
NRPB-R129 WSO, P.O. Box 569, London, January 1982.

U.S. Department of Health, Education and Welfare, 1975,* U.S.
Decennial Life Tables for 1969-1971, Vol. 1., No. 1., DHEW
Publication No. (HRA) 75-1150, Public Health Service, Health
Resources Administration, National Center for Health
Statistics, Rockville, Maryland.

International Commission on Radiological Protection, The
Metabolism of Compounds of Plutonium and Other Actinldes, ICRP
Publication 19, Pergamon Press, 1972.

International Commission on Radiological Protection, 1977,
Recommendations of the International Commission on
Radiological Protection, Ann. ICRP, Vol. 1, No. 1, Pergamon
Press-, 1977.
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ICRP79   International  Commission on Radiological  Protection, Limits
         for Intakes of Radionuclides by Workers,  ICRP Publication 30,
         Part 1, Annals of the ICRP, Z (3/4), Pergamon Press, 1979.

ICRP80   International  Commission on Radiological  Protection, Limits
         for Intakes of Radionuclides by Workers,  ICRP Publication 30,
         Part 2, Annals of the ICRP, £ (3/4), Pergamon Press, 1980.

ICRP81   International  Commission on Radiological  Protection, Limits
         for Intakes of Radionuclides by Workers,  ICRP Publication 30,
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Ki78     Killough G.G., Dunning D.E. Jr., and Pleasant J.C., INREM-II:
         A Computer Implementation of Recent Models for Estimating the
         Dose Equivalent to Organs of Man from an  Inhaled or Ingested
         Radionuclide,  ORNL/NUREG/TM-84, 1978.

Ko79     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, ORNL/NUREG/TM-283, 1979.

Ko81     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, Health Physics, 38, 543-621,  1981.

Mo66     Morrow P.E., Bates D.V., Fish B.R., Hatch T.F., and Mercer
         T.T., Deposition and Retention Models for Internal Dosimetry
         of the Human Respiratory Tract, Health Physics, 12, 173-207,
         1966.                          '                 — •

NAS72    National Academy of Sciences - National Research Council, The
         Effects on Populations of Exposures to Low Levels of Ionizing
         Radiation, Report of the Committee on the Biological Effects
         of Ionizing Radiations (BEIR Report), Washington, D.C., 1972.

NAS80    National Academy of Sciences - National Research Council, The
         Effects on Populations of Exposures to Low Levels of Ionizing
         Radiation, Committee on the Biological Effects of Ionizing
         Radiations (BEIR Report), Washington, D.C., 1980.

NAS83    National Academy of Sciences - National Research Council,
         Drinking Water and Health, Vol. 5, Safe Drinking Water
         Committee, Washington, D.C., 1983.
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Sn74     Snyder W.S., Ford M.R., Warner G.G., and Watson S.B., A
         Tabulation of Dose Equivalent per M1cr6cur1e-Day for Source
         and Target Organs of an Adult for Various Radlonuclldes,
         ORNL-5000, 1974.

Su81     Sullivan R.E., Nelson N.S., Ellett W.H., Dunning D.E. Jr.,
         Leggett R.W., Yalcintas M.G., and Eckerman K.F., Estimates of
         Health Risk from Exposure to Radioactive Pollutants,
         ORNL/TM-7745, 1981.
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