REVIEW DRAFT
                       DRINKING WATER CRITERIA DOCUMENT

                                      FOR

                     BETA AND GAMMA EMITTING RADIONUCLIDES
                                  Prepared by

                       Clement  International  Corporation
                              1201 Gaines Street
                            Ruston,  Louisiana 71270
                                      and

                            Wade Miller Associates
                             1911  North  Myer Drive
                          Arlington,  Virginia 22209
                                  July  1991
                                 Prepared for

                      Drinking Water  Standards  Division
                  Office of Ground Water  and  Drinking Water
                       and  Office of Radiation Programs
                     U.S.  Environmental Protection Agency
                             Washington, DC 20460
e*»
                                                                    Printed on Recycled Paper
U-3
CD

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                                   FOREWORD


      Section 1412 (b)(3)(A) of the Safe Drinking Water Act, as amended in
1986, requires the Administrator of the Environmental Protection Agency to
publish maximum contaminant level goals (MCLGs) and promulgate National
Primary Drinking Water Regulations for each contaminant, which, in the
judgment of the Administrator, may have an adverse effect on public health and
which is known or anticipated to occur in public water systems.  The MCLG is
nonenforceable and is set at a level at which no known or anticipated adverse
health effects in humans occur and which allows for an adequate margin of
safety.  Factors considered in setting the MCLG include health effects data
and sources of exposure other than drinking water.

      This document provides the health effects basis to be considered in
establishing the MCLG.  To achieve this objective, data on pharmacokinetics,
human exposure, acute and chronic toxicity to animals and humans, epidemiology
and mechanisms of toxicity are evaluated.  Specific emphasis is placed on
literature data providing dose-response information.   Thus, while the
literature search and evaluation performed in support of this document has
been comprehensive, only the reports considered most  pertinent in the
derivation of the MCLG are cited in the document.  The comprehensive
literature data base in support of this document includes information
published up to 1991; however, more recent data may have been added during the
review process.

      When adequate health effects data exist, Health Advisory values for less
than lifetime exposures (1-day, 10-day and longer-term, -10% of an
individual's lifetime) are included in this document.  These values are not
used in setting the MCLG, but serve as informal guidance to municipalities and
other organizations when emergency spills or contamination situations occur.

                                    James R. Elder
                                    Director
                                    Office of Ground  Water and Drinking Water
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                                 INTRODUCTION
      The Environmental Protection Agency (EPA) classifies all radionuclides
as Group A carcinogens based on their property of emitting ionizing radiation
(EPA 1991).  A Group A carcinogen is one in which there is sufficient evidence
from epidemiological studies to support a causal association between exposure
to the agent(s) and cancer.  The studies that provide this evidence indicate
that, depending on radiation dose and the pattern of exposure, ionizing
radiation can induce cancer in nearly any tissue or organ in the body (ATSDR
1990a,b,c).  Radiation-induced cancers in humans are found to occur in the
hemopoietic system, the lung, thyroid, liver, bone, skin, and other tissues.

      Man may be exposed to radionuclides by several routes, one of which is
through ingestion of drinking water containing these radionuclides.  Several
Drinking Water Criteria Documents for radionuclides have already been
completed, including those on naturally occurring radionuclides such as
radium, radon, and uranium.  These three radionuclides decay (transform)
primarily, by alpha emission.  This document estimates the risks of ingesting
drinking water containing radionuclides which decay by beta particles or gamma
rays.  Beta emitters decay by the emission of either a negative or positive
electron.  If the electron originates in the nuclides during the
transformation of a neutron into a proton (or the reverse reaction), the decay
is referred to as a beta decay.  A gamma ray is an energetic packet of
electromagnetic radiation (referred to as a "photon") produced in the nucleus
during a change in the energy level  of a nucleon (i-e., a proton or a
neutron).  Three beta or gamma-emitting radionuclides are discussed in depth
because drinking water, either surface or groundwater, are routinely monitored
for their presence.  These include strontium-90, tritium, and iodine-131.   For
these three radionuclides occurrence in drinking water, chemical and physical
properties, toxicokinetics, and health effects are discussed.  In addition,
discussions on mechanisms of toxicity and quantification of cancer effects are
presented.
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                               TABLE OF CONTENTS

                                                                           Page


FOREWORD   	     i

INTRODUCTION   	    ii

I.    SUMMARY	1-1

II.   NATIONAL OCCURRENCE OF BETA OR GAMMA  EMITTING
      ACTIVITY IN DRINKING WATER   	  II-l

      A.    INTRODUCTION	II-l

      B.    CURRENT STANDARDS AND COMPLIANCE  MONITORING REQUIREMENTS  .  .  11-2

      C.    MAN-MADE RADIONUCLIDE OCCURRENCE  DATA	11-5
            Environmental Radiation Data  Reports   	  II-5
            National Inorganics and Radionuclides  Survey (NIRS)  ....   11-10

      D.    CONCLUSIONS	   11-11

III.  PROFILES OF REPRESENTATIVE BETA OR  GAMMA  EMITTING RADIONUCLIDES .   III-l

      A.    INTRODUCTION	   I II-l

      B.    STRONTIUM	   111-2
            Physical and Chemical Properties   	   III-2
            Toxicokinetics  	   III-6
            Health Effects in Animals  	   III-8
            Health Effects in Humans   	  111-15

      C.    IODINE  	  111-17
            Physical and Chemical Properties   	  111-17
            Toxicokinetics  	  111-20
            Health Effects in Animals  	  ...  111-23
            Health Effects in Humans	111-27

      D.    TRITIUM 	  111-31
            Physical and Chemical Properties   	  111-31
            Toxicokinetics  	  111-34
            Health Effects in Animals  	  111-36
            Health Effects in Humans	111-40

      E.    BIOACCUMULATION AND RETENTION	111-41
            Hydrogen Model  	111-43
            Helium Model	111-43
            Lithium Model 	  111-43
            Beryllium Model	111-44
            Boron Model	111-44
            Carbon Model  	111-44
            Nitrogen Model	111-45


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             Oxygen  Model   	111-46
             Fluorine Model   	  111-46
             Neon  Model   	111-46
             Sodium  Model   	111-47
             Magnesium Model  	  111-47
             Aluminum Model   	111-47
             Silicon Model	111-48
             Phosphorus  Model   	  111-48
             Sulfur  Model   	111-49
             Chlorine Model   	  111-49
             Argon Model	111-50
             Potassium Model  	  111-50
             Calcium Model  	  111-51
             Scandium Model   	  111-51
             Titanium Model   	  111-52
             Vanadium Model   	  111-52
             Chromium Model   	  111-52
             Manganese Model  	  111-53
             Iron  Model   	111-53
             Cobalt  Model   	  111-54
             Nickel  Model   	  111-54
             Copper  Model   	111-55
             Zinc	111-55
             Gallium Model  	  111-56
             Germanium Model	111-56
             Arsenic Model  	  111-57
             Selenium Model   	  111-57
             Bromine Model	111-58
             Krypton Model	111-58
             Rubidium Model   	  111-59
             Strontium Model  	  111-59
             Yttrium Model  	  111-60
             Zirconium Model  	  111-60
             Niobium Model  	  111-61
             Molybdenum  Model	111-62
             Technetium  Model   	  111-63
             Ruthenium Model  	  111-63
             Rhodium Model	  111-64
             Palladium Model  	  111-64
             Silver  Model   	111-65
             Cadmium Model	111-65
             Indium  Model   	  111-66
             Tin Model  	  111-66
             Antimony	111-67
             Tellurium Model  	  111-67
             Iodine  Model   	 	  111-68
             Xenon Model	111-68
             Cesium  Model   	  111-69
             Barium  Model   	  111-69
             Lanthanide  (Rare Earth) Models  	  111-70
             Dysprosium   	  111-72
             Holmium 	  111-72
             Erbium   	  111-73
             Thulium 	•	  111-73
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            Ytterbium  	  	 111-74
            Lutetium   	 111-74
            Hafnium Model  	 111-75
            Tantalum Model   	111-75
            Tungsten Model   	 111-76
            Rhenium Model	111-76
            Osmium Model   	 111-77
            Iridium Model  	 111-77
            Platinum Model   	 111-78
            Gold Model	111-78
            Mercury Model	111-79
            Thallium Model   	 111-79
            Lead Model   	111-80
            Bismuth Model  '.	111-80
            Polonium Model   	 111-81
            Astatine Model   	 111-81
            Radon Model	111-82
            Francium Model   	111-82
            Radium Model   	111-83
            Actinium Model   	 111-83
            Thorium Model	111-84
            Protactinium Model   	 111-84
            Uranium Model	111-85
            Neptunium Model  	 111-85
            Plutonium Model	111-86
            Americium Model  	 .   . 111-87
            Curium Model   	 111-87

IV.   MECHANISM OF TOXICITY	IV-1

      A.    IONIZING ENERGY DEPOSITION   	 IV-1

      B.    RADIONUCLIDE DOSIMETRY   	 IV-3

V.    QUANTIFICATION OF TOXICOLOGICAL EFFECTS  	  V-l

      A.    NONCARCINOGENIC EFFECTS  	  V-l
            Method for Quantification of Noncarcinogenic Effects  ....  V-l
            Quantification of Noncarcinogenic  Effects  	  V-4

      B.    CARCINOGENIC EFFECT  	  V-4
            Method for Quantification of Carcinogenic  Effects 	  V-4
            Quantification of Cancer Risk for  Chemicals  	  V-5
            Quantification of Carcinogenic Effects   	  V-6

VI.  UNCERTAINTY ANALYSIS  	 VI-1

      A.    UNCERTAINTY IN ASSESSMENT OF NONCARCINOGENIC EFFECTS
            OF BETA AND GAMMA EMITTING RADIONUCLIDES   	 VI-1

      B.    UNCERTAINTY IN ASSESSMENT OF CARCINOGENIC  EFFECTS
            OF BETA AND GAMMA EMITTING RADIONUCLIDES   	 VI-1
            Uncertainty in Parameters Used in  the Metabolic Model  .... VI-1
            Uncertainty in Distribution of Isotope   .  .  .  .'	VI-2


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             Uncertainty in Dosimetric Calculations  	  VI-3
             Uncertainty in Risk Coefficients       	  VI-3
             Uncertainty in Other Factors Influencing Risk 	  vi-4
             Conclusion	VI-4

 VII.   REFERENCES	VI-5
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                                LIST OF TABLES

                                                                           Page

 II-l    Summary of Recent ERAMS Data on Beta Emitting
        Man-Made Radionuclides in Drinking Water   	    II-7

 III-l   Physical and Chemical Properties of Strontium  	   III-4

 III-2   Physical Properties of Iodine  	    111-18

 III-3   Atomic Properties of Hydrogen, Deuterium,  and  Tritium ....    111-32

 III-4   Physical Properties of Hydrogen, Deuterium,  and Tritium .  .  .    111-32

 V-l     50-Year Committed Absorbed Dose per Unit  Intake
        (millirad/pCi) from Beta and Gamma Emitters  in
        Drinking Water   	 V-8

 V-2     Organ-Specific Lifetime Cancer Risks Used  in the  RADRISK
        Model from High-LET and Low-LET Irradiation  	    V-ll

 V-3     Concentration of Beta and Gamma Emitters  In  Drinking
        Water to Yield a Specific Risk of Cancer  and Death
        for Lifetime Consumption  	    V-14
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                                LIST OF FIGURES
                                                                           Page
III-l   Half-Lives  and  Decay  Schemes of Strontium-89  and  -90   	  III-5
III-2   Half-Lives  and  Decay  Schemes of Iodine-129  and  -131  	   111-19
III-3   Half-Lives  and  Decay  Schemes of Tritium  	   111-33
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                                  I.   SUMMARY

      This document addresses potential  risks  of cancer from ingestion of man-
made radionuclides that decay by emitting beta particles or gamma rays.  Data
on distribution of these radionuclides in the environment are limited.
However,  some data on drinking water supplies monitored for strontium-90,
tritium,  and iodine-131, as well as gross gamma activity, are available.

      In drinking  water,  average concentrations  of  the  beta  emitting
radionuclides of concern are as follows:  <0.2 pCi/L (strontium-90),  100 to
300 pCi/L  (tritium), and <0.1 pCi/L (iodine-131).  None of the drinking water
samples monitored for gamma activity had measurable levels.   However, the
detection  limit for gamma activity was not reported.  These average
concentrations were obtained from the Environmental Radiation Ambient
Monitoring System (ERAMS).

      The potential  radiation dose  to  tissues  from  these radionuclides in
drinking water is dependent on the amount of the substance that may be
absorbed through the gastrointestinal  tract and distribution of the absorbed
amount to  potential target  tissues.  The beta emitting radionuclides  vary
widely in  their potential for absorption through the gut.  For example, about
15 to 36 percent of strontium-90 is absorbed,  while both iodine-131 and
tritium are very well  absorbed, with approximately 95 percent absorption from
the gut.

      Once absorbed  into  the  body,  each  of  these radionuclides  distributes
according  to a different pattern.  Strontium distributes preferentially to the
skeleton followed by lesser amounts distributed to soft tissues; while iodine-
131 distributes almost entirely to the thyroid gland.  Tritium in the form of
tritiated water behaves like ordinary water and distributes  throughout bodily
fluids and, thus,  uniformly throughout the body.

      Data on humans exposed  to  these  radionuclides  are limited.   In an
in vitro test using human blood cells  exposed  to strontium,  chromosomal
aberrations,  including dicentrics,  were induced.  No data on effects of
tritium exposure in humans  were located.  Several studies on effects of

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 iodine-131  exposure  in  humans were considered  in this document.  However, most
 of  these  studies  were on  individuals with preexisting thyroid problems and the
 iodine was  used as a diagnostic tool or used to destroy abnormal thyroid
 tissue.   In a  study  of  residents of the Marshall Islands who were exposed to
 radioactive iodine from fallout, hypothyroidism, thyroid nodules, and thyroid
 cancer were reported.   The  incidence of thyroid nodules was found to be
 statistically  significantly related to total radiation dose.

      In laboratory animals treated orally with strontium over many months,
 effects on  blood  and blood-forming tissues were most often reported.  These
 effects included  decreased  counts of numerous  types of blood cells, bone
 marrow hypoplasia or hyperplasia, and other forms of marrow proliferative
 disease.  In addition,  immune function was impaired in treated rats.  Dogs and
 swine administered strontium orally developed  bone tumors, tumors in the
 mouth, and  leukemia.

      In animal bioassays, all  effects  resulting from  exposure to  iodine-131
 were seen in the  thyroid  gland or adjacent tissues.  Oral doses to sheep (5 to
 15 mCi) have resulted in  damage to or complete destruction of the thyroid
 gland.  Oral exposure of  sheep, dogs, and rats has induced thyroid adenomas
 and/or carcinomas in all  three species.

      Long-term oral  exposure  of rats to  tritium resulted  in  numerous
 hematological  effects,  including various changes in white blood cells and
 decreased erythrocyte,  leukocyte, and reticulocyte counts.  Pregnant mice and
 rats receiving tritium  had  decreased reproductive capacity such as reduced
 litter size and offspring body weights.  Direct empirical information on
 possible carcinogenic effects of tritium is limited.  Male mice given tritium
 in drinking water sired offspring having intestinal adenocarcinomas, a tumor
which had not  been previously observed  in this particular strain of mice.
There is limited  evidence that exposure of rats in utero increased the
 incidence of ovarian tumors.

      Levels of these radionuclides  in  drinking water  estimated  to  result in  a
 risk of 1 cancer death  in 10,000 persons exposed have been calculated using
the RADRISK model.  For the three radionuclides specifically discussed in this

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document, the levels are as follows:  62 pCi/L  (strontium-90),  516  pCi/L
(iodine-131), and 5640 pCi/L (tritium).  Uncertainty  in  these estimates
results from uncertainty in the gastrointestinal absorption  factors  used,  the
kinetic behavior predicted by the model, and the risk factors derived  by  the
model.

      Because noncancer effects  have only been observed in animal bioassays
using test doses that exceed any potential doses from ingesting  drinking  water
containing these radionuclides, criteria for noncancer effects were  not
developed.
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              II.  NATIONAL OCCURRENCE OF BETA OR GAMMA EMITTING
                          ACTIVITY IN DRINKING WATER
A.    INTRODUCTION

      This report provides  current  monitoring  data  on  the presence of man-made
radionuclides in drinking water.  The main purpose of the information
presented in this report is to assist EPA in evaluating the potential impacts
of alternative monitoring requirements and Maximum Contaminant Levels (MCLs)
under consideration for a forthcoming proposal of national primary drinking
water regulations on radionuclides under the Safe Drinking Water Act  (SDWA).

      Two other  documents addressing  the  occurrence of man-made radionuclides
have previously been prepared for EPA's Office of Drinking Water.  A document
was prepared by Peeters (1985) for the EPA Office of Drinking Water that
focused primarily on identifying the important sources that could potentially
introduce man-made radionuclides into public drinking water supplies.  Four
major sources were discussed:

      •  DOE nuclear sites
      t  Commercial  nuclear power plants
      •  Institutional  sources (e.g., research facilities, hospitals,
         universities)
      •  Industrial  sources (e.g.,  pharmaceutical companies, commercial
         analytical  laboratories)

      Atmospheric fallout,  another frequently noted potential  source of man-
made radionuclides,  was also discussed briefly by Peeters.  Atmospheric
fallout is not currently considered a major source because of the moratorium
begun in 1958 suspending atmospheric weapons testing worldwide.

      Peeters (1985) provided an assessment of the potential for various
specific man-made radionuclides to be released from each of the four major
sources.  That assessment  included an estimate of the number of DOE facilities
that are potential sources  and a listing of specific man-made radionuclides
that may be released from  each facility.   It was concluded in the report,

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 however,  that  it  is  not  possible  to  make  any  generalizations  concerning  the
 type  of man-made  radionuclides  that  may result  as  drinking  water  contaminants
 from  any  of the four major  sources because  of the  widely  varying  nature  of
 activities  occurring at  specific  facilities in  each  category.

       The second  report  prepared  for the  Office of Drinking Water focused on
 available drinking water monitoring  data  on man-made radionuclides  (Ellis et
 al. 1986).   As indicated in  that  report,  the  amount  of actual monitoring data
 available on man-made radionuclides  in drinking water are very  limited.  The
 primary source for such  data is the  series  of "Environmental  Radiation Data"
 (ERD)  quarterly reports  prepared  by  EPA using data from the Environmental
 Radiation Ambient Monitoring System  (ERAMS).  In addition to  presenting  the
 available occurrence data on man-made radionuclides,  Ellis  et al.  (1986)
 provided  some estimates  of the  potential  radiation dose associated  with  those
 substances  in drinking water.

       This  document  is primarily  an  update of the  occurrence  data summary
 provided  in  the Ellis  et  al.  (1986)  report.   Specifically,  this report
 presents  a  summary of the ERAMS data that have  become available since the
 Ellis  et  al. report  was  prepared.  In addition, data  from the National
 Inorganics  and Radionuclides  Survey  (NIRS) are  presented; these data were not
 available when the Peeters and  Ellis reports  were  prepared.

 B.     CURRENT STANDARDS  AND  COMPLIANCE MONITORING  REQUIREMENTS

       To  provide a context for evaluating the man-made radionuclide occurrence
 information, it is useful to  summarize the existing drinking water  standards
 and compliance monitoring requirements.

       The category of  substances  referred to  as man-made radionuclides
 comprises more than  800  elements  of which approximately 200 are considered to
 be potential drinking water  contaminants  (Lowry and Lowry 1988).  Man-made
 radionuclides have been  regulated under SDWA  interim primary regulations since
 1976  (40  CFR 141.16).  Unlike most drinking water  regulations in  which a
drinking  water concentration of each contaminant regulated  is specified as the
MCL, the  regulation  for man-made  radionuclides  is  a categorical  standard that

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seeks to limit the combined health risk of all man-made radionuclides that may
be present in a given water supply.

      Under current regulations, the MCLs for man-made radionuclides are
defined in terms of "beta particle and photon radioactivity from man-made
radionuclides in community water systems."  Specifically, they  include all
radionuclides emitting beta particles and/or photons (except uranium-235 and
uranium-238) that are listed in the 1963 National Bureau of Standards (NBS)
Handbook 69 entitled, "Maximum Permissible Body Burden and Maximum Permissible
Concentration of Radionuclides in Air or Water for Occupational  Exposures."
The MCL states that the average annual concentration of beta particle and
photon radioactivity from man-made radionuclides in drinking water is not to
produce an annual dose equivalent to the total body or any organ greater than
4 millirem (mrem) per year.1   The regulation  specifies  the drinking water
levels assumed to produce the 4 mrem dose for only two specific man-made
radionuclides, namely tritium and strontium-90; for all other man-made
radionuclides, the 4 mrem equivalent level is to be calculated  from data on
dose to critical  organs provided in the NBS Handbook.

      Although the MCLs for man-made radionuclides apply to all public
community water supplies, only certain categories of supplies were
specifically required to monitor them.  The monitoring requirements that
accompany the MCL for man-made radionuclides  (40 CFR 141.26(b)) are depicted
in Figures II-l and II-2.  Only systems using surface water sources and
serving more than 100,000 people are specifically designated as having to
monitor man-made radionuclides under the Federal standards.  Those systems
must monitor gross beta activity, tritium and strontium-90, with more specific
monitoring to identify and quantify other man-made radionuclides "triggered"
if gross beta activity exceeds 50 pCi/L (see  Figure II-l).
          essentials  of the  radiochemistry  of man-made radionuclides,  the
practical utility of using gross beta as a screen or surrogate measure, and
the relationships between activity levels (measured in pCi/L) and dose levels
(measured in millirems per year) are discussed in detail in the 1986 ANPRM as
well as in other Agency documents, and are not repeated here.

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       In  addition  to  the  large surface water systems, the states were to have
identified other community water supplies "utilizing waters contaminated by
effluents from nuclear  facilities."  For those systems, gross beta, tritium,
strontium-90, and  iodine-131 were to be measured, again with additional
monitoring requirements applying if certain levels of gross beta activity are
exceeded  {see Figure  II-2).

       It  should be noted  that the man-made radionuclides interim regulations
were directed mainly  at surface water supplies.   Ground water has generally
been considered less  likely to be vulnerable to man-made radionuclides because
it is  not directly accessible to fallout.  Long-lived isotopes, such as
strontium-90 and cesium-137, are tightly bound by soil, and short-lived
isotopes decay before the water is used (Lowry and Lowry 1988).  However,
notwithstanding the implied emphasis on surface water systems, the interim
regulations do explicitly note that states have the discretion to require
monitoring for man-made radionuclides in supplies using only ground water
sources.

       In 1986, EPA published an Advance Notice of Proposed Rulemaking (ANPRM)
addressing radionuclides  (EPA 1986). Some changes to the man-made radionuclide
regulations were discussed in the ANPRM and public comment was solicited on
them.  The notable changes discussed for man-made radionuclides included the
elimination of the reference to the specific NBS Handbook list of man-made
radionuclides as being too limiting, suggesting instead the more generalized
definition be used to allow for the potential  development of new elements.
Also,  it was indicated that three additional substances may be included as
man-made radionuclides.  These are potassium-40 (a beta emitter that is
naturally occurring, but not part of the uranium or thorium decay series),  and
plutonium-239 and americium-241 (both man-made radionuclides that are alpha
rather than beta emitters).

      No changes were made in the use of the 4 mrem equivalent level  as the
MCL for man-made radionuclides, although more recent data on the activity
levels equivalent to 4 mrem for specific substances were presented.   Potential
changes to the monitoring requirements for man-made radionuclides were also
not discussed in the ANPRM.

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C.    MAN-MADE RADIONUCLIDE OCCURRENCE DATA

      As noted in the Introduction, the focus of this report is on the most
recent occurrence information on man-made radionuclides in drinking water
available from the ERAMS and NIRS.  One other potential source of drinking
water occurrence data that merits mention is the compliance monitoring data
required to be collected under the existing standards.  However, except for
showing that there have been no reports of gross beta activity levels
exceeding 50 pCi/L for surface water systems serving more than 100,000, the
available compliance monitoring data do not provide any specific information
on the levels of man-made radionuclides present in public water supplies.2

      In general, available data on the occurrence of man-made radionuclides
in drinking water are very limited.  As noted previously, the most important
source of relevant information is the ERAMS program, the data from which are
presented in the ERD reports published by EPA.

      In addition to the ERAMS, there are recent data available from the
National Inorganics and Radionuclides Survey (NIRS).  Although, as discussed
below, man-made radionuclides were not specifically included as analytes in
NIRS, gross beta activity levels were measured, and these data are presented
here.

Environmental  Radiation Data Reports

      The drinking water program of the ERAMS monitors ambient radiation
levels in drinking water grab samples from 78 sites that are either major
population centers or selected nuclear facility environs.  These sites all
     2There  are  approximately  275  surface  water  systems  serving 100,000 or
more people  required to perform compliance monitoring under the interim
regulations.  An attempt was made  to determine how many other water supplies
have been designated by the states as being affected by nuclear facilities.
No information on this is available at EPA.  Based on a limited number of
contacts made at the state level,  it appears that very few, if any, such water
supplies have been so designated.
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 involve  surface water sources.   Data  for  a  few  other  sites  are  also
 occasionally reported as  well.

       The  relevant  man-made  radionuclide  analyses performed  at  the ERAMS
 drinking water sites  are:

       •  tritium on a quarterly  basis
       •  gross beta,  strontium-90  and gamma radiation as annual composites
       •  iodine-131 on one quarterly  sample per year  for each station

       At the time that the Ellis et al. (1986) report was prepared, ERD
 reports  providing information on the occurrence of man-made  radionuclides in
 drinking water were only  available through March 1985.  Published ERD reports
 are now  available that cover the period through March 1989.  Table II-l
 presents a  summary  of the ERAMS data on "beta-emitting" man-made radionuclide
 levels found in  drinking water as  reported in the ERD reports covering the
 period from mid-1986  through March 1989.  The following sections summarize the
 ERAMS  data  by  parameter measured.3

       It should  be  noted that the data presented here for gross beta, tritium,
 strontium-90 and  iodine-131 taken  from the more recent ERAMS data do not
 differ markedly  from  the values reported  in the earlier ERD  reports and
 summarized  in  Ellis et al. (1986).

 GROSS  BETA

      Although  there  is currently no MCL  per ie for gross beta, gross beta
 activity measurements  are used in the compliance monitoring  scheme as a
     3Note that some ERAMS data presented in these tables are shown as
negative values.  As discussed in the ERD reports, negative values are a
result of the procedure for measuring radionuclides in which a previously
determined background level is subtracted from a measured sample value that
happens to fall below the background level.  Though having no real physical
meaning, these negative values when taken together with all other observations
can be used to describe the overall distribution of activity levels.  Also,
these values allow for better evaluations of trends in the data and facilitate
estimates of biases in the nuclide analytical methods.

DRAFT                                II-6

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Table II I   Summary "I Recent KItAMS Data on llcla Emitting Man-Made Uadiomiclides in Drinking Water"
KRAMS Site
AK: Pairbanks
Al.: Dolhan
Al.: Montgomery
Al.: Muscle Shoals
Al.: Scoltsboro
Alt: I.illle Itock
CA: Uerkelcy
CA: l.os Angeles
CO: Denver
CO: I'lalleville
CT: llarllord
DC: Washington
DI-: Dover
DE: Wilmington
PL: Miami
PL: Tampa
CiA: llaxley
CiA: Savannah
III: Honolulu
IA: Cedar Rapids
ID: Hoise
ID: Idaho Palls
II.: Morris
Gross Belab
Min Max Avg
2.2 3.0 2.7
1.6 3.0 2.2
1.6 1.7 1.6
0.7 2.7 1.5
2.1 2.K 23
O.I 1.9 I.I
0.7 1.5 1.1
0.0 6.4 3.8
1.2 2.0 1.7
6.5 7.6 6.9
0.5 1.5 1.1
2.0 3.0 2.6
3.5 5.4 4.3
0.0 2.9 1.5
0.9 2.1 1.5
1.8 4.8 3.2
1.8 1.8 1.8
1.2 2.7 1.7
1.2 2.1 1.6
2.8 3.3 3.0
0.4 1.7 1.0
2.6 4.7 3.9
16.1 17.2 16.6
Tritium0
Min Max Avg
0 300 180
100 300 150
100 300 150
2(K) 400 270
200 400 240
100 200 170
100 300 170
100 200 150
100 300 170
100 400 240
100 300 160
100 200 180
100 200 130

100 400 190
100 300 140
100 200 150
100 2500 1120
100 200 170
100 400 210
100 300 140
100 300 160
100 200 150
lodinc-131d
Min Max Avg
O.I 0.0 -0.1-
-0.2 0.1 -0.0
0.0 0.2 0.1
0.1 0.0 -0.1
0.2 0.3 0.1
O.I 0.1 0.1
-0.5 O.I -0.2
-0.1 0.1 0.0
-0.1 -0.1 -0.2
0.1 O.I 0.0
0.0 0.3 0.1
O.I 0.2 0.2
-0.3 0.1 -O.I

0.2 0.0 -O.I
-0.1 0.0 -0.1
2.5 0.0 -1.3
0.0 0.2 0.1
-0.3 0.0 -0.2
-0.2 0.1 0.0
-0.1 0.2 0.0
-0.4 0.3 -0.0
-0.1 0.2 0.1
Slrontium-90e
Min Max Avg
-0.2 0.2 0.0
-0.1 0.1 0.0
-0.2 0.3 O.I
-0.1 0.3 0.1
0.0 0.2 0.1
0.0 0.2 O.I
-0.2 0.2 0.0
-0.4 0.2 -0.0
-0.3 0.2 0.0
0.1 0.3 0.2
-0.1 O.I 0.0
O.I O.I 0.1
0.0 0.1 0.1
0.3 0.3 0.3
0.0 0.1 0.0
0.0 0.3 0.2
-0.1 -O.I -0.1
0.0 0.6 0.2
-0.1 0.2 0.0
-0.3 O.I -O.I
0.0 0.3 O.I
-0.3 0.3 0.0
-0.2 0.3 0.1

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Table ll-l.  (Continued)
CRAMS Site
IL: W. Chicago
K.S: Topeka
I.A: Nc\v Orleans
MA: 1 jiwrcnce
MA: Uowe
Ml): liallimore
MO: Conowingo
ME: Augusta
Ml: Detroit
Ml: Grand Rapids
MN: Minneapolis
MN: Ked Wing
MO: Jefferson City
MS: Jackson
MS: I'ort Gibson
MT: Helena
NC: Charlotte
NC: Wilmington
ND: liismnrck
NT,: Lincoln
Nil: Concord
N.I: Trenton
N.I: Warelown
Gross Helab
Min Max Avg
14.9 22.9 17.8
5.5 7.5 6.4
2.4 3.7 3.0
1.0 2.1 1.4
0.3 0.7 0.5
1.2 3.4 2.2
1.2 2.6 1.9
O.I 1.1 0.6
1.7 1.9 1.8
2.3 2.5 2.4
1.8 2.8 2.3
5.3 7.4 6.2
3.7 7.1 5.4
2.1 4.2 3.1
3.6 7.0 5.1
2.5 4.2 3.2
0.6 1.9 1.4
2.2 2.<> 2.4
2.4 4.7 3.3
10.4 11.7 11. 1
0.2 0.9 0.6
0.6 1.3 1.0
0.1 1.5 0.9
Triliumc
Min Max Avg
100 300 150
100 400 180
100 300 220
100 300 160
100 200 150
100 400 190
100 500 250
100 400 ' 210
200 400 260
200 500 250
200 300 220
100 200 150
100 200 150
100 200 170
100 300 150
100 300 240
300 1000 640
100 300 180
100 300 190
100 300 200
100 300 160
100 300 160
1(K) 200 120
Iodine-I31d
Min Max Avg
0.0 0.0 0.0
0.0 0.1 0.1
0.4 0.0 -0.2
0.0 0.3 0.2
0. 1 0.2 0.2
0.1 0.3 0.2
0.0 O.I 0.1
-0.2 0.1 -0.0
-0.2 0.1 -0.1
O.I 0.2 0.1
0.0 0.2 0.1
-O.I 0.1 0.0
0.3 0.3 0.3
0.0 0.3 0.1
0.1 0.2 0.0
-0.2 0.1 0.0
0.4 0.1 -0.1
-O.I 0.0 -0.1
0.0 0.2 0.1
0.1 0.2 0.1
-0.4 0.2 -0.1
O.I 0.3 0.2
0.0 0.1 0.0
Slronlium-90e
Min Max Avg
-0.2 O.I 0.0
-0.3 0.0 -0.2
0. 1 0.2 0. 1
-0.2 O.I -0.0
-0.5 O.I -O.I
-0.2 0.2 -0.0
-O.I 0.2 0.1
-0.1 0.1 0.0
0.5 0.8 0.7
-0.1 0.6 0.4
-0.4 0.1 -0.1
-0.6 0.4 -0.1
0.1 0.1 O.I
0.3 0.5 0.4
-0.2 O.I -0.1
-0.2 0.4 O.I
-0.5 0.2 -0. 1
0.0 0.1 O.I
-O.I 0.1 0.0
O.I 0.3 0.2
-0.3 O.I -O.I
-0.3 0.4 O.I
-0.2 0.1 0.0

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Table ll-l.  (Continued)
liKAMS Site
NM: S;int;i Te
NV: l,as Vegas
NY: Albany
NY: New York Cily
NY: Niagara Palls
NY: Syracuse
Oil: Cincinnati
Ol 1: Columbus
Oil: liasi Liverpool
Oil: I'ainesville
Oil: Toledo
OK: Oklahoma Cily
OR: Portland
1'A: Columbia
I'A: 1 larrisburg
I'A: I'illsburgli
1'R: Alteon
I'K: Coro/al
I'K: Cristobal
Kl: Providence
SC: llarnwell
SC: llnrnwell
S(.': Columbia
Gross »elab
Min Max Avg
1.9 7.6 4.';
3.0 6.7 5.4
0.1 1.3 0.8
0.6 1 . 1 (I.1;
I.I 2.5 1.6
1.6 2.4 2.0
2.2 3.1 2.5
3.4 18.2 8.4
1.3 3.1 2.3
1.6 4.1 2.7
1.7 2.8 2.2
2.1 2.7 2.3
0.6 0.9 0.7
1.2 2.9 2.2
0.6 1.2 0.9
1.3 3.4 2.1
0.1 0.8 0.6


1.0 1.5 1.2
0.4 1.5 1.1
2.2 2.2 2.2
2.0 2.0 2.0
Tritium'
Min Max Avg
100 200 120
100 200 180
100 300 160
100 300 170
100 300 180
KM) 400 210
100 300 200
100 300 190
KM) 200 150
200 300 210
100 300 210
100 200 180
100 200 150
100 300 180
100 300 180
100 300 170
100 200 130
400 400 400
100 100 100
100 200 140
100 200 150

200 600 370
lodine-131d
Min Max Avg
0.2 0.0 -0.1
-0.3 0.0 -0.1
-0.2 0.2 0.0
-O.I 0.2 0.0
0.0 0.2 0.1
00 O.I O.I
-0.2 0.4 0.2
0.0 0.1 0.0
0.0 0.4 0.2
-0.6 0.1 -0.2
0.0 0.1 0.1
-0.3 0.2 -0.1
0.0 0.3 0.1
O.I 0.3 0.2
-0.2 0.1 -0.0
-0.1 0.1 0.0
-O.I 0.3 O.I

-O.I -0.1 -0.1
-0.3 O.I -0.1
0.0 0.1 O.I
0.2 0.2 0.2
-0.2 0.1 -0.0
Stronlium-90c
Min Max Avg
-0.2 0.0 -O.I
0.1 0.6 0.4
-0.4 0.3 -0.0
0.1 0.3 0.2
O.I 0.7 0.4
0.2 0.6 0.4
0.0 0.3 0.1
-O.I O.I 0.0
-0.7 0.4 0.0
-0.2 0.9 0.3
0.1 0.6 0.3
-0.2 0.2 0.1
-0.3 0.2 0.0
0.1 0.7 0.3
0.0 0.2 0.1
0.0 0.5 0.2
-0.8 0.2 -0.2


-0.3 0.3 O.I
-1.3 0.0 -0.4
0.3 0.3 0.3
-0.4 0.3 -O.I

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                                                                              Table II-1.  (Continued)
ERAMS Site
SC: llarlsville
SC: Jcnkinsvillc
SC: Seneca
TN: Chattanooga
TN: Knoxvillc
'1'X: Austin
VA: Doswcll
VA: l.ynthburg
VA: Virginia Reach
VI: St. Thomas
WA. Kichland
WA: Seattle
Wl: Genoa City
Wl: Madison
WV: Wheeling
Gross Hciab
Min Max Avg
1.2 1.5 1.3
4.3 6.1 5.3
-1.2 1.2 0.3
2.0 3.9 2.8
1.5 2.7 1.9
2.8 4.4 3.5
4.3 6.1 5.0
0.6 1.5 1.0
2.6 3.2 3.0
O.I 0.7 0.3
1.3 1.9 1.6
0.5 1.2 0.8
0.8 1.7 1.2
1.0 1.2 1.1

Tritium0
Min Max Avg
100 200 140
100 300 190
100 300 200
100 500 300
100 300 180
100 400 190
100 300 190
100 300 170
100 200 130
100 300 150
100 600 250
100 200 130
100 200 130
100 200 150
100 100 100
lodine-131d
Min Max Avg
-0.2 0.1 -0.0
-0.1 0.0 -0.0
-0.2 0.2 0.0
0.0 0.4 0.2
•0.4 0.2 -0.0
-0.3 0.1 -O.I
-0.1 0.1 -0.0
-0.4 O.I -0.1
-O.I 0.4 0.1
-O.I -0.1 -0.1
-0.1 0.4 0.1
O.I 0.3 0.2
-0.3 0.0 -0.2
0.0 0.2 O.I

Slrontium-90e
Min Max Avg
-0.5 0.1 -O.I
-0.7 0.1 -0.2
-0.6 0.5 0.1
0.1 0.4 0.2
0.1 0.4 0.2
-0.7 0.2 -0.2
-0.3 O.I -O.I
-0.3 0.2 0.0
0.2 0.6 0.4
-0.6 0.2 -0.1
-0.4 0.2 -0.1
-0.4 0.4 0.0
-0.1 0.0 -0.0
-0.3 0.4 0.0

a All values in pCi/L; see Footnote 3 in text regarding negative values.
h Gross beta activity data are for annual composites 1985-1987 from EKD Reports 47, 51 and 54.
c Tritium activity data are for quarterly samples from ERD Reports 47 (July-Sept.  1986) through 57 (Jan.-March 1989).
d lodine-131 activity data are for one quarterly sample per year from ERD Reports 48 (1985), 53 (1987) and 57 (1988).
c Stronlium-90 activity data are for annual composites 1985-1987 from  ERD Reports 47, 51 and 54.

-------
screening device to determine whether a water supply should conduct more
detailed monitoring for specific man-made radionuclides.  There are two gross
beta "trigger values" in effect: 50 and 15 pCi/L.  Exceedance of the 50 pCi/L
level results in the requirement to conduct more comprehensive analyses to
identify the specific man-made radionuclides present and to determine the
annual dose from all such substances found for comparison with the 4 mrem/year
MCL.  The second screening value of 15 pCi/L is included only in the
monitoring scheme for those water supplies specifically designated as having
source water potentially contaminated by effluents from nuclear facilities.
Exceedance of the 15 pCi/L level in that scheme requires that additional
monitoring for strontium-89 and cesium-134 be conducted.

      The gross beta activity levels shown in Table II-l reflect the averages
of annual composites taken at the indicated sites for 1985 through 1987.  In
almost all cases, data were provided for all 3 years, although in a few cases
results were provided for only 1 or 2 years.  As indicated by these data, the
average gross beta levels at these sites ranged from 0.3 to 17.8 pCi/L, with
average values generally falling below 3 pCi/L.

      There were no instances in which the gross beta levels during this
period exceeded 50 pCi/L at any of these sites; however, there were a few
instances in which gross beta activity exceeded the 15 pCi/L value, most
notably at the Morris and West Chicago, Illinois sites where the gross beta
activities for the 3-year period ranged from 14.9 to 22.9 pCi/L.  No
information was provided in the ERD reports on these sites to explain the
relatively high gross beta levels.   However, a contact with the Illinois
Department of Nuclear Safety revealed that those relatively high gross beta
activity levels are apparently due to naturally occurring rather than man-made
radionuclides; however,  the specific nature of the naturally occurring sources
was not specified.
DRAFT                                11-8

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TRITIUM4

      The current drinking water regulations specify a tritium level of 20,000
pCi/L as the amount assumed to produce a total  body/organ dose of 4 mrem/year.
It should be noted that the Proposed Rule Making (PRM) shows a substantially
higher level of 60,000 pCi/L to be the 4 mrem/year equivalent.

      The available ERAMS data show that tritium levels are very low by
comparison to the 4 mrem/year equivalent levels.  As shown in Table II-l, the
range of the quarterly tritium levels reported  between 1985 and 1987 was 0 to
2,500 pCi/L, with average values generally falling in the 100 to 300 pCi/L
range.

STRONTIUM-90

      The current drinking water regulations specify a strontium-90 level of 8
pCi/L as the amount assumed to produce a total  body/organ dose of 4 mrem/year;
the ANPRM shows levels of 50 and 700 pCi/L as the 4 mrem/year equivalent.  As
shown in Table II-l, annual composite samples for strontium-90 for 1985 to
1987 do not approach any of those values, ranging from -1.3 to 0.9 pCi/L, with
typical average values falling below 0.2 pCi/L.

IODINE-131

      Although not having a 4 mrem per year equivalent level specified in the
current drinking water regulations as do tritium and strontium-90, the
compliance monitoring scheme indicates that an  iodine-131 level of 3 pCi/L is
the MCL compliance level (presumably derived from the NBS Handbook); the ANPRM
indicates that 700 pCi/L is the 4 mrem/year equivalent.  As shown in Table
II-l, the annual composite measurements for iodine-131 are far below these
levels, with a range of -2.5 to 0.4 pCi/L, and  typical average values falling
below 0.1 pCi/L (including many that are negative values).
     4Note that,  although tritium is a beta  emitter,  tritium levels  are not
reflected in the gross beta analyses because the calibration procedure for
gross beta analyses precludes detecting the low energy beta emissions from
tritium.
                                     II-9

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GAMMA RADIATION

      The interim drinking water standards include "photon radioactivity"  in
the definition of the MCL for man-made radionuclides.  Gamma radiation, which
provides the measure of photon radioactivity, is included as a parameter in
the annual composites at ERAMS sites.  For 1985 to 1987, all sites were
reported as having nondetectable (ND) levels for gamma radiation; however, no
information was given in the ERD reports on the detection limit for gamma
radiation in drinking water samples.

National Inorganics and Radionuclides Survey (NIRS)

      As noted in the Introduction, the NIRS results were not available at the
time Ellis et al. (1986) was prepared.  NIRS was designed to provide data  to
support the development of drinking water regulations for a wide range of
inorganic and radionuclide contaminants.  With regard to radionuclides,
however, the survey focused primarily on certain naturally-occurring
radionuclides (radon, radium-226, radium-228, and uranium).  In addition,  the
NIRS sample sites (approximately 1,000) were exclusively ground water supplies
which, as noted previously, are generally not considered to be at high risk of
contamination from man-made radionuclides.  Although there were no analyses
conducted for specific man-made radionuclides in NIRS, gross beta activity
analyses were performed.  The results of those analyses are summarized below.

      There were 990 sites in NIRS for which gross beta analyses were
reported.  Of these, 440 had levels above the minimum reporting level of 2.3
pCi/L.  There were nine sites (0.9%) reporting gross beta activity levels
above 50 pCi/L (maximum of 94 pCi/L), and 102 sites (10.3%) with levels above
15 pCi/L.  The mean gross beta activity for all  sample sites (assuming a value
equal to one-half the minimum reporting level for the "non-detects") was
approximately 6 pCi/L.

      Longtin (1988a) conducted a "beta activity balance" analysis to
determine the contribution of radium-228, the only beta emitter specifically
measured in NIRS,  to the total  gross beta levels observed.  Finding that the
bulk of the gross beta activity was not accounted for by radium-228, Longtin

DRAFT                                11-10

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(1988b) subsequently expanded the activity balance analysis to take into
consideration potential contributions of potassium-40 and rubidium-87, two
important naturally-occurring, non-series beta emitters.  Based on measured
potassium levels in the NIRS samples, and using the known relative isotopic
abundance of potassium-40, Longtin concluded that potassium-40 would generally
contribute more to the gross beta activity in the NIRS samples than radium-
228.  Based on crustal abundance considerations, Longtin concluded that
rubidium-87 would contribute only about an order of magnitude less activity
than potassium-40.  Even with those two sources considered along with radium-
228, however, there remained a considerable "deficit" of beta activity in the
NIRS samples (generally ranging from 50 to 90 percent of the gross beta
activity) that could not be accounted for by these specific substances.
Longtin concluded that the unaccounted for beta activity was most probably due
to beta emitting decay products of the uranium and thorium series and/or
errors in the gross beta analyses.  No suggestion of contributions by man-made
radionuclides was made by Longtin.

D.    CONCLUSIONS

      The absence of any violations of the current interim drinking water
regulations reported in the compliance monitoring data, together with the
consistently low levels of gross beta and specific man-made radionuclide
levels reported for the ERAMS sites, strongly suggest that there is little or
no occurrence of man-made radionuclides in surface water based drinking water
supplies at levels of concern relative to current MCL values.  The limited
data for ground water supplies are not sufficient for drawing conclusions
about man-made radionuclide occurrence, although other considerations suggest
that contamination is unlikely.

      It also appears that, with the current monitoring schemes, very few if
any public water supplies using surface water would find sufficiently high
levels of gross beta activity to require more specific monitoring.  The NIRS
data, however,  suggest that current screening levels for gross beta activity
of 50 pCi/L could, if applied to all ground water systems, result in about
1  percent of them being required to conduct further monitoring;  about
DRAFT                                11-11

-------
10 percent of ground water systems may exceed a gross beta activity screen of
15 pCi/L.

      It must be recognized,  however,  that the available data upon which these
conclusions are based are extremely limited.
DRAFT                                11-12

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     III.   PROFILES OF REPRESENTATIVE BETA OR GAMMA EMITTING  RADIONUCLIDES

A.    INTRODUCTION

      In the following sections  profiles  on  strontium,  iodine, and tritium are
provided.  For each radionuclide,  the profile  includes  a discussion of
physical and chemical  properties,  toxicokinetics,  health effects in animals,
and health effects in  humans.   Discussions of  the  toxicokinetics include
absorption, distribution,  bioaccumulation and  retention, and excretion.
Health effects sections  are organized in  the following  fashion:  first by
route of exposure (oral,  inhalation,  parenteral),  toxicological endpoint, and
species.  For all of these radionuclides, data on  toxicokinetics and health
effects following oral  exposure  are available.   These data are certainly  more
applicable than data from other  routes  of exposure for  estimating risks from
ingestion of radionuclides in  drinking  water.   However, since health effects
by other routes are generally  similar,  information on toxicokinetics and
health effects from exposure by  other routes is  also  presented.

      The relevance of information on other  routes of exposure to estimates of
potential health concerns  from the radionuclides  in drinking water is
dependent upon whether the pattern of distribution observed after exposure by
that route is similar  to  that  observed  after oral  exposure.  For example,
following oral exposure  to strontium,  distribution of the absorbed amount in
laboratory animals was primarily to the skeleton  followed by the liver and
other soft tissues.   Data  on distribution kinetics of strontium following
parenteral exposure were  not located;  however,  at  long  times following single
injections of high doses  of strontium,  hematological  effects (indicating
damage to bone marrow)  and other skeletal effects  (such as fractures, bone
marrow hypoplasia, and bone tumors) have  been  observed.  These effects are
similar to those observed  following high  oral  doses of  strontium.

      When compared to an  oral dose of  the same  radiological  activity,
intravenous exposure delivers  a  much  higher  dose  of strontium to these target
tissues resulting in effects much  more  severe  than should be expected
following oral exposure.   But  this example illustrates  that the main target
tissues are the same for  the two routes of exposure,  and, by. use of data on

DRAFT                                III-l

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absorption of  strontium from the gastrointestinal tract, relative
distribution,  dose equivalent, and cancer risks to these tissues may be
predicted.

      Use of data on toxicokinetics and health effects following inhalation
exposure is more complex due to the fact that distribution of beta/gamma
emitting radionuclides from the lung is largely dependent on the isotopic form
and solubility of the particular form administered.  However, depending upon
the particular isotope, distribution to other tissues than the lung, such as
the liver and  skeleton have been reported, as well as cancer in each of these
tissues.

      Therefore, even for  inhalation and injection routes, data on health
effects may be relevant when data on distribution, when compared to
distribution following oral exposure, are similar.

B.    STRONTIUM

Physical and Chemical Properties

Chemical Properties - Elemental

      Strontium is an alkaline earth element usually found as celestite or
strontianite.  The metal  may be prepared by reducing strontium oxide or by
electrolysis of the fused chloride mixed with potassium chloride.   Three
allotropic forms of strontium are known to exist with transition points at
235°C and 540°C.  Freshly cut strontium has a silvery appearance that quickly
changes to a yellowish color upon oxidation.  Finely divided strontium is
pyrophoric (Weast 1981).

      Strontium only forms divalent compounds,  and the solubility of its
compounds are  usually greater than those of barium (Carson et al.  1986).
Strontium chemistry resembles that of calcium;  however,  strontium has greater
base-forming characteristics than calcium but less than  those of barium
(Hampel  1968).   Because strontium is a reactive metal, exposure to air results
in an oxide coating which quickly covers the metal.  Two strontium oxides

DRAFT                                III-2

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known to exist are strontium oxide and the peroxide, strontium dioxide.
Strontium reduces halides and oxides of many metals at elevated temperatures,
thereby producing the corresponding metal  (Hampel 1968).  Strontium is an
active reducing agent that reacts violently with water to liberate hydrogen
and form strontium hydroxide.  Strontium reacted with acids forms hydrogen and
the strontium salt of the acid.  Strontium will burn when heated in air,
oxygen, chlorine, bromine gas, and sulfur, thus producing a bright crimson
color.  Strontium forms the nitride only in nitrogen at temperatures greater
than 380°C (Hampel 1968).

      Strontium compounds are analogous to the corresponding calcium
compounds.  Consequently, the strontium compounds of sulfide, chloride,
bromide, iodide, nitrate, etc. are soluble, whereas the carbonate, fluoride,
sulfate, oxalate and phosphate compounds are not.  The only major difference
occurring between the solubility of strontium compounds and calcium compounds
is that strontium hydroxide is very soluble in hot water (100°C) and calcium
hydroxide is not (Hampel 1968).

Physical Properties

      Strontium (atomic number 38, atomic  weight 87.62) is an alkaline earth
element located between calcium and barium in Group IIA of the Periodic Table
and its physical and chemical properties resemble both elements.  Strontium is
a hard, silver-white metal  softer than calcium, ductile and malleable, and
capable of being formed into wire.  Strontium has a melting and boiling point
of 769°C and 1384°C, respectively, and its specific gravity is 2.54 (Weast
1981).  Some chemical and physical properties of elemental  strontium are
listed in Table III-l,  adapted from Faure  and Powell (1972).
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      Table  III-l.   Physical and Chemical Properties of Strontium
       Properties
       Atomic number                                     38
       Atomic weight  (based on 12C)                      87.62
       Ionic radium  (A) (Pauling)                        1.13
       Radius ratio  (O2" = 1.40 A)                        0.81
	Electronegativity  (Pauling)	KO	

      Strontium occurs  naturally as a mixture of four stable isotopes:
strontium-84 (0.56 percent), strontium-86 (9.86 percent), strontium-87
(7.02 percent), and strontium-88 (82.56 percent).  In addition, 12 unstable
radioactive isotopes  are  known to exist, the most important being strontium-90
(half-life of 28 years) (Weast 1981) because of its presence in radioactive
fallout (Hampel 1968),  and strontium-89 (half-life of 50 days).  Strontium-89
and strontium-90 emit beta energies of 1.5 MeV and 0.61  MeV, respectively
(Hampel 1968).  Rubidium-89 decays to strontium-89 which subsequently decays
to the stable isotope of yttrium-89.  Strontium-90, a decay product of
rubidium-90, decays to  yttrium-90 which in turn decays to stable zirconium-90
(Brucer 1979).  Half-lives and decay schemes of strontium-89 and -90 may be
seen in Figure III-l, adapted from Brucer (1979).

Summary

      Strontium is a divalent alkaline earth element (Group IIA of the
Periodic Table) with physical and chemical properties similar to those of
calcium and barium.   It is a silver-white metal, ductile and malleable, and
readily oxidizes in air.  Strontium is an active reducing agent and reduces
halides and oxides of many metals at elevated temperatures, consequently
producing the corresponding metal.   Strontium compounds  are analogous to the
corresponding calcium compounds and include the soluble  sulfide, chloride,
bromide,  iodide, and nitrate compounds and the insoluble carbonate, fluoride,
sulfate,  oxalate, and phosphate compounds.

      Strontium occurs  naturally as a mixture of four stable isotopes:
strontium-84,  strontium-86, strontium-87,  and strontium-88. •Twelve

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                Figure 111-1. Half-Lives and Decay Schemes
                        of Strontium-89 and -90
              Sr -89 (a)
              50.5 d (b)
             B" = 1.489
              Y-89
             (Stable)
            Sr-90
            29.12 y
           B~ = .546
                                      Y -90 m -
                                      3.19 h
                                     B- = .480
                *  Y-90
                  2.67 d
                 B'= .2779
                                              Zr-90
                                             (Stable)
      a = half-life
      b = maximum B' decay energy in MeV
      m = metastable
      Brucer 1979
      ICRP1983
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radioactive  isotopes  of  strontium are known to exist, the most important being
strontium-90 because  of  its  presence in radioactive fallout and the fact that
it has the longest half-life (28 years) of the artificially produced strontium
isotopes.  Strontium-89  is another  important radioactive isotope and has a
half-life of 50 days.  The beta energies emitted by strontium-90 (decays to
xenon-90) and  strontium-89 (decays  to xenon-89) are 0.61 and 1.5 MeV,
respectively.

Toxicokinetics

Absorption

      In this  analysis strontium, unless otherwise noted, refers to strontium-
89 or -90.  Human gastrointestinal  absorption values ranging from 15 to 36
percent have been suggested  (Stara  et al. 1971, Spencer et al. 1972a).  ICRP
(1979) lists 30 percent  as the accepted value.  Strontium inhaled as strontium
chloride is rapidly absorbed into the bloodstream (McClellan et al. 1972).
Net strontium  absorption  in  young adults is similar to that found in older
persons (Spencer et al.  1972b).  Gastrointestinal absorption has been
determined to  be 11 percent  for dogs, 26 percent for cats, 16 percent for
monkeys, and 15 percent  for  rats (Stara et al. 1971).  Spencer et al. (1972b)
noted that calcium alone  and in conjunction with phosphorous decreased
strontium absorption  in  rats but, for reasons unknown, no such effect occurred
in humans.

Distribution

      Of the absorbed amount, initial fractional uptake to bone in humans is
reported to be 27 percent, while the reported uptake to other tissue is 73
percent (ICRP  1979).  Final  strontium distribution in adults is primarily to
the skeleton (uniformly  to within 10 percent) due to the fact that strontium
can substitute metabolically for calcium, though no time frame is given for
this or for the ICRP data (Stara et al.  1971, Kulp et al. 1959).   Strontium
distribution in the skeleton is relatively uniform throughout gestation and in
young children (Kawamura et  al. 1986, Kulp et al. 1959).  Since strontium is
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known to be a bone-seeker, 98 percent of the associated risk of cancer is from
the irradiation of the skeleton and bone marrow (Thorne and Vennart 1976).

      A study of strontium chloride in 452 beagle dogs exposed orally
beginning in utero (by oral exposure of the dam) and continuing to age 540
days found strontium distribution to be dependent on local bone turnover and
the beagle's age (Momeni et al. 1976).  Deposition was primarily to newly
forming bone surfaces or other areas of active bone formation (Stara et al.
1971).  Distribution was relatively uniform to all areas of the skeleton at
the end of the dosing period but, over time, became variable due to the uneven
rate of bone turnover (Pool et al.  1973).  Age of the subject was a factor
because younger organisms have more areas of active bone formation than mature
individuals.  During the feeding period strontium uptake to bone, plasma,
gastrointestinal tract,  and to soft tissues was uniform.  Thirty days after
the end of the feeding period in these beagles 78.5 percent of skeletal burden
of strontium was deposited in cortical (compact) bone, with a retention half-
life of 10.3 years, while the remainder was deposited in trabecular (spongy)
bone, with a retention half-life of 0.45 years (Momeni et al. 1976).  The
gastrointestinal tract,  plasma, and soft tissues retained a low level of
radioactivity (10 percent) at one year post-exposure.

      Strontium inhaled  as strontium chloride was distributed primarily to the
skeleton.  By 8 hours after exposure, 85 percent of the absorbed strontium was
found in the skeleton, while only 2.5 percent remained in the lungs (Gillett
et al. 1987, McClellan et al.  1972).  In beagles aged 1.5 years exposed via
single injection, 27 percent of the injected dose was retained after 30 days;
of this amount 46 percent had a retention half-life of 0.45 years (because of
its deposition in spongy bone) while the remainder (54 percent) had a
retention half-life of 7.6 years (because of its deposition in cortical bone)
(Momeni et al. 1976).  The rate of clearance from the skeleton showed no
relation to dose (Parks  1991).

Excretion

      Although little data are available regarding human excretion of
strontium, one relevant  study was located.  Warren and Spencer (1978) exposed

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 ten humans to 3.3 pCi strontium/day via the diet, and reported that about 84
 percent of the intake was excreted via the feces, while 14 percent was
 excreted in the urine.

 Bioaccumulation and Excretion

       See Section E.  In this section toxicokinetic models for beta or gamma
 emitting radionuclides are used to predict the potential  bioaccumulation and
 retention for these radionuclides.  Some of the metabolic models are based on
 extensive human and animal data,  some on primarily animal  data and some on
 similarity of elemental  characteristics.   The model  for strontium may be found
 on page 111-59.

 Summary

       Human absorption of strontium was  reported to  be  between 15 and 36
 percent,  though  30 percent was  the accepted value.   In  humans,  initial
 distribution  to  bone was 27 percent of the absorbed  amount,  with uniform
 distribution  to  all  areas of the  skeleton,  while final  distribution was
 primarily to  the  skeleton.   The distribution  varied  within the skeleton due to
 the  uneven  rate  of bone  turnover.   Excretion  of strontium  was  mainly via the
 feces  (84 percent),  with 14 percent excreted  in the  urine.

 Health  Effects  in  Animals

 Short-Term  Exposure

      Short-term exposure to  strontium has  been  associated with  hematopoietic
 changes,  bone marrow hypoplasia,  and liver  lesions.  A  study of  44  cats
 exposed by  gavage  to 25,  50,  or 100 (iCi strontium/day for  a month reported
 dose-related mortality,  hemorrhaging, depression of  platelet counts,  and  bone
 marrow  lesions, and  nondose-related bone marrow  hypoplasia and depression of
 lymphocyte  and neutrophil counts  (Nelson et al.  1972).  Hemorrhaging was  also
 reported  in pigs,  dogs,  mice, and cattle exposed to  strontium  (Ward  and Wright
 1972).  In  a group of  seven adult monkeys exposed orally to a  single dose of
 500 or  1,000 jiCi strontium, one monkey exposed to 1,000 nCi.died at  4 months

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post-exposure with pancytopenia, i.e., a decrease in all cellular components
of blood, while others developed tumors and leukemia (discussed in the section
on carcinogenicity) (Mays and Lloyd 1972).

      Few inhalation studies were located in which the soluble form of
strontium was used.  In one such study, 71 beagle dogs were exposed to a
single inhalation of strontium chloride resulting in initial body burdens of
2.5 to 250 pCi strontium/kg (Snipes et al . 1981).  Atrophy of the liver and
nonneoplastic liver lesions were reported (Snipes et al . 1981).  A related
study exposed dogs to 0.999 to 118.8 pCi strontium chloride/kg, and reported
the development of dose-dependent pancytopenia (Gillett et al . 1987).
      Beagles intravenously injected with 32.4 to 105.3 nCi strontium/kg
developed depressed platelet,  lymphocyte, and neutrophil counts, and anemia by
2 to 5 weeks after injection (Gillett et al .  1987).   Deaths due to bone marrow
hypoplasia were reported in the 64.8 and 105.3 jiCi treatment groups.  In a
further study, Taylor et al .  (1966)  determined that, in contrast to the
behavior of other radionucl ides,  a single injection of 100 ^Ci strontium/kg
seldom produced fractures in beagle  dogs at intervals up to 3,400 days post-
exposure.  Finkel et al . (1972),  however, found that a series of daily
injections of 5.8 jiCi of strontium given over 90 days to beagle dogs beginning
at 4 to 8 days postpartum resulted in many bone fractures.

      The injection of strontium in  mice caused prolonged hypoplasia of bone
marrow and impaired marrow hematopoiesis, resulting in a decrease in
lymphocyte counts (Ito et al .  1976).  A high  rate of cell death was noted in
lymphocyte populations,  as would be  expected  based on the radiosensitivity of
these cells (Stevenson et al .  1982).  Further, Monig et al . (1980) noted that
a single injection of strontium resulted in the disturbance of iron
incorporation into the peripheral  red blood cells of mice.  The incorporation
of iron reflects the level of  red  blood cell  production.  Red blood cell
production decreased initially but later increased to slightly above control
values.
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 Lonqer-Term Exposure

       Longer-term exposure to strontium has been associated with hematopoietic
 changes, bone marrow hypoplasia, excess growth of bone marrow, and a decrease
 in immune system function.  Shubik et al.  (1978) exposed rats to drinking
 water containing various concentrations of strontium or strontium chloride in
 an effort to study immune system response.  Rats exposed to 10,000 times the
 average annual permissible concentration (AAPC = 1.2xlO"8 Ci/1) of strontium
 showed the inhibition of nonspecific protection factors (including humoral
 factors such as lysozyme activity and cellular factors such as phagocytic
 activity of neutrophils),  while 1,000 times the AAPC resulted in  increased
 production of anti-tissue autoantibodies (which attack the  organism's own
 tissue).   These changes may affect the ability of the rat's immune system to
 function properly,  possibly allowing the development of malignant neoplasms
 and infectious complications  (Shubik et al.  1978).   Studies using beagle dogs
 orally exposed to strontium beginning j_n utero.  via  exposure of the  dam,
 continuing in  offspring to age 19 months at  0.081  to 118.8  jiCi/day have
 revealed  the development of dose-related myeloproliferative disease  (Gillett
 et  al.  1987).   A gradual and  persistent decrease in  leukocyte count  developed
 due to a  decrease in  neutrophils during the  first  1.5 years of exposure.   In
 animals  in the high-dose group,  the  maximum  depression of neutrophils was  47
 percent  (Gillett et al.  1987).

       An  ingestion study performed over the  lifetime of an  unknown number  of
 swine,  at  0.999  to 2,970 yCi  strontium/day,  resulted in  the development  of
 bone marrow  hypoplasia  and  myeloproliferative  disease  (Gillett  et  al.  1987).
 Ragan  et  al.  (1972) exposed more than  700  swine  to 1  to  3,100  jiCi
 strontium/day  over three generations  and noted the development  of  a dose-
 related decrease  in platelet,  neutrophil, and  lymphocyte counts,  in addition
 to  the development of myeloproliferative disease.

 Reproductive Effects

      No effects  on mortality, reproductive fitness,  or survival have been
noted at oral or  injected doses  up to and including  those subacutely  lethal to
the mother (Goldman and  Bustad 1972, Clarke et al. 1972).   Goldman and Bustad

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(1972) indicated that placenta!  and mammary barriers reduce strontium
concentration in the offspring,  relative to the maternal  concentration.
Following maternal  ingestion the placenta discriminates against the movement
of strontium across the placenta,  relative to calcium reducing the maternal-
fetal ratio by a factor of 5 (Delia Rosa et al. 1972).

Mutaoenicity

      Ito et al. (1976) studied  mice exposed via injection to strontium and
detected chromosomal aberrations in lymph nodes and bone  marrow.  Chinese
hamsters injected with 1 nCi of  strontium also incurred an increased frequency
of chromosomal aberrations of bone marrow (Volf 1972).

Carcinoqenicity

      In addition to the effects already discussed, exposure to strontium
resulted in tumor development and  leukemia in animals.   Wright et al.  (1972)
studied the effects of strontium ingested by mice for a period of 180 days,
beginning at conception or weaning.  Mice were exposed  to 20 or 60 yCi
strontium chloride/g of dietary  calcium/day.  Hematopoietic neoplasms, mainly
lymphatic leukemia, and bone tumors, primarily of the appendicular skeleton,
were the major causes of death.   Leukemia appeared early, while bone tumors
occurred after a latent period,  the length of which was not reported.

      Pool  et al. (1973) studied 373 dogs exposed via ingestion to 0.03 to 36
yCi strontium/day from in utero  to 1.5 years of age.  At  the high-dose, normal
bone formation was accompanied by  a high rate of osteocyte cell death and
cortical focal necrosis, to the  extent that the damage  was irreversible.  At
lower doses (12.5 ^Ci/day) repair  attempts were more "successful" and injury
developed more slowly, which may account for the longer latency period noted
at lower doses (Pool et al. 1973).  Dose-dependent bone tumors, osteosarcomas
(98 percent of which were malignant),  occurred first in high- dose animals and
later in lower dose groups, though the relative times to  tumor were not
reported.  Pool  et al. (1973) noted that this study and others in mice and
swine suggested  that attempts at repairing initial radiation injury may be a
prerequisite to  radiogenic tumor induction.

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      Parks et al . (1984) exposed 387 dogs via ingestion to 0.02 to 36
strontium/day for 1.5 years (21 days post-conception to 540 days) noting a
dose-related temporal effect on the development of squamous cell carcinoma
(SCC).  Dogs at higher doses developed SCC at an earlier age.  The highest
dose group was the exception presumably because animals died earlier with bone
tumors, primarily osteosarcomas, and leukemia.  In addition to significantly
higher numbers of animals with SCC, the percentages of carcinomas per location
in dosed groups differed from the percentages common in the controls.  In
controls, tumors were about evenly divided between tumors located near the
molars and pre-molars and tumors located toward the front of the mouth, 43 and
58 percent, respectively.  In dosed animals,  79 percent of the tumors were
located near the molars and pre-molars and 21 percent were located toward the
front of the mouth (Parks et a.l . 1984).  Another chronic ingestion study was
performed using 384 dogs exposed beginning in utero and continuing for 19
months to daily amounts of 0.081 to 118.8 jiCi strontium/day.  Gillett et al .
(1989) reported that, of the 46 primary bone  tumors developed by 41 dogs, 50
percent of the tumors were located in the appendicular skeleton.  In addition,
85 percent of the total number of tumors were osteoblastic osteosarcomas (bone
producing tumors) .
      The exposure of female swine via ingestion to 1 to 3,100
strontium/day resulted in the development of leukemia, but few bone tumors
(Clarke et al .  1972).  Ragan et al .  (1972) exposed swine orally to 1 to 3,100
nCi strontium and also noted a low incidence of bone tumors.  In contrast to
other studies where the primary effect was bone tumors, primary toxic effects
in swine were leukemogenic (causing leukemia) in bone marrow and
lymphoreticular systems (Clarke et al . 1972).  Monkeys exposed via ingestion
to 500 or 1,000 jiCi strontium developed bone tumors (osteosarcomas and
chondrosarcomas, cartilaginous tumors) and leukemia (Mays and Lloyd 1972).
Evidence compiled from studies using monkeys, swine, rats, mice, and dogs
indicated that strontium enhances the occurrence of the most common leukemia
in a species rather than eliciting a distinct type of leukemia.   In addition,
species with extremely low incidences of spontaneous leukemia appear more
resistant to the induction of leukemia by radiation (Clarke et al . 1972).
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      Following inhalation exposure to strontium chloride beagle dogs
developed bone tumors,  including hemangiosarcomas (tumors associated with
blood vessels), osteosarcomas,  and squamous cell carcinomas, and leukemia
(Benjamin et al .  1976,  Gillett  et al .  1989).   More specifically, Benjamin et
al .  (1974) noted that many of the 72  dogs exposed via inhalation to 2.5 to 250
\iC\  strontium chloride/kg developed mainly hemangiosarcomas and osteosarcomas.
The incidence of hemangiosarcomas was initially greater but the number of new
cases that developed declined over time.   Snipes et al .  (1981) found that
inhalation of strontium chloride also resulted in local  cancers, including
cancer of the lung, heart, and  tracheobronchial lymph nodes.  Most tumors
found in the tissues of these dogs were hemangiosarcomas.
      Dougherty et al .  (1972)  found that beagles injected with 64 to 98
strontium/kg developed  bone tumors, including hemangiosarcomas, osteosarcomas,
and squamous cell carcinomas,  after an average latency period of 1,243 days.
Nilsson (1972) studied  the effects of strontium in rodents.  The injection of
0.2 to 1.6 \id strontium/g in  mice resulted in leukemia and bone tumors.
Incidence of leukemia was highest in 0.2 to 0.4 yCi  strontium/g dose groups,
while osteoblastic and  fibroblastic (originating in  connective tissues)
osteosarcomas increased with dose to 1.6 nCi  strontium/g.  A clear relation
was seen between dose,  tumor incidence,  and time-to-tumor.  Those receiving
the high dose had more  tumors  (219) in a shorter period (an average of 267
days), while those receiving the low dose had fewer  tumors (8) and those
tumors had a longer latency period (an average of 485 days) (Nilsson 1972).
Ito et al . (1976) also  noted the development  of leukemia following strontium
injection in mice.  Bierke and Nilsson (1990) administered a single strontium
injection to mice and  reported the development of osteosarcomas, squamous cell
carcinomas, malignant  bone marrow lymphomas,  and liver tumors which progressed
to mal ignancy.

Summary

      Short-term exposure to strontium via ingestion, inhalation, and
injection resulted in  hematopoietic changes in cats,  monkeys, dogs and swine.
Among the most common changes  were the depression of lymphocyte and neutrophil
counts.   In addition, cats, dogs, and mice exposed to strontium exhibited bone

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marrow hypoplasia and, in many cases, myeloproliferative disease.  Researchers
using dogs exposed via inhalation reported liver lesions and atrophy of lobes
of the liver.

      Longer-term exposure resulted in similar effects including the
depression of lymphocyte and neutrophil counts and bone marrow hypoplasia and
myeloproliferative disease in dogs and swine exposed orally.  Rats exposed
orally exhibited a decrease in indicators of immune response, including
changes in factors of nonspecific protection and autoantibodies, possibly
indicative of reduced immune capabilities.

      No adverse reproductive effects were reported at levels below those
causing adverse effects in the dams.  Mutagenic  effects were seen in mice
exposed orally and in mice and hamsters exposed  via injection.  All three
groups exhibited an increase in the frequency of chromosomal aberrations in
bone marrow.

      Carcinogenic effects of radioactive strontium in animals are well
documented.  Oral exposure to strontium resulted in leukemia in mice, dogs,
monkeys, rats, and swine.  Mice reportedly developed dose-dependent
appendicular bone tumors, while dogs were reported to develop dose-dependent
squamous cell carcinomas (SCC) and appendicular  osteosarcomas.  The SCC
induced by strontium occurred in different percentages per location relative
to spontaneously occurring SCC in controls.  Exposure via the inhalation of
strontium chloride resulted in leukemia,  bone tumors, and local tumors in
beagle dogs.  Injections of strontium led to bone marrow tumors, liver tumors,
and leukemia in mice, as well  as bone tumors in  dogs.  Bone carcinomas in mice
occurred with a definite dose-relationship between tumor incidence and time-
to-tumor.  As with the ingestion study, higher doses resulted in more tumors
in a shorter period of time,  while lower doses led to fewer tumors after a
longer latency period.
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Health Effects in Humans

Clinical Case Studies

      Few case studies were located in which humans were exposed to strontium.
Human blood was irradiated (in vitro) using an external  source of strontium to
produce doses of between 13.8 and 276 rads.  Lymphocyte  aberrations, total
aberrations and the number of dicentrics (chromosomes with two centromeres)
per cell, increased with dose to 220 rads (Vulpis and Scarpa 1986).  The high
dose produced fewer total aberrations and dicentrics, perhaps because more
cells were killed at this dose.

Epidemioloqical Studies

      Stannard (1973) conducted a study of 103 luminous  dial painters exposed
to a compound containing strontium and radium-226 ratio  unreported.  The
incidence of chromosomal aberrations detected in the peripheral blood and bone
marrow of these individuals was twice that seen in the control group, which
reportedly consisted of healthy volunteers investigated  at the same time and
in the same manner.  Body burden estimates of strontium  in the exposed group
ranged from 0.1 to 1.9 jiCi (based on whole body counting and on strontium
excretion).  Pain in long bones and tendency toward subcutaneous hematomas was
noted in nearly half the subjects.  Evaluation of the hematology of the
subjects identified cases of leukopenia, neutropenia, and thrombocytopenia
(Volf 1972).  While these cases involve individuals also exposed to radium,
preventing any definitive correlations with the toxicity of strontium, these
effects correlate well with bioassay data derived from animals exposed to
strontium (Ito et al. 1976).

High-Risk Populations

      While there are currently no data available on the risk to young
children exposed to strontium, animal bioassay data suggested that this group
may be a high risk population for the development of bone tumors and of blood
disorders such as leukemia.  Evidence in mice, dogs, and pigs indicated that
the young may be up to four times as sensitive as adults to the induction of
                                    111-15

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bone tumors and may be more sensitive to the induction of blood disorders
(Mays and Lloyd 1972).

      In addition to possible increased sensitivity to strontium exposure, the
human fetus may be exposed to maternal concentrations of strontium via the
placenta.  Borisov (1972) studied skeletal ashes of human fetuses dying at
various stages of development in utero.  Based on average strontium blood
levels of women in Moscow and concentrations of strontium in the skeletal
ashes, Borisov determined that the placenta was not a strong barrier to the
movement of strontium.  In contrast, Warren (1972), using bone samples from
children whose mothers were exposed to nuclear fallout, determined that the
placenta  provided protection to the fetus by impeding the movement of
strontium.  This conclusion is supported by Kawamura et al.  (1986) who
determined the observed ratio of strontium in bone to strontium in diet for
adults to be 0.12 and the observed ratio of strontium in fetal bone to
strontium in maternal diet to be 0.055.

Summary

      Clinical case studies in vitro have revealed an increase in chromosomal
aberrations in human lymphocytes following irradiation with strontium.
Epidemiological studies of workers exposed to both strontium and radium-226
reported increased incidences of chromosomal aberrations in blood and bone
marrow of these individuals.  In addition, decreased leukocyte, neutrophil,
and platelet counts were noted.  Young children may be a high risk population
due their to increased sensitivity to the induction of bone tumors and blood
disorders following strontium exposure.  Studies suggested that the placenta!
membrane hindered the movement of strontium, reducing the concentration in the
fetus, relative to the maternal concentration, and thereby providing some
protection to the fetus.
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C.    IODINE

Physical and Chemical Properties

Chemical Properties - Elemental

      Iodine (I) is a member of the halogen family (Group VIIA of the Periodic
Table), and is a bluish-black,  lustrous, crystalline solid that volatilizes at
ordinary temperatures to a blue-violet gas (Weast 1981, Hawley 1981).  It
exhibits some metallic-like properties and is a semiconductor of electricity
(Mills 1968).  Although iodine  is nonmetallic, it dissolves in many organic
solvents including alcohol, chloroform, ether, carbon tetrachloride, glycerol,
carbon disulfide, and alkaline  iodide solutions;  however, it is only slightly
soluble in water and the least  soluble of the common halogens (Weast 1981,
Hawley 1981).  In solutions of  chlorides, bromides, and other salts, iodine is
somewhat more soluble.  No hydrates of iodine are known to exist (Mills 1968).
Iodine is the least reactive of the halogens but  will form compounds with all
the elements except the noble gases,  sulfur, and  selenium.  Unlike the
corresponding carbonyl, nitrosyl, or sulfuryl chlorides, iodine does not form
compounds with carbon monoxide,  nitrous oxide, or sulfur dioxide.  Iodine does
not react with carbon, nitrogen, or oxygen unless high temperatures and a
platinum catalyst are used (Mills 1968).

Physical Properties

      Elemental  iodine has an atomic weight of 126.9, atomic number of 53, and
a melting and boiling point of  113.5°C and 184.35°C, respectively.   The
density of the gas is 11.27 g/L  and its specific  gravity (solid) is 4.93 at
20°C.  Iodine can exist in valences of 1, 3, 5, and 7.  Physical properties of
iodine are listed in Table III-2, adapted from Mills (1968).  Iodine-127 is
the only stable isotope of iodine found in nature, although 23 isotopes are
known to exist.   Iodine-131 is  produced from the  radioactive decay of
tellurium-131 and decays to a stable isotope of xenon, xenon-131.  Iodine-131
has a radiological  half-life of  8.04 days and emits beta energy of 0.807 MeV
(Brucer 1979).   Iodine-129, a decay product of tellurium, is a radioactive
isotope with a half-life of 1.57xl07  years,  emits  beta energy  of 0.150  MeV,

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and decays to the stable xenon-129 (Brucer 1979).  Half-lives and decay

schemes of iodine-129 and -131 may be seen in Figure III-2, adapted from

Lederer and Shirley  (1978).

	Table  III-2.   Physical  Properties  of  Iodine	


 Atomic number                                 53
 Atomic weight                                 126.9044

 Solid Iodine

   Color                                       Bluish-black
   Melting point, °C                           113.6
   Density, g/cc, 20°C                         4.93
                  60°C                         4.886
   Crystal structure                           Orthorhombic
   Vapor pressure, mm Hg, 25°C                 0.31
                          113.6°C              90.5

 Liquid Iodine

   Color                                       Bluish-black
   Boiling point, °C                           185
   Critical temperature, °C                    553
   Critical pressure, atm                      116
   Density, g/cc, 120°C                        3.960
                  180°C                        3.736

 Gaseous Iodine

 Color                                         Violet
 Density, g/1, 185°C, 1 atm	6.75	


Summary


      Iodine is a non-metallic, crystalline solid that  volatilizes to a gas at

ordinary temperatures.  Although iodine is non-metallic,  it will  dissolve in

many organic solvents.  It is the least reactive of the halogens  but will form

compounds with most of the elements.   Only one stable isotope for iodine is

found in nature, iodine-127; however, 23 radioactive isotopes are known to

exist.  Two important radioactive isotopes are iodine-131  and iodine-127 with

half-lives of 8 days and 1.57xl07 years,  respectively.   Iodine-131  (beta

energy 0.807 MeV) decays to xenon-131 and iodine-129 (beta energy 0.150 MeV)

decays to xenon-129.
DRAFT                               111-18

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               Figure 111-2. Half-Lives and Decay Schemes
                        of lodine-129and -131
            -129
                 (a)
          1.6x107y(b)
          R-= .150
          Xe-129
          (Stable)
                   1-131
                   8.04 d
                  (T = .807
                 Xe-131
                 (Stable)
a = half-life
b = maximum B" decay energy in MeV
ICRP1983
DRAFT
111-19

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Toxicokinetics

Absorption

      Iodine is readily absorbed following oral, inhalation, or dermal
exposure.  Following oral iodine exposure, the majority was absorbed from the
stomach and the upper portion of the small intestine.  The oral rate of
absorption was approximately 5 percent of the administered dose per minute.
The USNRC (1975) has reported the absorption of iodine from the intestine at
95 percent.  Following inhalation exposure, between 50 and 90 percent of
deposited methyl iodine was taken up into the blood.  Deposition of iodine
particles in the lung was dependent on the physical properties of the
particulates (Johnson 1982).

Distribution

      Iodine is distributed to the thyroid almost immediately following an
oral or parenteral administration.  A maximum of 10 to 50 percent of the
administered oral or parenteral  dose was found in the thyroid within 1 to 2
days (Stara et al. 1971).  Following oral administration of iodine in women
with normal thyroid glands, uptake by the thyroid at 4 and 24 hours ranged
from 3 to 13 percent and 7 to 26 percent of the administered dose,
respectively (Schober and Hunt 1976).  Uptake to the thyroid following the
oral exposure of men with normal thyroid glands was 17.8 percent, slightly
less than that in the female (Ghahremani et al. 1971).  In addition to the
thyroid, iodine was also concentrated in the kidneys, gastric glands, mammary
glands,  and salivary glands of humans (Maier and Bihl 1987).  Twenty-four hour
iodine uptake into breast tissue was statistically significantly higher in
abnormal tissue, tissue with carcinoma or dysplasia (12.5 percent), compared
to histologically normal tissue (6.9 percent) (Eskin et al.  1974).  The
greatest tissue concentrations of iodine (those which exceeded concentrations
in the blood) in animals were found in the thyroid followed by the liver,
ovary, kidney,  adrenal, pituitary, lung, lacrimal gland, heart, pancreas,
spleen,  thymus, and brain (Stara et al.  1971).
DRAFT                               111-20

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      The amount of beta energy distributed to the thyroid gland is dependent
on the gland size, geometry, and the beta particle energy.  It has been
estimated that 70 percent of the total beta energy from absorbed iodine is
distributed to the thyroid of mice and rats, 90 percent to the thyroid of
human infants, and greater than 95 percent to the thyroid of adult humans (NAS
1990).  In workers exposed to iodine, a biological half-life in the thyroid of
48 to 75 days has been reported (Raghavendran et al.  1978).

      The uptake of orally administered radioactive iodine by the thyroid is
dependent on the amount of stable iodine in the diet.   Large amounts of stable
iodine in the diet may block the uptake of radioactive iodine by the thyroid.
During the 1950's, human studies determined that, in individuals with normal
thyroid function, 24 hour uptake to the thyroid was 28.6 percent, while
comparable studies conducted in the late 1960's reported the 24 hour uptake to
be 15.4 percent (Pittman et al. 1970).  This decrease in thyroid uptake seems
to be due to increased dietary intake of iodine in the more recent decade
(Pittman et al. 1970,  Oddie et al. 1970).  In rats fed a diet with a low
stable iodine level of 2 ng/day, the level of radioactive iodine in the
thyroid peaked at greater than 50 percent of intake in 6 hours.  The effective
half-life was 2.5 days.  When rats were fed a high stable iodine diet (15
ng/day), the maximum uptake of radioactive iodine, occurring at 24 hours, was
9 percent of the administered amount.  The effective half-life was 4 days.
Similar uptake by the  thyroid has been observed in sheep and chicks (Stara et
al. 1971).

      Inorganic iodine crossed the placental membrane and distributed from
maternal to fetal blood in humans (Johnson 1982).  In the fetus, the thyroid
began to accumulate iodine at about 90 days of age and this continued
throughout gestation.   The average absolute iodine dose to the fetal  thyroid
in hyperthyroid patients was predicted to be highest  when administration of
iodine occurred during the sixth month of gestation (Stabin et al.  1991).  The
concentration of iodine in fetal blood at term was approximately 75 percent of
that in maternal  blood.  With organic iodine, little  if any placental  transfer
has been observed (Johnson 1982).   No information was located on the transfer
of radioiodine across  the placenta.
DRAFT                               IH-21

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Excretion

       Iodine was excreted primarily in the urine of animals and man with a
urine:feces ratio of 27:1 in man.  In rats, fecal excretion was also an
important route (Stara et al. 1971).  In ten humans administered iodine to
destroy normal thyroid tissue in preparation for treatment of thyroid
carcinoma, 46 to 83 percent of the administered dose was excreted within
4 days (Andrews et al. 1954).  Small amounts of iodine have also been shown to
be excreted in humans via perspiration and exhalation (Nishizawa et al.  1980).
Iodine is eliminated exponentially with an effective half-life dependent on
species, thyroid function, and diet (Stara et al. 1971).

Bioaccumulation and Retention

      See Section E.  In this section toxicokinetic models for beta or gamma
emitting radionuclides are used to predict the potential bioaccumulation and
retention for these radionuclides.  Some of the metabolic models are based on
extensive human and animal data, some on primarily animal data and some on
similarity of elemental characteristics.  The model for iodine may be found on
page 111-68.

Summary

       Iodine is readily absorbed following all routes of exposure.  The oral
rate of absorption was approximately 5 percent of the administered dose per
minute and the absorption of iodine from the intestine was 95 percent of the
administered dose (USNRC 1975).   Distribution of iodine is primarily to the
thyroid.  An estimated 90 to 95 percent of the absorbed dose is distributed to
the thyroid of humans.  The distribution of iodine to the thyroid may be
influenced by the amount of stable iodine in the diet.  Iodine is excreted
primarily in the urine of both animals and humans.  In humans, the urine to
feces ratio is 27:1.  The excretion of iodine is dependent on thyroid function
and diet.
DRAFT                               111-22

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Health Effects in Animals

      The following discussion of health effects in animals is based on
experiments using iodine-131.

Short-term Exposure

      Oral exposure to iodine  in animals has resulted in damage to the thyroid
and effects on the hematological system.  Exposure to high parenteral doses
(50 mCi) resulted in complete  destruction of the thyroid gland and a lack of
epithelial regeneration.   With doses of 25 to 40 yCi, focal regenerative
hyperplasia progressed to benign nodule formation (Lindsay and Chaikoff 1964).
Exposure to lower doses resulted in damage to thyroid and parathyroid tissue,
skeletal abnormalities, and hematological effects.

        In adult sheep administered 1.25 mCi iodine by the oral route, no
damage was observed 60 days after administration (Goldberg et al.  1950).
Exposure to 5 mCi resulted in  severe damage to the thyroid, while 15 mCi
completely destroyed the  thyroid gland (Garner 1963).  Adult sheep
administered a single dose of  15 mCi iodine exhibited a transient depression
in lymphocytes and leukocytes  at 15 days after exposure which returned to
normal by 50 days (Garner 1963).

      No information was  located regarding the health effects of iodine in
animals following short-term inhalation exposure.

      In male Long-Evans  rats  administered a single intraperitoneal  injection
of 18 jiCi iodine, no evidence  of damage to any tissue was reported.   In
animals which received 300 or  525 ^Ci, damage to the thyroid occurred in five
phases: degeneration and  necrosis of epithelial  cells, vascular degeneration
and thrombosis,  inflammatory changes,  fibrotic changes, and epithelial
regeneration.  Similar effects occurred in animals receiving 875 ^Ci with the
exception that epithelial  regeneration did not occur.  Effects were seen as
early-as 12 hours after exposure to the two highest doses.  In animals
receiving 525 or 875 pCi,  fibrosis occurred in the peripheral  portions of the
parathyroid glands and slight  glomerular congestion and slight cloudy swelling

DRAFT                               111-23

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 was observed in the kidneys up to one week after exposure  (Goldberg et al.
 1950).

       Juvenile beagles were administered  intravenous  injections  of 0,  0.1,
 0.3,  0.6,  or 1 mCi  iodine/kg.   In dogs receiving 1  mCi/kg,  abnormal  skeletal
 development was observed within 3 to 4 months  and death  occurred in two of  the
 four dogs  within 12 to 15 months following exposure.   An absence of thyroid
 tissue  was seen in  the remaining two dogs  at autopsy  (30 months  after
 exposure).  Skeletal  growth retardation,  hypertrophy  of  the adrenal  medulla,
 lymph-node hyperplasia,  and neoplastic thyroid  tissue were  observed in dogs
 administered 0.3 or 0.6  mCi/kg.   These dogs also had  roughened and dry coats
 and excessive folding of the skin.   No effects  were observed  in  animals
 receiving  0.1 mCi/kg  (Andersen 1958).

       In mice administered 3 to  50  mCi  iodine/kg by subcutaneous injection,
 complete destruction  of  the thyroid occurred within 3  days  at the  high dose.
 Exposure to levels  as low as 3 to 4 mCi/kg resulted in 90 percent  destruction
 of  the  thyroid by 120 days.   The thyroid tissue  which  survived was  epithelial
 tissue  in  the isthmus and cranial apex.  By 120  days  after  injection of 3 to
 4 mCi/kg,  a total loss of the  parathyroids occurred (Gorbman  1947).

 Longer-term Exposure

      In sheep fed  1800  ^Ci  for  2 to 4 months or  240  ^Ci for 6 to  10 months,
 signs of hypothyroidism  were reported.  These included lethargy, clumsy
 movements,  bloating,  ulceration  of  the oral mucosa  and tongue, decreased milk
 production,  and  dry skin  and fleece  (Garner 1963).  In sheep fed 5 jiCi/day,  a
 depression  in  lymphocytes and  leukocytes was reported  (Garner 1963).

      No information  was  located on the health effects of iodine in animals
 following  longer-term exposure via other routes.

 Reproductive/Developmental  Effects

      Limited  information was  available on the reproductive/developmental
 effects of  iodine in  animals.  In lambs exposed j_n  utero by. feeding the dams

DRAFT                               111-24

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135 i»Ci to 1800 nCi iodine, hypothyroidism was observed at birth.  Ewes
exposed to 1800 jiCi or 240 jiCi during pregnancy gave birth to either dead
lambs or lambs which did not survive for more than a few days (Garner  1963).
In sheep receiving daily quantities of 1.5 or 5 yCi iodine from conception
(either j_n utero or in feed), thyroid adenomas were observed after 4 to 6
years (Lindsay and Chaikoff 1964).   Thyroid changes, including early fibrosis,
compensatory hyperplasia with adenoma formation, and colloid goiters,  have
been observed in the offspring of mouse dams administered iodine injections
during pregnancy (Lindsay and Chaikoff 1964).  No adverse effects on fertility
have been reported in hypothyroid sheep or cows (Garner 1963).

Mutagenicity

      No information on the mutagenic effects of iodine was located in the
reviewed literature.

Carcinogenicity

      Both benign and malignant thyroid neoplasms have been reported following
single or repeated exposure to iodine.  In sheep fed daily quantities  of 1.5
to 135 nCi beginning at 15 months of age,  thyroid adenomas were observed at 4
to 8 years of age (Lindsay and Chaikoff 1964).  In a separate study in sheep
fed 5 ^Ci per day for life, both thyroid adenomas and fibrosarcomas were
reported (Lindsay and Chaikoff 1964).  Three years after feeding adult sheep
45 nCi per day for 12 months or 135 ^Ci for 8 months, thyroid adenomas were
reported (Garner 1963).

      No information was located regarding the carcinogenicity of iodine in
animals following inhalation exposure.

      Juvenile beagles were administered single intravenous injections of 0,
0.1,  0.3, 0.6, or 1 mCi iodine/kg.   Thyroid adenomas were observed at
sacrifice (30 months after exposure) in five out of eight dogs which received
0.3 or 0.6 mCi iodine/kg and in one of two dogs receiving 1 mCi/kg (Andersen
1958).
DRAFT                               111-25

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      Levels of iodine as  low as 1 nCi have been reported to result in thyroid
tumors in Long-Evans rats  (Lindsay and Chaikoff 1964).  The highest incidence
of thyroid neoplasms reported has been in Long-Evans rats that received either
a single dose of 25 nCi or four doses of 10 ^Ci at weekly intervals (Lindsay
and Chaikoff 1964).  In male rats which received a single intraperitoneal
injection of 25 (iCi iodine or four injections of 10 jiCi at monthly intervals,
a statistically significant increase in follicular adenomas, papillary
adenomas and carcinomas, and follicular carcinomas of the thyroid were
observed (Potter et al. 1963).  Following three intraperitoneal injections of
10 nCi at monthly intervals in female rats, benign thyroid nodules or adenomas
were observed in 39 percent of the animals compared to 3 percent in controls.
The incidence of carcinomas in females was 7 percent compared to no carcinomas
in controls.  The incidence of carcinomas in females was lower than in males
(21 percent) which were treated with lower doses (Lindsay et al. 1963).  In
female Long-Evans rats administered 0.48 to 5.4 ^Ci iodine by intraperitoneal
injection,  a dose-related  increase in thyroid carcinomas was observed.  The
authors suggest that carcinoma induction was dependent on total dose and not
dose rate (Lee et al.  1982).

Summary

      Exposure to iodine by either the oral or parenteral route has been shown
to result in damage to the thyroid gland.  Depending on the dose administered,
effects on the thyroid ranged from epithelial degeneration, fibrotic changes,
and cancer, to complete obliteration of the gland.  Other effects which have
been reported include skeletal abnormalities, a decrease in lymphocytes and
leukocytes, damage to the parathyroid, and kidney effects.  Following longer-
term oral exposure, ulceration of the oral mucosa and tongue were also
reported.  Developmental effects which have been reported following exposure
of mouse and sheep dams included changes in the thyroid gland.   No adverse
effects on reproduction were reported.  Both benign and malignant thyroid
neoplasms have been reported following iodine exposure.  Repeated oral
exposure to iodine in sheep has been reported to result in thyroid adenomas
and fibrosarcomas as early as 3 years after exposure.  Levels of iodine as low
as 1 jiCi administered by injection have been reported to result in tumors in
rats.

DRAFT                               111-26

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 Health Effects in Humans

 Clinical  Case Studies

       Tenderness and swelling  of  the  salivary  glands,  as  well  as a decrease in
 salivary  flow, have been  reported in  humans  following  oral  doses of iodine
 high enough to destroy  thyroid tissue (Maier and  Bihl  1987).   Oral
 administration of 20 to 70 mCi  iodine in patients with carcinoma of the
 thyroid gland resulted  in a  "moderate"  increase in  red blood  cell  membrane
 permeability against hemoglobin in  peripheral  blood at 4  days  after
 administration.   The authors attributed this effect to beta radiation of the
 peripheral  blood resulting in  direct  damage  to the  formed elements (Geszti et
 al.  1973).   Chromosomal damage  (type  not specified)  was reported in one
 patient following  administration  of two 100  mCi doses  of  iodine  (Gestzi et al.
 1973).

       Oral  administration of 350  mCi  iodine  in a thirteen year old boy with
 thyroid cancer has  been reported  to result in testicular  damage,  including a
 lack of sperm in the semen (Ahmed and Shalet 1985).  In addition,  persistently
 elevated  basal  follicle stimulating hormone  level  was  reported.   Four years
 after treatment  there appeared to be  no recovery of  sperm production  in the
 boy  (Ahmed  and  Shalet 1985).   The possibility of a  reversal of this condition
 was  undetermined.

       In  patients administered greater than  100 mCi of  iodine-labeled
 monoclonal  antibodies by intraperitoneal injection, for the treatment of
 ovarian cancer, reversible bone marrow suppression was reported.   Neutropenia
 and  thrombocytopenia were reported 3 to 5 weeks following injection with the
 lowest  blood  counts observed  from days 30 to 40 (Stewart et al.  1989).

 Epidemiological Studies

      In patients with  Graves'  Disease,  a  form  of  thyrotoxicosis, who were
treated with  iodine, thyroid  nodules were  found in eight of 256 patients 5  to
 14 years following iodine  therapy.  Histological examination revealed typical
radiation  effects including nodules consisting  of  follicular atrophy,

DRAFT                               111-27

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perifollicular fibrosis, and mild chronic inflammatory infiltration.  Nodules
did not occur in patients who developed hypothyroidism following iodine
therapy for thyrotoxicosis which indicated that the gland was so severely
damaged that it was incapable of regeneration and nodule formation.  The
glands of these patients resembled those of rats receiving 400 pCi (Lindsay
and Chaikoff 1964).

      In a prospective study of 1,005 patients treated with iodine for
thyrotoxicosis, the risk of thyroid cancer was 9 fold greater compared to
patients who were treated surgically for this disease, but was not
statistically significant when compared with data from the Connecticut Cancer
Registry.  In 21,714 patients treated with iodine compared to 11,732 patients
treated surgically, the incidence of thyroid cancer was not significantly
increased.  In 4,557 iodine treated patients, the thyroid cancer incidence was
not increased compared with data from the Swedish Cancer Registry (NAS 1990).

      In a follow-up study of 10,133 patients who received diagnostic doses of
iodine, no evidence of an increased risk of thyroid cancer was observed.  A
separate study was conducted of 35,074 patients who survived 5 years or more
after receiving a mean diagnostic dose of 0.05 mCi iodine.  The mean follow-up
period was 20 years and the mean age at exposure was 44 years.  Fifty thyroid
cancers were observed in the exposed group compared to an expected 39.37
cases.  Of the 50 observed cases, ten were of a type not shown to be
associated with radiation exposure, six were from subjects 50 to 74 years of
age at time of exposure, and 15 cancers occurred after 5 to 9 years of
exposure suggesting that they were present at the time of exposure.
Therefore, the authors concluded that the data do not support an increased
risk of thyroid cancer from diagnostic doses of iodine (NAS 1990).

      Residents of the Marshall Islands were exposed to radioactive iodine
from fallout from the BRAVO test bomb.  Doses of ingested radionucl ides were
calculated from the iodine content of pooled urine samples taken 15 days after
the first exposure.  Doses were calculated to range from 0.3 to 15 Grays (30
to 1500 rads).  The prevalence of hypothyroidism, thyroid nodules, and thyroid
cancer appeared to increase with dose.  General radiation sickness, including
nausea and hair loss,  were reported within 2 weeks following exposure.  When

DRAFT                               111-28

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additional studies of the Islanders were undertaken,  a statistically
significant dose-related increase in thyroid nodules  was observed.  A
significant dependence of nodule prevalence on distance from the test site,
age at exposure, sex, and latitude was observed when  using logistic regression
analysis (MAS 1990).

      In school-age children who ingested milk contaminated with iodine from
atmospheric fallout resulting from atomic bomb tests, a suggestive 20 to 30
percent greater incidence in all thyroid abnormalities compared to unexposed
controls was reported.  The cumulative radiation doses to the thyroid were
estimated to average as high as 1 Gray (100 rads) (NAS 1990).

      No increase in reproductive problems, i.e., infertility, miscarriage,
prematurity, or birth defects,  were reported in 33 patients receiving a mean
dose of 196 mCi as children or adolescents (Sarkar et al. 1976).  However,
further examination of this and other data prompted Handelsman et al. (1980)
to note infertility in some men treated after puberty.  Toxicity of the testes
was seen in 3 of the 6 men in this category, including two men included in the
Sarkar et al. (1976) report (Handelsman et al. 1980,  Ahmed and Shalet 1985).
Total iodine dose administered (100 to 400 mCi) correlated positively with
serum follicle-stimulating hormone concentration and  negatively with sperm
density (Handelsman et al. 1980).  More detailed follow-up studies of
similarly treated individuals would be required to determine the reversibility
of this effect.
                                    111-29

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High-Risk Populations

      While little data were located concerning probable high-risk populations
following exposure to iodine, infants and children may be included in this
category.  Various incidents involving the treatment of pregnant women with
iodine have resulted in infants with depressed or absent thyroid function
(Stabin et al. 1991).  These effects were likely the result of iodine
accumulation in the fetal thyroid, which has been shown to begin at 90 days of
age.  In addition, iodine uptake to the thyroid in newborn infants is much
greater than that in adults, 62 percent compared to 16.9 to 26 percent
(depending on sex) (Fisher et al.  1962, Schober and Hunt 1976).  The decline
of thyroid absorption to adult values may occur within 5 days or require as
long as a year.

      Studies concerning other radionuclides, specifically strontium, have
shown children to be more sensitive to the induction of cancer following
exposure (Mays and Lloyd 1972).  The data suggest that children exposed to
radiation during the first five years of life have a considerably increased.
risk of cancer, compared to those exposed later (NAS 1990).  NAS (1990)
concludes that the risk of radiation-induced thyroid cancer in children is '
twice as great as that in adults.   Iodine radiosensitivity in children has not
yet been fully explored.  Pending further relevant studies, children should be
considered a high-risk population for iodine exposure.

Summary

      The effects of iodine exposure have been studied in patients receiving
large therapeutic doses, patients receiving smaller doses of iodine for
diagnostic purposes, and those exposed to environmental iodine fallout (NAS
1990).  Injury to the human thyroid gland, including cancer,  has occurred
following irradiation for thyrotoxicosis or thyroid carcinoma.  Effects
observed in the human thyroid gland at long times after administration of
large doses include chronic inflammation, interlobular and perifollicular
fibrosis, and foil icular atrophy (Lindsay and Chaikoff 1964).  Other effects
observed in humans include changes in blood cell membrane permeability and
chromosomal damage.  Effects observed in humans differ from.those in

DRAFT                               111-30

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laboratory animals in that the sequence of effects appears to occur more
rapidly  in animals.  In addition, the size of the organs  in small animals  in
relation to the path of the beta radiation is such that changes are more
commonly produced in adjoining structures, such as the parathyroids and
trachea  (Andrews et al. 1954).  Due to data concerning adverse effects in
infants exposed to iodine and the possible increased sensitivity of children
to  iodine exposure, infants and children should be considered a high-risk
population for iodine-induced effects.

D.    TRITIUM

Physical and Chemical Properties

Chemical Properties - Elemental

      Tritium, a radioactive isotope of hydrogen, may be  formed naturally  by
interactions of cosmic rays with gases in the upper atmosphere, or may be
prepared by the bombardment of lithium with low energy neutrons in nuclear
reactors, or by nuclear bombardment of deuterium with other hydrogen species.
Tritium is also present in effluents from nuclear reactors and weapons (Hawley
1981, Hobbs and McClellan 1986).

      With respect to chemical reactions, tritium reacts  similarly to ordinary
hydrogen.  However,  hydrogen isotopes are easily distinguished from one
another because of the relatively large differences in mass.   The reaction of
tritium to form tritiated water (HTO) is favored at room  temperature, and most
tritium present in the environment is in the form of tritiated water (Jacobs
1982).

Physical Properties

      Tritium (mass  number 3,  isotopic weight 3.017)  is the heaviest of the
three hydrogen isotopes  and has one electron outside  the nucleus and two
neutrons and one proton  inside the nucleus.   Tables III-3 and III-4, adapted
from Greenwood and Earnshaw (1984),  list atomic and physical  properties,
respectively,  for hydrogen,  deuterium, and tritium.   The binding energy
                                    111-31

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between the three elementary nuclear particles in tritium is relatively low.
Consequently, the nucleus  is not stable and will decay by emission of an
electron (beta particle) with energy up to 18.6 kev and a neutrino, where one
neutron transforms  into a  proton.  The nuclide gains an additional charge that
can hold a second electron  in orbit and thus undergo beta decay to a new
chemical identity,  primarily helium 3 (stable).  In this process an average of
approximately 11 ev of excitation may be added to the helium ion (Feinendegen
1967).  The half-life is 12.4 years and the decay constant, X,  equals 0.0565
per year, or 1.791xlO"9  per second.  The half-life  and decay  scheme for
tritium may be seen in Figure III-3, adapted from Lederer and Shirley (1978).
      Table III-3.   Atomic Properties  of Hydrogen,  Deuterium,  and  Tritium
Property
Relative atomic mass
Radioactive stability
Hydrogen
1.007825
Stable
Deuterium
2.014102
Stable
Tritium
3.016049
IT tv, 12.35 ya
18.6 keV;
                     5.7 keV.
     Table  III-4.   Physical  Properties  of Hydrogen,  Deuterium,  and  Tritium
Property3
Melting Point °C
Boiling Point °C
Heat of fusion/kJ mol"1
Heat of vaporization/kj mol"1
Critical temperature/K
Critical pressure/atmb
Hydrogen,
-259
-253
0.117
0.904
33.19
12.98
Deuterium,
-254
-249
0.197
1.226
38.35
16.43
Tritium,
-252
-248
0.250
1.393
40.6 (calc)
18.1 (calc)
   Data refer to H2 of normal  isotopic  composition  (i.e., containing 0.0156
   atom percent of deuterium,  predominantly as  HD).   All  data refer to the
   mixture of ortho- and para-forms that are in equilibrium at room
   temperature.
   1  atm = 101.325 kN m2 = 101.325  kPa.
DRAFT
                              111-32

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            Figure 111-3.  Half-Life and Decay Scheme
                          of Tritium
                            H -3  (a)
                           12.33y(b)
                         3-=0.0186
                           Helium
a = half life
b = maximum 3'decay energy in MeV
Lederer and Shirley 1978
                            111-33

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Summary

      Tritium is a radioactive isotope of hydrogen that has a half-life of
12.4 years, emits beta radiation up to 18.6 kev, and decays to helium-3.
Tritium reactions are similar to those involving hydrogen, and most of the
tritium present in the environment is in the form of tritiated water.  Tritium
is often used as tritium oxide (HTO, tritiated water), tritiated thymidine,
and other forms to label atoms or reactions for the purpose of following
mechanism pathways or to identify and analyze products.  Tritium atoms can
replace hydrogen atoms in many compounds, rendering the new molecule
radioactive and providing a means of monitoring the presence and concentration
of labeled compounds with beta-particle detecting devices (Andrews 1968).

Toxicokinetics

Absorption

      In this analysis all references to tritium refer to tritium oxide (HTO),
usually administered as tritiated water.   Tritium is easily absorbed from the
gastrointestinal tract, skin, and lungs into the bloodstream (Hobbs and
McClellan 1986).  Gastrointestinal  absorption is about 95 percent (Killough
and Rohmer 1978).  Pinson and Langham (1957) conducted an experiment in which
fasted adult males ingested 100 to 1000 milliliters (mL)  of tritiated water.
Absorption through the gastrointestinal tract began after 2 to 9 minutes and
was complete in 40 to 45 minutes (Pinson and Langham 1957).  Within the range
of 100 to 1000 ml, the volume of tritiated water transferred from the
intestine to the blood was linear with time and proportional to the water
volume ingested (Pinson and Langham 1957).  In humans 98  to 99 percent of
inhaled tritium was exchanged and absorbed through the respiratory tract, the
remainder being exhaled (Moskalev 1968).

Distribution

      Though limited definitive data are available, the distribution of
tritium has been described as follows.  An equilibrium distribution of tritium
in the bodily fluids of humans was established 2 to 4 hours.after ingestion or

DRAFT                               111-34

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 inhalation  of  tritium.   In  addition  to  its  presence  in  body  fluids,  0.5  to  4
 percent  of  the  tritium  activity may  be  incorporated  into  organic molecules  of
 the  body (Balonov et  al.  1984).   Subsequent to  intake,  tritium  content in the
 urine, saliva,  sweat, feces, and  exhaled  air was  the  same, indicating that
 tritiated water migrates  through  biological  barriers  at the  same rate as
 ordinary water  (Moskalev  1968).   According  to ICRP (1979) tritium distribution
 to soft  tissues is uniform.  However, since some  tissues  contain more water
 than others, the dose administered to tissue via  the  associated body water
 would be expected to  vary accordingly (Balonov  et al. 1984).  Moskalev (1968)
 reported that  in humans occupationally  exposed  to tritium (average specific
 activity in these individuals was 23 jiCi/L  body water), the  specific activity
 detected in certain organic components, specifically  in fat  and skin, was
 higher than the specific  activity detected  in the body water, though no
 explanation was offered as to why these components would  contain a higher
 specific activity.

 Excretion

      Data concerning the excretion of  tritium  are limited.  Since tritium  is
 incorporated into body water, most excretion is presumably via the urine,
 though some is  expired via respiration.  The rate of  tritium elimination
 increased slightly with age.  The biological half-life of tritium for persons
 20 to 29, 30 to 39,  40 to 49, and 50 to 59 years of age has been shown to be
 10.5, 9.5, 9.0, and 8.2 days, respectively  (Moskalev  1968).  Other factors
 influencing the elimination of tritium are  the  amount of water consumed and
 the rate of water turnover.

 Bioaccumulation and Retention

      See Section E.   In this section toxicokinetic models for beta or gamma
 emitting radionuclides are used to predict the potential bioaccumulation and
 retention for these radionuclides.  Some of the metabolic models are based on
 extensive human and animal data,  some on primarily animal  data and some on
 similarity of elemental  characteristics.  The model  for tritium (hydrogen) may
 be found on page 111-43.
DRAFT                               111-35

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Summary

      Tritium  is rapidly  absorbed  into  the  body water,  regardless  of  route of
administration  (Pinson  and  Langham 1957).   Humans  absorbed  98  to 99 percent of
inhaled tritium.  Tritium distribution  in humans was  uniform  in the body
water.  Distribution  in tissues, though  thought to be relatively uniform, may
vary depending  on the amount of  body water  contained  in  the tissue.   The  rate
of tritium excretion  has  been  shown to  increase with  age.   Excretion  may  also
vary with rate  of water turnover and amount of water  consumed.

Health Effects  in Animals

Short-term Exposure

      Data currently  available concerning health effects  in animals exposed to
tritium via ingestion or  inhalation are  limited.   A single  intraperitoneal
injection of 1400 jiCi tritium/g  body weight resulted  in  death  in all  treated
mice (Zhuravlev 1968).  Reported LD50/30s (the  dose  which was lethal  to 50
percent of the  animals in 30 days) for  injection in mice  ranged from  250  to
1000 tiCi/g body weight; however, the range  of 250  to  350  yCi/g was generally
agreed upon (Zhuravlev 1968).  The LD50/30 for rats  exposed via all  routes  is.
about 1,070 pCi/g body weight, confirming that the  toxicity of tritium for
rats is not dependent upon  the route of  exposure,  since  tritium is rapidly
absorbed and distributed  following exposure by any  route  (Zhuravlev 1968).

      Rats exposed via injection to 1,200 or 2,400  jiCi tritium/g body weight
(doses in excess of the LD50)  exhibited  an  immediate decrease  in erythrocyte
count.  However, in rats  dosed with 300  or 600 pCi  tritium/g there was an
initial increase in erythrocyte  count before the decrease began 3 to  5 days
after injection (Zhuravlev  1968).  Rats  injected with 300 to 2,400 ^Ci
tritium/g body weight exhibited  a decrease  in absolute leukocyte numbers  on
the first day after exposure.  Leukocyte count on days 7  to 10 was observed to
be 400 cells per cubic millimeter  (mm3), compared with 16,000 cells/mm3 before
injection.  By the end of a month leukocyte values  in the surviving animals
were between 5,500 and 9,000 cells/mm3.   Dogs exposed  via injection to 300
      body weight also exhibited decreases  in leukocyte,  platelet,
DRAFT                               111-36

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 erythrocyte,  and  lymphocyte  counts.   Zhuravlev  (1968)  reported  that the
 ability  of the  liver  to  synthesize  hippuric  acid was  inhibited  in  rats  exposed
 to  40  pCi  tritium/g body weight  and  dogs  exposed to 300  nCi  tritium/g  body
 weight.   The  production  of hippuric  acid  declined  to  50  and  55  percent  of the
 initial  output  for rats  and  dogs, respectively.  A gradual decrease in  the
 synthesis  of  hippuric  acid was seen  when  smaller doses were  administered  over
 a period of time.  Shal'nova (1968)  demonstrated that  tritium administered in
 single injections of  80  to 300,  10 to 300, and  150 to  300 nCi/g body weight,
 in  mice,  rats,  and dogs, respectively,  resulted in damage to immunological
 function.   All  three  species exhibited  disruption  of phagocytic activity  of
 neutrophils and all began to produce autoantibodies designed to attack  the
 organism's  tissue (Shal'nova 1968).

 Longer-term Exposure

       Repeated  oral doses of 5,  10,  and 40 jiCi tritium/g body weight
 administered  to rats produced a  gradual increase in toxicity (Zhuravlev 1968).
 In  rats, administration  of 40 jiCi tritium/g  resulted in changes in  the  white
 blood  cells,  including an increased  number of lysed cells, vacuolization  of
 the protoplasm, and fragmentation of the  nuclei of the neutrophils.
 Additional  effects observed  were a decrease  in the number of erythrocytes,
 leukocytes, and reticulocytes, and a  less distinct decrease  in  the  ability  of
 the liver to  synthesize  needed compounds.  At doses of 10 nCi tritium/g,  a
 gradual  inhibition of hematogenesis  (specifically  of erythrocytes and
 leukocytes) was observed.  No changes were seen in rats administered 5  nCi
 tritium/g for 2 months.

 Reproductive/Developmental  Effects

       Female germ cells  in some mammals have been  shown to be extremely
 sensitive to radiation,  such as that emitted by tritium (Dobson and  Kwan
 1977).   Pregnant mice  were given tritiated drinking water containing less than
 0.1  to more than 10 nCi/mL from conception to 14 days postpartum (Dobson
 et al.  1986).   Results indicated that the tritium-induced decrease of
 reproductive capacity  was dose-dependent but not directly proportional  to
decreased oocyte number  (Dobson et al. 1986).  No decrease in reproductive

DRAFT                                 111-37

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 capacity was seen unless early oocyte loss exceeded 50 percent.   Fecundity of
 exposed females tended to be normal during early reproductive life but  failed
 prematurely as oocytes diminished (Dobson et al .  1986).
       Rats were exposed to 0.01, 0.10,  1.0,  or 10.0 (iCi  tritium/mL drinking
 water from conception of the F1  generation through  delivery  of the  F2
 generation (offspring of the F,) (Laskey  et  al .  1973).   A 30  percent reduction
 in  the weight of testes of the F,  male  and decreased  litter  size and increased
 resorptions in the dam were observed following exposure  to  10 fiCi  tritium/mL
 (Laskey et al.  1973).  A similar study, using  only  intrauterine  exposures,
 produced statistically significant reductions  in litter  size and offspring
 body  weight.   The dose levels used in this second study  (though  not reported)
 were  10 to 100 times greater than  those used in the lifetime study  (Laskey
 et  al.  1973).
       Cahill  and  Yuile (1970) exposed pregnant  rats  to  1  to  100  nCi tritium/mL
of body  water5 throughout  pregnancy  and reported statistically significant
litter size  reduction  and  increased  resorptions.   Cahill  et  al .  (1975) exposed
pregnant rats  to  1,  10,  50,  or 100 jiCi  tritium/mL  of body water  to determine
late effects  of tritium  exposure.  No late  effects were reported at the two
lower  doses.   All  rats exposed in  utero to  the  two highest doses were sterile.
Cahill and Yuile  (1970)  exposed pregnant  rats to  1 to 100 nCi  tritium/mL of
body water throughout  pregnancy and  reported microencephaly,  sterility, and
stunting, all  of  which were  statistically significant.

       In addition to reproductive  effects,  tritium also affected the
offspring.  When  parents were exposed to  tritiated drinking  water, neonatal
effects  included  the reduction of  the brain to  body  weight ratio and decreased
body weight at doses as  low  as 0.1 and  1.0  pCi/mL, respectively  (Laskey et al .
1973).   Cahill et al .  (1975)  reported that  all  rats  exposed  in utero to 100
    tritium/mL had reduced mean life spans, when compared  to  controls.
       Females were injected with tritium with a high specific activity so
that when the tritium was diluted by the body water, the desired
concentrations were obtained.  Following the initial injection, tritiated
water was given ad libitum  to maintain the desired concentration.

DRAFT                               111-38

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 Mutaqenicitv

       Injection of  rats with  a  single dose of 75  or  100  jiCi  tritium/g  body
 weight  resulted in  a  statistically  significant  increase  in  chromosomal
 aberrations in bone marrow  cells within 24 hours  (Andreuta  and  Racoveanu
 1974).  A gradual decrease  in aberrations was seen 3  to  7 days  after
 administration.   In rats administered daily injections of 30 yCi/g  body weight
 for  18  days, an increase in the incidence of bone marrow cell aberrations  was
 reported (Andreuta  and Racoveanu 1974).

 Carcinoqenicity

       In addition to  noncarcinogenic effects, animals exposed to  tritium via
 drinking water developed tumors.  Following multigeneration  exposure of male
 mice to 10 (iCi tritium/mL of drinking water, a  heritable, multiple  intestinal
 adenocarcinoma (HMIA) was observed  in the offspring of five  successive
 generations.  This tumor type, not  previously seen in the C57 Black/6M strain,
 was detected in 44 percent of the males and 78  percent of the females  in the
 five generations  (Mewissen 1983).

      In a study performed by Cahill and Yuile  (1970), pregnant rats received
 1 to 100 jjCi tritium/mL of body water.  Within  270 days, five tumors (one  in
 the thymus gland,  two ovarian, and  two mammary) had arisen  in an  unreported
 number of animals exposed in utero  to 50 to 100 jiCi tritium/mL) compared to
 one benign facial  adenoma in a control.   Cahill et al . (1975) exposed pregnant
 rats to 1,  10, 50, or 100 (iCi  tritium/mL body water from conception  to birth
 of offspring.   Females exposed iji utero to 50 or 100 jiCi tritium/mL  had an
 increased incidence of ovarian tumors, compared to controls  (Cahill  et al .
 1975).  The controls had no ovarian tumors,  while rats receiving  50  and 100
  i tritium/mL developed five and two tumors,  respectively.
Summary

      Short-term exposure of rats and dogs to tritium has been reported to
cause hematological changes, such as the depression of erythrocyte and
leukocyte counts in both species and decreased platelet and lymphocyte counts

DRAFT                               111-39

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 in dogs.  In addition, the ability of the liver to synthesize hippuric acid
 was reduced, indicating some compromise in hepatic function.   Rats, mice,  and
 dogs reportedly developed damage to immunological  function,  such as the
 disruption of phagocytic activity of neutrophils.   Longer-term exposure has
 been shown to produce changes in white blood cells and to inhibit
 hematogenesis in rats.

       Reproductive studies in mice exposed to tritium j_n  utero have detected
 decreased reproductive capacity and oocyte death.   Studies  in rats have shown
 reduced testes  weight, brain to body weight ratio,  overall  body weight, and
 litter size.  Mutagenicity studies reveal  a significant increase in
 chromosomal  aberrations of bone marrow in  exposed  rats.   Carcinogenic  effects
 include the  observation of a heritable,  multiple  intestinal adenocarcinoma  in
 the offspring of exposed mice,  as  well  as  the development of  mammary and
 ovarian tumors  in exposed rats.

 Health Effects  in Humans

 C1inical  Case Studies

       There  are  currently  no  data  available  from clinical case  studies
 regarding  health effects resulting  from  human  exposure to tritium.

 Epidemiological  Studies

       There  are  currently  no  data  available  from clinical  case  studies
 regarding  health effects  resulting  from  human  exposure to tritium.

 High-Risk  Populations

       Female  germ cells  in some mammals have been shown to be extremely
 sensitive  to  radiation,  such  as that emitted by tritium (Dobson and Kwan
 1977).  However, germ  cell radiosensitivity in unborn females has not been
 studied extensively (Dobson et al.  1986).  For this reason females exposed in
utero may  be  a high-risk population for tritium induced damage to germ cells.
DRAFT                               111-40

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 Summary

      There are currently no data available from clinical  case  studies  or
 epidemiological studies regarding human health effects which  may  be associated
 with exposure to tritium.  Females exposed in utero may  be a  high risk
 population.

 E.    BIOACCUMULATION AND RETENTION

      The toxicokinetic models for beta and gamma radionuclide  uptake and
 retention are derived from a number of sources:  EPA  (1977),  Adams  et al .
 (1978), Bernard and Snyder (1975), ICRP (1973, 1979)  and Sullivan et al .
 (1981).  Some of the metabolic models are based on extensive  human  and  animal
 data, some on primarily animal data and some on similarity of elemental
 characteristics.  These radionucl ides include naturally occurring forms  such
 as:  uranium, radium and radon, which are described in other  criteria
 documents; tritium, carbon-14, etc. and some man-made radionucl ides such  as
 iodine-131 and cesium-137.

      In general, retention is defined as the amount  of a  substance remaining
 in a tissue or organ at some time after the intake of the  substance.  The
 retention function R(t) specifies the fraction of a substance remaining  in a
 tissue or organ at some time,  t,  after introduction.  The  retention function
 is frequently defined as a sum of terms of the form F x exp(-XBt) where each
 fraction, F, of a substance entering an organ or tissue has a corresponding
 biological removal  rate coefficient,  XB,  or equivalently a biological half-
 life TB.   TB and AB are related by the equation XB = (In 2)/TB.

      For a radionuclide with  a radiological decay constant,  XR, the retention
 function is modified by replacing each value of A.B  with the quantity
      Retention periods can be long for certain elements in some organs.
Under those conditions, the organ burden of a long-lived radionuclide may
include a significant fraction of all  previous uptake of the radionuclide at
that site.  For continuous intake,  this process of bioaccumulation can provide

DRAFT                               111-41

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an organ burden which  increases  significantly over  a  persons's entire
lifetime.  The bioaccumulation  is  proportional  to the convolution of intake
rate and retention.

      The numerical  values  for  F and TB are usually determined in studies
where there  is a  known  intake of a radionuclide.  The whole body or specific
organs or tissues  are  radioassayed to determine the amount of activity present
at various times  after  intake.   These data are  used to develop a retention
curve from which  the numerical values of parameters can be obtained.
Metabolic studies  to determine retention parameters are usually done in
laboratory animals;  however, for some radionuclides there are metabolic data
from both humans  and animals.

      The EPA models differ  from ICRP models in the treatment of radioactive
daughters produced  in the body  (Dunning et al.  1984).  ICRP assumes all
radioactive  progeny  produced in  the body follow the metabolic behavior of the
parent nuclide (ICRP 1979).  EPA permits each daughter, as it is formed, to
assume the metabolic properties  of that element.  For example, calculating the
ionizing energy deposition  in tissues associated with intake of alpha emitting
radionuclides involves metabolic models for all elements from curium to lead
and samarium, so that all progeny  can be evaluated and energy deposition
within tissues summed to calculate  the absorbed radiation dose.

      Toxicokinetic  models for all  elements may be used since almost every
element has  at least one beta or gamma emitting radioisotope.   Elements from
hydrogen to  curium are listed here.
DRAFT                               111-42

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 Hydrogen  Model
      The toxicokinetic model  for  hydrogen  is  taken  from Killough and Rohmer
 (1978).
      1.  Absorption  from  th.e  intestine  (f,)  is 0.95.
      2.  Fractional  tissue  uptake  (f'2)  is:   all tissues,  1.0.
      3.  Retention parameters:
          (a)  Assume a daily  intake of  350  g of 1H.
          (b)  Also assume the 3H/1H ratio in an organ is equivalent to that in
              the daily intake.
          (c)  If the fractional weight  of hydrogen in  an organ  is FH,  then the
              activity concentration of  H  in the organ  (pCi per  gram)  is
              (FH/350)(daily intake of UC in pCi).

 Helium Model
      There is no toxicokinetic model for helium  in  Sullivan et  al.  (1981).
 Isotope half-lives are too  short for internal dosimetry.

 Lithium Model
      There is no toxicokinetic model for lithium in Sullivan et  al.  (1981).
 Isotope half-lives are too  short for internal dosimetry.
DRAFT                               111-43

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Beryl 1ium Model
       The toxicokinetic  model  for  beryllium is  taken  from ICRP Publication  2
(1959).
       1. Absorption  from the intestine (f,)  is  0.002.
       2. Fractional  tissue uptake  (fl)  is:   bone,  0.32;  liver,  0.10;  kidneys,
         0.03;  spleen,  0.002;  other tissues, 0.548.
       3. Retention parameters:
                                      F                      TB
                                (Fraction  of         (Biological  half-
              Organ	organ  burden)	life  in  days)
Bone
Liver
Kidneys
Spleen
Other tissues
1.0
1.0
1.0
1.0
1.0
450
270
120
540
180
Boron Model
      There is no toxicokinetic model  for boron  in  Sullivan  et  al.  (1981).
Isotope half-lives are too  short for  internal dosimetry.

Carbon Model
      For carbon-11 and carbon-15  in  the case of carbon as C02, the following
is used:
      1. Absorption from  the  intestine (f,) is 0.95.
      2. Fractional tissue  uptake  (f^)  is:  bone, 0.008; other  tissues, 0.992.
      3. Retention parameters:
                                      F                      TB
                               (Fraction of          (Biological hal/-
      	Organ	organ  burden)	1 ife in days)'
       Bone
       Other tissues	
      *Data are not  available at  this time.
DRAFT                               111-44

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       For carbon-14, the specific  activity model of Killough  and  Rohmer (1978)

 is used:

       1. Absorption  from the  intestine  (f,) is 0.95.

       2. Fractional  tissue  uptake  (f'2)  is:  all tissues,  1.0.

       3. Retention parameters:

         (a)  Assume a daily  intake of  300 g of carbon.

         (b)  Also assume the UC/C ratio in  an organ  is equivalent to that in
              the daily intake.

         (c)  If the fractional weight  of carbon in an  organ  is Fc, then the
              activity concentration of  C  in  the  organ (pCi  per gram) is
              (Fc/300)(daily intake of UC in pCi).



 Nitrogen Model
       The toxicokinetic model for  nitrogen is taken from  ICRP  Publication  2

 (1959).

       1. Absorption  from the  intestine  (f,) is 0.95.

       2. Fractional  tissue  uptake  (f'2)  is:  all tissues,  1.0.

       3. Retention parameters:

                                     F                      TB
                               (Fraction of         (Biological half-
      	Organ	organ burden)	life in  days)	


       All  tissues                  1.0                     90
DRAFT                               111-45

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Oxygen Model
      The  toxicokinetic  model  for  oxygen  is  taken  from  ICRP Publication 2
(1959).
      1. Absorption from the intestine  (f,)  is 0.95.
      2. Fractional tissue uptake  (f'2)  is:   all tissues,  1.0.
      3. Retention parameters:
                                      f                      TB
                                (Fraction  of          (Biological  half-
      	Organ	organ  burden)	1 ife  in  days)	

       All  tissues	M)	14	

Fluorine Model
      There  is  no  toxicokinetic model for fluorine  in Sullivan et  al.  (1981)
The current  RADRISK toxicokinetic model for  fluorine is taken  from ICRP
Publication  30  (1980).
      1. Absorption from the intestine  (f,)  is 1.0.
      2. Fractional tissue uptake  (f'2) is:   bone,  1.0.
      3. Retention parameters:
                                      F                      TB
                                (Fraction of          (Biological  half-
      	Organ	organ  burden)	1 ife  in  days)	

       Bone	1.0	»	

Neon Model
      There  is  no  toxicokinetic model  for neon in Sullivan  et  al.  (1981).
DRAFT                               111-46

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Sodium Model
      The toxicokinetic model for  sodium  is taken  from  Adams  et  al.  (1978).
      1. Absorption  from  the  intestine  (f,) is 0.95.
      2. Fractional  tissue  uptake  (f'2)  is:  bone,  0.30; other tissues,  0.70.
      3. Retention parameters:
                                     F                      TB
                                (Fraction  of          (Biological  half-
              Or gan	organ burden)	1 ife  in days)
Bone
Other tissues
1.0
1.0
15
15
Magnesium Model
      There is no toxicokinetic model for magnesium  in  Sullivan  et  al.  (1981)
The current RADRISK toxicokinetic model for magnesium is taken from ICRP
Publication 30 (1981).
      1. Absorption from the  intestine  (f,) is 0.50.
      2. Fractional tissue uptake  (f'2)  is:  bone, 0.4;  other tissues, 0.4;
         excretion, 0.2.
      3. Retention parameters:
                                     F            .          T8
                               (Fraction of          (Biological  half-
              Organ	organ burden)	1 ife  in days)
Bone
Other tissues
1.0
1.0
100
100
Aluminum Model
      There is no toxicokinetic model for aluminum in Sullivan et al.  (1981)
The current RADRISK toxicokinetic model for aluminum is taken from  ICRP
Publication 30 (1981).
      1. Absorption from the intestine  (f,) is 0.01.
      2. Fractional tissue uptake (f'2) is:  bone, 0.30; other tissues, 0.70.
      3. Retention parameters:

DRAFT                               111-47

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                                (Fraction of          (Biological  half-
              Organ 	   organ  burden)	1 ife  in  days)
Bone
Other tissues
1.0
1.0
100
100
Silicon Model
      There  is no toxicokinetic model for silicon  in Sullivan et  al.  (1981)

The current  RADRISK toxicokinetic model for silicon is taken from ICRP

Publication  30 (1981).

      1. Absorption from the  intestine  (f,) is 0.01.

      2. Fractional tissue  uptake  (f'2)  is:  all tissues, 1.0.

      3. Retention parameters:

                                     F                      TB
                               (Fraction of         (Biological half-
              Organ	organ burden)	1 ife  in days)
All tissues
0.40
0.60
5
100
Phosphorus Model
      The toxicokinetic model for phosphorus is taken from ICRP Publication 30

(1979).

      1. Absorption  from  the  intestine  (f,) is 0.80.

      2. Fractional  tissue  uptake (f'2) is:  bone, 0.30; other tissues, 0.55;
         excretion,  0.15.

      3. Retention parameters:

                                     F                      T8
                               (Fraction of         (Biological half-
              Organ	organ burden)	life in days)
Bone
Other tissues

1.0
0.27
0.73
00
2
19
DRAFT                               111-48

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 Sulfur Model
      The  toxicokinetic model for  sulfur  is  taken  from Adams  et al .  (1978)
      1. Absorption  from  the  intestine  (f,)  is  0.95.
      2. Fractional  tissue  uptake  (f'2)  is:   all  tissues,  0.20;  excretion,
         0.80.
      3.  Retention  parameters:
                                                            TB
                                (Fraction of          (Biological  half-
              Organ	organ burden)	1 ife  in days)
All tissues
0.75
0.25
20
2000
Chlorine Model
      There is no toxicokinetic model for chlorine  in  Sullivan  et  al.  (1981)
The current RADRISK toxicokinetic model for chlorine  is  taken  from ICRP
Publication 30 (1980).
      1. Absorption from the intestine  (f,) is  1.0.
      2. Fractional tissue uptake  (f'2)  is:  all tissues,  1.0.
      3. Retention parameters:
                                     F                      TB
                               (Fraction of          (Biological  half-
      	Organ	organ burden)	1 ife  in days)	
       All  tissues                  1.0                     10
DRAFT                               111-49

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Argon Model
      The  toxicokinetic model  for argon  is  taken  from Bernard  and  Snyder
(1975).
      1.  Absorption from the intestine (f,)  is  1.0.
      2.  Fractional tissue uptake (f'z) is:   all tissues,  1.0.
      3.  Retention parameters:
                                      F                      TB
                                (Fraction  of          (Biological  half-
              Organ	organ  burden)	1 ife  in  days)
All tissues




0.885
0.092
0.021
1 . 5x10"^*
S.OxlO'4
5.3xlO'3
6.2xlO'4
5.7xlO'3
0.029
0.19
Potassium Model
      The toxicokinetic model  for  potassium  is  taken  from Adams  et  al.  (1978)
      1. Absorption  from  the intestine  (f,)  is  0.95.
      2. Fractional  tissue uptake  (fj)  is:   all tissues, 1.0.
      3. Retention parameters:
                                      F                      TB
                                (Fraction of         (Biological  half-
      	Organ	organ  burden)	1 ife  in days)	
       All tissues                  1.0                     30
DRAFT                               111-50

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Calcium Model
      There  is no toxicokinetic model for calcium  in Sullivan  et  al .  (1981).

The current  RADRISK toxicokinetic model for calcium is taken from Adams  et  al

(1978).

      1.  Absorption from the  intestine  (f,) is 0.30.

      2.  Fractional tissue uptake  (fl) is:  cortical bone, 0.33;  trabecular
          bone, 0.32; other tissues,  0.35.
      3.  Retention parameters:
                                                            TB
                               (Fraction of          (Biological  half-
              Organ 	organ burden)	1 ife  in  days)
Cortical bone


Trabecular bone


Other tissues


0.30
0.15
0.55
0.34
0.16
0.50
0.57
0.29
0.14
10
1100
10500
10
700
2900
1.5
45
100
Scandium Model
      The toxicokinetic model for scandium is taken from  ICRP  Publication  2

(1959).

      1. Absorption from the intestine (f^ is 0.0001.

      2. Fractional tissue uptake (f'2) is:  bone, 0.20; liver, 0.15; kidneys,
         0.02; other tissues, 0.63.

      3. Retention parameters:

                                     F                      TB
                               (Fraction of         (Biological half-
              Organ	organ burden)	1 ife in  days)
Bone
Liver
Kidneys
Other tissues
1.0
1.0
1.0
1.0
33
36
75
30
DRAFT                               111-51

-------
Titanium Model
      There is no toxicokinetic model  for  titanium  in  Sullivan  et  al.  (1981)
The ICRP (1981) toxicokinetic model  for  titanium  is  listed  below.
      1. Absorption  from the intestine (f,)  is 0.01.
      2. Fractional  tissue uptake  (f'2) is:   All tissues,  1.0.
      3. Retention parameters:
                                     f                     TB
                                (Fraction of          (Biological  half-
      	Organ	organ burden)	1 ife  in days)	
       All  tissues .	T.O	600	
Vanadium Model
      There is no toxicokinetic model  for  vanadium  in  Sullivan  et  al.  (1981).
The current RADRISK  toxicokinetic model  for  vanadium is taken from ICRP
Publication 30 (1981).
      1. Absorption  from the intestine (f,)  is 0.01.
      2. Fractional  tissue uptake  (f'z) is:   bone, 0.25; other tissues, 0.05;
         excretion,  0.70.
      3. Retention parameters:
                                     F                      TB
                               (Fraction of          (Biological  half-
              Organ	organ burden)	1 ife  in days)
Bone
Other tissues
1.0
1.0
10,000'
10,000
Chromium Model
      The toxicokinetic model for chromium is taken from Adams et al.  (1978)
      1. Absorption from the  intestine  (f,) is 0.10.
      2. Fractional tissue uptake (f'2) is:  bone, 0.05; other tissues, 0.65;
         excretion, 0.30.
      3. Retention parameters:
                                     F                      TB
                               (Fraction of         (Biological half-
      	Organ	organ burden)	1 ife .in days)	

DRAFT                                  111-52

-------
       Bone                          1.0                    1000

       Other tissues                0.62                     6
      	      0.38	80	


Manganese Model
      The toxicokinetic model for manganese is taken from  ICRP  Publication  30

(1979).

      1. Absorption  from  the  intestine  (f,) is 0.10.

      2. Fractional  tissue  uptake  (f'2) is:  bone, 0.35; liver,  0.25;  other
         tissues,  0.40.

      3. Retention parameters:

                                     F                      TB
                               (Fraction of         (Biological  half-
              Organ   	organ burden)	1 ife in days)
Bone
Liver

Other tissues

1.0
0.4
0.6
0.5
0.5
40
4
40
4
40
Iron Model
      The toxicokinetic model for iron is taken from Adams et al.  (1978).

      1. Absorption from the  intestine (f,) is 0.10.

      2. Fractional tissue uptake (f'2) is:  liver, 0.08; spleen, 0.013; other
         tissues, 0.907.

      3. Retention parameters:

                                     F                      TB
                               (Fraction of         (Biological half-
              Organ	organ burden)	life in days)
Liver
Spleen
Other tissues
1.0
1.0
1.0
2000
2000
2000
DRAFT                               111-53

-------
Cobalt Model
      The  toxicokinetic  model  for  cobalt  is  taken  from ICRP Publication 30
(1979).
      1. Absorption from the intestine  (f,)  is 0.05.
      2. Fractional tissue uptake  (f'2)  is:   kidneys,  0.05;  other  tissues,
         0.45;  excretion,  0.50.
      3. Retention parameters:
                                      F                      TB
                                (Fraction  of          (Biological half-
              Organ	organ  burden)	1 ife  in  days)
Kidneys


Other tissues


0.6
0.2
0.2
0.6
0.2
0.2
6
60
800
60
60
800
Nickel Model
      The toxicokinetic model for nickel is taken  from Adams  et  al.  (1978)
      1. Absorption  from  the  intestine  (f,) is 0.05.
      2. Fractional  tissue  uptake (fl) is:  kidneys, 0.97; other tissues,
         0.03.
      3. Retention parameters:
                                     F                      TB
                               (Fraction of          (Biological  half-
      	Organ	organ burden)	1 ife in days)	
       Kidneys                      1.0                     1
       Other tissues	1.0	10,000
DRAFT                               111-54

-------
Copper Model

      There is no toxicokinetic model for copper  in  Sullivan  et  al .  (1981).

The current RADRISK toxicokinetic model for copper is  taken from ICRP

Publication 30 (1980).

      1. Absorption from the  intestine  (f,) is 0.5.

      2. Fractional tissue  uptake  (f'2)  is:  liver, 0.1; brain, 0.1;  pancreas,
         0.006; other tissues, 0.794.
      3. Retention parameters:
                                                            TB
                               (Fraction of          (Biological  half-
              Organ   	organ burden)	1 ife  in days)
Liver
Brain
Pancreas
Other tissues
1.0
1.0
1.0
1.0
40
40
40
40
Zinc

      The toxicokinetic model for zinc is taken from Adams et al.  (1978).

      1. Absorption from the  intestine (f,) is 0.50.

      2. Fractional tissue uptake (f'2) is:  bone, 0.20; other tissues, 0.80.

      3. Retention parameters:

                                     F                      TB
                               (Fraction of         (Biological  half-
      	Organ	organ burden)	1 ife in days)	


       Bone                         1.0                    400

       Other tissues                0.3                     20
                                    0.7                    400
DRAFT                               111-55

-------
Gallium Model
      The  toxicokinetic  model  for  gallium  is taken from Adams et  al.  (1978).

      1. Absorption from the intestine  (f,) is 0.001.

      2. Fractional  tissue uptake  (f'2)  is:  bone, 0.30; liver, 0.25;  spleen,
         0.01;  other tissues,  0.44.

      3. Retention parameters:

                                      F                      TB
                                (Fraction of          (Biological half-
              Organ	organ  burden)	life  in days)
Bone
Liver
Spleen
Other tissues

1.0
1.0
1.0
0.5
0.5
40
5
40
5
40
Germanium Model

      There is no toxicokinetic model for germanium in Sullivan et al.  (1981)
The current RADRISK toxicokinetic model for germanium is taken from  ICRP

Publication 30 (1981).

      1. Absorption from  the  intestine  (f^ is 1.0.

      2. Fractional tissue  uptake  (f'2) is:  kidneys, 0.5; other tissues, 0.5.

      3. Retention parameters:

                                     F                      TB
                               (Fraction of         (Biological half-
      	Organ	organ burden)	1 ife in days)	


       Kidneys                      1.0                    0.2

       Other tissues                1.0                     1
DRAFT                                  111-56

-------
Arsenic Model
      The toxicokinetic model for arsenic is taken  from  ICRP  Publication  2
(1959).
      1. Absorption from the  intestine  (f,) is 0.03.
      2. Fractional tissue uptake (f'2) is:  liver,  0.03;  kidneys,  0.01; other
         tissues, 0.96.
      3. Retention parameters:
                               (Fraction of          (Biological  half-
              Organ	organ burden)	life  in  days)
Liver
Kidneys
Other tissues
1.0
1.0
1.0
550
550
280
Selenium Model
      The toxicokinetic model for selenium is taken from Adams  et  al .  (1978).
      1. Absorption from the intestine  (f,) is 0.95.
      2. Fractional tissue uptake (f'2) is:  bone, 0.10; liver,  0.20; kidneys,
         0.10; other tissues, 0.60.
      3. Retention parameters:
                                                            TB
                               (Fraction of          (Biological  half-
              Organ	organ burden)	1 ife  in days)
Bone


Liver


Kidneys


Other tissues


0.4
0.3
0.3
0.4
0.3
0.3
0.4
0.3
0.3
0.4
0.3
0.3
1
10
70
1
10
70
1
10
70
1
10
70
DRAFT                                  111-57

-------
Bromine Model
      There  is  no  toxicokinetic model  for bromine in Sullivan et al.  (1981)

The current  RADRISK toxicokinetic model  for bromine is taken from ICRP

Publication  30  (1980).

      1.  Absorption from the intestine (f,)  is  1.0.

      2.  Fractional tissue uptake (f'2)  is:   all  tissues,  1.0.

      3.  Retention parameters:

                                      F                       TB
                                (Fraction  of         (Biological  half-
      	Organ	organ  burden)	1 ife in days)	


       All tissues	1_10	10	



Krypton Model

      The toxicokinetic  model for krypton is  taken  from Bernard  and  Snyder

(1975).

      1.  Absorption from the intestine  (f,)  is  1.0.

      2.  Fractional tissue uptake (f'2)  is:   all  tissues,  1.0.

      3.  Retention parameters:

                                      F                       TB
                                (Fraction  of         (Biological  half-
      	Organ	organ  burden)	1 ife in days)	


       All tissues                 0.89                  8.8xlO"5
                                    0.09                  l.OxlO'3
                                    0.02                  9.5xlO'3
                                   2.9xlO"3                 0.049
                                   1.5xlO~3                 0.321
DRAFT                                   IH-58

-------
Rubidium Model
      The toxicokinetic model for rubidium  is taken  from  Adams  et al.  (1978)
      1. Absorption  from  the  intestine  (f,) is 0.95.
      2. Fractional  tissue  uptake  (f'z) is:  bone, 0.25; other tissues,  0.75.
      3. Retention parameters:
                                     F                      TB
                                (Fraction of          (Biological  half-
              Organ	organ burden)	life  in days)
Bone
Other tissues
1.0
1.0
40
40
Strontium Model
      The toxicokinetic model for strontium is taken  from Adams  et  al.  (1978)
and ICRP Publication 30 (1979).
      1. Absorption  from the  intestine  (f,) is 0.30.
      2. Fractional  tissue uptake (f'2) is:  bone, 0.27; other  tissues,  0.73.
      3. Retention parameters:
                                     F                      TB
                               (Fraction of         (Biological  half-
              Organ	organ burden)	1 ife  in  days)
Bone




Other tissues



0.393
0.0496
0.186
0.168
0.203
0.8
0.15
0.041
0.003
5
170
1100
2500
8800
1.8
30
200
. 1600
DRAFT                               111-59

-------
Yttrium Model
      The toxicokinetic  model  for yttrium  is  taken  from Adams  et  al.  (1978)

      1. Absorption  from the intestine (f,) is 0.0001.

      2. Fractional  tissue uptake  (f'2)  is:  bone, 0.50;  liver,  0.15;  other
         tissues,  0.10;  excretion,  0.25.

      3. Retention parameters:

                                      F.                      TB
                                (Fraction of          (Biological half-
              Organ	organ  burden)	life  in  days)
Bone
Liver
Other tissues
1.0
1.0
1.0
00
oo
30
Zirconium Model
      The toxicokinetic model for zirconium  is taken from  ICRP  Publication 30

(1979).

      1. Absorption  from  the  intestine  (f,)  is 0.002.

      2. Fractional  tissue  uptake  (f'2)  is:   bone, 0.50; other tissues, 0.50.

      3. Retention parameters:

                                     F                      TB
                               (Fraction of          (Biological half-
      	Organ	organ burden)	1 ife  in days)	


       Bone                         1.0                    8000

       Other tissues                1.0                     7
DRAFT                                  111-60

-------
Niobium Model

      The  toxicokinetic model  for  niobium  is  taken  from  ICRP Publication 30

(1979).

      1.  Absorption  from  the  intestine (f,) is  0.01.

      2.  Fractional  tissue  uptake  (f'2)  is:  bone, 0.71;  kidneys,  0.018;
          spleen,  0.01;  testes,  0.002;  other tissues,  0.26.

      3.  Retention parameters:

                                     F                      TB
                                (Fraction of         (Biological  half-
              Organ	organ burden)	1 ife  in  days)
Bone

Kidneys

Spleen

Testes

Other tissues

0.5
0.5
0.5
0.5
0.5
0.5
0.5
0.5
0.5
0.5
6
200
6
200
6
200
6
200
6
200
DRAFT                               111-61

-------
Molybdenum Model
      The toxicokinetic model for molybdenum is taken  from  ICRP  Publication 30
(1979).
      1. Absorption  from  the  intestine  (f,) is 0.80.
      2. Fractional  tissue  uptake  (f'2) is:  bone, 0.15; liver, 0.30; kidneys,
         0.05;  other tissues, 0.50.
      3. Retention parameters:
                                     F                      \
                               (Fraction of          (Biological  half-
              Organ	organ burden)	life  in days)
Bone

Liver

Kidneys

Other tissues

0.1
0.9
0.1
0.9
0.1
0.9
0.1
0.9
1
50
1
50
1
50
1
50
DRAFT                               111-62

-------
Technetium Model
      The toxicokinetic model for technetium  is  taken  from Adams  et al .

(1978).

      1. Absorption from the  intestine  (f.,) is 0.80.

      2. Fractional tissue uptake  (f'2)  is:  liver, 0.08;  kidneys,  0.01;
         thyroid, 0.02; other tissues,  0.89.
      3. Retention parameters:
                                                            TB
                                (Fraction of          (Biological  half-
              Organ    	organ burden)	1 ife  in  days)
Liver


Kidneys


Thyroid


Other tissues


0.76
0.20
0.04
0.76
0.20
0.04
0.76
0.20
0.04
0.76
0.20
0.04
1.6
3.7
22
1.6
3.7
22
1.6
3.7
22
1.6
3.7
22
Ruthenium Model

      The toxicokinetic model for ruthenium is taken  from  Adams  et  al.  (1978)

      .1. Absorption from the intestine  (f,) is 0.05.

      2. Fractional tissue uptake (f'2) is:  all tissues, 0.85; excretion,
         0.15.

      3. Retention parameters:

                                     F                      TB
                               (Fraction of          (Biological  half-
              Organ	organ burden)	1 ife in days)
All tissues


0.41
0.35
0.24
8
35
1000
DRAFT                               111-63

-------
Rhodium  Model
       The  toxicokinetic model  for rhodium is  taken  from Adams et al.  (1978)
       1.  Absorption from the intestine (f,) is  0.05.
       2.  Fractional tissue uptake (f'2)  is:  all  tissues,  0.85;  excretion,
          0.15.
       3.  Retention parameters:
                                      F                      TB
                                (Fraction  of          (Biological  half-
              Organ	organ  burden)	life  in days)
All tissues


0.41
0.35
0.24
8
35
1000
Palladium Model
      There  is no  toxicokinetic  model  for palladium  in  Sullivan  et  al.  (1981)
The current  RADRISK  toxicokinetic model  for palladium  is  taken  from ICRP
Publication  30 (1981).
      1. Absorption  from the intestine (f,) is 5xlO"3.
      2. Fractional  tissue uptake  (f'2)  is:  bone, 0.07; liver, 0.45;  kidneys,
         0.15; other tissues,  0.03;  excretion, 0.30.
      3. Retention parameters:
                                     F                      TB
                               (Fraction of          (Biological  half-
              Organ	organ burden)	1 ife  in days)
Bone
Liver
Testes
Other tissues
1.0
1.0
1.0
1.0
15
15
15
15
DRAFT                               111-64

-------
Silver Model
      The toxicokinetic model for silver is taken from Adams  et  al.  (1978).
      1. Absorption from the intestine  (f,) is 0.05.
      2. Fractional tissue uptake (f'2) is:   liver, 0.80; other tissues, 0.20.
      3. Retention parameters:
                                     F                      TB
                               (Fraction of          (Biological  half-
              Organ	organ burden)	life  in days)
Liver

Other tissues

0.10
0.90
0.10
0.90
3.5
50
3.5
50
Cadmium Model
      There is no toxicokinetic model for cadmium in Sullivan et  al.  (1981).
The current RADRISK toxicokinetic model  for cadmium is taken from ICRP
Publication 30 (1980).
      1. Absorption from the intestine (fj is 0.05.
      2. Fractional tissue uptake (f'2)  is:   liver, 0.30; kidneys,  0.30; other
         tissues, 0.40.
      3. Retention parameters:
                                     F                      TB
                               (Fraction of         (Biological half-
      	Organ	organ burden)	1 ife in days)	
       Liver                        1.0                     9131
       Kidneys                      1.0                     9131
       Other tissues                1.0                     9131
DRAFT                               111-65

-------
 Indium  Model

      The  toxicokinetic model  for indium is taken from Adams et al.  (1978).

      1.  Absorption from the intestine (f,) is  0.02.

      2.  Fractional tissue uptake (f^)  is:   bone,  0.30;  liver,  0.20;  kidneys,
          0.07; spleen, 0.01; other tissues, 0.42.

      3.  Retention parameters:

                                      F                       TB
                                (Fraction of         (Biological  half-
              Organ	organ burden)	life in days)
Bone
Liver
Kidneys
Spleen
Other tissues
1.0
1.0
1.0
1.0
1.0
00
00
00
00
00
Tin Model
      The  toxicokinetic  model  for  tin  is  taken  from  Adams  et  al.  (1978).

      1. Absorption from the intestine (f,)  is  0.05.

      2. Fractional  tissue uptake  (f'2)  is:   bone, 0.50; other  tissues,  0.50.

      3. Retention  parameters:

                                     F                     TB
                                (Fraction  of          (Biological half-
      	Organ	organ burden)	1 ife  in  days)	


       Bone                          1.0                     50

       Other tissues                 1.0                     50
DRAFT                               111-66

-------
Antimony
      The toxicokinetic model for antimony is taken from Adams et al.  (1978),

      1. Absorption from the intestine (f,) is 0.20.

      2. Fractional tissue uptake (f'2) is:  bone, 0.14; other tissues, 0.56;
         excretion, 0.30.

      3. Retention parameters:


                               (Fraction of         (Biological half-
              Organ	organ burden)	life in days)
Liver
Other tissues
1.0
1.0
20
20
Tellurium Model
      The toxicokinetic model  for tellurium is taken from ICRP Publication 30

(1979).

      1. Absorption from the intestine (f,) is 0.20.

      2. Fractional tissue uptake (f'2)  is:   bone,  0.25; other tissues, 0.25;
         excretion, 0.50.
      3.  Retention parameters:
                                                            TB
                               (Fraction of         (Biological half-
      	Organ	organ burden)	life in days)


       Bone                         1.0                    5000

       Other tissues                1.0                     20
                                    111-67

-------
 Iodine  Model
      The  toxicokinetic  model  for iodine is taken from the U.S.  Nuclear
 Regulatory Commission  (1975).

      1.  Absorption from the intestine (f,) is  0.95.

      2.  Fractional tissue uptake (f'2)  is:   thyroid,  0.30;  other tissues,
          0.70.

      3.  Retention parameters:

                                      F.                      TB
                                (Fraction of         (Biological  half-
              Organ	organ  burden)	1 ife in days)
Thyroid

Other tissues


0.05
0.95
0.996
-0.0725
0.0765
11.3
117
0.243
11.3
117
Xenon Model

      The toxicokinetic model for xenon  is  taken  from  Bernard  and  Snyder

(1975).

      1. Absorption  from  the  intestine  (f,)  is  1.0.

      2. Fractional  tissue  uptake  (f'2) is:   all tissues,  1.0.-

      3. Retention parameters:

                                      F                      TB
                                (Fraction of          (Biological  half-
      	Organ	organ  burden)	1 ife  in  days)	


       All  tissues                  0.87                  1.78xlO"4
                                   0.088                 2.1xlO'3
                                   0.037                  0.019
                                   0.0051                 0.097
                                   0.0028                 0.642
DRAFT                               111-68

-------
 Cesium Model
      The  toxicokinetic model  for  cesium  is  taken  from  ICRP Publication 30

 (1979).

      1. Absorption  from  the  intestine (f,)  is 0.95.

      2. Fractional  tissue  uptake  (f'2)  is:   all tissues,  1.0.

      3. Retention parameters:

                                      F                      TB
                                (Fraction  of          (Biological  half-
      	Organ	organ  burden)	life  in  days)	


       All tissues                  0.10                     2
      	0.90	110	


 Barium Model
      The  toxicokinetic model  for  barium  is  taken  from  Adams et  al.  (1978).

      1. Absorption  from  the  intestine  (f,)  is 0.10.

      2. Fractional  tissue  uptake  (f'2)  is:   bone,  0.60; other  tissues,  0.30;
         excretion,  0.10.

      3. Retention parameters:

                                      F                      TB
                                (Fraction  of          (Biological  half-
              Organ	organ  burden)	life  in  days)
Bone




Other tissues



0.83
0.10
0.08
0.0385
0.0235
0.73
0.13
0.1
0.017
0.2
3.5
390
1400
5500
0.8
18
130
1000
DRAFT                               IH-69

-------
 Lanthanide  (Rare  Earth)  Models
       The lanthanides  are  a  group  of  15  elements which  have  many  similar
 characteristics.   They are modeled in 3  groups.

  (A)   Lanthanum Model
       Cerium Model
       Praseodymium Model

       The toxicokinetic  model for  lanthanum, cerium and praseodymium  is taken
 from  ICRP Publication  30 (1979).
       1. Absorption from the intestine  (f,) is 0.0003.
       2. Fractional  tissue uptake  (f'z) is:  bone, 0.20; liver, 0.60;  spleen,
         0.05; other tissues, 0.15.
       3. Retention parameters:
                                     F                      TB
                                (Fraction of         (Biological half-
       	Organ	organ burden)	1 ife in days)	
       Bone                         1.0                    3500
       Liver                        1.0                    3500
       Spleen                       1.0                    3500
       Other tissues                1.0                    3500
DRAFT                               111-70

-------
       (B)     Neodvmium Model
              Promethium Model
              Samarium Model
              Europium Model
              Gadolinium Model
              Terbium Model

      The toxicokinetic model for neodymium, promethium,  samarium,  europium,
gadolinium and terbium is taken from Adams et. al.  (1978).
      1. Absorption  from the  intestine  (f,) is 0.0001.
      2. Fractional  tissue  uptake  (f'2)  is:  bone, 0.45; liver,  0.45;
         excretion,  0.10.
      3. Retention parameters:
                                                            TB
                               (Fraction of          (Biological  half-
              Organ	organ burden)	1 ife  in  days)
Bone
Liver
1.0
1.0
3500
3500
      (C)     Dysprosium Model
              Holmium Model
              Erbium Model
              Thulium Model
              Ytterbium Model
              Lutetium Model

      There is no toxicokinetic model for dysprosium, holmium, erbium,
thulium, ytterbium or lutetium in Sullivan et al. (1981).
DRAFT                               111-71

-------
Dysprosium
      The current  RADRISK toxicokinetic model for dysprosium  is  taken  from

ICRP Publication 30  (1981).
      1. Absorption  from the intestine  (f,)  is 3xlO"4.

      2. Fractional  tissue uptake  (f'2) is:   bone, 0.60; liver, 0.10; kidneys,
         0.02;  excretion, 0.28.
      3.  Retention  parameters:
                                                            TB
                                (Fraction of          (Biological  half-
              Organ	organ burden)	1 ife  in days)
Bone
Liver
Kidneys
1.0
1.0
1.0
3500
3500
10
Holmium

      The current RADRISK  toxicokinetic model for holmium  is taken  from  ICRP

Publication 30  (1981).

      1. Absorption  from  the  intestine  (f,) is 3xlO"4.

      2. Fractional  tissue uptake  (f'z) is:  bone, 0.40; liver, 0.40; pancreas/
         0.05;  excretion,  0.15.
      3. Retention  parameters:
                                                            TB
                                (Fraction of         (Biological half-
              Organ _ organ burden) _ 1 ife  in days)


       Bone                         1.0                    3500

       Liver                        1.0                    3500

       Pancreas                     1.0                .    3500
DRAFT                               111-72

-------
Erbium
      The current RADRISK toxicokinetic model  for  erbium  is  taken  from ICRP
Publication 30  (1981).
      1. Absorption  from the  intestine  (f,) is 3xlO"4.
      2. Fractional  tissue uptake  (f'2) is:  bone,  0.60; liver,  0.05;  other
         tissues, 0.10; excretion, 0.25.
      3. Retention parameters:
                                     F                      TB
                               (Fraction of          (Biological  half-
              Organ    	organ burden)	1 ife  in  days)
Bone
Liver
Other tissues
1.0
1.0
1.0
3500
3500
3500
Thulium
      The current RAORISK toxicokinetic model for thulium  is  taken  from ICRP
Publication 30 (1981).
      1. Absorption from the intestine  (f,) is 3xlO~4.
      2. Fractional tissue uptake  (f'2) is:  bone, 0.65; liver, 0.04;  other
         tissues, 0.10; excretion, 0.21.
      3. Retention parameters:
                                     F                      TB
                               (Fraction of          (Biological  half-
      	Organ	organ burden)	life  in days)
       Bone                         1.0                    3500
       Liver                        1.0                    3500
       Other tissues                1.0                    3500
DRAFT                               111-73

-------
 Ytterbium

       The current RADRISK toxicokinetic model  for ytterbium is taken from ICRP

 Publication 30 (1981).
       1.  Absorption from the intestine (f,)  is 3xlO"4.

       2.  Fractional tissue uptake (f^)  is:   bone,  0.5;  liver,  0.03;  kidneys,
          0.02; spleen,  0.005; excretion,  0.445.

       3.  Retention parameters:

                                      F                      TB
                                (Fraction  of          (Biological  half-
              Organ	organ  burden)	life  in  days)
Bone
Liver
Kidneys
Spleen
1.0
1.0
1.0
1.0
3500
3500
10
3500
Lutetium

      The current  RADRISK  toxicokinetic  model  for  lutetium  is  taken from ICRP

Publication  30  (1981).

      1. Absorption from the intestine  (f,)  is 3xlO"A.

      2. Fractional tissue uptake  (f'2) is:   bone,  0.6;  liver,  0.02; kidneys,
         0.005;  excretion, 0.375.

      3. Retention parameters:

                                      F                      T8
                                (Fraction of          (Biological half-
              Organ	organ  burden)	life  in  days)
Bone
Liver
Kidneys
1.0
1.0
1.0
3500
3500
10
DRAFT                               111-74

-------
Hafnium Model
      The toxicokinetic model for hafnium is taken from  ICRP  Publication  2
(1959).
      1. Absorption  from  the  intestine  (f,) is 0.0001.
      2. Fractional  tissue  uptake  (f^)  is:  bone, 0.15;  liver, 0.45;  kidneys,
         0.02;  spleen, 0.13;  other tissues, 0.25.
      3. Retention parameters:
                                     F                      TB
                               (Fraction of          (Biological  half-
              Organ	organ burden)	1 ife  in days)





Tantal
Bone
Liver
Kidneys
Spleen
Other tissues
urn Model
1.0
1.0
1.0
1.0
1.0

600
625
563
350
563

      There is no toxicokinetic model for tantalum in Sullivan et  al.  (1981),
The current RADRISK toxicokinetic model for tantalum is taken from ICRP
Publication 30 (1981).
      1. Absorption from the intestine  (f,) is 0.001.
      2. Fractional tissue uptake (f'2) is:  bone, 0.30; kidneys, 0.06; other
         tissues, 0.64.
      3. Retention parameters:
                                     F                      TB
                               (Fraction of         (Biological half-
              Organ	organ burden)	life  in days)
Bone
Kidneys
Other tissues
1.0
0.50
0.50
0.50
0.50
100
4
100
4
100
DRAFT                               111-75

-------
Tungsten Model
      The tungsten  (wolfram) model  is  taken  from  ICRP  Publication  2  (1959),
      1. Absorption from the  intestine (f,)  is 0.10.
      2. Fractional  tissue uptake (f'2)  is:   bone, 0.07;  liver,  0.06;  other
         tissues,  0.87.
      3.  Retention  parameters:
                                                            TB
                                (Fraction of          (Biological  half-
              Organ     	organ burden)	1 ife  in  days)
Bone
Liver
Other tissues
1.0
1.0
1.0
9
4
1
Rhenium Model
      There  is no toxicokinetic model for rhenium  in  Sullivan  et  al .  (1981).
The current  RADRISK toxicokinetic model for rhenium is  taken from ICRP
Publication  30 (1980).
      1. Absorption from  the  intestine  (f,) is 0.80.
      2. Fractional tissue  uptake  (f'z)  is:  thyroid,  0.04;  stomach wall, 0.10;
         liver,  0.03;  other tissues,  0.83.
3. Retention parameters:

                         (Fraction of         (Biological half-
                                                            TB
Organ
Thyroid
Stomach wall
Liver
Other tissues
organ burden)
1.0
0.75
0.20
0.05
0.75
0.20
0.05
0.75
0.20
0.05
1 ife in days)
0.5
1.6
3.7
22
1.6
3.7
22
1.6
3.7
22
DRAFT                               111-76

-------
Osmium Model
      There is no toxicokinetic model for osmium  in Sullivan  et  al  (1981)

The current RADRISK toxicokinetic model for osmium is  taken from ICRP

Publication 30 (1980).
      1.  Absorption from  the  intestine  (f,) is 0.01.

      2.  Fractional tissue  uptake  (f'2)  is:  liver, 0.20;  kidneys, 0.04;
          spleen, 0.02; other  tissues, 0.54; excretion,  0.20.

      3.  Retention parameters:

                                     F                      TB
                               (Fraction of         (Biological  half-
              Organ	organ burden)	1 ife in days)
Liver
Kidneys
Spleen
Other tissues
0.2
0.8
0.2
0.8
0.2
0.8
0.2
0.8
8
200
8
200
8
200
8
200
Iridium Model

      The iridium toxicokinetic model is taken from Furchner et  al.  (1971)

      1. Absorption from the  intestine  (f,) is 0.01.

      2. Fractional tissue uptake  (f'2) is:  liver, 0.20; kidneys,  0.04;
         spleen, 0.02; other  tissues, 0.54; excretion,  0.20.

      3. Retention parameters:

                                     F                      T8
                               (Fraction of         (Biological  half-
              Organ	organ burden)	life in days)
Liver
Kidneys
Spleen
Other tissues
0.20
0.80
0.20
0.80
0.20
0.80
0.20
0.80
8
200
8
200
8
200
8
200
DRAFT                               111-77

-------
Platinum Model
      There  is  no  toxicokinetic model  for platinum  in  Sullivan  et  al.  (1981)

The current  RADRISK toxicokinetic model for platinum is  taken from ICRP

Publication  30  (1981).

      1.     Absorption  from  the intestine (fj is 0.01.

      2.     Fractional  tissue uptake  (fl)  is:   kidneys, 0.1; liver, 0.1;
             spleen,  0.01;  adrenals, 0.001; other tissues, 0.589; excretion,
             0.2.

      3.     Retention parameters:

                                      F                      TB
                               (Fraction of         (Biological half-
              Organ	organ  burden)	life  in days)
Kidneys
Liver
Spleen
Adrenals
Other tissues
0.95
0.05
0.95
0.05
0.95
0.05
0.95
0.05
0.95
0.05
8
200
8
200
8
200
8
200
8
200
Gold Model
      There is no toxicokinetic model for gold in Sullivan et al.  (1981).  The

current RADRISK Toxicokinetic model for gold is taken from ICRP  Publication 30

(1980).
      1.    Absorption from the intestine (f,)  is 0.10.

      2.    Fractional tissue uptake (f'2)  is:   all  tissues,  1.0.

      3.    Retention parameters:

                                     F                      TB
                               (Fraction of         (Biological  half-
      	Organ	organ burden)	1 ife in days)	


       All tissues                  1.0                     3
DRAFT                               111-78

-------
 Mercury  Model

       The mercury  toxicokinetic  model  is  taken  from Adams et al .  (1978).

       1.    Absorption  from the  intestine (f,)  is 0.02.

       2.    Fractional  tissue  uptake  (f'2) is:   kidneys, 0.08; other  tissues,
            0.92.
      3.    Retention parameters:
                                             TB
                       (Fraction of    (Biological  half-
           Organ _ organ burden)     life  in days)

       Kidneys         0.95            40
                       0.05            10,000

       Other tissues   0.95            40
                       0.05            10,000
Thallium Model

      Thallium metabolism has been studied  in humans  and  animals.   The  model

is taken from Adams et al.  (1978).

      1.    Absorption from the intestine (f,) is 0.95.

      2.    Fractional tissue distribution  (f'2) is:  kidneys, 0.05  and  other
            tissues 0.95.

      3.    Retention parameters:

                            F                TB
                      (Fraction of   (Biological half-
      	Organ	organ burden)    life in days)

       Kidneys             1.0               7

       Other tissues       1.0               7
DRAFT                               111-79

-------
Lead Model
      The lead model used  is taken from Adams et al.  (1978).
      1.    Absorption from the  intestine  (f,) is 0.20.

      2.    Fractional tissue distribution  (f'2)  is:  bone 0.55; liver,  0.25;
            kidney, 0.02;  other  tissues 0.18.

      3.    Retention parameters:

                                     F                      TB
                               (Fraction of          (Biological half-
              Organ	organ burden)	1 ife  in  days)
Bone


Liver


Kidneys


Other tissues


0.60
0.15
0.25
0.80
0.18
0.02
0.80
0.18
0.02
0.80
0.18
0.02
12
180
12000
12
180
12000
12
180
12000
12
180
12000
Bismuth Model
      The bismuth model is taken from Adams et al. (1978).
      1.    Absorption from the intestine (f,)  is 0.05.

      2.    Fractional tissue uptake (fl)  is:  kidney, 0.40; other tissues,
            0.60.

      3.    Retention parameters:

                            F                TB
                      (Fraction of   (Biological half-
           Organ	organ burden)    life in days)
Kidneys

Other tissues

0.60
0.40
0.60
0.40
0.60
5
0.60
5
DRAFT                               111-80

-------
Polonium Model
      The  polonium model  is  taken  from  ICRP  30  (1979).

      1.    Absorption  from  the  intestine  (f,)  is 0.10.

      2.    Fractional  tissue uptake  (f^) is: liver, 0.10; kidney, 0.10;
            spleen, 0.10;  other  tissues, 0.70.

      3.    Retention parameters:

                                      F                      TB
                               (Fraction of          (Biological  half-
              Organ  	organ  burden)	life  in  days)
Bone
Liver
Kidneys
Spleen
Other tissues
1.0
1.0
1.0
1.0
1.0
50
50
50
50
50
Astatine Model
      The current RADRISK toxicokinetic model for astatine  is  taken  from  ICRP

Publication 30 (1981).

      1.    Absorption from the intestine (f,) is 1.0.

      2.    Fractional tissue uptake (f'2)  is:  all  tissues, 1.0.

      3.    Retention parameters:

                                     F                      TB
                               (Fraction of          (Biological half-
      	Organ	organ burden)	life  in  days)	


       All tissues                  1.0                     10
DRAFT                                  111-81

-------
 Radon Model
      The  radon  model  used  by  EPA  is  based on human and animal  studies using
 radon and  is  generally supported by human  and animal  studies with inert gases
 (Bernard and  Snyder  1975).
      1.    Absorption from the  intestine  (f,)  is  1.0.
      2.    Fractional  tissue  uptake  (f'2)  is:   all  tissues,  1.0.
      3.    Retention  parameters:
Organ
Bone
Other tissues
F
(Fraction of
organ burden)
0.70
0.30
0.874
0.0913
0.0198
0.00863
0.00612
TB
(Biological hal
life in days)
2.65xlO"4
00
2.65xlO"4
0.0031
0.0288
0.146
0.963
f-

Francium Model
      The current RADRISK toxicokinetic model  for  francium is  taken from ICRP
Publication 30  (1981).
      1.    Absorption from the  intestine  (f,) is  1.0.
      2.    Fractional tissue uptake  (f'2) is:  all tissues, 1.0.
      3.    Retention parameters:  Due to the  short  half-life  of
            francium  isotopes, francium is considered  to  transform in  the
            organ in which it is deposited.
DRAFT                               111-82

-------
Radium Model
      The  radium model  is based  on  human  and  animal  studies of radium.   The

radium model  is  taken from Adams et al.  (1978).

      1.    Absorption  from the  intestine (f,) is 0.20.

      2.    Fractional  tissue  uptake (f'2)  is: bone, 0.46; other  tissues,  0.54.
3.
4.



Bone




Other




Radon retention in bone is 0.
Retention parameters:
F
(Fraction of
Organ organ burden)
0.525
0.435
0.022
0.00875
0.013
tissues 0.16
0.54
0.11
0.046
0.009
30.

TB
(Biological half-
life in days)
0.023
3.6
1300
3500
9600
0.05
1.0
35
200
1400
Actinium Model

      The actinium model  is  taken  from Adams et al.  (1978).

      1.    Absorption  from  the  intestine  (f,) is 0.001.

      2.    Fractional  tissue distribution  (f'2) is:  bone 0.20; liver, 0.60;
            spleen, 0.05;  other  tissues, 0.15.

      3.    Retention parameters:

                                     F                      TB
                               (Fraction of          (Biological half-
              Organ	organ burden)	1 ife  in  days)
Bone
Liver
Spleen
Other tissues
1.0
1.0
1.0
1.0
3500
3500
3500
3500
DRAFT                                   111-83

-------
Thorium Model
      Thorium uptake and retention have been studied  in  humans  and  animals,

The thorium model is taken from ICRP 30 (ICRP  1979).

            Absorption from the intestine  (f,)  is 2xlO'4.
1.

2.
            Fractional tissue distribution  (fl) is: bone 0.70; liver, 0.04;
            other tissues, 0.16; excreta, 0.10.
      3.    Retention parameters:
              Organ
                         (Fraction of
                         organ burden)
(Biological half-
  life in days)
Bone
Liver
Other tissues
1.0
1.0
1.0
8000
700
700
Protactinium Model

      The protactinium model is based on the models for transuranium  elements

developed by EPA for "Proposed Guidance for Transuranium  Elements  in  the

Environment" (EPA 1977).

      1.    Absorption from the intestine (f,)  is 0.001.

      2.    Fractional tissue uptake (f'?)  is:   bone, 0.45; liver, 0.45;
            testes,  0.00035; ovaries, 0.00011; other tissues, 0.07; excretion,
            0.03.

      3.    Retention parameters:
              Organ
                         (Fraction of
                         organ  burden)
(Biological  half-
  life in days)
Bone
Liver
Testes
Ovaries
Other tissues
1.0
1.0
1.0
1.0
1.0
36525
14610
14610
14610
36525
DRAFT
                                 111-84

-------
Uranium Model
      The toxicokinetic  model  for  uranium  is based on human and animal  studies

of uranium administered  intravenously or orally  (ICRP 1979).   It  is taken  from

the EPA models  (Sullivan et  al.  1981, Dunning et al. 1984, Begovich et  al.

1981).
            Absorption from  the  intestine  (f,)  is 0.05 to 0.20.
1.

2.
            Fractional  tissue uptake  (f'2) is: bone, 0.22; kidneys, 0.12; other
            tissues,  0.12;  excretion, 0.54.
      3.    Retention  parameters:
              Organ
                         (Fraction of
                         organ burden)
(Biological  half-
  life in days)
Bone
Kidneys
Other tissues
0.9
0.1
0.996
0.004
0.996
0.004
20
5000
6
1500
6
1500
Neptunium Model
      The neptunium model  is based primarily on animal studies and taken from

the EPA model for transuranium elements  (EPA 1977).

      1.    Absorption from the  intestine (f,)  is 0.001.

      2.    Fractional tissue uptake  (f'2) is:   bone, 0.45; liver, 0.45;
            testes, 0.00035; ovaries, 0.00011; other tissues, 0.07; excretion,
            0.03.
      3.    Retention parameters:
              Organ
                         (Fraction of
                         organ burden)
(Biological  half-
  life in days)
Bone
Liver
Testes
Ovaries
Other tissues
1.0
1.0
1.0
1.0
1.0
36525
14610
14610
14610
36525
DRAFT
                              111-85

-------
Plutonium Model

      The plutonium model is based on extensive  animal  studies supported by

some  studies of accidental exposure  in humans.   It  is  taken from the EPA model
for transuranium elements (EPA 1977).

      1.    Absorption from the intestine  (f,) is 0.001; absorption  from the
            intestine (f,) for plutonium-239, plutonium-240  and  plutonium-242
            oxides only,  is 0.0001.

      2.    Fractional tissue uptake (f'2) is:  bone, 0.45;  liver, 0.45;
            testes, 0.00035; ovaries, 0.00011; other tissues,  0.07;  excretion,
            0.03.

      3.    Retention parameters:
Organ
Bone
Liver
Testes
Ovaries
Other tissues
(Fraction of
organ burden)
1.0
1.0
1.0
1.0
1.0
(Biological hal
1 ife in days)
36525
14610
14610
14610
36525
f-





DRAFT
111-86

-------
Americium Model
      The americium model  is  based primarily on  animal  studies with  some

support from studies of accidental exposure of humans.   It  is taken  from the

EPA model for transuranium elements  (EPA  1977).

      1.    Absorption from the  intestine  (f,)  is 0.001.

      2.    Fractional tissue uptake  (f^) is:   bone, 0.45; liver, 0.45;
            testes, 0.00035;  ovaries, 0.00011; other tissues, 0.07;  excretion,
            0.03.
      3.    Retention parameters:
                                                            TB
                                (Fraction of          (Biological half-
              Organ    	organ burden)	1 ife  in days)
Bone
Liver
Testes
Ovaries
Other tissues
1.0
1.0
1.0
1.0
1.0
36525
14610
14610
14610
36525
Curium Model
      The curium model is based primarily on animal studies and taken from the

EPA model for transuranium elements  (EPA 1977).

      1.    Absorption from the intestine (f,)  is 0.001.

      2.    Fractional tissue uptake (f^)  is:  bone, 0.45; liver,  0.45;
            testes, 0.00035; ovaries, 0.00011; other tissues, 0.07; excretion,
            0.03.

      3.    Retention parameters:

                                     F                      TB
                               (Fraction of         (Biological half-
              Organ  	organ burden)	life in days)
Bone
Liver
Testes
Ovaries
Other tissues
1.0
1.0
1.0
1.0
1.0
36525
14610
14610
14610
36525
DRAFT                               111-87

-------
      All of the models listed previously are used  in  the  an  overall  computer
program, RADRISK, to calculate the concentration of a  parent  radionuclide and
all subsequent daughters in body tissues (Dunning et al .  1980,  Sullivan et al .
1981).
      The activity in an organ at any time is calculated  as:
) Aiik + cllk (*; I]:! Bfj ZZ Ajr + Pik)  1  = 1 ...... ,  L
                                                                     1k
where:
      Ajlk =       rate of change of activity of isotope i in compartment 1
                  organ k
      Ljk    =     number of exponential  terms in the retention function for
                  isotope i in organ k
      Br    =     branching ratio of nuclide to nuclide i
      X*    =     rate coefficient (time"1)  for  radiological  decay  of isotope
                  i
      A.jllc   =     rate coefficient (time"1)  for  biological removal  of isotope
                  i ,  from compartment 1  of organ k
      CHk   =     fractional  coefficient for nuclide i  in the 1th compartment
                  of  organ k
      pjk    =     inflow rate of isotope i into organ k

      The function is evaluated for a constant  inflow rate per year,  1
pCi/year in most cases.
      Retention is calculated in a similar manner  (Sullivan  et al .  1981):
                                     _
where:
      R-k(t)  =   retention  of  isotope  i  at  time  t  after intake, in organ k.
      Concentration of activity or integrated activity  in an  organ  or  tissue
can be calculated using these computer programs.  Computed values are  stored
DRAFT                                111-88

-------
in a file and later passed to another program which calculates dose and dose
rate from the activity concentrations.   Dosimetric estimates calculated in
this way are used with age-specific risk coefficients to calculate the risk
from a specified radionuclide intake.  Further information on these
calculations can be found in Section IV and V.
                                    111-89

-------
                           IV.  MECHANISM OF TOXICITY

A.    IONIZING  ENERGY  DEPOSITION

      The potential  for  ionizing  radiation to cause tissue damage and cancer
was established  by  15  years  after the discovery of x-rays  (EPA 1989, Upton
1975).  Radiogenic  effects  in humans and animals following exposure to
ionizing radiation  from  x-rays and gamma rays and several specific
radionuclides such  as  radium, radon, thorium, and plutonium have been studied
extensively  (NAS  1972, 1988; UNSCEAR 1986, 1988).

      The interaction  of ionizing radiation with matter involves a number of
rapid radiochemical  reactions.  Absorption of energy from alpha and beta
particles induces ions and excited radicals in matter, while absorption of
energy from  x-  and  gamma radiations by atoms results in the ejection of
electrons from  the  atoms.  These  ejected high speed electrons then produce
ionizations  in  the  same  manner as the alpha and beta particles.

      Although  the  exact mechanisms of action of ionizing radiation are not
known with certainty,  radiation injury is considered to be related to the
production of these  ions and free radicals within the cells (Hobbs and
McClellan 1986).  One  mechanism by which radiogenic injury may occur is by the
interaction  of  radiation with cellular aqueous solutions resulting in the
formation of superoxide  (02~)  and  hydrogen  peroxide, and  free radicals,  such
as the hydroperoxyl  radical (H02-) or the hydroxyl radical  (OH").  These
reactive intermediates may then react with biologically important molecules in
the cell.  Further  chemical interactions can lead to bond scission, chain
scission, cross-linking,  development of adducts, single and double strand
breaks,  etc., in DNA and in nearby organic molecules.   Radiation effects have
been known to occur with  proteins, nucleic acids, lipids, and
carbohydrates.

      The intracellular  changes caused by radiation are numerous, varied and
complex and can be  similar to those seen with other types of cellular injury.
The response of individual cells  to radiation is variable and may depend on
such things as the  cycle  of the cell  and the oxygenation status of the cell

DRAFT                                IV-1

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(Hobbs and McClellan 1986).  The response of cells to radiation has been
extensively reviewed (Rubin and Casarett 1968, ICRP 1984, Mettler and Mosley
1985).  Ionizing radiation delivered at a sufficiently high dose and dose rate
may result in cell death, which, if extensive, may result in the death of the
organism.  At nonlethal doses and dose rate, cellular damage may undergo
either partial or total repair; however, unrepaired alterations may be
expressed as mutations or tumors at later times.

      For the purposes of radiation protection, radiogenic effects may be
classified as stochastic or nonstochastic (ICRP 1984).  Stochastic effects are
those for which the probability of occurrence of effect, and not its severity,
varies as a function of dose in the absence of a threshold (Hobbs and
McClellan 1986).  The major stochastic effects are cancer and heritable
effects (mutations).

      While the potential for carcinogenesis and mutagenesis has not been
investigated for every radionuclide, the results of studies that have been
performed are consistent with expected effects of ionizing radiation.  When
exposed to levels of ionizing radiation exceeding those in the environment,
mammalian cells in culture have been transformed; chromosomal aberrations have
been observed in cultured peripheral lymphocytes; even activation, by frame
shift due to a single base deletion in an oncogene, has been reported (EPA
1989).  Induction of enzymes of unscheduled DNA repair, perhaps signaling
error-prone repair, has also been noted (Tuschl et al. 1980, 1983; Olivieri et
al. 1984).

      Some epidemiological studies have shown increased cancer mortality in
persons exposed to x-rays, gamma rays and various internal alpha emitters,
such as radon, radium,  and thorium (EPA 1989).  Additional support comes from
the studies of mice, rats, hamsters, guinea pigs, cats, dogs, sheep, cattle,
pigs and monkeys that have demonstrated increased incidence of cancer
following exposure to a source of ionizing radiation (EPA 1989).
DRAFT                                IV-2

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B.     RADIONUCLIDE  DOSIMETRY

       Since  ionizing  radiation is known to induce cancer in many organs and
tissues,  risk  estimates  for internally deposited radionuclides can be
calculated  from  the distribution  of the radionuclides in tissues and the
ionizing  radiation  dose  associated with that  distribution.   The toxicokinetic
(metabolic)  models  used  to  estimate distribution have been  listed in Section
III, Part E.   As  explained  there, the  radionuclide concentration in various
organs  is calculated  for a  lifetime intake of 1  pCi/year.   For all organs or
tissues where  there is no organ-specific model,  the activity in the organ
compartment  "other" is considered to be uniformly distributed in all body
tissues not  specified.

      The absorbed  radiation dose rate is calculated as  follows:

       D5(X;t)  =  £k=1 Dj(X-Yk;t)

where:

       D,-(X;t)  =   Absorbed  dose rate to organ X  at time  t due to radionuclide
                  i in source organs Y,,  Y2	YM.
      D,(x-Yk;t)   =     S,  (X-Yk)  Aik(t)
and
      A,-k(t)  =     The activity at time t of radionuclide i  in source organ Yk
      S,(X-Yk)  =   The S  factor
      S,(X-Yk)  =   c L, f. Em*m(X-Yk)
      c   =  A  constant that  depends  on units  of  dose,  energy and time being
            used
and there is a summation  across all  events m  of:

      fm  =  Intensity of  decay event (number  per disintegration)
      Em  =  Average energy  of decay  event  in  MeV
      'UX-Yk)  =   Specific  absorbed  fraction,  i.e.,  the  fraction of emitted
                  energy  from source organ Yk absorbed by target organ X per
                  gram of X

DRAFT                                IV-3

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       The  S  factor  is  similar  to  the  SEE  factor used by the ICRP in ICRP
 Publication  30.   Both  S  factor and  SEE  are  dosimetric factors to account for
 the  fraction of  energy absorbed in  a  target organ  from emission of radiation
 from a source in another organ,  for example,  irradiation of a kidney by a
 radionuclide deposited in  the  bone.   However,  the  SEE factor includes a
 quality factor for  the type  of radiation  emitted during the transformation
 (disintegration)  (EPA  1989,  Dunning et  al .  1984).

       Summation  across all organs and tissues  is used to estimate the absorbed
 dose rate  in target organs due to one unit  of  activity of radionuclide i
 distributed  in source  organs Y1 ----  Yk.

       The  expression for this  dose  rate is:

                  ) - ZkL AJk(t) Sim(X-Yk).
      Alpha and beta particles are not  usually energetic  enough  to produce
significant cross-irradiation terms,  so m(X-Y) = 0.  The absorbed  fraction
for alpha and beta particles [4>m (X-X)j is assumed to be the  inverse  of  the
mass of organ X (EPA 1989).  Absorbed fractions for  beta  particles in skeletal
tissues are taken from ICRP Publication 30 (1980).   In the  case  of alpha
particles special calculations for active bone marrow and endosteal cells in
bone are based on the method of Thorne  (1977).

      A simplified model of the dose  rate estimate would  be (EPA 1989):

             D,.(t)  =  elf, (f;)E [l-e-x'M
                    mXE
where:

      D(t)  =     organ absorbed dose rate (rad/day)
      c =   proportionality constant  ([51.2 x 10"6 g  rad]  Ci~1 Mev"1 d"1)
      I =   radionuclide intake rate  (Ci/day)
      f,  =  fraction of ingested activity transferred to the  blood

DRAFT                                 IV-4

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      f'2 =  fraction  of  blood activity transferred to  the  target organ
      E =   energy  absorbed  by the target organ for each radioactive
            transformation
      m =   target  organ mass (grams)
      AE =  elimination  constant  (day"1)  ln2/TE or 0.693/TE
and
                                       TR TB
                                  TE  = ^-4-
      TB =  biological removal half-time
      TR =  radiological decay half-time

      Such a simplified estimate does not include cross-irradiation terms from
radionuclides deposited in other nearby organs.  These cross-irradiation terms
are included in the detailed calculation of radiation dose  (S factors)
performed by the RADRISK program employed by EPA for calculating radiation
dose.

      There are some differences between the EPA model and  the ICRP models as
noted earlier.  The EPA calculations carry forward high-LET and low-LET dose
rates as separate entities, whereas the ICRP combines high- and low-LET dose
rate through the use of a quality factor for high-LET.  The ICRP calculations
treat radioactive progeny in the body as following the metabolic behavior of
the parent nuclide, whereas the EPA model  assumes each of the progeny has the
metabolic behavior of the elements specific to the progeny.  The assumption
can have significant impact on the dose estimate (Dunning et al. 1884).

      EPA elected to assign the metabolic behavior of progeny on the basis of
the elemental form of the progeny.  This is clearly appropriate for soft
tissues where the elemental form of the progeny will govern their metabolic
behavior in the aqueous phase in tissues.   In skeletal tissues, however, the
progeny may be born and trapped in the crystal lattice of the hydroxyapatite.
They would, in this situation, continue to have the metabolic characteristics
more like the parent radionuclide (Neuman and Neuman 1958, McLean and Budy
                                     IV-5

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 1964).  That portion of the progeny born in skeletal tissues  outside  the
 crystal lattice would be expected to behave as their elemental characteristics
 direct them.  When radium transforms to radon-222 within  a crystal, 70 percent
 of the radon-222 escapes from the crystal (McLean and Budy 1964); very little
 of other radon isotopes born in the bone crystal can escape before decaying
 radiologically.

      In estimating radiation risk, EPA generally uses the risk coefficients
 derived from exposure to low-LET radiation for all tissues except bone, liver,
 and inhaled radon and radon daughters.  Bone and liver risk coefficients are
 derived from high-LET, radium and Thorotrast studies (MAS 1980).  Radon and
 radon daughter risk coefficients are derived from studies of  underground
 miners (NAS 1988).  The dosimetry for external x-rays and gamma rays  is well
 established and has minimal uncertainty due to the nature of  the radiation.
 The risk coefficients times the calculated radiation absorbed dose delivered
 by internally deposited radionuclides yield the risk.  The radiation  absorbed
 dose for internally deposited radionuclides, as noted above,  is based on
 pharmacokinetic models and radiation dosimetric calculations.

      The pharmacokinetic models assume uniform distribution  of radionuclides
 in organ or tissues.   While many studies have shown uneven distribution of
 radionuclides in tissues,  there are not sufficient data on any radionuclide to
 establish a detailed pharmacokinetic model  using non-uniform  tissue or organ
 nuclide distribution.  To the extent that the pharmacokinetic model cannot
 describe the microscopic distribution of deposited radionuclide within organs,
 the dose calculated and the risk estimated will be imprecise.

      Epidemiologic studies of ingested or injected radionuclides usually
 involve activity concentrations far in excess of expected environmental
 exposures.   A prime example of this situation can be found in epidemiological
 studies of persons exposed to radium-226 and radium-228 as dial painters or
 those injected with radium-226.

      The pharmacokinetic model  estimated for radium, but taken from studies
of persons  injected with radium,  differs appreciably from a model  estimate
based on environmental  exposure to radium (Stehney and Lucas  1956).   In

DRAFT                                IV-6

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addition,  gross  pathology,  including  peritrabecular fibrosis and
osteoradionecrosis  with  osteoporosis  and osteosaphyrosis  (softening and
fragility  of  bone),  has  been  noted  in many species, including humans,
following  elevated  doses of radiation to bone (Sharpe 1976, Lloyd and Henning
1983, Ackerman and  Spjut 1962,  Sikov  and Mahlum 1976, Wilson et al. 1976, Jee
et al.  1969,  Taylor and  Bensted 1969, Clarke 1962).  The  peritrabecular
fibrosis may  occur  within about 150 days post-exposure, following an abortive
attempt by osteoblasts to lay down  bone (Jee et al. 1969).  At the same time,
the microvasculature of  bone  and  bone marrow are disrupted.  Jee  (1971)
reported a 50 percent destruction of marrow vasculature within days of
injection  of  10  ^Ci  radium-226/kg.  The extensive  pathology reported by Jee
(1971)  following  radiation  exposure of bone demonstrates  that metabolism and
physiological responses  in  bone must be considered abnormal.

      The  circumstances  influencing pharmacokinetics, physiology and pathology
must be carefully evaluated for epidemiological  studies of internally
deposited  radionuclides.   In  particular, it is questionable whether bone with
abnormal physiology  and  metabolism  is suitable for estimating pharmacokinetics
and whether epidemiology of persons with such internal pathology can be
compared to environmental  situations.  The results of epidemiological studies
where atypical pathological conditions are prevalent must be regarded with
extreme caution.  Because data  are available on health effects following
exposure to lower doses  of  penetrating radiation (x- or gamma rays), risks at
environmental exposure levels are,  in some cases,   better estimated using risk
coefficients  derived  from penetrating radiation and pharmacokinetics models
than by applying data from  epidemiological  studies of persons exposed to
extremely  high activity  concentrations of radionuclides.

      For  many radionuclides  there  is no direct evidence for carcinogenesis in
humans.  Often, for  a specific  radionucl ide,  there is little evidence in
animal studies.  Nevertheless,  it must be presumed that such internally
deposited  radionuclides  can cause cancer since they deposit ionization energy
in tissues which is  no different in character than that which has been shown
to be carcinogenic.   In  such cases, it is prudent  to base risk estimates on
dosimetry models and  risk coefficients derived from other types of exposures
to ionizing radiation.

DRAFT                                IV-7

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       Risk  estimates for internally deposited radionuclides  should  be  based on
 positive  epidemiological studies where those are available,  but care must  be
 taken  in  extrapolating to low doses; in particular, tissue damage associated
 with high dose  levels may distort the results.  Where direct epidemiological
 data are  lacking, risk estimates can be calculated using the dosimetric
 method.   Where  epidemiological studies exist but show no statistical excess, a
 careful analysis should be conducted which considers the sensitivity and
 possible  shortcomings of the epidemiologic studies as well as uncertainties in
 the dosimetric  analysis.  However, even in the absence of direct
 epidemiological data, use of dosimetry models and risk coefficients is
 reasonable  since risk coefficients are based broadly on the  fact that  ionizing
 radiation is a  known carcinogen.
DRAFT                                IV-8

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                  V.  QUANTIFICATION OF TOXICOLOGICAL EFFECTS

      This  introductory  section  summarizes the general approach used to
evaluate  the  hazard of contaminants  in drinking water.  This text appears in
all criteria  documents to provide  information relevant to the basic issue of
how toxicological  effects are  quantified  for chemical toxicity assessment.

      The quantification  of toxicological effects of a chemical consists of
separate  assessments  of  noncarcinogenic and carcinogenic health effects.
Chemicals which  do  not produce carcinogenic effects are believed to have a
threshold dose below  which no  adverse, noncarcinogenic health effects occur,
while carcinogens  are assumed  to act without a threshold.

A.    NONCARCINOGENIC EFFECTS

Method for  Quantification of Noncarcinoqenic Effects

      In  the  quantification of noncarcinogenic effects, a Reference Dose (RfD)
(formerly called the  Acceptable Daily Intake (ADI)) is calculated.  The RfD is
an estimate of a daily exposure to the human population that is likely to be
without appreciable risk  of deleterious health effects, even if exposure
occurs over a lifetime.   The RfD is derived from a No-Observed-Adverse-Effect
Level (NOAEL), or  Lowest-Observed-Adverse-Effect Level (LOAEL), identified
from a subchronic or  chronic study, and divided by an uncertainty factor(s).
The RfD is  calculated as  follows:

                D,n     (NOAEL  or  LOAEL)              ,   .   . .
                RfD = —-	— =	mg/kg bw/day
                      Uncertainty Factor(s)
      Selection of the uncertainty factor to be employed in the calculation of
the RfD is based on professional judgment, while considering the entire data
base of toxicological effects for the chemical.  In order to ensure that
uncertainty factors are selected and applied in a consistent manner, the
Office of Water (OW) employs a modification to the guidelines proposed by the
National Academy of Sciences (NAS 1977, 1980) as follows:
DRAFT                                 V-l

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      •     An uncertainty factor of 10 is generally used when good chronic,
            or subchronic human exposure data identifying a NOAEL are
            available and are supported by good chronic, or subchronic
            toxicity data in other species.

      •     An uncertainty factor of 100 is generally used when good chronic
            toxicity data identifying a NOAEL are available for one or more
            animal species (and human data are not available), or when good
            chronic, or subchronic toxicity data identifying a LOAEL in humans
            are available.

      •     An uncertainty factor of 1,000 is generally used when limited or
            incomplete chronic, or subchronic toxicity data are available, or
            when good chronic,  or subchronic toxicity data identify a LOAEL,
            but not a NOAEL for one or more animal species are available.

      The uncertainty factor used for a specific risk assessment is based
principally on scientific judgment rather than scientific fact and accounts
for possible intra- and interspecies differences.  Additional  considerations
not incorporated in the NAS/OW guidelines for selection of an uncertainty
factor include the use of a less than lifetime study for deriving a RfD, the
significance of the adverse health effect and the counterbalancing of
beneficial effects.

      From the RfD, a Drinking  Water Equivalent (DWEL) can be calculated.  The
DWEL represents a medium specific (i.e.,  drinking water) 1ifetime exposure at
which adverse, noncarcinogenic  health effects are not anticipated to occur.
The DWEL assumes 100% exposure  from drinking water.   The DWEL provides the
noncarcinogenic health effects  basis for establishing a drinking water
standard.  For ingestion data,  the DWEL is derived as follows:

              DWEL ,    (RfD x (Body Weight in kg)    =	mg/|_
                     Drinking Water Volume in L/day
DRAFT                                V-2

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where:

      Body weight  =  assumed  to  be  70  kg for adult
      Drinking water volume  = assumed to be 2 liters per day  for an adult

      In addition  to the  RfD and the  DUEL, Health Advisories  (HAs) for
exposures of shorter duration (One-day, Ten-day and Longer-term) are
determined.  The HA  values are  used as informal guidance to municipalities and
other organizations  when  emergency spills or contamination situations occur.
The HAs are calculated using a  similar equation to the RfD and DWEL; however,
the NOAELs or LOAELs are  identified from acute or subchronic  studies.  The HAs
are derived as follows:
                   HA _  (NOAEL  or  LOAEL) x (bw) _ 	
                             (UF) x (L/day)
      Using the above equation, the following drinking water HAs are developed
for noncarcinogenic effects:

      1.    One-day HA for a 10-kg child ingesting 1 L water per day.
      2.    Ten-day HA for a 10-kg child ingesting 1 L water per day.
      3.    Longer-term HA for a 10-kg child ingesting 1 L water per day.
      ,4.    Longer-term HA for a 70-kg adult ingesting 2 L water per day.

      The One-day HA calculated for a 10-kg child assumes a single acute
exposure to the chemical and is generally derived from a study of less than
7 days duration.  The Ten-day HA assumes a limited exposure period of 1 to
2 weeks and is generally derived from a study of less than 30-days duration.
A Longer-term HA is derived for both the 10-kg child and a 70-kg adult and
assumes an exposure period of approximately 7 years (or 10% of an individual's
lifetime).  A Longer-term HA is generally derived from a study of subchronic
duration (exposure for 10 percent of animal's lifetime).
DRAFT                                 V-3

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Quantification of Noncarcinoqenic  Effects

      There  is little evidence for noncarcinogenic effects of exposure at
environmental levels to the beta or gamma emitting radionuclides of  interest
in this document  (see section III).  Numerous noncarcinogenic effects such as
hematopoietic effects, atrophy of  various tissues, and reproductive  effects
occur in laboratory animals only at doses exceeding the potential dose that
might result from drinking water containing these radionuclides.  Therefore,
EPA considers it  inappropriate to derive a Reference Dose for these  beta or
gamma emitting radionuclides in drinking water.

B.    CARCINOGENIC EFFECTS

Method for Quantification of Carcinogenic Effects

      The EPA categorizes the carcinogenic potential of a chemical,  based on
the overall weight-of-evidence,  according to the following scheme:

      •     Group A:  Human Carcinogen.  Sufficient evidence exists  from
            epidemiology studies to support a causal association between
            exposure to the chemical and human cancer.

      t     Group B:  Probable Human Carcinogen.  Sufficient evidence of
            carcinogenicity in animals with limited (Group Bl) or inadequate
            (Group B2) evidence in humans.

      •     Group C:  Possible Human Carcinogen.  Limited evidence of
            carcinogenicity in animals in the absence of human data.

      •     Group D:  Not classified as to Human Carcinogenicitv.  Inadequate
            human and animal  evidence of carcinogenicity or for which no data
            are available.

      •     Group E:  Evidence of Noncarcinogenicitv for Humans.  No evidence
            of carcinogenicity in at least two adequate animal tests in
DRAFT                                 V-4

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            different species or in both adequate epidemiologic and animal
            studies.

       If toxicological evidence leads to the classification of the contaminant
as a known, probable or possible human carcinogen, mathematical models are
used to calculate the estimated excess cancer risk associated with the
ingestion of the contaminant in drinking water.

Quantification of Cancer Risk for Chemicals

       For chemicals, the data used in these estimates usually come from
lifetime exposure studies  in animals.  In order to predict the risk for humans
from animal data, animal doses must be converted to equivalent human doses.
This conversion includes correction for noncontinuous exposure, less than
lifetime studies and for differences in size.  The factor that compensates for
the size difference is the cube root of the ratio of the animal and human body
weights.  It is assumed that the average adult human body weight is 70 kg and
that the average water consumption of an adult human is 2 liters of water per
day.

       For contaminants with a carcinogenic potential, chemical levels are
correlated with a carcinogenic risk estimate by employing a cancer potency
(unit  risk) value together with the assumption for lifetime exposure via
ingestion of water.  The cancer unit risk for chemicals is usually derived
from a linearized multistage model  with a 95 percent upper confidence limit
providing a low dose estimate;  that is, the true risk to humans, while not
identifiable,  is not likely to exceed the upper limit estimate and, in fact,
may be lower.   Excess cancer risk estimates may also be calculated using other
models such as the one-hit, Weibull,  logit and probit.   There is little basis
in the current understanding of the biological mechanisms involved in
chemically-caused cancer to suggest that any one of these models is able to
predict risk more accurately than any others.  Because each model  is based
upon differing assumptions, the estimates which were derived for each model
can differ by several  orders of magnitude.
DRAFT                                V-5

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      The scientific data base used to calculate and  support  the  setting of
cancer risk rate levels for chemicals has'an inherent uncertainty due to the
systematic and random errors in scientific measurement.   In most  cases, only
studies using experimental animals have been performed.   Thus, there is
uncertainty when the data are extrapolated to humans.  When developing cancer
risk rate levels, several other areas of uncertainty exist, such  as the
incomplete knowledge concerning the health effects of contaminants in drinking
water, the impact of the experimental animal's age, sex and species, the
nature of the target organ system(s) examined and the actual  rate of exposure
of the internal targets in experimental animals or humans.  Dose  response data
usually are available only for high levels of exposure, not for the lower
levels of exposure closer to where a standard may be set.  When there is
exposure to more than one contaminant, additional uncertainty results from a
lack of information about possible synergistic or antagonistic effects.

      For radionuclides, human epidemiologic data rather  than animal
experiments form the basis of the cancer risk rate levels, which  are derived
as best estimates rather than as 95% upper confidence limits  of the unit risk
from a linearized multistage model.  The true risks to humans may be higher or
lower than the predicted risks, but the overall uncertainty is probably less
than an order of magnitude.   Because human data are used, the individual sites
of cancer are predicted, as well  as the total risk.  Therefore, projections
can be made both of cancer incidence and of cancer fatality, which are related
for a given organ to site-specific survival data, which ranges from 90%
survival  (10% mortality) for thyroid cancer to 0% survival (100% mortality)
for liver cancer (EPA 1989).

Quantification of Carcinogenic Effects

Organ Doses and Risks from Ingestion of Beta and Photon Emitters in Drinking
Water Based on the RADRISK Model

      The risk calculations  in RADRISK are based on annual dose rates.   For
this purpose,  the dose rates  at specific ages are computed for an annual unit
intake of a radionuclide (Sullivan et al.  1981, Dunning et al. 1980,  EPA
1989).   The calculated dose  rate  in a given year for continuous intake is
DRAFT                                V-6

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numerically  equal  to  the  integrated lifetime dose for the cumulative  intake
until that year  (ICRP 1971).   For  illustration, Table V-l lists the 50th year
and the  70th year  doses  (integrated doses) for intake of beta and gamma
emitters.  (A  50 year period  is  standard for occupational exposure and 70
years is  recommended  by  ICRP  for environmental exposures.)

      As  noted earlier,  the RADRISK model differs from ICRP models in that no
quality  factors are used.  Instead, separate dose calculation files are
maintained for each organ, for high-LET and for low-LET radiations.

      The beta and gamma  emitters  are a diverse group of radionuclides
including examples from all elements.  Due to the large number of beta and
gamma emitters only selected  examples are given.   Isotopes selected are:
tritium,  a ubiquitous  radionuclide arising from both man-made and natural
sources;  cesium-137,  a nuclide in  both reactor effluents and weapons fallout;
strontium-90,  another  nuclide  in reactor effluents and fallout; iodine-131, a
nuclide present in reactor effluents and fallout  but also used in medical
practice  and some  laboratory  tests; and lead-210, one of the long-lived
daughters of radon-222.
DRAFT                                V-7

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                                   Table V-l


               50-year Committed Absorbed Dose per Unit Intake
         (millirad/pCi)  from  Beta  and  Gamma  Emitters  in Drinking Water
Orqan
Pulmonary
Lung
Stomach

Intestine

Kidneys

Liver

Breast

Pancreas

Red Marrow

Endosteum

Thyroid

All other

LET
Low
High
Low
High
Low
High
Low
High
Low
High
Low
High
Low
High
Low
High
Low
High
Low
High
Low
High

Lead-210
Isotope
Tritium-3*
2.400xlO"6(2.471xlO~6)** 8.360xlO"8
2.388xlO'5(2.475xlO'5)
1.380xlO"6(1.416xlO~6)
2.377xlO"5(2.463xlO'5)
9.948xlO~6(9.982xlO"6)
2.377xlO'5(2.464xlO~5)
5.008xlO'5(5.156xlO'5)
5. 192xlO'4(5. 382xlO~4)
1.081xlO'4(1.113xlO'4)
1.119xlO'3(1.160xlO~3)
2.389xlO'6(2.461xlO'6)
2.388xlO'5(2.475xlO'5)
2.397xlO'6(2.468xlO'6)
2.388xlO'5(2.475xlO'5)
5.155xlO'4(5.366xlO~4)
2.597xKT4(2.708xlO"4)
1.036xlO"3(1.079xlO'3)
3.962xlO"3(4.133xlO"3)
2.359xlO~6(2.429xlO'6)
2.388xlO'5(2.475xlO"5)
2.397xlO'6(2.468xlO'6)
2.388xlO'5(2.475xlO"5)

l.OSOxlO'7

1.187xlO"7

8.560xlO"8

8.280xlO"8

8.300xlO"8

8.060xlO'8

8.260xlO'8

6.560xlO'8

8.280xlO'8

8.300xlO'8


Iodine-131*
3.670xlO'7

1.091xlO'6

1.098xlO'6

1.745xlO"7

1.843xlO"7

4.468xlO"7

2.135xlO"7

3.506xlO"7

2.877xlO'7

1.670xlO"3

2.135xlO~7

*   Committed absorbed  dose  in  year 50 and year 70 are the same.
**  Committed absorbed  dose  in  the  70th year,  otherwise doses in the 50th year
    and 70th year are the  same.
DRAFT
V-8

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                             Table V-l (continued)

                50-year  Committed  Absorbed Dose per Unit  Intake
         (millirad/pCi)  from Beta and Gamma Emitters  in Drinking Water
Oroan
Pulmonary Lung
Stomach
Intestine
Kidneys
Liver
Breast
Pancreas
Red Marrow
Endosteum
Thyroid
All other
LET
Low
Low
Low
Low
Low
Low
Low
Low
Low
Low
Low
Isotope
Strontium-90
1.776xlO"7
9.653xlO"7
4.793xlO'5
1.776xlO"7
1.904xlO'7
1.776xlO'7
1.776xlO"7
2.167xlO'5(2.170xlO'5)**
4.794xlO~5(4.925xlO'5)**
1.776xlO'7
1.776xlO"7

Cesium-137*
4.438xlO"5
3.568xlO"5
2.928xlO'5
5.055xlO"5
4.786xlO'5
4.799xlO'5
4.440xlO"5
4.365xlO'5
3.052xlO"5
5.080xlO'5
4.440xlO'5
*   Committed absorbed dose in year 50 and year 70 are the same.
**  Committed absorbed dose in the 70th year, otherwise doses in the 50th year
    and 70th year are the same.
DRAFT

-------
       Isotopes in the natural radionuclide chains heavier than thallium,  if
they start as beta and gamma emitters, often have an alpha emitter as one of
their  progeny.  Lead-210 is an example of such a situation in that lead-210
and its daughter, bismuth-210, are essentially beta and gamma emitters; while
polonium-210, the daughter of bismuth-210, is an alpha emitter.  Lead-210,
therefore, has both low- and high-LET emissions associated with its decay.

       RADRISK contains a bookkeeping section of the program that sums
intakes, calculates dose rates (see Table V-l), and uses the calculated dose
rates  with risk coefficients (see Table V-2) to calculate lifetime risk by
organ  for high- and low-LET radiations for continuous intake of 1 pCi/year
(EPA 1989).  Since risk coefficients were based on cancer incidence/mortality
from the low-LET radiation, a relative biological effectiveness (RBE) of 8
should be used to estimate risk from high-LET radiation.  That is, the risk
per low-LET radiation listed in Table V-2 should be multiplied by a factor of
8 to obtain a high-LET risk coefficient (EPA 1989).

       Irradiation of bone marrow by low-LET radiation leads to leukemia in
humans and animals.  Leukemia has also been reported in patients receiving
thorium oxide and has been associated with enriched uranium exposure in
animals.  However, radium dial  painters with huge radium deposits in bone have
not developed leukemias,  but have developed bone sarcomas, sinus and mastoid
carcinomas.  Nor have ankylosing spondylitic patients treated with radium-224
developed an appreciable number of leukemias.

       In the case of internally distributed radioisotopes, the dose to
"sensitive" tissues is calculated from pharmacokinetic data and physics
dosimetry principles.   Compared to external  x- or gamma radiation which gives
a fairly uniform dose, internal  emitters,  particularly alpha emitters,  give an
irregular,  rather uncertain dose distribution.   In bone, for example,  target
DRAFT                                V-10

-------
                                   Table V-2

                      Organ-Specific  Lifetime Cancer Risks
                           Used in the RADRISK Model
                     from High-LET and Low-LET Irradiation
Organ
Pulmonary Lung
Stomach wall
Intestine
Kidneys
Liver
Breast
Pancreas
Red marrow
Bone surface
Thyroid
Esophagus
Lymphoma
All other tissue
LET
Low
High
Low
High
Low
High
Low
High
Low
High
Low
High
Low
High
Low
High
Low
High
Low
High
Low
High
Low
High
Low
High

Fatality
7.0xlO'5
5.7xlO/4
4.6xlO'5
3.7xlO'4
2.3xlCT5
l.SxlO'4
l.SxlO'5
1.4xlO~4
B.OxlO'5
4.0xlO'4
5.5xl(T5
4.4xlO'4
3.5xlO'5
2.8xlO'4
4.5xl(T5
3.6xlO'4
2.5xlO'6
2.0xlO"5
6.4xlO'6
B.lxlO'5
9.1xlO"6
7.3xlO'5
1.4xlO"5
l.lxlO'4
1.9xlO'5
1.6xlO'5
Risk/Rad
Incidence
7.5xlO"5
6.0xlO'4
6.0xlO'5
4.8xlO"4
4.3xlO"5
3.4xlO"4
4.3xlO"5
3.4xlO'4
S.OxlO'5
4.0xlO"4
1.4xlO'4
l.lxlO'3
3.8xlO"5
3.1xlO"4
4.5xlO"5
3.6xlO"4
2.5xlO"6
2.0xlO"5
6.4xlO"5
S.lxlO'4
9-lxlO"6
7.3xlO'5
1.9xlO"5
l.SxlO'4
3.4xlO'5
2.7xlO"4
Adapted from EPA (1989) Tables 6-6 and 6-7.
DRAFT
V-ll

-------
cells for osteosarcoma  induction are considered to be, and the dose estimated
for, cells up  to  10 jim  from bone surfaces.

      For leukemia induction,  the possible  non-uniform distribution of the
target cells in bone marrow is neglected.  Harley and  Pasternack  (1976)
calculated alpha  dose rate for radium-226  and its daughters  in uniformly
labelled bone  in  the tissues outside the mineral bone.  Noting Lloyd's report
(1970) of a 5  jim  thick  layer of osteoid between mineralized  bone  surfaces  and
cellular layers,  Harley and Pasternack (1976) adopted  a distance  of 10 jim  from
mineral bone as appropriate for calculating endosteal  dose.  On the other
hand, Scott (1967) indicated cell nuclei at a distance of 10 to 15 \im from
mineralized bone  surface in rats, and James and Taylor (1971) calculated dose
out to a distance of 20 ^m from bone surface.  ICRP  (1968) recommended
calculating endosteal dose rate over a distance 5 to  10 \im from the trabecular
surface.

     Mays and  Tueller  (1964)  calculated doses for radium-226 out  to 70  ^m
from bone surface and stated that the average dose rate for  soft  tissues from
0 to 10 urn was used because:  (a) osteosarcoma induction appeared  to occur  in
cells adjoining bone surfaces and (b) dose-rates were maximum at  bone
surfaces.  They also reported Owen's (1963) suggestion that cells located  over
1 cell-layer from bone surfaces were at risk.  Vaugan  (1972) had  shown a 5 to
20 \im thick cell  layer in rabbits and Lloyd and Henning (1983)  demonstrated a
single cell  layer 0.6 to ^8.1 \im thick in human bone.

      Bone exemplifies the dosimetry problems associated with alpha emitting
isotopes.  The short range of the alpha particle in tissue and the high rate
of deposition of energy make  the distance from source to target cells a very
important consideration.  The situation described for bone also applies to a
greater or lesser extent,  for all  tissues with a non-uniform distribution  of
radioisotope.   This complicates direct application of a risk coefficient
derived from gamma exposure with a  dose calculation using a pharmacokinetic
model.   It also increases  the uncertainty in the risk assessment.

      EPA does not list all beta and gamma emitters in the list of
radionuclides  in drinking  water.   Radioisotopes with very short half-lives,

DRAFT                                V-12

-------
which  are  not  members of decay  chains,  are  not  considered.   They will  not
exist  long enough to be a hazard  in  drinking water.   Those  radionuclides that
the  Agency deems  important are  tabulated  in Table  V-3.
DRAFT                                V-13

-------
                                   Table V-3

                   Concentration of Beta and Gamma Emitters
                  In  Drinking Water to Yield a  Specific Risk
           of Cancer and Death from Cancer  for Lifetime Consumption
            Ch = Concentration in water for 4 mrem/y Committed EDE
            Cm = Concentration in water for mortality risk = IxlO"4
            Ci = Concentration in water for incidence risk = IxlO"4
NUCLIDE
H-3
BE-7
N-13
C-ll
C-14
C-15
0-15
F-18
NA-22
NA-24
SI-31
P-32
P-33
S-35
CL-36
CL-38
K-40
K-42
CA-45
CA-47
SC-46
SC-47
SC-48
V-48
CR-51
MN-52
MN-54
MN-56
FE-55
FE-59
CO-57
CO-58
CO-58M*
CO-60
NI-59
NI-63
NI-65
CU-64
ZN-65
Ch(pCi/L)
6.09E+04
4.35E+04
1.52E+05
9.92E+04
3.20E+03
6.69E+06
4.95E+05
3.95E+04
4.66E+02
3.35E+03
1.02E+04
6.41E+02
1.87E+03
1.29E+04
1.85E+03
2.12E+04
3.02E+02
3.90E+03
1.73E+03
8.46E+02
8.63E+02
2.44E+03
7.66E+02
6.44E+02
3.80E+04
7.33E+02
2.01E+03
5.64E+03
9.25E+03
8.44E+02
4.87E+03
1.59E+03
6.49E+04
2.18E+02
2.70E+04
9.91E+03
8.81E+03
1.19E+04
3.96E+02
Cm(pCi/L)
5.64E+04
1.10E+05
7.69E+04
5.24E+04
3.28E+03
3.12E+06
2.36E+05
2.60E+04
4.39E+02
2.80E+03
1.34E+04
7.33E+02
4.32E+03
1.42E+04
1.73E+03
1.14E+04
2.89E+02
3.23E+03
2.33E+03
1.55E+03
2.09E+03
5.41E+03
1.74E+03
1.54E+03
7.76E+04
1.44E+03
2.67E+03
7.22E+03
1.04E+04
1.12E+03
5.09E+03
1.98E+03
9.96E+04
2.00E+02
3.58E+04
1.39E+04
1.13E+04
1.84E+04
3.73E+02
Ci(pCi/L)
3.55E+04
6.76E+04
5.81E+04
3.94E+04
2.14E+03
2.38E+06
1.80E+05
1.97E+04
2.86E+02
1.87E+03
8.83E+03
5.55E+02
3.46E+03
8.75E+03
1.08E+03
8.56E+03
1.81E+02
2.17E+03
1.96E+03
9.80E+02
1.23E+03
3.02E+03
1.03E+03
9.15E+02 .
4.60E+04
9.08E+02
1.82E+03
4.83E+03
7.05E+03
6.97E+02
3.34E+03
1.25E+03
6.01E+04
1.30E+02
2.22E+04
8.50E+03
7.51E+03
1.14E+04
2.27E+02
DRAFT
V-14

-------
Table V-3 (continued)

NUCLIDE
ZN-69
ZN-69M
GA-67
GA-72
GE-71
AS-73
AS-74
AS-76
AS-77
SE-75
BR-82
RB-82
RB-86
RB-87
RB-88
RB-89
SR-82
SR-85
SR-85M
SR-89
SR-90
SR-91
SR-92
Y-90
Y-91
Y-91M
Y-92
Y-93
ZR-93
ZR-95
ZR-97
NB-93M
NB-94
NB-95
NB-95M
NB-97
NB-97M
MO-99
TC-95
TC-95M
TC-96

Ch(pCi/L)
6.31E+04
4.22E+03
7.02E+03
1.19E+03
4.36E+05
7.85E+03
1.41E+03
1.06E+03
4.33E+03
5.74E+02
3.15E+03
4.36E+05
4.85E+02
5.01E+02
2.91E+04
5.27E+04
2.41E+02
2.83E+03
2.37E+05
5.99E+02
4.20E+01
2.16E+03
3.10E+03
5.10E+02
5.76E+02
1.32E+05
2.87E+03
1.20E+03
5.09E+03
1.46E+03
6.50E+02
1.05E+04
7.07E+02
2.15E+03
2.39E+03
2.35E+04
1.37E+06
1.83E+03
6.97E+04
3.12E+03
2.05E+03

Cm(pCi/L)
4.76E+04
7.53E+03
1.63E+04
2.44E+03
4.35E+05
1.12E+04
2.07E+03
1.83E+03
7.55E+03
4.64E+02
2.76E+03
2.06E+05
4.74E+02
7.66E+02
1.49E+04
2.75E+04
4.11E+02
3.98E+03
2.30E+05
9.99E+02
6.24E+01
3.70E+03
5.67E+03
1.11E+03
1.27E+03
1.23E+05
4.27E+03
2.33E+03
1.47E+04
3.44E+03
1.40E+03
2.33E+04
1.48E+03
5.08E+03
5.27E+03
2.20E+04
1.09E+06
1.66E+03
5.82E+04
2.79E+03
1.87E+03

Ci(pCi/L)
3.48E+04
4.47E+03
9.44E+03
1.46E+03
2.71E+05
6.75E+03
1.26E+03
1.08E+03
4.41E+03
3.06E+02
1.73E+03
1.57E+05
3.29E+02
5.65E+02
1.13E+04
2.07E+04
2.59E+02
2.54E+03
1.62E+05
6.46E+02
5.90E+01
2.27E+03
3.39E+03
6.13E+02
6.98E+02
8.68E+04
2.73E+03
1.36E+03
1.12E+04
1.99E+03
7.98E+02
1.30E+04
9.06E+02
3.02E+03
2.93E+03
1.56E+04
7.87E+05
1.14E+03
3.43E+04
1.09E+03
1.06E+03
        V-15

-------
                            Table V-3  (continued)

NUCLIDE
TC-96M
TC-97
TC-97M
TC-99
TC-99M
RU-97
RU-103
RU-105
RU-106
RH-103M
RH-105
RH-105M
RH-106
PD-100
PD-101
PD-103
PD-107
PD-109
AG-105
AG-108
AG-108M
AG-109M
AG-110
AG-110M
AG-111
CD-109
CD-115
CD-115M
IN-113M
IN-114
IN-114M
IN-115
IN-115M
SN-113
SN-121
SN-121M
SN-125
SN-126
SB-122

Ch(pCi/L)
1.76E+05
3.25E+04
4.45E+03
3.79E+03
8.96E+04
7.96E+03
1.81E+03
4.99E+03
2.03E+02
4.71E+05
3.72E+03
5.51E+06
1.24E+06
1.30E+03
1.34E+04
6.94E+03
3.66E+04
2.12E+03
2.70E+03
6.26E+05
7.23E+02
1.67E+07
1.84E+06
5.12E+02
1.08E+03
2.27E+02
9.58E+02
3.39E+02
5.24E+04
9.76E+05
3.23E+02
3.51E+01
1.64E+04
1.74E+03
6.06E+03
2.26E+03
4.46E+02
2.93E+02
8.10E+02

Cm(pCi/L)
1.46E+05
2.29E+04
3.13E+03
2.61E+03
8.22E+04
1.91E+04
3.78E+03
8.36E+03
3.55E+02
3.87E+05
7.94E+03
4.34E+06
5.78E+05
3.36E+03
2.71E+04
1.60E+04
7.83E+04
4.28E+03
3.69E+03
2.98E+05
7.27E+02
7.77E+06
8.52E+05
5.46E+02
2.03E+03
2.39E+02
2.00E+03
4.66E+02
5.71E+04
4.57E+05
5.48E+02
6.21E+01
2.63E+04
3.89E+03
1.28E+04
5.48E+03
9.78E-t-02
5.89E+02
1.71E+03

Ci(pCi/L)
8.47E+04
1.28E+04
1.70E+03
1.44E+03
3.83E+04
1.14E+04
2.18E+03
5.20E+03
2.04E+02
2.81E+05
4.47E+03
3.10E+06
4.42E+05
1.97E+03
1.66E+04
8.78E+03
4.32E+04
2.45E+03
2.64E+03
2.28E+05
5.51E+02
5.94E+06
6.51E+05
4.08E+02
1.21E+03
1.25E+02
1.10E+03
2.46E+02
3.96E+04
3.50E+05
3.34E+02
4.81E+01
1.66E+04
2.25E+03
7.18E+03
3.56E+03
5.43E+02
3.48E+02
9.68E+02
DRAFT
V-16

-------
                             Table  V-3  (continued)

NUCLIDE
SB-124
SB-125
SB-126
SB-126M
SB-127
SB-129
TE-125M
TE-127
TE-127M
TE-129
TE-129M
TE-131
TE-131M
TE-132
1-122
1-123
1-125
1-126
1-129
1-130
1-131
1-132
1-133
1-134
1-135
CS-131
CS-134
CS-134M
CS-135
CS-136
CS-137
CS-138
BA-131
BA-133
BA-133M
BA-137M
BA-139
BA-140
LA-140
CE-141
CE-143
CE-144

Ch(pCi/L)
5.63E+02
1.94E+03
5.44E+02
5.85E+04
8.18E+02
3.09E+03
1.49E+03
7.92E+03
6.63E+02
2.72E+04
5.24E+02
2.68E+04
9.71E+02
5.80E+02
2.11E+05
1.07E+04
1.51E+02
8.10E+01
2.10E+01
1.19E+03
1.08E+02
8.19E+03
5.49E+02
2.14E+04
2.34E+03
2.28E+04
8.13E+01
1.01E+05
7.94E+02
5.18E+02
1.19E+02
2.56E+04
2.95E+03
1.52E+03
2.62E+03
2.15E+06
1.38E+04
5.82E+02
6.52E+02
1.89E+03
1.21E+03
2.61E+02

Cm(pCi/L)
1.14E+03
3.86E+03
1.17E+03
3.58E+04
1.75E+03
5.32E+03
3.14E+03
1.44E+04
1.13E+03
2.39E+04
9.55E+02
2.37E+04
1.91E+03
1.25E+03
1.02E+05
1.59E+04
7.27E+02
3.87E+02
1.03E+02
1.76E+03
5.16E+02
7.98E+03
8.72E+02
1.43E+04
3.30E+03
2.15E+04
7.64E+01
6.79E+04
7.82E+02
4.76E+02
1.14E+02
1.39E+04
6.87E+03
2.47E+03
5.59E+03
1.08E+06
1.33E+04
1.29E+03
1.44E+03
4.22E+03
2.62E+03
5.68E+02

Ci(pCi/L)
6.77E+02
2.33E+03
6.98E+02
2.67E+04
9.97E+02
3.28E+03
2.27E+03
8.52E+03
8.72E+02
1.72E+04
6.14E+02
6.81E+03
5.13E+02
6.60E+02
7.75E+04
1.90E+03
7.46E+01
4.02E+01
1.04E+01
2.13E+02
5.37E+01
1.86E+03
9.36E+01
6.78E+03
4.57E+02
1.37E+04
4.66E+01
4.77E+04
4.90E+02
2.88E+02
7.01E+01
1.04E+04
4.11E+03
1.64E+03
3.15E+03
8.14E+05
9.37E+03
7.30E+02
8.32E+02
2.34E+03
1.47E+03
3.15E+02
DRAFT
V-17

-------
                             Table  V-3  (continued)

NUCLIDE
PR-142
PR-143
PR-144
PR-144M
ND-147
ND-149
PM-147
PM-148
PM-148M
PM-149
SM-151
SM-153
EU-152
EU-154
EU-155
EU-156
GD-153
GD-159
TB-158
TB-160
DY-165
DY-166
HO-166
ER-169
ER-171
TM-170
TM-171
YB-169
YB-175
LU-177
HF-181
TA-182
W-181
W-185
W-187
RE-183
RE-186
RE-187
RE-188
OS-185
OS-191
OS-191M

Ch(pCi/L)
1.04E+03
1.17E+03
4.70E+04
1.12E+05
1.25E+03
1.17E+04
5.24E+03
5.05E+02
5.75E+02
1.38E+03
1.41E+04
1.83E+03
8.41E+02
5.73E+02
3.59E+03
6.00E+02
4.68E+03
2.76E+03
1.25E+03
8.15E+02
1.51E+04
8.30E+02
9.81E+02
3.64E+03
3.80E+03
1.03E+03
1.27E+04
1.83E+03
3.11E+03
2.55E+03
1.17E+03
8.42E+02
1.90E+04
3.44E+03
2.66E+03
5.04E+03
1.88E+03
5.82E+05
1.79E+03
2.46E+03
2.38E+03
1.43E+04

Cm(pCi/L)
2.17E+03
2.58E+03
2.69E+04
7.02E+04
2.80E+03
1.51E+04
1.10E+04
1.12E+03
1.37E+03
2.98E+03
2.82E+04
3.99E+03
1.33E+03
9.57E+02
6.60E+03
1.37E+03
1.09E+04
5.75E+03
2.58E+03
1.89E+03
1.89E+04
1.89E+03
2.08E+03
8.01E+03
7.05E+03
2.27E+03
2.81E+04
4.28E+03
6.86E+03
5.65E+03
2.71E+03
1.96E+03
3.57E+04
6.85E+03
5.31E+03
6.55E+03
1.50E+03
4.00E+05
1.58E+03
4.96E+03
5.15E+03
2.91E+04

Ci(pCi/L)
1.23E+03
1.41E+03
2.03E+04
5.26E+04
1.55E+03
l.OOE+04
6.32E+03
6.23E+02
7.92E+02
1.65E+03
1.75E+04
2.22E+03
9.23E+02
6.46E+02
4.31E+03
7.73E+02
6.30E+03
3.26E+03
1.62E+03
1.08E+03
1.27E+04
1.03E+03
1.16E+03
4.40E+03
4.24E+03
1.25E+03
1.57E+04
2.45E+03
3.80E+03
3.12E+03 .
1.54E+03
1.13E+03
2.18E+04
3.80E+03
3.09E+03
2.42E+03
7.01E+02
2.21E+05
6.32E+02
3.08E+03
2.89E+03
1.66E+04
DRAFT
V-18

-------
                             Table V-3 (continued)

NUCLIDE
OS-193
IR-190
IR-192
IR-194
PT-191
PT-193
PT-193M
PT-197
PT-197M
AU-196
AU-198
HG-197
HG-203
TL-202
TL-204
TL-207
TL-208
TL-209
PB-203
PB-209
PB-210
PB-211
PB-212
PB-214
BI-206
BI-207
BI-210
BI-214
FR-223
AC-228
TH-231
TH-234
PA-233
PA-234
PA-234M
NP-236
NP-238
NP-239
NP-240
NP-240M
PU-243
AM-242

Ch(pCi/L)
1.69E+03
1.01E+03
9.57E+02
1.04E+03
3.81E+03
4.61E+04
3.02E+03
3.40E+03
1.75E+04
3.66E+03
1.31E+03
5.76E+03
2.39E+03
3.84E+03
1.68E+03
4.00E+05
2.83E+05
3.58E+05
5.06E+03
2.53E+04
1.01E+00
1.28E+04
1.23E+02
1.18E+04
6.56E+02
1.01E+03
8.53E+02
1.89E+04
3.41E+03
3.27E+03
4.07E+03
4.01E+02
1.51E+03
2.56E+03
9.30E+05
5.96E+03
1.39E+03
1.68E+03
2.31E+04
1.74E+05
1.64E+04
3.83E+03

Cm(pCi/L)
3.59E+03
2.37E+03
1.97E+03
2.15E+03
8.74E+03
9.94E+04
6.59E+03
7.03E+03
2.38E+04
8.38E+03
2.82E+03
1.26E+04
5.07E+03
3.53E+03
1.65E+03
1.93E+05
1.40E+05
1.89E+05
9.64E+03
3.47E+04
3.55E+00
1.44E+04
3.83E+02
1.52E+04
1.50E+03
2.27E+03
1.94E+03
1.92E+04
1.20E+04
6.10E+03
8.67E+03
8.87E+02
3.42E+03
4.61E+03
4.36E+05
1.36E+04
3.18E+03
3.71E+03
2.11E+04
8.93E+04
2.73E+04
8.66E+03

Ci(pCi/L)
2.01E+03
1.41E+03
1.15E+03
1.22E+03
5.11E+03
5.44E+04
3.64E+03
3.98E+03
1.55E+04
5.05E+03
1.59E+03
7.15E+03
2.85E+03
2.15E+03
9.39E+02
1.47E+05
1.06E+05
1.42E+05
6.06E+03
2.27E+04
2.99E+00
1.06E+04
2.70E+02
1.09E+04
8.89E+02
1.31E+03
1.01E+03
1.42E+04
9.11E+03
3.81E+03
4.87E+03
4.87E+02
1.91E+03
2.84E+03
3.33E+05
8.32E+03
1.82E+03
2.07E+03
1.51E+04
6.78E+04
1.69E+04
5.34E+03
* M = metastable.
DRAFT
V-19

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                           VI.  UNCERTAINTY ANALYSIS

      The types  of  health  effects  expected  following exposure to radiation in
general have  been established based on human data following high level
exposure and  supporting  animal  studies.  Much of the uncertainty in estimating
risk from exposure  to  radiation arises in evaluation of the relatively small
doses to target  organs that  result from environmental exposures.  The
remainder of  this section  briefly describes the assumptions and parameters
contributing  uncertainty to  the quantification of the toxicological effects of
beta and gamma emitting  radionucl ides found in drinking water.

A.    UNCERTAINTY IN ASSESSMENT OF NONCARCINOGENIC EFFECTS OF BETA AND GAMMA
      EMITTING RADIONUCLIDES
      It is assumed that noncancer health effects would not be of concern at
levels of exposure  from  beta  and gamma emitting radionuclides in drinking
water.  Noncancer health effects observed in animals and humans occur at high
levels of exposure  and do  not  appear to be more sensitive indicators of
adverse health effects than  cancer.  Therefore, consideration of
carcinogenicity  should be  sufficiently protective against other health
effects.

B.    UNCERTAINTY IN ASSESSMENT OF CARCINOGENIC EFFECTS OF BETA AND GAMMA
      EMITTING RADIONUCLIDES
      Assessment of the  carcinogenicity of beta and gamma emitting
radionuclides is uncertain in  several  areas.  These areas of uncertainty
include:  parameters used  in  the metabolic model,  including absorption,
distribution  and dosimetry;  the risk coefficients  used for calculating
lifetime risk; and  factors influencing both.

Uncertainty in Parameters Used in the Metabolic Model

      One issue  is the proper choice of the gastrointestinal  absorption factor
(f,)  for these radionuclides.  Because  the  number  of radionuclides  considered
in this analysis is large, and the data used to derive f1  factors  are  highly
variable, the degree of  confidence for the f,  factors chosen  also  varies.  In
assessing the uncertainty relating to f,,  one  should keep  in  mind  that  it  is
the dose to target organs  (or cells)  that is of interest and  not the f1  per

DRAFT                                VI-1

-------
se.  The organ doses depend also on rates of radioisotope  uptake  from  blood
(f'2) and of loss from the organ.  In principle, one can partly bypass  the
problem of determining these metabolic parameters and  assess  the  dose  to  an
organ or tissue for a given intake by simply measuring the organ  or  tissue
burden under  steady state conditions.  However, an important  limitation to
this approach is the difficulty in estimating  past intake.

      Estimates of body burden and the distribution of beta emitters among
organs vary widely (Dunning et al. 1984, Sullivan et al. 1981).   Uncertainty
in  organ burden influences estimates of total  body burden  and selection of
metabolic model parameters.  For a specific radionuclide,  the calculated  body
burden varies with the fraction absorbed, the  respective fraction  transferred
to  organs, and the retention of the radioisotope in these  organs.  If  intake
and body burden are specified, then varying any metabolic  parameter  requires
that some other parameter(s) change in compensation to maintain the  constant
body burden.  Because of their relatively short range, the dosimetry for  beta
particles depends on the precise localization  of the radionuclide  within  the
body; in contrast, the dose from gamma rays is less sensitive to  the detailed
distribution.  Consequently, dosimetry for the latter is generally more
certain than for the former.

Uncertainty in Distribution of Isotope

      Few of the beta emitting radionuclides have been well characterized with
respect to distribution in the human body.   Distribution within the  skeleton
has been reported in some studies (Stara et al. 1971, Pool  et al.  1973).
Distribution between and within soft tissues has also been reported  (Schober
and Hunt 1976, Moskalev 1968).  Uncertainty concerning the distribution within
organs will  influence dose and risk calculations.

      Estimating the degree of uncertainty for modeled dose estimates  for each
of the radionuclides is not only difficult,  but is also somewhat arbitrary.
No model  has been verified in  man for any long-term exposure scenario,  and the
data selected to establish the parameters used in  the model may not be
representative of the population being evaluated (EPA 1989).   Nevertheless,
EPA has characterized the potential  magnitude of dosimetric.uncertainties for

DRAFT                                VI-2

-------
the four groups  of  radionuclides:   1)  essential elements and their analogs,
2)  inert gases,  3)  well-studied  toxic metals, and 4) other elements.  The
section on Bioaccumulation  and  Retention  (Section  III.E) present models of
radionuclides  for all  four  of these groups.  EPA (1989)  states that for the
essential elements,  uncertainty  in dose is a factor of two or less in major
critical organs,  while  the  uncertainty for analogs is perhaps three or less in
the critical organs.   Because the  available information  on kinetics of the
well-studied toxic  metals varies widely among these compounds, the uncertainty
in dose for this  class  ranges from about  2 to 5, depending on the specific
radionuclide.  The  Group 4  radionuclides  include those for which kinetics
information is limited  and, therefore, EPA states that dose estimates may be
in error by at least an order of magnitude.  EPA considers these estimates to
represent the Agency's  best judgment but  also states that this quantification
should be considered rough  estimates.

Uncertainty in Dosimetric Calculations

      While calculations of average dose  deposited in a  tissue can be made,
these may not accurately reflect the dose to target cells.  This is
particularly true for some beta emitting  nuclides due to the short range of
beta particles in tissue.  For example, it is well  known that radioactive
iodine distributes primarily to the thyroid.  However, the degree to which
specific tissues  of the thyroid are irradiated is not well known.

      The pharmacokinetic models used assume uniform distribution of
radionuclides in  organs or tissues.  While many studies would indicate that
distribution is often non-uniform,  there  are not sufficient data on any
radionuclide to establish a detailed pharmacokinetic model using a non-uniform
distribution.   This limitation of the models results in some degree of
uncertainty.

Uncertainty in Risk Coefficients

      EPA (1989)   has derived risk coefficients for low-LET radiation  based on
data derived from atomic bomb survivors (NAS 1980).  New data and analyses on
irradiated  populations have recently become available (UNSCEAR 1988,  NAS

DRAFT                                VI-3

-------
 1990);  however, the resulting central estimates of risk from uniform, whole
 body  irradiation are in reasonable agreement with that based on EPA's current
 model  (to within a factor of 2).  For whole body irradiation, the uncertainty
 in the risk estimate is thought to be about a factor of 3 or less, but larger
 errors in the quantification of risk at very low doses and dose rates cannot
 be excluded.  In addition, the estimate of risk to specific irradiated target
 tissues is often more uncertain than the estimate for whole body irradiation.
 Hence, in cases where the radiation is concentrated in specific organs, the
 uncertainty in risk may be larger.

 Uncertainty in Other Factors Influencing Risk

      When considering a specific individual rather than population (average)
 risks, variability in physiological  parameters must be considered.  These will
 include such factors as age, genetic makeup, gender, and diet.  For example,
 uptake of radioactive iodine into the thyroid is dependent on the amount of
 stable iodine in an individual's diet (Pittman et al.  1970).

 Conclusion

      There are many uncertainties inherent is estimating the risk from
 ingestion of beta and gamma emitting radionuclides in drinking water.   These
 include uncertainties in internal  dosimetry and in the appropriate risk
 factors for specific tissues.   Overall,  EPA regards its risk estimate as a
 reasonable central  estimate but emphasizes that the actual  risk could be at
 least a factor of 3 higher or lower.
DRAFT                                VI-4

-------
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