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ICRP ref: 4889-2039-6370

Annals of the ICRPICRP PUBLICATION 1XX

Dose coefficients for intakes of radionuclides
by members of the public: Part 1
Editor-in-Chief
C.H. CLEMENT
Associate Editor
H. YU

Authors on behalf of ICRPF. Paquet, M.R. Bailey, R.W. Leggett, T. Smith, E. Blanchardon, A. Giussani,
J.W. Marsh, G. Ratia, C. Samuels, D. Gregoratto, V. Berkovski, D. Jokisch

PUBLISHED FOR
The International Commission on Radiological Protection
byPlease cite this issue as ‘ICRP, 202X. Dose coefficients for intakes of radionuclides bymembers of the public: Part 1. ICRP Publication 1XX, Ann. ICRP XX(X)’DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

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CONTENTS

38

ABSTRACT...................................................................................................................................... 739

MAIN POINTS ................................................................................................................................. 8

40

1.

INTRODUCTION .................................................................................................................... 941

1.1. Scope of this series of reports ................................................................................................. 942

1.2. Changes in Publication 103 that affect the calculation of equivalent and effective dose ......... 15

43

1.3. Biokinetic models implemented in this series of reports ........................................................ 1744

1.4. Dosimetry implemented in this series of reports .................................................................... 1745

1.5. Pregnancy and breast-feeding ............................................................................................... 1946

1.6. Structure of the report ........................................................................................................... 20

47

2.

BIOKINETIC AND DOSIMETRIC MODELS ....................................................................... 23

48

2.1. Introduction .......................................................................................................................... 2349

2.2. Human Respiratory Tract Model (HRTM) ............................................................................ 25

50

2.3. Human Alimentary Tract Model (HATM) ............................................................................ 43

51

2.4. Biokinetic models for systemic radionuclides........................................................................ 50

52

2.5. Summary of rules for treatment of radioactive progeny ......................................................... 52

53

2.6. Medical intervention ............................................................................................................. 53

54

2.7. Methodology for dose calculations – The ICRP dosimetry system......................................... 53

55

3.

GENERAL ASPECTS OF INTERNAL DOSE ASSESSMENT .............................................. 60

56

3.1. Introduction .......................................................................................................................... 60

57

3.2. Uncertainties in internal dose assessment .............................................................................. 60

58

3.3. Uncertainties in biokinetic models ........................................................................................ 61

59

3.4. Uncertainties in dosimetric models ....................................................................................... 65

60

4.

DATA PROVIDED FOR ELEMENTS AND RADIOISOTOPES ........................................... 67

61

4.1. Data provided in the printed reports and electronic annexes .................................................. 67

62

4.2. Quality assurance of data presented ...................................................................................... 67

63

5.

HYDROGEN (Z = 1) .............................................................................................................. 68

64

5.1. Routes of Intake ................................................................................................................... 68

65

5.2. Dosimetric data for tritium.................................................................................................... 74

66

6.

CARBON (Z = 6) ................................................................................................................... 75

67

6.1. Routes of Intake ................................................................................................................... 75

68

6.2. Dosimetric data for carbon .................................................................................................... 82

69

7.

PHOSPHORUS (Z = 15)......................................................................................................... 832

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7.1. Routes of Intake ................................................................................................................... 83

71

7.2. Dosimetric data for phosphorus ............................................................................................ 87

72

8.

SULPHUR (Z = 16) ................................................................................................................ 88

73

8.1. Routes of Intake ................................................................................................................... 88

74

8.2. Dosimetric data for sulphur................................................................................................... 93

75

9.

CALCIUM (Z = 20) ................................................................................................................ 94

76

9.1. Routes of Intake ................................................................................................................... 94

77

9.2. Dosimetric data for calcium .................................................................................................. 99

78

10. IRON (Z = 26) ...................................................................................................................... 100

79

10.1. Routes of Intake ............................................................................................................... 100

80

10.2. Dosimetric data for iron .................................................................................................... 106

81

11. COBALT (Z = 27) ................................................................................................................ 107

82

11.1. Routes of Intake................................................................................................................ 107

83

11.2. Dosimetric data for cobalt ................................................................................................. 111

84

12. NICKEL (Z = 28) ................................................................................................................. 113

85

12.1. Routes of Intake................................................................................................................ 113

86

12.2. Dosimetric data for nickel ................................................................................................. 117

87

13. ZINC (Z = 30)....................................................................................................................... 119

88

13.1. Routes of Intake................................................................................................................ 119

89

13.2. Dosimetric data for zinc .................................................................................................... 124

90

14. SELENIUM (Z = 34) ............................................................................................................ 125

91

14.1. Routes of Intake................................................................................................................ 125

92

14.2. Dosimetric data for selenium ............................................................................................ 128

93

15. STRONTIUM (Z = 38) ......................................................................................................... 129

94

15.1. Routes of Intake................................................................................................................ 129

95

15.2. Dosimetric data for strontium ........................................................................................... 135

96

16. YTTRIUM (Z = 39) .............................................................................................................. 137

97

16.1. Routes of Intake................................................................................................................ 137

98

16.2. Dosimetric data for yttrium ............................................................................................... 141

99

17. ZIRCONIUM (Z = 40) .......................................................................................................... 142

100

17.1. Routes of Intake................................................................................................................ 142

101

17.2. Dosimetric data for zirconium ........................................................................................... 146

102

18. NIOBIUM (Z = 41) ............................................................................................................... 147

103

18.1. Routes of Intake................................................................................................................ 147

104

18.2. Dosimetric data for niobuim ............................................................................................. 151

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19. MOLYBDENUM (Z = 42).................................................................................................... 152

106

19.1. Routes of Intake................................................................................................................ 152

107

19.2. Dosimetric data for molybdenum ...................................................................................... 156

108

20. TECHNETIUM (Z = 43)....................................................................................................... 157

109

20.1. Routes of Intake................................................................................................................ 157

110

20.2. Dosimetric data for technetium ......................................................................................... 161

111

21. RUTHENIUM (Z = 44)......................................................................................................... 163

112

21.1. Routes of Intake................................................................................................................ 163

113

21.2. Dosimetric data for ruthenium .......................................................................................... 167

114

22. SILVER (Z = 47) .................................................................................................................. 168

115

22.1. Routes of Intake................................................................................................................ 168

116

22.2. Dosimetric data for silver .................................................................................................. 171

117

23. ANTIMONY (Z = 51) ........................................................................................................... 172

118

23.1. Routes of Intake................................................................................................................ 172

119

23.2. Dosimetric data for antimony ............................................................................................ 176

120

24. TELLURIUM (Z = 52) ......................................................................................................... 177

121

24.1. Routes of Intake................................................................................................................ 177

122

24.2. Dosimetric data for tellurium ............................................................................................ 182

123

25. IODINE (Z = 53) .................................................................................................................. 184

124

25.1. Routes of Intake................................................................................................................ 184

125

25.2. Dosimetric data for iodine................................................................................................. 192

126

26. CAESIUM (Z = 55) .............................................................................................................. 194

127

26.1. Routes of Intake................................................................................................................ 194

128

26.2. Dosimetric data for caesium.............................................................................................. 200

129

27. BARIUM (Z = 56) ................................................................................................................ 202

13027.1. Routes of Intake................................................................................................................ 202

131

27.2. Dosimetric data for barium ............................................................................................... 206

132

28. IRIDIUM (Z = 77) ................................................................................................................ 207

133

28.1. Routes of Intake................................................................................................................ 207

134

28.2. Dosimetric data for iridium ............................................................................................... 210

135

29. LEAD (Z = 82) ..................................................................................................................... 211

136

29.1. Routes of Intake................................................................................................................ 211

137

29.2. Dosimetric data for lead .................................................................................................... 217

138

30. BISMUTH (Z = 83) .............................................................................................................. 219

139

30.1. Routes of Intake................................................................................................................ 219

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30.2. Dosimetric data for bismuth .............................................................................................. 223

141

31. POLONIUM (Z = 84) ........................................................................................................... 224

142

31.1. Routes of Intake................................................................................................................ 224

143

31.2. Dosimetric data for polonium ........................................................................................... 228

144

32. RADON (Z = 86) .................................................................................................................. 229

145

32.1. Routes of Intake................................................................................................................ 229

146

32.2. Dosimetric data for radon ................................................................................................. 235

147

32.3. Use of dosimetric data for radon ....................................................................................... 237

148

33. RADIUM (Z = 88) ................................................................................................................ 239

149

33.1. Routes of Intake................................................................................................................ 239

150

33.2. Dosimetric data for radium ............................................................................................... 244

151

REFERENCES.............................................................................................................................. 245

152

ANNEX A. SUPPLEMENTARY INFORMATION RELATING TO APPLICATION OF THE

153

HRTM TO ENVIRONMENTAL EXPOSURE .............................................................................. 264

154

A.1. Deposition in respiratory tract regions for Reference Individuals as a function of aerosol size

155

264

156

A.2. Reference values for regional deposition ............................................................................ 266

157

A.3. Progeny radionuclides formed in the respiratory tract ......................................................... 273

158

A.4. References ......................................................................................................................... 276

159

ANNEX B. EVOLUTION OF ICRP’S SYSTEMIC BIOKINETIC MODELS ............................... 277

160

B.1. Formulation of systemic models in modern ICRP reports ................................................... 277

161

B.2. Systemic model structures used in this report series ............................................................ 280

162

B.3. References ......................................................................................................................... 282

163

ANNEX C. SUPPLEMENTARY INFORMATION RELATING TO RADON .............................. 284

164

C.1. Fractional deposition of radon and thoron progeny in the respiratory tract .......................... 284

165

C.2. Biokinetic model for radon gas........................................................................................... 285

166

C.3. Dosimetric data for radon and thoron ................................................................................. 291

167

C.4. References ......................................................................................................................... 293

168

GLOSSARY ................................................................................................................................. 294

169

ACKNOWLEDGEMENTS ........................................................................................................... 297

170

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ICRP Publication 1XX

173

DOSE COEFFICIENTS FOR INTAKES OF RADIONUCLIDESBY MEMBERS OF THE PUBLIC: PART 1

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ICRP Publication XXX

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Approved by the Commission in 20YY

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Abstract– This report is the first in a series of documents giving age-dependent dosecoefficients for members of the public for environmental intakes of radionuclides by inhalationand ingestion. This series replaces the Publication 56 series of documents, update some datafrom Publication 119, and comes in addition to the series on occupational intakes ofradionuclides by workers (OIR series). The revised dose coefficients have been calculatedusing the Publication 100 Human Alimentary Tract Model (HATM) and the Publication 130
revision of the Human Respiratory Tract Model (HRTM). Revisions have also been made to
many of the models that describe the systemic biokinetics of radionuclides absorbed to blood,
making them more physiologically realistic representations of uptake and retention in organs
and tissues and of excretion. Changes have been implemented that were introduced in
Publication 103 to: the radiation weighting factors used in the calculation of equivalent doses
to tissues; the tissue weighting factors used in the calculation of effective dose; and the separate
calculation of equivalent doses to males and females with sex-averaging in the calculation ofeffective dose. Reference anatomical computational phantoms such as those in Publication 110
and Publication 143 (i.e. models of the human body based on medical imaging data), have
replaced many of the composite mathematical models used for previous calculations of organ
doses. Dose calculations were also improved by using updated radionuclide data in Publication
107 and specific absorbed fraction data in Publication 133 and Publication 1XX.

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© 20YY ICRP. Published by SAGE.

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Keywords: Environmental exposure; Internal dose assessment; Biokinetic and dosimetricmodels

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MAIN POINTS

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• This report is the first in a series of documents giving age-dependent dosecoefficients for members of the public for environmental intakes of radionuclides
by inhalation and ingestion. This series replaces the Publication 56 series of
documents and update some data from Publication 119.

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• The data provided are age-dependent dose coefficients for members of the public
for environmental intakes of radionuclides by inhalation and ingestion. As in the
Publication 56 series, dose coefficients are presented in this series of reports forintakes by 3-mo-old infants, 1-, 5-, 10-, and 15-y-old children, and adults.

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• The data provided in the printed reports are restricted to tables of committed
effective dose per intake (Sv Bq–1) for inhalation and ingestion. Data are provided
for all absorption types and for the most common isotope(s) of each element. The
electronic data that accompanies this series of reports contains a comprehensive setof committed effective and equivalent dose coefficients.

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• This first report provides the data above for some of the elements already describedin OIR Parts 2–3 (ICRP Publications 134, 137) i.e.: Hydrogen (H), Carbon (C),
Phosphorus (P), Sulphur (S), Calcium (Ca), Iron (Fe), Cobalt (Co), Nickel (Ni),Zinc (Zn), Selenium (Se), Strontium (Sr), Yttrium (Y), Zirconium (Zr), Niobium(Nb), Molybdenum (Mo), Technetium (Tc), Ruthenium (Ru), Silver (Ag),Antimony (Sb), Tellurium (Te), Iodine (I), Caesium (Cs), Barium (Ba), Iridium (Ir),
Lead (Pb), Bismuth (Bi), Polonium (Po), Radon (Rn), and Radium (Ra).

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1. INTRODUCTION

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1.1. Scope of this series of reports

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Environmental intakes of radionuclides by members of the public may occur as the resultof planned or accidental discharge from a range of industrial, medical, educational and researchfacilities. Dose coefficients have been calculated for radioisotopes of the elements which are
expected to be released into the environment as a result of human activities such as uranium
mining and milling, conversion, enrichment and fabrication, power station operations, fuelreprocessing, waste storage and disposal, and considered to be of significance forenvironmental radiation protection purposes. In addition, naturally occurring radionuclides arepresent in the environment and their concentrations may be modified by human activities.
Consequently, the range of radionuclides to be addressed includes those of natural origin,fission products, actinides, and activation products.
The chemical forms considered in this report series are those found in workplaces andalready described in the Occupational Intakes of Radionuclides (OIR) series (ICRP, 2015,2016a, 2017, 2019, 2022). Since most of the radionuclides released in the environment may be
gradually internalised in the food chain, an additional organic chemical form is taken into
consideration for ingestion by humans.
To provide dose coefficients for members of the public, it is necessary to take into
account the effect of age on the biokinetics of radionuclides and on anatomical andphysiological data. The biokinetic data used for the adults in this series of reports are takenfrom the OIR series (ICRP, 2015, 2016a, 2017, 2019, 2022). Additional data for infants andchildren are presented in this series for the calculation of a comprehensive set of dosecoefficients.
An adequate assessment of environmental internal exposure resulting from intakes ofradionuclides is essential for the design, planning and authorisation of a facility or activity, andfor the retrospective demonstration of compliance with regulatory requirements.
The protection quantities defined by ICRP, equivalent dose and effective dose, arefundamental to the application of ICRP recommendations. The concept of effective dose
provides a single quantity that may be used to characterise both internal and external individual
exposures in a manner that is independent of the individual’s body-related parameters, such assex, age (for adults), anatomy, physiology and race. In order to achieve wide applicability, theprotection quantities effective dose and equivalent dose are defined using computationalmodels with broad averaging of physiological parameter values. Specifically, Publication 89(ICRP, 2002a) defines the key parameters of the Reference Individuals (the mass, geometry
and composition of human organs and tissues), while this series of reports provides relevant
parameters for the Reference Members of the Public of each reference age, including an
associated set of ICRP reference biokinetic models.
Effective dose is not an individual-specific dose quantity, but rather the dose to a
Reference Person under specified exposure conditions. In the general case, the Reference
Person can be either a Reference Worker or a Reference Individual of a specified age.
After intake of radionuclides, doses received by organs and tissues are protracted overtime and so equivalent and effective doses are accumulated over time. The resulting quantities
are referred to as committed doses. Internal exposure of members of the public should beassessed in terms of the protection quantity committed effective dose.
This series of reports provides a comprehensive set of dose coefficients (i.e. committed
effective dose and committed equivalent doses to organs or tissues per intake). These data may

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be used for both prospective assessments and retrospective assessments. Prospective
assessments provide estimates of intakes and resulting doses using information on projected
exposures to radionuclides obtained at the design and planning stage of a facility or practice.
These assessments generally make use of default assumptions about exposure conditions anddefault values for parameters describing material-specific properties, such as the particle size
distribution of an inhaled aerosol or the absorption characteristics of a material after inhalation
or ingestion. Retrospective assessments use the results of individual monitoring andenvironmental monitoring to assess doses in order to demonstrate compliance with regulatory
requirements. These assessments may, in some circumstances, make use of specificinformation relating to the exposure, as discussed in Section 6 of Publication 130 (ICRP, 2015).
This series of reports contains detailed information on the ICRP reference models used
for the derivation of dose coefficients. The information provided in this first report of the series
includes overviews of the ICRP reference Human Respiratory Tract Model (HRTM) as revisedin Publication 130 (ICRP, 2015), and an overview of the ICRP reference Human Alimentary
Tract Model (HATM) (ICRP, 2006). Descriptions of the structures and parameter values of thereference systemic biokinetic models are also presented in this series of reports.
The material presented in this series of reports is not intended for applications beyond
the scope of environmental radiation protection. An example of such an application is theassessment of a case of substantial radionuclide intake, where organ doses can approach orexceed the thresholds for tissue reactions, and where medical treatment may require an
individual-specific reconstruction of the magnitude of absorbed doses and associatedparameters characterising the exposure. In such a case, the individual-related estimates ofabsorbed doses in organs or tissues should be made. Such individual-related assessments arebeyond the scope of this series of reports.
In some exceptional circumstances, when public exposure has occurred and absorbed
doses in organs or tissues are below the thresholds for tissue reactions, the data presented in
the OIR series of reports (ICRP, 2015, 2016a, 2017, 2019, 2022) could be used for planning of
bioassay monitoring programmes (usually based on the use of whole body and/or thyroid
monitors) and interpretation of bioassay monitoring data obtained for adult members of the
public.
The Publication 56 series: Publications 56, 67, 69, 71, 72, 88 and 95 (ICRP, 1990,
1993, 1995a, 1995b, 1995c, 2001, 2004) (Table 1.1) gave dose coefficients for members of the
public, for intakes of radionuclides by inhalation and ingestion, referencing the
Recommendations issued in Publication 60 (ICRP, 1991) and the anatomical and physiological
data in Publication 23 (ICRP, 1975). It applied the Publication 66 HRTM (ICRP, 1994b) for
inhaled radionuclides, the basic anatomical and physiological data for the skeleton in
Publication 70 (ICRP, 1995d) and systemic biokinetic models for selected isotopes of 31
elements given in Publications 56, 67, 69 and 71 (ICRP, 1990, 1993, 1995a, 1995b). The
biokinetic models for the gastrointestinal tract and systemic biokinetic models for otherelements were taken from Publication 30 and modified by addition of explicit excretion
pathways to improve dose estimates for the urinary bladder and colon walls. A compilation ofdose coefficients for intakes of radionuclides by workers and members of the public was thenproduced in Publication 119 (ICRP 2012).

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Table 1.1. Summary of previous reports on dose coefficients for members of the public from intakes of radionuclides .

ICRP
Publication
No. (year)

Application

Contents

56 (1989)

Inhalation*andingestion

Age-dependent biokinetic models with effective dose coefficients and tissue equivalent dose coefficients forselected radioisotopes of H, C, Sr, Zr, Nb, Ru, I, Cs, Ce, Pu, Am, and Np. Predates Publication 60 (ICRP, 1991)
hence used tissue weighting factors from Publication 26 (ICRP, 1977). Predates Publication 66 (ICRP, 1994b),
hence used lung model from Publication 30 (ICRP, 1979). The dose coefficients given in Publication 56 weresuperseded by those in Publications 67 and 71.

67 (1993)

Ingestion*

Age-dependent biokinetic models with effective dose coefficients and tissue equivalent dose coefficients foringestion of selected radioisotopes of S, Co, Ni, Zn, Mo, Tc, Ag, Te, Ba, Pb, Po, and Ra. Updated biokinetic models
are given for Sr, Pu, Am, and Np. Updated dose coefficients are given for H, C, Sr, Zr, Nb, Ru, I, Cs, Ce, Pu, Am,
and Np using tissue weighting factors from Publication 60 (ICRP, 1991).

69 (1995)

Ingestion*

Age-dependent biokinetic models with effective dose coefficients and tissue equivalent dose coefficients foringestion of selected radioisotopes for Fe, Sb, Se, Th, and U.

71 (1995)

Inhalation*

Effective dose coefficients and tissue equivalent dose coefficients for inhalation of the radioisotopes of elements
covered in Publications 56, 67, and 69, plus isotopes of Ca and Cm for which age-dependent biokinetic models arealso given. HRTM applied.

72 (1996)

Inhalationandingestion*

Effective dose coefficients for radioisotopes of the 31 elements covered in Publications 56, 67, 69, and 71, plus
radioisotopes of the further 60 elements covered in Publications 30 and 68. Intakes by both ingestion andinhalation. HRTM applied.

CD1(1999)

Inhalationandingestion*†

A database of effective and tissue equivalent dose coefficients for 10 aerosol particle sizes and 10 times after intake.
All radionuclides covered in Publications 68 and 72. Consistent with the dose coefficients in Publications 68 and72. Extensive help files also provided.

88 (2001)

Inhalationandingestion†

Fetal dose coefficients for intakes before and during pregnancy of the 31 elements covered in Publications 56, 67,
69, and 71, including doses to the embryo and fetus and to the child from activity retained at birth.

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315

*
†

ICRP
Publication
No. (year)

Application

Contents

CD2(2002)

Inhalationandingestion†

A database of effective and tissue equivalent fetal dose coefficients for 10 aerosol particle sizes and five times after
birth. All radionuclides covered in Publication 88. Consistent with the dose coefficients in Publication 88.
Extensive help files also provided.

95 (2004)

Inhalationandingestion†

Infant dose coefficients from intakes in maternal milk, for intakes by the mother, before and during pregnancy, andduring the period of breastfeeding, of the 31 elements covered in Publication 88, plus isotopes of Na, Mg, P and
K. For the four elements not included in Publication 88, doses to the embryo and fetus following maternal intakes
before and during pregnancy are also given.

CD3(2005)

Inhalationandingestion†

A database of effective and tissue equivalent dose coefficients from intakes in maternal milk, for acute and chronic
intakes by the mother, before and during pregnancy, and during the period of breastfeeding (more scenarios thanin Publication 95), for ingestion and inhalation of vapours and 10 aerosol particle sizes. All radionuclides coveredin Publication 95. Consistent with the dose coefficients in Publication 95, and also for additional intergration times.
Extensive help files also provided.

119 (2012)

Inhalationandingestion*†

Compilation of dose coefficients for intakes of radionuclides by workers and members of the public, andconversion coefficients for use in occupational radiological protection against external radiation from Publications
68, 72, and 74 (ICRP, 1994a, 1995c, 1996).

Age-dependent dose coefficients for members of the public (3 mo, 1, 5, 10, and 15 y, and adult).
Dose coefficients also given for workers.

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This series of reports provides revised age-dependent dose coefficients for membersof the public for intakes of radionuclides by inhalation and ingestion, replacing the Publication
56 series. As in the Publication 56 series, dose coefficients are presented in this series of reports
for intakes by 3-mo-old infants, 1-, 5-, 10-, and 15-y-old children, and adults. In most cases
the adult is taken to be aged 20 y. Exceptions are made for the alkaline earth elements, lead,thorium, uranium, neptunium, plutonium, americium and curium (ICRP, 1993, 1995a). For
these elements, the transfer rates for the adult apply to age 25 y, because some of the transfer
rates in the biokinetic models are equated with bone formation rates, which are expected toremain elevated up to about age 25 y. In the calculations of the activity in source regions of thebody, following intakes at these ages, continuous changes with age in the transfer rates
governing its distribution and retention are obtained by linear interpolation according to age.
This also applies to the transfer of activity from the small intestine to body fluids. For
application to other ages and protracted intakes, it is considered here, as in the Publication 56
series (e.g. ICRP, 1990) that tissue doses can be estimated by applying the age-specific dosecoefficients to the age ranges given below:
3 mo: from 0 to 12 mo of age
1 y: from 1 y to 2 y
5 y: more than 2 y to 7 y
10 y: more than 7 y to 12 y
15 y: more than 12 y to 17 y
Adult: more than 17 y
As in the Publication 56 series, a single Reference Person is used to represent eachage-group. Generally, biokinetic parameter values for males have been adopted because of theavailability of biokinetic data. Where there are known differences between sexes in the
biokinetics of an element, this is noted in the relevant section of the biokinetic data in OIR:
Parts 2‒5 (ICRP, 2016a, 2017, 2019, 2022) or in this volume. Energy absorption is consideredin models representing the Reference Male and Reference Female at each age.
These dose coefficients are provided for intake by inhalation and ingestion in a rangeof physico-chemical forms for each radionuclide, and in the case of inhalation, in a range ofaerosol particle size distributions.
While the generic definition of protection quantities remains unchanged in the mostrecent recommendations of (Publication 103, ICRP, 2007), there have been changes that affectcalculated values of dose per radiation exposure, including changes to radiation and tissue
weighting factors, updated and expanded sets of specific absorbed fractions (Publication 133,
ICRP, 2016, Publication 1XX, 202X) supported in large part by adoption of referencecomputational phantoms (Publication 110, ICRP, 2009, Publication 143, 2020), and thedevelopment of the new generation of reference biokinetic models.
The full data set of the report series is provided as an electronic annex. The printed
documents contain a selected set of data and materials. Data are presented in a standard format
for each element and its radioisotopes. Tabulated dose coefficients may be used to determine
committed effective dose from a known intake of a radionuclide. A full description of theinformation provided for each element and radioisotope is given in Section 4.
The revised dose coefficients have been calculated using the Publication 100 (ICRP,
2006) HATM and the revision of the Publication 66 (ICRP, 1994b) HRTM described in
Publication 130 (ICRP, 2015). The revisions made to the HRTM are described in Annex A of
Publication 130. In addition, information is provided in OIR: Parts 2‒5 (ICRP, 2016a, 2017,2019, 2022) and in this volume on absorption to blood following inhalation and ingestion ofdifferent chemical forms of elements and their radioisotopes. In selected cases, it is judged that13

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the data are sufficient to make material-specific recommendations. Revisions have been madeto many models for the systemic biokinetics of radionuclides, making them more
physiologically realistic representations of uptake and retention in organs and tissues and of
excretion.
Biokinetic models, reference physiological data, computational phantoms andradiation transport calculation codes are used for the calculation of dose coefficients (ICRP,
2007). ICRP publishes dose coefficients for the inhalation or ingestion of individual
radionuclides by members of the public, giving both equivalent doses to organs and tissues,and effective dose (ICRP, 1991, 2007). The steps in the calculation (Fig. 1.1) can besummarised as follows:
•

•

•
•
•

By use of the reference biokinetic models, the distribution and retention ofradionuclides in body organs and tissues of the Reference Member of the Public are
determined as a function of time after intake by inhalation or ingestion. For radiation
protection purposes, it is assumed that all biokinetic parameters of the Reference
Individual representing each age group are invariant on sex, anatomy, physiology, raceand other individual-related factors, but based on reference male parameter values
where sex-specific models are available. In this series of reports, the time-dependent
activity is calculated in each source region over a period following the intake, which istaken to be 50 y for adults and from intake to age 70 y for children;
Age and sex-dependent specific absorbed fractions are used to compute S-coefficients(ICRP, 2016b and forthcoming). The specific absorbed fractions are based on wholebody voxel phantoms (ICRP, 2009, 2020), skeletal models, and stylised models ofalimentary and respiratory tract geometries.
The radiation weighting factors are applied to determine sex-specific committed
equivalent dose coefficients to an organ or tissue;
The sex-specific committed equivalent dose coefficients are sex-averaged; andThe tissue weighting factors are then applied to determine the sex-averaged committed
effective dose coefficient, produced for different reference age-groups.
Quantified intake byinhalation or ingestion
Age-dependant
Biokinetic andDosimetric Models

Mean absorbed dose, DT,R
in an organ or tissue

Radiation weighting
factors, wR

Equivalent dose, HT,in an organ or tissue
Tissue weighting
factors, wT

395
396
397

Effective dose, E, forreference age-groups

Fig. 1.1. Calculation of absorbed dose and the protection quantities, equivalent and effective
dose – for intakes of radionuclides.
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398
399
400

The details of the computational procedure used in this report series are described in
Section 2.7.

401
402

1.2. Changes in Publication 103 that affect the calculation of equivalent andeffective dose

403
404
405
406
407
408
409
410
411
412
413
414
415
416
417
418

In the 2007 Recommendations issued in Publication 103 (ICRP, 2007), the concept
and use of equivalent and effective dose remain unchanged, but a number of revisions weremade to the methods used in their calculation. Changes were introduced in the radiation andtissue weighting factors, from the values previously recommended in Publication 60 (ICRP,
1991). Since radiation weighting factors (wR) for photons, electron and α particles areunchanged, the only difference of potential importance to internally deposited radionuclides isfor neutrons (Table 1.2). The changes made do not reflect the availability of additional data but
rather a reconsideration of the appropriate treatment of radiation weighting for protection
purposes. The abandonment of a step function for neutron wR as a function of energy is areflection of the fact that in practice, only a continuous function has been used. The majorchange in the continuous function is a lower wR value at low energies which more properlyreflects the low linear energy transfer contribution from secondary photons. In addition, there
are good theoretical reasons for assuming that wR values at high energies will converge withthat for protons.

419
420
421
422
423
424
425
426
427
428
429
430
431
432
433
434

Table 1.2. ICRP radiation weighting factors (ICRP, 2007)
Radiation Type
Radiation weighting factor, wR
Photons

1

Electrons and muons

1

Protons and charged pions

2

α particles, fission fragments, heavy ions20

Neutrons

Revised continuous function of neutron energy

The values of tissue weighting factors (wT) recommended in Publication 103 (ICRP,
2007) are shown in Table 1.3. Changes from values given in Publication 60 (ICRP, 1991)
reflect improved knowledge of radiation risks. The main sources of data on cancer risks are thefollow-up studies of the Japanese atomic bomb survivors, used to derive risk coefficientsaveraged over seven Western and Asian populations with different background cancer rates(ICRP, 2007). The new wT values are based on cancer incidence rather than mortality data,
adjusted for lethality, loss of quality of life and years of life lost. Weighting for hereditaryeffects is now based on estimates of disease in the first two generations rather than at theoreticalequilibrium. The main changes in wT values in the 2007 Recommendations are a decrease (from0.2 to 0.08) for gonads and an increase (from 0.05 to 0.12) for breast and for remainder, which
now includes more organs and tissues. The remainder dose is now calculated as the arithmetic
mean of the doses to the thirteen organs and tissues for each sex (Table 1.3). The so-called
splitting rule in the treatment of the remainder in Publication 60 (ICRP, 1991) is no longer usedand hence the effective dose is additive. Tissue weighting factors continue to represent averages
across the sexes and across all ages.
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436

437
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439
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441
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448
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450
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452
453
454
455
456
457
458
459
460
461
462
463
464
465
466

Table 1.3. Publication 103 (ICRP, 2007) tissue weighting factors
TissuewT∑ wT

Bone-marrow, breast, colon, lung, stomach,remainder tissues (13 for each sex*)

0.12

0.72

Gonads0.08

0.08

Urinary bladder, oesophagus, liver, thyroid

0.04

0.16

Bone surface, brain, salivary glands, skin

0.01

0.04

*

Remainder tissues: adrenals, ET regions of the respiratory tract, gall bladder, heart, kidneys, lymphatic nodes,
muscle, oral mucosa, pancreas, prostate (male), small intestine, spleen, thymus, uterus/cervix (female).

A further important change introduced in the 2007 Recommendations is that doses
from external and internal sources are calculated using reference computational phantoms of
the human body (ICRP, 2009, 2020). In the past, the Commission did not specify a particularphantom, and various mathematical phantoms such as hermaphrodite Medical Internal
Radiation Dose (MIRD)-type phantoms (Snyder et al., 1969), the sex-speciﬁc models of
Kramer et al. (1982), or the age-speciﬁc phantoms of Cristy and Eckerman (1987) have beenused. Voxel models, constructed from medical imaging data of real people, give a more realistic
description of the human body than afforded in mathematical (or stylised) phantoms. Thus, the
ICRP decided to use voxel models to define the reference phantoms to be used in thecalculations of dose distribution in the body for both internal and external exposures. Thesemodels (or computational phantoms), described in Publication 110 (ICRP, 2009) and in
Publication 143 (ICRP, 2020) , are representative of the Reference Members of the Public.
They are designed specifically for the calculation of the radiological protection quantities
corresponding to the effective dose concept of the 2007 Recommendations. These
computational phantoms have been supplemented with additional models when necessary andused to compute new specific absorbed fractions in Publication 133 (ICRP, 2016) andPublication 1XX (ICRP, 202X). The updated specific absorbed fractions include energydependent values for electrons and alpha particles representing a significant improvement toradiation protection dosimetry compared to non-energy dependent values in Publication 30(ICRP, 1982). For each age group, equivalent doses to organs and tissues, HT, are calculated
separately for the Reference Male and Female and then averaged in the calculation of effective
dose, E:𝐻 M + 𝐻TF

𝐸 = ∑𝑇 𝑤T [ T 2

]

(1.1)

where:
𝐻TM = ∑ 𝑤R 𝐷R,T (male)
𝑇

467
468

𝐻TF = ∑ 𝑤R 𝐷R,T (female)
𝑇

469
470
471

It is made clear in Publication 103 (ICRP, 2007) that effective dose is intended foruse as a protection quantity on the basis of reference values and relates to reference persons
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474
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476
477
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481

rather than specific individuals. The main uses of effective dose are in prospective dose
assessment for planning and optimisation in radiological protection, and retrospective
demonstration of compliance for regulatory purposes. Sex-averaging in the calculation ofequivalent and effective doses, implicit in the past use of hermaphrodite mathematicalphantoms, is now explicit in the averaging of equivalent doses to male and female phantoms.
Sex- and age-averaging in the derivation of tissue weighting factors can be seen to obscuredifferences in estimates of absolute radiation detriment between men and women and between
adults and children. However, practical protection would not be improved by calculating
effective dose separately for males and females and to do so might give a misleading impressionof the precision of these quantities.

482

1.3. Biokinetic models implemented in this series of reports

483
484
485
486
487
488
489
490
491
492
493
494
495
496

Biokinetic models for individual elements and their radioisotopes are used to calculate
the total number of transformations occurring within specific tissues, organs or body regions(source regions) during a given period of time (usually 50 y for adults, or to age 70 y forchildren) by determining the time-integrated activity in each source region. Dosimetric models
are used to calculate the deposition of energy in all important organs/tissues (targets) for
transformations occurring in each source region, taking account of the energies and yields ofall emissions (Section 2.7). Committed absorbed dose in target regions (in grays) can then be
calculated, knowing the number of decays occurring in source regions and energy depositionin target regions.
Biokinetic models of the alimentary and respiratory tracts are used to define themovement of radionuclides within these systems, resulting in absorption to blood and/or loss
from the body. The behaviour of radionuclides absorbed to blood is described by elementspecific systemic models that range in complexity. The models used in this series of reports aredescribed in Section 2.

497

1.4. Dosimetry implemented in this series of reports

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514
515

Dose calculations involve the use of nuclear decay data, anthropomorphic phantoms
that describe the human anatomy and codes that simulate radiation transport and energy
deposition in the body. The data provided in this report series are calculated using revised decay
data (Publication 107, ICRP, 2008), the ICRP reference computational phantoms of the adultand children based on medical imaging data (ICRP, 2009, 2020), separate models for theskeletal (Hough et al., 2011; O’Reilly et al., 2016; Pafundi et al., 2010), alimentary (ICRP,
2006), and respiratory tract anatomies (ICRP, 1994b), and well-established Monte Carlo codes(Kawrakow et al., 2006; Niita et al., 2010; Pelowitz, 2008). Radiation transport in the
anatomical phantoms and models provides age, radiation, and sex-dependent tables of specificabsorbed fractions (ICRP, 2016b and forthcoming; Schwarz et al., 2021a, 2021b).
For all dose calculations, radionuclides are assumed to be uniformly distributed
throughout source regions, although these can be whole organs (e.g. liver) or a thin layer within
a tissue (e.g. mucosa layers in the alimentary tract). Similarly, target cells are assumed to beuniformly distributed throughout target regions that vary in size from whole organs to layers ofcells. Doses from ‘cross-fire’ radiation between source and target regions are important for
penetrating photon radiation. For ‘non-penetrating’ α and β particle radiations, energy will inmost cases be largely deposited in the tissue in which the radionuclide is deposited. Photon andelectron transport are followed for most source and target combinations. Additionally, special
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517
518
519
520
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522
523

considerations are taken into account for α and β emissions in a number of important cases.
These include:• Doses to target cells in the walls of the respiratory tract airways from radionuclides in
the airways (ICRP, 1994b);• Doses to target cells in the alimentary tract from radionuclides in the lumen (ICRP,
2006); and• Doses to cells adjacent to inner bone surfaces (50-μm layer; see below) and all red
marrow from radionuclides on bone surfaces and within bone mineral.

524

1.4.1. Nuclear decay data, Publication 107

525
526
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530
531
532
533
534
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536
537
538
539
540
541
542
543

A fundamental requirement for dose calculations is reliable information on half-life,
modes of decay, and the energies and yields of the various radiations emitted by radionuclides
and their progeny (Eckerman et al., 1994; Endo et al., 2003, 2005). The calculations in thisreport use the nuclear decay data provided in Publication 107 (ICRP, 2008). This publication
replaces Publication 38 (ICRP, 1983) and consists of an explanatory text, with anaccompanying CD-ROM providing data on the radiation emissions of 1252 radioisotopes of 97
elements. Radioisotopes of elements of atomic number less than 101 were included in
Publication 107 if their half-lives exceed 1 min, or if they are the progeny of a selectedradionuclide and if the basic nuclear structure data enabled a meaningful analysis of theiremissions. CD-ROM use has enabled the complete listing of emitted radiations, and moredetails of Auger cascades and spontaneous fission data. The data given include: energies andintensities of emitted radiations; β, neutron, and Auger and Coster-Kronig (CK) electrons
spectra; spontaneous fission radiations and α recoil; half-lives, branching decay and chains; andno cut-off on the number of emissions.
In this series of reports, dose coefficients are presented for almost all radionuclides
included in Publication 107 (ICRP, 2008) that have half-lives equal to or greater than 10 min,and for other selected radionuclides. For radionuclides with decay chains, all parent
radionuclides with half-lives equal to or greater than 10 min are included, but no constraint isplaced on the half-lives of progeny radionuclides.

544

1.4.2. Adult reference computational phantoms, Publication 110

545
546
547
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551
552
553
554
555
556
557
558
559
560

As outlined above, the 2007 Recommendations (ICRP, 2007) adopted the use ofrealistic anatomical models to replace the stylised computational phantoms of human anatomy
previously used in the calculation of dose coefficients for both external and internal radiation
protection (Cristy, 1980; Cristy and Eckerman, 1987). These were indeed limited in their ability
to capture anatomic realism. The new reference phantoms are voxel models based on
segmented tomographic data of real individuals obtained from computed tomography (CT) or
magnetic resonance imaging.
Publication 110 (ICRP, 2009) describes the development and intended use of thecomputational phantoms of the Reference Adult Male and the Reference Adult Female. They
were constructed after modifying the voxel models of two individuals whose body height andmass closely matched reference values (Zankl et al., 2002, 2003, 2007). The report describes
the methods used for this process and the anatomical and computational characteristics of theresulting phantoms.
Publication 143 (ICRP, 2020) describes the development and intended use of the agedependent paediatric reference computational phantoms. CT images for the newborn werebased on prospective images of cadavers (Lee et al., 2007; Nipper et al., 2002). For other18

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reference ages, the CT images came from retrospective review and image retrieval fromradiology archives (Lee et al., 2010).
The reference computational phantoms are used, together with codes that simulate
radiation transport and energy deposition, for the assessment of the specific absorbed fractionof energy per unit mass, Φ, in an organ or tissue due to emissions in a source organ or region
from which equivalent doses and the effective dose are calculated successively.

567

1.4.3. Advances in skeletal dosimetry

568
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595

In Publication 130 (ICRP, 2015), the skeletal dosimetry models of Publication 30(ICRP, 1979) were substantially updated for all radiations emitted from internally depositedradionuclides – α particles, electrons, β particles, photons, and neutrons (e.g. from spontaneous
fission). Improvements over the Publication 30 models include a more refined treatment of thedependence of the absorbed fraction on particle energy, marrow cellularity, and bone-specificspongiosa micro-architecture. Two reference sets of skeletal images were established forradiation transport simulation. The first included 1-mm ex-vivo CT images of some 38 skeletalsites harvested from a 40-y old male cadaver (Hough et al., 2011). These images were used toestablish fractional volumes of cortical bone, trabecular spongiosa, and medullary cavities byskeletal site, and to serve as the macroscopic geometric model for particle transport. The second
included 30-µm microCT images of cored samples of trabecular spongiosa to establish
fractional volumes of trabecular bone and marrow tissues, and to serve as the microscopic
geometric model for particle transport. Both image sets were then combined during pairedimage radiation transport (PIRT) of internally emitted electrons (Shah et al., 2005). Source
tissues were: bone marrow (active and inactive), mineral bone surfaces (trabecular and cortical),and mineral bone volumes (trabecular and cortical). Target regions considered were: active
marrow (surrogate tissue for the hematopoietic stem and progenitor cells), and a revised 50-µ m
model of the skeletal endosteum (surrogate tissue for the osteoprogenitor cells) (see‘Endosteum’ in the Glossary). Absorbed fractions for internally deposited α particles andneutron-generated recoil protons were established based on path length-based transport
algorithms given in Jokisch et al. (2011; 2011). Values of absorbed fractions to active marrowand endosteum for internally-emitted photons and neutrons were obtained by first tallying
energy-dependent particle fluences within the spongiosa and medullary cavity regions of the
Publication 110 Reference Adult Male and Reference Adult Female voxel phantoms (ICRP,
2009) and then applying fluence-to-absorbed dose response functions (DRFs). Further details
on the derivations of these photon and neutron skeletal DRFs are given in Johnson et al. (2011)
and Bahadori et al. (Bahadori et al., 2011), respectively, as well as in Annexes D and E of
Publication 116 (ICRP, 2010a).

596

1.5. Pregnancy and breast-feeding

597
598
599
600
601
602
603
604
605

ICRP has provided information in Publications 88 and 95 (ICRP, 2001, 2004) on
doses to the embryo, fetus and newborn child following intake of radionuclides by female
members of the public and workers either before or during pregnancy or during lactation.
Comparisons of fetal dose coefficients given in Publication 88 with corresponding adult dosecoefficients showed that doses received by a woman from intakes before or during pregnancy
will in most cases be substantially greater than doses to her fetus. However, doses to theoffspring can exceed doses to the mother for a number of radionuclides. In particular, therequirements of skeletal development during fetal growth, particularly in late pregnancy, canlead to significant uptake of radioisotopes of phosphorus and of calcium and, to a lesser extent,
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612
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614
615
616
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618
619
620
621
622
623
624
625
626
627

other alkaline earth elements. Thus, offspring to adult dose ratios were up to factors ofapproximately 10–20 for isotopes of P and Ca and 2–6 for isotopes of Sr (ICRP, 2004; Stather
et al., 2003). Uptake of radioisotopes of iodine by the fetal thyroid can also lead to greater doses
to the fetus than to the mother following intakes late in pregnancy (dose ratios of up to
approximately 3) (Berkovski et al., 2003). Other radionuclides for which doses to the fetus canexceed doses to the mother include tritium as tritiated water, 14C and 35S. Offspring to adultdose ratios are greatest following ingestion or inhalation of soluble (Type F) forms. Values ofoffspring to adult dose ratios may change as a result of future calculations following from
Publication 103 (ICRP, 2007) and associated changes. Offspring protection may also be ofconcern when the dose ratio is <1, since an effective dose of 1 mSv to the embryo, fetus ornewborn child might be reached at otherwise acceptable levels of occupational dose (Phipps etal., 2001).
In general, doses to the infant from radionuclides ingested in breast milk are estimatedto be small in comparison with doses to the Reference Adult (ICRP, 2004). On the basis of themodels developed in Publication 95 (ICRP, 2004), it is only in the cases of tritiated water, 45Ca,75
Se and 131I that infant doses may exceed adult doses, by factors of between 1 and 3. Infant
doses are highest when maternal intakes by ingestion occur shortly after birth, because
maximum transfer occurs under these conditions. Ratios of infant to adult doses are generally
lower for intakes by inhalation than for ingestion. Comparisons with Publication 88 (ICRP,
2001) doses to the offspring due to in-utero exposures show that in most cases, these are more
important than doses that may result from breast feeding; exceptions include 60Co, 131I and210
Po. ICRP intends to provide a revision of these dose coefficients in a later report in this series.

628

1.6. Structure of the report

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This series of reports provides revised dose coefficients for EIR by inhalation andingestion, replacing the Publication 56 series, which gave doses to members of the public fromintake of radionuclides: Publications 56, 67, 69, 71, 72, 88 and 95 (ICRP, 1990, 1993, 1995a,
1995b, 1995c, 2001, 2004).
Section 2 of this report gives an overview of the biokinetic and dosimetric models
used to calculate dose coefficients and bioassay functions. It describes the main features of the
Publication 130 (ICRP, 2015) revision of the HRTM and the Publication 100 HATM (ICRP,
2006). Section 2 also provides an introduction to the models used in this report series to
describe the systemic biokinetics of elements and their radioisotopes. Dosimetric models andthe ICRP computational methodology are also explained.
Section 3 describes general aspects of internal dose assessment, including sources of
uncertainties.
Section 4 provides a brief outline of the types of information included in subsequentparts of this series of reports: biokinetic data and dose coefficients for individual elements andtheir radioisotopes. Each element section provides dose coefficients: committed effective doseper Bq intake (Sv Bq–1) for inhalation and ingestion of all relevant radioisotopes. Data areprovided in the printed reports of the series and in electronic annexes.
The data provided in the printed reports are restricted to tables of committed effective
dose per intake (Sv Bq–1). For intakes by inhalation, data are provided for all absorption typesof the most common isotope(s), and for an activity median aerodynamic diameter (AMAD) of
1 µm. In cases for which sufficient information is available (principally for actinides and forgas and vapour forms), lung absorption is specified for different chemical forms, and dose

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659
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661

coefficients are calculated accordingly. Dose coefficients for intake by ingestion are also given,for different chemical forms when sufficient information is available.
The electronic data that accompanies this series of reports and that are available on
the ICRP website contain a comprehensive set of committed effective and equivalent dosecoefficients, for most of the isotopes presented in Publication 107 (ICRP, 2008), and for arange of physico-chemical forms and aerosol AMADs and activity median thermodynamic
diameters (AMTDs).
The electronic data are made of a set of data files with dose coefficients and otherradionuclide-specific data which may be accessed by the user directly or by using theaccompanying Data Viewer. The Data Viewer permits rapid navigation of the dataset andvisualisation of the data in tabulated and graphical formats.

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662

2. BIOKINETIC AND DOSIMETRIC MODELS

663

2.1. Introduction

664
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This Section gives an overview of the biokinetic and dosimetric models used to
calculate dose coefficients and bioassay functions, as they apply to the general population. It
describes the main features of the Human Respiratory Tract Model (HRTM, ICRP, 1994b), as
updated in Publication 130 (ICRP, 2015), and of the Human Alimentary Tract Model (HATM,
ICRP, 2006). It provides an introduction to the models used in this series of reports to describe
the systemic biokinetics of elements and their radioisotopes. Dosimetric models andmethodology are also explained.
Radionuclide exposures in the environment can lead to intakes by a number of routes:
inhalation, ingestion, entry through intact skin and wounds. Fig. 2.1 summarises the routes ofintake, internal transfers, and routes of excretion.

675
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677
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681
682
683
684
685
686
687
688

Fig. 2.1. Summary of the main routes of intake, transfer and excretion of radionuclides in thebody.
Following inhalation, inhaled particles containing radionuclides deposit in the various
regions of the respiratory tract, with deposition in each being mainly dependent on particle size
(ICRP, 1994b, 2002b). Removal from the respiratory tract occurs mainly by dissolution andabsorption to blood, and the competing process of transport of particles to the throat followedby their entry into the alimentary tract. The proportions absorbed to blood or cleared by particle
transport depend on the speciation and the solubility of the material, and on the radioactive
half-life of the radionuclide. The HRTM is also applied here to gases and vapours and toinhalation of radon and its radioactive progeny.
For ingestion of radionuclides, the Publication 30 (ICRP, 1979) model of thegastrointestinal tract has been replaced by the Human Alimentary Tract Model (HATM)

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described in Publication 100 (ICRP, 2006), which is applied in this series of reports. The modelis also used for radionuclides in particles cleared to the throat from the respiratory tract after
inhalation. In the HATM, fractional absorption of radionuclides is specified by the alimentarytract transfer factor, fA, instead of the f1 value as given for the gastrointestinal model describedin Publication 30 (ICRP, 1979). The fA value describes total absorption from all regions of thealimentary tract, although the default assumption is that all absorption takes place in the small
intestine.
Intact skin is an effective barrier against entry of most substances into the body, andfew radionuclides cross it to any significant extent (see Section 3.4.1 of Publication 130 (ICRP,
2015)). Exceptions of practical importance include forms of tritium, carbon and iodine. Thereis no general model for absorption of radionuclides through the skin because of the wide rangeof possible exposure scenarios. Both the radiation dose to the area of skin contaminated andthe dose to the whole body as a result of absorption should be considered. ICRP (1991, 2007)
recommends that local skin doses should be calculated to sensitive cells, assumed to be at a
depth of 70 μm, or averaged over the layer of tissue 50 to 100 µm below the skin surface andaveraged over the most exposed 1 cm2 of skin tissue. This applies to activity either distributed
over the skin surface or aggregated in particles. No dosimetric models are recommended by
ICRP for calculating doses from radionuclides deposited on the skin and no dose coefficientsare given.
ICRP has generally not given advice on assessing doses from intakes of radionuclides
transferred from wound sites to blood and other organs and tissues. Internal exposure resulting
from wounds almost always arises because of accidents in the workplace, rather than as a resultof routine operations that are subject to the normal environmental controls. Uptake fromwounds can vary greatly depending on the circumstances of a particular incident, and inpractice, the assessment of internal contamination is treated on a case-by-case basis. As a result,provision of generic dose coefficients or bioassay functions would be of limited value.
Information on the transfer of radionuclides from wound sites has, however, been reviewed bya Scientific Committee of the U.S. National Council on Radiation Protection andMeasurements (NCRP), and these data have been used to develop a model to describe thetransfer of material from wounds after intakes in different physico-chemical forms (NCRP,
2006). Section 3.4 of Publication 130 (ICRP, 2015) summarises the main features of the NCRP
model. Dose coefficients for injection as the route of intake are given in the electronic annexe
to the OIR series of reports, which may assist in assessment of doses after wound contamination.
These coefficients are not given in this series of report, since contamination by wound is not acommon way of exposure for the members of the public.
For each route of intake, a portion of the radionuclide entering the body is absorbed
to blood and distributed systemically. The systemic distribution of radionuclides in the bodycan be diffuse and relatively homogeneous, as for the examples of tritiated water andradioisotopes of potassium and caesium, or may be localised in certain organs or tissues, as forthe examples of radioisotopes of iodine (thyroid), alkaline earth elements (bone), andplutonium (bone and liver). Systemic biokinetic models are used to describe the distribution
and excretion of radionuclides absorbed to blood. The systemic models for the elements havebeen reviewed and revised as necessary to take account of more recent information and provide
models that are appropriate for both dosimetry and bioassay interpretation.
Removal of deposited material from the body occurs principally by urinary and faecal
excretion although radionuclides may also be lost by exhalation or through the skin (e.g.
tritiated water). Urinary excretion is the removal in urine of radionuclides from blood following
filtration by the kidneys. Faecal excretion has two components: systemic (endogenous) faecal
excretion, which represents removal of systemic material via the alimentary tract due to biliary24

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

738
739
740
741
742
743

secretion from the liver and secretions at other sites along the alimentary tract; and direct(exogenous) faecal excretion, of the material passing unabsorbed through the alimentary tract
after ingestion or clearance to the throat from the respiratory system after inhalation. The
reference models outlined in this section are assigned reference parameter values, and used to
calculate body or organ content at specified times after acute or chronic intake. Together withdosimetric data, they are used to calculate reference dose coefficients.

744

2.2. Human Respiratory Tract Model (HRTM)

745
746
747
748
749
750
751
752
753
754
755
756
757
758
759
760
761
762
763
764
765
766
767
768
769
770
771
772
773
774
775
776
777
778
779
780
781
782
783

The HRTM is described in full in Publication 66 (ICRP, 1994b). It was applied to
calculate inhalation dose coefficients for workers and members of the public in Publications
68, 71, 72, 88 and 95 (ICRP, 1994a, 1995b, 1995c, 2001, 2004), and bioassay functions in
Publication 78 (ICRP, 1997). Further guidance on its use was given in ICRP Supporting
Guidance 3 (ICRP, 2002b).
The HRTM was updated in Publication 130 (ICRP, 2015) to take account of data
accumulated since its publication, although the basic features of the model remain unchanged.
The revised HRTM (ICRP, 2015) is used in this series of reports, as described below. Simple
changes from the original HRTM are noted in this section. The major changes made relate to
the clearance of deposited material by both particle transport and absorption to blood. Thesechanges involved review and analysis of relevant recent information, and judgements in
implementing the changes in the HRTM: they are described in Annex A of Publication 130(ICRP, 2015).
A summary of the main features of the revised HRTM is given here, in particular thoserelating to age dependence. The HRTM applies explicitly to all members of the population,
giving parameter values for 3-mo-old infants, 1-, 5-, 10- and 15-y-old children, and adults. The
principal age-specific aspects are unchanged from those described in Publication 71 (ICRP,
1995b). In this report, as in Publications 71 and 72 (ICRP, 1995b, 1995c), only one Reference
Individual is used to represent each age group. For those ages at which Publication 66 provides
separate parameter values for males and females (10 y and above), the male values are usedhere for the Reference Individual representing the age group. Nevertheless, tissue doses arecalculated for males and females separately, before being combined to calculate the effective
doses to Reference Individuals. If inhalation doses specific to females should be required, thendata given in Publication 66 enable them to be calculated. However, for a given exposure,differences in doses between males and females of the same age are small, because for females
both intake and body mass are smaller than for males by approximately 20% (ICRP, 1995b).
As in the original version of the HRTM, the respiratory tract is treated as two tissues:
the extrathoracic (ET) and the thoracic (TH) airways. The sub-division of these tissues into
regions was based mainly on differences in sensitivity to radiation. The TH regions arebronchial, (BB: trachea, airway generation 0, and bronchi, airway generations 1–8), bronchiolar(bb: airway generations 9–15), alveolar‒interstitial (AI: the gas exchange region, airway
generations ≥16); and the TH lymph nodes, LNTH. The ET regions are the anterior nasal passage,
ET1; the posterior nasal passages, pharynx and larynx, ET2; and the ET lymph nodes LNET (Fig.
2.2). For consistency with the HATM, the oral passage is now not included in region ET 2 as it
was in Publication 66. This does not affect results obtained with the model, because depositionin ET from air entering the mouth was taken to occur only in the larynx.
Values of dimensions of the airways, and scaling factors for subjects of different ages,
are specified in Publication 66 (ICRP, 1994b). In order to apply the model to different age
groups, dimensions of conducting and respiratory airways are scaled by body height and25

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

784
785
786
787
788

Functional Residual Capacity, respectively. It is assumed that the branching structure of the
airways (BB and bb) is complete at birth, and that the number of alveoli increases linearly withtime, from 40% of the adult total at 3 mo, to 80% at 1 y. The mass of the AI is scaled on thebasis of body mass. These dimensions are used with the deposition model to calculate regional
deposition, and are also used to derive masses of target tissues (see below).

789
790
791
792
793

Fig. 2.2. Respiratory tract regions defined in the HRTM. Note that the oral part of the pharynx
is no longer part of ET2. ET1: extrathoracic region including the anterior nasal passage; ET2
extrathoracic region including posterior nasal passage, pharynx and larynx; BB: bronchialregion; bb: bronchiolar region; AI: alveolar‒interstitial region. Taken from ICRP (1994b).

794

2.2.1. Physiology

795
796
797
798
799
800
801
802
803

This section is essentially unchanged from the corresponding section of Publication
71 (ICRP, 1995b). The HRTM enables inhalation dose coefficients to be calculated, and also
intake per exposure (time-integrated activity concentration in air), and hence doses per
exposure, which are frequently required for environmental dose assessments. Two factors relate
intake to exposure: inhalability and ventilation.
Inhalability is the ratio of the particle concentration in the air entering the respiratory
tract to that in the ambient air (taken to be 1 for particles with an aerodynamic diameter smaller
than approximately 1 μm). The inertia of larger particles increases the concentration in the air
entering the nose or mouth when facing into a wind, and reduces it otherwise, the average net

26

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

804
805
806
807
808
809
810

811
812
813
814
815
816
817
818
819
820
821
822
823
824
825
826
827
828
829
830
831
832
833
834
835
836
837
838

effect being to reduce it to approximately half that in the ambient air for particles withaerodynamic diameters greater than approximately 30 μm. For convenience, inhalability istaken into account in the calculation of regional deposition fractions, rather than being treatedseparately. Inhalability is assumed to be independent of age and sex.
Table 2.1. Ventilation parameters for Reference Individuals *. Taken from Table 4 of
Publication 71, (ICRP, 1995b)†.
Age
Exercise level
3 mo
1y
5y
10 y
15 y
Adult
(Male)(Male)(Male)SleepfR (min‒1)
38
34
23
17
14
12
3 ‒1
B (m h )
0.09
0.15
0.24
0.31
0.42
0.45
SittingfR (min‒1)
B (m3 h‒1)

‒
‒

36
0.22

25
0.32

19
0.38

15
0.48

12
0.54

Light exercise

fR (min‒1)
B (m3 h‒1)

48
0.19

46
0.35

39
0.57

32
1.12

23
1.38

20
1.5

Heavy exercise

fR (min‒1)
B (m3 h‒1)

‒
‒

‒
‒

‒
‒

44
2.22

36
2.92

26
3.0

*

Reference values, given to sufficient precision for calculational purposes, which may be greater than would bechosen to reflect the certainty with which the average value of each parameter is known.
†
Table 4 of Publication 71 (ICRP, 1995b) was based on Table B15 of Publication 66, (ICRP, 1994b).
fR = frequency, B = ventilation rate.

Ventilation, the breathing frequency and tidal volume, is the main factor in the modelthat depends on age and level of exercise. This is also the aspect for which there arecomprehensive data relating to women and children as well as men. Reference values of the
primary quantities, breathing frequency, fR, (breaths per min) and ventilation rate, B, (m3 h‒1),
are given in Table 2.1 for each age group and for four levels of exercise: sleep, sitting, light
exercise, and heavy exercise. For 3-mo-old infants, and for 1- and 5-y-old children, the valuesof fR and B are the same for males and females. For the other age groups, where there aredifferences, male values are given (see Para. (55)). However, the values for 10-y-old males
and females only differ for heavy exercise.
The HRTM enables deposition fractions to be calculated separately for nose breathing
and mouth breathing. Account can therefore be taken of the oro-nasal breathing that takes placein most individuals at heavy exercise, and in habitual mouth-breathers at all levels of exercise.
It is assumed [see Para. 158 and Table 11 of Publication 66, (ICRP, 1994b)] that the fractionof total ventilatory airflow passing through the nose in normal nasal augmenters (nosebreathers) is 100% at sleep, sitting and light exercise, and 50% at heavy exercise. These
fractions are taken to be independent of age and sex.
The results of habit surveys are summarised in Annexe B (Respiratory Physiology) of
Publication 66 (ICRP, 1994b). Table 2.2 gives the distribution of time spent in various
activities, taken from Table 4 of Publication 71 (ICRP, 1995b). For 3-mo-, 1-, 5- and 10-y-old
children, the time budgets in Table 2.2 are the same for males and females; and for the otherage groups, male values are given (see Para. (55)). These results have been used to provide
reference values, for calculating dose coefficients for environmental exposure, of the numberof hours per day spent at each of the four levels of exercise, which are given in Table 2.3. For

27

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

839
840
841
842
843
844
845
846
847

10-y-old children, the values in Table 2.3 (and hence the deposition fractions derived fromthem in Table 2.4) are the same for males and females, because the time budget for 10-y-old
children (Table 2.2) does not include heavy exercise, the only level at which there aredifferences in ventilation parameter values between males and females.
These parameter values can be used to determine intake per exposure, and are also usedwith the deposition model to determine regional deposition.

848
849
850
851
852
853
854
855
856
857
858

*

Table 2.2. Daily time budget (h) for environmental exposure of Reference Individuals. Taken
from Table 5 of Publication 71, (ICRP, 1995b)*.
Age
Location
3 mo
1y
5y
10 y
15 y
Adult
(Male) (Male)
Indoors
At home:
Asleep
17
14
12
10
10
8.5
†
‡
‡
‡
§
Awake
7
5
6
8
7
7‡
Elsewhere (eg. at work)
4‡
3‡
3‡
4§
6.5‡
‡
‡
‡
¶
Outdoors
1
3
3
3
2**
Table 5 of Publication 71 (ICRP, 1995b), was based on Table B16 of Publication 66 (ICRP, 1994b), but only
for the six Reference Individuals for which dose coefficients are given in Publication 71 and this series of reports.
†
Light exercise‡
One-third sitting + two-thirds light exercise§
One-half sitting + one-half light exercise¶
Two-thirds light exercise + one-third heavy exercise**
One-half sitting + three-eighths light exercise + one-eighth heavy exercise

Table 2.3. Daily time budget * and ventilation parameters† at each exercise level forenvironmental exposure of members of the public (Reference Individuals)‡ at various ages.
Taken from Table 6 of Publication 71, (ICRP, 1995b).
Exercise level
3 mo
1y
5y
3 ‒1
3
3 ‒1
3
h
m h m
h
m h m
h
m3 h‒1 m3
1. Sleep17.0 0.09 1.53
14.0 0.15 2.10
12.0 0.24 2.88
2. Sitting
3.33 0.22 0.73
4.0
0.32 1.28
3. Light exercise 7.0
0.19 1.33
6.67 0.35 2.33
8.0
0.57 4.56
4. Heavy exercise
Total
2.86
5.16
8.72
Exercise level
1. Sleep
2. Sitting
3. Light exercise
4. Heavy exercise
Total

859
860
861
862
863
864
865
866
867
868

h
10.0
4.67
9.33

10 y
m3 h‒1 m3
0.31 3.10
0.38 1.77
1.12 10.45

h
10.0
5.5
7.5
1.0

15.3

*

15 y(Male)m3 h‒1 m3
0.42 4.20
0.48 2.64
1.38 10.35
2.92 2.92
20.1

Adult (Male)hm3 h‒1 m3
8.0
0.45 3.60
6.0
0.54 3.24
9.75 1.5
14.63
0.25 3.0
0.75
22.2

The number of hours per day spent at each exercise level given above are reference values (see below).
Generally, they are based on the distributions of time given in Table 2.2, and rounded to the nearest 0.01 h. For
the adult male however, the time asleep has been rounded down from 8.5 h to 8 h for consistency with theReference Worker (Table 6 of ICRP Publication 66). The time spent sitting has been correspondingly increased
by 0.5 h.
†
The ventilation rates (m3 h‒1) are reference values taken from Table 2.1.
‡
The daily volumes inhaled (m3) at each exercise level are derived from the reference values of time spent at eachactivity, and of ventilation rate. See Para. (62).
§Reference values, given to sufficient precision for calculational purposes, which may be greater than would bechosen to reflect the certainty with which the average value of each parameter is known.

28

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

869

2.2.2. Deposition

870

2.2.2.1. Aerosols of (solid or liquid) particulate materials

871
872
873
874
875
876
877
878
879
880
881
882
883
884
885
886
887
888
889
890
891
892
893
894
895
896
897
898
899
900
901
902
903
904
905
906
907
908
909
910
911
912
913
914
915

Deposition refers to the initial processes that determine how much of the material in theinhaled air remains behind after exhalation. The deposition model described in Publication 66(ICRP, 1994b) evaluates fractional deposition of an aerosol in each region, for all aerosol sizesof practical interest (0.6 nm – 100 μm). For radionuclides inhaled in particulate form (aerosols),
it is assumed that entry and regional deposition in the respiratory tract of a given subject aregoverned only by the size distribution of the aerosol particles. Deposition fractions of gases
and vapours are determined by their chemical form: see below.
Deposition in the extrathoracic (ET) airways was determined empirically. Deposition
measurements in men were related to characteristic parameters of particle size and airflow. The
resulting deposition efficiencies were scaled by anatomical dimensions to predict deposition in
women and children. In Publication 66 (ICRP, 1994b) it was assumed that particles depositedin the nasal passage during inhalation are partitioned equally between ET 1 and the posterior
nasal passage, which is part of ET 2. (However, because of the way the deposition efficiencies
were calculated for polydisperse aerosols during inhalation and exhalation, for most aerosol
sizes of interest in radiation protection the deposition fractions given in Publications 66 (ICRP,
1994b) and 71 (ICRP, 1995b) are somewhat higher for ET2 than for ET1.)
For the thoracic (TH) airways, a theoretical model of gas transport and particle
deposition was used to calculate particle deposition in each of the BB, bb, and AI regions, andto quantify the effects of the subject’s lung size and breathing rate. To model particle deposition,
the regions were treated as a series of filters, during both inhalation and exhalation. The
efficiency of each was evaluated by considering aerodynamic (gravitational settling, inertial
impaction) and thermodynamic (diffusion) processes acting competitively. Regional deposition
fractions were calculated for aerosols having lognormal particle size distributions, withgeometric standard deviations taken to be a function of the median particle diameter, increasingfrom a value of 1.0 at 0.6 nm to a value of 2.5 above approximately 1 μm (Publication 66, Para.
170, ICRP, 1994b).
Deposition fractions for each individual subject and exercise level are given (to two
significant figures) in Publication 66, Annexe F, Tables F3 (sleep); F4 (sitting); F5 (light
exercise); F6 (heavy exercise) (ICRP, 1994b) and in Annex A of ICRP (2002b).
As described in Annex A of Publication 130, (ICRP, 2015), recent human experimental
studies showed that the distribution of the deposit in the ET airways is more accurately
characterised by mean deposition fractions of 65% to ET 1 and 35% to ET2. In this report, thedeposition values of ICRP Publication 66 (ICRP, 1994b) are adopted for the TH airways,
whereas the deposition in the ET airways is redistributed according to the new experimental
results. For particles inhaled through the nose, this is done by partitioning the total deposit in
the ET airways, [sum of ET1 and ET2, as calculated using the original HRTM (ICRP, 1994b)],
summing to give the total deposit in the ET airways, and then re-partitioning 65% to ET1 and
35% to ET2 (ANNEX A). For particles inhaled through the mouth (for example during heavy
exercise, when the HRTM assumes that 50% of the air is inhaled through the mouth by habitual
nose-breathers) there is no deposition in ET1 and the fraction deposited in ET2 remains ascalculated using the original HRTM
No changes are made here to the Publication 66 implementation of the deposition model
for aerosols, except for the re-distribution of the deposit in the ET airways between regions ET 1
and ET2 (see above). To calculate dose coefficients for inhalation of radionuclides by membersof the public, the subjects are taken to be normal nose-breathers whose time is spent according

29

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

916
917
918
919
920
921
922
923
924
925
926
927
928
929
930
931
932
933
934
935

to the distributions given in Table 2.3. For environmental exposure to most radionuclides, thedefault Activity Median Aerodynamic Diameter (AMAD) is taken to be 1 μm [Publication 66,
Para. 181 (ICRP, 1994b); Dorrian and Bailey (1996); Dorrian (1997); Section B9.2 of ICRP
(2002b)], in agreement with the fact that an AMAD of a few microns is characteristic ofaerosols produced by dispersion mechanisms. The short-lived progeny of radon, on the contrary,are formed as airborne free ions, which react rapidly with trace gases and vapours to form
particles approximately 1-nm diameter (̒unattached progenyʼ). These in turn may attach toexisting atmospheric aerosol particles (̒attached progenyʼ). Appropriate size distributions arerecommended in the radon inhalation section in OIR: Part 3 (ICRP, 2017).
Values of fractional deposition in each region of the respiratory tract of the Reference
Individual are given in Table 2.4 for aerosols of 1 μm AMAD. Values for aerosols of othersizes are given in ANNEX A. Generally, these deposition fractions do not vary markedly withage. The relatively high deposition in the BB region of the 15-y-old when compared to theother age-groups arises from the 1 h per day of heavy exercise, which is more than at otherages, and which involves oro-nasal breathing. Since deposition in the mouth is smaller than in
the nose, there is greater penetration to, and hence deposition in, the BB region.
Table 2.4. Regional deposition of inhaled aerosols with an activity median aerodynamic
diameter of 1 μm for the Reference Individuals * (% of inhaled activity). Based on Table A.1 inAnnex A.
Age
3 mo
1y
5y
10 y
15 y
Adult
(Male)(Male)
Deposition (%)†,‡

Region
ET1

31.31

31.44

25.81

26.40

20.49

21.94

ET2
BB

16.85
1.04

16.92
1.04

13.90
1.04

14.22
1.17

11.55
1.69

11.92
1.29

Bb

2.05

1.71

1.85

1.70

2.00

1.95

AI
Total

8.56
59.81

9.64
60.75

9.86
52.46

9.51
53.00

10.65
46.38

11.48
48.58

936
937
938
939
940
941
942
943
944
945
946
947

ET1: extrathoracic region including the anterior nasal passage; ET2 extrathoracic region including posterior nasal
passage, pharynx and larynx; BB: bronchial region; bb: bronchiolar region; AI: alveolar‒interstitial region. Basedon ICRP (1994b).
*
The Reference Individual was assigned the deposition and clearance parameter values of healthy, non-smoking,normal nose-breathers. The distributions of time spent at each of the four reference exercise levels are as given in
Table 2.3. The deposition fractions are volume-weighted average values for deposition at the four exercise levels(ANNEX A).
† Reference values, given to sufficient precision for calculation purposes, which may be greater than would bechosen to reflect the certainty with which the average value of each parameter is known.
‡ The particles are assumed to have density 3.00 g cm–3, and shape factor 1.5. The particle aerodynamic diameters
are assumed to be log-normally distributed with geometric standard deviation, σg of approximately 2.50 [the valueof σg is not a reference value, but is derived from the corresponding AMTD (ICRP, 1994b)].

948

2.2.2.2. Gases and vapours

949
950
951
952
953

For radionuclides inhaled as aerosols, the HRTM assumes that total and regional
deposits in the respiratory tract are determined only by the size distribution of the inhaledparticles. The situation is different for gases and vapours, for which deposition in the respiratory
tract depends entirely on the chemical form. In this context, deposition refers to how much of
the material in the inhaled air remains in the body after exhalation. Almost all inhaled gas
30

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

954
955
956
957
958
959
960
961
962
963
964
965
966

molecules contact airway surfaces, but usually return to the air unless they dissolve in, or react
with, the surface lining. The fraction of an inhaled gas or vapour that is deposited in each region
thus depends on its solubility and reactivity.
As for particulate forms of radionuclides, default parameter values are provided for use
in the absence of more specific information. The general defaults for gases and vapours are
100% total deposition in the respiratory tract (regional deposition: 20% ET 2, 10% BB, 20% bb
and 50% AI) with Type F absorption (Section 2.2.4). This classification is somewhat different
from that recommended in Publication 66, but simpler to apply. In particular, it is assumed bydefault that there is no deposition in ET 1. The SR-0, -1, -2, classification described in
Publication 66 and applied in Publication 71 was not found to be helpful and is not used here.
This series of reports covers gaseous and vapour forms of compounds of a number of
elements, including hydrogen, carbon, sulphur and iodine. In each case, parameter values are
given for total deposition, regional deposition and absorption.

967

2.2.3. Clearance: particle transport

968
969
970
971
972
973
974
975

The model describes several routes of clearance from the respiratory tract (Fig. 2.3).
Some material deposited in ET1 is removed by extrinsic means such as nose-blowing. In otherregions, clearance is competitive between the movement of particles towards the alimentarytract and lymph nodes (particle transport), and the absorption into blood of material from theparticles in the respiratory tract. Removal rates due to particle transport and absorption to blood
are taken to be independent of each other. It is further assumed that all clearance rates are
independent of age and sex.

976
977
978
979
980
981
982
983
984
985
986

Fig. 2.3. Routes of clearance from the respiratory tract. ET1: anterior nasal passage. Taken from
ICRP (2015).
As in the original HRTM, it is assumed that particle transport rates are the same for allmaterials. A generic compartment model is therefore provided to describe particle transport ofall materials. The revised particle transport model adopted in Publication 130 (ICRP, 2015),
and applied in this series of reports, is shown in Fig. 2.4. (Annex A of Publication 130 gives
details of the the revisions made.) Reference values of rate constants were derived, as far as
possible, from human studies, since particle transport rates are known to vary greatly among
mammalian species.

31

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

987
988
989
990
991
992
993
994
995
996
997
998
999
1000
1001
1002
1003
1004
1005
1006
1007
1008

1009
1010
1011
1012
1013
1014
1015
1016

The clearance rates for most of the material deposited in the conducting airways(regions ET1, ET2, BB and bb) are based on the results of human volunteer experiments. During
breathing through the nose, approximately 65% of the deposit in the ET airways is depositedin the anterior nasal passage, ET1, and is cleared with a half-time of approximately 8 h (rate of
2.1 d–1): approximately one-third by nose blowing, and two-thirds by transfer to ET2. This is
implemented with particle transport rates of 0.6 d–1 from compartment ET1 to the Environment
and 1.5 d–1 from ET1 to compartment ET′2 (Fig. 2.4). Most particles deposited in ET2, ortransferred to it from other regions (ET 1 and BB), are cleared rapidly by mucociliary action to
the throat and swallowed with a time scale of approximately 10 min. This is represented byclearance from the compartment ET′2 to the oesophagus at a rate of 100 d–1.
Throughout the bronchial tree (BB and bb regions), mucus velocities generally increase
towards the trachea, so that residence times range from a few days in the smallest, most distal,
bronchioles to less than 1 h in the trachea and main bronchi. This is represented by clearance
rates of 0.2 d–1 (half-time approximately 3.5 d) from compartment bb′ to compartment BB′, and10 d–1 (half-time approximately 2 hours) from BB′ to ET′2.
Experiments in several animal species have shown that a very small fraction of particles
deposited in the conducting airways is retained (sequestered) in the airway wall. To takeaccount of this, it is assumed that 0.2% of material deposited in regions ET 2, BB and bb isretained in the airway wall (compartments ET seq, BBseq, and bbseq respectively). Material iscleared from these compartments to regional lymph nodes at a rate of 0.001 d –1 (half-time
approximately 700 d).

Fig. 2.4. Compartment model representing time-dependent particle transport from each
respiratory tract region in the revised Human Respiratory Tract Model. Taken from ICRP
(2015). Rates shown alongside arrows are reference values in units of d–1. It is assumed that
0.2% of material deposited in the posterior nasal passage, pharynx, and larynx (ET2), bronchi(BB), and bronchioles (bb) is retained in the airway wall (ETseq, BBseq, and bbseq, respectively).
ET1: retention of material deposited in the anterior nose (region ET 1, which is not subdivided);
ETseq: long-term retention (t ½ approximately 700 d) in airway tissue of a small fraction of32

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

1017
1018
1019
1020
1021
1022
1023
1024
1025
1026
1027
1028
1029
1030
1031
1032
1033
1034
1035
1036
1037
1038
1039
1040
1041
1042
1043

particles deposited in the nasal passages; LN ET: lymphatics and lymph nodes that drain the ET
regions; LNTH: lymphatics and lymph nodes that drain the TH regions; ET′2 short-term
retention (t ½ approximately 10 min) of the material deposited in the posterior nasal passage,
larynx and pharynx (ET2 region) except for the small fraction (taken to be 0.002) retained in
ETseq; BB′: retention (t ½ approximately 100 min) of particles in the BB, with particle transport
to ET′2; bb′: retention (t½ approximately 3.5 d) of the particles in the bb, with particle transport
to BB′; BBseq: long-term retention (t ½ approximately 700 d) in airway walls of a small fractionof the particles deposited in the bronchial region; bbseq: long-term retention (t ½ approximately
700 d) in airway walls of a small fraction of the particles deposited in the bronchiolar region;
ALV: retention (t ½ approximately 250 d) of particles deposited in the alveoli. A fraction (0.67)
of the deposit is removed by particle transport to the ciliated airways (bb′), while the remainder
penetrates to the interstitium (INT); INT: very long-term retention (t ½ approximately 60 y) of
the particles deposited in the alveoli that penetrate to the interstitium: the particles are removed
slowly to the lymph nodes.
Human lung clearance has been quantified in several experimental studies for up to
approximately 1 y after inhalation, by which time approximately 50% of the deposit in the AI
region remained. Measurements of activity in the chest after occupational exposure, and ofactivity in the lungs at autopsy, show that some material can be retained in the lungs for decades(ICRP, 1994b). This is represented in the revised model by deposition in the alveolar
compartment (ALV), which clears at an overall rate of 0.003 d–1 (half-time of approximately
250 d): to the bronchial tree (compartment bb′) at a rate of 0.002 d –1 and to the interstitialcompartment (INT) at a rate of 0.001 d–1. Compartment INT clears very slowly to the regional
lymph nodes (rate of 0.00003 d–1). Thus, approximately 33% of the deposit in the AI region issequestered in the interstitium.
Fig. 2.4 as it stands would describe the retention and clearance of an insoluble material.
However, as noted above, there is in general simultaneous absorption to blood.

1044

2.2.4. Clearance: absorption to blood

1045
1046
1047
1048
1049
1050
1051
1052
1053
1054
1055
1056
1057
1058
1059
1060
1061
1062
1063

Absorption to blood depends on the physical and chemical form of the depositedmaterial. In both the original and revised HRTM, it is assumed (by default) to occur at the samerate in all regions (including the lymph nodes), except ET1 for which it is assumed that noabsorption takes place. It is recognised that absorption is likely to be faster in the AI region
where the air-blood barrier is thinner than in the conducting airways (ET, BB and bb regions),
but there is insufficient information available to provide a general systematic basis for taking
this into account, such as a scaling factor for different rates in different regions.
In the HRTM, absorption is treated as a two-stage process: dissociation of the particles
into material that can be absorbed into blood (dissolution); and absorption into blood of soluble
material and of material dissociated from particles (uptake). The clearance rates associated withboth stages can be time-dependent.
Dissolution: both the original and revised HRTM use the same simple compartment
model to represent time-dependent dissolution. It is assumed that a fraction (fr) dissolves
relatively rapidly, at a rate sr, and the remaining fraction (1 – fr) dissolves more slowly, at a rate
ss [Fig. 2.5(a)].
A limitation of this system is that it can only represent an overall dissolution rate that
decreases with time. To overcome this, Publication 66 also describes a more flexible system,
shown in Fig. 2.5(b). In this, the material deposited in the respiratory tract is assigned tocompartments labelled ‘Particles in initial state’ in which it dissolves at a constant rate sp.

33

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

1064
1065
1066
1067
1068
1069
1070
1071
1072
1073
1074

1075
1076
1077
1078
1079
1080
1081
1082
1083
1084
1085
1086
1087
1088
1089
1090
1091
1092
1093
1094
1095
1096
1097
1098
1099
1100
1101

Material is simultaneously transferred (at a constant rate spt) to a corresponding compartment
labelled ‘Particles in transformed state’ in which it has a different dissolution rate, st. With thissystem, the initial dissolution rate is approximately sp and the final dissolution rate isapproximately st. Thus, with a suitable choice of parameters, including st > sp, an increasing
dissolution rate can be represented. The ratio of sp to spt approximates to the fraction that
dissolves rapidly.
It may be noted that any time-dependent dissolution behaviour that can be represented
using the model shown in Fig. 2.5(a) can also be represented by the model shown in Fig. 2.5(b)with a suitable choice of parameter values. Thus, if the dissolution rate decreases with time, as
is usually the case, either system could be used, and would give the same results, with thefollowing values:
sp = ss + fr (sr – ss)(2.1)
spt = (1 – fr) (sr – ss)st = ss
However, the reverse is not true, as noted above.
The system shown in Fig. 2.5(b) was applied by default in earlier publications (ICRP,
1994a, 1995b, 1997). The additional flexibility it provides is, however, rarely required inpractice. The simpler approach, shown in Fig. 2.5(a), is therefore adopted now as the default,
with the more flexible approach retained as an alternative. Examples of materials that show
dissolution rates that increase with time, which have been represented by ‘particles in initialstate’ and ‘particles in transformed state’, including plutonium-238 dioxide, are given in theelement sections in OIR: Parts 3 and 4 (ICRP, 2017, 2019).
Uptake: uptake to blood of dissolved material is usually assumed to be instantaneous.
For some elements, however, part of the dissolved material is absorbed rapidly into blood, but
a significant fraction is absorbed more slowly because of binding to respiratory tract
components. To represent time-dependent uptake, it is assumed that a fraction (fb) of the
dissolved material is retained in the ‘bound’ state, from which it goes into blood at a rate sb,
while the remaining fraction (1 – fb) enters blood instantaneously (Fig. 2.5). In the model,material in the ‘bound’ state is not cleared by particle transport processes, but only by uptake
to blood. Thus, only one ‘bound’ compartment is required for each region, except for ET 1, fromwhich no absorption takes place.
The system shown in Fig. 2.5 applies to each of the compartments in the particle
transport model shown in Fig. 2.4. It is assumed that no absorption takes place from ET1, but
if the model in Fig. 2.5(a) is used, the ET1 deposit still has to be partitioned between fast andslow compartments because material is cleared from ET 1 to ET2, from which absorption doestake place.
For all elements, default values of parameters are recommended, according to whether
the absorption is considered to be fast (Type F), moderate (M) or slow (S). For gases or vapours,
instantaneous uptake to blood may be recommended: Type V (very fast).

34

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

1102
1103
1104
1105
1106
1107
1108
1109
1110
1111
1112
1113
1114
1115
1116
1117
1118
1119
1120
1121
1122
1123

Fig. 2.5. Alternative compartment models representing time-dependent absorption to blood(dissolution and uptake). In the model shown in Fig. 2.5(a), a fraction fr of the deposit is initiallyassigned to the compartment labelled ‘Rapid dissolution’, and the rest of the deposit (1 – fr) is
initially assigned to the compartment labelled ‘Slow dissolution’. In the model shown in Fig.
2.5(b), all the deposit is initially assigned to the compartment labelled ‘Particles in initialstate’, and material in the compartment labelled ‘Particles in transformed state’ is subject toparticle transport at the same rate as material in the compartment labelled ‘Particles in initialstate’. Material in the compartment labelled ‘Bound material’ is not subject to particle
transport and is cleared only by uptake into blood.
fr: fraction of the deposit that dissolves rapidly, at a rate sr; (1 – fr): fraction of deposit that
dissolves more slowly, at a rate ss; fb: fraction of the dissolved material that is retained in thebound state and from which it goes to blood at a rate sb; sr: rate of rapid dissolution; ss: rateof slow dissolution; sb: transfer rate from the bound state to the blood; spt: transfer rate ofmaterial from the compartment ‘Particles in initial state’ to the compartment ‘Particles intransformed state’; sp: dissolution rate of material from compartment ‘Particles in initialstate’; st: dissolution rate of material from the compartment ‘Particles in transformed state’.
The original default reference values for Types F, M and S given in Publication 66(ICRP, 1994b) were not based on reviews of experimental data but on comparison with particle
transport rates. For example, the value of 100 d–1 for the rapid dissolution rate, sr, was chosen
to equal the particle clearance rate from the nose (ET 2) to the throat.

35

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

1124
1125
1126
1127
1128
1129
1130
1131
1132
1133
1134
1135
1136
1137
1138
1139
1140
1141
1142
1143
1144
1145
1146
1147
1148
1149
1150
1151
1152
1153
1154
1155
1156
1157
1158
1159
1160
1161
1162
1163
1164
1165

In developing OIR: Parts 2 ‒ 5 (ICRP, 2016a, 2017, 2019, 2022), detailed reviews wereconducted of the absorption characteristics of inhaled materials relevant to radiologicalprotection. They are summarised in the inhalation sections of each element.
Where information was available, specific parameter values were derived fromexperimental data from both in-vivo and in-vitro studies. These provided a database to give
guidance on selecting values that are representative of materials that are generally considered
to clear at ‘fast’, ‘moderate’ or ‘slow’ rates. Values selected on that basis for default Type F,
M and S have been adopted in the revised HRTM used in this series of documents (see below).
Material-specific rates of absorption have been adopted in the element sections of the
OIR for a limited number of selected particulate materials, i.e. those for which:• There are in-vivo data from which specific parameter values can be derived;• Results from different studies are consistent;• It was considered that occupational exposure to the material is likely; and• The specific parameter values are sufficiently different from default Type F, M or S
parameter values to justify providing additional specific dose coefficients.
Relatively more use is made of material-specific parameter values for gases and vapours
than for particulate materials, because of the dependence of deposition in the respiratory tract
on chemical form.
Other materials were assigned to default types using suitable experimental data if
available, as reviewed in the element sections. Publication 66 (ICRP, 1994b) did not givecriteria for assigning materials to absorption types on the basis of experimental results. Criteria
were developed in Publication 71 (ICRP, 1995b) and their application was discussed further in
Supporting Guidance 3 (ICRP, 2002b). Type M is assumed for all particulate forms of mostelements in the absence of information on which assignment to an absorption type could be
made. A material is assigned to Type F if the amount absorbed into blood by 30 d after an acuteintake is greater than the amount that would be absorbed over the same period from ahypothetical material with a constant rate of absorption of 0.069 d–1 (corresponding to a halftime of 10 d) under identical conditions. Similarly, a material is assigned to Type S if theamount absorbed into blood by 180 d after an acute intake is less than the amount that would
be absorbed over the same period from a hypothetical material with a constant rate ofabsorption to blood of 0.001 d–1 (corresponding to a half-time of approximately 700 d) underidentical conditions. Particulate forms of each element were assigned to the HRTM default
absorption Types using these criteria. However, to make use of the limited information
available for many materials, some flexibility was applied (ICRP, 2015).
For soluble (Type F) forms of each element, estimates were made of the overall rate ofabsorption from the respiratory tract to blood, where information was available. It is assumed
that this can be represented by the rapid dissolution rate, sr, which is a characteristic of theelement. Because of the wide variation between elements in the estimated value of sr, elementspecific values were adopted in the OIR series and in this series of documents for thoseelements for which an estimate of the value could be made (Table 2.5).

36

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

1166
1167

Table 2.5. Element-specific absorption parameter values used in the OIR: Parts 2‒5 and in thisseries of reports.
Element

OIR Part Rapid
dissolution
rate, sr (d–1)

Hydrogen2
Beryllium
5
Carbon2
Fluorine
5
Sodium5
Magnesium 5
Aluminium 5
Silicon5
Phosphorus 2
Sulphur2
Chlorine
5
Potassium
5
Calcium
2
Scandium
5
Titanium
5
Vanadium5
Chromium
5
Manganese 5
Iron
2
Cobalt2
Nickel5
Copper
5
Zinc
2
Gallium
5Germanium 5
Arsenic
5
Selenium5
Bromine5
Rubidium
5Strontium
2
Yttrium
2
Zirconium
2
Niobium2
Molybdenum 2
Technetium 2
Ruthenium
3
Rhodium
5
Palladium5
Silver
5

100
30
100
30
30
30
30
30
1
30
30
30
70
30
30
30
30
30
100
1
3
30
30
30
30
30
30
30
30
30
1
30
30
30
100
30
30
30
1

Bound
fraction,fb

Uptake rate,sb (d–1)

0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0.03
0
0
0
0
0
0
0
0
0
0

–
–
–
–
–
–
–
–
–
–
–
–
–
–
–
–
–
–
–
0.002
–
–
–
–
–
–
–
–
–
–

0
0
0
0
0.5
0
0
0

–
–
–
–
0.1
–
–
–

37

Absorption from thealimentary tract*, fA
SolubleRelatively
insoluble
1
0.1
0.005
1
1
1
0.5
0.2
0.003
1×10‒4
0.5
0.01
0.8
1
0.1
1
1
0.4
0.001
0.001
0.2
0.01
0.01
0.05
0.1
0.1
0.05
0.05
0.01
0.5
0.5
0.001
1
1
0.3
0.8
1
1
0.25
0.01
‒4
1×10
0.002
0.01
0.9
0.05
0.9
0.05
0.05
0.005
0.05

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

1168
1169
1170
1171
1172

Bound
fraction,fb

Uptake rate,sb (d–1)

Element

OIR Part Rapid
dissolution
rate, sr (d–1)

Cadmium
IndiumTin
Antimony
Tellurium
IodineCaesium
Barium
Cerium‡Hafnium
Tantalum
Tungsten
Rhenium
OsmiumIridium
PlatinumGold
Mercury
Thallium
Lead
BismuthPolonium
Astatine
Radon
Francium
RadiumActinium
Thorium
Protactinium
Uranium
Neptunium
Plutonium§
Americium
CuriumBerkelium
Californium
Einsteinium
Fermium

5
5
5
3
3
3
3
3
4
5
5
5
5
5
3
5
5
5
5
3
3
3
5
3
5
3
4
3
4
3
4
4
4
4
4
4
4
4

0
0
0
0
0
0
0
0
0.07
0
0
0
0
0
0
0
0
0.24
0
0.5
0
0
0
0
0
0
0.002
0
0
0
0
0.002
0.002
0.002
0.002
0.002
0.002
0.002

–
–
–
–
–
–
–
–
0.02
–
–
–
–
–
–
–
–
2.1
–
1.7
–
–
–
–
–
–
0
–
–
–
–
0
0
0
0
0
0
0

30
30
30
30
50
100
100
20
1
30
30
30
30
30
30
30
30
30
30
100
1
3
30
30
10
0.4
50
50
10
30
0.4
0.4
0.4
0.4
0.4
0.4
0.4

*

Absorption from thealimentary tract*, fA
SolubleRelatively
insoluble
0.05
0.005
0.02
0.05
0.3
1
1
0.1
0.2
1×10‒4
5×10‒4
0.002
0.001
0.5
0.01
0.9
0.01
0.01
0.01
0.001
0.1
0.1
1
0.2
0.05
0.1
1
1
1
0.2
5×10‒4
5×10‒4
5×10‒4
0.02
0.002
‒4
5×10
5×10‒4
1×10‒5‒4
5×10
5×10‒4
5×10‒4
5×10‒4
5×10‒4
5×10‒4Adult values for ingested materials. Applies to all forms unless more than one value is given. In those cases
described in this table as ‘Soluble’ and ‘Relatively insoluble’; other values apply to some elements ingested indiet: see element section for details.
‡
Parameter values applied to the rest of the lanthanide series: lanthanum (Atomic number Z=57) to lutetium(Z=71).

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DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

1173
1174
1175
1176
1177
1178
1179
1180
1181
1182
1183
1184
1185
1186
1187
1188
1189
1190
1191
1192
1193
1194
1195
1196
1197
1198
1199
1200
1201

§

Plutonium respiratory tract parameter values are applied to the higher actinides series: americium (Z=95) tofermium (Z=100), and to actinium by analogy with americium.

Evidence for retention in the bound state, rather than by transformation into particulatematerial, may be in one or more forms: e.g. systemic uptake rather than faecal clearance of theretained material; slower clearance than for insoluble particles deposited in the same region of
the respiratory tract; or autoradiography showing diffuse rather than focal retention of activity.
The bound state was included in the model mainly to take account of slow clearance ofsoluble materials from the alveolar region. By default, it would be assumed that the same boundstate parameter values apply in all regions. In some cases (e.g. a long-term bound state for along-lived α-emitter), this could lead, unintentionally, to high calculated doses to the BB andbb regions. Because of the high weighting (apportionment factors) that these tissues are given,
this could in turn lead to high calculated equivalent doses to the lungs. Hence, in the OIR andin this series of documents, it is assumed that for those elements for which a bound state isadopted (fb> 0), it is applied in the conducting airways (ET 2, BB and bb regions) only if thereis experimental evidence to support that.
For some elements, for which there is little or no experimental data on absorption fromthe respiratory tract, element-specific absorption parameter values (sr, fb and sb) have been
based on chemical analogy, notable for some of the lanthanides and actinides (Table 2.5).
As noted above, the specific parameter values derived from experimental data (fromboth in-vivo and in-vitro studies) provided a database to give guidance on selecting values thatare representative of materials that are generally considered to clear at ‘fast’, ‘moderate’ or‘slow’ rates. This was not a representative survey from which central values could be derived
by objective statistical means. Rather, it provided a basis for informing judgements, as
described in Annex A of Publication 130 (ICRP, 2015). Updated default values for the revised
HRTM and applied in this series of documents are given in Table 2.6.
Table 2.6. Default absorption parameter values for Type F, M, and S materials *,† in the revised
Human Respiratory Tract Model.
Type
Fraction dissolved rapidly
Dissolution rates:
Rapid (d–1)
Slow (d–1)

1202
1203
1204
1205
1206
1207
1208
1209
1210
1211
1212
1213
1214
1215
1216
1217

fr

F(fast)1

M (moderate)
0.2

S (slow)
0.01

sr
ss

30‡
–

3§
0.005

3§
10–4

*Reference values, given with sufficient precision for calculation purposes, which may be greater than would bechosen to reflect the certainty with which the average value of each parameter is known.
†
The bound state is also used for default types of some elements (Table 2.5).
‡
Element-specific rapid dissolution rates are adopted for Type F forms of many elements (Table 2.5).
§
The element-specific value for Type F is also used for Types M and S if it is less than 3 d –1.

The default absorption rates, expressed as approximate half-times, and thecorresponding amounts of material deposited in each region that reach blood (from therespiratory tract) can be summarised as follows.
• Type V: 100% absorbed instantaneously. Regional deposition does not need to beassessed for such materials, because in dose calculations, they can be treated as if they
were injected directly into blood.
• Type F: For the general default value of 30 d–1 for sr, 100% absorbed with a half-timeof approximately 30 min. There is rapid absorption of almost all material deposited inbb and AI, approximately 80% of material deposited in BB, approximately 25% ofmaterial deposited in ET2, and approximately 20% of material deposited in ET 1. The

39

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

1218
1219
1220
1221
1222
1223
1224
1225
1226
1227
1228
1229
1230
1231
1232
1233
1234
1235
1236
1237
1238
1239
1240
1241
1242
1243

other material deposited in BB and ET 2 is cleared to the alimentary tract by particle
transport.
• Type M: For the general default value of 3 d–1 for sr, 20% absorbed with a half-time of
approximately 6 h and 80% with a half-time of approximately 140 d. There is rapid
absorption of approximately 20%, 5%, 0.5% and 0.4% of material deposited in bb, BB,
ET2 and ET1, respectively. Approximately 80% of the deposit in AI eventually reaches
blood.
• Type S: For the general default value of 3 d–1 for sr, 1% absorbed with a half-time of
approximately 6 h and 99% with a half-time of approximately 7000 d. There is rapid
absorption of approximately 1%, 0.25%, 0.03% and 0.02% of material deposited in bb,
BB, ET2 and ET1, respectively. Approximately 30% of the deposit in AI eventuallyreaches blood.
For absorption Types F, M, and S, some of the material deposited in ET 1 is removedby extrinsic means. Most of the material deposited in the respiratory tract that is not absorbed
is cleared to the alimentary tract by particle transport. The small amounts transferred to lymph
nodes continue to be absorbed into blood at the same rate as in the respiratory tract.
For material cleared from the respiratory tract to the alimentary tract, the default
assumption made is that fractional absorption in the alimentary tract is the product of fr and fA,
where fA is fractional absorption in the alimentary tract for relatively soluble forms of theelement (Section 2.3.3) and for the Reference Individual. This approach was based on theconsideration that fr represents the soluble fraction of the material, which is available forabsorption in the alimentary tract, and fA represents alimentary tract absorption of the soluble
fraction. In taking this approach, it was recognised that it is important not to overestimate
absorption in the alimentary tract greatly, because this could lead to overestimation of predicted
urinary excretion, and hence corresponding under-estimation of intakes from urine bioassay
measurements.

1244

2.2.5. Progeny radionuclides formed in the respiratory tract

1245
1246
1247
1248
1249
1250
1251
1252
1253
1254
1255
1256
1257
1258
1259
1260
1261
1262
1263

The following applies specifically to progeny formed in the respiratory tract after
inhalation of the parent radionuclide. Progeny radionuclides formed before inhalation andinhaled with the parent are generally treated as separate intakes, and so each progeny
radionuclide inhaled is assumed to adopt the biokinetics appropriate to the element of which it
is an isotope. Many issues relating to the behaviour of progeny in the respiratory tract arise inconnection with the natural decay series, which are therefore shown in ANNEX A, Figs. B.1(uranium-238 series), B.2 (uranium-235 series) and B.3 (thorium-232 series).
Publication 66 (Para. 272, ICRP, 1994b) noted that it would be expected that:• the rate at which a particle dissociates is determined by the particle matrix and therefore
the dissolution parameter values of the inhaled material would be applied to progeny
formed within particles in the respiratory tract (‘shared kinetics’);• progeny radionuclides formed as noble gases, including radon, would be exceptions
because they would diffuse from the particles; and• the behaviour of dissociated material would depend on its elemental form, and so, forexample, bound fraction parameter values for a progeny radionuclide would not be
those of the parent (‘independent kinetics’).
Nevertheless, in previous applications of the HRTM [e.g. Publications 71 and 72(ICRP, 1995b, 1995c)], with the exception of noble gases, the absorption parameter values ofthe parent were applied to all members of the decay chain formed in the respiratory tract (shared
40

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

1264
1265
1266
1267
1268
1269
1270
1271
1272
1273
1274
1275
1276
1277
1278
1279
1280

kinetics). After detailed consideration of the issues involved (Annex A of Publication 130,
ICRP, 2015), the same approach is taken in the OIR and in this series of documents.
Nevertheless, where experimental results are available which allow directcomparisons between the absorption behaviour of a parent radionuclide, and that of its
radioactive progeny, they are summarised in the inhalation section of the parent element (e.g.
uranium, thorium).
For calculation purposes, the assumption that noble gases, including radon, that areformed as progeny within the respiratory tract escape from the body at a rate of 100 d–1 isapplied in this series of documents.
For material cleared from the respiratory tract to the alimentary tract, fractional
absorption in the alimentary tract is assumed to be fr* fA (see above). In the case of progeny
formed in the respiratory tract, fr is taken to be that of the parent deposited in the respiratory
tract (reflecting the particle matrix), but the value of fA is taken to be that of the progeny
radionuclide entering the alimentary tract.
Following absorption to blood, progeny formed in the respiratory tract are assumed tobehave according to the systemic model applied to the element as a progeny of the parent
radionuclide.

1281

2.2.6. Respiratory tract dosimetry

1282
1283
1284
1285
1286
1287
1288
1289
1290
1291
1292
1293
1294
1295
1296
1297
1298
1299
1300
1301
1302
1303
1304
1305
1306
1307
1308
1309
1310

The HRTM dosimetric model is described in Chapter 8 of Publication 66 (ICRP,
1994b). For dosimetric purposes, the respiratory tract is treated as two tissues: the TH and ET
airways. These are sub-divided into regions, primarily based on considerations of differences
in sensitivity to radiation. The TH regions are BB, bb, AI, and LN TH. The ET regions are ET1,
ET2, and LNET (Fig. 2.2).
The dose to each respiratory tract region is calculated as the average dose to the target
region which contains the target cells at risk. In the AI region and lymph nodes (LN TH and
LNET), the cells at risk are thought to be distributed throughout the region, and the average doseto the whole lung and the lymph nodes, respectively, is calculated. For the regions making up
the conducting airways (ET1, ET2, BB and bb), the target cells are considered to lie in a layerof tissue at a certain range of depths from the airway surface and the average dose to this layer
is calculated. The target cells identified in ET 1, ET2, BB and bb, assumed to be independent ofage and sex, are given in Table 2.7. The masses of tissue containing target cells in each region,
for each age and sex, for use in dose calculations, are given in Table 2.8.
In each of these regions, there are also several possible source regions. For example,
in the bb region, particles retained in the airway wall (bb seq) are taken to be in a macrophagelayer at a depth of 20–25 μm (i.e. below the target cells); activity ‘bound’ to the epithelium is
uniformly distributed in it; and account is also taken of irradiation from activity present in the
AI region. In the original HRTM, there were two phases of mucociliary clearance: activity inthe fast phase of clearance was taken to be in a mucus layer above the cilia; and activity in theslow phase of clearance was taken to be in the mucus between the cilia. In the revised HRTM,
there is only one phase of clearance, and activity is distributed throughout the mucus as
specified below.
For each source/target combination, Publication 66 (ICRP, 1994b) provides absorbed
fractions for nonpenetrating radiations: α, β, and electrons; in each case, as a function of energy.
Since these absorbed fractions are not represented in the voxel phantoms because of inadequate
spatial resolution, the values given in Publication 66 (ICRP, 1994b) are used in the OIR and in
this series of reports. They were derived using a single cylindrical geometry to represent eachregion of the conducting airways (ET1, ET2, BB, bb): the representative bronchus for BB having

41

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

1311
1312
1313
1314
1315
1316
1317
1318
1319
1320
1321
1322
1323
1324
1325
1326
1327
1328
1329

a diameter of 5 mm and the representative bronchiole for bb having a diameter of 1 mm. The
absorbed fractions for the single phase BB and bb source regions were derived as the thicknessweighted sum of the slow and fast clearing source regions, as tabulated in Publication 66 (ICRP,
1994b). Absorbed fractions were considered to be age-independent. The age-dependence ofthe target mass created age-dependence in the specific absorbed fraction.
To take account of differences in sensitivity between tissues, the equivalent dose, Hi,
to each region, i, is multiplied by a detriment apportionment factor, the Assigned fraction, Ai,
representing the region's estimated sensitivity relative to that of the whole organ. The
recommended values of Ai are also given in Table 2.7. In Publication 103 (ICRP, 2007), theET and TH lymph nodes were included in the tissue ‘lymphatic nodes’, which is itself includedin the list of remainder tissues and organs (Table 1.3), and so are no longer included in the ET
and TH airways, respectively, as they were in the original HRTM. The fractions, Ai, of wT thatthey were assigned in Publication 66 are reassigned to other regions in Table 2.7. The weighted
sum of the equivalent dose, Hi, to each region, is the equivalent dose to the ET or TH airways,
respectively:
The tissue weighting factor, wT of 0.12 specified for lung in Publication 103 (ICRP,
2007) is applied to the equivalent dose to the TH region, HTH. The ET airways are included in
the list of remainder tissues and organs (Table 1.3).
𝐻ET = 𝐻ET1 𝐴ET1 + 𝐻ET2 𝐴ET2

(2.2)

𝐻TH = 𝐻BB 𝐴BB + 𝐻bb 𝐴bb + 𝐻AI 𝐴AI
Where: 𝐻BB =

1330

2

Table 2.7. Target regions of the respiratory tract (independent of age and sex).
TissueRegionTarget cells

ET

ET1
ET2

Basal
Basal

TH

BB

Secretory (BBsec)
Basal (BBbas)
Secretory

bb
AI

1331
1332
1333
1334
1335
1336
1337
1338
1339

𝐻𝐵𝐵𝑠𝑒𝑐 +𝐻𝐵𝐵𝑏𝑎𝑠

Mucus
thickness*
(μm)
‒
15

Epithelial
thickness*
(μm)
50
50

Depth oftarget cells*
(μm)
40‒50
40‒50

Assigned
fraction*
Ai of wT
0.001
0.999

5
5
2
‒

55
55
15
‒

10‒40
35‒50
4‒12

1/3

‡

1/3
1/3

ET, extrathoracic; TH, thoracic; ET1, anterior nasal passage; ET2, posterior nasal passage, pharynx and larynx;
BB: bronchial; bb: bronchiolar; AI: alveolar‒interstitial.
*
Reference values, given to sufficient precision for calculation purposes, which may be greater than would bechosen to reflect the certainty with which the average value of each parameter is known. For the BB, bb and AI
regions, each value of Ai is exactly one-third.
‡
Average dose to region calculated.

42

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

1340

Table 2.8. Masses of target regions in the respiratory tract in several Reference Individuals *Region
Age

3 mo

1y

Mass (kg)
10 y

1341
1342
1343
1344
1345
1346
1347
1348
1349
1350

15 y
Adult
Adult
(Male)(Male)(Female)ET1
2.792×10–6 4.133×10–6 8.284×10–6 1.263×10–5 1.852×10–5 2.000×10–5 1.729×10–5
ET2
6.28×10–5
9.30×10–5
1.864×10–4 2.843×10–4 4.166×10–4 4.500×10–4 3.890×10–4
BBsec‡
2.531×10–4 3.105×10–4 4.695×10–4 6.220×10–4 8.169×10–4 8.648×10–4 7.771×10–4‡
BBbas
1.266×10–4 1.553×10–4 2.348×10–4 3.110×10–4 4.085×10–4 4.324×10–4 3.885×10–4
bb
5.014×10–4 5.967×10–4 9.469×10–4 1.305×10–3 1.768×10–3 1.949×10–3 1.874×10–3
AI§
9.04×10–2
1.51×10–1
3.01×10–1
4.97×10–1
8.59×10–1
1.100
9.041×10–1
ET1, anterior nasal passage; ET2, posterior nasal passage, pharynx and larynx; BBsec secretory cells in the bronchialregion; BBbas; basal cells in the bronchial region; bb: bronchiolar; AI: alveolar‒interstitial.
*
Reference values, given to sufficient precision for calculation purposes, which may be greater than would bechosen to reflect the certainty with which the average value of each parameter is known.
†
Adult Male and Adult Female values were taken from Table 3.3 of Publication 130 (ICRP, 2015). Values forother subjects are taken from Table 10 of Publication 71 (ICRP, 1995b). These values are given to two significant
figures in Table 5 of ICRP Publication 66 (ICRP, 1994b).
‡
Masses for BBsec and BBbas are the masses of bronchial epithelium through which the secretory cells and basal
cells, respectively, are distributed and are based on reference values of airway dimensions.
§
The mass of AI includes blood but excludes lymph nodes.

1351

2.3. Human Alimentary Tract Model (HATM)

1352
1353
1354
1355
1356
1357
1358
1359
1360

The HATM described in Publication 100 (ICRP, 2006) has been used in this reportseries in replacement of the Publication 30 (ICRP, 1979) model of the gastrointestinal tract..
This replacement was motivated by a number of developments, including the availability of
improved information on the gut transit of materials, and developments in our understandingof the location of sensitive cells. The model structure is shown in Fig. 2.6, and parameter values
are shown in Table 2.10. As for the HRTM, an important feature of the HATM is the specificcalculation of doses to target regions containing sensitive cells for cancer induction, and theconsideration of specific absorption and/or retention values, where information is available.
The HATM and the HRTM are compatible and inter-connected, as shown in Fig. 2.6.

1361

2.3.1. Structure

1362
1363
1364
1365
1366
1367
1368
1369
1370
1371
1372

The HATM depicts the entry of a radionuclide into the oral cavity by ingestion or into
the oesophagus after particle transport from the respiratory tract. It describes the sequential
transfer through all alimentary tract regions, including the oral cavity, oesophagus, stomach,small intestine, and segments of the colon, followed by emptying in faeces. Doses arecalculated for all these regions. The colon is partitioned, for the purposes of dose calculations,
into right colon, left colon and rectosigmoid (the sigmoid colon and rectum) based on theavailability of transit time data. The rectum is included with the sigmoid colon, as therectosigmoid, because of difficulties in determining transit times separately and because therectum does not have a specific wT value. Total colon doses are combined as a mass-weighted
mean to include the right colon, left colon and rectosigmoid:
𝐻colon =5y

𝐻RC 𝑚RC + 𝐻LC 𝑚LC + 𝐻RS 𝑚RS
𝑚RC + 𝑚LC + 𝑚RS

1373

43

(2.2b)

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

1374
1375
1376
1377
1378

where mRC, mLC and mRS are the corresponding masses of three sections of the colon(Table 2.9).
Table 2.9. Typical values for masses of walls in the colon region (g) (from ICRP Publication
100)
SectionNewborn

1y

5y

Right colon

7

20

49

Left colon

7

20

Rectosigmoid

3

10

10 y

15 y

Adult

male

femalemale

female

85

122

122

150

145

49

85

122

122

150

145

22

40

56

56

70

70

1379

2.3.2. Model parameters

1380
1381
1382
1383
1384
1385

The HATM presents different transit times for solid foods, liquids, and total diet, inthe mouth, oesophagus and stomach. First-order kinetics is assumed. This is a considerable
simplification of the complex processes involved in transfer of material through the lumen of
the alimentary tract, but is expected to provide a reasonably accurate representation of the mean
residence time of a radionuclide in each segment of the tract.

1386
1387
1388
1389
1390

Fig. 2.6. Structure of the Human Alimentary Tract Model. The dashed boxes are included toshow connections between the HATM and the HRTM and systemic biokinetic models. Taken
from ICRP (2006).

44

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

1391

Table 2.10. Age-specific HATM transfer coefficients (per d) for total diet *,†Transfer coefficient‡ (d–1)
AgeAge
1 year
5–15 years
6480
6480

Adult male

From

To

O-cavity

Oesophag-c-FastAge
3 months
38,880O-cavity

Oesophag-c-Slow

4320

720

720

720

Oesophag-c-Fast

St-cont

21,60012,343

12,343

12,343

Oesophag-c-Slow

St-cont

2880

2160

2160

2160

St- cont

SI-cont

19.2

20.57

20.57

20.57

SI-cont

RC-cont

6

6

6

6

RC-cont

LC-cont

3

2.4

2.182

2

LC-cont

RSig-cont

3

2.4

2.182

2

RSig-contFaeces

2

2

2

2

6480

1392
1393
1394
1395
1396
1397
1398
1399
1400

*

1401

2.3.2.1. Modifying factors

1402
1403
1404
1405
1406
1407
1408

The default regional transit times given in the HATM are central estimates based oncollected data for a given sex, age group, and type of material (e.g. solids, liquids, caloric
liquids, or non-caloric liquids). As extensively illustrated in Publication 100 (ICRP, 2006),
transit of material through each of the major segments of the tract shows considerable interand intra-subject variability even under normal conditions. Extremely large deviations from thenorm may result from constipation, diarrhoea, unusual diet, pharmaceuticals, and a variety of
diseases that affect the nervous system or increase energy requirements, for example.

1409

2.3.2.2. Sex-specific values

1410
1411
1412
1413
1414
1415
1416

The HATM provides sex-specific parameter values for adults for dimensions andtransit times of contents through the regions. Although the dimensions of the stomach andintestines are generally smaller in females than males, the estimated central transit times
through these regions are approximately one-third greater in females than in males. However,taking into account the large variability in transit times through any region of the alimentarytract both in males and females, the Reference adult Individual is assigned the reference transit
times for the adult male.

1417

2.3.2.3. Material entering from the respiratory tract or in saliva

1418
1419
1420

Mucus and associated materials cleared from the respiratory tract enter the oesophagus
via the oropharynx. For ingested food and liquids, the HATM specifies two components ofoesophageal transit, representing relatively fast transfer of 90% of the swallowed material

Abbreviations: O-cavity = oral cavity content, Oesophag-c = oesophagus content, St = stomach, cont = content,
SI = small intestine, RC = right colon, LC = left colon, RSig = rectosigmoid.
†
Other transfer coefficients not given here are assumed to be zero unless specified in the relevant element section.
In most cases, uptake to blood from the alimentary tract is taken to occur from the SI contents, without retention
in
SI
wall.
The
correspondingtransfercoefficientis𝑓A ×𝜆SI,RC
‡

1− 𝑓A

, where λSI,RC is the transfer coefficient from SI contents to RC contents.

The degree of precision of the values given is for computational purposes and does not reflect the certainty withwhich the central values are known.

45

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

1421
1422
1423
1424

(mean transit time of 4 s (age 3 months) to 7 s (age 1 year and older) for total diet) and relatively
slow transit of the residual 10% (30 s (age 3 months) to 40 s (age 1 year and older) for totaldiet). It is assumed that the slower oesophageal transit time applies to all material cleared fromthe respiratory tract.

1425

2.3.3. Absorption from the alimentary tract

1426
1427
1428
1429
1430
1431
1432
1433
1434
1435
1436
1437
1438
1439
1440
1441
1442
1443
1444
1445
1446
1447
1448

Radionuclides may enter the alimentary tract: directly as a result of ingestion;
indirectly after inhalation and mucociliary escalation of particles from the respiratory tract tothe oropharynx and oesophagus; or in secretions such as saliva, bile, or gastric juice.
Alternatively, they may be produced in the alimentary tract by decay of a parent radionuclide.
The absorption of radionuclides to blood is specified in the HATM as a fraction of the amountentering the alimentary tract, with total absorption denoted as fA (ICRP, 2006). The model
structure allows for the use of data on absorption in any region, where information is available.
In most cases, no information will be available on the regional absorption of radionuclides, andthe default assumption is that all absorption takes place in the small intestine, i.e. fA= fSI. As adefault, it is also assumed that there is no recycling from the wall to the contents of thealimentary tract.
Some fA values recommended in this report are the same as the f1 values given
previously for use with the Publications 30, 56, 67 and 69 models (ICRP, 1979, 1980, 1981,
1988, 1990, 1993, 1995a) as there is not sufficient new information to warrant a revision in thevalue. Specific data of absorption from other regions are considered in the small number ofcases for which they were available, although in some cases (e.g. relatively long-lived isotopesof iodine), doses to alimentary tract regions and other tissues are insensitive to assumptions
regarding the site of absorption (ICRP, 2006).
The extent of absorption of radionuclides will depend on the element and its chemical
forms. Changes in chemical forms are likely to occur during digestive processes, beginning in
the mouth, but principally occurring in the stomach and the small intestine. These changes inchemical form or speciation will determine the availability of the radionuclide for absorption
and hence the extent of uptake through the intestinal epithelium to bloodstream (ICRP, 2006).

1449

2.3.3.1. Effect of chemical forms

1450
1451
1452
1453
1454
1455
1456
1457
1458
1459
1460
1461
1462
1463
1464
1465
1466

The values of f1 and fA recommended in Publication 30 (ICRP, 1979, 1980, 1981,1988) and in the OIR report series apply primarily to the intakes of chemical forms of theelements expected to be encountered in a workplace. These values are not necessarily
appropriate for environmental exposures. For example, occupational exposures may involve
ingestion of inorganic forms of radionuclides not normally present in the environment.
Environmental exposures mainly involve ingestion of radionuclides incorporated into foodmaterials, bound to organic constituents of food, and/or inorganic forms present in food and/or
water. It has been shown that incorporation of radionuclides into food, which contains
complexing agents such as citrates, phytates, and other organic acids, may lead in general togreater absorption than ingestion of inorganic forms of an element, although for some elements(e.g. molybdenum) the reverse is true. This factor should be considered when extrapolating theresult of animal studies performed with inorganic forms of elements to humans ingesting
radionuclides in mixed diets containing a variety of potential complexing agents. The
absorption of radionuclides from drinking water may be increased when ingested after a period
without food.
Environmental exposures have been reviewed in the Publication 56 series (ICRP,
1990, 1993, 1995a) and in Publication 100 (ICRP, 2006). For elements with absorption fraction
46

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

1467
1468
1469
1470
1471

greater than 0.5 in ICRP Publication 30 and for which there was no specific information on
absorption from food, Publication 67 (ICRP, 1993) applied an absorption fraction of 1. Specificvalues proposed in the present report are based on the content of the above mentioned ICRP
Publications as well as on any more recent information on the fractional absorption of organic
forms of ingested radionuclides available from the scientific literature.

1472

2.3.3.2. Effects of age on absorption parameters

1473
1474
1475
1476
1477
1478
1479
1480
1481
1482
1483
1484
1485
1486
1487
1488
1489
1490
1491
1492
1493
1494
1495
1496
1497

There is evidence from animal experiments and some supporting human data thatabsorption of many elements is substantially greater in newborn mammals than in adults. Dataon the effect of age and other factors on the intestinal absorption of radionuclides have beenreviewed in the Publication 56 series in order to specify values of absorption fraction for use
in the calculation of age-related dose coefficients for members of the public (Table 2.11). Dose
coefficients were given for radioisotopes of 31 elements, considered to be of potential
importance in terms of public exposures, and for a number of age groups including 3-monthold infants and 1-year-old children. Absorption is greatest immediately after birth and decreases
progressively over the suckling period. Thus, it was considered likely that adult values ofabsorption will apply in many cases to intakes by weaned infants later in the first year of life.
Nevertheless, the approach adopted had been to specify infant values of absorption for the 3month-old infant that were taken to apply as averages over the first year of life. This wasrecognised as a conservative assumption, particularly when applied to the consumption of solid
foods in the latter part of the first year. The most appropriate use of the 3-month-old infant’svalues of absorption is in the calculation of dose coefficients for radionuclide ingestion inmothers’ milk (ICRP, 2004) and concurrent intakes in other forms during the first 6 months oflife. In the Publication 56 series, where no age-specific human or animal data were available,
for elements with a fractional absorption in the adult of 0.001 or less, a value 10 times the value
for the adult was assumed for the first year of life; for absorption fraction values between 0.01
and 0.5 in the adult, an increase by a factor of 2 was assumed; for absorption values greaterthan 0.5 in the adult, complete absorption was assumed in the first year of life. The same
approach is applied in this series.

1498
1499

*

Table 2.11. Fractional absorption values for adults and infants as used in ICRP publication 56
series, (from ICRP, 2006)
Element
Adult
3-month-old infant
H, C, Cs, S, Mo, I
1
1
Se
0.8
1
Zn, Tc, Po
0.5
1
*
*
Te, Sr , Ca
0.3
0.6
*
*
*
Ba , Ra , Pb
0.2
0.6
*
*
Co , Fe
0.1
0.6
Sb
0.1
0.2
Ru, Ni, Ag
0.05
0.1
U
0.02
0.04
Zr, Nb
0.01
0.02
Ce, Th, Np, Pu, Am
0.0005
0.005
Intermediate values for 1-, 5-, 10-, and 15-year-old children: 0.4 for Sr, Ca, and Pb; 0.3 for Co, Ra and Ba; and0.2 for Fe.

47

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

1500

2.3.3.3. Absorption fraction for progeny radionuclides produced in the alimentary tract

1501
1502
1503
1504

The default absorption fraction fA for a radionuclide X produced in the alimentary tract
by decay of an ingested parent radionuclide Y is the reference fA for X as a parent. If X has
multiple reference values corresponding to different chemical or physical forms, then thedefault fA is the highest reference value provided for X.

1505

2.3.3.4. Ingestion of inhaled materials

1506
1507
1508
1509
1510
1511
1512
1513
1514
1515
1516
1517
1518
1519
1520

For inhaled particles reaching the alimentary tract after clearance from the respiratory
tract, it is appropriate to take account of solubility in the lungs in specifying fA values. For someelements exhibiting a range in solubility according to their physicochemical form, there isevidence that the reduced solubility of Type M or S materials is also associated with reduced
intestinal absorption. For a radionuclide that is transferred from the respiratory tract to thealimentary tract, the default fA value is determined as the product of the fraction of inhaledmaterial with rapid dissolution (fr) for the absorption type and the fA value for soluble forms of
the element.
The default absorption fraction fA for a progeny radionuclide produced in the
respiratory or alimentary tract by decay of a parent radionuclide inhaled is the product of fr forthe assigned absorption type and the reference fA for for the progeny radionuclide wheningested as a parent radionuclide. If the progeny radionuclide has multiple reference values offA when ingested as a parent, corresponding to different chemical or physical forms, then thedefault value of fA for the progeny radionuclide produced in the respiratory or alimentary tract
is the product of fr for the absorption type of the parent and the highest reference value provided.

1521

2.3.3.5. Reabsorption of material

1522
1523
1524
1525
1526
1527
1528
1529

Some of the biokinetic models used in this report series to predict the systemic
behaviour of radionuclides depict secretion from systemic compartments into the contents of
the alimentary tract. Activity transferred from systemic compartments into the small intestineor higher segments of the alimentary tract is assumed to be subject to reabsorption to blood. Insuch cases, the default absorption fraction fA for the secreted activity is the reference fA foringestion of the radionuclide. If multiple reference values of fA are given for different forms of
the ingested radionuclide X, the default fA for the secreted activity is the highest reference value
provided for X.

1530

2.3.4. Retention in the alimentary tract regions

1531
1532
1533
1534
1535
1536
1537
1538
1539
1540
1541
1542

The model structure allows, where information is available, for the use of data on
retention of radionuclides in different compartments. Human and animal data suggesting or
showing retention of ingested radionuclides on teeth or in mucosal tissues of the walls ofalimentary tract regions, principally the small intestine, can be used to refine calculation ofdoses to the alimentary tract. High levels of retention of radionuclides in the small intestine of
neonates have been shown to be associated with high levels of absorption in a number ofmammalian species (Fritsch et al., 1988; Nuclear Energy Agency (NEA), 1988; Sullivan,
Hardy, et al., 1984; Sullivan, Miller, et al., 1984; Sullivan, Ruemmler, et al., 1984). An example
given in Publication 100 (ICRP, 2006) for cadmium shows that retention of 115Cd on teeth
increases the estimated dose to the oral mucosa by almost two orders of magnitude comparedto that calculated using the Publication 30 model (ICRP, 1979, 1980). Similarly, retention of
59
Fe in the wall of the small intestine may increase the equivalent dose to the wall by48

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

1543
1544
1545
1546
1547

approximately a factor of two, compared to that calculated with the Publication 30 model(ICRP, 1979, 1980). However, in both examples, these increases in organ doses do not lead tosignificant changes in the committed effective doses, which are dominated by contributions
from other tissues (ICRP, 2006). Information on retention in alimentary tract tissues is given,
where available, in individual element sections of this and the OIR report series.

1548

2.3.5. Alimentary tract dosimetry

1549
1550
1551
1552
1553
1554
1555
1556
1557
1558
1559
1560
1561
1562
1563
1564
1565
1566
1567
1568
1569
1570
1571
1572
1573
1574
1575
1576
1577
1578
1579
1580
1581
1582
1583
1584
1585
1586
1587
1588
1589

The HATM allows explicit calculations of dose to target regions for cancer induction
within each alimentary tract region, considering doses from radionuclides in the contents of theregions, and considering mucosal retention of radionuclides when appropriate.
The oesophagus and oral cavity will receive very low doses from ingested
radionuclides because of short transit times in these regions (ICRP, 2006). However, they were
included because a specific wT is assigned to the oesophagus (ICRP, 2007), and because
retention in the mouth, on teeth for example, can result in a substantial increase in dose to theoral mucosa (which was added to the organs and tissues constituting the remainder in
Publication 103).
In general, the alimentary tract regions of greater importance in terms of doses andcancer risk are the stomach and particularly the colon. While the small intestine may receive
greater doses than the stomach, it is not sensitive to radiation-induced cancer and is not assigned
a specific wT value (ICRP, 2007). Small intestine is therefore included with the organs andtissues constituting the remainder (ICRP, 2007).
An important refinement in the HATM is the methodology used to calculate doses inthe various regions from non-penetrating α and electron radiations. In Publication 30 (ICRP,
1979), it was assumed that the dose to the wall of any gastrointestinal region from β- and αemitters in the contents was 100% and 1%, respectively, of the dose at the surface of thecontents. By contrast, the HATM takes account of the location of the target cells in the mucosal
layer of the wall of each gastrointestinal region and the depth of penetration of β and α particles
into the wall. The targets relating to cancer induction are taken in each case to be the epithelial
stem cells, located in the basal layers of the stratified epithelia of the oral cavity and oesophagus
and within the crypts that replenish the single cell layer epithelium of the stomach and small
and large intestines.
This new methodology generally results in substantially lower estimates of doses tothe colon from α- and β-emitting radionuclides in the colon contents than obtained using the
Publication 30 model (ICRP, 1979). This is because of the loss of the α particles and electronsenergies in the colon contents and in the mucosal tissue overlying the target stem cells (at adepth of 280–300 m at all ages). This reduces energy deposition in the target region forelectrons and results in zero contribution to dose in the target region from α particles emitted
within the contents. In the absence of retention of radionuclides in the alimentary tract wall,
doses from ingested α-emitters to all regions of the alimentary tract will be solely due to theirabsorption to blood and subsequent irradiation from systemic activity in soft tissues or to theemission of other types of radiation (e.g. electrons or photons).
The consequences of this decrease in local colon dose on the total committed effective
dose will vary according to the radionuclide. Examples given in Publication 100 (ICRP, 2006)
for 55Fe, 90Sr and 239Pu show that this decrease of local dose to the colon has little or no impact
on the effective dose since the dominating contributions are from equivalent doses to organs
and tissues from activity absorbed to blood. In general, the effect on effective dose is small forradionuclides with large fA values or long-lived radionuclides with long-term retention in the
body. However, for the example of 106Ru (fA = 0.05), there is a decrease in committed effective

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dose by approximately a factor two, due to the major contribution to effective dose fromequivalent doses to colon (decreased by a factor five) and other alimentary tract regions for thisradionuclide.
Calculations of doses in Publication 100 (ICRP, 2006) were based on preliminary
values of absorbed fractions of electrons and α particles to stem cell layers of each section of
the alimentary tract. In this report, new calculations have been performed for both particle types
and for both content and wall sources using improved absorption fraction values. Among others,
new models of segment folding have been implemented for regions within the small intestine.
Additional details are given in Publication 133 and Publication 143 (ICRP, 2016b, 2020).

1599

2.4. Biokinetic models for systemic radionuclides

1600

2.4.1. Parent radionuclides

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A model that describes the time-dependent distribution and excretion of a radionuclide
in the body after it reaches the systemic circulation is referred to here as a systemic biokinetic
model. In contrast to ICRP’s biokinetic models describing the behaviour of radionuclides in
the respiratory and alimentary tracts, ICRP’s systemic biokinetic models usually have been
element-specific models with regard to model structure as well as parameter values. A genericmodel structure that depicts all potentially important systemic repositories and paths of transfer
of all elements of interest in radiation protection would be too complex to be of much practicaluse. However, generic model structures have been used occasionally in previous ICRP
documents to describe the systemic biokinetics of small groups of elements, typically chemicalfamilies, known or expected to have qualitatively similar behaviour in the body. For example,
Publication 20 (ICRP, 1973) introduced a generic model formulation for the alkaline earth
elements calcium, strontium, barium, and radium, but provided element-specific values formost model parameters. In Parts 1–3 of Publication 30 (ICRP, 1979, 1980, 1981), a model
developed for plutonium, including parameter values as well as model structure, was applied
to most actinide elements. The biokinetic models for several of these actinide elements weremodified in Part 4 of Publication 30 (ICRP, 1988), where the model structure for plutonium
was used as a generic structure; a common set of parameter values was applied to plutonium,
americium and curium; and element-specific values were applied to selected parameters in themodels for other elements. The use of generic systemic model structures was increased in
ICRP’s reports on doses to members of the public from intake of radionuclides (ICRP, 1993,
1995a, 1995b, 2001, 2004) and was further expanded in the OIR series of documents (ICRP,
2015, 2016a, 2017, 2019, 2022) because it facilitates the development, description andapplication of systemic biokinetic models.
The systemic biokinetic models used in this series of reports generally follow aphysiologically descriptive modelling scheme applied on a more limited scale in the series of
ICRP reports on doses to members of the public from intake of radionuclides [referred to here
as the ‘Publication 56 series’ (ICRP, 1990, 1993, 1995a, 1995b, 1995c, 2001, 2004)]. That is,
the model structures include one or more compartments representing blood, depict feedback ofactivity from extravascular repositories to blood (i.e. they are recycling models), and as far aspractical, depict the main physiological processes thought to determine the systemic biokinetics
of individual elements.
The systemic biokinetic models for some elements, such as iodine and iron, aredeveloped within model structures specifically designed to describe the unique behaviour ofthese elements in the body. The models for most elements, however, have been constructedwithin one of the two generic model structures applied in the Publication 56 series to bone50

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seeking radionuclides (Figs. B.2 and B.3), or variations of those structures. This was done not
only for bone-seeking elements but also for a number of elements that show relatively low
deposition in bone (e.g. cobalt and ruthenium) because the main repositories and paths of
movement of those elements in the body are included in one or the other of these two structures.
In some cases, the model structure as applied in the Publication 56 series has been modified
slightly to accommodate specific characteristics of an element or simplified in view of thelimited information on certain aspects of the biokinetics of an element.
The systemic biokinetic models used in this report include explicit routes of biologicalremoval of systemic activity in urine and faeces. Additional excretion pathways, such as sweat,
are also depicted in the models for some elements.
The biokinetic model adopted for the urinary bladder is described in Publications 67
and 68 (ICRP, 1993, 1994a). To represent the kinetics of the bladder in terms of first-orderprocesses, the rate of elimination from the bladder is taken to be 40 d –1, 32 d–1 and 12 d–1 forthe 3 months infant, the 1 y child and the older age groups respectively.
In many of the systemic models used in the present series, activity is assumed to be
removed in faeces after transfer from systemic compartments into specified segments of thealimentary tract representing element-specific endogenous secretion pathways. The rates oftransfer of secreted material through different segments of the alimentary tract are elementindependent rates specified in the HATM. Activity transferred from systemic compartments
into the contents of the small intestine or higher segments of the tract is assumed to be reabsorbed in part, into blood. Activity assigned to the contents of the right colon or lower
sections of the tract is assumed not to be subject to re-absorption.

1658

2.4.2. Radioactive progeny

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A dose coefficient for a radionuclide that gives rise to a chain of radionuclides throughradioactive decay (called a ‘parent’ radionuclide) includes doses from radioactive progeny
produced in vivo following intake of the parent. The dose coefficient may depend strongly on
assumptions concerning the biokinetics of the progeny.
In Publications 30 and 68 (ICRP, 1979, 1994a), the general assumption was made thatchain members produced in systemic compartments following intake of a parent radionuclide
adopt the biokinetics of the parent. This is referred to as the assumption of ‘shared kinetics’.
The alternative assumption of ‘independent kinetics’ of chain members was made in
Publication 68 when the parent was an isotope of lead, radium, thorium or uranium, and also
for iodine progeny of tellurium and for noble gas isotopes arising in various chains. The
implementation of independent kinetics of progeny was based on a general pattern of behaviourof systemically produced progeny radionuclides suggested by a review of experimental studies
and follow-up of occupationally exposed workers (Leggett et al., 1984). That is, the datasuggested that most radioactive progeny produced in soft tissue or bone surface tended tomigrate from the parent and begin to follow their characteristic biological behaviour, while
radionuclides produced in bone volume tended to remain with the parent radionuclide in boneover the period of observation.
The assumption of independent kinetics is generally applied in this report series toprogeny radionuclides produced in systemic compartments other than bone volume
compartments, or absorbed to blood after production in the respiratory or alimentary tract. The
basic assumption is that a progeny radionuclide follows its characteristic behaviour from its
time of production in, or absorption into, the systemic pool. The implementation of thisassumption is not always straightforward due to structural differences in the systemic models
for many parent and progeny combinations. For example, a radionuclide may be born in an

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1711

explicitly designated tissue in the parent’s model that is not an explicitly designated tissue inthe progeny radionuclide’s characteristic model. When this happens, the rate of removal of theprogeny radionuclide from the tissue and the destination of the removed activity must be
defined before the model can be solved.
Even if the progeny radionuclide is produced in a tissue that is an explicitly designatedsource organ in the progeny radionuclide’s characteristic model, implementation of the default
treatment of independent kinetics may become somewhat arbitrary if the progeny
radionuclide’s model divides the tissue into compartments that are not identifiable withcompartments in the parent’s model. For example, this may occur if the division of the tissue
into compartments is based on physiological or anatomical considerations for the parent andon a kinetic basis for the progeny, or vice versa. Such issues of compartment identifiability are
addressed on a case-by-case basis.
Each of the element sections in this report series describes the implementation of theassumption of independent kinetics for dosimetrically significant progeny of radioisotopes ofthe element. The method of implementation depends on: the availability of specific informationon the behaviour of chain members produced in vivo, the sensitivity of dose estimates to
uncertainties in the behaviour of chain members, the lengths of radionuclide chains for thatelement, and the complexity and consistency of the characteristic systemic models for chain
members. In a number of cases, a simplified description of the systemic kinetics is used forradionuclides after their production in vivo. This is particularly true for short-lived progeny
radionuclides, which are assumed in some cases to decay at their site of production, or for noble
gases, for which the detailed mechanistic models applied in this report series as parent
radionuclides are replaced by much simpler models for application to their behaviour following
production in vivo. These simpler descriptions are judged adequate for practical purposes inview of the uncertainties in its short-term behaviour following production in vivo. In all cases,
the systemic model applied to an element X as a progeny of a parent element Y is the same forall chains headed by Y as the parent. For example, the systemic model applied to 224Ra produced
in a systemic pool following intake of 228Th is also applied to 223Ra produced in a systemic pool
following intake of 227Th.

1712

2.5. Summary of rules for treatment of radioactive progeny

1713
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1716
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1721
1722
1723
1724
1725
1726
1727

As in the OIR series of reports (ICRP, 2015, 2016a, 2017, 2019, 2022), the following
assumptions are made in this series of reports concerning the fate of progeny radionuclides
produced in the body by radioactive decay.
For all radionuclides with the exception of noble gases:• The parameter values describing absorption of the inhaled parent from the respiratory
tract to blood are applied to all members of the decay chain formed in the respiratory
tract.
• The systemic biokinetics of a progeny radionuclide produced by decay in a systemiccompartment, or absorbed to blood following production by decay in the respiratory
tract or alimentary tract, is defined in the element section for the parent, given in OIR:
Parts 2‒5 (ICRP, 2016a, 2017, 2019, 2022) or in this series of reports. As a rule withsome exceptions, the systemic biokinetics of the progeny is assumed to be independentof the systemic biokinetics of the parent. For decay chains whose members are all
isotopes of the same element, the progeny are assigned the same kinetics as the parent
throughout the body.

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DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

•

1728
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1749

The default absorption fraction fA for a progeny radionuclide produced by decay in thecontents of the alimentary tract (in the small intestine or a higher compartment)
following ingestion of a parent radionuclide, or produced in a systemic compartment
and subsequently transferred into the alimentary tract content, is the reference value offA for the progeny radionuclide when ingested as a parent. If the radionuclide has
multiple reference values corresponding to different chemical or physical forms, thenthe default value of fA is the highest reference value provided.
• The default absorption fraction, fA, for a progeny radionuclide produced in the
respiratory tract following inhalation of a parent, or produced in the alimentary tract
following transfer of activity from the respiratory tract to the alimentary tract, is the
product of the fraction of inhaled material with rapid dissolution (fr) for the assigned
absorption type and the reference value of fA for the progeny radionuclide wheningested as a parent radionuclide. If the progeny radionuclide has multiple reference
values of fA when ingested as a parent, corresponding to different chemical or physicalforms, then the default value of fA is the product of fr for the absorption type and thehighest reference value provided.
Noble gases produced in compartments of the respiratory tract and in the alimentarytract models by radioactive decay are assumed to escape from these compartments directly tothe environment at a rate of 100 d–1 without transfer to the blood compartment and withouttransfer between compartments of respiratory tract and alimentary tract models. It is assumed
that progeny of such noble gases formed within the body follow the rules of independent
kinetics stated in Para. (152).

1750

2.6. Medical intervention

1751
1752
1753
1754
1755
1756
1757

If medical treatment to prevent uptake or enhance excretion is administered, then thedata provided in the models summarised in this report series cannot be used directly to assess
committed effective doses from monitoring information (Bhattacharyya et al., 1992; IAEA,
1996; NCRP, 1980). In such circumstances, a programme of special monitoring (Section 5.5of Publication 130, ICRP, 2015) should be undertaken to follow the retention of the particular
contaminant in the person, and these data should be used to make a specific assessment ofcommitted dose.

1758

2.7. Methodology for dose calculations – The ICRP dosimetry system

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1767
1768

The ICRP dosimetry system is presented below as applied to assessment of organ
equivalent dose and effective dose following intakes of radionuclides. The system involves
numerical solution of reference biokinetic models, yielding the time-dependent number ofnuclear transformations in various source tissues. These solutions are then coupled withreference data on nuclear decay information, target tissue masses, and fractions of emitted
energy released from source tissue regions that are deposited in target tissue regions as definedin the reference phantoms in Publication 110 and Publication 143 (ICRP, 2009, 2020).
Presented below is the computational formalism of these dosimetry calculations consistent withthe protection quantities defined in Publication 103 (ICRP, 2007). More detailed data arepresented in ICRP Publication 133 (ICRP, 2016b).

1769

2.7.1. Computational solutions to the ICRP reference biokinetic models

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The HRTM (ICRP, 1994b, 2015), the HATM (ICRP, 2006), and the systemic
biokinetic models of this report describe the dynamic behaviour of radionuclides within the
body. Given the routes of intake, the models predict the subsequent uptake to the systemic
circulation, the distribution among tissues of the body, and the routes of elimination from thebody. Superimposed on these dynamics are in-situ radioactive decay and the ingrowth ofradioactive progeny. Consequently, the uptake, distribution and elimination of all progeny are
predicted, in addition to those of the parent radionuclide.
The compartment models of the respiratory and alimentary tract coupled with thoseof the systemic biokinetics define a system of first-order differential equations. The solution to
the set of equations is the time-dependent distribution of the radionuclide and its radioactive
progeny, if any, in mathematical compartments (pools) that are associated with anatomical
regions in the body.
If Ni,j(t) represents the number of atoms of radionuclide i in compartment j at time t,
the rate of change of these atoms is given in Eq. (2.3):

𝑀

𝑀

𝑖−1

𝑑𝑁i,j (𝑡)= ∑ 𝑁i,k 𝜆i,k,j − 𝑁i,j [∑ 𝜆i,j,k + 𝜆Pi ] + ∑ 𝑁h,j 𝜆Ph 𝛽h,i
𝑑𝑡
𝑘=1
𝑘=1
𝑘≠𝑗

(2.3)

ℎ=1

𝑘≠𝑗

1785

1786
1787
1788
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1797
1798
1799
1800
1801
1802
1803
1804
1805
1806
1807
1808
1809
1810

where:
M
is the number of compartments describing the kinetics;
𝑁i,kis the number of atoms of chain member i in donor compartment k and varies with time;
λi,j,kis the fractional transfer rate of chain member i from compartment j (donor
compartment) to compartment k (receiving compartment) in the biokinetic model which mayvary with age;p
𝜆i
is the physical decay constant of chain member i;𝑁h,jis the number of atoms of precursor nuclide h in compartment j and varies with time;P
𝜆his the physical decay constant of precursor chain member h; andβh,iis the fraction of the decays of chain member h forming member i.
Given the initial conditions specified for the compartments, Ni,j(0), Eq. (2.3) defines
the dynamic behaviour of the radionuclide and its progeny within the human body. The firstterm on the right-hand side of Eq. (2.3) represents the rate of flow of chain member i into
compartment j from all donor compartments. The second term represents the rate of removalof member i from compartment j both by transfer to receiving compartments and by physicaldecay. The third term addresses the ingrowth of member i within compartment j due to thepresence of its precursors h in the compartment. The number of atoms of the precursor
multiplied by its physical decay is the activity of the precursor, 𝐴h,j . Note that the members ofthe decay chain are assumed to be of order such that the precursors of member i have indexes
less than i. An ordered listing of the chain members can be obtained using the DECDATA
software distributed with Publication 107 (ICRP, 2008).
If all terms in Eq. (2.3) are multiplied by the physical decay constant of the chain
member being considered the rate of change of the activity of chain member i in compartment
j is obtained as shown in Eq. (2.4).

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𝑀

𝑀

𝑖−1

𝑑𝐴i,j (𝑡)= ∑ 𝐴i,k 𝜆i,k,j − 𝐴i,j [∑ 𝜆i,j,k + 𝜆Pi ] + ∑ 𝐴h,j 𝛽h,i 𝜆Pi
𝑑𝑡
𝑘=1
𝑘=1
𝑘≠𝑗

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1817
1818
1819
1820

(2.4)

𝑘=1

𝑘≠𝑗

The system of N × M ordinary first-order differential equations is generally solved
using suitable numerical methods, under the assumption that Ai,j(0) = 0 for all compartmentswith the exception of compartments of intake where nonzero initial conditions are only applied
to the parent nuclide (i.e. i=1).
To calculate the numerical values of the dose coefficients, it is necessary to associate
the biokinetic compartments of Eq. (2.4) with anatomical source regions indexed by rs. A
source region may or may not be a living tissue (for example, stomach content may be a source
organ but is not a living tissue) and may consist of more than one kinetic compartment. The
time-dependent activity in source region rs is the sum of the time-dependent activity in eachbiokinetic compartment j comprising the source region:𝑄

Ai (𝑟S , 𝑡) = ∑ 𝐴i,j (𝑡)

(2.5)

𝑗

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1831

where Q represents the total number of compartments comprising the source region
being considered.
For intakes in reference adults, dosimetric quantities are invariant with time and it isconvenient to integrate the activity in Eq. (2.5) over the 50-year commitment period to obtainthe total number of nuclear transformations as in the OIR series (ICRP 2015). For intakes inreference children the dosimetric quantities vary as reference child ages. The integration mustthen wait until after the time-varying activity is multiplied by a time-varying dose pertransformation (S-coefficient.)
Dividing the activity in Eq. (2.5) by the total initial activity taken into the body,∑𝑗 𝐴1,j (0), gives the rate of nuclear transformations per activity intake, ai (𝑟S , 𝑡):ai (𝑟S , 𝑡) = 𝐴

Ai (𝑟S ,𝑡)(2.6)

𝑒𝑥ℎ𝑎𝑙𝑒𝑑,0 +∑𝑗 𝐴1,j (0)

1832
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where the denominator includes the prompt exhaled activity 𝐴𝑒𝑥ℎ𝑎𝑙𝑒𝑑,0 , (pertinent for
inhalations, as only a fraction of the intake activity is deposited in the compartments of theHRTM) and the summation of parent activity (i=1) in all compartments at t = 0. Note that in
Publication 130, the denominator was erroneously described as excluding this exhaled activity.
This error was corrected in Publication 133.

1837

2.7.2. Computation of the ICRP reference dose coefficients for organ equivalent dose

1838
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The equivalent dose rate coefficient in target region rT of the Reference Male,ℎ̇M (𝑟T , 𝑡)and the Reference Adult Female, ℎ̇F (𝑟T , 𝑡), are given by:Mℎ̇M (𝑟T , 𝑡) = ∑ ∑ ai (𝑟S , 𝑡) 𝑆w(𝑟T ← 𝑟S , 𝑡)i
(2.7)
𝑖 𝑟
S

F
ℎ̇F (𝑟T , 𝑡) = ∑ ∑ ai (𝑟S , 𝑡) 𝑆w(𝑟T ← 𝑟S , 𝑡)i
𝑖

𝑟S

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(2.8)

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M
F
The S-coefficients, 𝑆w(𝑟T ← 𝑟S , 𝑡)i and 𝑆w(𝑟T ← 𝑟S , 𝑡)i give the radiation-weighted equivalentdose in target region 𝑟T due to a nuclear transformation of chain member i in source region 𝑟S[Sv (Bq)–1] for the male and female reference individuals, respectively. Note that the outersummation extends over the parent nuclide and its progeny.
The committed equivalent dose coefficients in each target region are given by
integrating the time-dependent equivalent dose rate coefficients over the commitment period
as shown in Eqs. (2.9) and (2.10). For intakes in the reference adult, the commitment period,
𝜏, is 50 years. For children the commitment period is found by subtracting the age at intake,
𝑡𝑜 , from 70 years.
𝑡𝑜 +𝜏

ℎTM (𝜏) = ∫ ℎ̇M (𝑟T , 𝑡) 𝑑𝑡

(2.9)

𝑡𝑜
𝑡𝑜 +𝜏

ℎTF (𝜏) =(2.10)∫ ℎ̇F (𝑟T , 𝑡) 𝑑𝑡
𝑡𝑜

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1855

A number of tissues listed in Table 1.3 used to compute the effective dose areconsidered to be represented by a single target region rT. In cases where more than one tissue
region defines the target tissue, fractional weighting of the equivalent dose must be made. The
committed equivalent dose coefficients for tissue T in the reference adult male, hM(), and adultfemale, hF(), are thus given as:ℎTM (𝜏) = ∑ 𝑓(𝑟T , 𝑇) ℎM (𝑟T , 𝜏)

(2.11)𝑟TℎTF (𝜏) = ∑ 𝑓 (𝑟T , 𝑇) ℎF (𝑟T , 𝜏)

(2.12)

𝑟T

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1869

where the target region fractional weights f(rT,T), are the proportions of the equivalent dose intissue T associated with target region rT. With the exception of the tissues addressed in Table
2.12, the tissues of Table 1.3 are represented by a single target region and thus for these tissuesf(rT,T) = 1. In Table 2.12, values of f(rT,T) for the ET and Thoracic (TH or Lung) regions aretaken to be equivalent to their risk apportionment factors as assigned in the revised HRTM(“Assigned fractions” in Table 2.7). These, at least, are assumed to be the same for children, in
the absence of information (ICRP, 1995b) (Table 2.7). For the colon, values of f(rT,T)f(rT , T)are taken to be the fractional masses of the stem cell layers within the alimentary tract
walls [see Table 7.8 of Publication 100 (ICRP, 2006)]. For the lymphatic nodes, values off(rT,T) are taken to be the fractional masses of lymphatic nodes (not lymphatic tissues) within
the ET, TH and non-respiratory regions consistent with data given previously in Publication
66 (ICRP, 1994b).
Table 2.12. Target region fractional weights, f(rT,T)
Tissue, T
ET
TH

Colon

rT
ET1
ET2
BB*
bb
AI
Right colonf(rT,T)
0.001
0.999
1/3
1/3
1/3
0.4

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Lymphatic nodes

Left colon
Rectosigmoid
LNET
LNTH
Lymph (systemic)

0.4
0.2
0.08
0.08
0.84

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ET, extrathoracic; TH, thoracic; ET1, anterior nasal passage; ET2, posterior nasal passage, pharynx, and larynx;
BB, bronchial; bb, bronchiolar; AI, alveolar–interstitial; LNET, ET lymph nodes; LNTH, TH lymph nodes.
*The basal and secretory cells are two target regions weighted equally.

1873

2.7.3. Computation of the ICRP reference dose coefficients for the effective dose

1874
1875

As defined in Publication 103 (ICRP, 2007), the committed effective dose coefficient,e(), is then:𝑒(𝜏) = ∑ 𝑤T [𝑇

ℎTM (𝜏) + ℎTF (𝜏)]2(2.13)

1876
1877
1878

where wT is the tissue weighting factor for tissue T of Table 1.3 and ℎTM (𝜏), and ℎTF (𝜏), are thecorresponding committed equivalent dose coefficients for these same tissues in the Reference
Male and Reference Female, respectively.

1879

2.7.4. Implementation of specific absorbed fractions within the ICRP dosimetry system

1880
1881

The time-dependent radiation-weighted S coefficient [Sv (Bq-s)–1] for a radionuclide
is calculated as:
𝑆w (𝑟T ← 𝑟S , 𝑡) = ∑ 𝑤R ∑ 𝐸R,i 𝑌R,i Φ(𝑟T ← 𝑟S, 𝐸R,i , 𝑡)
𝑅

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(2.14)𝑖where:• ER,i is the energy of the ith radiation of type R emitted in nuclear transformations of theradionuclide;• YR,i is the yield of the ith radiation of type R per nuclear transformation;• wR is the radiation weighting factor for radiation type R (Table 1.2); and• Φ(𝑟T ← 𝑟S, 𝐸R,i , 𝑡)is the specific absorbed fraction, defined as the fraction of energy
ER,i of radiation type R emitted within the source tissue rS that is absorbed per mass inthe target tissue rT at time t after intake.
The energies and yields of the emitted radiations, ER,i and YR,i, are taken from
Publication 107 (ICRP, 2008). For β emissions, the spectral data are used in the calculation of
Sw rather than mean values [i.e. the inner summation in Eq. (2.14) is replaced by the integral
over the spectrum].
For both sexes, the values of the specific absorbed fractions for all the radiations
emitted in nuclear transformations as tabulated in Publication 107 (ICRP, 2008) have been
published in Publications 133 and XXX (ICRP, 2016b, 20XX). Specific absorbed fractions at
the tabulated energies are found by piecewise cubic Hermite spline (PCHIP) interpolation(Fritsch and Carlson 1980).
For intakes in children, the S-coefficient varies with respect to time. Interpolation is
also performed to obtain S-coefficients at non-reference ages. At ages between 1 and 20 years

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1906

old, the same PCHIP interpolation technique described above is applied using S-coefficients ateach of the reference ages as input into the interpolation algorithm.
Publication 89 describes the complexities associated with growth rates in different
tissues in the first year of life. Accordingly, during the first year of life a weighted linear
interpolation is used as given in Eq. (2.15) where x is a fractional factor determined using Eq.
(2.16).

1907
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(2.15)𝑆𝑤 (𝑡) = 𝑥 [𝑆𝑤 (1𝑦) − 𝑆𝑤 (0𝑦)] + 𝑆𝑤 (0𝑦)
𝑥
100 𝑑
10
𝑡 [0.3+0.7(1−𝑡) ] ,0≤𝑡<(2.16)
365 𝑑
={
100
𝑑
5
𝑡 [0.16+0.84(1−𝑡) ] ,≤ 𝑡 < 1𝑦365 𝑑
In Eq. (2.16), t is given as the fraction of 1 year (365 days). Justification for thisinterpolation is provided in Publication XXX.
As described in Publication XXX the specific absorbed fractions for photons, electrons
and neutrons for many source and target geometries are based on Monte Carlo radiationtransport calculations (Zankl et al., 2012; Schwarz et al., 2021a,b) performed using thereference phantoms for the ICRP reference adult male and female described in Publication 110(ICRP, 2009) and the paediatric reference phantoms described in Publication 143 (ICRP, 2020).
These phantoms are constructed from tomographic images of real individuals.
For α particles, the specific absorbed fractions are the inverse of the mass of the target
region if rS = rT and 0 if rS ≠ rT. Exceptions occur for source and target regions within the
respiratory and alimentary tracts, in the skeleton, urinary bladder and gall bladder. In thesecases, only a fraction of the alpha energy emitted within the source region is deposited in thetarget region, and that fraction may be energy dependent. Separate models were used tocompute specific absorbed fractions in these regions.
In the alimentary and respiratory tracts, absorbed fractions for photons are derived
using the reference phantoms (ICRP, 2009, 2020). The absorbed fraction data for electrons andalpha particles in the alimentary tract of Publication 100 (ICRP, 2006) have been updated with
supplementary calculations included in Publication 133 (ICRP, 2016b) and Publication XXX(ICRP, 20XX). The absorbed fractions for electrons and alpha particles in the respiratory tract
given in Publication 66 (ICRP, 1994b) are presented in Publication 133 (ICRP, 2016b) andPublication XXX (ICRP, 20XX).
The biokinetic models consider that uptake occurs in the following skeletal source
regions:• trabecular bone surfaces and volumes;• cortical bone surfaces and volumes;
Surfaces of bone include:• Haversian canal within the cortical bone cortex surrounding all regions of trabecularspongiosa;• Haversian canal within the cortical bone of the long-bone shafts; and• surfaces separating medullary marrow cavities and cortical bone shafts of the longbones;• trabecular bone marrow, corresponding to the marrow within regions of trabecularspongiosa – both active and inactive marrow; and58

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•

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cortical bone marrow, corresponding to the marrow within the medullary marrow shaftsof the long bones, as well as the fluids within the Haversian canals of cortical bone. In
the adult, the marrow of the long bone shafts is inactive marrow.
The skeletal target regions are:• the 50-µm endosteal region (referred to as bone surface in Table 1.3); and• active (red) marrow.
The target tissue, bone surface, of Table 1.3 is the soft tissues within 50 µm of the surfaces ofmineral bone and is thought to be the region within which the osteoprogenitor cells associatedwith bone cancer reside. This target tissue is independent of the marrow cellularity (the fractionof bone marrow volume that is haematopoietically active). The systemic biokinetic models may
identify the ‘active marrow’ or the ‘trabecular marrow’ as source regions and specific absorbed
fractions are given for both source regions in Publications 133 and 143 (ICRP, 2016b, 2020) .

1952

2.7.5. Contribution of radioactive progeny to dose

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1961
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1963
1964
1965
1966
1967

As in earlier ICRP publications, the dose coefficients in this report series account for
ingrowth of radioactive progeny following the intake of the parent radionuclide. The
coefficients are for the intake of the parent nuclide: i.e. upon intake, the progeny are absent.
Inhalation of radon is an exception where the radioactive progeny are assumed to be present at
intake.
Generally, the systemic biokinetic model includes a compartment denoted as ‘Other’
which contains the systemic activity not explicitly assigned to compartments of identified
organs and tissues. ‘Other’ is the complement of the explicitly designated compartments; thatis, this compartment consists of all systemic tissues other than those associated with explicitly
identified compartments in the systemic biokinetic model. When independent kinetics are
assumed for progeny radionuclides, each member of the decay chain may have different setsof compartments, and as a result, the anatomic identity of the ‘Other’ compartment varies
among the chain members. Two alternative computational procedures to address this situation
were discussed in Annexe C.3 of Publication 71 (ICRP, 1995b).

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1968

3. GENERAL ASPECTS OF INTERNAL DOSE ASSESSMENT

1969

3.1. Introduction

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The effective dose calculated for protection purposes is determined from theequivalent doses to organs and tissues of the human body, which are in turn calculated fromthe mean absorbed doses to those organs and tissues (Section 1.2). Effective dose provides avalue which takes account of the given exposure conditions, but not of the characteristics of a
specific individual. In particular, the tissue weighting factors that are used to determine
effective dose are selected, rounded values representing averages over many individuals ofdifferent ages and both sexes. The equivalent doses to each organ or tissue of the Reference
Male and the Reference Female are averaged, and these averaged doses are each multipliedwith the corresponding tissue weighting factor to determine the sex-averaged effective dose for
the Reference Person (ICRP, 2007). It follows that effective dose does not provide an
individual-specific dose, but rather that for a Reference Person under given exposure conditions(ICRP, 2007).
There may be some circumstances in which parameter values may be changed fromthe reference values in the calculation of effective dose. It is therefore important to distinguishbetween those reference parameter values that might be changed in the calculation of effective
dose under particular circumstances of exposure, and those values that cannot be changed under
the definition of effective dose. As effective dose applies to a Reference Person, individualspecific parameter values should not be changed whereas material-specific parameter values
may be changed. Examples of individual-specific parameters include those describing thedosimetric phantom, respiratory tract model breathing and particle transport parameters,
HATM parameters other than the alimentary tract transfer factor, fA, and all systemic model
parameters. Examples of material-specific parameters include lung-to-blood absorption
parameters, aerosol parameters such as the AMAD of the inhaled aerosol, and fA.
In the majority of cases, assessed doses are low in comparison with dose limits, andfor such cases, it is likely that dose assessments will make use of the recommended default
values for material-specific parameters, and the tabulated dose coefficients that accompany thisseries of reports. However, in some circumstances, such as where assessed doses are likely to
be close to or exceed dose limits, material-specific parameter values other than therecommended defaults may be used. Further information and guidance is given in Section 6 of
Publication 130 (ICRP, 2015).
In unusual cases where doses to specified individuals may exceed dose limits
substantially and radiation risks need to be assessed, specific estimates of organ or tissue doses
are necessary to determine organ-specific risks. In such cases, absorbed dose in organs should
be calculated and used with the most appropriate biological effectiveness and risk factor data
(ICRP, 2007). This retrospective individual dose assessment should only be performed byprofessionals with recognised expertise, skills and practical experience. It is beyond the scopeof this publication to give advice on how to perform individualised retrospective dose and risk
assessments.

2008

3.2. Uncertainties in internal dose assessment

2009
2010

Publication 103 (ICRP, 2007) makes the following statement with respect to theassessment of uncertainties:

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In order to assess radiation doses, models are necessary to simulate the geometry of
the external exposure, the biokinetics of incorporated radionuclides, and the humanbody. The reference models and necessary reference parameter values are establishedand selected from a range of experimental investigations and human studies throughjudgements. For regulatory purposes, these models and parameter values are fixed byconvention and are not subject to uncertainty.
It follows that there is no requirement to assess or record the uncertainty associatedwith an individual dose assessment performed to demonstrate compliance with regulatory
requirements. Nevertheless, there are circumstances in which the assessment of uncertainties
associated with internal dose assessments may be useful. For example, the assessment of
uncertainties associated with a specified monitoring procedure might provide important
information for optimising the design of a monitoring programme. Where uncertainties inassessed effective dose are evaluated, uncertainties in material-specific model parameter values
should be considered, but individual-specific model parameter values should be taken to be
fixed at their reference values.

2026

3.3. Uncertainties in biokinetic models

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Biokinetic models are used in radiation protection to predict the time-dependent
distribution and retention of a radionuclide in the body and the rate of excretion of theradionuclide in urine and faeces. These models are used in this report series to derive dosecoefficients following intakes of radionuclides by inhalation or ingestion.
The following categorisation of the main types of information used to develop
biokinetic models and assess model reliability is taken from a paper by Leggett (2001).
Investigations of the reliability of many of the biokinetic models that have been used in ICRP
reports can be found in the following papers and reports published by Apostoaei et al., (1998);
Leggett et al., (2001; 1998, 2007, 2008); Harrison et al., (2001, 2002); Bolch et al., (2001,
2003); Skrable et al., (2002); Likhtarev et al. (2003); Apostoaei and Miller (2004); Sánchez(2007); Pawel et al., (2007); NCRP (2009), Li et al. (2014).

2038

3.3.1. Uncertainties associated with the formulation (structure) of a biokinetic model

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The confidence that can be placed in predictions of a biokinetic model for an element
or compound depends not only on uncertainties associated with parameter values of the model
but also on uncertainties associated with the model structure. Such uncertainties may arise
because the structure provides an oversimplified representation of the known processes,
because unknown processes have been omitted from the model, or because part or all of themodel formulation is based on mathematical convenience rather than consideration ofprocesses. Some combination of these limitations in model structure is associated with virtually
all biokinetic models for radionuclides. These limitations hamper the assignment of meaningful
uncertainty statements to the parameter values of a model because they cast doubt on theinterpretation of the parameter values.

2049

3.3.1.1. Types of information used to construct biokinetic models for elements

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Regardless of the model formulation or modelling approach, a biokinetic model for
an element or compound, particularly a systemic model, is usually based largely on somecombination of the following sources of information:

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•

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H1: direct information on humans, i.e. quantitative measurements of the element in
human subjects;• H2: observations of the behaviour of chemically similar elements in human subjects;• A1: observations of the behaviour of the element in non-human species; and• A2: observations of the behaviour of one or more chemically similar elements in nonhuman species.
H2, A1 and A2 data serve as surrogates for H1, (direct information on humans) which is thepreferred type of information on which to base a biokinetic model.
H1, H2, A1 and A2 data are sometimes supplemented with various other types of
information or constraints, such as quantitative physiological information (e.g. rates of bone
restructuring); considerations of mass balance; predictions of theoretical models based on
fundamental physical, chemical, and mathematical principles (e.g. a theoretical model ofdeposition of inhaled particles in the different segments of the lung); experimental data derived
with anatomically realistic physical models (e.g. hollow casts of portions of the respiratory tract
used to measure deposition of inhaled particles); and in-vitro data (e.g. dissolution ofcompounds in simulated lung fluid). Among these supplemental sources of information, massbalance and quantitative physiological data (data type P) have particularly wide use.

2070

3.3.2. Sources of uncertainty in applications of human data

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It is desirable to base a biokinetic model for an element or compound on observationsof the time-dependent distribution and excretion of that element in human subjects (H1 data).
Some degree of this type of direct information is available for most essential elements, as well
as for some important non-essential elements, such as caesium, lead, radium, uranium,
americium and plutonium. Depending on the degree of biological realism in the model
formulation, it may be possible to supplement element-specific information for human subjects
with quantitative physiological information for humans on the important processes controllingthe biokinetics of the element of interest. For example, in Publications 67, 69, and 71 (ICRP,
1993, 1995a, 1995b), long-term removal of certain radionuclides from bone volume isidentified with bone turnover.
Although it is the preferred type of information for purposes of model construction,
H1 data often have one or more of the following limitations: small study groups, coupled withpotentially large inter-subject variability in the biokinetics of an element; short observation
periods, coupled with potentially large intra-subject variability; use of unhealthy subjects
whose diseases may alter the biokinetics of the element; paucity of observations for womenand children; collection of small, potentially non-representative samples of tissue; inaccuracies
in measurement techniques; uncertainty in the pattern or level of intake of the element; atypical
study conditions; and inconsistency in reported values. In some cases, inconsistency in reported
values may provide some of the best evidence of the uncertain nature of the data.
An important tool in the development of biokinetic models for radionuclides has been
the use of reference organ contents of stable elements, as estimated from autopsy measurements
on subjects chronically exposed at environmental levels or at elevated levels encountered in
occupational exposures (ICRP, 1975). Such data are commonly used to adjust parameter valuesof biokinetic models or introduce new model components to achieve balance between reported
values of intake, total-body content, and excretion of stable elements. Balance considerations
can provide useful constraints on model parameters, provided that the data have been collectedunder carefully controlled conditions. However, balance considerations have often been based

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on data from disparate sources of information and unreliable measurement techniques, and insome cases, may have led to erroneous models or parameter values.
A confidence statement based on H1 data would reflect a variety of factors, such as
the reliability of the measurement technique(s), the number and state of health of the subjects,
representativeness of the subjects and biological samples, consistency in data from different
studies, knowledge concerning the level and pattern of intake, and the relevance of theinformation to the situation being modelled. For example, confidence in a parameter value
based on H1 data would be reduced if the data were determined in a study on any of thefollowing study populations: several seriously ill subjects with known intakes; several healthy
subjects with poorly characterised intakes; or one healthy subject with known intake.

2108

3.3.3. Uncertainty in interspecies extrapolation of biokinetic data

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Interspecies extrapolation of biokinetic data is based on the concept of a general
biological regularity across the different species with regard to cellular structure, organ
structure, and biochemistry. Mammalian species, with cellular structure, organ structure,biochemistry, and body temperature regulation particularly close to those of man are expected
to provide better analogies to man than do non-mammalian species with regard to biokinetics
of contaminants.
Despite the broad structural, functional, and biochemical similarities among
mammalian species, interspecies extrapolation of biokinetic data has proven to be an uncertain
process. Similarities across species are often more of a qualitative than quantitative nature, inthat two species that handle an internally deposited radionuclide in the same qualitative manner
may exhibit dissimilar kinetics with regard to that substance. Moreover, there are important
structural, functional and biochemical differences among the mammalian species, including
differences in specialised organs, hepatic bile formation and composition, level of biliary
secretion, urine volume and acidity, the amount of fat in the body, the magnitude of absorption
or secretion in various regions of the digestive tract, types of bacteria in the digestive tract, andmicrostructure and patterns of remodelling of bones.
In general, the choice of an animal model will depend strongly on the processes andsubsystems of the body thought to be most important in the biokinetics of the radionuclide in
humans, because a given species may resemble humans with regard to certain processes andsubsystems, but not others. For example, data on monkeys or baboons may be given relatively
high weight for purposes of modelling the distribution of a radionuclide in the skeleton due tothe close similarities in the skeletons of non-human primates and humans. Data on dogs may
be given relatively high weight for purposes of modelling the rate of loss of a radionuclide fromthe liver due to broad quantitative similarities between dogs and humans with regard to hepatic
handling of many radionuclides.
A physiologically based model provides the proper setting in which to extrapolate datafrom laboratory animals to man, in that it helps to focus interspecies comparisons on specificphysiological processes and specific subsystems of the body for which extrapolation may bevalid, even if whole-body extrapolations are invalid. Depending on the process being modelled,
it may be preferable in some cases to limit attention to data for a single species or small numberof species, and in other cases, to appeal to average or scaled data for a collection of species.
The degree of confidence that can be placed in a model value based on animal data
depends on the quality and completeness of the data and the expected strength of the animal
analogy for the given situation. Thus, one must consider potential experimental and statisticalproblems in the data as well as the logical basis for extrapolation of those particular data tohumans. Relatively high confidence might be placed in a model value based on animal data: if

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fairly extensive interspecies comparisons have been made and include observations on thespecies expected to be most human-like; if these comparisons suggest a strong basis forinterspecies extrapolation, either because the data are species-invariant or because thephysiological processes governing the biokinetics of the element in different species have beenreasonably well established; if the model structure allows meaningful extrapolation to man,usually on the basis of physiological processes; and if such processes have been well quantified
in humans (i.e. the central value for humans has been reasonably well established). A fairly
wide uncertainty interval is indicated if data are available only for species that frequently
exhibit qualitative differences from man (e.g. if data were available only for rats) or if nomeaningful basis for extrapolation to man has been established with regard to the quantity ofinterest. Whatever the quality of the animal data, the uncertainty interval should reflect the factthat some confidence in the predictive strength of the data is lost when the data are extrapolated
across species.

2158

3.3.4. Uncertainty in inter-element extrapolation of biokinetic data

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Biokinetic models for elements are often constructed partly or wholly from data forchemically similar elements, on the basis of empirical evidence that chemical analogues often
exhibit close physiological similarities. For example, the alkaline earth elements, calcium,
strontium, barium and radium, exhibit many physiological as well as chemical similarities(ICRP, 1993), and the alkali metals rubidium and caesium closely follow the movement of theirchemical analogue, potassium.
There are, however, counterexamples to the premise that chemical analogues are also
physiological analogues. For example, the alkali metals potassium and sodium share close
physical and chemical similarities but exhibit diametrically opposite behaviours in the body,with potassium being primarily an intracellular element and sodium being primarily an
extracellular element.
Moreover, some of the chemically similar elements that behave in a qualitatively
similar fashion in the body may exhibit quite different kinetics. For example, caesium appears
to follow the behaviour of potassium in the body in a qualitative sense, but is distributed
somewhat differently from potassium at early times after intake and exhibits a substantiallylonger whole-body retention time.
The level of confidence that can be placed in a model value based on human data fora chemically similar element depends on the quality and completeness of the data for the
analogue, as well as the expected strength of the analogy for the given situation. Whatever thequality of the data for the chemical analogue, the confidence interval should reflect the fact thatsome confidence in the predictive strength of the data is lost when the data are extrapolated
across elements.
The strength of the chemical analogy for a given element depends largely on the extent
to which the chemically similar elements have been found to be physiologically similar. Thatis, the analogy would be considered strong for a pair of elements if a relatively large set ofexperimental data indicates that these elements have essentially the same qualitative behaviourin the body and that their quantitative behaviour is either similar or differs in a predictablefashion. In view of counterexamples to the premise that chemically similar elements arenecessarily physiologically similar, the chemical analogy does not provide high confidence if
the elements in question have not been compared in animals or man.
If a chemical analogue has been shown to be a good physiological analogue, thenapplication of human data on the chemical analogue (H2 data) may be preferable to applicationof animal data on the element of interest (A1 data). For example, for purposes of constructing

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or evaluating a biokinetic model for americium in humans, use of quantitative human data on
the physiological analogue curium seems preferable to use of the best quantitative animal dataon americium. Similar statements can be made for radium and barium, rubidium and potassium,or other pairs of close physiological analogues. On the other hand, if two chemically similarelements show only broad physiological similarities, the animal analogy may be preferred tothe chemical analogy, particularly if element-specific data are available for a variety of animal
species (as is the case, for example, for uranium and calcium). In general, lower confidence
would be placed in animal data for a chemical analogue than in animal data for the element ofinterest.

2201

3.3.5. Uncertainty in central estimates stemming from variability in the population

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‘Uncertainty’ refers here to lack of knowledge of a central value for a population, and‘variability’ refers to quantitative differences between different members of a population.
Although uncertainty and variability are distinct concepts, the variability in biokinetic
characteristics within a population is often an important factor contributing to the uncertainty
in a central estimate of a biokinetic quantity. This is because such variability complicates the
problem of identifying the central tendency of these characteristics in the population due to thesmall number of observations generally available and the fact that usually, subjects of
biokinetic studies are not randomly selected.
Variability in the biokinetics of radionuclides, pharmaceuticals, or chemicals inhuman populations appears to result from many different physiological factors or modulating
host factors of an environmental nature, including age, sex, pregnancy, lactation, exercise,disease, stress, smoking and diet. Large inter-individual biokinetic variations sometimes persist
in the absence of appreciable environmental differences and suggest that these variations may
be genetically controlled. In real-world situations, genetic and environmental factors may
interact dynamically, producing sizable variations in the behaviour of substances taken into thehuman body.

2218

3.4. Uncertainties in dosimetric models

2219
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Dosimetric models are used to estimate the mean absorbed dose resulting fromradiations emitted by nuclear transformations of radionuclides present in the body. The
absorbed dose is computed for target regions (organs, tissues, or regions of tissues) considered
to be radiosensitive. Radiation weighting factors and tissue weighting factors are applied to themean absorbed dose to determine the equivalent and effective dose. The weighting factors are
assigned reference values, and as such, are not regarded as uncertain quantities. Thus, theuncertainties associated with an estimated equivalent dose to an organ, for example, areconsidered to be those associated with the underlying mean absorbed dose.
The physical and anatomical parameters contributing to uncertainties in the mean
absorbed dose for internal emitters are:• Energy and intensity of the nuclear and atomic radiations emitted by the radionuclide
and by any radioactive progeny;• Interaction coefficients of the emitted radiations in tissues;• Elemental composition of the tissues of the body;• Volume, shape, and density of the organs of the body; and65

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2265
2266
2267
2268
2269
2270
2271
2272
2273
2274
2275
2276
2277

•

Parameters describing the spatial relationship of the source regions (regions containing
the radionuclide) and the target regions (radiosensitive organs and tissues for which
dose values are desired).
Limitations are present in the computational model representing the anatomy and in
the numerical procedures used to calculate the energy absorbed in the target regions. The
magnitudes of these uncertainties vary with radiation type, the energy of the radiation, and thespecific source-target pair. The adoption of computational phantoms based upon medical
imaging data (often referred to as voxel phantoms) has reduced the uncertainties associatedwith cross-irradiation of tissues by photon and neutron radiations to some extent by providing
more realistic spatial relationships of some source and target regions (ICRP, 2009, 2020).
However, the absorbed dose is frequently dominated by the contributions from non-penetratingradiations. For source and target regions that cannot be resolved in the medical image data, e.g.
source and target regions in the respiratory and alimentary tracts and in the skeleton,
uncertainties are associated with the computational models used to represent these regions.
The anatomical models are static and thus do not address uncertainties in the spatial
position of the organs due to breathing and posture other than reclining.
The parameters of the dosimetric model contributing to uncertainties in the absorbed
dose are those physical parameters associated with the nuclear transformation processes that
determine the energy and intensity of the emitted radiation, and parameters which govern thetransport radiations in the body. Attenuation and absorption coefficients for photons involve
relatively small uncertainties, typically less than 10%, but somewhat higher uncertainties are
ascribed to soft tissue stopping power values for α particles and electrons. Improvements in thebasic nuclear data have reduced the uncertainties in the physical half-lives of radionuclides andthe branching fractions of decay modes. The simplified procedures used in the dosimetriccalculations to address the delayed β and gamma radiations of spontaneous fission cancontribute to substantial uncertainties in the mean absorbed dose in some tissues.
The dosimetric calculations must associate an anatomical region (source region) witheach biokinetic compartment. Many biokinetic models partition the systemic activity among a
few identified organs/tissues and include a compartment referred to as ‘Other tissue’ which
represents the residual activity (See Section 2.7). The dosimetric procedure distributes theactivity in the ‘Other tissue’ compartment uniformly among all tissues not explicitly identified
in the model. Substantial uncertainty may be associated with the mean absorbed dose for tissues
that are members of ‘Other tissue’. ‘Other tissue’ frequently includes tissues assigned an
explicit tissue weighting factor. For example, breast tissue is rarely explicitly identified as asource region in biokinetic models, and thus, its mean absorbed dose is often based on its
inclusion in ‘Other tissue’.
A number of numerical methods are capable of solving the set of potentially large
numbers (hundreds) of coupled differential ‘stiff’ equations that describe the kinetics, althoughfrequently the demands of numerical accuracy have to be balanced with computational time.
Compartment-model issues contributing to uncertainties in the mean absorbed dose include theassumed biokinetics of members of a decay chain (independent or shared kinetics), and therepresentation of ‘Other’ tissues when their anatomical identity varies among the decay chain
members [Section 2.7.5 and Annex C of Publication 71 (ICRP, 1995b)].

66

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

2278

4. DATA PROVIDED FOR ELEMENTS AND RADIOISOTOPES

2279
2280
2281
2282
2283
2284
2285
2286
2287
2288
2289
2290
2291
2292
2293
2294
2295
2296

This Section describes the information provided in subsequent parts of this series ofreports. The data provided are reference values for the purposes of radiation protection. The
biokinetic parameter values of the Reference Members of the Public and data provided here areinvariant with sex, race, health status and other individual-specific characteristics.
Each element section in the EIR series includes reviews of data on inhalation,
ingestion and systemic biokinetics and the structure and parameter values of the reference
systemic biokinetic model. (For inhalation, reviews of data in OIR Parts 2 – 5 are adopted.)
Dosimetric data provided include dose coefficients (committed effective dose and committed
equivalent dose to named organs or tissues, Sv Bq–1) for inhalation and ingestion of all relevantradioisotopes. Dosimetric data are calculated using the revised HRTM (ICRP, 2015), the
HATM (ICRP, 2006) and the reference systemic biokinetic models defined in this series ofreports for the Reference Individuals.
Committed effective dose and committed equivalent dose to named organs and tissues
per intake [or d̒ ose per intake coefficientʼ e(τ), Sv Bq–1] are provided for assessments of theeffective dose to each Reference Member of the Public. These coefficients should be used forthe assessments based on the activity of the intake; the activity intake can be assessed
prospectively (i.e. at the design or planning stage) or retrospectively (i.e. based on monitoringdata).

2297

4.1. Data provided in the printed reports and electronic annexes

2298
2299
2300
2301
2302
2303
2304
2305
2306
2307
2308
2309
2310
2311
2312
2313
2314
2315

The data provided in the printed reports are restricted to tables of committed effective
dose per intake (Sv Bq–1) for inhalation and ingestion. Data are provided for all absorption
types and for the most common isotope(s) of each element. In cases for which sufficient
information is available (principally for actinide elements), lung absorption is specified forcertain chemical forms, and dose coefficients are calculated accordingly. Dose coefficients arealso calculated for specific gas and vapour forms of some elements, because deposition in the
respiratory tract depends on chemical form. The sizes of particles inhaled by the Reference
Individuals are assumed to be log-normally distributed with an AMAD of 1 μm and geometricstandard deviation σg of approximately 2.5 (Paragraph 170, ICRP, 1994b). They are assumed
to have a density of 3.00 g cm–3, and a shape factor of 1.5 (Paragraph 181, ICRP, 1994b). An
exception is made for the short-lived progeny of radon, described in the inhalation section in
OIR: Part 3 (ICRP, 2017).
The electronic annex that accompanies this series of reports contains a comprehensive
set of committed effective and equivalent dose coefficients per intake. Data are presented foralmost all radionuclides included in Publication 107 that have half-lives equal to or greaterthan 10 min, and for other selected radionuclides. Data are provided for a range of physicochemical forms and for aerosols with median sizes ranging from an AMTD of 0.001 µm to an
AMAD of 20 µm. Data for intake by ingestion (for specified values of fA) are also provided.

2316

4.2. Quality assurance of data presented

2317
2318
2319
2320

The Commission attaches particular importance to quality assurance. The Task Groupof Committee 2 on Internal Dose Coefficients arranged for the quantities given in this series ofreports to be calculated independently at different laboratories, using different computer codes.
Any discrepancies in these calculations are investigated and resolved before publication.
67

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

2321

5. HYDROGEN (Z = 1)

2322
2323
2324
2325

Tritium may be released into the environment in three main chemical forms: tritium
gas, tritiated water, and organic compounds of tritium (organically-bound tritium, OBT). In theenvironment, tritium gas is gradually converted to tritiated water. In this section, dosimetricdata are given for tritium 3H.

2326

5.1. Routes of Intake

2327

5.1.1. Inhalation

2328
2329
2330
2331
2332
2333
2334
2335
2336
2337
2338
2339

Extensive information on absorption of tritium from the respiratory tract is available
from occupational exposures, and from human volunteer studies with inhaled tritium gas andtritiated water. Information is also available from experimental studies of tritiated organic
compounds and particulate forms (mainly metal tritides and luminous compounds), in rats andin vitro. For details see Section 2 of Publication 134 (ICRP, 2016a).
Absorption parameter values and types, and associated fA values for gas and vapour
forms of hydrogen (tritium) are given in Table 5.1 and for particulate forms in Table 5.2 (bothtaken from Section 2 of Publication 134). Exposures to gas or vapour forms of tritium are morecommon than exposures to particulate forms, and it is therefore recommended in this series of
documents that gas/vapour form is assumed in the absence of information.
Table 5.1. Deposition and absorption for gas and vapour forms of hydrogen (tritium) *,†Chemical form/origin

2340
2341
2342
2343
2344
2345
2346
2347
2348
2349
2350
2351
2352
2353
2354
2355
2356
2357
2358

Percentage deposited‡

Absorption*

Total

ET1

ET2

BB

bb

AI

Type

fA

Tritiated water (HTO)

100§

0

20

10

20

50

V

**

Tritium gas (HT)

0.01§

0

0.002

0.001

0.002

0.005

V

**

Tritiated methane (CH4–xTx)

0.3§

0

0.06

0.03

0.06

0.15

V

**

Unspecified†

100¶

0

20

10

20

50

F

1.0††

ET1, anterior nasal passage; ET2, posterior nasal passage, pharynx and larynx; BB, bronchial; bb, bronchiolar; AI,
alveolar-interstitial.
*
It is assumed that for tritium the bound state can be neglected, i.e. fb = 0.0. For intake of these forms of tritium
the systemic model for HTO is applied to absorbed activity.
†
For tritium in unspecified gas or vapour form (including unspecified organic vapours), the default option forgases and vapours is recommended: 100% total deposition in the respiratory tract; default distribution between
regions¶ and Type F absorption.
‡
Percentage deposited refers to how much of the material in the inhaled air remains in the body after exhalation.
Almost all inhaled gas molecules contact airway surfaces, but usually return to the air unless they dissolve in, or
react with, the surface lining. In the case of tritium gas and methane, a small fraction is absorbed into body fluids
and of that, a fraction is metabolised and the rest subsequently exhaled.
§
Since instantaneous absorption to blood is assumed, calculations can be performed assuming direct injection intoblood, and the regional deposition does not need to be considered. However, for completeness, the default
distribution is assumed¶.
¶
Default distribution between regions (20% ET2, 10% BB, 20% bb and 50% AI).
**Not applicable for absorption Type V, because all activity deposited in the respiratory tract is instantaneously
absorbed.
††
The value of fA = 1 is applicable to all age-groups.

68

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

2359
2360

Table 5.2. Absorption parameter values for inhaled particulate forms of tritium and for ingested
tritium.
*

Inhaled particulate materials
Specific parameter values‡
Biogenic organic compounds

frDefault parameter values§,¶
Absorption Type
Assigned forms
F
LaNi4.25Al0.75 tritide
M**
Glass fragments; luminous paint;titanium tritide; zirconium tritide
S
Carbon tritide; hafnium tritide

Absorption parameter values†sr (d–1)
ss (d–1)

1

100

–

1
0.2

100
3

–
0.005

0.01

3

1×10-4

Ingested materials††
Assigned forms*

Age-dependent absorption from the alimentary tract, fA
3 months 1 year 5 years 10 years
15 years Adult
Biogenic organic compounds‡
1
1
1
1
1
1
Tritiated water and other soluble 1
1
1
1
1
1
forms (as assigned to Type F forinhalation)
Relatively insoluble forms (Types 0.2
0.1
0.1
0.1
0.1
0.1
M and S)

2361
2362
2363
2364
2365
2366
2367
2368
2369
2370
2371
2372
2373
2374
2375
2376
2377
2378
2379

*

2380

5.1.2. Ingestion

2381

5.1.2.1. Tritiated water

2382
2383

Tritiated water is rapidly and completely absorbed to blood after ingestion with nodifference between ages.

2384

5.1.2.2. Organically-bound Tritium

2385
2386
2387

The major part of tritium intake by members of the public will occur by ingestion offood into which tritium has been incorporated through both plant and animal components. Suchorganically bound tritium (OBT) will be present in many different chemical compounds

The systemic model for HTO is applied to intake of all forms of tritium other than biogenic tritiated organic
compounds, for which the systemic model for OBT is applied.
†
It is assumed that for tritium the bound state can be neglected, i.e. fb = 0.0. The value of sr for Type F forms ofhydrogen (100 d–1) is element-specific. The values for Types M and S (3 d–1) are the general default values.
‡
See Section 2 of Publication 134 (ICRP, 2016a) for summary of information on which parameter values are
based, and on ranges of parameter values observed for individual materials. For biogenic organic compounds,
Type F default parameter values are used for absorption from the respiratory and alimentary tracts, but a specificsystemic model, OBT, for absorbed tritium.
§
Materials (e.g. “Glass fragments”) are generally listed here where there is sufficient information to assign to adefault absorption Type, but not to give specific parameter values (see Section 2 of Publication 134).
¶
For inhaled material deposited in the respiratory tract and subsequently cleared by particle transport to thealimentary tract, the default fA values for inhaled materials are applied: i.e. the product of fr for the absorption
Type and the fA value for ingested soluble forms of tritium applicable to the age-group of interest (1.0).
**
Default Type M is recommended for use in the absence of specific information on which the exposure material
can be assigned to an Absorption Type, e.g. if the form is unknown, or if the form is known but there is no
information available on the absorption of that form from the respiratory tract.
††
Activity transferred from systemic compartments into segments of the alimentary tract is assumed to be subject
to reabsorption to blood. The default absorption fraction fA for the secreted activity is the highest fA value foringestion of the radionuclide applicable to the age-group of interest (1.0).

69

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2388
2389
2390
2391
2392
2393
2394
2395
2396
2397

including proteins, carbohydrates, fats and nucleic acids. In the human alimentary tract,foodstuffs containing OBT will undergo digestion to yield small molecules which are readily
absorbed. A small proportion of the tritium will probably be present in indigestible fibres andwill be non-absorbable. However, it is assumed that non-absorbable OBT represents a verysmall proportion of the total dietary OBT.
In Publication 134 (OIR Part 2), an fA of 1 was adopted for both tritiated water andorganic compounds, although it was recognized that absorption may be substantially less thancomplete in the case of some organic compounds. In this report, an fA of 1 is adopted for tritiumin food and for all soluble forms. An fA of 0.1 is adopted for relatively insoluble forms of tritium
for adults. For 3-month-old infants, this values is increased to fA = 0.2.

2398

5.1.3. Systemic Distribution, Retention and Excretion

2399

5.1.3.1. Background

2400
2401
2402
2403
2404
2405
2406
2407
2408
2409
2410
2411
2412
2413
2414
2415
2416
2417
2418
2419
2420
2421
2422
2423
2424
2425
2426
2427

Two different systemic models are used in this report to develop dose coefficients for
two forms of tritium commonly encountered in the environment. These are referred to as the
HTO (tritiated water) and the OBT (organically bound tritium) models. OBT refers to carbonbound tritium formed in plants and animals through natural biological processes.
Studies of the fate of inhaled or ingested HTO in humans and laboratory animals
indicate that HTO is rapidly absorbed to blood and mixed with total-body water. A few percentof the absorbed amount is converted to OBT. The retention time for OBT appears to depend on
the metabolic activity of the tissue in which it deposits. The retention time of the unconverted
HTO presumably is determined by the rate of water turnover, which varies with age and may
be estimated on the basis of the mass of total-body water and total energy expenditure at a given
age. The average retention time of OBT appears from animal studies to be substantially longer
than that of unconverted HTO. Two phases of relatively long-term retention of tritium in the
body observed in persons exposed to tritium in the workplace (OIR Part 2, Publication 134)
are assumed to represent two phases of OBT retention.
Inaba et al. (1984) studied the tissue distribution and urinary excretion of tritium
administered as tritiated water via a stomach tube to rats of various ages. Younger animals
generally showed a shorter residence time of tritium in the body than did mature animals.
Incorporation of tritium in tissues was assessed both in the aqueous fraction and organic
components of the studied tissues, which included brain, liver, muscle, testis, and blood. Overthe first several days the activity concentration in tissue water decreased rapidly while that in
the organic portion decreased more slowly.
Ingested food containing OBT undergoes digestion in the gastrointestinal tract,yielding small molecules that are for the most part readily absorbed to blood. Studies in animals
administered various forms of OBT indicate relatively high concentrations of activity in fat,muscle, and brain (Pietrzak-Flis et al., 1978). The authors of Publication 56 (ICRP, 1990)
interpreted reported data for laboratory animals as indicating that 9-45% of ingested OBT isincorporated into organic constituents of tissues and, on average, about 9 times more OBT ispresent in body tissues after intakes of OBT than after intakes of HTO.

2428

5.1.3.2. HTO Model

2429
2430
2431
2432

The model for systemic HTO applied in Publication 134 (OIR Part 2) to workers isapplied here to adult members of the public. The model is extended to pre-adult ages byadjustment of a set of parameter values representing turnover of body water and a second setof parameter values representing turnover of a substantial portion of the body’s carbon content.
70

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

2433
2434
2435
2436
2437

2438
2439
2440
2441
2442
2443
2444
2445
2446
2447
2448
2449
2450
2451
2452
2453
2454
2455

The turnover rate of body water is assumed to be the same as the turnover rate of tritium
retained in the body as tritiated water. The turnover rate of carbon is assumed to be the sameas the rate of turnover of tritium retained in the body as OBT.
The structure of the HTO model is shown in Fig. 5.1. Parameter values are listed inTable 5.3.

Fig. 5.1. Structure of the HTO systemic model. Transfer from blood to excreta (or excretion
pathways) is divided as follows: 55% to urinary bladder contents; 4% to right colon contents;
12% exhaled with no retention in lungs; 29% removed through the skin (sweat plus insensibleloss) with no retention in skin.
The model includes compartments representing blood, extravascular body water thatexchanges rapidly with blood, and two components of retention of tritium converted in vivo to
OBT. Excretion is from the blood compartment only. The following partition of excreted
tritium (not shown in Fig. 5.1) is applied to all age groups on the basis of reference data forwater balance in adult humans (ICRP, 2002a): urine (via the urinary bladder contents), 55%;
faeces (via the right colon contents), 4%; exhalation, 12%; and loss through skin (sweat plus
insensible loss), 29%. For the worker or adult member of the public, the transfer coefficientfrom Blood to Excreta yields an initial removal half-time from the body of about 10 d, and thetransfer coefficients from compartments OBT-1 and OBT-2 back to Extravascular HTO
correspond to half-times of about 40 d and 1 y, respectively.
Table 5.3. Transfer coefficients for the HTO model*

Path

Blood to Extravascular HTO
Extravascular HTO to OBT-1
Extravascular HTO to OBT-2
Blood to urinary bladder contents
Blood to RC-contents
Blood to Excreta
Extravascular HTO to Blood
OBT-1 to Extravascular HTO
OBT-2 to Extravascular HTO

2456
2457

Transfer coefficient (d-1)
Infant
1y
5y
10 y
15 y
4.00E+02 4.00E+02 4.00E+02 4.00E+02 4.00E+02
1.32E-03 1.26E-03 1.26E-03 9.00E-04 6.60E-04
1.76E-04 1.68E-04 1.68E-04 1.20E-04 8.80E-05
3.85E-01 3.85E-01 3.85E-01 3.85E-01 3.85E-01
2.80E-02 2.80E-02 2.80E-02 2.80E-02 2.80E-02
2.87E-01 2.87E-01 2.87E-01 2.87E-01 2.87E-01
9.68E+01 9.24E+01 9.24E+01 6.60E+01 4.84E+01
6.93E-02 4.33E-02 4.33E-02 3.47E-02 2.08E-02
7.60E-03 4.75E-03 4.75E-03 3.80E-03 2.28E-03*

RC = right colon

71

Adult
4.00E+02
6.00E-04
8.00E-05
3.85E-01
2.80E-02
2.87E-01
4.40E+01
1.73E-02
1.90E-03

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

2458
2459
2460
2461
2462
2463
2464
2465
2466
2467
2468
2469
2470
2471
2472
2473
2474
2475
2476
2477
2478
2479
2480
2481
2482
2483
2484
2485
2486
2487
2488
2489
2490
2491
2492
2493
2494

Derivation of age-specific parameter values for HTO entering the systemic circulation
follows the same general assumptions applied in Publication 56 (ICRP, 1990) to model HTO
kinetics. The turnover rate of tritium in the compartment in Fig. 5.1 labeled ‘Extravascular
HTO’ is estimated from reference values for energy expenditure and the mass of total-bodywater, based on the physiological premise that 1 ml of water is required for each kcal of energy
expended (ICRP, 1975). The turnover rate of tritium in the compartments labeled ‘OBT-1’ and‘OBT-2’ are based on derived relative age-specific rates of carbon turnover.
The age- and sex-specific values for energy expenditure applied here are taken from
Table 2.29 of Publication 89 (ICRP, 2002a). The mass of total-body water is assumed to be
74% of total-body mass in the infant; 60% at ages 1, 5, and 10 y; 59% in the 15-y-old and adultmale; 56% in the 15-y-old female; and 50% in the adult female (Altman and Katz, 1961). Ageand sex-specific total-body masses are taken from Publication 89 (ICRP, 2002a). Age-specificwater turnover rates are derived separately for males and females and then sex-averaged (androunded) for each age to estimate a sex-independent turnover rate. For example, the rate ofturnover of body water for a male or female at age 10 y is estimated as (1 kcal ml-1 × 1900 kcald-1)/ (32,000 g × 0.6 × 1 g/ml) = 0.099 d-1, where 1900 kcal d-1, 32,000 g, and 0.6 are reference
values for energy expenditure, total-body mass, and body water as a fraction of total-body mass,
respectively, at age 10 y. The derived water turnover rates for the infant and ages 1, 5, 10, and15 years, normalized to a value of 1 for the adult to derive scaling factors for extension of adulttransfer coefficients to younger ages, are 2.2, 2.1, 2.1, 1.5, and 1.1, respectively. (Normalized
rather than absolute turnover rates for HTO are used here because this potentially biased
method of derivation of HTO turnover rates overestimates the observed average retention timeof HTO in adults by roughly 10%.) These scaling factors are applied to outflow rates from thecompartment ‘Extravascular HTO’ (transfer coefficients a, c, and f in Fig. 5.1) in the model forthe adult. For example, based on a scaling factor for age 10 y of 1.5 and adult value of 44 d-1
for transfer coefficient f, the value assigned to transfer coefficient f for age 10 y is 1.5 × 44 d-1= 66 d-1.
The reader is referred to the section on carbon biokinetics for a discussion of themethod of derivation of relative turnover rates of carbon at different ages. The following
multiplicative factors given in the section on carbon are used to scale transfer coefficients band d in Fig. 5.1 (outflow rates from OBT compartments) from adult values to values for ages
100 d, 1 y, 5 y, 10 y, and 15 y, respectively: 4.0, 2.5, 2.5, 2.0, and 1.2. For example, based ona scaling factor for age 10 y of 2.0 and an adult value of 0.01733 d -1 for transfer coefficient b(Fig. 5.1), the value assigned to transfer coefficient b for age 10 y is 2.0 × 0.01733 d-1 = 0.03466
d-1.
The outflow rate from Blood is assumed to be independent of age. That is, adult values
for transfer coefficients e and g (Fig. 5.1) are assigned to all ages.

2495

5.1.3.3. OBT model

2496
2497
2498
2499
2500
2501
2502
2503
2504

ICRP Publication 56 recommended a default model for OBT in which it is assumed
that 50% of OBT entering the systemic circulation enters into bonds with carbon and is clearedwith the same half-time as carbon. The remaining 50% is assumed to be rapidly metabolized
to HTO.
Similar assumptions are made here regarding the initial behaviour of OBT following
its uptake to blood. Specifically, it is assumed as indicated in Fig. 5.2 that 50% of organicallybound tritium is converted to tritiated water upon entering blood and 50% moves immediately
to the compartment representing intermediate-term retention of organically bound tritium(OBT-1 in Fig. 5.2). Subsequently the fate of deposited tritium is described by the age-specific72

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

2505
2506
2507

2508
2509
2510
2511
2512
2513
2514

model for tritiated water describe above. That is, the transfer coefficients summarized in Table
5.3 apply to OBT as well as HTO subsequent to assignment of 50% of the absorbed OBT tocompartment OBT-1 and the remaining 50% to Blood.

Fig. 5.2. Structure of the model for tritium initially entering blood as OBT. This differs fromthe model for HTO only in that 50% of tritium entering Blood is assumed to transfer
immediately to OBT-1.

73

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

2515

5.2. Dosimetric data for tritium

2516

Table 5.4. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 3H compounds
Effective dose coefficients (Sv Bq-1)
Inhaled gases or vapours

3 mo

1y

5y

10 y

15 y

Adult

Tritiated water (HTO)

1.1E-10

7.2E-11

3.6E-11

2.7E-11

2.1E-112.0E-11

Tritium gas (HT)1.1E-14

7.2E-15

3.6E-15

2.7E-15

2.1E-15

2.0E-15

Tritiated methane (CH4–xTx)

3.3E-13

2.2E-13

1.1E-13

8.2E-14

6.2E-14

5.9E-14

Unspecified gas or vapour form (including unspecified 1.1E-10
organic vapours)

7.2E-11

3.6E-11

2.7E-11

2.1E-112.0E-11

Inhaled particulate materials (1 µm AMAD aerosols)
Type F, Biogenic organic compounds (OBT)

9.6E-11

8.0E-11

3.6E-11

2.7E-11

2.1E-11

2.2E-11

Type F, LaNi4.25Al0.75 tritide

5.5E-11

3.7E-11

1.6E-11

1.2E-11

8.3E-128.2E-12Type M, Glass fragments, luminous paint, titanium 2.6E-10
tritide, zirconium tritide; all unspecified compounds

2.2E-10

1.2E-10

7.1E-11

5.0E-11

4.6E-11

Type S, Carbon tritide, hafnium tritide

1.4E-09

1.4E-09

9.0E-10

6.1E-10

5.4E-10

5.6E-10Adult fA = 1.0, Tritium in food and other soluble forms 1.1E-10(as assigned to Type F for inhalation)

7.2E-11

3.6E-11

2.7E-112.0E-11

1.9E-11

Adult fA = 0.1, Relatively insoluble forms (Types M 2.2E-11
and S)

7.2E-12

3.6E-122.7E-12

2.1E-122.0E-12Adult fA = 1.0, Biogenic organic compounds (OBT)

1.5E-10

7.8E-11

5.8E-11

5.1E-11

5.1E-11

Ingested materials

1.9E-102517
74

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

6. CARBON (Z = 6)

2518
2519

6.1. Routes of Intake

2520

6.1.1. Inhalation

2521
2522
2523
2524
2525
2526
2527
2528
2529
2530
2531

Some information on absorption from the respiratory tract is available for inhaledgases of carbon in man and in experimental animals. Some information is also available on the
behaviour of 14C-labelled compounds and particles, mainly in rats, and on forms of carbon
labelled with other radionuclides. For details see Section 3 of Publication 134 (ICRP, 2016a).
Absorption parameter values and types, and associated fA values for gas and vapour forms ofcarbon are given in Table 6.1 and for particulate forms in Table 6.2 (both taken from Section 3of Publication 134). Exposures to both gas/vapour forms and particulate forms of carbon arecommon, and it is therefore recommended in this series of documents that in the absence of
information 50% particulate; 50% gas/vapour should be assumed.
Table 6.1. Deposition and absorption for gas and vapour forms of carbon*
Chemical form/origin
Carbon monoxide (CO)Carbon dioxide (CO2)Methane (CH4)
Unspecified

2532
2533
2534
2535
2536
2537
2538
2539
2540
2541
2542
2543
2544
2545
2546
2547
2548
2549
2550
2551

Percentage deposited†
Total ET1 ET2 BB bb
40§
0
8
4
8
§
100
0
20
10
20
0.3§ 00.06 0.03 0.06
100¶ 0
20
10
20

AI
20
50
0.15
50

Absorption
Type fA
**
V
**
V
**
V
F
1.0††

Systemicmodel‡CO
CO2
MethaneC

ET1, anterior nasal passage; ET2, posterior nasal passage, pharynx and larynx; BB, bronchial; bb, bronchiolar; AI,
alveolar-interstitial.
*
For carbon in unspecified gas or vapour form (including unspecified organic vapours), the default option forgases and vapours is recommended: 100% total deposition in the respiratory tract; default distribution between
regions¶ and Type F absorption. It is assumed that for carbon the bound state can be neglected i.e. fb = 0.
†
Percentage deposited refers to how much of the material in the inhaled air remains in the body after exhalation.
Almost all inhaled gas molecules contact airway surfaces, but usually return to the air unless they dissolve in, or
react with, the surface lining. In the case of methane, a small fraction is absorbed into body fluids and of that, afraction is metabolised and the rest subsequently exhaled.
‡
CO = Systemic model for carbon monoxide; CO2 = Systemic model for carbon dioxide/bicarbonate; C = Genericsystemic model for other 14C compounds (Section 3.2.3.2. of Publication 134, ICRP, 2016a).
§
Since instantaneous absorption to blood is assumed, calculations can be performed assuming direct injection intoblood, and the regional deposition does not need to be considered. However, for completeness, the default
distribution is assumed¶.
¶
Default distribution between regions (20% ET2, 10% BB, 20% bb and 50% AI).
**Not applicable for absorption Type V, because all activity deposited in the respiratory tract is instantaneously
absorbed.
††
The value of fA = 1 is applicable to all age-groups.

75

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

2552
2553

Table 6.2. Absorption parameter values for inhaled particulate forms of carbon and for ingested
carbonAbsorption parameter values†
Inhaled particulate materials*
Specific parameter values‡
Barium carbonatefrsr (d–1)

ss (d–1)

1

100

–

Default parameter values§,¶
Absorption Assigned forms
Type
F
–
1
100
–
M**
–
0.2
3
0.005
S
Elemental carbon, carbon tritide
0.01
3
1×10-4††
Ingested materials
Assigned forms*
Age-dependent absorption from the alimentary tract, fA
3 months 1 year
5 years
10 years 15 years adult
Barium carbonate‡
1
1
1
1
1
1
All other forms
1
1
1
1
1
1

2554
2555
2556
2557
2558
2559
2560
2561
2562
2563
2564
2565
2566
2567
2568
2569
2570
2571
2572
2573

*

2574

6.1.2. Ingestion

2575
2576
2577
2578
2579
2580
2581
2582
2583

For the general public, 14C in foodstuffs is the most important source of thisradionuclide. The uptake of carbon from the alimentary tract is highly dependent on the form
in which it is ingested and can be almost complete (for more details, see section 3 of ICRP,
2016a). Publication 30 (ICRP, 1981) and Publication 134 (ICRP, 2016a) recommended that,in the absence of compound-specific information, organic compounds labelled with radioactive
isotopes of carbon should be assumed to be completely absorbed from the gastrointestinal tract.
This recommendation is retained here for all organic compounds, including proteins,carbohydrates, fats and nucleic acids. The fA value is taken to be 1 for all chemical forms andall ages.

2584

6.1.3. Systemic Distribution, Retention and Excretion

Following uptake into body fluids, the generic systemic model for carbon is used (Section 3.2.3.2. of Publication
134, ICRP, 2016a), with the exception of barium carbonate, for which the carbon dioxide/bicarbonate systemic
model (Section 3.2.3.2.) is applied to the absorbed carbon.
†
It is assumed that for carbon the bound state can be neglected i.e. fb = 0. The value of sr for Type F forms ofcarbon (100 d–1) is element-specific. The values for Types M and S (3 d–1) are the general default values.
‡
See Section 3 of Publication 134 for summary of information on which parameter values are based, and on rangesof parameter values observed for individual materials. For barium carbonate, Type F default parameter values areused for absorption from the respiratory and alimentary tracts, but a specific systemic model, carbon
dioxide/bicarbonate, for absorbed carbon.
§
Materials (e.g. elemental carbon) are generally listed here where there is sufficient information to assign to adefault absorption Type, but not to give specific parameter values (see Section 3 of Publication 134).
¶
For inhaled material deposited in the respiratory tract and subsequently cleared by particle transport to thealimentary tract, the default fA values for inhaled materials are applied: i.e. the product of fr for the absorption
Type and the fA value for ingested soluble forms of carbon applicable to the age-group of interest (1.0).
**
Default Type M is recommended for use in the absence of specific information on which the exposure material
can be assigned to an absorption type, e.g. if the form is unknown, or if the form is known but there is no
information available on the absorption of that form from the respiratory tract.
††
Activity transferred from systemic compartments into segments of the alimentary tract is assumed to be subject
to reabsorption to blood. The default absorption fraction fA for the secreted activity is the highest value foringestion of the radionuclide applicable to the age-group of interest (1.0).

76

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

2585

6.1.3.1. Background

2586
2587
2588
2589
2590
2591
2592
2593
2594
2595
2596
2597
2598
2599
2600
2601
2602
2603
2604
2605
2606
2607
2608
2609
2610
2611
2612
2613
2614

The biokinetics of systemic carbon depends on the carbon compound taken into thebody. Internally deposited 14C-labelled compounds have shown residence times varying froma few hours to several months in human volunteers. The distribution of radiocarbon in the bodyand the fractions of ingested or inhaled activity lost by exhalation, urinary excretion, and faecal
excretion also depend on the nature of the carbon compound taken into the body (Publication
134, ICRP, 2016a).
Results of animal studies indicate that the metabolism of some 14C-labelled
compounds varies with age. For example, metabolic incorporation and release of 14C fromlabelled glycine or stearic acid was more rapid in young rats than in mature rats (Medovar,
1976; Osipov, 1983). At 8-30 d following intraperitoneal injection of 14C-labeled carbonate,
the biological half-time of 14C in bone was 12-15 d in growing rats and 30-40 d in mature rats
(Schubert and Armstrong, 1949).
On the other hand, some 14C-labelled compounds have shown little if any variation
with age in 14C kinetics. For example, Leide-Svegborn et al. (1999) studied the biokinetics of
14
C in four adults and eight children (ages 7-14 y) undergoing 14C urea breath test for
Helicobacter pylori (HP) infection, and in four adult volunteers. After oral administration of
14
C-urea, samples of exhaled air were taken up to 180 d after administration and samples ofurine were collected up to 40 d. In 16 subjects including 11 patients who were not HP positive,~88% of the administered activity was excreted in urine over the first 3 d in both adults andchildren. Adults exhaled slightly more activity on average than did children over the first 20 d.
In Publication 56 (ICRP, 1990), a generic systemic biokinetic model was applied to
14
C-labelled compounds for which specific biokinetic data are not available. It was assumed
that inhaled or ingested 14C-labelled compounds are instantly and uniformly distributed
throughout all tissues of the body and removed from the body with biological half-time that
increases with increasing age. The half-time for a given age was based on balance
considerations. For example, the half-time for an adult was derived from the assumptions ofdaily carbon intake of 0.3 kg and a carbon pool of mass 16 kg in Reference Man (ICRP, 1975):
T1/2 = ln 2 × total body carbon / daily carbon intake = 0.693(16/0.3) ~ 40 d. Half-times of 8, 15,
19, 26, and 32 d were derived for the infant and ages 1, 5, 10, and 15 y, respectively.

2615

6.1.3.2. Biokinetic models for systemic carbon

2616
2617
2618
2619
2620
2621

In this publication, compound-specific biokinetic models are applied to carbon thatreaches the systemic circulation as carbon monoxide, carbon dioxide, bicarbonate, or methane.
A common model is applied to carbon dioxide and bicarbonate. A generic systemic model for
carbon is applied to unspecified forms of carbon. For example, the generic model is used todevelop dose coefficients for inhalation of particulate forms of carbon described as Type F,
Type M, or Type S material.

2622(a) Generic model

2623
2624
2625
2626
2627
2628
2629

The generic model for the adult member of the public is the same as the generic modelfor occupational intake of carbon applied in Publication 134 (OIR Part 2). The model isextended to pre-adults by introduction of age-specific parameter values that reflect fasterturnover of body carbon in infants, children, and adolescents than in adults.
The structure of the generic model and its connections to the respiratory andalimentary tract models are shown in Fig. 6.1. Age-specific transfer coefficients are listed inTable 6.3.
77

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

2630

2631
2632
2633
2634
2635
2636

Fig. 6.1. Structure of the generic model for radiocarbon labelled substances. HRTM is the
Human Respiratory Tract Model. HATM is the Human Alimentary Tract Model. Activity
transferred to Colon enters Right colon contents.
Table 6.3. Transfer coefficients for the generic model for systemic carbon *†PathBlood to Short-term tissue
Blood to Long-term tissue
Blood to UB contents
Short-term tissue to Blood
Short-term tissue to CO2 model‡
Short-term tissue to RC contentsLong-term tissue to CO2 model‡

2637
2638
2639
2640
2641
2642
2643
2644
2645
2646
2647
2648
2649
2650

Infant
1.20E+00
3.00E-01
1.50E+00
3.70E-01
2.77E-01
6.93E-02
3.96E-02

Transfer coefficient (d-1)
1y
5y
10 y
15 y
1.20E+00 1.20E+00 1.20E+00 1.20E+00
3.00E-01 3.00E-01 3.00E-01 3.00E-01
1.50E+00 1.50E+00 1.50E+00 1.50E+00
2.31E-01 2.31E-01 1.85E-01 1.11E-01
1.73E-01 1.73E-01 1.39E-01 8.32E-02
6.93E-02 6.93E-02 6.93E-02 6.93E-02
2.48E-02 2.48E-02 1.98E-02 1.19E-02

Adult
1.20E+00
3.00E-01
1.50E+00
9.24E-02
6.93E-02
6.93E-02
9.90E-03*

In addition to transfer coefficients in the CO2 model described in this section
UB = urinary bladder, RC = right colon‡
Initially enters Blood 1 in the CO2 model†

The behaviour of carbon that reaches blood is assumed to vary with age due to two
factors: (1) a decrease with increasing age in the turnover rate of relatively exchangeable carbon(assumed to be the carbon contained in soft tissues and bone surface) due to a decrease inenergy expenditure per unit mass of stable carbon, and (2) a decrease with increasing age in theturnover rate of carbon in bone volume due to a decreasing bone turnover rate. The distributionof carbon outflow from blood and the rate of movement of carbon from bone surface to bonevolume are assumed to be independent of age.
Differences with age in the rate of removal of carbon from systemic compartments
other than bone volume compartments are based on age- and sex-specific reference values forenergy expenditure, EA, at age A (infant, 1 y, 5 y, 10 y, 15 y, or adult) tabulated in Publication

78

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

2651
2652
2653
2654
2655
2656
2657
2658
2659
2660
2661
2662
2663
2664
2665
2666
2667
2668
2669

89 (ICRP, 2002a), and estimates of the stable carbon content CA of the total body minus bonevolume at age A. The mass of carbon transferred daily from soft tissues plus bone surface toblood is assumed to be proportional to energy expenditure with the proportionality constant kbeing independent of age. CA is based on a formula proposed by Kyere et al. (1982), in which
total-body carbon excluding that in bone mineral is estimated as (0.77 × F) + (3.25 × N), where
F is the mass of body fat and N is essentially the mass of body nitrogen excluding nitrogen inbone. Age-specific values of F and N applied here are based on Tables 2.3.1 and Table 13.2,
respectively, of Publication 89 (ICRP, 2002a). For a given sex and pre-adult age A, the rate ofremoval of carbon from a soft-tissue or bone-surface compartment relative to that for an adultof the same sex is estimated as (EA / CA) / (Eadult / Cadult), and the rounded average of relativevalues for males and females is used to scale selected parameter values (outflow rates fromcertain tissues to blood) from the adult to age A. Specifically, the following multiplicative
factors are used to scale transfer coefficients from soft tissues or bone surface to blood in adults
to corresponding transfer coefficients for ages 100 d, 1 y, 5 y, 10 y, and 15 y, respectively: 4.0,
2.5, 2.5, 2.0, and 1.2.
The rate of removal of carbon from trabecular or cortical bone volume at a given age
is assumed to be the same as the rate of bone turnover for that bone type at that age. Reference
age-specific trabecular and cortical bone turnover rates are taken from Publication 89 (ICRP,
2002a).

2670(b) Model for carbon monoxide

2671
2672

The systemic model for occupational inhalation of CO applied in Publication 134(OIR Part 2) is assigned here to all age groups.

2673(c) Model for carbon dioxide and bicarbonate

2674
2675
2676
2677
2678
2679
2680
2681
2682

A common model is applied here to systemic carbon taken into the body as carbon
dioxide or bicarbonate. The model structure is shown in Fig. 6.2. Age-specific parameter values
are listed in Table 6.4.
The model for the adult is the same as the systemic model applied in OIR Part 2(Publication 134) to inhalation of carbon dioxide by a worker. The method of extension ofparameter values for the adult to pre-adult ages is the same as that for the generic model for
carbon described above. In fact, this model for carbon dioxide is a sub-model of the genericmodel described above (see box labeled ‘CO2 model’ in Fig. 6.1).

79

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

2683
2684
2685
2686
2687
2688

Fig. 6.2. Structure of the systemic model used in this report for carbon taken into the body as
carbon dioxide or bicarbonate. Values in parentheses are removal half-times. ST0, ST1, ST2,and ST3 are soft tissue (ST) compartments.
Table 6.4. Transfer coefficients in the model for systemic carbon dioxide and bicarbonate*

Path

Blood 1 to environment
Blood 1 to ST0
Blood 1 to ST1
Blood 1 to ST2
Blood 1 to ST3
Blood 1 to Trabecular surface
Blood 1 to Cortical surface
Blood 1 to Trabecular volume
Blood 1 to Cortical volume
Blood 1 UB contents
Blood 1 to RC contents
ST0 to Blood 1
ST1 to Blood 1
ST2 to Blood 1
ST3to Blood 1
ST1 to Blood 2
ST2 to Blood 2
ST3 to Blood 2
Trabecular surface to Blood 1
Cortical surface to Blood 1
Trabecular volume to Blood 1

Infant
3.65E+01
6.00E+01
1.80E+00
3.00E-01
4.40E-01
9.00E-02
6.00E-02
6.00E-03
4.00E-03
6.50E-01
1.50E-01
2.00E+02
5.32E+00
8.87E-01
6.66E-02
2.22E-01
3.70E-02
2.77E-03
6.93E-02
6.93E-02
8.22E-03

1y
3.65E+01
6.00E+01
1.80E+00
3.00E-01
4.40E-01
9.00E-02
6.00E-02
6.00E-03
4.00E-03
6.50E-01
1.50E-01
1.25E+02
3.33E+00
5.55E-01
4.16E-02
1.39E-01
2.31E-02
1.73E-03
4.33E-02
4.33E-02
2.88E-03

80

Transfer coefficient (d-1)
5y
10 y
3.65E+01
3.65E+01
6.00E+01
6.00E+01
1.80E+00
1.80E+00
3.00E-01
3.00E-01
4.40E-01
4.40E-01
9.00E-02
9.00E-02
6.00E-02
6.00E-02
6.00E-03
6.00E-03
4.00E-03
4.00E-03
6.50E-01
6.50E-01
1.50E-01
1.50E-01
1.25E+02
9.98E+01
3.33E+00
2.66E+00
5.55E-01
4.44E-01
4.16E-02
3.33E-02
1.39E-01
1.11E-01
2.31E-02
1.85E-02
1.73E-03
1.39E-03
4.33E-02
3.47E-02
4.33E-02
3.47E-02
1.81E-03
1.32E-03

15 y
3.65E+01
6.00E+01
1.80E+00
3.00E-01
4.40E-01
9.00E-02
6.00E-02
6.00E-03
4.00E-03
6.50E-01
1.50E-01
5.99E+01
1.60E+00
2.66E-01
2.00E-02
6.65E-02
1.11E-02
8.32E-04
2.08E-02
2.08E-02
9.59E-04

Adult
3.65E+01
6.00E+01
1.80E+00
3.00E-01
4.40E-01
9.00E-02
6.00E-02
6.00E-03
4.00E-03
6.50E-01
1.50E-01
4.99E+01
1.33E+00
2.22E-01
1.66E-02
5.55E-02
9.24E-03
6.93E-04
1.73E-02
1.73E-02
4.93E-04

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
Cortical volume to Blood 1
Blood 2 to UB contents

8.22E-03 2.88E-03
1.00E+03 1.00E+03

1.53E-03
1.00E+03

9.04E-04
1.00E+03

5.21E-04 8.21E-05
1.00E+03 1.00E+03

2689

*

2690

(d) Model for methane

2691
2692
2693
2694
2695
2696
2697
2698
2699
2700

The age-specific biokinetic model for systemic carbon inhaled as methane extends themodel for occupational intake of methane applied in Publication 134 (OIR Part 2) to pre-adultages. The generic model structure for carbon (Fig. 6.1 and Fig. 6.2) is modified by the additionof a blood compartment that receives methane absorbed from the respiratory tract. For all age
groups it is assumed that carbon leaves this blood compartment with a half-time of 10 min,with 70% removed in expired air and 30% depositing in the short-term soft-tissue compartment
shown in Fig. 6.1. Outflow rates from all blood compartments are assumed to be independentof age. Other transfer coefficients in the model are taken from the age-specific generic model
for systemic carbon defined in Table 6.3. Transfer coefficients for the generic model forsystemic carbon*Table 6.3 and Table 6.4.

UB = urinary bladder, RC = right colon81

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

2701

6.2. Dosimetric data for carbon

2702

Table 6.5. Committed effective dose coefficients (Sv Bq -1) for the inhalation or ingestion of 14C compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled gases or vapours

3 mo

1y

5y

10 y

15 y

Adult

Carbon monoxide (CO)1.9E-11

1.2E-11

5.8E-12

3.5E-12

2.1E-12

1.8E-12

Carbon dioxide (CO2)

4.6E-11

4.6E-11

2.1E-11

1.4E-11

1.5E-11

1.3E-11

Methane (CH4)

4.6E-13

3.1E-13

1.6E-13

9.8E-14

5.9E-14

5.1E-14

Unspecified

5.4E-105.0E-10

2.6E-10

1.9E-10

1.7E-10

1.7E-10

Type F, Barium carbonate (CO2 model)

4.2E-11

3.8E-11

1.6E-11

1.0E-11

8.9E-128.0E-12Type F

2.8E-10

2.6E-10

1.2E-10

8.4E-11

6.7E-11

7.0E-11

Type M, All unspecified forms

4.0E-09

3.5E-09

2.0E-09

1.3E-09

1.0E-09

9.7E-10

Type S, Elemental carbon, carbon tritide

2.5E-08

2.4E-08

1.8E-08

1.3E-08

1.3E-08

1.3E-08

Adult fA = 1.0, All chemical forms

5.1E-10

4.7E-10

2.5E-10

1.8E-10

1.6E-10

1.6E-10Adult fA = 1.0, Bicarbonate

4.8E-11

4.8E-11

2.3E-11

1.5E-11

1.5E-11

1.3E-11

Inhaled particulate materials (1 µm AMAD aerosols)

Ingested materials

2703

82

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

7. PHOSPHORUS (Z = 15)

2704
2705

7.1. Routes of Intake

2706

7.1.1. Inhalation

2707
2708
2709
2710
2711
2712
2713
2714

Information on absorption from the respiratory tract is available from a few
experimental studies on the behaviour of inhaled phosphorus. However, most of it relates tophosphates for which the cation, rather than the phosphorus itself, was radiolabelled. For details
see Section 4 of Publication 134 (ICRP, 2016a). Absorption parameter values and types, andassociated fA values for particulate forms of phosphorus are given in Table 7.1 (taken from
Section 4 of Publication 134).
Table 7.1. Absorption parameter values for inhaled and ingested phosphorus
Absorption parameter values*sr (d–1)
ss (d–1)

Inhaled particulate materials
fr
Default parameter values†,‡
Absorption Assigned forms
TypeF
Sodium phosphate
1
1
–
§
M
Yttrium, stannic and zinc 0.2
10.005
phosphates
S
–
0.01
1
1×10-4¶
Ingested materials
Assigned forms
Age-dependent absorption from the alimentary tract, fA
3 months 1 year
5 years
10 years 15 years adultAll forms
1
0.9
0.9
0.9
0.9
0.8

2715
2716
2717
2718
2719
2720
2721
2722
2723
2724
2725
2726
2727
2728
2729

*

2730

7.1.2. Ingestion

2731

7.1.2.1. Adults

2732
2733
2734
2735

Dietary phosphorus in the form of inorganic phosphate and phosphorus-containing
biomolecules such as nucleic acids and phospholipids is well absorbed from the small intestine.
High calcium diets may precipitate calcium phosphate and reduce the availability of phosphate;
however, vitamin D, sodium phytate and fat counteract this tendency (For details see

It is assumed that for phosphorus the bound state can be neglected i.e. fb = 0. The values of sr for Type F, M and
S forms of phosphorus (1 d–1) are element-specific.
†
Materials (e.g. sodium phosphate) are listed here where there is sufficient information to assign to a default
absorption type, but not to give specific parameter values (see Section 4 of Publication 134, ICRP, 2016a).
‡
For inhaled material deposited in the respiratory tract and subsequently cleared by particle transport to thealimentary tract, the default fA values for inhaled materials are applied: i.e. the product of fr for the absorption
Type and the fA value for ingested soluble forms of phosphorus applicable to the age-group of interest (e.g. 0.8
for adults).
§
Default Type M is recommended for use in the absence of specific information on which the exposure material
can be assigned to an absorption type, e.g. if the form is unknown, or if the form is known but there is no
information available on the absorption of that form from the respiratory tract.
¶
Activity transferred from systemic compartments into segments of the alimentary tract is assumed to be subject
to reabsorption to blood. The default absorption fraction fA for the secreted activity is the highest fA value foringestion of the radionuclide applicable to the age-group of interest (e.g. 0.8 for adults).

83

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

2736
2737
2738

Publication 100, ICRP, 2006, and Section 4 of Publication 134, 2016a). In Publication 30(ICRP, 1979) and in the OIR Series (ICRP, 2016a) the recommended absorption fraction was
0.8 for all compounds of the element. This value is used here; that is, fA = 0.8 for all compounds.

2739

7.1.2.2. Children

2740
2741
2742
2743

The Food and Nutrition Board of the US Institute of Medicine reports somewhat
higher absorption values in infants and children than in adults (Institute of Medicine, 1997). A
value of fA = 0.9 is used here for 1-, 5-, 10- and 15-y-old children. For 3-month-old infants, anfA of 1 is adopted here.

2744

7.1.3. Systemic Distribution, Retention and Excretion2745

7.1.3.1. Age-specific data

2746
2747
2748
2749
2750
2751
2752
2753
2754
2755
2756
2757
2758
2759
2760
2761
2762
2763
2764
2765
2766
2767
2768

The behavior of phosphorus in bone closely resembles that of calcium. Rapid uptakeof both elements occurs on all bone surfaces. Calcium and phosphorus diffuse throughout bonevolume within a few hours to days after uptake to blood. Both elements can penetrate into theinterior of bone crystal. The exchangeable and non-exchangeable fractions of the total bonemineral are approximately the same for phosphorus and calcium (Neuman and Neuman, 1958;
Parfitt and Kleerekoper, 1980).
Uptake of calcium or phosphorus is much greater in forming or growing bone than inmature bone. Phosphorus and calcium show high concentration in forming osteons (Parfitt andKleerekoper, 1980). In rats injected intraperitoneally with 32P, skeletal uptake decreased withincreasing age at injection, from about 90% of the injected amount at age 15 d to about 17% at
age 170 d (Bonner, 1948).
Stather (1974) compared the distribution and retention of 32P and the alkaline earths
45
85
Ca, Sr, and 133Ba in the mouse skeleton. At 24 h after intraperitoneal injection into 8-weekold mice the distribution of the four radionuclides was virtually the same throughout theskeleton, but skeletal content as a percentage of injected activity differed from one radionuclide
to another: 32P, 21.6%; 45Ca, 61.5%; 85Sr, 37.3%; and 133Ba, 48.8%. The skeletal burden
represented about 37% of total-body 32P compared with about 90% of total-body 85Sr.
Bauer and Carlsson (1955) compared the uptake of 32P and 45Ca by bone (tibial shaft)and incisors in adult rats over the first 5 d after simultaneous subcutaneous injection of theseradionuclides. The percentage of the administered 45Ca found in bone was consistently about
2.3 times the percentage of administered 32P in the same bone samples at corresponding times
after administration. The ratio of uptake of 45Ca and 32P was about the same for incisors as for
bone.

2769

7.1.3.2. Systemic model

2770
2771
2772
2773
2774
2775
2776

The structure of the age-specific biokinetic model for systemic phosphorus and thetransfer coefficients for the adult member of the public are the same as in the model forphosphorus for the worker, adopted in Publication 134 (ICRP, 2016a). The model structure isshown in Fig. 7.1. Transfer coefficients for all six ages at intake are listed in Table 7.2.
The extension of transfer coefficients for phosphorus from mature adults to pre-adultages is based on the age-specific data summarized above together with analogy with the agespecific model for calcium applied in this report and in Publication 71 (ICRP, 1995b).

84

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

2777
2778
2779
2780
2781
2782
2783
2784
2785
2786
2787
2788
2789
2790

Fig. 7.1. Structure of the model for systemic phosphorus. Activity transferred from Plasma to
Alimentary tract contents enters Right colon contents. Activity transferred from Alimentarytract contents to Plasma represents activity absorbed from Small intestine contents to Plasma.
Abbreviations: exch = exchangeable, nonexch = non-exchangeable, RBC = red blood cells.

Deposition fractions for phosphorus on trabecular and cortical bone surfaces at a given
age are assumed to be 0.8 times corresponding values for calcium. Transfer coefficients
describing the translocation of calcium in the skeleton and removal from skeletal compartments
to blood are applied without change to phosphorus. Based on these assumptions the percentageof administered radiocalcium in bone will be roughly 2.3 times the percentage of administeredradiophosphorus beyond a few days post administration due to faster excretion and hence lower
recycling of phosphorus than calcium.

85

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

2791

2792
2793
2794

Table 7.2. Age-specific transfer coefficients for phosphorus

Patha

Infant1yTransfer coefficient (d-1)
5y
10 y
15 y

Plasma to UB-contents
Plasma to RC-contents
Plasma to Trab. surface
Plasma to Cort. surface
Plasma to ST0
Plasma to ST1
Plasma to ST2
Plasma to RBC
Plasma to Urinary path
Plasma to Other kidney tissue
Plasma to Liver 1
RBC to Plasma
ST0 to Plasma
ST1 to Plasma
ST2 to Plasma
Urinary path to UB-contents
Other kidney tissue to Plasma
Liver 1 to Liver 2
Liver 1 to Plasma
Liver 2 to Plasma
Cort. surface to Plasma
Cort. surface to Exch. Cort.
volumeTrab. surface to Plasma
Trab. surface to Exch. Trab.
volumeExch. Cort. volume to Cort.
surface
Exch. to Nonexch. Cort.
volumeExch. Trab. volume to Trab.
surface
Exch. to Nonexch. Trab.
volumeNonexch. Cort. volume to
PlasmaNonexch. Trab. volume to
Plasma

2.20E+00
1.00E-01
4.80E+00
1.92E+01
5.09E+00
5.09E+00

3.52E+00
1.60E-01
2.88E+00
1.15E+01
8.14E+00
8.14E+00

3.74E+00
1.70E-01
2.84E+00
9.96E+00
8.65E+00
8.65E+00

3.04E+00
1.38E-01
4.52E+00
1.34E+01
7.02E+00
7.02E+00

2.24E+00
1.02E-01
6.61E+00
1.71E+01
5.19E+00
5.19E+00

4.40E+00
2.00E-01
4.44E+00
3.56E+00
1.02E+01
1.02E+01

5.00E-02
1.20E+00
2.00E-01
7.00E-02
2.00E+00
6.93E-01

8.00E-02
1.92E+00
3.20E-01
1.12E-01
3.20E+00
6.93E-01

8.50E-02
2.04E+00
3.40E-01
1.19E-01
3.40E+00
6.93E-01

6.90E-02
1.66E+00
2.76E-01
9.66E-02
2.76E+00
6.93E-01

5.10E-02
1.22E+00
2.04E-01
7.14E-02
2.04E+00
6.93E-01

1.00E-01
2.40E+00
4.00E-01
1.40E-01
4.00E+00
6.93E-01

3.47E-01
3.47E-02
3.80E-04
6.93E-01
3.47E-02
3.47E-01
1.04E+00
3.47E-02
5.78E-01
1.16E-01

3.47E-01
3.47E-02
3.80E-04
6.93E-01
3.47E-02
3.47E-01
1.04E+00
3.47E-02
5.78E-01
1.16E-01

3.47E-01
3.47E-02
3.80E-04
6.93E-01
3.47E-02
3.47E-01
1.04E+00
3.47E-02
5.78E-01
1.16E-01

3.47E-01
3.47E-02
3.80E-04
6.93E-01
3.47E-02
3.47E-01
1.04E+00
3.47E-02
5.78E-01
1.16E-01

3.47E-01
3.47E-02
3.80E-04
6.93E-01
3.47E-02
3.47E-01
1.04E+00
3.47E-02
5.78E-01
1.16E-01

3.47E-01
3.47E-02
3.80E-04
6.93E-01
3.47E-02
3.47E-01
1.04E+00
3.47E-02
5.78E-01
1.16E-01

5.78E-01
1.16E-01

5.78E-01
1.16E-01

5.78E-01
1.16E-01

5.78E-01
1.16E-01

5.78E-01
1.16E-01

5.780E-01
1.160E-01

2.77E-03

2.77E-03

2.77E-03

2.77E-03

2.77E-03

2.77E-03

4.16E-03

4.16E-03

4.16E-03

4.16E-03

4.16E-03

4.16E-03

2.77E-03

2.77E-03

2.77E-03

2.77E-03

2.77E-03

2.77E-03

4.16E-03

4.16E-03

4.16E-03

4.16E-03

4.16E-03

4.16E-03

8.22E-03

2.88E-03

1.53E-03

9.04E-04

5.21E-04

8.21E-05

8.22E-03

2.88E-03

1.81E-03

1.32E-03

9.59E-04

4.93E-04

Adult

Abbreviations: UB = urinary bladder, RBC = red blood cells, Trab = trabecular, Cort = cortical, Exch =exchangeable, Non-exch = non-exchangeable, RC = Right colon

86

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

2795

7.2. Dosimetric data for phosphorus

2796
2797

Table 7.3. Committed effective dose coefficients (Sv Bq -1) for the inhalation or ingestion of 32P compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled particulate materials (1 µm AMAD aerosols) 3 mo

1y

5y

10 y

15 y

Adult

Type F, Sodium phosphate

1.3E-08

7.3E-09

3.1E-09

1.9E-09

1.4E-09

9.2E-10

Type M, Yttrium, stannic and zinc phosphates; allunspecified forms
1.1E-08

8.4E-09

4.5E-09

3.0E-09

2.3E-09

2.1E-09

Type S

1.1E-08

9.2E-09

5.1E-09

3.5E-09

2.6E-09

2.5E-09

2.4E-08

1.3E-08

6.2E-09

3.5E-09

2.9E-09

1.7E-09

Ingested materials
Adult fA = 0.8, All forms

2798

87

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

8. SULPHUR (Z = 16)

2799
2800

8.1. Routes of Intake

2801

8.1.1. Inhalation

2802
2803
2804
2805
2806
2807
2808
2809
2810
2811
2812
2813

Some information on absorption from the respiratory tract is available for inhaledgases of sulphur in man and in experimental animals. Most of the information available on
inhaled particulate forms of sulphur relates to sulphates. For details see Section 5 of Publication
134 (ICRP, 2016a).
Absorption parameter values and types, and associated fA values for gas and vapour
forms of sulphur are given in Table 8.1 and for particulate forms in Table 8.2,( taken from
Section 5 of of Publication 134).
Exposures to both gas/vapour forms and particulate forms of sulphur are common,and it is therefore recommended in this series of documents that in the absence of site-specificinformation 50% particulate; 50% gas/vapour should be assumed.
Table 8.1. Deposition and absorption for gas and vapour forms of sulphur *Chemical form/origin
Sulphur dioxide
Carbon disulphide
Hydrogen sulphide
Carbonyl sulphide
Other organic
Unspecified*

2814
2815
2816
2817
2818
2819
2820
2821
2822
2823
2824
2825
2826
2827
2828

Total
100§
100§
100§
100§
100§
100§

Percentage deposited†
ET1 ET2 BB bb
0
20
10
20
0
20
10
20
0
20
10
20
0
20
10
20
0
20
10
20
0
20
10
20

AI
50
50
50
50
50
50

Absorption
Type fA¶
F
1.0
F
1.0
F
1.0
F
1.0
F
1.0
F
1.0

Systemic model‡
Inorganic
Inorganic
Inorganic
Inorganic
Organic
Inorganic

ET1, anterior nasal passage; ET2, posterior nasal passage, pharynx and larynx; BB, bronchial; bb, bronchiolar; AI,
alveolar-interstitial.
*
For sulphur in unspecified gas or vapour form, the default option for gases and vapours is recommended: 100%
total deposition in the respiratory tract; default distribution between regions§ and Type F absorption. It is assumed
that for sulphur the bound state can be neglected i.e. fb = 0.
†
Percentage deposited refers to how much of the material in the inhaled air remains in the body after exhalation.
Almost all inhaled gas molecules contact airway surfaces, but usually return to the air unless they dissolve in, or
react with, the surface lining. For the forms of sulphur considered here, it is assumed that most, if not all, of theinhaled sulphur is absorbed into body fluids.
‡
Systemic models for inorganic sulphur and organic sulphur, Section 8.13.
§
Default distribution between regions (20% ET2, 10% BB, 20% bb and 50% AI).
¶The value of fA = 1 is applicable to all age-groups.

88

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

2829
2830
2831

Table 8.2. Absorption parameter values for inhaled particulate forms of sulphur and foringested sulphur*

Inhaled particulate materials
fr
Default parameter values‡,§
Absorption Assigned forms
Type
F
Caesium, nickel, strontium, thorium 1
sulphates¶**
M
Barium sulphate
0.2
S
—
0.01

Absorption parameter values†sr (d–1)
ss (d–1)

30

-

3
3

0.005
0.0001

Ingested materials††
Assigned forms

Age-dependent absorption from the alimentary tract, fA
3 months 1 year
5 years
10 years 15 years adult
Organic sulphur in food and 1
1
1
1
1
1
all soluble forms
Most forms of inorganic 1
1
1
1
1
1
sulphurSpecific inorganic sulphur: 0.2
0.1
0.1
0.1
0.1
0.1
Elemental
sulphurandthiosulphate

2832
2833
2834
2835
2836
2837
2838
2839
2840
2841
2842
2843
2844
2845
2846
2847

*

2848

8.1.2. Ingestion2849

8.1.2.1. Adults

2850
2851
2852
2853
2854
2855
2856
2857
2858
2859

Elemental sulphur and thiosulphate were found to be little absorbed after oral
administration. Some other inorganic forms of sulphur were shown to be completely absorbed.
Volwiler et al. (1955) reported that the fractional absorption of sulphur in adult men was
greater than 0.6 for organic compounds. Minski and Vennart (1971) measured absorption inrats and obtained a mean value for the absorption fraction of 35S 1-methionine of 0.92 ± 0.18(± 1 SD). Because there appears to be almost complete absorption of 35S ingested as aminoacids or other organic compounds, almost complete absorption of 35S incorporated in foodstuffs
is expected to occur. ICRP Publication 30 (ICRP, 1980) recommended absorption fractions of
0.8 for inorganic forms of sulphur and 0.1 for elemental sulphur. In Publication 134 (ICRP,
2016a), the recommended fA values were 1 for unspecified inorganic and organic compounds,

Following uptake into body fluids, the systemic model for inorganic sulphur is used, (see Section 8.1.3.1)
It is assumed that for sulphur the bound state can be neglected i.e. fb = 0. The values of sr for Type F, M and S
forms of sulphur (30, 3 and 3 d–1, respectively) are the general default values.
‡
Materials (e.g. caesium sulphate) are generally listed here where there is sufficient information to assign to adefault absorption type, but not to give specific parameter values (see Section 5 of Publication 134, ICRP, 2016a).
§
For inhaled material deposited in the respiratory tract and subsequently cleared by particle transport to thealimentary tract, the default fA values for inhaled materials are applied: i.e. the product of fr for the absorption type
and the fA value for ingested soluble forms of sulphur applicable to the age-group of interest (1.0).
¶
In the case of thorium sulphate the thorium is assigned to Type M and the sulphur to Type F.
**
Default Type M is recommended for use in the absence of specific information on which the exposure material
can be assigned to an absorption type, e.g. if the form is unknown, or if the form is known but there is no
information available on the absorption of that form from the respiratory tract.
††
Activity transferred from systemic compartments into segments of the alimentary tract is assumed to be subject
to reabsorption to blood. The default absorption fraction fA for the secreted activity is the highest fA value foringestion of the radionuclide applicable to the age-group of interest (1.0).
†

89

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

2860
2861
2862

and 0.1 for elemental sulphur and thiosulphate. For sulphur present in the diet, an absorption
fraction of 1 was adopted by Publication 67 (ICRP, 1993). The same value of fA = 1 is adopted
here. For ingestion of elemental sulphur and thiosulphate a lower fA = 0.1 is adopted.

2863

8.1.2.2. Children

2864
2865
2866
2867
2868
2869
2870
2871

There are few data available on the absorption of sulphur in infants and children. Shohland Sato (1923) showed that an 8-month-old baby lost about 3% of its dietary sulphur intake
in faeces, which indicates absorption of at least 97%. This value is consistent with available
data for adults. However, Wright et al. (1960) reported sulphur balance studies which indicatedthat 68-90% of dietary sulphur was absorbed by pre-adolescent girls, apparently depending on
dietary nitrogen levels. An f A value of 1 is adopted here for infants and children for sulphur
ingested in food and in soluble forms. An f A value of 0.2 is adopted for ingestion of elemental
sulphur and thiosulphate by 3 month old infants.

2872

8.1.3. Systemic Distribution, Retention and Excretion

2873
2874
2875
2876
2877
2878
2879
2880
2881
2882
2883
2884
2885
2886
2887
2888
2889
2890
2891
2892
2893
2894

By 15 min post intraperitoneal administration of 35S as sodium sulfate to 7-day-old
rats, radiographs revealed the highest activity concentration in cartilage at the epiphysealdiaphyseal junction of long bones and lower concentrations throughout the epiphysis(Dziewiatkowski, 1952). The pattern of deposition did not change over the first 24 h, and theconcentration in cartilage continued to increase during that time. The activity in articularcartilage appeared to decrease by roughly one-third from 1 to 4 days after injection.
Dziewiatkowski (1954) administered 35S-labeled sodium sulfate to 10-, 30-, and 300day-old rats by intraperitoneal injection and determined activity in fluids and tissues at 12, 24,
48, and 96 h. Over the first 24 hours about 51% and 64% of the administered activity was
excreted by 30- and 300-day-old rats, respectively. At 1 d the concentration of 35S in ends offemurs of 10-day-old rats was about 10 times that in 30-day-old rats and 25 times that in 300day-old rats. Measurements of activity in femurs and humeri indicated that activity had been
incorporated mainly into chondroitin sulfate of growing cartilage.
McElligott and Collins (1960) studied the in vitro uptake of 35S-labeled sulphate insamples of human articular and costal cartilage from human subjects. The samples werecollected at 44 necropsies on subjects ranging in age from 5 d to 83 y and by biopsy fromsubjects of age 23-68 y. Samples generally were collected during the first day or two after death.
A total of 54 costal cartilages and 32 articular cartilages were examined. Uptake of activity by
costal cartilage was high in infants a few days old, somewhat lower in older children, and much
lower in adult and elderly subjects, apparently due to increased cellularity and more active
individual cells in young cartilage. In articular cartilage, however, uptake was substantiallygreater in adults than in two pre-adult subjects.

2895

8.1.3.1. Systemic model for inorganic sulphur

2896
2897
2898
2899
2900
2901
2902
2903

The systemic model for inorganic sulphur applied in Publication 134 (OIR Part 2,
ICRP, 2016a) to workers is applied here to adult members of the public. The structure of themodel for sulphur entering the systemic circulation in inorganic form is shown in Fig. 8.1.
Parameter values are given in Table 8.3.
The systemic behaviour of sulphur is assumed to be independent of age except for ahigher uptake by cartilage in pre-adults than in adults, considering the importance of cartilage
as a repository for inorganic sulphur and the relatively large mass of cartilage in pre-adults
compared to total-body mass. The age-specific transfer coefficient of sulphur from blood to90

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

2904
2905
2906
2907
2908
2909
2910

cartilage is scaled from the adult value based on relative reference masses of cartilage as afraction of total body mass at different ages (ICRP, 2002a). This yields rounded scaling factorsof 3.0, 2.4, 2.1, 1.7, and 1.3 for infants and ages 1, 5, 10, and 15 y, respectively. The value 1.3
for age 15 y is an average of different values derived for males and females. The scaling factor
for the infant is rounded upward from the derived value of ~2.5 in view of the relatively highcellularity and sulphur concentration of cartilage early in life (ICRP, 1995d).

2911
2912
2913
2914
2915

Fig. 8.1. Structure of the systemic model for inorganic sulphur. Activity transferred from Bloodto Colon enters the Right colon contents.
Table 8.3. Transfer coefficients for the systemic model for inorganic sulphuraPathBlood to Red marrow
Blood to Cartilage
Blood to Other
Blood to Urinary bladder contents
Blood to Right colon contents
Red marrow to Blood
Cartilage to Blood
Other to Blood

Infant
7.50E-02
7.50E-01
1.75E-01
1.80E+00
2.00E-01
3.00E-01
1.00E-01
3.50E+00

Transfer coefficient (d-1)
1y
5y
10 y
15 y
7.50E-02 7.50E-02 7.50E-02 7.50E-02
6.00E-01 5.25E-01 4.25E-01 3.25E-01
1.75E-01 1.75E-01 1.75E-01 1.75E-01
1.80E+00 1.80E+00 1.80E+00 1.80E+00
2.00E-01 2.00E-01 2.00E-01 2.00E-01
3.00E-01 3.00E-01 3.00E-01 3.00E-01
1.00E-01 1.00E-01 1.00E-01 1.00E-01
3.50E+00 3.50E+00 3.50E+00 3.50E+00

Adult
7.50E-02
2.50E-01
1.75E-01
1.80E+00
2.00E-01
3.00E-01
1.00E-01
3.50E+00

2916
2917

8.1.3.2. Systemic model for organic sulphur

2918
2919
2920
2921
2922
2923
2924

The systemic model for organic sulphur applied in Publication 134 (OIR Part 2) toworkers is applied here to adult members of the public. Parameters for the adult are applied to
all age groups.
The model structure is shown in Fig. 8.2. Parameter values are listed in Table 8.4.

91

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

2925

2926
2927
2928
2929
2930

Fig. 8.2. Structure of the systemic model for organic sulphur.
Table 8.4. Transfer coefficients for the systemic model for organic sulphur
Path*
Blood 1 to Blood 2
Blood 1 to UB contents
Blood 2 to UB contents
Blood 2 to Excreta
Blood 2 to SI contents
Blood 2 to All tissues
All tissues to Blood 2

2931

*

Transfer coefficient (d-1)
Infant
1y
5y
10 y
15 y
8.30E+00 8.30E+00 8.30E+00 8.30E+00 8.30E+00
4.00E+00 4.00E+00 4.00E+00 4.00E+00 4.00E+00
1.10E-03 1.10E-03 1.10E-03 1.10E-03 1.10E-03
9.00E-04 9.00E-04 9.00E-04 9.00E-04 9.00E-04
2.00E-04 2.00E-04 2.00E-04 2.00E-04 2.00E-04
1.70E-02 1.70E-02 1.70E-02 1.70E-02 1.70E-02
4.20E-03 4.20E-03 4.20E-03 4.20E-03 4.20E-03

UB = Urinary bladder, SI = Small intestine

92

Adult
8.30E+00
4.00E+00
1.10E-03
9.00E-04
2.00E-04
1.70E-02
4.20E-03

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

2932

8.2. Dosimetric data for sulphur

2933

Table 8.5. Committed effective dose coefficients (Sv Bq -1) for the inhalation or ingestion of 35S compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled gases or vapours

3 mo

1y

5y

10 y

15 y

Adult

Sulphur dioxide, carbon disulphide, hydrogensulphide, carbonyl sulphide and other unspecified
inorganic gases and vapours
2.9E-10

2.1E-10

1.1E-107.0E-11

4.9E-11

5.5E-11

Other organic

9.6E-09

7.1E-09

3.7E-09

2.2E-09

1.3E-09

1.2E-09

Type F, Caesium, nickel, strontium and thorium
sulphates
1.2E-10

8.6E-11

3.6E-11

2.2E-11

1.4E-11

1.6E-11

Type M, Barium sulphates; all unspecified forms

2.3E-09

1.9E-09

1.1E-09

7.0E-10

5.6E-10

5.2E-10

Type S

3.6E-09

3.1E-09

1.8E-09

1.2E-09

9.1E-10

8.5E-10Adult fA = 1.0, Sulphur in food and all soluble forms

1.9E-10

1.3E-10

5.8E-11

3.3E-112.0E-11

2.7E-11

Adult fA = 0.1, Elemental sulphur and thiosulphate

4.1E-11

1.5E-11

7.5E-12

4.6E-12

2.9E-12

3.1E-12

Inhaled particulate materials (1 µm AMAD aerosols)

Ingested materials

2934

93

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

9. CALCIUM (Z = 20)

2935
2936

9.1. Routes of Intake

2937

9.1.1. Inhalation

2938
2939
2940
2941
2942
2943
2944

No information was found on the behaviour of inhaled calcium in man. Information
on absorption from the respiratory tract is available from experimental studies of calcium
chloride. For details see Section 6 of Publication 134 (ICRP, 2016a). Absorption parametervalues and types, and associated fA values for particulate forms of calcium are given in Table
9.1(taken from Section 6 of Publication 134).
Table 9.1. Absorption parameter values for inhaled and ingested calcium
Inhaled particulate materials
Default parameter values†,‡
Absorption Assigned forms
TypeF
Chloride§
M
S–
Ingested materials¶
Assigned forms
All forms

fr

1
0.2
0.01

Absorption parameter values*sr (d–1)
ss (d–1)

70
3
3

–
0.005
1×10-4Age-dependent absorption from the alimentary tract, fA
3 months 1 year
5 years
10 years 15 years adult
0.6
0.5
0.5
0.5
0.5
0.4

2945
2946
2947
2948
2949
2950
2951
2952
2953
2954
2955
2956
2957
2958

*

2959

9.1.2. Ingestion

2960

9.1.2.1. Adults

2961
2962
2963
2964

Calcium is an essential element and physiological mechanisms facilitate its intestinal
absorption. It has been measured in numerous volunteer studies and in most cases fractional
absorption was in the range 0.2 to 0.5, with some reported higher values and a large interindividual variation among healthy subjects. Calcium absorption is influenced by the

It is assumed that for calcium the bound state can be neglected i.e. fb = 0. The value of sr for Type F forms ofcalcium (70 d–1) is element-specific. The values for Types M and S (3 d–1) are the general default values.
†
Materials (e.g. chloride) are generally listed here where there is sufficient information to assign to a default
absorption Type, but not to give specific parameter values (see see Section 6 of Publication 134 (ICRP, 2016a) .
‡For inhaled material deposited in the respiratory tract and subsequently cleared by particle transport to thealimentary tract, the default fA values for inhaled materials are applied: i.e. the product of fr for the absorption type
and the fA value for ingested soluble forms of calcium applicable to the age-group of interest (e.g. 0.4 for adults).
§
Default Type M is recommended for use in the absence of specific information on which the exposure material
can be assigned to an absorption type, e.g. if the form is unknown, or if the form is known but there is no
information available on the absorption of that form from the respiratory tract.
¶
Activity transferred from systemic compartments into segments of the alimentary tract is assumed to be subject
to reabsorption to blood. The default absorption fraction fA for the secreted activity is the highest value foringestion of the radionuclide applicable to the age-group of interest (e.g. 0.4 for adults).

94

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

2965
2966
2967
2968
2969
2970
2971
2972
2973
2974

intraluminal concentration of ionized calcium and by morphological (positive correlation withbody size) and nutritional factors. Fractional calcium absorption is increased by high intakes ofvitamin D, by a high protein or carbohydrate diet, by calcium deficiency or low calcium intake
and by pregnancy or lactation. On the other hand, old age, sprue diseases, caffeine intake, oral
supplementation with magnesium, or ingestion of calcium binding agents such as EDTA or
citrate ions decreases calcium absorption in humans. Calcium absorption occurs mainly fromthe small intestine. However, a few percent of calcium may also be absorbed from other sites,such as the colon. In Publications 30 (ICRP, 1980) and 71 (ICRP, 1995b), an absorption
fraction of 0.3 was recommended. An fA value of 0.4 for all chemical forms was recommendedin Publication 134 (ICRP, 2016a). The same value fA = 0.4 is adopted here for adults.

2975

9.1.2.2. Children

2976
2977
2978
2979
2980
2981
2982
2983
2984
2985
2986
2987
2988
2989
2990
2991
2992
2993
2994
2995
2996
2997
2998

The developing rat has been used in a number of investigations of the ontogeny ofcalcium absorption after ingestion of simple salts (Ghishan et al., 1980; Halloran and DeLuca,
1980; Pansu et al., 1983; Taylor et al., 1962). In general, these studies demonstrated that during
the suckling period, ionic calcium is absorbed via a passive, non-vitamin-D-dependent process(Ghishan et al., 1980; Pansu et al., 1983) that contrasts with the adult mode of absorption which
involves an active vitamin-dependent process (Dostal and Toverud, 1984). Blake and Henning(1988) studied calcium absorption in 14- and 28-day-old rats and compared absorption of 45Cain milk and 45CaCl2. They showed that for suckling rats (14 days old), transport and absorptionof 45Ca from milk was slower during the first 3 h after introduction into the stomach than thatobserved for 45Ca administered as the chloride. By 6 h after intubation, absorption was similar
in both cases and was 90% of the ingested activity. Overall efficiency of 45Ca absorption from45
CaCl2 was significantly less in adult rats. It was postulated that in neonates, 45Ca from CaCl2
traverses the intestinal wall as ionic calcium and enters the mucosa passively, perhaps via
simple diffusion due to increased permeability of the brush border membranes (Dostal andToverud, 1984). In contrast, 45Ca in milk entering the small intestine remains associated withmilk protein. There are a number of reports of measurements of calcium absorption in infants
and children, using stable isotope techniques. Hillman et al. (1988) obtained a mean absorption
fraction of 0.5 for seven infants, about 2 weeks of age, with a range of 0.4-0.6. Values of up to
0.8 have been measured for premature infants (Ehrenkranz et al., 1985; Liu et al., 1989). For
six children ranging in age from 11 to 17 y, mean absorption was estimated as 0.4 with a rangeof 0.3-0.5 (Miller et al., 1989). Publication 71 used values of absorption fraction of 0.6 for 3mo-old infants and 0.4 for l-, 5-, 10- and 15-y-old children. The value fA = 0.6 is retained herefor 3-mo-old infants while a value fA = 0.5 is adopted for l-, 5-, 10- and 15-y-old children.

2999

9.1.3. Systemic Distribution, Retention and Excretion

3000

9.1.3.1. Summary of biokinetic data

3001
3002
3003
3004
3005
3006
3007
3008
3009

The biokinetics of calcium has been investigated extensively in physiological andclinical studies and to some extent in radiobiological studies. Biokinetic data for systemic
calcium are reviewed in Leggett (1992a), Publication 71 (ICRP, 1995b), and Publication 134(ICRP, 2016a).
The alkaline earth elements strontium, barium, and radium are physiologicalanalogues of calcium but exhibit somewhat different systemic kinetics from calcium and fromone another due to discrimination by biological membranes and hydroxyapatite crystals of bone
(ICRP, 1993; Leggett, 1992a). Strontium is a much closer biokinetic analogue of calcium thanis barium or radium.
95

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3010
3011
3012
3013
3014
3015
3016
3017
3018
3019
3020
3021
3022
3023
3024
3025
3026
3027
3028
3029
3030
3031
3032
3033
3034
3035
3036
3037
3038
3039
3040
3041
3042
3043
3044
3045
3046
3047
3048
3049
3050
3051

Data on the systemic behaviour of calcium in adults are reviewed in Publication 134.
Briefly, plasma disappearance curves for these elements indicate an outflow rate of several
hundred plasma volumes per day and rapid equilibration with an extravascular pool roughly
three times the size of the plasma pool. Soft tissues initially accumulate most of the systemic
burden, but bone becomes the primary systemic repository for calcium after a few days.
Following acute input of a stable calcium isotope into blood of an adult human, soft tissues are
estimated to contain nearly half of the injected amount at 1 d, one-fourth at 10 d and <1%beyond 100 d. Bone is projected to contain roughly a third of the injected amount at 1-100 dand to lose the accumulated amount with a half-time of a few years for trabecular bone and a
few decades for cortical bone. Available data suggest that the urinary excretion rate ismoderately higher than the faecal excretion rate.
Calcium entering bone initially deposits on bone surface, from which activity isremoved with an estimated half-time on the order of 1 d. Most of the calcium atoms leavingbone surface return to blood, but a portion diffuse into a bone volume pool referred to as
exchangeable bone volume. Calcium atoms entering exchangeable bone volume may return tobone surface or blood over a period of weeks or months or may transfer to nonexchangeablebone volume, meaning that they become firmly fixed in bone crystals. It appears that calcium,
strontium, barium, and radium are all about equally likely to transfer from bone surface toexchangeable bone volume but that the likelihood of becoming firmly fixed in bone crystal
decreases in the order calcium > strontium > barium > radium. Data from human and animalstudies indicate that the rate of loss of alkaline earth tracers from bone over the first few months
after acute uptake to blood increases in the order calcium < strontium < barium < radium.
Presumably these four elements are removed from trabecular or cortical non-exchangeablebone volume compartments at the rate of bone restructuring of that bone type, so that the rateof transfer from non-exchangeable bone volume is independent of the element.
There is a sizable literature on the age-specific kinetics of calcium, strontium, barium,
and radium in human subjects and laboratory animals (Anderson and Comar, 1968; Atherton
et al., 1965; Bauer et al., 1957; Bronner et al., 1956; Bruenger et al., 1983, 1989; Decker et al.,1964; Domanski et al., 1980; Glad et al., 1960; Henrichs et al., 1984; Kallfelz and Wentworth,
1969; Kereiakes et al., 1968; Kulp and Schulert, 1962; Lee et al., 1965; Likhtarev et al., 1975;
Lloyd, C.W. Jones, Bruenger, Atherton, et al., 1983; Macdonald et al., 1965; Osanov et al.,
1971; Parks et al., 1978; Parks and Keane, 1983; Stather, 1974; Wellman et al., 1970; Woodard
and Dwyer, 1972). It has been established that uptake of each of these elements is greater ingrowing bone than in mature bone. Changes with age in their fractional deposition in theskeleton are roughly proportional to the age-specific rate of calcium addition to bone resulting
from bone growth plus bone remodeling (Figure 9.1). At times remote from exposure, skeletal
burdens acquired during periods of growth tend to remain higher than those acquired by matureskeletons except for skeletal burdens acquired during or soon after infancy when there is aparticularly high rate of bone turnover. Both deposition and removal of the calcium-likeelements is greater in areas of bone undergoing rapid remodeling than in areas of relatively
slow remodeling. Greater deposition of these elements the younger skeleton results in lesssystemic radium available for excretion and distribution to soft tissues.

3052

9.1.3.2. Systemic model

3053
3054
3055

The age-specific model for systemic calcium is taken from Publication 67 (ICRP,
1993). The same model with parameter values for the adult was adopted in Publication 134 forapplication to workers.

96

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3056
3057
3058
3059
3060
3061
3062
3063
3064
3065
3066
3067
3068
3069
3070
3071
3072
3073

3074
3075
3076
3077
3078

The structure of the model is shown in Fig. 9.1. Transfer coefficients are listed inTable 9.2.
Extension of the calcium model to preadult ages is based on results of studies of theage-specific behavior of calcium and its physiological analogues strontium, barium, and radiumin human subjects and laboratory animals. These studies have demonstrated that deposition ofthese elements in bone is higher, and removal from bone is faster, at preadult ages than in adults.
The age-specific deposition fraction for bone, and the division of that deposition between
trabecular and cortical bone surface, are based on the estimated rates of calcium addition toeach of these bone types. For preadult ages the deposition fractions for soft tissues and excretion
pathways are reduced uniformly from the values for adults to reflect the elevated competition
from bone for circulating calcium. The removal half-times from bone surface and exchangeablebone volume compartments are assumed to be independent of age. The removal half-times frombone volume compartments to blood are reference age-specific bone turnover rates (ICRP,
2002a). Removal half-times from soft-tissue compartments are assumed to be independent ofage.
The reader is referred to Leggett (1992a), Publication 67 (ICRP, 1993), andPublication 71 (ICRP, 1995b) for more detailed descriptions of the basis for age-specificparameter values for calcium and physiologically related elements.

Fig. 9.1. Structure of the model for systemic calcium. exch = exchangeable, nonexch = nonexchangeable. Activity transferred to Colon enters Right colon contents.

97

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3079

Table 9.2. Transfer coefficients for the model for systemic calcium*

Path

Blood to Urinary bladder contents
Blood to Right colon contents
Blood to Trab surface
Blood to Cort surface
Blood to ST0
Blood to ST1
Blood to ST2
Trab surf to Blood
Trab surf to Exch Trab vol
Cort surf to Blood
Cort surf to Exch Cort volST0 to Blood
ST1 to Blood
ST2 to Blood
Exch Trab vol to Trab surf
Exch Trab vol to Nonexch Trab vol
Exch Cort vol to Cort surf
Exch Cort vol to Nonexch Cort vol
Nonexch Trab vol to Blood
Nonexch Cort vol to Blood

3080
3081

Infant2.00E-01
1.50E-01
2.25E+00
9.00E+00
2.90E+00
5.00E-01
2.50E-04
5.78E-01
1.16E-01
5.78E-01
1.16E-01
9.67E-01
1.73E-01
3.80E-04
2.77E-03
4.16E-03
2.77E-03
4.16E-03
8.22E-03
8.22E-03

1y4.40E-01
3.30E-01
1.35E+00
5.40E+00
6.38E+00
1.10E+00
5.50E-04
5.78E-01
1.16E-01
5.78E-01
1.16E-01
2.13E+00
1.73E-01
3.80E-04
2.77E-03
4.16E-03
2.77E-03
4.16E-03
2.88E-03
2.88E-03*

Transfer coefficient (d-1)
5y
10 y
15 y
4.80E-01 3.52E-01 2.08E-01
3.60E-01 2.64E-01 1.56E-01
1.33E+00 2.12E+00 3.10E+00
4.67E+00 6.28E+00 8.00E+00
6.96E+00 5.10E+00 3.02E+00
1.20E+00 8.80E-01 5.20E-01
6.00E-04 4.40E-04 2.60E-04
5.78E-01 5.78E-01 5.78E-01
1.16E-01 1.16E-01 1.16E-01
5.78E-01 5.78E-01 5.78E-01
1.16E-01 1.16E-01 1.16E-01
2.32E+00 1.70E+00 1.01E+00
1.73E-01 1.73E-01 1.73E-01
3.80E-04 3.80E-04 3.80E-04
2.77E-03 2.77E-03 2.77E-03
4.16E-03 4.16E-03 4.16E-03
2.77E-03 2.77E-03 2.77E-03
4.16E-03 4.16E-03 4.16E-03
1.81E-03 1.32E-03 9.59E-04
1.53E-03 9.04E-04 5.21E-04

Adult
6.00E-01
4.50E-01
2.08E+00
1.67E+00
8.70E+00
1.50E+00
7.50E-04
5.78E-01
1.16E-01
5.78E-01
1.16E-01
2.90E+00
1.73E-01
3.80E-04
2.77E-03
4.16E-03
2.77E-03
4.16E-03
4.93E-04
8.21E-05

Trab = Trabecular, Cort = cortical, surf = surface, vol = volume, Exch = Exchangeable, Nonexch =Nonexchangeable98DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3082

9.2. Dosimetric data for calcium

3083
3084

Table 9.3. Committed effective dose coefficients (Sv Bq -1) for the inhalation or ingestion of 45Ca compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled particulate materials (1 µm AMAD aerosols) 3 mo

1y

5y

10 y

15 y

Adult

Type F, Chloride

5.0E-09

2.8E-09

9.7E-10

5.6E-10

4.8E-10

2.2E-10

Type M, All unspecified forms

5.3E-09

4.2E-09

2.3E-09

1.5E-09

1.2E-09

1.0E-09

Type S

8.0E-09

7.0E-09

4.0E-09

2.6E-09

2.1E-09

1.9E-09

7.2E-09

3.5E-09

1.4E-09

7.7E-10

7.3E-10

2.7E-10

Ingested materials
Adult fA = 0.4, All forms

3085
3086

99

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

10. IRON (Z = 26)

3087
3088

10.1. Routes of Intake

3089

10.1.1. Inhalation

3090

10.1.1.1. Absorption Types and parameter values

3091
3092
3093
3094
3095
3096
3097
3098

Extensive information was found on the behaviour of iron inhaled in oxide form inboth animals and in man, because it has been used as a test material to study lung clearance.
Some information on absorption from the respiratory tract was also found on other forms, suchas the chloride. For details, see Section 7 of of Publication 134 (ICRP, 2016a).
Absorption parameter values and types, and associated fA values for particulate formsof iron are given in Table 10.1 (taken from Section 7 of Publication 134).
Table 10.1. Absorption parameter values for inhaled and ingested iron
Absorption parameter values*sr (d–1)
ss (d–1)

Inhaled particulate materials
fr
Default parameter values†,‡
Absorption
Assigned forms
Type
F
—
1
100
–
M§
Ferric chloride; ferric oxide
0.2
3
0.005
S
Corrosion products
0.01
3
1×10-4¶
Ingested materials
Assigned forms
Age-dependent absorption from the alimentary tract, fA
3 months 1 year
5 years
10 years 15 years adultAll forms
0.6
0.2
0.2
0.2
0.2
0.1

3099
3100
3101
3102
3103
3104
3105
3106
3107
3108
3109
3110
3111
3112

*

3113

10.1.2. Ingestion

3114

10.1.2.1. Adults

3115
3116
3117
3118

Inorganic iron, usually as ferric or ferrous salts, is present in many foods as a natural
constituent or after supplementation with iron, and as the major form of ambient iron present
in water and air. Biologically incorporated iron, usually in haem from haemoglobin, myoglobin,and cytochromes, is derived from animal tissues and/or their constituents present in the diet.

It is assumed that for iron the bound state can be neglected, i.e., fb = 0.0. The value of sr for Type F forms of iron(100 d–1) is element-specific. The values for Types M and S (3 d–1) are the general default values.
†
Materials (e.g. ferric chloride) are generally listed here where there is sufficient information to assign to a default
absorption Type, but not to give specific parameter values (see Section 7 of Publication 134, ICRP, 2016a).
‡
For inhaled material deposited in the respiratory tract and subsequently cleared by particle transport to thealimentary tract, the default fA values for inhaled materials are applied: i.e. the product of fr for the absorption
Type and the fA value for ingested soluble forms of iron applicable to the age-group of interest (e.g. 0.1 for adults).
§
Default Type M is recommended for use in the absence of specific information on which the exposure material
can be assigned to an absorption type, e.g. if the form is unknown, or if the form is known but there is no
information available on the absorption of that form from the respiratory tract.
¶
Activity transferred from systemic compartments into segments of the alimentary tract is assumed to be subject
to reabsorption to blood. The default absorption fraction fA for the secreted activity is the highest value foringestion of the radionuclide applicable to the age-group of interest (e.g. 0.1 for adults).

100

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3119
3120
3121
3122
3123
3124
3125
3126
3127
3128
3129
3130
3131
3132
3133
3134
3135
3136
3137
3138
3139
3140
3141
3142
3143
3144
3145
3146
3147
3148
3149
3150
3151
3152
3153
3154
3155
3156

Because of the nutritional significance of iron, its gastrointestinal absorption has been
investigated extensively in man and animals (Bothwell et al., 1979; Brozovic, 1975; ICRP,
1975; Nuclear Energy Agency (NEA), 1988). In numerous normal human subjects,
absorption fractions of 0.01-0.07 have been obtained when iron was ingested with a wide
variety of vegetable foods, whereas values of 0.1-0.2 are typically obtained when iron isadded to meat and fish. However, individual studies produced mean figures as great as 0.4 formen and 0.6 for women.
Iron absorption is influenced by the amount of iron in the diet, age, gender, the body's
state of iron repletion, the chemical form ingested, and substances in the diet andgastrointestinal secretions which act to alter iron absorption. Lowered iron status of theindividual results in increased iron uptake, as shown by menstruating women and sufferers
from anaemia. Uptake is also increased during pregnancy and lactation. These latter points,
associated to hormonal differences, result in higher iron absorption in females compared tomales (Brozovic, 1975; Fletcher et al., 1994; Woodhead et al., 1991). Iron absorption
measured in pregnant women gave absorption fractions of about 0.1, 0.25, and 0.3 in thefirst, second, and third trimester. Healthy older adults appear to absorb iron similarly toyounger adults (Freiman et al., 1963; Marx, 1979). Iron incorporated in food of animal origin
is generally better absorbed than that from vegetables (Layrisse and Martinez-Torres, 1971;
Martinez-Torres and Layrisse, 1973). Haem iron is usually better absorbed than non-haem ironin normal and iron-deficient subjects (Bjorn Rasmussen et al., 1974; Layrisse and MartínezTorres, 1972). Ferrous iron tends to be absorbed more efficiently than ferric because of its
greater solubility. In the alimentary tract, gastric hydrochloric acid, bile, and certain organic
and amino acids can augment iron absorption, whereas bicarbonate from pancreatic secretions,
phosphates, phytates, carbonates, tannates, oxalates, and/or EDTA can decrease iron absorption.
Ingestion of human milk and organic acids (ascorbic, lactic, citric…) are enhancers of ironabsorption, while dietary fibres (pectins, cellulose…), tannates in tea, polyphenols in coffee
and even calcium supplements in diet are potent inhibitors.
In normal iron balance, iron absorption occurs predominantly in the small intestineand is regulated such that absorption replaces loss. Iron is known to be, in some circumstances,
retained in the wall of the small intestine. Available data are consistent with a half-time ofintestinal retention of about 3 d for 20% of ingested iron, dependent on the iron status (ICRP,
2006).
In Publications 30 (ICRP, 1980), 69 (ICRP, 1995a) and 134 (ICRP, 2016a) an
absorption fraction of 0.1 for both males and females was recommended. This value
adequately represents iron absorption in many cases, e.g. in healthy adult male andpostmenopausal female subjects, with iron in inorganic forms, and in vegetarian diets.
For the adult dose coefficients given in this report an fA value of 0.1 is applied to all forms
of ingested iron.

3157

10.1.2.2. Children

3158
3159
3160
3161
3162
3163
3164
3165

Gorten et al. (1963) reported a fractional absorption of 59Fe of 0.32 (range 0.068-0.74)
following administration to healthy premature infants (1-2-week-old) as ascorbate in a milk
meal. In infants younger than 1.5 mo, values of fractional absorption of 0.56-0.91 were obtainedusing 59Fe citrate administered in a milk meal; in infants 1.5-3 mo of age, values obtained were0.15-0.38 (Garby and Sjolin, 1959). Children in the first year of life had a fractional
absorption of 0.48-0.7 of iron administered with breast milk (Saarinen et al., 1977), 0.030.3 of iron administered with infant formulas based on soya protein extract or cow's milk
(Rios et al., 1975; Saarinen and Siimes, 1977), and about 0.03 from carrier-free radioiron

101

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3166
3167
3168
3169
3170
3171
3172
3173
3174
3175
3176
3177
3178
3179
3180
3181
3182
3183
3184
3185
3186
3187
3188
3189
3190

activity (Rios et al., 1975; Saarinen et al., 1977; Saarinen and Siimes, 1977). Saarinen et al.
(1977) also compared the absorption of 59 Fe in 6-7-mo-old infants who had been exclusively
breast-fed or had been weaned from breast to cow's milk prior to the age of 2 mo. In eachcase, 59 Fe sulphate was administered during feeding after a 3 h fast and the absorption
values obtained were 0.5 ± 0.08 (SEM, n 11) for the breast-fed infants and 0.2 ± 0.05 (n =16) for those fed cow's milk. Iron absorption in infants and children is inversely related toage but has not usually been measured in direct comparison with that in adults (Cristy andLeggett, 1986). In one comparative study, children 4-52-mo-old absorbed approximately
0.1 of the 59Fe from a milk meal, in comparison with adult males who absorbed 0.028 froma similar meal (Schulz and Smith, 1958). The absorption of 59 Fe biologically incorporated
in eggs was approximately 0.11 in children 1-4.5 y of age and 0.06 in children 5-15 y ofage (Schulz and Smith, 1958). 59Fe-labelled ferrous ascorbate administered in lemonade
yielded mean absorption values of 0.08-0.16 in children 7-8 y of age, and 0.15-0.17 inchildren 9-10 y of age (Darby et al., 1947). The higher values obtained in the older children
in this experiment could be related to increased iron requirements during growth anddevelopment. After a 12 h fast, four normal children ages 6-11 y were given 59 Fe with 5 mg
of carrier iron, both in the form of ferrous sulphate. The percentage absorption values were
5, 8, 17, and 27% (mean 13.5%) (Erlandson et al., 1962). In adolescence enhanced
absorption of iron would also be expected; the daily requirement of iron in adolescent males
and females is respectively about 30 and 50% higher than in adults (Bothwell et al., 1979).
Although the published values of absorption are quite variable, those for children are
generally higher than those for adults, attributable in part to the relatively greater requirementsof iron for growth and development. For all forms of iron absorption fraction values of 0.6 for
3-mo-old infants, and 0.2 for 1-, 5-, 10-, and 15-y-old children were recommended in
Publication 69 (ICRP, 1995a). The same values are adopted here for fA.

3191

10.1.3. Systemic Distribution, Retention and Excretion3192

10.1.3.1. Adults

3193
3194
3195
3196
3197
3198
3199
3200
3201
3202
3203
3204
3205
3206
3207
3208
3209
3210
3211
3212

Publication 134 (ICRP, 2016a) describes the typical behavior of systemic iron in
healthy adult humans, based mainly on the authoritative review and analyses by Bothwell et al.
(1979) (See also Barton and Edwards, 2000; Green et al., 1968; Leggett et al., 2000; Munro
and Linder, 1978; Saito et al., 1964; Trubowitz and Davis, 1982)
The body’s iron content may be divided into two categories: essential (functional) ironand storage iron. Essential iron is the portion of the body’s iron that fulfills criticalphysiological functions, e.g., as components of oxygen carrying proteins and various enzymes
involved in metabolic processes. The adult human body typically contains 30-40 mg ofessential iron per kg of body mass. About 80-85% of this is found in haemoglobin within the
red blood cells (RBC), about 10-12% is found in myoglobin within muscle and other tissues,and the remainder is distributed throughout the body tissues as haem enzymes (2-3% of bodyiron) and non-haem enzymes (3-4% of body iron). Storage iron is an iron reserve in the bodythat assures an adequate supply of iron for normal physiological processes during periods of
low intake or rapid loss of iron. Storage iron is located mainly in the reticuloendothelial (RE)system and hepatic parenchyma. Essential and storage iron typically represent about 70% and30%, respectively, of total-body iron in adult males and about 85% and 15%, respectively, in
pre-menopausal adult females.
The iron content in the total body of a typical adult human is about 3.5-4.5 g in males
and 2.0-2.5 g in females. The following tissue distribution of iron is estimated for an adult malewith a total-body content of 3.9 g: erythrocytes, 2300 mg; liver hepatocytes, 400 mg; liver RE
102

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3213
3214
3215
3216
3217
3218
3219
3220
3221
3222
3223
3224
3225
3226
3227
3228
3229
3230
3231
3232
3233
3234
3235
3236

cells, 50 mg, RE cells of bone marrow, 320 mg; spleen (mainly RE cells), 80 mg; other RE
cells, 300 mg; erythroid marrow, 80 mg; plasma transferrin, 2.9 mg; remaining plasma, 0.4 mg;
and remainder of the body, 400 mg. The distribution in adult females is expected to be roughly
proportional to that in males with the main exception of iron storage sites such as the liver,which typically contain only about a third as much iron in females as in males.
Iron is distributed by blood plasma. Nearly all plasma iron is bound to the transport
protein transferrin. The removal half-time of transferrin iron from plasma to tissues is about 90
minutes. Most of the transferrin-bound iron leaving plasma enters a circuit starting in theerythroid marrow. Another portion enters the extravascular spaces and returns to plasma mainly
via the lymphatics. The rest is delivered to the parenchymal tissues, mainly the liver.
The mean hepatic non-haem iron concentration is roughly 0.1 mg/g liver in women,
compared with 0.3 mg/g liver in adult males. The average mass of storage iron in bone marrowis about 300 mg in adult males and 100 mg in adult females. The erythroid marrow takes uptransferrin iron from plasma for incorporation into haemoglobin. Most of this iron appears incirculating red blood cells (RBC) in the next few days and remains there for the life span of thecells, which is on the order of 110-120 d in adult humans. The portion that does not appear incirculating RBC consists of defective cells or extruded components of developing cells. This
portion, called the wastage iron of erythropoiesis, typically represents 20-30% of iron thatenters the erythroid marrow. This portion is collected by the body’s reticuloendothelial (RE)system, degraded, and returned to plasma.
Iron is lost very slowly from the body. Obligatory losses occur via the gastrointestinal
tract, skin, and genitourinary tract. Average daily loss of iron from the body has been estimatedas 12-14 μg/kg in the adult male. Average daily loss in the pre-menopausal adult female may
be about 50% higher due to loss of circulating iron via menstruation.

3237

10.1.3.2. Pre adults

3238
3239
3240
3241
3242
3243
3244
3245
3246
3247
3248
3249
3250
3251
3252
3253
3254
3255
3256

The average concentration of iron in the total body at birth is about 80 mg/kg. About
60-65% is contained in the blood as circulating hemoglobin, about 30% is storage iron divided
about equally between liver and other body tissues, and a few percent is contained in theerythroid cells of the marrow, in myoglobin, and in intracellular enzymes.
During the first 2 mo after birth erythropoiesis nearly ceases, and the hemoglobin
concentration in blood declines from about 17 g/dl to about 11 g/dl. As growth continues, thered cell mass increases so that nearly all storage iron has been used in the first few months. The
iron reserve gradually builds up to about 5 mg/kg during growth. In the male there is a further
increase between the ages of 15 to 30 y to about 12-15 mg/kg.
The rate of excretion of iron may be substantially higher in infants and children thanin adults, when expressed as daily loss per kg of body weight. Garby et al. (1964) estimateddaily losses in children to be 0.03 mg/kg in infants using a radioisotopic technique. Data of
Elian et al. (1966) on the rate of blood loss in faeces at ages 2-17 months indicates daily loss
on the order of 25 mg via the gastrointestinal tract alone. A similar rate of loss was estimatedby Hoag et al. (1961) using 59Fe-labeled red blood cells.
Fetal and neonatal red blood cells have a shorter life span than those in adults(Harrison, 1979; Pearson, 1967; Trubowitz and Davis, 1982). Reported measurements arevariable but indicate life spans in the fetus and infant no greater than about 70-90 d. The age at
which the adult value is attained does not appear to be known.

3257

10.1.3.3. Biokinetic model for systemic iron103

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3258
3259
3260
3261
3262
3263
3264
3265
3266
3267
3268
3269
3270
3271
3272

3273
3274
3275
3276
3277

The model for systemic iron applied in Publication 134 (ICRP, 2017) to workers isapplied here to adult members of the public. That model is designed to reproduce observationsof the short-term behavior of radio-iron in healthy adult males and the typical total-body
distribution of stable iron in adult males indicated earlier, based on reference values for dietaryintake and gastrointestinal absorption of iron.
The systemic model for the adult is extended to pre-adult ages based on the following
assumptions: the rate of loss of storage iron is inversely proportional to iron stores as a fractionof total-body iron; the rate of loss of iron from the body is twice as high through age 10 y as inadults but attains the adult value by age 15 y; and the life span of red blood cells 70 d in infants,
80 d at 1 y, 90 d at 5 y, 100 d at 10 y, and 110 d at 15 y, compared with 120 d in adults, Thetransfer coefficients describing all other aspects of iron metabolism are assumed to be
independent of age, i.e., the values for adults are assigned to all age groups.
The structure of the model for iron is shown in Fig. 10.1. Parameter values are given
in Table 10.2.

Fig. 10.1. Structure of the biokinetic model for systemic iron. RE = Reticoendothelial cells,
RBC = Red blood cells, SI = Small intestine.

104

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3278

Table 10.2. Transfer coefficients for the model for systemic iron*

Path

Other plasma to Plasma transferrin
Other plasma to UB contents
Other plasma to RC contents
Plasma transferrin to RM synthesis
Plasma transferrin to Liver 1
Plasma transferrin to EV transferrin
RBC to Other plasma
RBC to RM transit
RBC to RC contents
RBC to UB contents
RM synthesis to RBC
RM synthesis to RM transit
RM transit to Other plasma
RM transit to RM storage
RM transit to Liver 2
RM transit to Spleen
RM transit to Other RE
RM storage to RM transit
Liver 2 to RM transit
Spleen to RM transit
Other RE to RM transit
Liver 1 to Plasma transferrin
Liver 1 to SI contents
EV transferrin to Plasma transferrin
EV transferrin to Other parenchyma
Other parenchyma to EV transferrin
Other parenchyma to Excreta
Other parenchyma to UB contents

3279
3280

Infant7.00E+01
2.00E-02
2.00E-01
9.43E+00
5.55E-01
1.11E+00
1.43E-03
1.21E-02
6.86E-04
5.14E-05
2.43E-01
1.04E-01
1.39E+00
6.35E-02
1.06E-02
1.70E-02
6.35E-02
9.50E-03
9.50E-03
9.50E-03
9.50E-03
9.10E-03
3.70E-04
8.88E-01
2.22E-01
3.18E-03
1.14E-03
6.00E-05

1y
7.00E+01
2.00E-02
2.00E-01
9.43E+00
5.55E-01
1.11E+00
1.25E-03
1.06E-02
6.00E-04
4.50E-05
2.43E-01
1.04E-01
1.39E+00
6.35E-02
1.06E-02
1.70E-02
6.35E-02
7.60E-03
7.60E-03
7.60E-03
7.60E-03
7.28E-03
3.70E-04
8.88E-01
2.22E-01
2.54E-03
1.14E-03
6.00E-05*

Transfer coefficient (d-1)
5y
10 y
15 y
7.00E+01 7.00E+01 7.00E+01
2.00E-02 2.00E-02 1.00E-02
2.00E-01 2.00E-01 1.00E-01
9.43E+00 9.43E+00 9.43E+00
5.55E-01 5.55E-01 5.55E-01
1.11E+00 1.11E+00 1.11E+00
1.11E-03 1.00E-03 9.09E-04
9.43E-03 8.48E-03 7.95E-03
5.33E-04 4.80E-04 2.18E-04
4.00E-05 3.60E-05 1.64E-05
2.43E-01 2.43E-01 2.43E-01
1.04E-01 1.04E-01 1.04E-01
1.39E+00 1.39E+00 1.39E+00
6.35E-02 6.35E-02 6.35E-02
1.06E-02 1.06E-02 1.06E-02
1.70E-02 1.70E-02 1.70E-02
6.35E-02 6.35E-02 6.35E-02
7.60E-03 5.70E-03 4.18E-03
7.60E-03 5.70E-03 4.18E-03
7.60E-03 5.70E-03 4.18E-03
7.60E-03 5.70E-03 4.18E-03
7.28E-03 5.46E-03 4.00E-03
3.70E-04 3.70E-04 3.70E-04
8.88E-01 8.88E-01 8.88E-01
2.22E-01 2.22E-01 2.22E-01
2.54E-03 1.91E-03 1.40E-03
1.14E-03 1.14E-03 5.70E-04
6.00E-05 6.00E-05 3.00E-05

Adult
7.00E+01
1.00E-02
1.00E-01
9.43E+00
5.55E-01
1.11E+00
8.33E-04
7.29E-03
2.00E-04
1.50E-05
2.43E-01
1.04E-01
1.39E+00
6.35E-02
1.06E-02
1.70E-02
6.35E-02
3.80E-03
3.80E-03
3.80E-03
3.80E-03
3.64E-03
3.70E-04
8.88E-01
2.22E-01
1.27E-03
5.70E-04
3.00E-05

UB = Urinary bladder, RC = Right colon, RM = Red marrow, SI = Small intestine, EV = Extravascular, RBC =Red blood cells, RE = reticuloendothelial

105

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3281

10.2. Dosimetric data for iron

3282

Table 10.3. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 59Fe compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled particulate materials (1 µm AMAD aerosols) 3 mo

1y

5y

10 y

15 y

Adult

Type F

3.3E-082.0E-08

9.1E-09

6.6E-09

4.3E-09

4.0E-09

Type M, Ferric chloride, ferric oxide; all unspecified
forms
1.4E-08

9.3E-09

5.1E-09

3.5E-09

2.6E-09

2.6E-09

Type S, Corrosion products

1.1E-08

9.1E-09

5.2E-09

3.5E-09

2.7E-09

2.8E-09

4.6E-08

1.2E-08

6.3E-09

4.6E-09

3.2E-09

1.7E-09

Ingested materials
Adult fA = 0.1, All forms

3283
3284
3285
3286

106

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

11. COBALT (Z = 27)

3287
3288

11.1. Routes of Intake

3289

11.1.1. Inhalation

3290
3291
3292
3293
3294
3295
3296
3297
3298

There have been a number of reported studies of the lung retention of 60Co following
accidental inhalation, usually of an oxide. Information on absorption from the respiratory tract
is available from experimental studies of cobalt in a variety of forms, including nitrate, chloride,oxides, fused aluminosilicate particles (FAP) and polystyrene (PSL). For details see Section 8of Publication 134 (ICRP, 2016a). Absorption parameter values and types, and associated fA
values for particulate forms of cobalt are given in Table 11.1 (taken from Section 8 of
Publication 134).
Table 11.1. Absorption parameter values for inhaled and ingested cobalt
Inhaled particulate materials
Default parameter values†,‡
Absorption Assigned forms
TypeF
Nitrate, chloride
M§–
SOxide, FAP, PSL

fr

1
0.2
0.01

Absorption parameter values*sr (d–1)
ss (d–1)

1
1
1

–
0.005
1×10-4

Ingested materials¶
Assigned forms

Age-dependent absorption from the alimentary tract, fA
3 months 1 year
5 years
10 years
15 years
adult
Cobalt in diet and soluble 0.6
0.2
0.2
0.2
0.2
0.1
forms
Oxides
0.3
0.1
0.1
0.1
0.1
0.05
It is assumed that for cobalt the bound fraction fb is 0.03 with an uptake rate sb = 0.002 d–1 is applied to material
in the AI region and LNTH. It is assumed that fb = 0.0 for material in the ET2, BB and bb regions and LNET. The
values of sr for Type F, M and S forms of cobalt (1 d–1,) are element-specific.
†
Materials (e.g. nitrate) are listed here where there is sufficient information to assign to a default absorption Type,but not to give specific parameter values (see Section 8 of ICRP, 2016a).
‡
For inhaled material deposited in the respiratory tract and subsequently cleared by particle transport to thealimentary tract, the default fA values for inhaled materials are applied: i.e. the product of fr for the absorption type
and the fA value for ingested soluble forms of cobalt applicable to the age-group of interest (e.g. 0.1 for adults).
§
Default Type M is recommended for use in the absence of specific information on which the exposure material
can be assigned to an absorption type, e.g. if the form is unknown, or if the form is known but there is no
information available on the absorption of that form from the respiratory tract.
¶
Activity transferred from systemic compartments into segments of the alimentary tract is assumed to be subject
to reabsorption to blood. The default absorption fraction fA for the secreted activity is the highest value foringestion of the radionuclide applicable to the age-group of interest (e.g. 0.1 for adults).

3299
3300
3301
3302
3303
3304
3305
3306
3307
3308
3309
3310
3311
3312
3313

*

3314

11.1.2. Ingestion3315

11.1.2.1. Adults

107

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3316
3317
3318
3319
3320
3321
3322
3323
3324
3325
3326
3327
3328
3329
3330
3331
3332
3333
3334
3335
3336
3337
3338
3339
3340
3341
3342
3343
3344
3345
3346
3347

The gastrointestinal absorption of cobalt is variable and affected by the mass and thechemical form entering the body. Cobalt and iron share a joint absorption pathway andgenerally similar levels of absorption (Schade et al., 1970). A few percents of trace quantities
of insoluble forms like oxides are absorbed. About 10 - 30% is absorbed from large amountsof cobalt or carrier and from soluble inorganic forms like nitrate or chloride (for details, seesection 8 of ICRP, 2016a). A significantly higher uptake of ingested cobalt was observed by
Christensen et al. (Christensen et al., 1993) in females than in males. Increased cobalt
absorption is also observed in subjects suffering from iron deficiency (Pollack et al., 1965;
Valberg et al., 1969). The absorption of radioactive cobaltous chloride appears to diminish
when it is administered after a meal or pre-tagged to protein (Paley and Sussman, 1963). Taylor(1959, 1962) measured cobalt absorption in rats after administration of CoCl2, cobalt in cows’
milk, or lactose solutions and obtained values of approximately 0.3–0.4%. Nishimura et al.
(1976) administered 60Co chloride and 58Co vitamin B12 to rats and compared whole-bodyretention after oral and intravenous administration. Absorption was then estimated to be 3% forcobalt in its inorganic form and 70% for the vitamin-incorporated element. If fish or marine
algae are maintained in sea water containing radioactive 60Co before being fed to rats, fractional
absorption of the element is much higher than that of inorganic cobalt. Thus Inaba et al. (1982)
reported tissue retention in rats at 2 days after administration of 60Co incorporated in fish as
30% of the activity administered, whereas a value of 3% was obtained after administration of60
CoC12. For 60Co in crab meat, absorption by human volunteers was estimated to be about 5%(ICRP, 1993). The fractional absorption of 60Co from cockles collected on the Irish Sea coastin the UK was investigated in a human volunteer study by Hunt (1998), and a value ofapproximately 0.2 was obtained. In Publication 30 (ICRP, 1979) an absorption fraction valueof 0.3 was recommended for organically complexed cobalt compounds and for all inorganic
compounds of the element, excluding oxides and hydroxides. In Publication 67 (ICRP, 1993),
it was considered that the range of results reported in human studies suggested that in mostcases of normal adults the fractional absorption of trace quantities of cobalt was less than
0.1 and an absorption fraction of 0.1 was therefore adopted for intakes by adult members of
the public. In Publication 134, an fA value of 0.1 was adopted for ingestion of all chemical
forms but insoluble oxides for which an fA value of 0.05 was recommended. The fA value of 0.1
is adopted here for ingestion of soluble forms of cobalt and for cobalt in food. For oxides, thefA value of 0.05 is adopted.

3348

11.1.2.2. Children

3349
3350
3351
3352
3353
3354
3355
3356
3357
3358
3359
3360
3361
3362

The absorption of both 60Co chloride and 60 Co vitamin B12 following oral
administration can be much higher in young than in adult rats (Nishimura et al., 1976). At 3
days after administration as the chloride, retention by 7-day-old rats (10%) was approximately
30 times the adult value (0.3%). Retention of the element incorporated into the vitamin B 12
(nearly 100%) was almost double the adult value (55%). A study of cobalt balance in girls aged
between 6 and 10 years (Engel et al., 1967) gave an estimated absorption of 0.57. This
relatively high cobalt absorption could be associated with the stimulation of iron absorption
during periods of rapid growth. As there was evidence that absorption of cobalt may be
increased in childhood an absorption fraction of 0.3 was recommended in Publication 67
for children from 1 to 15 years. An absorption fraction of 0.6 was recommended in
Publication 67 as an average for the first year of life. The same values as for iron are adopted
here for cobalt in diet and for soluble cobalt: fA = 0.6 for 3-month-old infants and fA = 0.2 for
1- to 15-year-old children. Value fA = 0.3 for 3-month-old infants and fA = 0.1 for 1- to 15-yearold children are adopted for ingestion of oxides.

108

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3363

11.1.3. Systemic Distribution, Retention and Excretion

3364
3365
3366
3367
3368
3369
3370
3371
3372
3373
3374
3375
3376
3377
3378
3379
3380
3381
3382

The model for systemic cobalt applied in Publication 134 (ICRP, 2016a) to workers
is applied here to adult members of the public. That model was based mainly on data fromcontrolled studies of retention of activity in the total body, liver, and blood, and the rate of
excretion of activity in urine and faeces, in healthy human subjects administered radioisotopesof cobalt. The data for human subjects were supplemented with measurements of the timedependent distribution of systemic activity following administration of cobalt isotopes tolaboratory animals.
There is little information on age related changes in the biokinetics of systemic cobalt
in mammalian species. A study by Nishimura et al. (1976) on rats indicated greater retentionof 60Co in immature rats than in adult rats following ingestion of 60Co chloride or 58Co vitamin
B12, but this appeared to be due entirely to increased intestinal absorption of cobalt in immature
animals. The investigators concluded that retention of absorbed cobalt by the animals was
virtually independent of age.
The systemic behaviour of cobalt is assumed here to be independent of age except that
activity is assumed to be removed from trabecular or cortical bone volume to blood at the agespecific rate of turnover of that bone type.
The structure of the model for cobalt is shown in Fig. 11.1. Parameter values are given
in Table 11.2.

3383
3384
3385
3386
3387
3388
3389

Fig. 11.1. Structure of the systemic model for cobalt. Activity transferred from Blood 1 toAlimentary tract contents enters Right colon contents. Activity transferred from Liver 1 toAlimentary tract contents enters Small intestine contents. Activity transferred from Alimentarytract contents to Blood 1 represents absorption from the small intestine to blood.
Table 11.2. Transfer coefficients for the model for systemic cobalt*

Path

InfantTransfer coefficient (d-1)
5y
10 y
15 y

1y

109

Adult

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
Blood 1 to Liver 1
Blood 1 to Right colon contents
Blood 1 to ST0
Blood 1 to ST1
Blood 1 to ST2
Blood 1 to Cortical bone surf
Blood 1 to Trabecular bone surf
Blood 1 to Urinary path
Blood 1 to Other kidney tissue
Blood 1 to Blood 2
Blood 2 to Blood 1
Liver 1 to SI contents
Liver 1 to Blood 1
Liver 1 to Liver 2
Liver 2 to Blood 1
ST0 to Blood 1
ST1 to Blood 1
ST2 to Blood 1
Cortical surf to Blood 1
Cortical bone surf to Cortical vol
Trabecular bone surf to Blood 1
Trabecular surf to Trabecular vol
Cortical bone vol to Blood 1
Trabecular bone vol to Blood 1
Urinary path to UB contents
Other kidney tissue to Blood 1
Blood 1 to UB contents

3390

*

7.00E+01
4.00E+00
1.80E+01
1.00E+01
4.00E+00
6.00E+00
6.00E+00
9.00E+00
1.00E+00
1.20E+01
6.93E-01
9.24E-02
3.47E-01
2.31E-02
1.90E-03
9.90E-02
1.39E-02
9.50E-04
8.42E-02
1.49E-02
8.42E-02
1.49E-02
8.22E-03
8.22E-03
4.62E-01
1.90E-03
6.00E+01

7.00E+01
4.00E+00
1.80E+01
1.00E+01
4.00E+00
6.00E+00
6.00E+00
9.00E+00
1.00E+00
1.20E+01
6.93E-01
9.24E-02
3.47E-01
2.31E-02
1.90E-03
9.90E-02
1.39E-02
9.50E-04
8.42E-02
1.49E-02
8.42E-02
1.49E-02
2.88E-03
2.88E-03
4.62E-01
1.90E-03
6.00E+01

7.00E+01
4.00E+00
1.80E+01
1.00E+01
4.00E+00
6.00E+00
6.00E+00
9.00E+00
1.00E+00
1.20E+01
6.93E-01
9.24E-02
3.47E-01
2.31E-02
1.90E-03
9.90E-02
1.39E-02
9.50E-04
8.42E-02
1.49E-02
8.42E-02
1.49E-02
1.53E-03
1.81E-03
4.62E-01
1.90E-03
6.00E+01

UB = Urinary bladder, surf = surface, vol = volume, SI = Small intestine110

7.00E+01
4.00E+00
1.80E+01
1.00E+01
4.00E+00
6.00E+00
6.00E+00
9.00E+00
1.00E+00
1.20E+01
6.93E-01
9.24E-02
3.47E-01
2.31E-02
1.90E-03
9.90E-02
1.39E-02
9.50E-04
8.42E-02
1.49E-02
8.42E-02
1.49E-02
9.04E-04
1.32E-03
4.62E-01
1.90E-03
6.00E+01

7.00E+01
4.00E+00
1.80E+01
1.00E+01
4.00E+00
6.00E+00
6.00E+00
9.00E+00
1.00E+00
1.20E+01
6.93E-01
9.24E-02
3.47E-01
2.31E-02
1.90E-03
9.90E-02
1.39E-02
9.50E-04
8.42E-02
1.49E-02
8.42E-02
1.49E-02
5.21E-04
9.59E-04
4.62E-01
1.90E-03
6.00E+01

7.00E+01
4.00E+00
1.80E+01
1.00E+01
4.00E+00
6.00E+00
6.00E+00
9.00E+00
1.00E+00
1.20E+01
6.93E-01
9.24E-02
3.47E-01
2.31E-02
1.90E-03
9.90E-02
1.39E-02
9.50E-04
8.42E-02
1.49E-02
8.42E-02
1.49E-02
8.21E-05
4.93E-04
4.62E-01
1.90E-03
6.00E+01

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3391

11.2. Dosimetric data for cobalt

3392

Table 11.3. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 57Co compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled particulate materials (1 µm AMAD aerosols) 3 mo

1y

5y

10 y

15 y

Adult

Type F, Nitrate, chloride

1.4E-09

7.1E-10

4.0E-10

2.7E-10

1.9E-10

1.8E-10

Type M, All unspecified forms

2.2E-09

1.9E-09

1.0E-09

7.1E-10

5.2E-10

5.6E-10

Type S, Oxide, FAP, PSL

4.3E-09

3.9E-09

2.3E-09

1.5E-09

1.2E-09

1.3E-09

Adult fA = 0.1, Cobalt in diet and soluble forms

2.2E-09

6.9E-10

4.1E-102.8E-102.0E-10

1.2E-10Adult fA = 0.05, Oxides

1.2E-09

4.4E-10

2.6E-10

1.8E-10

1.3E-108.8E-11

Ingested materials

3393
3394

Table 11.4. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 58Co compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled particulate materials (1 µm AMAD aerosols) 3 mo

1y

5y

10 y

15 y

Adult

Type F, Nitrate, chloride

3.9E-09

2.1E-09

1.2E-09

8.0E-10

5.5E-10

5.3E-10

Type M, All unspecified forms

6.3E-09

5.1E-09

3.0E-09

2.0E-09

1.5E-09

1.7E-09

Type S, Oxide, FAP, PSL

8.7E-09

7.5E-09

4.4E-09

3.0E-09

2.2E-09

2.6E-09

Adult fA = 0.1, Cobalt in diet and soluble forms

6.1E-09

2.5E-09

1.5E-09

1.0E-09

7.1E-10

5.4E-10Adult fA = 0.05, Oxides

3.8E-09

1.9E-09

1.1E-09

7.9E-10

5.5E-10

4.6E-10

Ingested materials

3395
111

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3396

Table 11.5. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 60Co compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled particulate materials (1 µm AMAD aerosols) 3 mo

1y

5y

10 y

15 y

Adult

Type F, Nitrate, chloride

3.0E-08

1.6E-08

9.7E-09

6.7E-09

5.3E-09

5.2E-09

Type M, All unspecified forms

3.7E-08

3.1E-08

1.9E-08

1.3E-08

1.0E-08

1.1E-08

Type S, Oxide, FAP, PSL

1.2E-07

1.2E-078.2E-08

5.9E-08

5.6E-08

6.3E-08

Adult fA = 0.1, Cobalt in diet and soluble forms

4.7E-08

1.5E-08

9.8E-09

6.8E-09

5.4E-09

3.2E-09

Adult fA = 0.05, Oxides

2.5E-08

9.1E-09

5.8E-09

4.1E-09

3.2E-09

2.1E-09

Ingested materials

3397

112

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

12. NICKEL (Z = 28)

3398
3399

12.1. Routes of Intake

3400

12.1.1. Inhalation

3401
3402
3403
3404
3405
3406
3407
3408
3409
3410
3411
3412
3413
3414
3415

Inhalation of nickel radioisotopes is not generally of major concern, but because of
the recognised chemical toxicity of nickel, numerous studies have been conducted on its
behaviour following deposition in the respiratory tract (see e.g. Goodman et al., 2011; National
Research Council (NRC) and Committee on Medical and Biological Effects of Environmental
Pollutants, 1975; Sivulka, 2005). Information is available from experimental studies of nickel
compounds including carbonyl, chloride, sulphate, sulphides, and oxide: mostly in rats, with afew studies in dogs or monkeys. For details see Section 15 of Publication 151 (ICRP, 2022).
Absorption parameter values and types, and associated fA values for gas and vapour
forms of nickel are given in Table 12.1 and for particulate forms in Table 12.2 (both taken from
Section 15 of Publication 151). Exposures to gas or vapour forms of nickel are relatively
unusual compared to exposures to particulate forms, and it is therefore recommended in thisseries of documents that particulate form should be assumed in the absence of information(ICRP, 2002b).
Table 12.1. Deposition and absorption for gas and vapour forms of nickel.
Chemical form/origin
Nickel carbonyl

Total

Percentage deposited (%)*
ET1 ET2
BB
bb

AI

Absorption
Type

100†

0

50

F

20

10

20

Age-dependent absorption from the alimentary tract, fA
3 months
1 year
5 years
10 years 15 years Adult
Chemical form/origin
Nickel carbonyl

3416
3417
3418
3419
3420
3421
3422

0.5

0.05

0.05

0.05

0.05

0.05

ET1, anterior nasal passage; ET2, posterior nasal passage, pharynx and larynx; BB, bronchial; bb, bronchiolar; AI,
alveolar-interstitial.
*Percentage deposited refers to how much of the material in the inhaled air remains in the body after exhalation.
Almost all inhaled gas molecules contact airway surfaces, but usually return to the air unless they dissolve in, or
react with, the surface lining.
†
Default distribution between regions: 20% ET2, 10% BB, 20% bb and 50% AI.

113

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3423
3424

Table 12.2. Absorption parameter values for inhaled and ingested nickel.
Inhaled particulate materials
Default parameter values†,‡
Absorption
Assigned forms
TypeF
Chloride, sulphate, monosulphide,subsulphide§
M
Nickel metal
S
Oxide

fr

Absorption parameter values*sr (d–1)
ss (d–1)

1

3

–

0.2
0.01

3
3

0.005
1×10‒4

Ingested materials¶
Assigned forms

Age-dependent absorption from the alimentary tract, fA
3 months 1 year
5 years
10 years 15 years Adult
Nickel in diet, soluble and 0.5
0.05
0.05
0.05
0.05
0.05
unspecified forms
Nickel metal
0.1
0.01
0.01
0.01
0.01
0.01
Nickel oxide
5×10‒3
5×10‒4
5×10‒4
5×10‒4
5×10‒4
5×10‒4

3425
3426
3427
3428
3429
3430
3431
3432
3433
3434
3435
3436
3437
3438

*

3439

12.1.2. Ingestion

3440

12.1.2.1. Adults

3441
3442
3443
3444
3445
3446
3447
3448
3449

Numerous studies have been conducted on the behaviour of ingested nickel.
Information is available from studies of human volunteers, accidental and environmental
exposure, experimental studies of nickel compounds including citrate, carbonate, oxalate,nitrate, chloride, sulphate, sulphides, metal and oxide in rats, calves and dogs. For details see
Publication 151 (ICRP, 2022). In Publications 30 (ICRP, 1981) and 67 (ICRP, 1993) anabsorption fraction of 0.05 was recommended for all nickel compounds ingested by adults. As
indicated in Table 12.3, a value of fA = 0.05 is adopted here for nickel in drinking water and in
food. For ingestion of nickel metal and oxide, lower fA values of 0.01 and 5×10-4 arerespectively recommended for adults.

3450

12.1.2.2. Children

3451
3452
3453

Paquet et al (1998) demonstrated an increased absorption of nickel chloride in rats
with decreasing age: 1- to 7-d-old neonates absorbed 40 times more nickel than adults. 14-dold rats absorbed 10 times more than adults and the values for 21-d-old, close to weaning age,

It is assumed that for nickel the bound state can be neglected, i.e. fb = 0.0. The value of sr for Type F forms ofnickel (3 d–1) is element-specific. The values for Types M and S (3 d–1) are the general default values.
†
Materials (e.g. chloride) are generally listed here where there is sufficient information to assign to a default
absorption Type, but not to give specific parameter values (see Section 15 of Publication 151 (ICRP, 2022)).
‡
For inhaled material deposited in the respiratory tract and subsequently cleared by particle transport to thealimentary tract, the default fA values for inhaled materials are applied: i.e. the product of fr for the absorption ype
and the fA value for ingested soluble forms of nickel applicable to the age-group of interest (e.g. 0.05 for adults).
§
Default Type M is recommended for use in the absence of specific information on which the exposure material
can be assigned to an absorption type, e.g. if the form is unknown, or if the form is known but there is no
information available on the absorption of that form from the respiratory tract.
¶
Activity transferred from systemic compartments into segments of the alimentary tract is assumed to be subject
to reabsorption to blood. The default absorption fraction fA for the secreted activity is the highest value for any
form of the radionuclide applicable to the age-group of interest (e.g. 0.05 for adults).

114

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3454
3455
3456
3457
3458

were not significantly different from adults. In Publications 30 and 67, an absorption fractionof 0.1 was recommended for infants. In this publication, for soluble forms, unspecified forms
and nickel in diet, an fA = 0.5 is adopted for 3-month-old infants. For nickel metal and oxide,fA values of 0.1 and 5×10-3 respectively are adopted for ingestion by 3-month-old infants. For
children of 1 year and older the same fA values as for adults are recommended.

3459

12.1.3. Systemic distribution, retention and excretion

3460
3461
3462
3463
3464
3465
3466
3467

An updated systemic model for occupational intake of nickel is described in
Publication 151 (ICRP, 2022). Due to a paucity of information on age related changes in thesystemic behavior of nickel, that model is applied here to members of the public of ages exceptthat activity is assumed to be removed from trabecular or cortical bone volume to blood at theage-specific rate of turnover of that bone type.
The structure of the model for nickel is shown in Fig. 12.1. Parameter values are given
in Table 12.3.

3468
3469
3470
3471
3472
3473

Fig. 12.1. Structure of the model for nickel. UB = urinary bladder, RBC = red blood cells, SI= small intestine. Activity transferred from Plasma to Colon contents enters Right colon
contents.
Table 12.3. Transfer coefficients for the model for systemic nickel*

Path

Plasma to Kidneys 1
Plasma to SI contents
Plasma to Liver 1
Plasma to Cort bone surf
Plasma to Trab bone surf
Plasma to ST0
Plasma to ST1
Plasma to RBC
Plasma to Excreta
RBC to Plasma

Infant
1.27E+01
1.80E-01
4.50E-01
6.75E-01
6.75E-01
7.20E+00
1.20E+00
7.50E-02
3.40E-01
2.31E-01

1y
1.27E+01
1.80E-01
4.50E-01
6.75E-01
6.75E-01
7.20E+00
1.20E+00
7.50E-02
3.40E-01
2.31E-01

115

Transfer coefficient (d-1)
5y
10 y
1.27E+01 1.27E+01
1.80E-01
1.80E-01
4.50E-01
4.50E-01
6.75E-01
6.75E-01
6.75E-01
6.75E-01
7.20E+00 7.20E+00
1.20E+00 1.20E+00
7.50E-02
7.50E-02
3.40E-01
3.40E-01
2.31E-01
2.31E-01

15 y
1.27E+01
1.80E-01
4.50E-01
6.75E-01
6.75E-01
7.20E+00
1.20E+00
7.50E-02
3.40E-01
2.31E-01

Adult
1.27E+01
1.80E-01
4.50E-01
6.75E-01
6.75E-01
7.20E+00
1.20E+00
7.50E-02
3.40E-01
2.31E-01

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
Kidneys 1 to Plasma
Kidneys 1 to UB contents
Kidneys 1 to Kidneys 2
Kidneys 2 to Plasma
Liver 1 to Plasma
Liver 1 to Liver 2
Liver 1 to SI contents
Liver 2 to Plasma
ST0 to Plasma
ST1 to PlasmaCort bone surf to PlasmaCort bone surf to Cort bone vol
Trab bone surf to Plasma
Trab bone surf to Trab bone volCort bone vol to Plasma
Trab bone vol to Plasma

3474

3.50E+01
1.50E+01
1.30E-03
1.73E-03
1.90E+00
2.90E-01
1.46E+00
1.73E-03
1.90E+00
1.73E-03
1.90E+00
1.92E-02
1.90E+00
1.92E-02
8.22E-03
8.22E-03

3.50E+01
1.50E+01
1.30E-03
1.73E-03
1.90E+00
2.90E-01
1.46E+00
1.73E-03
1.90E+00
1.73E-03
1.90E+00
1.92E-02
1.90E+00
1.92E-02
2.88E-03
2.88E-03*

3.50E+01
1.50E+01
1.30E-03
1.73E-03
1.90E+00
2.90E-01
1.46E+00
1.73E-03
1.90E+00
1.73E-03
1.90E+00
1.92E-02
1.90E+00
1.92E-02
1.53E-03
1.81E-03

3.50E+01
1.50E+01
1.30E-03
1.73E-03
1.90E+00
2.90E-01
1.46E+00
1.73E-03
1.90E+00
1.73E-03
1.90E+00
1.92E-02
1.90E+00
1.92E-02
9.04E-04
1.32E-03

3.50E+01
1.50E+01
1.30E-03
1.73E-03
1.90E+00
2.90E-01
1.46E+00
1.73E-03
1.90E+00
1.73E-03
1.90E+00
1.92E-02
1.90E+00
1.92E-02
5.21E-04
9.59E-04

3.50E+01
1.50E+01
1.30E-03
1.73E-03
1.90E+00
2.90E-01
1.46E+00
1.73E-03
1.90E+00
1.73E-03
1.90E+00
1.92E-02
1.90E+00
1.92E-02
8.21E-05
4.93E-04

SI = small intestine, Cort = cortical, Trab = trabecular, surf = surface, vol = volume, UB = urinary bladder

116

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3475

12.2. Dosimetric data for nickel

3476

Table 12.4. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 59Ni compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled gases or vapours

3 mo

1y

5y

10 y

15 y

Adult

Nickel carbonyl

1.1E-09

7.3E-10

4.4E-10

2.6E-10

1.8E-10

1.6E-10

3.9E-10

1.5E-10

8.6E-11

5.1E-11

3.6E-11

3.5E-11

Type M, Nickel metal; all unspecified forms

4.7E-10

3.7E-102.0E-10

1.2E-108.8E-11

8.1E-11

Type S, Oxide

2.8E-09

2.9E-09

2.1E-09

1.6E-09

1.6E-09

1.6E-09

Adult fA = 0.05, Nickel in diet, soluble and unspecified
forms
6.1E-10

5.5E-11

3.2E-112.0E-11

1.3E-11

1.1E-11

Adult fA = 0.01, Nickel metal

1.3E-10

1.6E-11

8.6E-12

5.5E-12

3.4E-122.8E-12Adult fA = 5.0E-04, Nickel oxide

1.3E-11

6.3E-123.0E-12

2.1E-12

1.1E-12

6.7E-13

Inhaled particulate materials (1 µm AMAD aerosols)
Type F, Chloride,
subsulphidesulphate,monosulphide,

Ingested materials

3477
3478

Table 12.5. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 63Ni compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled gases or vapours

3 mo

1y

5y

10 y

15 y

Adult

Nickel carbonyl

3.0E-09

2.1E-09

1.2E-09

7.4E-105.0E-10

4.7E-10117

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
Inhaled particulate materials (1 µm AMAD aerosols)
Type F, Chloride,
subsulphidesulphate,monosulphide,
1.1E-09

4.1E-10

2.4E-10

1.4E-109.9E-11

9.8E-11

Type M, Nickel metal; all unspecified forms

1.4E-09

1.1E-09

6.2E-10

3.9E-10

2.9E-10

2.7E-10

Type S, Oxide

3.7E-09

6.6E-09

4.7E-09

3.5E-09

3.3E-09

3.4E-09

Adult fA = 0.05, Nickel in diet, soluble and unspecified
forms
1.7E-09

1.4E-108.0E-11

4.8E-11

3.2E-11

3.0E-11

Adult fA = 0.01, Nickel metal

3.4E-10

2.7E-11

1.6E-11

9.6E-12

6.4E-12

6.0E-12Adult fA = 5.0E-04, Nickel oxide

1.7E-11

1.4E-12

8.1E-13

4.8E-13

3.2E-133.0E-13

Ingested materials

3479
3480

118

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

13. ZINC (Z = 30)

3481
3482

13.1. Routes of Intake

3483

13.1.1. Inhalation

3484

13.1.1.1. Absorption Types and parameter values

3485
3486
3487
3488
3489
3490
3491
3492

Little information was found on the behaviour of inhaled zinc in man. Information on
absorption from the respiratory tract is available from experimental studies of several
compounds of zinc or associated with corrosion products. For details see Section 9 of
Publication 134 (ICRP, 2016a). Absorption parameter values and Types, and associated fA
values for particulate forms of zinc are given in Table 13.1 (taken from Section 9 of Publication
134).
Table 13.1. Absorption parameter values for inhaled and ingested zinc
Inhaled particulate materials
Default parameter values†,‡
Absorption Assigned forms
Type
F
Oxide, chromate
M§
Nitrate, phosphate
S
Corrosion products
Ingested materialse
Assigned forms
All forms

fr

1
0.2
0.01

Absorption parameter values*sr (d–1)
ss (d–1)

30
3
3

–
0.005
1×10-4Age-dependent absorption from the alimentary tract, fA
3 months
1 year
5 years
10 years 15 years adult
1
0.5
0.5
0.5
0.5
0.5

3493
3494
3495
3496
3497
3498
3499
3500
3501
3502
3503
3504
3505
3506

*

3507

13.1.2. Ingestion3508

13.1.2.1. Adults

3509
3510
3511
3512

Zinc absorption in humans is influenced by numerous factors including fasting, meal
composition, the amount of daily dietary zinc and the state of health. Volunteer studies showed
gastrointestinal absorption of inorganic zinc of about 0.2, increased to 0.4 - 0.9 in fasting
subjects. Tracer studies in which either stable or radioactive zinc isotopes were incorporated

It is assumed that for zinc the bound state can be neglected i.e. fb = 0. The values of sr for Type F, M and S formsof zinc (30, 3 and 3 d–1, respectively) are the general default values.
†
Materials (e.g. zinc oxide) are listed here where there is sufficient information to assign to a default absorption
Type, but not to give specific parameter values (see Section 9 of Publication 134 (ICRP, 2016a)).
‡
For inhaled material deposited in the respiratory tract and subsequently cleared by particle transport to thealimentary tract, the default fA values for inhaled materials are applied: i.e. the product of fr for the absorption type
and the fA value for ingested soluble forms of zinc applicable to the age-group of interest (e.g. 0.5 for adults).
§
Default Type M is recommended for use in the absence of specific information on which the exposure material
can be assigned to an absorption type, e.g. if the form is unknown, or if the form is known but there is no
information available on the absorption of that form from the respiratory tract.
¶
Activity transferred from systemic compartments into segments of the alimentary tract is assumed to be subject
to reabsorption to blood. The default absorption fraction fA for the secreted activity is the highest value foringestion of the radionuclide applicable to the age-group of interest (e.g. 0.5 for adults).

119

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3513
3514
3515
3516
3517
3518
3519
3520
3521
3522
3523
3524
3525

in meals fed to normal adult volunteers have produced individual absorption values ranging
up to about 60%, with a value of about 30% being typical (Sandstrom et al., 1989; Sandström
et al., 1987; Solomons and Cousins, 1984). It has been suggested that some foods, such as milk
and beef may enhance dietary zinc uptake (Evans and Johnson, 1980; Solomons et al., 1982),
while bran and phytate reduce it (Sandstrom and Cederblad, 1980; Turnlund et al., 1984).
Studies in which human volunteers have ingested crab meat containing 65 Zn gaveabsorption fractions of about 0.15 (ICRP, 1993), and an average value of 0.35 (range 0.250.45) was obtained in seven volunteers for 65 Zn in fish (Honstead and Brady, 1967). In
Publication 30 (ICRP, 1980), an absorption fraction of 0.5 was recommended for all forms of
Zn. The same value was recommended in Publication 67 (ICRP, 1993) for dietary intakes,
although it may be an overestimate for zinc in some foods. An fA of 0.5 was also
recommended in Publication 134 (ICRP, 2016a) for all chemical forms of zinc. The same fA =0.5 is adopted here for dietary forms of zinc ingested by adults.

3526

13.1.2.2. Children

3527
3528
3529
3530
3531
3532
3533
3534
3535
3536

Sullivan et al. (1984) showed an increase by a factor 4 in gastrointestinal absorption
and tissue retention (67%) in 2-day-old neonatal rats compared with adult rats (16%). Ballou
and Thompson (1961) showed that absorption fell abruptly after weaning in rats. Studies by
Sherif et al. (1981) with rats showed a progressive decrease of gastrointestinal absorption withage from the weaning period (17-20 days) to 80 days. Ghishan et al. (1982) observed 90%
absorption in suckling rats compared with 45% in adolescent rats given 65ZnCl2 solution.
Similar results have been reported for mice (ICRP, 1993). An absorption fraction of 1 wasrecommended in Publication 67 for 3-month-old infants. For children of 1 year and older theabsorption fraction for the adult (0.5) was used in Publication 67. The same values are adopted
here for fA.

3537

13.1.3. Systemic Distribution, Retention and Excretion3538

13.1.3.1. Summary of biokinetic data

3539
3540
3541
3542
3543
3544
3545
3546
3547
3548
3549
3550
3551
3552
3553
3554
3555
3556
3557

Biokinetic data for zinc in adult humans were reviewed in Publication 134 (ICRP,
2016a). Briefly, 60% or more of absorbed or intravenously injected zinc isotope rapidly
accumulates in the liver. High concentrations are also seen in the kidneys and pancreas at earlytimes. The label gradually shifts largely to skeletal muscle and bone, which have low rates ofaccumulation but extended retention of zinc. Faecal loss is the primary route of endogenous
excretion and appears to arise from pancreatic secretions together with smaller losses in liverbile, saliva, and other secretions. External measurements of 65Zn in human subjects following
intravenous or oral administration indicate two main components of systemic retention withhalf-times on the order of 1-3 wk (15-30%) and 300-450 d (70-85%). Biokinetic studies onhuman subjects have been too short to identify any components of long-term retention that may
arise, for example, from binding of zinc to bone mineral (ICRP, 2016a). Results of autopsy
studies indicate that muscle contains about 55-65% and bone about 20-30% of zinc in the adulthuman body.
Griffin et al. (2000) investigated the biokinetics of zinc in 7 healthy girls of age 8-11
y. 67Zn and 70Zn were measured in blood, urine, and faeces over a 6-day period following
ingestion of 67Zn and intravenous injection of 70Zn. The data were used to develop transfer
coefficients for a first-order compartmental model containing systemic compartments
representing plasma, red blood cells, tissues with relatively fast turnover, and tissues withrelatively slow turnover. The systemic model was connected to an alimentary tract model
120

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3558
3559
3560
3561
3562
3563
3564
3565
3566
3567
3568
3569
3570
3571
3572
3573
3574
3575
3576
3577
3578
3579
3580
3581
3582
3583
3584
3585
3586
3587
3588
3589
3590
3591
3592
3593
3594

depicting the stomach, small intestine, and colon. The derived mean transfer coefficients andmodel predictions were compared with those of a previously derived model for adult females
based on similar techniques (Lowe et al., 1997). The investigators concluded that the transfer
coefficients between plasma and tissue compartments were similar for children and adults
except for transfer from plasma to the fast-turnover tissue compartment, which was judged tobe significantly higher in children than in adults.
Haumont (1961) examined the distribution of zinc in bones of young adult dogs andimmature rats and found elevated concentrations of zinc at sites undergoing calcification. Zinc
was detected in the haversian systems of compact bone and in endochondral bone recently
deposited in the metaphysis. Following intravenous administration of 65Zn to rats of different
ages, the highest activity concentrations were found in liver, kidneys, and pancreas at earlytimes and in bone at late times (Ballou and Thompson, 1961). In rats fed 65Zn by gavage at age
6, 14, 19, 26, 36, or 94 d, the mean content of the femur at 1 d was 0.48, 2.0, 1.8, 1.4, 1.6, and
1.0% of the retained amount (Ballou and Thompson, 1961). Calhoun et al. (1970) observed asignificantly increased uptake of intravenously administered 65Zn in healing bones of rats
compared with healthy bones of control rats, apparently related to the increased bone formation
rate. Bergman et al. (1972) examined the importance of zinc to cell proliferation in
endochondral growth sites of bone in white rats using zinc-deficient feeding andautoradiography. The results of the study suggest that zinc is required in bone formation,
especially in the synthesis of the organic matrix. Data of Sullivan et al. (1984) for ingestion of65
Zn by rats indicate that the ratio of activity in liver to that in skeleton was not affected by age.
Studies on weanling and 7-week-old mice were conducted to investigate whether boneserves as a reservoir of available zinc (Murray and Messer, 1981). The results indicated thatavailability of bone zinc depended on the rate of bone resorption. In calcium deficiency there
was an increased deposition of zinc in bone, suggesting limited substitution of zinc for calcium
in bone mineral.
Bawden and Hammarström (1977) studied the distribution of 65Zn in young rats byautoradiography following intraperitoneal injection. The liver showed a high activity
concentration within a few hours. The activity concentration eventually became higher in boneand dentine than in other tissues.
Liu-Sheng et al. (1991) studied the absorption and systemic kinetics of 65Zn insuckling (1-20 d old), adolescent (20-70 d), young adult (70-100 d), and mature adult (>100 d)
mice administered a 65Zn solution by stomach tube or intraperitoneal injection. Systemic
activity was found mainly in the liver, muscle, lung, kidneys, and bone (femora). The residence
time of 65Zn in the total body increased with age. Whole-body retention could be described bya sum of 2-3 exponential terms. Among the studied tissues, bone showed the longest componentof retention.

3595

13.1.3.2. Systemic model

3596
3597
3598
3599
3600
3601
3602
3603

The model for systemic zinc applied in Publication 134 (ICRP, 2016a) to workers isapplied here to adult members of the public. The model for adults is modified as follows forapplication to pre-adult ages: (1) the deposition fractions for trabecular and cortical bone
surface are increased by 50% over the adult value for all pre-adult ages, (2) the deposition
fraction for intermediate-term soft tissue in the adult is reduced for pre-adult ages to balance
the increased deposition on bone surface, and (3) activity is assumed to be removed fromtrabecular or cortical bone volume to blood at the age-specific rate of turnover of that bone
type.

121

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3604
3605
3606

3607
3608
3609

The structure of the model for zinc is shown in Fig. 13.1. Parameter values are given
in Table 13.2.

Fig. 13.1. Structure of the systemic model for zinc. RBC = red blood cells; SI = small intestine.

122

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3610

Table 13.2. Transfer coefficients for the model for systemic zinc*

Path

Plasma to Liver 1
Plasma to Kidneys
Plasma to Pancreas
Plasma to Muscle
Plasma to RBC
Plasma to ST0
Plasma to ST1
Plasma to ST2
Plasma to UB contents
Plasma to Excreta
Plasma to SI contents
Plasma to Trab bone surf
Plasma to Cort bone surf
Liver 1 to Plasma
Liver 1 to SI contents
Liver 1 to Liver 2
Liver 2 to Plasma
Kidneys to Plasma
Pancreas to Plasma
Pancreas to SI contents
Muscle to Plasma
RBC to Plasma
ST0 to Plasma
ST1 to Plasma
ST2 to Plasma
Trab bone surf to PlasmaCort bone surf to Plasma
Trab bone surf to Trab bone volCort bone surf to Cort bone vol
Trab bone vol to PlasmaCort bone vol to Plasma

3611
3612

Infant
6.00E+01
4.00E+00
3.00E+00
2.00E+00
1.50E+00
4.00E+01
2.98E+01
4.00E-01
1.30E-01
1.30E-01
2.00E-01
2.25E-01
4.50E-01
1.00E+01
6.70E-02
1.00E+01
6.00E-01
7.00E-01
1.50E+00
1.00E+00
5.00E-03
1.40E-01
1.00E+01
3.00E+00
1.00E-02
1.00E-02
1.00E-02
5.30E-04
5.30E-04
8.22E-03
8.22E-03

1y
6.00E+01
4.00E+00
3.00E+00
2.00E+00
1.50E+00
4.00E+01
2.98E+01
4.00E-01
1.30E-01
1.30E-01
2.00E-01
2.25E-01
4.50E-01
1.00E+01
6.70E-02
1.00E+01
6.00E-01
7.00E-01
1.50E+00
1.00E+00
5.00E-03
1.40E-01
1.00E+01
3.00E+00
1.00E-02
1.00E-02
1.00E-02
5.30E-04
5.30E-04
2.88E-03
2.88E-03*

Transfer coefficient (d-1)
5y
10 y
6.00E+01 6.00E+01
4.00E+00 4.00E+00
3.00E+00 3.00E+00
2.00E+00 2.00E+00
1.50E+00 1.50E+00
4.00E+01 4.00E+01
2.98E+01 2.98E+01
4.00E-01
4.00E-01
1.30E-01
1.30E-01
1.30E-01
1.30E-01
2.00E-01
2.00E-01
2.25E-01
2.25E-01
4.50E-01
4.50E-01
1.00E+01 1.00E+01
6.70E-02
6.70E-02
1.00E+01 1.00E+01
6.00E-01
6.00E-01
7.00E-01
7.00E-01
1.50E+00 1.50E+00
1.00E+00 1.00E+00
5.00E-03
5.00E-03
1.40E-01
1.40E-01
1.00E+01 1.00E+01
3.00E+00 3.00E+00
1.00E-02
1.00E-02
1.00E-02
1.00E-02
1.00E-02
1.00E-02
5.30E-04
5.30E-04
5.30E-04
5.30E-04
1.81E-03
1.32E-03
1.53E-03
9.04E-04

15 y
6.00E+01
4.00E+00
3.00E+00
2.00E+00
1.50E+00
4.00E+01
2.98E+01
4.00E-01
1.30E-01
1.30E-01
2.00E-01
2.25E-01
4.50E-01
1.00E+01
6.70E-02
1.00E+01
6.00E-01
7.00E-01
1.50E+00
1.00E+00
5.00E-03
1.40E-01
1.00E+01
3.00E+00
1.00E-02
1.00E-02
1.00E-02
5.30E-04
5.30E-04
9.59E-04
5.21E-04

Adult
6.00E+01
4.00E+00
3.00E+00
2.00E+00
1.50E+00
4.00E+01
3.00E+01
4.00E-01
1.30E-01
1.30E-01
2.00E-01
1.50E-01
3.00E-01
1.00E+01
6.70E-02
1.00E+01
6.00E-01
7.00E-01
1.50E+00
1.00E+00
5.00E-03
1.40E-01
1.00E+01
3.00E+00
1.00E-02
1.00E-02
1.00E-02
5.30E-04
5.30E-04
4.93E-04
8.21E-05

RBC = red blood cells, UB = Urinary bladder, Trab = trabecular, Cort = cortical, surf = surface, vol = volume,
SI = Small intestine123

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3613

13.2. Dosimetric data for zinc

3614

Table 13.3. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 65Zn compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled particulate materials (1 µm AMAD aerosols) 3 mo

1y

5y

10 y

15 y

Adult

Type F, Oxide, chromate

2.4E-08

1.1E-08

6.1E-09

4.0E-09

2.8E-09

2.7E-09

1.1E-08

6.7E-09

4.0E-09

2.7E-09

2.0E-09

2.1E-09

9.4E-09

8.5E-09

5.2E-09

3.6E-09

2.8E-09

3.2E-09

4.7E-08

1.5E-08

9.5E-09

6.2E-09

4.6E-09

4.3E-09

Type M, Nitrate,compounds

phosphate;

Type S, Corrosion products

allunspecified

Ingested materials
Adult fA = 0.5, All forms

3615
3616

124

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

14. SELENIUM (Z = 34)

3617
3618

14.1. Routes of Intake

3619

14.1.1. Inhalation

3620

14.1.1.1. Absorption Types and Parameter Values

3621
3622
3623
3624
3625
3626
3627
3628
3629

No information was found on the behaviour of inhaled selenium in man. Information
on absorption of selenium from the respiratory tract is available from experimental studies offorms of selenium including selenious acid (H2SeO3) and elemental selenium, which wereconducted mainly to investigate the potential health hazard of selenium emitted during fossil
fuel combustion. For details see Section 20 of Publication 151 (ICRP, 2022).
Absorption parameter values and Types, and associated fA values for particulate forms
of selenium are given in Table 14.1 (taken from Section 20 of Publication 151).
Table 14.1. Absorption parameter values for inhaled and ingested selenium
Inhaled particulate materials
Default parameter values†,‡
Absorption type Assigned forms
F
Selenium dioxide, selenious acid,elemental selenium
§
M
—
S
—
Ingested materials¶
Assigned forms
selenium in dietfr

Absorption parameter values*sr (d–1)
ss (d–1)

1

30

–

0.2
0.01

3
3

0.005
0.0001Age-dependent absorption from the alimentary tract, fA
3 months 1 year
5 years
10 years
15 years
adults
1
0.8
0.8
0.8
0.8
0.8

It is assumed that for selenium the bound state can be neglected i.e. fb = 0. The value of sr for Type F (30 d–1) iselement-specific. The values for types M and S (3 d–1) are the general default values.
†
Materials (e.g. selenium dioxide) are generally listed here where there is sufficient information to assign to adefault absorption Type, but not to give specific parameter values (see Section 20 of ICRP, 2021).
‡
For inhaled material deposited in the respiratory tract and subsequently cleared by particle transport to thealimentary tract, the default fA values for inhaled materials are applied: i.e., the product of fr for the absorption
type and the fA value for ingested soluble forms of selenium applicable to the age-group of interest (e.g. 0.8 for
adults).
§Default Type M is recommended for use in the absence of specific information on which the exposure material
can be assigned to an absorption type, e.g. if the form is unknown, or if the form is known but there is no
information available on the absorption of that form from the respiratory tract.
¶
Activity transferred from systemic compartments into segments of the alimentary tract is assumed to be subject
to reabsorption to blood. The default absorption fraction fA for the secreted activity is the highest value foringestion of the radionuclide applicable to the age-group of interest (e.g. 0.8 for adults).

3630
3631
3632
3633
3634
3635
3636
3637
3638
3639
3640
3641
3642
3643
3644

*

3645

14.1.2. Ingestion3646

14.1.2.1. Adults

125

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3647
3648
3649
3650
3651

The behaviour of dietary selenium has been studied in balance studies, stable isotope
and radiotracer human volunteer experiments. The gastrointestinal absorption of some otherorganic and inorganic forms of selium has also been evaluated in humans, monkeys, rats, miceand dogs. For details, see Section 20 of Publication 151 (ICRP, 2022). A fA value = 0.8 isadopted here for ingestion of selenium in diet by adult members of the public.

3652

14.1.2.2. Children

3653
3654
3655
3656
3657

Limited data are available on the absorption of selenium in young animals. Nishimura
et al. (1991) reported that in 6-d-old rats given 75Se as selenite, fractional absorption was muchgreater than in adults (> 0.6). In 14-d-old rats intermediate values were obtained. Like in
Publication 69 (ICRP, 1995a), the same fA value as is adopted for adults (0.8) is used here forl-, 5-, l0-, and 15-y-old children. For 3-mo-old infants an fA of 1 is adopted.

3658

14.1.3. Systemic Distribution, Retention and Excretion

3659
3660
3661
3662
3663
3664

No information was found on age related changes in the systemic kinetics of selenium.
An updated systemic biokinetic model for occupational intake of selenium is described in
Section 20 of Publication 151 (ICRP, 2022). That model is applied here to intake of selenium
at any age.
The model structure is shown in Fig. 14.1. The transfer coefficients are listed in Table
14.2.

3665
3666
3667
3668
3669

Fig. 14.1. Structure of the model for systemic selenium. Activity transferred from Plasma to
Colon contents enters Right colon contents. SI = Small intestine.
Table 14.2. Transfer coefficients for the model for systemic seleniumaPath

Plasma to Liver
Plasma to Kidneys
Plasma to Pancreas
Plasma to Spleen
Plasma to Testes

Infant
1.20E+00
6.00E-01
8.00E-02
1.10E-01
4.00E-02

Transfer coefficient (d-1)
1y
5y
10 y
1.20E+00 1.20E+00 1.20E+00
6.00E-01 6.00E-01 6.00E-01
8.00E-02 8.00E-02 8.00E-02
1.10E-01 1.10E-01 1.10E-01
4.00E-02 4.00E-02 4.00E-02

126

15 y
1.20E+00
6.00E-01
8.00E-02
1.10E-01
4.00E-02

Adult
1.20E+00
6.00E-01
8.00E-02
1.10E-01
4.00E-02

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
Plasma to Ovaries
Plasma to ST1
Plasma to ST2
Plasmato
UBcontents
PlasmatoRCcontents
Plasma to Trab bone
surf
Plasma to Cort bone
surf
Plasma to RBC
Liver to Plasma
Kidneys to Plasma
Spleen to Plasma
Pancreas to Plasma
Testes to Plasma
Ovaries to Plasma
ST1 to Plasma
ST2 to Plasma
RBC to Plasma
Trab bone surf to
PlasmaCort bone surf to
Plasma3670

a1.30E-02
5.20E+00
5.00E-01
1.00E+00

1.30E-02
5.20E+00
5.00E-01
1.00E+00

1.30E-02
5.20E+00
5.00E-01
1.00E+00

1.30E-02
5.20E+00
5.00E-01
1.00E+00

1.30E-02
5.20E+00
5.00E-01
1.00E+00

1.30E-02
5.20E+00
5.00E-01
1.00E+00

4.00E-01

4.00E-01

4.00E-01

4.00E-01

4.00E-01

4.00E-01

2.00E-01

2.00E-01

2.00E-01

2.00E-01

2.00E-01

2.00E-01

2.00E-01

2.00E-01

2.00E-01

2.00E-01

2.00E-01

2.00E-01

5.00E-01
8.00E-02
8.00E-02
8.00E-02
8.00E-02
8.00E-02
8.00E-02
8.00E-02
5.00E-03
3.50E-02
1.50E-02

5.00E-01
8.00E-02
8.00E-02
8.00E-02
8.00E-02
8.00E-02
8.00E-02
8.00E-02
5.00E-03
3.50E-02
1.50E-02

5.00E-01
8.00E-02
8.00E-02
8.00E-02
8.00E-02
8.00E-02
8.00E-02
8.00E-02
5.00E-03
3.50E-02
1.50E-02

5.00E-01
8.00E-02
8.00E-02
8.00E-02
8.00E-02
8.00E-02
8.00E-02
8.00E-02
5.00E-03
3.50E-02
1.50E-02

5.00E-01
8.00E-02
8.00E-02
8.00E-02
8.00E-02
8.00E-02
8.00E-02
8.00E-02
5.00E-03
3.50E-02
1.50E-02

5.00E-01
8.00E-02
8.00E-02
8.00E-02
8.00E-02
8.00E-02
8.00E-02
8.00E-02
5.00E-03
3.50E-02
1.50E-02

1.50E-02

1.50E-02

1.50E-02

1.50E-02

1.50E-02

1.50E-02

UB = urinary bladder, RC = right colon, Trab = trabecular, Cort = cortical, RBC = red blood cells, surf = surface

127

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3671

14.2. Dosimetric data for selenium

3672
3673

Table 14.3. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 75Se compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled particulate materials (1 µm AMAD aerosols) 3 mo

1y

5y

10 y

15 y

Adult

Type F, Selenium dioxide, selenious acid, elemental
selenium
8.4E-09

6.1E-09

3.3E-09

2.3E-09

1.2E-09

1.2E-09

Type M, All unspecified forms

5.2E-09

4.2E-09

2.4E-09

1.7E-09

1.1E-09

1.2E-09

Type S

5.7E-09

5.0E-09

2.9E-09

2.0E-09

1.5E-09

1.7E-09

1.6E-08

1.1E-08

6.6E-09

4.6E-09

2.7E-09

2.5E-09

Ingested materials
Adult fA = 0.8, Selenium in diet

3674
3675

Table 14.4. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 79Se compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled particulate materials (1 µm AMAD aerosols) 3 mo

1y

5y

10 y

15 y

Adult

Type F, Selenium dioxide, selenious acid, elemental
selenium
1.4E-08

9.9E-09

5.3E-09

3.5E-09

1.2E-09

9.2E-10

Type M, All unspecified forms

8.5E-09

6.9E-09

4.0E-09

2.6E-09

1.6E-09

1.4E-09

Type S

2.7E-08

2.7E-08

1.9E-08

1.5E-08

1.4E-08

1.4E-08

2.7E-08

1.7E-08

1.0E-087.0E-09

2.7E-09

1.9E-09

Ingested materials
Adult fA = 0.8, Selenium in diet

3676
128

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

15. STRONTIUM (Z = 38)

3677
3678

15.1. Routes of Intake

3679

15.1.1. Inhalation

3680
3681
3682
3683
3684
3685
3686
3687
3688

Some information is available on the behaviour of inhaled strontium in man following
accidental intakes of several compounds. Information on absorption from the respiratory tract
is available from experimental studies of strontium as chloride, sulphate, titanate, irradiatedfuel fragments, or in fused aluminosilicate particles (FAP) and polystyrene (PSL). For details
see Section 10 of of Publication 134 (ICRP, 2016a).
Absorption parameter values and types, and associated fA values for particulate formsof strontium are given in Table 15.1 (taken from Section 10 of Publication 134).
Table 15.1. Absorption parameter values for inhaled and ingested strontium
Absorption parameter values*sr (d–1)
ss (d–1)

Inhaled particulate materials
fr
Default parameter values†,‡
Absorption Assigned forms
TypeF
Chloride, sulphate and carbonate
1
30
–
M§
Fuel fragments
0.2
3
0.005
S
FAP, PSL, Strontium titanate
0.01
3
1 x 10-4¶
Ingested material
Assigned forms
Age-dependent absorption from the alimentary tract, fA
3 months 1 year
5 years
10 years 15 years adult
Strontium in diet and in soluble 0.6
0.4
0.4
0.4
0.4
0.25
forms
Insoluble forms (assigned as 0.02
0.01
0.01
0.01
0.01
0.01
type S)

3689
3690
3691
3692
3693
3694
3695
3696
3697
3698
3699
3700
3701
3702
3703

*

3704

15.1.2. Ingestion

3705

15.1.2.1. Adults

It is assumed that for strontium the bound state can be neglected i.e. fb = 0. The values of sr for Type F, M and S
forms of strontium (30, 3 and 3 d–1, respectively) are the general default values.
†
Materials (e.g. chloride) are generally listed here where there is sufficient information to assign to a default
absorption Type, but not to give specific parameter values (see Section 10 of Publication 134 (ICRP, 2016a)).
‡
For inhaled material deposited in the respiratory tract and subsequently cleared by particle transport to thealimentary tract, the default fA values for inhaled materials are applied: i.e. the product of fr for the absorption type
and the fA value for ingested soluble forms of strontium applicable to the age-group of interest (e.g. 0.25 for
adults).
§Default Type M is recommended for use in the absence of specific information on which the exposure material
can be assigned to an absorption type, e.g. if the form is unknown, or if the form is known but there is no
information available on the absorption of that form from the respiratory tract.
¶
Activity transferred from systemic compartments into segments of the alimentary tract is assumed to be subject
to reabsorption to blood. The default absorption fraction fA for the secreted activity is the highest value foringestion of the radionuclide applicable to the age-group of interest (e.g. 0.25 for adults).

129

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3706
3707
3708
3709
3710
3711
3712
3713
3714
3715
3716
3717
3718
3719
3720
3721
3722
3723
3724
3725
3726
3727
3728

Due to the presence of strontium isotopes in fall-out material and its long-term
retention in bone as a calcium analogue, the metabolism of strontium has been the subject of anumber of human volunteer studies. Similar fractional absorption values, typically in the range
0.1 – 0.4 (Harrison et al., 2001) with a central value around 0.2, were obtained from studies inwhich inorganic forms of radiostrontium was administered orally in solution and fromexperiments where known quantities of radiostrontium incorporated in food were ingested. An
exception was strontium titanate (SrTiO3) which shows low levels of absorption of about 0.01.
A number of factors have been found to increase strontium absorption, including fasting, lowdietary levels of calcium, magnesium and phosphorus, milk diets and vitamin D. By contrast,
sex, age at exposure in adult groups, smoking, exercise or use of oral contraceptives in young
females do not seem to significantly change the intestinal absorption of strontium. Radioactive
strontium has been shown to accumulate in teeth. Most of this deposit comes fromgastrointestinal absorption and subsequent systemic distribution but a small part may also be
adsorbed directly from the oral cavity onto the dental plaque and enamel during mastication.
Unfortunately not enough information is available to derive robust parameters for Sr adsorption
and retention on teeth. (For more details see Section 10 of Publication 134, ICRP, 2016a). In
Publication 30 (ICRP, 1979), the recommended absorption values were 0.01 for SrTiO 3 and
0.3 for all other compounds. In Publication 67 (ICRP, 1993), a value of 0.3 was recommended
for dietary intakes by adults. Due to the strong link between strontium and calcium absorption
and the known discrimination in favour of calcium, a default fA value of 0.25 was recommendedin Publication 134 for all chemical forms but strontium titanate. The same value of 0.25 for fA
is adopted here for adults and for strontium in food and in other soluble forms. For ingestionof strontium titanate and other type S forms, an fA of 0.01is adopted.

3729

15.1.2.2. Children

3730
3731
3732
3733
3734
3735
3736
3737
3738
3739
3740
3741
3742
3743
3744
3745

Results obtained by Widdowson et al. (1960) suggest that absorption of strontium in
7-day-old infants fed with cows' milk is greater than 73%. Bedford et al. (1960) reported thatabsorption in 5-15-year-old children was the same as in adults. However, studies on beagles
and rats have shown that the period of increased absorption of strontium extends beyond thetime of weaning. In the beagle, retention values for strontium at 3-9 days after ingestion were20%, 15% and 8% in 48-, 80- and 140-day-old animals, respectively (Della Rosa et al., 1965).
The absorption of strontium in 35- and 75-day-old rats was estimated as 70-90% by Gran
(1960) compared with 12% in 270-day-old rats. Taylor et al. (1962) obtained absorption valuesof 0.95±0.004 (standard error, n = 31) for 14–18-day-old rats and 0.74 ± 0.024 (standard error,n = 5) for 22-day-old animals. A value of 0.6 was recommended in Publication 67 for infants.
For ages 1-15 years a value of 0.4 was chosen in Publication 67, based on the considerationthat there may be elevated absorption of strontium throughout the period of growth. Harrison
et al. (2001) proposed confidence intervals of 0.1–0.5 for 10-year-old children, and 0.15–0.75
for 3-month-old infants. The values of f A 0.6 for 3-month-old infants and 0.4 for ages 1-15
years are adopted here. For ingestion of strontium titanate and other type S forms by 3-monthold infants, an fA of 0.02 is adopted.

3746

15.1.3. Systemic Distribution, Retention and Excretion3747

15.1.3.1. Age-specific data

3748
3749
3750

Strontium is a chemical and physiological analogue of calcium but has somewhat
different biokinetics from calcium due to discrimination between these elements by biologicalmembranes and hydroxyapatite crystals of bone. For example, strontium is less effectively
130

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3751
3752
3753
3754
3755
3756
3757
3758
3759
3760
3761
3762
3763
3764
3765
3766
3767
3768
3769
3770
3771
3772

absorbed from the intestines and more effectively excreted by the kidney than calcium and islost from bone at a higher rate than calcium over the first few months after deposition in bone
(Bauer et al. 1955, Spencer et al. 1960, Barnes et al. 1961, Cohn et al. 1963, Decker et al. 1964,
Harrison et al. 1967).
The biokinetics of strontium has been studied extensively in human subjects andlaboratory animals. Differences with age in the systemic behavior of strontium in humans arereasonably well understood from studies of the uptake and retention of environmental 90Sr inpersons of all ages; control studies of the fate of strontium isotopes in humans and laboratory
animals at different stages of life; and comparison with age-specific data for chemical andphysiological analogues of strontium.
A large database related to the transfer of 90Sr from food and milk to the humanskeleton was developed in the 1950s and 1960s (Fig. 15.1). Interpretation of the environmental
data with regard to systemic biokinetics is complicated by the gradual accumulation of 90Sr in
the body and uncertainties in the level of uptake of ingestion 90Sr to blood at any age. Moreeasily interpreted age-specific human data are available from controlled human studies (Fig.
15.2), but such data are limited for children and generally involved unhealthy children. Agespecific data on retention of strontium in laboratory animals, particular beagles (Fig. 15.3), help
to clarify the behavior of strontium at early times after intake as well as relative patterns ofbuildup and decline of strontium in bone at different stages of bone development. Because
strontium is a close physiological analogue of calcium, data from controlled studies of calciumin humans provide supporting information for selection of age-specific parameter values forstrontium.

3773
3774
3775

Fig. 15.1. Observed differences with age in the concentration of 90Sr in bone in persons exposed
to environmental 90Sr from fallout (after Leggett et al., 1982).

131

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3776
3777
3778
3779

Fig. 15.2. Observed differences with age in total-body retention of strontium as a function oftime after intravenous injection (after Leggett, 1992a; data collected from several sources).

3780
3781
3782
3783
3784

Fig. 15.3. Observed differences with age in total-body retention of strontium in dogs as afunction of time after intravenous injection. Figure from (Leggett, 1992a); data collected fromseveral studies.

3785

15.1.4. Systemic model

3786
3787
3788
3789

A number of age-specific biokinetic models for strontium have been developed(Aarkrog, 1971; Bennett, 1975; Harley, 1966; ICRP, 1990, 1993; Kulp and Schulert, 1962;
Leggett, 1992a; Leggett et al., 1982; Papworth and Vennart, 1984; Rivera, 1967; Shagina et al.,2003, 2015). Although different conceptual frameworks have been used, the various models

132

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3790
3791
3792
3793

3794
3795
3796
3797
3798
3799

yield broadly consistent estimates with regard to accumulation and retention of ingested
strontium in bone, the dominant repository for systemic strontium.
The systemic model adopted in Publication 67 (ICRP, 1993) is applied in this report.
The model structure is shown in Fig. 15.4. Transfer coefficients are listed in Table 15.2.

Fig. 15.4. Structure of the biokinetic model for systemic strontium. Abbreviations: exch =exchangeable, nonexch = non-exchangeable. Activity transferred from Blood to Colon contents
enters Right colon contents.

133

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3800

Table 15.2. Age-specific transfer coefficients for strontium

Pathway
Blood to UB contents
Blood to Right colon contents
Blood to Trabecular bone surf
Blood to Cortical bone surf
Blood to ST0
Blood to ST1
Blood to ST2
Trabecular bone surf to Blood
Trab bone surf to Exch trab bone volCort bone surf to Blood
Cort bone surf to Exch cort bone volST0 to Blood
ST1 to Blood
ST2 to Blood
Exch trab bone vol to trab bone surf
Exch to Non-exch trab bone volExch cort bone vol to cort bone surf
Exch to Non-exch cort bone volNon-exch cort bone vol to Blood
Non-exch trab bone vol to Blood

Transfer coefficient (d-1)
100 d
1y
5y
10 y
15 y
5.77E-01 1.27E+00 1.38E+00 1.02E+00 6.00E-01
1.75E-01 3.85E-01 4.20E-01 3.08E-01 1.82E-01
2.25E+00 1.35E+00 1.33E+00 2.12E+00 3.10E+00
9.00E+00 5.40E+00 4.67E+00 6.28E+00 8.00E+00
2.50E+00 5.50E+00 6.00E+00 4.40E+00 2.60E+00
5.00E-01 1.10E+00 1.20E+00 8.80E-01 5.20E-01
1.00E-03 2.20E-03 2.40E-03 1.80E-03 1.00E-03
6.01E-01 6.01E-01 6.01E-01 6.01E-01 6.01E-01
9.24E-02 9.24E-02 9.24E-02 9.24E-02 9.24E-02
6.01E-01 6.01E-01 6.01E-01 6.01E-01 6.01E-01
9.24E-02 9.24E-02 9.24E-02 9.24E-02 9.24E-02
8.33E-01 1.83E+00 2.00E+00 1.47E+00 8.67E-01
1.16E-01 1.16E-01 1.16E-01 1.16E-01 1.16E-01
3.80E-04 3.80E-04 3.80E-04 3.80E-04 3.80E-04
4.30E-03 4.30E-03 4.30E-03 4.30E-03 4.30E-03
4.30E-03 4.30E-03 4.30E-03 4.30E-03 4.30E-03
4.30E-03 4.30E-03 4.30E-03 4.30E-03 4.30E-03
4.30E-03 4.30E-03 4.30E-03 4.30E-03 4.30E-03
8.22E-03 2.88E-03 1.53E-03 9.04E-04 5.21E-04
8.22E-03 2.88E-03 1.81E-03 1.32E-03 9.59E-04

3801

134

Adult
1.73E+00
5.25E-01
2.08E+00
1.67E+00
7.50E+00
1.50E+00
3.00E-03
5.78E-01
1.16E-01
5.78E-01
1.16E-01
2.50E+00
1.16E-01
3.80E-04
4.30E-03
4.30E-03
4.30E-03
4.30E-03
8.21E-05
4.93E-04

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3802

15.2. Dosimetric data for strontium

3803

Table 15.3. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 85Sr compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled particulate materials (1 µm AMAD aerosols) 3 mo

1y

5y

10 y

15 y

Adult

Type F, Chloride, sulphate and carbonate

4.0E-09

1.7E-09

8.2E-10

6.8E-10

6.2E-10

2.7E-10

Type M, Fuel fragments; all unspecified forms

3.6E-09

2.6E-09

1.5E-09

1.0E-09

8.0E-10

7.9E-10

Type S, FAP, PSL, Strontium titanate

4.3E-09

3.6E-09

2.1E-09

1.4E-09

1.1E-09

1.2E-09

Adult fA = 0.01, Insoluble forms (assigned as Type S) 1.0E-09

8.2E-10

4.6E-10

3.3E-10

2.4E-10

2.1E-10Adult fA = 0.25, Strontium in diet and in soluble forms 6.4E-09

2.3E-09

1.3E-09

1.0E-09

9.7E-10

3.8E-10

Ingested materials

3804
3805

Table 15.4. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 89Sr compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled particulate materials (1 µm AMAD aerosols) 3 mo

1y

5y

10 y

15 y

Adult

Type F, Chloride, sulphate and carbonate

2.4E-08

9.3E-09

3.2E-09

2.0E-09

2.3E-09

7.0E-10

Type M, Fuel fragments; all unspecified forms

2.1E-08

1.6E-08

8.5E-09

5.6E-09

4.6E-09

4.0E-09

Type S, FAP, PSL, Strontium titanate

2.5E-08

2.1E-08

1.2E-08

8.1E-09

6.3E-09

6.1E-09

Adult fA = 0.01, Insoluble forms (assigned as Type S) 3.1E-09

1.8E-09

1.1E-09

7.4E-10

5.1E-10

4.0E-10Adult fA = 0.25, Strontium in diet and in soluble forms 3.7E-08

1.1E-08

4.7E-09

3.0E-09

3.5E-09

8.9E-10

Ingested materials

3806
135

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3807

Table 15.5. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 90Sr compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled particulate materials (1 µm AMAD aerosols) 3 mo

1y

5y

10 y

15 y

Adult

Type F, Chloride, sulphate and carbonate

2.4E-07

9.2E-08

4.2E-08

6.1E-08

9.5E-08

2.5E-08

Type M, Fuel fragments; all unspecified forms

1.4E-07

9.9E-08

5.6E-08

5.0E-08

5.9E-08

3.2E-08

Type S, FAP, PSL, Strontium titanate

6.0E-07

6.2E-07

4.8E-07

3.9E-074.0E-07

4.1E-07

Adult fA = 0.01, Insoluble forms (assigned as Type S) 1.3E-08

3.5E-09

1.9E-09

2.4E-09

3.6E-09

1.1E-09

Adult fA = 0.25, Strontium in diet and in soluble forms 3.7E-07

1.1E-07

5.6E-08

8.2E-08

1.3E-07

2.4E-08

Ingested materials

3808

136

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

16. YTTRIUM (Z = 39)

3809
3810

16.1. Routes of Intake

3811

16.1.1. Inhalation

3812
3813
3814
3815
3816
3817
3818

Information on absorption from the respiratory tract is available from experimental
studies of yttrium mainly as chloride or in fused aluminosilicate particles (FAP). For details
see Section 11 of Publication 134 (ICRP, 2016a). Absorption parameter values and types, andassociated fA values for particulate forms of yttrium are given in Table 16.1 (taken from Section
11 of Publication 134).
Table 16.1. Absorption parameter values for inhaled and ingested yttrium
Absorption parameter values*sr (d–1)
ss (d–1)

Inhaled particulate materials
Default parameter values†,‡
Absorption
Assigned forms
TypeF
Chloride
M§
Oxide, phosphate

fr

1
0.2

1
1

–
0.005

S

0.01

1

1×10-4FAP

Ingested material¶
Assigned forms
All chemical forms

Age-dependent absorption from the alimentary tract, fA
3 months 1 year
5 years
10 years 15 years adult1 × 10-3
5 × 10-4
5 × 10-4
5 × 10-4
5 × 10-4
1 × 10-4

3819
3820
3821
3822
3823
3824
3825
3826
3827
3828
3829
3830
3831
3832
3833

*

3834

16.1.2. Ingestion

3835

16.1.2.1. Adults

3836
3837
3838
3839

There is little information on absorption of ingested yttrium but it appears to be very
low. In Publications 30 and 134 (ICRP, 1987, 2016a) an absorption fraction of 1 × 10-4 wasrecommended. The same fA value of 1 × 10-4 is adopted here for all chemical forms ingested
by adult members of the public.

It is assumed that for yttrium the bound state can be neglected i.e. fb = 0. The values of sr for Type F, M and S
forms of yttrium (1 d–1, respectively) are element-specific.
†
Materials (e.g. Chloride) are listed here where there is sufficient information to assign to a default absorption
type, but not to give specific parameter values (see Section 11 of Publication 134, ICRP, 2016a).
‡
For inhaled material deposited in the respiratory tract and subsequently cleared by particle transport to thealimentary tract, the default fA values for inhaled materials are applied: i.e. the product of fr for the absorption
type and the fA value for ingested soluble forms of yttrium applicable to the age-group of interest (e.g. 1×10-4 foradults).
§Default Type M is recommended for use in the absence of specific information on which the exposure material
can be assigned to an absorption type, e.g. if the form is unknown, or if the form is known but there is no
information available on the absorption of that form from the respiratory tract.
¶
Activity transferred from systemic compartments into segments of the alimentary tract is assumed to be subject
to reabsorption to blood. The default absorption fraction fA for the secreted activity is the highest value foringestion of the radionuclide applicable to the age-group of interest (e.g. 1×10-4 for adults).

137

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3840

16.1.2.2. Children

3841
3842
3843

Consistently with the approach of Publication 56 (ICRP, 1990), an fA = 10-3 is adopted
here for 3 month old infants and an intermediate value of 5 × 10-4 is adopted here for 3 month
old infants to 15 year old children.

3844

16.1.3. Systemic Distribution, Retention and Excretion3845

16.1.3.1. Biokinetic model for systemic yttrium

3846
3847
3848
3849
3850
3851
3852
3853
3854
3855
3856
3857
3858
3859
3860
3861
3862
3863
3864
3865
3866
3867
3868
3869
3870
3871

The model for systemic yttrium applied in Publication 134 (ICRP, 2016a) to workers
is applied here to adult members of the public. That model is based on results of a controlled
study of retention and excretion of intravenously administered 88Y in healthy human subjects,
supplemented with results of biokinetic studies of yttrium isotopes in laboratory animals.
Yttrium is considered a bone seeker and by analogy with more extensively studiedbone seekers is expected to have higher deposition in growing bone than in mature bone.
Studies on laboratory animals indicate, however, that changes with age in uptake by bone may
be less pronounced for yttrium than for some bone seekers such as strontium or lead
(MacDonald et al., 1952; Stevenson, 1975).
In the age-specific model for yttrium applied in this report, fractional deposition of
yttrium in bone is assumed to be 50% higher in infants than in adults (i.e., the deposition
fraction in bone is assumed to be 0.6 in infants compared with 0.4 in adults) and 25% higher inpersons of age 1-15 y than in adults. Bone deposits are assumed to be equally divided between
trabecular and cortical bone surfaces. The skeletal behaviour of yttrium deposited on bone
surfaces is described by the generic model for bone-surface-seekers (Annex B of ICRP, 2015),
except that yttrium biologically removed from bone is assumed to return to blood rather thanto be channeled through bone marrow.
For a given pre-adult age the deposition fractions for soft tissues and excretion
pathways are reduced from the adult value to account for elevated competition for circulating
yttrium from bone surfaces at the pre-adult age. The deposition fraction for a soft-tissue or
excretion pathway at a given pre-adult age is the value for the adult multiplied by the ratio(1-B)/(1-A) where A and B are fractional depositions in bone in the adult and the given preadult age, respectively.
The structure of the model for systemic yttrium is shown in Fig. 16.1. Parametervalues are given in Table 16.2.

138

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3872
3873
3874

Fig. 16.1. Structure of the biokinetic model for systemic yttrium. SI = Small intestine.

139

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3875

Table 16.2. Transfer coefficients for the model for systemic yttriuma

Path

Blood 1 to Blood 2
Blood 1 to Liver 0
Blood 1 to Kidneys
Blood 1 to ST0
Blood 1 to ST1
Blood 1 to UB contents
Blood 1 to SI contents
Blood 1 to Trab bone surf
Blood 1 to Cort bone surf
Blood 2 to Blood 1
Liver 0 to SI contents
Liver 0 to Liver 1
Liver 0 to Blood 1
Liver 1 to Blood 1
Kidneys to Blood 1
ST0 to Blood 1
ST1 to Blood 1
Trab bone surf to Blood 1
Trab bone surf to Trab bone vol
Trab bone vol to Blood 1
Cort bone surf to Blood 1
Cort bone surf to Cort bone volCort bone vol to Blood 1

3876

a

Infant
3.32E-01
1.11E+00
1.11E-01
2.43E+00
8.85E-01
1.66E+00
1.11E-01
4.98E+00
4.98E+00
4.62E-01
2.31E-02
1.16E-01
9.24E-02
1.90E-03
1.90E-03
2.31E-01
1.90E-03
8.22E-03
8.22E-03
8.22E-03
8.22E-03
8.22E-03
8.22E-03

1y4.15E-01
1.38E+00
1.38E-01
3.04E+00
1.11E+00
2.08E+00
1.38E-01
4.15E+00
4.15E+00
4.62E-01
2.31E-02
1.16E-01
9.24E-02
1.90E-03
1.90E-03
2.31E-01
1.90E-03
2.88E-03
2.88E-03
2.88E-03
2.88E-03
2.88E-03
2.88E-03

Transfer coefficient (d-1)
5y
10 y
15 y
4.15E-01 4.15E-01 4.15E-01
1.38E+00 1.38E+00 1.38E+00
1.38E-01 1.38E-01 1.38E-01
3.04E+00 3.04E+00 3.04E+00
1.11E+00 1.11E+00 1.11E+00
2.08E+00 2.08E+00 2.08E+00
1.38E-01 1.38E-01 1.38E-01
4.15E+00 4.15E+00 4.15E+00
4.15E+00 4.15E+00 4.15E+00
4.62E-01 4.62E-01 4.62E-01
2.31E-02 2.31E-02 2.31E-02
1.16E-01 1.16E-01 1.16E-01
9.24E-02 9.24E-02 9.24E-02
1.90E-03 1.90E-03 1.90E-03
1.90E-03 1.90E-03 1.90E-03
2.31E-01 2.31E-01 2.31E-01
1.90E-03 1.90E-03 1.90E-03
1.81E-03 1.32E-03 9.59E-04
1.81E-03 1.32E-03 9.59E-04
1.81E-03 1.32E-03 9.59E-04
1.53E-03 9.04E-04 5.21E-04
1.53E-03 9.04E-04 5.21E-04
1.53E-03 9.04E-04 5.21E-04

Adult
4.98E-01
1.66E+00
1.66E-01
3.65E+00
1.33E+00
2.49E+00
1.66E-01
3.32E+00
3.32E+00
4.62E-01
2.31E-02
1.16E-01
9.24E-02
1.90E-03
1.90E-03
2.31E-01
1.90E-03
4.93E-04
2.47E-04
4.93E-04
8.21E-05
4.11E-05
8.21E-05

UB = Urinary bladder, Trab = trabecular, Cort = cortical, surf = surface, vol = volume, SI = Small intestine140

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3877

16.2. Dosimetric data for yttrium

3878

Table 16.3. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 90Y compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled particulate materials (1 µm AMAD aerosols) 3 mo

1y

5y

10 y

15 y

Adult

Type F, Chloride

3.4E-09

2.4E-09

1.1E-09

7.5E-10

5.2E-10

4.1E-10

Type M, Oxide, phosphate; all unspecified forms

4.5E-09

3.4E-09

1.8E-09

1.2E-09

8.6E-10

7.9E-10

Type S, FAP

4.8E-09

3.6E-09

1.9E-09

1.3E-09

9.5E-108.9E-10

3.1E-09

2.4E-09

1.5E-09

1.0E-09

6.5E-10

5.6E-10

Ingested materials
Adult fA = 0.0001, All chemical forms

3879

141

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

17. ZIRCONIUM (Z = 40)

3880
3881

17.1. Routes of Intake

3882

17.1.1. Inhalation

3883
3884
3885
3886
3887
3888
3889
3890

Some information was found on the behaviour of inhaled zirconium in man, mainly
associated with irradiated fuel. Information on absorption from the respiratory tract is available
from experimental studies of zirconium as oxalate, oxide, and irradiated uranium dioxide. For
details see Section 12 of Publication 134 (ICRP, 2016a). Absorption parameter values andtypes, and associated fA values for particulate forms of zirconium are given in Table 17.1 (takenfrom Section 12 of Publication 134).
Table 17.1. Absorption parameter values for inhaled and ingested zirconium
Inhaled particulate materials
Default parameter values†,‡
Absorption
Assigned forms
Type
F
–
§
M
OxalateS
Carbonate, oxide, tritide
Ingested material¶
Assigned forms
Zirconium in foodAll other chemical forms

fr

1
0.2
0.01

Absorption parameter values*sr (d–1)
ss (d–1)

30
3
3

–
0.005
1x10-4Age-dependent absorption from the alimentary tract, fA
3 months 1 year
5 years
10 years 15 years adult
0.02
0.01
0.01
0.01
0.01
0.01
0.02
0.002
0.002
0.002
0.002
0.002

3891
3892
3893
3894
3895
3896
3897
3898
3899
3900
3901
3902
3903
3904
3905

*

3906

17.1.2. Ingestion3907

17.1.2.1. Adults

3908
3909
3910

Based on human and animal data, the gastrointestinal absorption of inorganic formsof zirconium appears to be less than one percent (for more details see Section 12 of Publication
134, ICRP, 2016). Publications 30 and 134 (ICRP, 1979, 2016a) recommended an absorption

It is assumed that for zirconium the bound state can be neglected i.e. fb = 0. The values of sr for Type F, M and S
forms of zirconium (30, 3 and 3 d–1, respectively) are the general default values.
†
Materials (e.g. zirconium oxalate) are listed here where there is sufficient information to assign to a default
absorption type, but not to give specific parameter values (see Section 12 of Publication 134, ICRP, 2016).
‡
For inhaled material deposited in the respiratory tract and subsequently cleared by particle transport to thealimentary tract, the default fA values for inhaled materials are applied: i.e. the product of fr for the absorption type
and the fA value for ingested soluble (excluding dietary) forms of zirconium applicable to the age-group ofinterest(e.g. 0.002 for adults).
§
Default Type M is recommended for use in the absence of specific information on which the exposure material
can be assigned to an absorption type, e.g. if the form is unknown, or if the form is known but there is no
information available on the absorption of that form from the respiratory tract.
¶
Activity transferred from systemic compartments into segments of the alimentary tract is assumed to be subject
to reabsorption to blood. The default absorption fraction fA for the secreted activity is the highest value foringestion of the radionuclide applicable to the age-group of interest (e.g. 0.01 for adults).

142

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3911
3912
3913
3914
3915
3916
3917

fraction of 0.002 for all chemical forms of zirconium. Because an absorption fraction of 0.01
was recommended in Publication 30 for niobium, a chemically similar element, and because
zirconium uptake might be higher for biologically incorporated forms of the element present in
low concentrations in the diet, an absorption fraction of 0.01 was recommended in Publication
56 (ICRP, 1990) for calculating dose coefficients for the ingestion of zirconium by adults inthe population. The same value fA = 0.01 is adopted here for ingestion by adults of zirconium
in food. For all other chemical forms, an fA of 0.002 is adopted.

3918

17.1.2.2. Children

3919
3920
3921
3922
3923
3924
3925
3926
3927
3928
3929
3930
3931

Studies by Matsusaka et al. (1969) with newborn mice and by Shiraishi and Ichikawa(1972) with newborn rats both showed increased absorption and intestinal retention in theimmediate postnatal period. Estimates of absorption from the results of Shiraishi and Ichikawa(1972) were 2% and 1% for 5 day and 16 day old rats, respectively, compared with less than
0.1% in adults. Retention in the gut wall attributable to pinocytotic uptake into intestinal
epithelial cells accounted for about 10% of the dose administered to rats under 14 days of age
but fell off rapidly, consistent with closure of the gut towards the end of the suckling period.
Suppression of pinocytosis by administration of cortisone decreased both retention andabsorption. These results indicate a higher absorption of zirconium in the newborn infant andan absorption fraction of 0.02 was therefore recommended for the 3 months old infant by
Publication 56. Publication 56 recommended a value of 0.01 for children of 1 year and older.
The same values of fA are adopted here for dietary intakes of zirconium by children. For 3month-old infants, a higher fA value of 0.02 is adopted for all chemical forms.

3932

17.1.3. Systemic Distribution, Retention and Excretion

3933
3934
3935
3936
3937
3938
3939
3940
3941
3942
3943
3944
3945
3946
3947
3948
3949
3950
3951
3952
3953
3954
3955

The model for systemic zirconium applied in Publication 134 (ICRP, 2016a) toworkers is applied here to adult members of the public. That model depicts the following
general behavior of zirconium in mature humans or laboratory animals. About half ofzirconium atoms entering blood transfer to tissues and excretion pathways within a few hours,
and the remainder bind to plasma proteins and are cleared more slowly from blood. More than
95% of zirconium atoms leaving blood deposit in tissues. The remainder enter excretion
pathways, primarily the urinary bladder contents. Soft tissues initially contain most of theextravascular zirconium, but bone eventually accumulates >90% of the systemic burden due toa much slower turnover than soft tissues. Zirconium atoms that reach blood have a longresidence time in the body due to its low excretion rate and tenacious retention in bone.
The effect of age on absorption and retention of zirconium was studied in rats
(Shiraishi and Ichikawa, 1972), but the results are difficult to interpret regarding comparative
systemic kinetics at different ages. Based on findings for more extensively studied bone seekers,
zirconium is expected to have higher deposition in growing bone than in mature bone. Basedon analogy with niobium, zirconium’s neighbor in the period table, fractional deposition of
zirconium in bone is assumed to be 50% higher in infants than in adults and 25% higher at ages
1-15 y than in adults. This moderate decline with increasing age in skeletal deposition of
niobium is based on studies of changes with age in the systemic kinetics of niobium in swine
and sheep (Mraz and Eisele, 1977b). Bone deposits of zirconium are assumed to be equallydivided between trabecular and cortical bone surfaces. The skeletal behaviour of zirconium
deposited on bone surfaces is described by the generic model for bone-surface-seekers (ICRP,
2015), except that zirconium removed from bone is assumed to return to blood rather than to
be channeled through bone marrow.

143

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3956
3957
3958
3959
3960
3961
3962
3963
3964

3965
3966
3967

For a given pre-adult age the deposition fractions in soft tissues and excretion
pathways are reduced from the adult value to account for elevated competition from bone
surfaces for circulating zirconium. The deposition fraction for a soft-tissue or excretion
pathway at a given pre-adult age is the value for the adult multiplied by the ratio (1-B)/(1-A)
where A and B are fractional depositions in bone in the adult and the given pre-adult age,respectively.
The structure of the model for zirconium is shown in Fig. 17.1. Parameter values are
given in Table 17.2.

Fig. 17.1. Structure of the biokinetic model for systemic zirconium. SI = Small intestine.

144

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3968

Table 17.2. Transfer coefficients for the model for systemic zirconiuma

Path

Blood 1 to Blood 2
Blood 1 to Liver 0
Blood 1 to Kidneys
Blood 1 to ST0
Blood 1 to ST1
Blood 1 to UB contents
Blood 1 to SI contents
Blood 1 to Trab bone surf
Blood 1 to Cort bone surf
Blood 2 to Blood 1
Liver 0 to SI contents
Liver 0 to Liver 1
Liver 0 to Blood 1
Liver 1 to Blood 1
Kidneys to Blood 1
ST0 to Blood 1
ST1 to Blood 1
Trab bone surf to Blood 1
Trab bone surf to Trab bone vol
Trab bone vol to Blood 1
Cort bone surf to Blood 1
Cort bone surf to Cort bone volCort bone vol to Blood 1

3969

a

Infant
1.82E+00
6.84E-02
1.14E-02
1.82E+00
3.42E-02
9.12E-02
2.28E-02
5.63E-01
5.63E-01
4.62E-01
1.16E-01
4.62E-01
1.16E-01
1.00E-02
1.00E-02
4.62E-01
2.00E-02
8.22E-03
8.22E-03
8.22E-03
8.22E-03
8.22E-03
8.22E-03

Transfer coefficient (d-1)
1y
5y
10 y
1.91E+00 1.91E+00 1.91E+00
7.17E-02
7.17E-02 7.17E-02
1.19E-02
1.19E-02 1.19E-02
1.91E+00 1.91E+00 1.91E+00
3.58E-02
3.58E-02 3.58E-02
9.56E-02
9.56E-02 9.56E-02
2.39E-02
2.39E-02 2.39E-02
4.69E-01
4.69E-01 4.69E-01
4.69E-01
4.69E-01 4.69E-01
4.62E-01
4.62E-01 4.62E-01
1.16E-01
1.16E-01 1.16E-01
4.62E-01
4.62E-01 4.62E-01
1.16E-01
1.16E-01 1.16E-01
1.00E-02
1.00E-02 1.00E-02
1.00E-02
1.00E-02 1.00E-02
4.62E-01
4.62E-01 4.62E-01
2.00E-02
2.00E-02 2.00E-02
2.88E-03
1.81E-03 1.32E-03
2.88E-03
1.81E-03 1.32E-03
2.88E-03
1.81E-03 1.32E-03
2.88E-03
1.53E-03 9.04E-04
2.88E-03
1.53E-03 9.04E-04
2.88E-03
1.53E-03 9.04E-04

15 y
1.91E+00
7.17E-02
1.19E-02
1.91E+00
3.58E-02
9.56E-02
2.39E-02
4.69E-01
4.69E-01
4.62E-01
1.16E-01
4.62E-01
1.16E-01
1.00E-02
1.00E-02
4.62E-01
2.00E-02
9.59E-04
9.59E-04
9.59E-04
5.21E-04
5.21E-04
5.21E-04

Adult
2.00E+00
7.50E-02
1.25E-02
2.00E+00
3.75E-02
1.00E-01
2.50E-02
3.75E-01
3.75E-01
4.62E-01
1.16E-01
4.62E-01
1.16E-01
1.00E-02
1.00E-02
4.62E-01
2.00E-02
4.93E-04
2.47E-04
4.93E-04
8.21E-05
4.11E-05
8.21E-05

UB = Urinary bladder, Cort = cortical, Trab = trabecular, surf = surface, vol = volume, SI = Small intestine

145

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3970

17.2. Dosimetric data for zirconium

3971

Table 17.3. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 95Zr compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled particulate materials (1 µm AMAD aerosols) 3 mo

1y

5y

10 y

15 y

Adult

Type F

1.7E-08

1.4E-08

6.7E-09

3.7E-09

3.0E-09

2.7E-09

Type M, Oxalate; all unspecified forms

1.4E-08

1.2E-08

6.6E-09

4.2E-09

3.4E-09

3.4E-09

Type S, Carbonate, oxide, tritide

1.7E-08

1.5E-08

8.7E-09

5.9E-09

4.5E-09

4.8E-09

Adult fA = 0.002, All other chemical forms

2.7E-09

1.2E-09

7.0E-10

4.9E-10

3.4E-10

3.2E-10Adult fA = 0.01, Zirconium in food

2.7E-09

1.7E-09

9.5E-10

6.3E-10

4.6E-10

4.2E-10

Ingested materials

3972

146

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

18. NIOBIUM (Z = 41)

3973
3974

18.1. Routes of Intake

3975

18.1.1. Inhalation

3976
3977
3978
3979
3980
3981
3982
3983

Some information was found on the behaviour of inhaled niobium in man, mainly
associated with irradiated fuel. Information on absorption from the respiratory tract is available
from experimental studies of niobium as oxalate, oxide, and irradiated uranium dioxide. For
details see Section 13 of Publication 134 (ICRP, 2016a). Absorption parameter values andtypes, and associated fA values for particulate forms of niobium are given in Table 18.1 (takenfrom Section 13 of Publication 134).
Table 18.1. Absorption parameter values for inhaled and ingested niobium
Inhaled particulate materials
Default parameter values†,‡
Absorption Assigned forms
Type
F
M§
OxalateS
Carbonate, oxide
Ingested materials¶
Assigned forms
All forms

fr

1
0.2
0.01

Absorption parameter values*sr (d–1)
ss (d–1)

30
3
3

–
0.005
1x10-4Age-dependent absorption from the alimentary tract, fA
3 months 1 year
5 years
10 years 15 years adult
0.02
0.01
0.01
0.01
0.01
0.01

3984
3985
3986
3987
3988
3989
3990
3991
3992
3993
3994
3995
3996
3997

*

3998

18.1.2. Ingestion

3999

18.1.2.1. Adults

4000
4001
4002
4003

Data on the gastrointestinal absorption of niobium are available from a number ofanimal studies and indicate absorbed fractions from 4 × 10-4 to 4 × 10-2 depending on chemical
forms and animal species (see section 13 of Publication 134 for more details). Publications 30 ,56 and 134 (ICRP, 1979, 1990, 2016a) recommended a default value of 0.01 for all chemical

It is assumed that for niobium that the bound state can be neglected, i.e. fb = 0.0. The values of sr for Type F, M
and S forms of niobium (30, 3 and 3 d–1, respectively) are the general default values.
†
Materials (e.g. niobium oxalate) are listed here where there is sufficient information to assign to a default
absorption type, but not to give specific parameter values (see Section 13 of Publication 134, ICRP, 2016).
‡
For inhaled material deposited in the respiratory tract and subsequently cleared by particle transport to thealimentary tract, the default fA values for inhaled materials are applied: i.e. the product of fr for the absorption type
and the fA value for ingested soluble forms of niobium applicable to the age-group of interest (e.g. 0.01 for adults).
§
Default Type M is recommended for use in the absence of specific information on which the exposure material
can be assigned to an absorption type, e.g. if the form is unknown, or if the form is known but there is no
information available on the absorption of that form from the respiratory tract.
¶
Activity transferred from systemic compartments into segments of the alimentary tract is assumed to be subject
to reabsorption to blood. The default absorption fraction fA for the secreted activity is the highest value foringestion of the radionuclide applicable to the age-group of interest (e.g. 0.01 for adults).

147

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

4004
4005

forms. This value of fA = 0.01 is also adopted here for the ingestion of niobium in food by adults
in the population.

4006

18.1.2.2. Children

4007
4008
4009
4010
4011
4012
4013
4014
4015
4016
4017
4018
4019
4020

Absorption of niobium is increased in suckling animals and falls to adult values by
about the time of weaning. Variable results have been obtained, however, for different species.
Mraz and Eisele (1977a) measured absorption of about 5.5% and 4% in newborn and 7 day old
rats respectively, compared with about 0.1% in 21 day old weaned rats. Higher values of about
40% and 35% were obtained for 1 day old pigs and sheep respectively, compared with valuesof less than 0.5% in weaned animals (Mraz and Eisele, 1977b). Harrison et al. (1990) haveshown that in 2 day old guinea pigs absorption of 95Nb administered as the citrate is about 1.5%
compared with 0.8% in adults. Further results on absorption and intestinal retention of niobium
in neonatal mammals were published by Naylor et al. (1989). Paquet et al. (1998) observed thatwhen 95Nb oxalate was given to 1-day-old rats, absorption was increased by a factor of 200, as
compared to adult rats. In Publication 56, an absorption fraction of 0.02 was recommended for
3-month-old infants and a value of 0.01 was recommended for children of 1 year and older.
The same fA values are adopted here for absorption of niobium in food by children. For the 3month-old infants, an fA of 0.02 is adopted here.

4021

18.1.3. Systemic Distribution, Retention and Excretion

4022
4023
4024
4025
4026
4027
4028
4029
4030
4031
4032
4033
4034
4035
4036
4037
4038
4039
4040
4041
4042
4043
4044
4045
4046
4047
4048
4049

The model for systemic niobium applied in Publication 134 (ICRP, 2016a) to workers
is applied here to adult members of the public. That was based on results of biokinetic studiesof laboratory animals exposed to radioisotopes of niobium. The data indicate that half or moreof niobium atoms entering blood transfer to tissues and excretion pathways within a few hours,
and the remainder clears much more slowly due to binding with plasma proteins. Excretion ismainly in urine. Niobium distributes somewhat uniformly throughout the body but is retainedmuch longer in bone than in other tissues, so that bone eventually contains a large portion of
the total-body content. Niobium depositing in bone appears to be retained largely on bone
surfaces. Total-body retention generally has been described in terms of two retention
components of roughly equal size. The short-term component typically has a biological halftime of a few days, and the long-term component has a half-time of at least a few months.
Reported biokinetic studies have not been sufficiently long to characterize longer-term
components of retention such as may be present in bone.
Mraz and Eisele (1977b) compared the behavior of niobium in newborn and weaned
swine and sheep. the skeletons of newborn and weaned swine contained 66% and 51%,
respectively, of intravenously administered 95Nb. The corresponding values for newborn andweaned sheep were 67% and 43%, respectively. Based on these findings, it is assumed herethat the fraction of absorbed niobium that deposits in bone decreases moderately with age after
infancy. The fraction of outflow from blood to bone surface is assumed to be 25% greater atages 1-15 y than in adults and 50% greater in infants than in adults. Bone deposits of niobium
are assumed to be equally divided between trabecular and cortical bone surfaces. The skeletal
behaviour of niobium deposited on bone surfaces is described by the generic model for bonesurface-seekers (Annex B of Publication 130, ICRP, 2015), except that niobium biologicallyremoved from bone is assumed to return to blood rather than to be channeled through bonemarrow.
For a given pre-adult age the adult deposition fractions for soft tissues and excretion
pathways are reduced from the adult value to account for elevated competition for circulating
niobium from bone surfaces. The deposition fraction for a soft-tissue or excretion pathway at a148

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

4050
4051
4052
4053

4054
4055
4056
4057

given pre-adult age is the value for the adult multiplied by the ratio (1-B)/(1-A) where A and
B are fractional depositions in bone in the adult and the given pre-adult age, respectively.
The structure of the model for niobium is shown in Fig. 18.1. Parameter values are given in
Table 18.2.

Fig. 18.1. Structure of the biokinetic model for systemic niobium. SI = Small intestine.

149

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

4058

Table 18.2. Transfer coefficients for the model for systemic niobiumaPathBlood 1 to Blood 2
Blood 1 to Liver 0
Blood 1 to Kidneys
Blood 1 to ST0
Blood 1 to ST1
Blood 1 to UB contents
Blood 1 to SI contents
Blood 1 to Trab bone surf
Blood 1 to Cort bone surf
Blood 2 to Blood 1
Liver 0 to SI contents
Liver 0 to Liver 1
Liver 0 to Blood 1
Liver 1 to Blood 1
Kidneys to Blood 1
ST0 to Blood 1
ST1 to Blood 1
Trab bone surf to Blood 1
Trab bone surf to Trab bone vol
Trab bone vol to Blood 1
Cort bone surf to Blood 1
Cort bone surf to Cort bone vol
Cortical vol to Blood 1

4059

a

Infant
3.15E+00
2.36E-01
3.94E-02
3.15E+00
1.18E-01
8.66E-01
7.88E-02
1.80E-01
1.80E-01
1.39E+00
5.78E-02
2.31E-01
5.78E-02
5.00E-03
5.00E-03
1.39E+00
1.00E-02
8.22E-03
8.22E-03
8.22E-03
8.22E-03
8.22E-03
8.22E-03

1y3.18E+00
2.38E-01
3.97E-02
3.18E+00
1.19E-01
8.73E-01
7.94E-02
1.50E-01
1.50E-01
1.39E+00
5.78E-02
2.31E-01
5.78E-02
5.00E-03
5.00E-03
1.39E+00
1.00E-02
2.88E-03
2.88E-03
2.88E-03
2.88E-03
2.88E-03
2.88E-03

Transfer coefficient (d-1)
5y
10 y
3.18E+00 3.18E+00
2.38E-01 2.38E-01
3.97E-02 3.97E-02
3.18E+00 3.18E+00
1.19E-01 1.19E-01
8.73E-01 8.73E-01
7.94E-02 7.94E-02
1.50E-01 1.50E-01
1.50E-01 1.50E-01
1.39E+00 1.39E+00
5.78E-02 5.78E-02
2.31E-01 2.31E-01
5.78E-02 5.78E-02
5.00E-03 5.00E-03
5.00E-03 5.00E-03
1.39E+00 1.39E+00
1.00E-02 1.00E-02
1.81E-03 1.32E-03
1.81E-03 1.32E-03
1.81E-03 1.32E-03
1.53E-03 9.04E-04
1.53E-03 9.04E-04
1.53E-03 9.04E-04

15 y
3.18E+00
2.38E-01
3.97E-02
3.18E+00
1.19E-01
8.73E-01
7.94E-02
1.50E-01
1.50E-01
1.39E+00
5.78E-02
2.31E-01
5.78E-02
5.00E-03
5.00E-03
1.39E+00
1.00E-02
9.59E-04
9.59E-04
9.59E-04
5.21E-04
5.21E-04
5.21E-04

Adult
3.20E+00
2.40E-01
4.00E-02
3.20E+00
1.20E-01
8.80E-01
8.00E-02
1.20E-01
1.20E-01
1.39E+00
5.78E-02
2.31E-01
5.78E-02
5.00E-03
5.00E-03
1.39E+00
1.00E-02
4.93E-04
2.47E-04
4.93E-04
8.21E-05
4.11E-05
8.21E-05

UB = Urinary bladder, Cort = cortical, Trab = trabecular, surf = surface, vol = volume, SI = Small intestine150

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

4060

18.2. Dosimetric data for niobuim

4061

Table 18.3. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 95Nb compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled particulate materials (1 µm AMAD aerosols) 3 mo

1y

5y

10 y

15 y

Adult

Type F

2.5E-09

1.9E-09

1.0E-09

6.6E-10

4.7E-10

4.6E-10

Type M, Oxalate; all unspecified forms

4.2E-09

3.4E-09

1.9E-09

1.3E-09

9.9E-10

1.1E-09

Type S, Carbonate, oxide

5.3E-09

4.3E-09

2.5E-09

1.7E-09

1.3E-09

1.4E-09

1.3E-09

1.1E-09

6.3E-10

4.5E-10

3.1E-103.0E-10

Ingested materials
fA = 0.01, All forms

4062

151

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

19. MOLYBDENUM (Z = 42)

4063
4064

19.1. Routes of Intake

4065

19.1.1. Inhalation

4066
4067
4068
4069
4070
4071
4072

Little information is available on the behaviour of inhaled molybdenum in man
following accidental intakes, or from experimental studies in animals. For details see Section
14 of Publication 134 (ICRP, 2016a). Absorption parameter values and types, and associatedfA values for particulate forms of molybdenum are given in Table 19.1 (taken from Section 14
of Publication 134).
Table 19.1. Absorption parameter values for inhaled and ingested molybdenum
Inhaled particulate materials
Default parameter values†,‡
Absorption
Assigned forms
TypeF
Chlorideandmolybdate
M§
Oxide
S
–
Ingested materials¶
Assigned forms
Molybdenum in food
Molybdenum in water
Sulfideframmonium 1
0.2
0.01

Absorption parameter values*sr (d–1)
ss (d–1)

30

–

3
3

0.005
0.0001Age-dependent absorption from the alimentary tract, fA
3 months 1 year
5 years
10 years 15 years adult
1
0.6
0.6
0.6
0.6
0.6
1
0.9
0.9
0.9
0.9
0.9
0.1
0.05
0.05
0.05
0.05
0.05

4073
4074
4075
4076
4077
4078
4079
4080
4081
4082
4083
4084
4085
4086
4087

*

4088

19.1.2. Ingestion

4089
4090
4091

Molybdenum is an essential trace element naturally present in soils and waters. It is
generally absorbed fairly readily from the gastrointestinal tract except for molybdenum
disulphide which is only poorly absorbed. The gastrointestinal absorption of molybdenum

It is assumed that for molybdenum the bound state can be neglected i.e. fb = 0. The values of sr for Type F, M
and S forms of molybdenum (30, 3 and 3 d–1, respectively) are the general default values.
†
Materials (e.g. molybdenum chloride) are listed here where there is sufficient information to assign to a default
absorption type, but not to give specific parameter values (see Section 14 of Publication 134, ICRP, 2016).
‡
For inhaled material deposited in the respiratory tract and subsequently cleared by particle transport to thealimentary tract, the default fA values for inhaled materials are applied: i.e. the product of fr for the absorption type
and the fA value for ingested soluble forms of molybdenum applicable to the age-group of interest (e.g. 0.9 for
adults).
§Default Type M is recommended for use in the absence of specific information on which the exposure material
can be assigned to an absorption type, e.g. if the form is unknown, or if the form is known but there is no
information available on the absorption of that form from the respiratory tract.
¶
Activity transferred from systemic compartments into segments of the alimentary tract is assumed to be subject
to reabsorption to blood. The default absorption fraction fA for the secreted activity is the highest value foringestion of the radionuclide applicable to the age-group of interest (e.g. 0.9 for adults).

152

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

4092
4093

depends on its concentration in the diet, the amounts of copper and sulphur present, and the age(for more details, see section 14 of Publication 134, ICRP, 2016).

4094

19.1.2.1. Adults

4095
4096
4097
4098
4099
4100
4101
4102
4103
4104
4105
4106
4107
4108
4109
4110
4111
4112
4113
4114
4115

The intestinal absorption of molybdenum from aqueous solutions and labelledfoodstuffs was investigated with stable isotopes in a number of human volunteer studies(Cantone, Bartolo, et al., 1997; Cantone, De Bartolo, et al., 1997; Giussani, 2008; Giussani etal., 2006, 2007; Giussani, Heinrichs, et al., 1998; Giussani, Roth, et al., 1998; Sievers, Dörner,
et al., 2001; Sievers, Oldigs, et al., 2001; Turnlund et al., 1999; Turnlund, Keyes and Peiffer,
1995; Turnlund, Keyes, Peiffer, et al., 1995; Werner et al., 1998). The fractional absorption of
inorganic forms of molybdenum (chloride and ammonium-molybdate) from aqueous solutions
was greater than 0.85 for administration of up to 40 μg Mo kg−1 body weight, then it decreased
with increasing tracer amount, being about 0.6 at 80 μg Mo kg −1 body weight (Giussani et al.,2006; Turnlund, Keyes and Peiffer, 1995; Turnlund, Keyes, Peiffer, et al., 1995; Werner et al.,1998). For molybdenum intrinsically incorporated in foodstuffs (salad, beans, tomatoes) theabsorbed fraction was between 0.3 and 0.6, and the absorption from a composite meal wasaround 0.5 (Giussani et al., 2006, 2007; Giussani, Heinrichs, et al., 1998; Turnlund et al., 1999;
Werner et al., 1998).
Previous balance studies in humans (Engel et al., 1967; Robinson et al., 1973; Tipton
et al., 1966, 1969) had shown intestinal absorption from complete meals to be between 0.3 and
0.8, in reasonable agreement with the stable tracer studies. However, results of these balance
studies are biased by the contribution of endogenous molybdenum to the faecal excretion, andby the fact that increased levels of molybdenum in the diet were partially obtained by additional
administration of molybdenum in liquid solutions, for which intestinal absorption is known tobe very high.

4116

19.1.2.2. Children

4117
4118
4119
4120
4121
4122
4123
4124
4125
4126
4127
4128
4129
4130
4131

A study conducted with 10 infants with gestational age 30-39 weeks (Sievers, Dörner,
et al., 2001) found that absorbed fraction of molybdenum from milk and baby formulas is0.975% (0.96-0.99). Metabolic balance data were obtained for 36 pre-adolescent girls, aged
6-10 years, which showed that there is considerable variation in retention of molybdenum
from various diets (Engel et al., 1967). An absorbtion fraction of 0.63 - 0.78 was derived
from the data on excretion for this group of children (Coughtrey and Thorne, 1983), howeverthese values are subject to the aforementioned biases.
In Publication 30 (ICRP, 1979), the recommended absorption fraction for adults were0.05 for the sulphide and 0.8 for all other compounds of the element. The value of 1 was adopted
in Publication 67 (ICRP, 1993) for dietary intakes. In Publication 134 (ICRP, 2016a), therecommended values for adults were 0.05 for sulphide and 0.9 for all other compounds. The fA
values adopted in this report for adults and children of 1 year and older are 0.05 for sulphide,
0.6 for dietary molybdenum, 0.9 for compounds other than sulphide in aqueous form. For 3month-old infants, fA values of 0.1 and 1 are adopted for the sulphide and for all other forms ofmolybdenum respectively.

4132

19.1.3. Systemic Distribution, Retention and Excretion

4133
4134
4135

The model for systemic molybdenum applied in Publication 134 (ICRP, 2016a) toworkers is based largely on results of biokinetic studies on healthy volunteers administeredstable isotopes of molybdenum as tracers (Cantone et al., 1995; Giussani, 2008; Giussani et al.,153

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

4136
4137
4138
4139
4140
4141
4142
4143
4144
4145
4146
4147

4148
4149
4150
4151
4152

2007; Giussani, Heinrichs, et al., 1998; Turnlund, Keyes and Peiffer, 1995; Turnlund, Keyes,
Peiffer, et al., 1995; Werner et al., 2000). Blood, liver, and kidneys are the only explicitly
depicted regions (Fig. 19.1). The model predicts that most of the systemic activity is containedin the liver from a few hours to several weeks after acute uptake of a molybdenum radioisotope
to blood.
Limited data for rats indicate a shorter retention time for molybdenum in young
animals than in mature animals (ICRP, 1993). However, the rat may not be a suitable laboratorymodel for human biokinetics of molybdenum due to much different requirements formolybdenum in humans and rats.
The model for systemic molybdenum applied in Publication 134 to workers is applied
here to members of the public of all ages. The age-independent parameter values are listed inTable 19.2.

Fig. 19.1. Structure of the biokinetic model for systemic molybdenum. Activity transferredfrom Liver to Colon contents enters Right colon contents.

154

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

4153

Table 19.2. Transfer coefficients for the model for systemic molybdenumaPathBlood 1 to Blood 2
Blood 1 to LiverBlood 1 to UB contents
Blood 2 to Kidneys 1
Blood 2 to Kidneys 2
Blood 2 to Other
Liver to RC contents
Liver to Blood 2
Kidneys 2 to Blood 2
Kidneys 1 to UB contents
Other to Blood 2

4154

a

Infant
1.25E+01
1.42E+01
6.50E+00
1.70E+00
1.15E-01
1.73E+00
4.80E-03
1.22E-02
4.74E-02
1.40E+00
3.23E-02

Transfer coefficient (d-1)
1y
5y
10 y
1.25E+01 1.25E+01 1.25E+01
1.42E+01 1.42E+01 1.42E+01
6.50E+00 6.50E+00 6.50E+00
1.70E+00 1.70E+00 1.70E+00
1.15E-01
1.15E-01 1.15E-01
1.73E+00 1.73E+00 1.73E+00
4.80E-03
4.80E-03 4.80E-03
1.22E-02
1.22E-02 1.22E-02
4.74E-02
4.74E-02 4.74E-02
1.40E+00 1.40E+00 1.40E+00
3.23E-02
3.23E-02 3.23E-02

UB = Urinary bladder, RC = Right colon

155

15 y
1.25E+01
1.42E+01
6.50E+00
1.70E+00
1.15E-01
1.73E+00
4.80E-03
1.22E-02
4.74E-02
1.40E+00
3.23E-02

Adult
1.25E+01
1.42E+01
6.50E+00
1.70E+00
1.15E-01
1.73E+00
4.80E-03
1.22E-02
4.74E-02
1.40E+00
3.23E-02

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

4155

19.2. Dosimetric data for molybdenum

4156

Table 19.3. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 99Mo compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled particulate materials (1 µm AMAD aerosols) 3 mo

1y

5y

10 y

15 y

Adult

Type F, Chloride and ammonium molybdate

1.7E-09

1.2E-09

5.3E-10

3.7E-10

2.1E-10

1.9E-10

Type M, Oxide; all unspecified forms

2.4E-09

1.8E-09

9.5E-10

6.6E-10

4.8E-10

4.4E-10

Type S

2.6E-09

1.9E-09

1.0E-09

7.2E-10

5.4E-105.0E-10Adult fA = 0.05, Sulphide

3.0E-09

2.0E-09

1.1E-09

7.7E-10

5.1E-10

4.4E-10Adult fA = 0.6, Molybdenum in food

3.0E-09

1.7E-09

9.7E-10

6.6E-10

4.3E-10

3.7E-10Adult fA = 0.9, Molybdenum in water

1.4E-09

1.1E-09

6.6E-10

4.7E-103.0E-10

2.6E-10

Ingested materials

4157
4158

156

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

20. TECHNETIUM (Z = 43)

4159
4160

20.1. Routes of Intake

4161

20.1.1. Inhalation

4162
4163
4164
4165
4166
4167
4168
4169

Most of the experimental information available on the behaviour of technetium
following deposition in the respiratory tract relates to pertechnetate, or materials labelled with99m
Tc, especially diethylenetriaminepentaacetic acid (DTPA). Some information is alsoavailable from accidental human intakes. For details see Section 15 of Publication 134 (ICRP,
2016a). Absorption parameter values and types, and associated fA values for particulate formsof technetium are given in Table 20.1 (taken from Section 15 of Publication 134, ICRP, 2016a).
Table 20.1. Absorption parameter values for inhaled and ingested technetium
Inhaled particulate materials
Default parameter values†,‡
Absorption
Assigned forms
Type
F
Pertechnetate, Tc-DTPA
§
M
–
S
–
Ingested material¶
Assigned forms
Technetium in food
Pertechnetate

fr

1
0.2
0.01

Absorption parameter values*sr (d–1)
ss (d–1)

100
3
3

–
0.005
0.0001Age-dependent absorption from the alimentary tract, fA
3 months 1 year
5 years
10 years 15 years adult
1
0.5
0.5
0.5
0.5
0.5
1
0.9
0.9
0.9
0.9
0.9

4170
4171
4172
4173
4174
4175
4176
4177
4178
4179
4180
4181
4182
4183
4184

*

4185

20.1.2. Ingestion

4186

20.1.2.1. Adults

4187
4188
4189

The most stable species of technetium in aqueous solution is the pertechnetate ion(TcO4 ). Pertechnetate appears to be the most likely form prevailing in the environment (Till etal., 1979). Technetium administered as pertechnetate is generally well absorbed by human

It is assumed that for technetium the bound state can be neglected, i.e. fb = 0.0. The value of sr for Type F formsof technetium (100 d-1) is element specific. The values for Types M and S (3 d–1) are the general default values.
†
Materials (e.g. pertechnetate) are generally listed here where there is sufficient information to assign to a default
absorption type, but not to give specific parameter values (see Section 15 of Publication 134 (ICRP 2016b)).
‡
For inhaled material deposited in the respiratory tract and subsequently cleared by particle transport to thealimentary tract, the default fA values for inhaled materials are applied: i.e. the product of fr for the absorption type
and the fA value for ingested soluble (excluding dietary) forms of technetium applicable to the age-group of interest(e.g. 0.9 for adults).
§
Default Type M is recommended for use in the absence of specific information on which the exposure material
can be assigned to an absorption type, e.g. if the form is unknown, or if the form is known but there is no
information available on the absorption of that form from the respiratory tract.
¶
Activity transferred from systemic compartments into segments of the alimentary tract is assumed to be subject
to reabsorption to blood. The default absorption fraction fA for the secreted activity is the highest value foringestion of the radionuclide applicable to the age-group of interest (e.g. 0.9 for adults).

-

157

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

4190
4191
4192
4193
4194
4195
4196
4197
4198
4199
4200
4201
4202
4203

subjects with fractional absorption up to 0.95 (Publication 134, ICRP, 2016a). In Publication
134, an fA value of 0.9 was recommended for all chemical forms in the workplace.
Incorporation into foods appears to reduce technetium absorption. The fractional absorption oftechnetium from the gut is reduced to half of that following administration of pertechnetate,when soya-bean and animal tissue with incorporated technetium were fed to rats and guinea
pigs (Sullivan et al., 1978). Similar results in rats and sheep fed technetium either aspertechnetate or incorporated in maize have been obtained by Gerber et al. (1989). The
fractional absorption of 99Tc from cockles collected on the Irish Sea coast in the UK wasinvestigated in a human volunteer study by Hunt (1998), and a value of approximately 0.6 was
obtained. A low value of around 0.1 was also obtained in a volunteer study of absorption of99
Tc from lobster flesh (Harrison and Phipps, 2001; Hunt, 1998). As technetium in food wasless readily absorbed than the pertechnetate, an absorption fraction of 0.5 was recommended in
Publication 67 (ICRP, 1993). The same value of fA = 0.5 is adopted here for ingestion by adultsof technetium in food. For ingestion of pertechnetate an fA = 0.9 is adopted.

4204

20.1.2.2. Children

4205
4206
4207
4208
4209

Technetium gavaged in the form of pertechnetate is well absorbed by both adult andneonatal rats (Sullivan, Miller, et al., 1984). In Publication 67, a value of 1 was applied for 3month-old infants. For children of 1 year and older the absorption fraction for the adult (0.5)
was used. The same values are adopted here for fA of technetium in food. For ingestion ofpertechnetate by 3-month-old infants, an fA of 1 is adopted.

4210

20.1.3. Systemic Distribution, Retention and Excretion

4211
4212
4213
4214
4215
4216
4217
4218
4219
4220
4221
4222
4223
4224
4225
4226
4227
4228
4229
4230
4231
4232

The model for systemic technetium applied in Publication 134 (ICRP, 2016a) toworkers is applied here to adult members of the public. That model is based primarily on datafrom biokinetic studies of technetium administered in the commonly encountered form
pertechnetate (TcO4-). As discussed in Publication 134, the initial distribution of pertechnetate
resembles that of inorganic iodide. Pertechnetate and iodide are selectively concentrated in the
thyroid, salivary glands, and stomach wall. In contrast to iodide, pertechnetate trapped by the
thyroid is not organically bound in the thyroid but is mainly released back to blood over a
period of hours. Over time the pertechnetate ion and iodide exhibit markedly different excretion
patterns. Iodide is excreted primarily in urine. In adults, roughly 30% of technetium
intravenously administered as pertechnetate is excreted in urine over the first day, but thereafter
the urinary excretion rate decreases markedly while cumulative faecal excretion increases andmay eventually exceed cumulative urinary excretion. Most of the absorbed or injected
pertechnetate is lost from the body within a few days, but a small percentage is retained forweeks or longer. During extended intake, relatively high concentrations are found in bone,kidneys, liver, skin, hair, and thyroid.
No useful information was found on age related changes in the systemic behavior oftechnetium. It is assumed here that the systemic behaviour of technetium is independent of age
except that activity is assumed to be removed from trabecular or cortical bone volume to bloodat the age-specific rate of turnover of that bone type.
The structure of the model for technetium is shown in Fig. 20.1. Parameter values are given in
Table 20.2.

158

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

4233
4234
4235
4236
4237

Fig. 20.1. Structure of the biokinetic model for systemic technetium. Activity transferred toColon contents enters Right colon contents. St = Stomach, SI = Small intestine, cont = contents
Table 20.2. Transfer coefficients for the model for systemic technetiuma

Path

Blood to Thyroid 1
Blood to ST0
Blood to ST1
Blood to ST2
Blood to UB contents
Blood to Salivary glands
Blood to St wall
Blood to Urinary path
Blood to Other kidney tissue
Blood to Liver 1
Blood to RC wall
Blood to Cort bone surf
Blood to Trab bone surf
Thyroid 1 to Blood
Thyroid 1 to Thyroid 2
Thyroid 2 to Blood
ST0 to Blood
ST1 to Blood
ST2 to Blood
Salivary glands to Oral cavity
St wall to St contents
Urinary path to UB contents
Other kidney tissue to BloodLiver 1 to Blood

Infant7.00E+00
7.19E+01
3.00E+00
1.80E-01
1.70E+00
2.60E+00
4.30E+00
7.00E-01
4.00E-02
4.50E+00
3.40E+00
3.50E-01
3.50E-01
1.00E+02
1.00E+00
1.00E+00
5.00E+01
4.62E-01
3.47E-02
5.00E+01
5.00E+01
8.32E+00
3.47E-02
8.23E+00

1y
7.00E+00
7.19E+01
3.00E+00
1.80E-01
1.70E+00
2.60E+00
4.30E+00
7.00E-01
4.00E-02
4.50E+00
3.40E+00
3.50E-01
3.50E-01
1.00E+02
1.00E+00
1.00E+00
5.00E+01
4.62E-01
3.47E-02
5.00E+01
5.00E+01
8.32E+00
3.47E-02
8.23E+00

159

Transfer coefficient (d-1)
5y
10 y
15 y
7.00E+00 7.00E+00 7.00E+00
7.19E+01 7.19E+01 7.19E+01
3.00E+00 3.00E+00 3.00E+00
1.80E-01
1.80E-01
1.80E-01
1.70E+00 1.70E+00 1.70E+00
2.60E+00 2.60E+00 2.60E+00
4.30E+00 4.30E+00 4.30E+00
7.00E-01
7.00E-01
7.00E-01
4.00E-02
4.00E-02
4.00E-02
4.50E+00 4.50E+00 4.50E+00
3.40E+00 3.40E+00 3.40E+00
3.50E-01
3.50E-01
3.50E-01
3.50E-01
3.50E-01
3.50E-01
1.00E+02 1.00E+02 1.00E+02
1.00E+00 1.00E+00 1.00E+00
1.00E+00 1.00E+00 1.00E+00
5.00E+01 5.00E+01 5.00E+01
4.62E-01
4.62E-01
4.62E-01
3.47E-02
3.47E-02
3.47E-02
5.00E+01 5.00E+01 5.00E+01
5.00E+01 5.00E+01 5.00E+01
8.32E+00 8.32E+00 8.32E+00
3.47E-02
3.47E-02
3.47E-02
8.23E+00 8.23E+00 8.23E+00

Adult
7.00E+00
7.19E+01
3.00E+00
1.80E-01
1.70E+00
2.60E+00
4.30E+00
7.00E-01
4.00E-02
4.50E+00
3.40E+00
3.50E-01
3.50E-01
1.00E+02
1.00E+00
1.00E+00
5.00E+01
4.62E-01
3.47E-02
5.00E+01
5.00E+01
8.32E+00
3.47E-02
8.23E+00

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
Liver 1 to Liver 2
Liver 2 to Blood
RC wall to RC contents
Cort bone surf to Blood
Cort bone surf to Cort bone vol
Trab bone surf to Blood
Trab bone surf to Trab bone volCort bone vol to Blood
Trab vol to Blood

4238
4239

8.32E-02
3.47E-02
1.39E+00
4.57E-01
4.62E-03
4.57E-01
4.62E-03
8.22E-03
8.22E-03

8.32E-02
3.47E-02
1.39E+00
4.57E-01
4.62E-03
4.57E-01
4.62E-03
2.88E-03
2.88E-03a8.32E-02
3.47E-02
1.39E+00
4.57E-01
4.62E-03
4.57E-01
4.62E-03
1.53E-03
1.81E-03

8.32E-02
3.47E-02
1.39E+00
4.57E-01
4.62E-03
4.57E-01
4.62E-03
9.04E-04
1.32E-03

8.32E-02
3.47E-02
1.39E+00
4.57E-01
4.62E-03
4.57E-01
4.62E-03
5.21E-04
9.59E-04

8.32E-02
3.47E-02
1.39E+00
4.57E-01
4.62E-03
4.57E-01
4.62E-03
8.21E-05
4.93E-04

UB = Urinary bladder, RC = Right colon, Cort = cortical, Trab = trabecular, St = Stomach, Trab = Trabecular,
Cort = Cortical, surf = surface, vol = volume

160

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

4240

20.2. Dosimetric data for technetium

4241

Table 20.3. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 99Tc compounds.
Effective dose coefficients (Sv Bq -1)
Inhaled particulate materials (1 µm AMAD
aerosols)
3 mo
1y
5y
10 y
15 y
Adult
Type F, Pertechnetate, Tc-DTPA

1.8E-09

1.2E-09

4.5E-10

2.5E-10

1.6E-10

1.3E-10

Type M, All unspecified forms

8.1E-09

7.1E-09

4.0E-09

2.6E-09

2.0E-09

1.9E-09

Type S

5.4E-08

5.5E-08

4.1E-08

3.1E-08

3.1E-08

3.1E-08

Adult fA = 0.5, Technetium in food

3.4E-09

1.2E-09

5.2E-10

2.9E-102.0E-10

1.5E-10Adult fA = 0.8, Pertechnetate

3.4E-09

2.0E-09

9.2E-105.0E-10

3.5E-10

2.7E-10

Ingested materials

4242
4243

Table 20.4. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 99mTc compounds.
Effective dose coefficients (Sv Bq -1)
Inhaled particulate materials (1 µm AMAD
aerosols)
3 mo
1y
5y
10 y
15 y
Adult
Type F, Pertechnetate, Tc-DTPA

4.9E-11

3.6E-11

1.6E-11

9.9E-12

6.4E-12

5.5E-12Type M, All unspecified forms

5.0E-11

3.7E-112.0E-11

1.4E-11

1.1E-11

1.0E-11

Type S

4.9E-11

3.7E-112.0E-11

1.4E-11

1.1E-11

1.0E-11

1.1E-10

5.6E-11

3.0E-112.0E-11

1.4E-11

1.3E-11

Ingested materials
Adult fA = 0.5, Technetium in food161

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

Adult fA = 0.8, Pertechnetate

1.1E-10

7.2E-114244

162

3.8E-11

2.4E-11

1.6E-11

1.4E-11

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

21. RUTHENIUM (Z = 44)

4245
4246

21.1. Routes of Intake

4247

21.1.1. Inhalation

4248
4249
4250
4251
4252
4253
4254
4255
4256
4257
4258
4259

Some information is available on the behaviour of inhaled ruthenium in man following
accidental intakes as an oxide or in irradiated fuel fragments. Information on absorption fromthe respiratory tract is available from experimental studies of ruthenium as tetroxide, chloride,
citrate, dioxide, and irradiated uranium dioxide. For details see Section 2 of Publication 137(ICRP, 2017). Absorption parameter values and types, and associated fA values for gas andvapour forms of ruthenium are given in Table 21.1 and for particulate forms in Table 21.2
(taken from Section 2 of Publication 137). Exposures to gas and vapour forms of ruthenium
are relatively unusual compared to exposures to particulate forms, and it is therefore
recommended in this series of documents that particulate form is assumed in the absence of
information.
Table 21.1. Deposition and absorption for gas and vapour forms of ruthenium.
Chemical
form/origin
Ruthenium
tetroxide
Chemical
form/origin
Ruthenium
tetroxide

4260
4261
4262
4263
4264
4265
4266
4267
4268
4269

Total

Percentage deposited (%)*
ET1
ET2
BB
bb

AI

fr

100b

40

1

0.5

3 months
0.02

40

12

7

Absorption†sr (d–1) ss (d–1)
1

0.001

Age-dependent absorption from the alimentary tract, fA
1 year
5 years
10 years
15 years
Adult
0.01
0.01
0.01
0.01
0.01

ET1, anterior nasal passage; ET2, posterior nasal passage, pharynx and larynx; BB, bronchial; bb, bronchiolar; AI,
alveolar-interstitial.
*
Percentage deposited refers to how much of the material in the inhaled air remains in the body after exhalation.
Almost all inhaled gas molecules contact airway surfaces, but usually return to the air unless they dissolve in, or
react with, the surface lining.
†
It is assumed that for ruthenium the bound fraction fb is 0.05 with an uptake rate sb = 0.1 d–1, and that this applies
throughout the respiratory tract (ET2, BB, bb and AI regions, and associated lymph nodes LNET and LNTH).

Table 21.2. Absorption parameter values for inhaled particulate forms of ruthenium and foringested ruthenium.
Inhaled particulate materials
Default parameter values†,‡
Absorption
Assigned forms
TypeF
Chloride, oxalate
M§
CitrateS
DioxideIngested material¶
Assigned forms

fr

1
0.2
0.01

Absorption parameter values*sr (d–1)
ss (d–1)

30
3
3

–
0.005
1×10-4Age-dependent absorption from the alimentary tract, fA
3 months 1 year
5 years
10 years
15 years
adult

163

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
All forms

0.1

0.05

0.05

0.05

0.05

0.05

It is assumed that for ruthenium the bound fraction fb is 0.05 with an uptake rate sb = 0.1 d–1, and that this applies
throughout the respiratory tract (ET2, BB, bb and AI regions, and associated lymph nodes LNET and LNTH). The
values of sr for Type F, M and S forms of ruthenium (30, 3 and 3 d–1, respectively) are the general default values.
†
Materials (e.g. ruthenium chloride) are listed here where there is sufficient information to assign to a default
absorption type, but not to give specific parameter (see Section 2 of Publication 137, ICRP, 2017).
‡
For inhaled material deposited in the respiratory tract and subsequently cleared by particle transport to thealimentary tract, the default fA values for inhaled materials are applied: i.e. the product of fr for the absorption type
and the fA value for ingested soluble forms of ruthenium applicable to the age-group of interest (e.g. 0.05 for
adults).
§Default Type M is recommended for use in the absence of specific information on which the exposure material
can be assigned to an absorption type, e.g., if the form is unknown, or if the form is known but there is no
information available on the absorption of that form from the respiratory tract.
¶
Activity transferred from systemic compartments into segments of the alimentary tract is assumed to be subject
to reabsorption to blood. The default absorption fraction fA for the secreted activity is the highest value foringestion of the radionuclide applicable to the age-group of interest (e.g. 0.05 for adults).

4270
4271
4272
4273
4274
4275
4276
4277
4278
4279
4280
4281
4282
4283
4284
4285

*

4286

21.1.2. Ingestion

4287

21.1.2.1. Adults

4288
4289
4290
4291
4292
4293
4294

Results from a number of human and animal studies show fractional absorption in therange 0.8 – 15% depending on the physical and chemical form administered and the nutritional
status of the subject (for more details, see section 2 of Publication 137, ICRP, 2017). In
Publication 30 (ICRP, 1980), an absorption fraction of 0.05 was recommended for all chemical
forms of ruthenium. This value was also recommended in Publication 56 (ICRP, 1990) for
dietary intakes as well as in Publication 137. The same value fA = 0.05 is adopted here forruthenium ingested in food by adults in the population.

4295

21.1.2.2. Children

4296
4297
4298
4299
4300
4301
4302
4303
4304
4305
4306

Few data are available on the absorption of ruthenium in the young. Newborn miceabsorbed about 7% of 106Ru administered as the chloro-complex in dilute HCl (Matsusaka etal., 1969) but 21 days old and adult mice absorbed less than 1%. Inaba et al. (1984) found 0.8%
absorption of carrier free 103Ru in suckling (5 days old) rats after administration as the chloride
compared with 0.5% in adults. These results suggest that for young infants a higher absorption
fraction than is applied to adults is appropriate. For the 3 months infant an absorption fractionof 0.1 was recommended in Publication 56 for isotopes of ruthenium in food. For children of
1 year and older an absorption fraction of 0.05 was recommended in Publication 56. Harrison
et al. (2001) proposed confidence intervals of 0.005 to 0.1 for adults, 0.005–0.15 for 10year-old children, and 0.005–0.2 for 3-month-old infants. The same values as in Publication
56 are adopted here for children : fA = 0.1 for 3-mo-old and fA = 0.05 for older children.

4307

21.1.3. Systemic Distribution, Retention and Excretion

4308
4309
4310
4311
4312

The model for systemic ruthenium applied in Publication 137 (ICRP, 2017) toworkers is applied here to adult members of the public. That model is based where feasible on
biokinetic data derived in controlled studies of ruthenium kinetics in human subjects. However,most transfer coefficients are based at least in part on observations of the distribution, retention,and excretion of ruthenium isotopes in laboratory animals, particularly dogs.

164

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

4313
4314
4315
4316
4317
4318

4319
4320
4321
4322

No useful information was found regarding age related changes in the biokinetics ofsystemic ruthenium. The systemic behaviour of ruthenium is assumed to be independent of age
except that activity is assumed to be removed from trabecular or cortical bone volume to bloodat the age-specific rate of turnover of that bone type.
The structure of the model for ruthenium is shown in Fig. 21.1. Parameter values are
given in Table 21.3.

Fig. 21.1. Structure of the biokinetic model for systemic ruthenium. SI = Small intestine.

165

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

4323

Table 21.3. Transfer coefficients for the model for systemic rutheniuma

Path

Blood 1 to SI contents
Blood 1 to UB contents
Blood 1 to Liver 1
Blood 1 to Urinary path
Blood 1 to Other kidney tissue
Blood 1 to Blood 2
Blood 1 to ST0
Blood 1 to ST1
Blood 1 to ST2
Blood 1 to Cort bone surf
Blood 1 to Trab bone surf
Blood 2 to Blood 1
Liver 1 to Blood 1
Liver 1 to SI contents
Liver 1 to Liver 2
Liver 2 to Blood 1
Urinary path to UB contents
Other kidney tissue to Blood 1
ST0 to Blood 1
ST1 to Blood 1
ST2 to Blood 1
Cort bone surf to Blood 1
Trab bone surf to Blood 1
Cort bone surf to Cort bone vol
Trab bone surf to Trab bone volCort bone vol to Blood 1
Trab bone vol to Blood 1

4324

a

Infant3.00E+00
1.70E+01
1.20E+01
7.76E+00
2.40E-01
2.70E+01
1.50E+01
5.00E+00
5.00E+00
2.00E+00
6.00E+00
6.93E-01
9.70E-02
3.47E-02
6.93E-03
3.80E-03
1.39E-01
3.80E-03
9.90E-02
2.31E-02
9.50E-04
7.92E-02
7.92E-02
1.98E-02
1.98E-02
8.22E-03
8.22E-03

1y
3.00E+00
1.70E+01
1.20E+01
7.76E+00
2.40E-01
2.70E+01
1.50E+01
5.00E+00
5.00E+00
2.00E+00
6.00E+00
6.93E-01
9.70E-02
3.47E-02
6.93E-03
3.80E-03
1.39E-01
3.80E-03
9.90E-02
2.31E-02
9.50E-04
7.92E-02
7.92E-02
1.98E-02
1.98E-02
2.88E-03
2.88E-03

Transfer coefficient (d-1)
5y
10 y
3.00E+00 3.00E+00
1.70E+01 1.70E+01
1.20E+01 1.20E+01
7.76E+00 7.76E+00
2.40E-01 2.40E-01
2.70E+01 2.70E+01
1.50E+01 1.50E+01
5.00E+00 5.00E+00
5.00E+00 5.00E+00
2.00E+00 2.00E+00
6.00E+00 6.00E+00
6.93E-01 6.93E-01
9.70E-02 9.70E-02
3.47E-02 3.47E-02
6.93E-03 6.93E-03
3.80E-03 3.80E-03
1.39E-01 1.39E-01
3.80E-03 3.80E-03
9.90E-02 9.90E-02
2.31E-02 2.31E-02
9.50E-04 9.50E-04
7.92E-02 7.92E-02
7.92E-02 7.92E-02
1.98E-02 1.98E-02
1.98E-02 1.98E-02
1.53E-03 9.04E-04
1.81E-03 1.32E-03

15 y
3.00E+00
1.70E+01
1.20E+01
7.76E+00
2.40E-01
2.70E+01
1.50E+01
5.00E+00
5.00E+00
2.00E+00
6.00E+00
6.93E-01
9.70E-02
3.47E-02
6.93E-03
3.80E-03
1.39E-01
3.80E-03
9.90E-02
2.31E-02
9.50E-04
7.92E-02
7.92E-02
1.98E-02
1.98E-02
5.21E-04
9.59E-04

Adult
3.00E+00
1.70E+01
1.20E+01
7.76E+00
2.40E-01
2.70E+01
1.50E+01
5.00E+00
5.00E+00
2.00E+00
6.00E+00
6.93E-01
9.70E-02
3.47E-02
6.93E-03
3.80E-03
1.39E-01
3.80E-03
9.90E-02
2.31E-02
9.50E-04
7.92E-02
7.92E-02
1.98E-02
1.98E-02
8.21E-05
4.93E-04

UB = Urinary bladder, SI= Small intestine, Trab = Trabecular, Cort = Cortical, surf = surface, vol = volume

166

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

4325

21.2. Dosimetric data for ruthenium

4326

Table 21.4. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 106Ru compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled gases or vapours

3 mo

1y

5y

10 y

15 y

Adult

Ruthenium tetroxide

3.4E-08

2.7E-08

1.6E-08

1.0E-08

7.6E-09

7.0E-09

Type F, Chloride, oxalate

4.2E-08

3.5E-08

1.8E-08

1.1E-08

8.1E-09

6.7E-09

Type M, Citrate; all unspecified forms

9.2E-08

8.3E-08

4.9E-08

3.2E-08

2.6E-08

2.6E-08

Type S, Dioxide

2.2E-07

2.1E-07

1.3E-078.7E-08

7.2E-08

7.4E-08

2.2E-08

1.2E-08

6.9E-09

4.3E-09

3.0E-09

2.6E-09

Inhaled particulate materials (1 µm AMAD aerosols)

Ingested materials
Adult fA = 0.05, All forms

4327
4328

167

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

22. SILVER (Z = 47)

4329
4330

22.1. Routes of Intake

4331

22.1.1. Inhalation

4332
4333
4334
4335
4336

A few studies give information on absorption of silver from the respiratory tract. For
details see Section 25 of Publication 151 (ICRP, 2022). Absorption parameter values and types,
and associated fA values for inhaled particulate forms of silver are given in Table 22.1.
Table 22.1. Absorption parameter values for inhaled and ingested silver
Inhaled particulate materials
Default parameter values†,‡
Absorption
Assigned forms
TypeF
NitrateM§
IodideS—
Ingested materials¶
Assigned forms
All chemical forms

3 months
0.1

fr

1
0.2
0.01

Absorption parameter values*sr (d–1)
ss (d–1)

1
1
1

–
0.005
1x10–4Age-dependent absorption from the alimentary tract, fA
1 year
5 years
10 years
15 years
adults
0.05
0.05
0.05
0.05
0.05

4337
4338
4339
4340
4341
4342
4343
4344
4345
4346
4347
4348
4349
4350
4351

*

4352

22.1.2. Ingestion

4353

22.1.2.1. Adults

4354
4355
4356

There is very little information on the gastrointestinal absorption of silver. For details
see Section 25 of Publication 151 (ICRP, 2022). The value of fA = 0.05 is adopted here for
dietary intakes of silver.

4357

22.1.2.2. Children

4358
4359

110m

It is assumed that for silver the bound state can be neglected i.e. fb = 0. The values of sr for Type F, M and S
forms of silver (1 d–1) are element-specific.
†
Materials (e.g. Nitrate) are listed here where there is sufficient information to assign to a default absorption type,but not to give specific parameter values (see Section 25 of Publication 151, ICRP, 2022).
‡
For inhaled material deposited in the respiratory tract and subsequent cleared by particle transport to thealimentary tract, the default fA values for inhaled materials are applied: i.e., the (rounded) product of fr for theabsorption type and the fA value for ingested soluble forms of silver applicable to the age-group of interest (e.g.
0.05 for adults).
§
Default Type M is recommended for use in the absence of specific information on which the exposure material
can be assigned to an absorption type, e.g. if the form is unknown, or if the form is known but there is no
information available on the absorption of that form from the respiratory tract.
¶
Activity transferred from systemic compartments into segments of the alimentary tract is assumed to be subject
to reabsorption to blood. The default absorption fraction fA for the secreted activity is the highest value foringestion of the radionuclide applicable to the age-group of interest (e.g. 0.05 for adults).

Inaba et al. (1984) have reported data for rats on the age-dependent biokinetics of
AgN03 after oral administration. Their results indicate an enhancement of absorption of168

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

4360
4361
4362

silver in suckling rats compared with adults. Like in Publication 67 (ICRP, 1993), an fA valueof 0.1 is adopted here for 3-month-old infants. For children of 1 year and older the fA value forthe adult (0.05) is used.

4363

22.1.3. Systemic Distribution, Retention and Excretion

4364
4365
4366
4367
4368
4369

No information was found on age related changes in the systemic kinetics of silver.
An updated systemic biokinetic model for occupational intake of silver is describedin Section 25 of Publication 151 (ICRP, 2022). That model is applied here to intake of silver
at any age.
The structure of the model for systemic silver is shown in Fig. 22.1. Parameter values
are listed in Table 22.2.

4370
4371
4372

Fig. 22.1. Structure of the biokinetic model for systemic silver. SI = Small intestine.

169

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

4373

Table 22.2. Transfer coefficients for the model for systemic silveraPathBlood 1 to Blood 2
Blood 1 to Kidneys
Blood 1 to Liver 1
Blood 1 to Trab bone surf
Blood 1 to Cort bone surf
Blood 1 to ST0
Blood 1 to ST1
Blood 1 to UB contents
Blood 2 to Blood 1
Kidneys to Blood 1
Liver 1 to SI contents
Liver 1 to Liver 2
Liver 2 to Blood 1
ST0 to Blood 1
ST1 to Blood 1
Trab bone surf to Blood 1
Cort bone surf to Blood 1

4374

a

Infant
7.20E-01
1.20E+00
3.00E+01
1.20E+00
1.20E+00
1.28E+01
1.28E+01
1.30E-01
2.31E-01
8.00E-01
1.00E+00
9.00E+00
2.00E-01
8.00E+00
4.00E-01
7.00E-02
7.00E-02

1y
7.20E-01
1.20E+00
3.00E+01
1.20E+00
1.20E+00
1.28E+01
1.28E+01
1.30E-01
2.31E-01
8.00E-01
1.00E+00
9.00E+00
2.00E-01
8.00E+00
4.00E-01
7.00E-02
7.00E-02

Transfer coefficient (d-1)
5y
10 y
7.20E-01
7.20E-01
1.20E+00 1.20E+00
3.00E+01 3.00E+01
1.20E+00 1.20E+00
1.20E+00 1.20E+00
1.28E+01 1.28E+01
1.28E+01 1.28E+01
1.30E-01
1.30E-01
2.31E-01
2.31E-01
8.00E-01
8.00E-01
1.00E+00 1.00E+00
9.00E+00 9.00E+00
2.00E-01
2.00E-01
8.00E+00 8.00E+00
4.00E-01
4.00E-01
7.00E-02
7.00E-02
7.00E-02
7.00E-02

15 y
7.20E-01
1.20E+00
3.00E+01
1.20E+00
1.20E+00
1.28E+01
1.28E+01
1.30E-01
2.31E-01
8.00E-01
1.00E+00
9.00E+00
2.00E-01
8.00E+00
4.00E-01
7.00E-02
7.00E-02

Trab = trabecular, Cort = cortical, surf = surface, UB = urinary bladder, SI = small intestine

170

Adult
7.20E-01
1.20E+00
3.00E+01
1.20E+00
1.20E+00
1.28E+01
1.28E+01
1.30E-01
2.31E-01
8.00E-01
1.00E+00
9.00E+00
2.00E-01
8.00E+00
4.00E-01
7.00E-02
7.00E-02

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

4375

22.2. Dosimetric data for silver

4376

Table 22.3. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 110mAg compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled particulate materials (1 µm AMAD aerosols) 3 mo

1y

5y

10 y

15 y

Adult

Type F, Nitrate

1.8E-08

1.3E-08

7.5E-09

5.1E-09

3.8E-09

4.2E-09

Type M, Iodide; all unspecified forms

3.0E-08

2.6E-08

1.5E-08

1.0E-08

7.9E-09

9.0E-09

Type S

5.2E-08

4.8E-08

2.9E-082.0E-08

1.6E-08

1.8E-08

1.4E-08

7.7E-09

4.5E-09

3.2E-09

2.2E-09

2.3E-09

Ingested materials
fA = 0.05, All chemical forms

4377

171

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

23. ANTIMONY (Z = 51)

4378
4379

23.1. Routes of Intake

4380

23.1.1. Inhalation

4381
4382
4383
4384
4385
4386
4387
4388
4389

Information on absorption from the respiratory tract is available from experimental
studies of antimony inhaled by laboratory animals as chloride, tartrate or oxide. Some
information is also available on the behaviour of inhaled 125Sb in man. For details, see Section
3 of Publication 137 (ICRP, 2017). Absorption parameter values and types, and associated fA
values for particulate forms of antimony are given in Table 23.1 (taken from Section 3 of
Publication 137).

Table 23.1. Absorption parameter values for inhaled and ingested antimony.
Inhaled particulate materials
Default parameter values†,‡
Absorption
Type
F
Chloride, tartrate
M§
Trioxide
S—
Ingested materials¶
Assigned forms
Antimony in food
Other chemical forms

4390
4391
4392
4393
4394
4395
4396
4397
4398
4399
4400
4401
4402
4403

fr

1
0.2
0.01

Absorption parameter values*sr (d–1)
ss (d–1)

30
3
3

–
0.005
1×10–4Age-dependent absorption from the alimentary tract, fA
3 months 1 year
5 years
10 years 15 years adult
0.2
0.1
0.1
0.1
0.1
0.1
0.1
0.05
0.05
0.05
0.05
0.05

*

It is assumed that for antimony the bound state can be neglected, i.e. fb = 0.0. The values of sr for Type F, M and
S forms of antimony (30, 3 and 3 d–1, respectively) are the general default values.
†
Materials (e.g. Chloride) are generally listed here where there is sufficient information to assign to a default
absorption Type, but not to give specific parameter values (see Section 3 of Publication 137, ICRP, 2017).
‡
For inhaled material deposited in the respiratory tract and subsequently cleared by particle transport to thealimentary tract, the default fA values for inhaled materials are applied: i.e. the product of fr for the absorption type
and the fA value for ingested soluble (excluding dietary) forms of antimony applicable to the age-group of interest(e.g. 0.05 for adults).
§
Default Type M is recommended for use in the absence of specific information on which the exposure material
can be assigned to an absorption type, e.g., if the form is unknown, or if the form is known but there is no
information available on the absorption of that form from the respiratory tract.
¶
Activity transferred from systemic compartments into segments of the alimentary tract is assumed to be subject
to reabsorption to blood. The default absorption fraction fA for the secreted activity is the highest value foringestion of the radionuclide applicable to the age-group of interest (e.g. 0.1 for adults).

4404
4405

23.1.2. Ingestion

4406

23.1.2.1. Adults

4407
4408

No controlled studies on antimony absorption in humans have been carried out, butbioassay measurements following accidental exposure and animal experiments suggested
172

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

4409
4410
4411
4412
4413
4414
4415
4416
4417
4418
4419
4420
4421
4422
4423

variable absorption values, nearly all less than 5% of ingested antimony, except for a somewhat
higher absorption of antimonyl potassium tartrate (tartar emetic) (Publication 137, ICRP, 2017).
For more details, see Section 3 of Publication 137. In Publication 137, a single fA value of 0.05
was recommended for all occupational exposures where specific information was not available.
Inaba et al. (1984) reported fractional absorption in adult rats as 0.5 of 125Sb biologicallyincorporated into blood cells. In a further study in which 125Sb was mixed with blood, fractional
absorption was only about 0.01; however, hydrolysis may have occurred which would have
reduced uptake. Coughtrey and Thorne (1983) have suggested an upper limit for the absorption
fraction of about 0.1, based on estimates of the daily dietary intake and the body content of
stable antimony. The data indicate there may be considerable differences in absorption for therange of chemical forms of antimony encountered in the environment. Because ingestion ofradioantimony by the general public is likely to occur principally in food or drink, Publication
69 (ICRP, 1995a) assumed a higher value of 0.1 for the fractional absorption of antimony. Thisvalue is also adopted here for ingestion by adult of antimony in food. For ingestion of otherforms, an fA of 0.05 is adopted.

4424

23.1.2.2. Children

4425
4426
4427
4428
4429
4430
4431
4432
4433

Few data seem to be available on the absorption of antimony in young animals. Inabaet al. (1984) administered 125SbCl3 to 5-d-old suckling rats and to adult rats, and compared theirwhole body retention of 125Sb. Retention of antimony on the fifth day after administration was
about 40% for suckling animals and 0.2% for adults. For 15-d-old suckling animals, retention
on the fifth day was 20% and for 25-d-old weanlings it was about the same as for adults (JiroInaba et al., 1984). In view of the limited data available, Publication 69 recommended anabsorption fraction for the 3-mo-old infant of 0.2. The same value of fA = 0.2 for 3-mo-old
infants is adopted here for antimony in food and an fA of 0.1 is adopted for all other chemical
forms.

4434

23.1.3. Systemic Distribution, Retention and Excretion

4435
4436
4437
4438
4439
4440
4441
4442
4443
4444
4445
4446
4447
4448
4449
4450
4451
4452
4453
4454

Antimony generally occurs in nature either in the trivalent or pentavalent state, withthe trivalent state being the more stable state in biological fluids. Trivalent and pentavalent
antimony initially show different biokinetics after entering the systemic circulation. For
example, Sb(III) is excreted in urine at a lower rate and accumulated by red blood cells at ahigher rate than Sb(V) in the first day or two after intravenous or intramuscular injection. Thereis evidence of some reduction of Sb(V) to Sb(III) in vivo and convergence of the systemic
biokinetics of these two initial forms over time.
The model for systemic antimony applied in Publication 137 (ICRP, 2017) to workers
is applied here to adult members of the public. That model is based where feasible on resultsof controlled biokinetic studies of antimony tracers in a few human subjects. Due to the sparsityof such data, however, the model relies heavily on findings for laboratory animals, particularly
dogs. The transfer coefficients are based on data for trivalent antimony, which has been studied
more than pentavalent antimony and which is expected to be the primary form of antimony inthe body except perhaps for a relatively brief period after exposure to Sb(V). For radioisotopesof antimony entering the systemic circulation as pentavalent antimony, the model is expected
to underestimate the initial rate of biological removal from the body and overestimate
cumulative nuclear transformations in systemic tissues and fluids.
No information was found on age related changes in the systemic behaviour ofantimony in human subjects. In rats, total-body retention of 125Sb administered as the chloride
appeared to be independent of age (J. Inaba et al., 1984).
173

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

4455
4456
4457
4458
4459
4460

The systemic behaviour of antimony is assumed here to be independent of age exceptthat activity is removed from trabecular or cortical bone volume to blood at the age-specificrate of turnover of that bone type.
The structure of the model for antimony is shown in Fig. 23.1. Parameter values are
given in Table 23.2.

4461
4462
4463
4464
4465

Fig. 23.1. Structure of the biokinetic model for systemic antimony. SI = Small intestine, RBC= Red blood cells.
Table 23.2. Transfer coefficients for the model for antimonyaPath

Plasma to UB contents
Plasma to RBC
Plasma to ST0
Plasma to ST1
Plasma to ST2
Plasma to Liver 1
Plasma to Kidneys
Plasma to Cort bone surf
Plasma to Trab bone surf
Plasma to Thyroid
Thyroid to Plasma
RBC to Plasma
ST0 to Plasma
ST1 to Plasma
ST2 to Plasma
Liver 1 to SI contents
Liver 1 to Plasma
Liver 1 to Liver 2
Liver 2 to Plasma

Infant
9.00E+00
3.00E+00
7.49E+01
4.50E+00
4.00E-02
4.00E+00
2.50E-01
2.00E+00
2.00E+00
3.00E-01
1.39E-01
6.93E-01
1.39E+00
1.39E-02
6.93E-04
2.43E-01
4.37E-01
1.39E-02
6.93E-04

1y
9.00E+00
3.00E+00
7.49E+01
4.50E+00
4.00E-02
4.00E+00
2.50E-01
2.00E+00
2.00E+00
3.00E-01
1.39E-01
6.93E-01
1.39E+00
1.39E-02
6.93E-04
2.43E-01
4.37E-01
1.39E-02
6.93E-04

174

Transfer coefficient (d-1)
5y
10 y
9.00E+00 9.00E+00
3.00E+00 3.00E+00
7.49E+01 7.49E+01
4.50E+00 4.50E+00
4.00E-02 4.00E-02
4.00E+00 4.00E+00
2.50E-01 2.50E-01
2.00E+00 2.00E+00
2.00E+00 2.00E+00
3.00E-01 3.00E-01
1.39E-01 1.39E-01
6.93E-01 6.93E-01
1.39E+00 1.39E+00
1.39E-02 1.39E-02
6.93E-04 6.93E-04
2.43E-01 2.43E-01
4.37E-01 4.37E-01
1.39E-02 1.39E-02
6.93E-04 6.93E-04

15 y
9.00E+00
3.00E+00
7.49E+01
4.50E+00
4.00E-02
4.00E+00
2.50E-01
2.00E+00
2.00E+00
3.00E-01
1.39E-01
6.93E-01
1.39E+00
1.39E-02
6.93E-04
2.43E-01
4.37E-01
1.39E-02
6.93E-04

Adult
9.00E+00
3.00E+00
7.49E+01
4.50E+00
4.00E-02
4.00E+00
2.50E-01
2.00E+00
2.00E+00
3.00E-01
1.39E-01
6.93E-01
1.39E+00
1.39E-02
6.93E-04
2.43E-01
4.37E-01
1.39E-02
6.93E-04

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
Kidneys to PlasmaCort bone surf to Plasma
Trab bone surf to PlasmaCort bone surf to Cort bone vol
Trab bone surf to Trab bone volCort bone vol to Plasma
Trab bone vol to Plasma

4466

a

2.31E-01
3.43E-01
3.43E-01
3.47E-03
3.47E-03
8.22E-03
8.22E-03

2.31E-01
3.43E-01
3.43E-01
3.47E-03
3.47E-03
2.88E-03
2.88E-03

2.31E-01
3.43E-01
3.43E-01
3.47E-03
3.47E-03
1.53E-03
1.81E-03

2.31E-01
3.43E-01
3.43E-01
3.47E-03
3.47E-03
9.04E-04
1.32E-03

2.31E-01
3.43E-01
3.43E-01
3.47E-03
3.47E-03
5.21E-04
9.59E-04

2.31E-01
3.43E-01
3.43E-01
3.47E-03
3.47E-03
8.21E-05
4.93E-04

UB = Urinary bladder, SI= Small intestine, Trab = Trabecular, Cort = Cortical, surf = surface, vol = volume

175

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

4467

23.2. Dosimetric data for antimony

4468

Table 23.3. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 124Sb compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled particulate materials (1 µm AMAD aerosols) 3 mo

1y

5y

10 y

15 y

Adult

Type F, Chloride, tartrate

1.1E-08

8.3E-09

4.3E-09

2.5E-09

1.7E-09

1.4E-09

Type M, Trioxide; all unspecified forms

2.1E-08

1.7E-08

9.9E-09

6.6E-09

5.0E-09

5.2E-09

Type S

2.9E-08

2.5E-08

1.5E-08

9.9E-09

7.5E-09

7.9E-09

Adult fA = 0.05, Other chemical forms

7.2E-09

4.7E-09

2.7E-09

1.8E-09

1.2E-09

1.1E-09

Adult fA = 0.1, Antimony in food

1.1E-08

6.1E-09

3.5E-09

2.2E-09

1.5E-09

1.4E-09

Ingested materials

4469
4470

Table 23.4. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 125Sb compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled particulate materials (1 µm AMAD aerosols) 3 mo

1y

5y

10 y

15 y

Adult

Type F, Chloride, tartrate

5.6E-09

4.5E-09

2.4E-09

1.4E-09

9.4E-10

8.5E-10

Type M, Trioxide; all unspecified forms

1.4E-08

1.2E-08

6.9E-09

4.5E-09

3.5E-09

3.5E-09

Type S

4.4E-08

4.2E-08

2.7E-08

1.8E-08

1.5E-08

1.6E-08

Adult fA = 0.05, Other chemical forms

3.0E-09

1.6E-09

9.4E-10

6.0E-10

4.1E-10

3.7E-10Adult fA = 0.1, Antimony in food

5.2E-09

2.5E-09

1.4E-09

8.8E-10

6.1E-10

5.4E-10

Ingested materials

4471
176

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

24. TELLURIUM (Z = 52)

4472
4473

24.1. Routes of Intake

4474

24.1.1. Inhalation

4475
4476
4477
4478
4479
4480
4481
4482
4483
4484
4485
4486
4487
4488
4489

A few experimental studies of the behaviour of radio-labelled tellurium (i.e. tracer
level) following deposition in the respiratory tract have been identified in the literature. Some
information is also available from measurements following inadvertent intakes of irradiatedtellurium oxide, from studies of tellurium-132 inhaled by people after the Chernobyl accident,
and from toxicology studies of stable tellurium compounds. For details, see Section 4 of
Publication 137 (ICRP, 2017).
Absorption parameter values and types, and associated fA values for gas and vapour
forms of tellurium are given in Table 24.1 and for particulate forms in Table 24.2 (taken from
Section 4 of Publication 137). Common forms of tellurium (e.g. dioxide) are solids at room
temperature. Exposures to gas or vapour forms of tellurium are therefore probably relatively
unusual compared to exposures to particulate forms, and it is therefore recommended in thisseries of documents that particulate form should be assumed in the absence of specificinformation.
Table 24.1. Deposition and absorption for gas and vapour forms of tellurium.
Chemical form/origin
All unspecified compounds

Total

Percentage deposited (%)*
ET1
ET2
BB
bb

AI

Absorption
Type†

100b

0

50

F

20

10

20

Age-dependent absorption from the alimentary tract, fA
3 months
1 year
5 years
10 years 15 years Adult
Chemical form/origin
All unspecified compounds

4490
4491
4492
4493
4494
4495
4496
4497
4498
4499

0.6

0.3

0.3

0.3

0.3

0.3

ET1, anterior nasal passage; ET2, posterior nasal passage, pharynx and larynx; BB, bronchial; bb, bronchiolar; AI,
alveolar-interstitial.
*
Percentage deposited refers to how much of the material in the inhaled air remains in the body after exhalation.
Almost all inhaled gas molecules contact airway surfaces, but usually return to the air unless they dissolve in, or
react with, the surface lining. The default distribution between regions is assumed: 20% ET 2, 10% BB, 20% bb
and 50% AI.
†
It is assumed that for tellurium the bound state can be neglected i.e. fb = 0.

Table 24.2. Absorption parameter values for inhaled particulate forms of tellurium and foringested tellurium.
Inhaled particulate materials
Default parameter values†,‡
Absorption
Assigned forms
TypeF
Chloride, Dioxide
M§
Elemental tellurium,
tellurideS—

fr

Absorption parameter values*sr (d–1)
ss (d–1)

1
cadmium 0.2

50
3

–
0.005

0.01

3

1×10–4

177

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
Ingested materials¶
Assigned forms
All forms

Age-dependent absorption from the alimentary tract, fA
3 months 1 year
5 years
10 years 15 years adult
0.6
0.3
0.3
0.3
0.3
0.3

4500
4501
4502
4503
4504
4505
4506
4507
4508
4509
4510
4511
4512
4513

*

4514

24.1.2. Ingestion

4515

24.1.2.1. Adults

4516
4517
4518
4519
4520
4521
4522
4523

Taking into account experimental data from several animal species Publication 30(ICRP, 1979) recommended an absorption fraction of 0.2. Kron et al. (1991) studied the renal
excretion of stable tellurium by healthy volunteers after oral administration of Te as sodium
tellurate (TeO3), sodium tellurite (TeO2) and metallic colloid and proposed that a fractional
absorption value of 0.25 should be applied for radiological protection purposes. Based on thisstudy and on recent animal experiments, a value of 0.3 was recommended in Publication 67(ICRP, 1993) and in Publication 137 (ICRP, 2017). The value of fA = 0.3 is adopted here for
dietary intakes of tellurium.

4524

24.1.2.2. Children

4525
4526
4527
4528
4529

No information appears to be available from experimental animals or studies inhumans for assessing any possible changes with age of tellurium gastrointestinal absorption.
Following its general approach, Publication 67 recommended an absorption fraction for
tellurium of 0.6 for the 3-month-old infant. For children of 1 year and older Publication 67
recommended to use the value for adults (0.3). The same values are adopted here for fA.

4530

24.1.3. Systemic Distribution, Retention and Excretion4531

24.1.3.1. Summary of biokinetic data

4532
4533
4534
4535
4536
4537
4538

Kron et al. (1991) studied urinary excretion of tellurium in five healthy volunteers
after oral administration of tellurium in different forms: tellurite (Na 2TeO4), tellurate(Na2TeO3), metallic form, and intrinsically bound in cress (Lepidium sativum). Cress was
consumed both with and without oil and vinegar dressing. The three-day urinary excretion
varied between 3 and 25%. Urinary excretion was higher for tellurate (9-25%) than for tellurite(<8%) or metallic tellurium (4-9%). After ingestion of tellurium with cress, the amountexcreted over three days was in the range 6-16%, and was reduced to 3% when dressing was

It is assumed that for tellurium the bound state can be neglected i.e. fb = 0. The value of sr for Type F forms oftellurium is element-specific. The values for Types M and S (3 d–1) are the general default values.
†
Materials (e.g. Chloride) are listed here where there is sufficient information to assign to a default absorption
type, but not to give specific parameter values (see Section 4 of ICRP, 2017).
‡
For inhaled material deposited in the respiratory tract and subsequently cleared by particle transport to thealimentary tract, the default fA values for inhaled materials are applied: i.e. the product of fr for the absorption type
and the fA value for ingested soluble forms of tellurium applicable to the age-group of interest (e.g. 0.3 for adults).
§
Default Type M is recommended for use in the absence of specific information on which the exposure material
can be assigned to an absorption type, e.g., if the form is unknown, or if the form is known but there is no
information available on the absorption of that form from the respiratory tract.
¶
Activity transferred from systemic compartments into segments of the alimentary tract is assumed to be subject
to reabsorption to blood. The default absorption fraction fA for the secreted activity is the highest value foringestion of the radionuclide applicable to the age-group of interest (e.g. 0.3 for adults).

178

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

4539
4540
4541
4542
4543
4544
4545
4546
4547
4548
4549
4550
4551
4552
4553
4554
4555
4556
4557
4558
4559
4560
4561
4562
4563
4564
4565
4566
4567
4568
4569
4570
4571
4572
4573
4574
4575
4576
4577
4578
4579
4580
4581
4582
4583
4584
4585
4586

added. For tellurate and metal tellurium most of the excretion occurred in the first 24 h afteradministration, whereas for cress and tellurite the excretion curve was delayed.
Schroeder et al. (1967) measured the concentration of tellurium in human tissues andcalculated that a total body content of ~600 mg in a reference adult, approximately 90% of
which was contained in bone
The systemic behaviour of tellurium at early times after intake has been investigatedin laboratory animals including rats (Agnew and Cheng, 1971; Barnes et al., 1955; DeMeio andHenriques Jr., 1947; Health Council of the Netherlands: Committee on Updating ofOccupational Exposure Limits, 2002; Hollins, 1969; Morgan et al., 1997; Valkonen and
Savolainen, 1985), rabbits (DeMeio and Henriques Jr., 1947), dogs (DeMeio and Henriques Jr.,
1947), guinea pigs, (Barnes et al., 1955), sheep (Casey et al., 1963; Wright and Bell, 1966),
swine (Wright and Bell, 1966), cattle (Mullen and Stanley, 1974). The collective data indicatethat a substantial portion of the administered activity is contained in the liver, kidneys, andbone during the first few days after administration. A relatively high concentration is also foundin the thyroid gland, but the thyroid content represents only a small percentage of the systemic
content due to its small mass. A substantial portion of the absorbed or injected amount isremoved in urine in the first few days.
Casey et al. (1963) administered a mixture of radionuclides of tellurium and iodine tolactating sheep and found relatively low transfer of tellurium to milk (two to three orders ofmagnitude less than for iodine). Retained tellurium was found mainly in the liver, kidney, lungs.
The highest concentration was found in the thyroid, but the total content of the thyroid wassmall due to its small mass.
Wright and Bell (1966) compared the kinetics of 127mTe in sheep and swine following
its intravenous administration as Na2TeO3. Activity cleared readily from plasma in both sheep
and swine. Only a small portion of the administered activity was recovered in the cell fraction
in sheep, In swine the corpuscular fraction rose with time to 3% of the injected amount at 5 d.
At 5 d the liver and kidneys contained about 8% and 7%, respectively, in sheep and 7% and2%, respectively, in swine. No information was given about skeleton or thyroid. Both species
excreted about 11% of the injected 127mTe in the faeces and 34% in the urine over five d. About
two-thirds of the urinary excretion occurred in the first 24 h.
Hollins (1969) studied the metabolism of 127mTe administered orally or
intraperitoneally as tellurous acid to rats. Retention after intraperitoneal injection could be
described as a bi-exponential function with half-times of 0.8 d (49%) and 13 d (51%),
respectively. The highest activity concentrations were observed in the kidneys, blood, liver,spleen, femur, and lung. Tellurium in blood was almost entirely bound to the protein content
of the red blood cells. The tissues could be divided into three classes according to the retention
half-time: lung, blood, liver and heart with a half-time of approximately 10 d; muscle, spleen,
and kidney with a half-time of approximately 20 d; and femur (skeleton) with a half-time thatwas much longer than the duration of the experiment (200 d) and could therefore not be
determined with much confidence. About 27% of the injected tellurium was excreted in urine
during the first 24 h, and 6% was excreted in faeces. Less than 0.25% of the administered dose
was eliminated in the breath in the first 24 h.
Barnes et al. (1955) administered 132Te orally to rats and guinea pigs and determinedthe distribution of tellurium in the body at 3-4 d. In guinea pigs the concentration in liver,kidneys, and bone were substantially higher than in pelt, blood, and carcass. About 5.5% and6.5% was excreted in the urine over 4 d by the guinea pigs and rats, respectively. Faecal
excretion plus activity present in the gut amounted to about 93% in the guinea pigs and 80% in
the rats.

179

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

4587
4588
4589
4590
4591
4592
4593
4594
4595
4596
4597
4598
4599

Morgan et al. (1997) administered cadmium telluride intra-tracheally to rats. Afterabsorption of tellurium into the systemic circulation, relatively high concentrations were foundin the spleen (maximum, 82.8±10.2 µgg-1 tissue), kidney (maximum, 8.1±1.3 µgg-1 tissue),liver (maximum, 8.8±0.6 µgg-1 tissue), femur (maximum 3.5±0.5 µgg-1 tissue) and blood(maximum, 5.3±0.2 µgg-1 tissue). The maximum concentration was reached at day 14 afteradministration in all tissues except liver, where the maximum was reached at day 7.
Mullen and Stanley (1974) studied absorption, distribution and milk secretion ofradiotellurium in dairy cows and calves. The transfer of tellurium to milk was low (about 0.25%
of the orally administered activity in 13 d). Retained tellurium was found mainly in the liver,bone, and organs of the digestive/ruminal tract. The activity concentration in the thyroid was
similar to that in the liver.
No information was found regarding the effect of age on the biokinetics of systemic
tellurium.

4600

24.1.3.2. Systemic model

4601
4602
4603
4604
4605
4606
4607
4608
4609
4610
4611
4612
4613
4614
4615

A variation of the generic model structure for bone-surface-seeking radionuclides isapplied to tellurium, with the introduction of the thyroid as a separate compartment. The modelfor the adult member of the public is the same as the model for occupational intake of tellurium
used in Publication 137 (ICRP, 2017). Transfer coefficients for adults are based predominantly
on human data with regard to whole body retention and urinary excretion and on data forlaboratory animals (particularly swine and guinea pigs) with regard to the system distribution.
Due to paucity of age-specific biokinetic data for tellurium the transfer coefficients for adults
are applied to all age groups with the exception for the assumption generally made in this reportseries that activity is removed from trabecular or cortical bone volume to blood at the reference
age-specific rate of turnover of that bone type (ICRP, 2002a).
The model structure is shown in Fig. 24.1. Transfer coefficients are listed in Table
24.3.

4616
4617
4618
4619

Fig. 24.1. Structure of the biokinetic model for systemic tellurium.
Table 24.3. Age-specific transfer coefficients for tellurium.
Transfer coefficient (d-1)

180

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
Pathwaya
Blood 1 to Urinary bladder contents

100 d
7.51E-01

1y
7.51E-01

5y
7.51E-01

10 y
7.51E-01

15 y
7.51E-01

Adult
7.51E-01

Blood 1 to Kidneys

4.04E-02

4.04E-02

4.04E-02

4.04E-02

4.04E-02

4.04E-02

Blood 1 to Liver

1.21E-01

1.21E-01

1.21E-01

1.21E-01

1.21E-01

1.21E-01

Blood 1 to Blood 2

1.01E-01

1.01E-01

1.01E-01

1.01E-01

1.01E-01

1.01E-01

Blood 1 to Other

7.68E-02

7.68E-02

7.68E-02

7.68E-02

7.68E-02

7.68E-02

Blood 1 to Cort bone surface

2.02E-02

2.02E-02

2.02E-02

2.02E-02

2.02E-02

2.02E-02

Blood 1 to Trab bone surface

4.04E-02

4.04E-02

4.04E-02

4.04E-02

4.04E-02

4.04E-02

Blood 1 to Thyroid

4.00E-03

4.00E-03

4.00E-03

4.00E-03

4.00E-03

4.00E-03

Blood 2 to Blood

6.93E-02

6.93E-02

6.93E-02

6.93E-02

6.93E-02

6.93E-02

Liver to Small intestine contents

6.93E-02

6.93E-02

6.93E-02

6.93E-02

6.93E-02

6.93E-02

Thyroid to Blood 1

6.93E-02

6.93E-02

6.93E-02

6.93E-02

6.93E-02

6.93E-02

Kidneys to Blood 1

6.93E-02

6.93E-02

6.93E-02

6.93E-02

6.93E-02

6.93E-02

Other to Blood 1

6.93E-02

6.93E-02

6.93E-02

6.93E-02

6.93E-02

6.93E-02

Cort bone surf to Blood 1

1.16E-02

1.16E-02

1.16E-02

1.16E-02

1.16E-02

1.16E-02

Trab bone surf to Blood 1

1.16E-02

1.16E-02

1.16E-02

1.16E-02

1.16E-02

1.16E-02

Cort bone surf to Cort bone volume

6.93E-04

6.93E-04

6.93E-04

6.93E-04

6.93E-04

6.93E-04

Trab bone surf to Trab bone volume

6.93E-04

6.93E-04

6.93E-04

6.93E-04

6.93E-04

6.93E-04

Cort bone vol to Blood 1

8.22E-03

2.88E-03

1.53E-03

9.04E-04

5.21E-04

8.21E-05

Trab bone vol to Blood 1

8.22E-03

2.88E-03

1.81E-03

1.32E-03

9.59E-04

4.93E-04

4620

a

4621

24.1.3.3. Treatment of radioactive progeny

4622
4623

The treatment of radioactive progeny produced in systemic compartments after intake
of a radioisotope of tellurium is described in Section 4.2.3.3. of Publication 137 (ICRP, 2017).

Cort = Cortical, Trab = Trabecular181

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

4624

24.2. Dosimetric data for tellurium

4625

Table 24.4. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 129Te compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled gases or vapours

3 mo

1y

5y

10 y

15 y

All unspecified compounds

2.9E-10

2.2E-10

1.3E-109.0E-11

6.4E-11

1.4E-101.0E-10

4.5E-11

3.3E-11

2.1E-11

Type M, Elemental tellurium, cadmium telluride; allunspecified forms
1.9E-10

1.4E-10

6.9E-11

5.2E-11

3.7E-11

Type S

1.9E-10

1.4E-10

6.9E-11

5.2E-11

3.8E-11

3.3E-10

2.7E-10

1.8E-10

1.3E-108.9E-11

Inhaled particulate materials (1 µm AMAD aerosols)
Type F, Chloride, Dioxide

Ingested materials
Adult fA = 0.3, All forms

4642
4643

4626
4627
Adult4628
4629
5.8E-11
4630
4631
4632
1.6E-11
4633
4634
4635
2.9E-114636
2.9E-11
4637
4638
4639
4640
6.1E-114641

Table 24.5. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 132Te compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled gases or vapours

3 mo

1y

5y

10 y

15 y

Adult

All unspecified compounds

3.0E-08

2.5E-08

1.4E-08

6.9E-09

4.7E-09

3.4E-09

1.3E-08

1.0E-08

4.9E-09

2.6E-09

1.6E-09

1.2E-09

Inhaled particulate materials (1 µm AMAD aerosols)
Type F, Chloride, Dioxide

182

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
Type M, Elemental tellurium, cadmium telluride; allunspecified forms
7.5E-09

5.5E-09

2.9E-09

1.9E-09

1.3E-09

Type S

6.3E-09

4.9E-09

2.6E-09

1.8E-09

1.3E-09

2.1E-08

1.2E-08

6.6E-09

3.6E-09

2.5E-09

Ingested materials
Adult fA = 0.3, All forms

4652
4653
4654
4655
4656
4657
4658
4659
4660
4661
4662

183

4644
4645
1.3E-094646
1.3E-09
4647
4648
4649
4650
1.9E-094651

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

25. IODINE (Z = 53)

4663
4664

25.1. Routes of Intake

4665

25.1.1. Inhalation

4666
4667
4668
4669
4670
4671
4672
4673
4674
4675
4676
4677

Detailed information on the behaviour of inhaled gases and vapours of iodine isavailable from studies in human volunteers. Some information on absorption from therespiratory tract is available on inhaled particulate forms of iodine: as iodide from animal
experiments; and associated with irradiated fuel fragments from human exposures. For details,
see Section 5 of Publication 137 (ICRP, 2017). Absorption parameter values and types, andassociated fA values for gas and vapour forms of iodine are given in Table 25.1 and forparticulate forms in Table 25.2 (taken from Section 5 of Publication 137). Exposures to both
gas/vapour forms and particulate forms of iodine are common, and it is therefore recommended
in this series of documents that in the absence of information 50% particulate; 50% gas/vapour
should be assumed.
Table 25.1. Deposition and absorption for gas and vapour forms of iodine *.
Chemical form/origin
Elemental iodine, I2
Methyl iodide, CH3I;
ethyl iodide, C2H5I
Unspecified*

4678
4679
4680
4681
4682
4683
4684
4685
4686
4687
4688
4689
4690
4691
4692
4693
4694

Total
100
70‡

ET1
0
0

100

0

Fraction deposited (%)†
ET2
BB
bb
50
50
0
14
7
14
50

50

0

AI
0
35

Absorption
Type fA
F
1.0¶
§
V

0

F

1.0¶

ET1, anterior nasal passage; ET2, posterior nasal passage, pharynx and larynx; BB, bronchial; bb, bronchiolar; AI,
alveolar-interstitial.
*
For iodine in unspecified gas or vapour form, the behaviour assumed is the same as that for elemental iodine:
100% deposition (50% ET2 and 50% BB) with Type F absorption. It is assumed that for iodine the bound state
can be neglected i.e. fb = 0.
†
Fraction deposited refers to how much of the material in the inhaled air remains in the body after exhalation.
Almost all inhaled gas molecules contact airway surfaces, but usually return to the air unless they dissolve in, or
react with, the surface lining.
‡
Since instantaneous absorption to blood (Type V) is assumed, calculations can be performed assuming direct
injection into blood, and the regional deposition does not need to be considered. Nevertheless, for completeness,the deposits in each region are assumed to be distributed in the same proportions as in the default distribution forgases and vapours: 20% ET2, 10% BB, 20% bb and 50% AI.
§
Not applicable for absorption Type V, because all activity deposited in the respiratory tract is instantaneously
absorbed.
¶
The value of fA = 1 is applicable to all age-groups.

184

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

4695
4696

Table 25.2. Absorption parameter values for inhaled particulate forms of iodine and foringested iodine.
Inhaled particulate materials
Default parameter values†,‡
Absorption
Assigned forms
TypeF§
Sodium iodide; caesium chloride
vector, silver iodide
M—
S—
Ingested materials¶
Assigned forms
All chemical forms

fr

Absorption parameter values*sr (d–1)
ss (d–1)

1

100

–

0.2
0.01

3
3

0.005
1×10-4Age-dependent absorption from the alimentary tract, fA
3 months 1 year
5 years
10 years
15 years
adult
1
1
1
1
1
1

4697
4698
4699
4700
4701
4702
4703
4704
4705
4706
4707
4708
4709
4710

*

4711

25.1.2. Ingestion

4712

25.1.2.1. Adults

4713
4714
4715
4716
4717
4718
4719
4720
4721
4722

The absorption of iodide from the alimentary tract of humans is virtually complete,
while subject to changes of the redox conditions in the alimentary tract. For other chemical
forms, absorption is less complete but commonly above 70%. (For details see Section 5 of
Publication 137, ICRP, 2017). Iodine absorption occurs in the stomach as well as the proximal
small intestine (Berkovski, 1999). However, assuming half of ingested iodine to be absorbed
from the stomach would increase thyroid and effective doses by less than 1% for common
isotopes (ICRP, 2006). In Publication 30 (ICRP, 1979), an absorption fraction of 1 wasrecommended for all chemical forms of iodine. This value was recommended in Publication
56 (ICRP, 1990) for dietary intakes and in Publication 137 (ICRP, 2017) for all forms. A valueof fA = 1 is also adopted here for adults and for all chemical forms.

4723

25.1.2.2. Children

4724
4725
4726
4727

Similar results have been obtained in both young children and adolescents (Cuddihy,
1966; van Dilla and Fulwyler, 1963). No differences in uptake between iodine in aqueous media
and milk have been found (Comar et al., 1963; Cuddihy, 1966). It is, therefore, assumed thatfor all ages absorption of iodine is complete when incorporated in foodstuffs (i.e. fA = 1).

It is assumed that for iodine the bound state can be neglected i.e. fb = 0. The value of sr for Type F forms of iodine(100 d–1) is element-specific. The values for Types M and S (3 d–1) are the general default values.
†
Materials (e.g. sodium iodide) are generally listed here where there is sufficient information to assign to a default
absorption ype, but not to give specific parameter values (see Section 5 of Publication 137, ICRP, 2017).
‡
For inhaled material deposited in the respiratory tract and subsequently cleared by particle transport to thealimentary tract, the default fA values for inhaled materials are applied: i.e. the product of fr for the absorption type
and the fA value for ingested soluble forms of iodine applicable to the age-group of interest (1.0).
§
Default Type F is recommended for use in the absence of specific information on which the exposure material
can be assigned to an absorption type, e.g. if the form is unknown, or if the form is known but there is no
information available on the absorption of that form from the respiratory tract.
¶
Activity transferred from systemic compartments into segments of the alimentary tract is assumed to be subject
to reabsorption to blood. The default absorption fraction fA for the secreted activity is the highest value foringestion of the radionuclide applicable to the age-group of interest (1.0).

185

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

4728

25.1.3. Systemic Distribution, Retention and Excretion4729

25.1.3.1. Age specific data

4730(a) Thyroidal uptake of iodine

4731
4732
4733
4734
4735
4736
4737
4738
4739
4740
4741
4742
4743
4744
4745
4746
4747
4748
4749

Fractional uptake of ingested iodine by the thyroid is substantially greater in the firstfew days of life than at higher ages. Twenty-four hour uptake of intramuscularly injected 131I
in seven infants of age 2-3 d ranged from 46 to 97% and averaged 70% (Van Middlesworth,1954). In 25 infants 0.5-2 d of age, uptake of intravenously injected 131I at 24 h ranged from35 to 88% and averaged 61% (Fisher et al., 1962). In seven premature infants 0.4-3 d old,
uptake ranged from 46 to 100% and averaged 73% (Fisher et al., 1962). Thyroidal uptake
averaged 70% in 17 infants of age <1.5 d following intramuscular injection and 50% in 8 infantsof age <1.5 d following oral administration (Morrison et al., 1963). According to Fisher et al.
(1964), “Thyroid function during the first weeks of life is characterized by hyperactivity as
measured by increased radioiodine uptake, increased serum hormonal iodine values, andincreased erythrocyte triiodothyronine 131I uptake. This neonatal thyroid hyperactivity subsides
within one to two weeks, and the elevated test results have returned to normal childhood levels
by 8 to 12 weeks of age.”
Regional studies of radioiodine uptake by the thyroid in different age groups suggestthat there is little if any age dependence in uptake beyond early infancy except perhaps for amodest decline after the fifth or sixth decade (Cuddihy, 1966; Gaffney et al., 1962; Oliner etal., 1957; Quimby et al., 1950; Rosenberg, 1957, 1958; Schober and Hunt, 1976; van Dilla andFulwyler, 1963). Age-specific uptake values determined in one relatively large set of euthyroid
subjects (60 subjects ages 2.5 mo to 18 y and 64 adults) are shown in .

4750
4751
4752
4753

Fig. 25.1. Comparison of thyroidal uptake of 131I at 24 h in euthyroid children and adults fromthe same region (Oliner et al., 1957).

4754(b) Biological half-time in the thyroid

4755
4756

In the model for adults (Leggett, 2010) the baseline biological half-time of iodine in
the thyroid is 90 d, based on a wide range of reported values. The large variability in the half-

186

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

4757
4758
4759
4760
4761
4762
4763
4764
4765
4766
4767
4768
4769
4770
4771
4772
4773
4774
4775
4776
4777
4778
4779
4780
4781
4782
4783

time presumably is related to variation in dietary intake and related thyroid stores of stableiodine.
Observed half-times for pre-adult ages are also highly variable (Fig. 25.2.). For
newborn infants, data of Karhausen (1974) for two subjects suggest a half-time of the order of
3 d; Morrison et al. (1963) estimated a half-time of the order of 15-25 d based on “a few”
studies; Fisher et al. (1962) determined a mean half-time of approximately 11 d (range 4-40 d)based on “prolonged thyroid 131I decay curves” for 9 premature infants; and Ogborn et al.
(1960) and Quimby et al. (1958) estimated half-times of 6 d and 23 d, respectively. Data of
Karhausen (1974) indicate a mean half-time of about 9 d (2.5-13 d) in 5 subjects of age 2.5-5mo; 14 d (4-39 d) for 5 subjects of age 1-2 y; and 64 d (21-142 d) for 12 subjects of age 10-14
y. Data of Cuddihy (1966) indicate mean half-times of 31 d (range, 19-41 d) for four subjectsof age 6-9 y and 44 d (39-53 d) for three subjects of age 12-16 y. Longer mean half-times inchildren and adolescents were determined by Van Dilla and Fulwyler (1963): 85 d (range, 59163 d) in 7 subjects of age 4-8 y, and 96 d (73-142 d) in 4 subjects of age 10-14 y.
On the basis of a review and analysis of biological half-times reported in the literature,Dunning and Schwarz (1981) estimated means of 16 d (range, 6-23 d) for infants; 13 d (4-39d) for ages 0.5-2 y; 50 d (19-118 d) for ages 6-16 y; and 85 d (21-372 d) for ages >18 y. Medianvalues determined by Dunning and Schwarz were 13 d for infants, 10 d for ages 0.5-2 y, 44 d
for ages 6-16 y, and 72 d for ages >18 y.
Overall, the reported data on biological half-times of iodine in the thyroid suggest asizable increase between birth and about age 5-6 y and then a more gradual increase to early
adulthood. There appears to be little if any change in the half-time from early adulthood until
at least the fifth or sixth decade, after which there may be a moderate decline.
Selected baseline biological half-times for use in the iodine model are 10 d in infants(age 100 d), 15 d at age 1 y, 30 d at age 5 y, 50 d at age 10 y, 65 d at age 15 y, and 90 d inyoung or middle-aged adults. These are the age groups addressed in the ICRP’s age-specificbiokinetic models for members of the public.

4784(c) Rate of secretion of organic iodine by the thyroid

4785
4786
4787
4788
4789
4790
4791

Results of clinical and experimental studies indicate that the mass of organic iodine
secreted daily by the thyroid increases with age from infancy to early adulthood, remains steadyfrom young adulthood through the fifth or sixth decade of life, and declines thereafter (Fisher
et al., 1965; Gregerman et al., 1962; Haddad, 1960; Herrmann et al., 1981; Karhausen, 1974;
Mariotti et al., 1995; Oddie et al., 1965, 1966; Sawin, 2005). Representative results from fivestudies including central estimates based on a review of the literature (Oddie et al., 1966) are
shown in Fig. 25.3.

187

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

4792
4793
4794

Fig. 25.2. Measured and modeled biological half-time of iodine in the thyroid.

4795(d) Rate of degradation of extrathyroidal organic iodine

4796
4797
4798
4799
4800
4801
4802
4803

The biological half-time of extrathyroidal T4 increases with age throughout life (Anbar
et al., 1965; Gregerman et al., 1962; Oddie et al., 1966). Central half-times estimated fromcollected data are 4 days in infants, 5 days in children, 6 days in adolescents, 7 days in young
adults, 8 days in middle-aged adults, and 9 days in elderly adults. The half-time ofextrathyroidal T4 essentially determines the half-time of extrathyroidal hormonal iodine. The
following reference values are used to develop baseline transfer coefficients describing the
behavior of extrathyroidal organic iodine at different ages: 4 d in infants, 4.5 days at age 1 y,
5 d at age 5 y, 5.5 d at age 10 y, 6 d at age 15 y, and 7 d in adults.

4804

25.1.3.2. Systemic model

4805
4806
4807
4808

The structure of the age-specific biokinetic model for iodine, and the transfer
coefficients for the adult member of the public are the same as in the model for iodine in theworker adopted in Publication 137 (ICRP, 2017). The model structure is shown in Fig. 25.4.
Transfer coefficients for all six ages at intake are listed in

188

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

4809

4810
4811
4812
4813
4814

4815
4816
4817
4818
4819
4820
4821
4822
4823

Table 25.3.

Fig. 25.3. Measured and modeled rate of secretion of T 4 by the thyroid in males from birth toearly adulthood. In the model, secretion of iodine as T 4 is assumed to be 93% of total secretionof hormonal iodine by the thyroid.

Fig. 25.4. Structure of the biokinetic model for systemic iodine.
The transfer coefficients that vary with age are the coefficient describing transfer oforganic iodine from Thyroid 2 to Blood Organic Iodine, and values describing movement of
extrathyroidal organic iodine. The transfer coefficients for these paths are calculated asfollows: (1) the transfer coefficient from Thyroid 2 to Blood Organic Iodine at a given age isln(2)/T1/2, where ln(2) = 0.69315 and T1/2 refers to the biological half-times of iodine in the
thyroid discussed earlier (e.g., 7 d in infants and 50 d at age 10 y); (2) all parameter values
189

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

4824
4825
4826
4827
4828
4829
4830
4831
4832
4833
4834
4835
4836
4837

describing the movement of extrathyroidal organic iodine at a given age (the last 12 values ineach column in Table 1) are (7/T) times the corresponding value for adults, where T is the agespecific turnover time of extrathyroidal organic iodine discussed earlier, (e.g., 4 d in infantsand 5.5 d at age 10 y).
A transfer coefficient developed for adults was applied to children unless there wasclear evidence of age dependence. As summarized above, clear evidence of age dependence
was found for: (1) the rate of removal of organic iodine from the thyroid to blood, expressed
either as a removal half-time or mass of iodine removed per unit time; and (2) the rate ofturnover of extrathyroidal organic iodine. It appears that there is little if any age dependence inthe rate of transfer of inorganic iodide from blood to the thyroid. Data were insufficient todetermine whether other aspects of the kinetics of inorganic iodide changes with age. Hence,
the biokinetics of inorganic iodide in the body is assumed to be invariant with age.

190

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

4838

Table 25.3. Age-specific transfer coefficients for systemic iodine
Pathway
Blood Iodide to Thyroid 1
Blood Iodide to UB contents
Blood Iodide to Salivary
glandsBlood Iodide to St Wall
Blood Iodide to Other 1
Blood Iodide to Kidneys 1
Blood Iodide to Liver 1
Salivary glands to Oral cavity
St Wall to St contents
Thyroid 1 to Thyroid 2
Thyroid 1 to Blood Iodide
Thyroid 2 to Blood Organic
Thyroid 2 to Blood Iodide
Other 1 to Blood Iodide
Other 1 to Other 2
Other 2 to Other 1
Kidneys 1 to Blood Iodide
Liver 1 to Blood Iodide
Blood Organic to Other 3
Other 3 to Blood Organic
Other 3 to Other 4
Other 4 to Other 3
Other 4 to Blood Iodide
Blood Organic to Kidneys 2
Kidneys 2 to Blood Organic
Kidneys 2 to Blood Iodide
Blood Organic to Liver 2
Liver 2 to Blood Organic
Liver 2 to Blood Iodide
Liver 2 to Right colon
contents

4839

100 d
1y
7.26E+00 7.26E+00
1.18E+01 1.18E+01

Transfer coefficient (d-1)
5y
10 y
15 y
7.26E+00 7.26E+00 7.26E+00
1.18E+01 1.18E+01 1.18E+01

Adult
7.26E+00
1.18E+01

5.16E+00
8.60E+00
6.00E+02
2.50E+01
1.50E+01
5.00E+01
5.00E+01
9.50E+01
3.60E+01
6.93E-02
0.00E+00
3.30E+02
3.50E+01
5.60E+01
1.00E+02
1.00E+02
2.63E+01
3.68E+01
2.10E+00
1.09E+00
2.45E-01

5.16E+00
8.60E+00
6.00E+02
2.50E+01
1.50E+01
5.00E+01
5.00E+01
9.50E+01
3.60E+01
4.62E-02
0.00E+00
3.30E+02
3.50E+01
5.60E+01
1.00E+02
1.00E+02
2.33E+01
3.27E+01
1.87E+00
9.64E-01
2.18E-01

5.16E+00
8.60E+00
6.00E+02
2.50E+01
1.50E+01
5.00E+01
5.00E+01
9.50E+01
3.60E+01
2.31E-02
0.00E+00
3.30E+02
3.50E+01
5.60E+01
1.00E+02
1.00E+02
2.10E+01
2.94E+01
1.68E+00
8.68E-01
1.96E-01

5.16E+00
8.60E+00
6.00E+02
2.50E+01
1.50E+01
5.00E+01
5.00E+01
9.50E+01
3.60E+01
1.39E-02
0.00E+00
3.30E+02
3.50E+01
5.60E+01
1.00E+02
1.00E+02
1.91E+01
2.67E+01
1.53E+00
7.89E-01
1.78E-01

5.16E+00
8.60E+00
6.00E+02
2.50E+01
1.50E+01
5.00E+01
5.00E+01
9.50E+01
3.60E+01
1.07E-02
0.00E+00
3.30E+02
3.50E+01
5.60E+01
1.00E+02
1.00E+02
1.75E+01
2.45E+01
1.40E+00
7.23E-01
1.63E-01

5.16E+00
8.60E+00
6.00E+02
2.50E+01
1.50E+01
5.00E+01
5.00E+01
9.50E+01
3.60E+01
7.70E-03
0.00E+00
3.30E+02
3.50E+01
5.60E+01
1.00E+02
1.00E+02
1.50E+01
2.10E+01
1.20E+00
6.20E-01
1.40E-01

6.30E+00
3.68E+01
2.45E-01
3.68E+01
3.68E+01
2.45E-01

5.60E+00
3.27E+01
2.18E-01
3.27E+01
3.27E+01
2.18E-01

5.04E+00
2.94E+01
1.96E-01
2.94E+01
2.94E+01
1.96E-01

4.58E+00
2.67E+01
1.78E-01
2.67E+01
2.67E+01
1.78E-01

4.20E+00
2.45E+01
1.63E-01
2.45E+01
2.45E+01
1.63E-01

3.60E+00
2.10E+01
1.40E-01
2.10E+01
2.10E+01
1.40E-01

1.40E-01

1.24E-01

1.12E-01

1.02E-01

9.33E-02

8.00E-02

UB = Urinary bladder, St = Stomach

191

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

4840

25.2. Dosimetric data for iodine

4841

Table 25.4. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 125I compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled gases or vapours

3 mo

1y

5y

10 y

15 y

Adult

Elemental iodine, I2; unspecified forms

3.5E-08

4.4E-08

3.6E-08

2.1E-08

1.6E-08

1.3E-08

Methyl iodide, CH3I; Ethyl iodide, C2H5I

2.5E-08

3.1E-08

2.5E-08

1.5E-08

1.2E-08

8.9E-09

Type F, Sodium iodide; caesium chloride vector, silver
iodide; all unspecified forms
1.8E-08

2.3E-08

1.6E-08

9.7E-09

6.6E-09

5.3E-09

Type M

5.6E-09

6.6E-09

4.7E-09

2.8E-09

2.0E-09

1.7E-09

Type S

2.0E-09

1.8E-09

9.9E-10

6.4E-10

4.5E-10

4.3E-10

3.5E-08

4.3E-08

3.6E-08

2.1E-08

1.6E-08

1.3E-08

Inhaled particulate materials (1 µm AMAD aerosols)

Ingested materials
Adult fA = 1.0, All chemical forms

4842
4843

Table 25.5. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 129I compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled gases or vapours

3 mo

1y

5y

10 y

15 y

Adult

Elemental iodine, I2; unspecified forms

1.2E-07

1.6E-07

1.7E-07

1.2E-07

1.0E-07

9.4E-08

Methyl iodide, CH3I; Ethyl iodide, C2H5I

8.6E-08

1.1E-07

1.2E-07

8.4E-08

7.2E-08

6.6E-08

Inhaled particulate materials (1 µm AMAD aerosols)

192

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
Type F, Sodium iodide; caesium chloride vector, silver
iodide; all unspecified forms
6.2E-08

8.5E-08

7.5E-08

5.4E-08

4.2E-08

4.0E-08

Type M

2.7E-08

3.3E-08

2.9E-082.0E-08

1.7E-08

1.7E-08

Type S

4.3E-08

4.4E-08

3.4E-08

2.7E-08

2.6E-08

2.7E-08

1.2E-07

1.6E-07

1.6E-07

1.2E-07

1.0E-07

9.4E-08

Ingested materials
Adult fA = 1.0, All chemical forms

4844
4845

Table 25.6. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 131I compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled gases or vapours

3 mo

1y

5y

10 y

15 y

Adult

Elemental iodine, I2; unspecified forms

1.2E-07

1.2E-07

7.5E-08

3.6E-08

2.4E-08

1.7E-08

Methyl iodide, CH3I; Ethyl iodide, C2H5I

8.2E-08

8.6E-08

5.2E-08

2.5E-08

1.7E-08

1.2E-08

Type F, Sodium iodide; caesium chloride vector, silver
iodide; all unspecified forms
5.9E-08

6.2E-08

3.3E-08

1.6E-08

9.7E-09

6.9E-09

Type M

1.5E-08

1.5E-08

8.3E-09

4.2E-09

2.7E-09

2.1E-09

Type S

3.8E-09

3.1E-09

1.7E-09

1.1E-09

8.3E-10

7.7E-10

1.2E-07

1.2E-07

7.4E-08

3.5E-08

2.4E-08

1.6E-08

Inhaled particulate materials (1 µm AMAD aerosols)

Ingested materials
Adult fA = 1.0, All chemical forms

4846
4847

193

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

26. CAESIUM (Z = 55)

4848
4849

26.1. Routes of Intake

4850

26.1.1. Inhalation

4851
4852
4853
4854
4855
4856
4857
4858
4859

There is some information on the behaviour of inhaled caesium in man following
accidental intakes. Information on absorption from the respiratory tract is also available fromexperimental studies of caesium in ionic forms (chloride, nitrate), in irradiated fuel fragments
and other contaminated dusts associated with nuclear facilities, and in fused aluminosilicate
particles (FAP). For details, see Section 6 of Publication 137 (ICRP, 2017). Absorption
parameter values and types, and associated fA values for particulate forms of caesium are given
in Table 26.1 (taken from Section 6 of Publication 137).
Table 26.1. Absorption parameter values for inhaled and ingested caesium.
Inhaled particulate materials
Default parameter values†,‡
Absorption
Assigned forms
TypeF
Chloride, nitrate, sulphateM§
Irradiated fuel fragments
S—
Ingested materials¶
Assigned forms

*

4875

26.1.2. Ingestion

1
0.2
0.01

100
3
3

0.005
1×10-4Age-dependent absorption from the alimentary tract, fA
3 months 1 year
5 years
10 years
15 years adult
1
1
1
1
1
1

Caesium chloride, nitrate, sulphate;caesium in food, all unspecified
compounds
Relatively
insoluble
forms 0.2
(irradiated fuel fragments)

4860
4861
4862
4863
4864
4865
4866
4867
4868
4869
4870
4871
4872
4873
4874

fr

Absorption parameter values*sr (d–1)
ss (d–1)

0.1

0.1

0.1

0.1

0.1

It is assumed that for caesium the bound state can be neglected, i.e. fb = 0.0. The value of sr for Type F forms of
caesium (100 d–1) is element-specific. The values for Types M and S (3 d–1) are the general default values.
†
Materials (e.g. chloride) are generally listed here where there is sufficient information to assign to a default
absorption ype, but not to give specific parameter values (see Section 6 of Publication 137, ICRP 2017).
‡
For inhaled material deposited in the respiratory tract and subsequently cleared by particle transport to thealimentary tract, the default fA values for inhaled materials are applied: i.e. the product of fr for the absorption type(or specific value where given) and the fA value for ingested soluble forms of caesium applicable to the age-groupof interest (1.0).
§
Default Type M is recommended for use in the absence of specific information on which the exposure material
can be assigned to an absorption type, e.g. if the form is unknown, or if the form is known but there is no
information available on the absorption of that form from the respiratory tract.
¶
Activity transferred from systemic compartments into segments of the alimentary tract is assumed to be subject
to reabsorption to blood. The default absorption fraction fA for the secreted activity is the highest value foringestion of the radionuclide applicable to the age-group of interest (1.0).

194

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

4876
4877
4878
4879
4880
4881
4882
4883
4884
4885
4886
4887
4888
4889
4890
4891
4892
4893
4894

Caesium absorption has been shown to occur mainly in the ileum (Majle et al., 1991).
Human data and the results of animal experiments indicate that inorganic soluble compoundsof caesium are rapidly and almost completely absorbed from the alimentary tract. However
134
Cs and 137Cs incorporated into insoluble particles such as inorganic sedimentary material,
glass microspheres or irradiated reactor fuel may be less available for absorption. In
Publications 30 (ICRP, 1979) and 137 (ICRP, 2017) complete absorption from the alimentarytract was assumed for all chemical forms of caesium, except in situations where it wasconsidered that the material was insoluble and a lower fA value of 0.1 was appropriate. (Fordetails, see section 6 of Publication 137). Henrichs et al. (1989) measured the uptake of 137Cs
in 10 volunteers following the consumption of venison contaminated as a result of theChernobyl accident. Absorption varied from about 56% to 90% (mean 78%). Hunt (1998)
investigated the fractional absorption of 137Cs from cockles (Cerastoderma edule) collected on
the Irish Sea coast of the UK. He found that fractional absorption was in the range of 0.08–
0.43. Uptake of caesium from food may thus not always be complete. However, since there
were insufficient data on the uptake of caesium incorporated in foods, an absorption fraction
value of 1 was recommended by Publication 56 (ICRP, 1990) for caesium in food for all ages.
The same value of fA = 1 is adopted here for all ages and for all forms, except insoluble
inorganic material for which the value of fA = 0.2 is applied for 3-mo-old and fA = 0.1 is applied
to other ages.

4895

26.1.3. Systemic Distribution, Retention and Excretion4896

26.1.3.1. Age-specific data

4897
4898
4899
4900
4901
4902
4903
4904
4905
4906
4907
4908
4909
4910
4911
4912
4913
4914
4915
4916
4917
4918
4919
4920
4921
4922

The systemic behavior of caesium in humans has been well characterized on the basisof experimental studies involving human volunteers, follow-up of subjects receiving
occupational or environmental exposure to 137Cs, and autopsy measurements of the distributionof 137Cs in the body. Whole-body retention of acutely ingested 137Cs has been followed in a
number of adult males until little of the intake remained in the body. Results of 14 studies ofthe long-term half-time in healthy adult males yield mean long-term half-times in the range 79133 d with an overall mean of about 97 d. Inter-subject variability within a given study
generally was small, with a typical coefficient of variation of about 20% and a typical geometricstandard deviation of about 1.2 (ICRP, 1989; Leggett, 1986; Leggett et al., 1998, 2003; Lloyd
et al., 1973).
In at least eight studies, retention half-times have been measured in adult female aswell as adult male subjects. Although there is some overlap in individual half-times for maleand female subjects, the mean half-time for the female subjects is 15-35% lower than that for
male subjects in each of these studies. The long-term half-time of cesium in the body usuallyis reduced during pregnancy to about two-thirds of the value when not pregnant, perhaps due
to increased aldosterone levels in blood during pregnancy (ICRP, 1989; Leggett, 1986; Lloyd
et al., 1966; Melo et al., 1997; Thornberg and Mattsson, 2000; Zundel et al., 1969).
Schwartz and Dunning (1982) collected data from the literature on the equivalent
biological half-time of 137Cs in the human body. The equivalent half-time is estimated fromsimultaneous measurement of the total body content and the excretion rate and assumes that
total-body 137Cs is a well-mixed pool. They determined means of 96 ± 23 d (range 47-152 d)from data 116 adult males and 65 ± 29 d (range 30-141 d) for 29 adult females.
Variation with age in the retention time of radiocesium in the human body has been
investigated in controlled studies, in subjects exposed to contamination from the Chernobyl
accident or other sources of environmental contamination, and in subjects exposed in theaccident in Goiania, Brazil. Data from three studies (Lebedev and Yakovlev, 1993; Lloyd et195

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

4923
4924
4925

4926
4927
4928
4929
4930
4931

al., 1973; Melo et al., 1997) are shown in Fig. 26.1. Typical long-term half-times as a functionof age and gender are given in Table 26.2 (Lebedev and Yakovlev, 1993; Leggett, 1986;
Leggett et al., 1998; Lloyd et al., 1973; McCraw, 1965; Melo et al., 1997).

Fig. 26.1. Measured 137Cs whole-body retention half-times at different ages.
Table 26.2. Central estimates for age- and gender-specific long-term retention half-times for
cesium in the human body
Age
Infant (100 d)
1y
2y
5y
10 y
15 y
35 y
60 y

Males
17
19
22
32
46
75
97
85

Long-term half-time (d)Females
17
19
22
32
46
65
75
65

4932
4933

26.1.3.2. Systemic model

4934
4935
4936
4937
4938
4939
4940
4941
4942
4943
4944

The systemic model for cesium used in this report is an extension of the model for
workers applied in Publication 137 (ICRP, 2017). The model structure is shown in Fig. 26.2.
Transfer coefficients are listed in Table 26.3.
Transfer coefficients for pre-adults depict lower residence times of cesium in the total
body, a reduced portion of total-body cesium in the relatively smaller mass of skeletal muscle,and higher uptake of cesium by the skeleton at younger age (Leggett et al., 2003). The following
approach, modified slightly from a scheme applied to cesium in NCRP Report 161, Part II(2009), was used to extend the parameter values for adults to pre-adult ages:• The transfer rate from plasma to skeletal muscle at ages 100 d, 1 y, 5 y, and 10 y isassumed to be 0.5, 0.5, 0.7, and 0.85, respectively, times the transfer rate for the adultbased on changes with age in muscle mass as a percentage of total-body mass.

196

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

•

4945
4946
4947
4948
4949
4950
4951
4952
4953
4954
4955
4956
4957

For infants and children through age 10 y, the transfer rated from plasma to bone surface
compartments and the compartment representing cartilage is assumed to be twice thevalue for the adult.
• The transfer rate from plasma to the compartment Other 1 is modified to maintain aconstant total outflow rate from plasma at all ages, i.e, to balance the changes in transferfrom plasma to skeletal muscle, bone surfaces, and cartilage.
• All flow rates out of tissue compartments are increased by the following factors, chosen
to approximate central estimates of the long-term biological half-time in males: 4 at age
100 d, 3.5 at age 1 y, 2.5 at age 5 y, 2.0 at age 10 y, and 1.3 at age 15 y.
The resulting age-specific model predicts the following long-term biological halftimes in the total body: 17, 19, 32, 45, 74, and 96 d for intake at ages 100 d, 1 y, 5y, 10 y, 15 y,
and adult, respectively. These values are based on the time required for the total-body content
to decline from 50% to 25% of an acute input to blood.

4958

26.1.3.3. Treatment of progeny

4959
4960
4961
4962
4963
4964

The model for 137mBa as 137Cs progeny in the adult is extended to pre-adult age byassuming the ouflow rate from plasma is invariant with age, the age-specific deposition
fractions on bone surface are proportional to corresponding values applied in the model forbarium as a parent radionuclide, and the deposition fractions in soft tissue and excretion
pathways are proportional to values for adults.

4965
4966
4967
4968
4969
4970
4971

Fig. 26.2. Structure of the model for systemic caesium and its exchange with caesium in thealimentary tract. Abbreviations: Trab = trabecular, Cort = cortical, surf = surface, UB = urinary
bladder, cont = content, RBC = red blood cells, St = stomach, SI = small intestine, RC = rightcolon, LC = left colon, RS = rectosigmoid colon.
Table 26.3. Age-specific transfer coefficients for systemic caesium
Pathway

100 dTransfer coefficient (d-1)
5y
10 y
15 y

1y

197

Adult

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
Blood to heart wall
Blood to LiverBlood to Kidneys
Blood to Muscle
Blood to Stomach wall
Blood to SI wall
Blood to RC wall
Blood to LC wall
Blood to RS wall
Blood to Stomach contents
Blood to SI contents
Blood to RC contents
Blood to Spleen
Blood to Pancreas
Blood to Brain
Blood to Red marrow
Blood to Trab bone surf
Blood to Cort bone surf
Blood to Cartilage
Blood to Skin
Blood to Lung tissue
Blood to Other 1
Blood to Other 2
Blood to RBC
Blood to Adipose tissue
Heart wall to BloodLiver to BloodLiver to SI contents
Kidneys to UB contents
Kidneys to Blood
Muscle to Blood
Stomach wall to Blood
Stomach wall to Liver
Stomach wall to contents
SI wall to Blood
SI wall to Liver
SI wall to contents
RC wall to Blood
RC wall to Liver
RC wall to contents
LC wall to Blood
LC wall to Liver
LC wall to contents
RS wall to Blood
RS wall to Liver

1.41E+01
1.95E+01
6.71E+01
1.50E+01
3.53E+00
3.53E+01
5.65E+00
5.65E+00
2.83E+00
4.52E+00
1.05E+00
2.00E-02
5.30E+00
1.77E+00
4.24E-01
5.30E+00
3.18E+00
2.12E+00
6.00E+00
4.42E+00
4.42E+00
1.91E+01
3.53E-03
1.80E+00
8.83E+00
3.23E+01
8.56E+00
4.52E-01
6.72E+00
1.28E+02
3.00E-01
1.66E+01
8.76E-01
8.40E-01
3.95E+01
2.08E+00
8.40E-01
2.74E+01
1.44E+00
8.40E-01
2.74E+01
1.44E+00
8.40E-01
2.74E+01
1.44E+00

1.41E+01
1.95E+01
6.71E+01
1.50E+01
3.53E+00
3.53E+01
5.65E+00
5.65E+00
2.83E+00
4.52E+00
1.05E+00
2.00E-02
5.30E+00
1.77E+00
4.24E-01
5.30E+00
3.18E+00
2.12E+00
6.00E+00
4.42E+00
4.42E+00
1.91E+01
3.53E-03
1.80E+00
8.83E+00
2.82E+01
7.49E+00
3.96E-01
5.88E+00
1.12E+02
2.63E-01
1.46E+01
7.67E-01
7.35E-01
3.45E+01
1.82E+00
7.35E-01
2.40E+01
1.26E+00
7.35E-01
2.40E+01
1.26E+00
7.35E-01
2.40E+01
1.26E+00

198

1.41E+01
1.95E+01
6.71E+01
2.10E+01
3.53E+00
3.53E+01
5.65E+00
5.65E+00
2.83E+00
4.52E+00
1.05E+00
2.00E-02
5.30E+00
1.77E+00
4.24E-01
5.30E+00
3.18E+00
2.12E+00
6.00E+00
4.42E+00
4.42E+00
1.31E+01
3.53E-03
1.80E+00
8.83E+00
2.02E+01
5.35E+00
2.83E-01
4.20E+00
7.98E+01
1.88E-01
1.04E+01
5.48E-01
5.25E-01
2.47E+01
1.30E+00
5.25E-01
1.72E+01
9.03E-01
5.25E-01
1.72E+01
9.03E-01
5.25E-01
1.72E+01
9.03E-01

1.41E+01
1.95E+01
6.71E+01
2.55E+01
3.53E+00
3.53E+01
5.65E+00
5.65E+00
2.83E+00
4.52E+00
1.05E+00
2.00E-02
5.30E+00
1.77E+00
4.24E-01
5.30E+00
3.18E+00
2.12E+00
6.00E+00
4.42E+00
4.42E+00
8.56E+00
3.53E-03
1.80E+00
8.83E+00
1.61E+01
4.28E+00
2.26E-01
3.36E+00
6.38E+01
1.50E-01
8.32E+00
4.38E-01
4.20E-01
1.97E+01
1.04E+00
4.20E-01
1.37E+01
7.22E-01
4.20E-01
1.37E+01
7.22E-01
4.20E-01
1.37E+01
7.22E-01

1.41E+01
1.95E+01
6.71E+01
3.00E+01
3.53E+00
3.53E+01
5.65E+00
5.65E+00
2.83E+00
4.52E+00
1.05E+00
2.00E-02
5.30E+00
1.77E+00
4.24E-01
5.30E+00
1.59E+00
1.06E+00
3.00E+00
4.42E+00
4.42E+00
9.71E+00
3.53E-03
1.80E+00
8.83E+00
1.05E+01
2.78E+00
1.47E-01
2.18E+00
4.15E+01
9.76E-02
5.41E+00
2.85E-01
2.73E-01
1.28E+01
6.75E-01
2.73E-01
8.92E+00
4.69E-01
2.73E-01
8.92E+00
4.69E-01
2.73E-01
8.92E+00
4.69E-01

1.41E+01
1.95E+01
6.71E+01
3.00E+01
3.53E+00
3.53E+01
5.65E+00
5.65E+00
2.83E+00
4.52E+00
1.05E+00
2.00E-02
5.30E+00
1.77E+00
4.24E-01
5.30E+00
1.59E+00
1.06E+00
3.00E+00
4.42E+00
4.42E+00
9.71E+00
3.53E-03
1.80E+00
8.83E+00
8.07E+00
2.14E+00
1.13E-01
1.68E+00
3.19E+01
7.51E-02
4.16E+00
2.19E-01
2.10E-01
9.87E+00
5.19E-01
2.10E-01
6.86E+00
3.61E-01
2.10E-01
6.86E+00
3.61E-01
2.10E-01
6.86E+00
3.61E-01

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
RS wall to contents
Spleen to Blood
Spleen to Liver
Pancreas to Blood
Pancreas to Liver
Skin to Blood
Skin to Excreta
Brain to Blood
Red marrow to Blood
Trab bone surf to Blood
Cort bone surf to Blood
Cartilage to Blood
Lung tissue to Blood
Other 1 to Blood
Other 2 to Blood
Adipose to Blood
RBC to Blood

8.40E-01
2.01E+01
1.06E+00
6.72E+00
3.53E-01
3.47E+00
6.36E-02
3.39E-01
2.82E+00
8.48E-01
8.48E-01
8.00E-01
5.88E+00
3.05E+00
5.64E-03
7.08E+00
1.03E+00

7.35E-01
1.76E+01
9.28E-01
5.88E+00
3.09E-01
3.03E+00
5.57E-02
2.97E-01
2.47E+00
7.42E-01
7.42E-01
7.00E-01
5.15E+00
2.67E+00
4.94E-03
6.20E+00
9.00E-01

4972

199

5.25E-01
1.26E+01
6.63E-01
4.20E+00
2.21E-01
2.17E+00
3.98E-02
2.12E-01
1.77E+00
5.30E-01
5.30E-01
5.00E-01
3.68E+00
1.91E+00
3.53E-03
4.43E+00
6.43E-01

4.20E-01
1.01E+01
5.30E-01
3.36E+00
1.77E-01
1.73E+00
3.18E-02
1.70E-01
1.41E+00
4.24E-01
4.24E-01
4.00E-01
2.94E+00
1.52E+00
2.82E-03
3.54E+00
5.14E-01

2.73E-01
6.54E+00
3.45E-01
2.18E+00
1.15E-01
1.13E+00
2.07E-02
1.10E-01
9.18E-01
2.76E-01
2.76E-01
2.60E-01
1.91E+00
9.91E-01
1.83E-03
2.30E+00
3.34E-01

2.10E-01
5.03E+00
2.65E-01
1.68E+00
8.83E-02
8.67E-01
1.59E-02
8.48E-02
7.06E-01
2.12E-01
2.12E-01
2.00E-01
1.47E+00
7.62E-01
1.41E-03
1.77E+00
2.57E-01

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

4973

26.2. Dosimetric data for caesium

4974

Table 26.4. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 134Cs compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled particulate materials (1 µm AMAD aerosols) 3 mo

1y

5y

10 y

15 y

Adult

Type F, Chloride, nitrate, sulphate

1.2E-08

9.9E-09

7.0E-09

5.6E-09

5.3E-09

5.9E-09

Type M, Irradiated fuel fragments; all unspecified
forms
2.6E-08

2.3E-08

1.4E-08

9.9E-09

8.0E-09

8.8E-09

Type S

7.6E-08

7.2E-08

4.6E-08

3.2E-08

2.7E-083.0E-08

Adult fA = 1.0, Chloride, nitrate, sulphate; caesium infood; all unspecified compounds
2.3E-08

1.9E-08

1.5E-08

1.2E-08

1.3E-08

1.4E-08

Adult fA = 0.1, Relatively insoluble forms (irradiatedfuel fragments)
6.6E-09

4.0E-09

2.8E-09

2.1E-09

1.9E-09

2.0E-09

Ingested materials

4975
4976

Table 26.5. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 137Cs compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled particulate materials (1 µm AMAD aerosols) 3 mo

1y

5y

10 y

15 y

Adult

Type F, Chloride, nitrate, sulphate

1.1E-08

9.1E-09

5.7E-09

4.7E-09

4.6E-09

5.8E-09

Type M, Irradiated fuel fragments; all unspecified
forms
2.6E-08

2.3E-08

1.4E-08

9.4E-09

7.8E-09

8.4E-09

Type S

1.6E-07

1.3E-07

9.9E-08

9.9E-08

1.0E-07

1.6E-07

Ingested materials

200

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
Adult fA = 1.0, Chloride, nitrate, sulphate; caesium infood; all unspecified compounds
2.2E-08

1.7E-08

1.3E-08

1.0E-08

1.1E-08

1.4E-08

Adult fA = 0.1, Relatively insoluble forms (irradiatedfuel fragments)
5.5E-09

2.8E-09

1.9E-09

1.5E-09

1.4E-09

1.6E-09

4977
4978
4979
4980
4981

201

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

27. BARIUM (Z = 56)

4982
4983

27.1. Routes of Intake

4984

27.1.1. Inhalation

4985
4986
4987
4988
4989
4990
4991
4992

No information was found on the behaviour of inhaled barium in man. Information on
absorption from the respiratory tract is available from experimental studies of barium aschloride, sulphate or in fused aluminosilicate particles (FAP). For details see Section 7 of
Publication 137 (ICRP, 2017). Absorption parameter values and types, and associated fA values
for particulate forms of barium are given in Table 27.1 (taken from Section 7 of Publication
137).
Table 27.1. Absorption parameter values for inhaled and ingested barium.
Inhaled particulate materials
fr

Default parameter values†,‡
Absorption
Assigned forms
TypeF
Chloride, carbonate§
M
Sulphate
S
—

1
0.2
0.01

Absorption parameter values*sr (d–1)
ss (d–1)

20
3
3

0.005
1×10-4

Ingested materials¶
Assigned forms

Age-dependent absorption from the alimentary tract, fA
3 months 1 year
5 years
10 years 15 years adult
Soluble forms, including barium 0.6
0.3
0.3
0.3
0.3
0.2
in dietInsoluble
forms(sulphate, 1×10-3
1×10-4
1×10-4
1×10-4
1×10-4
1×10-4titanate)

4993
4994
4995
4996
4997
4998
4999
5000
5001
5002
5003
5004
5005
5006
5007

*

5008

27.1.2. Ingestion5009

27.1.2.1. Adults

It is assumed that for barium the bound state can be neglected, i.e. fb = 0.0. The value of sr for Type F forms ofbarium (20 d–1) is element-specific. The values for Types M and S (3 d–1) are the general default values.
†
Materials (e.g. chloride) are listed here where there is sufficient information to assign to a default absorption
type, but not to give specific parameter values (see Section 7 of Publication 137, ICRP, 2017).
‡
For inhaled material deposited in the respiratory tract and subsequently cleared by particle transport to thealimentary tract, the default fA values for inhaled materials are applied: i.e. the product of fr for the absorption type(or specific value where given) and the fA value for ingested soluble forms of barium applicable to the age-groupof interest (e.g. 0.2 for adults).
§
Default Type M is recommended for use in the absence of specific information on which the exposure material
can be assigned to an absorption type, e.g. if the form is unknown, or if the form is known but there is no
information available on the absorption of that form from the respiratory tract.
¶
Activity transferred from systemic compartments into segments of the alimentary tract is assumed to be subject
to reabsorption to blood. The default absorption fraction fA for the secreted activity is the highest value foringestion of the radionuclide applicable to the age-group of interest (e.g. 0.2 for adults).

202

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

5010
5011
5012
5013
5014
5015
5016
5017
5018
5019
5020
5021

Barium absorption, studied in humans and animals, depends on its chemical form.
Barium sulfate is poorly absorbed from the gastrointestinal tract of adults while acid-solublebarium salts are readily dissolved in gastric acid and absorbed as a few percents of ingested
quantity. Fasting and low calcium concentration in the gut may increase barium absorption bya factor 2 to 3 (Publication 137, ICRP, 2017). In Publication 30 (ICRP, 1979), fractional
absorption was taken to be 0.1 for all forms of barium. However, as concluded by Leggett(1992b), absorption for soluble forms of barium may be higher. On the basis of chemicalsimilarity with radium, and similar absorption values reported for the two elements, a value of
0.2 was recommended in Publication 67 (ICRP, 1993). An fA of 0.2 for adults wasrecommended in Publication 137 for direct ingestion of soluble forms of barium. The value of
fA = 0.2 is adopted here for ingestion of barium in food. For insoluble forms such as barium
sulfate or titanate, an fA of 1 × 10-4 is recommended.

5022

27.1.2.2. Children

5023
5024
5025
5026
5027
5028
5029
5030
5031
5032
5033
5034
5035
5036
5037
5038

There appear to be no direct measurements of barium absorption in children.
However, data from animals indicate that the gastrointestinal absorption of barium is greater in
immature than in mature animals, as is the case for other alkaline earth elements. In rats, there
was an inverse relationship of barium absorption with age after administration as the chloride(Taylor et al., 1962). In suckling rats 14-18 days of age, the absorption of both barium andradium was about 80% and in young adult rats (6-8 weeks) about 10%. These results suggestthat the high fractional absorption in suckling infants decreases rapidly with increasing age.
Della Rosa et al. (1967) reported that following oral administration of 133Ba to beagle dogs of
43, 150 and 250 days of age retention at 30 days after administration was 2.3%, 2.0% and 0.8%,
respectively, and 0.4-0.6% in adult dogs. Cuddihy and Griffith (1972) estimated from thesedata that gastrointestinal absorption may have been 0.7-1.5% in the adult dogs and as high as
7% in the younger animals. In Publication 67, based on the consideration that there may beelevated absorption of barium throughout the period of growth, a fractional absorption of
barium of 0.6 was recommended for the infant for solubles forms. For ages 1-15 years, a valueof 0.3 was recommended. The values are adopted here for children fA. For insoluble forms, anfA of 0.001 is adopted in this report for 3 month old infants.

5039

27.1.3. Systemic Distribution, Retention and Excretion

5040

27.1.3.1. Summary of biokinetic data

5041
5042
5043
5044
5045
5046
5047
5048
5049
5050
5051
5052
5053
5054

The alkaline earth element barium is a physiological analogue of the alkaline earths
calcium, strontium, and radium but exhibits somewhat different kinetics from those elementsin the human body due to discrimination by biological membranes and hydroxyapatite crystalsof bone. The biokinetics of barium resembles that of radium more closely than that of calcium
or strontium.
The biokinetics of systemic barium has been investigated in a variety of studies
involving human subjects or laboratory animals. Reviews and bibliographies can be found in
Publication 20 (ICRP, 1973), Publication 67 (ICRP, 1993), and Publication 137 (ICRP, 2017),
and in an article by Leggett (1992a). Plasma disappearance curves for barium and other alkaline
earth elements indicate an outflow rate of several hundred plasma volumes per day and rapid
equilibration with an extravascular pool roughly three times the size of the plasma pool. Basedon controlled studies on adult human subjects it is estimated that about a third of barium atoms
leaving blood deposit in excretion pathways, predominantly in the colon contents. Observationsof retention of injected barium tracers in human soft tissues are largely qualitative but indicate
203

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

5055
5056
5057
5058
5059
5060
5061
5062
5063
5064
5065
5066
5067
5068
5069
5070
5071
5072
5073
5074
5075
5076
5077
5078
5079
5080
5081
5082
5083

that little activity remains in soft tissues by a few days after injection. Despite the initially low
retention of injected barium in soft tissues, a non-trivial portion of total-body barium has beenfound in human soft tissues after chronic exposure, presumably representing small, relatively
insoluble deposits of barium sulphate. Skeletal retention of barium in mature adults typicallydecreases from 25% or more of injected activity in the first day or two after injection to roughly
10% after 1 month and 5% after 1 year.
Barium entering bone initially deposits on bone surface, from which activity is largely
removed over a few days. Most of the barium atoms leaving bone surface return to blood, but
a portion diffuse into a bone volume pool referred to as exchangeable bone volume. Barium
atoms entering exchangeable bone volume may return to bone surface or blood over a periodof weeks or months or may transfer to nonexchangeable bone volume, meaning that they
become firmly fixed in bone crystals. It appears that calcium, strontium, barium, and radium
are all about equally likely to transfer from bone surface to exchangeable bone volume but thatthe likelihood of becoming firmly fixed in bone crystal decreases in the order calcium >strontium > barium > radium. Data from human and animal studies indicate that the rate of lossof alkaline earth tracers from bone over the first few months after acute uptake to bloodincreases in the order calcium < strontium < barium < radium. Presumably these four elements
are removed from trabecular or cortical non-exchangeable bone volume compartments at therate of bone restructuring of that bone type, so that the rate of transfer from non-exchangeablebone volume is independent of the element.
Age dependence in the biokinetics of barium has been investigated in laboratory
animals (Cuddihy and Griffith, 1972; Della Rosa et al., 1967; Domanski et al., 1980; Ellsasser
et al., 1969; Farnham and Rowland, 1965; Hardy et al., 1969; Stather, 1974; Wood et al., 1970)
and in a study involving administration of a barium trace to human infants, children and adults(Bauer et al., 1957). It has been established from these studies and similar studies of calcium,
strontium, and radium kinetics, that fractional deposition of alkaline earth elements in bone issubstantially greater, and the turnover rate is substantially higher, for immature bone than formature bone. Greater deposition of barium in the younger skeleton results in less systemic
barium available for excretion and distribution to soft tissues.

5084

27.1.3.2. Systemic model

5085
5086
5087
5088
5089
5090
5091
5092
5093
5094
5095
5096
5097
5098
5099
5100
5101

The age-specific model for systemic barium is taken from Publication 67 (ICRP,
1993). The same model with parameter values for the adult was adopted in Publication 137(ICRP, 2017) for application to workers.
The structure of the model is shown in Fig. 27.1. Transfer coefficients are listed inTable 27.2.
Extension of the barium model to preadult ages is based on results of studies of theage-specific behavior of barium and its physiological analogues in human subjects andlaboratory animals, indicating that deposition in bone is higher, and removal from bone is faster,at preadult ages than in adults. The age-specific deposition fraction for bone, and the divisionof that deposition between trabecular and cortical bone surface, are based on the estimated rates
of calcium addition to each of these bone types. For preadult ages the deposition fractions forsoft tissues and excretion pathways are reduced uniformly from the values for adults to reflect
the elevated competition from bone for circulating barium. The removal half-times from bone
surface and exchangeable bone volume compartments are assumed to be independent of age.
The removal half-times from bone volume compartments to blood are reference age-specificbone turnover rates (ICRP, 2002a). Removal half-times from soft-tissue compartments are
assumed to be independent of age.

204

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

5102
5103

5104
5105
5106
5107
5108
5109

The reader is referred to Leggett (1992a) and Publication 67 for more detailed
descriptions of the basis for age-specific parameter values for barium.

Fig. 27.1. Structure of the model for systemic barium. Abbreviations: exch = exchangeable,
nonexch = non-exchangeable. Activity transferred from Blood to Colon contents enters Rightcolon contents.
Table 27.2. Transfer coefficients for the model for systemic barium

Patha

InfantBlood to Urinary bladder contents
7.47E-01
Blood to Right colon contents
6.72E+00
Blood to Trab bone surface
1.05E+01
Blood to Cort bone surface
4.20E+01
Blood to ST0
7.67E+00
Blood to ST1
2.33E+00
Blood to ST2
4.66E-02
Trab bone surf to Blood
5.78E-01
Trab bone surf to Exch Trab bone vol
1.16E-01
Cort bone surf to Blood
5.78E-01
Cort bone surf to Exch Cort bone vol
1.16E-01
ST0 to Blood
2.56E+00
ST1 to Blood
6.93E-01
ST2 to Blood
3.80E-04
Exch Trab bone vol to Trab bone surface 9.70E-03
Exch Trab bone vol to Nonexch Trab vol 4.20E-03
Exch Cort bone vol to Cort bone surface 9.70E-03
Exch Cort bone vol to Nonexch Cort vol 4.20E-03
Nonexch Trab bone vol to Blood
8.22E-03
Nonexch Cort bone vol to Blood
8.22E-03

5110

a

1y
1.64E+00
1.48E+01
6.30E+00
2.52E+01
1.69E+01
5.13E+00
1.03E-01
5.78E-01
1.16E-01
5.78E-01
1.16E-01
5.62E+00
6.93E-01
3.80E-04
9.70E-03
4.20E-03
9.70E-03
4.20E-03
2.88E-03
2.88E-03

Transfer coefficient (d-1)
5y
10 y
1.79E+00 1.31E+00
1.61E+01 1.18E+01
6.22E+00 9.88E+00
2.18E+01 2.93E+01
1.84E+01 1.35E+01
5.60E+00 4.11E+00
1.12E-01 8.22E-02
5.78E-01 5.78E-01
1.16E-01 1.16E-01
5.78E-01 5.78E-01
1.16E-01 1.16E-01
6.13E+00 4.50E+00
6.93E-01 6.93E-01
3.80E-04 3.80E-04
9.70E-03 9.70E-03
4.20E-03 4.20E-03
9.70E-03 9.70E-03
4.20E-03 4.20E-03
1.81E-03 1.32E-03
1.53E-03 9.04E-04

15 y
7.77E-01
6.99E+00
1.45E+01
3.74E+01
7.97E+00
2.43E+00
4.86E-02
5.78E-01
1.16E-01
5.78E-01
1.16E-01
2.66E+00
6.93E-01
3.80E-04
9.70E-03
4.20E-03
9.70E-03
4.20E-03
9.59E-04
5.21E-04

Trab = Trabecular, Cort = cortical, vol = volume, Exch = Exchangeable, Nonexch = Nonexchangeable

205

Adult
2.24E+00
2.02E+01
9.72E+00
7.78E+00
2.30E+01
7.00E+00
1.40E-01
5.78E-01
1.16E-01
5.78E-01
1.16E-01
7.67E+00
6.93E-01
3.80E-04
9.70E-03
4.20E-03
9.70E-03
4.20E-03
4.93E-04
8.21E-05

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

5111

27.2. Dosimetric data for barium

5112

Table 27.3. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 133Ba compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled particulate materials (1 µm AMAD aerosols) 3 mo

1y

5y

10 y

15 y

Adult

Type F, Chloride, carbonate

9.4E-09

3.1E-09

1.8E-09

2.5E-09

4.7E-09

1.0E-09

Type M, Sulphate; all unspecified forms

1.1E-08

8.8E-09

5.1E-09

4.0E-09

4.3E-09

2.9E-09

Type S

4.7E-08

4.6E-08

3.2E-08

2.4E-08

2.4E-08

2.5E-08

Adult fA = 0.2, Soluble forms, including barium in diet 1.5E-08

3.6E-09

2.2E-09

3.0E-09

5.7E-09

1.0E-09

Adult fA = 0.0001, Insoluble forms (sulphate, titanate) 8.2E-10

7.5E-10

4.2E-103.0E-10

2.1E-102.0E-10

Ingested materials

5113
5114

Table 27.4. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 140Ba compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled particulate materials (1 µm AMAD aerosols) 3 mo

1y

5y

10 y

15 y

Adult

Type F, Chloride, carbonate

1.3E-08

4.3E-09

1.7E-09

1.2E-09

1.2E-09

4.8E-10

Type M, Sulphate; all unspecified forms

1.5E-08

1.1E-08

5.8E-09

3.9E-09

3.0E-09

2.9E-09

Type S

1.6E-08

1.3E-08

7.3E-09

4.9E-09

3.7E-09

3.8E-09

Adult fA = 0.2, Soluble forms, including barium in diet 2.0E-08

5.1E-09

2.4E-09

1.7E-09

1.7E-09

7.1E-10Adult fA = 0.0001, Insoluble forms (sulphate, titanate) 2.2E-09

2.0E-09

1.2E-09

8.4E-10

5.6E-10

5.3E-10

Ingested materials

5115
206

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

28. IRIDIUM (Z = 77)

5116
5117

28.1. Routes of Intake

5118

28.1.1. Inhalation

5119
5120
5121
5122
5123
5124
5125
5126

Some information was found on the behaviour of inhaled iridium in man following
accidental intakes. Information on absorption from the respiratory tract is available fromexperimental studies of iridium chloride and elemental iridium. For details see Section 8 of
Publication 137 (ICRP, 2017). Absorption parameter values and types, and associated fA values
for particulate forms of iridium are given in Table 28.1 (taken from Section 8 of Publication
137).
Table 28.1. Absorption parameter values for inhaled and ingested iridium.
Inhaled particulate materials
Default parameter values†,‡
Absorption Assigned forms
TypeF
Chloride
§
M
–

fr

1
0.2

Absorption parameter values*sr (d–1)
ss (d–1)

30
3

–
0.005

S
Elemental iridium
0.01
3
1×10-4
Ingested materials¶
Assigned forms
Age-dependent absorption from the alimentary tract, fA
3 months 1 year
5 years
10 years
15 years
adult
all forms
0.02
0.01
0.01
0.01
0.01
0.01

5127
5128
5129
5130
5131
5132
5133
5134
5135
5136
5137
5138
5139
5140

*

5141

28.1.2. Ingestion

5142
5143
5144
5145
5146
5147
5148

No human data are available on the absorption of iridium from the gastrointestinal
tract. In Publication 30 (ICRP, 1979) and in Publication 137 (ICRP, 2017), an absorption
fraction of 0.01 was recommended on the basis of animal data. Since no new data on thegastrointestinal absorption seem to be available, an fA value of 0.01 is adopted here for all
chemical forms ingested by adult members of the public. Consistently with the approach of
Publication 56 (ICRP, 1990), an fA = 0.02 is adopted for 3-mo-old infants and fA = 0.01 is
adopted for 1-15 y-old children.

It is assumed that for iridium the bound state can be neglected i.e. fb = 0. The values of sr for Type F, M and S
forms of iridium (30, 3 and 3 d–1, respectively) are the general default values.
†
Materials (e.g. chloride) are listed here where there is sufficient information to assign to a default absorption
type, but not to give specific parameter values (see Section 8 of Publication 137, ICRP, 2017).
‡
For inhaled material deposited in the respiratory tract and subsequently cleared by particle transport to thealimentary tract, the default fA values for inhaled materials are applied: i.e. the product of fr for the absorption type
and the fA value for ingested soluble forms of iridium applicable to the age-group of interest (e.g. 0.01 for adults).
§
Default Type M is recommended for use in the absence of specific information on which the exposure material
can be assigned to an absorption type, e.g. if the form is unknown, or if the form is known but there is no
information available on the absorption of that form from the respiratory tract.
¶
Activity transferred from systemic compartments into segments of the alimentary tract is assumed to be subject
to reabsorption to blood. The default absorption fraction fA for the secreted activity is the highest value foringestion of the radionuclide applicable to the age-group of interest (e.g. 0.01 for adults).

207

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

5149

28.1.3. Systemic Distribution, Retention and Excretion

5150
5151
5152
5153
5154
5155
5156
5157
5158
5159
5160
5161
5162
5163
5164

The model for systemic iridium applied in Publication 137 (ICRP, 2017) to workers
is applied here to adult members of the public. The model is based on biokinetic studies of
iridium in rodents, monkeys, and dogs. Three phases of excretion of absorbed or intravenously
injected iridium are indicated: a rapid phase of loss, primarily in urine, with a half-time of afew hours; an intermediate phase of loss with a half-time on the order of 1-2 wk; and a slow
phase of loss with a half-time of several months. The fraction of uptake associate with each ofthese phases depends to some extent on the form of iridium reaching blood. The rate of loss
from individual tissues roughly parallels that in the whole body. Concentrations of iridium inthe liver and kidneys are much higher than those in most other tissues.
Due to lack of age-specific data for iridium, the transfer coefficients in the model forthe adult are applied to all age groups except that iridium is assumed to be removed fromtrabecular or cortical bone volume to blood at the age-specific turnover rate for that bone type.
The structure of the model for iridium is shown in Fig. 28.1. Parameter values are
given in
Table 28.2.

5165
5166
5167
5168

Fig. 28.1. Structure of the biokinetic model for systemic iridium. SI = Small intestine.
Table 28.2. Transfer coefficients for the model for systemic iridiuma

PathBlood 1 to SI contents
Blood 1 to UB contents
Blood 1 to Liver 1
Blood 1 to Urinary path
Blood 1 to Other kidney tissue
Blood 1 to Blood 2
Blood 1 to ST0
Blood 1 to ST1Infant
4.00E+00
1.20E+01
1.20E+01
4.00E+00
2.00E+00
2.70E+01
1.50E+01
1.50E+01

1y
4.00E+00
1.20E+01
1.20E+01
4.00E+00
2.00E+00
2.70E+01
1.50E+01
1.50E+01

208

Transfer coefficient (d-1)
5y
10 y
4.00E+00 4.00E+00
1.20E+01 1.20E+01
1.20E+01 1.20E+01
4.00E+00 4.00E+00
2.00E+00 2.00E+00
2.70E+01 2.70E+01
1.50E+01 1.50E+01
1.50E+01 1.50E+01

15 y
4.00E+00
1.20E+01
1.20E+01
4.00E+00
2.00E+00
2.70E+01
1.50E+01
1.50E+01

Adult
4.00E+00
1.20E+01
1.20E+01
4.00E+00
2.00E+00
2.70E+01
1.50E+01
1.50E+01

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
Blood 1 to ST2
Blood 1 to Cortical surf
Blood 1 to Trabecular surf
Blood 2 to Blood 1
Liver 1 to Blood 1
Liver 1 to SI contents
Liver 1 to Liver 2
Liver 2 to Blood 1
Urinary path to UB contents
Other kidney tissue to Blood 1
ST0 to Blood 1
ST1 to Blood 1
ST2 to Blood 1
Cortical surf to Blood 1
Trabecular surf to Blood 1
Cortical surf to Cortical vol
Trabecular surf to Trabecular vol
Cortical vol to Blood 1
Trabecular vol to Blood 1

5169

a

1.00E+00
2.00E+00
6.00E+00
6.93E-01
2.31E-02
4.62E-02
6.93E-02
6.93E-03
1.39E-01
6.93E-03
6.93E-02
6.93E-03
9.50E-04
1.85E-02
1.85E-02
4.62E-03
4.62E-03
8.22E-03
8.22E-03

1.00E+00
2.00E+00
6.00E+00
6.93E-01
2.31E-02
4.62E-02
6.93E-02
6.93E-03
1.39E-01
6.93E-03
6.93E-02
6.93E-03
9.50E-04
1.85E-02
1.85E-02
4.62E-03
4.62E-03
2.88E-03
2.88E-03

1.00E+00
2.00E+00
6.00E+00
6.93E-01
2.31E-02
4.62E-02
6.93E-02
6.93E-03
1.39E-01
6.93E-03
6.93E-02
6.93E-03
9.50E-04
1.85E-02
1.85E-02
4.62E-03
4.62E-03
1.53E-03
1.81E-03

1.00E+00
2.00E+00
6.00E+00
6.93E-01
2.31E-02
4.62E-02
6.93E-02
6.93E-03
1.39E-01
6.93E-03
6.93E-02
6.93E-03
9.50E-04
1.85E-02
1.85E-02
4.62E-03
4.62E-03
9.04E-04
1.32E-03

1.00E+00
2.00E+00
6.00E+00
6.93E-01
2.31E-02
4.62E-02
6.93E-02
6.93E-03
1.39E-01
6.93E-03
6.93E-02
6.93E-03
9.50E-04
1.85E-02
1.85E-02
4.62E-03
4.62E-03
5.21E-04
9.59E-04

1.00E+00
2.00E+00
6.00E+00
6.93E-01
2.31E-02
4.62E-02
6.93E-02
6.93E-03
1.39E-01
6.93E-03
6.93E-02
6.93E-03
9.50E-04
1.85E-02
1.85E-02
4.62E-03
4.62E-03
8.21E-05
4.93E-04

UB = Urinary bladder, SI= Small intestine, Trab = Trabecular, Cort = Cortical, surf = surface, vol = volume

209

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

5170

28.2. Dosimetric data for iridium

5171

Table 28.3. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 192Ir compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled particulate materials (1 µm AMAD aerosols) 3 mo

1y

5y

10 y

15 y

Adult

Type F, Chloride

9.5E-09

7.6E-09

3.8E-09

2.4E-09

1.7E-09

1.5E-09

Type M, All unspecified forms

1.3E-08

1.1E-08

6.4E-09

4.2E-09

3.2E-09

3.3E-09

Type S, Elemental iridium

1.9E-08

1.6E-08

9.2E-09

6.2E-09

4.7E-09

4.9E-09

2.4E-09

1.7E-09

1.0E-09

7.0E-10

4.9E-10

4.5E-10

Ingested materials
Adult fA = 0.01, All forms

5172

210

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

29. LEAD (Z = 82)

5173
5174

29.1. Routes of Intake

5175

29.1.1. Inhalation

5176
5177
5178
5179
5180
5181
5182
5183
5184
5185
5186
5187
5188
5189
5190

Information on absorption from the respiratory tract is available from experimental
studies of the behaviour of lead inhaled in a variety of forms by both animals and man. In
particular, studies have been conducted to improve assessment of risks from exposure toradioisotopes of lead inhaled as progeny radionuclides of radon, and from exposure to stable
lead as an atmospheric pollutant, e.g. from petrol engine exhaust. For details see Section 9 of
Publication 137 (ICRP, 2017). Absorption parameter values and Types, and associated fA
values for particulate forms of lead are given in Table 29.1 (taken from Section 9 of Publication137).
For radiation protection purposes, the most important exposures to radioisotopes oflead are as progeny radionuclides of radon. Dose coefficients for isotopes of lead inhaled asradon progeny are given in the radon section, where factors such as the relevant aerosol size
distribution are addressed. Otherwise, exposures to radioisotopes of lead occur most often as
progeny radionuclides associated with intakes of uranium, thorium or radium.
Table 29.1. Absorption parameter values for inhaled and ingested lead.
Inhaled particulate materials
Specific parameter values‡
Lead as a progeny of radon

fr

Default parameter values†,§
Absorption
Assigned forms
TypeF¶
Dichloride, dibromide, difluoride,hydroxide, nitrate, oxide
M
S—

Mineral dusts

Ingested material**
Assigned forms
All forms

5191
5192
5193
5194
5195
5196
5197
5198
5199
5200
5201

Absorption parameter values*sr (d–1)
ss (d–1)

0.1

100

1.7

1

100

–

0.2
0.01

3
3

0.005
0.0001Age-dependent absorption from the alimentary tract, fA
3 months 1 year
5 years
10 years 15 years adult
0.6
0.3
0.3
0.3
0.3
0.2

It is assumed that for lead the bound fraction fb is 0.5 with an uptake rate sb = 1.7 d–1, and that this applies
throughout the respiratory tract (ET2, BB, bb and AI regions, and associated lymph nodes LNET and LNTH). The
value of sr for Type F forms of lead (100 d–1) is element-specific. The values for Types M and S (3 d–1) are thegeneral default values.
†
For inhaled material deposited in the respiratory tract and subsequently cleared by particle transport to thealimentary tract, the default fA values for inhaled materials are applied: i.e. the product of fr for the absorption type(or specific value where given) and the fA value for ingested soluble forms of lead applicable to the age-group ofinterest (e.g. 0.2 for adults).
‡
See Section 9 of Publication 137 (ICRP, 2017) for summary of information on which parameter values are based,
and on ranges of parameter values observed in different studies. For lead as a progeny of radon, specific parametervalues are used for dissolution in the lungs, but a default value of fA (footnote †).
*211

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

5202
5203
5204
5205
5206
5207
5208
5209
5210

§

5211

29.1.2. Ingestion

5212

29.1.2.1. Adults

5213
5214
5215
5216
5217
5218
5219
5220
5221
5222
5223

Lead absorption has been studied extensively in man and animals. (For more details,
see reviews by ICRP, 1975, 1993, 2017; Leggett, 1993; Moore, 1986). Factors shown to affectabsorption of lead include ingestion of milk, calcium and iron status, protein deficiency,
vitamin D, and fasting. In normally fed adults, the absorption fraction ranges from 0.03 to 0.14.
Lead is absorbed more readily in fasting subjects than when it is ingested with food (range ofabsorption fraction 0.1-0.76). Heard and Chamberlain (1982) showed that fasting values ofabsorption of approximately 0.4–0.5 could be reduced to approximately 0.1–0.2 by giving leadwith tea, coffee, or beer rather than water. Publication 30 (ICRP, 1980) recommended anabsorption fraction of 0.2 that was applied in Publication 67 (ICRP, 1993) for dietary intakes
and in Publication 137 (ICRP, 2017) for direct ingestion of all forms of lead. The same valueof fA = 0.2 is adopted here for dietary intakes of lead by adults.

5224

29.1.2.2. Children

5225
5226
5227
5228
5229
5230
5231
5232
5233
5234
5235
5236
5237
5238
5239
5240

Ziegler et al. (1978) reported repeated 3-day balance studies of lead in six normal
infants of ages ranging from 14 to 746 days, most being in the range 150 - 300 days. In subjects
ingesting more than 5 pg of lead kg-1 body weight day-1, the net absorption averaged 42%. Ineight children of ages 3 months to 8 years with daily intakes of 5-17 µg kg-1 body weight,
Alexander et al. (1974) reported absorption of 53% and retention of 18%. There are a numberof uncertainties in these estimates and true absorption could have been greater due toendogenous faecal excretion of absorbed lead. However, the results suggest that the fractional
absorption of lead in children may remain high for at least the first 8 years of life. Results for
non-human primates are qualitatively consistent with these data for humans (Pounds et al.,
1978; Willes et al., 1977). Studies in chickens, rats and sheep demonstrate clearly that there isan inverse relationship of age and the capacity to absorb lead (Conrad and Barton, 1978; Gerberand Deroo, 1975; Kostial et al., 1974; Mykkänen and Wasserman, 1981; Quarterman andMorrison, 1978). An absorption fraction of 0.6 was recommended in Publication 67 for the 3month-old infant. For ages l - l5 years a value of 0.4 was recommended. Values of fA = 0.6 for
3-mo-old and fA = 0.3 for older children are adopted here for consistency with radium andbarium.

5241

29.1.3. Systemic Distribution, Retention and Excretion5242

29.1.3.1. Summary of biokinetic data

5243(a) Mature human subjects and laboratory animals

Materials (e.g. dichloride) are listed here where there is sufficient information to assign to a default absorption
Type, but not to give specific parameter values (see Section 9 of Publication 137).
¶
Default Type F is recommended for use in the absence of specific information on which the exposure material
can be assigned to an absorption type, e.g. if the form is unknown, or if the form is known but there is no
information available on the absorption of that form from the respiratory tract.
**
Activity transferred from systemic compartments into segments of the alimentary tract is assumed to be subject
to reabsorption to blood. The default absorption fraction fA for the secreted activity is the highest value foringestion of the radionuclide applicable to the age-group of interest (e.g. 0.2 for adults).

212

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

5244
5245
5246
5247
5248
5249
5250
5251
5252
5253
5254
5255
5256
5257
5258
5259
5260
5261
5262
5263
5264
5265
5266
5267
5268
5269
5270
5271
5272
5273
5274
5275
5276
5277
5278
5279
5280
5281
5282
5283
5284
5285
5286
5287
5288
5289
5290
5291
5292

Following intravenous administration of radiolead to adult human subjects, theinjected activity initially cleared from blood at a rate of 1 min -1 or greater (Chamberlain et al.,
1978; Wells et al., 1975). The content of lead in blood declined to about one-third of the injectedamount within 2-3 min, at which time roughly three-fourths of activity in blood resided in red
blood cells (RBC). Increasing activity in blood was then seen for 24-48 h as the tracer returned
from extravascular spaces and accumulated in RBC (Booker et al., 1969; Chamberlain et al.,
1978; Wells et al., 1975). Within a few hours after injection, 99% or more of activity in blood
was bound to RBC (Booker et al., 1969; Chamberlain et al., 1978; DeSilva, 1981; Everson and
Patterson, 1980; Heard and Chamberlain, 1984; Hursh et al., 1969; Manton and Cook, 1984;
Wells et al., 1975). At 1-2 d after introduction of radiolead into adult humans by injection or
inhalation, the blood contained 40-75% (mean 58 ± 12%) of the amount reaching the circulation(Booker et al., 1969; Chamberlain et al., 1978; Heard and Chamberlain, 1984; Hursh et al.,
1969; Hursh and Suomela, 1968; Morrow et al., 1980; Wells et al., 1975). Over the next few
weeks, activity was cleared from blood with a biological half-time on the order of 15-20 d(Heard and Chamberlain, 1984; Rabinowitz et al., 1973, 1974, 1976; Wells et al., 1975).
The liver contained about 10-15% of administered radiolead at 1 d after intravenous
administration to adult humans (Heard and Chamberlain, 1984), baboons (Cohen et al., 1970),
or dogs (Lloyd et al., 1975). Most of the activity deposited in the liver was removed with abiological half-time of a few weeks. Loss of lead from the liver was due in part to its biliary
secretion into the contents of the small intestine (Ishihara and Matsushiro, 1986; Rabinowitz etal., 1976). Autopsy measurements on adult humans chronically exposed to environmental leadindicate that the liver typically contains about 2-3% of total-body lead (Barry, 1975, 1981;
Gross et al., 1975; Zhu et al., 2010).
In baboons receiving radiolead by intravenous injection, the kidneys contained about
4% of the administered amount after 1 d, 0.6% after 30 d, and 0.1% after 60 d (Cohen et al.,1970). In dogs receiving 210Pb by intravenous injection, the kidneys contained about 0.5% of
the administered activity at 1 month (Lloyd et al., 1975).
Gradual loss of lead from RBC, liver, kidneys, and other soft tissues over the first few
weeks can be accounted for by a slow loss in urine and faeces and a continual increase inskeletal lead. Typically, 3-5% of injected or absorbed lead is lost in urine during the first day.
The urinary to faecal excretion ratio is about 2 during d 3-14 after absorption of lead to bloodin humans. About 30% of intravenously injected radiolead is removed in urine and faeces
during the first 20 d (Booker et al., 1969; Chamberlain et al., 1978; Heard and Chamberlain,
1984; Hursh et al., 1969; Hursh and Mercer, 1970; Hursh and Suomela, 1968; Wells et al.,1975).
In studies on baboons (Cohen et al., 1970) and human subjects (Heard andChamberlain, 1984), there was evidence of rapid skeletal uptake of about 10-15% of
intravenously administered lead. The skeletal content remained nearly constant over the next
2-3 d and then slowly increased over an extended period as activity returned from RBC andsoft tissues to plasma. In human subjects the skeleton contained roughly 20% of the injectedamount after 20 d. Autopsy data for persons chronically exposed to environmental lead indicatethat the skeletal content of lead increases throughout life and represents 90% or more ofsystemic lead by the fifth decade (Barry, 1975, 1981; Gross et al., 1975; Leggett, 1993; Tipton
and Cook, 1963; Zhu et al., 2010).
Skeletal behaviour of lead appears to be qualitatively similar to that of the alkaline
earth elements and quantitatively similar to that of barium or radium, if account is taken of theslower deposition of lead in the skeleton due to competition from RBC (Domanski and
Trojanowska, 1980; Heard and Chamberlain, 1984; Hursh, 1973; Lloyd et al., 1975). Lead has
been used frequently as a marker of bone growth and osteon formation, and a close resemblance

213

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

5293
5294
5295
5296
5297
5298
5299
5300
5301
5302
5303
5304
5305
5306
5307
5308
5309
5310
5311
5312
5313
5314
5315
5316
5317

to calcium has been demonstrated in such studies (Hong et al., 1968; Lacroix, 1960; Scheiman‐
Tagger and Brodie, 1964; Vincent, 1957; Yen and Shaw, 1977). Lead is incorporated into the
crystalline structure of bone, where it replaces calcium ions (MacDonald et al., 1951; Miyake
et al., 1986; Verbeeck et al., 1981).
Autoradiographs of bone sections from baboons injected with 210Pb indicate that a
portion of skeletal activity remains near bone surfaces at 1 to 2 months after administration, as
appears to be the case for radium and barium. Studies on human subjects indicate that the
distribution of lead in bone may be skewed toward bone surfaces for at least a few months after
exposure, but the subjects generally have been exposed to heavy levels of lead that could affectbone metabolism (Flood et al., 1988; Lindh et al., 1978). Burial of lead beneath the surfaces inregions of bone formation has been observed, and there is evidence that lead is eventuallydistributed throughout the bone volume (Hong et al., 1968; Hu et al., 1989; Lacroix, 1960;
Lindh et al., 1978; Scheiman‐Tagger and Brodie, 1964; Vincent, 1957; Yen and Shaw, 1977).
In beagles, long-term skeletal retention of lead is similar to that of strontium and radium (Hursh,
1973; Lloyd et al., 1975). Because lead is incorporated into the bone crystal, long-term losses
from bone presumably are largely controlled by the rate of bone resorption.
In a study of the comparative behaviour of injected lead, calcium, and barium in boneof rabbits, Domanski and Trojanowska (1980) found that the build-up of lead in bone is similar
to that of barium and greater than that of calcium when related to integrated activity in plasma.
Similar results for lead and calcium were obtained by Heard and Chamberlain (1984) for
humans injected with radioisotopes of these two elements. A relatively low uptake of lead by
the skeleton at early times compared with radium, for example, apparently reflects acompetition by RBC for lead that does not occur to a significant extent for the alkaline earth
elements. The later build-up in the skeleton results from the gradual release of activity from
RBC and the relatively longer retention of lead in the skeleton than in RBC.

5318(b) Immature human subjects and laboratory animals

5319
5320
5321
5322
5323
5324
5325
5326
5327
5328
5329
5330
5331
5332
5333

Autopsy data for persons of all ages exposed only to environmental lead indicate thatthe content of lead in bone increases gradually from birth to adulthood. The bones of infants
may contain roughly one-quarter to one-third of total-body lead and those of young children
and teenagers one-half to two-thirds, compared with a value of 90% or more for middle-aged
and older persons (Barry, 1973, 1975, 1981; Leggett, 1992a). Data for non-human primates(Kneip et al., 1983; Pounds et al., 1978; Willes et al., 1977) and rodents (Jugo et al., 1975,
1980; Keller and Doherty, 1980; Kello and Kostial, 1978; Kostial et al., 1978; Momčilović andKostial, 1974) indicate that retention of a lead tracer is greater in growing than in mature
animals and that much of the variation with age is due to elevated uptake and/or retention oflead by the immature skeleton. Some differences in uptake and/or retention of lead by the brain,
liver and kidneys have been observed between immature and mature rodents (Keller andDoherty, 1980; Momčilović and Kostial, 1974). The combined age-specific data for laboratory
animals and environmentally exposed humans are reasonably consistent with assumptions ofhigher uptake and faster release of lead by the immature than the mature skeleton andsubstantial retention of lead by blood and soft tissues at all ages.

5334

29.1.3.2. Systemic model

5335
5336
5337

The model for systemic lead applied in Publication 137 (ICRP, 2017) to workers isapplied here to adult members of the public. The systemic behaviour of lead is assumed to be
independent of age.

214

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

5338
5339
5340

5341
5342
5343
5344
5345
5346

The structure of the model for systemic lead is shown in Fig. 29.1. Transfer
coefficients are listed in Table 29.2.

Fig. 29.1. Structure of the model for systemic lead. Activity transferred from Plasma to Coloncontents enters Right colon contents. Abbreviations: RBC = Red Blood Cells, SI = Small
intestine, Exch = Exchangeable, Nonexch = Non-exchangeable.
Table 29.2. Age-specific transfer coefficients for lead.
Transfer coefficient (d-1)
PathwayaBlood to Urinary bladder contents

100 d
1.25E+00

1y
1.55E+00

5y
1.60E+00

10 y
1.44E+00

15 y
1.26E+00

Adult
1.75E+00

Blood to Right colon contents

5.00E-01

6.20E-01

6.40E-01

5.76E-01

5.04E-01

7.00E-01

Blood to Trab bone surface

5.25E+00

3.15E+00

3.11E+00

4.94E+00

7.23E+00

4.86E+00

Blood to Cort bone surface

2.10E+01

1.26E+01

1.09E+01

1.47E+01

1.87E+01

3.89E+00

Blood to ST0

1.58E+01

1.96E+01

2.03E+01

1.82E+01

1.60E+01

2.22E+01

Blood to ST1

5.00E-01

6.20E-01

6.40E-01

5.76E-01

5.04E-01

7.00E-01

Blood to ST2

1.00E-01

1.24E-01

1.28E-01

1.15E-01

1.01E-01

1.40E-01

Blood to Liver 1

3.50E+00

4.34E+00

4.48E+00

4.03E+00

3.53E+00

4.90E+00

Blood to Kidneys 1

1.75E+00

2.17E+00

2.24E+00

2.02E+00

1.76E+00

2.45E+00

Blood to Kidneys 2

1.75E-02

2.17E-02

2.24E-02

2.02E-02

1.76E-02

2.45E-02

Blood to Blood 1

2.00E+01

2.48E+01

2.56E+01

2.30E+01

2.02E+01

2.80E+01

Blood to Excreta

3.00E-01

3.72E-01

3.84E-01

3.46E-01

3.02E-01

4.20E-01

Blood 1 to Blood

1.39E-01

1.39E-01

1.39E-01

1.39E-01

1.39E-01

1.39E-01

Trab bone surf to Blood

6.50E-01

6.50E-01

6.50E-01

6.50E-01

6.50E-01

5.00E-01

Trab bone surf to Trab bone volume 1

3.50E-01

3.50E-01

3.50E-01

3.50E-01

3.50E-01

5.00E-01

Cort bone surf to Blood

6.50E-01

6.50E-01

6.50E-01

6.50E-01

6.50E-01

5.00E-01

Cort bone surf to Cort bone volume 1

3.50E-01

3.50E-01

3.50E-01

3.50E-01

3.50E-01

5.00E-01

215

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
Trab bone vol 1 to Trab bone surface

1.85E-02

1.85E-02

1.85E-02

1.85E-02

1.85E-02

1.85E-02

Trab bone vol 1 to Trab bone volume 2

4.60E-03

4.60E-03

4.60E-03

4.60E-03

4.60E-03

4.60E-03

Cort bone vol 1 to Cort bone surface

1.85E-02

1.85E-02

1.85E-02

1.85E-02

1.85E-02

1.85E-02

Cort bone vol 1 to Cort bone volume 2

4.60E-03

4.60E-03

4.60E-03

4.60E-03

4.60E-03

4.60E-03

Trab bone vol 2 to Blood

8.22E-03

2.88E-03

1.81E-03

1.32E-03

9.59E-04

4.93E-04

Cort bone vol 2 to Blood

8.22E-03

2.88E-03

1.53E-03

9.04E-04

5.21E-04

8.21E-05

Liver 1 to Blood

3.12E-02

3.12E-02

3.12E-02

3.12E-02

3.12E-02

3.12E-02

Liver 1 to SI-contents

3.12E-02

3.12E-02

3.12E-02

3.12E-02

3.12E-02

3.12E-02

Liver 1 to Liver 2

6.93E-03

6.93E-03

6.93E-03

6.93E-03

6.93E-03

6.93E-03

Liver 2 to Blood

6.93E-03

6.93E-03

6.93E-03

1.90E-03

1.90E-03

1.90E-03

Kidneys 1 to Urinary bladder contents

1.39E-01

1.39E-01

1.39E-01

1.39E-01

1.39E-01

1.39E-01

Kidneys 2 to Blood

6.93E-03

6.93E-03

6.93E-03

1.90E-03

1.90E-03

1.90E-03

ST0 to Blood

5.28E+00

6.54E+00

6.75E+00

6.08E+00

5.32E+00

7.39E+00

ST1 to Blood

4.16E-03

4.16E-03

4.16E-03

4.16E-03

4.16E-03

4.16E-03

ST2 to Blood

3.80E-04

3.80E-04

3.80E-04

3.80E-04

3.80E-04

3.80E-04

ST1 to Excreta

2.77E-03

2.77E-03

2.77E-03

2.77E-03

2.77E-03

2.77E-03

5347

a

5348

29.1.3.3. Treatment of radioactive progeny

5349
5350

The treatment of radioactive progeny produced in systemic compartments after intake
of a radioisotope of lead is described in Section 9.2.3.3. of Publication 137 (ICRP, 2017).

Trab = Trabecular, Cort = Cortical216

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

5351

29.2. Dosimetric data for lead

5352

Table 29.3. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 210Pb compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled particulate materials (1 µm AMAD aerosols)

3 mo

1y

5y

10 y

15 y

Adult

Type F, Dichloride, dibromide, difluoride, hydroxide,
nitrate, oxide; all unspecified forms
5.7E-06

3.2E-06

1.7E-06

1.4E-06

7.2E-07

4.9E-07

Type M

4.9E-06

4.1E-06

2.4E-06

1.6E-06

1.1E-06

9.8E-07

Type S, Mineral dusts

3.4E-05

3.4E-05

2.4E-05

1.7E-05

1.6E-05

1.6E-05

8.0E-06

2.5E-06

1.5E-06

1.2E-06

6.9E-07

3.2E-07

Ingested materials
Adult fA = 0.2, All forms

5353
5354

Table 29.4. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 212Pb compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled particulate materials (1 µm AMAD aerosols)

3 mo

1y

5y

10 y

15 y

Adult

Type F, Dichloride, dibromide, difluoride, hydroxide,
nitrate, oxide; all unspecified forms
1.0E-06

8.0E-07

3.8E-07

2.7E-072.0E-07

1.8E-07

Type M

4.8E-07

3.5E-07

2.2E-07

1.5E-07

1.3E-07

1.2E-07

Type S, Mineral dusts

4.9E-07

3.6E-07

2.3E-07

1.6E-07

1.4E-07

1.2E-07

1.5E-07

5.0E-08

2.5E-08

1.4E-08

8.6E-09

5.6E-09

Ingested materials
Adult fA = 0.2, All forms

5355

217

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

5356

Table 29.5. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 214Pb compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled particulate materials (1 µm AMAD aerosols)

3 mo

1y

5y

10 y

15 y

Adult

Type F, Dichloride, dibromide, difluoride, hydroxide,
nitrate, oxide; all unspecified forms
6.5E-08

5.2E-08

2.6E-08

1.9E-08

1.6E-08

1.3E-08

Type M

4.4E-08

3.3E-082.0E-08

1.5E-08

1.5E-08

1.2E-08

Type S, Mineral dusts

4.4E-08

3.3E-082.0E-08

1.5E-08

1.5E-08

1.2E-08

1.0E-09

4.2E-10

2.5E-10

1.7E-10

1.1E-10

7.7E-11

Ingested materials
Adult fA = 0.2, All forms

5357
5358
5359
5360
5361

218

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

30. BISMUTH (Z = 83)

5362
5363

30.1. Routes of Intake

5364

30.1.1. Inhalation

5365
5366
5367
5368
5369
5370
5371
5372
5373
5374
5375
5376
5377

Very little information from which parameter values can be assessed is available fromexperimental studies of the behaviour of bismuth deposited in the respiratory tract. For details
see Section 10 of Publication 137 (ICRP, 2017). Absorption parameter values and types, andassociated fA values for particulate forms of bismuth are given in Table 30.1 (taken from
Section 10 of Publication 137,).
For radiation protection purposes, the most important exposures to radioisotopes ofbismuth are as progeny radionuclides of radon. Dose coefficients for isotopes of bismuth
inhaled as radon progeny radionuclides are given in the radon section, where factors such as
the relevant aerosol size distribution are addressed. Otherwise, exposures to radioisotopes ofbismuth occur most often as progeny radionuclides associated with intakes of uranium, thorium
or radium.
Table 30.1. Absorption parameter values for inhaled and ingested bismuth.
Inhaled particulate materials
Default parameter values†,‡
Absorption
Assigned forms
TypeF
Bismuth as a progeny of radon—
M§—
S
Ingested material¶
Assigned forms
All forms

5378
5379
5380
5381
5382
5383
5384
5385
5386
5387
5388
5389
5390
5391
5392

*

5393

30.1.2. Ingestion

fr

1
0.2
0.01

Absorption parameter values*sr (d–1)
ss (d–1)

1
1
1

–
0.005
1×10-4Age-dependent absorption from the alimentary tract, fA
3 months 1 year
5 years
10 years 15 years adult
0.1
0.05
0.05
0.05
0.05
0.05

It is assumed that for bismuth the bound state can be neglected, i.e. fb = 0. The values of sr for Type F, M and S
forms of bismuth (1 d–1) are element-specific.
†
For inhaled material deposited in the respiratory tract and subsequently cleared by particle transport to thealimentary tract, the default fA values for inhaled materials are applied: i.e. the product of fr for the absorption type(or specific value where given) and the fA value for ingested soluble forms of bismuth applicable to the age-groupof interest (e.g. 0.05 for adults).
‡
Materials (e.g. bismuth as a progeny of radon) are listed here where there is sufficient information to assign to adefault absorption type, but not to give specific parameter values (see Section 10 of Publication 137, ICRP, 2017).
§
Default Type M is recommended for use in the absence of specific information on which the exposure material
can be assigned to an absorption type, e.g. if the form is unknown, or if the form is known but there is no
information available on the absorption of that form from the respiratory tract.
¶
Activity transferred from systemic compartments into segments of the alimentary tract is assumed to be subject
to reabsorption to blood. The default absorption fraction fA for the secreted activity is the highest value foringestion of the radionuclide applicable to the age-group of interest (e.g. 0.05 for adults).

219

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

5394
5395
5396
5397
5398
5399
5400
5401
5402
5403

There are some available data on bismuth absorption in human and animals. It has
been shown that inorganic forms of bismuth are only poorly absorbed (less than 1% of ingested
quantity) from the gastrointestinal tract (for more details, see Section 10 of Publication 137,
ICRP, 2017) and suggested that the fractional absorption of dietary bismuth from thegastrointestinal tract is about 8% (ICRP, 1975). Publications 30 (ICRP, 1980) and 137 (ICRP,
2017) recommended an absorption fraction of 5% to apply to all chemical forms. The samevalue fA = 0.05 is adopted here for dietary intakes of bismuth by adult members of the public.
Consistently with the approach of Publication 56 (ICRP, 1990), the value fA = 0.1 is adopted
for 3-month-old infants. The adult value of fA = 0.05 is also applied here to 1-15 year-old
children.

5404

30.1.3. Systemic Distribution, Retention and Excretion5405

30.1.3.1. Summary of biokinetic data

5406
5407
5408
5409
5410
5411
5412
5413
5414
5415
5416
5417
5418
5419
5420
5421
5422
5423
5424
5425
5426
5427
5428
5429
5430
5431
5432
5433

Bismuth has been used since the late 1700s as a therapeutic agent for a number ofdisorders of the human body. The systemic biokinetics of bismuth has been found to vary withthe route of administration and the form administered.
Most forms of bismuth show high deposition in the kidneys and subsequent clearance
to urine (Durbin, 1959; Eridani et al., 1964; Matthews et al., 1964; Pieri and Wegmann, 1981;
Russ et al., 1975; Slikkerveer and de Wolff, 1989). Human subjects injected with bismuth
citrate excreted a third or more of the administered bismuth in urine during the first day(Coenegracht and Dorleyn, 1961; Newton, 2001).
Newton et al. (2001) studied the biokinetics of bismuth in a healthy male volunteer
after intravenous injection with 207Bi citrate. They estimated that the liver contained 60% of the
body content at 3 d. An estimated 55% of the administered amount was lost in excreta, primarily
urine, during the first 2 d. The remaining amount was lost more slowly. Approximately 0.6%of the injected amount remained at 924 d. The long-term half-time was estimated as 1.9 y.
Extended retention of a few percent of administered bismuth has been reported for
relatively insoluble bismuth compounds used in clinical applications (Sollmann, 1957). Buijs
and coworkers (1985) found 207Bi (T1/2 = 38 y) remaining in two human subjects treated aquarter century earlier with 206Bi injections contaminated with small amounts of 207Bi. They
estimated from measurements of the rate of decline of total-body 207Bi and from assumptions
on the early rate of excretion of bismuth that 7% of injected bismuth was retained with a halftime close to 20 y. Autopsy measurements on subjects treated with bismuth compounds
indicated that the kidneys and liver each contained nearly 10% of the total found in the body(Sollmann, 1957).
Results of animal studies indicate elevated deposition in the kidneys and in some cases
the liver (Publication 137, ICRP, 2017). Deposition of bismuth in bone has also been observedin rats, but uptake and retention are highly variable and may depend on the administered formof bismuth (Publication 137).
No information was found regarding the effect of age on the biokinetics of systemic
bismuth.

5434

30.1.3.2. Systemic model

5435
5436
5437

The model for systemic bismuth applied in Publication 137 (ICRP, 2017) to workers
is applied here to adult members of the public. The systemic behaviour of bismuth is assumed
to be independent of age.

220

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

5438
5439

5440
5441
5442
5443
5444

The structure of the model for systemic bismuth is shown in Fig. 30.1. Transfer
coefficients are listed in Table 30.2.

Fig. 30.1. Structure of the model for systemic bismuth. Activity transferring from Plasma to
Colon contents enters Right colon contents.
Table 30.2. Age-specific transfer coefficients for bismuth.
Transfer coefficient (d-1)

Pathway

100 d

1y

5y

10 y

15 y

Adult

Blood to Urinary bladder contents

2.00E+01

2.00E+01

2.00E+01

2.00E+01

2.00E+01

2.00E+01

Blood to Right colon contents

4.00E+00

4.00E+00

4.00E+00

4.00E+00

4.00E+00

4.00E+00

Blood to Blood 1

5.00E-01

5.00E-01

5.00E-01

5.00E-01

5.00E-01

5.00E-01

Blood to ST0

3.00E+02

3.00E+02

3.00E+02

3.00E+02

3.00E+02

3.00E+02

Blood to ST1

4.20E+00

4.20E+00

4.20E+00

4.20E+00

4.20E+00

4.20E+00

Blood to ST2

1.30E+00

1.30E+00

1.30E+00

1.30E+00

1.30E+00

1.30E+00

Blood to Liver 1

3.00E+01

3.00E+01

3.00E+01

3.00E+01

3.00E+01

3.00E+01

Blood to Kidneys 1

3.00E+01

3.00E+01

3.00E+01

3.00E+01

3.00E+01

3.00E+01

Blood to Kidneys 2

5.00E+00

5.00E+00

5.00E+00

5.00E+00

5.00E+00

5.00E+00

Blood to Cortical bone surface

2.50E+00

2.50E+00

2.50E+00

2.50E+00

2.50E+00

2.50E+00

Blood to Trabecular bone surface

2.50E+00

2.50E+00

2.50E+00

2.50E+00

2.50E+00

2.50E+00

Blood 1 to Blood

1.73E-01

1.73E-01

1.73E-01

1.73E-01

1.73E-01

1.73E-01

ST0 to Blood

6.65E+01

6.65E+01

6.65E+01

6.65E+01

6.65E+01

6.65E+01

ST1 to Blood

3.47E-02

3.47E-02

3.47E-02

3.47E-02

3.47E-02

3.47E-02

ST2 to Blood

1.16E-03

1.16E-03

1.16E-03

1.16E-03

1.16E-03

1.16E-03

Liver 1 to Small intestine contents

2.08E-01

2.08E-01

2.08E-01

2.08E-01

2.08E-01

2.08E-01

Liver 1 to Liver 2

1.39E-01

1.39E-01

1.39E-01

1.39E-01

1.39E-01

1.39E-01

Liver 2 to Blood

6.93E-02

6.93E-02

6.93E-02

6.93E-02

6.93E-02

6.93E-02

221

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
Kidneys 1 to Urinary bladder contents

6.93E-01

6.93E-01

6.93E-01

6.93E-01

6.93E-01

6.93E-01

Kidneys 2 to Blood

1.39E-01

1.39E-01

1.39E-01

1.39E-01

1.39E-01

1.39E-01

Cortical bone surface to Blood

3.47E-02

3.47E-02

3.47E-02

3.47E-02

3.47E-02

3.47E-02

Trabecular bone surface to Blood

3.47E-02

3.47E-02

3.47E-02

3.47E-02

3.47E-02

3.47E-02

5445
5446

30.1.3.3. Treatment of radioactive progeny

5447
5448

The treatment of radioactive progeny produced in systemic compartments after intake
of a radioisotope of bismuth is described in Section 10.2.3.3. of Publication 137 (ICRP, 2017).

222

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

5449

30.2. Dosimetric data for bismuth

5450

Table 30.3. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 210Bi compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled particulate materials (1 µm AMAD aerosols) 3 mo

1y

5y

10 y

15 y

Adult

Type F, Bismuth as a decay product of radon

4.7E-08

3.1E-08

1.8E-08

1.2E-08

5.1E-09

3.7E-09

Type M, All unspecified forms

2.3E-072.0E-07

1.1E-07

7.4E-08

5.4E-08

4.9E-08

Type S

3.9E-07

3.5E-072.0E-07

1.3E-07

9.9E-08

9.4E-08

2.7E-08

1.0E-08

5.9E-09

4.1E-09

1.6E-09

1.1E-09

Ingested materials
Adult fA = 0.05, All forms

5451
5452

Table 30.4. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 214Bi compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled particulate materials (1 µm AMAD aerosols) 3 mo

1y

5y

10 y

15 y

Adult

Type F, Bismuth as a decay product of radon

4.2E-08

3.3E-08

1.9E-08

1.4E-08

1.3E-08

1.1E-08

Type M, All unspecified forms

4.3E-08

3.3E-08

1.9E-08

1.4E-08

1.3E-08

1.1E-08

Type S

4.3E-08

3.3E-08

1.9E-08

1.4E-08

1.3E-08

1.1E-08

2.7E-10

2.1E-10

1.4E-101.0E-10

6.6E-11

4.7E-11

Ingested materials
Adult fA = 0.05, All forms

5453
5454

223

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

31. POLONIUM (Z = 84)

5455
5456

31.1. Routes of Intake

5457

31.1.1. Inhalation

5458
5459
5460
5461
5462
5463
5464
5465
5466
5467
5468
5469
5470
5471
5472
5473
5474

Information is available on the behaviour of polonium following deposition in the
respiratory tract from animal experiments with several chemical forms, and from some
accidental human intakes. However, the behaviour of ionic (soluble) Po following depositionin the respiratory tract is difficult to determine because ionic solutions (e.g. chloride) areunstable at neutral pH and in many biological media, resulting in colloid formation. For details,
see Section 11 of Publication 137 (ICRP, 2017). Absorption parameter values and types, andassociated fA values for particulate forms of polonium are given in Table 31.1 (taken from
Section 11 of Publication 137).
The most important widespread exposures to radioisotopes of polonium are asprogeny radionuclides of radon. The alpha-emitting isotopes 218Po (half-life 3 min) and 214Po(half-life 160 µs) give rise to most of the dose from inhalation of the short-lived progeny
radionuclides of 222Rn, as do 216Po (half-life 0.15 s) and 212Po (half-life 300 ns) for those of220
Rn (thoron). For the decay schemes see the radon Section of this report. Dose coefficientsfor isotopes of polonium inhaled as short-lived radon progeny radionuclides are given in theradon section, where factors such as the relevant aerosol size distribution are addressed.
Table 31.1. Absorption parameter values for inhaled and ingested polonium.
Inhaled particulate materials
Default parameter values†,‡
Absorption
Assigned forms
Type
F
—
M§
Chloride, hydroxide,
polonium
S—
Ingested material¶
Assigned forms
polonium in diet
All other chemical forms

5475
5476
5477
5478
5479
5480
5481
5482
5483
5484
5485

fr

Absorption parameter values*sr (d–1)
ss (d–1)

1
volatilised 0.2

3
3

–
0.005

0.01

3

1×10–4Age-dependent absorption from the alimentary tract, fA
3 months 1 year
5 years
10 years 15 years adult
1
0.5
0.5
0.5
0.5
0.5
0.2
0.1
0.1
0.1
0.1
0.1

*

It is assumed that for polonium the bound state can be neglected, i.e. fb = 0.0. The value of sr for Type F forms ofpolonium (3 d–1) is element-specific. The values for Types M and S (3 d–1) are the general default values.
†
Materials (e.g. polonium chloride) are generally listed here where there is sufficient information to assign to adefault absorption type, but not to give specific parameter values (see Section 11 of Publication 137, ICRP, 2017).
‡
For inhaled material deposited in the respiratory tract and subsequently cleared by particle transport to thealimentary tract, the default fA values for inhaled materials are applied: i.e. the product of fr for the absorption type
and the fA value for ingested soluble (excluding dietary) forms of polonium applicable to the age-group of interest(e.g. 0.1 for adults).
§
Default Type M is recommended for use in the absence of specific information on which the exposure material
can be assigned to an absorption type, e.g. if the form is unknown, or if the form is known but there is no
information available on the absorption of that form from the respiratory tract.

224

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

5486
5487
5488
5489

¶

5490

31.1.2. Ingestion

5491

31.1.2.1. Adults

5492
5493
5494
5495
5496
5497
5498
5499
5500
5501
5502
5503
5504
5505
5506
5507
5508
5509

Fractional absorption of 210Po from the alimentary tract has been measured in humansubjects and in animals at levels in the order of 1- 15% for inorganic forms (see reviews by
Harrison et al., 2007; ICRP, 2017; Scott, 2007). In Publications 30 (ICRP, 1979) and 137(ICRP, 2017) an absorption fraction of 0.1 was recommended for all chemical forms in theworkplace. Fractional absorption in animals seems to be identical in males and females. Data
from humans consuming meat from reindeer exposed to 210Po suggest that polonium
incorporated in food may have an absorption fraction of 5-25 times that of inorganic polonium
compounds, values of around 0.3 to 0.5 having been estimated (Hill, 1965; Kauranen and
Miettinen, 1967; Ladinskaya et al., 1973). Rats absorbed approximately 50% of polonium
biologically incorporated into goat’s milk. This value is higher than is typically observed forinorganic polonium absorption in rats (McInroy et al., 1972). Similarly, experiments in rats
ingesting polonium biologically incorporated into rat liver yielded absorption fractions of 0.100.12 which are at least twice those which have been obtained using inorganic polonium
compounds (Naylor et al., 1991). In a human volunteer study of the absorption of 210Po fromcrabmeat, Hunt and Allington (1993) estimated fractional absorption to be about 0.8. In
Publication 67 (ICRP, 1993), an absorption fraction of 0.5 has been recommended for dietaryintakes of polonium by adult members of the public. The same value fA = 0.5 is adopted here
for polonium in food for adult. fA for other chemical forms is equal to 0.1.

5510

31.1.2.2. Children

5511
5512
5513
5514
5515
5516
5517

There appear to be no data available for estimating an absorption fraction for polonium
in infants and children. Following the approach of Publication 56 (ICRP, 1990), an absorption
fraction of 1 was recommended in Publication 67 for the 3-month-old infant. For children of 1
year and older the absorption fraction for the adult (0.5) was recommended in Publication 67.
The same values are adopted here for fA for polonium in food. When ingested as any otherchemical form, an fA of 0.2 is adopted for 3 month old infants and an fA of 0.1 is adopted forchildren of 1 year old and older.

5518

31.1.3. Systemic Distribution, Retention and Excretion5519

31.1.3.1. Summary of biokinetic data

5520
5521
5522
5523
5524
5525
5526
5527
5528

Leggett and Eckerman (2001) reviewed records of about 1500 former polonium
workers and estimated urinary half-times for numerous cases of apparently elevated, acuteexposure. Approximately 95% of the derived effective half-times were in the range 8-52 d,corresponding to a range of biological half-times of 8.5-83 d. The mean, median, and mode ofthe effective half-times were approximately 30 d, 30 d, and 34 d, corresponding to biologicalhalf-times of 38 d, 38 d, and 45 d, respectively.
Retention and excretion of 210Po has been studied in workers exposed acutely via
wounds or intact skin (Cohen et al., 1989; Sheehan, 1964; Silverman, 1944; Testa, 1972;
Wraight and Strong, 1989) or inhalation (Foreman et al., 1958; Jackson and Dolphin, 1966;

Activity transferred from systemic compartments into segments of the alimentary tract is assumed to be subject
to reabsorption to blood. The default absorption fraction fA for the secreted activity is the highest value foringestion of the radionuclide applicable to the age-group of interest (e.g. 0.5 for adults).

225

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

5529
5530
5531
5532
5533
5534
5535
5536
5537
5538
5539
5540
5541
5542
5543
5544
5545

Naimark, 1948, 1949; Scott and West, 1975; Sheehan, 1964; Spoerl, 1951). A phase of
relatively rapid phase removal of activity from the body generally was observed in cases where
measurements were begun soon after exposure. Estimates of the long-term biological half-timewere generally in the range 13-42 d for cases of entry through a wound or intact skin and 2060 d in inhalation cases.
Silberstein et al. (1950) measured 210Po in the urine, faeces, and blood of four
lymphosarcoma or leukemia patients who were administered 210Po chloride by intravenous
injection and in a leukemia patient administered 210Po chloride by ingestion. Biological halftimes fitted to the time-dependent concentration of 210Po in urine, faeces, or blood of thesesubjects varied with the observation period. Urinary excretion data for the first week afteradministration yielded biological half-times as short as 3 d. For three subjects followed forseveral weeks or months, urinary excretion data indicated half-times of 30-50 d for the period
starting 1 wk after exposure; faecal excretion data indicated half-times of 33-52 d for thisperiod; and data for red blood cells indicated half-times of 12-48 d for this period.
Measurements on 14 children or adolescents (age range, 6-15 y) exposed to 210Po
indicated a retention half-time of about 40 days (Guskova et al., 1964; Kalmykov et al., 1969).
This value is near the mean or median value indicated by data on adults summarized above.

5546

31.1.3.2. Systemic model

5547
5548
5549
5550
5551

The model for systemic polonium applied in Publication 137 (ICRP, 2017) to workers
is applied here to adult members of the public. The systemic behaviour of polonium is assumed
to be independent of age.
The structure of the model for systemic polonium is shown in Fig. 31.1. Transfer
coefficients are listed in Table 31.2.

5552
5553
5554
5555
5556
5557
5558

Fig. 31.1. Structure of the model for systemic polonium. Polonium absorbed from thealimentary tract and repiratory tract is assigned to Plasma 1 and Plasma 2, respectively.
Polonium transferred from Liver 1 to the alimentary tract contents enters Small intestinecontents. RBC = red blood cells.
Table 31.2. Age-specific transfer coefficients for polonium.

226

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
Transfer coefficient (d-1)
Pathway

100 d

1y

5y

10 y

15 y

Adult

Plasma 2 to Blood

8.00E+02

8.00E+02

8.00E+02

8.00E+02

8.00E+02

8.00E+02

Plasma 2 to Kidneys 1

2.00E+02

2.00E+02

2.00E+02

2.00E+02

2.00E+02

2.00E+02

Plasma 1 to RBC

6.00E+00

6.00E+00

6.00E+00

6.00E+00

6.00E+00

6.00E+00

Plasma 1 to Plasma 3

4.00E+00

4.00E+00

4.00E+00

4.00E+00

4.00E+00

4.00E+00

Plasma 1 to Other

3.24E+01

3.24E+01

3.24E+01

3.24E+01

3.24E+01

3.24E+01

Plasma 1 to Liver 1

1.75E+01

1.75E+01

1.75E+01

1.75E+01

1.75E+01

1.75E+01

Plasma 1 to Liver 2

1.75E+01

1.75E+01

1.75E+01

1.75E+01

1.75E+01

1.75E+01

Plasma 1 to Kidneys 1

5.00E+00

5.00E+00

5.00E+00

5.00E+00

5.00E+00

5.00E+00

Plasma 1 to Kidneys 2

5.00E+00

5.00E+00

5.00E+00

5.00E+00

5.00E+00

5.00E+00

Plasma 1 to Spleen

2.00E+00

2.00E+00

2.00E+00

2.00E+00

2.00E+00

2.00E+00

Plasma 1 to Red marrow

4.00E+00

4.00E+00

4.00E+00

4.00E+00

4.00E+00

4.00E+00

Plasma 1 to Trab bone surface

7.50E-01

7.50E-01

7.50E-01

7.50E-01

7.50E-01

7.50E-01

Plasma 1 to Cort bone surface

7.50E-01

7.50E-01

7.50E-01

7.50E-01

7.50E-01

7.50E-01

Plasma 1 to Testes

1.00E-01

1.00E-01

1.00E-01

1.00E-01

1.00E-01

1.00E-01

Plasma 1 to Ovaries

5.00E-02

5.00E-02

5.00E-02

5.00E-02

5.00E-02

5.00E-02

Plasma 1 to Skin

5.00E+00

5.00E+00

5.00E+00

5.00E+00

5.00E+00

5.00E+00

RBC to Blood

9.90E-02

9.90E-02

9.90E-02

9.90E-02

9.90E-02

9.90E-02

Plasma 3 to Blood

9.90E-02

9.90E-02

9.90E-02

9.90E-02

9.90E-02

9.90E-02

Other to Plasma 1

9.90E-02

9.90E-02

9.90E-02

9.90E-02

9.90E-02

9.90E-02

Spleen to Plasma 1

9.90E-02

9.90E-02

9.90E-02

9.90E-02

9.90E-02

9.90E-02

Liver 1 to Small intestine contents

1.39E-01

1.39E-01

1.39E-01

1.39E-01

1.39E-01

1.39E-01

Liver 2 to Plasma 1

9.90E-02

9.90E-02

9.90E-02

9.90E-02

9.90E-02

9.90E-02

Kidneys 1 to Urinary bladder contents

1.73E-01

1.73E-01

1.73E-01

1.73E-01

1.73E-01

1.73E-01

Kidneys 2 to Plasma 1

9.90E-02

9.90E-02

9.90E-02

9.90E-02

9.90E-02

9.90E-02

Red marrow to Plasma 1

9.90E-02

9.90E-02

9.90E-02

9.90E-02

9.90E-02

9.90E-02

Trab bone surf to Plasma 1

2.31E-02

2.31E-02

2.31E-02

2.31E-02

2.31E-02

2.31E-02

Cort bone surf to Plasma 1

2.31E-02

2.31E-02

2.31E-02

2.31E-02

2.31E-02

2.31E-02

Skin to Plasma 1

6.93E-03

6.93E-03

6.93E-03

6.93E-03

6.93E-03

6.93E-03

Skin to Excreta

6.93E-03

6.93E-03

6.93E-03

6.93E-03

6.93E-03

6.93E-03

Testes to Plasma 1

1.39E-02

1.39E-02

1.39E-02

1.39E-02

1.39E-02

1.39E-02

Ovaries to Plasma 1

1.39E-02

1.39E-02

1.39E-02

1.39E-02

1.39E-02

1.39E-02

5559
5560

31.1.3.3. Treatment of radioactive progeny

5561
5562

The treatment of radioactive progeny produced in systemic compartments after intake
of a radioisotope of polonium is described in Section 11.2.3.3. of Publication 137 (ICRP, 2017).

227

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

5563

31.2. Dosimetric data for polonium

5564

Table 31.3. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 210Po compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled particulate materials (1 µm AMAD aerosols) 3 mo

1y

5y

10 y

15 y

Adult

Type F

5.1E-06

3.1E-06

1.8E-06

1.2E-06

4.5E-07

3.2E-07

Type M, Chloride, hydroxide, volatilised polonium;
all unspecified forms
8.5E-06

6.9E-06

4.1E-06

2.7E-06

1.9E-06

1.8E-06

Type S

1.2E-05

1.1E-05

6.3E-06

4.1E-06

3.2E-06

3.0E-06

Adult fA = 0.1, All other chemical forms

5.6E-06

2.1E-06

1.2E-06

8.7E-07

2.8E-07

1.8E-07

Adult fA = 0.5, Polonium in diet

2.8E-05

1.0E-05

6.1E-06

4.4E-06

1.4E-06

9.2E-07

Ingested materials

5565

228

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

32. RADON (Z = 86)

5566
5567

32.1. Routes of Intake

5568

32.1.1. Inhalation of short-lived radon and thoron progeny

5569
5570
5571
5572
5573
5574
5575
5576
5577
5578
5579

Absorption parameter values for radon progeny are addressed in the inhalation
sections of the elements (lead, bismuth and polonium) of Publication 137 (ICRP, 2017). These
values are summarised in Annex A of Publication 137 and in Table 32.1 below. As describedin Publication 130, OIR part 1, section 3.2.3 (ICRP, 2015), shared kinetics are assumed in the
respiratory tract.
Following deposition in the respiratory tract and subsequent clearance by particle
transport to the alimentary tract, the default age-dependent fA values given in Table 32.1 areapplied. These values are taken from the inhalation sections for lead, bismuth and polonium inthis report.
Table 32.1. Absorption parameter values for inhaled radon progeny.
Inhaledprogeny
Polonium
Lead
Bismuthradon

Polonium
Lead
Bismuth

5580
5581
5582
5583
5584
5585
5586
5587
5588
5589
5590
5591
5592

Dissolution parameter values
Uptake parameter valuessr (d–1) ss (d–1)
fbsb (d–1)
3
–
0
–
100
1.7
0.5
1.7
1
–
0
–
Age-dependent absorption from the alimentary tract, fA
3 months
1 year
5 years
10 years
15 years
Adult
0.2
0.1
0.1
0.1
0.1
0.1
0.6
0.3
0.3
0.3
0.3
0.2
0.1
0.05
0.05
0.05
0.05
0.05
fr
1
0.1
1

Aerosol characteristics need to be defined in order to calculate doses from inhaledradon or thoron progeny. The activity size distribution of the radon progeny aerosol can be veryvariable and depends upon the exposure scenario. In Publication 137, reference aerosolparameter values were given for indoor workplaces, mines and tourist caves for the purposesof dose calculations for workers (ICRP, 2017). For dose calculations for members of the public,
aerosol parameter values are given for home exposures following exposure to radon ( 222Rn) or
thoron (220Rn) progeny (Table 32.2). They are similar to the values assumed for indoor
workplaces, because the parameter values for workplaces were based on data for homes as well
as for workplaces when available (ICRP, 2017). Any differences are justified below.
Table 32.2. Reference aerosol parameter values for home exposures for radon ( 222Rn) progeny
and thoron (220Rn) progeny.
Nuclidesfp*

Equilibrium
factor, F

Radon(222Rn)progeny
Thoron(220Rn)progeny

0.1

0.4

0.02

-

Attached aerosol characteristics in the ambient air †Mode, i
fpi
AMTDi
σgi
hgfi‡
(nm)
n
0.2
30
2.0
1.75
a
0.8
200
2.0
1.75
n
a

0.14
0.86

229

40
200

2.0
1.8

1.75
1.75

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

5593
5594
5595
5596
5597
5598
5599
5600
5601

fp = unattached fraction in terms of the potential alpha energy concentration (PAEC); fpi = fraction of attached
PAEC for mode i; AMTD = activity median thermodynamic diameter; gi = geometric standard deviation of modei; hgfi = hygroscopic growth factor for mode i.
*The unattached progeny are assumed to have an AMTD of 1.0 nm with g = 1.3, and unit density and shapefactor.
†Indices i = ‘n’ and ‘a’ represent the nucleation and accumulation modes, respectively.
‡It is assumed that the AMTD increases by hgf instantaneously as the particle enters the nose or the mouth. For
simplicity, the hygroscopically enlarged particles are assumed to have unit density and shape factor.

5602

32.1.1.1. Radon progeny

5603
5604
5605
5606
5607
5608
5609
5610
5611
5612
5613
5614
5615
5616
5617
5618
5619
5620
5621
5622
5623
5624
5625
5626
5627
5628
5629
5630
5631
5632
5633
5634
5635
5636
5637
5638
5639
5640
5641

The aerosol parameter values for radon progeny are mainly based on the publicationsof Marsh et al. (2002) and Porstendörfer (2001). They are also consistent with the measurement
results from other researchers summarised in Publication 137 (ICRP, 2017) and in ICRU
Report 88 (ICRU, 2012).
The unattached fraction, fp depends inversely on the ambient particle concentration.
This depends on the ventilation rate and whether additional sources are present. The mean valueof fp measured in dwellings range between 0.04 and 0.2 with some values greater than 0.4(ICRP, 2017; ICRU, 2012). Compared with indoor workplaces, the air is assumed to be ‘cleaner’(i.e. a lower particle concentration), for example in the bedroom while asleep. Thus, a slightly
higher fp value of 0.1 is assumed for homes (Marsh et al., 2002, 2005; Marsh and Bailey, 2013).
The fraction of the attached potential alpha energy concentration (PAEC) of radon
progeny in the nucleation mode, fpn is assumed to be 0.2, the same as for indoor workplaces(ICRP, 2017). Measurements have shown that the nucleation mode is present when small
aerosols are produced, for example, by cooking, candle burning and gas combustion (ICRP,
2017; ICRU, 2012). However, activity size measurements performed in a house in Germany,
without additional aerosols (i.e. for an aged aerosol), also showed a nucleation mode with fpn
of about 0.2 (Reineking et al., 1994). In addition, measurements in a dwelling in Okinawa,
Japan showed a nucleation mode with an activity fraction of 0.14 (Kranrod et al., 2009). It is
acknowledged that for an aged aerosol, the presence of the nucleation mode is not always
measured (Huet et al., 2001). Without a nucleation mode the effective dose would decrease by
about 20% (Annex C, para. C.20 and Table C.9).
Measurements of the activity median diameter (AMD) of the accumulation mode in
dwellings show a wide range of values, typically between 90 nm to 350 nm (El-Hussein et al.,
1998; Huet et al., 2001; ICRU, 2012; Kranrod et al., 2009; Mohamed, 2005; Porstendörfer,
2001; Tokonami et al., 1997; Tu et al., 1991; Tu and Knutson, 1988). The mean of the average
AMD values in each of these studies is about 190 nm. Porstendörfer (2001) summarised activity
size measurements in dwellings and reported activity median diameters (AMD) of 20 to 40 nm
for the nucleation mode and 210 nm (120-350 nm) for the accumulation mode. A central valueof 200 nm is assumed here for the accumulation mode and 30 nm for the nucleation mode.
Some of the ambient aerosols, to which radon progeny attach, are hygroscopic and areassumed to grow very quickly on inhalation. For modelling purposes and simplicity, it isassumed that the activity median diameter increases by the hygroscopic growth factor (hgf)
instantaneously as the particle enters the nose or mouth. In Publication 137, a hgf of 2.0 was
assumed based on growth measurements of atmospheric aerosols as the relative humidity (RH)
increases from zero to 99% (ICRP, 2017). For example, Li and Hopke (1993) measured
average hgf between 1.5 and 1.9 for various types of indoor aerosols. Sinclair et al. (1974)
showed that atmospheric particles, which originated from an industrial area close to the sea,
increase by a factor of 2 due to hygroscopic growth. Because these measurements start withdried aerosols, they represent maximum growth (United Nations Scientific Committee on the230

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

5642
5643
5644
5645
5646
5647
5648

Effects of Atomic Radiation (UNSCEAR), 2020). The data of Sinclair et al. (1974) also showedthat the atmospheric particles would increase by factors of 1.5 and 1.8 as the humidity increases
from the RH of indoor air (30-50%) to 99% RH in the respiratory tract. Compared with
Publication 137, a lower hgf of 1.75 is assumed here, recognising that growth starts from the
RH of indoor air rather than for the experimentally dried aerosol. Assuming a hgf of 1.75 rather
than 2.0 only increases the effective dose per unit exposure by a few percent (Marsh andBirchall, 2000).

5649

32.1.1.2. Thoron progeny

5650
5651
5652
5653

In Publication 137, the aerosol parameter values assumed for thoron progeny forindoor workplaces are based on the measurements of Reineking et al. (1992) and on the values
recommended by Porstendörfer (2001). As these measurements were carried out in houses, thesame values are assumed for home exposures.

5654

32.1.1.3. Average breathing rates at home

5655
5656
5657
5658
5659
5660
5661
5662
5663
5664
5665
5666
5667
5668
5669
5670

For a given concentration of radon progeny the intake is directly proportional to theaverage breathing rate. To a lesser extent, the fraction of the intake deposited in the respiratory
tract (i.e. regional depositions) also depends on the breathing rate. At higher respiratory
frequencies during increased physical activities, the residence time in the airways decreases,
resulting in lower deposition by diffusion.
In Publication 66 (ICRP, 1994b), the ‘time-activity-ventilation’ approach was used to
calculate mean breathing rates for each reference individual. In this approach, the ventilation
rates for the four reference levels of exercise (sleep, sitting, light exercise and heavy exercise)are combined with the time spent in each level of exercise. The daily time budgets at home forthe reference individuals are given in Table 2.2, Section 2.2.1. Using these values, the fractionsof time spent in each activity at home are given in Table 32.3. The mean breathing rates arealso given in Table 32.3, obtained by combing these fractions with the reference ventilation
rates for each level of exercise (Table 2.1, Section 2.2.1).
Table 32.3. Mean breathing rates and distribution of time spent in various activities at home
for Reference Individuals.
Age

3 mo
1y
5y
10 y
15 y (Male)
Adult (Male)

Fraction of time spent in each level of exercise at
home
Sleep
SittingLight exercise
0.71
0.29
0.73
0.09
0.18
0.67
0.11
0.22
0.55
0.15
0.30
0.58
0.21
0.21
0.55
0.15
0.30

Mean
breathingrates (m3 h-1)
0.12
0.19
0.32
0.56
0.63
0.78

5671

32.1.2. Ingestion

5672
5673
5674
5675
5676
5677

Radon is soluble in water and volunteer experiments have shown that radon is readily
absorbed from the alimentary tract into blood. It has not been clearly established whether someabsorption takes place in the stomach or not. For details, see section 12 of Publication 137(ICRP, 2017). In the biokinetic model adopted in Publication 137 and in this document, it isassumed that radon gas does not diffuse from Stomach contents to Stomach wall, but that radonis absorbed to blood only via the small intestine.
231

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

5678
5679

32.1.3. Systemic Distribution, Retention and Excretion5680

32.1.3.1. Summary of biokinetic data

5681
5682
5683
5684
5685
5686
5687
5688
5689
5690
5691
5692
5693
5694
5695
5696
5697
5698
5699
5700
5701
5702
5703
5704
5705
5706
5707
5708
5709
5710
5711
5712
5713
5714
5715
5716
5717
5718
5719
5720
5721

The noble gases are chemically inert but are absorbed to blood from the lungs or
gastrointestinal tract and retained in systemic tissues to some extent, due in part to theirsolubility in blood and tissues. Radon returns from tissues to blood at tissue-specific rates andis recycled through the lungs and partly removed by exhalation and partly recycled to tissues.
It is almost entirely removed from the body over a few hours after intake. Loss of radon by
pathways other than inhalation (e.g., via skin, urine, or faeces) appears from experimental
studies to be small.
As described in Publication 137 (ICRP, 2017), the rate of transfer of radon from blood
to a tissue can be related to the fraction of cardiac output received by the tissue. The rate of
return from a tissue to blood can be estimated from the blood perfusion rate and the relative
solubility of the gas in blood and the tissue, represented by a gas-specific tissue-to-blood
partition coefficient. The partition coefficient for two compartments is defined as the ratio of
the concentrations of the gas in the compartments at equilibrium. Some experimentally
determined tissue-to-blood partition coefficients for radon and other noble gases are listed inTable 12.2 of Publication 137. Derived half-times for the build-up or washout of radon are a
few minutes for tissues with a rich blood supply and relatively low partition coefficients but
are much greater for fatty tissues because of their poor blood supply and relatively high tissueto-blood partition coefficient.
Measurements of 222Rn in breath and external measurements of the short-lived chain
member 214Bi have been used to estimate whole-body retention of radon in adult humansubjects after ingestion or inhalation of elevated levels (Andersson and Nilsson, 1964; Brown
and Hess, 1992; Fernau and Smereker, 1933; Gosink et al., 1990; Harley et al., 1951, 1994;
Hursh et al., 1965; Meyer, 1937; Suomela and Kahlos, 1972; Vaternahm, 1922; von Döbeln
and Lindell, 1964). The reader is referred to Publication 137 (ICRP, 2017) for descriptions ofseveral studies. The results of these studies on adult humans have been used as model-freedeterminations of total-body retention of radon as well as a check on the theoretical method ofmodeling the kinetics of radon in the body using partition coefficients.
Reported rates of loss of radon from the human body are variable, presumably due inlarge part to differences in experimental conditions such as the timing of intake of radon relative
to meals, the level of physical activity of the subjects after intake of radon, the percentage ofbody fat, and the length of the observation period. Retention half-times in the range 30-70 min
have been reported in several studies involving relatively short observation periods. Multiple
retention components with half-times varying from a few minutes to several hours have been
determined in some studies with relatively long observation periods.
Age-specific lung “washout” rates have been determined in persons inhaling air mixed
with xenon or krypton for several respiratory cycles (Treves et al. 1974; Ciofetta et al. 1980;
Treves and Packard 1995; Goo et al. 2013). Those data are assumed to be applicable to radon,
because observed washout times for xenon (Susskind et al. 1977) and krypton (Ellis et al. 1977)
in adults are consistent with washout times observed for radon in adults (Harley et al. 1994).
The removal half-time of xenon or krypton from lung air to the environment appears to increasenearly linearly from about 4-6 s in the first year of life to about 20-30 s in young adults.

5722

32.1.3.2. Biokinetic model for systemic radon

232

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

5723
5724
5725
5726

5727
5728
5729
5730
5731

The structure of the radon model applied in this report is shown in Figure 32.1. Agespecific transfer coefficients are listed in Table 32.4 for males and Table 32.5 for females. The
basis for the model is discussed in Annex C.

Figure 32.1. Structure of the biokinetic model for systemic radon. Abbreviations: RT-air =respiratory tract air; Blood-A = arterial blood; Blood-V = venous blood; Breast-g = glandular
breast tissue; Breast-a = adipose tissue in breast.

233

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

5732

Table 32.4. Age-specific transfer coefficients for males (d-1).
From

To

Environment
RT-airBlood-A
Blood-A
Blood-A
Blood-A
Blood-A
Blood-A
Blood-A
Blood-A
Blood-A
Blood-A
Blood-A
Blood-A
Fat 1
Fat 2
KidneysLiver

RT-airEnvironment
Fat 1
Fat 2
KidneysLiver
TB volume
CB volume
Y-Marrow 1
Y-Marrow 2
Red marrow
Breast-g
Breast-a
Other
Blood-V
Blood-V
Blood-V
Blood-V

TB volume
CB volume

Blood-V
Blood-V

Y-Marrow 1
Y-Marrow 2

Blood-V
Blood-V

Red marrow
Breast-g
Breast-a
Other

Blood-V
Blood-V
Blood-V
Blood-V

Other
Blood-V

Liver
RT-air

100 d

1y

5y

10 y

15 y

Adult

*
1.33E+04
4.91E+02
1.23E+02
2.33E+03
7.98E+02
2.21E+02
1.47E+02
1.52E-01
3.81E-02
3.68E+02
1.04E-02
1.07E-02
7.79E+03
5.58E+00*
1.20E+04
5.12E+02
1.28E+02
2.43E+03
8.32E+02
2.30E+02
1.54E+02
4.13E-01
1.03E-01
3.84E+02
2.39E-02
2.02E-02
8.13E+03
5.06E+00*
7.49E+03
5.18E+02
1.30E+02
2.46E+03
8.42E+02
2.33E+02
1.55E+02
3.34E+00
8.36E-01
3.89E+02
5.33E-02
4.41E-02
8.22E+03
9.44E+00*
5.44E+03
4.44E+02
1.11E+02
2.11E+03
7.22E+02
2.00E+02
1.33E+02
1.13E+01
2.82E+00
3.33E+02
3.58E-01
2.75E-01
7.04E+03
8.77E+00*
3.52E+03
2.89E+02
7.23E+01
1.37E+03
4.70E+02
6.51E+01
4.34E+01
1.73E+01
4.31E+00
2.17E+02
2.74E-01
5.93E-01
4.68E+03
7.52E+00*
2.60E+03
2.62E+02
6.54E+01
1.24E+03
4.25E+02
5.89E+01
3.92E+01
2.62E+01
6.54E+00
1.96E+02
3.11E-01
9.97E-01
4.22E+03
4.96E+00

1.39E+00
8.46E+03

1.27E+00
7.39E+03

2.36E+00
1.33E+04

2.19E+00
1.20E+04

1.88E+00
1.05E+04

1.24E+00
9.04E+03

2.16E+03
1.46E+03
2.50E+02
4.26E-01
1.06E-01
1.17E+03

1.96E+03
1.20E+03
2.04E+02
6.16E-01
1.54E-01
9.98E+02

3.21E+03
1.66E+03
2.75E+02
1.74E+00
4.36E-01
1.25E+03

3.24E+03
1.37E+03
2.28E+02
2.57E+00
6.41E-01
9.90E+02

2.52E+03
4.89E+02
8.14E+01
3.13E+00
7.82E-01
7.05E+02

1.94E+03
4.03E+02
6.72E+01
3.34E+00
8.34E-01
6.93E+02

8.59E+00
1.55E+00

1.37E+01
1.51E+00

3.91E+01
3.91E+00

5.95E+01
5.11E+00

8.54E+01
6.76E+00

1.14E+02
6.85E+00

4.65E+02
1.99E+02

3.86E+02
1.65E+02

5.61E+02
2.39E+02

4.90E+02
2.10E+02

3.34E+02
1.40E+02

2.78E+02
1.21E+02

4.54E+03
2.97E+03

4.73E+03
2.60E+03

4.79E+03
2.35E+03

4.11E+03
1.78E+03

2.67E+03
1.21E+03

2.42E+03
1.04E+03

RT-airBlood-A
1.92E+01
2.06E+01
2.06E+01
2.06E+01
2.06E+01
2.06E+01
ST contents
SI contents
5.99E+03
5.99E+03
5.99E+03
5.99E+03
5.99E+03
5.99E+03
SI contents
Liver−1* The rate that activity enters the RT air space is assumed to equal 𝜆𝐶𝑒𝑛𝑣 𝑉𝑅𝑇−𝑎𝑖𝑟 [𝐵𝑞 𝑑 ], where λ is the transfer coefficientfrom the RT-air space to the environment, Cenv is the radon concentration in the environment and VRT-air is the averagevolume of respiratory tract air space (Table 32.7).
TB = Trabecular bone; CB = cortical bone; Y-Marrow = yellow marrow; ST = stomach; SI = small intestine

5733
5734
5735

Table 32.5. Age-specific transfer coefficients for females (d-1)
From

To

Environment
RT-air

RT-airEnvironment

Blood-A

Fat 1

100 d

1y

5y

10 y

15 y

Adult

*
1.33E+04
4.91E+02*
1.20E+04
5.12E+02*
7.49E+03
5.18E+02*
5.44E+03
4.44E+02*
3.52E+03
6.70E+02*
2.60E+03
5.49E+02234

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
Blood-A
Blood-A
Blood-A
Blood-A
Blood-A
Blood-A
Blood-A
Blood-AFat 2
KidneysLiver
TB volume
CB volume
Y-Marrow 1
Y-Marrow 2
Red marrow

Blood-A
Blood-A

Breast-g
Breast-aBlood-A
Fat 1

Other
Blood-V

Fat 2
Kidneys

Blood-V
Blood-VLiver
TB volume
CB volume
Y-Marrow 1
Y-Marrow 2
Red marrow

Blood-V
Blood-V
Blood-V
Blood-V
Blood-V
Blood-V

Breast-g
Breast-a
Other
Other
Blood-V
RT-airBlood-V
Blood-V
Blood-V
Liver
RT-airBlood-A

1.23E+02
2.33E+03
7.98E+02

1.28E+02
2.43E+03
8.32E+02

1.30E+02
2.46E+03
8.42E+02

1.11E+02
2.11E+03
7.22E+02

1.68E+02
1.68E+03
6.41E+02

1.37E+02
1.37E+03
5.24E+02

2.21E+02
1.47E+02

2.30E+02
1.54E+02

2.33E+02
1.55E+02

2.00E+02
1.33E+02

8.87E+01
5.92E+01

7.26E+01
4.84E+01

1.52E-01
3.81E-02

4.13E-01
1.03E-01

3.34E+00
8.36E-01

1.13E+01
2.82E+00

3.02E+01
7.56E+00

3.23E+01
8.07E+00

3.68E+02
1.04E-02

3.84E+02
2.39E-02

3.89E+02
5.33E-02

3.33E+02
3.58E-01

2.96E+02
1.14E+01

2.42E+02
2.00E+01

1.07E-02
7.79E+03
5.58E+00
1.39E+00
8.46E+03
2.16E+03

2.02E-02
8.13E+03
5.06E+00
1.27E+00
7.39E+03
1.96E+03

4.41E-02
8.22E+03
9.44E+00
2.36E+00
1.33E+04
3.21E+03

2.75E-01
7.04E+03
8.77E+00
2.19E+00
1.20E+04
3.24E+03

8.33E+00
6.20E+03
7.75E+00
1.94E+00
9.80E+03
2.67E+03

1.23E+01
5.05E+03
5.84E+00
1.46E+00
8.28E+03
2.40E+03

1.46E+03
2.50E+02
4.26E-01
1.06E-01
1.17E+03
8.59E+00
1.55E+00
4.65E+02
1.99E+02
4.54E+03
2.97E+03
1.92E+01
5.99E+03

1.20E+03
2.04E+02
6.16E-01
1.54E-01
9.98E+02
1.37E+01
1.51E+00
3.86E+02
1.65E+02
4.73E+03
2.60E+03
2.06E+01
5.99E+03

1.66E+03
2.75E+02
1.74E+00
4.36E-01
1.25E+03
3.91E+01
3.91E+00
5.61E+02
2.39E+02
4.79E+03
2.35E+03
2.06E+01
5.99E+03

1.37E+03
2.28E+02
2.57E+00
6.41E-01
9.90E+02
5.95E+01
5.11E+00
4.90E+02
2.10E+02
4.11E+03
1.78E+03
2.06E+01
5.99E+03

5.35E+02
8.91E+01
4.31E+00
1.08E+00
7.61E+02
7.41E+01
5.63E+00
4.04E+02
1.87E+02
3.65E+03
1.39E+03
1.52E+01
5.99E+03

5.03E+02
8.39E+01
4.17E+00
1.04E+00
8.18E+02
7.69E+01
4.58E+00
3.69E+02
1.71E+02
2.98E+03
1.17E+03
1.52E+01
5.99E+03

ST contents
SI contents
SI contents
Liver* The rate that activity enters the RT air space is assumed to equal 𝜆𝐶𝑒𝑛𝑣 𝑉𝑅𝑇−𝑎𝑖𝑟 [𝐵𝑞 𝑑−1 ], where λ is the transfer
coefficient from the RT-air space to the environment, Cenv is the radon concentration in the environment and VRT-air
is the average volume of respiratory tract air space (Table 32.7).
TB = Trabecular bone; CB = cortical bone; Y-Marrow = yellow marrow; ST = stomach; SI = small intestine

5736
5737

32.1.3.3. Treatment of radioactive progeny

5738
5739

The treatment of radioactive progeny produced in systemic compartments after intake
of a radioisotope of radon is described in Section 12.3.3.3. of Publication 137 (ICRP, 2017).

5740

32.2. Dosimetric data for radon

5741

32.2.1. Effective dose coefficient from ingestion of radon gas

5742
5743
5744
5745

The effective dose coefficients for members of the public following ingestion of 222Rn
gas are given in
Table 32.6. Age-dependent effective dose coefficients following ingestion of radon
222Rn() gasǂ (Sv Bq-1).

235

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

5746
5747
5748
5749
5750
5751
5752
5753
5754

5755
5756
5757

Effective dose coefficients following ingestion of 222Rn gas (Sv Bq-1)
Age
3 months
1y
5y
10 y
15 y
Adult
4.0E-09
2.1E-09
1.2E-09
8.6E-10
7.5E-10
7.7E-10ǂDose coefficients for ingestion of thoron gas are not given in this report due to its short halflife.
The corresponding equivalent doses to organs per activity of 222Rn ingested are givenin the accompanying electronic annex. Dose coefficients for ingestion of 220Rn gas are not givenin this report due to its short half-life.
Table 32.6. Age-dependent effective dose coefficients following ingestion of radon ( 222Rn) gasǂ(Sv Bq-1).
Effective dose coefficients following ingestion of 222Rn gas (Sv Bq-1)
Age
3 months
1y
5y
10 y
15 y
Adult
4.0E-09
2.1E-09
1.2E-09
8.6E-10
7.5E-10
7.7E-10ǂDose coefficients for ingestion of thoron gas are not given in this report due to its short halflife.

5758
5759

32.2.2. Effective dose coefficients from inhalation of radon gas with its progeny and frominhalation of thoron progeny

5760
5761
5762
5763
5764
5765
5766
5767
5768
5769
5770
5771
5772
5773
5774
5775
5776
5777
5778
5779
5780
5781
5782
5783

Error! Reference source not found. provides age-dependent effective doses for theinhalation of radon (222Rn) in the home, expressed in units of mSv per Bq h m-3, mSv per mJ h
m-3, and mSv WLM-1. Dose coefficients are given for (i) the inhalation of radon gas alone, (ii)inhalation of the airborne radon progeny and (iii) their sum (gas + progeny). The assumed
aerosol parameter values for home exposures are given in Table 32.2. Calculations apply toreference members of the public at home with average breathing rates as given in Table 32.3.
Further details of the calculations of doses from radon and radon progeny are given in Annex
A of Publication 137 (ICRP, 2017).
In general, it is the inhalation of the airborne radon progeny rather than the inhalationof the radon gas that dominates the lung dose and the effective dose. The dose from inhaling
222
Rn gas is only a small fraction of the total effective dose: about 2% for adults at homeassuming F=0.4. (Table 32.7).
The effective dose per unit exposure to radon progeny is relatively insensitive to age(< 15%) because competing effects tend to cancel each other out. For example, children havelower breathing rates, so this decreases the intake and dose for a given activity air
concentration. However, this is partly compensated by the smaller target tissue masses, which
in turn increases the dose. Children have smaller airways which increase deposition bydiffusion, but this is compensated in part by smaller residence times (i.e. higher respiratory
frequencies) that decrease deposition by diffusion (Marsh and Birchall, 2000; National
Research Council (NRC), 1991; United Nations Scientific Committee on the Effects of Atomic
Radiation (UNSCEAR), 2020).
Table 32.7. Age-dependent effective doses per exposure to radon (222Rn) gas, radon progeny
and radon gas + progeny for homes.
Age

Effective dose per exposure*236

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
222

3 mo
1y
5y
10 y
15 y
Adult

5784
5785
5786
5787
5788
5789
5790
5791
5792
5793
5794
5795
5796
5797
5798
5799
5800
5801
5802

Rn gasmSv per mSv per
Bq h m-3
mJ h m-3 †9.8E-08
4.4E-02
1.1E-07
4.9E-02
1.4E-07
6.3E-02
1.6E-07
7.3E-02
1.7E-07
7.7E-02
1.9E-07
8.5E-02

Rn progeny‡
mSv per mSv per
Bq h m-3 † mJ h m-3
7.20E-06
3.24
8.46E-06
3.81
8.17E-06
3.67
9.54E-06
4.29
8.18E-06
3.68
9.32E-06
4.19
222

Total (222Rn gas + progeny)
mSv per mSv per mSv per
Bq h m-3
mJ h m-3
WLM
7.3E-06
3.3
12
8.6E-06
3.9
14
8.3E-06
3.7
13
9.7E-06
4.4
15
8.4E-06
3.8
13
9.5E-06
4.3
15*

For radon (222Rn), 1 mJ h m-3 = (1.80 × 105/F) Bq h m-3 where the equilibrium factor, F=0.4; 1 WLM=3.54 mJ h
m-3.
‡
The degree of precision of the values given is for computational purposes and does not reflect the certainty withwhich the central values are known.
†
Value calculated assuming F=0.4.

The age-dependent effective doses per exposure to radon (222Rn) progeny as a functionof the unattached fraction, fp and the fraction of the attached PAEC associated with thenucleation mode, fpn are given in the Annex C.
Table 32.8 gives the age-dependent effective dose coefficients following inhalation ofthoron (220Rn) progeny in homes. The dose coefficients are expressed in units of mSv per
WLM, mSv per mJ h m-3, and mSv per Bq h m-3 of equilibrium equivalent concentration (EEC)of 220Rn. The assumed aerosol parameter values for home exposures and the age-dependent
breathing rates are given in Tables 32.2 and 32.3 respectively. For thoron, no reference Fvalue is recommended. This is because thoron gas activity concentrations in air varysignificantly with position in a room due to its very short half-life (56 s), leading to a positiondependent relationship between thoron gas and its airborne progeny (ICRU, 2012).
Table 32.8. Age-dependent effective doses per exposure to thoron (220Rn) progeny for homes.
Age
Effective dose per exposure*Thoron (220Rn) progeny-3
nSv per Bq h m of EEC mSv per mJ h m-3
mSv per WLM
3 mo
76
1.0
3.6
1y
88
1.2
4.1
5y
81
1.1
3.8
10 y
90
1.2
4.2
15 y
78
1.0
3.6
Adult
86
1.1
4.0

5803
5804

*

5805

32.3. Use of dosimetric data for radon

5806
5807
5808
5809
5810
5811
5812
5813
5814

Protection of the public against radon in homes is based on measurement of radon gas,
the application of reference levels and optimisation (ICRP, 2014). Nevertheless, in somecircumstances, dose estimates are required in assessing public exposures and are also used incomparisons of sources of public exposure.
The effective dose coefficient per unit exposure to radon gas and progeny can bederived either by dosimetric calculations or by epidemiological comparisons. The
epidemiological approach gives values of 3.3 mSv per mJ h m-3 (12 mSv per WLM) for workers
and 2.5 mSv per mJ h m-3 (9 mSv per WLM) for members of the public (ICRP, 2017). In
comparison, effective dose coefficients calculated with ICRP reference biokinetic and

For thoron (220Rn), 1 WLM=4.68 × 104 Bq h m-3 of equilibrium equivalent concentration (EEC) of 220Rn; 1
WLM=3.54 mJ h m-3.

237

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

5815
5816
5817
5818
5819
5820
5821
5822
5823
5824
5825
5826
5827
5828
5829
5830
5831
5832
5833
5834
5835
5836
5837
5838
5839
5840
5841
5842
5843
5844
5845
5846
5847
5848
5849

dosimetric models gives values of 3 to 4 mSv per mJ h m-3 (11 to 14 mSv WLM-1) for workers
in mines, sedentary indoor workers and exposures in homes (ICRP, 2017). These values are
consistent with the recent review of radon epidemiology and dosimetry conducted by theUnited Nations Scientific Committee on the Effects of Atomic Radiation (Harrison, 2021;
Marsh et al., 2021; United Nations Scientific Committee on the Effects of Atomic Radiation(UNSCEAR), 2020).
The present situation shows good consistency between coefficients obtained bydosimetric calculations and conversion coefficients based on epidemiological comparisons.
However, the underlying uncertainties in both approaches should be recognised.
Taking account of both methods, Publication 137 recommended for workers a single
rounded value of 3 mSv per mJ h m-3 (approximately 10 mSv WLM-1) to be used in mostcircumstances of occupational exposure, with no adjustment for aerosol characteristics. A
second higher value of 6 mSv per mJ h m-3 (approximately 20 mSv per WLM) was referred toin ICRP Publication 137, for specific situations of indoor work involving substantial physicalactivity and for workers in tourist caves. However, this may be seen as an example of the need
to use site-specific data for more realistic dose calculations when warranted. Publication 137
provides additional dosimetric data for such calculations. ICRP recognises the difficulty indefining substantial physical activity for regulatory purposes and in most cases, it is notpractical to distinguish between workers with medium and high physical activities.
The dose coefficients given here for inhalation of radon by members of the public at
different ages (Table 32.7) are quite similar to the Publication 137 reference value (3 mSv permJ h m-3) for workers, with only small differences according to age at exposure. Taking accountof all available data, the Commission recommends the use of the same effective dose coefficientfor the inhalation of radon by members of the public in homes as for workers, that is 3 mSv permJ h m-3 (approximately 10 mSv per WLM).
In terms of measurements of 222Rn gas exposure, the dose coefficient of 3 mSv per mJ
h m-3 corresponds to 6.7 × 10-6 mSv per Bq h m-3, assuming an equilibrium factor, F, of 0.4.
With exposure parameters (F=0.4, occupancy of 7000 h y-1), an annual average radon
concentration at the upper reference level for homes of 300 Bq m-3 (Publication 126, ICRP,
2014) corresponds to an effective dose of 14 mSv.
Dose coefficients for the inhalation of thoron progeny in homes also show only small
differences according to age at exposure (Table 32.8). Based on these calculations, it isrecommended that a rounded value of 1 mSv per mJ h m-3 (approximately 4 mSv WLM-1 orabout 80 nSv per Bq h m-3 of EEC of 220Rn) is used for indoor public exposures at all ages.

238

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

33. RADIUM (Z = 88)

5850
5851

33.1. Routes of Intake

5852

33.1.1. Inhalation

5853
5854
5855
5856
5857
5858
5859
5860
5861
5862

Several studies have been reported on the behaviour of inhaled radium in man
following accidental intakes, especially of the sulphate, which was used in powder form in
gamma-ray sources. However, it is difficult to estimate the contribution of absorption to lungclearance in such cases, because the systemic excretion of radium is predominantly by the
faecal route. Information on absorption from the respiratory tract is available from experimental
studies of radium as nitrate, or in fly ash. For details, see Section 13 of Publication 137 (ICRP,
2017). Absorption parameter values and types, and associated fA values for particulate formsof radium are given in Table 33.1. (taken from Section 13 of Publication 137).
Table 33.1. Absorption parameter values for inhaled and ingested radium.
Inhaled particulate materials
Default parameter values†,‡
Absorption
Assigned forms
TypeF
Nitrate§M—
S—Ingested materials¶
Assigned forms
All chemical forms

fr

1
0.2
0.01

Absorption parameter values*sr (d–1)
ss (d–1)

10
3
3

–
0.005
0.0001Age-dependent absorption from the alimentary tract, fA
3 months 1 year
5 years
10 years
15 years
adult
0.6
0.3
0.3
0.3
0.3
0.2

5863
5864
5865
5866
5867
5868
5869
5870
5871
5872
5873
5874
5875
5876
5877

*

5878

33.1.2. Ingestion

5879

33.1.2.1. Adults

5880
5881
5882

Radium is a good chemical analogue of barium and calcium, Fasting and low calcium
intake increase its absorption. Results from human ingestion studies of radium soluble salt or224
RaSO4 in mock dial paint suggested fractional absorption in the order of 0.2-0.3 (For more

It is assumed that for radium the bound state can be neglected, i.e. fb = 0.0. The value of sr for Type F forms ofradium (10 d–1) is element-specific. The values for Types M and S (3 d–1) are the general default values.
†
Materials (e.g. nitrate) are generally listed here where there is sufficient information to assign to a default
absorption ype, but not to give specific parameter values (see Section 13 of Publication 137, ICRP, 2017).
‡
For inhaled material deposited in the respiratory tract and subsequently cleared by particle transport to thealimentary tract, the default fA values for inhaled materials are applied: i.e. the (rounded) product of fr for theabsorption type and the fA value for ingested soluble forms of radium applicable to the age-group of interest (e.g.
0.2 for adults).
§
Default Type M is recommended for use in the absence of specific information on which the exposure material
can be assigned to an absorption type, e.g. if the form is unknown, or if the form is known but there is no
information available on the absorption of that form from the respiratory tract.
¶
Activity transferred from systemic compartments into segments of the alimentary tract is assumed to be subject
to reabsorption to blood. The default absorption fraction fA for the secreted activity is the highest value foringestion of the radionuclide applicable to the age-group of interest (e.g. 0.2 for adults).

239

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

5883
5884
5885
5886
5887
5888

details, see Section 13 of Publication 137, ICRP, 2017). Data from balance studies reviewed
by the ICRP Task Group on Alkaline Earth Metabolism in Adult Man (ICRP, 1973) indicatedthe fraction of radium absorbed from food or drinking water to be between 0.15 and 0.21
(Stehney and Lucas Jr, 1956). In Publications 30 (ICRP, 1979), 67 (ICRP, 1993) and 137 (ICRP,
2017) an absorption fraction of 0.2 was recommended for all forms of radium. The same valueof fA = 0.2 is adopted here for adults.

5889

33.1.2.2. Children

5890
5891
5892
5893
5894
5895
5896
5897
5898
5899
5900
5901
5902
5903
5904

There is considerable evidence of elevated gastrointestinal absorption of the alkaline
earth elements by both laboratory animals and humans during periods of rapid growth, but there
is relatively little radium-specific information. Results reported by Muth and Glöbe1 (1983)
for 226Ra in food, water and human bone suggest a much higher rate of transfer of 226Ra fromdiet to bone during periods of rapid growth than during adulthood or periods of relatively slow
growth during childhood. In a study of variation with age in absorption of alkaline earths fromthe gastrointestinal tract of the rat, Taylor et al. (1962) determined that absorption of radium
averaged 79% in suckling rats, 11% in young adult rats and 3% in old rats. Similarly, data of
Della Rosa et al. (1967) suggest considerably greater gastrointestinal absorption of radium inimmature than in mature beagles. The available data for radium and other alkaline earth
elements, mainly strontium, suggest that two controlling factors may be variation with age ingastrointestinal absorption and corresponding changes in deposition and retention in theskeleton. In the absence of more specific information, fractional absorptions of radium of 0.6
for the infant and 0.3 for ages 1-15 years were recommended in Publication 67. The samevalues are adopted here for fA during childhood.

5905

33.1.3. Systemic Distribution, Retention and Excretion5906

33.1.3.1. Summary of biokinetic data

5907
5908
5909
5910
5911
5912
5913
5914
5915
5916
5917
5918
5919
5920
5921
5922
5923
5924
5925
5926

The alkaline earth element radium is a physiological analogue of the alkaline earths
calcium, strontium, and barium but has somewhat different biokinetics from those elements
due to discrimination by biological membranes and hydroxyapatite crystals of bone (ICRP,
1973; Leggett, 1992a). The biokinetics of radium resembles that of barium more closely thanthat of calcium or strontium.
Data on the systemic behaviour of radium in adults are reviewed in Publication 137(ICRP, 2017). Briefly, the biokinetics of radium and its physiological analogues barium,
strontium, and calcium has been studied extensively in adult human subjects with elevatedintakes of radioisotopes of radium and in more detailed investigations involving laboratory
animals, particularly dogs. Plasma disappearance curves indicate an outflow rate of several
hundred plasma volumes per day and rapid equilibration with an extravascular pool roughly
three times the size of the plasma pool. Based on controlled studies on adult human subjects it
is estimated that about a third of radium atoms leaving blood deposit in excretion pathways,
predominantly in the colon. Soft tissues initially accumulate a substantial portion of retained
systemic radium but lose most of the accumulated activity within a few days. After intravenous
administration of radium isotopes to adult dogs, soft tissues contained roughly 60% of retained
activity at one hour, 30% at 1 d, and 12% at 7 d. In adult dogs, the liver and kidneys containedroughly one-third of soft-tissue radium from 7 to 1200 d after intravenous administration. Bone
typically becomes the primary systemic repository of radium within the first day or two after
acute uptake to blood. Skeletal retention of radium in mature adult humans is estimated to240

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

5927
5928
5929
5930
5931
5932
5933
5934
5935
5936
5937
5938
5939
5940
5941
5942
5943
5944
5945
5946
5947
5948
5949
5950
5951
5952
5953
5954
5955
5956
5957
5958
5959

decrease from about 25-30% of injected activity in the first day or two after injection to roughly
8% after 1 month and 3% after 1 year.
Radium entering bone initially deposits on bone surface, from which activity isremoved over a period of hours or days back to blood and to a lesser extent to a trabecular or
cortical bone volume pool referred to as exchangeable bone volume. Activity entering this pool
may return to bone surface or blood over a period of weeks or months or they may enter a nonexchangeable bone volume pool, i.e., they may become firmly fixed in bone crystals andretained there until removed by relatively slow bone restructuring processes. It appears thatcalcium, strontium, barium, and radium are all about equally likely to transfer from bone
surface to exchangeable bone volume but that the likelihood of becoming firmly fixed in bone
crystal decreases in the order calcium > strontium > barium > radium. Data from human andanimal studies indicate that the rate of loss of alkaline earth tracers from bone over the first few
months after acute uptake to blood increases in the order calcium < strontium < barium <radium. Presumably these four elements are removed from trabecular or cortical nonexchangeable bone volume compartments at the rate of bone restructuring of that bone type, sothat the rate of transfer from non-exchangeable bone volume is independent of the element.
Information is available on the systemic behaviour of radium in immature humans(ICRP, 1973; Keane and Schlenker, 1987; Muth and Glōbel, 1983; Parks et al., 1978; Parks
and Keane, 1983). More detailed data on the age-specific behaviour of systemic radium areavailable for laboratory animals, particularly beagle dogs (Bruenger et al., 1983, 1989; Lloyd,
Bruenger, Jones, et al., 1983; Lloyd, Bruenger, Mays, et al., 1983; Lloyd, C.W. Jones, Bruenger,
Atherton, et al., 1983; Lloyd et al., 1982; Lloyd, G.N. Taylor, Jones and Mays, 1983; Lloyd,Mays and Atherton, 1976; Lloyd, Mays, Atherton, et al., 1976). Differences with age in thesystemic behaviour of radium are consistent with findings for other alkaline earth elements.
That is, retention of radium is greater in growing bone than in mature bone. Changes with age
in uptake of radium by the skeleton are roughly proportional to the age-specific rate of calcium
addition to bone from bone growth plus bone remodelling (Fig. 33.1). At times remote fromexposure, skeletal burdens acquired during periods of growth tend to remain higher than thoseacquired by mature skeletons except for skeletal burdens acquired during or soon after infancy,
when bone shows a particularly high rate of turnover. Both deposition and removal of radium
appear to be greater in areas of bone undergoing rapid remodelling than in areas of relatively
slow remodelling. Greater deposition of radium in the younger skeleton results in less systemic
radium available for excretion and distribution to soft tissues.

5960
5961
5962

Fig. 33.1. Comparison of the rate of calcium addition to bone with observations of total-bodyretention of 226Ra at 30 d after injection for different ages at injection. The calcium addition
241

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

5963
5964

rate is normalized to observed retention in a 17-year-old subject.

5965

33.1.3.2. Systemic model

5966
5967
5968
5969
5970
5971
5972
5973
5974
5975
5976
5977
5978
5979
5980
5981
5982
5983
5984
5985
5986
5987

The model for systemic radium applied in this report is a modification of the model
adopted in Publication 67 (ICRP, 1993). In the earlier version of the model the liver was
represented as a single compartment, and the kidneys were not depicted explicitly but were
included as part of Other soft tissues. In the present version of the model the kidneys are also
depicted explicitly, and both the liver and kidneys are modelled as two compartments
representing relatively fast and relatively slow loss of radium.
The structure of the model for systemic radium is shown in Fig. 33.2. Transfer
coefficients are listed in Table 33.2.
Transfer coefficients for adults are the same as those applied to workers in Publication
137 (ICRP, 2017). Extension of the model to preadult ages is based on results of studies of theage-specific behavior of radium in humans and laboratory animals, indicating that depositionof radium in bone is higher, and removal of radium from bone is faster, at preadult ages thanin adults. The age-specific deposition fraction for bone, and the division of that deposition
between trabecular and cortical bone surface, are based on the estimated rates of calcium
addition to each of these bone types. For preadult ages the deposition fractions for soft tissues
and excretion pathways are reduced uniformly from the values for adults to reflect the elevatedcompetition from bone for circulating radium. The removal half-times from bone surface andexchangeable bone volume compartments are assumed to be independent of age. The removal
half-times from bone volume compartments to blood are reference age-specific bone turnoverrates (ICRP, 2002a). Removal half-times from soft-tissue compartments are assumed to be
independent of age.

5988
5989
5990
5991
5992

Fig. 33.2. Model for systemic radium used in this report. Activity transferred from Blood toColon contents enters Right colon contents. SI = Small intestine.

242

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

5993

Table 33.2. Age-specific transfer coefficients for radium.

a

Path

Blood to Urinary bladder contents
Blood to Right colon contents
Blood to Trab bone surface
Blood to Cort bone surface
Blood to ST0
Blood to ST1
Blood to ST2
Blood to Liver 1
Blood to Kidneys 1
Trab bone surf to Blood
Trab bone surf to Exch trab bone volCort bone surf to Blood
Cort bone surf to Exch trab bone volST0 to Blood
ST1 to Blood
ST2 to BloodLiver 1 to BloodLiver 1 to Liver 2
Liver 2 to Blood
Kidneys 1 to Blood
Kidneys 1 to Kidneys 2
Kidneys 2 to Blood
Exch trab bone vol to Trab bone
surface
Exch to Nonexch trab bone volExch cort bone vol to Cort bone
surface
Exch to Nonexch cort bone vol
Nonexch cort bone vol to Blood
Nonexch trab bone vol to Blood

5994

a

100 d
2.02E-01
7.26E+00
1.05E+01
4.20E+01
6.98E+00
1.17E+00
2.33E-02
1.40E+00
4.67E-01
5.78E-01
1.16E-01
5.78E-01
1.16E-01
6.98E+00
6.93E-*01
3.80E-04
6.91E-01
2.08E-03
1.90E-03
2.07E+00
6.24E-03
1.90E-03
1.85E-02

1y
4.44E-01
1.60E+01
6.30E+00
2.52E+01
1.53E+01
2.57E+00
5.13E-02
3.08E+00
1.03E+00
5.78E-01
1.16E-01
5.78E-01
1.16E-01
6.98E+00
6.93E-01
3.80E-04
6.91E-01
2.08E-03
1.90E-03
2.07E+00
6.24E-03
1.90E-03
1.85E-02

Transfer coefficient (d-1)
5y
10 y
4.85E-01
3.56E-01
1.74E+01
1.28E+01
6.23E+00
9.87E+00
2.18E+01
2.93E+01
1.67E+01
1.23E+01
2.80E+00
2.05E+00
5.60E-02
4.11E-02
3.36E+00
2.46E+00
1.12E+00
8.21E-01
5.78E-01
5.78E-01
1.16E-01
1.16E-01
5.78E-01
5.78E-01
1.16E-01
1.16E-01
6.98E+00
6.98E+00
6.93E-01
6.93E-01
3.80E-04
3.80E-04
6.91E-01
6.91E-01
2.08E-03
2.08E-03
1.90E-03
1.90E-03
2.07E+00
2.07E+00
6.24E-03
6.24E-03
1.90E-03
1.90E-03
1.85E-02
1.85E-02

4.60E-03
1.85E-02

4.60E-03
1.85E-02

4.60E-03
1.85E-02

4.60E-03
1.85E-02

4.60E-03
1.85E-02

4.60E-03
1.85E-02

4.60E-03
8.22E-03
8.22E-03

4.60E-03
2.88E-03
2.88E-03

4.60E-03
1.53E-03
1.81E-03

4.60E-03
9.04E-04
1.32E-03

4.60E-03
5.21E-04
9.59E-04

4.60E-03
8.21E-05
4.93E-04

15 y
2.10E-01
7.55E+00
1.44E+01
3.74E+01
7.26E+00
1.21E+00
2.43E-02
1.46E+00
4.85E-01
5.78E-01
1.16E-01
5.78E-01
1.16E-01
6.98E+00
6.93E-01
3.80E-04
6.91E-01
2.08E-03
1.90E-03
2.07E+00
6.24E-03
1.90E-03
1.85E-02

Adult
6.06E-01
2.18E+01
9.72E+00
7.78E+00
2.09E+01
3.50E+00
7.00E-02
4.20E+00
1.40E+00
5.78E-01
1.16E-01
5.78E-01
1.16E-01
6.98E+00
6.93E-01
3.80E-04
6.91E-01
2.08E-03
1.90E-03
2.07E+00
6.24E-03
1.90E-03
1.85E-02

Trab = Trabecular, Cort = cortical, vol = volume, Exch = Exchangeable, Nonexch = Nonexchangeable

243

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

5995

33.2. Dosimetric data for radium

5996

Table 33.3. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 226Ra compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled particulate materials (1 µm AMAD aerosols) 3 mo

1y

5y

10 y

15 y

Adult

Type F, Nitrate

2.9E-06

8.8E-07

4.2E-07

4.2E-07

5.2E-07

1.5E-07

Type M, All unspecified forms

1.0E-05

8.3E-06

4.9E-06

3.2E-06

2.6E-06

2.3E-06

Type S

5.0E-05

4.9E-05

3.5E-05

2.6E-05

2.4E-05

2.4E-05

4.7E-06

9.5E-07

4.9E-07

5.0E-07

6.5E-07

1.3E-07

Ingested materials
Adult fA = 0.2, All forms

5997
5998

Table 33.4. Committed effective dose coefficients (Sv Bq-1) for the inhalation or ingestion of 228Ra compounds.
Effective dose coefficients (Sv Bq-1)
Inhaled particulate materials (1 µm AMAD aerosols) 3 mo

1y

5y

10 y

15 y

Adult

Type F, Nitrate

2.3E-05

5.5E-06

2.0E-06

2.0E-06

2.2E-06

3.7E-07

Type M, all unspecified forms

1.6E-05

1.1E-05

5.5E-06

3.6E-06

3.0E-06

2.0E-06

Type S

8.8E-05

8.8E-05

5.9E-05

4.1E-05

3.8E-05

4.0E-05

3.8E-05

6.2E-06

2.5E-06

2.5E-06

2.8E-06

3.4E-07

Ingested materials
Adult fA = 0.2, All forms

5999

244

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

6000

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ANNEX A. SUPPLEMENTARY INFORMATION RELATING TOAPPLICATION OF THE HRTM TO ENVIRONMENTALEXPOSURE

6979
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A.1. Deposition in respiratory tract regions for Reference Individuals as afunction of aerosol size

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(A 1) In the original HRTM, it was assumed that particles deposited in the nasal passages
during inhalation are partitioned equally between ET 1 and the posterior nasal passage, whichis part of ET2. [However, because of the way the deposition efficiencies were calculated forpolydispersed aerosols during inhalation and exhalation, for most aerosol sizes of interest inradiation protection the deposition fractions given in Publication 66 (ICRP, 1994) aresomewhat higher for ET2 than for ET1]. In the revised HRTM, it is assumed that for nose
breathing, the deposit in the ET airways is distributed 65% to ET1 and 35% to ET2. To calculate
the fractions of inhaled material deposited in ET1 and ET2 in the revised HRTM, the fractions
deposited in ET1 and ET2 (calculated using the original HRTM) were summed to give the total
deposit in the ET airways, and then re-partitioned 65% to ET1 and 35% to ET2.For mouth
breathing, there is no deposition in ET1 and the fraction deposited in ET2 remains as calculatedusing the original HRTM.
(A 2) Table A.1 gives values of fractional deposition in each region of the respiratory tract
as a function of aerosol size, for each Reference Individual and for the time budget andventilation parameter values used in this series of reports for environmental exposure (Main
Text, Table 2.3). Values for the Reference Individuals for aerosols of 1 μm AMAD inhaledfor environmental exposure are given in the Main Text (Table 2.4). Tables of fractional
deposition for each Reference Individual at each exercise level are provided in a supplementary
file.
Table A.1. Fractional deposition in regions of the respiratory tract for environmental exposure
as a function of aerosol size *,†,‡.
(a) Infant 3 mo old (breathing rate = 0.12 m3 h–1)
µm
ET1
ET2
BB
AMTD
0.001
5.520×10‒1 2.972×10‒1 1.187×10‒1
0.003
3.519×10‒1 1.895×10‒1 1.827×10‒10.01
1.383×10‒1 7.446×10‒2 8.727×10‒2
0.03
5.918×10‒2 3.187×10‒2 3.742×10‒2
0.1
5.480×10‒2 2.951×10‒2 1.970×10‒2
AMAD
0.3
1
3
5
10
20

7005
7006

1.038×10‒1
3.131×10‒14.908×10‒1
5.177×10‒14.931×10‒14.311×10‒1

5.588×10‒2
1.686×10‒12.643×10‒12.788×10‒12.655×10‒12.321×10‒11.432×10‒2
1.042×10‒2
1.021×10‒2
8.978×10‒36.050×10‒33.066×10‒3(b) Infant 1 y old (breathing rate = 0.22 m3 h–1)
µm
ET1
ET2
BB

264

bb

AI

Total

2.124×10‒2
1.989×10‒12.707×10‒11.530×10‒17.764×10‒23.060×10‒51.687×10‒2
2.365×10‒13.500×10‒12.126×10‒19.892×10‒1
9.398×10‒18.072×10‒1
6.314×10‒1
3.942×10‒15.144×10‒22.045×10‒2
9.462×10‒3
6.335×10‒33.057×10‒3
1.085×10‒3

1.541×10‒18.562×10‒24.645×10‒22.910×10‒2
1.169×10‒2
3.274×10‒33.795×10‒15.981×10‒18.212×10‒18.408×10‒17.795×10‒16.707×10‒1

bb

AI

Total

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

7007
7008

AMTD
0.001
0.003
0.01
0.03
0.1

5.434×10‒13.406×10‒11.322×10‒15.746×10‒2
5.479×10‒22.926×10‒11.834×10‒1
7.121×10‒2
3.094×10‒22.950×10‒2

1.124×10‒11.460×10‒16.436×10‒22.758×10‒2
1.459×10‒2

3.911×10‒2
2.318×10‒12.439×10‒11.304×10‒16.476×10‒2

2.319×10‒4
3.787×10‒23.215×10‒14.105×10‒12.377×10‒1

9.878×10‒19.396×10‒18.332×10‒1
6.569×10‒14.013×10‒1

AMAD
0.3
1
3
5
10
20

1.047×10‒1
3.144×10‒14.910×10‒15.176×10‒14.930×10‒14.311×10‒1

5.638×10‒2
1.693×10‒12.644×10‒12.787×10‒12.655×10‒12.321×10‒11.109×10‒2
1.041×10‒2
1.147×10‒21.014×10‒26.757×10‒33.355×10‒34.250×10‒21.707×10‒28.506×10‒3
5.898×10‒3
2.936×10‒3
1.056×10‒3

1.708×10‒19.636×10‒2
5.314×10‒2
3.329×10‒2
1.329×10‒2
3.673×10‒33.854×10‒16.075×10‒18.286×10‒18.457×10‒17.815×10‒16.713×10‒1

bb

AI

Total

5.396×10‒22.434×10‒12.261×10‒11.240×10‒16.050×10‒2

6.077×10‒4
5.398×10‒2
3.514×10‒1
3.679×10‒11.958×10‒19.835×10‒1
9.296×10‒1
8.273×10‒16.060×10‒1
3.380×10‒1

3.977×10‒21.851×10‒2
1.253×10‒29.703×10‒3
5.389×10‒3
2.107×10‒31.420×10‒19.855×10‒2
6.861×10‒2
4.684×10‒22.068×10‒2
6.249×10‒3

3.118×10‒15.245×10‒17.822×10‒18.193×10‒17.724×10‒16.690×10‒1

bb

AI

Total

7.860×10‒2
2.523×10‒12.016×10‒11.090×10‒1
5.219×10‒22.590×10‒3
9.347×10‒2
4.169×10‒1
3.789×10‒1
1.918×10‒19.835×10‒19.355×10‒1
8.483×10‒15.954×10‒1
3.248×10‒1

3.418×10‒21.702×10‒2
1.299×10‒2
1.041×10‒2
5.957×10‒32.381×10‒3

1.371×10‒19.513×10‒26.757×10‒2
4.667×10‒2
2.099×10‒2
6.478×10‒33.056×10‒15.300×10‒17.862×10‒1
8.213×10‒1
7.729×10‒16.690×10‒1

bb

AI

Total

9.531×10‒22.561×10‒15.717×10‒3
1.124×10‒19.814×10‒19.334×10‒1(c) Child 5y old (breathing rate = 0.36 m3 h–1)
µm
ET1
ET2
BB
AMTD
0.001
5.395×10‒1 2.905×10‒1 9.893×10‒2
0.003
3.356×10‒1 1.807×10‒1 1.161×10‒10.01
1.304×10‒1 7.021×10‒2 4.931×10‒2
0.03
5.973×10‒2 3.216×10‒2 2.212×10‒2
0.1
4.551×10‒2 2.451×10‒2 1.164×10‒2
AMAD
0.3
1
3
5
10
20

7009
7010

4.235×10‒21.390×10‒12.406×10‒12.624×10‒12.580×10‒12.295×10‒19.022×10‒31.035×10‒2
1.372×10‒2
1.294×10‒2
9.292×10‒3
4.926×10‒3(d) Child 10 y old (breathing rate = 0.64 m3 h–1)
µm
ET1
ET2
BB
AMTD
0.001
5.293×10‒1 2.850×10‒1 8.804×10‒2
0.003
3.233×10‒1 1.741×10‒1 9.244×10‒2
0.01
1.249×10‒1 6.723×10‒2 3.782×10‒2
0.03
5.863×10‒2 3.157×10‒2 1.722×10‒2
0.1
4.658×10‒2 2.508×10‒2 9.166×10‒3
AMAD
0.3
1
3
5
10
20

7011
7012

7.864×10‒22.581×10‒1
4.468×10‒14.874×10‒14.791×10‒1
4.262×10‒18.224×10‒22.640×10‒1
4.483×10‒14.871×10‒14.781×10‒14.256×10‒14.428×10‒2
1.421×10‒12.414×10‒12.623×10‒12.574×10‒12.292×10‒17.774×10‒3
1.167×10‒2
1.595×10‒2
1.484×10‒2
1.042×10‒2
5.419×10‒3(e) 15 y male (breathing rate = 0.84 m3 h–1)
µm
ET1
ET2
BB
AMTD
0.001
4.911×10‒1 3.017×10‒1 8.757×10‒20.003
3.000×10‒1 1.792×10‒1 8.582×10‒2

265

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

7013
7014

0.01
0.03
0.1

1.161×10‒15.471×10‒23.770×10‒2

6.872×10‒2
3.252×10‒22.182×10‒2

3.443×10‒2
1.571×10‒28.451×10‒3

1.948×10‒11.048×10‒15.002×10‒2

4.331×10‒13.772×10‒11.889×10‒18.472×10‒1
5.848×10‒1
3.069×10‒1

AMAD
0.3
1
3
5
10
20

6.037×10‒22.049×10‒13.792×10‒14.250×10‒1
4.298×10‒13.896×10‒13.381×10‒2
1.155×10‒12.233×10‒12.569×10‒12.689×10‒12.505×10‒17.770×10‒3
1.689×10‒22.965×10‒2
2.991×10‒22.254×10‒21.201×10‒2

3.320×10‒2
1.995×10‒2
1.938×10‒2
1.658×10‒21.002×10‒2
4.127×10‒3

1.367×10‒11.065×10‒18.596×10‒2
6.236×10‒2
2.968×10‒2
9.589×10‒32.718×10‒1
4.638×10‒17.376×10‒17.907×10‒1
7.609×10‒16.657×10‒1

bb

AI

Total

9.028×10‒2
2.633×10‒12.002×10‒11.066×10‒15.105×10‒2

3.595×10‒3
1.056×10‒14.459×10‒14.051×10‒12.062×10‒19.844×10‒19.422×10‒18.676×10‒1
6.148×10‒13.265×10‒13.387×10‒2
1.951×10‒2
1.766×10‒2
1.483×10‒2
8.872×10‒3
3.669×10‒3

1.498×10‒11.148×10‒19.004×10‒2
6.456×10‒23.035×10‒29.724×10‒3

2.898×10‒14.858×10‒17.554×10‒18.028×10‒1
7.662×10‒1
6.673×10‒1(f) 20 y (male) (breathing rate = 0.93 m3 h–1)
µm
ET1
ET2
BB
AMTD
0.001
5.182×10‒1 2.877×10‒1 8.460×10‒2
0.003
3.152×10‒1 1.738×10‒1 8.430×10‒2
0.01
1.212×10‒1 6.668×10‒2 3.369×10‒2
0.03
5.669×10‒2 3.121×10‒2 1.524×10‒2
0.1
3.953×10‒2 2.163×10‒2 8.126×10‒3
AMAD
0.3
1
3
5
10
20

6.421×10‒2
2.194×10‒14.049×10‒1
4.529×10‒14.571×10‒14.136×10‒1

3.486×10‒2
1.192×10‒12.222×10‒12.501×10‒12.545×10‒12.320×10‒1

7.082×10‒3
1.286×10‒22.071×10‒22.049×10‒2
1.536×10‒2
8.328×10‒3

7015
7016
7017
7018
7019
7020
7021
7022
7023
7024
7025
7026
7027
7028
7029
7030
7031

*Reference values are given to a greater degree of precision than would be chosen to reflect the certainty withwhich the average value of each parameter is known.
†
The particles are assumed to have density 3.00 g cm –3, and shape factor 1.5 (typical of compact, irregular, i.e.
non-spherical particles). The particle diameters are assumed to be log-normally distributed with geometricstandard deviation, σg increasing from a value of 1.0 at 0.6 nm to a value of 2.5 above approximately 1 μm
[Publication 66 (ICRP, 1994), Paragraph 170]. The value of σg is not a reference value, but is derived from thecorresponding AMTD (ICRP, 1994).
‡
The distribution of time spent at each of the four reference exercise levels are as given in Table 2.3. The
deposition fractions are volume-weighted average values for deposition at the four exercise levels.

7032

A.2. Reference values for regional deposition

7033
7034
7035
7036

(A 4) Tables A.2-A.5 provide fractional deposition in each region of the respiratory tractfor each Reference Individual at each exercise level (sleep, rest, light exercise and heavy
exercise) as a function of aerosol size.

(A 3) For aerosols with an AMAD below approximately 0.3 µm, deposition in the
respiratory tract is dominated by thermodynamic mechanisms (i.e. diffusion) and as a result,deposition fractions are mainly dependent on the AMTD. Table A.1 therefore tabulates
deposition fractions against the AMTD in this size range. For aerosols with an AMAD above
approximately 0.3 µm, deposition in the respiratory tract is dominated by impaction andsedimentation, and so deposition fractions are mainly dependent on the AMAD. Therefore, inthis size range, Table A.1 tabulates deposition fractions against AMAD.

266

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

7037
7038
7039

Fractional depositions for environmental exposure (Table A.1) are calculated as volumeweighted average values for deposition at the four exercise levels (Tables A.2-A.5). For eachregional deposition DE:
47040

𝐷𝐸 = ∑ 𝑤𝑖 𝐷𝐸𝑖

7041

where DEi is the fractional deposition at exercise level i and the volume-weight is
𝐵𝑗 𝑡𝑗
𝑤𝑗 = 4∑𝑖=1 𝐵𝑖 𝑡𝑖
where Bi and ti are the breathing rate and the time spent at the exercise level i. The breathing
rate (m3 h‒1) and the distribution of time spent (h) at each of the four reference exercise levels
are given in Table 2.3 for each Reference Individual.

𝑖=1

7042
7043
7044
7045
7046
7047
7048
7049
7050
7051
7052
7053

Deposition data contained in Tables A.1-A.5 may also be accessed by the user by using theData Viewer.
Table A.2. Fractional deposition in regions of the respiratory tract for sleeping subjects (normal
nose breathers) as a function of aerosol size *,†.
(a) Infant 3 mo old (breathing rate = 0.09 m3 h–1)
µm
ET1
ET2
BB
AMTD
0.001
5.592E-01 3.011E-01 1.168E-01
0.003
3.616E-01 1.947E-01 2.016E-01
0.01
1.436E-01 7.734E-02 1.012E-01
0.03
6.122E-02 3.297E-02 4.365E-02
0.1
4.695E-02 2.528E-02 2.299E-02
AMAD
0.3
1
3
5
10
20

7054
7055

8.272E-02
2.718E-01
4.621E-01
4.993E-01
4.854E-01
4.286E-01

4.454E-02
1.464E-01
2.488E-01
2.688E-01
2.613E-01
2.308E-01

1.636E-02
1.040E-02
1.002E-02
9.121E-03
6.523E-03
3.511E-03(b) Infant 1 y old (breathing rate = 0.15 m3 h–1)
µm
ET1
ET2
BB
AMTD
0.001
5.528E-01 2.977E-01 1.139E-01
0.003
3.527E-01 1.900E-01 1.676E-01
0.01
1.387E-01 7.470E-02 7.788E-02
0.03
5.973E-02 3.216E-02 3.345E-02
0.1
4.511E-02 2.429E-02 1.761E-02
AMAD
0.3
1
3
5
10
20

7.864E-02
2.622E-01
4.537E-01
4.934E-01
4.827E-01
4.277E-01

4.234E-02
1.412E-01
2.443E-01
2.657E-01
2.599E-01
2.304E-01

1.277E-02
9.810E-03
1.103E-02
1.030E-02
7.442E-03
3.999E-03

267

bb

AI

Total

1.156E-02
1.708E-01
2.841E-01
1.678E-01
8.667E-02

1.224E-06
6.617E-03
1.779E-01
2.972E-01
1.871E-01

9.887E-01
9.354E-01
7.841E-01
6.029E-01
3.690E-01

5.821E-02
2.464E-02
1.242E-02
8.574E-03
4.276E-03
1.563E-03

1.394E-01
8.720E-02
5.332E-02
3.490E-02
1.475E-02
4.318E-03

3.412E-01
5.404E-01
7.867E-01
8.207E-01
7.723E-01
6.688E-01

bb

AI

Total

2.268E-02
2.065E-01
2.657E-01
1.480E-01
7.484E-02

1.479E-05
1.658E-02
2.491E-01
3.604E-01
2.179E-01

9.871E-01
9.334E-01
8.061E-01
6.337E-01
3.797E-01

4.989E-02
2.153E-02
1.181E-02
8.493E-03
4.414E-03
1.657E-03

1.619E-01
1.052E-01
6.665E-02
4.397E-02
1.866E-02
5.448E-03

3.455E-01
5.399E-01
7.875E-01
8.219E-01
7.731E-01
6.692E-01

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

7056
7057

(c) Child 5 y old (breathing rate = 0.12 m3 h–1)
µm
ET1
ET2
BB
AMTD
0.001
5.503E-01 2.963E-01 1.045E-01
0.003
3.493E-01 1.881E-01 1.395E-01
0.01
1.371E-01 7.383E-02 6.226E-02
0.03
6.120E-02 3.296E-02 2.758E-02
0.1
3.869E-02 2.083E-02 1.448E-02
AMAD
0.3
1
3
5
10
20

7058
7059

1.051E-02
9.099E-03
1.248E-02
1.261E-02
1.001E-02
5.849E-03

4.609E-02
1.630E-01
3.508E-01
4.149E-01
4.417E-01
4.121E-01

2.482E-02
8.775E-02
1.889E-01
2.234E-01
2.379E-01
2.218E-01

9.649E-03
8.594E-03
1.312E-02
1.395E-02
1.181E-02
7.334E-03(e) 15 y male (breathing rate = 0.42 m3 h–1)
µm
ET1
ET2
BB
AMTD
0.001
5.470E-01 2.945E-01 9.608E-02
0.003
3.449E-01 1.857E-01 1.182E-01
0.01
1.351E-01 7.275E-02 5.110E-02
0.03
6.179E-02 3.328E-02 2.307E-02
0.1
3.444E-02 1.855E-02 1.203E-02
AMAD
0.3
1
3
5
10
20

7062
7063

3.051E-02
1.077E-01
2.122E-01
2.422E-01
2.482E-01
2.261E-01(d) Child 10 y old (breathing rate = 0.31 m3 h–1)
µm
ET1
ET2
BB
AMTD
0.001
5.493E-01 2.958E-01 1.004E-01
0.003
3.481E-01 1.874E-01 1.295E-01
0.01
1.366E-01 7.355E-02 5.704E-02
0.03
6.169E-02 3.322E-02 2.551E-02
0.1
3.593E-02 1.935E-02 1.336E-02
AMAD
0.3
1
3
5
10
20

7060
7061

5.667E-02
2.001E-01
3.942E-01
4.497E-01
4.609E-01
4.198E-01

4.027E-02
1.398E-01
3.202E-01
3.888E-01
4.260E-01
4.053E-01

2.168E-02
7.528E-02
1.724E-01
2.093E-01
2.294E-01
2.182E-01

8.691E-03
8.216E-03
1.382E-02
1.525E-02
1.352E-02
8.732E-03(f) 20 y (male) (breathing rate = 0.45 m3 h–1)
µm
ET1
ET2
BB

268

bb

AI

Total

3.271E-02
2.254E-01
2.560E-01
1.443E-01
7.211E-02

4.233E-05
2.418E-02
2.817E-01
3.505E-01
1.984E-01

9.838E-01
9.264E-01
8.109E-01
6.165E-01
3.445E-01

4.826E-02
2.426E-02
1.795E-02
1.439E-02
8.373E-03
3.446E-03

1.498E-01
1.199E-01
9.449E-02
6.765E-02
3.168E-02
1.011E-02

2.957E-01
4.611E-01
7.313E-01
7.865E-01
7.592E-01
6.653E-01

bb

AI

Total

3.685E-02
2.321E-01
2.545E-01
1.442E-01
7.177E-02

5.550E-05
2.668E-02
2.906E-01
3.449E-01
1.919E-01

9.824E-01
9.237E-01
8.123E-01
6.095E-01
3.323E-01

4.841E-02
2.758E-02
2.436E-02
2.065E-02
1.276E-02
5.529E-03

1.466E-01
1.309E-01
1.156E-01
8.679E-02
4.318E-02
1.459E-02

2.756E-01
4.178E-01
6.928E-01
7.597E-01
7.473E-01
6.614E-01

bb

AI

Total

4.267E-02
2.376E-01
2.450E-01
1.383E-01
6.836E-02

9.551E-05
3.199E-02
3.030E-01
3.379E-01
1.836E-01

9.803E-01
9.184E-01
8.069E-01
5.943E-01
3.170E-01

4.644E-02
2.983E-02
3.019E-02
2.659E-02
1.708E-02
7.658E-03

1.401E-01
1.319E-01
1.255E-01
9.751E-02
5.075E-02
1.790E-02

2.572E-01
3.850E-01
6.622E-01
7.375E-01
7.367E-01
6.578E-01

bb

AI

Total

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

7064
7065
7066
7067
7068
7069
7070
7071
7072
7073
7074
7075

AMTD
0.001
0.003
0.01
0.03
0.1

5.463E-01
3.441E-01
1.345E-01
6.099E-02
3.385E-02

2.942E-01
1.853E-01
7.241E-02
3.285E-02
1.823E-02

9.632E-02
1.172E-01
5.036E-02
2.252E-02
1.176E-02

4.523E-02
2.468E-01
2.525E-01
1.411E-01
6.997E-02

9.859E-05
3.317E-02
3.164E-01
3.621E-01
1.994E-01

9.821E-01
9.266E-01
8.262E-01
6.195E-01
3.332E-01

AMAD
0.3
1
3
5
10
20

3.903E-02
1.350E-01
3.133E-01
3.828E-01
4.224E-01
4.038E-01

2.102E-02
7.269E-02
1.686E-01
2.061E-01
2.275E-01
2.174E-01

8.516E-03
8.189E-03
1.405E-02
1.562E-02
1.398E-02
9.102E-03

4.780E-02
3.163E-02
3.257E-02
2.877E-02
1.853E-02
8.329E-03

1.529E-01
1.448E-01
1.381E-01
1.073E-01
5.592E-02
1.975E-02

2.693E-01
3.923E-01
6.667E-01
7.406E-01
7.383E-01
6.584E-01*Reference values are given to a greater degree of precision than would be chosen to reflect the certainty withwhich the average value of each parameter is known.
†
The particles are assumed to have density 3.00 g cm –3, and shape factor 1.5 (typical of compact, irregular, i.e.
non-spherical particles). The particle diameters are assumed to be log-normally distributed with geometricstandard deviation, σg increasing from a value of 1.0 at 0.6 nm to a value of 2.5 above approximately 1 μm
[Publication 66 (ICRP, 1994), Paragraph 170]. The value of σg is not a reference value, but is derived from thecorresponding AMTD (ICRP, 1994).

Table A.3. Fractional deposition in regions of the respiratory tract for resting (sitting) subjects(normal nose breathers) as a function of aerosol size. *(a) Infant 1 y old (breathing rate = 0.22 m3 h–1)
µm
ET1
ET2
BB
AMTD
0.001
5.448E-01 2.934E-01 1.147E-01
0.003
3.420E-01 1.842E-01 1.494E-01
0.01
1.329E-01 7.155E-02 6.556E-02
0.03
5.717E-02 3.078E-02 2.783E-02
0.1
5.153E-02 2.775E-02 1.467E-02
AMAD
0.3
1
3
5
10
20

7076
7077

9.833E-02
3.065E-01
4.881E-01
5.165E-01
4.930E-01
4.312E-01

5.295E-02
1.650E-01
2.628E-01
2.782E-01
2.654E-01
2.322E-01

1.102E-02
1.019E-02
1.150E-02
1.028E-02
6.913E-03
3.440E-03(b) Child 5 y old (breathing rate = 0.32 m3 h–1)
µm
ET1
ET2
BB
AMTD
0.001
5.442E-01 2.930E-01 1.033E-01
0.003
3.413E-01 1.838E-01 1.265E-01
0.01
1.328E-01 7.152E-02 5.426E-02
0.03
5.961E-02 3.209E-02 2.399E-02
0.1
4.118E-02 2.217E-02 1.261E-02
AMAD
0.3
1

6.676E-02
2.313E-01

3.594E-02
1.245E-01

9.420E-03
9.661E-03

269

bb

AI

Total

3.566E-02
2.353E-01
2.515E-01
1.329E-01
6.600E-02

8.444E-05
3.193E-02
3.196E-01
4.269E-01
2.532E-01

9.887E-01
9.428E-01
8.411E-01
6.755E-01
4.131E-01

4.338E-02
1.731E-02
8.392E-03
5.737E-03
2.807E-03
9.896E-04

1.842E-01
1.065E-01
5.858E-02
3.638E-02
1.428E-02
3.861E-03

3.899E-01
6.055E-01
8.294E-01
8.471E-01
7.824E-01
6.717E-01

bb

AI

Total

4.426E-02
2.439E-01
2.428E-01
1.326E-01
6.541E-02

1.465E-04
3.834E-02
3.331E-01
3.864E-01
2.141E-01

9.849E-01
9.337E-01
8.345E-01
6.347E-01
3.555E-01

4.332E-02
2.050E-02

1.589E-01
1.172E-01

3.143E-01
5.032E-01

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
3
5
10
20

7078
7079

1.331E-02
1.297E-02
9.724E-03
5.349E-03

5.147E-02
1.835E-01
3.758E-01
4.352E-01
4.530E-01
4.166E-01

2.772E-02
9.881E-02
2.023E-01
2.344E-01
2.440E-01
2.243E-01

8.890E-03
9.030E-03
1.392E-02
1.442E-02
1.171E-02
6.952E-03(d) 15 y male (breathing rate = 0.48 m3 h–1)
µm
ET1
ET2
BB
AMTD
0.001
5.441E-01 2.930E-01 9.487E-02
0.003
3.412E-01 1.837E-01 1.122E-01
0.01
1.332E-01 7.174E-02 4.778E-02
0.03
6.131E-02 3.302E-02 2.163E-02
0.1
3.489E-02 1.879E-02 1.127E-02
AMAD
0.3
1
3
5
10
20

7082
7083

2.293E-01
2.549E-01
2.547E-01
2.285E-01(c) Child 10 y old (breathing rate = 0.38 m3 h–1)
µm
ET1
ET2
BB
AMTD
0.001
5.450E-01 2.935E-01 9.875E-02
0.003
3.424E-01 1.844E-01 1.198E-01
0.01
1.337E-01 7.198E-02 5.142E-02
0.03
6.099E-02 3.285E-02 2.313E-02
0.1
3.707E-02 1.996E-02 1.208E-02

0.3
1
3
5
10
20

7080
7081

4.258E-01
4.734E-01
4.731E-01
4.243E-01

4.298E-02
1.519E-01
3.368E-01
4.031E-01
4.346E-01
4.090E-01

2.315E-02
8.180E-02
1.814E-01
2.170E-01
2.340E-01
2.202E-01

8.237E-03
8.542E-03
1.446E-02
1.569E-02
1.353E-02
8.481E-03(e) 20 y (male) (breathing rate = 0.54 m3 h–1)
µm
ET1
ET2
BB
AMTD
0.001
5.424E-01 2.921E-01 9.541E-02
0.003
3.390E-01 1.826E-01 1.104E-01
0.01
1.317E-01 7.093E-02 4.638E-02
0.03
5.963E-02 3.210E-02 2.060E-02
0.1
3.411E-02 1.837E-02 1.077E-02
AMAD
0.3
1
3
5
10

4.231E-02
1.502E-01
3.343E-01
4.011E-01
4.336E-01

2.279E-02
8.088E-02
1.801E-01
2.159E-01
2.335E-01

7.949E-03
8.673E-03
1.497E-02
1.626E-02
1.402E-02

270

1.397E-02
1.085E-02
6.063E-03
2.386E-03

8.445E-02
5.814E-02
2.584E-02
7.826E-03

7.668E-01
8.103E-01
7.694E-01
6.683E-01

bb

AI

Total

4.511E-02
2.429E-01
2.429E-01
1.355E-01
6.666E-02

1.341E-04
3.663E-02
3.215E-01
3.563E-01
1.934E-01

9.825E-01
9.261E-01
8.215E-01
6.087E-01
3.292E-01

4.454E-02
2.413E-02
2.018E-02
1.677E-02
1.008E-02
4.236E-03

1.456E-01
1.234E-01
1.036E-01
7.601E-02
3.667E-02
1.201E-02

2.782E-01
4.389E-01
7.158E-01
7.768E-01
7.555E-01
6.641E-01

bb

AI

Total

4.837E-02
2.442E-01
2.377E-01
1.328E-01
6.516E-02

1.662E-04
3.912E-02
3.236E-01
3.461E-01
1.853E-01

9.805E-01
9.204E-01
8.140E-01
5.948E-01
3.154E-01

4.396E-02
2.718E-02
2.658E-02
2.314E-02
1.461E-02
6.423E-03

1.402E-01
1.281E-01
1.183E-01
9.060E-02
4.626E-02
1.600E-02

2.585E-01
3.975E-01
6.775E-01
7.496E-01
7.430E-01
6.601E-01

bb

AI

Total

5.381E-02
2.591E-01
2.454E-01
1.338E-01
6.594E-02

2.054E-04
4.395E-02
3.541E-01
3.953E-01
2.170E-01

9.839E-01
9.351E-01
8.485E-01
6.414E-01
3.462E-01

4.469E-02
2.800E-02
2.734E-02
2.373E-02
1.493E-02

1.656E-01
1.509E-01
1.369E-01
1.040E-01
5.244E-02

2.833E-01
4.187E-01
6.936E-01
7.610E-01
7.485E-01

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
20

7084
7085
7086
7087
7088
7089

8.780E-03

6.540E-03

1.793E-02

6.620E-01

Table A.4. Fractional deposition in regions of the respiratory tract for subjects (normal nose
breathers) engaged in light exercise as a function of aerosol size. *(a) Infant 3 mo old (breathing rate = 0.19 m3 h–1)
µm
ET1
ET2
BB
AMTD
0.001
5.437E-01 2.928E-01 1.209E-01
0.003
3.406E-01 1.835E-01 1.609E-01
0.01
1.321E-01 7.115E-02 7.123E-02
0.03
5.685E-02 3.061E-02 3.025E-02
0.1
6.384E-02 3.437E-02 1.592E-02

1.280E-01
3.605E-01
5.239E-01
5.388E-01
5.020E-01
4.340E-01

6.893E-02
1.941E-01
2.821E-01
2.901E-01
2.703E-01
2.337E-01

1.196E-02
1.043E-02
1.044E-02
8.813E-03
5.507E-03
2.554E-03(b) Infant 1 y old (breathing rate = 0.35 m3 h–1)
µm
ET1
ET2
BB
AMTD
0.001
5.346E-01 2.879E-01 1.103E-01
0.003
3.292E-01 1.773E-01 1.255E-01
0.01
1.262E-01 6.796E-02 5.181E-02
0.03
5.550E-02 2.988E-02 2.223E-02
0.1
6.452E-02 3.474E-02 1.185E-02
AMAD
0.3
1
3
5
10
20

7092
7093

2.200E-01

See notes of Table A.2.

AMAD
0.3
1
3
5
10
20

7090
7091

4.087E-01*

1.301E-01
3.638E-01
5.256E-01
5.397E-01
5.024E-01
4.341E-01

7.007E-02
1.959E-01
2.830E-01
2.906E-01
2.705E-01
2.338E-01

9.604E-03
1.102E-02
1.184E-02
9.950E-03
6.093E-03
2.749E-03(c) Child 5 y old (breathing rate = 0.57 m3 h–1)
µm
ET1
ET2
BB
AMTD
0.001
5.314E-01 2.862E-01 9.418E-02
0.003
3.253E-01 1.752E-01 9.832E-02
0.01
1.254E-01 6.755E-02 3.974E-02
0.03
5.884E-02 3.168E-02 1.816E-02
0.1
5.104E-02 2.748E-02 9.586E-03
AMAD
0.3
1
3

9.586E-02
3.023E-01
4.859E-01

5.161E-02
1.628E-01
2.616E-01

7.970E-03
1.133E-02
1.462E-02

271

bb

AI

Total

3.236E-02
2.312E-01
2.553E-01
1.358E-01
6.724E-02

6.438E-05
2.867E-02
3.039E-01
4.107E-01
2.419E-01

9.899E-01
9.448E-01
8.337E-01
6.642E-01
4.233E-01

4.366E-02
1.563E-02
6.057E-03
3.759E-03
1.656E-03
5.350E-04

1.710E-01
8.380E-02
3.853E-02
2.242E-02
8.170E-03
2.072E-03

4.235E-01
6.645E-01
8.610E-01
8.639E-01
7.877E-01
6.728E-01

bb

AI

Total

5.497E-02
2.534E-01
2.218E-01
1.138E-01
5.530E-02

4.734E-04
5.889E-02
3.872E-01
4.504E-01
2.506E-01

9.882E-01
9.442E-01
8.550E-01
6.718E-01
4.170E-01

3.558E-02
1.297E-02
5.564E-03
3.613E-03
1.647E-03
5.348E-04

1.746E-01
8.521E-02
3.927E-02
2.271E-02
8.149E-03
2.018E-03

4.200E-01
6.689E-01
8.652E-01
8.666E-01
7.888E-01
6.732E-01

bb

AI

Total

7.011E-02
2.546E-01
2.025E-01
1.087E-01
5.177E-02

1.094E-03
7.718E-02
4.005E-01
3.738E-01
1.890E-01

9.830E-01
9.306E-01
8.357E-01
5.912E-01
3.289E-01

3.342E-02
1.432E-02
8.696E-03

1.324E-01
7.981E-02
4.782E-02

3.213E-01
5.706E-01
8.187E-01

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
5
10
20

7094
7095

1.314E-02
8.718E-03
4.225E-03

9.819E-02
3.076E-01
4.895E-01
5.174E-01
4.931E-01
4.311E-01

5.288E-02
1.656E-01
2.636E-01
2.786E-01
2.655E-01
2.322E-01

7.028E-03
1.304E-02
1.712E-02
1.517E-02
9.793E-03
4.590E-03(e) 15 y male (breathing rate = 1.38 m3 h–1)
µm
ET1
ET2
BB
AMTD
0.001
5.203E-01 2.802E-01 7.953E-02
0.003
3.122E-01 1.681E-01 7.319E-02
0.01
1.196E-01 6.439E-02 2.827E-02
0.03
5.707E-02 3.073E-02 1.303E-02
0.1
4.387E-02 2.363E-02 6.966E-03
AMAD
0.3
1
3
5
10
20

7098
7099

2.774E-01
2.650E-01
2.320E-01(d) Child 10 y old (breathing rate = 1.12 m3 h–1)
µm
ET1
ET2
BB
AMTD
0.001
5.207E-01 2.804E-01 8.256E-02
0.003
3.126E-01 1.683E-01 7.680E-02
0.01
1.199E-01 6.455E-02 2.981E-02
0.03
5.732E-02 3.086E-02 1.376E-02
0.1
5.136E-02 2.766E-02 7.428E-03
AMAD
0.3
1
3
5
10
20

7096
7097

5.151E-01
4.922E-01
4.308E-01

7.840E-02
2.644E-01
4.560E-01
4.949E-01
4.831E-01
4.277E-01

4.221E-02
1.424E-01
2.456E-01
2.665E-01
2.601E-01
2.304E-01

6.487E-03
1.287E-02
1.883E-02
1.751E-02
1.201E-02
5.967E-03(f) 20 y (male) (breathing rate = 1.50 m3 h–1)
µm
ET1
ET2
BB
AMTD
0.001
5.192E-01 2.796E-01 7.855E-02
0.003
3.110E-01 1.674E-01 7.156E-02
0.01
1.187E-01 6.393E-02 2.745E-02
0.03
5.638E-02 3.036E-02 1.258E-02
0.1
4.302E-02 2.317E-02 6.758E-03
AMAD
0.3
1
3
5
10
20

7.657E-02
2.601E-01
4.523E-01
4.923E-01
4.819E-01
4.273E-01

4.123E-02
1.401E-01
2.435E-01
2.650E-01
2.595E-01
2.301E-01

6.378E-03
1.304E-02
1.930E-02
1.801E-02
1.241E-02
6.185E-03

272

6.420E-03
3.315E-03
1.184E-03

3.052E-02
1.229E-02
3.367E-03

8.425E-01
7.816E-01
6.715E-01

bb

AI

Total

9.667E-02
2.598E-01
1.789E-01
9.407E-02
4.392E-02

3.759E-03
1.229E-01
4.705E-01
3.929E-01
1.915E-01

9.840E-01
9.405E-01
8.636E-01
5.889E-01
3.219E-01

2.820E-02
1.269E-02
8.401E-03
6.297E-03
3.240E-03
1.132E-03

1.328E-01
7.971E-02
4.720E-02
2.978E-02
1.174E-02
3.132E-03

3.191E-01
5.787E-01
8.259E-01
8.472E-01
7.834E-01
6.721E-01

bb

AI

Total

9.987E-02
2.615E-01
1.780E-01
9.329E-02
4.369E-02

4.032E-03
1.266E-01
4.783E-01
4.002E-01
1.962E-01

9.839E-01
9.416E-01
8.685E-01
5.943E-01
3.144E-01

2.838E-02
1.437E-02
1.111E-02
8.740E-03
4.750E-03
1.749E-03

1.387E-01
9.368E-02
6.304E-02
4.191E-02
1.766E-02
5.019E-03

2.942E-01
5.277E-01
7.946E-01
8.296E-01
7.776E-01
6.708E-01

bb

AI

Total

1.037E-01
2.670E-01
1.799E-01
9.370E-02
4.399E-02

4.225E-03
1.302E-01
4.909E-01
4.167E-01
2.057E-01

9.852E-01
9.472E-01
8.808E-01
6.097E-01
3.226E-01

2.864E-02
1.465E-02
1.138E-02
8.949E-03
4.858E-03
1.789E-03

1.458E-01
9.938E-02
6.733E-02
4.488E-02
1.897E-02
5.411E-03

2.986E-01
5.272E-01
7.938E-01
8.292E-01
7.777E-01
6.707E-01

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

7100
7101
7102
7103
7104
7105
7106

*

See notes of Table A.2.

Table A.5. Fractional deposition in regions of the respiratory tract for subjects (normal nose
augmenters) engaged in heavy exercise as a function of aerosol size. *(a) 15 y male (breathing rate = 2.92 m3 h–1)
µm
ET1
ET2
BB
AMTD
0.001
2.595E-01 3.966E-01 9.724E-02
0.003
1.553E-01 2.048E-01 6.013E-02
0.01
6.096E-02 7.557E-02 2.024E-02
0.03
3.016E-02 3.733E-02 9.265E-03
0.12.305E-02 2.285E-02 6.018E-03
AMAD
0.3
1
3
5
10
20

7107
7108

4.110E-02
1.357E-01
2.303E-01
2.488E-01
2.421E-01
2.140E-01

3.111E-02
1.084E-01
2.558E-01
3.270E-01
3.883E-01
3.954E-01

1.057E-02
5.116E-02
1.045E-01
1.078E-01
8.098E-02
4.131E-02(b) 20 y (male) (breathing rate = 3.0 m3 h–1)
µm
ET1
ET2
BB
AMTD
0.001
2.596E-01 3.970E-01 9.953E-02
0.003
1.555E-01 2.050E-01 6.173E-02
0.01
6.013E-02 7.447E-02 2.043E-02
0.03
2.927E-02 3.621E-02 9.213E-03
0.1
2.194E-02 2.200E-02 5.938E-03
AMAD
0.3
1
3
5
10
20

3.855E-02
1.297E-01
2.251E-01
2.452E-01
2.405E-01
2.135E-01

2.930E-02
1.017E-01
2.442E-01
3.152E-01
3.793E-01
3.906E-01

1.018E-02
4.985E-02
1.052E-01
1.104E-01
8.502E-02
4.444E-02

bb

AI

Total

1.973E-01
2.737E-01
1.434E-01
7.183E-02
3.240E-02

2.480E-02
2.438E-01
5.593E-01
3.800E-01
1.738E-01

9.754E-01
9.378E-01
8.595E-01
5.286E-01
2.581E-01

2.148E-02
1.902E-02
2.661E-02
2.405E-02
1.439E-02
5.398E-03

1.216E-01
9.600E-02
8.106E-02
5.873E-02
2.697E-02
8.026E-03

2.259E-01
4.103E-01
6.983E-01
7.663E-01
7.527E-01
6.641E-01

bb

AI

Total

2.016E-01
2.867E-01
1.488E-01
7.383E-02
3.375E-02

2.274E-02
2.409E-01
5.862E-01
4.276E-01
2.012E-01

9.805E-01
9.498E-01
8.900E-01
5.761E-01
2.848E-01

2.243E-02
1.925E-02
2.658E-02
2.414E-02
1.463E-02
5.586E-03

1.428E-01
1.158E-01
9.953E-02
7.279E-02
3.393E-02
1.028E-02

2.433E-01
4.163E-01
7.006E-01
7.678E-01
7.533E-01
6.644E-01

7109

*

7110

A.3. Progeny radionuclides formed in the respiratory tract

7111
7112
7113
7114

(A 5) As noted in Section 3.3.1 of the Main Text, many issues relating to the behaviour ofprogeny in the respiratory tract arise in connection with the natural decay series, which are
therefore shown in Figs. A.1 (uranium-238 series), A.2 (uranium-235 series) and A.3 (thorium232 series).

See notes of Table A.2.

273

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

7115
7116
7117

Fig. A.1. Natural decay series: Uranium-238 (ICRP, 2008).

274

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

7118
7119
7120

Fig. A.2. Natural decay series: Uranium-235 (ICRP, 2008).

275

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

7121
7122
7123

Fig. A.3. Natural decay series: Thorium-232 (ICRP, 2008).

7124

A.4. References

7125
7126
7127
7128
7129

ICRP, 1994. Human respiratory tract model for radiological protection. ICRP Publication 66. Ann.
ICRP 24(1–3).
ICRP, 2008. Nuclear Decay Data for Dosimetric Calculations. ICRP Publication 107. Ann. ICRP 38(3).

276DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

7130
7131

ANNEX B. EVOLUTION OF ICRP’S SYSTEMIC BIOKINETIC
MODELS

7132

B.1. Formulation of systemic models in modern ICRP reports

7133
7134
7135
7136
7137
7138
7139
7140
7141
7142
7143
7144
7145
7146
7147
7148
7149
7150
7151
7152
7153
7154
7155
7156
7157
7158
7159
7160
7161
7162
7163
7164
7165
7166
7167
7168
7169
7170
7171
7172
7173
7174

(B 1) Publication 30 (ICRP, 1979, 1980, 1981, 1988) provided a comprehensive set of systemic
biokinetic models for radionuclides commonly encountered in occupational settings. The
models were generally in the form of retention functions (e.g. sums of exponential terms) that
may be interpreted as first-order compartmental models with one-directional flow. Thesemodels were designed mainly to estimate the cumulative activities of each radionuclide in its
main repositories in the body. They do not depict realistic paths of movement of radionuclides
in the body, but describe only the initial distribution of elements after uptake to blood and thenet biological half-times of elements in source organs. Activity absorbed from thegastrointestinal or respiratory tract or through wounds is assumed to enter a transfer
compartment, from which it transfers to source organs with a specified half-time, typically 0.25
d or longer. Retention in a source organ is usually described in terms of one to three first-orderretention components, with multiple biological half-times representing retention in multiple
hypothetical compartments within a source organ. Feedback of activity from tissues to blood
is not treated explicitly in Publication 30 with the exception of the model for iodine (ICRP,
1979). It is generally assumed that activity leaving an organ moves directly to a collective
excretion compartment, i.e. radioactive decay along actual routes of excretion is not assessed.
Relatively short-lived radionuclides (half-lives up to 15 d) depositing in bone are generally
assigned to bone surface, and longer-lived radionuclides are assigned either to bone surface orbone volume, depending on their main sites of retention in bone as indicated by available data.
(B 2) The systemic biokinetic models of the Publication 30 series (ICRP, 1979, 1980,
1981, 1988) were intended primarily for calculation of dose per intake coefficients for planningpurposes rather than for retrospective evaluation of doses. For some elements, these systemic
biokinetic models were developed separately from ICRP’s concurrent bioassay models. For
example, urinary and faecal excretion models for plutonium, americium, and curium
recommended in Publication 54 (ICRP, 1989) were derived independently of the concurrent
systemic biokinetic model for these elements, shown in Fig. B.1.
(B 3) A series of ICRP reports on doses to members of the public from intake ofradionuclides (ICRP, 1990, 1993, 1995a,b,c, 2001, 2004) provide age-specific systemic
biokinetic models for selected radioisotopes of 31 elements: hydrogen, carbon, sulphur,calcium, iron, cobalt, nickel, zinc, selenium, strontium, zirconium, niobium, molybdenum,
technetium, ruthenium, silver, antimony, tellurium, iodine, caesium, barium, cerium, lead,polonium, radium, thorium, uranium, neptunium, plutonium, americium and curium. Those
reports are referred to here as the Publication 56 series, after the first document in the series(ICRP, 1990). Most of the systemic biokinetic models in the Publication 56 series (ICRP, 1990,
1993, 1995a,b,c) follow the same modelling scheme as applied in the Publication 30 series(ICRP, 1979, 1980, 1981, 1988) and illustrated in Fig. B.1, except that explicit excretion
pathways are included in reports completed after the issue of Publication 60 (ICRP 1991).
These pathways are included to allow the assessment of doses to the urinary bladder and colon,
both of which are assigned tissue weighting factors in Publication 60 (ICRP, 1991). A different
modelling scheme involving more realistic paths of movement of systemic radionuclides isapplied in the Publication 56 series (ICRP, 1990, 1993, 1995a,b,c, 2001, 2004) to iron and thefollowing ‘bone-seeking’ elements: calcium, strontium, barium, lead, radium, thorium,

277

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

7175
7176
7177
7178
7179
7180
7181
7182

7183
7184
7185
7186
7187
7188
7189
7190
7191
7192
7193
7194
7195
7196
7197
7198
7199
7200
7201
7202
7203
7204
7205
7206
7207
7208
7209
7210
7211
7212
7213

uranium, neptunium, plutonium, americium and curium. The model structures for theseelements and the structure for iodine, carried over from Publication 30, depict feedback ofmaterial from organs to blood and, where feasible, physiological processes that determine thebiokinetics of radionuclides. Examples of such physiological processes are bone remodelling,which results in removal of plutonium or americium from bone surface, and phagocytosis ofaging erythrocytes by reticuloendothelial cells, which results in transfer of iron from blood toiron storage sites.

Fig. B.1. Systemic biokinetic model for plutonium, americium, and curium recommended in
Publication 30, Part 4 (ICRP, 1988). This illustrates the one-directional flow of systemic
activity depicted in models of Publication 30 series (ICRP, 1979, 1980, 1981, 1988) and, formany radionuclides, in later ICRP documents on occupational or environmental exposure toradionuclides.
(B 4) The physiologically based modelling scheme applied in the Publication 56 series is
illustrated in Fig. B.2, which shows the generic model structure used for the actinide elements
thorium, neptunium, plutonium, americium and curium. The systemic tissues and fluids are
divided into five main components: blood, skeleton, liver, kidneys, and other soft tissues. Bloodis treated as a uniformly mixed pool. Each of the other main components is further divided intoa minimal number of compartments needed to model the available biokinetic data on these fiveelements or, more generally, ‘bone-surface-seeking’ elements. The liver is divided into
compartments representing short- and long-term retention. Activity entering the liver isassigned to the short-term compartment (Liver 1), from which it may transfer back to blood, tothe intestines via biliary secretion, or to the long-term compartment from which activity slowly
returns to blood. The kidneys are divided into two compartments, one that loses activity tourine over a period of hours or days (Urinary path) and another that slowly returns activity toblood (other kidney tissue). The remaining soft tissue other than bone marrow is divided into
compartments ST0, ST1, and ST2 representing rapid, intermediate, and slow return of activity
to blood, respectively. ST0 is used to account for a rapid build-up of activity in soft tissues andrapid feedback to blood after acute input of activity to blood and is regarded as part of theactivity circulating in blood. The skeleton is divided into cortical and trabecular fractions, andeach of these fractions is subdivided into bone surface, bone volume, and bone marrow.
Activity entering the skeleton is assigned to bone surface, from which it is transferred gradually
to bone marrow and bone volume by bone remodelling processes. Activity in bone volume istransferred gradually to bone marrow by bone remodelling. Activity is lost from bone marrow
to blood over a period of months and is subsequently redistributed in the same pattern as theoriginal input to blood. The rates of transfer from cortical and trabecular bone compartments
to all destinations are functions of the turnover rate of cortical and trabecular bone, assumed to278

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

7214
7215
7216
7217
7218
7219
7220
7221
7222
7223
7224
7225
7226
7227
7228
7229
7230
7231

7232
7233
7234
7235
7236
7237

be 3% and 18% per year, respectively. Other parameter values in the model are elementspecific.
(B 5) A variation of the model structure shown in Fig. B.2 was applied in the Publication
56 series to calcium, strontium, barium, radium, lead and uranium (Fig. B.3). These elements
behave differently from the bone-surface seekers addressed above in that they diffuse
throughout bone volume within hours or days after depositing in bone. After reaching bonevolume, these elements may migrate back to plasma (via bone surface in the model) or they
may become fixed in bone volume and then gradually transfer to blood at the rate of bone
remodelling. The compartments in Fig. B.2 representing bone-marrow and gonads are omitted
from the model for bone-volume seekers because generally these are not sites of elevatedaccumulation of these elements. Some of the compartments shown in Fig. B.3 are notapplicable to all bone-volume seekers. For example, the liver, kidneys and red blood cells are
not important sites of accumulation of calcium and strontium but are important repositories forlead. If a particular compartment or pathway shown in Fig. B.3 is not important for a given
element, it is not considered separately in the model for that element. For example, in the model
for calcium, blood is treated as a single well-mixed pool, and the liver and kidneys are assumed
to be part of ‘Other soft tissues’.

Fig. B.2. Model structure applied in the Publication 56 series to the bone-surface seekers
thorium, neptunium, plutonium, americium and curium. This structure (or its modest
variations) is applied to a number of elements in this series of reports, including elements notregarded as bone-seekers. GI, gastrointestinal.

279

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

7238
7239
7240
7241
7242
7243
7244
7245
7246
7247
7248
7249
7250
7251
7252
7253
7254
7255
7256
7257

Fig. B.3. Model structure applied in the Publication 56 series (ICRP, 1990, 1993, 1995a,b,c,
1996) to calcium, strontium, barium, lead, radium and uranium.
This structure (or modest variations of it) is applied to a number of elements in this series ofreports, including elements not regarded as bone-seekers. Exch, exchangeable; Nonexch,
nonexchangeable; RBC, red blood cells; GI, gastrointestinal.
(B 6) The systemic models used in Parts 2–4 of the Publication 56 series (ICRP 1993,
1995a,b) were applied in Publication 68 (ICRP, 1994a), along with ICRP’s HRTM (ICRP,
1994b), to update dose coefficients for occupational intake of radionuclides based onrecommendations in Publication 60 (ICRP, 1991). For elements not addressed in Parts 2–4 of
the Publication 56 series (ICRP 1993, 1995a,b), the systemic biokinetic models applied in
Publication 68 (ICRP, 1994a) were taken from Publication 30 series (ICRP, 1979, 1980, 1981,1988) and modified to include specific excretion pathways to address doses to the urinary
bladder and colon.
(B 7) The biokinetic models applied in Publication 68 (ICRP, 1994a) were used in
Publication 78 (ICRP, 1997) to update recommendations concerning interpretation of bioassay
data for workers for selected radioisotopes of 15 elements. The systemic models for nine of the
15 elements addressed in Publication 78 (ICRP, 1997) were physiologically based models
adopted in the Publication 56 series (ICRP 1993, 1995a,b,c, 2001, 2004).

7258

B.2. Systemic model structures used in this report series

7259
7260
7261
7262
7263

(B 8) It is now generally recognised that the physiologically descriptive model structures
introduced for selected elements in the Publication 56 series (ICRP 1990, 1993, 1995a,b,c,
2001, 2004) have a number of potential advantages over the retention-function models
traditionally used in radiation protection. For example, a physiological descriptive model
structure:

280

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

7264
7265
7266
7267
7268
7269
7270
7271
7272
7273
7274
7275
7276
7277
7278
7279
7280
7281
7282
7283
7284
7285
7286
7287
7288
7289
7290
7291
7292
7293
7294
7295
7296
7297
7298
7299
7300
7301
7302
7303
7304
7305
7306
7307
7308
7309
7310

•

facilitates the use of physiological information and physiologically reasonableassumptions as a supplement to radiobiological data in the development of model
parameter values;• provides a basis for extrapolating beyond the radiobiological database to different
subgroups of the population and to times outside the period of observation: for example,
a parameter value found to depend on the rate of bone remodelling can be varied withage on the basis of age-specific data on bone remodelling rates;• facilitates the extrapolation of biokinetic data from laboratory animals to man, in that ithelps to focus interspecies comparisons on specific physiological processes and specificsubsystems of the body for which extrapolation may be valid, even if whole-body
extrapolations are not;• facilitates the extrapolation of biokinetic data from an element to its chemical
analogues, in that the degree of physiological similarity of chemical analogues mayvary from one physiological process to another: for example, the alkaline earth elements
show similar rates of transfer from blood to bone but much different rates of transfer tonon-exchangeable sites in bone;• links excretion with exchanges of activity among body tissues and fluids, so that thesame model can be used for dose calculation and bioassay interpretation;• allows modelling of the differential biokinetics of parent radionuclides and theirradioactive progeny produced in the body; and• allows the addition of compartments and pathways to the model for purposes ofextending the model to new applications, as was demonstrated in the ICRP documentson doses to the embryo and fetus (ICRP, 2001) and to the nursing infant (ICRP, 2004)
from intakes of radionuclides by the mother.
(B 9) On the other hand, the level of physiological realism in the systemic biokinetic
models currently used in radiation protection, including those recommended in the present
report, should not be overstated. Even the most sophisticated models represent a compromise
between biological realism and practical considerations regarding the quantity and quality of
information available to determine parameter values. For example, the recycling models
applied to bone-seeking radionuclides in the Publication 56 series all include soft-tissuecompartments representing fast, intermediate, and slow exchange with blood for all soft tissues
not explicitly identified in the models. These soft tissue compartments are typically defined ona kinetic basis rather than a physiological basis: i.e. the compartment sizes and turnover rates
are set for reasonable consistency with data on accumulation and loss of elements by soft
tissues. For some elements, these soft tissue compartments appear to be associated with specificsites or processes, but the associations are not generally confirmed by available information.
For example, biokinetic studies of calcium suggest, but do not establish that: the rapid-turnover
pool in soft tissues may correspond roughly to interstitial fluids plus some rapidly exchangeable
cellular calcium (Harrison et al., 1968; Hart and Spencer, 1976; Heaney, 1964); theintermediate turnover rate may stem from a composite of several pools with slower exchange
rates, including mitochondrial calcium, cartilage calcium and exchangeable dystrophic calcium(e.g. arterial plaque and calcified nodes) (Borle, 1981; Heaney, 1964); and long-term retention
in soft tissues may be associated with relatively nonexchangeable dystrophic calcium that
gradually accumulates in the human body (Heaney, 1964).
(B 10) For many elements, it is not feasible to develop genuine physiological systemmodels due to inadequate information on the processes that determine the systemic behaviourof these elements. Even for relatively well understood elements, the model components are

281

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

7311
7312
7313
7314
7315
7316
7317
7318
7319
7320
7321
7322
7323
7324
7325
7326
7327

often intended only to represent the net result of multiple processes. For example, in the model
for bone-surface-seeking radionuclides shown in Fig. B.2 and its precursors (Leggett, 1985,
1992), the depiction of burial of activity in bone volume is intended to approximate the net
result over time of a number of known or suspected burial processes occurring at different rates.
Activity depositing in bone remodelling units, either in the formation period or in thetransitional period between resorption and formation, may be buried relatively quickly.
Delayed burial of surface activity may result from ‘local recycling’ during bone restructuring
processes: that is, some of the surface activity removed by osteoclasts during bone remodelling
may be redeposited almost immediately at closely adjacent sites of new bone formation thatare supplied by the same blood vessels. Such local redeposition of mineral ions is thought tooccur, particularly in cortical bone (Parfitt and Kleerekoper, 1980). Burial of surface deposits
may also occur as a result of ‘bone drift’, a phenomenon in which new bone is deposited on
previously formed bone without any prior resorption process. Bone drift occurs on a larger
scale in immature bone than in mature bone, but drift within bones and expansion of bonevolume via periostial-endosteal drift continues throughout life in humans (Epker and Frost,
1965a,b; Frost 1986; Priest et al., 1992). ‘Drifting osteons’ are observed at all ages withinhuman cortical bone, and their count is used in forensics for age-at-death estimation.

7328

B.3. References

7329
7330
7331
7332
7333
7334
7335
7336
7337
7338
7339
7340
7341
7342
7343
7344
7345
7346
7347
7348
7349
7350
7351
7352
7353
7354
7355
7356
7357
7358

Borle,
A.B.,
1981.
Control,
Modulation,andregulationofcell
calcium.
Rev. Physiol. Biochem. Pharmacol. 90, 13–153.
Epker, B.N., Frost, H.M., 1965a. Correlation of Bone Resorption and Formation with the PhysicalBehavior of Loaded Bone. J. Dent. Res. 44(1), 33–41.
Epker, B.N., Frost, H.M., 1965b. The direction of transverse drift of actively forming osteons in humanrib cortex. J. Bone Jt. Surg. 47, 1211–1215.
Frost, H.M., 1986. Intermediary Organization of the Skeleton. Volumes I & II. Boca Raton, CRC Press,
FL, USA.
Harrison, G.E., Carr, T.E.F., Sutton, A., 1968. Distribution of radioactive calcium, strontium, bariumand radium following intravenous injection into a healthy man. Int. J. Radiat. Biol. 13(3), 235–247.
Hart, H.E., Spencer, H., 1976. Vascular and extravascular calcium interchange in man determined withradioactive calcium. Radiat. Res. 67(1), 149–161.
Heaney, R.P., 1964. Interpretation of calcium kinetic data. In: Pearson OH and Joplin GF (eds) Dynamic
Studies of Metabolic Bone Disease. Oxford, Blackwell, pp. 11–23.
ICRP, 1979. Limits for intakes of radionuclides by workers, ICRP Publication 30, Part 1. Ann. ICRP
2(3/4).
ICRP, 1980. Limits for intakes of radionuclides by workers. ICRP Publication 30, Part 2. Ann. ICRP
4(3/4).
ICRP, 1981. Limits for intakes of radionuclides by workers. ICRP Publication 30, Part 3. Ann. ICRP
6(2/3).
ICRP, 1988. Limits for intakes of radionuclides by workers: an addendum. ICRP Publication 30, Part
4. Ann. ICRP 19(4).
ICRP, 1989. Individual Monitoring for Intakes of Radionuclides by Workers. ICRP Publication 54. Ann.
ICRP 19(1–3).
ICRP, 1990. Age-dependent Doses to Members of the Public from Intake of Radionuclides - Part 1.
ICRP Publication 56. Ann. ICRP 20(2).
ICRP, 1991. 1990 Recommendations of the International Commission on Radiological Protection.
ICRP Publication 60. Ann. ICRP 21(1–3).
ICRP, 1993. Age Dependent Doses to Members of the Public from Intake of Radionuclides: Part 2,
Ingestion Dose Coefficients. ICRP Publication 67. Ann. ICRP 23(3/4).

282

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

7359
7360
7361
7362
7363
7364
7365
7366
7367
7368
7369
7370
7371
7372
7373
7374
7375
7376
7377
7378
7379
7380
7381
7382
7383
7384
7385
7386

ICRP, 1994a. Dose coefficients for intake of radionuclides by workers. ICRP Publication 68. Ann.
ICRP 24(4).
ICRP, 1994b. Human respiratory tract model for radiological protection. ICRP Publication 66. Ann.
ICRP 24(1–3).
ICRP, 1995a. Age-Dependent Doses to Members of the Public from Intake of Radionuclides: Part 3.
Ingestion Dose Coefficients, ICRP Publication 69. Ann. ICRP 25(1).
ICRP, 1995b. Age-Dependent Doses to Members of the Public from Intake of Radionuclides: Part 4.
Inhalation Dose Coefficients, ICRP Publication 71. Ann. ICRP 25(3/4).
ICRP, 1995c. Age-Dependent Doses to the Members of the Public from Intake of Radionuclides - Part
5 Compilation of Ingestion and Inhalation Coefficients. ICRP Publication 72. Ann. ICRP 26(1).
ICRP, 1997. Individual monitoring for internal exposure of workers. ICRP Publication 78. Ann. ICRP
27(3/4).
ICRP, 2001. Doses to the Embryo and Fetus from Intakes of Radionuclides by the Mother. ICRP
Publication 88. Ann. ICRP 31(1-3).
ICRP, 2004. Doses to Infants from Ingestion of Radionuclides in Mothers’ Milk. ICRP Publication 95.
Ann ICRP 34(3-4).
Leggett, R.W., 1985. A model of the retention, translocation and excretion of systemic Pu. Health Phys.
49(6), 1115–1138.
Leggett, R.W., 1992. A generic age-specific biokinetic model for calcium-like elements.
Radiat. Prot. Dosim. 41(2–4), 183–198.
Parfitt, A.M., Kleerekoper, M., 1980. The divalent ion homeostatic system: physiology and metabolism
of calcium, phosphorus, magnesium and bone. In: Maxwell MH and Kleeman CR (eds) Clinical
Disorders of Fluid and Electrolyte Metabolism, 3rd Edition. McGraw-Hill, New York, pp. 269–398.
Priest, N.D., Haines, J.W., Humphreys, J.A.M., et al., 1992. The bone volume effect on the dosimetryof plutonium-239 and americium-241 in the skeleton of man and baboon. J. Radioanal. Nucl. Chem.
156(1), 33–53.

283

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

7387
7388

ANNEX C. SUPPLEMENTARY INFORMATION RELATING TO
RADON

7389
7390

C.1. Fractional deposition of radon and thoron progeny in the respiratory
tract

7391
7392
7393
7394
7395
7396
7397
7398
7399
7400
7401

(C 1) Table C.1. gives values of fractional deposition for each Reference Individual and in eachregion of the respiratory tract as a function of aerosol size for home exposures for radon ( 222Rn)
and thoron (220Rn) progeny. The AMTD values given in Table C.1 are the reference aerosol
sizes in the ambient air (Table 32.2). For the attached modes, it is assumed that the AMTD
increases by the hygroscopic growth factor instantaneously as the particle enters the nose or
mouth.

7402
7403

7404
7405

7406
7407

7408
7409

Table C.1. Fractional deposition in regions of the respiratory tract for inhalation of radon
progeny as a function of aerosol size *,†a) Infant 3 mo old (breathing rate = 0.12 m3 h–1)
µm
ET1
ET2
BB
AMTD
1
5.484×10‒1 2.953×10‒1 1.184×10‒130
4.442×10‒2 2.392×10‒2 2.818×10‒240
3.792×10‒2 2.042×10‒2 2.344×10‒2200
9.182×10‒2 4.944×10‒2 9.035×10‒3b) Infant 1 y old (breathing rate = 0.19 m3 h–1)
µm
ET1
ET2
BB
AMTD
1
5.426×10‒1 2.922×10‒1 1.117×10‒130
4.359×10‒2 2.347×10‒2 2.203×10‒2403.710×10‒2 1.998×10‒2 1.832×10‒2200
8.454×10‒2 4.552×10‒2 7.318×10‒3c) Child 5 y old (breathing rate = 0.32 m3 h–1)
µm
ET1
ET2
BB
AMTD
1
5.387×10‒1 2.901×10‒1 9.890×10‒230
4.462×10‒2 2.403×10‒2 1.763×10‒2403.730×10‒2 2.009×10‒2 1.464×10‒2200
5.797×10‒2 3.121×10‒2 5.803×10‒3d) Child 10 y old (breathing rate = 0.56 m3 h–1)
µm
ET1
ET2
BB
AMTD
1
5.285×10‒1 2.846×10‒1 8.812×10‒230
4.380×10‒2 2.359×10‒2 1.369×10‒240
3.676×10‒2 1.979×10‒2 1.135×10‒2200
6.311×10‒2 3.398×10‒2 5.085×10‒3e) 15 y male (breathing rate = 0.63 m3 h–1)
µm
ET1
ET2
BB

284

bb

AI

Total

2.594×10‒21.140×10‒19.516×10‒2
2.899×10‒21.370×10‒42.856×10‒12.542×10‒19.420×10‒29.882×10‒14.961×10‒14.311×10‒12.735×10‒1

bb

AI

Total

3.957×10‒21.002×10‒18.316×10‒2
2.483×10‒24.709×10‒43.161×10‒12.782×10‒11.022×10‒19.865×10‒15.054×10‒1
4.368×10‒12.644×10‒1

bb

AI

Total

5.385×10‒2
9.468×10‒2
7.813×10‒22.280×10‒2

1.035×10‒32.764×10‒12.368×10‒18.626×10‒29.826×10‒14.574×10‒13.870×10‒12.040×10‒1

bb

AI

Total

7.748×10‒2
8.264×10‒26.777×10‒2
1.931×10‒2

3.719×10‒3
2.768×10‒12.330×10‒18.137×10‒29.824×10‒14.405×10‒13.687×10‒12.029×10‒1

bb

AI

Total

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
AMTD
1
30
40
200

7410
7411

5.310×10‒1
4.398×10‒2
3.647×10‒2
4.299×10‒22.860×10‒12.368×10‒2
1.964×10‒22.315×10‒28.690×10‒21.370×10‒2
1.136×10‒2
4.693×10‒3f) 20 y (male) (breathing rate = 0.78 m3 h–1)
µm
ET1
ET2
BB
AMTD
1
5.268×10‒1 2.837×10‒1 8.436×10‒230
4.297×10‒2 2.314×10‒2 1.237×10‒240
3.570×10‒2 1.922×10‒2 1.026×10‒2200
4.629×10‒2 2.493×10‒2 4.489×10‒3

7.389×10‒2
8.528×10‒2
6.999×10‒22.044×10‒2

3.128×10‒32.720×10‒12.293×10‒18.251×10‒29.809×10‒14.386×10‒1
3.668×10‒1
1.738×10‒1

bb

AI

Total

8.438×10‒28.207×10‒2
6.726×10‒2
1.961×10‒2

4.072×10‒3
2.942×10‒12.480×10‒18.883×10‒2

9.833×10‒1
4.548×10‒13.804×10‒11.841×10‒1

7412
7413
7414

*

7415

C.2. Biokinetic model for radon gas

7416
7417
7418
7419
7420
7421
7422
7423
7424
7425
7426
7427
7428
7429
7430
7431
7432
7433
7434
7435
7436
7437
7438
7439
7440
7441
7442
7443
7444
7445
7446

(C 2) Several compartmental biokinetic models including the model for radon adopted in
Publication 137 (2017) have been developed for inert gases on the basis of physical laws
governing transfer of a non-reactive and soluble gas between materials. In these models the
kinetics of an inert gas is assumed to be determined by the blood-to-air partition coefficient(ratio of concentrations of the gas in blood and air) and the blood perfusion rates, tissue-toblood partition coefficients, and volumes of the tissues represented by the compartments of themodel. It is assumed that gas entering respiratory air (RT-air) after inhalation, or pulmonary
blood after ingestion, equilibrates rapidly between RT-air and pulmonary blood with relative
concentrations determined by the blood-to-air partition coefficient. Part of the gas in pulmonary
blood is assumed to be removed from the body in expired air and the remainder is assumed totransfer to arterial blood and distribute to tissues in proportion to the percentage of cardiac
output received by each tissue. It is assumed that the perfusion of the gas in tissues isinstantaneous, allowing equilibrium to be achieved between venous blood and tissue. The gas
is carried in the venous blood to the pulmonary blood, and the cycle is repeated. In the case of
acute intake of radon, virtually all of the inhaled or ingested radon is removed from the bodywithin a few hours.
(C 3) The age-specific biokinetic model for radon used in this report is based on theidealized system described above, together with empirical age-specific removal half-times ofradon from lung air to the environment. The structure of the model and age- and sex-specifictransfer coefficients can be found in the main text (Figure 32.1, Table 32.4, and Table 32.5).
The reader is referred to the radon section in Publication 137 (ICRP, 2017) for a more detailed
discussion of the rationale for the modelling approach and the methods for deriving the transfer
coefficients from physical principles.
(C 4) The partition coefficients used in the derivation of age-specific transfer coefficientsfor the radon model used in this report are listed in Table C.2. These values are taken from
Table 12.2 of Publication 137 (ICRP, 2017) or derived from values listed in that table in thecase of model compartments representing a mixture of tissues addressed in that table. The
partition coefficients are assumed to be independent of age with one exception: the partition
coefficient for adipose breast tissue (Breast-a in Figure 32.1) increases with age up to adulthood
because its fractional content of fat is assumed to increase with age. The age-specific tissue
volumes (Table C.3) are based on age-specific tissues masses given in Publication 89 (2002)

Reference values are given to a greater degree of precision than would be chosen to reflect the certainty withwhich the average value of each parameter is known.
†
Aerosol parameter values used in the calculations are given in Table 32.2, Section 32.1.1.

285

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

7447
7448
7449
7450
7451
7452
7453

(Table C.4) and tissue densities (Table C.5) given in Publication 23 (1975) and Publication 89(2002). It is assumed that bone is 80% cortical bone and 20% trabecular bone by mass for all
ages. A density of 1.04 g/cc is applied to soft tissues other than fat and adipose tissue. The agespecific density of trabecular bone is assumed to be the same as that of cortical bone, which
has been studied more extensively. Age-specific blood flow rates are listed in Table C.6.
Table C.2. Reference partition coefficients (tissue/blood) *
100 d

1y

5-y

10-y

15-y
Male Female

Adult
Male
Female

Fat
Fat 1
Fat 2
Yellow marrow
Yellow marrow 1
Yellow marrow 2

11
11
11
8.9
8.9
8.9

11
11
11
8.9
8.9
8.9

11
11
11
8.9
8.9
8.9

11
11
11
8.9
8.9
8.9

11
11
11
8.9
8.9
8.9

11
11
11
8.9
8.9
8.9

11
11
11
8.9
8.9
8.9

11
11
11
8.9
8.9
8.9

KidneysLiver
Trabecular volume
Cortical volume
R-marrow
Breast

0.66
0.71
0.36
0.36
0.36

0.66
0.71
0.36
0.36
0.36

0.66
0.71
0.36
0.36
0.36

0.66
0.71
0.36
0.36
0.36

0.66
0.71
0.36
0.36
0.36

0.66
0.71
0.36
0.36
0.36

0.66
0.71
0.36
0.36
0.36

0.66
0.71
0.36
0.36
0.36

1.4
5.1

1.4
6.7

1.4
7.3

1.4
7.8

1.4
8.3

1.4
8.3

1.4
8.9

1.4
8.9

0.36

0.36

0.36

0.36

0.36

0.36

0.36

0.36

Tissues

Breast-g
Breast-a
Other

7454
7455
7456
7457

Blood/Air
0.43
0.43
0.43
0.43
0.43
0.43
0.43
0.43
Values taken from Table 12.2 of Publication 137 (2017) and see discussions in text of partition coefficients foryellow marrow and breast.
*

286

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

7458

Table C.3. Reference tissue volumes* (L)
100 d
Fat
Fat 1
Fat 2
Yellow marrow
Yellow marrow 1
Yellow marrow 2
KidneysLiver
Trabecular volume
Cortical volume
Red marrow
BreastBreast-g
Breast-a
Other
Blood†
Blood-A
Blood-V

7459
7460
7461
7462
7463
7464
7465

1y

5y

10 y

15 y

Adult

1.6E+00
7.8E-01
7.8E-01
7.8E-03
3.9E-03

2.5E+00
1.2E+00
1.2E+00
2.0E-02
1.0E-02

3.8E+00
1.9E+00
1.9E+00
1.6E-01
8.2E-02

6.0E+00
3.0E+00
3.0E+00
6.4E-01
3.2E-01Male
8.5E+00
4.2E+00
4.2E+00
1.5E+00
7.6E-01

Female1.4E+01
7.0E+00
7.0E+00
1.4E+00
7.0E-01Male
1.4E+01
6.9E+00
6.9E+00
2.5E+00
1.3E+00

Female1.8E+01
9.0E+00
9.0E+00
1.8E+00
9.2E-01

3.9E-03
4.1E-02

1.0E-02
6.7E-02

8.2E-02
1.1E-01

3.2E-01
1.7E-01

7.6E-01
2.4E-01

7.0E-01
2.3E-01

1.3E+00
3.0E-01

9.2E-01
2.6E-01

2.0E-01
4.1E-02

3.2E-01
7.2E-02

5.5E-01
1.5E-01

8.0E-01
2.6E-01

1.3E+00
4.5E-01

1.3E+00
4.1E-01

1.7E+00
5.8E-01

1.3E+00
4.2E-01

1.6E-01
8.5E-02

2.8E-01
1.4E-01

5.9E-01
3.3E-01

1.1E+00
6.1E-01

1.8E+00
1.0E+00

1.6E+00
9.6E-01

2.3E+00
1.1E+00

1.7E+00
8.7E-01

2.1E-04
8.3E-05
1.3E-04
3.2E+00

4.3E-04
1.7E-04
2.7E-04
5.5E+00

9.5E-04
3.6E-04
5.9E-04
1.1E+01

7.2E-03
2.7E-03
4.5E-03
1.8E+01

1.6E-02
2.7E-03
1.3E-02
3.3E+01

2.5E-01
9.6E-02
1.6E-01
2.7E+01

2.6E-02
2.7E-03
2.3E-02
4.1E+01

5.1E-01
1.9E-01
3.2E-01
2.8E+01

3.6E-01
9.7E-02

5.0E-01
1.4E-01

1.4E+00
3.8E-01

2.4E+00
6.5E-01

4.5E+00
1.2E+00

3.3E+00
8.9E-01

5.3E+00
1.4E+00

3.9E+00
1.1E+00

2.6E-01

3.7E-01

1.0E+00

1.8E+00

3.3E+00

2.4E+00

3.9E+00

2.8E+00

1.7E-01 2.9E-01 9.0E-01 1.7E+00 3.1E+00 2.7E+00 3.9E+00 3.1E+00
Lung-air volǂBased on reference tissue masses and specific gravities listed in Tables C.4 and C.5, respectively.
†
Blood volumes given in ICRP Publication 89 for ages 1 year old to adult. Value for infant based on mass anddensity listed in Tables C.4 and C.5 respectively.
ǂ
Adult value based on value given in ICRP Publication 68 (1994a) and other ages scaled by age-specific functional
residual capacity (ICRP Publication 66, 1994b).
*

Table C.4. Reference tissue masses* (g)

Fat†
Fat 1
Fat 2
Yellow marrow
Yellow marrow 1
Yellow marrow 2
KidneysLiver
Trabecular volume
Cortical volume
Red marrow
Breastǂ
Breast-g§
Breast-a

5.5E+0315 y
MaleFemale7.8E+03 1.3E+04

Adult
Male
Female1.3E+04 1.7E+04

2.7E+03
2.7E+03
6.3E+02
3.2E+02
3.2E+02
1.8E+02
8.3E+02
4.6E+02
1.8E+03
6.3E+02
7.1E+00
2.8E+00
4.3E+00

3.9E+03
3.9E+03
1.5E+03
7.4E+02
7.4E+02
2.5E+02
1.3E+03
8.1E+02
3.2E+03
1.1E+03
1.5E+01
2.8E+00
1.2E+01

6.3E+03
6.3E+03
2.5E+03
1.2E+03
1.2E+03
3.1E+02
1.8E+03
1.1E+03
4.4E+03
1.2E+03
2.5E+01
2.8E+00
2.2E+01

100 d

1y

5y

10 y

1.4E+03

2.3E+03

3.5E+03

7.2E+02
7.2E+02
7.7E+00
3.8E+00
3.8E+00
4.2E+01
2.1E+02
6.8E+01
2.6E+02
8.8E+01
2.1E-01
8.6E-02
1.3E-01

1.1E+03
1.1E+03
2.0E+01
1.0E+01
1.0E+01
7.0E+01
3.3E+02
1.2E+02
4.7E+02
1.5E+02
4.3E-01
1.7E-01
2.6E-01

1.7E+03
1.7E+03
1.6E+02
8.0E+01
8.0E+01
1.1E+02
5.7E+02
2.5E+02
1.0E+03
3.4E+02
9.4E-01
3.8E-01
5.6E-01287

6.4E+03
6.4E+03
1.4E+03
6.9E+02
6.9E+02
2.4E+02
1.3E+03
7.4E+02
3.0E+03
1.0E+03
2.5E+02
1.0E+02
1.5E+02

8.3E+03
8.3E+03
1.8E+03
9.0E+02
9.0E+02
2.8E+02
1.4E+03
8.0E+02
3.2E+03
9.0E+02
5.0E+02
2.0E+02
3.0E+02

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
Other¶

7466
7467
7468
7469
7470
7471
7472
7473
7474
7475
7476

3.3E+03 5.8E+03 1.1E+04 1.9E+04 3.4E+04 2.8E+04 4.2E+04 2.9E+04
Total Body
6.0E+03 1.0E+04 1.9E+04 3.2E+04 5.6E+04 5.3E+04 7.3E+04 6.0E+04
Blood
3.8E+02 5.3E+02 1.5E+03 2.5E+03 4.8E+03 3.5E+03 5.6E+03 4.1E+03*
Based on reference values ICRP Publication 89 for ages 1 through adult. For age 100 d, masses are based on
growth trends indicated in Publication 89 for total body and, where available, individual tissues.
†
Mass of fat taken as mass of storage fat minus mass of fat assigned to yellow marrow compartments. See text
on the assumptions of the % of fat in yellow marrow.
ǂThe reference breast masses for infant to 10 year old are extrapolated from data given in Publication 89.
§
Assumes mass of glandular breast is 40% of total breast apart from ages after 10 years old for males where theglandular breast stops growing.
¶
Mass of “other” calculated as mass of total body minus masses of tissues and fluids explicitly identified insystemic model and contents of stomach, intestines, gallbladder, and urinary bladder.

Table C.5. Reference tissue densities*
100 d

1y

5y

10 y

15 y
Male Female

Adult
Male
Female

0.92
0.92
0.92
0.98

0.92
0.92
0.92
0.98

0.92
0.92
0.92
0.98

0.92
0.92
0.92
0.98

0.92
0.92
0.92
0.98

0.92
0.92
0.92
0.98

0.92
0.92
0.92
0.98

0.92
0.92
0.92
0.98

Yellow marrow 1
Yellow marrow 2

0.98
0.98

0.98
0.98

0.98
0.98

0.98
0.98

0.98
0.98

0.98
0.98

0.98
0.98

0.98
0.98

Kidneys†
Liver†
Trabecular volumeǂ

1.04
1.04
1.65
1.65
1.04

1.04
1.04
1.66
1.66
1.04

1.04
1.04
1.70
1.70
1.04

1.04
1.04
1.75
1.75
1.04

1.04
1.04
1.80
1.80
1.04

1.04
1.04
1.80
1.80
1.04

1.04
1.04
1.90
1.90
1.04

1.04
1.04
1.90
1.90
1.04

1.04
0.99

1.04
0.97

1.04
0.96

1.04
0.96

1.04
0.95

1.04
0.95

1.04
0.94

1.04
0.94

Fat
Fat 1
Fat 2
Yellow marrow

Cortical volume
Red marrow†
BreastBreast-g†
Breast-a§

7477
7478
7479
7480
7481
7482
7483

Other
1.04
1.04
1.04 1.04
1.04
1.04
1.04
1.04
Blood
1.06
1.06
1.06 1.06
1.06
1.06
1.06
1.06
*
Based on data in ICRP Publication 23 (1975) and Publication 89 (2002).
†
The reference soft tissue density of 1.04 g/cc was applied to kidneys, liver, red marrow, glandular breast and‘other’.
ǂ
The age-specific density of trabecular bone was assumed to be the same as that of cortical bone.
§
The age-specific density of adipose breast takes account of the change in fat content with age.

Table C.6. Reference blood flow rates to tissues (% of cardiac output)*

5.0E+00
4.0E+00
1.0E+00
1.3E-01
1.0E-01

15 y
MaleFemale5.0E+00 8.5E+00
4.0E+00 6.8E+00
1.0E+00 1.7E+00
3.0E-01 3.8E-01
2.4E-01 3.1E-01

Adult
Male
Female5.0E+00 8.5E+00
4.0E+00 6.8E+00
1.0E+00 1.7E+00
5.0E-01 5.0E-01
4.0E-01 4.0E-01

2.5E-02
1.9E+01

6.0E-02
1.9E+01

1.0E-01
1.9E+01

100 d

1y

5y

10 y

5.0E+00
4.0E+00
1.0E+00
1.6E-03
1.2E-03

5.0E+00
4.0E+00
1.0E+00
4.0E-03
3.2E-03

5.0E+00
4.0E+00
1.0E+00
3.2E-02
2.6E-02

3.1E-04
1.9E+01

8.1E-04
1.9E+01

6.5E-03
1.9E+01

Tissue
Fat
Fat 1
Fat 2
Yellow marrow†
Yellow marrow 1
Yellow marrow 2
Kidneys288

7.7E-02
1.7E+01

1.0E-01
1.7E+01

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
Liver
Arterial
Total
Trabecular volumeǂ
Cortical volumeǂ

6.5E+00
2.6E+01

6.5E+00
2.6E+01

6.5E+00
2.6E+01

6.5E+00
2.6E+01

6.5E+00
2.6E+01

6.5E+00
2.7E+01

6.5E+00
2.6E+01

6.5E+00
2.7E+01

1.8E+00
1.2E+00

1.8E+00
1.2E+00

1.8E+00
1.2E+00

1.8E+00
1.2E+00

9.0E-01
6.0E-01

9.0E-01
6.0E-01

9.0E-01
6.0E-01

9.0E-01
6.0E-01

Red marrow
Breast§3.0E+00
1.7E-04

3.0E+00
3.4E-04

3.0E+00
7.5E-04

3.0E+00
5.7E-03

3.0E+00
1.2E-02

3.0E+00
2.0E-01

3.0E+00
2.0E-02

3.0E+00
4.0E-01

Breast-g

8.5E-05
8.7E-05

1.9E-04
1.6E-04

4.1E-04
3.4E-04

3.2E-03
2.5E-03

3.8E-038.2E-03

1.2E-01
8.4E-02

4.8E-03
1.5E-02

2.5E-01
1.5E-01

6.3E+01

6.3E+01

6.3E+01

6.3E+01

6.5E+01

6.3E+01

6.4E+01

6.3E+01

Breast-a
Other¶

7484
7485
7486
7487
7488
7489
7490
7491
7492
7493
7494
7495
7496
7497
7498
7499
7500
7501
7502
7503
7504
7505
7506
7507
7508
7509
7510
7511
7512
7513
7514
7515
7516
7517
7518
7519
7520

Cardiacoutput(L/min)
0.83
1.2
3.4
5.0
6.1
6.1
6.5
5.9
*
Blood flow rates for adults taken from ICRP Publication 89 (2002).
†
The total blood flow rate to yellow marrow at different ages was scaled by mass from the reference value for
adult given in ICRP Publication 89 (2002).
ǂ
The percentage of cardiac output received by bone in infants and children through age 10 y is assumed to be
twice the percentage received by bone in adults.
§
The blood flow rate (i.e. % of cardiac output) to breast at different ages and for males were scaled from the value
for the adult non-pregnant female breast based on mass. The fraction of this blood flow rate to ‘breast-a’ reflects
the varying percentages of fat in adipose breast with age.
¶
The percentage of cardiac output to “other” is calculated as 100% minus the % of cardiac output to the tissues
explicitly identified in systemic model (i.e. fat, yellow marrow, kidneys, liver (arterial), trabecular and corticalvolume, red marrow and breast).

(C 5) The model structure shown in Figure 32.1 differs from the structure applied toworkers in Publication 137 (2017). The modification was made for greater consistency
between the source regions depicted in the biokinetic model for radon and the target regions
addressed in the ICRP’s current dosimetry system. With the model structure applied to workers
in Publication 137, the dose estimates for red marrow were imprecise because the compartment
named “Red marrow” in that model included some non-hematopoietic tissue. In the modified
structure used in this report, the compartment named “Red marrow” includes only
hematopoietic tissue. Two compartments representing two phases of retention of radon inyellow marrow have been added to the model used in Publication 137. These two phases ofretention are based on the division and half-times of the two compartments of the model
representing fat.
(C 6) Some modifications of the parameter values for adult males used in Publication 137(2017) resulted from modifications in this report regarding the mass, density, or compositionof tissues. Assumptions used to develop the parameter values in the present model aresummarized below.
(C 7) The flow rates between blood and breast are assumed to be the same for males andfemales through age 10 y. For assignment of transfer coefficients to breast at higher ages it istaken into account that, beginning at puberty, the increased testosterone levels cause involutionof the glandular tissue in the male breast (Chen et al. 2006). Data for U.S. subjects indicate thatthe onset of puberty for boys may be around age 10 y (Herman-Giddens et al. 2012). It is
assumed in the model that growth of the male breast after age 10 y results only from an increasein the mass of adipose tissue.
(C 8) For all age groups, the total mass of the compartments labelled Fat 1 and Fat 2 inFigure 32.1 was calculated from reference values for storage fat given in Publication 89 (2002)
minus the mass of fat in bone marrow. For age 100 d, total fat including breast and marrow fat

289

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

7521
7522
7523
7524
7525
7526
7527
7528
7529
7530
7531
7532
7533
7534
7535
7536
7537
7538
7539
7540
7541
7542
7543
7544
7545
7546
7547
7548
7549
7550
7551
7552
7553
7554
7555
7556
7557

is assumed to be 24% of the total body weight (Fomon et al. 1982, Fomon and Nelson 2002).
For other ages the mass of Fat 1 + Fat 2 is based on reference masses of storage fat given in
Publication 89.
(C 9) For each age the compartment named “Breast-a” representing adipose tissue in thebreast is assumed to contain the same percentage of fat as total adipose tissue for that age.
Adipose tissue excluding yellow marrow is assumed to be 45% fat for age 100 d (Fomon and
Nelson, 2002). For ages 1 y and greater the percentage of fat in adipose tissue other than yellow
marrow were taken from Publication 89 (60% at 1 y, 65% at 5 y, 70% at 10, 75% at 15 y, and
80% in adults). It is assumed that fat represents 80% of the mass of yellow marrow at all ages
based on the lipid content of yellow marrow estimated for adults (Publication 23, Guillerman
2013, Chan 2016, Karampinos 2018) and the lack of clear evidence of an age dependence ofthe lipid content of yellow marrow. The age-specific masses of red marrow (active marrow)
were taken from Publications 70 and 89 (1995, 2002). The compartment named “Breast-g”
representing glandular breast is assumed to contain 10% intraglandular fat for each age (ICRP,
2017).
(C 10) The blood flow rates to individual tissues expressed as a percentage of cardiac output
were modified from reference values for adult given in Publication 89 (2002). As in the agespecific model for systemic caesium described in this report, the percentage of cardiac output
received by bone in infants and children through age 10 y is assumed to be twice the percentage
received by bone in adults. Blood flow rates were also adjusted for a given age to reflect theage-specific composition and masses of some tissues, e.g., for the varying percentages of fat
and other soft tissue in adipose tissue.
(C 11) For example, the blood flow rate to breast was scaled from the reference value fornon-pregnant adult female breast based on mass. Thus, the age- and sex-specific percentage of
cardiac output received by breast is given by:
0.4 ×

𝑚breast

(C.1)

500

where 0.4 is the % of cardiac output to non-pregnant adult female breast with a reference massof 500 g (ICRP, 2002), and mbreast is the reference age- and sex-specific mass of the breast given
in Table C.3.
(C 12) The distribution of blood flow to breast between adipose breast (breast-a) andglandular breast (breast-g), was based on the relative blood perfusion rates of fat and ‘other’and the age-specific fat content of breast-a and breast-g. Thus, the fraction of the % of cardiac
output to breast that goes to ‘breast-a’ is calculated as follows:𝑓fat ×%𝐶𝑂storage fat (1−𝑓fat )×%𝐶𝑂other+)𝑚storage fat𝑚other𝑚breast−a ×(

7558
7559
7560
7561
7562
7563
7564
7565
7566

((1−𝑓fat )×𝑚breast−a+0.9×𝑚breast−g )×%𝐶𝑂other(𝑓fat ×𝑚breast−a+0.1×𝑚breast−g )×%𝐶𝑂storage fat+𝑚storage fat𝑚other

(C.2)

where
mbreast-a, mbreast-g, mstorage fat, and mother are the masses of adipose breast, glandular breast, storage
fat and other, respectively (Table C.3).
ffat is the age-specific fraction of fat in adipose tissue.
%COstorage fat is the reference blood flow rate to storage fat for adult (5% for males and 8.5%
for females).

290

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

7567
7568
7569
7570
7571
7572
7573
7574
7575
7576
7577
7578
7579
7580
7581
7582
7583
7584
7585
7586
7587

%COother is the % of cardiac output to Other (Table C.5)

7588

C.3. Dosimetric data for radon and thoron

7589

Inhalation of radon or thoron gas

7590
7591
7592
7593
7594
7595
7596
7597
7598
7599
7600
7601
7602
7603
7604
7605
7606

The remaining fraction of the % of cardiac output to breast goes to breast-g.
(C 13) For pre-adults the partition coefficients for individual tissues are consistent withvalues for adult and, where applicable, reflect the relative amounts of different tissues thatmake up a compartment of the model. The partition coefficients for yellow marrow are basedon a composition of 80% fat and 20% other soft tissue; for the compartment named Breast-g(glandular breast tissue) are based on an assumed composition of 10% fat and 90% other soft
tissue; and for the compartment named Breast-a (adipose tissue of breast) are based on theassumed age-specific percentage of fat in adipose tissue.
(C 14) Age-specific removal half-times of radon from lung air to the environment are basedon measured washout rates of xenon and krypton in infants and children (Treves et al. 1974,
Ciofetta et al. 1980). The following reference half-times were selected: 4.5 s for infants, 5 s forage 1 y, 8 s for 5 y, 11 s for 10 y, 17 s for 15 y, and 23 s for adults. The half-time assigned tothe adult male is the same as in the Rn model for workers used in Publication 137 (ICRP, 2017).
(C 15) The average volume of the RT-air space for an adult male is 3.858 l (Bailey, et al.,
1996; ICRP, 1994b). This was scaled downward to other ages using the age-specific functional
residual capacity (FRC) values from Table 15 of Publication 66 (ICRP, 1994a). In other words,
the age-specific FRC values are multiplied by (3.858/3.30).
(C 16) The revised model described here for the adult male replaces the model given in
Publication 137 (ICRP, 2017).

(C 17) The age-dependent equilibrium effective dose rates for continuous chronic exposure
to unit concentration of 222Rn (or 220Rn) are given in Table C.7. In other words, these are theeffective dose rates following chronic exposure to unit concentration of radon (or thoron) after
the radon (or thoron) concentration in organs and tissues have reached saturation (i.e.
equilibrium).
(C 18) The effective dose coefficients in terms of Sv Bq -1 intake of radon gas are also given
in Table C.7. and the corresponding equivalent doses to organs are given in the accompanying
electronic annex. These values can be converted to the effective dose per exposure (Sv per Bq
h m-3) by multiplying the Sv Bq -1 value by (𝜆 × 𝑉̅𝑅𝑇−𝑎𝑖𝑟 × 1/24), where λ is the transfer
coefficient (d-1) from the the RT-air space to the environment in the radon gas biokinetic model(Table 32.4 or 32.5), and 𝑉̅𝑅𝑇−𝑎𝑖𝑟 (m3) is the sex-average volume of RT-air space for thereference age group (Table C.3). It is noteworthy that unlike the inhalation of radon progeny,
the dose per exposure (Sv per Bq h m-3) from inhaling 222Rn gas is approximately independentof the breathing rate.
Table C.7. Age-dependent effective dose coefficients following inhalation of radon (222Rn) or
thoron (220Rn) gas alone.
Age

3 mo
1y
5y

Sv Bq-1
1.0E-09
7.6E-105.0E-10

Effective dose coefficients
Radon (222Rn) gas
Thoron (220Rn) gas
mSv per Bq h m-3 *Sv Bq-1
mSv per Bq h m-3 *9.8E-08
3.5E-10
3.4E-08
1.1E-07
2.6E-10
3.8E-08
1.4E-072.0E-10
5.7E-08291

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
10 y
15 y
Adult

7607
7608
7609

1.7E-10
1.6E-10
1.8E-10

6.6E-08
6.8E-08
6.7E-08

This is the effective dose rate following chronic exposure to unit concentration of radon (or thoron) after theradon (or thoron) concentration in organs and tissues have reached saturation (i.e. equilibrium).

Inhalation of radon or thoron progeny(C 19) Table C.8. lists effective dose coefficients (Sv Bq-1) for inhalation of individual
short-lived radon (222Rn or 220Rn) progeny. Values are calculated for each mode of the assumed
aerosol distribution for homes (Table 32.2). The progeny addressed in Table C.8. are those thatgenerally dominate the estimated lung dose and effective dose from exposure to radon andaccompanying progeny. The tabulated values can be used to calculate values of effective dose
per potential alpha energy exposure (ICRP, 2017).
Table C.8. Effective dose coefficients (in Sv Bq -1) for inhaled radon (222Rn) or thoron (220Rn)progeny. Values are given for each mode of the assumed aerosol distribution for homes*
Mode
NuclideRadon (222Rn) progeny
unattachedPo-218
Pb-214Bi-214nucleation
Po-218
Pb-214Bi-214
accumulation Po-218
Pb-214Bi-214
Thoron (220Rn) progeny
unattachedPb-212
Bi-212
nucleation
Pb-212
Bi-212
accumulation Pb-212
Bi-212

7620
7621
7622
7623
7624
7625
7626
7627
7628
7629
7630
7631

1.6E-07
1.7E-07
1.9E-07

*

7610
7611
7612
7613
7614
7615
7616
7617
7618
7619

4.1E-10
4.0E-105.0E-10*3 mo

Effective dose coefficients (Sv Bq-1)
Age
1y
5y
10 y
15 y

Adult

3.9E-08
2.2E-07
2.1E-07
2.8E-08
1.3E-07
1.1E-07
8.4E-09
4.3E-08
3.7E-08

3.2E-08
1.8E-07
1.7E-072.0E-08
9.5E-08
7.9E-08
5.9E-09
3.0E-08
2.6E-082.0E-08
1.1E-07
1.0E-07
1.1E-08
5.4E-08
4.5E-08
3.2E-09
1.6E-08
1.4E-08

1.5E-08
8.3E-08
7.5E-08
7.1E-09
3.4E-08
2.8E-08
2.1E-09
1.0E-08
8.9E-09

1.1E-08
6.3E-08
5.7E-08
5.5E-09
2.6E-08
2.2E-08
1.6E-09
7.8E-09
6.6E-09

1.1E-08
6.1E-08
5.5E-08
4.9E-09
2.3E-08
1.9E-08
1.4E-09
7.1E-09
6.0E-09

1.4E-06
4.5E-07
1.2E-06
2.4E-07
4.4E-078.7E-08

1.2E-06
3.6E-079.0E-07
1.7E-07
3.1E-07
6.1E-08

7.7E-07
2.3E-07
5.1E-079.8E-08
1.7E-07
3.3E-08

6.2E-07
1.7E-07
3.2E-07
6.1E-08
1.0E-07
2.1E-08

4.6E-07
1.3E-07
2.5E-07
4.7E-08
7.9E-08
1.6E-08

4.6E-07
1.2E-07
2.2E-07
4.2E-08
7.1E-08
1.4E-08

Assumed aerosol distributions are given in Table 32.2.

(C 20) The age-dependent effective doses per exposure to radon ( 222Rn) progeny as afunction of the unattached fraction, fp and the fraction of the attached PAEC associated with
the nucleation mode, fpn are given in Table C.9. Values of effective dose coefficients with fp=0.1
and fpn = 0.2 are also shown. Here, the doses from inhaling 222Rn gas are excluded. If there isno nucleation mode present (i.e. fpn =0) then the dose reduces by about 20% for exposures at
home.
Table C.9. Age-dependent effective doses per exposure to radon (222Rn) progeny as a functionof the unattached fraction, fp and the fraction of the attached potential alpha energy
concentration (PAEC) associated with the nucleation mode, fpn.
Age

Effective dose per exposure to radon (222Rn) progeny*
mSv per mJ h m-3
nSv per Bq h m-3 of EEC† of 222Rn

292

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3 mo
1y
5y
10 y
15 y
Adult

a fp + (1- fp)[b fpn + c(1- fpn)]
a
b
c
8.4
5.8
1.9
11
6.6
2.1
12
6.3
1.9
15
6.8
2.1
13
6.0
1.8
16
6.6
2.0

Calculated
valueǂ
3.2
3.8
3.7
4.3
3.7
4.2

a fp + (1- fp)[b fpn + c(1- fpn)]
a
b
c
47
32
10
61
37
12
64
35
11
84
38
12
72
33
10
86
36
11

Calculated
valueǂ
18
21
20
24
20
23

7632
7633
7634
7635
7636

*

Doses from inhaling 222Rn gas are excluded.

7637

C.4. References

7638
7639
7640
7641
7642
7643
7644
7645
7646
7647
7648
7649
7650
7651
7652
7653
7654
7655
7656
7657
7658
7659
7660
7661
7662
7663
7664
7665
7666
7667

Bailey, M. R., Birchall, A., Marsh, J.W., et al., 1996. Application of the new ICRP Respiratory Tract
Model to gases and vapours in ICRP Publication 68. NRPB Memorandum, NRPB-M688. Public
Health England, Chiltoin, Didcot.
Chan, B.Y., Gill, K.G., Rebsamen, S.L., et al., 2016. MR imaging of pediatric bone marrow.
Radiographics 36(6), 1911–1930.
Chen, L., Chantra, P.K., Larsen, L.H., et al., 2006. Imaging characteristics of malignant lesions of themale breast. Radiographics 26(4), 993–1006.
Ciofetta, G., Silverman, M., Hughes, J.M.B., 1980. Quantitative approach to the study of regional lungfunction in children using krypton 81m. Brit. J. Radiol. 53(634), 950–959.
Fomon, S.J., Nelson, S.E., 2002. Body composition of the male and female reference infants.
Annu. Rev. Nutr. 22, 1–17.
Fomon, S.J., Haschke, F., Ziegler, E.E., et al., 1982. Body composition of reference children from birth
to age 10 years. Am. J. Clin. Nutr. 35(5 Suppl.), 1169–1175.
Guillerman, R.P., 2013. Marrow: Red, yellow and bad. Pediatr. Radiol. 43(SUPPL. 1), S181–S192.
Herman-Giddens, M.E., Steffes, J., Harris, D., et al., 2012. Secondary sexual characteristics in boys:
Data from the pediatric research in office settings network. Pediatrics 130(5), e1058–e1068.
ICRP, 1975. Report of the Task Group on Reference Man. ICRP Publication 23. Pergamon Press,
Oxford.
ICRP, 1994a. Dose coefficients for intake of radionuclides by workers. ICRP Publication 68. Ann.
ICRP 24(4).
ICRP, 1994b. Human respiratory tract model for radiological protection. ICRP Publication 66. Ann.
ICRP 24(1–3).
ICRP, 2002a. Basic anatomical and physiological data for use in radiological protection: reference
values. ICRP Publication 89. Ann. ICRP 32(3–4).
ICRP, 2017. Occupational intakes of radionuclides: Part 3. ICRP Publication 137. Ann. ICRP 46(3/4).
Karampinos, D.C., Ruschke, S., Dieckmeyer, M., et al., 2018. Quantitative MRI and spectroscopy ofbone marrow. J. Magn. Reson. Imaging 47(2), 332–353.
Treves, S., Ahnberg, D.S., Laguarda, R., et al., 1974. Radionuclide evaluation of regional lung function
in children. J. Nucl. Med. 15(7), 582–587.

†

EEC = equilibrium equivalent concentration; 1 h Bq m −3 of EEC exposure of 222Rn = 1.57 × 10−6 WLM = 5.56
× 10−6 mJ h m−3. EEC of 222Rn = F × Radon gas activity concentration (Bq m-3), where F is the equilibrium factor.
ǂ
Effective dose per unit exposure to radon progeny calculated with fp=0.1 and fpn = 0.2.

293

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCEGLOSSARY

7668
7669
7670
7671
7672

Active (bone) marrow

7673
7674
7675

Blood

7676
7677
7678
7679
7680
7681
7682
7683

Bone marrow. See also ‘Active (bone) marrow’ and ‘Inactive (bone) marrow’

7684
7685
7686

Clearance

7687
7688
7689
7690
7691

Committed effective dose, E(). See also ‘Effective dose’.
In this series of reports, the integration time  following the intake is taken to be 50 y for adults
and from intake to age 70 y for children. The committed effective dose E() is calculated with

7692

Active marrow is haematopoietically active and gets its red colour from the large numbers oferythrocytes (red blood cells) being produced. Active bone marrow serves as a target region forradiogenic risk of leukaemia.

Corresponds to the transfer compartment in the biokinetic models. Also called ‘transfer
compartment’ or ‘body fluids’ in previous ICRP publications.

Bone marrow is a soft, highly cellular tissue that occupies the cylindrical cavities of long bones
and the cavities defined by the bone trabeculae of the axial and appendicular skeleton. Totalbone marrow consists of a sponge-like, reticular, connective tissue framework called stroma,
myeloid (blood-cell-forming) tissue, fat cells (adipocytes), small accumulations of lymphatic
tissue, and numerous blood vessels and sinusoids. There are two types of bone marrow: active(red) and inactive (yellow) where these adjectives refer to the marrow’s potential for blood cellelement production (haematopoiesis).

The removal of material from the respiratory tract by particle transport and by absorption intoblood.

the use of male and female committed equivalent doses to individual target organs or tissues, T
according to the expression:

𝐸 (𝜏) = ∑ 𝑤T [
𝑇

7693
7694
7695
7696
7697
7698
7699
7700
7701
7702

𝐻TM (𝜏) + 𝐻TF (𝜏)]2

The SI unit for committed effective dose is the same as for absorbed dose, J kg–1, and its specialname is sievert (Sv).

Committed equivalent dose HT(). See also ‘Equivalent dose’.
In this series of reports, the equivalent dose to an organ or tissue region is the time integral of
the equivalent dose rate in a target organ or tissue T of the Reference Individual. This iscalculated using reference biokinetic and dosimetric models following the intake of radioactive
material into the body of the Reference Individual. The integration period  following the intake
is taken to be 50 y for adults and from intake to age 70 y for children:𝜏𝐻T (𝜏) = ∫ Ḣ(𝑟T , 𝑡)𝑑𝑡
0

7703
7704
7705
7706

For both sexes, the equivalent dose rate Ḣ (rT, t) in target region rT at time t after an acute intake
is expressed as:

7707

Ḣ(𝑟T , 𝑡) = ∑ 𝐴(𝑟S , 𝑡) ∙ 𝑆w (𝑟T ← 𝑟S , 𝑡)𝑟S

294

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

7708
7709
7710
7711
7712
7713
7714
7715
7716
7717

where:

7718
7719
7720
7721
7722
7723

Compartment

7724
7725
7726
7727
7728

Dose coefficient

7729
7730
7731
7732

Dose per intake coefficient. See also ‘Dose coefficient’

7733
7734
7735

Endogenous excretion

7736
7737
7738
7739

Extrathoracic (ET) airways

7740
7741
7742
7743

Inactive (bone) marrow

7744
7745
7746
7747
7748
7749

Nasal augmenter

7750

Normal nose breather See ‘Nasal Augmenter’A(rS,t) is the activity of the radionuclide in source region rS at time t after intake, in Bq, as
predicted by the reference biokinetic models for the Reference Individual,
Sw(rS←rT) is the radiation weighted S coefficient; i.e. the equivalent dose to target region rT per
nuclear transformation in source region rS, in Sv (Bq s)–1, for the Reference Individual.
The SI unit for committed equivalent dose is the same as for absorbed dose, J kg–1, and its
special name is sievert (Sv).

In this series of reports: mathematical pool of radioactive materials in the body which can becharacterised by first order kinetics. Activity is considered to be uniformly distributed in acompartment. One or more compartments can be associated with an organ (e.g. the liver), a partof an organ (e.g. the bronchial region of the lungs), a tissue (e.g. the bone), a part of a tissue(e.g. the bone surface) or another substance of the body (e.g. the blood).

In this series of reports, a dose coefficient is defined as either the committed equivalent dose inorgan or tissue T per intake, hT(), or the committed effective dose per intake, e(), where  isthe dose-commitment period in years over which the dose is calculated. Note that elsewhere
the term ‘dose per intake coefficient’ is sometimes used for dose coefficient.

In this series of reports: the committed effective dose per radionuclide intake, e(), or
committed equivalent dose to the tissue or organ rT per radionuclide intake, hT(rT,), where  isthe dose-commitment period over which the dose is calculated.

Term used to specify the excretion of materials from blood to the alimentary tract, applying tobiliary excretion and passage of materials through the alimentary tract wall.

Part of the respiratory tract, consisting of the anterior nose (the ET 1 region) and the posterior
nasal passages, pharynx and larynx (the ET 2 region). Note that the oral part of the pharynx is
no longer part of ET2 because it is included in the HATM.

In contrast to the active marrow, the inactive marrow is haematopoietically inactive (i.e. does
not directly support haematopoiesis). It gets its yellow colour from fat cells (adipocytes) which
occupy most of the space of the bone marrow framework.

A person who breathes entirely through the nose at the exercise levels of ‘sleep’, ‘sitting’ and‘light exercise’, but oro-nasally (partly through the nose and partly through the mouth) during‘heavy exercise’. Also known as a ‘normal nose breather’, because most people breathe
according to this pattern. All Reference Individuals defined in this series of reports are assumed
to be Nasal Augmenters.

295

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

7751
7752
7753
7754
7755

Reference Man

7756
7757
7758
7759
7760
7761
7762

Reference Member of the Public

7763
7764
7765

S-coefficient (radiation-weighted) Sw(rT ← rS, t)

An individual with the anatomical and physiological characteristics previously defined in thereport of the ICRP Task Group on Reference Man (ICRP, 1975) and now given in Publication
89 (ICRP, 2002a). Publication 89 gives reference anatomical and physiological values for maleand female individuals of six age groups: newborn, 1 y, 5 y, 10 y, 15 y, and adults.
A newborn, 1 y, 5 y, 10 y, 15 y old or adult Reference Person combined with the reference
biokinetic and dosimetric models and their parameter values, as defined in this report seriessystemic biokinetic models (HRTM, HATM, and dosimetric models). The structure andparameter values of biokinetic models of the Reference Member of the Public are invariant
on the sex, race and other individual-specific characteristics, but depend on its age group andare based on reference male parameter values where sex-specific models are available.

The equivalent dose to target region rT per nuclear transformation of a given radionuclide insource region rS, Sv (Bq s)–1, for the Reference Individual of age t.

𝑆w (𝑟T ← 𝑟S , 𝑡) = ∑ 𝑤R ∑ 𝐸R,i 𝑌R,i Φ(𝑟T ← 𝑟S, 𝐸R,i , 𝑡 )

7766

𝑅

𝑖

7767
7768
7769
7770
7771
7772

where:
ER,iis the energy, in joules, of the ith radiation of type R emitted in nuclear transformationsof the radionuclide;YR,iis the yield of the ith radiation of type R per nuclear transformation, (Bq s)–1,wR
is the radiation weighting factor for radiation type R (Table 1.2),
Φ(rT ← rS, ER,i, t) is the specific absorbed fraction (SAF), defined as the

7773
7774
7775
7776
7777
7778
7779

fraction of energy ER,i ER,i of radiation type R emitted within the source region rS that isabsorbed per mass in the target region rT for the reference individual of age t, kg–1.
Note that anatomical parameters depend on the age-group. In case of intake of long-lived
radionuclides during childhood, Sw will vary with respect to time. S-coefficients for times in
between the 6 reference individual ages are obtained via interpolation. Its value represents
either the equivalent dose rate (Sv s–1) per activity (Bq), or the equivalent dose (Sv) per nuclear
transformation (Bq s) in the target region.

7780
7781
7782

Specific absorbed fraction (SAF), Φ(rT ← rS, ER,i, t)

7783
7784
7785
7786
7787
7788
7789
7790
7791
7792

Spongiosa

Fraction of radiation R of energy ER,i emitted within the source region rS that is absorbed permass in the target region rT for the reference individual of age t .

Term referring to the combined tissues of the bone trabeculae and marrow tissues (both active
and inactive) located beneath cortical bone cortices across regions of the axial and appendicularskeleton. Spongiosa is one of three bone regions defined in the Publication 110 (ICRP, 2009)reference phantoms, the other two being cortical bone and medullary marrow of the long bone
shafts. As the relative proportions of trabecular bone, active marrow, and inactive marrow varywith skeletal site, the homogeneous elemental composition and mass density of spongiosa are
not constant but vary with skeletal site (see Publication 110 and Publication 143 (ICRP, 2020)).
.

296

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCEACKNOWLEDGEMENTS

7793
7794
7795
7796
7797
7798
7799
7800
7801
7802
7803
7804
7805
7806
7807
7808
7809
7810
7811
7812
7813
7814
7815
7816

This report is the first in a series of documents replacing the Publication 56 series (ICRP, 1989,
1993, 1995b,c, 1996a, 2001, 2004) to provide revised age-dependent dose coefficients formembers of the public for environmental intakes of radionuclides by inhalation and ingestion.
The revised dose coefficients have been calculated using the Publication 100 (ICRP, 2006)
Human Alimentary Tract Model (HATM) and the revision of the Publication 66 (ICRP, 1994a)
Human Respiratory Tract Model (HRTM) described in Publication 130 (ICRP, 2015).
Revisions have been made to many of the models that describe the systemic biokinetics ofradionuclides absorbed to blood, making them more physiologically realistic representationsof uptake and retention in organs and tissues and of excretion.
This first report in the series provides an introduction to the report series and includes Sections
on biokinetic and dosimetric models plus data on individual elements and their radioisotopes,
including biokinetic data and models, and dose coefficients. Additional data accompanying thisseries are available on the ICRP website and give extensive additional information. This current
report provides the above data for the elements already described in OIR Parts 2–5(Publications 134, 137, 141, 151) i.e.: Hydrogen (H), Carbon (C), Phosphorus (P), Sulphur (S),Calcium (Ca), Iron (Fe), Cobalt (Co), Zinc (Zn), Strontium (Sr), Yttrium (Y), Zirconium (Zr),
Niobium (Nb), Molybdenum (Mo), Technetium (Tc), Ruthenium (Ru), Antimony (Sb),
Tellurium (Te), Iodine (I), Caesium (Cs), Barium (Ba), Iridium (Ir), Lead (Pb), Bismuth (Bi),Polonium (Po), Radon, (Rn), and Radium (Ra).
Subsequent reports will provide data for most of the remaining elements.

7817
7818

ICRP thanks all those involved in the development of this publication for their hard work anddedication over many years.

7819
7820
7821
7822
7823
7824
7825
7826
7827
7828

Task Group 95 members (2014-present)

7829

Main Commission critical reviewers

F. Paquet (Chair)
M. R. Bailey
V. Berkovski
L. Bertelli
E. Blanchardon
S. Lamart
E. Davesne
G. Etherington

M. KaiJ.W. Marsh
T. Fell
A. Giussani
D. Gregoratto
D. JokischT. Smith
M.A. Lopez
R. W. Leggett

D. Melo
D. Noβke
G. Ratia

S. Romanov

7830

Editorial members

7831
7832
7833

C.H. Clement (Scientific Secretary and Annals of the ICRP Editor-in-Chief)
H. Yu (Assistant Scientific Secretary and Annals of the ICRP Associate Editor)
T. Yasumune (Assistant Scientific Secretary and Annals of the ICRP Associate Editor)

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DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

7834

Committee 2 members during preparation of this publication

7835(2017-2021)

7836
7837
7838
7839
7840
7841

J.D. Harrison (Chair)
F. Paquet (Vice-Chair)
W.E. Bolch (Secretary)
M. Antonia Lopez
V. Berkovski
E. Blanchardon

7842(2021-2025)

7843
7844
7845
7846
7847
7848

F. Bochud (Chair)
F. Paquet (Vice-chair)
M.A. Lopez (Secretary)
M. Andersson
V. Berkovskyy
D. de Souza Santos

7849

Committee 2 emeritus members

7850

K. Eckerman

7851

Main Commission members at the time of approval of this publication

7852
7853
7854
7855
7856
7857
7858
7859
7860
7861
7862

Chair: W. Rühm, Germany
Vice-Chair: D.A. Cool, USA
Scientific Secretary: C.H. Clement, Canada; sci.sec@icrp.org*

7863
7864

*

K.E. Applegate, USA
F. Bochud, Switzerland
S. Bouffler, UK
K.W. Cho, Korea
G. Hirth, Australia
M. Kai, Japan
D. Laurier, France

A. Giussani
D. JokischC.H. Kim
R. Leggett
J. Li
N. Petoussi-Henss

T. SatoT. Smith
A. Ulanowski
F. Wissmann

A. Giussani
D. JokischC.H. Kim
M.S. Kulkarni
S. Lamart
C. LeeJ. Li
J.W. Marsh
N. Petoussi-Henss
T. SatoT. Smith
A. Ulanowski

S. Liu, China
S. Romanov, Russia
T. Schneider, France
A. Wojcik, Sweden

Emeritus members
R.H. Clarke, UK
F.A. Mettler Jr, USA
R.J. Pentreath, UK
R.J. Preston, USA
C. Streffer, Germany
E. Vañó, Spain

Although formally not a Main Commission member since 1988, the Scientific Secretary is an
integral part of the Main Commission.

7865

298