3. HEALTH EFFECTS CAUSED BY RADIATION AND BASIS FOR RADIOLOGICAL
PROTECTION
3.1. Introduction
When ionizing radiation passes through matter, some of its energy is imparted to the matter by
means of ionization and excitation of atoms and molecules. Impartment of radiation energy to
matter is the start point for developing radiation health effects in human, animals, plants and
microorganisms – in all alive beings.
Tissues and organs are composed by cells of different kinds and radiation damage of these cells
leads to development of radiation health effects. The target for most biological effects of ionising
radiation is the genome of the cell, the DNA, which is the macromolecule of deoxyribonucleic
acid. That molecule has very complicated structure, which primary structure could be imagined
as double helix. Two stands of DNA helix contain complimentary copies of cell genome
information, which plays the key role of the cell reproduction. Even a single ionization by a
particle or a photon can cause a break in the DNA molecule. If it is a break in one strand of the
DNA only (a single strand break) it will most probably be perfectly repaired with no
consequences for the cell genome. Cells have tremendous ability to repair damage. As a result,
not all radiation damages of DNA are irreversible. In many instances, the cells are able to
completely repair any damage and function normally. If, however, both DNA strands are broken
close to each other, repair mechanisms are likely to fail and the cell genome may be modified. In
some case, as shown in Figure 03-1, the damage is severe enough that the cell dies or loss ability
for reproduction (cell division). In other instances, the cell is damaged but it still able to
reproduce. The daughter cell, however, may be lacking some critical life sustaining components,
and they die. Finally, the cell may be affected in such a way that it does not die but is simply
mutated. The mutated cell reproduces and thus perpetuates the mutation. This could be the
beginning of the malignant tumour.
Figure 03-1. Outcomes of DNA damage
Generally, cells are most sensitive to radiation when they are in stage of cell division, so that the
most radiosensitive tissues are the blood, the intestinal wall, the skin, and the foetus. Cells of that
tissues and organs demonstrate the high reproduction intensity. Conversely, the most
radioresistant tissues are muscle, nerves, and the adult brain, where the intensity of cell
reproduction is minimal.
1
Probability of development of DNA damage after irradiation is grooving up with concentration
of ionizations and excitations in the media, which defines the absorbed dose of ionizing
radiation. The absorbed dose D R is the energy imparted to matter by ionizing radiation R per
unit mass of irradiated material at the place of interest. The unit of absorbed dose is J×kg-1,
called the gray (Gy).
Table 03-01 presents a list of radiation-induced health effects that would be critical during an
emergency. Experience and research indicate that evaluation of the dose to the target organs
presented in the table should provide a basis for criteria for making decisions that will address
the full range of potential adverse health effects in emergency exposure situation.
Table 03-1. Critical radiation-induced health effects during a radiation emergency
Health effect
Fatal
Haematopoietic syndrome
Gastrointestinal syndrome
Target organ or entity
Severe deterministic health effects
Red marrow (a)
Small intestine for external exposure (a) or
Colon for internal exposure (b)
Lung (a), (c)
Embryo/foetus in all periods of gestation
Pneumonitis
Embryo/foetal death
Nonfatal
Moist desquamation
Skin (d)
Necrosis
Soft tissue (e)
Cataract
Lens of the eye (a), (f)
Acute radiation thyroiditis
Thyroid (a)
Hypothyroidism
Thyroid (a)
Permanently suppressed ovulation Ovary (a)
Permanently suppressed sperm
Testes (a)
counts
Severe mental retardation
Embryo/foetus 8–25 weeks of gestation
Verifiable reduction in IQ
Embryo/foetus 8–25 weeks of gestation
Malformation
Embryo/foetus 3–25 weeks of gestation [#543]
Growth retardation
Embryo/foetus 3–25 weeks of gestation [#543]
Stochastic health effects
Thyroid cancer
Thyroid
All stochastic health effects
All organs taken into account in definition of effective
dose
(a)
External exposure to the red marrow, lung, small intestine, gonads, thyroid and lens of eye
from irradiation in a uniform field of strongly penetrating radiation is addressed by AD red
marrow.
(b)
(c)
(d)
(e)
(f)
Different targets for gastrointestinal syndrome are proposed because of difference in dose
formation in small intestine and colon in case of internal exposure. This is due to difference
in the kinetics of ingested material in the gastrointestinal (GI) tract, which leads to much
higher doses in colon than in small intestine after intake.
For the gas-exchange (alveolar interstitial (AI)) region of the respiratory system.
Skin structures at a depth of 50 mg/cm2 (or 0.5 mm) under the surface and over an area of 100
cm2
To a depth of 0.5 cm in tissue.
Lens structures at a depth of 300 mg/ cm2 (or 3 mm) under the surface.
2
The health effects of ionizing radiation need a time for development from physical act of energy
absorption to medical syndrome. Figure 03-2 presents the time perspective of development
biological effects. This time perspective plays the important role in evaluation of causality of
health effects and exposure.
TIME SCALE
EFFECTS
Fractions of
seconds
Energy absorption
Changes in biomolecules (DNA, membranes)
Seconds
Biological repair
Change of information in cell
Minutes
Hours
Weeks
Germ
cell
Cell
death
Days
Organ
failure
Mutations
Somatic
cell
Clinical
changes
Months
Years
Leukaemia or
solid cancer
Decades
Hereditary
effects
Generations
Figure 03-2. Biological effects of radiation in time perspective.
Another aspect of time perspective is the competition of deterministic and stochastic effects in
causation of untimely death after exposure. Because of short time for development, the
deterministic effects win in case of high dose exceeding the threshold level. The overexposed
individual will die because of development of deterministic effects before the stochastic effect
becomes apparent. Therefore


At high doses cell death and loss of ability for reproduction reproductive leads to
development of deterministic health effects (organ death or clinical changes). Such an
effect is described as a severe deterministic effect if it is fatal or life threatening or results
in a permanent injury that reduces quality of life.
At low doses, when probability of cell survival after irradiation is high, the development
of mutated cell could give a rise for stochastic health effects of radiation (hereditary
effects or cancers).
3.2. Dosimetric quantities for use in characterization of emergency exposure situation
Biological effects of radiation are correlated with the energy absorbed by ionization and
excitation in unit mass of tissue (the absorbed dose). The effects are modified by microscopic
spatial distribution of energy of radiation imparted to matter, which depends on quality of
radiation. It also can be modified by dose rate, concentration of oxygen in tissue as well as by
other factors determining radiosensitivity of biological object concerned.
The absorbed dose in organ or tissue provides the dosimetric basis for evaluating the risk of
development of stochastic and deterministic effects after the exposure. The average absorbed
dose in organ or tissue D R ,T (absorbed organ dose) is the dosimetric quantity, which
3
characterises the energy absorbed by ionization and excitation in unit mass of tissue or organ T
[#502]:
D R ,T 
E R ,T
,
(03- 1)
mT
where E R ,T is the energy absorbed in tissue or organ T and mT is the mass of that organ or
tissue. The unit of absorbed dose is J×kg-1, called the gray (Gy).
The dosimetric quantities of effective dose, equivalent dose, and RBE weighted absorbed dose
are used in evaluating radiation induced consequences in emergency exposure situations. The
dosimetric quantities of personal dose equivalent and ambient dose equivalent are used in
individual and areal monitoring in emergency. These quantities are listed in Table 03-2. The
Figure 03-3 [#501] illustrates links between absorbed organ dose and other dosimetric quantities.
Table 03-2. Dosimetric quantities used to characterise of emergency exposure situation
Operational
quantities
Radiation protection
quantities
Dosimetry quantity
RBE weighted
absorbed dose in
organ or tissue
Equivalent dose
in organ or tissue
Symbol
Purpose
Unit
AD T
For evaluating deterministic health effects
induced due to exposure of an organ or tissue
Gy
HT
For evaluating stochastic health effects induced
due to exposure of an organ or tissue
Sv
Effective dose
Personal dose
equivalent
H P (d)
For evaluating detriment related to the
occurrence of stochastic health effects in an
exposed population
For monitoring external exposure of an
individual
Ambient dose
equivalent
H*(d )
For monitoring a radiation field at the site of an
emergency
E
Sv
Sv
Sv
The radiation protective quantities of effective dose, equivalent organ dose, and RBE weighted
organ dose could not be directly measured. They have to be calculated on the base of
characteristics of exposure pathways and exposed person. Radiation protection quantities are
used for purposes of radiation protection and safety to express the criteria of safe conditions for
life and work.
4
Intake of
radionuclide
I,
Bq
RBE weighted
dose in tissue
or organ T,
ADT [Gy]
RBER,T
Risk
of deterministic
effects
Absorbed dose in
tissue or organ T,
DT [Gy]
Radiation
fluence
F,
[cm-2]
Equivalent
dose
Equivalent
dose
tissue
Equivalent
dose
inin
tissue
oror
organ
in tissue
or
organ
T,T,
[Sv]
organ
T T,
HTH[Sv]
HT [Sv]
WR
Effective dose,
E [Sv]
Radiation
detriment
QR
Personal dose
equivalent,
HP(d) [Sv]
Individual
monitoring
QR
Ambient dose
equivalent,
H*(d) [Sv]
Area
monitoring
WT
Absorbed dose
D [Gy]
at surface of
body
Absorbed dose
D [Gy]
at a point
Risk
of stochastic
effects
Figure 03-3. Dosimetric quantities and their application in an emergency exposure situations.
The RBE weighted dose in an organ or tissue (RBE weighted average absorbed dose) AD T is
defined as a product of averaged absorbed dose D R ,T of radiation (R) in organ or tissue (T) and
the relative biological effectiveness ( RBE R ,T ):
AD T   D R ,T  RBE R ,T
(03- 2)
The relative biological effectiveness is a measure of the relative effectiveness of different
radiation types at inducing a specified health effect, expressed as the inverse ratio of the
absorbed doses of two different radiation types that would produce the same degree of a defined
biological end point. Values of relative biological effectiveness in causing the development of
deterministic effects are selected to be representative of the severe deterministic effects that are
significant to emergency preparedness and response. The tissue specific and radiation specific
values of RBE R ,T for the development of selected severe deterministic effects are as shown in
the Table 03-3 [#501], [#511], [#512]. The RBE weighted dose is intended to account for
differences in biological effectiveness in producing deterministic health effects in organs or
tissues of reference man due to the quality of radiation. The unit of the RBE weighted dose in SI
is Jkg-1 and is called the gray (Gy) [#501], [#502].
R
5
Table 03-3. Tissue- and radiation-specific values of RBE for developing selected severe
deterministic health effects.
Health effect
Critical organ
Haematopoietic syndrome
Red marrow
Pneumonitis
Lung (b)
GI Syndrome
Colon
Exposure (a)
RBE
External and internal 
External and internal n0
Internal 
Internal 
External and internal 
External and internal n0
Internal 
Internal 
External and internal 
1
3
1
2
1
3
1
7
1
External and internal n0
3
Internal 
1
0 (c)
Internal 
1
External , 
Necrosis
Soft tissue (d)
0
External n
3
1
External , 
Moist desquamation
Skin (e)
External n0
3
(f)
Intake of iodine isotopes
0.2
Hypothyroidism
Thyroid
Other thyroid seekers
1
(a)
External ,  exposure includes the dose from bremsstrahlung produced within the source
materials;
(b)
Tissue of alveolar-interstitial gas exchange region of respiratory tract;
(c)
For alpha-emitters uniformly distributed in the contents of the colon, it is assumed that
irradiation of the walls of the intestine is negligible;
(d)
Tissue at a depth of 0.5 cm;
(e)
Tissue at a depth of 0.5 mm below skin surface over an area of more than 100 cm2;
(f)
Uniform irradiation of the tissue of the thyroid gland is considered to be five times more likely
to produce deterministic health effects than internal exposure to low energy beta-emitting
isotopes of iodine such as 131I, 129I, 125I, 124I and 123I. Thyroid seeking radionuclides have a
heterogeneous distribution in thyroid tissue. 131I emits low energy beta-particles that lead to a
reduced effectiveness of irradiation of critical thyroid tissues due to the dissipation of
particles’ energy in other tissues.
The RBE weighted organ dose is used for characterizing high-dose exposure to evaluate the
likelihood of development of severe deterministic effects after external exposure and intake of
radioactive material. The guidelines for evaluation of the likelihood of development of severe
deterministic effects are provided in Refs. [#511], [#512], [#555], [#530].
The equivalent dose in organ or tissue (radiation weighted averaged absorbed dose in organ or
tissue) H T is defined as the product of the averaged absorbed dose in the organ or tissue (D) and
the radiation weighting factor w R [#502]:
H T   D R ,T  w R
R
(03- 3)
It is an organ-specific quantity that may be used for assessment of the risk of any radiationinduced cancer in an organ. The equivalent dose is intended to account for differences in
6
biological effectiveness in producing stochastic health effects in organs or tissues of reference
man due to the quality of radiation. Equivalent dose is a measure of the dose to a tissue or organ
designed to reflect the amount of harm caused. The values of an equivalent dose to a specified
tissue from any type of radiation can therefore be compared directly. The unit of the equivalent
dose in SI is Jkg-1 and is called the sievert (Sv) [#502]. Values of w R are shown in Table 03-4.
Table 03-4. Radiation weighting factors for evaluation equivalent dose in tissue or organ
Radiation
Radiation weighting factor
Photons, electrons, positrons
and muons
Protons and charged pions
Alpha particles, fission
fragments, heavy ions
Neutrons
1
2
20
A continuous function of neutron energy:
2.5  18.2 exp( [ln( E n )] 2 / 6),
E n  1 MeV

2
w R  5.0  17.0 exp( [ln( 2E n )] / 6), 1 MeV  E n  50 MeV

2
E n  50 MeV
2.5  3.25 exp( [ln( 0.04E n )] / 6),
The equivalent organ dose is used for characterizing low-dose exposure to evaluate the
likelihood of development of stochastic effects after external exposure and intake of radioactive
material. The guidelines for evaluation of the likelihood of development of stochastic effects are
provided in Refs. [#519], [#533], [#547].
The effective dose is defined as the product of the equivalent dose in a tissue (T) and the tissue
weighting factor ( w T ) representing its proportion of the detriment resulting from irradiation of
tissue (T) to the total detriment when the whole body is irradiated uniformly [#502].
E   HT  w T
(03- 4)
T
The effective dose is intended to account for differences in biological effectiveness in producing
stochastic health effects due to the quality of radiation and its distribution in the body of
reference man. The values of w T currently recommended by the ICRP are as given in Table 035.
The total effective dose for the specified period (e.g., day, year, etc.) is widely used to formulate
the regulatory requirements. It is the sum of the relevant doses from external exposure in the
specified period and the relevant committed doses from intakes in the same period; the period for
calculating the committed dose shall be 50 years for intakes by adults and to age 70 years for
intakes by children. Values of effective dose from any type(s) of radiation and mode(s) of
exposure could be compared directly.
7
Table 03-5. Tissue weighting factors for evaluation effective dose
wT
Tissue
Bone-marrow (red), colon, lung, stomach, breast, remainder tissues
Gonads
Bladder, oesophagus, liver, thyroid
Bone surface, brain, salivary glands, skin
w
T
(a)
0.12
0.72
0.08
0.08
0.04
0.16
0.01
0.04
Total
1.00
(a)
The w T for the remainder tissues (0.12) applies to the arithmetic mean dose of the 13 organs
and tissues for each sex listed below. Remainder tissues: adrenals, extrathoracic (ET) region, gall
bladder, heart, kidneys, lymphatic nodes, muscle, oral mucosa, pancreas, prostate (male), small
intestine, spleen, thymus, uterus cervix (female).
The organ weighting factors were chosen by the ICRP to reflect the relative detriment from
cancer or occurrence of sever hereditary effects in the first generations after uniform whole-body
exposure. The radiation detriment is the product of probability of occurrence and severity of
injury or damage, which lead to a shortening duration of a normal life. The concept of radiation
detriment have been introduced in the 1990 Recommendations of the ICRP [#552] and was
upgraded in the 2007 Recommendations of the ICRP [#522].
Cancer needs a long period for latent developing. The shortest latent period is about 4-5 years for
leukaemia. The first wave in Error! Reference source not found. presents development of
leukaemia after brief exposure of red marrow. The wave in Error! Reference source not found.
presents development of solid cancers (malignant tumours). The latent period for these cancers is
several decades.
Figure 03-4. Development of the stochastic effects in exposed group after brief uniform exposure
of whole body.
The Error! Reference source not found. shows the dynamics of development of radiation
induced cancers after brief whole body exposure. The value of R T is a risk of development fatal
cancer in organ T. It depends on dose, dose rate, time passed after exposure, and organ
concerned. The value of TLat is the latent period, which depends on organ concerned. Cancer
needs a long period for latent developing. The shortest latent period is about 4-5 years for
leukaemia. The first wave in Error! Reference source not found. presents development of
leukaemia after brief exposure of red marrow. The wave in Error! Reference source not found.
presents development of solid cancers (malignant tumours). The latent period for these cancers is
several decades.
8
Organs of the human body have different radiosensitivity. The severity of manifestations of the
stochastic effect of irradiation of this organ is characterized by the average number of years of
normal life lost because of cancer. The lower the latency period for cancer - the more years of
life may be lost and the greater the severity of this effect. Without medical care, development of
cancer leads to death quite quickly. The difference between life expectancy and latent period (
TLat ) is the lost period of normal life for victim ( TLost ). The value of TLost is used for
evaluation of radiation detriment. Table 03-6 presents values of TLost used in evaluation of w T
[#552].
Table 03-6. Life expectancy lost from stochastic effects
Loss of lifespan,
years
Organ where stochastic effect is developed
Red marrow
30
Gonads, Breasts
20
Bone surfaces, Liver, Skin, Thyroid, Lung, Colon, Remainder organs
15
Esophagus, Stomach, Urinary bladder
10
Reference stochastic effect
15
The radiation detriment is the product of probability of occurrence and severity of injury or
damage, which lead to a shortening duration of a normal life. Severity of injury is measured in
terms of years of a normal life, which loosed due to developing a radiation health effect. Its value
characterizes the reference man. Value of radiation detriment cannot be measured. Radiation
detriment is a quantity, which could be calculated on the base of estimating an effective dose.
Limitation of radiation detriment is the basis for framework of radiation protection and safety.
The effective dose was invented by the ICRP to account differences in biological effectiveness in
producing harm, due to the quality of radiation and its distribution in the body of exposed
individual. The effective dose (E) is widely used for justifying and optimizing protective actions
[#502].
Effective dose is intended for use as a radiation protection quantity and therefore should not be
used for epidemiological evaluations, nor should it be used for any specific investigation of
human exposure. The 2007 Recommendations of the International Commission on Radiological
Protection [#522] in paragraphs 153-154 determine the area for use of effective dose as follows.
(153) The main and primary uses of effective dose in radiological protection for both
occupational workers and the general public are:


prospective dose assessment for planning and optimisation of protection; and
retrospective dose assessment for demonstrating compliance with dose limits, or for
comparing with dose constraints or reference levels.
(154) In this sense, effective dose is used for regulatory purposes worldwide. In practical
radiological protection applications, effective dose is used for managing the risks of stochastic
effects in workers and the public. The calculation of effective dose or corresponding conversion
coefficients for external exposure, as well as dose coefficients for internal exposure, are based
on absorbed dose, weighting factors ( w R and w T ), and reference values for the human body
and its organs and tissues. Effective dose is not based on data from individual persons (see
9
Annex B). In its general application, effective dose does not provide an individual-specific dose
but rather that for a Reference Person under a given exposure situation.
(155) There may be some circumstances in which parameter values may be changed from the
reference values in the calculation of effective dose. It is, therefore, important to distinguish
between 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 (e.g., the weighting factors). Thus, in the assessment of effective
dose in occupational situations of exposure, changes may be made that, for example, relate to
the characteristics of an external radiation field (e.g., direction of exposure) or to the physical
and chemical characteristics of inhaled or ingested radionuclides. In such cases it is necessary
to clearly state the deviation from the reference parameter values.
The effective dose is used for expression of dose limitations, e.g. dose limits, dose constraints or
reference levels to control the exposure of the members of the public and workers. To estimate
the radiation detriment due to use of radiation sources, the ICRP determined the detrimentadjusted nominal risk coefficients [#522]. This risk coefficient is the likelihood of loss of 15
years of normal life per 1 sievert of effective dose. Table 03-7 provides the detriment-adjusted
nominal risk coefficients of effective dose for developing reference stochastic effect after
exposure to radiation at low dose rate.
Table 03-7. Detriment-adjusted nominal risk coefficients for developing reference stochastic
effect after exposure to radiation at low dose rate
Exposed population
Total
Cancer
Heritable effects
The general public
5.7×10-2 Sv-1
5.5×10-2 Sv-1
0.2×10-2 Sv-1
Occupational workers
4.2×10-2 Sv-1
4.1×10-2 Sv-1
0.1×10-2 Sv-1
In accordance to the ICRP, as mentioned above, the effective dose should not be used for
evaluation of medical consequences of radiation exposure of the person. The detriment-adjusted
nominal risk coefficients of effective dose from Table 03-7 provides basis for assessment of
expected collective loss of life span by the members of certain exposed cohort. The collective
exposure of cohort is expressed in terms of collected effective dose, which is the sum of effective
doses received by the members of certain cohort
S   En .
(03- 5)
n
The unit of collective dose is man-sievert (man-Sv).
Product of detriment-adjusted nominal risk coefficient and collective dose provides estimation of
collective loss of life span as follows.
Expected detriment = Collective effective dose
× Detriment-adjusted nominal risk coefficients for stochastic effects
× Expected loss of lifespan
For instance, the expected collective detriment of group of workers with collective dose of 1
man-Sv will be 0.63 man-y:
1 man-Sv × (4.2×10-2 Sv-1×15 y) = 0.63 man-y.
10
(03- 6)
The assessment of collective dose and collective detriment could be used in cost-benefit analysis
for optimization of radiation protection. It also used in comparison of different sources of harm
[#569].
The operational quantities of personal dose equivalent and ambient dose equivalent are directly
measurable quantities characterizing the exposure of reference person in actual radiation field.
They are used for purposes of radiation protection and safety to express the operational criteria:


ambient dose equivalent ( H*(d) ), i.e. the dose equivalent that would be produced by the
corresponding aligned and expanded field in the ICRU sphere at a depth d on the radius
opposing the direction of the aligned field; and
personal dose equivalent ( H P (d) ), i.e. the dose equivalent in soft tissue below a specified
point on the body at an appropriate depth d.
Their units in SI are Jkg-1 and are expressed as sievert (Sv).
Ambient dose equivalent and personal dose equivalent are the operational quantities based on the
dosimetric quantity of dose equivalent. The dose equivalent is the product of the absorbed dose
at a point in the tissue or organ and the appropriate quality factor for the type of radiation giving
rise to the dose [#558]:
H   DR  QR
(03- 7)
R
The quality factor QR was introduced as a weighting factor to modify the absorbed dose and to
define the dose equivalent with an objective to account the dependence of probability of
development of stochastic effects on the quality of radiation. This dimensionless factor is given
as a function of the unrestricted linear energy transfer as shown in Figure 03-5. Quality factors
are the product of the relative biological effectiveness, (RBE's), averaged over several types of
tissue, and certain other linear energy transfer (LET) factors expressing biological differences
resulting from radiation absorption of the radiation type of interest and the reference radiation
(200-250 keV X rays); they are assumed to be independent of type of organ exposed.
Figure 03-5. Quality factor of radiation as a function of LET.
11
Any statement of personal dose equivalent or ambient dose equivalent should include a
specification of the reference depth, d, with the value expressed in mm [#558]:



If depth of 10 mm is employed; the operational quantities of H P (10) and H*(10) provide
the best estimation of effective dose of external exposure in uniform parallel field of
penetrating radiation;
If a depth of 0.07 mm is employed, the operational quantity of H P (0.07) provides the
best estimation of equivalent dose in basal layer of skin;
If a depth of 3 mm is employed, the operational quantity of H P (3) provides the best
estimation of equivalent dose in lens of eye.
The table 03-02 shows that units of some dosimetric quantities, e.g. equivalent organ dose and
effective dose, are similar. That situation should be kept in mind and any statement of dose value
should include the reference to the dosimetric quantity used for characterization of exposure
conditions. For instance, the statement of “1 mSv of effective dose” instead of “exposure dose of
1 mSv” shall be used.
3.3. Health effects caused by ionizing radiation
Deterministic health effects
The scientific knowledge about deterministic effects is based on radiobiological research and
evaluation of clinical observation of people overexposed in radiation accidents or received high
radiation doses in course of radiation therapy. In 1944 – 2010, about 260 radiation accidents
were reported worldwide in which about 3000 people were exposed with RBE weighted whole
body dose of above 0.25 Gy or organ dose above 0.75 Gy. These accidents were resulted in 168
registered fatalities [#509]. That number does not include fatalities in 9 reported nuclear
submarine emergencies.
Massive cell death in irradiated organ or tissue causes development of deterministic health
effects of radiation (deterministic effect). The deterministic heath effect is a radiation effect for
which generally a threshold level of dose exists above which the severity of the effect is greater
for a higher dose. Cell survival after exposure is a stochastic process with probability depends
on the exposure dose and dose rate. The higher dose and dose rate, the less probability of
survival the fewer portions of cells in the organ survived after exposure [#504]. The effect will
usually also decrease with dose rate, because a more protracted dose causes the cell damage to be
spread out in time, allowing for more effective repair or repopulation. Deterministic effects occur
at high doses when enough cells in an organ or tissue are killed or prevented from reproducing
and functioning normally and there is a loss of organ function. A threshold dose exists above
which the effects on an organ or biological system are clinically observable. Above the
appropriate threshold, the effect becomes more severe as the radiation dose increases, reflecting
the number of cells damaged. The threshold value reflects the minimal portion of survived cell
that may be enough for relatively normal function of organ or tissue in organism. If exposure
dose is below threshold, the loss a portion of cells of particular organ or tissue may be
compensated by more intensive work of other organs or tissues. In general, the dose-response
function for tissues, i.e. the plot on linear axes of the probability of harm against dose, is sigmoid
in shape. When dose is over threshold, a portion of survived cells is so small, that the system
compensation of cell death could not be effective and the clinical effect of concern is developing.
Dose-response function for deterministic effects is given in Figure 03-6(a). The onset of the
symptoms usually shortens (from weeks to hours) and their severity increases with increasing a
dose. Severe deterministic effects if developed leads to radiation induced death of exposed
person. Causation of deterministic effects and exposure to ionizing radiation has a deterministic
character. The time of appearance of tissue damage ranges from a few hours to many years after
12
the exposure, depending on the type of effect and the characteristics of the particular tissue. Cell
death is an end-point of biological processes developing in time. The time period between
exposure and developing radiation induced clinical effect is comparable with cell reaction to
exposure or with life span of cell and varies from hours to months.
Formerly, deterministic effects were termed "non-stochastic" effects. Now the new term “tissue
reaction” is used by the ICRP for such kind of health effects [#551].
(a)
(b)
Figure 03-6. Dose-response dependence for radiation–induced health effects. (a) Deterministic
effects; (b) Stochastic effects.
Deterministic health could be classified as sever and non-severe. Such an effect is described as a
‘severe deterministic effect’ if it is fatal or life threatening or results in a permanent injury that
reduces quality of life.
Vomiting is an example of non-severe deterministic effect caused by total body irradiation. Time
of its manifestation reflects severity of that effect and depends over the dose.
Figure 03-7. Manifestation of emesis after brief whole body external exposure
The quantitative characteristic of its severity is the time to onset of vomiting: the lover time to
onset, the more severe the level of whole body exposure and injury is. Time to onset of vomiting
is a function of a torso dose. Dose in red marrow could be assumed equal to this quantity in case
of preliminary characterizing the emergency exposure. This dependence is useful for dose
assessment in case of emergency exposure to photons. The Figure 03-7 presents a median RBE
weighted dose in torso as a function of time to onset of vomiting [#506], [#507]:
AD Torso 50  a  t b ,
(03- 8)
where AD Torso 50 is the median estimate of RBE weighted dose in torso (Gy), a = 4.47±0.16, and
b = -0.57±0.045 and t - time to first emesis (hours).
13
In case of criticality emergency, the RBE of neutrons for this effect is about 1 [#507].
Confidence limits (yellow area) represent one SE from the fitted line (solid dark blue).
Whole body radiation dose of greater than 1 Gy received in a short time results in the clinical
"acute radiation syndrome". The symptoms include headache, dizziness, nausea, diarrhea,
insomnia, decrease in white blood cells and platelets. This syndrome, which is dose related, can
result in disruption of the functions of the bone marrow system (>1 Gy), the gastro-intestinal
system (>5 Gy), and the central nervous system (>20 Gy). An acute dose over 3 Gy could be
lethal if no qualified medical care is provided.
Severity of the effects is characterized by probability of radiation induced premature death and
time of occurrence and realization of effect in radiation-induced death. Figure 03-8 from Ref
[#505] illustrates an increasing severity of radiation effects with increasing dose. The range
depends on the non-uniformity of the dose distribution and individual radiosensitivity.



4 Gy – threshold (5% probability of death) for the haematopoietic syndrome;
6-8 Gy – threshold for radiation pneumonitis;
50 Gy – very fast death.
It is recommended to briefly outline the general characteristics of the haematopoietic,
gastrointestinal and neurovascular syndromes.
Figure 03-8. Severity of acute radiation syndrome after brief whole body external exposure
Information on humans and animals has made it possible to describe the symptomatology
associated with the acute radiation syndrome (ARS) caused by more or less uniform irradiation
of whole body. In humans, ARS is defined as the symptoms manifested after whole body
exposure to ionizing radiation, and is often called radiation sickness. From a physiological
standpoint, ARS is a combination of subsyndromes. They appear in stages and are directly
related to the level of received dose as given in Figure 03-8 [#505]. These subsyndromes begin
to occur within hours after exposure and may last for several weeks.
Patients who vomit greater than 4 hours post-accident are likely to have, at worst, a mild acute
radiation syndrome. Patients who experience radiation-induced emesis within one hour after a
radiation incident require extensive and prolonged medical intervention, and an ultimately fatal
outcome is expected in many cases. The median dose for this case is found to be 6.5 Gy with an
interquartile (25%-75%) range of approximately 5-11 Gy.
14
Figure 03-9. Median lethal dose as a function of dose rate of whole body exposure
Risk models and associated parameters were developed using the available data on animal
experiments and analysis of human exposures as described in detail in [#510]. The Figure 03-9
shows the estimated median lethal RBE weighted dose (AD50) to the human relative to the dose
rate for humans, based on data collected in [#510] to confirm the risk model for haematopoietic
syndrome. This data also illustrates the strong dependence of risk on dose rate:

LANGHAM 67 estimates based on linear probit model for exposure for 0–1 day and 1–7
days.
 HIROSHIMA: estimate for Hiroshima with AD50 dose at about 900 meters from
hypocentre; dose estimate modified based on DS86 dosimetry and new transmission
factors.
 MEXICAN FAMILY: Mexican family unknowingly exposed intermittently in their home
to orphan 60Co source; 4 out of the 5 died.
 JAPANESE FISHERMEN: Seven of the 23 fishermen exposed to fallout gamma
radiation had estimated total-body doses greater than 4 Gy; none died from marrowsyndrome mode.
 OTA 80: Judgment of AD50 provided by the Office of Technology Assessment for a one
week exposure period.
 BIR REPORT: Judgment of AD50 provided by the British Institute of Radiology for a one
month exposure period (1982).
Values of quantitative characteristics of the risk of development the fatal or nonfatal
deterministic effects depends on irradiation history presented by time dependence of dose rate
[#501], [#511], [#512]. The threshold doses attributing the fatal deterministic effects for brief
exposure are presented in the Table 03-8.
Table 03-8. Threshold dose of brief exposure
Syndrome
Critical organ or tissue
AD05, Gy
Embryo 0–18 d
0.3
Embryo / foetus 18–150 d
0.6
Foetus > 150 d
2
Haematopoietic
Red marrow
3
Gastrointestinal
Small intestine
12
Embryo or foetal death
15
Syndrome
Critical organ or tissue
AD05, Gy
Soft tissue
25 (a)
Necrosis
Derma of skin
10 (b)
(a)
The dose delivered to 100 cm2 at a depth of 0.5 cm under the body surface due to close contact
with a radioactive source;
(b)
The dose is to the 100 cm2 dermis (skin structures at a depth of 40 mg/cm2 (or 0.4 mm) below
the surface).
Nonfatal deterministic effects of exposure should be taken into account in response to
radiological or nuclear emergency. The threshold doses attributing the nonfatal deterministic
effects for brief exposure are presented in the Table 03-9.
Table 03-9. Nonfatal deterministic effects of external exposure of embryo and foetus
Symptom
Malformation
Possible verifiable
reduction in IQ
Growth retardation
Severe mental
retardation
Period of embryo / foetus gestation
8-25 weeks
8-25 weeks
AD05, Gy
0.1
0.1
8-25 weeks
8-15 weeks
16-25 weeks
0.25
0.6
0.9
The action of penetrating radiation on the whole-body was the main reason of the development
of clinical syndromes of ARS such as bone-marrow and intestinal syndromes and their
combinations, which are characteristic for dose range 1-16 Gy. Less penetrating, only to the
depth of skin, beta irradiation at the doses at least 10 to 20 times higher than average whole-body
dose became the cause of the vast radiation injuries of the skin in more than 50% of the patients.
These injuries significantly aggravated the clinical course of sickness and greatly influenced the
outcomes. Sometimes on the background of shallow radiation injuries, the isolated centres of
more deep local radiation injuries (LRI) have arisen because of local application or contact with
the objects contaminated by radionuclides such as the wet clothes or boots [#508].



134 cases of ARS among responders (emergency workers):
28 died in 1986 from a combination of high external doses of -exposure and skin burns
due to -emitters
17 died in 1987-2004 from various causes, not all directly linked to radiation
No cases of acute radiation syndrome have been recorded among the general public. Table 03-10
presents outcomes of high dose exposure of the Chernobyl emergency workers. Most of fatal
deterministic effects in Chernobyl emergency workers were caused by combination of high
doses of external exposure to penetrating radiation and spacious skin burns caused by heavy
contamination of wet protective closes by fission products, presumably by Ru-106 and Rh-106
[#508].
16
Table 03-10. Responders with ARS following the Chernobyl accident
Degree of ARS
Range of whole body
RBE weighted
dose, Gy
Number of patients
treated
N of deaths
Mild (I)
0.8-2.1
41
-
Moderate (II)
2.2-4.1
50
1
Severe (III)
4.2-6.4
22
7
Very severe (IV)
6.5-16
21
20
Total
0.8-16
134
28
Stochastic health effects
The scientific knowledge about stochastic effects is based on radiobiological research and
evaluation of clinical observation of survives of A-bombing of Hiroshima and Nagasaki, and
people received significant doses in course of radiation therapy or unintended intake of
radioactive material by dial workers and uranium miners in course of work.
Stochastic effects could occur at all dose levels because of cell mutations caused by damage to
the DNA. A modified cell that is still able to perform mitosis can give rise to a clone of cells that
may eventually result in a cancer in the exposed person. Such effects develop in the long term,
often decades after the exposure. The probability that effects will occur either in the exposed
person (somatic effects) or in descendants (hereditary effects) increases in proportion to a dose.
Causation of stochastic effects from exposure to ionizing radiation has a probabilistic character.
It is based on comparison of cancer mortality or morbidity for adequate groups of exposed and
intact persons. Validity of this approach is limited due to natural fluctuations of cancer morbidity
and mortality. So in case of human exposure with very low dose the development of radiation
induced cancers additional to natural ones could not be proved and, therefore, detected, because



All radiation-induced stochastic effects are similar to those developing in non-irradiated
population;
There are no signs or characteristics that may indicate that the cancer in the exposed
person or hereditary effect in his or her progeny is caused by irradiation;
One can only estimate probability of causation of diagnosed effect
From the common point of view, initial damaged cell must pass through number of phases for
developing malignant tumour from one mutated cell. They are the cell initiation; dysplasia;
benign tumour and malignant tumour. These processes are developing in time, so the time
between cell initiation and developing radiation induced cancer may be comparable with life
span of exposed human or animal. Development of malignant tumour during this time has not
any clinical effects and this period is named a latent period of cancer development.
Stochastic effect is the radiation-induced health effect, occurring without a threshold level of
dose, whose probability is in many cases proportional to the dose and whose severity is
independent of the dose. These effects include radiation-induced cancers and hereditary effects,
and are characterized by very long period of latent development of the disease after exposure.
All radiation-induced stochastic effects are similar to those developing in non-irradiated
population. There are no signs or characteristics that may indicate that the cancer in the exposed
person or hereditary effect in his or her progeny is caused by irradiation. Stochastic effects are
not immediately evident or certain to occur, but the likelihood that they will occur increases as
17
the dose increases as given in Figure 03-6(b). The induction of cancer is recognized as the most
important long-term stochastic health effect from emergency exposure of the public. Cancer
needs a long period for latent development. The shortest latent period is about several years.
The scientific knowledge about stochastic effects is mainly based on evaluation of health status
of people survived after atomic bombing of Hiroshima and Nagasaki in 1945.
From among about 284 000 A-bomb survivors in both Hiroshima and Nagasaki confirmed by the
1950 national census, a basic cohort called the Life Span Study (LSS) was organized in 1958. It
consists of, 1) all of the heavily exposed A-bomb survivors, 2) a selected population of the less
exposed, matched by age and sex with the first group, and 3) non-exposed residents of both cities
selected on the basis of matched age and sex with the first group, with the total number of study
subjects reaching about 120 000. Until 2002, the radiation doses were reconstructed for 86 611
of them.
Cancer is a common disease. In economically developed countries, over one third of the
population develops cancer at some time during their lives and between one fifth and one-quarter
of individuals eventually dies of malignant disease. In addition, cancer is becoming more
important as a major cause of disability and death in less developed countries.
Epidemiological studies of relatively large populations exposed to significant levels of acute
radiation exposure, in particular the studies of the cohort of Japanese survivors of the atomic
bombings of Hiroshima and Nagasaki, have established that such exposure can cause most forms
of cancer. They have also shown that the excess risk is modified by other factors (such as sex or
age at exposure) and how this excess risk is expressed over time. For example, the studies show
that the risk of radiation-induced acute leukaemia is significantly greater at younger ages at
exposure. The excess risk is manifest as a “wave” over time since exposure, beginning at about
two years after exposure, rising to a peak between five and ten years after exposure and then
falling away to a low level some 20 years after exposure. Thus, if the convolution of size and
dose of an exposed population is large enough, the epidemiological study of such a population
allows the number of cases of cancer that may be attributed to irradiation to be determined and
how this varies with other factors such as age and gender. Risk models have been developed to
describe the expression of radiation-induced cancer risk in terms of important determinants of
risk, for example the organ-specific cumulative equivalent dose, from which the excess relative
risk may be derived for a particular set of individual circumstances. Here, the excess relative risk
is the proportional increase in the risk of the particular cancer that is due to exposure to radiation
for the specific set of individual circumstances; this proportional increase is with respect to the
background risk of the specific cancer in the absence of the additional dose of radiation [#504].
Table 03-11. Life Span Study mortality (1950-2002)
Deaths
observed
expected
excess
Attributable
fraction
Solid cancer
6 718
6 205
513
8.3%
Leukaemia
317
219
98
44.7%
Diseases
The Table 03-11 presents data of 52 years follow-up of the atomic bomb survivors to among
these people, the leukaemia incidence started to increase two years after exposure and then
gradually faded. The maximum increase occurred less than ten years after exposure. In contrary,
the incidence for solid tumours started to increase later, about 5 years after exposure, but the
18
increase is still going on and seems to continue to the end of life. It is actually accentuated when
the exposed population gets older and natural cancer incidence increases.
In 2002, the Dosimetry System 2002 was completed [#513]. It contains the reassessment of the
atomic bomb radiation dosimetry for Hiroshima and Nagasaki. It includes records of 86 611
people with evaluated dose. Among them 38 509 with Colon dose < 5 mSv (mean = 0.2 mSv)
and 37 401 with Red marrow dose < 5 mSv [#514].
A substantial increase in thyroid cancer incidence has occurred in the three republics (the whole
of Belarus and Ukraine, and the four most affected regions of the Russian Federation) since the
Chernobyl accident among those exposed as children or adolescents. Between 1991 and 2005 the
5,127 cases of thyroid cancer were reported amongst those under age 14 years in 1986, and 6,848
cases amongst those under age 18 years in 1986.
It was demonstrated, that in Belarus, after the Chernobyl accident in 1986, thyroid cancer
incidence rates among children under age of 10 years increased dramatically in comparison with
pre-Chernobyl level and subsequently declined, specifically for those born after 1986. This
pattern suggests that the increase in incidence in 1991-1995 was associated with the accident.
The increase was primarily among the children under age 10 years at the time of the accident.
For those born after 1986, there was no evidence for an increase in the incidence of thyroid
cancer. The increase in the incidence of thyroid cancer among children and adolescents began to
appear about 5 years after the accident and persisted up until 2005. The background rate of
thyroid cancer among children under age 10 years is approximately 2 to 4 cases per million per
year.
Table 03-12. Thyroid dose in entire population at affected territory in 1986
Persons in age group
Quantity
0-17 y
Adults
All ages
Total
26,330,000
71,576,000
97,896,000
Hthy< 50 mSv
23,032,000
68,319,000
91,351,000
Hthy > 50 mSv
3,288,000
(12.5 %)
3,257,000
(4.6 %)
6,545,000
(6.7 %)
Estimates for the dose to the thyroid are presented in Table 03-12 [#520] for four age categories
and the total population according to the region/oblast or city of residence and for contaminated
areas of the three countries (all of Belarus and Ukraine and 19 regions of the Russian
Federation). The estimates of the collective dose to the thyroid are presented according to 8
individual dose intervals, ranging from less than 0.05 Gy to more than 5 Gy. The Figure 03-10
presents thyroid cancer incidence rate among those exposed as children and adolescents (age
under 18 years in 1986) in Belarus [#564], [#565].
19
Figure 03-10. Thyroid cancer incidence in 1986-2002 among Belarusians of 18 years old and
younger in 1986.
Linear Non-Threshold hypothesis
Until now, biological markers of radiation-induced cancer were not found. Therefore, the only
way to confirm the risk estimates is to use an epidemiological investigation of the affected
population. Power of epidemiological consideration depends on the number of the affected
population, expected number of excess radiation-induced cancers, background level of the same
type of cancer and on a variation of this background level in population equivalent to the one
under study.
The number of excess radiation-induced cancers depends on the exposure dose, time of the
follow-up, and size of the affected group (sample size of the irradiated and controlled cohorts).
Contribution of total cancer mortality to the mortality statistics in developed countries is about
20-30%. This high level of background cancer incidence is characterized by a wide variation. It
is similar to year-by-year variation of total annual mortality, which can be higher than 3%. The
nature of these variations is not clear, but it is much higher than expected statistical fluctuations
of background level of cancer mortality.
Radiogenic and natural cancers are similar and the only way to detect excess cancers in exposed
group is to compare cancer incidence in it with that in control group. The control and exposed
groups must have the same age and gender composition.
The simplest way to detect this difference is to apply common methods of mathematical statistics
to results of the epidemiology of cancer in given groups. It is assumed in this approach, that the
groups are composed of individuals for whom development of a cancer is a random Poisson
process, and Poisson distribution [#517] describes cancer incidence. In this assumptions level of
detectability of difference between two groups is the only matter of number of “items” in control
and affected group. The similar approach is used in nuclear physics when activity of a sample is
measured in presence of background contamination.
20
Figure 03-11. Non-Poisson variation of annual mortality in France.
Number of people in study
and control cohorts
Reality is more complicated than simple statistical model. The Poisson distribution could not
present the statistics of total and cancer mortality. The Figure 03-11 presents the effect of 4%
variation of total mortality in thousands death per year in 100,000 people observed in France
with total population of 55,000,000 inhabitants in 1976-2000 [#516]. Non-Poisson variation of
background cancer mortality is similar to that presented in Figure 03-11 and could not be
reduced by expanding the number of people in examined cohort. Because of non-Poisson
variation of cancer mortality, the excess radiation induced cancers could not be detected in
exposed cohort if their level does not exceed 4% of the background level. These variations and a
high level of background incidence, which is about 25% in developed countries, are the major
factors limiting the statistical power of epidemiological investigations. The statistically
determined sample size of the irradiated and controlled cohorts needed to detect a significant
increase in total cancer risk from whole body exposure of 100 mSv is about 100,000 (of each
cohort) [#511].
Area of
detectability
Equivalent dose in whole body, Sv
Figure 03-12. Statistical limitation of detectability of stochastic health effects in exposed
population.
Therefore, threshold of detectability is an average dose of public exposure that, if exceeded,
leads to an additional (above the background level) total number of stochastic health effects in
the irradiated population that theoretically may be confirmed by means of current
epidemiological methods with a 95% level of confidence. For the case of developing any cancer
excluding leukaemia and thyroid cancers, the epidemiological estimate of number of people in
study and control group, which is needed to detect an increase in solid cancer mortality in case of
brief whole body exposure to penetrating radiation, is shown in Figure 03-12:
N
10 9
H WB 2
, H WB  100 mSv ,
(03- 9)
21
where H WB is the whole body equivalent dose in mSv. Value of N could not be defined if
H WB  100 mSv [#518].
Considering a 4% variation of background mortality with time, which has a non-statistical nature
as discussed earlier, whole body exposure of 100 mSv should be treated as the minimal level of
exposure which cause a detectable increase of cancer incidence [#516]. This level cannot be
decreased by simply expanding the control of test groups as discussed above. The conclusion of
the UNSCEAR regarding detectability of radiogenic cancers [#519], [#520], [#521] supports that
evaluation of threshold for detectability of increase of a number of all cancers in case of uniform
exposure of people, when all internal organs are exposed to the same dose.
The concept of detectability of radiation-induced cancer is also valid for a case of exposure of a
single organ, e.g. thyroid after intake of I-131 or red marrow after intake of Sr-90. For such case
the level of detectability will be another then for case of whole body exposure as show in Ref.
[#511].
The undetectability of radiation induced health effects at low doses raised up in 1970-s, when the
firs lessons were learning from Life Span Study of A-bomb survives. In the same time, the need
to have some simple instrument to assess risks of exposure to low doses became actual because
of significant improvement of working conditions in radiation industry, and decrease of
individual doses of radiation workers worldwide. To solve the problem, the ICRP introduced the
Linear Non-Threshold (LNT) hypothesis of developing the stochastic health effects. The LNT
was formulated in paragraph 27 of the 1977 Recommendations of the ICRP [#523] as follows.
(27) ... For radiation protection purposes it is necessary to make certain simplifying
assumptions. One such basic assumption underlying the Commission’s recommendations is that,
regarding stochastic effects, there is, within the range of exposure conditions usually
encountered in radiation work, a linear relationship without threshold between dose and the
probability of an effect.
LNT proposes that the risk of stochastic effects is directly proportional to the dose for all levels
of dose and dose rate (below those at which deterministic effects occur). It stats that any nonzero dose implies a non-zero risk of stochastic effects. This is the working hypothesis on which
the IAEA safety standards (and ICRP’s Recommendations) are based. It is not proven — indeed,
it is probably not provable — for low doses and dose rates, but it is considered the most
defensible assumption on which to base safety standards.
The 1977 Recommendations of the ICRP [#515] were superseded by 1990 Recommendations of
the ICRP [#552] and then by 2007 Recommendations of the ICRP [#522], but the key concept
based on the Linear Non-Threshold (LNT) hypnosis was remained unchanged.
This paragraph 27 of the ICRP publication 26, several hundreds of words, is the only technical
basis for assessment the radiation risks in a very low dose area, below 10 mSv of whole body
equivalent dose. However, this hypothesis plays the key role in framework of radiation
protection.
Concept of a dose as the only characteristic of exposure, which is needed for risk assessment is
most valuable conclusion the Linear Non-Threshold hypnosis. The “summation” concept is, and
will be a technical bass for radiation protection dosimetry in low dose area.
22
Figure 03-13. Use of Linear non-threshold hypothesis
Thus, although proof of development of additional cancers at small doses is not found, it has
been accepted, that the increase of frequency of development of stochastic effects in group of
equally irradiated people is proportion to any dose received by them above the normal
background. The Figure 03-13 is an illustration of such dependence. It shows increment of risk
of development of any cancer after exposure as a function of increment of equivalent dose in
whole body. Thus, it is assumed that there is no dose threshold below which stochastic effects do
not occur.
The LNT hypothesis results in a highly overestimated estimation of danger due to low doses.
The accepted decision entirely is caused by the desire to simplify methods for estimation values
of small doses in organs or tissues and thus to secure the personnel and the public from possible
radiation induced risk even at those levels of an exposure at which development of radiation
health effects is not proved yet.
Likelihood of harmful effect
The radiation protection dosimetric quantities of RBE weighted organ dose, equivalent organ
dose and effective dose might be calculated for any exposure conditions, but each of these
quantities was invented for use in only certain field of exposure assessment. The field of
exposure assessment is the range of exposure conditions, which could be properly characterized
in terms of considered dosimetric quantity to evaluate the likelihood of harmful radiation health
effect. Figure 03-14 provides an example of the field of exposure assessment of these quantities
in event of brief exposure to external penetrating radiation.
Equivalent dose in whole body, Sv
Figure 03-14. Probability of severe health effects as a function of brief exposure of whole body
to external penetrating radiation.
23
The fields are not exactly distinguished. For instance, the development of radiogenic cancers and
severe deterministic effects have to be considered when determining risk of harmful health
effects if the equivalent whole body dose is around 1-2 Sv. For this exposure conditions the
equivalent organ dose has to be determined to evaluate the risk of development of stochastic
effects and RBE weighted organ dose – to evaluate the risk of development of deterministic
effects. Characterization of those exposure conditions in terms of effective dose will be nonproductive. Analogously, characterization of low dose brief exposure in terms of RBE weighted
organ dose will be also non-productive.
Therefore,




In case of high dose exposure, when the equivalent dose in whole body is greater than
2 Sv, contribution of stochastic effects to total probability of premature death is
negligible, and only the RBE weighted dose should be used as the characteristic of
human exposure in that field of exposure assessment;
In the case, when the equivalent dose in whole body is in the range of 1-2 Sv,
contribution of deterministic and stochastic effects to total probability of premature death
is comparable, and it is reasonable to use equivalent organ dose and RBE weighted organ
dose as the characteristics of human exposure in that field of exposure assessment;
In case of intermediate dose exposure, when the equivalent dose in whole body is in the
range of 1-0.1 Sv, contribution of deterministic effects to total probability of premature
death is negligible, and it is reasonable to use only equivalent organ dose as the
characteristics of human exposure in that field of exposure assessment;
In case of low dose exposure, when the equivalent dose in whole body is less than 0.1 Sv,
the development of undetectable effects is expected, so the effective dose is usually in
use as the characteristic of human exposure in that field of exposure assessment to set
limitations for human’s exposure.
24
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[#502] INTERNATIONAL ATOMIC ENERGY AGENCY, Radiation Protection and Safety of
Radiation Sources: International Basic Safety Standards. Interim edition, General Safety
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[#503] INTERNATIONAL ATOMIC ENERGY AGENCY, The Radiological Accident in
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25
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[#515] INTERNATIONAL COMMISSION ON RADIOLOGICAL PROTECTION,
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