Transcript IAEA Training Material on Radiation Protection in Diagnostic and Interventional Radiology RADIATION PROTECTION IN DIAGNOSTIC AND INTERVENTIONAL RADIOLOGY L 3: Biological effects of ionizing.

IAEA Training Material on Radiation Protection in Diagnostic and Interventional Radiology
RADIATION PROTECTION IN
DIAGNOSTIC AND
INTERVENTIONAL RADIOLOGY
L 3: Biological effects of ionizing radiation
IAEA
International Atomic Energy Agency
Introduction
• Subject matter: radiobiology
• The mechanisms of different types of
biological effects following exposure to
ionizing radiation
• Types of models used to derive risk
coefficients for estimating the detriment
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3 : Biological effects of ionizing radiation
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Topics
•
•
•
•
Classification of radiation health effects
Factors affecting radio sensitivity
Dose-effect response curve
Whole body response: acute radiation
syndrome
• Effects of antenatal exposure and delayed
effects of radiation
• Epidemiology
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Overview
• To become familiar with the mechanisms of
different types of biological effects following
exposure to ionizing radiation. To be aware
of the models used to derive risk coefficients
for estimating the detriment.
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IAEA Training Material on Radiation Protection in Diagnostic and Interventional Radiology
Part 3: Biological effect of ionizing
radiation
Topic 1: Classification of radiation health effects
IAEA
International Atomic Energy Agency
Radiation health effects
TYPE
OF
EFFECTS
CELL DEATH
CELL TRANSFORMATION
DETERMINISTIC
STOCHASTIC
Somatic
Clinically attributable
in the exposed
individual
somatic & hereditary
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epidemiologically
attributable in large
populations
BOTH
ANTENATAL
somatic and
hereditary expressed
in the foetus, in the live
born or descendants
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Biological effects of ionizing radiation
• Deterministic
• e.g. Lens opacities, skin
injuries,
• infertility, epilation, etc
• Stochastic
• Cancer, genetic effects.
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Deterministic effects
• Deterministic
(Threshold or nonstochastic)
• Existence of a dose
threshold value (below
this dose, the effect is
not observable)
• Severity of the effect
increases with dose
• A large number of cells
are involved
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Radiation injury from an industrial source
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Threshold Doses for Deterministic Effects
• Cataracts of the lens of the eye 2-10 Gy
• Permanent sterility
• males
• females
3.5-6 Gy
2.5-6 Gy
Severity of
effect
• Temporary sterility
• males
• females
0.15 Gy
0.6 Gy
dose
threshold
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Stochastic Effects
• Stochastic(Non-Threshold)
• No threshold
• Probability of the effect increases with dose
• Generally occurs with a single cell
e.g., cancer, genetic effects
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No change
DNA mutation
radiation
hit cell
nucleus!
DIRECT ACTION
INDIRECT ACTION
Viable Cell
Mutation
repaired
Cell death
Unviable Cell
DNA Mutation
Cancer ?
Cell survives
but mutated
Outcomes after cell exposure
DAMAGE TO DNA
DAMAGE
REPAIRED
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CELL DEATH
(APOPTOSIS)
TRANSFORMED
CELL
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Outcomes after cell exposure
DAMAGE TO DNA
DAMAGE
REPAIRED
CELL
NECROSIS
TRANSFORMED
CELL
OR
APOPTOSIS
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How DNA is
repaired ?
Altered base
Enzyme Glycosylases recognizes
lesion and releases damaged base
AP-endunuclease makes incision
and releases remaining sugar
DNA-polymerase fills resulting gap
but nick remains
DNA ligase seals the nick
Repair completed
DNA has been repaired with no
loss of genetic information
Repair of DNA damage
• RADIOBIOLOGISTS
ASSUME THAT THE
REPAIR SYSTEM IS
NOT 100%
EFFECTIVE.
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ADAPTIVE
RESPONSE
Conditioning dose
Response
Challenging dose
Response
Conditioning dose
Challenging dose Response
Outcomes after cell exposure
DAMAGE TO DNA
DAMAGE
REPAIRED
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CELL
NECROSIS OR
APOPTOSIS
TRANSFORMED
CELL
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Normal human
lymphocyte:
chromosomes
uniformly
distributed
Apoptotic cell:
chromosomes
and nucleus
fragmented
and collapsed
into apoptotic
bodies
Effects of cell death
Probability of cell
death
100%
Acute dose
(in mSv)
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5000
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Outcomes after cell exposure
DAMAGE TO DNA
DAMAGE
REPAIRED
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CELL
NECROSIS OR
APOPTOSIS
TRANSFORMED
CELL
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Chromosomal deletions
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Chromosomal translocations
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CANCER INITIATION
STEAM
CELL
TUMOR
PROMOTION
MALIGNANT
PROGRESSION
NECROSIS OR
APOPTOSIS
MUTATION
MALIGNANT
TRANSFOMATION
DIVISION
METASTASIS
NORMAL TISSUE
CELL INITIATION
An initiating event
creates a mutation in
one of the basal cells
DYSPLASIA
More mutations occurred.
The initiated cell has
gained proliferative
advantages.
Rapidly dividing cells
begin to accumulate
within the epithelium.
BENIGN TUMOR
More changes within
the proliferative cell
line lead to full tumor
development.
MALIGNANT TUMOR
The tumor breaks trough
the basal lamina.
The cells are irregularly
shaped and the cell line
is immortal. They have
an increased mobility
and invasiveness.
METASTASIS
Cancer cells break through
the wall of a lymphatic
vessel or blood capillary.
They can now migrate
throughout the body and
potentially seed new
tumors.
A simple generalized scheme for multistage oncogenesis
Damage to chromosomal DNA
of a normal target cell
Failure to correct
DNA repair
Appearance of specific
neoplasia-initiating mutation
Promotional growth
of pre-neoplasm
Conversion to overtly
malignant phenotype
Malignant progression
and tumour spread
10-15
Energy deposition
Excitation/ionization
10-12
Initial particle tracks
10-9
Radical formation
PHYSICAL INTERACTIONS
Diffusion, chemical reactions
Initial DNA damage
TIME (sec)
10-6
10-3
1 ms
100
1 second
Repair processes
Damage fixation
3
PHYSICO-CHEMICAL INTERACTIONS
DNA breaks / base damage
10
1 hour Cell killing
106
1 day Mutations/transformations/aberrations
Proliferation of "damaged" cells
1 year Promotion/completion
109
100 years
Timing of
events
leading to
radiation
effects.
BIOLOGICAL RESPONSE
Teratogenesis
MEDICAL EFFECTS
Cancer
Hereditary defects
IAEA Training Material on Radiation Protection in Diagnostic and Interventional Radiology
Part 3: Biological effect of ionizing
radiation
Topic 2: Factors affecting the radiosensitivity
IAEA
International Atomic Energy Agency
Radiosensitivity [RS] (1)
• RS = Probability of a cell,
tissue or organ of suffering
an effect per unit of dose.
• Bergonie and Tribondeau
(1906): “RS LAWS”: RS
will be greater if the cell:
• Is highly mitotic.
• Is undifferentiated.
• Has a high cariocinetic
future.
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Radiosensitivity (2)
High RS
Bone Marrow
Spleen
Thymus
Lymphatic
nodes
Gonads
Eye lens
Lymphocytes
Medium RS
Skin
Mesoderm
organs (liver,
heart, lungs…)
Low RS
Muscle
Bones
Nervous
system
(exception to the RS laws)
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• Physical
• LET (linear energy transfer):  RS
• Dose rate:  RS
• Chemical
% survivor cells
Factors affecting the radiosensitivity
 LET
 LET
• Increase RS: OXYGEN, cytotoxic drugs.
• Decrease RS: SULFURE (cys, cysteamine…)
• Biological
G0
M
• Cycle status:
G2
•  RS: G2, M
•  RS: S
G1
• Repair of damage (sub-lethal damage
may be repaired e.g. fractionated dose)
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IAEA Training Material on Radiation Protection in Diagnostic and Interventional Radiology
Part 3: Biological effect of ionizing
radiation
Topic 3: Dose-effect response curve
IAEA
International Atomic Energy Agency
Systemic effects
• Effects may be morphological and/or functional
• Factors:
• Which Organ
• How much Dose
• Effects
• Immediate (usually reversible): < 6 months e.g.:
inflammation, bleeding.
• Delayed (usually irreversible): > 6 months e.g.: atrophy,
sclerosis, fibrosis.
• Categorization of dose
• < 1 Gy: LOW DOSE
• 1-10 Gy: MODERATE DOSE
• > 10 Gy: HIGH DOSE
• Regeneration means replacement by the original tissue while
Repair means replacement by connective tissue.
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Skin effects
• Following the RS laws (Bergonie and
Histologic view of the skin
EPIDERMIS
Tribondeau), the most RS cells are
those from the basal stratum of the
epidermis.
• Effects are:
• Erythema: 1 to 24 hours after irradiation of
•
DERMIS
From “Atlas de Histologia...”. J. Boya
Basal stratum cells, highly
mitotic, some of them with
melanin, responsible of
pigmentation.
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•
•
•
about 3-5 Gy
Alopecia(*): 5 Gy is reversible; 20 Gy is
irreversible.
Pigmentation: Reversible, appears 8 days
after irradiation.
Dry or moist desquamation: traduces
epidermal hypoplasia (dose  20 Gy).
Delayed effects: teleangiectasia (**),
fibrosis.
(*):alopecia: loss or absence of hair
(**): ectasia: swelling of part of the body
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Skin reactions
Injury
Early transient erythema
Temporary epilation
Main erythema
Permanent epilation
Dry desquamation
Invasive fibrosis
Dermal atrophy
Telangiectasis
Moist desquamation
Late erythema
Dermal necrosis
Secondary ulceration
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Threshold
Weeks to
Dose to
Onset
Skin (Sv)
2
3
6
7
10
10
11
12
15
15
18
20
<<1
3
1.5
3
4
>14
>52
4
6-10
>10
>6
3 : Biological effects of ionizing radiation
Skin damage
from prolonged
fluoroscopic
exposure
46
Skin injuries
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Skin injuries
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Effects in eye
Histologic view of eye:
• Eye lens is highly RS.
• Coagulation of proteins
occur with doses
greater than 2 Gy.
• There are 2 basic
effects:
Effect
From “Atlas de Histologia...”. J. Boya
Eye lens is highly RS,
moreover, it is surrounded by
highly RS cuboid cells.
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Detectable
opacities
Visual
impairment
(cataract)
Sv single brief
exposure
Sv/year for
many years
0.5-2.0
> 0.1
5.0
> 0.15
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Eye injuries
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IAEA Training Material on Radiation Protection in Diagnostic and Interventional Radiology
Part 3: Biological effect of ionizing
radiation
Topic 4: Whole body response: acute radiation
syndrome
IAEA
International Atomic Energy Agency
Whole body response: adult
Acute irradiation
syndrome
1-10 Gy
Chronic irradiation
syndrome
Steps:
10 - 50 Gy
> 50 Gy
1. Prodromic
(onset of
disease)
2. Latency
BONE
MARROW
3. Manifestation
GASTRO
INTESTINAL
CNS
Lethal dose 50 / 30
•Mechanism:
Neurovegetative
disorder
•Similar to a sick
feeling
•Quite frequent in
fractionated
radiotherapy
(central nervous
system)
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Dose
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Lethal dose 50 / 30
• “Dose which would
cause death to 50% of
the population in 30
days”.
• Its value is about 2-3
Gy for humans for
whole body irradiation.
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IAEA Training Material on Radiation Protection in Diagnostic and Interventional Radiology
Part 3: Biological effect of ionizing
radiation
Topic 5: Effects of antenatal exposure and
delayed effect
IAEA
International Atomic Energy Agency
Effects of antenatal exposure (1)
• As post-conception time increases RS decreases
• It is not easy to establish a cause-effect relation because
there are a lot of teratogenic agents, effects are unspecific
and not unique to radiation.
• There are 3 kinds of effects: lethality, congenital anomalies
and large delay effects (cancer and hereditary effects).
%
Congenital anomalies
Lethality
Pre-implantation
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Organogenesis
Foetus
3 : Biological effects of ionizing radiation
Time
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Effects of antenatal exposure (2)
• Lethal effects can be induced by relatively small
doses (such as 0.1 Gy) before or immediately after
implantation of the embryo into the uterine wall. They
may also be induced after higher doses during all the
stages during intra-uterine development.
%
0.1 Gy
Lethality
Time
Pre-implantation
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Organogenesis
Foetus
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Effects of antenatal exposure (3)
• Mental retardation:
• ICRP establishes that mental retardation can be induced
by radiation (Intelligence Quotient score < 100).
• It occurs during the most RS period: 8-25 week of
pregnancy.
• Risks of antenatal exposure related to mental retardation
are:
8-15 week
15-25 week
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Severe mental
retardation with a
risk factor of
Severe mental
retardation with a
risk factor of
0.4/Sv
0.1/Sv
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Delayed effects of radiation
• Classification:
• SOMATIC: they affect the health of the
irradiated person. They are mainly different
kinds of cancer (leukemia is the most
common, with a delay period of 2-5 years, but
also colon, lung, stomach cancer…)
• GENETIC: they affect the health of the
offspring of the irradiated person. They are
mutations that cause malformation of any
kind (such as mongolism)
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IAEA Training Material on Radiation Protection in Diagnostic and Interventional Radiology
Part 3: Biological effects of ionizing
radiation
Topic 6: Epidemiology
IAEA
International Atomic Energy Agency
Epidemiology I
• Irradiated populations can be studied by
• following cohorts of exposed and non-exposed
people
• back-tracing patients suffering from the disease
with regard to possible exposure (case
controls)
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Epidemiology II
• Irradiated populations are
• people exposed from the atomic bomb
•
•
•
•
explosions
people exposed during nuclear and other
radiation accidents
patients exposed for medical reasons
people exposed to natural radiation
workers in radiation industries
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Epidemiology III
• Most valid data come from high dose / high
dose rate exposure to low LET radiation,
including some radionuclides [iodine131I],
and from high LET internal exposure to a
emitters in lung, bone and liver.
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Epidemiology IV
• Information is scanty on:
• Consequences of low doses delivered at low dose
rates
• To detect an increase from a 20% spontaneous cancer
incidence to 25% (corresponding to an exposure to ~1
Sv) > 1300 persons must be studied
• Consequences of external high LET radiation
• (neutrons) and several radionuclides
• Presence and influence of confounding factors
• especially if different populations are to be compared
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Epidemiology V
• Modifying influence of cancer background
incidence
• does radiation-induced cancer increase at a fixed level
or in proportion to existing cancer additive vs.
multiplicative risk model ?
• Is, for example, the risk greater in:
• European women which have a higher background
breast tumor rate than Japanese women ?
• Smokers exposed to radon in homes or mines than in
non-smokers ?
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Detectability limits in Radioepidemiology
10 4
REGION OF DETECTABILITY
Theoretical limit of detectability due
to statistical causes
(90%
confidence interval)
EFFECTIVE DOSE (mSv)
10 3
10 2
101
CHERNOBYL
DOSES
10 0
10-1
10 0
REGION OF UNDETECTABILITY
101
10 2
10 3
104
105
106
107
108
109
10 10
Number of people in study and control groups
1011
High and Low Spontaneous Cancer
Rates Incidence (ICRP 105)
Tissue
Nasopharynx
Esophagus
Stomach
Colon
Liver
Lung+Bronchus
Skin melanoma
Breast female
Cervix
High
Male / Female
23.3
9.5
20.1
8.3
95.5
40.1
35.0
29.6
46.7
11.5
110.8 29.6
33.1
29.8
103.7
53.5
Low
Male /Female
0.2
0.1
0.5
0.2
5.2
2.2
1.8
1.3
0.7
0.3
10.3 2.4
0.2
0.2
14.6
3.0
from UNSCEAR 2000
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Data on irradiated populations
Population
Approximate Size
Atomic bomb survivors Japan:
86 000
Atomic tests:Semipalatinsk/Altai
30 000
Marshallese islanders
2 800
Nuclear accidents: intervention teams Chernobyl (total)
> 200 000
population Chernobyl (>185 kBq /m2 137Cs) 1 500 000
population Chelyabinsk (total)
70 000
Medical procedures:
low LET
iodine treatment and therapy
~ 70 000
chest fluoroscopy
64 000
children hemangioma treatment
14 000
high LET thorotrast angiography
4 200
Ra-224 treatment
2 800
Prenatal exposure (fetal radiography, atomic bombs)
6 000
Occupational exposure: workers nuclear industry (Japan, UK) 115 000
uranium miners
21 000
radium dial painters
2 500
radiologists
10 000
Natural exposure (Chinese, EC and US studies)
several 100 000
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Populations Studied for Specific
Cancers (I)
• Leukemia: atomic bomb survivors,
radiotherapy for ankylosing spondylitis and
cervix cancer, radiologists, people at the
Majak plant, Chelyabinsk and the Techa
river, prenatal radio-diagnostics (Oxford
survey)
• Lung cancer: atomic bomb survivors,
uranium and other miners in USSR, Canada,
USA, Germany, Sweden
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Populations Studied for Specific
Cancers (II)
• Breast cancer: atomic bomb survivors,
fluoroscopy TB patients, radiotherapy mastitis
• Thyroid cancer: radiotherapy thymus
enlargement, tinea capitis skin hemangioma,
fallout at Marshall islands, children near the
Chernobyl accident
• Liver cancer: Thorotrast angiography
• Osteosarcoma: 224Ra (226Ra) treatment, 226Ra
(watch) dial painters.
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Excess Solid-Tumor Deaths among
Atomic-Bomb Survivors
Estimated relative risk at 1 Gy
Relative Mortality Risks at Different
Times After Exposure
20
Leukaemia ( ~10.7%/y)
10
5
2
All cancers except
leukaemia (+ 4.8%/y)
1
0.5
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1950- 1955- 1959- 1963- 1967- 1971- 1975- 19791954 1958 1962 1966 1970 1974 1978 1982
Interval of follow-up Atomic bomb survivors
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Relative Risks of Radon from Indoor
Exposure and from Mining
2
Relative risk
1.5
,
, &
&
1
&
&
&
,
,
&
miner studies (cohorts)
indoor studies (case controls)
log-linear fit to indoor studies
estimated from correlation
study in different regions
0.6
0.5
0.4
0.3
0
100
200
300
400
500
Radon concentration Bq/m3
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Observed/expected breast cancers
Breast Cancer in Women Exposed to
Fluoroscopy
4
,
3
,
2
,
1
,
,
0
0
1
2
3
4
Mean absorbed dose (Gy)
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Thyroid Tumors in Irradiated Children
10
,
Relative risk
8
Thyroid Cancer
6
4
,
,
,
2
,
,
,
Thyroid benign
tumors
0
0
0.05
0.1
0.15
0.2
0.25
Mean dose (Gy)
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Thyroid Cancer Cases in Children
after the Chernobyl Accident
100
Children under 15 years of age at diagnosis
$
80
$
$
$
$
60
Belarus
$
"
"
"
40
"
$
"
"
Ukraine
$
"
"
"
20
0
$
"
$
&
"
$
&
"
$
86
87
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Russian Fed.&
"
&
$
&
&
&
88
89
90
91
&
92
&
&
&
93
94
95
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96
&
97
98
75
Thyroid Cancer in Children in the
Chernobyl Region
Region
No of Cases
before the accident after the accident
Belarus
(1977-1985) 7
(1986-1994) 390
Ukraine
(1981-1985) 24
(1986-1995) 220
Russia (Bryansk and Kaluga region only) (1986-1995) 62
The data represent incidences (not mortality) and are
preliminary results.
Most excess cancers occurred since 1993.
Thyroid cancer has a high rate of cure >90%, but many of the
cancers found are of the aggressive papillary type.
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Risk Estimates from Occupational
Exposure
Study
Excess relative risk per Sv
All cancer
Leukemia
UK National Registry
Radiation Workers
0.47 (-0.12-1.20) 4.3 (0.4-13.6)
1,218,000 person years
34 mSv average dose
US Workers
-1.0 (<0-0.83
<0 (<0-3.4)
705,000 person years
32 mSv average dose
Atomic Bomb Survivors 0.33 (0.11-0.6) 6.2 (2.7-13.8)
2,185,000 person years
251 mSv average dose
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Doses and Risks for in Utero
Radiodiagnostics
Exposure
Mean foetal dose Hered. Disease
(mGy)
X Ray
Abdomen
2.6
Barium enema
16
Barium meal
2.8
IV urography
3.2
Lumbar spine
3.2
Pelvis
1.7
Computed tomography
Abdomen
8.0
Lumbar spine
2.4
Pelvis
25
Nuclear medicine
Tc bone scan
3.3
Tc brain scan
4.3
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Fatal cancer
to age 14 y
6.2 10-5
3.9 10-4
6.7 10-5
7.7 10-5
7.6 10-5
4.0 10-5
7.7 10-5
4.8 10-4
8.4 10-5
9.6 10-5
9.5 10-5
5.1 10-5
1.9 10-4
5.7 10-5
6.1 10-4
2.4 10-4
7.1 10-5
7.7 10-4
7.9 10-4
1.0 10-5
1.0 10-4
1.3 10-4
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Extrapolation by Additive and
Multiplicative Risks Models
45
35
25
Following exposure to 2 Gy at an age of 45 years
Spontaneous risks: increase with age:
Radiation risks become apparent after a lag period
(5) -10 years
Additive risk models: imply constant risk
independent of background.
Multiplicative risk models: imply an increase
proportional to background risk
15
5
55
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60
65
Age Years
70
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79
Risk Probability Coefficients (ICRP)
Probability of fatal Cancer (10-2/Sv)
Population
Workers
Bladder
0.30
0.24
Bone marrow
0.50
0.40
Bone surface
0.05
0.04
Breast
0.20
0.16
Colon
0.85
0.68
Liver
0.15
0.12
Lung
0.85
0.68
Esophagus
0.30
0.24
Ovary
0.10
0.08
Skin
0.02
0.02
Stomach
1.10
0.88
Thyroid
0.08
0.06
Remainder
0.50
0.40
Total all cancers
5.00
4.00
Genetic effects weighted
1.00
0.50
Tissue
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Proportion of Fatal Cancers
Attributable to Different Agents
Agent or Class
Percentage of all Cancer Disease
Best estimate
Range
Smoking
31
29 - 33
Alcoholic beverages
5
3-7
Diet
35
20 - 60
Natural hormones
15
10 - 20
Infection
10
5 - 15
Occupation
3
2-6
Medicines, medical practices
1
0.5 - 2
Electromagnetic radiation
8
5 -10
Ionizing (85% from natural radiation*) 4.5
Ultraviolet
2.5
Lower frequency
<1
Industrial products
<1
<1 - 2
Pollution
2
<1 - 4
Other
?
?
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Tissue risk factor (1)
• RISK FACTOR: The quotient of increase in
probability of a stochastic effect and the
received dose. It is measured in Sv-1 or
mSv-1.
 probability
 dose
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 probability
Risk =
factor
 dose
Dose
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Tissue risk factor (2)
• EXAMPLE: A risk factor of 0.005 Sv-1 for bone
marrow (lifetime mortality in a population of all
ages from specific fatal cancer after exposure to
low doses) means that if 1,000 people would
receive 1 Sv to the bone marrow, 5 will die from a
cancer induced by radiation.
 probability
 dose
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 probability
Risk
factor
=
 dose
Dose
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Indicators of relative organ tissue risk
TISSUE OR ORGAN
Gonads
Bone marrow (red)
Colon
Lung
Stomach
Bladder
Breast
Liver
Oesophagus
Thyroid
Skin
Bone surface
Remainder
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wT
0.20
0.12
0.12
0.12
0.12
0.05
0.05
0.05
0.05
0.05
0.01
0.01
0.05
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Summary
• Effects of ionizing radiation may be
deterministic and stochastic, immediate or
delayed, somatic or genetic
• Some tissues are highly radiosensitive
• Each tissue has its own risk factor
• Risk from exposure may be assessed
through such factors
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Where to Get More Information (1)
• The 2007 Recommendations of the International
Commission on Radiological Protection, ICRP 103,
Annals of the ICRP 37(2-4):1-332 (2007)
• UNSCEAR 2008 Report to the General Assembly,
with scientific annexes, United Nations Scientific
Committee on the Effects of Atomic Radiation,
United Nations, Vienna, Austria, 2008
• Avoidance of radiation injuries from medical
interventional procedures. ICRP Publication 85.
Ann ICRP 2000;30 (2). Elsevier
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