Biological Effects of Radiation IAEA

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
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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
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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3 : Biological effects of ionizing radiation 3
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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Part 3: Biological effect of ionizing radiation

Topic 1: Classification of radiation health effects
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Radiation health effects

TYPE OF EFFECTS CELL DEATH DETERMINISTIC
Somatic Clinically attributable in the exposed individual
CELL TRANSFORMATION
BOTH ANTENATAL
somatic and hereditary expressed
in the foetus, in the live born or descendants
STOCHASTIC
somatic & hereditary
epidemiologically attributable in large populations
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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(Thres
hold/non-stochastic)
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
Threshold Doses for Deterministic Effects
Cataracts of the lens of the eye 2-10 Gy

Permanent sterility
males females males females
3.5-6 Gy 2.5-6 Gy
Severity of effect
Temporary sterility
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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DIRECT ACTION
INDIRECT ACTION
Outcomes after cell exposure
DAMAGE TO DNA
DAMAGE REPAIRED CELL DEATH (APOPTOSIS) TRANSFORMED CELL
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DAMAGE TO DNA
DAMAGE REPAIRED
CELL NECROSIS
OR
TRANSFORMED CELL
APOPTOSIS
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How DNA is
repaired ?
Repair of DNA damage

RADIOBIOLOGISTS
ASSUME THAT THE REPAIR SYSTEM IS NOT 100% EFFECTIVE.
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DAMAGE TO DNA DAMAGE REPAIRED 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
DAMAGE TO DNA
DAMAGE REPAIRED
CELL NECROSIS OR APOPTOSIS
TRANSFORMED CELL
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Chromosomal deletions
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Chromosomal translocations
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CANCER INITIATION
TUMOR PROMOTION
MALIGNANT PROGRESSION
STEAM CELL
NECROSIS OR APOPTOSIS MUTATION

MALIGNANT TRANSFOMATION
METASTASIS
DIVISION
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

through 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
-15 10 -12 10
Energy deposition Excitation/ionization Initial particle tracks Radical formation
PHYSICAL INTERACTIONS
-9 10 -6 10
Diffusion, chemical reactions

Initial DNA damage
PHYSICO-CHEMICAL INTERACTIONS
TIME (sec)
-3 10 0 10 3
1 ms
DNA breaks / base damage
1 second Repair processes Damage fixation
10
1 hour Cell killing
BIOLOGICAL RESPONSE
6 10
1 day Mutations/transformations/aberrations Proliferation of "damaged" cells 1 year Promotion/completion
109 100 years
Teratogenesis MEDICAL EFFECTS Cancer Hereditary defects
Timing of events leading to radiation effects.

Topic 2: Factors affecting the radiosensitivity
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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
(exception to the RS laws)
Medium RS Skin Mesoderm organs (liver, heart, lungs)
Low RS Muscle Bones Nervous system
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Factors affecting the radiosensitivity

LET (linear energy transfer): RS Dose rate: RS
% survivor cells
Physical Chemical
LET LET
Increase RS: OXYGEN, cytotoxic drugs. Decrease RS: SULFURE (cys, cysteamine)
Biological
Cycle status:
RS: G2, M RS: S
G2
G0
M
G1
Repair of damage (sub-lethal damage

may be repaired e.g. fractionated dose)
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S

Topic 3: Dose-effect response curve
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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
Tribondeau), the most RS cells are those from the basal stratum of the epidermis. Effects are:
Erythema: 1 to 24 hours after irradiation of
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
From Atlas de Histologia.... J. Boya
Basal stratum cells, highly mitotic, some of them with melanin, responsible of pigmentation.
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Skin reactions
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
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
>14 >52 4 6-10 >10 >6
Skin damage from prolonged fluoroscopic exposure
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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
Sv single brief exposure 0.5-2.0 Sv/year for many years > 0.1
From Atlas de Histologia.... J. Boya
Eye lens is highly RS, moreover, it is surrounded by highly RS cuboid cells.
Detectable opacities Visual impairment (cataract)
5.0
> 0.15
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Eye injuries
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Topic 4: Whole body response: acute radiation syndrome
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Whole body response: adult

Acute irradiation syndrome
1-10 Gy
10 - 50 Gy > 50 Gy
BONE MARROW
Chronic irradiation syndrome

Whole body clinic of a partial-body irradiation Mechanism: Neurovegetative disorder Similar to a sick feeling Quite frequent in fractionated radiotherapy
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Steps:
1. Prodromic
(onset of disease)
2. Latency
GASTRO INTESTINAL
3. Manifestation
CNS
(central nervous system)
Lethal dose 50 / 30
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Dose
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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Topic 5: Effects of antenatal exposure and delayed effect
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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
Organogenesis
Foetus
Time
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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 Organogenesis Foetus
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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
Severe mental retardation with a risk factor of
Severe mental retardation with a risk factor of
0.4/Sv
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0.1/Sv
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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Part 3: Biological effects of ionizing radiation

Topic 6: Epidemiology
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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 [iodine 131I], and from high LET internal exposure to a emitters in lung, bone and liver.
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Epidemiology IV
Information is scanty (not much,less than needed)
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
EFFECTIVE DOSE (mSv)
10 3
Theoretical limit of detectability due to statistical causes (90% confidence interval)
10 2
101
CHERNOBYL DOSES
10 0
REGION OF UNDETECTABILITY
101 10 2 10 3 10 4 105 106 107 108 109 10 10 1011
10-1 10 0
Number of people in study and control groups
High and Low Spontaneous Cancer Rates Incidence/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, U and other miners in CSSR, 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
Relative Mortality Risks at Different Times After Exposure

Estimated relative risk at 1 Gy
20 10
Leukaemia ( ~10.7%/y)
5
2 1 0.5
1950- 1955- 1959- 1963- 1967- 1971- 1975- 19791954 1958 1962 1966 1970 1974 1978 1982 All cancers except leukaemia (+ 4.8%/y)
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Interval of follow-up Atomic bomb survivors

Relative Risks of Radon from Indoor Exposure and from Mining

2
1.5
, & &
, &
&
& ,
&
Relative risk
1 0.6 0.5 0.4 0.3 0
miner studies (cohorts) indoor studies (case controls) log-linear fit to indoor studies estimated from correlation study in different regions
100
200
300
400
500
72
Radon concentration Bq/m3

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Breast Cancer in Women Exposed to Fluoroscopy

Observed/expected breast cancers 4
,
3 2
, , ,
0
1 0
,
1 2 3 4
Mean absorbed dose (Gy)

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Thyroid Tumors in Irradiated Children

10 8
,
Thyroid Cancer
Relative risk
,
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
$ $ $ $ $ $
Belarus
" "
$ "
60 40
$ "
" "
$ " "
Ukraine
"
20 0
" $ & " $ & " $ & " $ & &
Russian Fed. &

& & &
& &
&
86
87
88
89
90
91
92
93
94
95
96
97
98
75
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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. IAEA
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)
6.2 10-5 3.9 10-4 6.7 10-5 7.7 10-5 7.6 10-5 4.0 10-5 1.9 10-4 5.7 10-5 6.1 10-4
Fatal cancer to age 14 y

7.7 10-5 4.8 10-4 8.4 10-5 9.6 10-5 9.5 10-5 5.1 10-5 2.4 10-4 7.1 10-5 7.7 10-4
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 IAEA
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

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
45
35
25 15
5 55 60 65 Age Years 70 75
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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 ? ? IAEA
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 Risk = factor dose
probability dose
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Dose
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 Risk factor
=
probability dose
dose
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Dose
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
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)

1990 Recommendations of the ICRP. ICRP
Publication 60. Pergamon Press 1991 Radiological protection of the worker in medicine and dentistry. ICRP Publication 57. Pergamon Press 1989 Sources and Effects of Ionizing Radiation. United Nations Scientific Committee on the Effects of Atomic Radiation UNSCEAR 2000 Report to the General Assembly, with Scientific Annexes. New York, United Nations 2000.
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Where to Get More Information (2)

Avoidance of radiation injuries from medical
interventional procedures. ICRP Publication 85. Ann ICRP 2000;30 (2). Pergamon Manual of clinical oncology 6th edition. UICC. Springer-Verlag. 1994 Atlas de Histologia y organografia microscopica. J. Boya. Panamericana. 1998 Tubiana M. et al. Introduction to Radiobiology. London: Taylor & Francis, 1990. 371 pp. ISBN 085066-763-1.
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IAEA Training Material on Radiation Protection in Diagnostic and Interventional Radiology

RADIATION PROTECTION IN DIAGNOSTIC AND INTERVENTIONAL RADIOLOGY

3 : Biological effects of ionizing radiation

3 : Biological effects of ionizing radiation

IAEA Training Material on Radiation Protection in Diagnostic and Interventional Radiology

Part 3: Biological effect of ionizing radiation

Radiation health effects

3 : Biological effects of ionizing radiation

Biological effects of ionizing radiation

3 : Biological effects of ionizing radiation

Radiation injury from an industrial source

3 : Biological effects of ionizing radiation

Threshold Doses for Deterministic Effects

Cataracts of the lens of the eye 2-10 Gy

3 : Biological effects of ionizing radiation

Outcomes after cell exposure

3 : Biological effects of ionizing radiation

Outcomes after cell exposure

3 : Biological effects of ionizing radiation

Repair of DNA damage

3 : Biological effects of ionizing radiation

Outcomes after cell exposure

DAMAGE TO DNA DAMAGE REPAIRED CELL NECROSIS OR APOPTOSIS TRANSFORMED CELL

3 : Biological effects of ionizing radiation

Normal human lymphocyte:

Effects of cell death

Acute dose (in mSv)

Outcomes after cell exposure

CELL NECROSIS OR APOPTOSIS

3 : Biological effects of ionizing radiation

3 : Biological effects of ionizing radiation

3 : Biological effects of ionizing radiation

NECROSIS OR APOPTOSIS MUTATION

CELL INITIATION An initiating event creates a mutation in

one of the basal cells

More mutations occurred.

within the epithelium.

The tumor breaks

shaped and the cell line

Cancer cells break

capillary. They can now

A simple generalized scheme for multistage oncogenesis

Damage to chromosomal DNA of a normal target cell

Energy deposition Excitation/ionization Initial particle tracks Radical formation

Diffusion, chemical reactions

DNA breaks / base damage

1 second Repair processes Damage fixation

1 hour Cell killing

1 day Mutations/transformations/aberrations Proliferation of "damaged" cells 1 year Promotion/completion

109 100 years

Teratogenesis MEDICAL EFFECTS Cancer Hereditary defects

Timing of events leading to radiation effects.

IAEA Training Material on Radiation Protection in Diagnostic and Interventional Radiology

Part 3: Biological effect of ionizing radiation

Radiosensitivity [RS] (1)

3 : Biological effects of ionizing radiation

Medium RS Skin Mesoderm organs (liver, heart, lungs)

Low RS Muscle Bones Nervous system

3 : Biological effects of ionizing radiation

Factors affecting the radiosensitivity

Repair of damage (sub-lethal damage

IAEA Training Material on Radiation Protection in Diagnostic and Interventional Radiology

Part 3: Biological effect of ionizing radiation

3 : Biological effects of ionizing radiation