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This medical PowerPoint presentation is about radiobiology, the study of the effects of ionizing radiation on living organisms, including the biological effects of radiation exposure at the molecular, cellular, tissue, and organismal levels.

Radiation can cause damage to biological molecules such as DNA, proteins, and lipids, which can result in a wide range of effects, including cell death, mutations, chromosomal abnormalities, and cancer. Radiobiologists study the mechanisms underlying these effects and develop strategies to minimize radiation damage and improve the effectiveness of radiation therapy in cancer treatment.

Radiobiology also plays an important role in radiation protection, helping to establish safe exposure limits and guidelines for radiation workers and the general public. The field draws on expertise from a range of disciplines, including physics, chemistry, biology, and medicine, and has applications in areas such as nuclear medicine, radiation therapy, and radiation safety.

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Published on : Jun 20, 2023 | Views : 1783 | Downloads : 4

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Slide 1-

Radiobiology
Slide 2-

Course content Physical effect of radiation - ionization and excitations - interaction between moving charged particle and stationary electron - stopping power and range of radiation in the medium Radiation chemistry - physical events - radiolysis of water
Slide 3-

Effect of radiation on DNA molecules and chromosomes Cell survival curve - cell death - intrinsic cellular radiosensitivity - cell survival and repair Radiation effect on normal tissue - from cellular effect to tissue damage - late effect The effect of radiation on tumors, the biological bases of radiotherapy
Slide 4-

Hypoxic cells and their importance in radiotherapy - the oxygen effect - the hypoxic cells - methods of selectively attaching hypoxic cells
Slide 5-

Introduction Scientists have studied radiation for over 100 years and a great deal of information is known about it. Radiation is part of nature. All living creatures, from the beginning of time, have been, and are still being, exposed to radiation. We Live (And Have Always Lived) in a “Sea of Radiation”
Slide 6-

Definition of Radiation “Radiation is an energy in the form of electro-magnetic waves or particulate matter, traveling in the air.”
Slide 7-

Ionizing Radiation Definition: “ It is a type of radiation that is able to disrupt atoms and molecules on which they pass through, giving rise to ions and free radicals”.
Slide 8-

Basic Model of a Neutral Atom. Electrons (-) orbiting nucleus of protons (+) and neutrons. Same number of electrons as protons; net charge = 0. Atomic number (number of protons) determines element. Mass number (protons + neutrons)
Slide 9-

Radioactivity If a nucleus is unstable for any reason, it will emit and absorb particles. There are many types of radiation and they are all pertinent to everyday life and health as well as nuclear physical applications.
Slide 10-

Ionization - Ionizing radiation is produced by unstable atoms. Unstable atoms differ from stable atoms because they have an excess of energy or mass or both. - Unstable atoms are said to be radioactive. In order to reach stability, these atoms give off, or emit, the excess energy or mass. These emissions are called radiation.
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TYPES OF RADIATIONS
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Types of Radiation
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Absorbed Dose Depends on: Whether material is inside or outside body How long material remains in the body How much radioactive material there is The type of radiation it emits What its half-life is
Slide 15-

Natural and Man-Made Radiation Sources
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Natural Background Radiation Cosmic Radiation Terrestrial Radiation Internal Radiation
Slide 17-

Cosmic Radiation The earth, and all living things on it, are constantly being bombarded by radiation from outer space (~ 80% protons and 10% alpha particles). Charged particles from the sun and stars interact with the earth’s atmosphere and magnetic field to produce a shower of radiation. The amount of cosmic radiation varies in different parts of the world due to differences in elevation and to the effects of the earth’s magnetic field.
Slide 18-

Terrestrial Radiation (Uranium, Actinium, Thorium decay series) Radioactive material is found throughout nature in soil, water, and vegetation. Important radioactive elements include uranium and thorium and their radioactive decay products which have been present since the earth was formed billions of years ago. Some radioactive material is ingested with food and water. Radon gas, a radioactive decay product of uranium is inhaled. The amount of terrestrial radiation varies in different parts of the world due to different concentrations of uranium and thorium in soil.
Slide 19-

Internal Radiation People are exposed to radiation from radioactive material inside their bodies. Besides radon, the most important internal radioactive element is naturally occurring K-40, but uranium and thorium are also present as well as H-3 and C-14. The amount of radiation from potassium-40 does not vary much from one person to another. However, exposure from radon varies significantly from place to place depending on the amount of uranium in the soil. On average, in the United States radon contributes 55% or all radiation exposure from natural and man-made sources. Another 11% comes from the other radioactive materials inside the body.
Slide 20-

Radioactive material is used in: Medicine - diagnostic (X-ray, CAT) Medicine - therapeutic (Co-60, Linac) Medical research (radio-pharmaceuticals, accel.) Industry - (X-ray density gauges, well logging) Man-Made Radiation
Slide 21-

Radiation in Medicine Radiation used in medicine is the largest source of man-made radiation. Most exposure is from diagnostic x-rays.
Slide 22-

Man-Made Radiation Sources Exposure of selected groups of the public: diagnostic radiology (X-rays) nuclear medicine (radiopharmaceuticals) radiotherapy (Co-60)
Slide 23-

Interaction of radiation with matter
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Elastic Scattering hnin = hnout No loss of photon energy
Slide 25-

Elastic Scattering Elastic scattering is also known as called “Coherent” or “Rayleigh” scattering Photon scattering angle depends on Z and hn* hn 0.1 MeV 1 MeV 10 MeV Al 15o 2o 0.5o Pb 30o 4o 1.0o Occurs mainly at low energies Large Z materials Contributes nothing to KERMA or dose, no energy transferred, no ionisation, no excitation No real importance in radiotherapy * F. H. Attix, Introduction to Radiological Physics and Radiation Dosimetry
Slide 26-

The Photoelectric Effect Ee: maximum kinetic energy of the outgoing electron W: energy needed to remove electron Ee = hn - W Incoming photon
Slide 27-

The Photoelectric Effect Photoelectron emitted leaving atom in unstable, excited state Atom relaxes by X-ray emission Auger electron emission (The Auger Effect)
Slide 28-

The Photoelectric Effect Process = attenuation and absorption Interaction of a photon with bound atomic electrons Total absorption of photon energy Photoelectron emitted , max. kinetic energy: Ee = hn - W Produces characteristic X-rays and/or Auger electrons Predominates at low energies Is highly Z dependent Example: tPb/rPb is 300 times greater than tbone/rbone
Slide 29-

The Photoelectric Effect If the photon energy is slightly higher than the energy required to remove an electron form a particular shell (e.g. K, L, M) around the nucleus, there is a sharp increase in t/r. This increase is called an absorption edge.
Slide 30-

The Photoelectric effect Absorption edges important: 1. In radiology because it influences the choice of material used in intensifying screens, photographic film, contrast agents 2. In radiation protection because it influences the choice of shielding materials In radiotherapy because it influences the choice of filtering material Example
Slide 31-

The Photoelectric Effect Number of X-rays produced/no. of vacancies = Fluorescent Yield (w) Fluorescent Yield is high for high Z, low for low Z Low Z materials give low energy X-rays => X-rays absorbed locally For low Z materials, Auger electrons more probable Fluorescent yield (K-shell vacancy)* * H. Johns & J. Cunningham, The Physics of Radiology, 4th Edition
Slide 32-

The Compton Effect Incoming photon Outgoing electron Outgoing photon q f
Slide 33-

The Compton Effect Interaction of photon with unbound atomic electrons Scatter + partial absorption of photon energy Scattered electron + scattered photon Change in photon wavelength depends on angle of scattered photon lout- lin = constant x (1- Cos q) lin: wavelength of the outgoing electron, lout: energy of incoming photon If photon makes a direct hit: Electron will be scattered straight on with maximum energy Photon will be scattered backwards i.e. q = 180o with minimum energy Scattered photon energy
Slide 34-

The Compton Effect
Slide 35-

The Compton Effect
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The Compton Effect Dominates over a wide range of X-ray energies Depends on electron density (re) Independent of Z /r  e / hn
Slide 37-

Pair Production – Type 1 hn ³ 1.022 MeV hn – 1.022 = E- + E+ E-, E+ are the kinetic energies of the electron and positron resp.
Slide 38-

Pair Production – Type 1 Photon interacts with Coulomb field of atomic nucleus and is absorbed Electron/Positron pair produced if hn ³ 1.022 MeV Example of conversion of energy into mass: E = mc2 Energy equivalent of one electronic mass is 0.511 MeV As e+ & e- produced, incoming photon must have energy: 2 x 0.511 MeV e+ and e- can receive any fraction of photon energy Dominates at high photon energies Dependent on Z
Slide 39-

Pair Production – Type 1 e+ produced in Pair Production dissipates energy locally Energy lost through excitation and ionisation of atoms along its track until it comes to rest It is annihilated by combining with a free electron producing two photons of energy 0.511 MeV
Slide 40-

Pair production –Type 2 Otherwise called Triplet Production Incident photon interacts with Coulomb field of atomic electrons & is absorbed Incident photon transfers energy to Host e- and e-/e+ pair produced Conservation of momentum => threshold energy for this process is 4mc2 hn=1.022 MeV+E1-+E2-+E+
Slide 41-

Summary Pb, W H Ca Zr Al Sn
Slide 42-

Photonuclear Interactions High energy photon interacts with atomic nucleus resulting in emission of a proton (p) or a neutron (n) Occurs for incident photons with energy > few MeV If p emitted, effect can contribute to dose. But relative importance is low If n emitted, there can be consequences for radiation protection must take account in shielding designs n can escape shielding more readily than photons n may activate accelerator hardware e.g. in target Biological effect in radiotherapy patient negligible compared with effects of photons
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The Auger Effect (Revisited) Mono-energetic Auger electrons will carry away any surplus energy of excited atom Multiple Auger electrons can be emitted resulting in an Auger shower. Vacancies continue to move to less tightly bound shells until they are eventually filled by conduction band (free) electrons K L M hn = EK-EL X-ray Auger e- E = hn - EM E = EK – EL - EM holes in L- and M-shell Initial state: hole in K-shell
Slide 44-

Scattered Radiation = By-product of the interaction of radiation with matter Scattered radiation = radiation (particulate or EM radiation) that has changed direction with or without a change in energy during its passage through intervening matter. EXAMPLE: In radiotherapy, scattered radiation comes from the interaction of the primary beam with the flattening filters, primary and secondary collimators, monitor chamber, the patient.
Slide 45-

Scattered Radiation If energy of incoming radiation high  scatter mostly in forward direction. Example: Therapy range (MV) If energy of incoming radiation low  scatter in backwards direction (= backscatter) increases. Example: Therapy range (50 – 160 kV) or Diagnostic Imaging (typically 40 – 80 kVp) Spatial distribution of scattered x-rays
Slide 46-

Scattered Radiation Effects of Scattered Radiation: In imaging it acts as a mask over the image. In radiotherapy, adds to patient dose and has radiation protection issues for staff
Slide 47-

Secondary Electrons When primary radiation interacts with matter, electrons may be produced – these electrons are called “secondary electrons” Secondary electrons are emitted close to the original point of interaction. If the secondary electron is given enough energy, it can create its own separate track depositing energy along the way – d-ray d-rays do not deposit energy in the immediate vicinity  consequences for determining Absorbed Dose NOTE: Electrons follow tortuous paths undergoing many interactions before coming to a stop. Photons travel in straight lines.
Slide 48-

Range versus Energy The furthest distance radiation travels in a medium is called “the range”. An electron follows a tortuous path undergoing many interactions before coming to a stop
Slide 49-

Range versus Energy The range depends on: the type and energy of the radiation the density of the traversing medium Data from: F. Attix, Introduction to Radiological Physics and Radiation Dosimetry EXAMPLE: Electron range in tissues
Slide 50-

Linear Energy Transfer The LET is the rate at which energy is transferred to the medium and therefore the density of ionisation along the track of the radiation. LET also referred to as “restricted stopping power” (LD) LET is expressed in terms of keV per micron dE = energy lost by radiation dX = length of track Radiation that is easily stopped has a high LET and vice versa
Slide 51-

Interaction of Charged Particles with Matter - General charged particles (e-, protons, a-, b-particles) lose energy in a manner very different from uncharged radiation (X-rays, g-rays, neutron). charged-particles are surrounded by an electrostatic field (= Coulomb field) they interact with electrons/nuclei of practically every atom they pass The force between two particles is  Ze2/r2 probability of charged particle passing through a medium without interaction is ZERO Example: a 1 MeV charged-particle typically undergoes 105 interactions before losing all its kinetic energy (K.E.)
Slide 52-

Interaction of Charged Particles with Matter – Energy Loss HOW? “soft collision” when b >> a “hard collision” when b ~ a “Coulomb-force interactions with the external nuclear field” when b << a Interactions characterised by: “impact parameter, b” vs “atomic radius, a”
Slide 53-

Interaction of Charged Particles with Matter – Energy Loss Soft Collisions (b >> a): Excitation and Ionisation The electric field of the charged particle interacts with atomic electrons causing them to accelerate and gain energy. Excitation: If the gain in electron energy is equal to the difference in energy between its own energy level and a higher energy level, then the electron is excited to the higher energy level. Ionisation: If the gain in energy is greater than the binding energy for the electron, then an electron is removed from its orbital. The atom is “ionised”. Net effect: transfer of a small amount of energy (few eV) to atom of absorbing medium
Slide 54-

Interaction of Charged Particles with Matter – Energy Loss Soft Collisions (b >> a) Large b more probable than small b  “soft” collisions more likely than any other type of interaction  approx. 1/2 particle energy transferred to absorbing medium Cerenkov radiation in the core of a reactor Two additional effects: Polarisation of atoms in absorbing medium Cerenkov radiation = emission of bluish light (< 0.1 % of particle energy spent in this way.
Slide 55-

Interactions of Charged Particles with Matter – Energy Loss Hard Collisions (b ~ a): Ionisation, d-rays, char. X-rays + Auger e- When b ~ a, more likely for CP to interact with single atomic e-  “hard” collisions result in ejection of e-  e- emitted with large K.E. = d-ray  d-rays have sufficient energy to ionise other atoms  d-rays dissipate energy along separate track = spur d-ray
Slide 56-

Interactions of Charged Particles with Matter – Energy Loss Hard Collisions (b ~ a): Ionisation, d-rays, char. X-rays + Auger e-  char. X-rays and Auger electrons also emitted  some energy transferred to medium by d-rays, char. x-rays and Auger e- transported away from primary particle track  no. of hard collisions is small  BUT fraction of energy spent in hard + soft collision comparable L-shell to K-shell = Ka radiation M-shell to K-shell = Kb radiation
Slide 57-

Interaction of Charged Particles with Matter – Energy Loss Mean Energy Expended per Ion Pair, W In measuring the energy absorbed extensive use is made of ionisation. Mean energy expended to form an ion pair: W = E/N where E = initial K.E. of the charged particle N = mean no. of ion pairs formed when all energy is used EXAMPLE: W for dry air is 34 eV
Slide 58-

Interaction of Charged Particles with Matter – Energy Loss Coulomb-force interactions with the external nuclear field” (b << a): Bremsstrahlung When charged particle comes very close to nucleus, its electric field interacts with that of the nucleus. Most important for electrons because: Prob.  Z2 , 1/m2 Most cases, elastic scattering results i.e. electron changes direction but loses no energy 2-3% of cases, charged particle decelerates thereby losing energy and changing direction Up to 100 % particle energy lost as X-rays = Bremsstrahlung  continuous spectrum of Bremsstrahlung radiation
Slide 59-

Interaction of Charged Particles with Matter – Energy Loss Electrons The interaction of electrons with matter is different from other charged particles because the electron is very small: me = 9.11 e-31 kg mp = 1.67 e-27 kg Therefore, two important effects observed for electrons: Relativistic effects  large changes in energy and angle Rapid deceleration  Bremsstrahlung
Slide 60-

Stopping Power, S Stopping Power, S: The rate of energy loss per unit path length by a charged particle having K.E. in a medium of atomic number Z Units: MeV/cm Mass Stopping Power = S/r (independent of density) Total Stopping Power  collision losses + radiative losses Stopping Power depends on the absorbing medium, the particle charge, the particle energy, and the particle mass
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BIOLOGICAL EFFECTS OF IONIZING RADIATION AT MOLECULES AND CELLS
Slide 62-

The stage of action of ionizing radiation
Slide 63-

Effect of radiation on atom and molecules
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Effects of ionizing radiation at atomic level Ionization Excitation
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Mechananisms of damage at molecular level
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Direct action of ionizing radiation Ionizing radiation + RH R- + H+ OH I R – C = NH imidol (enol) O II R – C = NH2 amide (ketol)   Tautomeric shifts Bond breaks
Slide 67-

e- X ray  ray P+ O H H OH- H+ Ho OHo Indirect action of ionizing radiation
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Radiolysis of H2O molecule Shared electron Shared electron H-O-H  H+ + OH- (ionization) H-O-H  H0 + OH0 (free radicals)
Slide 69-

Reaction of H2O molecule radiolysis Н2О + h  Н2О+ + е- Н2О + h  Н2О*  Но + НОо Н2О + е-  е-  Но + НО- Н2О + е-  Н2О*  Но + ОНо Н2О  Н+ + ОНо е- + Н+  Но Н2О+ + ОН-  Н2О + ОНо Н2О+ + Н2О  Н3О+ + ОНо Н3О+ + е-  Н2О + Но
Slide 70-

Effects of oxygen on free radical formation Oxygen can modify the reaction by enabling creation of other free radical species with greater stability and longer lifetimes H0 + O2  HO20 (hydroperoxy free radical) R0 + O2  RO20 (organic peroxy free radical)
Slide 71-

Reactions with free radicals H0 + OH0  H2O H0 + H0  H2 OH0 + OH0  H2O2 RH + OH0  R0 + H2O RH + H0  R0 + H2 R0 + OH  ROH R0 + H  RH R0 + O2  ROO0 ROO0 + RH  ROOH + R0
Slide 72-

Lifetimes of free radicals 3nm Because short life of simple free radicals (10-10sec), only those formed in water column of 2-3 nm around DNA are able to participate in indirect effect Ho OHo Ho OHo HO2o RO2o
Slide 73-

Relation between linear energy transfer (LET) and type of action Direct action is predominant cause of damage with high LET radiation, e.g. alpha particles and neutrons Indirect action is predominant with low LET radiation, e.g. X and gamma rays
Slide 74-

Effects of Ionizing Radiation on DNA Single strand break Double-Strand Break Double-Strand Break in Same Rung of DNA Mutation
Slide 75-

Single-Strand Break If ionizing radiation interacts with a DNA macromolecule, the energy transferred can rupture one of its chemical bonds, possibly severing one of the sugar-phosphate chain side rails or strands of the ladderlike molecular structure (single-strand break). This type of injury to DNA is called a point mutation. Gene mutations may result from a single alteration along the sequence of nitrogenous bases. Point mutations commonly occur with low-LET radiations. Repair enzymes, however, are capable of reversing this damage.
Slide 76-

Double-Strand Break Further exposure of the affected DNA macromolecule to ionizing radiation may result in additional breaks in the sugar-phosphate molecular chain(s). These breaks might also be repaired, but double-strand breaks (one or more breaks in each of the two sugar-phosphate chains) are not repaired as easily as single-strand breaks. If repair does not take place, further separation may occur in the DNA chains, threatening the life of the cell. Double-strand breaks occur more commonly with densely ionizing (high-LET) radiations and often are associated with the loss or gain of one or more nitrogenous bases. When high-LET radiation interacts with DNA molecules, the ionization interactions may be so closely spaced that, by chance, both strands of the DNA chain are broken. If both strands are broken at the same nitrogenous base “rung,” the result is the same as if both side rails of the ladder were cut at the same step or rung—the ladder would be cut into two pieces. If the DNA is cut into two pieces, the chromosome, which is composed of a long chain of twisted strands of DNA ladders, is itself broken. Thus some types of chromosomal damage that are particularly associated with high-LET radiation are related to double-strand breaks of DNA. Because the chance of repairing this damage is much slighter, the possibility of inducing a lethal alteration of nitrogenous bases within the genetic sequence is far greater.
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Double-Strand Break in Same Rung of DNA When two interactions (hits), one on each of the two sugar-phosphate chains, occur within the same rung of the DNA ladder like configuration, the result is a cleaved or broken chromosome, with each new portion containing an unequal amount of genetic material. If this damaged chromosome divides, each new daughter cell will receive an incorrect amount of genetic material. This will culminate in the death or impaired functioning of the new daughter cell.
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Mutation In general, the interaction of high-energy radiation with a DNA molecule causes either a loss of or change in a nitrogenous base on the DNA chain. The direct consequence of this damage is an alteration of the base sequence. Because the genetic information to be passed on to future generations is contained in the strict sequence of these bases, the loss or change of a base in the DNA chain is a mutation. It may not be reversible and may cause acute consequences for the cell but, more important, if the cell remains viable, incorrect genetic information will be transferred to one of the two daughter cells when the cell divides.
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Covalent Cross-Links Covalent cross-links are chemical unions created between atoms by the single sharing of one or more pairs of electrons. Covalent cross-links involving DNA are another effect initiated by high-energy radiation. At low energies, however, covalent cross-links are probably caused by the process of indirect action. Following irradiation, some molecules can produce small, spurlike molecules that become very interactive (“sticky”) when exposed to radiation. This can cause these molecules to attach to other macromolecules or to other segments of the same macromolecule chain.
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Cross-linking can occur in many different patterns. For example, a cross-link can form between two places on the same DNA strand. This joining is termed an intrastrand cross-link. Cross-linking may also occur between complementary DNA strands or between entirely different DNA molecules. These joinings are termed interstrand cross-links. Finally, DNA molecules also may become covalently linked to a protein molecule. All these linkages are potentially fatal to the cell if they are not properly repaired.
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Biochemical reactions with ionizing radiation DNA is primary target for cell damage from ionizing radiation
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Radiation induced DNA damage
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The most important types of radiation induced lesions in DNA Single-strand breaks 500-1000 per 1 Gy Double strand breaks 40-50 per 1 Gy Base damage: 1000-2000 per 1 Gy
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Mechanisms of base excision and nucleotide excision repair
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Mechanism of single-strand breaks DNA repair Exonuclease
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DNA restoration failure Unrejoined DNA double strand breaks Incorrect repair of DNA damage Cytotoxic effect Mutations
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Radiation induced membrane damage Biological membranes serve as highly specific mediators between the cell and the environment. Radiation changes within the lipid bilayers of the membrane may alter ionic pumps. This may be due to changes in the viscosity of intracellular fluids associated with disruptions in the ratio of bound to unbound water. Such changes would result in an impairment of the ability of the cell to maintain metabolic equilibrium and could be very damaging even if the shift in equilibrium were quite small. Alterations in the proteins that form part of a membrane’s structure can cause changes in its permeability to various molecules, i.e. electrolytes.
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Effect of radiation on cells
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Types of cellular damage Interphase cell death Changes of metabolism & function Mitotic cell death Norma repair Mutation
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Cell cycle
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NORMAL IRRADIATED Mitotic death
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The most ‘radiosensitive’ cells are actively proliferating (dividing) at the time of exposure undifferentiated (non-specialized in structure and function) Bergonié and Tribondeaus’ ‘law’ (1906)
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Pyknosis: The nucleus becomes contracted, spheroidal, and filled with condensed chromatin. Karyolysis: The nucleus swells and loses its chromatin. Protoplasmic Coagulation: Irreversible gelatin formation occurs in both the cytoplasm and nucleus. Karyorrhexis: The nucleus becomes fragmented and scattered throughout the cell. Cytolysis: Cells swell until they burst and then slowly disappear. Apoptosis: Programmed cell death, usually be fragmentation Morphological forms of cell death
Slide 97-

Block of Mitotic Cycle: Mitosis may be delayed or inhibited following radiation exposure. Disruptions in Cell Growth: Cell growth may also be retarded, usually after a latent period. Permeability Changes: Irradiated cells may show both increased and decreased permeability. Changes in Cell Motility: The motility of a cell may be decreased following irradiation. Changes of cell metabolism and function
Slide 98-

Radiation induced chromosome damage Chromosomes
Slide 99-

Effects of Ionizing Radiation on Chromosomes Large-scale structural changes in a chromosome brought about by ionizing radiation may be as grave for the cell as are radiation-induced changes in DNA. When changes occur in the DNA molecule, the chromosome exhibits the alteration. Because DNA modifications are discrete, they do not inevitably result in observable structural chromosome alterations.
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Radiation-Induced Chromosome Breaks After irradiation and during cell division, some radiation-induced chromosome breaks may be viewed microscopically. These alterations manifest themselves during the metaphase and anaphase of the cell division cycle, when the length of the chromosomes is visible.
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Because the events that have happened before these phases of cell division are not visible, they can only be assumed to have occurred. What can be seen, however, is the effect of these events—the gross or visible alterations in the structure of the chromosome. Both somatic cells and reproductive cells are subject to chromosome breaks induced by radiation.
Slide 102-

Chromosomal Fragments After chromosome breakage, two or more chromosomal fragments are produced. Each of these fragments has a fractured extremity. These broken ends appear sticky and have the ability to adhere to another such sticky end. The broken fragments may rejoin in their original configuration, fail to rejoin and create an aberration (lesion or anomaly), or rejoin other broken ends and create new chromosomes that may not look structurally altered compared with the chromosome before irradiation
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Chromosome Anomalies Two types of chromosome anomalies have been observed at metaphase. They are called (1) chromosome aberrations and (2) chromatid aberrations. Chromosome aberrations result when irradiation occurs early in interphase, before DNA synthesis takes place. In this situation, the break caused by ionizing radiation is in a single strand of chromatin; during the DNA synthesis that follows, the resultant break is replicated when this strand of chromatin lays down an identical strand adjacent to itself if repair is not complete before the start of DNA synthesis.
Slide 104-

This leads to a chromosome aberration in which both chromatids exhibit the break. This break is visible at the next mitosis. Each daughter cell generated will have inherited a damaged chromatid as a consequence of a failure in the repair mechanism. Chromatid aberrations, on the other hand, result when irradiation of individual chromatids occurs later in interphase, after DNA synthesis has taken place. In this situation, only one chromatid of a pair might suffer a radiation-induced break. Therefore only one daughter cell is affected.
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Structural Changes in Biologic Tissue Caused by Ionizing Radiation Ionizing radiation interacts randomly with matter. Because of this phenomenon, exposure to radiation produces a variety of structural changes in biologic tissue. Some of these changes are as follows: •A single-strand break in one chromosome •A single-strand break in one chromatid •A single-strand break in separate chromosomes •A strand break in separate chromatids •More than one break in the same chromosome •More than one break in the same chromatid •Chromosome stickiness, or clumping together
Slide 106-

Consequences to the Cell from Structural Changes in Biologic Tissue: 1.Restitution, whereby the breaks rejoin in their original configuration with no visible damage . In this case no damage to the cell occurs because the chromosome has been restored to the condition it was in before irradiation. The process of healing by restitution is believed to be the way in which 95% of single-chromosome breaks mend. 2.Deletion, whereby a part of the chromosome or chromatid is lost at the next cell division, creating an aberration known as an acentric fragment.
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3.Broken-end rearrangement, whereby a grossly misshapen chromosome may be produced. Ring chromosomes, dicentric chromosomes, and anaphase bridges are examples of such distorted chromosomes. 4.Broken-end rearrangement without visible damage to the chromosomes, whereby the chromosome's genetic material has been rearranged even though the chromosome appears normal. Translocations are an example of such rearrangements. Changes such as these inevitably result in mutation because the positions of the genes on the chromosomes have been rearranged, thus altering the heritable characteristics of the cell.
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Restitution
Slide 109-

Deletion
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The process of broken-end rearrangement may result in no visible damage to the chromosome, although the chromosome's genetic material has been rearranged—a result that will drastically alter its function within the cell, probably leading to cell death or failure to replicate.
Slide 111-

Target Theory Amid the many different types of molecules that lie within the cell, a master, or key, molecule that maintains normal cell function also is believed to be present. This master molecule is necessary for the survival of the cell. Because this molecule is unique in any given cell, no similar molecules in the cell are available to replace it; if the master molecule is inactivated by exposure to radiation, the cell will die. Experimental data strongly support this concept and indicate that DNA is the irreplaceable master, or key,
Slide 112-

molecule that serves as the vital target. Destruction of some of the molecules that are plentiful in the cell does not result in cell death. The reason for this is simply that cells have an abundance of similar molecules to take over and perform necessary functions for them in the event of their demise. If only a few non-DNA cell molecules are destroyed by radiation exposure, the cell will probably not show any evidence of injury after irradiation.
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CELLULAR EFFECTS OF IRRADIATION Ionizing radiation can adversely affect the cell. Damage to the cell's nucleus reveals itself in one of the following ways: 1.Instant death 2.Reproductive death 3.Apoptosis, or programmed cell death (interphase death) 4.Mitotic, or genetic, death 5.Mitotic delay 6.Interference of function 7.Chromosome breakage
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SURVIVAL CURVES FOR MAMMALIAN CELLS Cells vary in their radiosensitivity. This fact is particularly important in determining the type of cancer cells that will respond to radiation therapy. A classic method of displaying the sensitivity of a particular type of cell to radiation is the cell survival curve. A cell survival curve is constructed from data obtained by a series of experiments. First, the cells are made to grow “in culture,” meaning in a laboratory environment such as a Petri dish.
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Then the cells are exposed to a specified dose of radiation. After radiation exposure, the ability of the cells to divide, or form new “colonies” of cells, is measured. The fraction of cells that are able to form new colonies through cell division is then reported as the fraction of cells that have survived irradiation. The process is repeated for a range of radiation doses, and the results are graphed with the logarithm of the surviving fraction on the vertical axis and the dose on the horizontal axis.
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Vegetative Cells: these cells, comprising differentiated functional cells of a large variety of tissues, are generally the most radiosensitive. Differentiating Cells: these cells are somewhat less sensitive to radiation; they are relatively short‑lived and include the first generation produced by division of the vegetative mitotic cells. Totally Differentiated Cells: these cells are relatively radioresistant; they normally have relatively long lifespans and do not undergo regular or periodic division in the adult stage, except under abnormal conditions such as following damage to or destruction of a large number of their own kind. Fixed Nonreplicating Cells: these cells are most radioresistant; they are highly differentiated morphologically and highly specialized in function. Relative cellular radiosensitivity
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Radiosensitivity varies in different types of tissue. While all cells can be destroyed by a high radiation dose, highly radiosensitive cells or tissue exhibit deleterious effects at much lower doses than others, rapidly dividing, undifferntiated cells in tissue are the most sensitive to radiation effects. Highly radiosensitive tissue - lymphoid, bone marrow elements, gastrointestinal epithelium, gonads (testis and ovary), and foetal tissue. Moderately radiosensitive tissue - skin, vascular endothelium, lung, kidney, liver, lens and thyroid in childhood. Least radiosensitive tissue - central nervous system, endocrine (except gonad), thyroid in adults, muscle, bone and cartilage, and connective tissue. The least radiosensitive tissue, although radioresistant, is less capable of cell renewal than highly sensitive tissue. Some - especially neurons, glial cells of the brain, and muscle cells - has essentially no ability to regenerate. Once these cells are killed, the area is repaired by fibrosis or scarring.
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Factors affecting cell radiosensitivity 1- cell maturity and specialization: immature cells are nonspecialized and undergo rapid cell division so they are radiosensitive 2- amount of radiation energy transferred to biologic tissue (LET) 3- oxygen enhancement effect: oxygen increases the cell radiosensitivity, more free radicals are formed in the presence of oxygen
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4- Low of Beronie’ and Tribondeau: the radiosensitivity is a function of the metabolic state of the cell receiving the exposure. It state that the radiosensitivity of the cells is directly proportional to their reproductive activity and inversely proportional to their degree of differentiation.
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Effect of ionizing radiation on human cells Blood cells - hematologic depression: ionizing radiation affect blood cells by depressing the number of cells in the peripheral circulation a whole body dose of 25 rad produce measurable hematologic depression. - Depletion of immature blood cells: most blood cells are produced in the bone marrow radiation causes decrease in the number of immature blood cells
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If the bone marrow cells have not been destroyed by exposure they can repopulate after a period of recovery, the recovery time depend on the magnitude of the radiation dose received ( repopulation). Effect on stem cells of the hematopoietic system: radiation affects primarily the stem cells of the hematopoietic ( blood forming) system erythrocytes are among the most sensitive of human tissue, as with all cells that transform from an immature, undifferentiated state to a mature functional state
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The mature red blood cells are less radiosensitive. Because the population of circulating RBCs is high and their life span is long depletion of red cells is not usually the cause of death in high dose, death is more typically caused by infection that cannot be overcome by the immune system because of destruction of myeloblasts (type of WBCs) and internal bleeding resulting from destruction of magakaryoblasts ( precursors of platelets)
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Whole body dose in excess of 5 Gy (500 rad) Body exposure more than 5 Gy might result in death within 30-60 days because of effect related to initial depletion of stem cells of hematopoietic system. The use of antibiotics or isolation from pathogens in the environment feeding only sterilized food has been shown to limit these effects in animals and humans. Lethal dose in animals is usually specified as LD50/30 ( dose that produce s death of 50% of exposed group in 30 days
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The lethal dose in human beings is usually given as LD 50/60 because humans recovery is slower than that of the laboratory animals. The lethal dose for human beings estimated to be 3-4 GY without treatment and higher if medical intervention is available. Effect of radiation on lymphocytes: white blood cells are called leukocytes, lymphocytes are subgroup of WBCs these cells defend the body against antigens by forming antibodies to fight the disease, they live only for 24 hours
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Lymphocytes manufactured in the bone marrow are the most sensitive blood cells in the human body, a radiation dose of 0.25 GY (25 rad) is sufficient to depress the number of cells present in the circulating blood, when significant number of lymphocytes are damaged the body loses its natural ability to fight infection and become more susceptible to infection by bacteria and viruses. This also applied to neutrophils and granulocytes
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Effect of ionizing radiation on thrombocytes (platelets): platelets initiate blood clotting and prevent hemorrhage they have life span of 30 days a dose of radiation greater than 0.5 Gy lessens the number of platelets in the circulating blood, death from internal bleeding might occur. Radiation exposure during diagnostic imaging procedures: diagnostic procedures should not result in high exposure to blood forming organs, however studies indicate chromosomal abrasion in lymphocytes that receive radiation dose during diagnostic procedure,
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Patients with high level fluoroscopic procedures like cardiac catheterization. Occupational radiation exposure monitoring: film badge or TLD can be used to detect exposures in mSv and can be used to discover potentially hazardous working conditions, a periodic blood count is not recommended as a method of monitoring occupational exposure because biologic damage has already been sustained when irregulatory is seen in the blood counts
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Muscle tissue: these tissues are highly specialized and do not divide they are relatively insensitive to radiation Nervous tissue: in adults nerve cells are highly specialized and perform specific functions, in the nucleus of one of these cells is destroyed the cell will die and never restored. If axon or dendrites damaged by radiation control and communication with some areas of the body may be disrupted.
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Nerve tissue in the embryo-fetus: developing nerve cells in the embryo-fetus are more radiosensitive than mature nerve cells of the adult, irradiation of the embryo may lead to CNS anomalies, microcephaly and mental retardation, maximum sensitivity extends from 8-15 weeks after gestation during this period exposure of 0.1 Sv (10 rem) fetal EqD is associated with as much as 4% risk of mental retardation
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Reproductive cells: Spermatogonia: human germ cells are relatively radiosensitive, the male testes contain both mature and immature Spermatogonia, the mature spermatogonia are specialized and do not divide they are relatively insensitive to radiation, the immature spermatogonia are rapidly dividing they are extremely radiosensitive, radiation dose of 2Gy may cause temporary sterility for 12 months and 5-6 Gy exposure may cause permanent sterility, small doses 0.1 Gy may depress male sperm population. Male reproductive cells that have been exposed to 0.1 Gy or more may cause genetic mutation in future generation.
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Ova: is the mature female germ cells that do not divide constantly, radiosensitivity of ova varies considerably throughout the life time of the germ cells immature ova are very radiosensitive, after irradiation a mature ovum can still unit with a male germ cell, these irradiated cells may contain damaged chromosomes, genetic damage may be passed on to the offspring resulting in congenital anomalies. During diagnostic imaging gonadal shielding is essential to limit radiation damage to the reproductive organs. Radiation exposure also may cause female sterility depending on the age of the subject the ovaries of female fetus and young child are very radiosensitive because they contain large number of stem cells.
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Summary Cells going through the division phase (M and S) are generally the most sensitive to ionizing radiation. Exceptions: lymphocytes and some bone marrow stem cells, which exhibit interphase death Bone marrow consists of progenitor and stem cells, the most radiosensitive cells in the human body and the most important in controlling infection
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Early and late effect of radiation 1- early effect: when biologic effects of radiation occur relatively soon after human exposure to a high does of radiation
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Early Somatic Effects This appears within minutes, hours, days, or weeks, of the time of radiation exposed A sever amount of dose can cause a pattern of symptoms which referred to as radiation syndrome. Nausea, Fatigue, Erythema, and Blood Disorder
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The amount Somatic and genetic damage depends on 1- the quantity of ionizing radiation to which the body is exposed 2- the ability of ionizing radiation to cause ionizations of human tissue 3- the amount of body area exposed 4- the specific body part exposed
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Somatic effects: when human body exposed to radiation experience biological damage, the effects of this exposure is classified as somatic effect. Depending on the length of time from the exposure to the first appearance of symptoms of radiation damage. The effects are classified as either early or late somatic effects
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If these effects are cell-killing and directly related to the dose received they are called deterministic somatic effects, as dose increased the severity of early effects are also increased. A substantial dose of ionizing radiation is required to produce biological effect soon after exposure, the severity of these effects is dose dependent the higher the dose the more severe is the damage
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Acute radiation syndrome (ARS): occur in human after whole body exposure to large doses of ionizing radiation in short period of time. Symptoms of ARS: three separate dose related syndromes occur as part of the total body syndrome Hematopoietic syndrome Gastrointestinal syndrome Cerebrovascular syndrome
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Response stages of ARS - prodromal Latent period Manifest illness Recovery or death Prodromal or initial stage occur within hours after whole body absorbed dose of 1 Gy or more this stage is characterized by nausea, vomiting, diarrhea, fatigue, and leukopenia >5000/ cubic mm.
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Latent period: occur about 1 week after exposure during which no visible symptoms occur, during this period either recovery or lethal effects begin Manifest illness: the period when symptoms that affect the hematopoietic, gastrointestinal, and Cerebrovascular systems become visible. Some of these symptoms are apathy, confusion, decrease in the number of RBCs and WBCs and platelets in the circulating blood, dehydration, epilation, exhaustion, vomiting , severe diarrhea, infection hemorrhage, and cardiovascular collapse.
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Lethal dose LD: LD 50/30 means the whole body dose of radiation that can kill 50% of the exposed population within 30 days. The LD 50/30 for adult human is estimated to be 3-4 Gy without medical support, for x-ray and gamma ray this is equal to an equivalent dose of 3-4 Sv, whole body does greater than 6 Gy may cause the death of the entire population in 30 days.
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LD 50/30
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Hematologic Syndrome Radiation doses in the range of approximately 200 to 1000 rad (2 to 10 Gyt) produce the hematologic syndrome. The patient initially experiences mild symptoms of the prodromal syndrome, which appear in a matter of a few hours and may persist for several days. The latent period that follows can extend as long as 4 weeks and is characterized by a general feeling of wellness. There are no obvious signs of illness, although the number of cells in the peripheral blood declines during this time.
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The period of manifest illness is characterized by possible vomiting, mild diarrhea, malaise, lethargy, and fever. Each of the types of blood cells follows a rather characteristic pattern of cell depletion. If the dose is not lethal, recovery begins in 2 to 4 weeks, but as long as 6 months may be required for full recovery. If the radiation injury is severe enough, the reduction in blood cells continues unchecked until the body's defense against infection is nil. Just before death, hemorrhage and dehydration may be pronounced. Death occurs because of generalized infection, electrolyte imbalance, and dehydration.
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Gastrointestinal (GI) Syndrome Radiation doses of approximately 1000 to 5000 rad (10 to 50 Gy) result in the GI syndrome. The prodromal symptoms of vomiting and diarrhea occur within hours of exposure and persist for hours to as long as a day. A latent period of 3 to 5 days follows, during which no symptoms are present. The manifest illness period begins with a second wave of nausea and vomiting, followed by diarrhea. The victim experiences a loss of appetite (anorexia) and may become lethargic. The diarrhea persists and becomes more severe, leading to loose and then watery and bloody stools. Supportive therapy cannot prevent the rapid progression of symptoms that ultimately leads to death within 4 to 10 days of exposure.
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Intestinal cells are normally in a rapid state of proliferation and are continuously being replaced by new cells. The turnover time for this cell renewal system in a normal person is 3 to 5 days. Radiation exposure kills the most sensitive cells—stem cells; this controls the length of time until death. When the functional cells are completely removed from intestinal lining, fluids pass uncontrollably across the intestinal membrane, electrolyte balance is destroyed, and conditions promote infection.
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Central Nervous System (CNS) Syndrome After a radiation dose in excess of approximately 5000 rad (50 Gyt) is received, a series of signs and symptoms occur that lead to death within a matter of hours to days. First, severe nausea and vomiting begins, usually within a few minutes of exposure. During this initial onset, the patient may become extremely nervous and confused, may describe a burning sensation in the skin, may lose vision, and can even lose consciousness within the first hour. This may be followed by a latent period that lasts up to 12 hours, during which earlier symptoms subside or disappear.
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The latent period is followed by the period of manifest illness, during which symptoms of the prodromal stage return but are more severe. The person becomes disoriented; loses muscle coordination; has difficulty breathing; may go into convulsive seizures; experiences loss of equilibrium, ataxia, and lethargy; lapses into a coma; and dies. Regardless of the medical attention given to the patient, the symptoms of manifest illness appear rather suddenly and always with extreme severity. At radiation doses high enough to produce CNS effects, the outcome is always death within a few days of exposure.
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The ultimate cause of death in CNS syndrome is elevated fluid content of the brain. The CNS syndrome is characterized by increased intracranial pressure, inflammatory changes in the blood vessels of the brain (vasculitis), and inflammation of the meninges (meningitis). At doses sufficient to produce CNS damage, damage to all other organs of the body is equally severe. The classic radiation-induced changes in the GI tract and the hematologic system cannot occur because there is insufficient time between exposure and death for them to appear.
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Acute radiation lethality follows a nonlinear, threshold dose-response relationship. At the lower dose of approximately 100 rad (1 Gyt), no one is expected to die. Above approximately 600 rad (6 Gyt), all those irradiated die unless vigorous medical support is available. Above 1000 rad (10 Gyt), even vigorous medical support does not prevent death. As the whole-body radiation dose increases, the average time between exposure and death decreases. This time is known as the mean survival time.
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All early radiation responses—local tissue damage is a good example—follow a threshold-type dose-response relationship. This is characteristic of a deterministic radiation response. A minimum dose is necessary to produce a deterministic response. Once that threshold dose has been exceeded, the severity of the response increases with increasing dose. local tissues that can be affected immediately by the radiation are: skin, gonads, and bone marrow.
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Radiation effects Early (deterministic only) Local Radiation injury of individual organs: functional and/or morphological changes within hrs-days-weeks Common Acute radiation disease Acute radiation syndrome Late Deterministic Radiation dermatitis Radiation cataract Teratogenic effects Stochastic Tumours Leukaemia Genetic effects
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Late effect of radiation High radiation doses can induce cancer in human, low radiation doses such as those received in occupationally exposed individuals are not known to cause malignancy, however the risk for radiation induced cancer in radiation workers is not really measurable at low doses encountered in diagnostic radiology
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Radiation Dose-Response Relationship Also known as the dose response curves, which is graphically determined by a curve that diagrams the observed effects of radiation exposure in relation to the dose of the radiation given.
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Dose-Response curves different in two ways: They can either be linear or non linear linear (straight line) nonlinear (curved to some degree) They can also be either threshold or nonthreshold
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Nonlinear Nonlinear can be described as a relationship or function that is not exactly proportional. For Example: An observed response that is not directly proportional to the dose. Doubling the dose of radiation, does not double the response.
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Threshold Threshold is the point at which something begins or changes. (Starting Point) In this case, it assumes that there is a radiation level reached below which no effects can be observed.
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Nonlinear Dose-Response Also known as the Sigmoid Dose Response Curve. Sigmoid meaning S-shaped (curve) This curve is mainly applied to the high dose effects observed in radiotherapy. There is usually a Threshold below which no visible effects happen.
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Nonthreshold Means that any radiation dose will produce biologic effect, no radiation dose is believed to be absolutely safe, some biologic response will be caused in living organisms by even the smallest dose of ionizing radiation, A linear-quadratic dose response is a relationship between dose and biological response that is curved. This implies that the rate of change in response is different at different doses. The response may change slowly at low doses, for example, but rapidly at high doses
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Dose Response Relationship Threshold assumes that there is a radiation level reached below which there would be no effects observed. Nonthreshold assumes that any radiation dose produces an effect. Linear Quadratic Dose Response Linear Nonthreshold Dose Response Linear Threshold Dose Response Nonlinear Dose Response (sigmoid curve)
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Factors Effecting the Dose Models and Theories The time period over which the dose is delivered Age of the exposed individual State of health of the exposed individual The time period between multiple exposures
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Somatic effect : when living organisms that have been exposed to radiation sustain biologic damage the effects of the exposure are classified as somatic effects. Late somatic effects : are effects that appear months or years after exposure to ionizing radiation, these effects may result from previous whole or partial body acute high radiation doses, or may be due to individual low level doses sustained over several years.
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Late effects that can be directly related to the dose received and occur months or years after high level radiation exposure are classified as late deterministic somatic effects ( cataract, fibrosis, organ atrophy, reduced fertility, sterility). Late effects that do not have threshold occur in an arbitrary or probabilistic manner have a severity that does not depend on dose, and occur months or years after high level radiation exposure
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Are classified as late stochastic somatic effects ( cancer, embryonic effects( birth defects)).
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Long Term Effects Malignant disease Induction of cataracts of the eye lenses Local tissue damage Life-span shortening Genetic damage Potential effects to fetus
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Bone Cancer Radium dial painters Ingested radium Radium deposited in bones Increased incidence of osteogenic sarcoma and osteoporosis Radon is very high LET radiation Alpha and Beta particles emitted
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Studies Showing Evidence Of Carcinogenesis In Humans Atomic Bomb Survivors Leukemia, Thyroid, Breast Marshall Islanders Some thyroid cancer Radium Dial Painters Bone cancer Early Radiologists Leukemia, skin cancer Multiple Chest Fluoroscopy Breast cancer Infants W/Enlarged Thymus Thyroid cancer Thorotrast Leukemia, Liver cancer In Utero Exposures Leukemia Iodine 131 Therapy ForThyroid Some leukemia Uranium Miners Lung cancer
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Conclusions About Radiation-Induced Cancer Single exposure can be enough to elevate cancer incidence several years later There is no radiounique cancer Almost all cancers are associated with radiation Breast, bone marrow, and thyroid are especially radiosensitive The most prominent radiogenic tumor is leukemia Solid tumors have a latent period of 10 years Leukemia’s latent period is thought to be about 5 - 7 years Age of irradiated individual is most important factor Percentage increase in cancer incidence/rad varies between organs and types of cancers Dose-effect curves are best assumed to be linear
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Cytogenetic damage Increased spontaneous abortions or still birth Altered sex ratios Leukemia and other neoplasms Increased infant mortality Increased congenital effects Decreased life expectancy Dominant inherited diseases Dwarfism, Polydactly, Huntington’s Chorea Recessive inherited diseases Cystic fibrosis, Tay-Sachs, hemophilia, albinism
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Skin Highly vascular organ Basal layer is constantly regenerating Most radiosensitive layer Late changes in skin sunburn, aging atrophy fibrosis change in pigmentation ulceration necrosis
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Skin Cancer Skin cancer usually begins with the development of a radiodermatitis. Significant data have been developed from several reports of skin cancer induced in radiation therapy recipients treated with orthovoltage (200 to 300 kVp) or superficial x-rays (50 to 150 kVp). Radiation-induced skin cancer follows a threshold dose-response relationship.
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Eyes Cataractogenesis Latent period may take up to 30 years About 200 rads All will develop cataracts at 1000 rads The dose-response relationship for radiation induced cataracts is nonlinear, threshold.
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If the lens dose is high enough, in excess of approximately 1000 rad (10 Gyt), cataracts develop in nearly 100% of those who are irradiated. The precise level of the threshold dose is difficult to assess. Most investigators would suggest that the threshold after an acute x-ray exposure is approximately 200 rad (2 Gyt). The threshold after fractionated exposure, such as that received in radiology, is probably in excess of 1000 rad (10 Gyt). Occupational exposures to the lens of the eye are too low to require protective lens shields for radiologic technologists. It is nearly impossible for a medical radiation worker to reach the threshold dose. Radiation administered to patients who are undergoing head and neck examination by fluoroscopy or computed tomography can be significant. In computed tomography, the lens dose can be 5 rad (50 mGyt) per slice. In this situation, however, usually no more than one or two slices intersect the lens. In either case, protective lens shields are not normally required. However, in computed tomography, it is common to modify the examination to reduce the dose to the eyes
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LIFE-SPAN SHORTENING Many experiments have been conducted with animals after both acute and chronic exposures that show that irradiated animals die young. Figure below, shows that the relationship between life span shortening and dose is apparently linear, nonthreshold. When all animal data are considered collectively, it is difficult to attempt a meaningful extrapolation to humans
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The theory of radiation hormesis suggests that very low radiation doses are beneficial. Some evidence supports the principle of radiation hormesis. Radiation hormesis suggests that low levels of radiation—less than approximately 10 rad (100 mGyt)—are good for you! Such low doses may provide a protective effect by stimulating molecular repair and immunologic response mechanisms. Nevertheless, radiation hormesis remains a theory at this time, and until it has been proved, we will continue to practice ALARA—as low as reasonably achievable.
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Genetically Significant Dose The dose equivalent to the reproductive organs that would bring about genetic injury to the population if received by the total population The estimated GSD for the US is about 20 mrem
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Radiation Effects On Fetal Development Three basic stages in fetal development Preimplantation Conception to 10 days post conception Organogenesis Cells implanted in uterine wall Cells begin differentiating into organs Fetal or growth stage Sixth week after conception Growth rather than new development
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Principle Effects Of Radiation On Embryo Or Fetus Embryonic or fetal death Malformations Growth retardation Congenital defects Cancer induction Doses of less than 10 rad No indication to terminate a pregnancy Doses between 10 and 25 rad Gray area for terminating pregnancy Doses above 25 rad Termination should be considered
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Radiation Damage In Terms Of When Irradiated Cataracts 0-6 gestation days Herniation of the brain 0 - 37 days Embryonic death 4 - 11 days Anencephaly or microcephaly 9 - 90 days Anophthalmia 16 - 32 days Cleft palate 20 - 37 days Skeletal disorders 25 - 85 days Growth disorders 54 +
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Doses To Embryo Per Procedure Based on overhead films only Average number of films/examination Barium Enema - 800 mrad Cholecystrogram - 80 mrad IVP - 800 mrad Pelvis - 200 mrad UGI - 50 mrad
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Objective of radiation protection 1- to prevent any clinically important radiation induced deterministic effect from occurring by adhering to dose limits that are below threshold level 2- to limit the risk of stochastic response to a conservative level as weighted against societal needs, values, benefits acquired, and economic consideration
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ALARA concept: national council on radiation protection and measurements (NCRP) put this principle that radiation exposure should be kept as low as reasonably achievable with consideration for economic and social factors. The continuation of good radiation protection program and practices which traditionally have been effective in keeping the average and individual exposures for monitored workers well below the limit.
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For the radiographer and the radiologist the ALARA concept should serve as a guide for the selection of technical radiographic and fluoroscopic exposure factors for all patient imaging procedure. The reason for this concept in radiologic practice is to keep radiation exposure and consequent dose to the lowest possible level.
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Responsibility for Maintaining ALARA It is the responsibility of the employer to provide the necessary resources and appropriate environment in which to execute an ALARA program. To determine that proper lowered radiation exposure are being applied, management should perform periodic exposure audits. Radiation workers with appropriate education and work experience must function with awareness of rules governing the work situations.
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EQUIVALENT DOSE AND EFFECTIVE DOSE Equivalent Dose (EqD)– A quantity that attempts to take into account the variation in biologic harm that is produced by different types of radiation. Equivalent Dose (Eqd) enables the calculation of the Effective Dose (EfD) Effective Dose (EfD) – A quantity that attempts to summarize the overall potential for biologic damage to a human due to exposure to ionizing radiation Effective dose takes into account organ weighting factors and represents the whole body dose that would give an equivalent biologic response. EfD and EqD are both expressed in sieverts (Sv), used by the International System of Units (SI), or rem, which adopts the traditional measuring system
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NCRP Recommendations Annual occupational effective dose limits should not exceed 50mSv (5 rem) for whole body dose Cumulative effective dose limits refers to lifetime effective dose age in years multiplied by 10mSv for whole body dose Collective effective dose in description with population or group exposure using an averaging the effective dose
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NCRP Recommendations (cont) Limits of nonoccupationally exposed individuals are set at 1mSv annually for medical exposure and 5mSv for natural exposure Limits for pregnant female radiation workers are 0.5mSv per month and entire pregnancy dose limit of 5mSv Limits for education and training purpose for individuals under 18years of age is 1mSv annually Negligible individual dose is 0.01mSv Limits for tissue and organs are set differently depending on sensitivity of the organ or tissue. Lens of the eye 150mSv(15rem) Localized skin 500mSv(50rem)
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Occupational Dose Limits Action limits are set by health care facilities to ensure radiographers do not reach a dose limit that can be harmful Effective dose limits for radiation workers are 20mSv (2 rem) annually Special limits are set for highly sensitive areas of the body such as the lens of the eye and localized areas of the skin, hands, and feet to prevent nonstochastic effects