[Cat 1] Demonstrate knowledge of the function and interpret the values of specific dose measurement methods used for radiological procedures. Explain the implications of measured dose parameters, both in terms of overall risk and the risk to specific tissues and organs. Be aware of the relative radiation doses from different radiological procedures, and how they compare to natural background radiation doses.
[Cat 1] Examine the mechanism of how radiation interacts with tissue to cause biological damage, and the parameters used to quantify this damage.
[Cat 1] Demonstrate knowledge of the hereditary and genetic implications of radiation exposure.
[Cat 1] Demonstrate knowledge of the stochastic effects of radiation and the factors which influence it. Assess the approximate risk from a radiation exposure and explain how to convey this risk in a simple manner to patients and other staff.
[Cat 1] Demonstrate knowledge of the deterministic effects of radiation and the factors which influence it.
[Cat 1] Identify the procedures that may deliver large doses of radiation.
[Cat 1] Demonstrate knowledge of the effects of radiation on the developing embryo and foetus at various stages of gestation. To be aware of which procedures may deliver large doses to the embryo/foetus, and the actions to be taken in considering dose to a pregnant patient, prospectively or retrospectively.
[Cat 2] Explain the importance and application of the dose descriptors:
• Dose-area product (DAP)
• CT Dose Index (CTDI)
• Dose length product (DLP)
1. Introduction
Recall that photoelectric absoprtion of a single x-ray or gamma-ray photon can result in the production of over 1,000 low-energy secondary electrons known as delta rays. These delta rays can cause additional excitation or ionisation events in the tissue, ultimately depositing energy along the track.
1.1. Terminology
Excitation occurs when a photon transfers sufficient energy to promote an orbital electron to a higher energy level within the atom.
Ionisation occurs the electron receives enough energy to be ejected completely from the atom with kinetic energy, forming an ion pair.
Somatic effects affects the exposed (irradiated) individual.
Hereditary effects affects subsequent generations of the exposed individual, arising from irradiation of the gonads
2. Type of Interactions
The biologic effects of radiation result principally from damage to deoxyribonucleic acid (DNA), the double-helical macromolecule containing the genetic code for the development, functioning, growth and reproduction of organisms. DNA can be damaged via two different interactions of radiation with tissue, classified as either direct or indirect.
2.1. Direct interactions
When energy from photons or charged particles is absorbed by biological material, there is a possibility for direct interaction with the critical target in the cells (such as DNA), causing ionisation or excitation which leads to observable biological effects.
This process is the dominant process in radiation types with high linear energy transfer (such as neutrons or α particles.
2.2. Indirect interactions
Indirect effects occur when irradiation of tissue creates highly energetic and unstable chemically reactive species, such as free radicals, which then interact with macromolecules causing damage. Free radicals are uncharged molecules containing a single unpaired orbital electron and can be created from the radiolysis (or decomposition) of water. As water is the predominant molecule in the body, the principal effect of radiation on humans is through indirect interaction.
3. DNA Damage
3.1 Types of DNA lesions
The number and type of DNA lesions per cell detected immediately following 1 Gy of x-ray:
| Type of DNA Lesion | Incidence | Notes |
| Base damage | > 2,000 | Base alteration or abasic site |
|
Single-strand breaks (point mutation) |
1,000 |
More likely with low LET radiation. Can be enzymatically repaired |
| Double-strand breaks | 40 |
More likely with high LET radiation. Widely space lesions potentially reparable Closely spaced lesions unlikely to be repaired |
| DNA-DNA crosslinks | 30 |
The interaction of two double-strand breaks can result in cell killing, carcinogenesis or mutation and may occur by both direct ionisation or free radical.
DNA double-strand breaks constitute the most dangerous type of DNA damage induced by ionising radiation.
Types of Effects
Deterministic
Deterministic effects result from radiation-induced cell loss or damage in a non-random pattern of occurrence, where severity increases with doses.
- Importantly, these effects only occur above a certain threshold dose.
- There is a large number of cells involved.
- Deterministic effects are rare as high skin and organ doses are needed
Absorbed dose the is more relevant quantity for deterministic effects, given they are generally skin effects.
| Effect | Threshold dose (mGy) | Time to Manifest |
| Early transient erythema | 2,000 | 2 – 24 hours |
| Main erythema | 6,000 | 10 days |
| Epilation |
Reversible: 3,000 – 5,000 Irreversible: 20,000 |
Temporary epilation: 3 weeks |
| Necrosis | 18,000 | 10 weeks |
| Observable reactions in eye lens | 500 | Several years |
- Skin effects
- 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.
- Epilation
- Tissue necrosis
- Cataractogenesis
- Radiation sickness
- Depression of blood cell formation 0.5Sv whole body
- Chronic occupation dose > 0.4 Sv/yr
e.g. opacification of lens 2 – 10 g, skin injuries,
permanent infertility,
- males 3.5-6 Gy
- females 2.5-6 Gy
- Temporary sterility
- males 0.15 Gy
females 0.6 Gy epilation
threshold, severity of effect increases with dose
large number of cells involved
Stochastic
Due to cell modification (DNA damage) rather than cell death. It is long term (late effects)
Linear no-threshold model: Above the prevalent background dose, an increment in dose results in a proportional increment in the proability of incurring stochastic effect. Cancer induction can occur at any dose
Kinear Quadratic Response
Low dose = linear, high dose = quadratic component. Leukaemic may follow this response.
Latency period: time between exposure and onset of effects.
The probability, not severity, of an effect occurring increases with dose
Effective dose is the more relevant quantity for stochastic effects as it represents whole body dose which takes into account radiation weight factors and tissue weighting factors
The genetically significant dose is an index of the presumed genetic impact of radiation-induced mutation in germ cells in an exposed population. The sensitivity of a population to radiation-induced genetic damage can be measured by the doubling dose.
The doubling dose is the radiation dose (i.e. absorbed dose to the gonads) required per generation to double the spontaneous mutation rate.
Stochastic
no threshold, probability of effect increases with dose, occurs with single cell
cancer, gentic effects
somatic & hereditary
Somatic effects affect the exposed individual
Hereditary effects affects subsequent generations. Damage arises from irradiation of the gonads
Lose doses of radiation may cause damage to the germinal cells in the gonads which may lead to DNA damage, conseqeuntly to gene mutations in the exposed cells
These mutations may lead to an increase in hereditary disease in the children of exposed parents.
Genetically significant dose: the fraction of the radiation exposure to the population is absorbed in the gonads of persons who subsequently produce children
epidemiologically attributable in large populations
Antenatal
somatic and hereditary expressed in the foetus, in the live born or descendants
Total lifetime risk of radiation=induced fatal cancer for general population
5% per Sv or 1 in 20,000 per mSv
ICRP Framework
Principles of Radiation Protection
Justification
- The benefit must be greater than the risk
Optimisation
- Keep doses As Low as Reasonably Achievable (ALARA) principle)
Limitation
- Dose limits must not be exceeded (not applicable to medical exposures/patient examinations)
Diagnostic Reference Levels
- Choose commonly performed, well-defined exmination e.g. CT non-con brain
- Ask all hospitals to collect data for this exams for 20 patients per CT Scanner
- Take the median value for each set of data (i.e. 50th percentile)
- Take the 75th percentile of the median values and this is set as national DRL
This means that 75% of hospital are able to achieve an average below this median value.
Hospitals need to collect data for 20 patients per examination per C scanner. Calculate the median dose and ocmpare this to the natrional DRL
The national DRL is not a limit. Some individual patient doses will exceed the DRL (e.g. obese patients, complex or multi-phase scans).
CTDIvol
- CTDI is the average dose per slice or rotation (mGy)
- The scanner displays CTDIvol: the weighted CTDI corrected by pitch
DLP
- DLP = CTDIvol x scan length (mGyxcm)
DAP/KAP
- DAP meter is a transmission ionisiation chamber (radiotransparent) which measures the product of air kerma and field size (Gyxcm2)
- Positioned over the x-ray tube and collimator assembly
CAK
- Cumulative air kerma
- An indication of total entrance skin dose
- Can be used to determine whether a patient is likely to experience deterministic effects e.g. erythema
Dose limits
Occupational: 20mSv per year, avera,ge over defined period of 5 years
- 50 mSv permisslbe in a single year, but total over 5 years must be <100mSv
Public
1mSv in a year