University Of Cape Town

Transport And Shielding Of Ionising Radiation

Radiation Protection Assignment One Report
2013
Courage Mahuvava (MHVCOU001)
April 5, 2013

Question 1 : Radiation dose

Part (a)
Describe the successive refinement of radiation dose from absorbed dose to the
protection quantities equivalent dose and effective dose.

The effective dose (sievert), accurately quantifies the risk of radiation-related cancer and when
dose rates are low. At higher dose rates, and when the health effect is deterministic tissue
reactions, the absorbed dose(gray) is used. Let

DT,R = Average absorbed dose deposited in organ/tissue T by ionising radiation of type R; It

quantifies the average amount of energy imparted to the medium per unit mass and is used for
high dose rates. This quantity is given by:
d
DT,R =
dm
where d is the energy and dm is the mass.
wR = Radiation weighting factor for ionising radiation type R;
wT = Tissue weighting factor;
HT = Average equivalent dose in organ or tissue T

In order to determine the radiation level and possible deterministic and stochastic effects, we
introduce the protection quantities; equivalent dose and effective dose to describe the detriment
to the body due to the radiation. The protection quantity equivalent dose in an organ or
tissue, HT , is then defined as :
X
HT = wR DT,R (1)
Where the sum is performed over all types R of radiations involved. Usually, more than one
tissue T is exposed, and thus necessary to use tissue weighting factors. The application of both
the radiation and the tissue weighting factors to the tissue absorbed doses leads to the effective
dose. The effective dose E is defined as

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 " #
X X X
E= [wT HT ] Or E= wT [wR DT,R ] (2)
T T R

Therefore from the absorbed dose, we can calculate the equivalent dose and from the equivalent
dose, we can calculate the effective dose.

Explain which weighting factors are introduced.

In order to improve correlation between dose quantities applied in radiation protection and the
effects considered, two types of weighting factors have been introduced, these are :
1. The radiation weighting factor, wR

2. The tissue weghting factor, wT

These factors are needed for calculation of the effective dose. The radiation weighting factor
wr quantifies the effect of the microdeposition of radiation energy in tissue, on its carcinogenic
potential, and is intimately related to the structure of DNA, and the fact that carcinogenesis is
related to unrepaired or misrepaired radiation insult to DNA. The tissue weighting factor wT
quantifies the empirically determined radiosensitivities of tissues, based on clinical observation
and results from radiobiology and radio-epidemiology. The values of the tissue weighting fac-
tors are a quantification of the susceptibilities of different tissues to the development of primary
radiation-related cancers.

On what are the numerical values of these weighting factors based?

The values of the radiation weighting factors wR for radiation type R, rely on the fact that life
is organised in cells, that cells contain DNA, that DNA insult by ionising radiation is carcino-
genic, that the DNA molecule has two strands, and that the carcinogenic potential of ionising
radiation is related to the relationship between the mean distance between ionisation events
and the distance between the strands in the DNA molecule, because double-strand breaks in
DNA are far less repairable and more carcinogenic than single-strand breaks in DNA.

Tissue weighting factors wT are based on cancer incidence data, and takes account of the
lethality rate, the years of life lost and of a weighted contribution from the non-fatal cancers
and from hereditary disorders. The values of wT are normalised to add up to 1, that is, values
have only relative meanings and no absolute meaning.

The concept LET and its importance

The linear energy transfer (LET, i.e. the energy transferred per unit path length) is a measure
of the intensity with which the particle interacts with matter, and determines the ionisation
density, i.e. the number of ion pairs produced per unit path length.
Radiations that cause dense ionisation along their track (such as neutrons) are called high-
linear energy-transfer (high-LET) radiation, a physical parameter to describe average energy
released per unit length of the track. Low-LET radiations produce ionisations only sparsely
along their track and hence, almost homogeneously within a cell. Thus, high-LET radiations
are more destructive to biological material than low-LET radiations such as ionising photons
because at the same dose, the low-LET radiations induce the same number of radicals more
sparsely within a cell, whereas the high-LET radiations such as neutrons and alpha particles
transfer most of their energy to a small region of the cell. The localized DNA damage caused

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by dense ionisations from high-LET radiations is more difficult to repair than the diffuse DNA
damage caused by the sparse ionisations from low-LET radiations.

Examples of high and low LET ionising Radiation

Photons and electrons are low-LET radiation types. Protons interact directly with atomic
electrons so proton therapy is classified as low-LET radiotherapy. Neutrons and alpha particles
are examples of high-LET radiation.

Describe why effective dose is not a pure physics quantity.

The effective dose is a dosimetric protection quantity that is not directly measurable with
instruments and its SI unit, the sievert, is not a physics unit either. The definition for E
weighs the physics quantity DT,R by weighting factors derived from radiobiology and radio-
epidemiology. The effective dose is a protection quantity, a convolution of physics, radiobiology
and radioepidemiology. For this reason, effective dose can in no way be classified as a physics
quantity.

Part (b)
The protection quantity effective dose and its associated weighting factors wR and wT has been
designed to optimally quantify the risk of radiation-related cancer

Part (c)
A radiation accident occurred, and exposures are in the range where tissue reac-
tions are the dominant concern. Will the quantity effective dose be a good measure
of harm? Explain your answer.

No. The effective dose should only be used when one focuses on the risk of radiation-related
cancer and when dose rates are low. An accident would usually imply high dose rates, that is,
the radiation was applied over a short time period. Since at higher dose rates, and when the
health effect in question is deterministic tissue reactions, the quantity absorbed dose and its SI
unit, the gray, would be the correct quantity to work with.

Question 2 : External dosimetry & uptake dosimetry

Part (a)
Set forth the performance characteristics of an ideal personal dosimeter.

Personal dosimeters are used to measure effective doses (and, in certain cases, also the equiva-
lent doses to particular parts of the body, e.g. the hand) received by persons exposed to ionising
radiation, and should therefore possess the following performance characteristics:
• Energy response-a personal dosimeter must have a near-flat energy response over a wide
energy range. A graph of relative response vs. energy should be as flat as possible over the
energy range of interest.
• Dose range-A typical personal dosimeter should be able to measure doses over the dose

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range 10 µSv 10 Sv in a 4-week wearing period.(i.e should be able to accurately measure low
doses, because any dose is detrimental, and high doses in order to be able to yield vital dose
information in the event of radiation accidents.)
• Angular dependence-The reading of the dosimeter should not be excessively dependent on
the angle of incidence of the ionising radiation.
• Fading-The dosimeter should retain its reading without fading for an extended period of
time, e.g. for up to several months.
• Resistance against heat & humidity-Extreme temperatures and humidity should not
affect the reading excessively.
• Re-readibility- If the need arises, a dosimeter should be re-readable. This is a problem
with TLDs-the process of determining the dose destroys the dose-record. OSL dosimeters can
be reread several times.
• Accuracy-Only if the dosimeter is adequate in all the above characteristics, the reading will
be accurate and trustworthy.

Part (b)
Describe the method of operation of OSL dosimeters as well as TLDs.

Optically Stimulated Luminescence (OSL) personal dosimeters operate as follows. A special

phosphoric detector material is used-usually aluminium oxide, which has the property that
ionising radiation excites electrons from the valence band, and these electrons end up in traps.
After the wearing period, during which the OSL phosphor has accumulated trapped electrons
proportional to the absorbed dose of ionising radiation, the OSL phosphor is ”interrogated” by
irradiating it with laser light of a specific frequency. In response to the interrogative irradiation,
the OSL phosphor responds by emitting light of a different wavelength. It is caused by the
trapped electrons being excited by the stimulating optical irradiation, and then releasing their
excitation energy as the luminescence signal. The amount of emitted light is proportional to
the absorbed dose. The stimulated electrons return to the electron traps-dose information is
not lost by the reading process; OSL dosimeter can be re-read as the need arises. The OSL
radiation detector inside the Landauer LUXEL dosimeter, is a thin strip of specially formulated
aluminium oxide (Al2 O3 ) crystalline material. The aluminium oxide is doped with a carbon
impurity to produce stable electron traps in the energy gap in the crystalline structure. During
analysis in the laboratory, the Al2 O3 strip is stimulated with selected frequencies of laser light
(usually green), causing it to luminesce (blue light) in proportion to the absorbed dose. Hence
the name: Optically Stimulated Luminescence (OSL) emission dosimeter. Re-readability:
the Al2 O3 detector can be re-stimulated numerous times to confirm the accuracy of a radiation
dose measurement. A full re-analysis is automatically performed for every measurement yield-
ing a dose above 5 mSv.

Thermoluminescent dosimeters (TLDs) operate on the following principle: Some crystalline

materials possess a phosphoric quality known as thermoluminescence- they absorb radiation
energy during exposure and, upon being heated to a temperature of about 200 degrees celcius,
release this stored energy as visible light (i.e. they luminesce). The total amount of light that
is emitted is proportional to the dose that was absorbed during the wearing period. Ionising
radiation transfers energy to electrons of the phosphor atoms. The energised electrons are
detached from the atoms; after a period of motion in the crystal, many of these electrons be-

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come trapped at luminescence centres, usually an impurity atom added to the phosphorescent
crystal during manufacture. The impurities are carefully chosen to produce relatively stable
electron traps of the desired energy. When the phosphor is heated, the thermal energy enable
the trapped electrons to escape from the traps, i.e. forbidden energy transitions become pos-
sible. The electrons return to their ground state, i.e. they become re-attached to the atoms
of the phosphorescent material. In dropping from a higher to a lower energy state, the energy
difference is emitted as a photon; this photon is in the visible light region. When the electron is
bound to a phosphor atom, it is in the valence band. When it is energised by ionising radiation,
it enters the conduction band. The energy gap between the valence band and the conduction
band, is called the forbidden energy gap. The trapping centres are located inside the forbid-
den energy gap. The absorbed dose deposited in the phosphorescent material, determines the
number of electrons that are trapped. When heated, all the traps release their electrons, so
that the integral intensity of the light flash is directly proportional to the absorbed dose. TLDs
can be designed and calibrated to measure ionising photons or neutron doses. The ability of
TLDs to measure neutron doses accurately, is severely limited by a energy-response curve that
deviates very far from the desired value of 1, especially in the thermal neutron energy range.

Question 3 : Scientific fundamentals of radiation protection

Part (a)
Discuss the nature, associated commandment(s) and practical implementation of
the following fundamental principles of radiation protection.

Source Barrier.
The source barrier principle has as commandment, ”keep it in”. Examples of the implemen-
tation of the source barrier principle to limit intakes and ontakes (skin contamination) of
radioactive material, include:

1. Sealing potentially dangerous sources in multiple containers.

2. Performing radiation work in hotcells, glove-boxes and fume hoods.

3. Effluent treatment, e.g. water and air filtration.

4. Putting contaminated items in sealed plastic bags.

5. Covering contaminated surfaces.

Personal Barrier.
The personal barrier principle is: ”keep it out”. People are isolated from the radiation or
radioactive material by using a personal barrier. Protecting the individual from external radia-
tion fields is done through the use of personal protective equipment (PPE). Examples include:
(i) Lead aprons.
(ii)Wearing thick gloves when working with electron-emitting nuclides, e.g beta particle sources.
Protecting the individual against intakes and ontakes of radioactive material involves the use
of PPE in the form of, e.g. wearing personal protective clothing such as overalls, overshoes,
breathers that offer respiratory protection, gloves, etc. The personal barrier principle is how-
ever a method of last resort. In a well designed, properly shielded well ventilated and regularly
cleaned work-area, it is unnecessary to rely heavily on the personal barrier principle of radiation

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protection.

Effect mitigation.
Effect mitigation seeks to reduce the biological effect of a given dose from external radiation,
or a given intake of a radionuclide. There are several agents that can mitigate the effects of a
given dose or a given intake of a radionuclide. Anti-oxidants or free-radical scavengers such as
Vitamin E, Superoxide dismutase, Carotenoids, Vitamin A & C, Selenium, Zn, Mn, Cu, green
tea, Pycnogenol, Red wine, grape seed extract, etc are agents that reduce oxidative damage,
and are excellent effect-mitigators as well as excellent protectors against cancer, heart disease
and strokes. Any action that will diminish one’s ”background cancer risk” will also diminish
the carcinogenic potential of a given dose of ionising radiation.

Optimal technology.
One should choose the best available technology (BAT). Choosing the optimal technology may
mean using an ionising radiation technology that produces a lower dose, or modifying an ex-
isting technology to produce a lower dose and in some cases, using a technology that does not
involve ionising radiation at all. An example of using methods involving lower radiation levels,
is switching from the use of 131 I to 123 I with half-lives 8.04 days and 13h respectively. Using
an optimal technology will maximise the risk-benefit-cost figure-of merit.

Limitation of other exposures.

This principle involves limiting exposures to other agents that may work in concert with ionis-
ing radiation, such as genotoxic agents or those that cause initiation, promotion or progression
of tumours. Don’t compound risks. Radiation workers implement this principle by avoiding
smoking tobacco which contains a relatively high concentration of radionuclides.

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The following table summarises the foundational principles and commandments of
practical radiation protection.

Principle Commandment

Maximise absorption of radiation in a shield; Minimise release

Source barrier
(contain & confine radioactive material).

Minimise entry into the body of radiation and radioactive

Personal barrier
materials.
Limit the damage by optimising exposures over time and
Effect mitigation
among persons; scavenge free radicals; induce repair

Use a technology that results in lower dose; Modify existing

Optimal technology
technology to produce lower dose.

Minimise exposures to other carcinogens

Limitation of other exposure
( e.g tobbacco smoke).

Question 4 : Health risk of ionising radiation

Part (a)
What is cancer?
Cancer is an over-proliferation of non-functional, parasitic cells in a body organ.

What are the main differences between a healthy cell and a cancer cell?

Normal cells in the body are:

(1) Differentiated & specialised;
(2) Perform a useful function;
(3) Divide only when necessary;
(4) Remain anchored where they should be;
but cancer cells lose all the above properties of normal, healthy cells. They become functionless
and parasitic, divide continually without restraint, and can spread metastatically throughout
the body.

How does cancer begin & develop in the human body?

Cancer may have a monoclonal origin, i.e. that it may result from damage to the control
system of a single cell, causing it to lose its differentiation and specialisation, and escape re-
straints on mitotic proliferation and anchorage dependence. The defect is transmitted to the
daughter cells by mitotic cloning so that the population of abnormal, non-functional cells builds
up to the detriment of the normal cells in the organ. The estimation of the increased risk of
cancer is complicated by the long and variable latent period, from about 5 to 30 years or more,
between exposure and appearance of the cancer, and by the fact that radiation-related cancers
are not normally distinguishable from those which arise spontaneously. The course of cancer is
as follows :

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• A mistake happens in a cell. Sooner or later, exposure to carcinogens damages one of the
genes in the DNA of a cell. In most cases, this does not lead to cancer.
• The genetic mistakes add up. It becomes harder and harder for the cells to maintain normal
growth, as genes that should be on get turned off, and genes that should be off, are turned on.
These genes are:
(i) DNA repair genes manufacture proteins that correct errors that sometimes occur whenever
a cell copies its DNA. If DNA repair genes can not do their job, genetic mistakes start to
accumulate.
(ii) Tumour suppressor genes-these genes restrain cell growth and cell division. Their absence
or inactivation takes the brakes off cell multiplication.
(iii) Growth genes-if these genes, which regulate normal cell growth and cell division become
stuck in the on position, growth continues unabated.
• The cells turn cancerous. Free of normal restraints on proliferation, the now malignant cells
break all the rules. They divide uncontrollably, become less attached to their neighbours and
invade the space occupied by normal cells.
• The tumour’s appetite grows. In a process called angiogenesis, malignant cells secrete chem-
icals that attract and promote the formation of new blood vessels. With a steady supply of
nutrients, the tumour can grow without limits.
• The cancer spreads. Tumour cells break off and, in a process termed metastasis, migrate
through the blood and lymphatic systems. Eventually, the runaway cells colonise other parts
of the body and give rise to distant or satellite tumours.

Define the concept ”carcinogen” and name a few carcinogens.

Carcinogens are agents which damage genes involved in controlling cell proliferation and migra-
tion. Carcinogenesis is a multistaged process that transforms a normal cell into a cancer cell.
In other words, in a cell, any single event by itself is not sufficient to turn a normal cell into
a cancer cell. Only when the correct number, combination, and types of aberrant alterations
have accumulated in one cell will a cancer cell develop.
Examples of carcinogens are:
(i) tobacco smoke;
(ii) radon gas;
(iii) ionising radiation;
(iv) persistent organic pollutants (POPS) such as organochlorine pesticides.
(v) Free radicals

How does cancer spread?

Cancerous tissue continually enlarges as a result of the ability of cancer cells to proliferate
at a high rate, and indefinitely. The tumour cells invade surrounding normal tissue and may
spread throughout the body when cancer cells break away from the primary tumour, voyaging
through the circulatory system and establish colonies at distant sites-the process of metasta-
sis. Cancer cells are rogues that trespass aggressively into other tissues. Whereas normal cells
stay where they are supposed to be, cancer cells detach from their original location, invade
blood or lymphatic vessels, travel in the circulatory system to a distant site, and establish a
new, malignant cellular colony. As a result of oncogenes, i.e. mutated proto-oncogenes, cancer
cells are anchorage-independent. Cancer cells also release enzymes that dissolve extracellular
membranes. This allows them to invade a blood or lymphatic vessel and be carried to a new site.

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Why is cancer so deadly and difficult to cure?

One reason why it is so difficult to cure cancer, is that tumour cells differ only minimally
from healthy ones. Thus, normal friend and malignant foe are woven of very similar fabric, and
any fire directed against the enemy may do almost as much harm to normal tissue as to the
intended target. New cancer therapies will have to home in on the few and subtle genetic and
molecular differences between cancerous and normal cells.

A malignant cell’s ability to escape apoptosis (the programmed cellular suicide response to
damage) may endanger patients not only by contributing to the expansion of a tumour but also
by making the resulting tumours resistant to therapy. Radiation and many chemotherapeu-
tic treatments often harm DNA to a relatively minor extent. Nevertheless, the affected cells
perceive that the inflicted damage can not be repaired easily and they actively kill themselves.
This discovery implies that cancer cells, being able to evade apoptosis, will be less responsive
to treatment. By the same token, it suggests that therapies which restore a cell’s capacity for
suicide could combat cancer by improving the effectiveness of existing radiation and chemother-
apeutic treatment strategies.

Anoxic tumours and anoxic parts of tumours are resistant to radiotherapy. Well oxygenated
tumour cells in the periphery of a tumour are significantly more sensitive to ionising radiation
than cells located centrally in a necrotic tumourthese cells are anoxic or hypoxic, are more
resistant to radiation and can survive higher radiation doses. The ability of oxygen to enhance
radiation damage, is called the oxygen effect.

Describe future cancer therapy prospects

• Antigrowth drugs aim to block the biological signals that promote cancer-cell growth.
• Drugs are being developed to activate pathways of cell destruction, so that cancer cells will
commit cellular suicide. Gene therapy re-introduces functional protein p53 into cancer cells;
combined with radiotherapy
• Immune booster: Cancer cells somehow evade the immune system. New vaccines are devel-
oped to goad white blood cells into attacking cancer cells.
• Microradiation: Treatments are developed to combine the specificity of a monoclonal anti-
body with the lethality of a radionuclide.
• Anti-angiogenesis. Use drugs that attack the tumour’s blood supply in an effort to choke off
the flow of nutrients to the tumour.
• Surgery- early detection leads to less invasive operations and more cures.
• Chemotherapy-though less toxic than before, these poisons still kill both healthy and cancer-
ous cells.
• Radiation-even though radiation beams are localised, they still kill and damage lots of healthy
cells. New directions in radiotherapy include ”chemical brachytherapy”-a radionuclide is bound
to a nutrient that is preferentially absorbed by cancer cells.

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Part (b)
Describe the generic nature of radio-epidemiological studies.
The aim of radio-epidemiological studies is to determine-qualitatively and quantitatively-the
health risks posed by ionising radiation. The typical methodology of a radio-epidemiological
study is:
• Select a cohort of persons exposed to substantially above-background doses of ionising radi-
ation. The dose received by each person must be known with reasonable accuracy.
• Compare the long-term health of this cohort and their children, with that of a carefully se-
lected control group of individuals only exposed to natural background radiation levels.
• Determine how many excess, i.e. more than expected, negative health endpoints are observed
in the exposed cohort. Express this as a dose-effect relationship and radiation risk factors, also
called nominal probability coefficients.
The exposure rate effect that is at stake when comparing risks of populations exposed to a
very short exposure with those exposed to the same total level of exposure, but protracted over
several years, is one of the major questions presently under study.

Set forth the PYR measure for the comparative statistical power of radioepidemi-
ological studies.
The ability of radio-epidemiological studies to yield statistically reliable information on the
health risk of ionising radiation, may be compared by calculating the following product :

PYR = Persons at risk × Years of follow up × Mean Radiation Dose received (Sv) (3)

For the Radiation Effects Research Foundation (RERF) Japanese atomic bomb survivor Life-
span study (LSS),

PYR ≈ 500000 (4)

in the year 2000. The PYR value for the RERF LSS is at least 5 to 10 times larger than the
PYR values for most other radio-epidemiological studies. This is why the RERF LSS study
provides the most authoritative quantification of the health detriment of ionising radiation, of
all radio-epidemiological studies-it has the highest statistical power. To evaluate the statistical
power of a radio-epidemiological study, it is useful to express its PYR value as a percentage of
the PYR of the RERF study.

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How does radiation-related cancer risk from exposure to ionising radiation depend
on age at exposure?.

Relative Risk for radiation-related solid-cancer mortality, is significantly higher for exposures
at younger ages; Radiation related cancer mortality risk is lowest for exposure at advanced
ages, as shown below.

Figure 1: Estimated attributable lifetime risk from a single small dose of radiation as a function
of age at exposure. Note the dramatic decrease in radiosensitivity with age.

Part (c)
During the 50 year follow-up period, 1 October 1950-31 December 2000, there have been an
estimated 572 radiation-related cancer deaths in the RERF Life Span Study (LSS) cohort of
86,611 nuclear bomb survivors; these were: 479 radiation-related deaths as a result of solid
cancers, and 93 radiation related leukaemia (blood cancer) deaths.

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Part (d)
Describe the health effects of ionising radiation on persons exposed in-utero. State
on the time periods during which 4 risk categories will dominate, and give values
for dose thresholds above which syndromes are observed, where applicable

Radiation risks are most significant during organo-genesis and in the early foetal period, some-
what less in the 2nd trimester, and least in the 3rd trimester. The principal health risks of
ionising radiation to an unborn child, are:
• Pre-natal death. Risk peaks in the first 2 weeks of pregnancy;
• Neuro-cognitive defects: brain damage, lowering of intelligence (dose threshold 100 mSv),
mental retardation (dose threshold 500 mSv) and psychiatric disorders. Risk peaks from weeks
8 to 15, and remains substantial until the end of week 25;
• Congenital disorders are neo-natal diseases and abnormalities that exist at birth and often
before birth; of these congenital diseases, those characterized by structural deformities are
termed malformations and abnormalities. Risk for malformations and abnormalities peaks for
radiation exposure from weeks 2-6(dose threshold 100 mSv);
• Increased cancer risk-as high as 50% excess relative risk per 10 mGy;
• Growth retardation.

These radiation risks only become substantial at doses significantly higher than the legal dose
limit of 1 mSv to the conceptus for the known part of pregnancy. At doses below the legal limit
of 1 mSv for the known duration of the pregnancy, risk is low or practically absent.

Describe practical radiation protection measures that should be followed and en-
forced when radiation workers become pregnant.

• Any pregnant female radiation worker should announce the fact that she is pregnant to
her supervisor without delay.
• At a meeting between the pregnant woman, her supervisor and a member of the Radiation
Safety Division, the pregnant radiation worker must choose whether she still desires to perform
radiation work during the remainder of the pregnancy.
• The pregnant woman’s professional activities should not be unduly disrupted.
• The special dose limits that apply to pregnancy may not be exceeded-the fetus should receive
less than 1 mSv from the detection of pregnancy until birth, and radionuclide intake restrictions
are 20 times more stringent than for non-pregnant radiation workers.
• Pregnant radiation workers may work in a radiation environment as long as there is reason-
able assurance that the foetal dose can be kept below 1 mGy during the pregnancy-1 mGy is
approximately the dose that all persons receive annually from penetrating natural background
radiation.
• In addition to her dosimeter of legal record, the pregnant radiation worker should be issued
with an alarming Electronic Personal Dosimeter (EPD) and should wear it at waist level, so
that she always has an audible idea of the intensity of the ambient radiation field.
• Should the pregnant worker choose to continue performing radiation work, she may only
perform specific types of radiation work, where there is virtually no risk of accidental overex-
posure. The types of radiation work that she may perform should accordingly be characterised
by low exposure risks and low, predictable dose rates. Dose rate constraints may be set, e.g. a
constraint that pregnant radiation workers may not work where dose rates are above 10 Sv per
hour.

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• Pregnant worker’s EPDs should be set to alarm at significantly lower dose and dose rate levels
compared to the EPDs issued to non-pregnant radiation workers.
• The pregnant radiation worker may not receive an effective dose exceeding 0.5 mSv per month.
If there is any possibility of contamination, the pregnant radiation worker should monitor her
hands and feet every time she leaves surface contamination areas. Any unusually high readings
should be reported to the Office for Radiation Protection without delay.

Part (e)
What tissue reaction symptoms & syndromes will be observed for exposures of the whole body
to penetrating ionising radiation, for acute doses of :

(i) 250 mSv

Excellent prognosis, no signs of acute radiation syndromes.

(ii) 2000 mSv

Good prognosis,moderate leukopenia, Hematologic syndrome(also bone marrow syndrome or
hematopoietic syndrome). At ionising radiation doses below about 6000 mSv, the hematolog-
ical syndrome is the main cause of suffering and death. The first stage of the hematologic
syndrome involves the prodromal NVD syndrome-nausea, vomiting and diarrhea. Then follows
the period of latency, whose duration depends on dose magnitude- during this period the only
sign of the disease is the declining numbers of red and white blood cells and platelets in the
circulating blood. The next phase is termed manifest illness-Symptoms include generalised
malaise, anaemia, haemorrhage and infections. Patients will show signs or increased evidence
of hemorrhagic disease and increased susceptibility to infection. Patients lose weight, may lose
hair and ultimately die from overwhelming infection and haemorrhage unless sufficient regen-
eration of the marrow occurs. In summary:
• Bone Marrow Syndrome (BMS);
• Circulating white blood cells killed;
• Stem cells in bone marrow killed;
• Blood cell & platelet forming process impaired;
• Immune system suppressed;
• Slow recovery if patient survives 1st 60 days;
• Long-term health prospects markedly affected.

(iii) 8000 mSv

Weak prognosis, haemorrhage, infection, fever, epilation.
• Gastro-Intestinal (GI) Syndrome dominates the BMS;
• Stem cells in small intestines - crypt cells - are depleted;
• Intestinal villi disintegrate; blood and digested food mingle;
• massive dehydration, bleeding & systemic septic shock results;
• Not survivable;
• Death usually results within 2 weeks.

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For dose range: 6 Gy - 40 Gy: regardless of the dose involved, the gastrointestinal syndrome
has a very serious prognosis because it is almost always accompanied by non-recoverable bone-
marrow. After the prodromal phase, which may last up to 1 day, follows a latent phase lasting
3 to 5 days. A second wave of NVD inaugurates the manifest illness stage. The onset of the
clinical phase of the gastrointestinal syndrome occurs earlier than that of the hematopoietic
syndrome. After a short latent period of a few days to a week or so, the characteristic severe
fluid losses, haemorrhage and diarrhea begin. The pathologic basis for this syndrome is an
early physiologic derangement of the epithelial cells followed by a combination of severe loss
of intestinal mucosa and injury to the fine vasculature of the submucosa. The lining of the
gastro-intestinal tract is depopulated and finally removed, which results in dehydration and
infection. Medical intervention can not prevent the progression of the syndrome, and death
will typically result in less than a week.

(iv) 20000 mSv

Hopeless prognosis.
• Gastro-Intestinal (GI) Syndrome dominates the BMS;
• Stem cells in small intestines crypt cells are depleted;
• Intestinal villi disintegrate; blood and digested food mingle;
• massive dehydration, bleeding & systemic septic shock results;
• Not survivable;
• Death usually results within 2 weeks.
• If (Dose > 20 000 mSv), cerebro-vascular or Central Nervous System (CNS) syndrome dom-
inates both the BMS and GI syndromes; death will usually within 2 days.

Long-term health effects & concerns in survivors

Late or delayed effects of radiation occur following a wide range of doses and dose rates. De-
layed effects may appear months to years after irradiation and include a wide variety of effects
involving almost all tissues or organs. Some of the possible delayed consequences of radiation
injury are life shortening, carcinogenesis, cataract formation, chronic radiodermatitis, decreased
fertility, and genetic mutations.

Part (f )
(i) Briefly present the modern classification of tissue radiosensitivities, and use it
to answer the following questions:

VIM (Vegetative Inter-Mitotic) cells are most radiosensitive. These cells divide regularly.
Examples include primitive stem cells of the bone marrow and Gastro-intestinal (GI) tract, as
well as spermatogonia, granulosa cells of the ovary, and basal cells of dermoid tissues.
DIM (Differentiating Inter-Mitotic) cells are somewhat less radiosensitive compared to VIM
cells. DIM cells are usually short-lived before cell division, and some degree of differentiation
may occur. Included in this category are the more differentiated spermatogonia and sperma-
tocytes as well as the dividing, differentiating cells of the bone marrow.
MCT (Multi-potential Connective Tissue) cells include the cells of the microcirculation, es-
pecially endothelial cells, fibroblasts and mesenchymal cells.
RPM (Reverting Post-Mitotic) cells are relatively resistant to ionising radiation and have rel-
atively long lives. They undergo division only under certain unusual circumstances. Included
are epithelial parenchymal cells, and the duct cells of the following organs: the liver, kidneys,

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pancreas, salivary glands and endocrine glands.
FPM ( Fixed Post-Mitotic) cells are the most radio-resistant type of cell. These are cells that
have lost the ability to divide. This category include long-lived neural tissue and muscle, red
blood cells (erythrocytes) and granulocytes.

In summary, we can classify the tissue radiosensitivites as follows : FPM-lowest, RPM-low,

MCT-intermediate, DIM-higher, VIM-highest.

(ii) A radiotherapy beam traverses muscle tissue. Briefly describe the expected
short-term and long-term tissue reactions.

The muscle tissue falls under the most radio-resistant FPM category. The mechanism for
injury is initial edema and inflammation in the HBB (walls of the arteries & veins) followed by
microcirculation occlusion and fibrosis that causes the death of FPM cells.
Short term : As it is relatively radiation resistant, no changes may be noted during the acute
period, but still clinical radiation damage will result. Vascular changes as a result of arteriolar
narrowing may occur later, with associated complications. Underlying radiation damage in the
parenchymal cells may become manifest as clinically significant problems.
Long term : During the chronic clinical period (1-5 years), the muscle may show further
deterioration of vascularity and secondary degradation of the parenchyma. In the late clinical
period (after 5 years), there will be slow progression of residual radiation damage and the for-
mation of a dense fibrous tissue as the result of hypo-perfusion (decreased blood flow through
the muscle tissue). During this late period, there may be radiation carcinogenesis.

(iii) A radiotherapy beam traverses a section of the small intestines, a bone con-
taining marrow, as well as muscle tissue. Briefly describe the expected short-term
and long-term tissue reactions.
Among the most radiosensitive tissues are the bone marrow and the small intestines. The short
term reaction would be damage and loss of function in these tissues.
Deterioration of micro circulation occurs after some time and the organs may fail relatively
quickly. Abnormalities may also be seen in the tissue. By the time the radiation traverses
the radio-resistant muscle tissue it is already attenuated and there may be no muscle tissue
reactions.

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