CT (Computed Tomography) imaging is an extremely useful

CT (Computed
Tomography) imaging is an extremely useful diagnostic tool, it comes with
benefits that are well known in diagnosing different type’s diseases and
trauma, however, those benefits aren’t without risks (Pearce el al., 2012). The
risks from radiation that’s associated with computed tomography are quite minor
when it’s compared to the clinical benefits that reliable diagnosis and
treatment can provide (Nickoloff and Alderson, 2001). Nevertheless, unnecessary
radiation exposure to patients throughout medical procedures should always be
avoided. This is especially concerning for paediatric patients, who are usually
more sensitive to radiation and have more years remaining of life for cancer to
start developing compared to adults (Nickoloff and Alderson, 2001). This essay
will discuss the biological effects and health risks towards ionising
radiation. Additionally, the interaction process that’s associated with
ionising radiation. The factors that affect radiosensitivity of tissues within
the human body will also be discussed. Evidence suggests that children are more
radiosensitive, compared to adults and vulnerable to the potential cancer risks
that exist within ionising radiation associated with CT. Research into
epidemiology studies and theories will be evaluated, in order to support this

There are two
different types of electromagnetic radiation: ionising and non- ionising (Reisz
et al., 2014). Non- ionising radiation refers to the insufficient energy to
remove an electron from the shells of the atom. This includes radio waves,
microwaves and visible light. The radiation from CT scans uses ionising
radiation called x-rays. This form of ionising radiation has similar properties
to gamma rays, however of a lower energy. X-rays are an electromagnetic wave
that travels in a straight line, they also have a short wavelength, meaning
they’ll have a higher frequency and higher energy level (Reisz et al., 2014).
Therefore, by having a short wavelength this enables x-rays to penetrate living
tissue, it allows visualisation of dense areas like bones within the human

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absorption is the interaction between the incident photon and inner-shell
electron. This process occurs when an x-ray photon collides with a tightly
bound orbital electron (inner-shell electron) of an atom of the absorber. This
leads to the ejection of the electron from its inner-shell and becomes recoil
electron (photoelectron). The incident photon gives up its energy entirely. The
ejected electron (photoelectron) with kinetic energy is equal to the energy of
the incident photon, less the binding energy that previously held the electron
with the inner-shell of an electron. This process usually occurs in soft tissue
with low energy photons (White and Pharoah, 2014).      

radiation may cause deletions or breaks in the DNA chain. Photons from x-rays
transfers’ energy to electron via the Compton Effect and photoelectric
absorption, which causes biological damage through ionisation (Mettler and
Guiberteau, 2012). Compton Effect is the interaction of x-ray photons in the
diagnostic energy range with soft tissue (Bushberg et al., 2012). This process
occurs when an x-ray photon interacts with an outer-shell electron. The ejected
electron receives kinetic energy and recoils from the site of the collision.
The x-ray photon is deflected from its original path and scattered in a new
direction from the point of impact (White and Pharoah, 2014). Thus, the
scattered photon equals the energy of the incident photon minus the sum of the
kinetic energy obtained by the recoil electron. High energy x- ray photons have
a significantly higher probability of penetrating matter while low energy x-ray
photons have a greater chance of being absorbed.  

The adverse
health effects of ionising radiation were noticed shortly after the discovery
of x-rays by Roentgen in 1895 (Little, 2003). When living tissue is exposed to
radiation, the amount of cellular damage will depend on the photon energy
carried by the radiation. Ionising radiation is energetic and penetrating.
Therefore it carries sufficient amount of energy to cause damage to cells
(Desouky et al., 2015). The process of ionisation within living tissue has the
ability to interfere with the molecular level of the cell. Hence, this could
possibility lead to cell death and losing the ability to repair adequately.
Another outcome is that the cell’s Deoxyribonucleic acid (DNA) can get damaged,
however still able to reproduce itself in its modified form. This could cause
somatic cells to become cancerous. Whereas, if it’s a germ cell it could lead
to inherited diseases (Little, 2003).

damage to the cell can be caused by either the direct or indirect action of
ionising radiation on the DNA molecule (Desouky et al., 2015). In the direct
action, the ionising radiation collides with DNA molecules directly, disrupting
the molecular structure. The biologic molecules absorb energy from the
radiation and form unstable free radicals. This could cause double strand
breaks and frameshifts mutations of the DNA. Therefore, abnormities of the
chromosomes may arise (Hall, 2000). Direct ionisation can compromise the
biological and chemical function of the macromolecule. This could result in the
inability to pass on information, abnormal replication of cells and cell death.
If somatic cells are directly affected by radiation, it can have adverse
effects on the DNA and chromosome. Resulting in a radiation-induced malignancy.
High linear energy transfer (LET) radiations, such as alpha particles are more
likely to do damage by direct action (Hall, 2000).  

The Indirect
action involves the ionisation of water molecules in the cell. Free radicals
such as, hydroxyl and alkoxy are produced, which can damage important biologic
molecules. Free radical molecules are characterised by an unpaired electron
structure, which is highly reactive. The free radicals can combine with
molecular oxygen to form highly reactive hydroperoxyl, this is toxic to the DNA
molecule (Hall, 2000).This can produce biological damage and transfer excess
energy to other molecules, resulting in chemical bonds being broken. Indirect
action has a greater effect than direct. It has been discovered that most
ionising radiation-induced damage is from the indirect interaction. This is
mainly because of water forms around 70% of the cell. Thus, the majority of
ionising radiation interactions are indirect (Desouky et al., 2015). Children
are more vulnerable to an indirect interaction of ionising radiation. Alzen and
Benz-Bohm (2011) emphasised that children have a high content of water with
their tissues compared to adults. This suggests that more radiation is absorbed
and dispersed, therefore an increased dose may be required to penetrate the layer
of tissue.


The biological
effects of exposure to ionising radiation can be classified as either
deterministic or stochastic. The deterministic effects are caused by radiation-
induced cell death. The deterministic effect occurs when radiation exposure is
very high, causing it to exceed the threshold dose (Bushberg et al., 2012).
This results in severe biological effects, as it can impair and compromise the
functions of organs and tissues. A threshold is essential for damage to be
observable. The amount of damage caused usually depends on the dose rate,
absorbed dose and the quality of radiation. Thus, the severity of the
deterministic effects increases as the dose of exposure increases (Little,
2003). Examples of deterministic effects usually include skin erythema,
irreversible skin damage and cataract.

In contrast to
deterministic effects, the stochastic effects occur at low doses of ionising
radiation that possibly causes damage to the genetic material within cells.
This may result in radiation- induced cancers to develop years later after
exposure. There isn’t a reasonable safe dose for stochastic effect as it’s
believed not to have a threshold. The reason is that damage to a few cells or
single cell can theoretically result in the development of cancers and
production of disease (Bushberg et al., 2012). The risk of stochastic
biological effect within humans, after being exposed to low doses of ionising
radiation is mainly assessed based on the linear no-threshold model (LNT)
(Scott, 2005). Since it implies that any dose including really low doses can
pose a thread for genetic defects or cancer to arise. The linear no-threshold
hypothesis (LNT) assumes that each photon has the potential to cause DNA
mutation. The theory believes there is a linear relationship between DNA damage
within the form of double-strand breaks (Desouky et al., 2015), that each
double-strand break will most likely have the same probability of cell
transformation. Therefore, each cell that is transformed will have the same probability
of becoming cancerous.

A factor that
affects radiosensitivity of tissues and organs is age. Humans are usually more
radiosensitive at birth, however, this generally decreases with age.Children
are usually more prone to biological damages from ionising radiation (Sinnott
et al., 2010).This is because children’s tissues are still growing and cells
are dividing more rapidly (high mitosis rate). The radiosensitivity of the
thyroid glands is significantly greater in children. (Sinnott et al., 2010). The
findings from epidemiological studies of the Chernobyl disaster showed a high
increase of thyroid cancer in people that received high thyroid doses as
children, after a few years after the Chernobyl incident (Zablotska et al.,
2010). The increase of receiving thyroid cancer was high in children around age
1-5. However, there were no reports of the increase of thyroid cancer in

Kufe et al.,
(2003) stated carcinogenesis is a stochastic process. Carcinogenesis is caused
by the cellular damage by ionising radiation. Ionising radiation is a known
carcinogen which children are especially vulnerable. The cell may not be
adequately repaired, this can prevent the cell from surviving, reproducing or
mutation of a cell occurs. When exposed to ionising radiation from CT scans,
children can receive higher doses than adults, due to a greater intake and
accumulation. Sensitivity to ionising radiation is particularly highest at the
early stages of life. This is linked to the greater cell division in developing
tissues. Children have a longer life expectancy compared to adults, meaning
there’s an increased chance of repeated exposures and accumulated damage to
cells. Thus, leads to an increased chance of cancer risk for children (Kufe et
al., 2003).   

A cohort study
was funded by the UK Department of Health and US National Cancer Institution to
investigate the “radiation exposure from CT (Computed Tomography) scans in
childhood and subsequent risk of leukaemia and brain tumours” (Pearce el al.,
2012). The researchers that conducted the study, examined the medical records
of around 175,000 patient that were under 22 years of age, who had a CT scan
within NHS (National Health Service) between 1985 and 2001. According to Pearce
el al. (2012), the study discovered that children that received a bone marrow
dose from CT (Computed Tomography) scans of ?30
mGy were at three times more likely to develop leukaemia whereas children that
received a brain dose of ?50 were at 2.8 times more likely
to develop brain cancer. This well-conducted study suggests that children who
are exposed to higher levels of ionising radiation during CT scans are more
prone to developing certain types of radiation-induced cancer.

The risks of
leukaemia are best described by the non- linear threshold model; risks are
higher for exposures that occur in childhood. However, it usually tends to
begin to decrease 10 to 15 years late (Matsumoto et al., 2009).  

To support the
reliability of this study, results from epidemiological studies, including the
cohort study of Japanese survivors of the atomic bomb in Hiroshima and Nagasaki
also referred to “the life span study” and the UN Scientific Committee on the
Effects of Atomic Radiation (UNSCEAR) agreed that children are usually more
sensitive than adults to ionising radiation for most cancer types, such as
leukaemia and brain tumours (Charles, 2009). The atomic bomb survivor’s
life-span study is stated to support the linear no-threshold hypothesis (LNT)
of ionising radiation carcinogenesis (Scott, 2005). This is because the linear
no-threshold hypothesis was acquired by using statistically significant dose
response, in a relationship between the ionising radiation dose received by the
atomic survivors of Hiroshima and Nagasaki. Additionally, it was derived from
the observation of hereditary disorders and cancers (Desouky et al., 2015).

The non-linear
threshold model is accepted by most regulatory requirements that authorise
activities that use ionising radiation such as industry, health (radiography
organisers), and scientific research (Matsumoto et al., 2009). The non-linear
threshold model is used in establishing radiation protection guidelines. There
have been discussions about the validity of the LNT model. The international
commission on radiological protection (ICRP) 2007 review, challenged the LNT
model. Nevertheless, it concluded that for reasons of radiation protection,
it’s scientifically acceptable to assume the possibilities of cancer risks at
low levels of radiation exposure (Desouky et al., 2015). The Biological effects
of ionising radiation (BEIR VII) report concluded that the biological and
effects of low dose data support the LNT model risk model (Morgan and Blair,
2013). This model states that even the smallest of ionising 

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