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SECTION 5 - BIOLOGICAL EFFECTS AND RISKS OF RADIATION

A. The Cell - Basic Unit of Structure

This section will be devoted to the effects of ionizing radiation on

the human body. The structure of the body is quite complex, and it is
often of value to deal with effects at certain levels of organization
within the body. Thus, the human body contains many organs, each of which
is composed of two or more types of tissue. In turn, a tissue is composed
of similar cells, there being four types of tissues in the body:
epithelial, connective, muscle, and nerves. The job of a tissue is to
perform a special body function. The cell, which makes up the tissues of
the body, is the basic unit of structure and function in the body. A cell
contains many elements; hydrogen, oxygen, carbon and nitrogen are the main
components. Human cells vary in size from approximately 3-100 pm.
A cell is normally composed of a nucleus surrounded by cytoplasm,
both encased in membranes. Although highly complex in structure, the
nucleus and cytoplasm contain about 70 percent water.' The vital part of
the cell is the nucleus, usually an oval body located near the center of
the cell. From a chemical standpoint, the nucleus is quite active. The
normal growth of the cell is controlled by the nucleus. Also, it initiates
cell division and controls the repair of injured cells. The cytoplasm is a
more or less colorless liquid substance. It secretes enzymes, and controls
absorption and excretion in the cell.
Among the complex structures found in the cell are carbohydrates,
fats, proteins and nucleic acids. Carbohydrates serve as food for the cell
and as structural units. Fats store chemical energy. Proteins, which
differ from each other by the number, sequence, length and arrangement of
amino acid chains, are involved in all the metabolic activities (chemical
reactions) which sustain cell life. Amino acids are composed of NH2
groupings and about 20 amino acids are found in the proteins of mammals.
The nucleic acids, DNA (deoxyribonucleic acid) and RNA (ribonucleic acid)
function together to produce the cell's proteins. Most of the DNA is found
in the nucleus. The DNA molecules are thought to carry the genetic code
necessary for proper cell reproduction. 2 The RNA is distributed
throughout the cell and is thought to be the messenger which translates
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the information contained in the DNA into instructions for protein

production.
Many body cells have only a limited life span. In order that their
functions be carried on, cells divide at a certain stage in their life
(mitosis). The daughter cell then takes over the functions of the parent
cell. As a cell divides, there appear in the nucleus threadlike structures
called chromosomes. The chromosome number is fixed for a given species (23
pairs in human cells). Arranged linearly along the chromosomes are the
genes which determine hereditary characteristics. Prior to cell division,
the number of chromosomes is temporarily doubled. When a cell divides, the
daughter cell receives a duplicate set of chromosomes from the parent as
well as identical genes. If the process is normal, no alterations or
changes occur. However, any changes which do occur in the chromosomes
and/or genes are called mutations. These changes or mutations can then
affect either the daughter cell or future cells.
The development of an organ then proceeds from mitosis, the term
used to designate cell division. In a bisexual species, the union of two
cells (gametes) - one from the male and the other from the female -
produces an original cell from which the species will be reproduced.
This cell then undergoes a number of divisions which increase its
number. In the embryonic state, all the cells look alike. However, changes
in the structure of the cells begin to take place. The changes enable the
cells to perform specialized functions. This process of change is referred
to as differentiation. The result of this process is the development of
differential cell types or lines. One of these lines is the germ line, the
rest are called somatic. The germ line gives rise to either male or female
gametes. The somatic lines develop into the tissues of the individual.
Since only the gametes can be transmitted to future generations of
the species, damage to somatic cells is limited to the individual. Damage
to the offspring of an individual may occur when there is damage to the
cells of the germ line.
A great many agents can cause injuries to the cells. When such
injury occurs, the effects are the same regardless of the agent which
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caused the damage. Ionizing radiation produces damage to cells, but in a

mostly nonspecific way; that is, other physical and chemical substances
cause the same effects because the body responds the same to certain cell
damage regardless of the cause.
Radiation passing through living cells will directly ionize or
excite atoms and molecules in the cell structure. These changes affect the
forces which bind the atoms together into molecules. If the molecule
breaks up (dissociates), some of the parts will be charged. These
fragments are called free radicals and ions, and are not chemically
stable. Free radicals are electrically neutral structures with one
unpaired electron. 3 Because the cell has a higher water content, the
most important free radicals are those formed from water molecules. For
example, an excited H20* molecule may dissociate into

H20*+H" + OH",

in which the hydrogen radical H" has an unpaired e- and the OH" radical
will have nine e-, one of which will be unpaired. The free radicals are
very reactive chemically, and when combining can produce hydrogen peroxide
W202>, which is a chemical poison, and the HO" radical which is more
2
damaging than peroxide. Further effects are produced when the
radicals and ions interact with other cell material. In this way, damage
is caused in a direct and indirect manner. 2 The role that each type of
action plays in the total damage to the cell is still an unsolved problem.
Of the damage which is done, the effects are greatest in the nucleus of
the cell, but injury to the cytoplasm can also cause serious effects in
the cell.
The total effect on cell processes is a function of the dose of
radiation. The cell processes will be affected in varying degrees up to
the ultimate result-cell death. Some damage to the cell may be repaired.
This can be accomplished by action of the cell itself, or by replacement
of badly injured cells in a given tissue through mitosis of healthy cells.
On the other hand, if the extent of the damage to an organ is quite large,
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the organ may not be able to repair itself, That is, damaged cells may
show confused growth but eventually be unable to divide. Or the cells may
begin to exhibit uncontrolled growth. Although many factors are important
in assessing the total damage, it seems likely that most cell functions
and structures are somewhat impaired by radiation.

B. Radiosensitivity

Since the cells which make up the tissues of the body differ both in
appearance and function, one might suspect that their response to
radiation would also differ. Such is the case, and this property is known
as the radiosensitivity of the cell. The first statement about this
property was given by Bergonie and Tribondeau. They found that the
radiosensitivity of a tissue is directly proportional to the reproductive
capacity and varies inversely with the degree of differentiation. Since
then, other factors have been found which affect the radiosensitivity.
Among these are the metabolic state of the cell, the state of cell
division, and the state of nourishment. It turns out that to produce a
given effect, the necessary radiation dose varies inversely as the
relative sensitivity of the given tissue.
Thus, cells which are most active in reproducing themselves, cells
which have a high metabolic rate (rate of chemical changes) in the cell,
and those cells which are more nourished than others are more sensitive to
radiation. 4 Also, there is evidence that cells are more susceptible to
radiation at certain stages of division than at others. Moreover, cells
not fully mature will also be more harmed by radiation than mature cells.
In the body, bone marrow, lymphoid tissues, and the reproductive organs
rank among the most radiosensitive. Muscle and bone cells are the least
radiosensitive.

C. Radiation Damage

As has been pointed out, damage to somatic cells is limited to the

individual whereas damage to germ cells may result in damage to the
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offspring of an individual. One may broadly classify biological effects in

man as somatic or hereditary. Somatic effects include any and all types of
damage which affect only the individual; hereditary effects are those
which can be transmitted to a future generation 125 . Thus, damage to the
genes of a somatic cell may produce damage to a daughter cell, but this
would be a somatic effect, not hereditary. The term genetic damage refers
to effects caused by chromosome and/or gene mutations. This may lead to
hereditary effects only when the damage affects the germ line since only
then can these effects be transmitted to a future generation.

D. Factors Influencing Radiation Effects

The radiation effects in man and animals are usually discussed in

terms of total body and partial body irradiation, and with reference to
damage to an organ. Because of the importance of some organs in the body,
certain damage to these can induce effects in other organs. A number of
physical factors are important in the determination of radiation effects:

1) sensitivity of the individual-for a select group, the effects

may differ greatly from those in a heterogeneous group;

2) nature or tYPe of radiation-some types of radiation are more

effective in producing damage;

3) the absorbed dose-this is a function of the energy absorbed per

gram of tissue;

4) time distribution or fractionation-a lethal dose given in a

short time may not be lethal if protracted over a long time;

5) dose distribution-is the total body involved or only a specific

organ?

6) age at irradiation-response is altered during growth in some

systems.

The nature, severity and duration of biological effects depend upon

the above and-other factors. The combination of factors makes the effects
on different organs differ for changes in the number of relevant
parameters.
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1. Individual Sensitivity - Dose-Effect Curve

Because a number of factors enter into the response of

individuals to radiation, one might expect an effect to be seen in some at
a lower dose than others. This may be due to certain host factors in the
individual 6 , such as general health, previous exposure to other agents,
etc. Such a variation is seen, so that, if one studies the fraction of
individuals which exhibit a given effect as the dose is varied, a
dose-effect curve (Figure 5.1) is obtained. In the figure, for very low
doses, no effects are seen. As dose is increased, the % affected increases
with increased dose. Above 50% affected, the rate of increase slows, and
larger doses are required to produce the effect in the remaining popula-
tion. In the study of radiation effects, the dose D at which 50% of the
population is affected is generally used as the reference dose. If the
effect is death, the symbol ID50 called the median lethal dose (lethal

80

20

0
DOSE (Gy)
Figure 5.1 Dose -effect relationship.
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dose to 50% of the exposed), is used. Moreover, since the time for an
effect to show up may also vary, the symbol LD50,30 (lethal dose to 50%
of the exposed within 30 days of irradiation) may be used.
Getting back to the dose-effect curve, we note that at D50,
half of the exposed would show the particular biological effect. This
means that a single value of the dose cannot adequately describe the
probability for &LJ individuals. That is, almost half of those exposed
show the effect for less than D50. On the other hand, half have not yet
shown the effect at D50. This type of statistical behavior is typical of
the response to radiation seen in mammals and implies a normal
distribution of sensitivity with respect to dose. 2

2. Tvne of Radiation

As discussed in Section 4.B, the damage done by radiation

depends upon the type of radiation. Not all radiation types are equally
effective in producing biological damage. In radiobiology, the effective-
ness is determined by the relative biological effectiveness (RBE). This
quantity can be determined if one can establish the effect and control the
conditions of the exposure. For this case,

RBE = Dose of 200-250 kV x rays to produce the effect of interest

Dose of comparison radiation to produce the same effect

In radiation protection work, one cannot control the conditions of

exposure or concentrate on one effect. Thus, the quality factor, Q, an
assigned value, is used to denote that the degree of response is modified
for the type of radiation. Both the quality factor and the RBE are related
to the LET. In general, for high values of LET one finds high values of

BE, and high LET radiation is more effective in producing damage then low
LET.
For low LET radiation (electrons), the ion density is low so
that recombination of ions and radicals is less likely. This allows ions
and radicals to diffuse through the medium easily to form other products.
This would increase the contribution of indirect effects. In addition, the
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the small electrons colliding with large DNA macromolecules tend to

produce only small bond breaks. This tends to lessen the effect of direct
action.
In the case of high LET radiation (protons and other heavy
recoils), the ion density is greater promoting more recombination and less
diffusion. This would work to reduce indirect action. The much larger
protons colliding with DNA would tend to produce many large fragments, and
even damage the macromolecule beyond repair. This would enhance the effect
of direct action.
If one looks at cells exposed to both low LET and high LET
radiation, the survival curve will look something like Figure 5.2. In
curve A, a similar set of cells are irradiated by high LET particles. The
simple exponential implies that cells become inactivated following a hit.
That is, single events are important. In curve B, cells of both high and
low sensitivity are irradiated. The initial dropoff suggests the rapid

DOSE

Figure 5.2 Survival curves for low LET and high LET radiation.

.
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inactivation of the high sensitivity cells. The latter straight portion

represents the removal of the low sensitivity cells. Curve C is typical of
most types of similar cells irradiated by low LET radiation (60Co).'
The initial shoulder portion implies that cells sustain non-lethal damage
at first, followed by more damage which inactivates the cell. ;
Many models have been suggested to explain the shape of the
survival curves. 8 The simplest model explains curve A by assuming an
exponential in which the slope of the line is a constant-l/D. This model
is compatible with the assumption of direct action (or single hits) being
the important reactions. Curve C is better explained by assuming a
multi-target, single hit model.' In this view, a number, n, of targets
must all be hit at least once to kill the cell. This is consistent with
the shoulder portion of the curve C, which indicates more interactions are
necessary to inactivate cells. That is, sublethal damage is followed by
lethal damage.
Some qualitative results which apply to high LET radiation are:

1) a smaller dose is required to achieve a given degree of

effect,

2) the exponential survival curve implies little recovery

from sublethal damage,

3) fractionation of dose seems to have little effect, and

4) the degree of damage is not affected greatly by dose rate.

For low LET, the following apply:

1) there is some recovery of sublethal damage,

2) fractionation of dose results in less effect, and

3) a dose rate dependence is seen, the effects of low dose

rate are l/3 to l/6 those at high dose rate.

3. Absorbed Dose

The basic parameter, which can be associated with biological

damage, is the energy absorbed per unit mass. However, we have seen that
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the damage produced is also related to the type of radiation. But, in a

given system, the absorbed dose for a given radiation type will acquire
added significance in a small tissue mass. Moreover, for a very large
energy deposition per unit mass, the absorbed dose will override the LET
considerations.

4. Time Distribution or Fractionation

If a dose of some value is delivered in a number of smaller

fractions, the effectiveness of the radiation is often reduced. This
sparing effect is attributed to repair of sublethal damage and replacement
of cells suffering lethal damage. For low LET damage, it is assumed that
sublethal damage occurs before cell inactivation results. Since successive
low LET doses, separated in time, are less effective than their sum
delivered in a single, short dose, sublethal damage is somewhat
repairable. 7 When irradiation is given over many doses, repair occurs
after each dose. In addition to repair, cell replacement is also able to
offset cell death. Although little is known about the dose rate at which
cell replacement counterbalances cell death, it is known that this effect
acts to mitigate the effect of cell killing.

5. Dose Distribution

When the whole body is irradiated, the total effect is more

severe for a given dose than if that dose were given to a specific organ,
This indicates that when the tissue volume is reduced, the severity of the
response is also reduced. The magnitude of this sparing effect has not
been adequately measured.

6. Age At Irradiation

In addition to the fact that effects are more pronounced in the

young, there is also an increased sensitivity in the unborn.4 Certain
organs, such as bone and cartilage, show a definite response during growth
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but are relatively radioresistant when mature. 7 Whereas, for the ovary,
sensitivity for sterility decreases with age. Damage to the germ cells is
of concern only during the period of child bearing. Some effects are ir-
relevant when the life expectancy of the individual is much less than the
latent period required for the effect to show up.

E. Earlv Somatic Effects - Acute Radiation Svndrome

The somatic effects which are observed can be loosely divided into
early and late effects. Although quite an arbitrary grouping, early
effects are classed as those which appear within a few weeks after the
exposure. The range of these effects as well as their duration depend upon
the dose. For very high whole body doses, there are three basic forms of
early or acute damage. In the range above about 20 Gy (2000 rad), the dose
is fatal within a day or tw~.~ The same symptoms appear when the head
suffers severe irradiation, which points to a breakdown of the central
nervous system. This type of acute radiation syndrome is thus referred to
as central nervous svstem death (CNS death).
For the range 5-20 Gy (500-2000 rad), symptoms may appear within
hours. Death often occurs within a week or so. In this mode, the damage to
the lining of the intestinal tract is the most severe. This form is called
gastrointestinal tract death (GI death). At the lower end of this dose
range, it is possible for one to survive this mode of death only to fall
victim to the effects which prevail at lower doses.
At doses < 5 Gy (500 rad), the most important effect is damage to
the blood forming organs. Since these centers are located in the bone
marrow, this mode of death is often called bone-marrow death. The first
signs may appear within a few days, depending upon the dose, and the total
effect may not develop for a few weeks. Severe changes occur when the dose
is > 2 Gy (200 rad). In the range above 3 Gy (300 rad), the damage is
severe enough so that death becomes more and more probable.
In the preceding sections, the results are based on x and 7 ray
data. As such, the conversion to rem for other types of radiation is not
justified in this instance.
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The main clinical effects which follow acute exposure to total body
doses of ionizing radiation are nausea, vomiting, loss of appetite and
fatigue for doses > 1 Gy (100 rad) or so. 3 As indicated above, the time
of onset, the severity and the duration of the effects depend on the dose
and the exposed organs. A summary of clinical effects for acute doses is
given in Table 5.1 and may be used as a rough guide. Note the virtual
absence of any symptoms in the dose range below 1 Sv (100 rem). Some
people would be expected to have mild symptoms in the range 0.5-l Sv (50-
100 rem), because of differences among individuals. Below 0.5 Sv (50 rem),
however, no symptoms at all are expected. In fact, special techniques are
needed to detect doses this low. 4
Death occurs in a larger fraction of cases as the dose increases. If
the dose becomes large enough, all cases of exposure result in death. In
the range where survival is possible, the concept of the median lethal
dose (LD50) is used. For man, the best estimate places the LD50 in the
range of 3 to 5 Gy (300-500 rad). Of course, in this range all would have
severe symptoms. Note that this dose refers to short-term total body
radiation.

F. Late Somatic Effects

The problem in the study of late effects resulting from exposure to

radiation is that the elapsed time may be rather long, thus making it hard
to relate the cause to the effect. Since the late effects may be caused by
many other agents besides radiation, there can be no positive assignment
of the cause in most cases. At best, it can be shown that radiation
increases the incidence of these nonspecific injuries.

The main late effects are discussed in the following.

1. Cancers

In its 1980 report,6 the Committee on the Biological Effects

of Ionizing Radiation (BEIR) indicated that cancer was considered to be
the most important somatic effect of low-dose ionizing radiation. Cancer
 Therapeutic Range - 1 to 10 Sv Lethal Range - Over 10 Sv

Subclinical to 2 6 to 10 .Sv 10 to 50 sv over 50 sv

Range: oto1Sv
1 Sv 2 to 6 sv

Incidence of None
1 Sv: 5%
3 sv: 100% 100% 100% 100%
Vomltlng: 2 sv: 50%

Delay Time: 3 Hours 2 Hours 1 Hour 30 mln 30mln

Central
Leadlng Organ: None Hematopoletic Tissue G.I.Tract
Nervous System

Diarrhea, Fever,
Severe Leukopenla, Hemorrhage, Infection, Convulsions, Tremor,
Characterlstlc None Moderate Leukopenla Disturbance of
signs: Purpura, Epilatlon Above 3 Sv Electrolyte Balance Ataxla, Lethargy

Crltlcal Period 4-6 Weeks 5 to 14 Days 1 to 48 Hours

Post-Exposure:

Reassurance, Consider Bone-Marrow Maintenance of

Blood Transfusions,
Therapy: Reassurance Hematologlc Sedatives
Antibiotics Transplantation Electrolytic Balance
Surveillance

Good Guarded Hopeless

Prognosls: Excellent Excellent
Therapy Effective Therapy Promlslng Therapy Palliative

>onvalescent Perlod: Several Weeks 1 to 12 Months Long

lncldence of Death: None 0 to 80% (Variable) 80 to 100% (Variable) 80 to 100%

Death 2 Months 2 Weeks 2 Days

Occurs Wlthln:

Respiratory Failure
Cause of Death: Hemorrhage, Infection Circulatory Failure
Brain Edema

Table 5.1 Summary of Clinical Effects of Acute Ionizing Radiation D~ses.~

. . .. . .
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may be induced by radiation in nearly all human tissue. The main sites of
solid tumors are the breast in women, thyroid, lung and some digestive
organs. These tumors have long latent periods (approximately 10 to > 30
years) and occur in larger numbers than leukemia.6 Leukemia (abnormal
increase in white blood cells) has a much shorter latent period. The
incidence peaks within a few years of exposure and returns to normal
levels after about 25 years.l' Reference 6 contains an extensive
discussion on radiation induced cancers and presents data on the incidence
in specific organs. The ICRPl' has estimated that the fraction of all
cancers, for both sexes and all ages, is 1.25~10-~ Sv-l
(1.25~10~~ rem-l).

2. Tissue Effects

Among the more prominent late effects in tissues are cata-

racts (see 5.1.7) and sterility (see 5.1.4). Radiation-induced cataracts
are slowly progressive over a period of time, but may stop or even
regress.' Sterility is a late effect which may be either permanent or
temporary. In some cases, fertility will return in a few years.6

3. Life-span

Information on life-shortening effects in man is still inade-

quate. The effects of long-term, low-level irradiation on longevity cannot
be predicted. With the exception of tumor induction, there is no evidence
of life shortening. 6,lO

4. Growth and Development

Effects on the embryo depend upon the dose as well as the age
of the embryo. The younger the embryo, the more it is affected.1 Here,
as in the case of other late effects, the results of damage are the same
as those caused by other agents. The effects on the fetus are so much more
important since minor damage may be amplified during growth into a major
anomaly. Relatively high doses can cause death, malformation, growth
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retardation and impairment of function.6 Susceptibility to certain

cancers appears to be higher during prenatal and childhood periods. 6,lO
The incomplete status of these problems at the present time
reflects the lack of needed information. Such data are very hard to
obtain, and require careful work and analysis. In each case of late
effects, extensive data are needed before any real firm conclusions may be
drawn. As the dose rate is reduced, one approaches background levels and
any effects produced by the applied dose rates may be masked by effects
produced by other agents or background radiation.

G. Hereditarv Effects

The study of hereditary effects attempts to discover the traits

which can be transmitted from generation to generation in a given species.
The genes are the determinants of the inherited traits. Any change or
mutation of a gene, which is usually quite stable, can result in an
altered trait. Such changes can be produced by radiation, as well as other
agents. The study of radiation-induced mutations is thus hampered by the
fact that other substances also act to produce the same effects. Since the
change is not unique, radiation only serves to increase the frequency of
the effect. Increases in the rate are small even for high doses. Thus, the
study requires the use of large numbers of subjects studied over many
generations. In the case of man, the study is very difficult, since large
numbers are seldom available and the time between generations is so long.
To date, there has been no demonstration of radiation induced mutations in
man."
For this reason, much of the present knowledge is based on work with
animals. 6 At all doses and dose rates used up to the present, radiation
is known to induce mutations in all species studied. Because of this, any
increase of radiation to humans should bring about an increase in the
mutation rate. Sometimes the application of animal data to man can result
in error. However, in this case, the effects on some other species are
similar enough to those in man.
Studies have shown that some hereditary effects in man are caused by
chromosome damage. IL UP to the present time, the lack of knowledge about
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the harmful traits has made estimates of the magnitude of these effects
uncertain. When more diseases and effects can be related to certain types
of mutations, then better estimates can be made. -
Genes may be dominant or recessive. When genes differ-; the tr&-
which results may be determined by either gene_,. or some intermediate trait

may occur. If the trait is determined by one or the other of the genes,
this gene is then a dominant gene. The other is a recessive gene.
Mutations in dominant genes give rise to damage in the offspring of the
first generation. Damage to offspring caused by recessive genes occurs
only if the same altered gene is received from each parent. Unless these
changes occur frequently, recessive damage won't show up for many
generations.
It is estimated that already about 10% of human liveborn offspring
suffer from serious disorders of genetic origin. In evaluating radiation
induced genetic effects in humans, mouse data must be used.6 The
estimates of the increased serious genetic disorders in humans due to
radiation exposure are small relative to the natural incidence cited
above. That is, the ICRPl' has estimated that the fraction of effects to
be expected, in the first two generations, can be taken as about 4x
10q3 Sv-l (4x10m5 rem-l).

H. Stochastic and Nonstochastic Effects-Risk

For some of the effects that have been mentioned, the relative
damage or severity of the effect increases with increased dose. Higher
doses produce . a greater degree of that type of damage. On the other hand,
for some effects, increasing the dose increases the chance, or probability
of the effect occurring. The terms "nonstochastic" and "stochastic"
effects have been employed by the ICRPl' to distinguish between these.
Nonstochastic effects are those in which the severity of the effect varies
with the dose. For these types of effects, a threshold dose may exist.
That is, if the dose is kept below the threshold dose, the effect will not
be observed. Nonstochastic effects are considered to result from the
collective injury of a substantial number of cells in the tissue. 7
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Examples of such effects are cataracts, skin ulcerations or burns,

depletion of blood-forming cells in bone marrow, and impairment of
fertility.
Stochastic effects are those in which the probability of the effect
occurring increases with dose, without threshold. Any dose, therefore, has
a certain probability, however low, of causing the effect. Stochastic
effects may result from injury to a single cell or a small number of
cells. 8 Carcinogenic (cancer) and heritable effects are examples of
stochastic effects. In these, once the effect is induced, the severity is
already determined by the nature of the effect.
From a protection standpoint, preventing nonstochastic effects may
be achieved if the dose limit is set low enough so that the threshold dose
is not exceeded. In this case, the risk of producing nonstochastic effects
could be reduced to zero. The ICRP has recommended dose limits intended to
prevent detrimental nonstochastic effects." However, since stochastic
effects have some chance of occurring no matter how low the dose, the ICRP
limits intend to limit the probability of stochastic effects occurring to
an acceptable level. That is, any exposure to radiation involves a risk,
and no risk should be undertaken without the expectation of a net
benefit." Since the setting of limits involves judgments that cannot
wholly be based on scientific knowledge, the concept "acceptable risk" has
evolved. The basis for an acceptable level of risk in radiation work is
comparison to the risks in other occupations considered to have high
safety standards. 10 The average annual mortality in these occupations is
10m4. The risk factor of 10m4 represents 1 chance in 10,000
that an accidental death due to occupational hazards will occur during the
year. The risk factors used by the ICRP are the estimated probability of
occurrence of stochastic effects per unit dose, that is, the sum of the
risk factor for all radiation induced cancers (1.25~10~~ Sv-l)
and the average risk factor for hereditary effects (4x10-3
sv-1). The average annual dose equivalent in cases of occupational
exposure is about 5 mSv (.5 rem). lo So, the averape annual risk would
be (1.65 x 1O-2 sv- 1) (5x10-3 Sv) = 8.25~10-~,
approximately 1x10m4 or comparable to other safe industries.
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For more discussions on risk and risk factors, for both radiation
workers as well as risks in everyday living, one may consult References 11
and 12, respectively.
The ICRP makes a further point in their recommendations. They
recommend that all necessary exposures be kept as low as reasonably
achievable, taking into account economic and social factors. lo This part
of the recommendations is referred to as optimization. That is, achieving
the optimum net benefit such that the increased protection cost to reduce
exposures is balanced by the reduction in the expected harm (detriment).

I. Biological Responses of Soecific Organs

With respect to specific damage in various organs of the body, some

effects may be stochastic or nonstochastic. For the stochastic effects,
the risk factors from Reference 10 will be given. For nonstochastic
effects, the threshold doses from Reference 7 are quoted. The sensitivity
of the method for detecting damage is an important factor. For this
reason, the threshold dose is defined as the amount of radiation required
to cause a particular effect in at least l-5% of those exposed. 7 With
the exception of tissues such as skin, which respond for short-term
irradiation, data is lacking for reactions to long-term protracted
exposures in all organs. Knowledge of the radiosensitivity of different
tissues regarding nonstochastic effects is based mainly on therapy
experience. The thresholds are based on therapy irradiation conditions;
typically, 20-35 exposures to x or 7 rays over a 4-7 week period, a
occupational exposure conditions. The following summary points out some of
the specific aspects of biological response in specific tissues and organs
of the body:

1. Blood and Bone Marrow

The blood is composed of three major types of cells, namely,

the erythrocytes (red cells), the leukocytes (white cells), and platelets,
suspended in a fluid called plasma. The red cells supply other body cells
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with food and oxygen, and remove waste products. White cells help to
combat infections, and the platelets aid in blood-clotting action. Plasma
is a viscid liquid which contains water, proteins, salts, and free ions.
Blood contains about 45% red cells, approximately 1% white cells and
platelets, and 54% plasma.
Bone centers are filled with marrow, either red or yellow. Red
marrow is found in the skull, breastbone, ribs, pelvis, and spine of
adults. The red marrow provides the blood-forming function. Yellow marrow
provides fat storage.
White cells are the first to be affected by radiation. Although
there are subtypes of white cells which differ in their sensitivity, the
net effect of irradiation is to reduce the number of white cells. This
lack of white cells is known as leukopenia. For acute whole body doses > 1
Gy (100 rad), the maximum drop in the leukocytes is seen within 2-5 weeks.
The platelets drop in number somewhat more slowly. A few weeks later, a
loss of red cells (anemia) occurs.
The loss of white cells affects resistance to infection. The
drop in the platelet number affects clotting action, so that open wounds
may not heal. Anemia causes a general weakness in the individual. Recovery
will take place if the damage to the bone marrow is not too great. The
marrow will regenerate and produce new blood cells to replace the cells
which were lost. When the damage to the red marrow is too great, the
effects are likely to be permanent. The LD50j60 is not known precisely,
but is estimated to lie in the range 2.5-5 Gy (250-500 rad).
For fractionated or protracted doses, the effects are not as
severe due mainly to replacement and some repair. Although dose rate
influence on damage is not well known for humans, it is believed that the
blood forming system can withstand 3-10 Gy (300-1000 rad) if protracted
over several months. The threshold dose for nonstochastic effects is 2 Gy
(200 rad).
With respect to leukemia, the red bone marrow is believed to be
the main tissue involved. The risk factor is taken as 2~10~~
sv- 1 (2x10m5 rem-l).
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2. Lvmnhatic System

The lymphatic system is a network of small tubes which permeate

the body tissues. A fluid called lymph, somewhat like plasma but with less
proteins, drains from tissues into the lymphatic system. The lymph picks
up waste products from the tissues. Along the course of a lymph vessel are
oval-shaped glands (lymph nodes) which filter out foreign substances from
the lymph. Thus purified, the lymph is passed back into the blood stream.
The spleen contains the largest mass of lymphatic tissue in the
body. The spleen filters dead blood cells from the blood and is a source
of white blood cells. Also, the spleen stores red blood cells.
The lymph nodes show the first signs of hemorrhaging and infec-
tion after acute irradiation. The spleen may exhibit weight loss and
damage to lymphocytes (a subtype of white blood cells). A complication in
the function of lymphoid tissues is a drop off in the body's immune
response to infection.

3. Digestive Tract (GI Tract)

The digestive tract, or alimentary canal, consists of the

mouth, pharyrur , esophagus, stomach, and the small and large intestines.
This system is often called the GI tract. In an adult man, the canal may
be as much as 9 m in length. The cells which line the walls of the
intestines secrete substances which act on food to make absorption into
the blood stream possible. The stomach is the reservoir in which the major
chemical phases of digestion occur. The radiosenstivities of the many
sections of the canal vary greatly. The small intestine is quite radio-
sensitive, whereas the stomach and esophagus are much less radiosensitive.
The symptoms of damage to the canal are nausea and vomiting.
The initial effects are impaired secretion and discontinued cell
production. When cell breakdown occurs, the dead cells are released from
the walls of the tract. This debris clutters up the intestine. The
exposure of tissues under the surface layer may lead to ulcers. The
threshold dose for ulceration is estimated as 45 Gy (4500 rad). In fatal
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cases, infection, failure of food absorption, and dehydration from

diarrhea are the causes. As indicated earlier, the LD50 for acute whole
body exposures is in the range 5-20 Gy (500-2000 rad).

4. Renroductive Organs

Since the reproductive organs are the source of germ cells,

damage to these cells can result both in somatic and hereditary effects.
For the present, our concern is only with the somatic effects.The
response of germ cells to radiation differs slightly in the male and
female. These cells are highly radiosensitive, while other cells of the
reproductive system are relatively radioresistant. Radiation can produce
sterility in both sexes, but the degree depends upon the dose delivered.
In man, partial sterility can be induced at doses as low as 0.15 Gy (15
rad). Based on dog experiments, it is inferred that the human testes can
tolerate 1 mGy d -1 (0.1 rad/d) for an indefinite period of time without
fertility impairment. It requires a larger dose to produce permanent
sterility in the male than in the female. Acute exposure of the ovaries to
0.65-1.5 Gy (65-150 rad) may cause prompt impairment of fertility and
acute doses > 3 Gy (300 rad) will cause permanent sterility. Threshold
doses for testes of 5-15 Gy (500-1500 rad), and for ovaries of 2-3 Gy
(200-300) have been estimated.
Germ cells which survive damage can transmit any genetic
changes caused by the radiation. For this reason, the total effect of
radiation on the gonads may not be seen for several generations. The
estimated risk factor for the first two generations is 4~10~~ Sv"
(4~10'~ rem-l).

5. Nervous Svstem

The nervous system, composed of the brain, spinal cord, and the
peripheral nerves, acts to coordinate body activity. The spinal cord and
peripheral nerves are highly radioresistant, but the brain is more
sensitive than often supposed. Lesions and functional impairment have been
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observed for brain doses above 10 Gy (1000 rad) in adults. In children,

doses from l-6 Gy (100-600 rad) have produced detectable physical and
functional changes.8 Necrosis of the brain has an estimated threshold
dose of 50 Gy (5000 rad), the damage occurring directly or through lack of
blood supply due to blood vessel damage. Inflamation of the spinal cord
producing numbness, tingling, weakness or paralysis can be caused by
radiation damage depending on dose, irradiated tissue volume and nerve
location. The estimated threshold dose is 50 Gy (5000 rad). Peripheral
nerves have been damaged at doses > 60 Gy (6000 rad) during conventional
radiotherapy.

6. Thyroid Gland

The thyroid, a gland located at the base of the throat,

secretes a hormone known as thyroxine, which helps to control basal
metabolism. The action of the thyroid seems to be closely connected with
the functions of the pituitary and adrenal glands. Thyroxine contains
about 65 percent iodine, and is essential for growth and development.
Damage to the thyroid, or to the other two glands, have marked effects in
the body.
The thyroid is radioresistant from the standpoint of external
radiation. It can be severely damaged if radioiodine is inhaled, since
iodine will concentrate in the thyroid. Damage causes a decrease in
production of thyroxine (hypothyroidism) which produces a lower metabolism
rate. Muscle tissue may then fail to absorb enough oxygen and health can
be badly impaired. The threshold dose is estimated to be 45 Gy (4500 rad).
The sensitivity of the thyroid to cancer induction appears to
be higher than that for leukemia induction. However, the tumors are slowly
progressive so that treatment is generally successful. So, the mortality
(death rate) for thyroid cancers is much lower than that for leukemia. The
mortality risk factor is taken as 5x10-4 sv-l (5x10-6
rem-l).
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7. Eves

The lens ofthe eye is highly susceptible to irreversible

damage by radiation. The lens cells of the eye are not replaced by
regrowth. The retina is much less sensitive than the lens.
When the cells of the lens become damaged, the cells lose their
transparency. The opacities which may occur will appear after a latent
period. The term cataract is applied to these lens opacities. The
formation of cataracts is generally a late somatic effect. Acute effects
in other eye structures occur only after high doses. At high doses,
cataracts may develop within months, while at low doses, the latent period
may be years.
In the early stages of development, radiation induced cataract
may be distinguished from that due to other causes.I" The initial
opacity appears as almost a dot near the center of the lens, whereas
spontaneous cataracts tend to begin at the periphery of the lens. The
central opacity grows larger, developing a clear center, so that it
resembles a doughnut. As it continues to progress it becomes similar in
appearance to other types of cataracts, and therefore can no longer be
distinguished. It is possible for the lesion to grow for a time and then
remain stationary. The lowest dose observed to cause a progressive
cataract in radiotherapy patients was 5 Gy (500 rads). For the case of
occupational exposure, extrapolation suggests that > 8 Gy (800 rads) of
low LET radiation would be necessary to produce a vision impairing
opacity.
For high energy neutrons (7.5 MeV) in fractionated doses, the
threshold for visual impairment appeared to be 3-5 Gy (300-500 rad). On
this basis, the ICRP has recommended that no change is required for the
neutron quality factor relative to cataract formation. In relation to the
lens, other parts of the eye are radioresistant. In terms of the threshold
dose, the estimate is 5 Gy (500 rad) with respect to cataract production.
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8. Lungs

The lungs are cone-shaped organs made up of very small air sacs
called alveoli. When a person breathes, the air is directed down the
trachea (wind pipe). From there, two large tubes (bronchi) direct the air
toward each lung section. Many small tubes (bronchioles) branch out from
the bronchi to connect with the alveoli in the lungs.
During breathing, each air sac is expanded and compressed by
lung muscles, and is thus filled and emptied. Air passes through the walls
of the alveoli into tiny blood vessels (capillaries).
The effects produced in the lung by radiation are the result of
damage to the air sacs. The lungs are not normally affected by external
radiation. As in the case of the thyroid, the greater hazard occurs from
internal radiation from inhaled dust and vapors. However, when a major
portion of the lungs are irradiated at high dose, a fatal pneumonia may
result. The LD5() in man for acute exposure is about 8-10 Gy (800-1000
rad) for gamma rays. The damage which occurs is to the alveoli and the
lung blood vessels. The tissues of the upper respiratory tract are
relatively less radiosensitive. The threshold dose for nonstochastic
damage in the lung is 40 Gy (4000 rad).
Cancer of the lung has been observed in miners exposed to high
radon concentrations. There is also evidence that external irradiation can
induce lung cancer in man. The risk factor for lung cancer is 2~10~~
sv- 1 (2x10W6 rem-l).

9. Liver and Gall Bladder

The liver is radioresistant as compared with other organs. The

liver, the largest gland in the body, secretes bile for digestion. The
gall bladder stores and concentrates the bile secreted by the liver. When
bile is needed, it passes from the gall bladder to the intestine.
External radiation is not too effective in causing damage to
these organs. Most damage is caused by internal exposure from radionu-
elides which concentrate in the liver. Impairment of liver function occurs
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for exposure of the entire liver to 30 Gy (3000 rad) of conventional

therapeutic irradiation. The damage is indicated by decreased liver
function and fluid accumulation (ascites). The threshold dose for
nonstochastic effects in liver is 35 Gy (3500 rad).

10. Kidnevs

The kidneys help to control the concentration and content of

the blood by excreting water and waste products. The waste products pass
from the kidneys through small tubes (ureters) into the bladder (this
system is called the urinary tract). Impairment of renal functions does
not add to mortality in the case of total body radiation. Damage to the
kidney is indicated by an increase in amino acids in the urine. These
effects occur mostly from internal radiation. The appearance of blood in
the urine is an indication of severe renal damage. The dose to cause
injury in the system, is lowest for the kidneys, highest for the ureters.
The threshold dose for a fatal kidney infection (nephritis) is estimated
to be approximately 23 Gy (2300 rad) when delivered in fractionated doses.
The tolerance of the bladder is higher than that of the kidney, with a
threshold of 55-60 Gy (5500-6000 rad) when fractionated over 4 weeks.

11. Circulatory System

The heart and blood vessel system are damaged seriously only
for very high doses of radiation. The heart is not highly radiosensitive,
but can be damaged by doses in the range 40-60 Gy (4000-6000 rad). The
threshold for inducing inflammation of the lining surrounding the heart
(pericarditis) is 40 Gy (4000 rad). Blood vessels show damage after 40-60
Gy (4000-6000 rad). In many cases, vascular damage in advance of tissue
effects suggests that this is an important factor in tissue injury.

12. Skin

The degree of skin damage varies with the dose and the species
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of animal. Skin is easily damaged but has a tremendous capacity for

repair. Various structures of the skin show quite different sensitivities.
The damage seems to be greater for less penetrating radiations.
Slight damage to the skin may result in an erythema (redden-
ing). With increasing dose, loss of hair (epilation), dry, scaly skin and
death of tissue in the epidermis (outermost skin layer) may occur. For
increased damage, ulceration may result. The threshold dose for skin
ulceration is estimated to be 55 Gy (5500 rad).
Skin cancer is a late effect of chronic irradiation at very
high dose rates. However, skin is less likely to develop fatal cancer. 10
The ICRP feels that the nonstochastic limit for skin will prevent the
occurrence of skin cancer.

13. Hair

Irradiation can lead to temporary baldness (epilation). This

condition may last for a few weeks. The hair begins to return, but the new
hair may have different characteristics, such as a new color.
With respect to hair follicles, an acute dose of low LET of 3-5
GY (300-500 rad) can cause temporary epilation. The threshold for
permanent epilation for acute exposure is about 7 Gy (700 rad).

14. Bones

Bone is composed of living cells which are distributed in a

matrix of fibers and bone salts. Although the marrow of the bone is very
radiosensitive, the bone cells, fibers, and salts are relatively radio-
resistant.
When radionuclides, such as strontium or plutonium, are
internally deposited in the bone marrow or bone tissue, then great damage
can be done. These effects again are late effects since the damage may
take years to show up.
In children, the developing bone cells and cartilage show a
greater response. For doses as low as 1 Gy (100 rad), some retardation of
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growth may be seen. Mature bone in adults can withstand fractionated doses
of 65 Gy (6500 rad) in a 6-8 week period.
In adults, the developing bone cells lining the bone cavity are
the radiosensitive cells at risk with respect to cancer. The risk factor
is taken as 5~10~~ Sv-l (5~10~~ rem).

15. Muscle

Mature muscle is relatively radioresistant, but in children

when muscle is growing, the radiation response is greater. Contraction and
delayed healing show up for doses of approximately 60 Gy (6000 rad)
fractionated. The threshold dose is estimated to be > 100 Gy (10,000 rad).

16. Breast

The breast in females is one of the more radiosensitive organs

with respect to cancer induction. 6y10 The latent period seems to be
related strongly to age at exposure. An estimate of the latent period is 5
years for women 25 years or older.6. The risk factor is taken as
2.5x10- 3 Svm2 (2.5~10-~ rem-l).

REFERENCES

1. Norwood, W.D., HEALTH PROTECTION OF RADIATION WORKERS, Charles C.

Thomas, Springfield, IL (1975).

2. Casarett, A.P., RADIATION BIOLOGY, Prentice-Hall, Inc., Englewood

Cliffs, NJ (1968).

3. Andrews, H.L. RADIATION BIOPHYSICS, 2nd ed, Prentice-Hall, Inc.,

Englewood Cliffs, NJ (1974).

4. NCRP Report No. 39, Basic Radiation Protection Criteria, NCRP

Publications, Bethesda, MD (1971).

5. REPORT OF THE UNITED NATIONS SCIENTIFIC COMMITTEE ON THE EFFECTS OF

ATOMIC RADIATION, Seventeenth Session, Supplement No. 16 (A/5216),
United Nations, NY (1962).
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6. Committee on the Biological Effects of Ionizing Radiation, THE

EFFECTS ON POPULATIONS OF EXPOSURE TO LOW LEVELS OF IONIZING
RADIATION: 1980, National Academy Press, Washington, D.C. (1980).

7. ICRP Publication 41, Nonstochastic Effects of Ionizing Radiation,

Annals of the ICRP l4, No. 3, Pergamon Press, Oxford, England
(1984).

8. REPORT OF THE UNITED NATIONS SCIENTIFIC COMMITTEE ON THE EFFECTS OF

ATOMIC RADIATION, Ionizing Radiation: Sources and Biological
Effects, Report to the General Assembly, with Annexes, United
Nations, New York, NY (1982).

9. Glasstone, S., Editor, THE EFFECTS OF NUCLEAR WEAPONS, U.S.

Government Printing Office, Washington, D.C. (1962).

10. ICRP Publication 26, Recommendations of the International Commission

on Radiological Protection, Annals of the ICRP 1, No. 3, Pergamon
Press, Oxford, England (1977).

11. Lapp, R.E. and Russ, G.D., RADIATION RISKS FOR NUCLEAR WORKERS,
Atomic Industrial Forum, Inc., Public Affairs and Information
Program, Washington, D.C. (1979).

12. Cohen, B.L. and Lee, I., A Catalog of Risks, Health Physics 36,
707-722 (1979).

BIBLIOGRAPHY

ICRP Publication 14, Radiosensitivity and Spatial Distribution of Dose,

Pergamon Press, Oxford, England (1969).

ICRP Publication 27, Problems Involved in Developing an Index of Harm,

Annals of the ICRP 1, No. 4, Pergamon Press, Oxford, England (1977).

ICRP Publication 37, Cost-Benefit Analysis in the Optimization of

Radiation Protection, Annals of the ICRP l-0, No. 2/3, Pergamon Press,
Oxford, England (1983).

NCRP Report No. 64, Influence of Dose and its Distribution in Time on
Dose-Response Relationships for Low-LET Radiation, NCRP Publications,
Bethesda, MD (1980).

Cember, H., INTRODUCTION TO HEALTH PHYSICS, 2nd ed, Pergamon Press,

Oxford, England (1983).

Lloyd, D.C. and Purrott, R.J., Chromosome Aberration Analysis in

Radiological Protection Dosimetry, Rad. Prot. DOS. 1, No. 1, 19-28 (1981).
 Operational
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NCRP Report No. 80, Induction of Thyroid Cancer by Ionizing Radiation,

NCRP Publications, Bethesda, MD (1985).

NCRP Report No. 53, Review of NCRP Radiation Dose Limit for Embryo and
Fetus in Occupationally Exposed Women, NCRP Publications, Bethesda, MD
(1977) .

Cohen, B.L., Failures and Critique of the BEIR III Lung Cancer Risk
Estimates, Health Physics 42, 267-284 (1982).

ICRP Publication No. 18, The RBE for High-LET Radiations with Respect to
Mutagenesis, Pergamon Press, Oxford, England (1972).

NCRP Report No. 54, Medical Radiation Exposure of Pregnant and Potentially
Pregnant Women, NCRP Publications, Bethesda, MD (1977).

Pochin, E., NUCLEAR RADIATION: RISKS AND BENEFITS, Clarendon Press,

Oxford, England (1983).

Rossi, H.H., Microscopic Energy Distribution in Irradiated Matter, in

RADIATION DOSIMETRY, 2nd ed., Vol. 1, edited by F. H. Attix and W. C.
Roesch, Academic Press, New York, NY (1968).

Voelz, G.L., A 37-year Medical Follow-up of Manhattan Project Pu Workers,

Health Physics 48, 249-259 (1985).

NCRP Proceedings No. 6, Some Issues Important in Developing Basic Radia-

tion Protection Recommendations, NCRP Publications, Bethesda, MD (1985).

Proceedings of International Conference, Radiobiology of Radium and the

Actinides in Man, Edited by J. Rundo, P. Failla and R. A. Schlenker,
Health Physics 44, Supp. 1 (1983).

Rees, D.J., HEALTH PHYSICS, The MIT Press, Cambridge, MA (1967).

Morgan, K.Z. and Turner, J.E., Editors, PRINCIPLES OF RADIATION

PROTECTION, Chapters 11-13, John Wiley & Sons, Inc., New York, NY (1967).

USNRC ) Instruction Concerning Risks from Occupational Radiation Exposure,

Regulatory Guide 8.29, U.S. Nuclear Regulatory Commission, Washington, DC
(1981).

QUESTIONS

5.1 What is the basic unit of structure in the body?

5.2 What are main component elements of the basic unit of structure in
the body?

5.3 What are the two principal parts of a cell? What does each part do?
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5.4 What tiny parts in the nucleus of a cell determine the hereditary
traits of a daughter cell? To what are they attached?

5.5 What term is given to changes in the chromosomes or genes of cell?

5.6 Correlate the items in list A. with those in list B.

List A List B

cell division differentiation, gametes,

ba: bisexual cells somatic cells, hereditary
C. process of cell change cells, mitosis
d. cell damage limited to
the individual
e. germ line

5.7 Name two changes to atoms or molecules that will occur when radia-
tion passes through living cells.

5.8 What terms are given to the fragments of molecules that result from
radiation?

5.9 In what part of a cell is radiation damage most likely to be

serious?

5.10 What term indicates that dose of radiation below which no effects
are observed?

5.11 What term is used to indicate the different response of cells to

radiation?

5.12 List some of the factors affecting or determining the radiosensi-

tivity of cells.

5.13 Compare genetic damage with somatic damage to cells.

5.14 Define the term "median lethal dose" and indicate its symbol. What
level of dose does this term represent in man?

5.15 Explain the term RBE.

5.16 How is LET of the radiation related to the biological damage?

5.17 What are survival curves?

5.18 List some of the qualitative results that apply to high LET and low
LET radiation.

5.19 Under what conditions is sublethal damage of a cell repairable?

. l
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5.20 Explain the terms

a> CNS death

b) GI death
c> Bone-marrow death

5.21 List the late somatic effects.

5.22 Explain a) stochastic effects

b) nonstochastic effects

5.23 What is the basis for an acceptable level of risk?

5.24 List the three types of blood cells and the fluid that transports
them through the body. Indicate the principal function of each.

5.25 Indicate the effects that occur upon loss of

a> white cells,

b) platelets and
c> red cells

5.26 Indicate three functions of the spleen.

5.27 Which part of the digestive tract is highly radiosensitive?

5.28 What is the result of a high radiation dose to the reproductive

organs?

5.29 Which organ of the nervous system is the most radiosensitive?

5.30 What radionuclide presents the greatest internal hazard to the

thyroid gland?

5.31 What hazard do neutrons and x ray present to the eye?

5.32 From what does the greater radiation hazard to the lungs occur?

5.33 To what does the term "epilation" refer?

5.34 What organ of the body is easily damaged by radiation, but has a
tremendous capacity for repair?

5.35 Which part of the bone is the most radiosensitive?

5.36 Explain why the study of hereditary effects resulting from radiation
is difficult.
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PROBLEMS

5.1 The following table is adapted from the National Safety Council,
Accident Facts, 1979. Calculate the risk (the probability of death
per person/year) for each profession. How do these compare with
cancer risk due to radiation?

PROBABILITY OF ACCIDENTAL DEATH BY TYPE OF OCCUPATION

Number of Accidental
Occupation Deaths for 10,000 Workers
for 40 Years

a. Mining 252

b. Construction 228

C. Agriculture 216

d. Transportation and 116

Public Utilities

e. Government 44

Answers: a. 6.3x10-4/person-year
b. 5.7x10-4/person-year
C. 5.4x10-4/person-year
d. 2.9x10-4/person-year
e. l.lx10-4/person-year

5.2 According to the "absolute-risk projection model" of the 1980 BEIR

Report, if l,OOO,OOO people, representative of the U.S. population,
receive a single exposure of 0.1 Gy due to low LET radiation, there
would be 766 eventual cancer deaths as a result of the radiation.
Calculate the risk estimator. How does this compare with the risk
factor suggested by ICRP?

Answer: 7.66~10-~ cancer deaths/person-Gy

5.3 A town's population of 60,000 is exposed to radiation due to passage

of a radioactive cloud after an accident. The average gamma dose is
estimated to be 0.04Gy. What are the predicted cancer deaths

a> by BEIR model above, and

b) by ICRP risk factor?

Answer: a) - 18 b)- 30