CONTINUING EDUCATION

Basic Review of Radiation Biology and Terminology*

Norman E. Bolus, MSPH, MPH, CNMT, FSNMMI-TS

Nuclear Medicine Technology Program, University of Alabama at Birmingham, Birmingham, Alabama

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more radioresistant. A cell that is radiosensitive would be

The purpose of this paper is to review basic radiation biology and more inclined to die after exposure to ionizing radiation
associated terminology to impart a better understanding of the than a radioresistant cell (1). Although new terms such as
importance of basic concepts of ionizing radiation interactions “more or less radioresponsive” are now being used, the
with living tissue. As health care workers in a field that utilizes
basic tenets of their hypothesis hold true for living tissue
ionizing radiation, nuclear medicine technologists are concerned
about the possible acute and chronic effects of occupational reactions to ionizing radiation (2). Therefore, cells under-
radiation exposure. Technologists should have a clear under- going active mitosis are more likely to have an effect from
standing of what they are exposed to and how their safety could ionizing radiation, and stem cells (bone marrow, stomach
be affected. Furthermore, technologists should be knowledgeable mucosa, germ layer of the skin) are much more radiosen-
about radiation effects so that they can adequately assuage sitive than neurons, which either never replicate or do so
possible patient fears about undergoing a nuclear medicine very slowly. Experiments in fruit flies and mice have
procedure. After reading this article, the nuclear medicine
shown that the effects of ionizing radiation can cause mu-
technologist will be familiar with basic radiation biology con-
cepts; types of interactions of radiation with living tissue, and tations in progeny, but these mutations are not specific to
possible effects from that exposure; theoretic dose–response radiation. Such mutations are similar to ones that have
curves and how they are used in radiation biology; stochastic already been found to occur spontaneously in nature. Fur-
versus nonstochastic effects of radiation exposure, and what thermore, the experiments showed that the effects of ion-
these terms mean in relation to both high- and low-dose radi- izing radiation depend on total dose and exposure rate. A
ation exposure; and possible acute and chronic radiation expo- large dose given in a short amount of time is more dam-
sure effects.
aging than the same dose given over a longer period of
Key Words: radiation biology; radiation exposure; stochastic time (3).
radiation effects; nonstochastic radiation effects; acute radiation
The interaction of radiation with cells is a probability
effects; chronic radiation effects
function. Because cellular repair usually takes place, perma-
J Nucl Med Technol 2017; 45:259–264
nent damage will not necessarily result from an interaction of
DOI: 10.2967/jnmt.117.195230
ionizing radiation with living tissue. Energy deposition to a
cell occurs very quickly, in some 10218 s, with the energy
being deposited in the cell in a random fashion. All interac-
tions happen on a cellular level, which in turn may affect the
B asic radiation biology concepts include the traditional
assumptions of Bergonie and Tribondeau, who stated in
organ and the entire system. In addition, there is no unique
cellular damage associated with radiation. Any damage to a
1906 that any cells that are immature, undifferentiated, cell due to radiation exposure may also happen due to chem-
and actively dividing (e.g., stomach mucosa, basal layer ical, thermal, or physical damage. After radiation exposure to
of skin, and stem cells) are more radiosensitive. They re- a cell, there is a latent period before any observable response.
spond by exhibiting some effect from radiation exposure The latent period could be decades for low radiation doses but
that causes cell injury or death. Cells that are mature, dif- only minutes or hours for high radiation exposure. These basic
ferentiated, and not actively dividing (e.g., neurons) are generalizations form the foundation on which radiation biol-
ogy is based (4).
For correspondence or reprints contact: Norman E. Bolus, University of
Alabama at Birmingham, 1705 University Blvd., SHPB, Room 446, RADIATION INTERACTIONS WITH HUMAN CELLS
Birmingham, AL 35294.
E-mail: [email protected] What happens in a cell when ionizing radiation interacts
*This basic review article was previously published in Journal of Nuclear
Medicine Technology in June 2001.
with it? There are really only 2 possibilities: direct interaction
COPYRIGHT © 2017 by the Society of Nuclear Medicine and Molecular Imaging. or indirect interaction in a cell.

RADIATION BIOLOGY AND TERMINOLOGY REVIEW • Bolus 259

Direct Interaction TABLE 1
In direct interaction, a cell’s macromolecules (proteins or Hydrolysis of Water (5)
DNA) are hit by the ionizing radiation, which affects the cell
H2O (molecule) 1 ionizing radiation → H1 1 OH− 5 (hydroxyl,
as a whole, either killing the cell or mutating the DNA (2). free radical)
There are many target and cell survival studies showing that it Recombination of:
is harder to permanently destroy or break double-stranded DNA H1 1 H1 → H2 5 hydrogen gas (not a problem)
H1 1 OH− → H2O 5 water (not a problem)
than single-stranded DNA. Although humans have 23 pairs of
Antioxidants can recombine with the OH− free radical and
double-stranded chromosomes, some cells react as if they con- block hydrogen peroxide formation. If not, then the 2
tain single-stranded, nonpaired chromosomes and are more ra- hydroxyl ions could do the following:
diosensitive. Many different types of direct hits can occur, and OH− 1 OH− → H2O2 5 hydrogen peroxide formation
the type of damage that occurs determines whether the cell can H2O2 → H1 1 HO2− 5 unstable peroxide
HO2− 1 organic molecule → stable organic peroxide
repair itself. Generally, if a direct hit causes a complete break in Stable organic peroxide → lack of essential enzyme →
the DNA or some other permanent damage, the cell dies im- eventual cell death is possible
mediately or will die eventually (5). However, humans have an
abundance of cells, and somatic cellular reproduction (mitosis)
is always occurring to replace cells that die. Therefore, it is only
when this system of replacing cells falters that radiation effects dependent delay in cell division; reproductive failure, when
are seen. This occurs at higher doses of radiation. cells fail to complete mitosis either immediately or after
Actively dividing cells are more radiosensitive than nondi- one or more generations; and interphase death, a relatively
viding cells. There are 4 phases of mitosis: M phase, in which prompt death caused by the apoptosis mechanism. The last
cells divide into two; G1 phase (gap 1), in which cells prepare is seen most commonly with lymphocytes, although some
for DNA replication; S phase, in which DNA doubles by cancer cells show apoptosis in response to radiation.
replication; and G2 phase (gap 2), in which cells prepare for In division delay, mitotic division is delayed but later
mitosis. Of these, M phase, in which the chromosomes are returns to near normal for unknown reasons. This is seen in
condensed and paired, is the most radiosensitive. More DNA doses greater than 0.5 Gy (50 rad) up to approximately 3
is present in one area at this point in the cycle, which is why it Gy (300 rad). This is the first observable effect from
is theorized that this is the most radiosensitive time. It is also ionizing radiation exposure. At more than 3 Gy (300 rad),
thought that increased chromatin in cancer cells is why these the mitotic rate does not recover and the division may never
cells, which have unusually high mitotic rates, are more happen, thus killing the cell.
radiosensitive than normal cells (6). Reproductive failure of a cell is based on the dose. At
levels at or below 1.5 Gy (150 rad), reproductive failure is
Indirect Interaction
random and nonlinear. At doses above 1.5 Gy (150 rad),
The other type of interaction is indirect cellular interaction. it is linear and nonrandom. As dose increases, so does re-
Indirect interaction occurs when radiation energy is deposited productive death.
in the cell and interacts with cellular water rather than with In interphase death, cell death can occur many genera-
macromolecules within the cell. The reaction that occurs is tions from the initial radiation exposure. It is thought either
hydrolysis of the water molecule, resulting in a hydrogen
that this is a natural process of aging cells (apoptosis) or
molecule and a hydroxyl (free radical) molecule. If the 2
that a critical mechanism of cell replication has been
hydroxyl molecules recombine, they form hydrogen peroxide,
altered. It depends on the type of cell affected and the
which is highly unstable in the cell. This will form a peroxide
dose to the cell. Generally, rapidly dividing, undifferenti-
hydroxyl, which readily combines with some organic com- ated cells exhibit interphase death at lower doses than
pound, which then combines in the cell to form an organic nondividing, differentiated cells.
hydrogen peroxide molecule, which is stable. This may result Any of these types of cellular injury can happen as a
in the loss of an essential enzyme in the cell, which could lead result of either direct or indirect cellular interactions with
to cell death or a future mutation of the cell (Table 1) (5).
radiation (5).
Antioxidants, about which there has been much research and
publicity, block hydroxyl (free radical) recombination into hy-
DOSE–RESPONSE MODELS
drogen peroxide, preventing stable organic hydrogen peroxide
compounds from occurring. This is one way in which the body There are many different theoretic types of dose–
can defend itself from indirect radiation interactions on a cel- response models used to explain the effects of radiation
lular level and is one reason that antioxidants have received so exposure. Different models suggest different possibilities
much attention as a cancer prevention agent (7). of response to radiation exposure. These range from linear–
no threshold, which suggests any exposure (even back-
ground radiation) is harmful, to the possibility that low-
CELLULAR INJURY dose radiation exposure is beneficial (radiation hormesis).
There are 3 ways for cellular injury to occur after Three dose–response models used in radiation biology are
ionizing radiation exposure: division delay, with dose- linear no-threshold, linear threshold, and linear quadratic.

260 JOURNAL OF NUCLEAR MEDICINE TECHNOLOGY • Vol. 45 • No. 4 • December 2017

These dose–response models are used to extrapolate high- may make the most sense to use, because it is generally
dose effects (which are known) to the low-dose range accepted that there are no clinical effects seen from radia-
(which has not been reliably detected) (Fig. 1). tion exposure at or below 0.5 Gy (50 rad). In 1996, the
Health Physics Society released the following position
Linear No-Threshold Model
statement on low-level radiation (10): “In accordance with
For any known carcinogen at any level of exposure (e.g.,
current knowledge of radiation health risks, the Health
benzene, asbestos, or high-dose radiation) a linear no-
Physics Society recommends against quantitative estima-
threshold dose–response model is used across all industries.
tion of health risks below an individual dose of 0.05 Sv
This model states that any radiation exposure, no matter how
(5 rem) in one year, or a lifetime dose of 0.1 Sv (10 rem)
small, can induce cancer. While this is a possibility, generally
in addition to background radiation. Risk estimation in this
no clinical effects are seen below approximately 0.5 Gy (50
dose range should be strictly qualitative accentuating a
rad). The linear no-threshold dose–response model is used for
range of hypothetical health outcomes with an emphasis
regulatory purposes, whenever a xenobiotic or other carci-
on the likely possibility of zero adverse health effects.
nogenic agent is known at any dose level (8).
The current philosophy of radiation protection is based on
At high doses, or more than 0.5 Gy (50 rad), clinical
the assumption that any radiation dose, no matter how
symptoms of radiation start to appear; at much higher doses,
small, may result in human health effects, such as cancer
radiation exposure is clearly a known carcinogen, primarily
and hereditary genetic damage. There is substantial and
because of its mutagenic effect on cells. The greatest
convincing scientific evidence for health risks at high dose.
association is with leukemia (9). However, it is difficult to
Below 0.1 Sv (10 rem) (which includes occupational and
say that any cancer is caused solely by radiation exposure, as
environmental exposures) risks of health effects are either
cancer may be caused by a combination of factors. Because
too small to be observed or are nonexistent.” Although this
it is best to err on the side of caution, the “as low as reason-
position statement suggests levels 5-fold less for clinical
ably achievable” (ALARA) principle and the linear no-
effects, it still indicates that a threshold does exist to a
threshold dose–response model are used.
certain degree in radiation exposure. This statement favors
Linear Threshold Model a linear threshold dose–response model with a threshold of
The linear threshold dose–response model consists of a 0.1 Sv (10 rem).
known threshold below which no effects are seen. At the
Linear Quadratic Model
threshold level, effects are noticeable and increase linearly
The linear quadratic dose–response model is used for
as the dose increases. This is the dose–response model that
overall human response to radiation exposure. Response at
low levels of radiation exposure are linear, whereas higher
doses are quadratic. There is no threshold in this dose–
response model. In cell survival theories, the linear quadratic
dose–response model is used to represent the multiple-target/
single-hit theory. This theory best explains the reaction of
human cells to ionizing radiation exposure.
Summary of Dose–Response Models
It is important to remember that for all dose–response
models, the dose makes the poison. Perhaps this was best
stated by Paracelsus, who is considered the father of toxi-
cology: “All substances are poisons; there is none which is
not a poison. The right dose differentiates a poison from a
remedy” (11). Generally, as the dose increases, response
increases to a toxic point; in other words, anything in ex-
cess can be toxic. Radiation dose–response models vary
depending on what is being analyzed. It is important to
remember that there is evidence to suggest a possible
threshold for radiation exposure that would favor the linear
threshold dose–response model. Also, any dose–response
model for radiation in the lower levels is extrapolated from
what is known at high-dose levels. Thus, any lower-level
response from radiation is only theorized, not proven. The
FIGURE 1. This figure shows dose curves that correspond to only dose–response model accepted by the Nuclear Regu-
dose models described in text. Data are measured at high dose
levels and then, using curve-fitting techniques, extrapolated to latory Commission is the linear no-threshold dose–response
estimate low-dose portion of curve. Low-dose data points model, which suggests that any radiation exposure can lead
shown on these curves are thus estimated, not measured. to cancer induction.

RADIATION BIOLOGY AND TERMINOLOGY REVIEW • Bolus 261

 TABLE 2
Summary of Nonstochastic (Deterministic) Effects (5)

Syndrome Summary

Hematologic Dose: Approximately 1–10 Gy (100–1,000 rad)

Clinical symptoms: General injury of blood-forming cells in bone marrow, which increases with increasing
dose, leading to pancytopenia. This results in bleeding, anemia, hemorrhage, malaise, and severe,
often fatal, infection.
Treatment:
0–1 Gy (0–100 rad)—Reassurance
1–2 Gy (100–200 rad)—Reassurance and hematologic surveillance
2–6 Gy (200–600 rad)—Blood transfusion and antibiotics
6–10 Gy (600–1,000 rad)—Consider bone marrow transplant
Without treatment, no one has survived a single abrupt dose of 5 Gy (500 rad) or higher. It is possible to
survive the hematologic syndrome with a bone marrow transplant, but at higher doses all subjects
will die from the gastrointestinal syndrome.
Gastrointestinal Dose: Approximately 2–50 Gy (200–5,000 rad)
Clinical symptoms: Nausea, vomiting, and diarrhea; prolonged diarrhea; dehydration; electrolyte
imbalance; lethargy; anorexia; death above 10 Gy (1,000 rad) with no treatment.
Treatment:
2–6 Gy (200–600 rad)—Blood transfusion and antibiotics
6–10 Gy (600–1,000 rad)—Consider bone marrow transplant
10–50 Gy (1,000–5,000 rad)—Maintenance of electrolyte balance
At about 2 Gy (200 rad), classic radiation sickness (nausea, vomiting, and diarrhea) may begin because of
radiation injury to the gastric and intestinal mucosa.
Central nervous system Dose: .50 Gy (.5,000 rad)
Clinical symptoms: Ataxia, convulsions, lethargy, coma, death
Treatment: Sedatives

STOCHASTIC VERSUS NONSTOCHASTIC EFFECTS OF (deterministic) effects include hematologic syndrome (pan-
RADIATION EXPOSURE cytopenia), erythema, gastrointestinal syndrome (radiation
Stochastic means random in nature. There is a statistical sickness), and central nervous system syndrome (Table 2).
accounting for all diseases that could be caused by any of One concept used to gauge toxicity is that of the lethal
several different xenobiotics or carcinogens; any random oc- dose to 50% of the population (LD50) exposed to the agent
currence of a disease that cannot be attributed solely to ra- observed at a specific time. The LD50 at 30 d (LD50/30) for
diation is stochastic. As far as cancer is concerned, it is humans due to ionizing radiation exposure is approximately
extremely difficult to say whether a particular cancer is at- 2.5–4.5 Gy (250–450 rad). This estimate for humans varies
tributable to a specific exposure because most cancers have a between different sources and is primarily empiric. There-
20-y latency period from exposure to manifestation. There- fore, concrete data are not available. In other organisms, the
fore, chronic low-dose radiation exposure effects are seen as LD50/30 factor has been established through experiments
stochastic. At diagnostic levels, where doses are low, sto- (Table 3) (5).
chastic effects are random and the odds of having any effect
ACUTE VERSUS CHRONIC EFFECTS
are extremely low. A few people may experience an effect
from the radiation exposure, but this cannot be predicted. Acute Radiation Effects
Radiation risks from diagnostic imaging are considered to Acute ionizing radiation exposure is “harmless” at back-
be stochastic. Also, heredity effects and carcinogenesis are ground or diagnostic levels but is nonstochastic and harm-
considered to be stochastic (5). ful at high-dose levels. At or above approximately 0.5 Gy
Ionizing radiation at high doses causes certain specific
effects. Therefore, at certain doses, certain predictable
TABLE 3
outcomes can be determined. These are called nonstochas-
LD50/30 Values for Different Species (5)
tic, or deterministic, effects. These effects are very predict-
able and range from blood and chromosome aberrations to Species LD50/30
radiation sickness to certain death, depending on the dose,
Cockroach 50 Gy (5,000 rad)
dose rate, age, immune capacity of an individual, and type Rabbit 8 Gy (800 rad)
of radiation exposure. Goldfish 7.5 Gy (750 rad)
For g- and x-ray radiation, exposure measured in grays Rat 6 Gy (600 rad)
and sieverts (rads and rems) is equal; however, this is not true Mouse 4.5 Gy (450 rad)
Monkey 4.5 Gy (450 rad)
of neutron radiation or when the quality factor is greater than Human ∼2.5–4.5 Gy (250–450 rad)
1 for the conversion between rads and rems. Nonstochastic

262 JOURNAL OF NUCLEAR MEDICINE TECHNOLOGY • Vol. 45 • No. 4 • December 2017

 TABLE 4
Summary of Acute Clinical Effects of Ionizing Radiation (9)
Radiation exposure range

Subclinical Therapeutic Lethal

(0–1 Sv 10–50 Sv
Parameter [0–100 rem]) 1–2 Sv (100–200 rem) 2–6 Sv (200–600 rem) 6–10 Sv (600–1,000 rem) (1,000–5,000 rem) .50 Sv (.5,000 rem)

Treatment required Reassurance Reassurance and Blood transfusion Consider bone Maintenance of Sedatives
hematologic surveillance and antibiotics marrow transplant electrolyte balance
Overall treatment plan None needed Observation Effective Therapy promising Palliative Palliative
Incidence of vomiting None 5% at 1 Sv (100 rem); 100% at 3 Sv (300 rem) 100% 100% 100%
50% at 2 Sv (200 rem)
Delay time prior to N/A 3h 2h 1h 30 min 30 min
vomiting
Leading organ affected None Blood-forming tissue Blood-forming tissue Blood-forming tissue Gastrointestinal tract Central nervous system
Characteristic signs None Mild leukopenia Severe leukopenia; Severe leukopenia; Diarrhea; fever; Convulsions; tremor;
hemorrhage; hair loss infections; erythema electrolyte ataxia; lethargy
above 3 Sv (300 rem) imbalance
Critical period N/A N/A 4–6 wk 4–6 wk 5–14 d 1–48 h
after exposure
Prognosis Excellent Excellent Good Guarded Hopeless Hopeless
Incidence of death None None 0%–80% 80%–100% 90%–100% 90%–100%
Cause of death N/A N/A Hemorrhage and infection Hemorrhage and infection Circulatory collapse Respiratory failure and
brain edema

TABLE 5
Staging of Acute Radiation Syndromes (5)

Phase Description

Prodromal (“running before”) Signs and symptoms include nausea, vomiting, and diarrhea; hair loss above 3 Gy (300 rad);
skin erythema above 6 Gy (600 rad)
Latent Period of no signs or symptoms
Manifest Nausea, vomiting, and diarrhea return; hematologic syndrome; gastrointestinal syndrome;
central nervous system syndrome; signs and symptoms return to prodromal levels or worse
Recovery If good treatment is provided and the affected individual received less than a 10-Gy (1,000-rad)
dose, recovery is possible after the manifest phase

(50 rad), acute effects are predictable and follow a linear lens of the eye can cause formation of cataracts. At lower
path. Some chromosome aberrations may be seen under a doses, damage is similar to senile cataracts but is less severe.
microscope at or below 0.5 Gy (50 rad), but no clinical Another possible chronic stochastic effect is shortening of
symptoms have been found to manifest from this observa- the life span. Although there is no conclusive evidence of
tion. However, this can be used as a bioassay technique such, it is theorized in some literature (8).
years after an acute exposure. Table 4 shows the generally As a stochastic effect, leukemia has been associated with
accepted acute effects and symptoms these dose ranges can chronic radiation exposure at doses as low as 50–100 cGy
be expected to manifest (8). There are sequelae of acute (50–100 rad). Between 100 and 500 cGy (100–500 rad),
ionizing radiation exposure from which certain well- there is a linear correlation between dose and leukemia
defined syndromes can be expected (Table 5) (5).
In radiation therapy, acute nonstochastic effects of TABLE 6
radiation exposure include radiation fibrosis in the lung Average Annual Effective Dose Equivalent to a Member of
when normal lung tissue is exposed. Other tissues that show the U.S. Population (14,16)
effects are the kidney, brain, and spinal cord. Because tissue
Source Effective/whole-body dose
injury is known to occur if a certain threshold is exceeded,
there are well-established guidelines in radiotherapy to Average annual dose to 6.2 mSv (0.62 rem)
avoid exceeding a specific dose (12). U.S. population from all
sources
Chronic Radiation Effects Radon & thoron 2.28 mSv (0.228 rem)
Conventional radiography & 0.33 mSv (0.033 rem)
Chronic effects of ionizing radiation exposure are primar-
fluoroscopy
ily stochastic. The chief concern is possible cancer induction. Computed tomography 1.47 mSv (0.147 rem)
However, noncancerous effects are possible, such as cataract Nuclear medicine 0.77 mSv (0.077 rem)
formation in the eye. This would be a possible stochastic Consumer products 0.13 mSv (0.013 rem)
chronic effect, with a probability that increases with in- Cosmic radiation 0.33 mSv (0.033 rem)
Terrestrial radiation 0.21 mSv (0.021 rem)
creasing dose. Radiation doses of 500–800 R directed at the

RADIATION BIOLOGY AND TERMINOLOGY REVIEW • Bolus 263

 TABLE 7 CONCLUSION
Whole-Body Patient Doses from Nuclear Medicine
This brief synopsis of radiation biology is intended as a
Procedures (15)
review of terminology and concepts. Unfortunately, con-
Radiopharmaceutical cGy/mCi (rad/mCi) clusive information is elusive at the low-dose levels of
67Ga-citrate
radiation exposure that technologists encounter. Stochastic
0.26
201Tl-chloride 0.21 low-dose radiation exposure effects are only theorized from
18F-FDG 0.04 extrapolating data from known responses of high-dose
123I-iodide 0.03 radiation exposure. High-dose radiation effects are well
99mTc-sulfur colloid 0.019
99mTc-MIBI
established and follow nonstochastic (deterministic) re-
0.017
99mTc-DTPA 0.016
sponses. In the safety industry, protection of personnel
99mTc-DISIDA 0.016 working with known carcinogens is paramount. The radiation
99mTc-MAA 0.015 industry is no different from other industries that have
99mTc-HMPAO 0.013
99mTc-pertechnetate
threshold limit values and biologic exposure indices for
0.011
99mTc-MDP 0.007
worker exposure. These allowed limits offer a guideline
99mTc-MAG3 0.007 for acceptable exposure, below which no ill effects are
expected. In the radiation industry, these are known as
total effective dose equivalents (Table 8).
incidence. Data suggest that the incidence of leukemia in- Radiation biology is a diverse field that covers many
creases at a rate of 1–2 cases per million per year per cen- areas of knowledge, including cell biology, chemistry,
tigray (1 rad) as a result of exposure. There is an average radiation physics, human physiology, radiation safety,
latency period of 14 y from exposure to onset of disease. epidemiology, biostatistics, and toxicology. Information
Higher doses of ionizing radiation have also been associated about this topic continues to evolve as more knowledge is
with thyroid, bone, lung, and various other cancers (8). obtained about ionizing radiation interactions with cells. It
Interestingly, there is no conclusive evidence that can be confusing to delve into radiation biology without
chronic low-dose radiation exposure causes any long-term understanding the basic concepts outlined in this article. Be
ill health effects in workers in the medical field (13). aware that this overview barely begins to discuss all of the
Furthermore, there is no evidence to suggest that regular information available about radiation biology.
background amounts of radiation exposure cause any
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