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CHAPTER 8 Early Tissue Reactions and Their Effects on Organ Systems
147

Effects on the Reproductive System

Some of the early tissue reactions from ionizing radiation have been discussed in Chapter 7.
Human germ cells are relatively radiosensitive. Doses as low as 0.1 Gyt can depress the male sperm population, and this same dose has the potential to cause genetic
mutations in future generations. In females, a gonadal
dose of 0.1 Gyt may delay or suppress menstruation.
Animal experiments and data from irradiated hu­man populations have provided important information on gonadal response to radiation exposure. Irradiated human populations include:
• Patients who have undergone radiation therapy
• Radiation accident victims
• Volunteer convicts
The testes of the male and the ovaries of the female do not respond in the same manner to irradiation be­cause of the differences in the method in which these cells are produced and progress from elementary stem cells to mature cells. The spermatogonia, the stem cells of the testes, continually reproduce. They evolve and become spermatocytes. The latter cells then multiply and develop into spermatids that eventually differenti­ate and become spermatozoa, or sperm, which are the functionally mature germ cells (Fig. 8.8). The develop­ment of the male stem cell into a functionally mature germ cell takes 3 to 5 weeks.
In the female, the oogonia, the ovarian stem cells, multiply to millions of cells only during fetal develop­ment, before birth, and then they steadily decline in number throughout life. During the latter part of fetal development, the oogonia become encapsulated by nu­merous primordial (primary) follicles that grow around them (see Fig. 8.8). The oogonia then become oocytes,
Male:
Spermatogonia
Female:
8,9
5
Spermatocyte Spermatid Sperm
which contain follicles that are nests of cells, some of which eventually mature during the reproductive life of a woman. Before these primary oocyte-containing fol­licles grow into mature follicles, they remain dormant until puberty. Then, just before puberty, the oocytes are reduced in number to only several hundred thousand. Some of the cells of the primary follicles proliferate in response to stimulation by hormones from the pituitary gland, and these cells begin to mature. At the same time, the ovum contained within each of the follicles under­goes meiosis. As puberty begins, the developed ova, or mature female germ cells*, within the follicles are ejected when the follicles themselves rupture. Usually, only one follicle will fully mature and move toward the surface of the ovary to be expelled, and the others disin­tegrate. This process occurs at regular time intervals of approximately 28 days. Of the mature ova that are actu­ally enclosed within the follicles, only 400 to 500 are produced, matured, and made available for fertilization during a woman’s reproductive life.
Follicles range in size from small to large. Of these, the intermediate-size follicles are the most radiosensi­tive, and the small follicles are the least radiosensitive. Large, mature follicles possess only a moderate degree of radiosensitivity.10 During the female menstrual cycle, a mature follicle releases an ovum during the period of ovulation, when a ripe egg is expelled from an ovary into the pelvic cavity. If a waiting male sperm does not fertilize that ovum in the uterus, it will be lost during menstruation and not replaced.

Hematologic Effects

As a brief review, recall that during the 1920s and 1930s, periodic blood counts were the only means of radiation exposure monitoring for radiation workers engaged in radiologic practices. The use of personnel dosimeters for monitoring occupational exposure made the simplistic practice obsolete. When blood counts were used to monitor the effects of radiation exposure among those who worked with radiation, a whole-body radiation dose of 0.25 Gyt would be required to produce a measur­able hematologic depression. Such a dose could cause enough of a decrease in the number of lymphocytes in
Primordial
follicle
Fig. 8.8 Development of the germ cell from the stem cell
phase to the mature cell.
Mature follicle Corpus luteum Ovum
*Mature female germ cells or eggs are those that have entered stage M2 of meiosis. The end result of meiosis is the halving of the number of chromosomes and genetic material.
148
CHAPTER 8 Early Tissue Reactions and Their Effects on Organ Systems
the blood to render the body vulnerable to infection by foreign invaders. This method therefore, was com­pletely unfounded for modern principles of radiation protection.
Hematopoietic System. The hematopoietic system
consists of:
• Bone marrow
• Circulating blood
• Lymphoid organs (lymph nodes, spleen, and thymus gland) Cells of this system develop from a single precursor
cell, the pluripotential stem cell. The following are other types of cells that originate from this one type of primary cell: lymphocytes, granulocytes, thrombocytes or platelets, and erythrocytes. Fig. 8.9 demonstrates the progressive development of these cells from a single pluripotential stem cell. Most of these blood cells are manufactured in bone marrow at different intervals, and when they mature, they enter the blood capillaries and the peripheral circulation. Even though blood cells are continually being produced, the life span of each type of blood cell differs, varying, on average, from only a few hours (e.g., lymphocytes) to almost 120 days (e.g., erythrocytes).
The human body may experience health-related con-
sequences throughout life if there is a decrease in the numbers of these various cells. Some of these conse­quences will be increased susceptibility to aggressive
infectious organisms, higher risk of hemorrhage, and anemia.
Radiation doses resulting from diagnostic imaging procedures during which appropriate radiation protec­tion methods have been employed for patients and all personnel result in negligible damage to the blood and the blood-forming organs. However, in this dose range, some chromosomal changes in circulating lymphocytes have been observed.

Cytogenetic Effects

In simple terms, cytogenetics may be defined as the study of cell genetics with an emphasis on cell chromo­somes. The techniques used to study and observe the chromosomes of each human cell have contributed sig­nificantly to advancing genetic analysis and the under­standing of the influence of radiation on genetics.
Cytogenetic analysis of chromosomes may be ac­complished through the use of a chromosome map called a karyotype. This map consists of a photograph or photomicrograph, of the human cell nucleus during metaphase, when each chromosome can be individually perceived. The karyotype is constructed by extracting the individual chromosomes and pairing them on the map with their sister chromosomes. These chromosome pairs are usually aligned by size, beginning with the largest pair and ending with the smallest pair (Fig. 8.10).
Metaphase is the phase of cell division in which
chromosome damage caused by radiation exposure can
Reticulocyte Pronormoblast
Erythrocytes
Stem cell
Myeloblast
Neutrophilic
granulocytes
Fig. 8.9 Progressive development of various cells from a single pluripotential stem cell.
Eosinophilic
granulocytes
Megakaryoblast
Platelet-producing megakaryoblast
Lymphoblast
Thrombocytes
(platelets)
Lymphocyte
CHAPTER 8 Early Tissue Reactions and Their Effects on Organ Systems
149
A
1
C
6
D
13
F
19
Fig. 8.10 A photomicrograph of the human cell nucleus at metaphase that shows each chromosome indi-
vidually demonstrated. The karyotype is constructed by cutting out the individual chromosomes and pairing them with their sister chromosomes. These chromosome pairs are usually aligned by size, beginning with the largest pair and ending with the smallest pair. The left karyotype is male, and the right is female. (From Carolyn Caskey Goodner, Identigene, Inc.)
2
8
7
14
20 21 22
15
G
B
3
9 10
E
16
4
11
17 18
Sex
chromosomes
X Y
5
12
be evaluated. Chromosome aberrations (deviation from normal development or growth of structures that con­tain genetic material) and chromatid aberrations have been observed at metaphase.
Both low and high radiation doses can cause chro­mosomal damage that may not be apparent immedi­ately. The majority of chromosomal damage results from the process of indirect action of ionizing radiation on vital biologic macromolecules.
Almost every type of chromosome aberration can be caused by exposure to ionizing radiation. However, some aberrations can “only” be produced by radiation exposure.5 The total radiation dose delivered to a so­matic or genetic cell and the duration in which the dose was delivered determine the rate of production of chro­mosome aberrations.
Attempts have been made to measure chromosome aberrations after diagnostic x-ray imaging procedures, but successful results have not been achieved in these studies. For imaging procedures that involve much higher radiation dose rates, studies demonstrated that radiation­induced chromosome imperfections were observed shortly after the imaging procedure was completed.
Increased frequency of chromosome translocations is an established radiation biomarker and may also
A
1
C
6
D
13
F
19
2
8
7
14
20 21 22
15
G
B
3
9
E
4
10
16
11
17 18
Sex
X Y
chromosomes
5
12
suggest increased cancer risk.11 An occupational epi­demiologic study of 146,000 US radiologic technolo­gists began in 1982 and is still in progress. This study is a collaborative effort of the University of Minnesota School of Public Health, the National Can­cer Institute, and the American Registry of Radiologic Technologists.
12,13
The purpose of the research is “to determine whether their personal cumulative expo­sure to diagnostic x-rays was associated with in­creased frequencies of chromosome translocations”11 and possible associated cancer risk. Included in the study were mail surveys, telephone interviews, and a collection of 150 blood samples for testing purposes. Results of the blood tests indicated increased chromo­some damage as a consequence of cumulative work­related exposure from routine x-ray procedures.11 For patients, computed tomography (CT) and nuclear medicine procedures can contribute substantially to higher radiation exposure. “Some studies have found increased chromosome abnormalities immediately after radiation exposure from CT scanning”
11,14
or in patients with unusually high numbers of diagnostic procedures.
11,15
These studies, however, have failed to show similar levels for low dose CT versions of the same scan.
150

S U M M A R Y

CHAPTER 8 Early Tissue Reactions and Their Effects on Organ Systems
• Biologic effects that occur relatively soon after hu­mans receive high doses of ionizing radiation are generally referred to as early effects.
• Early tissue reactions are not common in diagnostic radiology.
• Somatic effects are effects upon the body that was irradiated.
• Genetic effects are effects upon future generations due to the irradiation of germ cells in previous generations.
• Somatic tissue reactions include cell killing and are directly related to the dose of radiation received. As dose increases, so does the severity of these early tissue reactions.
• Early tissue reactions vary depending on the duration of time after exposure to ionizing radiation. They may appear within minutes, hours, days, or weeks after receiving a high dose of ionizing radiation.
• Possible high radiation dose consequences generally include nausea and fever, extreme fatigue, erythema, epilation, and blood and intestinal disorders. Also, temporary or permanent sterility in the male and female and injury to the central nervous system (at extremely high radiation doses) can occur.
• Acute radiation syndrome (ARS) occurs in humans after large whole-body doses of ionizing radiation delivered over a short period.
• ARS can manifest as hematopoietic syndrome,
gastrointestinal syndrome, and cerebrovascular syndrome.
• ARS presents in four major response stages: pro-
dromal, latent period, manifest illness, and recov­ery or death.
• LD (lethal dose) 50/30 signifies the whole-body dose of ionizing radiation that can be lethal to 50% of an exposed population within 30 days.
• LD 50/30 for adult humans is estimated to be 3 to
4 Gyt without medical support.
• When cells are exposed to sub-lethal doses of ion-
izing radiation, repair and recovery are possible.
• After receiving a sub-lethal dose of radiation,
surviving cells will be able to divide and thereby begin to repopulate in the irradiated region.
• Approximately 90% of radiation-induced damage
may be repaired over time; 10% is irreparable.
• High radiation doses to any part of the human body can result in local tissue damage.
• Significant cell death usually results after substantial radiation exposure, leading to potential atrophy of involved organs and tissues.
• Depending on the types of cells included and the dose of radiation received, recovery may be partial or complete, or it may not occur, resulting in failure of the irradiated biological structure.
• Factors such as radiosensitivity, reproductive charac­teristics, and growth rate govern organ and tissue response to radiation exposure.
• Many early radiologists and dentists developed ra­diodermatitis as a consequence of radiation exposure to the skin that eventually led to the development of cancerous lesions.
• Human skin consists of three layers and several
accessory structures, all of which are actively involved in the response of tissue to radiation exposure.
• A single absorbed dose of 2 Gyt can cause radia-
tion-induced skin erythema within 24 to 48 hours after irradiation.
• High radiation doses to the skin can cause moist
skin pealing, and then dry desquamation.
• Moderate radiation doses to the scalp can cause
temporary hair loss, and large radiation doses can result in permanent hair loss.
• Significant evidence of skin damage as a conse-
quence of exposure to orthovoltage radiation therapy comes from oncology patients who un­derwent such treatments in earlier years for deep­seated tumors.
• The use of high-level fluoroscopy for extended
periods can result in radiation-induced skin inju­ries for patients.
• Human germ cells are relatively radiosensitive.
• In males, a radiation dose to the gonads of 0.1 Gyt
can depress the sperm population and possibly cause genetic mutations in future generations.
• In females, a gonadal dose of 0.1 Gyt may delay or
suppress menstruation.
• Personnel dosimeters have replaced periodic blood counts as an accurate means to monitor occupa­tional radiation exposure.
• When blood counts were used to monitor the effects of radiation exposure among those who worked with radiation, a whole-body radiation dose of 0.25 Gyt
CHAPTER 8 Early Tissue Reactions and Their Effects on Organ Systems
151
would be required to produce a measurable hemato­logic depression.
• The mapping of chromosomes is karyotyping.
• Karyotyping is performed during metaphase, when each chromosome can be individually perceived and radiation-induced chromosome and chroma­tid aberrations can be observed.
• Chromosomal damage can be caused by both low
• Chromosome aberrations have been observed in

G E N E R A L D I S C U S S I O N Q U E S T I O N S

1. Although early tissue reactions are not common in
diagnostic radiology, what type of diagnostic imag­ing procedure could possibly produce a radiation dose sufficient to cause such a reaction?
2. In what do unacceptable high x-ray exposures in
radiology primarily result?
3. How can a cytogenetic analysis of chromosomes be
accomplished?
4. What are genetic effects?
5. How have scientists become aware of radiation-
induced skin damage in early pioneers?
6. What are the three separate dose-related syndromes
that occur as part of acute radiation syndrome, and what are the four major response stages?
7. What is radiodermatitis?
8. After the reception of a single absorbed dose of
9. How has information on the gonadal response to
10. How significant is the chance of causing sterility in
11. What are the somatic effects of radiation exposure?
12. From where does the term somatic originate?
and high radiation doses.
individuals after completion of some imaging procedures.
2 Gyt of radiation, approximately how long will it take to cause radiation-induced skin erythema?
radiation exposure been acquired?
imaging personnel who perform routine procedures?

R E V I E W Q U E S T I O N S

1. The total radiation dose given to a somatic or genetic
cell and the period of time in which that dose was delivered determine the rate of production of:
A. Cell division B. Chromosome aberrations C. Genetic analysis D. Karyotyping
2. Acute radiation syndrome presents in four major
response stages. In what order do these stages occur?
A. Latent period, prodromal, manifest illness, recovery
or death
B. Manifest illness, prodromal, latent period, recovery
or death
C. Prodromal, latent period, manifest illness, recovery
or death
D. Manifest illness, latent period, prodromal, recovery
or death
3. Which of the following systems is the most radiosen-
sitive vital organ system in human beings?
A. Cerebrovascular B. Gastrointestinal
C. Hematopoietic D. Skeletal
4. When cells are exposed to sub-lethal doses of ioniz-
ing radiation, approximately _____ of radiation­induced damage may be repaired over time and about ______ is irreparable.
A. 25%, 75% B. 50%, 50% C. 75%, 25% D. 90%, 10%
5. As radiation dose increases, the severity of early
tissue reactions:
A. Also increases B. Gradually decreases C. Increases sharply and then gradually decreases D. Remains constant
6. Prolonged exposure to x-rays in the diagnostic en-
ergy range results in high radiation dose to the skin while underlying tissues receive:
A. A much greater dose B. A slightly greater dose
152
CHAPTER 8 Early Tissue Reactions and Their Effects on Organ Systems
C. No dose D. A substantially less dose
7. In 1898 after personally developing burns attributed
to radiation exposure, this Boston dentist began in­vestigating the hazards of radiation exposure and became the first advocate of radiation protection. Who is this person?
A. William Herbert Rollins B. Wilhelm Conrad Roentgen C. Thomas Alva Edison D. Clarence Madison Dally
8. In the female, the ovarian stem cells:
A. Begin as a single cell during fetal development,
before birth, and then gradually increase in num­ber throughout life
B. Multiply to a few hundred cells during fetal life,
before birth, and then gradually increase in num­ber throughout life
C. Multiply to millions of cells only during fetal de-
velopment, before birth, and then steadily decline in number throughout life
D. Multiply to millions of cells only during fetal
development, before birth, and then steadily continue to increase in number throughout life
9. Which of the following types of cells develop from
single precursor cell, the pluripotential stem cell?
1. Lymphocytes and granulocytes
2. Thrombocytes and erythrocytes
3. Platelets A. 1 only B. 2 only C. 3 only D. 1, 2, and 3
10. With regard to radiation exposure, which part of
the gastrointestinal tract is most severely affected?
A. Esophagus B. Stomach C. Small intestine D. Large intestine
Stochastic Effects and Late Tissue
Reactions of Radiation in Organ Systems

O B J E C T I V E S

After completing this chapter, the reader will be able to perform the following:
• Define all key terms.
• Explain how scientists use epidemiologic studies to predict the risk of cancer in human populations ex­posed to low doses of ionizing radiation.
• Explain the purpose of a radiation dose–response curve.
• Draw diagrams demonstrating various dose–response relationships.
• Explain the reason regulatory agencies continue to use the linear dose–response model for establishing radiation protection standards.
• Differentiate between the threshold and nonthresh­old relationships.
9
• List and describe the various late tissue reactions and stochastic effects of ionizing radiation on living systems.
• Describe the concept of risk for radiation-induced malignancies, and explain the models that are used to provide risk estimates.
• Identify ionizing radiation-exposed human popula­tions or groups that prove radiation induces cancer.
• Explain how spontaneous mutations occur.
• Discuss the concept and processes of radiation­induced genetic effects.
• Differentiate between dominant and recessive gene mutations.
• Explain the doubling dose concept, and provide an example of how the number of mutations increases as dose increases.
C H A P T E R O U T L I N E
Epidemiology Carcinogenesis Radiation Dose–Response Relationship
Dose–Response Curves Threshold and Nonthreshold Relationships Risk Models Used to Predict Cancer Risk and
Heritable Damage in Human Populations
Risk Models Used to Predict Leukemia, Breast
Cancer, and Heritable Damage
Risk Model Used to Predict High-Dose Cellular
Response
The Rationale for Risk Model Selections
Somatic Effects
Late Somatic Effects Risk Estimate for Contracting Cancer From
Low-Level Radiation Exposure
Low-Level Effects Summary Major Types of Late Effects Risk Estimates for Cancer Life Span Shortening Cataractogenesis Embryologic Effects (Birth Defects)
Genetic (Hereditary) Effects
Irradiation Mutations Natural Mutations Other Agents of Genetic Mutations Incapacities of Mutant Genes Dominant or Recessive Point Mutations Ionizing Radiation as a Possible Cause of Genetic
(Hereditary) Effects
Doubling Dose Concept
Summary
153
154
CHAPTER 9 Stochastic Effects and Late Tissue Reactions of Radiation

K E Y T E R M S

absolute risk carcinogenesis cataractogenesis doubling dose embryologic effects (birth
defects) epidemiology genetic, or hereditary, effects
late somatic effects late tissue reactions linear nonthreshold curve linear-quadratic nonthreshold
curve nonthreshold organogenesis
radiation dose-response
relationship relative risk sigmoid, or S-shaped (nonlinear)
threshold curve stochastic effects threshold
Radiation-induced damage at the cellular level may lead to measurable somatic and hereditary damage in the living organism as a whole later in life. These late effects are the long-term results of radiation exposure. Some examples of measurable delayed biologic damage are:
• Cataracts
• Leukemia
• Genetic mutations Cataracts are considered to be a late tissue reaction
that is nonrandom, whereas leukemia and genetic mu­tations are viewed as delayed stochastic or random consequences that, if these reactions do appear, they do not do so for extended periods. This chapter focuses on the organic system-level damage from ionizing radiation that occurs months or years after radiation exposure.

EPIDEMIOLOGY

Epidemiology is a “science that deals with the inci-
dence, distribution, and control of disease in a popula­tion.”1 Epidemiologic studies consist of observations and statistical analysis of data, such as the incidence of disease within groups of people. The latter studies in­clude the risk of radiation-induced cancer. The incident rates at which these irradiation-related malignancies occur are determined by comparing the natural inci­dence of cancer occurring in a human population with the prevalence of cancer occurring in an irradiated population. Risk factors are then identified for the general human population.
Epidemiologic studies are of significant value to ra-
diobiologists who use the information from these stud­ies to formulate dose–response estimates for predicting the risk of cancer in human populations exposed to low doses of ionizing radiation.

CARCINOGENESIS

Carcinogenesis, also called tumorigenesis, is the for­mation of a cancer. Cancer is the name used for a sub­stantial group of diseases in which healthy cells have been transformed into nonstandard cells that divide uncontrollably. The process leads to an expansive growth of abnormal structures within various loca­tions in the body and the destruction of surrounding body tissues such as bone marrow. The altered or can­cer cells readily demonstrate the potential to invade or spread to other parts of the body. Cancer is the most significant late stochastic effect caused by exposure to ionizing radiation.

RADIATION DOSE–RESPONSE RELATIONSHIP

Dose–Response Curves

The radiation dose–response relationship is demon- strated graphically through a curve (the dose–response [DR] curve) that maps the observed effects of radiation exposure in relation to the dose of radiation received. The “effect” in question may be the incidence of a dis­ease (e.g., cases of cancer per million in a population or fatalities due to cancer per million in a population), or the effect may be its degree of acuteness, such as the severity of cataracts as dose increases. The DR curve is either linear (straight line) or nonlinear (curved to some degree), and it depicts either a threshold dose or a nonthreshold dose (Fig. 9.1).

Threshold and Nonthreshold Relationships

The term threshold is defined as a point or level at which a response or reaction to an increasing stimula­tion first occurs. Regarding ionizing radiation, this
CHAPTER 9 Stochastic Effects and Late Tissue Reactions of Radiation
Response to radiation
1
155
Response to radiation
(expressed in biologic effects observed)
A
Response to radiation
(expressed in biologic effects observed)
B
Fig. 9.1 (A) 1 represents a linear (straight-line) nonthreshold
curve of radiation dose–response relationship; 2 represents a linear threshold curve of radiation dose–response relationship; 3 represents a nonlinear threshold curve of radiation dose– response relationship. (B) Sigmoid (S-shaped, hence nonlinear) threshold curve of radiation dose–response relationship gener­ally employed in radiation therapy to demonstrate high-dose cellular response.
Radiation dose received
(Threshold)
Radiation dose received
2
3
(expressed in biologic effects)
Radiation dose
Fig. 9.2 Linear nonthreshold curve of radiation dose–response
relationship. The straight-line curve passing through the origin in this graph indicates both that the response to radiation (in terms of biologic effects) is directly proportional to the dose of radiation and that no known level of radiation dose exists below which the chance of sustaining biologic damage is zero. In contrast to a cell-survival curve (Fig. 7.17), as seen in Chapter 7, both the vertical and horizontal axes of a dose–response curve are ordinary linear scales.
means that below a certain absorbed radiation dose, no biologic effects are observed. The biologic effects begin to occur only when the threshold dose is reached. A
nonthreshold relationship indicates that a radiation
absorbed dose of any magnitude has the capability of producing a biologic effect. Therefore, if the DR curve is as shown in Fig. 9.2, biologic effect responses will be caused by ionizing radiation in living organisms in a directly proportional manner at any dose above zero. This behavior is referred to as a linear nonthreshold (LNT) relationship. LNT proclaims that no radiation dose can be considered absolutely “safe,” with the inci­dence of the biologic effects increasing directly with the magnitude of the absorbed dose.

Risk Models Used to Predict Cancer Risk and Heritable Damage in Human Populations

In a 1980 report, the Committee on the Biological Ef­fects of Ionizing Radiation (BEIR), under the auspices of the National Academy of Sciences, studying atomic bomb survivors concluded that most stochastic effects (e.g., cancer) and hereditary effects at low-dose levels
156
Response to radiation
Response to radiation
(expressed in biologic effects)
Fig. 9.3 Linear-quadratic nonthreshold dose–response relation-
ship. The curve estimates the risk associated with low-dose levels from low LET radiation.
CHAPTER 9 Stochastic Effects and Late Tissue Reactions of Radiation
c
Linear
e
n
i
L
Radiation dose
i
t
a
r
d
a
u
q
-
r
a
from low LET radiation, such as the type of radiation used in diagnostic radiology, appear to follow a linear­quadratic nonthreshold dose–response curve (LQNT DR) (Fig. 9.3). The term linear-quadratic implies that the equation that best fits the data has components that depend on dose to the first power (linear or straight-line behavior) and also on dose squared (quadratic or curved behavior). Since the 1980 report, newer risk models and updated dosimetry techniques have provided a more useful follow-up study of Hiroshima and Nagasaki atomic bomb survivors. In 1990 the BEIR Committee’s revised risk estimates indicated that the risk from radia­tion exposure was about three to four times greater than previously projected. Currently, the committee recom­mends the use of the linear nonthreshold curve of ra­diation dose–response (LNT DR) for most types of cancers. With the LNT DR curve, if the absorbed dose is doubled, the biologic response probability, and there­fore its actual occurrence in a large population sample, is also doubled (see Fig. 9.2).
humans are exposed to radiation during diagnostic imag­ing procedures. Another nonthreshold risk estimate curve is the LQNT DR curve (see Fig. 9.3). This curve displays a more conservative dose–response outcome for low-level radiation. The 1990 BEIR Committee consid­ered the LQNT relationship to be an improved reflection of stochastic and genetic effects at low-dose levels from low-LET radiation. The following health concerns are presumed to follow this DR curve:
• Leukemia
• Breast cancer
• Heritable damage For leukemia, the LQNT hypothesis appears to be
supported by an analysis of the leukemia occurrences in Nagasaki and Hiroshima that utilized a more recent re­evaluation of the radiation dose distribution in these two cities.
2,3

Risk Model Used to Predict High-Dose Cellular Response

Acute reactions from significant radiation exposure, such as skin erythema and hematologic depression, may be demonstrated graphically through the use of a radia­tion linear threshold dose–response curve (LT DR) as shown in Fig. 9.4. In this model, a biologic response does not occur below a specific dose level. Laboratory
(Linear)
(expressed in biologic effects)

Risk Models Used to Predict Leukemia, Breast Cancer, and Heritable Damage

Currently, advocates of LNT theorize that because all radiation exposure levels possess the potential to cause biologic damage, radiographers must never fail to employ aggressive radiation safety measures whenever
Threshold
Radiation dose
dose
Fig. 9.4 Linear threshold curve of radiation dose–response.
This depicts those cases for which a biologic response does not occur below a specific radiation dose.