Understanding Biological Effects Of Nuclear Radiation Biology Essay

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An understanding of the biological effects of nuclear and Xray radiation is important for evaluating many potential uses and dangers. This is pertinent in the present scenario of technology advances wherein the use of Xrays in the form of CT scans, PET-CT scans and radioisotopes in diagnosis and thrapy are being used extensively.

Some types of radiation are more damaging than others. Alpha radiation is the most damaging to human tissues because its particles are strongly ionising. Neutrons are also damaging to cells, because they interact very easily with body tissue which contains a lot of water. They are a highly penetrating form of radiation. Beta and gamma radiation are the least damaging forms of nuclear radiation but they are able to penetrate deeper into the body than alpha radiation. Gamma radiation and Xrays pass through the body easily.

It is important to know that one is constantly being exposed to a variety of natural and man made background radiations. Gamma rays from space and from the earth as cosmic radiation which is equal to 1mSv/yr on earth and in space 27mSv/yr. Cosmogenic radionucleides ( C14,Be7and He3 )account for 0.28mSv/yr and natural radon in the air exposures are 0.1mSv/yr. Radioactive potassium 40 atoms are naturally present in the body and undergo several thousand nuclear disintegrations every second. This accounts for 0.26mSv/yr. Medical exposures account for 20% , and natural background exposures for 80% of average exposures to world populations.

Ionising Radiation.

A wide variety of ionizing radiations can interact with biological systems, but there are only five types of radiation of importance, they are gamma, neutron, beta, alpha and Xrays.

Gamma Radiation.

Gamma radiation which emanates from the nucleus of an atom is highly energetic , penetrating so that a significant part will pass through the human body without interaction. This energy deposition may occur anywhere along a given photon's path. Because of its penetrating ability, the effects of gamma irradiation can be independent of the location of the source, (i.e., internal or external to the body).

Gamma rays are commonly used for diagnostic and therapy purposes.

Neutron Radiation.

Since neutrons are uncharged particles and can react only with the nuclei of target atoms, the probability of interaction of neutrons in the energy range is roughly comparable to that of low-energy gamma photons. The energy deposition will not be uniform.

Its present clinical application is in neutron beam therapy in some forms of cancer treatment.

Beta Radiation.

High speed electrons in the form of beta radiation lose most of their energy after penetrating only a few millimeters of tissue. If the beta emitting material is on the surface of the skin, the resulting beta irradiation causes damage to the basal stratum of the skin. Damaged cells may be of greater significance to the total organism than killed cells, particularly if they go on to become malignant or otherwise malfunction. Killed cells are replaced quickly in most tissues with any degree of reserve capacity and do not cause significant overall clinical effects unless the cells involved are highly critical or the fraction of cells killed in a given organ is large.

Beta rays are used in radioisotope therapies.

Alpha Radiation

The energy of these relatively heavy, positively charged particles is fully absorbed within the first 20 micrometers of an exposed tissue mass. Because of this, alpha radiation is not an external hazard. If alpha emitting material is internally deposited, all the radiation energy will be absorbed in a very small volume of tissue immediately surrounding each particle . These rays are highly effective in targeted radioisotope therapies.

There is now a significant progress in development of radioisotope therapies which are internally administered and are effectively targeted to the cancerous tissues. In such situations beta and alpha rays which can deposit their energy in a small volume of tissue will be useful and can reduce radiation exposure to the normal surrounding tissues. .


X-rays , whose origin is from the electron shells of the nucleus of an atom are a type of penetrating radiation that, depending on the dose, can reduce cell division, damage genetic material, and harm unborn children.

Xrays are extensively used for diagnostic purposes.

Interaction of ionizing radiation with matter or tissues .

When radiation interacts with target atoms, energy is deposited, resulting in ionization or electron excitation. This ionization or excitation must involve certain critical molecules or structures in a cell. It has been theorized that this localization of absorbed energy in critical molecules could be either a direct or an indirect action.

However, the most reasonable hypothesis is that in an indirect reaction ,water, both intracellular and extracellular, is the primary site of radiation energy deposition and that the energy deposited in the water would be transferred to and affect sensitive molecules indirectly. This is done through the production of a variety of free radicals such as superoxides, oxygen, hydrogen and hydrogen peroxide radicals which are highly reactive and which damage chemical bonds in molecules. Direct action is at the level of the chromosomes of the cell nucleus.

Units of Exposure and Dose

The need to quantify radiation damage became increasingly evident, despite obvious difficulties in doing so. The first two units introduced dealt with radiation in the air, and as it is absorbed in living tissue. The two corresponding quantities are called "exposure" and "absorbed dose".

The unit of radiation "exposure", adopted by the International Congress on Radiology in 1931, was the Roentgen. A roentgen is a quantity of x-rays or gamma rays which will cause a precisely defined degree of ionization in one kg of dry air.

The roentgen unit does not apply to any particulate radiation (such as alpha, beta, neutron or high-speed ions), nor does it involve biological tissue. To rectify these shortcomings, the concept of "absorbed dose" was introduced. The unit of absorbed dose is called a Rad (an acronym for Radiation Absorbed Dose).

One rad is that quantity of ionizing radiation of any type that will deposit 100 ergs of energy in each gram of absorbing tissue.

The relation between "exposure" and "absorbed dose" depends on the tissue involved. The rad has now been replaced by the Gray (Gy) which equals 100 rads.

Relative Biological Effectiveness (RBE)

Equal doses of ionizing radiation are not always equally effective in causing biological damage. Such observations have led to the concept of Relative Biological Effectiveness (RBE). In any given situation, when two different doses of ionizing radiation produce the same measurable biological result (e.g. number of mutations, reduction in lymphocytes, incidence of cancer, degree of mental retardation, percentage of animals killed promptly) is the RBE of radiation.

Linear Energy Transfer (LET)

One important consideration affecting RBE is the "quality" of the ionizing radiation being used. In general, a given dose of alpha or neutron radiation is much more effective in causing biological damage than an equal dose of beta, gamma or x-radiation. This difference in effectiveness is related to a physical quantity called Linear Energy Transfer (LET) noted as high and low LET radiations.

Units of Dose Equivalence:   the Quality Factor (Q)

In an attempt to account for such differences in biological effectiveness, a new unit of "dose equivalence" was introduced, called a Rem (an acronym for "Roentgen Equivalent Man"). This unit is intended to indicate, however roughly, the relative degree of biological damage caused by a particular exposure to ionizing radiation. The rem is now superceded by the Sievert (Sv); 1 Sv = 100 rem.

What is an effective dose of radiation?

Finally, the biological effect of radiation depends on the type of tissue being irradiated.

When radioactive materials are incorporated into the body by inhalation, ingestion, and absorption through the skin and retained, significant radiation injury can be sustained by specific tissues in which the materials are concentrated or in some instances by the whole body. The primary factors which determine the type and degree of injury are the types and amounts of the isotopes deposited and the nature and energies of the radiation emitted.

In the context of a growing use of radioisotopes for diagnosis and therapy one needs to understand the kinetics of the administered radioisotope which is generally tagged to compounds for specific purposes.

A radioactive material internally administered must be eliminated from the body to remove its hazard.

include renal excretion for most soluble materials,

elimination in the feces for materials which are retained in the gut or which can be secreted in the bile, and

exhalation for volatile materials and gases.

The rate at which a material is eliminated is usually expressed as the biological half-life. This is the time it takes for one-half of a given amount of material to be excreted or eliminated. The biological half-time may be variable. Effective half-life will be a function of their physical and biological half-lives considered together.

In the event of excess radioisotope either due to misadministration or accidents methods for detoxification are needed.

Chelating agents, e.g., calcium or zinc DTPA (diethylenetriamine pentaacetic acid), if administered soon after exposure, are effective in enhancing the elimination of certain radioisotopes not fixed in tissues. Potassium iodide or iodate if given prior to or soon after an intake of radioiodine, will reduce the uptake of radioiodine by the thyroid gland. Similarly, orally administered Prussian Blue will reduce the absorption of cesium from the gut and Alginate will reduce strontium absorption.

Cellular Effects of Radiation

Mechanisms of Damage

Injury to living tissue results from the transfer of energy to atoms and molecules in the cellular structure. Ionizing radiation causes atoms and molecules to become ionized or excited. These excitations and ionizations can:

Produce free radicals.

Break chemical bonds.

Produce new chemical bonds and cross-linkage between macromolecules.

Damage molecules that regulate vital cell processes (e.g. DNA, RNA, proteins).

The cell can repair certain levels of cell damage. At low doses, such as that received every day from background radiation, cellular damage is rapidly repaired.

 At higher levels, cell death results. At extremely high doses, cells cannot be replaced quickly enough, and tissues fail to function.

Tissue Sensitivity

An important factor which is an individual response of a cell to radiation induced changes at the cell level is the parameter called tissue sensitivity. Hence all individuals will not react identically to the same dose of radiation . Some individuals will be more sensitive to radiation than others .Hence this aspect needs to be understood especially when therapy with radiation is considered.

The probable reason is a balance between damage to tissue and the capability for tissue repair. Some individuals will have a better ability for repair than others and the final outcome would be reflection of this balance in an individual.

Radiation sensitivity of a tissue is:

proportional to the rate of proliferation of its cells

inversely proportional to the degree of cell differentiation

In general, actively proliferating cells are most sensitive to radiation. Thus, cellular radiosensitivity tends to vary inversely with the degree of differentiation. Vegetative cells comprising of differentiated functional cells of a large variety of tissues are generally the most radiosensitive. Examples include: Free stem cells of hematopoietic tissue, cells deep in the intestinal crypts, primitive spermatogonia, granulosa cells of developing and mature ovarian follicles, basal germinal cells of the epidermis, germinal cells of the gastric glands, large and medium sized lymphocytes and mesenchymal cells.

The most sensitive are therefore blood forming cells , followed by skin ,bone, teeth ,muscle and nervous system. This also means that a developing embryo is most sensitive to radiation during the early stages of differentiation, and an embryo/fetus is more sensitive to radiation exposure in the first trimester than in later trimesters.

Differentiating Cells are somewhat less sensitive to radiation. The best examples of this type of cell are the dividing and differentiating cells of the granulocytic and erythrocytic series in the bone marrow, differentiated spermatogonia and spermatocytes in the seminiferous tubules and the ovocytes.

Totally Differentiated Cells. These cells are relatively radioresistant. This class includes hepatocytes, cells of interstitial gland tissue of the gonads, smooth muscle cells, and vascular endothelial cells.

Fixed Nonreplicating Cells. These cells are most radioresistant. This group includes the long-lived neurons, striated muscle cells, short-lived polymorphonuclear granulocytes and erythrocytes, spermatids and spermatozoa, and the superficial epithelial cells of the alimentary tract.

Observed cellular effects of radiation, whether due to direct or indirect damage, are basically similar for different kinds and doses of ionizing radiation..

The manifestations of radiation damage is dose dependant and the absorbed energy deposited. It is important to understand these concepts as in diagnostic applications one needs to minimize cell damage as much as possible while for therapy one needs to ensure cell death is the predominant effect to be obtained.

One of the simplest effects to observe is cell death, the course of which can be described by various terms.

(1) Pyknosis. The nucleus becomes contracted, spheroidal, and filled with condensed chromatin.

(2) Karyolysis. The nucleus swells and loses its chromatin.

(3) Protoplasmic Coagulation. Irreversible gelatin formation occurs in both the cytoplasm and nucleus.

(4) Karyorrhexis. The nucleus becomes fragmented and scattered throughout the cell.

(5) Cytolysis. Cells swell until they burst and then slowly disappear.

Nonlethal changes in cellular function can occur as a result of lower radiation doses. These includes

delays in certain phases of the mitotic cycle, this inhibition occurs before prophase in the mitotic cycle, at a time disrupted cell growth, resulting in depletions of all populations

permeability changes. Irradiated cells may show both increased and decreased permeability.

and changes in motility.

At a molecular level there is damage to enzymes, DNA and biological pathways. Damage to cell membranes , nucleus and chromosomes occur at a subcellular level. Cellular effects are observed as cell death, inhibition of cell division, and carcinogenesis.

Systemic disruption occurs at the tissue level and death with shortening of life is a manifestation of whole body radiation. If a population is involved there are genetic changes in individuals.

Radiation-Induced Chromosome Damage.

Cell nuclei contain chromosomes which in turn contain the genes controlling cellular somatic and reproductive activity. These chromosomes are composed of deoxyribonucleic acid (DNA), the macromolecule containing the genetic information. This is a large, tightly coiled, double-stranded molecule and is sensitive to radiation damage. Radiation effects range from

complete breaks of the nucleotide chains of DNA,

to point mutations which are essentially radiation induced chemical changes in the nucleotides which may not affect the integrity of the basic structure.

Intermediate effects, such as abnormal bonding between adjacent molecules and alterations in viscosity resulting in translocations, trisomies, truncation and other abnormalities.

Genetic Effects.

Laboratory studies in animals indicate increased mutation rates with small doses of radiation. As radiation dose increases, mutation induction also increases. Mutations per unit dose decrease at low dose rates. However, viable mutations are still extremely rare. Most of the mutations are lethal and thus self-limiting. It must be kept in mind that radiation doses increase natural mutation rates and that the mutations produced, and not visibly detected, are permanent in regard to future generations.

Bystander effects due to untargeted cells not hit by direct radiation resulting from exposures to cells in the vicinity. The effects can lead to genomic instability, cell death, apoptosis , mutations, chromosomal aberrations and other cellular changes.

At low doses bystander effects may be more important than targeted effects . Targeted effects are predominant in high dose exposures. This means that the effects are more wide spread in the surrounding tissues as well as in the tissues directly exposed to the ionizing radiation due to the bystander phenomenon,

The transmission of damaging effects to the non-targeted tissues are by signals mediated via plasma and factors. The exact mechanism is yet to be proved.

Clinical manifestation of radiation effects

Each of the numerous cell renewal systems making up an animal's total cellular mass is normally in an equilibrium state between cell formation, proliferation, maturation, and death. Some systems, such as the adult central nervous system in higher animals, are stabilized at the end point of maturation, and the functional cells of such a system are not replaced if lost or destroyed. Other organ systems, such as the liver, which do not normally replace cells at a rapid rate, have the potential to regenerate large numbers of cells if needed. Other organ systems, such as the skin, the reproductive system, the gastrointestinal tract, and the hematopoietic system in the bone marrow, maintain a continuous high cell turnover rate. Bone marrow also has a large reserve capacity in the adult. A large fraction of it is normally nonfunctioning but has the potential to be functional if required. Failure of a particular organ system may or may not lead to death of the animal, depending on the importance of that system's functions, i.e., failure of gonadal function would not be lethal, whereas failure of bone-marrow function would be.

The stem cells of the various cell lines are almost all relatively sensitive to radiation whereas the mature functional cells are relatively resistant. As a result, following radiation, injured stem cells are not likely to mature. When the mature cells die or are otherwise lost they will not be replaced and the overall population of cells in the system will be decreased.

If the radiation injury is repairable, recovery of the ability of a stem cell population to mature will result in a gradual return of a mature, functional population. If the damage is irreversibly severe, there will be no recovery.

Table 1 Dose and effects of Radiation Syndrome.



<50 rads (0.5Gys)

Generally no clinical effect. Subject asymotomatic

50-100 rads(0.5-1Gys)

Mild nausea. WBCs increased and then decreased.


Nausea, vomiting, fatigue. WBCs increased and then decreased. Recovery in 2- 4 days.


2-3 days of nausea, vomiting, fatigue. WBCs markedly decrease , platelets decrease. Epilation, diarrhea, bleeding .

Recovery in 1-3 weeks. Some die in 4-6 weeks.

300-500 rads (3-5Gys).

LD 50 .Dose lethal to 50% of persons exposed.

400-600rads (Gys)

Severe nausea, vomiting , diarrhea and sore throat. WBCs vey low, platelets very low

Recovery period brief or absent. Symptoms recur with bleeding and diarrhea.

Death occurs in less than 30 days.

600-1000 rads(6-10Gys)

Severe and continuous nausea, diarrhea , and vomiting.

Death occurs in 1-10 days.

>1000 rads(>10Gys).

Severe illness, disorientation, ataxia, burning sensations and shock.

Death occurs in 10-36 hours.

Lethality. (LD50).

When comparing the effects of various types or circumstances, that dose which is lethal to 50% of a given population is a very useful parameter. The term is usually defined for a specific time, being limited, generally, to studies of acute lethality. The common time periods used are 60 days for large animals and humans. Medically, other figures of interest are the dose that will kill virtually no one, (LD5), and the dose that will kill virtually every one (LD95). Approximations of those doses are within the ranges 200-300 cGy (free in air) and 600-700 cGy (free in air), respectively.

Recovery processes

Understanding the process of recovery from radiation damage is necessary in determining the protocols for radiation therapy. If there is time between therapy fractions and repair takes place effective results will not be seen.

A variety of recovery processes may reduce radiation damage to a varying extent. For example, when a chromosome is broken, the broken ends tend to rejoin thus reconstituting the chromosome, but occasionally the broken ends seal over before rejoining thus leaving permanent chromosome damage. If two (or more) chromosomes are broken within the same cell, rejoining of inappropriate broken ends can occur and so may lead to permanent chromosomal change of a different kind. Repair of the broken ends of chromosomes, like all other repair processes following radiation damage, is not specific in respect of radiation damage.

Intracellular repair occurs when individual irradiated cells have the ability to repair themselves as long as the amount of intracellular damage does not exceed a threshold value.

Repopulation brought about by stem cell proliferation is a particularly important recovery mechanism in both the bone marrow and the gastrointestinal tract whenever the radiation exposure has been large enough.

Repair is a biological process specific to a particular kind of damage which comes into play whatever the agent which causes that damage. The third, a combination of the first two types of recovery, can be very approximately quantified for lethality in humans by the use of the operational equivalent dose formula in cases where the irradiation period is protracted over several hours or longer

Delayed Effects.

The above description is the early effects of radiation observed. However radiation effects can manifest several years later and hence it is important to ensure when radiation of any form is used in the diagnostic and therapeutic management of patients to be aware of consequences which might occur many years later .Hence the risk factors for a particular type of manifestation of delayed effects should be kept in mind when exposing a patient to radiation.

The present increase in the life span of persons all over the world can be a hazard for development of higher incidences of delayed radiation effects.


Late or delayed effects of radiation occur following a wide range of doses and dose rates. Delayed effects may appear months to years after irradiation and include a wide variety of effects involving almost all tissues or organs. Some of the possible delayed consequences of radiation injury are

life shortening,


cataract formation,

chronic radiodermatitis,

decreased fertility,

and genetic mutations.


Irradiation of almost any part of the body increases the probability of cancer. The type formed depends on such factors as area irradiated, radiation dose, age, and species. Irradiation may either increase the absolute incidence of cancer or accelerate the time or onset of cancer appearance, or both. There is a latent period between the exposure and the clinical appearance of the cancer. In the case of the various radiation-induced cancers seen in mankind, the latency period may be several years. Latent periods for induction of skin cancers in people have ranged from 12 to 56 years after x irradiation. Fifteen years is reported as a latent period for bone tumors from radium.

A leukemogenic effect was expected and found among Hiroshima and Nagasaki survivors. Peak incidence occurred 6 years after exposure and was less marked for chronic granulocytic leukemia than acute leukemia. The incidence was inversely related to distance from the hypocenter.

British persons receiving radiotherapy for spondylitis showed a dose response relationship for leukemia, with peak incidence occurring 5 years after the first exposure. Studies have demonstrated that ionizing radiation can induce more than one kind of leukemia in people, but not chronic lymphocytic leukemia.

Predisposing factors for tumor development include heredity, age, hormones, and prior exposure to physical trauma, chemical agents and ionizing radiation. The actual processes by which cancer is induced are not known. Somatic mutations, virus infections, and precancerous abnormalities in tissue organization and vascular supply have all been postulated.

Cells that divide quickly are very sensitive to x-ray exposure. Unborn children are particularly sensitive to x-rays because their cells are rapidly dividing and developing into different types of tissue. Exposure of pregnant women to sufficient doses of x-rays could possibly result in birth defects or illnesses such as leukaemia later in life.

Cataract Formation.

A late effect of eye irradiation is cataract formation. It may begin anywhere from 6 months to several years after exposure. While all types of ionizing radiation may induce cataract formation, neutron irradiation is especially effective in its formation, even at relatively low doses. Cataract formation begins at the posterior pole of the lens and continues until the entire lens has been affected. The threshold for detectable cataract formation in 2 Sv (sievert) (200 REM (roentgen equivalent, man)) for acute radiation doses and 15 Sv (1500 REM) for protracted doses.

Chronic Radiodermatitis.

Delayed, irreversible changes of the skin usually do not develop as a result of sublethal whole-body irradiation, but instead follow higher doses limited to the skin. These changes are a common complication in radiation therapy. Erythema occurs at low doses ranging from 60-80Sv followed by skin necrosis and ulceration at higher doses. Chronic exposure over 20Sv can lead to dermatitis with skin cancers.

Genetic, or heritable effects appear in the future generations of the exposed person as a result of radiation damage to the reproductive cells. Genetic effects are abnormalities that may occur in the future generations of exposed individuals. They have been extensively studied in plants and animals, but risks for genetic effects in humans are seen to be considerably smaller than the risks for somatic effects. Therefore, the limits used to protect the exposed person from harm are equally effective to protect future generations from harm.

Genetically Significant dose(GSD) is that dose if received by any member of the population which would be expected to produce the same number of genetic abnormalities as are produced by the actual doses received in various individuals. GSD for natural background is 3.6 mSv/yr ,medical exposures is 0.4 mSv and nuclear medicine procedures is 0.14 mSv.

Dose and Effect

Stochastic Effects: These effects have no threshold and the severity of the effect does not vary with the dose. The probability of occurrence, however, increases as the dose increases. Cancer is a stochastic effect, particularly leukemia which has a latent period of 2 to 10 years post exposure. The risk for leukemia is significantly increased above acute doses of 40 rads (0.4 Gy). There is a longer latent period for solid tumors (10 to 40 years) such as squamous cell carcinoma of the skin and adenocarcinoma of the breast or lung. There may be some associated increased risk for childhood cancer following exposure in utero. Genetic effects are also considered under this category.

Non-stochastic Effects or deterministic effects .The severity of the effect varies with the dose and the effects are not seen below a certain threshold level of radiation. A minimum dose of 200 rem (2 Sv) is required for the development of cataracts. The threshold for developing a vision impairing cataract under conditions of prolonged, fractionated exposure is felt to be 800 rem. Temporary sterility in males can be seen following acute doses of 15 rem (0.15 Sv), while permanent sterility can be seen after doses of 350 rem (3.5 Sv). In females, permanent sterility can be seen following doses of 250 to 600 rem (2.5-6.0 Sv).

The Dose Response Curve

It is believed that at low dose rates, defence mechanisms in the cells can operate to repair some of the damage caused by radiation. In this region of low dose, the effect (i.e., the probability of producing cancerous cells) is thought to be proportional to the dose. At higher dose rates, greater than 100 mGy/h, two or more ionising events might occur in the critical parts of cells before the repair mechanism would have a chance to operate. At this point, the slope of the dose/effect curve increases and the effect will depend on the square of the dose, D2, rather than just on D.

This means that if the whole body is exposed to 1 Sv of ionising radiation  an extra 4% chance of contracting a cancer  that will be fatal many years after the exposure. The word `extra' is used because one normally has a 20 to 25% chance of dying from cancer.

Other stochastic effects also occur. Radiation can cause changes in DNA, the "blueprints" that ensure cell repair and replacement produces a perfect copy of the original cell. Changes in DNA are called mutations.

Sometimes the body fails to repair these mutations or even creates mutations during repair. The mutations can be teratogenic or genetic. Teratogenic mutations are caused by exposure of the fetus in the uterus and affect only the individual who was exposed. Genetic mutations are passed on to offspring.

Potential Effects of In Utero Exposure:

Prenatal death occurs if the radiation is received during perimplantation. The most sensitive period for neonatal death to occur following radiation exposure is between 3 to 5 weeks gestation. The most sensitive period for congenital abnormalities is during the period of organogenesis. Growth retardation can also be seen in irradiated fetuses. Long term effects of the radiation include sterility, genetic effects, the induction of malignancies, and neurologic impairment.

Mental Retardation: Mental retardation can be seen following in utero radiation exposure and is the most commonly documented abnormality in humans who are prenatally exposed. The fetus is most susceptible to radiation delivered during the 8 to 15 week period, and somewhat less susceptible between 16 and 25 weeks. The risk of mental retardation is dose related and is only about 4% for a 10 rem (0.1 Sv) dose, while it may be as high as 43% for a 100 rem (1 Sv) dose. There may be a threshold for retardation between 20 and 40 rem (0.2-0.4 Sv), but this has not yet been proven.

Malignancy: The increased risk of cancer in the fetus is estimated to be approximately 500 deaths before age 10 years among 1 million children exposed shortly before birth to 1 rad (2 x 10 [to the -4] per rad). The leukemia risk for the child is greatest if radiation was received during the first trimester.

Considerations for pregnancy termination 

Threshold dose for developmental effects approximately 0.1 Gy

Normal rate of preclinical loss >30%. At  0.1 Gy , increase of  0.1-1%

The foetal absorbed dose > 0.5 Gy at 7-13 weeks: substantial risk of IUGR and CNS damage

0.25-0.5 Gy at 7-13 weeks:  parental decision with physician's guidance  

      Minimizing health effects of ionizing radiation

Life style abnormalities, natural disasters and accidents are greater risk factors than exposure to small amounts of radiation as encountered in medical exposures and in radiation workers.

Some scientists assert that low levels of radiation are beneficial to health (this idea is known as hormesis)

Although exposure to ionizing radiation carries a risk, it is impossible to completely avoid exposure. Radiation has always been present in the environment and in our bodies.

We can however avoid exposure .Although one cannot sense ionizing radiation , there is a range of simple, sensitive instruments capable of detecting small amounts of radiation from natural and man-made sources.

Dosimeters measure an absolute dose received over a period of time. The TLD is normally used to obtain your official dose of record. TLDs are processed routinely at the end of each calendar quarter. TLDs are sensitive to beta, gamma, and neutron radiation.

Self Reading Pocket Dosimeters - SRPDs The term Self Reading Pocket Dosimeter applies to any of a variety of devices which can be read by the wearer to determine the dose received. The SRPD is usually used as a supplemental device to aid in dose tracking during activities where elevated doses are possible.

Pocket Ion Chambers - (PIC) These are small instruments which operate on the electroscope principle. Typically, the range of the PIC is 0-200 mR. This is one of the most common supplemental dosimeters used in Radiation Areas.

Electronic dosimeters (ED) are sometimes used instead of and in addition to PICs when it is helpful to have additional capability of dose or dose rate alarm functions..

Geiger counters and scintillometers measure the dose rate of ionizing radiation directly

Film badge dosimeters enclose a photographic film which will get exposed to radiaition

In addition there are 3 ways for personal protection:

Time: Limiting or minimizing the exposure time to reduce the dose

Distance : The intensity of exposure reduces as a square of the distance from the source

Shielding : Barriers of lead, concrete or water are protective against radiation such as gamma and neutrons. That is why certain radioactive materials are stored or handled under water or by remote control in rooms constructed of thick concrete or lined with lead. There are special plastic sheets for stopping betas and air will stop alpha particles.

It should be noted that the setting of a dose limit is equivalent to specifying a maximum acceptable level of risk. It is not acceptable to be exposed to the full extent of the limit if a lower dose can be reasonably achieved ( ALARA)The average dose received by an occupationally exposed worker is < 0.2 mSv per year.


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Radiation and Life http://www.uic.com.au/ral.htm

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Are X-rays Safe? http://www.medinfo.ufl.edu/other/cameron/rads.html

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V), Washington, DC, National Academy Press, 1990

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*CANDU Owners Group, Staff & Consultants, **McMaster University

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13) Health and Environmental Issues Linked to the Nuclear Fuel Chain

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Multiple choice questions

1.What is the difference between Xrays and gamma rays

Xrays are produced extranuclearly while gamma rays are produced by nuclear decay

Xrays have higher energies than gamma

Xrays react differently than gamma rays in matter

2. A free radical is

any charged particle

an atom or molecule with an unpaired electron in the outer shell

an atom with an even pair of electrons

a chemically stable atom

3. All types of radiation can produce biological effects by direct or indirect action



4.Which of the following statements is false

Cataract is denoted by any detectable change in the normally transparent lens of the eye

Cataracts can be caused by irradiation of the lens

Cell division of the lens continues throughout life

Lens has the same mechanism of removal as other tissues.

5.What is the most important lesion in chromosomal DNA produced by exposure to ionizing radiation.

Single strand break

Well separated breaks on both strands

Breaks on both strands which are separated by a few bases or opposite each other

Multiple breaks on the same strand

6.Chromosomal aberrations are caused by

Single strand breaks

Double strand breaks


7.Radiation damage is divided into a)lethal b)sublethal c) potential lethal (PLD). Which of the statement is true

PLD will cause death under ordinary circumstances

PLD cannot be repaired under normal circumstances

PLD repair is less likely to occur if mitosis is delayed

8.Total body doses in excess of 100 Gy which cause death within 24-48 hours of exposure are connected to

Cerebrovascular syndrome

Gastrointestinal syndrome

Hemopoetic syndrome

9. By LD 50/30 is meant

Death occurs in 50% population in 30 days after exposure to radiation

Dose required to produce sublethal changes in 50% population when exposed to a beam of LET value of 30

Dose required to cause death in 30-50% of the population

10. A deterministic effect has

A threshold in dose but the severity of the effect is dose independant

A threshold in dose and the severity of effect increases with dose

No threshold in dose and the severity is a constant function of dose

Has no threshold in dose and the severity of effect is dose dependant

11. The most sensitive stage of lethal effects of radiaition is


Early organogenesis

Late organogenesis

Fetal period