Biological Effects of Ionizing Radiation Quiz

PDF page 1537: We hear many seemingly contradictory things about the biological effects of ionizing radiation. It can cause cancer, burns, and hair loss, yet it is used to treat and even cure cancer. How do we understand these effects? Once again, there is an underlying simplicity in nature, even in complicated biological organisms. All the effects of ionizing radiation on biological tissue can be understood by knowing that ionizing radiation affects molecules within cells, particularly DNA molecules. Let us take a brief look at molecules within cells and how cells operate. Cells have long, double-helical DNA molecules containing chemical codes called genetic codes that govern the function and processes undertaken by the cell. It is for unraveling the double-helical structure of DNA that James Watson, Francis Crick, and Maurice Wilkins received the Nobel Prize. Damage to DNA consists of breaks in chemical bonds or other changes in the structural features of the DNA chain, leading to changes in the genetic code. In human cells, we can have as many as a million individual instances of damage to DNA per cell per day. It is remarkable that DNA contains codes that check whether the DNA is damaged or can repair itself. It is like an auto check and repair mechanism. This repair ability of DNA is vital for maintaining the integrity of the genetic code and for the normal functioning of the entire organism. It should be constantly active and needs to respond rapidly. The rate of DNA repair depends on various factors such as the cell type and age of the cell. A cell with a damaged ability to repair DNA, which could have been induced by ionizing radiation, can do one of the following:

PDF page 1537: • The cell can go into unregulated cell division leading to tumors and cancers.

PDF page 1537: Since ionizing radiation damages the DNA, which is critical in cell reproduction, it has its greatest effect on cells that rapidly reproduce, including most types of cancer. Thus, cancer cells are more sensitive to radiation than normal cells and can be killed by it easily. Cancer is characterized by a malfunction of cell reproduction, and can also be caused by ionizing radiation. Without contradiction, ionizing radiation can be both a cure and a cause. To discuss quantitatively the biological effects of ionizing radiation, we need a radiation dose unit that is directly related to those effects. All effects of radiation are assumed to be directly proportional to the amount of ionization produced in the biological organism. The amount of ionization is in turn proportional to the amount of deposited energy. Therefore, we define a radiation dose unit called the rad, as of a joule of ionizing energy deposited per kilogram of tissue, which is 32.1 For example, if a 50.0-kg person is exposed to ionizing radiation over her entire body and she absorbs 1.00 J, then her whole-body radiation dose is 32.2 If the same 1.00 J of ionizing energy were absorbed in her 2.00-kg forearm alone, then the dose to the forearm would be 32.3 and the unaffected tissue would have a zero rad dose. While calculating radiation doses, you divide the energy absorbed by the mass of affected tissue. You must specify the affected region, such as the whole body or forearm in addition to giving the numerical dose in rads. The SI unit for radiation dose is the gray (Gy), which is defined to be 32.4 However, the rad is still commonly used. Although the energy per kilogram in 1 rad is small, it has significant effects

PDF page 1539: Absorbed dose Gray (Gy) 1 J/kg rad

PDF page 1537: Since ionizing radiation damages the DNA, which is critical in cell reproduction, it has its greatest effect on cells that rapidly reproduce, including most types of cancer. Thus, cancer cells are more sensitive to radiation than normal cells and can be killed by it easily. Cancer is characterized by a malfunction of cell reproduction, and can also be caused by ionizing radiation. Without contradiction, ionizing radiation can be both a cure and a cause. To discuss quantitatively the biological effects of ionizing radiation, we need a radiation dose unit that is directly related to those effects. All effects of radiation are assumed to be directly proportional to the amount of ionization produced in the biological organism. The amount of ionization is in turn proportional to the amount of deposited energy. Therefore, we define a radiation dose unit called the rad, as of a joule of ionizing energy deposited per kilogram of tissue, which is 32.1 For example, if a 50.0-kg person is exposed to ionizing radiation over her entire body and she absorbs 1.00 J, then her whole-body radiation dose is 32.2 If the same 1.00 J of ionizing energy were absorbed in her 2.00-kg forearm alone, then the dose to the forearm would be 32.3 and the unaffected tissue would have a zero rad dose. While calculating radiation doses, you divide the energy absorbed by the mass of affected tissue. You must specify the affected region, such as the whole body or forearm in addition to giving the numerical dose in rads. The SI unit for radiation dose is the gray (Gy), which is defined to be 32.4 However, the rad is still commonly used. Although the energy per kilogram in 1 rad is small, it has significant effects

PDF page 1537: Since ionizing radiation damages the DNA, which is critical in cell reproduction, it has its greatest effect on cells that rapidly reproduce, including most types of cancer. Thus, cancer cells are more sensitive to radiation than normal cells and can be killed by it easily. Cancer is characterized by a malfunction of cell reproduction, and can also be caused by ionizing radiation. Without contradiction, ionizing radiation can be both a cure and a cause. To discuss quantitatively the biological effects of ionizing radiation, we need a radiation dose unit that is directly related to those effects. All effects of radiation are assumed to be directly proportional to the amount of ionization produced in the biological organism. The amount of ionization is in turn proportional to the amount of deposited energy. Therefore, we define a radiation dose unit called the rad, as of a joule of ionizing energy deposited per kilogram of tissue, which is 32.1 For example, if a 50.0-kg person is exposed to ionizing radiation over her entire body and she absorbs 1.00 J, then her whole-body radiation dose is 32.2 If the same 1.00 J of ionizing energy were absorbed in her 2.00-kg forearm alone, then the dose to the forearm would be 32.3 and the unaffected tissue would have a zero rad dose. While calculating radiation doses, you divide the energy absorbed by the mass of affected tissue. You must specify the affected region, such as the whole body or forearm in addition to giving the numerical dose in rads. The SI unit for radiation dose is the gray (Gy), which is defined to be 32.4 However, the rad is still commonly used. Although the energy per kilogram in 1 rad is small, it has significant effects

PDF page 1538: since the energy causes ionization. The energy needed for a single ionization is a few eV, or less than . Thus, 0.01 J of ionizing energy can create a huge number of ion pairs and have an effect at the cellular level. The effects of ionizing radiation may be directly proportional to the dose in rads, but they also depend on the type of radiation and the type of tissue. That is, for a given dose in rads, the effects depend on whether the radiation is x-ray, or some other type of ionizing radiation. In the earlier discussion of the range of ionizing radiation, it was noted that energy is deposited in a series of ionizations and not in a single interaction. Each ion pair or ionization requires a certain amount of energy, so that the number of ion pairs is directly proportional to the amount of the deposited ionizing energy. But, if the range of the radiation is small, as it is for s, then the ionization and the damage created is more concentrated and harder for the organism to repair, as seen in Figure 32.6. Concentrated damage is more difficult for biological organisms to repair than damage that is spread out, so short-range particles have greater biological effects. The relative biological effectiveness (RBE) or quality factor (QF) is given in Table 32.2 for several types of ionizing radiation—the effect of the radiation is directly proportional to the RBE. A dose unit more closely related to effects in biological tissue is called the roentgen equivalent man or rem and is defined to be the dose in rads multiplied by the relative biological effectiveness. 32.5

PDF page 1538: created by is more concentrated and harder for the organism to repair. Thus, the RBE for s is greater than the RBE for s, even though they create the same amount of ionization at the same energy. So, if a person had a whole-body dose of 2.00 rad of radiation, the dose in rem would be . If the person had a whole-body dose of 2.00 rad of radiation, then the dose in rem would be . The s would have 20 times the effect on the person than the s for the same deposited energy. The SI equivalent of the rem is the sievert (Sv), defined to be , so that 32.6 The RBEs given in Table 32.2 are approximate, but they yield certain insights. For example, the eyes are more sensitive to radiation, because the cells of the lens do not repair themselves. Neutrons cause more damage than rays, although both are neutral and have large ranges, because neutrons often cause secondary radiation when they are captured. Note that the RBEs are 1 for higher-energy s, s, and x-rays, three of the most common types of radiation. For those types of radiation, the numerical values of the dose in rem and rad are identical. For example, 1 rad of radiation is also 1 rem. For that reason, rads are still widely quoted rather than rem. Table 32.3 summarizes the units that are used for radiation.

PDF page 1538: created by is more concentrated and harder for the organism to repair. Thus, the RBE for s is greater than the RBE for s, even though they create the same amount of ionization at the same energy. So, if a person had a whole-body dose of 2.00 rad of radiation, the dose in rem would be . If the person had a whole-body dose of 2.00 rad of radiation, then the dose in rem would be . The s would have 20 times the effect on the person than the s for the same deposited energy. The SI equivalent of the rem is the sievert (Sv), defined to be , so that 32.6 The RBEs given in Table 32.2 are approximate, but they yield certain insights. For example, the eyes are more sensitive to radiation, because the cells of the lens do not repair themselves. Neutrons cause more damage than rays, although both are neutral and have large ranges, because neutrons often cause secondary radiation when they are captured. Note that the RBEs are 1 for higher-energy s, s, and x-rays, three of the most common types of radiation. For those types of radiation, the numerical values of the dose in rem and rad are identical. For example, 1 rad of radiation is also 1 rem. For that reason, rads are still widely quoted rather than rem. Table 32.3 summarizes the units that are used for radiation.

PDF page 1538: created by is more concentrated and harder for the organism to repair. Thus, the RBE for s is greater than the RBE for s, even though they create the same amount of ionization at the same energy. So, if a person had a whole-body dose of 2.00 rad of radiation, the dose in rem would be . If the person had a whole-body dose of 2.00 rad of radiation, then the dose in rem would be . The s would have 20 times the effect on the person than the s for the same deposited energy. The SI equivalent of the rem is the sievert (Sv), defined to be , so that 32.6 The RBEs given in Table 32.2 are approximate, but they yield certain insights. For example, the eyes are more sensitive to radiation, because the cells of the lens do not repair themselves. Neutrons cause more damage than rays, although both are neutral and have large ranges, because neutrons often cause secondary radiation when they are captured. Note that the RBEs are 1 for higher-energy s, s, and x-rays, three of the most common types of radiation. For those types of radiation, the numerical values of the dose in rem and rad are identical. For example, 1 rad of radiation is also 1 rem. For that reason, rads are still widely quoted rather than rem. Table 32.3 summarizes the units that are used for radiation.

PDF page 1538: created by is more concentrated and harder for the organism to repair. Thus, the RBE for s is greater than the RBE for s, even though they create the same amount of ionization at the same energy. So, if a person had a whole-body dose of 2.00 rad of radiation, the dose in rem would be . If the person had a whole-body dose of 2.00 rad of radiation, then the dose in rem would be . The s would have 20 times the effect on the person than the s for the same deposited energy. The SI equivalent of the rem is the sievert (Sv), defined to be , so that 32.6 The RBEs given in Table 32.2 are approximate, but they yield certain insights. For example, the eyes are more sensitive to radiation, because the cells of the lens do not repair themselves. Neutrons cause more damage than rays, although both are neutral and have large ranges, because neutrons often cause secondary radiation when they are captured. Note that the RBEs are 1 for higher-energy s, s, and x-rays, three of the most common types of radiation. For those types of radiation, the numerical values of the dose in rem and rad are identical. For example, 1 rad of radiation is also 1 rem. For that reason, rads are still widely quoted rather than rem. Table 32.3 summarizes the units that are used for radiation.

PDF page 1540: Immediate effects are explained by the effects of radiation on cells and the sensitivity of rapidly reproducing cells to radiation. The first clue that a person has been exposed to radiation is a change in blood count, which is not surprising since blood cells are the most rapidly reproducing cells in the body. At higher doses, nausea and hair loss are observed, which may be due to interference with cell reproduction. Cells in the lining of the digestive system also rapidly reproduce, and their destruction causes nausea. When the growth of hair cells slows, the hair follicles become thin and break off. High doses cause significant cell death in all systems, but the lowest doses that cause fatalities do so by weakening the immune system through the loss of white blood cells. The two known long-term effects of radiation are cancer and genetic defects. Both are directly attributable to the interference of radiation with cell reproduction. For high doses of radiation, the risk of cancer is reasonably well known from studies of exposed groups. Hiroshima and Nagasaki survivors and a smaller number of people exposed by their occupation, such as radium dial painters, have been fully documented. Chernobyl victims will be studied for many decades, with some data already available. For example, a significant increase in childhood thyroid cancer has been observed. The risk of a radiation-induced cancer for low and moderate doses is generally assumed to be proportional to the risk known for high doses. Under this assumption, any dose of radiation, no matter how small, involves a risk to human health. This is called the linear hypothesis and it may be prudent, but it is controversial. There is some evidence that, unlike the immediate effects of radiation, the long-term effects are cumulative and there is little self-repair. This is analogous to the risk of skin cancer from UV exposure, which is known to be cumulative. There is a latency period for the onset of radiation-induced cancer of about 2 years for leukemia and 15 years for most other forms. The person is at risk for at least 30 years after the latency period. Omitting many details, the overall risk of a radiation-induced cancer death per year per rem of exposure is about 10 in a million, which can be written as . If a person receives a dose of 1 rem, his risk each year of dying from radiation-induced cancer is 10 in a million and that risk continues for about 30 years. The lifetime risk is thus 300 in a million, or 0.03 percent. Since about 20 percent of all worldwide deaths are from cancer, the increase due to a 1 rem exposure is impossible to detect demographically. But 100 rem (1 Sv), which was the dose received by the average Hiroshima and Nagasaki survivor, causes a 3 percent risk, which can be observed in the presence of a 20 percent normal or natural incidence rate. The incidence of genetic defects induced by radiation is about one-third that of cancer deaths, but is much more poorly known. The lifetime risk of a genetic defect due to a 1 rem exposure is about 100 in a million or , but the normal incidence is 60,000 in a million. Evidence of such a small increase, tragic as it is, is nearly impossible to obtain. For example, there is no evidence of increased genetic defects among the offspring of Hiroshima and Nagasaki survivors. Animal studies do not seem to correlate well with effects on humans and are not very helpful. For both cancer and genetic defects, the approach to safety has been to use the linear hypothesis, which is likely to be an overestimate of the risks of low doses. Certain researchers even claim that low doses are beneficial. Hormesis is a term used to describe generally favorable biological responses to low exposures of toxins or radiation. Such low levels may help certain repair mechanisms to develop or enable cells to adapt to the effects of the low exposures. Positive effects may occur at low doses that could be a problem at high doses. Even the linear h

PDF page 1540: Immediate effects are explained by the effects of radiation on cells and the sensitivity of rapidly reproducing cells to radiation. The first clue that a person has been exposed to radiation is a change in blood count, which is not surprising since blood cells are the most rapidly reproducing cells in the body. At higher doses, nausea and hair loss are observed, which may be due to interference with cell reproduction. Cells in the lining of the digestive system also rapidly reproduce, and their destruction causes nausea. When the growth of hair cells slows, the hair follicles become thin and break off. High doses cause significant cell death in all systems, but the lowest doses that cause fatalities do so by weakening the immune system through the loss of white blood cells. The two known long-term effects of radiation are cancer and genetic defects. Both are directly attributable to the interference of radiation with cell reproduction. For high doses of radiation, the risk of cancer is reasonably well known from studies of exposed groups. Hiroshima and Nagasaki survivors and a smaller number of people exposed by their occupation, such as radium dial painters, have been fully documented. Chernobyl victims will be studied for many decades, with some data already available. For example, a significant increase in childhood thyroid cancer has been observed. The risk of a radiation-induced cancer for low and moderate doses is generally assumed to be proportional to the risk known for high doses. Under this assumption, any dose of radiation, no matter how small, involves a risk to human health. This is called the linear hypothesis and it may be prudent, but it is controversial. There is some evidence that, unlike the immediate effects of radiation, the long-term effects are cumulative and there is little self-repair. This is analogous to the risk of skin cancer from UV exposure, which is known to be cumulative. There is a latency period for the onset of radiation-induced cancer of about 2 years for leukemia and 15 years for most other forms. The person is at risk for at least 30 years after the latency period. Omitting many details, the overall risk of a radiation-induced cancer death per year per rem of exposure is about 10 in a million, which can be written as . If a person receives a dose of 1 rem, his risk each year of dying from radiation-induced cancer is 10 in a million and that risk continues for about 30 years. The lifetime risk is thus 300 in a million, or 0.03 percent. Since about 20 percent of all worldwide deaths are from cancer, the increase due to a 1 rem exposure is impossible to detect demographically. But 100 rem (1 Sv), which was the dose received by the average Hiroshima and Nagasaki survivor, causes a 3 percent risk, which can be observed in the presence of a 20 percent normal or natural incidence rate. The incidence of genetic defects induced by radiation is about one-third that of cancer deaths, but is much more poorly known. The lifetime risk of a genetic defect due to a 1 rem exposure is about 100 in a million or , but the normal incidence is 60,000 in a million. Evidence of such a small increase, tragic as it is, is nearly impossible to obtain. For example, there is no evidence of increased genetic defects among the offspring of Hiroshima and Nagasaki survivors. Animal studies do not seem to correlate well with effects on humans and are not very helpful. For both cancer and genetic defects, the approach to safety has been to use the linear hypothesis, which is likely to be an overestimate of the risks of low doses. Certain researchers even claim that low doses are beneficial. Hormesis is a term used to describe generally favorable biological responses to low exposures of toxins or radiation. Such low levels may help certain repair mechanisms to develop or enable cells to adapt to the effects of the low exposures. Positive effects may occur at low doses that could be a problem at high doses. Even the linear h

PDF page 1540: Immediate effects are explained by the effects of radiation on cells and the sensitivity of rapidly reproducing cells to radiation. The first clue that a person has been exposed to radiation is a change in blood count, which is not surprising since blood cells are the most rapidly reproducing cells in the body. At higher doses, nausea and hair loss are observed, which may be due to interference with cell reproduction. Cells in the lining of the digestive system also rapidly reproduce, and their destruction causes nausea. When the growth of hair cells slows, the hair follicles become thin and break off. High doses cause significant cell death in all systems, but the lowest doses that cause fatalities do so by weakening the immune system through the loss of white blood cells. The two known long-term effects of radiation are cancer and genetic defects. Both are directly attributable to the interference of radiation with cell reproduction. For high doses of radiation, the risk of cancer is reasonably well known from studies of exposed groups. Hiroshima and Nagasaki survivors and a smaller number of people exposed by their occupation, such as radium dial painters, have been fully documented. Chernobyl victims will be studied for many decades, with some data already available. For example, a significant increase in childhood thyroid cancer has been observed. The risk of a radiation-induced cancer for low and moderate doses is generally assumed to be proportional to the risk known for high doses. Under this assumption, any dose of radiation, no matter how small, involves a risk to human health. This is called the linear hypothesis and it may be prudent, but it is controversial. There is some evidence that, unlike the immediate effects of radiation, the long-term effects are cumulative and there is little self-repair. This is analogous to the risk of skin cancer from UV exposure, which is known to be cumulative. There is a latency period for the onset of radiation-induced cancer of about 2 years for leukemia and 15 years for most other forms. The person is at risk for at least 30 years after the latency period. Omitting many details, the overall risk of a radiation-induced cancer death per year per rem of exposure is about 10 in a million, which can be written as . If a person receives a dose of 1 rem, his risk each year of dying from radiation-induced cancer is 10 in a million and that risk continues for about 30 years. The lifetime risk is thus 300 in a million, or 0.03 percent. Since about 20 percent of all worldwide deaths are from cancer, the increase due to a 1 rem exposure is impossible to detect demographically. But 100 rem (1 Sv), which was the dose received by the average Hiroshima and Nagasaki survivor, causes a 3 percent risk, which can be observed in the presence of a 20 percent normal or natural incidence rate. The incidence of genetic defects induced by radiation is about one-third that of cancer deaths, but is much more poorly known. The lifetime risk of a genetic defect due to a 1 rem exposure is about 100 in a million or , but the normal incidence is 60,000 in a million. Evidence of such a small increase, tragic as it is, is nearly impossible to obtain. For example, there is no evidence of increased genetic defects among the offspring of Hiroshima and Nagasaki survivors. Animal studies do not seem to correlate well with effects on humans and are not very helpful. For both cancer and genetic defects, the approach to safety has been to use the linear hypothesis, which is likely to be an overestimate of the risks of low doses. Certain researchers even claim that low doses are beneficial. Hormesis is a term used to describe generally favorable biological responses to low exposures of toxins or radiation. Such low levels may help certain repair mechanisms to develop or enable cells to adapt to the effects of the low exposures. Positive effects may occur at low doses that could be a problem at high doses. Even the linear h