Hazard Classification
External Radiation Exposure
Biological Effects
Immediate Somatic Effects/ Acute Radiation Syndrome
Delayed Somatic Effects
Genetic Effects
Internal Radiation Exposure
Radiation Exposure during Pregnancy
Biological Hazards from Radioactive Compounds

In radiation safety, the major goal is to insure that most of the ionizations which occur as a result of a radiation's energy deposition do not occur in either radiation workers or in the general public. Radiation which can deposit energy within healthy tissue may carry some risk. In assessing the radiation work area it is important to distinguish between the two types of radiation hazards, external and internal.

An external radiation hazard is a type of radiation which has sufficient energy that, from outside of the body, it is capable of penetrating through the protective layer of the skin and deposit its energy deep (>0.07 cm) inside the body. External hazards are type and energy dependent. There are three major types of external hazards: (1) X- and ?-rays, (2) neutrons and (3) higher energy (>200keV) ß particles. Each of these types of radiation is considered penetrating. While the high energy ß particles are capable of penetrating the skin, the uncharged particles and rays can also interact with tissues deep in the body.

An internal radiation hazard arises from radioactive material being taken into the body either by inhalation, ingestion, or absorption through the skin, then metabolized and stored in body compartments which utilize the particular chemical or elemental form. For example, radioiodine in the form of NaI, is capable of volatilizing. If inhaled, approximately 20% to 30% will be metabolized and stored in the thyroid gland. Radioactive material stored in the body is capable of irradiating surrounding healthy tissues. While all radiations pose a potential hazard, it has been found that the types of radiations which are not penetrating (e.g., a- and low energy ß-particles) have the greatest potential to damage those tissues if ingested, inhaled or absorbed.

As we have seen, the principal difference between nuclear radiation and other types of radiation such as heat or light is that nuclear radiation deposits its energy which produces ion pairs (ionizations) as it passes through matter. The ionization of living cells can lead to molecular changes which damage the cell's chromosomes. Radiation can cause several different types of damage to cells such as small physical displacement of molecules or the production of ion pairs. If the energy deposited is high enough, biological damage can occur (e.g., chemical bonds can be broken and cells can be damaged or killed). There are several possible results from cellular radiation interactions:

• The damaged cells can repair themselves so no damage is caused. This is the normal outcome for low doses of radiation commonly encountered in the workplace.
• The cells can die, like millions of normal cells, and be replaced through the normal biological process.
• A change may occur in the cell's reproductive stucture in which the cell may mutate and subsequently be repaired with no effect, or they can form precancerous cells,which may then become cancerous.

Generally, the most radiosensitive cells are those that are rapidly dividing and undifferentiated. Examples include immature blood cells, intestinal crypt cells, etc. Damage to these cells is manifested by clinical symptoms such as decreased blood counts, radiation sickness, cataracts or, in the long term, cancer.

The effects on the human body as the result of damage to individual cells are divided into two classes, somatic and genetic. Somatic effects are dose dependent, arising from damage to the body's cells and are only seen in the irradiated person. Genetic effects result from damage to reproductive cells where it is possible to pass on the damage to the irradiated person's children and to later generations.

As previously mentioned, somatic effects are entirely dose dependent. To date, detrimental effects have only been seen for acute exposures, large doses of radiation received in a short period of time. Acute whole body exposures in excess of 100 rem (i.e., much higher that is allowed for workers to receive in a lifetime of radiation work) may damage a sufficient number of radiosensitive cells to produce symptoms of radiation sickness within a short period of time, perhaps a few hours to a few weeks. These symptoms may include blood changes, nausea, vomiting, hair loss, diarrhea, dizziness, nervous disorders, hemorrhage, and maybe death. Without medical care, half of the people exposed to a whole body acute exposure of 400 rem may die within 60 days (LD50/60). Regardless of care, persons exposed to a whole body acute exposure exceeding 700 rem are not likely to survive (LD100). Exposed individuals who survive acute whole body exposure may develop other delayed somatic effects such as cataracts and/or cancers.

Radiation damage to somatic cells may result in cell mutations and the manifestation of cancer. However, these delayed effects cannot be measured at low radiation doses received by radiation workers. In fact, radiation worker populations exposed to currently allowed standards (see Chapter 4) have not been shown to have increased cancer rates when compared to the rest of the population. The estimate of any (statistically) small increased cancer risk is complicated by the facts that:

• there is a long, variable latent period (about 5 to 30 years or more) between radiation exposure and cancer manifestation
• a radiation-induced cancer is indistinguishable from spontaneous cancers
• the effects vary from person to person
• the normal incidence of cancer is relatively high (i.e., the fatal cancer risk from all causes in the U.S. is about 20% or one person in five)

Most regulators take a conservative approach to radiation-induced cancer risk, assuming the risk from radiation is linearly related to the radiation exposure and that there is no threshold for effects. For that reason, workers should aim to keep their exposure ALARA (As Low As Reasonably Achievable). As an estimate, a single exposure of 1 rem carries with it an increased chance of eventually producing cancer in 2 - 4 of 10,000 exposed persons. Lengthening the time for the same exposure should lower the expected number of cancers because of cellular repair (a factor not considered in the establishing the dose limits). To compare radiation risks to other risks, refer to Chapter 3, Radiation Exposure Risks.

Genetic effects from radiation exposure could result from damage of chromosomes in the exposed person's reproductive cells. These effects may then show up as genetic mutations, birth defects or other conditions in the future children of the exposed individual and succeeding generations. Again, as with cancer induction, radiation-induced mutations are indistinguishable from naturally occurring mutations. Chromosome damage is continually occurring throughout a worker's lifetime from natural causes and mutagenic agents such as chemicals, pollutants, etc. There is a normal incidence of birth defects in approximately 5 - 10% of all live births. Excess genetic effects clearly caused by radiation have not been observed in human populations exposed to radiation. However, because ionizing radiation has the potential to increase this mutation rate (e.g., an exposure of 1 rem carries with it an increased chance for genetic effects of 5 - 75 per 1,000,000 exposed persons), it is essential to control the use of radioactive materials, prevent the spread of radiation from the work place, and ensure that exposure of all workers is maintained ALARA.

Mutations become genetic effects as they are carried through to succeeding generations by genes. Exposure to radiation of a person beyond child bearing age will have no genetic effect on future populations because they cannot pass on damaged chromosomes to their offspring.

As previously discussed, not all radiation is equally penetrating. When exposed to external sources of ionizing radiation, only high-energy beta particles and gamma/X-rays are potentially hazardous. Table 8 lists some commonly encountered, low-energy beta emitting radioisotopes which are not external hazards. Generally, beta emitters which have maximum beta energies of less than 200 keV are not external radiation hazards.

However, once inside the body, radioisotopes emitting particulate radiations are extremely hazardous. Radioisotopes can enter the body by workers eating or drinking in an area where radioactive materials are used, by breathing in vapors or aerosols from volatile radioactive compounds, or absorption into the body through cuts or wounds in the skin. The body treats these radioisotopes as it does similar, non-radioactive elements. Some is excreted through normal body processes, but some may be metabolized and incorporated in organs which have an affinity for that element.

The hazard an internal radionuclide poses is directly related to the length of time it spends in the body. Radioactive material not incorporated in an organ is rapidly excreted, thus the hazard is less than if it remains inside the body for a long time as part of the body tissue. Radioisotopes incorporated in organs are more slowly excreted. Different organs have different affinities for certain radionuclides, so the excretion rate depends on the organ involved. This natural elimination rate, the biological half-life, is the time required for the body to naturally reduce the amount of a chemical or elemental substance in the body to one-half of its original amount.

However, all the time the radioisotope is in the body it is also decaying so, even if none of the isotope is excreted the amount in the body is still continually decreasing. Specific organs may have different biological half-lives, and the biological half-life and the physical half-life can be different. The combination of the biological half-life and the physical half-life is called the effective half-life. Table 9 gives the physical, biological and effective half-lives of some common radioisotopes. The value listed as the biological half-life is the whole body half-life, not organ specific.

The embryo/fetus is especially sensitive to radiation during the first three months of pregnancy when there is rapid cell division and organ development taking place. Radiation damage at this time could produce abnormalities that would result in birth defects or fetal death.

Most of the research on fetal radiation effects has been performed on laboratory animals exposed to very high radiation levels. Some studies of children who were exposed to low levels of radiation (during medical procedures or tests) as fetuses have suggested that even at the levels allowed for radiation workers (5 rem TEDE/year) there may be an increased risk for fetal damage. Therefore, Federal regulatory agencies require that the radiation dose to the embryo/fetus as a result of the occupational exposure to the expectant mother should not exceed .5 rem TEDE (10% of the normal limit) during the duration of the pregnancy. Workers who are pregnant or are trying to become pregnant can inform the Radiation Safety Officer. Once a worker has declared her pregnancy in writing, Radiation Safety Program staff will provide additional information on actions to take to ensure that the "declared" pregnant worker maintains her radiation exposure ALARA, and within the 500 mrem limit. Additional information on the various risks to the fetus from radiation and other information on the University's "Declared Pregnant Worker Policy" can be found in Appendix A. This information is extracted from several of the Nuclear Regulatory Commission's pregnancy guides, including Regulatory Guide 8.13, "Instruction Concerning Prenatal Radiation Exposure."

Much of the research conducted at the University uses compounds which have radioactive elements as components (i.e., ³H steroids, ^32P nucleic acids) of the compound. This type of material is specially synthesized to provide information about metabolism or other cell processes. If taken into the body these compounds, unlike "pure" radioactive elements, will then be processed by the body differently and perhaps will be stored for even longer periods of time. For example, it is estimated that ³H ingested in the form of thymidine is 9 times more hazardous than ³H ingested in the form of water. Thus, those radionuclides which are incorporated into nucleic acids are of particular concern in radiation safety.

Damage to a cell's genetic material, particularly to the DNA, is the major harmful effect of radiation and can lead to cell death, mutations, and other detrimental effects. Compounds which contain radiolabeled nucleic acids have the potential, if ingested by a worker or entering the body through cuts, needle sticks, or breaks in the skin, of exposing the worker's DNA to radiation that may affect cell replication or cause a change in genetic function. The nucleic acids which use ³H, ¹⁴C, ³²P, ³⁵S and ¹²⁵I are of concern not only because the radioactive material can be incorporated into a cell's nucleus, but also because the radiation emitted will be absorbed primarily within the cell, increasing the possibility that harmful effects will occur. Therefore, individuals who work with these radioactive compounds must take great caution to ensure the material remains outside the body where they pose only a minor hazard. Good housekeeping and cleanliness are crucial. Wear gloves and never mouth pipette any solutions, radioactive or otherwise. Additionally, at the completion of work with a radioactive compound, wash your hands and forearms thoroughly and use appropriate radiation survey instruments to check your hands, feet, clothing, and work area for radioactive contamination before leaving the lab.