Florida Dental Hygienist Ebook Continuing Education

Stochastic effects involve biologic responses to radiation in which the probability or incidence of such effects occurring increases as the radiation dose increases. Stochastic effects result from damage to DNA. These effects are associated with repeated low-dose radiation exposures received over a long period and are not dependent on a threshold dose. The primary stochastic effects are cancers or genetic (heritable) changes. With regard to stochastic effects, no radiation dose is considered safe. The idea that the probability of experiencing effects of

radiation goes up as the dosage goes up over time – called the linear nonthreshold ( LNT , or linear no-threshold ) hypothesis – has been widely accepted for establishing policy in radiation safety and protection with the sum of several small radiation exposures causing the same damage as one large exposure (Connor, 2019a). Stochastic effects are therefore more important than deterministic effects when considering risk in maxillofacial diagnostic imaging.

OTHER FACTORS THAT INFLUENCE THE EFFECTS OF RADIATION

Several other factors influence the effects of radiation on the human body. The type of tissue exposed, the sensitivity of the tissue to radiation, and the area of exposure are all important considerations. Two basic types of tissues make up the body: somatic and genetic . Somatic tissues are all the tissues of the body except those involved in reproduction. The effects of radiation exposure on somatic tissues follow a nonlinear threshold dose response model. This means that above a certain threshold or dose level the effects are observed clinically, and below the threshold no damage is visible. As the dose increases beyond the threshold, more severe damage is produced and observed clinically. Genetic tissues include reproductive and embryonic tissues. Whereas radiation injury to somatic tissues affects only the exposed person, injury to genetic tissues may impact future generations. Genetic or heritable effects may result in mutations or effects on the embryo that are passed on but may not be expressed for years. In contrast to the effects of exposures to somatic tissue, the effects on genetic tissue follow an LNT dose- response model, in which no dose is considered safe. However, as genetic exposures increase, so does the degree of mutation. As demonstrated by genetic exposures, some cells and tissues are more sensitive to the effects of radiation than others. The law of Bergonié and Tribondeau describes radiosensitivity as a function of the degree of metabolism and maturation (Mallari, 2019). Radiosensitive tissues exhibit particular characteristics: They have a high rate of cell division (Sciacca, 2019; Iannucci & Howerton, 2017), a high rate of cellular metabolism (Iannucci & Howerton, 2017; Mallari 2019), a primitive or immature nature (Radiology Key, 2016), and they are nonspecialized (Radtechonduty, 2018). Iannucci & Howerton, 2017). Table 1 provides examples of the cells and tissues that have high, intermediate, and low sensitivity to ionizing radiation. Finally, the volume of tissue exposed to radiation influences the effects of radiation. The body can better tolerate high doses of radiation delivered to a localized area than to the whole body. Radiation oncology, which fractionates a high total

dose into multiple small doses to allow for tissue repair and recovery between doses, employs this knowledge. By contrast, high doses delivered to the whole body are debilitating, if not fatal. For example, the nuclear reactor meltdown at Chernobyl, Ukraine, produced lethal whole-body exposures to firemen and cleanup workers (International Atomic Energy Agency, n.d.). Table 1: Relative Radiosensitivity of Cells and Tissues High Sensitivity Intermediate Sensitivity Low Sensitivity

Note. Adapted from White, S. C., & Pharoah, M. J. (2014). Oral radiology: Principles and interpretation (6th ed.). St. Louis, MO: Mosby.

SHORT- AND LONG-TERM EFFECTS OF RADIATION EXPOSURE

For the most part, radiation effects are not observed immediately. The delay, or time lag, between the exposure to radiation and the first clinical signs of biologic damage is known as the latent period . The length of the latent period is dependent upon the total dose of radiation received and the rate at which the dose was delivered. In general terms, the greater the amount of radiation received and the faster its delivery, the shorter the latent period. Short-term , early , or acute effects of radiation occur within minutes, days, or weeks following the latent period. Typically, short-term effects are the result of high doses of radiation delivered to the entire body, as when a nuclear power plant melts down or a nuclear weapon explodes. In these rare instances of high-level whole-body exposure, a particular sequence of biologic responses known as acute radiation syndrome occurs. This syndrome involves a subset of three syndromes: hematological, gastrointestinal, and central nervous system death. A person with acute radiation syndrome will typically proceed through three stages (prodromal, latent,

manifest illness) before reaching the final stage, which is recovery or death. During the prodromal period, the clinical symptoms may include nausea, vomiting, diarrhea, and leukopenia. After the initial period of radiation sickness, a latent period occurs in which there is absence of illness and seeming recovery. The latent period is followed by manifest illness, a dose-related period during which the three syndromes occur. It is important to emphasize that short-term or acute effects are not associated with diagnostic imaging, including dental radiographic exposures. Radiation effects that occur months, years, or decades after the exposure are referred to as long-term , late , or chronic effects. Chronic effects are the result of small amounts of radiation absorbed repeatedly and cumulatively over a long period. Receipt of these repeated low levels of radiation may result in the development of cancer or genetic abnormalities much later in life or the presence of birth defects in the affected person’s offspring.

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