Stochastic radiation exposure

Stochastic radiation effects are typically associated with those that occur over many months or years (i.e., are typically chronic instead of acute). Chronic doses are typically on the order of background doses (0.3 rem [0.003 Sv] or less) and are not necessarily associated with larger doses that could result from a terrorist attack with radiological weapons. However, stochastic health effects are defined here as effects that occur many years after chronic or acute exposure to radiological contaminants. Stochastic effects are categorized as cancers and hereditary effects. Because no case of hereditary effects (e.g., mutation of future generations) has been documented, this discussion focuses on cancer risk. 

UCL takes into account measurement uncertainty in the study used to estimate the dose-response relationship, such as the statistical uncertainty in the number of tumors at each administered dose, but it does not take into account other uncertainties, such as the relevance of animal data to humans. It is important to emphasize that UCL gives an indication of how well the model fits the data at the high doses where data are available, but it does not indicate how well the model reflects the true response at low doses. The reason for this is that the bounding procedure used is highly conservative. Use of UCL has become a routine practice in dose-response assessments for chemicals that cause stochastic effects even though a best estimate (MLE) also is available (Crump, 1996 Crump et al., 1976). Occasionally, EPA will use MLE of the dose-response relationship obtained from the model if human epidemiologic data, rather than animal data, are used to estimate risks at low doses. MLEs have been used nearly universally in estimating stochastic responses due to radiation exposure. 

Table 3.3—Nominal probability coefficients for stochastic responses due to radiation exposure of the general public.a...

As depicted in Figure 3.11, the principles of optimization (ALARA) and dose limitation embodied in the radiation paradigm may be thought of as defining a top-down approach to management of stochastic risks. Given that radiation exposures have been justified, the radiation paradigm has two basic elements ... 

The chemical paradigm for management of stochastic risks is applied to control of exposures to stochastic chemicals under authority of several environmental laws. The chemical paradigm also applies to control of radiation exposures when these exposures are regulated under authority of any laws other than AEA. 

Fatalities. In the second option, the common measure of stochastic response from exposure to radionuclides and hazardous chemicals would be fatalities, without any modifications to account for such factors as differences in lethality fractions for responses in different organs or tissues or expected years of life lost per fatality. This option is particularly advantageous for radionuclides, because fatalities is the measure of response provided by the most scientifically defensible database on stochastic radiation effects in humans. Fatalities is the measure of response normally emphasized in radiation risk assessments. 

Two kinds of radiation exposure are distinguished, stochastic exposure (the effects are distributed statistically over a large population), and deterministic exposure (the effects are inevitable or intended, as in the case of deliberate irradiation, e.g. in radiotherapy). 

Exposure to radiation can cause detrimental health effects. At large doses, radiation effects such as nausea, reddening of the skin or, in severe cases, more acute syndromes are clinically expressed in exposed individuals within a short period of time after the exposure such effects are called deterministic because they are certain to occur if the dose exceeds a threshold level. Radiation exposure can also induce effects such as malignancies, which are expressed after a latency period and may be epidemiologically detectable in a population this induction is assumed to take place over the entire range of doses without a threshold level. Hereditary effects due to radiation exposure have been statistically detected in other mammalian populations and are presumed to occur in human populations also. These epidemiologically detectable effects—malignancies and hereditary effects—are termed stochastic effects because of their random nature. 

Unlike stochastic effects, non-stochastic effects are characterized by a threshold dose below which they do not occur. In addition, the magnitude of the effect is directly proportional to the size of the dose. Furthermore, for non-stochastic effects, there is a clear causal relationship between radiation exposure and the effect. Examples of non-stochastic effects include sterility, erythema (skin reddening), ulceration, and cataract formation. Each of these effects differs from the other in both its threshold dose and in the time over which this dose must be received to cause the effect (i.e. acute vs. chronic exposure). 

In general, the guidelines established for radiation exposure have had as their principle objectives (1) the prevention of acute radiation effects (e.g., erythema, sterility), and (2) the limiting of the risks of late, stochastic effects... 

Kossenko MM, Hoffman DA, Thomas TL. 2000. Stochastic effects of environmental radiation exposure in populations living near the Mayak Industrial Association Preliminary report on study of cancer morbidity. Health Phys 79(l) 55-62. 

Radiation exposure limits are set at such levels that stochastic effects are minimized and become acceptable in view of the benefits derived from the exposure. 

The stochastic effects of radiation exposure (e.g. an increased risk of cancer) are not quantified in the derivation of the D values. However, given that the risk of stochastic effects increases with exposure, higher category sources will, in general, present a higher risk of stochastic effects. Furthermore, the deterministic effects resulting from an accident or malicious act are likely in the short term to overshadow any increased risk of stochastic effects. The... 

The effects of exposure to significant doses of radiation can be both immediate and/or delayed. Stochastic effects are those where the probability of the effect (but not the degree) is related to the dose. Nonstochastic effects are those where the severity of the effect is related to the dose. In both cases, however, less exposure is safer. In species other than humans (but not in humans), it has been demonstrated that abnormalities of offspring are related to radiation exposure in parents. Radiation is also known to have a teratogenic effect on fetuses and embryos. 

Health effects from exposure to radiation fall into two categories stochastic (based on probability) and acute. Stochastic effects typically take several years to materialize (e.g., cancer appearing 20 years after an exposure) while acute effects such as nausea or reddening of the skin may take only weeks, days, or even hours to materialize. Stochastic and acute effects are described in more detail in the following sections. First, however, a brief discussion describes how radiation damages human tissue and why exposure may produce one or a combination of the described health effects. 

Specific health effects resulting from an acute dose appear only after the victim exceeds a dose threshold. That is, the health effect will not occur if doses are below the threshold. (Note that this is significantly different from the LNT model used to predict stochastic effects.) After reaching the acute dose threshold, a receptor can experience symptoms of radiation sickness, also called acute radiation syndrome. As shown in Table 3.2, the severity of the symptoms increases with dose, ranging from mild nausea starting around 25-35 rad (0.25-0.35 Gy) to death at doses that reach 300-400 rad (3-4 Gy). Table 3.2 shows that the range of health effects varies by both total dose and time after exposure. 

The basic assumption of the International Commission on Radiological Protection (ICRP) is that for stochastic effects, a linear relationship without threshold is found between dose and the probability of an effect within the range of exposure conditions usually encountered in radiation work. However, ICRP cautions that if the dose is highly sigmoid, the risk from low doses could be overestimated by linear extrapolation from data obtained at high doses. Furthermore, ICRP... 

Given the models for estimating external or internal radiation doses in specific organs or tissues, the following sections consider the responses resulting from a given dose by any route of exposure. As is the case with hazardous chemicals, both stochastic and deterministic radiation effects can occur. 

In spite of uncertainties in the dose-response relationship for radiation discussed above, it is generally believed that radiation risks in humans can be assessed with considerably greater confidence than risks from exposure to most hazardous chemicals that cause stochastic effects. The state of knowledge of radiation risks in humans compared with risks from exposure to chemicals that cause stochastic effects is discussed further in Section 4.4.2. 

The acceptable risks for substances that induce stochastic responses discussed in this Section are values in excess of unavoidable risks from exposure to the undisturbed background of naturally occurring agents that cause stochastic responses, such as many sources of natural background radiation and carcinogenic compounds produced by plants that are consumed by humans. This distinction is based on the assumption of a linear, nonthreshold dose-response relationship for substances that cause stochastic responses and the inability to control many sources of exposure. Risk management can address exposures to naturally occurring substances that induce stochastic responses, but only when exposures are enhanced by human activities or can be reduced by reasonable means. 

Radiation Dose Limits. For routine exposure of individual members of the public to all man-made sources of radiation combined (i.e., excluding exposures due to natural background, indoor radon, and deliberate medical practices), NCRP currently recommends that the annual effective dose should not exceed 1 mSv for continuous or frequent exposure or 5 mSv for infrequent exposure. The quantity effective dose is a weighted sum of equivalent doses to specified organs and tissues (ICRP, 1991), which is intended to be proportional to the probability of a stochastic response for any uniform or nonuniform irradiations of the body (see Section 3.2.2.3.3). 

For the purpose of developing a risk-based hazardous waste classification system, prevention of deterministic responses should be of concern only for hazardous chemicals, but not for radionuclides. Deterministic responses from exposure to radionuclides can be ignored because radiation dose limits for the public intended to limit the occurrence of stochastic responses are sufficiently low that the doses in any organ or tissue would be well below the thresholds for deterministic responses (see Section 3.2.2.1). 

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