Radiation risks

The Leggett (1992) model was developed to predict tissue doses and whole-body dose to people who may be exposed to americium. The model is considered an updated version of the ICRP (1989) model for americium, which has been used to establish risk-based limits of intake of241 Am (ICRP 1989). The Leggett (1992) and ICRP (1989) models predict similar long-term average doses of americium to the liver and skeleton for an injection exposure and would be expected to predict similar radiation risks and risk-based intake limits (Leggett 1992). Descriptions of applications of the Leggett (1992) model in risk assessment have not been reported. 

Brodsky A. 1996. Review of radiation risks and uranium toxicity with application to decisions associated with decommissioning clean-up criteria. Hebron,Connecticut RSA Publications. 

HPS, Radiation Risk in Perspective, Position Statement of the Health Physics Society, adopted January 1996. 

Radiation-induced genomic instability and bystander effects are now well-established consequences of exposure of living cells to ionizing radiation. Cells not directly traversed by radiation may still exhibit radiation effects. This phenomenon, known as bystander effect, has become a major activity in radiation biology and in some cases has challenged the conventional wisdom. An example is the currently accepted models used for low-dose extrapolation of radiation risks. The currently used models assume that cells in an irradiated population respond individually rather than collectively. If bystander effects have implications for health risks estimates from exposure to ionizing radiation, then the question of whether this is a general phenomenon or solely a characteristic of a particular type of cell and the radiation under test becomes an important issue. 

The Low Dose Radiation Risks is part of The Sixth Framework Program of the European Union, http //www.cordis.lu/fp6... 

In carcinogenic risk assessments for chemicals, as in those for radiation, risks should be expressed in ways that place them in perspective and make them broadly intelligible. Such an approach will facilitate their interpretation and use. 

Boice, J.D., Jr., Beebe, G.M. and Land, C.E. (1985a). Absolute and relative time-response models in radiation risk estimation, page 22 in the Proceedings of the Tluentieth Annual Meeting of the NatioruU Council on Radiation Protection and Measurements, NCRP Proceedings, No. 6, (National Council on Radiation Protection and Measurements, Bethesda, Maryland). 

On this matter, there is some excuse for the media because the scientific community is still split on the issue of application of the LNT to low-level radiation risks. But as evidence accumulates, I believe there is a good chance that scientific opinions will soon consolidate in rejecting the LNT. When that happens, I hope the media will decide that a good headline would be mo st radiation found be harmless. That should attract the public attention they so crave. 

Because of the difficulties in obtaining any significant quantities of francium, use of ihe element is confined to scientific investigations. " Fr is used for the measurement ofAc. Studies have shown that francium fixes itself jn induced sarcomas in rats. Because of the short half-lives of - Fr and 2l Fr. which would cause mi radiation risk to organisms, the property could become useful for the early diagnosis of certain kinds of cancers. 

Beardsley, T, Fallout New Radiation Risk Estimates Prompt Calls for Tighter Controls. Sci. Amer., 35 (March 1990). 

McKinlay, A. F., and Diffey, B. L. (1987) A reference action spectrum for ultraviolet induced erythema in human skin, in W. F. Passchier and B. F. M. Bosnajakovic (eds.). Human Exposure to Ultraviolet Radiation Risks and Regulations, Elsevier, New York, pp. 83-87. 

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. 

Measures of Radiation-Induced Responses. This Section discusses the measures of response from radiation exposure generally used in radiation protection and assessments of radiation risk in general terms. 

Measures of stochastic responses. The primary measure of stochastic responses used in radiation protection and radiation risk assessment by ICRP and NCRP has been fatalities (i.e., fatal cancers and severe hereditary effects). Fatalities have been emphasized essentially because this was the only health-effect endpoint for which data generally were available, both for study populations... 

Until recently, fatalities (especially latent cancer fatalities) was the only measure of stochastic response used in radiation protection and assessments of radiation risks in general terms (ICRP, 1977 NCRP, 1987a). No consideration was given to radiation-induced non-fatal stochastic responses or to the relative severity of different types of fatal responses (e.g., the expected length of life lost per fatality). 

Second, the primary measure of stochastic response used in radiation protection and in most radiation risk assessments has been fatalities. In contrast, the measure of response for chemicals causing... 

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. 

This option does not appear to be advantageous for either radionuclides or chemicals that cause stochastic responses. In radiation protection, total detriment is used mainly to develop the tissue weighting factors in the effective dose (see Section 3.2.2.3.3), but ICRP and NCRP have continued to emphasize fatal responses as the primary health effect of concern in radiation protection and radiation risk assessments. Since total detriment is based on an assumption that fatalities are the primary health effect of concern, the same difficulties described in the previous section would occur if this measure of response were used for chemicals that induce stochastic responses. Other disadvantages of using total detriment include that detriment is not a health-effect endpoint experienced by an exposed individual and the approach to weighting nonfatal responses in relation to fatalities is somewhat arbitrary. Furthermore, total detriment is not as simple and straightforward to understand as either incidence or fatalities. 

EPA (1992a). U.S. Environmental Protection Agency. Commentary on harmonizing chemical and radiation risk-reduction strategies, Letter report prepared by Science Advisory Board s Radiation Advisory Committee, EPA-SAB-RAC-COM-92-007 (May 18) (U.S. Environmental Protection Agency, Washington). 

Sir Edward Pochin (1978) Why be Quantitative about Radiation Risk Estimates Hymer L. Friedell (1979) Radiation Protection-Concepts and Trade Offs Harold O. Wyckoff (1980) From Quantity of Radiation and Dose to Exposure and Absorbed Dose -An Historical Review James F. Crow (1981) How Well Can We Assess Genetic Risk Not Very Eugene L. Saenger (1982) Ethics, Trade-offs and Medical Radiation Merril Eisenbud (1983) The Human Environment-Past, Present and Future Harald H. Rossi (1984) Limitation and Assessment in Radiation Protection John H. Harley (1985) Truth (and Beauty) in Radiation Measurement Herman P. Schwan (1986) Biological Effects of Non-ionizing Radiations ... 

Seymour Jablon (1987) How to be Quantitative about Radiation Risk Estimates Bo Lindell (1988) How Safe is Safe Enough ... 

The only estimate of dominant effects in humans comes from mouse data. BEIR III and UNSCEAR both used skeletal anomalies and cataracts as a basis for human radiation-risk estimates. With chemicals, there are greater uncertainties in extrapolating from mouse to man. The skeletal and cataract systems have not been used widely enough for their validity to be assessed, but at present there is little choice but to use these if an estimate must be made. We suggest that the human impact in the first 5-10 generations be estimated as 4 times the first-generation estimate, as explained in Chapter 7. As is also discussed in Chapter 7, there is no feasible way to estimate the total genetic impact. 

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