Radiation chronic effects

The reader should note tliat since many risk assessments have been conducted on the basis of fatal effects, there are also uncertainties on precisely what constitutes a fatal dose of thennal radiation, blast effect, or a toxic chemical. Where it is desired to estimate injuries as well as fatalities, tlie consequence calculation can be repeated using lower intensities of exposure leading to injury rather titan dcatli. In addition, if the adverse healtli effect (e.g. associated with a chemical release) is delayed, the cause may not be obvious. Tliis applies to both chronic and acute emissions and exposures. 

In some circumstances such as may be encountered after a terrorist attack, acute doses may be more important than potential chronic effects. More specifically, high doses of radiation may be immediately dangerous to life and health and could lead to severe injury including sickness, irreparable tissue damage, and death, although the more severe effects would likely only be observed after a nuclear explosion. For the purpose of this discussion, acute exposures are defined as those that occur in a relatively short time (over several days or less) and result in a dose of at least 25-35 rad (0.25-0.35 Gy).6-7... 

UV radiation has both acute and delayed adverse effects on the human skin. The acute effects are inflammation and sunburn, and the delayed or chronic effects are primarily photoaging and photocarcinogenesis. 

M.J. Behrenfeld, J.T. Hardy, H.I. Lee (1992). Chronic effects of ultraviolet-B radiation on growth and cell volume of Phaeodactylum tricornutum (Bacillariophyceae). J. Phycol., 28, 757-760. 

Moulder and Medhora (2011) noted that the effects of exposure to radiation are two-fold 1) acute and 2) chronic. According to these authors, a therapy developed to treat the acute effects will not be effective if there is no therapy for the chronic effects that manifest in people exposed to high amounts of radiation. On the other hand, the therapies developed for the chronic effects are of little use in the absence of effective therapies for acute effects. ... 

Other effects of irradiation on endothelial cells are cytotoxic effects that participate in the antitumor treatment. As a chronic effect of radiation exposure to blood vessels, histopathologic investigation reveals a capillary rarefication, which means a markedly reduced density of capillaries in irradiated tissues, which can occur, depending on the tissue type, even after many years. The depletion of capillaries and mircrovessels is supposed to be the consequence of an impaired cellular function leading to destruction of capiUaries. The exact mechanisms are still not known (Trott 2002). 

An area of considerable interest is the antioxidant function of ascorbic acid. Ascorbic acid is probably the most effective and least toxic antioxidant present in the human body. Therefore, ascorbic acid may be important in protecting against oxidative stress-related diseases, including cancer, coronary heart disease, cataract formation, and aging. Chapters are devoted to these and other associations of ascorbic acid with disease. A related chapter is devoted to the radiation protective effect of ascorbic acid. One chapter is devoted entirely to the role of ascorbic acid in aging, while another chapter reviews the extensive epidemiological evidence for the relationship between ascorbic acid and chronic health risk. 

A number of studies have shown that vitamins moderate the induction of chromosomal aberrations by radiation. Vitamins C and E given orally to mice either 2 h before, immediately after, or 2 h after 1 Gy (100 rad) of y-ray TBI significantly reduce the frequencies of micronuclei and chromosomal aberrations in BM cells. Vitamin E is the more effective (95). Administration of vitamins C and E within 5 min of irradiation is as effective as pretreatment. Protection by vitamin C has also been shown in humans. Whereas chronic treatment of rats using vitamin C (100 or 300 mg/(kg/d)) for six months prior to TBI protects against chromosomal aberrations, vitamin E is not radioprotective in this setting (96). 

Bissett DL, Chatterjee R, Hannon DP (1990) Photoprotective effect of superoxide-scavenging antioxidants against ultraviolet radiation-induced chronic skin damage in the hairless mouse. Photodermatol Photoimmunol Photomed 7 56-62... 

Radiation causes dominant lethal mutations in the medaka (Oryzias latipes) (Shima and Shimada 1991). Mosquitofish (Gambusia spp.) from radionuclide-contaminated ponds in South Carolina differed from conspecifics in reference ponds, as judged by the frequency of DNA markers, and this is consistent with the hypothesis that these DNA markers may originate from genetic elements that provide a selective advantage in contaminated habitats (Theodorakis et al. 1998). Ionizing radiation at low-level chronic exposure reportedly has no deleterious genetic effects on aquatic populations because exposure is compensated by density-dependent responses in fecundity (IAEA 1976). However, this needs verification. 

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. 

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