Late Effects of Fast Neutrons and Gamma-Rays in Mice as Influenced by the Dose Rate of Irradiation: Induction of Neoplasia
TL;DR: The influence of dose and dose rate on the oncogenic effectiveness of 1-MeV neutrons, 5-meV neutron, 250-kVp x-rays, and 60 Co gamma-rays was investigated in male and female RF mice exposed to various doses of whole-body radiation at dose rates of 10-6 to $10^{2}\ \text{rads}/{\rm min}$, beginning at 10 weeks of age as mentioned in this paper.
Abstract: The influence of dose and dose rate on the oncogenic effectiveness of 1-MeV neutrons, 5-MeV neutrons, 250-kVp x-rays, and60 Co gamma-rays was investigated in male and female RF mice exposed to various doses of whole-body radiation at dose rates of 10-6 to $10^{2}\ \text{rads}/{\rm min}$, beginning at 10 weeks of age. Incidence of myeloid leukemia and of thymic lymphoma increased with dose, also varying with dose rate of gamma-rays but not of neutrons. Neutrons were equally or slightly less leukemogenic than x- or gamma-rays at high dose rates but several times as leukemogenic as gamma-rays at low dose rates. Incidence of ovarian tumors also varied as a function of dose and dose rate in gamma-irradiated mice, but relatively few such tumors were induced by neutrons. The cumulative incidence of nonthymic lymphomas and lung tumors was increased by gamma-irradiation at low dose rates but was decreased at high dose rates, the decrease being greater and less dependent on intensity with neutrons than with x- and ...
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TL;DR: The effect of ionising radiation is influenced by the dose, the dose rate, and the quality of the radiation as mentioned in this paper, which is the main objective of the present report, as well as the underlying relative biological effectiveness (RBE) values.
Abstract: The effect of ionising radiation is influenced by the dose, the dose rate, and the quality of the radiation. Before 1990, dose-equivalent quantities were defined in terms of a quality factor, Q(L), that was applied to the absorbed dose at a point in order to take into account the differences in the effects of different types of radiation. In its 1990 recommendations, the ICRP introduced a modified concept. For radiological protection purposes, the absorbed dose is averaged over an organ or tissue, T, and this absorbed dose average is weighted for the radiation quality in terms of the radiation weighting factor, wR, for the type and energy of radiation incident on the body. The resulting weighted dose is designated as the organ- or tissue-equivalent dose, HT. The sum of the organ-equivalent doses weighted by the ICRP organ-weighting factors, wT, is termed the effective dose, E. Measurements can be performed in terms of the operational quantities, ambient dose equivalent, and personal dose equivalent. These quantities continue to be defined in terms of the absorbed dose at the reference point weighted by Q(L). The values for wR and Q(L) in the 1990 recommendations were based on a review of the biological and other information available, but the underlying relative biological effectiveness (RBE) values and the choice of wR values were not elaborated in detail. Since 1990, there have been substantial developments in biological and dosimetric knowledge that justify a re-appraisal of wR values and how they may be derived. This re-appraisal is the principal objective of the present report. The report discusses in some detail the values of RBE with regard to stochastic effects, which are central to the selection of wR and Q(L). Those factors and the dose-equivalent quantities are restricted to the dose range of interest to radiation protection, i.e. to the general magnitude of the dose limits. In special circumstances where one deals with higher doses that can cause deterministic effects, the relevant RBE values are applied to obtain a weighted dose. The question of RBE values for deterministic effects and how they should be used is also treated in the report, but it is an issue that will demand further investigations. This report is one of a set of documents being developed by ICRP Committees in order to advise the ICRP on the formulation of its next Recommendations for Radiological Protection. Thus, while the report suggests some future modifications, the wR values given in the 1990 recommendations are still valid at this time. The report provides a scientific background and suggests how the ICRP might proceed with the derivation of wR values ahead of its forthcoming recommendations.
463 citations
369 citations
01 Jan 1987
TL;DR: Leukemia as a cause of death among survivors has continued to decrease and now differs from the control group only in Hiroshima and Nagasaki, and radiation-induced cancers other than leukemia seem to develop proportionally to the natural cancer rate for the attained age.
Abstract: For nonleukemic cancers the relative risk seen in those who were young when exposed has decreased with time, while the smaller risks for those who were older at exposure have tended to increase. While the absolute excess risks of radiation-induced mortality due to nonleukemic cancer have increased with time for all age-at-exposure groups, both excess and relative risks of leukemia have generally decreased with time. For leukemia, the rate of decrease in risk and the initial level of risk are inversely related to age at exposure. ? 1987 Academic Press, Inc.
260 citations
TL;DR: Data show that the time delay between receipt of dose and cancer death increases with decreasing dose, which means that, with low level radiation, death from natural causes will often occur first, which implies an effective threshold.
Abstract: We present a wide variety of experimental data indicating that linear no-threshold theory (LNT) greatly exaggerates the cancer risk from low level radiation LNT is based on cancer initiating hits on DNA molecules, but many other factors affect the progression from DNA damage to a fatal tumor, such as availability of DNA repair enzymes, immune response, and cell suicide Data are presented to show that these are generally stimulated by low level radiation (LLR) and suppressed by high doses that serve as calibrations for LNT Since the great majority of cancers are caused by natural chemical processes, the protection against these provided by LLR may make LLR beneficial rather than harmful Genes turned on and turned off by LLR are often different from those affected by high doses Direct studies of cancer risk vs dose are reviewed: animal experiments generally indicate that LNT exaggerates the risk of low level radiation, and the same is true of most data on humans except possibly where dose rates are very high Data show that the time delay between receipt of dose and cancer death increases with decreasing dose, which means that, with low level radiation, death from natural causes will often occur first This implies an effective threshold Responses to this type of information by various official and prestigious groups charged with estimating cancer risks from radiation are reviewed
199 citations
TL;DR: In the studies reported here the prevalence of tumors as the result of pituitary isografts was not enhanced after irradiation with 56Fe ions, and it remains to be seen how effective pituitaries are for enhancement of radiogenic neoplasia from other ions at different LET values.
Abstract: The potential for radiogenic neoplasia from charged-particle irradiation has been estimated using the Harderian gland of the mouse as a test system. Particles ranging in Z from Z = 1 (proton) to Z = 41 (niobium), in energy from 228 to 670A MeV, and in LET from 0.4 to 464 keV/microns were produced at the Lawrence Berkeley Laboratory BEVALAC. Expression of the tumorigenic potential of the initiated cells was enhanced by hormones from isogeneic grafts of pituitaries. The goal of the studies was to estimate the initial slope of the relationship between increased tumor prevalence at 16 months after irradiation and the dose received. Initial slopes were measured with good precision for 60Co gamma rays and the Bragg plateau beams of 228A MeV 4He ions, 600A MeV 56Fe ions, and 350A MeV 56Fe ions. The ratio of the initial slope for these ions to that of 60Co gamma rays give an estimate of the maximum RBE for radiogenic neoplasia. These values were 2.3 for the 4He ions, 40 for 600A MeV 56Fe, and 20 for 350A MeV 56Fe. In the studies reported here the prevalence of tumors as the result of pituitary isografts was not enhanced after irradiation with 56Fe ions. It remains to be seen how effective pituitary isografts are for enhancement of radiogenic neoplasia from other ions at different LET values. A risk analysis was undertaken using particle fluence rather than dose as the independent variable. This analysis provides a value for a "cross section" expressed in microns 2. This parameter expresses as the increase in proportion of mice with one or more Harderian gland tumors per unit increase in particle fluence. The plot of the cross section (risk coefficient) as a function of LET is monotonic, with no clear evidence of a maximum value of the risk coefficient for even the highest LET particle used.
192 citations