Environmental Standards for Ionizing Radiation: Theoretical Basis for Dose-Response Curves

Abstract

The types of injury attributable to ionizing radiation are subdivided, for purposes of risk assessment and radiological protection, into two broad categories: stochastic effects and nonstochastic effects. Stochastic effects are viewed as probablistic phenomena, varying in frequency but not severity as a function of the dose, without any threshold; nonstochastic effects are viewed as deterministic phenomena, varying in both frequency and severity as a function of the dose, with clinical thresholds. Included among stochastic effects are heritable effects (mutations and chromosome aberrations) and carcinogenic effects. Both types of effects are envisioned as unicellular phenomena which can result from nonlethal injury of individual cells, without the necessity of damage to other cells.For the induction of mutations and chromosome aberrations in the low-to-intermediate dose range, the dose-response curve with high-linear energy transfer (LET) radiation generally conforms to a linear nonthreshold relationship and varies relatively little with the dose rate. In contrast, the curve with low-LET radiation generally conforms to a linear-quadratic relationship, rising less steeply than the curve with high-LET radiation and increasing in slope with increasing dose and dose rate. The dose-response curve for carcinogenic effects varies widely from one type of neoplasm to another in the intermediate-to-high dose range, in part because of differences in the way large doses of radiation can affect the promotion and progression of different neoplasms. Information about doseresponse relations for low-level irradiation is fragmentary but consistent, in general, with the hypothesis that the neoplastic transformation may result from mutation, chromosome aberration or genetic recombination in a single susceptible cell.

Epidemiology of Radiation-Induced Cancer

“…This mathematical formulation fits closely the experimental data presented by Upton (2). The ratio of the constant b to constant a, which I take to be about 0.01 when the dose D is in rads, is close to the value given by Upton for this ratio of the quadratic and linear component.…”

“…Radiation provides a useful model of ways of evaluating risks from all environmental agents, because we have more information about health effects of radiation in human populations than we have for any other environmental agent of which I am aware (2). Radiation provides a useful model of ways of evaluating risks from all environmental agents, because we have more information about health effects of radiation in human populations than we have for any other environmental agent of which I am aware (2).…”

“…I would like to begin by presenting some theoretical concepts which follow a point made by Upton (2). With respect to cellular effects of radiation on DNA, and we believe radiation carcinogenesis is at least associated with phenomena having to do with cellular DNA, if E represents an incremental effect of radiation, say, on cancer incidence, then we can express E as a to radiation dose.…”

Chemical carcinogens: a review of the science and its associated principles. U.S. Interagency Staff Group on Carcinogens.

“…It is important when making estimations of risk for chemical agents that we realize that many of the tenets upon which these estimations are made are based upon information from radiation carcinogenesis. For example, the hypothesized mechanisms of the action of radiation, while not the primary concern of this document, have served, and continue to serve, as the basis for some of the primary models for chemical carcinogenesis (156,157). Much evidence that damage to the cellular DNA is a step in the induction of tumors comes from studies using radiation.…”