A laser Doppler technique which provides a means of obtaining absolute measurements of the speed of red blood cells (RBCs) flowing in individual retinal vessels is described. Doppler-shift frequency spectra of laser light scattered from the RBCs are obtained for two directions of the scattered light. Each spectrum exhibits a cutoff frequency that is directly related to the maximum RBC speed (V(max)). The difference in cutoff frequencies is used to obtain an absolute measure of V(max) that is independent of the exact orientation of the vessel and of the relative direction of the incident and scattered beams with respect to the flow direction. Preliminary measurements obtained using a prototype instrument are presented.
Experimental evidence shows that if the probability of biological response is plotted against the absorbed dose from ionizing radiation, and if both dose and response are determined at the same level of biological organization (e.g., cell or organ-organism) the result appears as a sigmoid, medical-toxicological type of "dose-response" function when plotted using linear coordinates. However, if the biological response expressed at the cellular level is similarly plotted against the average absorbed dose expressed at the organ-organism level, a linearly proportional, "non-threshold" function is obtained. To explain this marked difference in curve shape, the absorbed dose at the organ level in terms of its meaning at the cellular level was examined, and both dose and response were put on the latter level. The result is consistent with the conclusion that absorbed dose at the organ-organism level can be treated, at the cellular level, as the product of two quantities: 1) the mean energy concentration or dose in a cell from a deposition event, i.e., "hit size" (the frequency-averaged specific energy in a reference cell target), and 2) the number of deposition events, or "hits," on the exposed cells. When the mean hit size for a given radiation remains constant, and the number of hits is increased, the total number of responses follows a linearly proportional "hit number response function." However, if the hit number is held constant or normalized to a given value, and the hit size is varied, the resulting probability of cell response again plots as the apparently sigmoid curve mentioned above, which has been termed the "hit size effectiveness function." With decreasing hit size, the probability of a cellular response appears to decrease asymptotically, and become indistinguishable from zero before zero dose is reached. It follows from this inherent relationship between the two kinds of functions that a sufficiently extensive set of data on a population of cells permits either type of function to be produced at will. These findings bear on the interpretation of the "linear, non threshold" hypothesis.
Two equally useful dosimetric quantities, both of which are called dose, are used in toxicology. With radiation measurement, only one-the energy per unit mass D-is called dose. The other-the total energy in the irradiated system-is here distingished from D by assigning it the name collective energy, E. The collective energy is a more complete statement of dose because it is the product of the energy concentration D and the mass irradiated m. Especially in radioepidemiology, in which e is the total energy imparted to all persons irradiated, the quantity m must be specified because it is situation specific and thus highly variable. At present, radioepikemiological dose-response curves are given only in terms of the toxicological model-i.e., the fraction (probability) of radiation-attributable cancers occurring as a function of D. Because this relation does not involve the number of persons at each value ofD, it fosters the illusion that any dose, no matter how small, can result in cancer. However, we show that if the dose-response relationship is expressed in terms ofthe absolute number of attributable cancers as a function of E, cancer occurs, on average, only if the collective energy exceeds a relatively large minimum value, the ma de of which will be ated. Therefore, we conclude that the nonthreshold aspect of the linear hypothesis is misleading and quite probably invalid. For example, in or around a facility in which exposure of humans to relatively low values of D occurs, attributable cancers are most unlikely to appear unless the e to the irradiated population exceeds this minimum value. Dose-response curves for ionizing radiation were first developed to predict its acute, early effects on normal organs and mammals (humans) and on cancers in connection with radiotherapy. These relationships determined the fraction (probability) of persons responding quantally as a function of absorbed dose [a quantal response is a definably either/or change of state such as an irreversible level of injury, the appearance of a cancer, or death (1)]. The purpose and usefulness of these functions was to estimate these probabilities, thus permitting the radiotherapist to prescribe a dose, or course of doses, that would maximize the probability of controlling the tumor while minimizing the chance of unacceptable collateral damage to normal tissues that were unavoidably irradiated. The curves corresponded to those used generally in toxicology and therapeutic medicine-i.e., they had a -threshold and were nonlinear.Subsequent findings in cell systems and in human radioepidemiological studies suggested that cancer could result from relatively small absorbed doses. However, it was evident that at least the initial portion of the dose-response curve was often consistent with a linear, nonthreshold relationship. Nonetheless, the identical variable quantities developed earlier in connection with the toxicological model were carried over directly to describe the linear, nonthreshold relationships (2,3). It is the function based on...
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