In the accompanying tabulation are listed the several sources of information underlying the maximum permissible exposure level from external sources of radiation (by this phrase, I mean radiation sources external to the body). The primary source of data for man has been the

medical uses of radiation, particularly radiology installations. Secondary sources of data in man are the doses clearly associated with definite changes. These come from radiation therapy and occasional accidental exposure, and could be considered as providing a ceiling for any exposure. A “floor” is provided by the background radiation levels which Dr. Eisen — bud and others have discussed earlier in this volume. These data in man are supplemented and augmented by animal experiments. Long-term studies have been supported over the last twenty years — many of them by the Atomic Energy Commission and the Public Health Service, some by state laboratories and others — to provide assistance in situations where data for man cannot be obtained.

Source of Data Human exposure

Primary: radiology installations over past 40 years.,

Secondary: doses associated with definite changes Secondary: background radiation levels “floor”

Animals

Large number of long-term experiments…………………….. assistance and

range-finding

The primary human data useful for determining maximum permis­sible exposure levels for individuals are derived from experience with radiologists and other radiation workers. Retrospective analyses have been made of the radiation levels in many installations of the 1920’s and even of World War I. Where there had been no effects in long-term employees, the levels so estimated were judged to be “safe.” On the other side of the coin, changes incidental to the use of radiation in patients and also the exposures of the Japanese and to a lesser extent the Marshallese have contributed human data where effects are seen clearly. Thus, working down from levels where effects are seen and correlating the “safe” radi­ology installations with these give a first approximation of maximum permissible dose (mpd). Because the data pertain always to the exposed individual, these levels are pertinent only to somatic effects — not to ge­netic effects.

The chart on page 92 shows, similarly, sources of information for maximum permissible exposure to radioisotopes. Here again, human ex­perience is rather considerable. The luminous dial painters and radium workers, many of them having worked from the time of World War I onward, have supplied clear evidence of effects which can be correlated with their body burden of the isotope. The radium patients differ from the radium-dial painters, luminous-dial painters, and radium workers in some details. These patients received radium as a nostrum in the late twenties

Basis for Maximum Permissible Exposures to Radioisotopes

Source of Data Provides

Human exposure

Luminous dial painters, radium workers, and

radium patients…………………………………………………. Reliable and

relatively complete picture

Patients receving isotopes in therapy………………….. Assistance

Accidental exposures including calculated and measured effects or fallout from nuclear

weapons tests…………………………………………………….. Primarily inferential

assistance except

Animal experiments

Several long-term experiments…………………………….. Important influence

“Metabolism” of isotopes…………………………………….. Essential

Empirical toxicity ratios……………………………………… Important influence

Calculations from external radiation data………………… With the metabolic

data provide majority of figures except for bone seekers

and early thirties, when radium was considered a rather general “tonic”; they received pure radium and its daughters, not a mixture as did the dial workers.

Accidental exposures provide another level of human experience. And finally, the levels for many radioisotopes are determined by calcula­tion from external radiation figures by the use of data on the metabolism (i. e., tissue distribution and excretion) of the isotope using as the basis a “critical” organ (ordinarily, the one with the highest concentration of the radioisotope). Thus, standards for radioisotopes are determined in part by direct observation and in part by experience in the external radiation field. This has led to something of a “double standard,” one applying primarily to the bone seekers, the other to soft tissue seekers. Work with animals provides directly empirical toxicity data, the approach of the pharmacologist extrapolated into the field of radiobiology.

On page 93 there appears an abbreviated and incomplete summary, taken largely from experimental work, of the doses of radiation associated with detectable changes in a number of important biological processes. In most cases the dose at which effects may possibly occur is given as well as the dose at which they clearly occur. The purpose of this survey is to show that in only one or two instances are clear effects seen (sometimes

Summary of Doses of Radiation Associated with Detectable Change in Certain Biological Processes”’’ Dose Dose Clearly Possibly Detectable Change Associated Associated Lymphocyte count (man and animals)………… <25 rad 5 rad Morphology of lymphocyte……………………….. Incidence of leukemia (man) 0.2 rad in 1 wkc 0.1 rad in 1 wk’ In utero radiation…………………………………. 6-10 rad 2-3 rad Ankylosing spondylitis cases…………………… 200 rad ? Thymus irradiation cases……………………….. 200 rad ? Radiologists…………………………………………. c. 1,000 rad4 c. 500 rad4 Japanese — several criteria……………………….. >100 rad’ >50 rad’ Marshallese — thyroid changes…………………. Incidence of cataract 500-1,000 rad c. 350 rad Man…………………………………………………….. c. 200 rad ? Mouse (neutron exposure) …………………….. 1-5 rad 0.5 rad Incidence of osteogenic sarcoma (calculated doses) Radium cases (“Ra)………………………………. 1,200 rad c. 500 rad “Sr (man, calculated) …………………………… 500-17,000 rad ? Incidence of lung cancer (calculated doses) 250-500 rad >125 rad Cell division rate in grasshopper embryo…. Cell division rate in embryonic tissue 10 rad 5 rad (general) ………………………………………………… 25 rad 10 rad Chromosome breaks in tissue culture………….. 10 rad ? Sperm count and morphology of male beagles………………………………………………………………. 150-300 rad at 3 rad/wkf ?

"The doses are reasonably well established in the animal experiments, but the transfer of information from animal to man introduces a factor of uncertainty which depends on the process under consideration. With the human data the ef­fects are clear but dosimetry is more approximate — for example, the dose must be calculated on the basis of deposition of a radioisotope, must be reconstructed in the case of the Japanese and the radiologists, and so forth. Nonetheless, they show the relation of current mpd’s to those at which overt somatic changes occur. ” Pertains to potential somatic effects only. Not intended to be more than illustra­tive.

“ Dosimetry difficult but correct within an order of magnitude.

4 Estimated long-term cumulative dose.

‘ Dosimetry reconstructed and had components of both low and high linear energy transfer radiation; is very approximate. f Very dependent on dose rate.

in a single exposure) at dosage levels approaching those discussed in this volume as representing the mpd levels. The lowest is that associated with minimal changes in the morphology of the circulating lymphocyte, a change which may or may not be regarded as “damage.”* * Dosimetry for these particular experiments was difficult. Nevertheless, the error would be unlikely to be sufficient to bring the doses appreciably higher than other “sensitive” processes in the table.

This summary could be misleading. Many of these are doses at which something is seen clearly after a single exposure. What we are interested in in setting mpd’s is at the other end of the scale — very low levels of ex­posure over long periods of time. Here there are two important con­siderations.

First, is fractionation of the dose important in developing the somatic effects of radiation? Clearly, it is. Fractionation of the dose will decrease effect if recovery can take place between exposures. On this premise, a total dose of much more than the single dose can be withstood without even noticeable effect if the dose is sufficiently fractionated. Since a total dose which is lethal if given in a single exposure is easly withstood, in terms of acute effects, if protracted, the presence of recovery is quite gen­erally assumed to occur with the somatic effects of radiation. But there are exceptions: radiation of high linear energy transfer rates —such as that associated with neutron exposures, alpha particles, fission fragments — does not seem to exhibit the marked effect of dosage fractionation seen with X or gamma radiation. Also, we know little about the presence or absence of recovery in those processes with long latent periods such as carcinogenesis.

The second important question is whether or not somatic effects in general follow a “threshold” relation to dose. This is illustrated in the accompanying figure. In many cases, the effects, especially acute, short­term ones, do appear to be related to dose, as in the line marked threshold in the figure. But the incidence of cancer, leukemia, and genetic changes (to be discussed later) may follow a non-threshold relation to dose, as in

Dose-response relationships of two types commonly encountered in measuring the biological effects of radiation. The scale is arbitrary. It is not known whether the line marked nonthreshold actually extrapolates to the origin.

the second line of the figure. With genetic effects such as mutating the evidence is clear. For the others there are still differences of opinion.

Application to Nuclear Reactor Problems

What does all of this have to do with the subject of this volume, nu­clear power and the public? Considering still only somatic risks to the in­dividual, I shall examine first exposures at relatively high levels of radia­tion.