ML20065A936

Testimony of Ji Fabrikant on Contentions 42,111 & 112 Re Radiation Exposure.Natl Committee for Radiation Protection Recommendations on Dose Limit for Exposure to Pregnant Women Provides Protection Against Teratogenic Effects

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Issue date:	02/15/1983
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OUTLINE OF JACOB I. FABRIKANT'S TESTIMONY ON CONTENTIONS 42, 111, and 112 I. Dr. Fabrikant is a physician and radiologist,-professor, and researcher who has served on many committees in the area of radiation and health and has published numerous articles on that subject.

II. The 1980 NAS-BEIR committee preferred a linear quadratic hypothesis, and its determination of the excess cancer risk per rem, of generally 1 in 10,000, does not appreciably differ from the 1977 UNSCEAR Report.

A. The current estimates of risks associated with exposure to low dose, low-LET radiation were adopted over 10 years ago.

B. In 1980 NAS-BEIR Committee placed emphasis on the methods of estimation of the cancer risk coefficient rather than emphasizing the numerical estimates derived.

C. The 1980 BEIR Committee reached an agreement on the magnitude of the risk associated with low levels of radiation exposure.

III. The scientific community usually endorses the linear dose-response model for radiation protection purposes because it is the most conservative.

A. The supralinear hypothesis does not fit the data for cancer induction following exposure to low dose, lot-LET radiation.

B. Low doses of low-LET radiation do not produce more cancers per unit dose than high doses.

C. More malignancies will not occur if a given number of person-rems is distributed among a greater number of people.

D. Because of the dose rate effectiveness factor, linear interpolation from high doses may over-estimate the effects of either low doses or doses delivered at low dose rates by a factor of 2 to 10.

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IV. Some reports on epidemiological studies claim the linear hypothesis is not conservative but no expert advisory committee has agreed with such claims.

A. The Mancuso, Steward, and Kneale (1977) study on the cancer mortality rate for workers at the Hanford Nuclear Facility has serious flaws and their results are inconsistent with known radiobiological evidence.

B. The Najarian and Colton (1978) study on the Portsmouth Navel Shipyard workers also suffers from serious methodological flaws.

C. Bross' conclusion that susceptible subgroups in the general population exist which are especially sensitive to radiation damage is not supported by the evidence.

D. Bross and Driscoll's (1981) study on lung cancer deaths in the Portsmouth Navel Shipyars workers uses unconventional statistical methods and has methodological flaws.

E. Modan's study on Israeli children who had been treated with radiation for ringworm of the scalp has substantial dosimetry uncertainties.

F. Dr. K.Z. Morgan's claims that low level exposure to radiation is more hazardous per unit of absorbed dose than exposure to high doses at high dose rates ~ fails to differentiate between the effects of high-LET and low-LET radiation.

G. Dr. Morgan's various publications and talks provide no new information on the risks of low dose, low-LET radiation exposure.

V. Reliable epidemiological studies exist that allow risk estimates to be made on the effects of low-dose, low-LET radiation.

A. Any changes that have been made in the scientific dose response hypothesis and the risk estimates are results of new knowledge derived from epidemiological studies and have not been made because those studies demonstrate that the risk per rad of low-LET radiation is greater at low doses than at high doses.

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. 1 B. The NAS-BEIR Committee used the Hiroshima and Nagasaki atomic-bomb survivor studies as a chief source of data, especially for low to intermediate doses of radiation.

1. The Japanese atomic-bomb survivor study does not support the hypothesis that the cancer risk from low level exposure to radiation is

greater than what was previously believed.

2. The Japanese atomic-bomb survivor studies will not solve the controversies surrounding potential low dose health effects but still will play an important role in testing alternative dose-response models because of the studies' population size and dose dis-tribution.

3. The Japanese atomic-bomb survivor studies represent normal populations.

4. The dosimetry of the Hiroshima and Nagasaki studies currently is being reassessed, but the reassessment is not expected to yield significant changes in the low dose, low-LET cancer risks estimates reported by BEIR, UNSCEAR, and other councils.

VI. Sensitive subpopulations to cancer induction exist

! on the basis of age and sex, but present radiation protection guides already take into account the exist-

ence of these small, unidentifiable subpopulations.

l VII. Dr. Fabrikant believes the NCRP recommendations on dose l limitation for exposure to declared pregnant women

provide adequate protection against potential teratogenic effects.

i VIII. Skin cancer is not considered to be an especially radiogenic cancer.

IX. Calculating of internal dose and dose commitments over a 50-year period provides an adequate estimation of the dose commitment to an occupationally exposed worker.

X. Dr. Fabrikant believes that the present ICRP recommended standards of dose limitation for the general public and radiation worker populations are not without risk, but it will not be possible to detect any excess i

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instances of cancer or genetic ill-health, if they do occur, caused by such exposures because the' doses are so small and because the probability of occurrence is i so infrequent.

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TESTIMONY OF JACOB I. FABRIKANT

1. Q. State your name, occupation, and present position.

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A. My name is Jacob I. Fabrikant. I am a physician  !

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4 and radiologist, research biophysics scientist, l

1 teacher and' university professor in radiology and in biophysics at the University of California, San Francisco School of Medicine, University of 1

California, Berkeley, and the Lawrence Berkeley Laboratory, University of California, Berkeley.

2. Q. Briefly describe your education, including dates of degrees received, academic and-other honors, 1

professional societies and professional experience.

A. I hold a Bachelor of Science degree in chemistry and mathematics, McGill University (1952); a Doctor of Medicine degree and a Master of Surgery degree,

' both from McGill University (1956); and a Doctor

! of Philosophy degree in biophysics, University of

London (1964). I am a Fellow of the American College of Radiology (1978). I did post-doctoral i

I training in surgery and pathology at Duke Univer-sity Hospital and trained in radiology at The Johns Hopkins Hospital. I am certified by the

! American Board of Radiology in diagnostic radiology, therapeutic radiology and nuclear medicine. I have

. been Professor and Head of the Department of Radiology, University of Connecticut School of Medicine; and Professor and Chairman, Department of Diagnostic Radiology, McGill University Faculty of Medicine. I am presently Professor of Radi-ology, University of California School of Medicine at San Francisco; Staff Senior Scientist at Lawrence Berkeley Laboratory, University of California, Berkeley; Physician-in-charge of the Donner Pavilion, Cowell Memorial Hospital, University of California, Berkeley; and Professor and Member of the Graduate Biophysics Group, Department of Biophysics and Medical Physics, University of California, Berkeley.

I devote all my professional and academic activi-ties to patient care, primarily diagnostic and therapeutic radiology and nuclear medicine; to research in the radiological sciences, primarily cancer research; and to teaching in radiology and biophysics, primarily in the radiological sciences in the medical school and in the graduate school at the University of California. These are all l

l documented in my curriculum vitae which is attached 1

to this testimony.

3. Q. Have you ever been appointed to or served on, or do you presently serve on, any recognized national or l

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international committees, commissions, or groups dealing with the radiological sciences in general and radiation and health in particular?

A. Yes, I have served on seven committees of the National Academy of Sciences - National Research Council, including the 1972 BEIR I, 1976 BEIR II, and 1980 BEIR III Committees. I served on the 1982 National Academy of Sciences Committee on a National Institute for Occupational Safety and Health ("NIOSH") study of the Portsmouth Naval Shipyard workers. I presently am consultant to the National Academy of Sciences Board of Radio-active Waste Management. I was the Director of Public Health and Safety of the President's Com-mission on the Accident at.Three Mile Island (1979). I have served on scientific advisory committees of the President's Commission, USPHS, NIH, NCI, BRH, NASA, American College of Radiology, the NRPB of Canada and England, and other scien-tific bodies dealing with radiation and health and cancer research. I am a member of the Interna-tional Commission on Radiological Protection. I am a member of the Nuclear Regulatory Commission's Harvard University Scientific Committee for the 1

Reevaluation of the WASH-1400 Radiological Health Effects Model, i

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4. Q. Have you ever published in the scientific literature dealing with medicine, cancer research, and radia-tion and health?

A.

Attached to my testimony is a complete bibliography of my publications. My publications now number in excess of 200 scientific articles, reports, chapters, and reviews in the open literature. They are all in the fields of the radiological sciences, medicine and surgery, radiobiology, radiation sciences and health, cancer biology, and related disciplines.

5. Q. Briefly describe the BEIR Committee, NCRP, ICRP, the relationship between them, and your personal participation in each committee.

A. The BEIR Committee is a standing expert scientific advisory committee on radiation and health effects of radiation of the National Academy of Sciences -

National Research Council, viz., the Committee on the Biological Effects of Ionizing Radiations.

The National Council on Radiation Protection and Measurements ("NCRP") is an expert scientific advisory committee on radiation and health effects chartered by the U.S. Congress in 1964 (originally l

dating back to 1929) with designated responsibility l to collect and analyze scientific data and to develop recommendations about protection against radiation and on radiation measurements, quantities,

. and units. The International Commission on Radi-ological Protection ("ICRP") is the oldest expert scientific advisory body on radiation and health; it dates to 1928. The ICRP is represented by scientists from some 15-20 countries throughout the world with responsibilities to evaluate the health risks of radiation, particularly concerning radioisotopes and medical applications, estimate the extent of these risks, and recommend limits on radiation exposures to worker populations and the general population. These advisory committees on radiation of international and national compo-sition have, for these many years, met and served effectively to discuss, to review, to evaluate, and to report on three important matters of societal concern: (1) to place into perspective the actual and potential harm to the health of man and his descendants in the present and in the future from those societal activities involving the use of ionizing radiations; (2) to develop quantitative indices of harm based on dose-response relationships to provide a scientific basis for the evaluation of somatic and genetic risk so as to better protect human populations exposed to low-level radiation; and (3) to identify the sources and levels of radiation which could cause harm, to assess their relative importance,

and to provide a framework on how to reduce unnec-essary radiation exposure to human populations.

I was a member of the 1972 BEIR I Committee

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and was on the Subcommittee on Somatic Effects.. I was Vice-Chairman of the 1976 BEIR II Committee.

I was a member of the 1980 BEIR III Committee, on

the Subcommittee of Somatic Effects, and Chairman of the Ad Hoc Committee to estimate radiation cancer risks of low-dose, low-LET, whole-body radiation. I am on the ICRP and a member of Committee 1, which deals with risk estimation and all health effects of exposure to ionizing radia-tions.

6. Q. What is the scope and purpose of your testimony?

A. The scope and purpose of my testimony is to respond those portions of Contentions 42, 111, and-112 of the Rockford League of Women Voters (the

" League") which are within my scientific and medical expertise. Contention 42 generally allegec

! the.t no assurance exists that Byron can be operated so that proper radiation exposure levels to the employees and workers are maintained. Contention 111 asserts that the in-plant monitoring systems at Byron are inadequate and that Byron's design base will not keep radiation exposure levels as low as is reasonably achievable. Contention 112 J

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. generally claims that Commonwealth Edison' Company

(" Edison") has not accurately assessed the effects of radiation exposure on plant workers.

In creating this testimony, I have considered both the specific language of the contentions and supplementary information which the League pro-vided in response to discovery requests by both Edison and the NRC Staff. A basic thrust of these contentions to which this testimony responds is that new scientific data are available which demonstrate that occupational radiation exposures within the limits of applicable NRC regulations and in accordance with as-low-as-reasonably achiev-able ( "ALARA") principles have more serious health effects than previously believed. This position is articulated in many different ways, but perhaps most clearly as follows:

spreading out a given man-rem dose to more persons . . . [causes) more cancers because the lethal cancers per man-rem are more at low doses than at high doses . . . .

League's Response to the NRC Staff's Interrogatories,

p. 42-3.

7. Q. Describe the characteristics of ionizing radiation which are associated with routine exposures to radioactivity by workers in nuclear power plants in the United States.

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A. Under normal operating conditions, the radiation resulting from the routine release of radioactive isotopes is primarily gamma radiation, but beta, alpha, and neutron radiations also exist in very minute amounts.

8. Q. In the scientific community, what are generally regarded as high, low, and intermediate doses of radiation?

A. The NCRP (1980) Report provides a reasonable working definition: " low" doses of sparsely ionizing radiation are arbitrarily defined as 0-20 rads; "high" doses exist at "150-350" rads;

" intermediate" doses are defined as between the two; and " ultra high" doses are anything greater than 350 rads.

9. Q. What is the definition of low-LET radiation and how does it differ from high-LET radiation?

A. Linear energy transfer ("LET") is defined as the average amount of energy lost per unit of ionizing particle spur-track length. Low-LET radiation is sparsely ionizing radiation and is characteristic of electrons, x-rays, and gamma rays. Low-LET radiations are those encountered primarily in the routine operation of nuclear power plants.

. High-LET radiation is characteristic of alpha particles and fast neutrons. These are commonly encountered in the operation of high energy accelerators.

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10. Q. What are the observed biological effects cf low-LET

radiation in human beings?-

A. Briefly, low-LET radiation can affect the cells and tissues of the body in three important ways.

First, if the damage is caused in the DNA molecule and occurs in one or a few cells, such as those of the blood-forming tissues, the irradiated cell can occasionally transform into a cancer cell, and, after a period of time, there is an increased risk of cancer developing in the exposed individual.

This biological effect is carcinogenesis; and the health effect, cancer. Second, if the embryo or i

fetus is exposed during gestation, injury can occur i

in the proliferating and differentiating cells and tissues, leading to abnormal growth. This bio-loc' et effect is teratogenesis; and the health

. ect, developmental abnormality in the newborn.

Thiru, if the macromolecular lesion occurs in the l

reproductive cell of the testis or the ovary, the hereditary genome of the germ cell can be altered, i.

, and the injury can be expressed in the descendants of the exposed individual. This biological effect i

1 is mutagenesis; the health effect, genetically related ill-health.

There are a number of other important biological effects of ionizing radiation, such as induction of cataracts in the lens of the eye or impairment of fertility, but these three important delayed or late biological effects - carcinogenesis, tera-togenesis and mutagen sis - stand out as those of greatest concern.

11. Q. How have these biological effects been observed?

A.

A considerable amount of scientific information is now known from epidemiological studies of exposed human populations and from laboratory animal experiments. Furthermore, the scientific evidence indicates that any exposure to such delayed or late radiation, even at low levels of dose, carries some rist of such health effects. And as the dose of radiation increases above very low levels, the risk of these delayed or late health effects increases in exposed human populations.

12. Q. What are the observed health effects of low-LET radiation on human beings?

A. A number of important observations on the late health effects of low-LET radiation have now emerged, about which there is general scientific agreement.

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. These observations are based primarily on evalua-tion of epidemiological surveys of exposed human populations, on extensive research in laboratory animals, on analysis of dose-response relationships of carcinogenesis, teratogenesis and genetic effects, and on known mechanisms of cell and tissue injury in vivo and in vitro. Cancer-induction is considered to be the most important late somatic effect of low-dose, low-LET ionizing radiation. The different tissues appear to vary greatly in their relative rusceptibility to cancer-induction by radiation. Influences affecting the cancer risk include: age at the time of irradia-tion and at the time of the expression of the disease, sex, and radiation factors and types such as LET and relative biological effectiveness.

Effects of growth and development in the irradiated embryo and fetus have been observed and these i

effects are related to the gestational stage at which exposure occurs. It appears that a threshold level of radiation dose and dose rate may exist below which gross teratogenic effects will not be observed.

l Estimation of the radiation risks of genetically

related ill-health are based mainly on laboratory

) animal obs3rvations - primarily from laboratory i

mouse experiments.- because of the paucity of data on exposed human populations. Genetic effects due 4 to ionizing radiations have never been directly observed in human beings. Our knowledge of funda-mental mechanisms of radiation injury at the genetic level is far more complete than, for example, of mechanisms of radiation carcinogenesis, thereby permitting greater assurance in extrapolat-ing information on genetic mutagenesis from laboratory animals to man.

13. Q. At what' level of radiation doses have these health effects been observed?

A. Epidemiological surveys of exposed human populations are highly uncertain in regard to the forms of the dose-response relationships for radiation-induced cancer in man. This is especially the case for low-level radiation. It has been necessary to estimate human cancer risk from low radiation doses primarily from observations of relatively high doses, frequently greater than 100 rads.

While radiation-induced cancer in man has been observed at levels below 50 rads, the epidemio-logical surveys are too uncertain to provide reli-able dose-response data. Surveys of developmental abnormality in the newborn demonstrate teratogenic

. health effects in the 10-19 rad dose range.

Genetic effects in exposed human populations have never been demonstrated, even after high-level exposure.

14. Q. Describe the relationship between a rem and a rad.

A.

A rad is the unit of absorbed dose of radiation =

100 ergs / gram. The rem is the unit of dose equivalent (used in radiological protection) =

absorbed dose (in rads) times quality factor times distribution factor times any other necessary modifying factors; it represents a quantity of radiation that is equivalent - in biologic damage of a specified sort - to 1 rad of 250-kVp x-rays.

15. Q. Do you agree with the position expressed in Con-tentions 42, 111, rnd 112: that the health effects of occupational exposure to radiation from routine operation of nuclear power plants in accordance with NRC regulations and ALARA are greater than set forth in the curre-t scientific reports by standard setting bodies?

A. No.

16. Q. How does the most recent NAS-BEIR Committee Report express the health effects of low-dose exposures to low-LET radiation?

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, I A. Table V-4 of-the 1980 BEIR Report is a table which lists " Comparative Estimates of Lifetime Risk of Cancer Mortality Induced by Low-LET Radia-tion - Excess Deaths per Million, Average Value per Rad by Projection Model, and Type of Exposure."

To compare the risk estimates with those of the 1972 BEIR Report and the 1977 United Nations Scientific Committee on the Effects of Atomic Radiation ("UNSCEAR") Report, the NAS-BEIR (1980)

Report found it convenient to express the risk estimates as cancer deaths per million persons (including both sexes) per rad of continuous lifetime exposure. In this form, the risks were based on average values per rad recieved over a lifetime and are not (stimates of the1 excess for a single dose of 1 rad. For continuous lifetime exposure to 1 rad / year, the relative-risk projec-l-

tion in the 1980 BEIR Report is 182 excess cancer deaths per million persons exposed per rad, and the absolute-risk projection is 67 deaths.

The 1980 NAS-BEIR Committee preferred a con-strained linear-quadratic, rather than the linear, dose-response model for low-dose, low-LET, whole-body radiation and preferred not to assume a fixed relationship between the effects of high- and low-LET radiation. The BEIR Committee chose to express

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the incremental cancer risk estimates as the number of excess cancers or of excess cancer deaths in an exposed population of one million people followed from the onset of exposure to the end of life. These numbers also may be expressed as percentages of the number of cancers normally expected for a population cohort of that size over the period under consideration and in the absence of any additional radiation exposure. The expres-sion of excess cancer risk per rad generally is avoided in the published 1980 BEIR Report tables (Chapter V) because it would suggest a commitment to the linear hypothesis that some members of the Committee wished to ' void because they believe that the effect per rad is most probably variable:

that is, an increasing function of dose in the region from zero rads up to the point where cell-killing becomes important.

The 1980 BEIR Committee linear-quadratic estimates do not differ appreciably from those in the'1977 UNSCEAR Report. These values indicate that the lifetime excess cancer risk per rem is generally 1 in 10,000 and may be considerably less.

, 17. Q. Does the scientific community now believe that the.

risks of low-dose, low-LET radiation exposure are much greater than was thought a few years ago?

A. No. The current estimate of tae risks associated with exposure to low-dose, low-LET radiation was i

adopted by the BEIR Committee in 1972. In addition, the present protection guides for maximum dose limitations were set by the ICRP over two decades ago.

18. Q. Are there any risk estimates of health effects from low-dose, low-LET radiation as great as 10-3, i

or one chance in one thousand, that have been endorsed by any radiation protection standard setting commission or council?

A. No.

19. Q. Did the 1980 NAS-BEIR Committee state that its numerical estimates of the cancer risk coeffi-cients for exposure to low-dose, low-LET radia-tion were exact?

A. No. The 1980 BEIR Committee, in its report (NAS-BEIR 1980), emphasized that the numerical estimates for risk coefficients for low-dose, low-LET radia-tion are imprecise and should not be considered as firm numerical values because of numerous uncer-tainties. The quantitative estimation of the t

. carcinogenic risk of low-dose, low-LET radiation is subject to numerous uncertainties. The great-i est of these involves the shape of the dose-response curve. Other uncertainties include the length of the latent period, the RBE for fast neutrons and alpha radiation relative to gamma and X radiation, the period during which the radiation s

risk is expressed, the model used in projecting risk beyond the period of observation, the effect of dose rate or dose fractionation, and the influ-ence of differences in the natural incidence of specific forms of cancer. In addition, uncertain-i ties are introduced by biological risk factors, e.g., the effect of age at irradiation, the influ-ence of any disease for which the radiation was r

given therapeutically, and the influence of length of followup. Moreover, these uncertainties, unlike sampling variation, cannot be summarized in probabilistic terms. Instead, their collective influence denies any great credibility to estimates that can be made for low-dose, low-LET radiation.

Therefore, the 1980 NAS-BEIR Committee placed emphasis on the methods of estimation rather than on any numerical estimates derived thereby.

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, 20. Q. Did the 1980 BEIR Committee reach an agreement on the magnitude of the risk from low-level radiation exposure?

A. Yes. The lowest dose levels of low-LET radiation for which estimates of excess cancer risk were calculated included a single exposure (whole-bcdy) to 10 rads to a population of 1 million people and continuous exposure to 1 rad per year for periods up to a lifetime in a population of 1 million people. The 1980 BEIR Committee agreed that the epidemiological data available were not sufficiently reliable - either with regard to the size of the study populations or to the completeness of radia-tion dosimetry - for estimation of excess cancer risks at dose levels below those cited. The excess cancer risk estimates were calculated using four dose-response relationships: linear, linear-quadratic, a modified form of the linear-quadratic, and a pure quadratic, and were pre-sented as an envelope of risks. In this envelope, the linear relationship presented the highest risk, the quadratic the lowest, and the linear-quadratic relationships intermediate between the two. There was no disagreement that this envelope of risks adequately described the range of dose-response relationship at low doses.

, 21. Q. Why does the scientific community usually endorse the linear dose-response model for radiation protection purposes?

A. Although the weight of the experimental evidence generally favors the linear-quadratic dose-response i model for low-LET radiation (NCRP, 1980), extra-polation from animals to humans is always hazardous,

and for example with breast cancer, the human data provide fairly strong support for the linear model. Moreover, all of the models fit the data with approximately the same success and a con-servative model is preferred when the level of uncertainty is high and when human life and health  !

are at stake. The linear model also has an advantage in that the scientific uncertainty about dose-response models chiefly concerns the region lying below the linear regression line. The simplicity and ease of cpplication of the linear model are important advantages. Furthermore, because the use of the linear model does not require observations over a wide range of doses, it obviates the necessity for depending so heavily on the experience of only one epidemiological survey, such as the Japanese atomic-bomb survivors study. The linear model is also a more flexible tool, permitting use to be made of all available

, epidemiological data representing different exposure situations and populations.

Application of the linear model for radiological protection of workers in the workplace or the general population is prudent. Under this model, the risk of radiation-induced cancer remains the same derived from the population collective dose equivalent -- in other words, the risk is the same whether 100,000 people receive a dose of 1 rem, 10,000 people receive a dose of 10 rems, or 1,000 people receive a dose of 100 rems.

22. Q. Following exposure to low-dose, low-LET radiation, does the sup: alinear hypothesis fit the data for cancer induction better than the linear hypothesis?

A. No. The GAO Report (1981) describes alternative dose-response models and comments as follows on the supralinear model (see Chapter 2, page 37, GAO, 1981):

The square root of dose-response model (such as the supralinear dose-response model as the most representative) pre-dicts a 40 percent increase in radiation-caused-cancer if radiation exposure doubles. According to this model, lower doses of radiation are much more harmful than predicted by the linear model. The analysis of a few recent epidemiological studies have been cited by some to support the square root model. These studies have been seriously criticized on statis-tical and/or methodological grounds.

For a more detailed analysis of many of those

, studies, see the answers to questions 29 through 43 of this testimony.

23. Q. Do low doses of low-LET radiation produce more cancers.per unit dose than high-doses?

A. No. The best reliable evidence available to the scientific community strongly suggests that the linear model probably tends to over-estimate the risk of most radiation-induced cancers in man as a-result of exposure to low-LET radiation. The linear model can be used to define the upper limits of the risk associated with exposure to low-LET radiation and implies that these risks-rise proportionately as the amount of the dose increases.

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! 24. Q. Will more malignancies occur if a given number of I

person-rems are distributed among a greater number J

of people?

A. No. This is another way of saying that the risk I

per rem at low doses of low-LET radiation is 1 greater than for high doses and that the linear, i

no-threshold dose-response relationship is not i

! conservative because it underestimates the risk i

at low doses. No convincing scientific evidence exists for these conclusions.

The consideration of the processes of repair and recovery of radiation injury in the cells and tissues of the body and of dose-rate effectiveness factors (NCRP, 1980) leads to the conclusion that the linear hypothesis generally overestimates the risk of low-LET radiation exposure at low doces.

In experimental systems, the risk per unit dose of low-LET radiation for cell killing, for the induc-tion of chromosome aberrations, mutations, teratogenic effects, tumor formation, and for the shortening of life consistently depends upon both the magnitude of the dose and its temporal distribution. In general, the dose-response curves for low-LET radiation for late (carcinogenesis) and genetic effects increase in slope with increasing dose and dose rate. Thus, linear interpolation between the naturally-occurring spontaneous incidence and the intermediate-to-high doses and dose rates generally overestimates the risk of low-LET radiation at low doses and low-dose rates. This observation f

also has been reported by the ICRP (1977), NCRP (1980), and UNSCEAR (1977, 1982).

25. Q. What is a dose-rate effectiveness factor?

A.

The existence of dose-rate effectiveness facrors has long been recognized from clinical experience and from studies of both genetic and somatic

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effects (e.g. cancer induction) in experimental animals. From the studies on somatic effects in animals (NCRP, 1980), the effectiveness per unit dose of low-LET radiation for cancer induction is  ;

lower at low doses and low dose-rates than at high doses and high dose-rates. The effectiveness per unit dose of high- vs. low-dose and dose-rate exposure ranges from a factor of about 2 to about

10. In other words, linear interpolation from high doses (150 to 350 rads) may overestimate the effects of either low doses (20 rads or less) or of any dose delivered at dose-rates of the order of 5 rad per year or less by a factor of 2 to 10.

This factor is referred to as the Dose-Rate Effec-tiveness Factor ("DREF") (NCRP, 1980).

Although extensive data from human beings permit reasonable risk assessments to be made for exposures to intermediate-to-high doses of low-LET radia-i tion, these data are not adequate to demonstrate conclusively that a dose rate effect either does or does not exist. The experimental evidence from many different biological effects, including carcinogenesis, and for many species of animals in support of a dose rate effect is so extensive, however, that it would be extraordinary if such dependence did not apply to the same endpoints in the human being as well. Because of the complexity 4

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, and wide spectrum of the tumorigenic responses to radiation in the experimental animal, however, NCRP Report No. 64 (1980).is reluctant-at the present time to go beyond providing a range of factors within which a single factor for the total yield of tumors in man after exposure of the whole body probably would lie. The DREF range is estimated to be 2 to 10 when the actual absorbed dose is 20 rads or less or when the dose rate is 5 rads per year or less.

26. Q. Do any recent reports on epidemiological studies claim that the linear hypothesis is not conserva-tive?

A. Yes, but all reports of expert scientific advisory comittees, including the NCRP, ICRP, BEIR, and GAO j (1981) committees, disagree with such claims.

I Current scientific evidence does not support those claims. Although some of those studies and reports may be worthy of further investigation, they currently are not considered convincing enough to argue effectively against the conservatism of the linear hypothesis for effects of exposure to low-I t

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dose, low-LET radiation in man.

In addition, none of those reports are new to the scientific community or to international and

national groups or councils constitued to provide expert advice on radiation and health, such as the ICRP, NCRP, NAS-BEIR Committee, or UNSCEAR.

Most of those reports pre-date the scientific reports which analyze all the available data (e.g., UNSCEAR, 1977, 1982; NAS-BEIR, 1980; NCRP, 1980) and are quoted and reviewed in these reports.

Although some scientific papers have been published or presented at meetings in the past year, they do not provide new information but rather give the authors' current personal interpretation of old data which have been available for years or decades.

Many of these have never been published in the i

open literature through the critical peer-review process.

Furthermore, no paper claiming any such.effect goes unnoticed by the scientific community or goes without critical evaluation. Committee 1 of the ICRP continually reviews all published epidemio-logical surveys on exposed populations, including 1

all studies on human population groups exposed to low doses. The Committee continues to conclude

, that the Tvailable information on low-dose radia-tion and cancer induction in humans is insufficient to enable conclusions to be drawn regarding the dose-responde relationship for doses below 10 rads of low-LET radiation. The results of new

. epidemiological studies of occupationally exposed groups are consistent with previously available information.

27. Q. Please describe these studies which challenge the conservatism of the linear hypothesis.

1 A. The following reports are among those which have been interpreted by their authors, or a few other people, to indicate that the currently applied radiation risk estimates, primarily based on the ICRP (1977), UNSCEAR (1977, 1982), and NAS-BEIR Committee (1980) reports, underestimate the risks of low-LET radiation exposure at all dose levels:

Mancusco, Stewart, and Kneale, 1977; Bross and Natarajan, 1972, 1977, 1979; Bross and Driscoll, 1981; Najarian and Colton, 1978; and Morgan, 1975.

28. Q. Please de;cribe the basis for your knowledge of these studies.

. A. I have not personal]y reviewed the raw data which underlies these studies. All of these studies, however, have been discussed in considerable detail in meetings of the NAS-BEIR, ICRP, and other scientific committees to which I belong; I am therefore familiar with these studies. Disting-

uished members of those committees have in fact reviewed the raw data underlying those studies and

4 - +-4 -- <4 >

s

. J reported their findings to the committee. I personally critically reviewed the studies them-selves and contributed to the scientific and other committee reports which analyze and criticize these studies in great detail. In many instances, the methodological and statistical' 1

flaws are apparent from the study itself.

29. Q. What data were the basis of the Mancuso, Stewart, i

and Kneale (1977) epidemiological survey?

A. Mancuso, Stewart, and Kneale (1977) studied the cancer mortality rate for the workers at the

. Hanford Nuclear Facility at Richland, Washington j between 1943 and 1971. Their report was based on j the work experience of 24,939 male workers with 3,520 certified deaths (death certificates) and an unspecified number of female workers with 412 certified deaths. Their preliminary report came out in 1977 and primarily was an analysis of the cancer mortality data for the 3,520 male deaths l for which death certificates were available.. In that report, the authors claimed that their 3 analysis demonstrated a greater number of 1

radiation-induced cancers than the linear dose-response hypothesis would indicate. Leading epidemiologists and statisticians have, however, widely criticized this analysis because of its serious deficiencies in methodology, statistical

formulations, and conclusions. 'In addition, other

- analysea of the data have been performed which show little or no radiation induction effect. See NCRP, 1980; Hutchison, et al., 1979; NAS-BEIR, 1980; Reissland, 1978; GAO, 1981; Anderson, 1978; Mole, 1978;' Gilbert and Marks, 1979; and Darby and Reissland (1981).

30. Q. What are the serious methodological flaws in the Mancuso, Stewart, and Kneale (1977) analysis?

A. The methodological flaws in that report involve inadequacies of radiation dosimetry, confounding factors which could have caused cancer in the workers in the absence of radiation exposure, selection bias, and inconsistencies with the spontaneous incidence of cancer in the exposed population. Their report did not give the actual individual radiation doses the Hanford workers who died of' cancer received but instead only provided mean cumulative radiation doses.

Their analysis also did not. consider the calendar year in which the cancer began in the individual and in the study population. It made no correction for the fact that the United States population as a whole had an increasing number of cancers of the types observed in the Hanford workers during the study period. Thus, this study's conclusion that

, an increase in cancer occurs with increasing dose accumulated over increasing time fails to take into account that a similar increase in cancer incidence in the entire United States population occurred, even in the absence of increasing doses of radiation, when the incidence of cancer in the general population is plotted against increasing

, time.

Gilbert and Marks (1979) and Hutchison, et al.

(1979) have analyzed the same data used in the Mancuso, Stewart, and Kneale (1977) report and concluded that cancer of the pancreas and multiple myeloma are possibly associated with the work experience of the study population. In these studies, no radiation relationship exists for

, lymphatic or cancers of the blood-forming tissues other than multiple myeloma. Thus, no excess of i

leukemias existed which experience, such as with l the Japanese atomic-bomb survivors, suggests j should have been most observable where radiation is a factor.

l Because the recorded radiation doses in the Hanford workers were very small, perhaps only a few rads, the very low cancer-doubling dose esimates reported by Mancuso, Stewart, and Kneale f

l (1979) are spurious. Numerous scientists have strongly disputed those doubling-dose estimates because their values are inconsistent with known

- and established radiobiological evidence. If the estimated small dose in the worker population actually caused a doubling of the spontaneous rate of cancers, natural background radiation in the p United States would produce more than the actual number of cancer cases observed in the entire United States population. Such a result is, of course, impossible. Thus, if the Mancuso, Stewart, ,

and Kneale (1977) cancer-doubling doses are correct, something other than radiation was the cause of the observed cancers in the Hanford workers. As a result of these criticisms, Mancuso, Stewart, and Kneale have modified their original estimates of cancer-doubling doses in the range of 2-7 rads and presently are quoting doubling doses of 2-150 rads in the worker population. The latter range, however, still is inconsistent with existing knowledge and experience in cancer epidemiology and statistics.

31. O. What did the Najarian and Colton (1978) study involve?

A. Najarian and Colton (1978) studied employees at ,

the Portsmouth Naval Shipyard in New England which has serviced nuclear-powered ships since 1959. In their initial report, the authors estimated that 20,000 people had been employed at the shipyard in

.u-- - J

, the past twenty years and that twenty per cent of those workers were exposed to radiation. By studying the workers' death certificates from 1959

to 1977, they estimated that 1,450 former shipyard p- employees died under the age of 80. The authors I

then telephoned relatives of the decedents to determine whether these former employees were radiation-exposed workers. They obtained tele-phone information on 525 cases, and relatives of 146 of these former employees claimed the deceased probably was exposed to radiation at the Ports-mouth Naval Shipyard. By comparing this informa-i tion to the mortality rate of United States white i

) males in 1973, the authors concluded that the i

observed numbers of cancers and leukemias in the selected worker population were considerably greater than those expected. The actual number of cancers and leukemias was, however, quite small, and the conclusions based upon those numbers are erroneous.

l

32. Q. Does that study also suffer from serious methodo-logical flaws?

A. Yes. Much of the criticism of the Najarian and Colton (1978) study already has been recorded.

The flaws in that study include bias in worker selection, worker history, radiation dosimetry, 1

i

_. ._. _,- _n.

'. and confounding factors such as exposure to other carcinogens in the workplace. See Hamilton (1979).

Even Najarian and Colton (1978) listed the important inadequacies of their survey in their

, report. Their study was an analysis of cancer deaths only and provided no information on the total worker population at risk. A significant bias in the information supplied by relatives exists because this was recall information. The study did not incorporate data on how long the employees worked at the shipyard, how long the nuclear workers were exposed to radiation, or the amounts of radiation the workers received.

Dosimetry data were not provided. The authors did not consider any confounding factors such as the carcinogenic effects of other toxic agents, includ-ing asbestos, smoking, or industrial solvents, which could have acted along with radiation to cause the apparent excess deaths from cancer and leukemia either in an additive fashion or through l

i a multiplicative mechanism.

Further serious statistical and methodological inadequacies in the Najarian and Colton (1978) survey exist (Hamilton, 1979). For example, to exclude the effects of carcinogens other than radiation, the authors should have shown that the l

. cancer frequencies in the study population increased with increasing radiation exposure. Information on the lifetime-accumulated doses of former employees, however, was not available. More p importantly, the radiation work at the Portsmouth Naval Shipyard began only in 1959. It is unlikely that changes in overall cancer frequency induced by radiation would appear before a minimum latent period of 10 years after tha initial exposure or after 5 years f _ leukemia. These are roughly the minimum latent periods for cancer and leukemia induction in other studies of exposed populations.

Thus, the Najarian ano Colton (1978) data analysis should be divided into two periods: cancer deaths occurring during the period from 1959-1969 when radiation effects would not be expected to appear, and cancer deaths occurring from 1970-1977 when radiation effects might be expected to appear.

Of all of the Portsmouth Naval Shipyard workers who died between' 1959-1969, about 25% had cancer listed on their death certificates as the cause of death. Only thirty-three radiation workers died l

during this period, however, and about 40% of their deaths were recorded as due to cancer. For all shipyard workers who died between 1970-1977, approximately 25% had cancer listed as the cause of death. Of the 113 radiation workers who died

during the 1970-1977 period, about 40% were due to cancer -- no more than during the previous. ten year period. Thus, no differences existed in the incidence of cancer deaths in all workers or for

, the radiation workers during the two periods.

Najarian and Colton's conclusions, therefore, are not concordant with well-established medical epidemiological data on the effect of the latency period of cancers on the expression of risk of radiation-induced cancer. This absence of the apparent latent period effect casts considerable doubt on any conclusions by Najarian and Colton (1978) and others who have chosen to cite these conclusions as evidence that very low-level doses of radiation contributed to the unexplained high numbers of cancer deaths among the radiation workers (Reissland and Dolphin, 1978).

When radiation dosimetry data were made avail-able to Najarian and Colton, a number of serious inconsistencies in their analysis became apparent.

For example, one-third of the leukemia cases reported in their original paper had no history of radiation and another one-third had negligible levels of exposure. With the new dosimetry data, statistical analyses showed no significant differ-ences in the cancer incidence in the different exposure levels.

, 33. Q. Do any other significant factors exist which cast

! considerable doubt on the conclusions made by I

Najarian and Colton (1978)?

A. Yes. The list of chemical and physical agents .

P probably present at the Portsmouth Naval Shipyard during the past 25 years incJudes over 40 poten-tially harmful chemicals. The common occupational carcinogens affecting the health of workers in the United States are quite well known. The presence of so many chemical carcinogens in the workplace underscores the difficulty in assessing the effects of low levels of radiation in this and other nuclear worker populations.

34. Q. Has any other study been made of the Portsmouth Naval Shipyard workers?

A. Yes. The final report of the U.S. Department of Health and Human Services, Public Health Service Centers for Disease Control, NIOSH's Epidemiologic Study of Civilian Employees at the Portsmouth Naval Shipyard, based on a total cohort of 24,545 civilian white males employed at the Portsmouth Naval Shipyard between 1952 and 1977, is now available (Rinsky, et al., 1982).

I

. ~36-l

35. Q. What were the findings of that study?

A. The report found no excess deaths due to malignant neoplasms or due specifically to neoplasms of the blood and blood-forming tissues (leukemias) in p civilian workers at the Portsmouth Naval Shipyard.

This NIOSH study found no relationship between exposure to radiation and mortality from any cause among the worker population when compared to the United States white male population. Furthermore, no excess in leukemia mortality was observed in the radiation exposed population when compared to the non-radiation exposed employees of the Portsmouth Naval Shipyard. A National Academy of Sciences -

National Research Council (NAS-NRC, 1982) scientific advisory committee has reviewed this report, and the committee did not disagree with the NIOSH study findings.

l l

36. Q. What conclusions has Bross made in his Bross and Natarajan, 1972, 1977 and Bross, et al., 1979 studies?

A. Bross claims that the risk for cancer-induction to pregnant women and all adults following diagnostic l X-ray exposure, which is low-level radiation ex-posure, is greater than the risk at high doses and at high dose rates. Bross also claims that he has i

, identified susceptible subgroups in the general population which are especially sensitive to radiation damage.

p 37. Q. Do you agree with Bross' observations?

A. No. Bross' belief that especially sensitive subgroups exist is derived from his analysis of the Tri-State Leukemia Survey (Graham, et al. ,

1966; Gibson, et al., 1972) wherein he studied what he termed as certain " indicators of suscep-tibility" (e.g., viral infections, bacterial infections and allergies) shown by the leukemic child from birth until diagnosis of leukemia.

Bross concluded "the apparently harmful effects of antenatal irradiation are greatly increased in certain susceptible subgroups of children possess-ing the indicators associated with a slightly higher intrinsic risk of leukemia" (Bross and I

l Natarajan, 1972). Re-analysis of Bross' observa-tions (Smith, et al., 1973) showed, however, that children with leukemia are simply more prone to viral and bacterial infections and allergies before the clinical onset of the leukemic disease.

Thus, these " indicators" characterize the disease l itself and do not relate to the child's inherent l

susceptibility or sensitivity to leukemia. The occurrence of these " indicator" diseases as part I

t

'. of the pre-leukemia phase of leukemia in children is well known in pediatric medicine and in clini-cal hematology. Analysis of Bross' data shows that the incidence of these " indicator" diseases p before the clinical onset of leukemia is the same in children who had received no irradiation in utero as those who had. Bross' hypothesis, that a susceptible portion of the population exists that has a higher risk of leukemia, also has been challenged on the grounds that Bross' methods do not allow the identification of susceptible individuals ahead of time and, therefore, do not allow his thesis to be tested (Smith, et al.,

1973).

More recently, Bross has claimed that the rela-tively small radiation exposures (in the millirad range) from diagnostic X-rays in adults signi-ficantly increases the risk of leukemia (Bross, et al., 1979). In coming to this conclusion, it appears that Bross erroneously assumes that, in the absence of diagnostic X-rays, the incidence of heart disease and leukemia in the general popula-tion would be zero. Of course, this is not the case. Also, below the ten rad exposure level, his

" dose-response" curves for adults exposed to diagnostic X-rays are flat. This suggests that a

threshold exists in the dose-response relation-ship. Indeed, a more conventional relative risk analysis recently done (Boice and Land, 1979) found little or no increase in the risk of leukemia

, from a small number of diagnostic X-rays in 3ross' selected Tri-State study populations.

Bross also erroneously assumes that the relative risks are fixed and that the " percentage of the population affected" varies with the dose, i.e.,

he assumes that the basic response variable is the proportion of the irradiated population affected by radiation rather than the dose. Conventional relative-risk analysis assumes that everyone is affected and that the relative risks vary with dose. The reason for Bross' unconventional methodological approach is unclear. This position taken by Bross in his 1979 study (Bross et al.,

1979) appears to be at odds with his earlier paper (Bross and Natarajan, 1972) in which he postulated the existence of a sensitive, fixed size subgroup of people whose relative risk of leukemia increased rapidly with increasing X-ray dose.

In addition, the leukemia risk (or " percent affected") in Bross' analysis increases dramati-cally only in males and only after a large number of diagnostic X-rays. Females, however, appear to be unaffected. No radiation dosimetry was performed

---

..e , - - - ,n.,-- , , _- ,_

. in the Tri-State Survey. The cause-effect rela-tionship is obscured because if a person is receiving very large numbers of diagnostic X-rays - 40 or more within 10 years - it implies P that a disease state is present and perhaps is deriving from heart disease or a preleukemic sensitivity to infections.

Further interpretations of the Tri-State leukemia study data introduced by Bross (Bross and Natara-jan, 1972, 1977; Bross, et al., 1979) have sub-sequently been criticized in the ccientific litera-ture (Smith, et al. ,1973; Land, 1977, 1979; Oppenheimer, 1977; Boice and Land, 1979, Rothman, 1977; MacMahon, 1972; Hamilton, 1979), as have the conclusions Bross has drawn.

Although small subpopulations which are abnormally sensitive to radiogenic cancer apparently exist, the evidence does not support Bross' conclusions that such groups may exist and be identified on the basis of the presence of certain diseases or on the existance of conditions other than age or sex. See also my response to question 55 of this testimony.

38. Q. Has Bross performed any other similar radiation study analyses?

i

• A. Yes. Recently, Bross took data from the Najarian and Colton survey and concluded that the Portsmouth Naval Shipyard workers sustained very large numbers of lung cancer deaths as a result of

, exposure to low-level radiation (Bross and Dris-coll, 1981).

39. Q. Do you agree with that observation?

A. No. This Bross report has many methodological errors and uses unconventional statistical methods.

Bross and Driscoll (1981) also make unsubstan-tiated claims on the existence of subpopulations which are especially sensitive or susceptible to radiation damage. Furthermore, in their attempt to re-analyze the data from the Portsmouth Naval Shipyard study, Bross and Driscoll (1981) claim that the official publication of Rinsky, et al.

(1981) was purposely misleading and underestimated the lung cancer risk by a factor of 20 to 200. By regrouping selected data for lung cancer, which do not appear in the Rinsky, et al. (1981) paper, Bross reached the conclusion that above the 1-rem exposure range, with more than a 15-year follow-up, a two-fold increase of lung cancer exists.

This would mean an excess of 189 deaths per million people exposed per year per rem compared with the ICRP (1977) and NAS-BEIR (1980) estimates of about

l

, ~42-1 lung cancer deaths per million people exposed per year per rem. Because no detailed denomi-nators, basis for expected cases, or host factors are given or corrected for in the Lross analysis, p his conclusions cannot be evaluated or substan-tiated. Finally, smoking, the leading cause of lung cancer, was not examined in any detail as an important confounding factor in Bross' analysis.

40. Q. What conclusions can be drawn from Modan's study of Israeli children who had been treated with radiation for ringworm of the scalp (Modan, et al., 1977)?

A. Certain human thyroid tumor data derived from that study (Modan, et al., 1977) appear to show that the risk coefficients at low doses are greater than or equal to the risk coefficients at high doses and high dose rates. Substantial uncer-tainties, however, exist in the dosimetry. Any interpretation of the low-dose thyroid cancer effect in the Modan study (Modan, et al. ,1977) must considar the possibility that: (1) imprecise irradiation techniquer or restless children could have resulted in direct thyroid exposure; (2) pituitary irradiation may have increased the number of thyroid cancers; and (3) the radiation may have interacted with other factors such as

, ethnic background, nutritional deficiencies, or goiter to alter the risk. Also, Modan's con-clusions must be balanced against the lack of thyroid tumors in other similar series and the p lack of such an increase in thyroid tumor incid-ence in children in Utah who apparently received much larger thyroid doses from fallout radioiodine than those reported in the Modan series.

41. Q. Are you familiar with Dr. K. Z. Morgan's con-clusions about low-level radiation effects?

A. Yes. Dr. Morgan c] aimed that low-level exposure may be more hazardous per unit of absorbed dose than exposure to high doses at high dose rates (Morgan, 1975). He has persisted in that claim since then.

42. Q. Do you agree with those claims?

A. No. In his assessment, Dr. Morgan did not dif-ferentiate between the effects of high-LET and low-LET radiation. As a consequence, Dr. Morgan has never demonstrated that his claim holds true for low-LET radiation. Indeed, in his study he emphasized the potential effects of high-LET radiation at high doses from internally-deposited radioisotopes. Thus, Dr. Morgan's analysis does

. not provide any information on the low-level dose range of low-LET radiation exposure.

43. Q. Do Dr. K. Z. Morgan's publications and talks p provide any new facts or new information on the risks of low-dose, low-LET radiation exposure?

A. No. I have reviewed the publications listed in the League's Response to Edison's Second Set of Interrogatories, pages 9-1 to 9-3. Dr. Morgan's papers, articles, and talks provide no information not already known to the ICRP (1977), NCRP (1980),

UNSCEAR (1977, 1982), and NAS-BEIR (1980) commit-tees. Dr. Morgan is a well-known health physicist who has been a member of national and international radiation and health committees, and his writings and statements do not go uanoticed. Most of his writings and statements listed are his own opinions,

unreviewed by his scientific peers, and frequently l

merely interpret other people's data or reports l

and analyses by authors who have been thoroughly i

discredited (e.g., Mancuso, Stewart and Kneale, 1977; Kneale, et al., 1978; Kneale et al., 1981; Bross and Natarajan, 1972, 1977; Bross, et al.,

1979; Stewart, et al., 1980).

44. O. Have the changes in scientific hypotheses and cancer risk estimates in recent years occurred l

> ~ . _ . - _ . - -__ - . . _ - , _ _ _ . _ - _ . - -- . _ - _ _ -

- because of the existence of new scientific infor-mation that the risk per rad of low-dose exposure to low-LET radiation is greater than at high doses?

p A. No. Changes in the scientific dose-response hypotheses and the risk estimates are results of new knowledge derived in the last ten to fifteen years from epidemiological studies of exposed human populations and new scientific laboratory observations. Quantitative epidemiology based on '

current statistical methods is a relatively new science of medicine. Until such studies were instituted with sufficiently large study popula-tions, for periods of 10 to 20 years or more, and with sufficient information on accurate radiation dosimetry, risk estimation for excess cancer induction could not be precisely determined.

Therefore, after many years of follow-up, long latent periods, and new insight into the mechanisms of radiation carcinogenesis, greater reliability and precision of risk estimation can be obtained.

Even with these great advances in our knowledge, however, no new information derived from either laboratory experiments or epidemiological studies has reliably demonstrated that the risk per rad of low-LET radiation is greater at low doses than at high doses. On the contrary, the evidence is

. compelling that for exposure to low-LET radiation, the risk per unit dose at low doses generally appears to be less than at high doses (see NCRP, 1980; NAS-BEIR, 1980) because of the more effi-p cient repair mechanisms of cells and tissues of the body at low doses and low-dose rates and because of dose rate effectiveness factors (NCRP, 1980).

45. Q. Do reliable epidemiological studies exist that allow risk estimates to be made on the effects of low doses of low-LET radiation?

A. Yes. In fact, it is remarkable how many careful and detailed epidemiological studies have been J

made on the effects of ionizing radiation in man (see UNSCEAR, 1977, 1982; NAS-BEIR, 1980). Good '

information on the probability with which cancer is likely to be induced by moderate absorbed doses in the region of 100 rads and, in a few cases, by much lower doses of tens of rads is now available.

This information allows risk estimates to be made with reasonable confidence for ten or more individual body organs or tissues, with the likelihood that these are the more sensitive ones to cancer induc-tion, and an adequate estimate can be made of the total risk of cancer induction following uniform whole-body irridation.

- J

46. Q. What use of the Hiroshima and Nagasaki atomic-bomb survivor studies was made by the NAS-BEIR committee?

A. The chief sources of data used in the NAS-BEIR Report (1980) were the populations exposed to P whole-body irradiation in Hiroshima and Nagasaki, patients with ankylosing spondylitis treated with x-rays in England and Wales, other patients who were exposed to partial-body irradiation thera-peutically or for diagnostic reasons, and various occupationally-exposed populations such as uranium miners and radium-dial painters. But most epide-miologic data do not systematically cover the range of low to intermediate doses, and the Japanese data appear to be fairly strong for that dose range. Analysis in terms of dose response must, therefore, rely heavily on the Japanese atomic-bomb survivor data.

The comparatively large neutron component of the dose in Hiroshima and its correlation with gamma dose, however, limit the relevance of the more numerous Hiroshima data for the estimation of risk from low-LET radiation. The Nagasaki data, for which the neutron component of dose was very small, are weaker for doses below 100 rads. Thus, I

t it is necessary to obtain the maximum benefit from the Hiroshima data. In any analysis of the Japanese l

'. data that attempts to separate the effects of neutrons and gamma rays, however, the gamma-ray coefficients (low-LET radiation) are determined mainly by the Nagasaki data.

P

47. Q. Do the epidemiological studies of either the Japanese atomic-bomb survivors or the ankylosing spondylitis patients of England and Wales support the hypothesis that the cancer risk from low-level exposure to radiation is greater than what was believed previously?

A. No. It is recognized that neither epidemiological survey involves a study population that will necessarily provide a better understanding of the carcinogenic effects of low-level radiation (see Beebe, 1981a, 1981b; Smith and Doll, 1981). They represent, however, the two most important epide-miological studies existing of large populations exposed to higher levels of radiation. These two studies are important because the irradiated populations are sufficiently large enough and the radiation doses are sufficiently high enough to provide reliable statistical analyses.

They are not, however, epidemiological studies of low-level radiation cancer effects. The Japanese atomic-bomb survivor study has a cohort study

, population (Life Span Study sample) of 110,000.

survivors with radiation doses estimated as high as 400 to 600 rads (kerma) (Beebe, 1981a). The mean dose estimated for the leukemia patients in p the atcmic-bomb survivors is 86 rads (Beebe, 1981b). The British ankylosing spondylitis patient population under study comprises 14,560 persons, and the estimated mean bone marrow dose is 321 rads with some patients receiving thousands of rads to certain tissues (Smith and Doll, 1982).

These are not low-level radiation exposures.

]

! 48. O. How will the Japanese atomic-bomb survivor studies and the British ankylosing spondylitis studies contribute to the scientific knowledge regarding the effects of low-level radiation?

A. The epidemiological investigations of the Japanese atomic-bomb survivors and the British ankylosing

spondylitis patients will never solve the contro-versies surrounding the potential low-dose health

[

l effects no matter how long these studies continue.

Direct estimates of the low-dose risk in these studies will and should be made, but their statis-tical instability gives them little practical value for purposes of radiological protection.

The Japanese atomic-bomb data also cannot reflect

the influence of dose-rate and dose-fractionation which are especially important in analyzing the potential cancer risks of low-doses in occupationally exposed workers or the general public. Although

, the effect of a single dose of ionizing radiation will always be of great importance, some of the most important questions being asked in radiological protection involve ;ontinuous low dose and low dose rate exposure. The continuation of the Japanese atomic-bomb survivors and the British ankylosing spondylitis patient studies will, however, play an important role in testing alter-native dose-response models. No other populations of such size and dose distribution exist that could be expected to assist in defining with greater precision dose-response relationships in the low-dose region.

49. Q. Do the two studies discussed above represent normal populations?

A. The issue of whether the populations studied are

" normal" is not important to the scientific results obtained from the study. To claim that such important epidemiological studies are incorrect or spurious because they do not involve " normal populations" implies that either other populations exist that do not contain any confounding factors

. or the limitations of the present radiation epi-3emiological studies are not taken into considera-tion by the scientists or the national and international committees and groups concerned with p radiation and health. Neither situation is true.

50. Q. Does evidence exist to support the statement that the atomic-bomb dosimetry in the Hiroshima and Nagasaki studies needs to be reassessed?

A. Yes. Criticism of the T-63D dosimetry system used in the Japanese atomic-bomb survivor epidemiological studies since 1967 has occurred recently. The entire basis for the dosimetry is now under restudy in several of the national laboratories of the

. Department of Energy and in other scientific laboratories. The preliminary findings indicate that a major reduction in the neutron component of the Hiroshima doses may be required with some compensating increase in the gamma component. Any changes in the Nagasaki doses, however, would be far less extensive.

l l 51. Q. Does this mean that the reevaluation of the

{

l Japanese data will show that the risk estimates for cancer are grossly underestimated?

A. No. Until the present uncertainties of the Japanese atomic-bomb survivor data are resolved, no precise

. ~

, statement can be made as to the effect of any of the necessary changes in risk estimation. The present indications are, however, that low-dose, low-LET radiation excess cancer risk estimates

, will not change uniformly for the various effects.

Instead, those risk estimates may atay the same in some instances, may increase by less than 10 percent in other situations, and may double under the linear or linear-quadratic models of dose-response in very limited situations.

52. Q. If there is a change in the risk estimates calcu-lated from the Japanese atomic-bomb survivor studies / wou]d you expect a significant change in the low-dose, low-LET cancer risk estimates reported by BEIR, UNSCEAR and radiation-protection standard-setting commissions and councils?

A. No. The excess cancer risk estimates for the largest proportion of the organs and tissues of the body exposed (cited in the NAS-BEIR (1980),

UNSCEAR (1977, 1982), ICRP (1977), and NCRP (1980) reports) are not based solely on the Japanese atomic-bomb survivor studies. Instead, they are based primarily on a large number of epidemiological studies of human population groups exposed to medical radie -d on or to occupational radiation.

These latter two groups are studied with their own individual dosimetry. The Japanese data only

augment these. Almost all excess cancer risk estimates for the different organs and tissues of the body (except for bone cancer and bone marrow cancers) are based on linearity of dose-response

, and, therefore, are conservative (NAS-BEIR, 1980).

In the NAS-BEIR (1980) Report, the cancer risk estimates for low-dose, low-LET whole-body expo-sure are based primarily on the Nagasaki survivor leukemia data, and those dosimetry estimates may not change appreciably and perhaps not at all.

53. Q. How will this reassessment of the Japanese atomic-bomb dosimetry data affect the risk coefficients-for radiation carcinogenesis among the Japanese atomic-bomb survivors?

A. At the present time, it is not known. It would be premature to attempt reanalysis of observed effects until the revision of dose estimation is completed. This revision is expected to last two years or more and will include reassessments of individual shielding factors and organ dose cal-culations.

It is recognized, however, that any changes in i

l the Nagasaki doses in the reassessment will be far less than those of the Hiroshima doses and poss-

! ibly will result in negligible effects on the l

! Nagasaki estimates of carcinogenic risk in the i

i I

'. exposed atomic-bomb survivors (Bartlett, 1982).

Neutron and gamma tissue dose values as a function of distance from the hypocenters of the atomic-bomb explosions of Hiroshima and Nagasaki, p however, have been recalculated by Loewe and Mendelsohn (1980; 1981) of the Lawrence Livermore National Laboratory. These calculations are supported by those of Pace (Oak Ridge National Laboratory), Scott (Scientific Applications, Inc.), and Bartlett (1982).

Fc- values of neutron dose, the differences between the new estimates and the T-65D estimates can be broadly attributed to the effect of the moisture content of the air and to the methods of calculation, including the use of a different neutron energy distribution than presently known j

to be correct spectra. Humidity effects give rise to a factor of about two in reduction of neutron dose, the neutron spectra to the remainder. The reductions in dose due to the latter is greater in l

the casc of Hiroshima.

Considerable uncertainties remain in the results of these new calculations, and firm conclusions at the present time are unwarranted (Bartlett, l

l 1982). The reassessment is still in progress and will need to include recalculations of shielding

factors for the effects of terrain and buildings, 1

'. a consideration of organ dose conversion factors, and the possible contribution to doses to persons from other sources. It is premature, therefore, to derive risk factors, RBEs, or dose-response p functions using these new, but preliminary, dose estimates.

54. Q. Do all radiation epidemiological studies have uncontrolled variables such as those which exist in the atomic-bomb survivor studies?

A. Yes, but this will not necessarily reduce the value of the study. Investigators reporting their results, and those who depend on those results, should be aware of the possibility that host factors, such as age, sex, nutrition, infection, other illnesses, and carcinegens other than radia-tion, may be present and may influence the results in some unexpected way. The host or environmental factors may interact with radiation to exaggerate or minimize the effect of radiation or some charac-teristic associated with exposure to radiation may independently affect the normal expectation of the effect under study. For example, the results of the study of British ankylosing spondylitis patients treated by X-ray (Smith and Doll, 1982),

valuable as they were seen to be from the time

. they were first reported, were regarded with some reserve until it was shown that ankylosing spondylitis patients not treated by X-ray probably have a normal cancer experience (Smith et al., 1977) p except possibly for cancer of the colon where some correlation between that cancer and ankylosing spondylitis exists through their mutual association with ulcerative colitis (Beebe, 1981b). These host and environmental factors do not, however, eliminate the value of the study as long as the researchers are aware of the possibility of their existance.

55. Q. Does scientific evidence support the theory that some people may have increased susceptibility or sensitivity to cancer induction by ionizing radia-tion?

A. Data on sensitive subpopulations provide one of the strongest direct pieces of evidence for the existence and importance of repair (and hence of dose-rate dependence) in radiation carcinogenesis in man. Data also aid in the identification of small population groups which apparently are abnormally sensitive to radiogenic cancer. Dif-ferences in sensitivity to radiogenic cancer obviously occur as a function of age and of sex, and therefore, sensitive subpopulations do exist

'. on this basis. Additionally, Bross has claimed that such groups may exist on the basis of other conditions or the presence of certain diseases, such as allergy prone or virus infection of a

, mother while an individual was in utero, but Bross' claims have been shown to be unsupported by the data.

A notable development during the past decade is l the increasing recognition that human genotypes exist that confer both increased susceptibility or resistance to DNA damage and increased cancer risk after exposure to carcinogenic agents, including ionizing radiation. The role of constitutional susceptibility to cancer induction is not well enough understood, however, for it to be used as a factor to modify risk estimates (NAS-BEIR, 1980). The risk estimates developed for the BEIR Report (1980) are averages for large capulations that include many genotypes. Thus, it is unlikely that the present risk estimates would be notably altered if data representing very small subsets of abnormally radiosensitive persons could be recog-nized and excluded from the calculations of the NAS-BEIR (1980) Committee cancer risk estimates.

If population subsets can be identified as having a substantially greater risk of radiation car-cinogenesis, and at the present this has not been

J the case, their risk will require separate estima-tion. At the present time, the incidence and sensitivity differentials of these diseases, particularly for ionizing radiation, appear to be a so low that even their increased sensitivity to radiation would not be likely to detectably influ-ence the dose-effect response of a large, random population containing a normal number of such individuals. Accordingly, present radiation protection guides already take into account both the existence of small, unidentifiable susceptible sub-populations and the existence of various susceptibilities of the tissues and organs of the body to cancer-induction.

56. Q. Does the potential risk of teratogenic damage to the developing child in utero justify a prohibi-tion against women of childbearing age and young men working jobs that could potentially expose them to radiation?

A. No. Teratogenic effects, by definition, can occur only in the developing embryo and fetus. Therefore, teratogenic effects cannot occur unless a woman is pregnant. I believe the NCRP recommendations on dose-limitation for exposure to pregnant women in the workplace of 500 millirem for the entire gestation period provide adequate protection

- against potential teratogenic effect. Because men cannot become pregnant, teratogenic effects cannot be considered relevant to radiation protection of young men who are occupationally exposed.

P

57. Q. Is skin cancer, particularly malignant melanoma, considered to be an especially radiogenic cancer?

A. No. The skin is not considered to De a sensitive organ to radiation-induced cancer. Doses of radiation as high as 1500 to 2000 rads are required before malignant lesions will occur in the skin.

Such doses are far beyond the levels of exposure a nuclear power plant worker can expect to receive in his entire lifetime (NAS-BEIR, 1980; UNSCEAR, 1977, 1982; ICRP, 1977).

In addition, malignant melanoma is one skin cancer in which ionizing radiation is not consid-ered to be a risk factor (Austin et al., 1981).

l The epidemiological study at the Lawrence Livermore i National laboratory (Austin et al., 1981) has demonstrated no causal relationship between radia-tion exposure and the increase of malignant melanoma i

in workers. These scientists studied over 5,000 l

l employees of the Lawrence Livermore National Laboratory and noted a statistically significant excess of malignant melanoma among male workers.

l The cancers were, however, found to be unrelated 1

to either the length of employment or to the type of radiation exposure. It was highest among the group of employees classified as chemists. The study did not give detailed exposure comparisons,

, but the authors attributed the excess malignant melanoma of the skin to the life style of the exposed persons and not to the radiation.

58. Q. Do internal dose and dose commitments that are calculated over a 50 year period provide an adequate estimation of the internal dose and dose commit--

ments that an occupationally exposed worker will receive?  :

A. Yes. This 50 year period was established by the NRC and represents an appropriate length of time the average person works in a lifetime. This period is used for the general population as well.

Because the rate of accrual of a committed dose in the worker population tends to decrease over time, l

the percentage of a person's total dose which he l

would receive after the 50 year period would be quite small. In addition, the average age of the general population, the likelihood that a worker will not be employed at the same job for more than 50 years, the normal operating lifespan of a i nuclear power plant, and the probability that a person will not live his entire life in the same t

". geographical location, all make it extremely unlikely that large numbers of people will be continually exposed to radiation, in the workplace or in the areas surrounding a normal operating

, nuclear power plant, for periods of more than 50 years in their lifetime.

59. Q. In your opinion, what levels of low-LET radiation exposure are sufficiently low as to properly protect the healuh and safety of the workers at the Byron Station?

A. Epidemiological studies primarily involve studies of people after exposure to intermediate-to-high doses and dose rates. Linear interpolation of dose-response between the naturally-occurring spontaneous incidence and the incidence observed following exposure at intermediate-to-high doses and dose rates generally overestimates the risk of low-LET radiation at low doses and low dose rates and may be considered as an upper bound. The ICRP (1977), NCRP (1975), UNSCEAR (1977, 1982), and NAS-DEIR (1980) reports all incorporate this observation.

On this basis, some potential risk of carcinogenic a or genetic effects of low-dose, low-LET radiation exposure exists which is estimated to be no greater

'. than a lifetime risk of one in ten thousand per average rem to large populations and could be much less (ICRP, 197 7 ; NCRP , 1980; UNSCEAR, 1977, 1982; NAS-BEIR, 1980). This is a conservative estimate, e and the existing epidemiological data will not support any greater risk estimate. Quite apart from current NRC or EPA regulatory positions, no epi-demiologic data exist to support any suggestion that maximum levels of 25 mrem (whole-body) and 75 mrem (thyroid) per year are necessary to protect the public health.

The present ICRP (1977) recommended standards of dose-limitation - 0.5 rem per year for the general public and 5 rem per year for the radiation worker populetion - are not to be considered without risk. Such a concept does not exist, because the

" linear, no-threshold hypothesis" does not accept the possibility that no risk exists. The practical questions of concern, however, are whether these current recommended standards adequately protect the general public and worker populations taking into account all factors, including a comparison of risks that society normally accepts in every day life.

The question of interest for this proceeding is:

For the radiation worker population in industry, l will delayed or late health effects occur at

levels of exposure in the range of 0.5 to 5 rems per year? The NAS-BEIR (1980) Committee concluded that delayed health effects could occur in those radiation workers who are exposed to an amount of p radiation close to the maximum permissible dose during their entire occupational lifetime.

Such health effects, however, are unlikely to ever be observed in these occupationally exposed populations. This is so for at least two reasons.

First, as stated previously, the current risk

, estimates for radiation protection standards, recommended by the ICRP and NCRP, are based on the linear hypothesis which is considered to represent the upper bound of the risk; the scientific evid-ence is compelling that the actual risk would be considerably less even for an accumulated dose in the range of 100-150 rems working lifetime of low-dose, low-LET radiation exposure at low dose-rates. Furthermore, any estimation of risk based on the linear hypothesis does not take into account known biological processes of cell and tissue repair and recovery following exposure to low levels of low-LET radiation delivered at low dose-rates. Accordingly, and as mentioned pre-viously in this testimony, a dose rate effective-ness factor of from 2 to 10 can be predicted to

. decrease the potential risk due to these normal processes of cell and tissue repair and recovery.

Second, one must keep in mind that any potential incremental risk of cancer-induction or genetic p ill-health due to exposure to low-LET radiation at dose-rates between .5 and 5 rems per year would be extremely small when superimposed on the present risks to the population of spontaneous cancer induction or genetic ill-health due to natural causes and in the absence of any excess radiation.

Hence, it would not be possible to actually detect any excess incidences of cancer or genetic ill-health, if these do occur, caused by exposures in the range described, because the radiation dosec are so small and the probability of occurance is so infrequent.

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CURRICULUM VITAE JACOB I. FABRIKANT

( New York, New York Bi rth_ February 9,1928 ,

Education 1948-52 McGill University, Montreal B.Sc. (magna cum laude; Chemistry) .

- ., p Faculty of Arts and Science McGill University, Montreal M.D., C.M.

~ '1952-56 Faculty of Medicine 1961-64 University of London, England Ph.D. (Biophysics) -

Faculty of Science 1978 - CAmerican College of Radiology Fellow (F. A.C.R.)

Academic Appointments ,

1956-57 Duke University Hospital and Intern in Surgery

- School of Medicine, Durham

'1957 Duke University Hospital and Assistant in Pathology ~

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School of Medicine 1957-58 Duke University Hospital and Fellow in Surgery School of Medicine 1958-61 The Johns Hopkins Hospital, Resident in Radiology Baltimore 1958-61 The Johns Hopkins University . Fellow in Radiology School of Medicine, Baltimore  ;

1961-64 Department of Physics Advanced Fellow in Academic Institute of Cancer Research Radiology of the James Picker University of London, England Foundation, National Academy of Sciences-National Research Council 1964-65 The Johns Hopkins University Advanced Fellow in Acad'emic ,

School of Medicine and School Radiology of the James Picker of Hygiene and Public Health, Foundation, National Academy of -

Baltimore ,

Sciences-National Research Council 1964-68 The Johns Hopkins University Assistant Professor of Radiology School of Medicine 1964-70 The Johns Hopkins Hospital Radiologist L .

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' JACOB I. FABRIKANT Academic Appointments (cont.)

(- 1965-68 The Johns Hopkins University School of Hygiene and Public Assistant Professor of Radiological Science Heal th 1958-70 The Johns Hopkins University Associate Professor of Radiology

, School of Medicine

_ 1969-70 The Johns Hopkins University Associate Professor of P School of Hygiene and Public Radiological Science Heal th 1970-75 The University'of Connecticut Professor and Head School of Medicine, Farmington Department of Radiology 1973-75 The Royal Society Special Consultant for the

. London, England Advisory Comittee on the Biological Effects of Ionizing Radiations, National Academy of Sciences-National Research Council, U.S. A.

1973-75 Royal Postgraduate Picker Sabbatical Study Year Medical School James Picker Foundation University of London, England National Academy of Sciences-National Research Council, U.S.A.

1973-75 Royal Pos'tgra'duate Visiting Colleague Medical School Department of Diagnostic Radiology University of London, England 1973-75 Hammersmith Hospital Honorary Consultant Radiologist Royal Postgraduate Department of Diagnostic Radiology Medical School London, England 1975-78 McGill University Professor of Diagnostic Radiology Faculty of Medicine Department of Diagnostic Radiology

! Montreal, Canada 1975-78 The Montreal General Hospital Diagnostic Radiologist-in-Chief Montmal, Canada Department of Diagnostic Radiology i 1976-78 McGill University Professor & Chairman Faculty of Medicine Department of Diagnostic Radiology -

Diagnostic Radiologist-in-Chief ,

1978- University of California Professor of Radiology School of Medicine San Francisco, California k

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,' 3A' COB 1. FABRIKANT Academic Appointments _ (cont.)

( 1978-80 University of California, Staff Scientist Berkeley Research Medicine and Radiology Donner Laboratory 1979 President's Commission on the Di metor, Accident at Three Mile Island, Public Health and Safety The White House, Washington, D.C.

1980- University of California,- Staff Senior Scientist Berkeley Lawmnce Berkeley Laboratory 9

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' JACOB I. FABRIKANT

( Academic and Professional Organizations American College of Radiology,1972-; Member, 1972-78; Fellow, 1978-Society of Chairmen of Academic Radiology Departments, 1970-75, 1976-78 Association of University Radiologists,1967-British Institute of Radiology,1961-Society of Nuclear Medicine, The Academic Council,1970-Canadian Association of Radiologists, 1975-80; Committee on Basic Research

, 1975-78 The New England Roentgen Ray Society, 1972-78

- Radiological Society of Connecticut, 1971-75 Association for Radiation Research (UJK.),1964-Radiation Research Society,1965-; Councillor in Medicine, 1973-76 Sigma Xi, 1971-Cell Kinetics Society,1978-Connecticut State Medical Society, 1971-75 The Johns Hopkins Medical and Surgical Association,1965-Maryland Medical and Chirurgical Society, 1958-70 American Association for the Advancement of Science, 1966-75 American Institute of Biological Sciences, 1968-75 .

Alpha Omega Alpha,1955-Nu Sigma Nu Medical Fraternity,1953-Academic Honors Alpha Omega Alpha Honorary Medical Society, McGill University Faculty of Medicine, Montreal , 1955 -

Wood Gold Medal, McGill University Faculty of Medicine, Montreal,1956 Advanced Fellow in Academic Radiology of the Janes Picker Foundation, National Academy of Sciences-National Research Council, 1961-65 Special Consultant, Committee on the Biological Effects of Ionizing Radiations, National Academy of Sciences-National Research Council, The Royal Society, London, England, 1973-75 .

j Picker Sabbatical Study Year Award of the Jaces Picker Foundation, National Academy of Sciences-National Research Council, 1973-75 Visiting Colleague in Diagnostic Radiology, Royal Postgraduate Medical School, England, 1973-75 Fellow of the American College of Radiology (F. A.C.R.),1978 j Visiting Professorships l

Visiting Professor of Radiology, Bowman Gray School of Medicine,1968 Visiting Professor of Oncology, Clinical Cancer Program, Georgetwon University School of Medicine and Hospital,1969 Visiting Radiation Biologist, American Institute of Biological Sciences, 1969-75 William O'Brien Professor of Radiation Science, University of Minnesota School of Medicine and Hospitals,1970

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' JACOB I. FABRIKANT ,

9 Visiting Professorships _ (Continued) bI Visiting Professor of Radiology, University of Vemont College of Medicine, 1970, 1977-78 Visiting Scientist, Gray Laboratory, Cancer Research Campaign, Mt. Vernon Hospi tal, England,1971 Visiting Lectumr, Cambridge University Medical School, Addenbrooke's Hospital, England,1971 Visiting Professor of Radiology, University of Southern Florida College of

' Medicine, 1973

, { Visiting Professor of Radiology, University of Montmal, Faculty of Medicine, Montreal ,1977

-- -- Visiting Lecturer, Oxford University Medical School, The Radcliffe Infimary, Oxford, England,1979 Visiting Lectumr, University of London, Institute of Cancer Research, London, Engl and,1979 Visiting Professor of Radiation Medicine, Brown University,1979 Scientific Advisory Committees Comission on Radiation and Infection, Armed Forces Epidemiological Board, Liaison Member, 1965-66 Comittee on Radiology, Division of Medical Sciences, National Academy of Sciences-National Research Council, Member, 1967-74 X-Ray Image Production and Related Facilities Advisory Comittee, DHEW, USPHS, Membe r, 1968-69 Medical Radiation Advisory Comittee, Bureau of Radiological Health, DHEW, USPHS, Member, 1969-74 Long-Tem Radiation Effects Advisory Committee, DHEW, USPHS, Member, 1969-74 Neurology A Study Section, National Institutes of Health, DHEW, Member, 1969-72 Comittee on the Biological Effects of Ionizing Radiations, National Academy of Sciences-National Research Council, Member,1973-;

Vice-Chairman, 1973-77; Subcomittee on Medical Radiation, Member, 1973-77 Subcomittee on Somatic Effects, Member,1977-Ad hoc Subcomittee on Somatic Effects, Chairman,1979-Comittee on Genetic and Carcinogenic Effects, Division of Radiotherapeutic Research, Commission on Radiation Therapy. American College of Radiology, Membe r, 1972-76 Comittee on Medical Uses of Radiation and the Radiation Exposure of Patients, National Radiological Protection Board, United Kingdom, Member, 1974-75 Associate Comittee on Scientific Criteria for Environmental Quality, Sub-committee on Physical Energy, National Research Council, Canada, Member,-

1976-78 Committee on Radiation Risks to Space Workers (Space Powered Satellite), . .

National Aeronautics Space Administration, Member,1979- '-

Comittee on Federal Research into the Biological Effects of Ionizing Radiation, National Institutes of Health, DHEW, Member,1979-President's Comission on the Accident at Three Mile Island, The White House, Washington, D.C.; Director, Public Health and Safety,1979 International Commission on Radiological Protection, Committee 1 on Radiation b Effects, Member,1980-Committee on NIOSH Portsmounth Naval Shipyard Workers Study, National Academy of Sciences-National Research Council, Washington, D.C.,1982-

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JACOB I. FABRIKANT

-. Extramural Research and Education Review Committees National Academy of Sciences-National Research Council, Committee on Radiology, Division of Medical Sciences, Member, 1967-74 U.S. Atomic Energy Commission, Division of Biology and Medicine, Consultant, 1968-75 National Science Foundation, Division of Developmental Biology, Consultant, 1970 State of Connecticut, Commission on Higher Education, Standing Committee on r p Accreditation, Connecticut Council on Higher Education, Consultant, 1971-73

- Connecticut Cancer Epidemiological Program, Planning Committee, Secretary, 1972-73

_ . American Cancer Society, Connecticut Division, Board of Directors, Member, 1972-73 National Academy of Sciences-National Research Council Assembly of Life Sciences, Division of Medical Sciences, Consultant, 1972-75 U.S. Energy Research and Developnent Agency, Consultant, 1975-76 McGill University, University Senate Senator, 1976-78 McGill University, Faculty of Graduate Studies and Research, Faculty Council, The Graduate Council, Councillor, 1975-78 McGill University, Faculty of Medicine, Postgraduate Training Committee, Member, 1975-78 McGill University Faculty of Medicine, Department'of Diagnostic Radiology, Postgraduate Training Committee, Program Di rector, 1976-78 Scientific Journal Review Cell and Tissue Kinetics,1968-; Member, Editorial Board,1972-Investigative Radiology,1973-; Member, Editorial Board, 1973-76 ,

Journal of the Canadian Association of Radiologists,1976-; Member, Editorial Board, 1976-78 McGill Medical Journal, 1952-56; Managing Editor, 1954-55; Editor, 1955-56

• Cancer Research,1968- .

Journal of the National Cancer Institute,1969-Biology of Reproduction,1970-Radiology, 1970-Science,1970-Medicine,1970-Bioscience, 1970-

{ Cance r,1971-Radiation Research,1972-International Journal of Applied Radiation and Isotopes,1973-o

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JACOB 1. FABRIKANT Hospital Appointment's

( 1964-70 The Johns Hopkins Hospital Baltimore, Maryland Radiologist 1970-73 University of Connecticut Hospital Head, Department of Radiology Hartford, Connecticut 1973-75 University of Connecticut Hospital Attending Radiologist Hartford, Connecticut r p

-- 1970-73 Veterans Adininistration Hospital Acting Chief, Department of

_ Newington, Connecticut Radiology; Consultant in Radiology 1971-75 New Britain General Hospital

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Consultant in Radiology New Britain, Connecticut 1971-75 William W. Backus Hospital Consultant in Radiology Norwich, Connecticut 1972-75 Hartford Hospital ' Consultant in Radiology Hartford, Connecticut ,

1972-75 Mount Sinai Hospital Consultant in Radiology Hartford, Connecticut 1973-75 Hammersmith Hospital Honorary Consultant Radiologist

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London, England Department of Diagnostic Radiology 1975-78 The Montreal General Hospital Diagnostic Radiologist-in-Chief Montreal, Canada Department of Diagnostic Radiology 1975-78 The Montreal General Hospital Director, Department of Montreal, Canada - Diagnostic Radiology 1978- Cowell Memorial Hospital .

Physician present University of California, Berkeley 1978- University of California Medical Radiologist, Clinical Faculty present Center, San Francisco 9 e e

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. JACOB 1. FABRIKANT I Certi fi cation _

1962 American Board of Radiology

'Medict' icensure- ,

. 1957 National Board of Medical Exr'ners (No. 36999)

"1956 . Maryland (No. D 1511)

• 1971 Connecticut (No.14808)

- 1973-75 Great Britain 1976-78 Quebec, Canada (No.76-033) 1978 California (No. G 36656)

Military Service _

World War II, Veteran, United States Navy Marital Status _

Irene B. Fabrikant, Wife (McGill University)

B.Sc.

M.Sc. (McGill University, Bacteriology and Imunology)

Ph.D. (University of Maryland, Microbiology) 1966-70 Instructor, Departrmnt of Microbiology University of Maryland School of Medicine 1970-75 Assistant Professor of Medicine, Department of Medicine The University of Connecticut School of Medicine 1973-75 Honorary Research Fellow (Imunology)

Department of Zoology and Comparative Anatorny University College, London, England 1975-78 Assistant Professor, Department of Microbiology & Immunology Faculty of Medicine, McGill University, Montreal 1977-78 Executive Secretary, McGill University BiohazardsComittee McGill University, Montreal 1978-79 Research Fellow, U.S. Public Health Service, DHEW .

Center for Disease Control, San Juan Laboratories, Puerto Rico 1979- Research Associate, University of California, Berkeley, School of Public Health, Department of Biomedical & Environmental Health Sciences . .

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' JACOB I. FABRIKANT BIBLIOGRAPHY _

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l. Fabrikant, J.I. The Osler Society. (Editorial) McGill Med. J. 24:128, 1955.

, 2. Fabrikant, J.I. The Dean. (Editorial) McGill Med. J. 24:180, 1955.

3. Fabrikant, J.I. A concept of the term " anxiety". McGill Med. J. 24:201-207, p

1955.

~ 4. Fabrikant, J.I. Pediatric problems in clinical practic. (Book Review) McGill

- Med. J. 24:114-115,1955.

5. Anylan, W.G. , Delaughter, G.D. , Jr. , Fabrikant, J.I. , Sullenberger, J.W. and Weaver, W.T. The management of acute venous thromboembolism. JAMA 168:

725-729, 1958.

6. Anylan, W.G. , Baylin, G.J. , Fabrikant, J.I. and Trumbo, R.B. Studies in coronary angiography. Surgery 45:8-18, 1959.

7. 'Fabrikant, J. I. Colcstomy--A short revi ew. 11. Quart. 2:23-33,1959.

8. Sullenberger, J.W. , Weaver, W.T. , Fabrikant, J.I. and Anylan, W.G. A study of the pressor effects of serotonin and its possible role in massive thromboembolism. Surgical Forum 9:127-130, 1959. s

9. Fabrikant, J.I. Reflections on illness. II. Quart. 3:6-8, 1959.

10. Fabrikant, J.I. , Anlyan , W.G. , Baylin , G.J. and Trumbo, R.B. A comparison of vcrious techniques for a safe and reliable method of coronary arterio-graphy. Surgical Forum 9:233-237, 1959.

11. Fabrikant , J. I . , 'Anlyan , W.G. and Creadi ck, R.N. The management of radiation injuries to the intestines. South. Med. J. 52:1186-1191, 1959.

,12. Fabrikant, J.I. The ileal bladder. II. Quart. 3:43-47, 1959.

13. Fabrikant, J.I. , Anlyan , W.G. , Baylln, G.J. and Trumbo, R.B. A comparison of techniques for visualization of the coronary arteries. Ame r. J.

Roentgenol. Rad. Therapy and Nuclear Med. 81:764-771, 1959.

14. Fabrikant, J.I. The wet colostomy. 11. Quart. 4:1-5, 1959. .

15. Koehler, P.R. , Fabrikant, J.I. and Dana, E.R. Gastric retention during oral cholecystography due to underlying lesions of the stomach and .

duodenum. Surg. Gynet. and Obstet. 110:409-412, 1960. .

16. Fabrikant, 1. I . , Anlyan , W. G. and Creadi ck , R.N. Management of intestinal injuries caused by pelvic irradiation. Modern Med. 28:117-118, 1960.

f 17. Fabrikant, J.I. An improved ileostomy appliance. AMA Arch. Surg. 89:416-L 418, 1960.

. JACOB I. FABRIKANT 10.

18. Anlyan, W.G. , Baylin, G.J. , Fabrikant, J.I. and Trumbo, R.B. Studies in coronary arteriography. (In) Year Book of Radiology, Eds. , Holt, J.F. ,

s(-s Whitehouse, W.M. , Jacox, H.W. and Kligerman, M.M. , pp. 123-125, Year Book Medical, Chicago,1960.

19. Fabrikant, J.I. Specialists at your service: The radiologist. II. Quart. 5:

. 29-32, 1961.

20. Fabrikant, J.I. , Richards, G.J. , Jr. , Brack, C.B. and Goodwin, P.N. A

- vaginal applicator for radium therapy of carcinoma in the vagina.

• Radiology 77:987-989, 1961.

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21. Fabrikant, J.I. , Cockey, T.B. and Goodwin, P.N. A simple pituitary localizer for radiation therapy. Amer. J. Roentgenol. , Rad. Therapy and Nuclear Med. 86:649-650,1961.

22. Fabrikant, J. I. Reflections upon illness. Nursing News 12:3-5, 1961.

23. Fabrikant, J.I. , Anlyan, W.G. , Baylin, G.J. and Isley, J.K. Isotope studies for the evaluation of venous disease of the lower extmmity. J. Nuclear Med. 2:136-148,1962.

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24. Koehler, P.R. , Fabrikant, J.I. and Dickson, R.J. Observations on the behavior of testicular tumors with coments on racial incidence. J. Urol . 87:

577-579, 1962.

Fabrikant, J.I. , Richards , G.J. , Jr. , Tucker, G.F. , Jr. and Dickson, R.J.

25.

Contrast laryngography in the evaluation of laryngeal neoplasms. Amer.

J. Roentgenol. , Rad. Therapy and Nuclear Med. 87:822-835, 1962.

26. Fabrikant, J.I. , Richards , G.J. , Jr. , Tucker, G.F. , Jr. and Dickson , R.J.

Aid to diagnosis of laryngeal cancer. Modern Med. 31:212, 1962.

27. Fabrikant, J.I. Radiological changes in experimental animals following the administration of bone-seeking radionuclides. (ab) Intern. Congr Radiation Res. 2:212,1962.

28. Fabrikant, J.I. Cellular msponse and cell population kinetics unter con-tinuous irradiation. Radiologic changes ir. bone following irradiation.

(In) James Picker Foundation, Annual Report, pp. 23-25, New York,1962.

29. Fabrikant, J.I. and Dickson, R.J. Contrast cinefluorographic studies of the Q la rynx. (ab) Intern. Congr. Radiology 10:261, 1962.

30. Fabrikant, J.I. and Dickson, R.J. Clinical observations on radiation carci-nogenesis. (ab) Intem. Congr. Radiology 10:243, 1362.

31. Fabrikant, J.I. and Smith, C.L.D. Radiological changes in experimental animals following the administration of bone-seeking radionuclides. (In)

Radiation Effects in Physics, Chemistry, and Biology, Eds. , Ebert, M.

and Howard, A. , p. 472, North-Holland, Amsterdam,1963.

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32. Fabrikant, J.I. Regenerating liver. (In) Report of the Institute of Cancer Research: Royal Cancer Hospital, Annual Report, p.122, London,1963.

h., 33. Fabrikant, J.I. , Richards, G.J. , Jr. , Brack, C.B. and Goodwin, P.N. Vaginal applicator for radium. therapy of carcinoma in vagina. (In) Year Book of Radiology, Eds. , Holt, J.F. , Whitehouse, W.M. , Jacox, H.W. and Kligerman, M.M., p. 315, Year Book Medical, Chicago,1963.

34. Fabrikant, J.I . Studies of ~ cellular reponse and cell population kinetics

. under continuous irradiation. (In) James Picker Foundation, Annual

" Report, pp. 26-27, New York,1963.

35. ' Fabrikant , J. I . Cell proliferation studies in normal, continuously irradiated and malignant tissues. Regenerating liver. (In) Report of the Institute of Cancer Research: Royal Cancer Hospital, British Empire Cancer Cam-paign for Researth, Annual Report 41:152-153, 1964.

36. Fabrikant, J.I. and Smith, C.L.D. Radiographic changes following the admini-stration of bone-seeking radionuclides. Brit. J. Radiol . 37:53-62, 1964.

37. Fabrikant, J.I. and Roylance , P.J. Cinefluorographic anatomy of the larynx and hypopharynx. Proc. Anat. Soc. Great Britain and Ireland 33:25, 1964.

38. Fabrikant, J.I. Investigation of cellular reponse and cell population kinetics in tissues under continuous irradiation. (In) James Picker Foundation, Annual Report, pp. 28-29, New York,1964.

39. Fabrikant, J. I. Studies of cell proliferation in the regenerating liver and the effect of prior continuous irradiation. Ph.D. Thesis, University of London, 1964.

40. Fabrikant, J.I. , Dickson, R.J. and Fetter, B.F. Mechanisms of radiation carcinogenesis at the clinical level. Brit. J. Cancer 18:459-477, 1964.

41. Fabrikant, J.I. and Dickson, R.J. The use of cinefluorography for the radio-logical examination of the: larynx and hypopharynx in cases of suspected carcinoma. Brit. J. Radiol. 38:28-38, 1965.

42. Fabrikant, J.I. and Roylance, P.J. Cinefluorographic functional anatomy of the nonnal and diseased larynx. J. Anat. 99:209,1965.

43. Fabrikant, J.X. and Koburg, E. 'RSntgen-Kontrastuntersuchungen von Larynx und Hypopharyna n Verbindung mit Bildverst5rkung. HN0 Wegw. f. fach.

Praxis 13:16-19.1H5.

44. Fabrikant, J.I. and Lamerton, L.F. The effect of prior continuous irradiation . ,,

on cell proliferation in the mgenerating liver. Exc. Med. Intern. -

Congr. 89:347, 1965. _

l

45. Fabrikant, J.I. , Dickson, R.J. and Fetter, B.F. Mechanisms of radiation car-cinogenesis at clinical level. (In) Year Book of Radiology, Eds., Holt, J.F. , Whitehouse, W.M. and Latourette, H.B. , pp. 384-386, Year Book Medical, Chicago, 1966. '

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JACOB I. FABRIKANT

46. Fabrikant, J.I. Cell cycle of regenerating hepatocytes after continuous

{.)

i rradiation. (ab) Intern. Congr. Radiation Res. 3:79, 1966. .

47. Fabrikant, J.I. Cell population kinetics in the mgenerating liver in nonnal and continuously irradiated mice. (ab) Intern. Congr. Radiation Res. 3:

- 80, 1966. .

48. Fabrikant, J.I. Radiation-induced chromosome aberrations in the mgenerating

.- liver under continuous irradiation. (ab) Intern. Congr. Radiation Res. 3:

L 80, 1966.

3. '49. Fabrikant, .J.I. and Dickson, R.J. Use of cinefluorography for radiologic examination of larynx and hypopharynx in cases of suspected carcinoma.

(In) Year Book of Cancer, Eds. , Clark, R.L. and Cumley, R.W. , pp. 384-387, Year Book Medical, Chicago,1966.

50. Fabrikant, J.I. The spatial distribution of parenchymal cell proliferation during regeneration of the liser. J. Hopkins Med. J. 120:137-147, 1967.

51. Fabri kant, J.I. The,effect of prior continuous irradiation on the G 2, M and S phases of pmliferating parenchymal cells in the regenerating liver.

Radiation Res. 31:304-314, 1967.

52. Fabrikant, J.I. Radiation sterilization in man. JAMA 200:201-202, 1967.

53. Fabrikant, J.I. The kinetics of cellular proliferation in conditional celf renewal systems under continuous irradiation. (ab) Assn. Univ. Radiolo-gists 15:24,1967.

54. Fabrikant, J.I. The accumulation of chromosome damage under continuous low dose-rate exposure. Radiology 88:767-774, 1967.

55. Fabrikant, J.I . The ileal bladder. Colorado St. Dept. Public Health, Suppl . ,

pp.1-4, Denver,1967.

56. Lamerton, L.F. and Fabrikant, J.I. Repair of cellular radiation injury in the liver of continuously irradiatdd C57BL mice. (ab) Radiation Res. 31:

664-665, 1967.

57. Fabrikant, J.I. The effect of radiation-free intervals after continuous exposure on the yield of chromosome aberrations in the regenerating liver.

~

l (ab) Radiation Res. 31:665, 1967.

58. Fabrikant, J.I . Cell proliferation in the mgenerating liver of continuously irradiated mice. Brit. J. Radiol. 40:487-495, 1967. ,,

59. Fabrikant, J. I. and Wisseman, C.L. , III. Cell proliferation in n Smal and l malignant tissues. I. In vitro incorporation of thymidine-H . (ab)

Radiol . Soc. N. Amer. 37:41, 1967.

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JACOB I. FABRIKANT

~,

60. Fabrikant, J.I. Cell proliferation in the regenerating liver and the effect f~

i of prior continuous irradiation. Radiation Res. 32:804-826, 1967.

61. Fabrikant, J.I. , Peterson, W.E. and Donner, M.W. Biographical note. (In)

Russell H. Morgan, A Tribute. Eds. , Fabrikant, J.I. and Donner, M.W. ,

pp. xi-xii, duPont, Wilmington, Delawam,1967.

62. Fab ri kant , J. I . The analysis of cell population kinetics in a conditional renewal system under continuous irradiation. (In) Russell H. Morgan, A

-

• Tribute. Eds. , Fabrikant, J.I. and Donner, M.W. , pp.93-100, du Pont,

- Wilmington, Delaware,1967. .

~ 63. Fabrikant, J.I. Kinetic analysis of hepatic regeneration. Growth 34:311-315, 1967.

64. Morreels, C.L. , Jr. , Cherry, J. and Fabrikant, J.I. Ossified arytenoid cartilage masquerading as a foreign body; A case report. Ame r. J .

Roentgenol . , Rad. Therapy and Nuclear Med. 101:837-838, 1967.

65. Fabrikant, J.I. The kinetics of cellular proliferation in regenerating liver. J. Cell. Biol. 36:551-565, 1968.

66. Fabrikant, J.I. and Wisseman, C.L. , III. In vitro incorporation of tri-tiated thymidine in normal and neoplastic tissues. Radiology 90:361-363, 1968. s

67. Morreels, C.L. , Jr. , Cherry, J. and Fabrikant, J.I. Masquerader. (ab)

Modern Med. 36:103, 1968.

68. Fabrikant, J.I. Rate of cell proliferation in the regenerating liver.

Brit. J. Radiol . 41:71, 1968.

69. Foster, B.R. and Fabrikant, J.I. Studies on lymphoid cell proliferation in the nornlal and continuously irradiated mouse thymus by repeated labeling with tritiated thymidine. (ab) Radiation Res. 35:486, 1968.

70. Fabrikant, J.I. Cell proliferation during lymphopoiesis in nomal and continu-ously irradiated mice. (ab) (In) Symposium on the Effect of Radiation on Cellular Proliferation and Differentiation, I AEA, Vienna, SM-103/41, 1968.

71. Fabrikant, J.I. Radiation effects on a conditional cell renewal systrem under continuous low dose rate exposure. Amer. J. Roentgenol . , Rad. Therapy and Nuclear Med. 102:811-821, 1968.

72. Fabrikant, J.I. Cell proliferation in normal and malignant human tissues. (In).

James. Picker Foundation, Annual Report,1967, New York, pp. 44-45, 1968.

73. Fabrikant, J.I. Cell proliferation during lymphopoiesis in normal and continu-ously irradiated mice. (In) Symposium on Effects of Radiation on Cellular Proliferation and Differentiation, SM-103/41, pp.1-24, I AEA, Vienna,

( 1968.

14, JACOB 1. FABRIKANT

74. Fabrikant, J.I. Influence of cell cycle stage on radiation response in vivo.

1 l

16:27, 1968.

$ (ab) Assn. Univ. Radiologists,

(.

75. Fabrikant, J.I. Cell proliferation in the regenerating liverBrit. of continuously J. Radiol . ,

irradiated mice; effect of a radiation-free interval.

41:369-374, 1968.

C.L., III. The kinetics of cellular

76. Fabrikant, J.I., Vitak, M.J..and Wisseman, IV. Nucleic acid synthesis and the cell (ab) proliferation in human tissues. cycle in relation to normal, inflammatory a Radiol . Soc. N. Amer. , E4:47,1968.

~ ~ Objective evaluation of cleft palate speech.

77. Hoopes, J.E. and Fabrikant, J.I.42:214-224, 1968.

Plast. Reconstr. Surg.,

78. Fabrikant, J.I. The kinetics of lymphoid cell proliferation under continuous 54:149, 1968.

irradiation. (ab) Radiol . Soc. N. Amer. ,

Radiographic evaluation of x radiation induced

79. Knudson, D.H. and Fabrikant, J.I. 54:180, 1968.

bone tumors. (ab) Radiol. Soc. N. Amer.,

80. Fabrikant, J.I. Cell proliferation during lymphopoiesis in the thymus of continuously irradiated mice. (In) Effects of Radiation 269-393, I . A.E. A.on Cellular

, Vienna,1968.

proliferation and Differentiation, pp.

The kinetics of cellular

81. Fabrikant, J.I., Wisseman, C.L., III, and Vitak, M.J. II. An in vitro method proliferation in normal and malignant tissues.for incorporation of tri 92:1309-1320, 1969.

Fabrikant, J.I.

Studies on cell population kinetics in regenerating liver.30:169-183, 82.

(In) Human Tumor Cell Kinetics, Nat. Cancer Inst. Monogr. No.

1969.

The kinetics of cellular proliferation in

83. Fabrikant, J.I. and Cherry, J. normal and malignant tissues. III. Cell proliferation Ann Otol . , Rhinol . , Laryngol . , 78:326-341, 1969.

The locus of

84. Hoopes, J.E. , Dellon, A.L. , Fabrikant. J.I. and Soliman, H. levato incompetence. Plastic Reconstr. Surg., 44:155-160, 1969.

The kinetics of lymphoid cell proliferation

85. Fabrikant, J.I. and Foster, B.R. Radiation Res., 39:544, during radiation lymphomogenesis in C57BL mice.

1969.

The kinetics of cellular proliferation in

86. Fabrikant, J.I . and Cherry, J. V. Analysis of labeling indices and normal and malignant tissues. J. Surg.

potential doubling times in human tumor cell populations.

Oncol . , 1 : 27-51, 1969.

Exp.

Fabrikant, J.I. Size of proliferating pools in regenerating liver.

87.

Cell Res., 55:277-279, 1969.

I l

- ~ ~ _ _ _ _ _ _ _ . - _ .

I . -

JACOB I. FABRIKANT 15.

88. Fabrikant, J.I. Radiation response in relation to the cell cycle in vivo.

( Amer. J. Roentgenol. , Rad. Therapy and Nuclear Med. 105:734-745, 1969.

89. Fabrikant , J.I. Studies on cell population kinetics in radiation leukemo-genesis. Assn. Univ. Radiologists 17:88, 1969.

90. Fabrikant, J.I. and Foster, B.R. Cell cycle of lymphocytes in mouse thymus.

Die Naturwissenschaften' 57:567,1969.

'91. >Fabri kant, J.I . Cell proliferation in continuously irradiated mammals; Effect of age. (In) Radiation Biology of the Fetal and Juvenile Mamal,

- - Sikov, M. and Mahlum, D.D. , eds. USAEC, CONF. 690501, pp. 621-628, Oak Ridge, Tenn. ,1969.

92. Hoopes , J.E. , Dellon , A.L. , Fabrikant, J.I . , Edge rton , M.T. and Soliman, A.H.

Cineradiographic definition of the functional anatomy and pathophysiology of the velopharynx. (ab) Intem. Congr. Cleft Palate, 42, Houston, Texas, 1969.

(

93. Fabrikant, J.I. The kinetics of cellular proliferation in the seminiferous epithelium under continuous irradiation. XII Intern. Congr. Radiology 12:98, 1969.

94. Fabrikant, J.I. Radiation effects on lymphopoiesis under continuous low l dose-rate exposure. Radiology 93:887-893, 1969. ~

95. Hoopes, J.E. and Fabrikant, J.I. Objective evaluation of cleft palate speech.

(ab) Cleft Palate J. 6:181, 1969.

l 96. Fabrikant, J.I. Research on cell proliferation in normal and malignant

( human tissues. (In) James Picker Foundation Annual Report,1968, pp. 45-50, 1969.

97. Fabrikant, J.I. The kinetics of cellular proliferation in normal and I malignant tissues. VIII. Studies on cell population kinetics in normal, inflammatory and neoplastic tissues in man. (ab) XII Intern.

Congr. Radiology 12:442,1969.

l 98. Fabrikant, J.I. Cell proliferation in normal and malignant human tissues.

l (In) James Picker Foundation Annual Report,1969, pp. 40-42,1969.

99. Fabrikant, J.I. and Wisseman, C.L. , III. In vitro incorporation of tritiated thymidine in normal and neoplastic tissues. (In) Year Book of Radiology, Holt, J.F. , Whitehouse, W.M. and Latourette, H.B. , eds. ,

pp. 383-384, Year Book Medical, Chicago,1969. .

100. Fabrikant, J.I. The kinetics of cellular proliferation in human tissues.

IX. Estimation of DNA synthesis time in normal and malignant tissues.

(ab) Radiol. Soc. N. Amer. 55:44, 1969.

/

l l

v .

~ 16.

JACOB I. FABRIKANT 1 01. Fabrikant, J.I. Tumor cell population kinetics during radiation lymphomo-(* genesis. (ab) Radiol. Soc. N. Amer. 55:124, 1969.

Hoopes, J.E. , Dellon, A.L. , Fabrikant, J.I. and Soliman, A.H. Cineradio-102.

graphic assessment of combined island flap pushback and pharyngeal flap in the surgical management of submucous cleft palate. Brit. J.

- Plast. Surg. 23:39-44, 1970. .

103. Fabrikant, J.I. and Kovar, D.S. Spennatogonial cell renewal under continu-

- ous irradiation at l'.8 rads / day. (ab) Radiation Res. 18:233, 19/0.

9

_ 1 04.

Dannenberg, A.M. , Jr. , Shima, K. , Chandrasekhar, S. and Fabrikant, J.I.

Macrophage proliferation, maturation, and function in rabbit BCG lesions. (ab) Fed. Proc. 29:501, 1970.

105. Fabrikant, J.I. Thymus cell population studies during radiation leukemo-genesis. Amer. J. Roentgenol. , Rad. Therapy and Nuclear Med.108:

729-735, 1970.

106. Fabrikant, J.I. The kinetics of cellular proliferation in normal and malig-nant tissues. XI. Estimation of DNA synthesis time in human tissues.

Radiology 95:691-693, 1970.

107. Hoopes , J.E. , Dellon , A.H. , Fabrikant, J.I. and Soliman , A.H. Idiopathic hypernasality: Cineradiographic evaluation and etiologic considera-ti ons. J. Speech Hearing Dis. 35:44-50, 1970. ..

108. Fabrikant, J.I. The kinetics of cellular proliferation in normal and' malignant tissues. IV. Nucleic acid synthesis in human tissues. (ab)

Invest. Radiol . 5:281, 1970.

109. Hoopes , J.E. , Dellon , A.L. , Fabrikant, J.I. and Soliman , A.H. The locus of levator palatini function as a measure of velopharyngeal incompetence.

(ab) Cleft Palate J. 7:357, 1970.

110. Fabrikant, J.I. and Cherry, J.I. The kinetics of cellular proliferation in normal and malignant tissues. X. Cell proliferation in respiratory epithelium of the nose and adjoining cavities. Ann. Otol., Rhinol.,

Laryngol. 79:572-578, 1970. t 111. Fabrikant, J.I. Environmental radioactivity: Inclusion at the cellular level. Envi ronmental Radioactivity Symposium, Clopton, J.C. , ed. ,

pp.35-106, The Johns Hopkins University Press , Baltimord, Md. ,1970.

112. Fabrikant, J.I. Report of the United Nations Scientific Committee on the *

• Effects of Atomic Radiation. Supplement 13, 1969. (Book Review) .'

Social Biol. 17:238-241, 1970.

l 113. Fabrikant, J.I. Radiation response in relation to the cell cycle in vivo.

I (ab) Radiology 94:247, 1970.

L-

17.

" JACOB. I. FABRIKANT 114. Fabrikant, J.I. Human tumor cell kinetics. (In) Tine and Dose Relation-h ships in Radiation Biology as Applied to Radiotherapy, Bond, V.P.,

Seit, H.D. and Marcial, V. , eds. , pp. 334-337, BNL 50203(C-57) Brook-haven National Laboratory, Upton, N.Y. ,1970.

115. Hoopes, J.E. , Dellon, A.L. , Fabrikant, J.I. , Edgerton , M.T. and Soliman, j A.H. Cineradiographic definition of the functional anatomy and patho-physiology of the velopharynx. Cleft Palate J. 7:443-454, 1970.

-h* 16. Sabrikant, J.I. Cell proliferation (ab) in the seminiferous epithelium under IV Congr. Intern. Radiobiol. Physico-continuous irradiation.

- Chimie Rayon. 4:68, 1970.

117. Fabrikant, J.I. Effects of rapidly and slowly proliferating cell renewal systems. Sixth Annual San Francisco Cancer Symposium, (ab) 5:26, 1970.

118. Dannenberg, A.M.', Jr. , Shima, K. , Kambara, T. , Meyer, 0.T. , Ester!v, J.R.

and Fabrikant, J.I. Imunity in tuberculosis, illustrated by its

< pathogenesis. (ab) Tuberculosis Conference, NI AID, US-Japan Program, 7, 1970.

Hoopes, J.E. , Dellon, A.L. , Fabrikant, J.I. and Soliman, A.H. Cineradio-119.

graphic definition of the anatomical variables responsible for cleft palate speech. Brit. J. Plast. Surg. , 24:158-162, 1971.

120. Fabrikant, J.I. Radiation response in relation to the cell cycle in vivo. .,

- (In) Year Book of Radiology, Holt, J.F. , Whitehouse, W.M. and Latourette, H.B. , eds. , p. 392, Year Book ' Medical, Chicago,1970.

121. Fabrikant, J.I. The kinetics of cellular proliferation in human tissues.

VII. Determination of duration of DNA synthesis using double labeling autoradiography. Brit. J. Cancer 24:122-127, 1970. .

122. Fabrikant, J.I. Thymus cell population studies during radiation leukemo-genesis. (ab) Sadiology 97:742, 1970.

123. Fabrikant, J.I. Radiation effects on cell renewal systems. (ab) (In)

Frontiers of Radiation Therapy and Oncology, Vaeth, J.M. , ed. , 5:6-8, 1970.

124. Fabrikant, J.I. The kinetics of cellular proliferation in normal and -

malignant tissues. XII. In vitro label. (In) The Growth Kinetics of Solid Tumors, Williambsburg, Va. , February 8-11, 1971, Summary The Report of the Meeting. Mendelsohn,Cell M.L.Tissue and Shackney, S.E.

Kinet. 3:401-414, 1971. . , , . .

growth kinetics of solid tumors. ~.

• 125. Fabrikant, J.I. The kinetics of ceIlular proliferation in nonnal and malignant tissues. XV. A review of methodology and the analysis of Amer. J. Roentgenol . ,

cell population kinetics in human tissues.

Rad. Therapy and Nuclear Med. 111:700-711, 1971.

C

/

l

18.

JACOB I. FABRIKANT (In) Symposium on Cell 126. Fabrikant, J.I. Spermatogonial cell renewal.

( Renewal Systems. (ab) Radiation Res. 19:46-47, 1971.

127. Delahunty, J.E. and Fabrikant, J.I. Experimental laryngeal arteriography.

Ann. Otol., Rhinol., Laryngol. 80:744-749, 1971.

128. Fabrikant, J.I. Cell population (In) kinetics in thymus lymphocytes under con-Biological Aspects of Radiation Protection, tinuous irradiation.

. p Sugahara, E. and Hug, 0., eds., pp. 74-80, Igaku Shoin, Tokyo, r Japan , 1971.

129. Fabrikant, J.I. Biological effects of small doses of radiation. (ab)

Amer. Assn. Physicists Med. Quart. Bull. 5:115, 1971.

130. Fabrikant, J.I. Spennatogonial cell-renewal under continuous low dose irradiation. Invest. Radiol . 6:343, 1971.

Radiation Biology of the Fetal and Juvenile Mamml. Proc.

1 31 . Fabrikant, J.I. Radiology 97:

Ninth Ann. Hanford Biol. Symposium. (Book Review).

659-660, 1970.

132. Fabrikant, J.I. and Foster, B.R. The cell cycle and gmwth kinetics during radiation leukemogenesis in C57BL mice. (ab) Radiol. Soc. N. Amer.

57:244, 1971.

13'3. Chandrasekhar, S. , Shima, K. , Dannenberg , A.M. , Jr. , Kambara, T. , Fabrikant, J.I. and Roessler, W.G. Radiation, infection and macrophage function.

IV. Effect of radiation on the proliferative abilities of mononuclear Infection and Immunity phagocytes in tuberculosis lesions of rabbits.

3:254-259, 1971.

1 34. Fabrikant, J.I. and Cherry, J. The kinetics of cellular proliferation in Doubling times in primary and nonnal and malignant tissues. XIII.

metastatic tumors in the same patient. (ab) Radiol. Soc. N. Amer. 57:

46, 1971.

135. Fabrikant, J.I. , Wisseman, C.L. , III and Vitak, M.J. The kinetics of cellular proliferation in normal and malignant tissues. VI. Nucleic acid metabolism in m1ation to the cell cycle in human tissues. Growth 36:

173-183, 1972.

(Ip) Reduction 1 36. Fabrikant, J.I. The effects of small doses of radiation.

of Radiation Dose in Diagnostic X-Ray Procedures, pp. 3-32. Proceedings of a Symposium held in Houston, Texas, July 8,1971. Amer. Assoc.

Phys. Med. , USDHEW Publ . No. (FDA) 73-8009, Bureau of Radiological ,

Health, Rockville, Md. ,1972.

137. Fabrikant, J.I. Spermatogonial cell mnewal under continuous low dose i rradiation. Amer. J. Roentgenol . , Rad. Therapy and Nuclear Med, 114:792-802, 1972.

L

19, JACOB 1. FABRIKANT 138. Fabrikant, J.I. Radiation effects on rapidly and slowly proliferating cell renewal systems. Discussion. Front. Radiation Ther Oncol. 6:524-( 526, 1972.

139. Hsu, T.H.S. and Fabrikant, J.I. Spermatogonial Kinetics cell' renewal under continu-of cellular depopulation ous low level irradiation. 'VII.

under 45 rads per day.~ (ab) Radiation Res. 51:544, 1972.

140. Fabrikant, J.I. and Foster, B.R. Lymphoid cell renewal' under' low-level irradiation. XI. The cell cycle and growth kinetics during radiation

- p leukemogenesis of C57BL mice. Radiology 104:203-204, 1972.

Fabrikant, J.I. Radiation effects on rapidly and slowly proliferating cell

_ .141. (In) Frontiers of Radiation Therapy and Oncology, renewal systems.

Vaeth, J.M., ed., Vol. 6, pp. 57-78, Karger, Basel, 1972.

142. Fabrikant, J.I. Medical Radiation ' Biology. (Book Review)'. Radiology 105:

434, 1972.

143. Fabrikant, J.I. Cell population kinetics in'the seminiferous epithelium under continuous low dose rate irradiation. (.Inl Advances.in Radiation Research. Biology and Medicine. Vol. II. Duplan, J.F. and Chapiro, A. eds. pp. 805-814, Gordon and Breach, New York,1972.

144. Fabrikant, J.I. and Foster, B.R. Cell population kinetics in mouse and rat thymus. J. Hopkins Med. J. 130:208-215, 1972.

145. Fabrikant, J.I. Lymphoid cell renewal under low level irradiation. XII.'

Regulation of thymus. cell proliferation under cont.inuous exposure.

(ab) Radiation Res. 51:471, 1972.

146. Fabrikant, J.I., Hsu, T.H.S., Knudson, D.H. and Smith, C.L.D. Effect of LET on radiation carcinogenesis.. ', Comparison of single and fractionated doses of plutonium-239, americium-241, phosphorus-32 and x-rays on the production of osteosarcomas in rats. (ab) 12th Hanford Biology Symposium on Radionuclide Carcinogenesis, Richland, Wash., May 11-13, 1972.

l ,

147. Fabrikant, J.I. and Cherry, J. The kinetics .of cellular proliferation in normal and malignant tissues. XIV. Analysis of tumor cell kinetics in primary and metastatic ~ lesions. (ab) Assn.' Univ. Radiologists 20:

34, 1972. Invest. Radiol. 7:436-437, 1972.

l Fabrikant, J.I . , Hsu , T.H.S. , Knudson , D.H. and Smi th, C.L.D. LET and

! 148.

radiation carcinogenesis. The effects of fractionation of dose of plutonium-239, americium-241, phosphorus-32 and x-rays o'n the produc-tion of osteosarcomas in rats. (In) Radionuclide Carcinogenesis, 12th . .

Hanford Biology Symposium, pp. 322-346, C.L. Sanders, R.H. Busch, J.E.

Ballou, D.D. ~ Mahlum, eds. CONF-720505, USAEC, Oak Ridge, Tenn. 1973.

149. Fabrikant, J.I. Public health considerations of the biological effects of small doses of medical radiation. .(abl Health Physics Society, San Juan, P.R., 7:4, 1972.

{

• 20.

JACOB I. FABRICANT Fabrikant, J.I. Radiation dosimetry of heavily irradiated sites in patients 150.

p g. treated for ankylosing spondylitis. (In) The Effects on Populations Report of the U of Exposure to Low Levels of Ionizing Radiation.

i Advisory Comittee on Biological Effects of Ionizing Radiations, pp.

190-195. National Academy of Sciences-National Research Council, Washington, D.C. ,1972.

151. Fabrikant, J.I. The kinetics of cellular proliferation in normal and malignant tissue. XVI. Cell population kinetics in primary and

.- metastatic tumors. (ab) Europ. Soc. Radiation Biol . , Rome, 9:47, 1972.

Lymphoid cell renewal under low level irradiation. XIII.

I

. . P-

, 1.52. Fabrikant, J.I.

Homeostatic control of cell mproduction under continuous exposure.

' (ab) Europ. Soc. Radiation Biol. , Rome, 9:46, 1972.

153. Fabrikant, J.I. and Hsu, T.H.S. Spermatogonial cell renewal under low level irradiation. VII. Cellular response and cell population kinetics in i

the seminiferous epithelium during mcovery after continuous exposum 1 at 45 rads / day. (ab) Europ. Soc. Radiation Biol . , Rome, 9:49, 1972.

4 l 154. Shima, K. , Dannenberg, A.M. , Jr. , Ando, M. , Chandrasekhar, S. , Seluzicki, J.

and Fabrikant, J.I. Macrophage accumulation, division, maturation, and digestive and microbial capacities of tritiated thymidine and their t,

content of lysomal enzymes and bacilli. Amer. J. Path. 66:143, 1972.

Delahunty, J.E. and Fabrikant, J.I. Experimental laryngeal arteriography.

155. -

Radiology 103:227, 1972.

156. Fabrikant, J.I. Lymphoid cell renewal under continuous low level irradiation.

XIV. Regulation of cell proliferation and differentiation. (ab) f Radiol. Soc. N. Amer. 58:47, 1972.

I Spermatogonial cell mnewal under low level 157. Hsu, T.H.S. and Fabrikant, J.I. Cellular response and cell population kinetics during irradiation. X.

mcovery of the testes after continuous irradiation at 45 rads / day.

(ab) Radiation Res. 55:560, 1973.

158. Fabrikant, J.I. and Foster, B.R. Lymphoid cell renewal under low level irradiation. XVII. Cell kinetic analysis of radiation leukemogenesis.

I l

(ab) Radiation Res. 55:587, 1973.

159. Fabrikant, J.I. Public health considerations of the biological effects of small doses of medical radiation. (In) Health Physics in the Healing Arts, pp. 31-42, DHEW Publication (FDA) 73-8029, Food and Drug Admini-stration, Bumau of Radiological Health, NTIS, Springfield, Va.,1973. .

l 160. Fabrikant, J.I. , Hsu, T.H.S. , Kovar, D.H. and Smi th, C.L.D. Radiation-induced osteosarcomas in rats. Delayed effects of bone-seeking radio-nuclides and x-rays. Invest. Radiol. 8:269, 1973.

161. Fabrikant, J.I. Tumor cell population kinetics under continuous irradiation.

(In) Symposium on the Radiobiological Effect and RBE of Minimum Doses of P3diation. (ab) Proc. XIII Intern. Congr. Radiology, p. 473, Madrid,

( Spain,1973.

l e

__.---..,--m. + , , , - . . - . - . - - ..m__m..,,u. y-, y,.- ,,...-,.m., ,,,,,,,,--,,_%y...,m,-%, -,.m , , , - . . .,y-, .r.

21.

. JACOB I. FABRIKANT Lymphoid cell renewal under low level irradiation. XIV.

( 162. Fabrikant, J.I.

(In) Symposium Regulation of lymphopoiesis under continuous exposure.

on Long-Tenn Effects--Low Level Radiation Doses. Proc. XIII Interna-tional Congress of Radiology, p. 518, Madrid, Spain,1973.

1.63.

Hsu, T.H.S. , Fabrikant, J.I. and Kovar, D.S. Spermatogonial cell mnewal under low level irradiation. XII. Effect of dose rate on cellular response under continuous exposure. (ab) J. Hopkins Med. Surg. Assn.,

Radiology Sec. , Baltimore , Md. ,1973.

' 164. " Fabrikant, J.I . The cell cycle in lymphoid tissues. (ab) (In) The Cell

- - Cycle in Malignancy and Immunity. Thirteenth Hanford Biology Symposium, Richland, Wash. 13:59-60, 1973.

165. Hsu, T.H.S. , Kovar, D.S. and Fabrikant, J.I . Spermatogonial cell renewal under low level irradiation. XI. Analysis of stem cell population kinetics in mice. (ab) Radiat. Res. Soc. Work-in Progmss Session, Twenty-third Ann. Mtg. , St. Louis, Mo. , May 1,1973.

166. Fabrikant, J.I. Some implications of the 1972 Report of the Advisory Com-mittee on the Biological Effects of Ionizing Radiations (The BEIR

- Report) of the National Academy of Sciences-National Research Council.

(In) Report of the Eleventh Meeting of the Medical Radiation Advisory Committee, Bureau of Radiological Health, FDA, DHEW, Rockville, M6, September 13-14, 1973.

167. Fabrikant, J.I. The cell cycle in lymphoid tissues and the immune respons'e'.

(In) The Cell Cycle in Malignancy and Immunity, Hampton, J. , ed. ,

Thirteenth Hanford Biology Symposium, pp. 504-530, . (CON F-731005 ) .

NTIS, Springfield, Va. ,1974.

168. Fabrikant, J.I. The biological effects of low levels of radiation dose:

Implications for diagnostic radiology. (ab) Postgraduate Weekend Course, The Faculty of Radiologists, London, England, May 1974.

169. Hsu, T.H.S. and Fabrikant, J.I. ' Spermatogonial cell renewal under continu-ous irradiation. XII. Stem cell renewal. (ab) V. Intern. Congr.

l Radiation Res. , Seattle, Wash. , July 1974.

170. Fabrikant, J.I. Tumor cell population kinetics under continuous irradiation.

Proc. XIII International Congress of Radiology, Madrid,1973, pp. 585-589, Excerpta Medica, Amsterdam,1975. .

171. Fabrikant, J.I . Medical Radiation. Second Report to the Advisory Committee on the Biological Effects of Ionizing Radiations, National Academy of , ,

Sciences-National Research Council , 59 pp. , Washington, D.C. ,1974. .

i 172. Fabrikant, J.I. Concepts: Cost-Benefit Analysis and Medical Radiation.

Report to the Advisory Comittee on the Biological Effects of Ionizing l Radiations, National Academy of Sciences-National Research Council, l

18 pp. , Washington, D.C. ,1975.

l

./

22.

JACOB I. FABRIKANT 173. Hsu, T.H.S. and Fabri kant, J.I . Spermatogonial cell renewal under continu-ous irradiation at 1.8 and 45 rads per day. (In) Proceedings of the C- Symposium on Low Level Radiation, International Atomic Energy Agency, IAEA-SM-202/214, Chicago, Ill., 1975.

174. Fabrikant, J.I. The significance to diagnostic radiology of the effects Clinical Radiol.

- of exposure to low levels of ionizing radiations.

33:172-179, 1975.

Benefit-Risk-Cost Analysis for Medical Radiation. Chapter 475.* Fabrikant,

.. VI. J.I.(In) Considerations of Health Benefit-Risk-Cost Analysis for Activities Involving Ionizing Radiation Exposure and Altematives.

Report of the Advisory Conmittee on the Biological Effects of Ionizing Radiations, National Academy of Sciences-National Research Council, 147 pp. , Washington, D.C. ,1976.

176. Hsu, T.H.S. and Fabrikant, J.I. Spermatogonial cell renewal under con-tinuous irradiation at 1.8 and 4.5 rads per day. (In) Biological and Envimnmental Effects of Low-level Irradiation. Vol. 1, pp. 157-168, I AEA-SM-202/214, International Atomic Energy Agency, Vienna,1976.

177. Fabrikant, J.I. and Hsu, T.H.S. Spermatogonial cell renewal under low-level irradiation. XVI. Stem cell proliferation. (ab) Radiat. Res.

70:620, 1977.

178. Hsu, T.H.S. and Fabrikant, J.I. Kinetics of spermatogonial cell renewal '

under continuous irradiation at 1.8 and 4.5 rads per day. (ab)

Radiat. Res. 70:620, 1977.

179. Fabrikant, J.I. and Hilberg, A.W. Benefit-cost analysis for medical radia-ti on. (ab) Radiat. Res. 70:670-671, 1977.

180. Fabrikant, J.I. Benefit-cost analysis in diagnostic radiology. (In) Panel on Efficiency, Cost-Benefit Analysis and Health Resource Allocation in Radiology. James Picker Foundation Conference, The Radiologist in Society--Prospects and Problems for the 1980s. Kay Biscayne, Florida, April 1977.

181. Fabrikant, J.I. and Hsu, T.H.S. Spermatogonial cell renewal under low-level i rradiation. XV. Stem cell proliferation in the seminiferous epi-thelium under 1.8 rads per day. (ab) XIV International Congress of -

Radiology, Rio de Janeiro, Brasil,1977, In Press. ,

182. Fabrikant, J.I. and Hilberg, A.W. Benefit-cost analysis for diagnostic radiology in medicine. (In) Symposium on Risks and Benefits in Medical Radiation Applications. XIV International Congress of Radiology, '.,*

Rio de Janeiro, Brasil,1977, In Press.

183. Fabrikant, J.I. and Anderson, N.D. Immunchematopoietic cell renewal under low level irradiation. XVIII. Hematopoietic stem cell kinetics. (ab)

(In) Symposium on Immunological Consequences of Radiotherapy. XIV International Congress of Radiology, Rio de Janeiro, Brasil,1977,

( In Press.

. 23.

JACOB 1. FABRIKANT 184. Fabrikant, J.I. and Hilberg, A.W. The effects of low level radiation dose to

( human populations; The significance for diagnostic radiology. (ab) XIV International Congress of Radiology, Rio de Janeiro, Brasil,1977, In Press.

185.. Fabrikant, J.I. Lymphoid cell renewal under low level irradiation. XIX.

- Cell proliferation in the spleen germinal center during the primary imune reaction under 45 rads per day. (ab) XIV International Congress of Radiology, Rio de Janeiro, Brasil,1977, In Pmss.

186." Fabrikant, J.I. and Hilberg, A.k'. Mamorgraphy: Benefit-cost analysis of mass screening procedures. (ab) XIV International Congress of Radiology, Rio de Janeiro, Brasil,1977, In Prc.a.

187. Fabrikant, J.I. Respiratory function in ischemic myocardial disease: The value of pulmonary radiology. (ab) XIV International Congress of

s. ~ Radiology, Rio de Janeiro, Brasil,1977, In Press.

188. Fabrikant, J.I. Radiation protection and safety in diagnostic ultrasound.

l (ab) XIV International Congress of Radiology, Rio de Janeiro, Brasil, 1977, In Press.

189. Fabrikant, J.I. Safety in Diagnostic Ultrasound. (In) CRC Critical Reviews in Diagnostic Imaging, Wang, Y. , ed. CRC Press , Inc. , Vol .10, pp. 219-234, 1977.

190. Fabrikant, J.I. Perspectives of decisi.on-making and estimation of risk in (In) Symposium populations exposed to low levels of ionizing radiation. AAAS Annual

' on Epidemiology Studies of Low Level Radiation Exposure.

Meeting, Houston, Texas, January 1979. Lawrence Berkeley Laboratory Report LBL-8667, pp.1-40, Lawrence Berkeley Laboratory, University of i California, Berkeley, California, January 1979.

Fabrikant, J.I. Cell cycle of spennatogonia in mouse testes. Invest.

191.

Radiol. 14:189-191, 1979.

I 192. Fabrikant, J.I. The 1979 Report of the Advisory Committee on the Biological Effects of Ionizing Radiation (The BEIR Report). The Effects on Implications Populations to Exposure to Low levels of Ionizing Radiation.

for Nuclear Energy and Medical Radiation. (In) Symposium on Known

Effects of Low Level Radiation Exposures, (National Cancer Institute), -

Pittsburgh, Pennsylvania, April 1979, Lawrence Berkeley Laboratory -

Report, LBL-9084, pp.1-42, In Press.

193. Fabrikant, J.I. and Anderson, N.D. Imunchematopoietic cell renewal under low level irradiation. XI X. CFU stem cell kinetics. (ab) VI Inter-

' national Congmss of Radiation Research, Tokyo, May 13-19,1979, p. 309, '-

1979.

Fabrikant, J.I. Spermatogonial stem cell renewal following irradiation. (In) 194.

Symposium on Radiation and Stem Cells, (ab) VI Intemational Congress l

of Radiation Research, Tokyo, May 13-19,1979, p. 44,1979.

- - , , . . . . - - . , - , . , , . - ~ , , , - , + - - . . . ,.,--.-,---.n,

, - , . -,,, ---- - +,

,- 's 24.

JACOB 1. FABRIKANT 195. Fai rikant, J.I . Spermatogonial stem cell renewal following irradiation.

(In) Symposium on Radiation and Stem Cells. VI International Congress of Radiation Research. Proceedings of the Congress, Tokyo, May 13-

{ 19,1979, LBL-8667,1979.

196. Fabrikant, J.I. and Hilberg, A.W. Benefit-risk analysis for diagnostic radi ology. (ab) VI International Congress of Radiation Research, Tokyo, May 13-19,1979, p.183,1979.

197. Lyman, J.T. and Fabrikant, J.I. Estimation of absolute risk of leukemias p

and cancers of heavily irradiated sites in single-course radiotherapy

-'~

patients treated for ankylosing spondylitis in England and Wales. (ab)

VI International Congress of Radiation Research, Tokyo, May 13-19, 1979, p.180,1979. _

198. Tobias , C. A. , Benton , E.V. , Holley, W.R. , Fabrikant, J.I. , and Henke, R.P.

Heavy-ion computed tomography. (ab) VI International Congress of Radiation Research, Tokyo, May 13-19,1979, p.135,1979.

199. Vitak, M.J. , Hsu, T.H.S. , Kovar, D. , and Fabrikant, J.I. Lymphoid cell renewal under low level irradiation. XX. B-cell population kinetics of the cellular imune response. (ab) VI International Congress of Radiation Research, Tokyo, May 13-19,1979, p. 212,1979.

200. Fabrikant, J.I. Degeneration and regeneration of the spermatogonial stem-cell system after exposure to ionizing radiation. Lawrence Berkeley Laboratory Report No. LBL-8850, pp.1-25, University of California, s Berkeley, California, February 1979.

201. Fabrikant, J.I. Perspectives of decision-making and estimation of risk in populations exposed to low levels of ionizing radiations. (In) Sym-posium on Epideiniology Studies of Low-level Radiation Exposure, AAAS Annual Meeting, Houston, Texas, January 3-8, 1979; Lawrence Berkeley Laboratory Rerart LBL 8667, pp.1-40, January 1979.

202. Fabrikant, J.I. Fertility. (In) Chapter V. Somatic Effects: Effects Other Than Cancer: The Effects on Populaticns of Exposure to Low Levels _

of Ionizing Radiation: 1980. Report of the Committee on the Biological Effects of Ionizing Radiations, pp. 493-498, National Academy of Sciences-National Research Council, Washington, D.C.,1980, Lawrence Berkeley Laboratory Report LBL-8704,-January 1979.

203. Fabrikant, J.I. Salivary Glands. (In) Chapter V. Somatic Effects: Cancer.

The Effects on Populations of Exposure to Low Levels of lonizing Radiation: 1980. Report of the Committee on the Biological Effects of Ionizing Radiations, pp. 392-396, National Academy of Sciences-National Research Council, Washington, D.C., 1980, Lawrence Berkeley .

Laboratory Report LBL-8708, January 1979.

L

" 25.

JACOB I. FABRIKANT 204. Fabrikant, J.I. and Lyman, J.T. Estimates of radiation doses in tissues

([ and organs in the single-course radiotherapy patients treated for ankylosing spondylitis in England and Wales. (In) Chapter V. Somatic Effects: Cancer. The Effects on Populations of Exposure to Low Levels of Ionizing Radiation: 1980. Report of the Committee on the Biological Effects of Ionizing Radiations, pp. -160-167, National Academy of Sciences-National Research Council, National Academy Press, Washington, D.C.,

1980, Lawrence Berkeley Laboratory Report LBL-8708. January 1979.

e 9-Fabrikant, J.I. and Land, C.E. Pancreas. (In) Chapter 5. Somatic Effects:

205.

Cancer. The Effects on Populations of Exposure to Low Levels of Ionizing

- ~

Radiation: 1980. Report of the Committee on the Biological Effects of Ionizing Radiations, pp. 384-389, National Academy of Sciences-National Research Council, Washington, D.C., 1980, Lawrence Berkeley Laboratory Report LBL-8710. January 1979.

Pharynx, hypopharynx, and larynx. (In) Chapter V. Somatic 206. Fabrikant, J.I.

Effects: Cancer. The Effects on Populations of Exposure to Low Levels of Ionizing Radiatian: 1980. Report of the Committee on the Biological Effects of Ionizing Radiations, pp. 389-392, National Academy of Sciences-National Research Council, Washington, D.C., 1980, Lawrence Berkeley Laboratory Report LBL-8711. January 1979.

207. Fabrikant, J.I. Somatic Effects - Cancer. II. Introductory Material.

A. Mechanisms of Radiation Carcinogenesis. B. Concepts of Somatic ~

Effects. . (In) The Effects on Populations of Exposure to Low Levels of Ionizing Radiation: 1980. Report of the Comm ttee on the Biological Effects of Ionizing Radiations, National Academy of Sciences-National Research Council, Washington, D.C., pp.1-14, Lawrence Berkeley Laboratory Report LBL-8715. January 1979.

208. Fabrikant, J.I. Ovary. (In)ChapterV. Somatic Effects: Cancer. The Effects on Populations of Exposure to Low Levels of Ionizing Radiation: 1980 Report of the Committee on the Biological Effects of Ionizing Radiations, pp. 406-409, National Academy of Sciences-National Research Council, Washington, D.C.,1980, Lawrence Berkeley Laboratory Report LBL-8743.

January 1979.

209. Fabrikant, J.I. Degeneration add regeneration of the spermatogonial stem-cell system after exposure to ionizing radiation. Presented at the Symposium on Rcdiation and Stem Cells. VI Intern. Congr. Radiation t

Res., Tokyo, Japan, May 13-19, 1979. Lawrence Berkeley Caboratory Report LBL-8850, pp. 1-25. February 1979.

Fabrikant, J.I. Health Effects of low-level ionizing radiation. Presented ,

21 0.

before the U.S. Senate Committee on Human Resources, Subcommittee on Health and Scientific Research. Official Record ofLawrence the U.S. Berkeley Senate Hearings of April 4,1979, GPO, Washington, D.C.

Laboratory Report LBL-9018. April 1979.

f <W.

o

- 's JACOB I. FABRIKANT 26.

211. Fabrikant, J.I. Applications of dose-response functions to observed data.

{~ (In)ChapterII. Scientific Principles of Radiation Effects. The Effects on Populations of Exposure to Low Levels of Ionizing Radiation: 1980.

Report of the. Committee on the Biological Effects of Ionizing Radiations, pp. 21-23, National Academy of Sciences-National Research Council, Washington, D.C., 1980.

21 2. Fabrikant, J.I. Perspectives of decision-making and estimation of risk in

_ ,. , populations exposed to low levels of ionizing radiation. Presented at the AAAS Annual Meeting. Symposium of Epidemiology Studies of Low-Level Radiation Exposure, Houston, Texas. January 3-8, 1979. Report LBL-8667,

~

pp.1-40, Lawrence Berkeley Laboratory, University of California, Berkeley, California, January 1979.

213. Tobias, C.A., Fabrikant, J.I., Holley, W.R., and Benton, E.V. Heavy-ion radiography. Lawrence Berkeley Laboratory Report, LBL-10022, UC-48, pp. 63-67, 1979.

214. Holley, W.R. , Henke, R.P. , Gauger, G.E. , Jones , B. , Benton, E.V. , Fabrikant, J.I., and Tobias, C.A. Heavy particle computed tomography. (In) Sixth Symposium on Computer Radiology, 1979 IEEE, pp. 64-70, June 1979.

215. Fabrikant, J.I. Summary of the Public Health and Safety Task Force Report to The President's Commission on the Accident at Three Mile Island.

(In) Public Health and Safety Task Force Report to The President's s Commission on the Accident at Three Mile Island. (Fabrikant,J.I.,Ed.)

32 pp. Government Printing Office, Washington, D.C., October 1979.

216. Axelrod , D. , Bluestone , M. , Densen, P.M. , Fabrikant, J. I . , Fowinkle, E.W. ,

Johnson, K.G., Jones, E.W., and Seltser, R. Technical Staff Analysis Report on Public Health and Epidemiology. (In) Public Health and Safety Task Force Report to The President's Commission on the Accident at Three Miles Island. (Fabrikant, J.I. , Ed. ) 147 pp. Government Printing Office, Washington, D.C., October 1979.

217. Abrahamson, S., Bair, W.J., Bender, M.A., Bloom, A.D., Bond, V.P., Casarett, G.W., and Fabrikant, J.I. Technical Staff Analysis Report on Report l of the Radiation Health Effects Task Group. (In) Public Health and Safety Task Force Report to The President's Commission on the Accident at Three Mile Island. (Fabrikant, J.I., Ed.) 98 pp. Government Printing -

Office, Washington, D.C., October 1979. -

1

! 218. Fabrikant, J.I. The BEIR-III Report and the health effects of low-level l radiation. (In) Symposium on Nuclear Reactor Safety: A Current Per-Lawrence Berkeley -

spective. AAAS, San Francisco, 1980. Science. ,

Laboratory Report LBL-10383. January 1980.

I b

.i l

- JACOB I. FABRIKANT 27.

e 3

h219. Fabrikant, J.I. The 1979 Report of the Advisory Committee on the Biological Effects of Ionizing Radiation (The BEIR Report). The Effects on Popula-tions of Exposure to Low Levels of Ionizing Radiation. Implications for Nuclear Energy and Medical Radiation. (In) Known Effects of Low Level Radiation Exposure Health Implications of TMI Acciden (Shrivastava, P.N., Ed.) pp.79-104. Division of Cancer Control and Rehabilitation of the National Cancer Institute, Mideast Center for Radiological

. Physics, Pittsburgh, Pennsylvania, April 25, 1979, NIH Publication 80-2087.

. Lawrence Berkeley Laboratory Report LBL-9084. 1980.

9

~

a:.

'220. Fabrikant, J. I. The BEIR-III Report and its implications for radiation d protection and public health policy. (In) Proceedings of the Inter-national Radiation Protection Association, Fifth International Congress, Jerusalem, March 9-14, 1980. In press. Lawrence Berkeley Laboratory 7 Report LBL-10494,1980.

221. Fabrikant, J.I., Tobias, C.A., Benton, C.V., and Capp, M.P. Heavy ion imaging I applied to medicine, (ab.). (In) Proc. SPIE, IEEE, Medicine VIII, p. 64, -

Las Vegas, Nevada. April 1980.

3 222. Fabrikant, J.I. Current understanding of the relation between radiation 5 exposure and the induction of developmental disabilities. Presented at W Symposium on Prevention of Mental Retardation: Opportunities and Obstacles 1980, III. Environmental Hazards; Special Concerns, American Association 7 on Mental Deficiency,104th Annual Meeting, San Francisco, May 14, 1980, -

in press.

223. Fabrikant, J. I., Tobias, C.A., Capp, M.P., Benton, E.V. and Holley, W.R.  ?

Heavy-ion imaging applied to medicine. SPIE Vol. 233, Application of A

! Optical Instrumentation in Medicine VIII, pp. 255-263, 1981. Lawrence 3 Berkeley Laboratory Report LBL-10543, 1981. -

l m

224. Fabrikant, J.I.  %

Health effects of the nuclear accident at Three Mile Island. ~

Presented at Conference on Environmental Regulation of the Nuclear T Industry: A new Decade. Atomic Industrial Forum, San Francisco, i California, May 18-21, 1980, in press. 15 T

i 225. Fabrikant, J.I. The BEIR-III controversy. Radiation Research Society, $

l New Orleans, Louisiana. June 1, 1980. University of California, 7,';

i LBL-ll268, June 1980. .

j 226. Fabrikant, J.I., Tobias, C.A., Capp, M.P., Benton, e and Holley, W.R. '

Heavy-ion imaging applied to medicine. Amer. . -

ntgenol., Nuclear r Medicine and Rad. Therapy, 1981, in press.

227. Tobias, C. A. , Fabrikant, J.I. , Benton, E.V. and Holley, W.R. Projection radiography and tomography. (In) Biological and Medical Research with Accelerated Heavy Ions at the Bevalac 1977-1930. (Pirruccello, M. and Tobias, C. A. , eds. ) pp. 335-346. Lawrence Berkeley Laboratory Report

. LBL-ll220, 1980. ..

( - a

';:0 g

l l

V

• t JACOB I. FABRIKANT 28.

Fabrikant, J.I. , Tobias, C. A. , Capp, M.P. , Holley, W.R. , Woodruff, K.H. and Sickles, S. A. Heavy-ion mammography and breast cancer. (In) Biological 228.

and Medical Research with Accelerated Heavy Ions at the Bevalac 1977-1980.

Lawrence Berkeley (Pirruccello, M. and Tobias, C.A., eds.) pp. 347-357.

- Laboratory Report LBL-11220.1980.

229. Chen, G.T.Y. , Fabrikant, d.I. , _ Holley, W.R. , Tobias, C. A. and Castro, J.R.

~

Heavy-ion radiography applied to charged particle radiotherapy. (In)

., Biological and Medical Research with Accelerated Heavy Ions at the pp. 359-366.

Bevalac 1977-1980. (Pirruccello, M. and Tobias, C.A., eds.)

Lawrence Berkeley Laboratory Report LBL-11220.1980.

230. Llacer, J. , Chu, W.T. , Tobias, C. A. , Fabrikant, J.I. , and (In) Alonzo, J.R. Active heavy-ion radiography and computerized tomography. Biological and Medical Research with Accelerated Heavy Ions at the Bevalac 1977-1980.

Lawrence Berkeley (Pirruccello, M. and Tobias, C.A., eds.) pp. 367-374.

Laboratory Report LBL-11220.1980.

231. Fabrikant, J. I. , Budinger, T.F. , Tobias, C. A. , and Born, J.L. Focal lesions in the central nervous system. (In) Biological and Medical Research with Accelerated Heavy Ions at the Bevalac 1977-1980. (Pirruccello, M. and Tobias, C. A. , eds. ) pp. 399-405. Lawrence Berkeley Laboratory Report LBL-11220.

232. Fabrikant, J.I . , Beebe, G.W. , Bender, M. A. , Brill , A.R. , Land, C.E. ,

Moeller, D.W. , and Webster, E.W. Estimating the Total Cancer Risk of Low-Dose, Low LET, Whole-Body Radiation. Chapter V, Section 3, l

pp.176-226. (In) The Effects on Populations of Exposure to Low Levels of Ionizing Radiation,1980. Report of the Committee on the Biological Effects of Ionizing Radiations, National Academy of Sciences-National Research Council, Washington, D.C., 1980.

233. Fabrikant, J.I. Health effects of the nuclear accident at Three Mile Island.

Health Phys. 40:151-161, 1981. Lawrence Berkeley Laboratory Report LBL-11297, 1980. -

234. Fabrikant, J.I. The BEIR-III controversy. Radiat. Res. 84:361-368, 1980.

235. Holley, W.R. , Tobias, C. A. , Fabrikant, J.I. , Llacer, J. , Chu, W.T. and Benton, E.V. Computerized heavy-ion tomography. SPIE Vol. 27,3, Application of

Optical Instrumentation in Medicine IX, pp. 283-293, 1981. Lawrence Berkeley Laboratory Report LBL-12304.

236. Fabrikant, J.I. The contribution of modern medical imaging technology to .

radiation health effects in exposed populations. IEEE Transactions on Nuclear Science, Vol. NS-28, No.1, pp. 40-46, February 1981. Lawrence Berkeley Laboratory Report LBL-11728, November 1980.

b

3ACOB1.FABRIKANT 246. Fabrikant, J.I. Impact of the 1980 BEIR-III Report on low-level radiation:

Risk assessment, radiation protection guides, and public health policy.

(, (In) Proceedings Selected Topics in Reactor Health Physics, Fourth Annual HPS Summer School, Lexington, Kentucky, June 1981. To be published, 1981. Lawrence Berkeley Laboratory Report LBL-13408, 247. Fabrikant, J.I. Biological effects of ionizing radiation: Epidemiological surveys and laboratory animal experiments. Implications for risk

- 'e evaluation and decision processes. (In)ProceedingsoftheSeminaire des Evaluations des Risques et Processus de Decision, National Academy P of Sciences-National Research Council (USA) and Mouvement Universel de la Responsibilite Scientifique-Academie Francais, Orsay, France, December 17-19, 1980. To be published,1981. Lawrence Berkeley Laboratory Report LBL-12555.

248. Fabrikant, J.I. Nuclear energy, public health and public policy. Amer.

Jour. Public Health,1981. To be published. Lawrence Berkeley Laboratory Report LBL-13469.

249. Fabrikant, J. I. Influence of dose and its distribution in time on dose-response relationships for low-LET radiations. NCRP Report 64, National Health Council on Radiation Protection and Measurements (Book Review).

Physics, 1981, in press.

1 e

e h

JACOB I. FABRIKANT BOOKS AND CHAPTERS

1. Fabrikant, J.I. Studies on Cell Proliferation in the Regenerating Liver

{' ' , and the Effect of Prior Continuous Irradiation. Ph.D. Thesis, University of London, London,1964.

2. Fabrikant, J.I. and Donner, M.W., Eds. Russell H. Morgan, A Tribute duPont, Wilmington, Delaware,1967.

3. Fabrikant, J.I. The Effects of Continuous Irradiation. (In) Pathology of Irradiation. Berdjis, C.C., Ed., Chapter 4, pp. 50-85, Williams "p and Wilkins, Baltimore, Maryland,1971.

4. Fabrikant, J.I. The Effects of Irradiation on the Kinetics of Proliferation in Cell Renewal Systems. (In) CRC Critical Reviews in Radiological Sciences. Wang, C. , Ed. Vol . 2, pp. 525-576, CRC Press Inc. Cleveland, Ohio, 1971.

1

5. Fabrikant, J.I. Radiobiology Year Book Medical Publishers, Chicago, Illinois,1972.

6. Fabrikant, J.I. The Kinetics of Cell Proliferation in Normal Tissue, Malignant Tumors of the Upper Air Passages. (In) The Biological and Clinical Basis of Radiosensitivity. Friedman, M. , Ed. , Chapter 13, pp. 274-313, Charles C. Thomas Publishers, Springfield, Illinois,1974.

7. Fabrikant, J.I. Safety in Diagnostic Ultrasound. (In) CRC Critical Reviews in Diagnostic Imaging. Wang, C.. Ed. Vol. 10, pp. 219-234, CRC Press Inc., Cleveland, Ohio, 1977.

8. Fabrikant, J.I. Summary of the Public Health and Safety Task Force Report to The President's Commission on the Accident at Three Mile Island.

32 pp. Government Printing Office, Washington, D.C., October 1979, in press.

9. Axelrod, D. Bluestone, M. , Densen, P.M. , Fabrikant, J.I . , Fowinkle, E.W. ,

Johnson, K.G. , Jones , E.W. , and Seltser, R. Technical Staff Analysis Report on Public Health and Epidemiology. (In) Report of the Public Health and Safety Task Force Report to The President's Commission on The Accident at Three Mile Island.132 pp. Government Printing Office, Washington, D.C. , October 1979, in press.

i

10. Abrahamson, S. , Bair, W.J. , Bender, M. A. , Bloom, A.D. , Bond, V.P. , Casarett, G.W., and Fabrikant, J.I. Technical Staff An@ds Report on Report of the Radiation Health Effects Task Group. 'I b ort of The Public l

Health and Safety Task Force Report to The Presuen. s Commission on The Accident at Three Mile Island. 98 pp. Government Printing Office, .

j Washington, D.C., October 1979.

11. Auxier, J. A. , Berger, C.D. , Eisenhauser, C.M. , Gesell, T.F. , Jones, A.R. ,

and Masterson, M.E. Report of the Task Group on Health Physics and Dosimetry. (In) Report of the Public Health and Safety Task Force to The President's Commission the Accident at Three Mile Island l

1 h (Fabrikant, J.I., Ed.) 196 pp. Government Printing Office, Washington, D.C. , October 1979.

l

s e t

• J,. COB I. FABRIKANT

12. Dohrenwend, B.P., Dohrenwend, B.S., Kas1, S.V. and Warheit, G.J. Technical

(?.

Staff Analysis Repcrt on Behavrioral Effects. (In)ReportofthePublic Health and Safety Task Force to The President's Commission on the Accident at Three Mile Island. (Fabrikant, J.I., Ed.) 81 pp. Government Printing Office, Washington, D.C., October 1979.

13. Fabrikant, J.1. , Beebe, G.W. . Bender, M. A. , Brill , A.R. , Land, C.E. , Moeller, D.W., and Webster, E.W. Estimating the Total Cancer Risk of Low-Dose,

- p Low LET, Whole-Booy Radiation. Chapter V., Section 3. (In) The Effects

. on Populations of Exposure to Low Levels of Ionizing Radiation: 1980.

Report of the Committee on Biological Effects of Ionizing Radiations, pp. 176-226, National Academy of Sciences-National Research Council, Washington, D.C., 1980.

e f

( ..

O

r -

a

' JACOB I. FABRIKANT 29.

(' 237. Fabrikant, J.I. The BEIR-III Report: Origin of the controversy. AJR 136:209-214, 1981. Lawrence Berkeley L% oratory Report LBL-13409,1981.

238. Fabrikant, J.I. and Lyman, J.T. Estimates of absolute risk of excess leukemias and cancers arising in heavily irradiated sites in the single-course radiotherapy patients treated for ankylosing spondylitis in England and Wales. Brit. J. Radiol. , in press.

239, Fabrikant, J.I. Public health implications and decision-making during nuclear reactor accidents---the Three Mile Island experience. (In)

Symposium on Preparing for the Issues of the 1980's. Annual Meetin;;.

Association of State and Territorial Health Officials, Atlanta, Georgia, April 1980. To be published.

240. Fabrikant, J.I., Tobias, C. A., and Pirruccello, M.C. Medical imaging using heavy-ion radiography. (In) Proceedings of the Conference on Biological Imaging, Scripps Clinic and Research Foundation, La Jolla, California, November 1980. To be published. Lawrence Berkeley Laboratory Report LBL-12517,1981.

241. Fabrikant, J.I. Risk estimation and decision-making: Implications of the 1980 BEIR-III Report. (In) Proceedings of the Conference on Radiation Exposure on Pediatric Dentistry, American Academy of Pedodontics, Cincinnati, Ohio, April 1981. Pediatric Dentistry, 1981. In press. '

Lawrence Berkeley Laboratory Report LBL-13407.

242. Fabrikant, J.I. Epidemiological studies on radiation carcinogenesis in human populations following acute exposure: Nuclear explosions and medical radiation. (In) Proceedings of the Symposium on Effects on Humans of Exposure to Low Levels of Ionizing Radiation, Yale University School of Medicine, New Haven, Connecticut, May 1981. Yale Journal Biol. Med., 1981.

In press. Lawrence Berkeley Laboratory Report LBL-13416.

243. Fabrikant, J.I. The effects of low-level radiation on human health: Epidemio-i logical studies. The Walter W. Herbert Memorial Symposium: Is Low-dose l Radiation Harmful? (In) Diagnostic Radiology 1981. (Margulis,A.R.and Gooding,G.A.,eds.) pp. 451-455. University of California, San Francisco 1981. i 244. Fabrikant, J.I. and Tobias, C.A. Heavy-ion radiography and. cancer. Donner Laboratory, Lawrence Berkeley Laboratory, University of California, Berkeley, PUB-5051. February 1981.

245. Fabrikant, J.I. Controversial issues confronting the BEIR-III Committee---implir cations for radiation protection. Thirteenth Annual National Conference on Radiation Control, Little Rock, Arkansas, May 1981. To be published.

Lawrence Berkeley Laboratory Report LBL-13444.

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