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Testimony for the GESMO Hearings 

Submitted by 

The Public Interest Research Group 
1346 Connecticut Ave, N.W., Suite 419A 
Washington , D. C. 20036 

Prepared by 

John W. Gofman, M.D., Ph.D.* 
Professor Emeritus , Medical Physics 
Division of Medical Physics 
University of California, Berkeley 
Berkeley, California 94720 

February 21, 1977 


* John W. Gofman is also Chairman, Committee for Nuclear Responsibility. 
This is CNR Report 1977-1. 
Committee for Nuclear Responsibility, Inc. 
P.O.B. 332. Yachats, Oregon 97498 
Correspondence address: P.O.8. 11207, San Francisco, California 94101 



Testimony by John W. Gofman for the NRC GESMO Hearings 

The testimony presented here addresses the considerations of the 
toxicity of plutonium. It addresses GESMO, Volume 3, Section lV-J, 
Radiological Health Assessment. There are other sections of GESMO 
which also address or mention the toxicity of plutonium. To the 
extent that this is so, this testimony addresses those sections as 
well. 

Contents of áTestimony 

1. General Response to All Critiques of John W. Gofman's Estimates of 
the Lung Cancer Hazard of Plutonium                           pp 1-14 

2. APPENDIX: Responses by J.W. Gofman to the Minor Issues Raised in 
the ERDA Lab Critiques                                        pplS-26 

3. "The Cancer Hazard from Inhaled Plutonium" by John W. Gofman, 
May 14, 1975, CNR-lR, The Committee for Nuclear Responsibility, 
M.P.O. Box 11207, San Francisco, California 94101. 

4. "Estimated Production of Human Lung Cancers By Plutonium from 
Worldwide Fallout" by John W. Gofman, July 10,1975, CNR 1975-2, 
The Committee for Nuclear Responsibility, M.P.O. Box 11207, San 
Francisco, California 94101. 

5. "The Plutonium Controversy" by John w. Gofman, Journal of the 
American Medical Association, Vol. 236, No.3, pp 284-286, July19, 
1976. 

Note: All five items listed above are integral parts of this testimony. 




General Response to All Critiques 
of 
John W. Gofman's Estimates of the Lung Cancer Hazard of Plutonium 

Introduction: 

The estimates of the lung cancer hazard of inhaled 
plutonium are set forth in three papers by John W. Gofman. These are 

(1) The Cancer Hazard From Inhaled Plutonium, CNR Report 1975-lR, 
dated May 14, 1975 

(2) Estimated Production of Human Lung Cancers By Plutonium 
from Worldwide Fallout, CNR Report 1975-2, dated July 10, 1975 

(3) The Plutonium Controversy, JAMA, 236, No.3, pp284-286, July 
19,1976. 

For simplicity in the ensuing discussion, reference to these reports 
of a general character will be by the term "Gofman-Pu papers". References 
of a specific character will be to "CNR-1R", or "CNR-2", or "JAMA". 

Before the appearance of the Gofman-Pu papers, the general 
"wisdom" was that the lung cancer potential of plutonium could be 
adequately described by consideration of the deposition and retention 
of Puo 2 aerosols ( or other insoluble Pu compounds as aerosols) in the 
lung tissue of the bronchiole-alveolar regions, with neglect of any 
potential effect on more proximal bronchial tissues, that is tissues 
proximal to the terminal bronchioles. The models used in achieving that 
"wisdom" predicted no significant long-term retention of plutonium 
would occur in the bronchial tissues proximal to the terminal bronchioles. 
Hence it was predicted that there would be no significant dose to 
such more proximal bronchi. Gofman raised the question as to 
whether the conventional "wisdom" might be in error, which it certainly 
seems to be. Since even a small percentage retention in the 
proximal bronchial tissues could drastically increase the lung cancer 
hazard of plutonium aerosols, it becomes of extreme importance to 
know just how much plutonium is subject to long-term retention in 
the bronchial tissues proximal to the bronchiole-alveolar region. 
The plain fact is that no studies have been accomplished to describe 
such retention of plutonium in either of two major classes of humans, 
cigarette smokers and non-smokers. It is regrettable that such studies 
have not been accomplished .It is further an indication of the lack 
of competence of AEC and ERDA that in all their highly-funded studies 
of plutonium, these crucial questions have not been addressed, particularly 
when one considers the central importance of the issues in



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volved. 

In the Gofman-Pu papers it was pointed out that the major part 
of the mechanism counted upon to remove Pu rapidly from the bronchi 
was the set of cilia lining the bronchial ' cells. These cilia beat in 
a direction such that material is propelled in the direction of the 
nasopharynx. The actual material being propelled is, at least in part, 
mucus secreted by goblet cells in the á bronchial lining, such mucus 
probably incorporating part of the particulate material being cleared. 
Part of the clearance mechanism may also be the propulsion of cells of 
the macrophage class by cilia. The cilia are severely damaged in humans 
who smoke cigarettes. Such damage is two-fold in character, namely 
actual denuding of the cilia of cells and functional impairment of 
ciliary action in those retaining cilia. Additionally the smokers have 
replacement of the normal bronchial epithelium by metaplastic epithelium 
'innumerous regions. Similar alterations occur in non-smokers 
but to a far lesser degree. JAMA presents the references both to the 
studies of Ide and of Auerbach on these issues. 

No one really knows why Pu0 2 aerosols are retained so tenaciously 
in the bronchiole-alveolar region, tenaciously enough to give 
T~clearance times of the order of 500 days from this region. But there 
is no doubt that the clearance time is long. Many who have commented 
on the long-term retention in this region have ascribed it to the 
absence of cil i ated cells, so that the so-called "muco-ciliary escalator" 
doesn't work there as it does in the more proximal bronchi. 

If the cilia are absent in 25-30 % of the bronchial cells and 
if the cells are altered to rnetaplastic epithelium, what has happened 
in such regions to the ability to clear Pu0 2 aerosols? As Gofman 
pointed out carefully in the Pu papers, there simply are no data on 
humans ( nor any valid experimental animal model) to answer this 
crucial question. No data at all. Gofman therefore suggested that, 
as a first approximation, the best estimate is that clearance from 
such regions of ciliary absence and metaplasia will become equivalent 
to that for the non-ciliatEd bronchiolo-alveolar á region , yielding T~ 
values of the order of 500 days. To be sure, altered bronchial epithelium 
is not identical with bronchioloalveolar tissue. It may be, 
as Gofman pointed out, that altered bronchial epithelium is more 
capable, equally capable , or less capable in Puo 2 clearance compared 
with bronchiole-alveolar epithelium. It is the height of public health 
irresponsibility to assume that clearance is unaltered in the damaged 


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bronchial epithelium. Such an assumption emanating from laboratories 
supported by ERDA or NRC should be totally suspect, in view of the 
vested interest of those laboratories in a low order of plutonium 
toxicity. 

The Criticisms of the Gofman Hypothesis 

In five separate reports, the ERDA laboratories have produced 
critiques of the Gofman-Pu papers. While I shall deal with 
each of those reports separately below, the substance of the 
criticism has to do with two points: 

(a) The T~ clearance time utilized by Gofman -for the injured 
bronchial epitheium just "must be too high", and 
(b) Gofman has used a much higher figure for the relative risk 
of lung cancer per rem of ionizing radiation than the BEIR committee 
and this accounts in part for his high toxicity of plutonium. 
I shall deal with these two points in this general response. 
As for the remainder of the criticisms, they are so far over on the 
side of absurdity that they_,hardly deserve any comment whatever. This 
will be demonstrated in the responses to the specific critiques. 

Criticism . (a) 

Other than wishful thinking, the five ERDA lab critiques have 
provided .nothing at all to challenge the Gofman value of T~ of clearance 
from injured bronchial epithelium. They have, therefore,assumed 

( not presenting any basis whatever) that even after cilia have been 
lost and damaged, after normal cell epithelium is replac .ed by metaplastic 
epithelium, this bronchialepithelium will still be far more 
efficient in clearing Puo 2 particulates than the non-ciliated epithelium 
of the bronchioalveolar region. In the absence of any evidence 
to support their position, they simply choose to be optimistic 
about the lung cancer potential of plutonium. This is public health 
irresponsibility at its worst! To the extent that ERDA and / or NRC 
accept(s) such nonsense as science , they are being totally derelict 
in their legal responsibilities concerning the health and safety of 
the public. All estimates of the hazard of the nuclear fuel cycle, 
of reprocessing, of mixed oxide fuel fabrication, of appropriate 
standards for so-called" permissible" exposure either to the public 
or to occupational workers are simply worthless until the question 
of plutonium retention in the bronchial epithelium is resolved. Gofman 


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¥. ..~ 
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has made the very reasonable ( and modestly conservative} suggestion 
that áconversion of ciliated bronchial epithelium to non-ciliated 
epithelium plus some metaplastic epithelium makes them act , with 
respect to Pu02 retention, like non-ciliated bronchiolo-alveolar 
epithelium. Moreover, he suggested that metaplastic epithelium might 
be more active, by phagocytosis or endocytosis, than is the case for 
the bronchiole-alveolar region, and that this could indeed make his 
estimate inadequately conservative. Gofman emphasized that the 
burden of proof that his proposed behavior does not represent reality 
rests upon á those who choose to believe a more "optimistic" behavior 
will occur. This is clearly and unequivocally as it should be in such 
matters of public health importance, a . point not apparently appreciated 
in any of the five ERDA lab critiques. While such lack of appreciation 
cannot be condoned, it can be understood in the light. of the desire 
not to bite the á hand that feeds them. 

Meanwhile, in striking contrast to the opportunistic gobbledygook 
presented in the five ERDA lab critiques, there has appeared a 
most valuable study of human material by Radford and Martell. This 
paper bears directly upon the clearance of insoluble particulates 
from bronchial tissue. The paper is" PolOnium-210: Lead-210 ratios 
As An Index of Residence Times of Insoluble Particles From Cigarette 
Smoke in Bronchial Epithelium" by Edward P . Radford and Edward A. 
Martell, and was presented at The Fourth International Symposium on 
Inhaled Particles and Vapors, Edinburgh, 22-26 September 1975. 

á. á ( in .press, Pergamon Press Ltd . ) . The introduction to this paper, 
appearing just a few months after the CNR-1 and CNR-2 papers, reiterates 
and confirms the points made by Gofman, and it does that so 
succinctly, that I think it important to reproduce that introduction 
here as follows: (I now quote Radford and Martell } 

"Up to the present, models of the deposition, retention, and 
clearance of insoluble particles from pulmonary tissues have 
emphasized processes within the lung parenchyma, with the bronchi 
being considered primarily conduits through which mucociliary 
clearance occurs. There is recognition that pr~ferential deposition 
of some inhaled particles occurs by impaction at special locations 
in the bronchial tree, such as at bifurcations of the trachea and 
major bronchi, and there is also evidence that localized regions 
of the epithelium may have inefficient ciliary clearance becauae 
of splitting of the mucociliary stream at bifurcations, develop~ 
ment of squamous metaplasia and loss of ciliary function in small 
areas, or other mechanisms affecting mucociliar y competence. For 
these reasons, one would conclude that in some regions 


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(Radford-Martell quote continued) 

of the bronchial epithelium, especially at bifurcations, localized 
concentration of insoluble inhaled particles might accumulate, 
both by direct deposition or after entrainment in the mucociliary 
stream and subsequently becoming trapped in regions of 
of inefficient clearance . Especially in relation to development 
of bronchial cancer, certainly one of the most serious consequences 
of inhalation of particles, the failure of current lung clearance 
models to take account of the retention of materials in the 
bronchial epithelial structures is one of the most serious limi tations 
of these models." 

This quotation expresses precisely the same type of thinking 
presented in the Gofman-Pu papers .. The experimental data of Radford 
and Martell are used to try to estimate the residence time (mean 
value) for the Lead-210-containing insoluble particles in mainstream 
cigarette smoke. These authors point out that the presence of some 
soluble Lead-210 in bronchial tissues will have the effect of giving 
too low a mean residence time for the insoluble particles by their 
method of analysis. Yet, in spite of this, they estimate a mean residence 
time of 3 to 5 months for the insoluble particles. This , in 
days , is between 90 and 150 days. Taking a middle value of 120 days 
this would be some six times lower than the mean residence time 
Gofman estimated for Puo 2 aerosols in the injured part of the bronchial 
epithelium ( 500 / 0.693 is approximatel y 700 days). I t must be 
noted that the Radford-Martell va lues are for overall bronchial 
tissue samples, not the injured regions alone. Thus over and above 
the Lead-210 (soluble) error which t~nds to make their residence times 
too low they are including some normal bronchial t i ssue which may 
have a very much shorter residence time than the injured tissue. When 
these t wo factors are taken into account, their experimental evidence 
on human material may finally suggest an even lo nger T~ f or injured 
bronchial tissue than that suggested by Gofman. These data ,preliminary 
as they are, are enormously closer to the estimates of Gofman 
than to the optimistic suggestions of a fraction of a day or a day 
for T~ in injured bronchial epithelium to be found in the ERDA l ab 
c ritiques. 

Dr. J . Martin Brown ( Health, Safety , and Social Issues of 
Nuclear Power and the Nucl ear Initiative, Chap te r 4 in "The California 
Nucl ear Initiative" , Stanford Unive rsit y Inst itu te for Energy Studie s, 
April 1976) stated, concerning t he ERDA c ritiques, the following; 

"How ever, none of the critics seems to be awar e of recent data 


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showing the extensive holdup of insoluble particles of polonium 

(an atpha-emitter~ like plutonium, that is concentrated on 
topacco leaf hairs) in the bronchial tree of smokers. This, at 
least qualitatively, supports Gofman's hypothesis and certainly 

suggests further study is urgently needed." 
Dr. Brown is referring to the Radford-Martell studies cited above. 
Of all the five ERDA lab critiques, only one, áthat by Healy 
and co-workers,shows even a glimmer of appreciation of the problem 
of plutonium retention in the bronchi. In their conclusion they 
state 
" In our review of his papers we have concluded that the 
speculations of Gofman require the arbitrary acceptance 

of too many numerical parameters and unconfirmed mechanisms 
to be acceptable as even an approximate numerical estimate of 
potential lung carcinogenesis by plutonium. There is, indeed, 
a paucity of direct measurements of clearance rates for intact 
and damaged bronchial ciliated epithelium but current information 
would indicate that the problem is not as serious as 
postulated by Gofman. We would recommend that measurements 
continue with more emphasis on the absolute bronchial retention, 
and that until such evidence is available , the Gofman predictions 
be regarded as interesting and imaginative speculations 
which should serve to stimulate increased interest in certain 
phases of current studies. However, we cannot concur with his 
often state:3.position that speculation, no matter how poorly 
founded, is a proper basis for public health decisions." 

It is of some importance to dissect this amazing paragraph 
of admission of ignorance concerning the clearance of plutonium by 
intact and damaged epithelium. Starting with the gratuitous insult 
at the end of their quote, I might point out that it will rain 40 inches 
per day in the Sahara Desert before the Healy group will be able to 
show a single instance where Gofman suggested that speculation , no 
matter how poorly founded , is a proper basis for public health 
decisions , let alone" his often stated position" . Nevertheless, one 
must be tolerant in such matters. Here is one of ERDA's set of experts 
on plutonium toxicity publicly admitting that there is absolutely no 
way that they can help refute Gofman's estimates, admitting th~t 
Gofman is correct concerning the absence of the crucial measurements, 
advising that the measurements Gofman says are essential must be given 
high priority. It is easy to understand their frustrations about their 
admissions which lead them to use insults when they have no science to 
offer in refutation. 

There is one additional point in the Healy et al critique that 
deserves translation. That is in the quote above where they say "current 


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information would indicate the problem is not as serious as 

postulated by Gofman~ On a matter of such transcendent importance 

one would expect scientists, in possession of such "current information", 

would tell us how serious the problem is, if it is not as serious 
as postulated by Gofman. On this, they are silent. One cannot help 
thinking, since they do net provide the" current information", that 
what they mean is current wishful thinking that might please ERDA. 

Criticism (b): 

The essence of this second criticism is that Gofman used too high 
a value for the relative risk of lung cancer development per rem of 
exposure . Cited as evidence that Gofman used too high a value are a 
value of 0.20 for the relative risk and a value of 0.29 for the rela


both 

tive risk ; in the BEIR Report. I shall return to the excellent reasons 
why Gofman r ejecte d these values. At this point I should like to take 
up the reason why Gofman quoted the BEIR statement that the relative 
risk might be 0.5% or even higher---and even so Gofman rejected that 
value as four times too low. Much of this discussion is in a sense 
moot since new evidence is now available from the Hiroshima -Nagasaki 
studies (1975) and they not only show that Gofman's choice of 2% per 
rem was the proper choice at the time, but also the new evidence indicates 
that even the Gofm an estimate of relative risk per rem might 
be too low, NOT too high. 

The relative risk method suggests that radiation acts as a multiplier 
on the risk of carcinogenesis from so-called "spontaneous" or 
"natural" causes. Now, virtually everyone in th:e cancer field considers 
that the so-called "spontaneous" causes of cancer are ,at least 
to the extent of some 90% of all causes, environmental factors of a 
variety of sorts. á In the case of lung cancer in man, it is widel y 
accepted that the environmental factor is the smoking of cigarettes , 
and it is widely considered that cigarette smoking is responsible for 
90 % of all human lung cancers. To my knowledge the onl y contrary 
opinion is th at of the tobacco ~industry, which is hardly the surprise 
of the century . If radiation acts as a multiplier of "spontaneous" 
cancer, the corollary is that it will, in general, act as a multiplier 
of the cancers caused by the environmental factors that are the basis 
for so-called "spontaneous" cancers. Is thi s reasonable? Particularly 
in the case of lung cancer induced by alpha part ic le radiation which 


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is at iss~e here, is . this reasonable? The answer is overwhelmingly 

in the affirmative. An excellent study was reported by Lundin et al 

(Lundin, F.E., Jr.,Wagoner, J.K.,Archer, V.E. "Radon Daughter Exposure 

and Respiratory Cancer:Quantitative and Temporal Aspects" NIOSH-NIEHS 
Joint Monograph No.l US DHEW,1971.) 

contrasting the effect of alpha particle irradiation of uranium miners 

in the production of lung cancer in cigarette smokers versus non


smokers . They demonstrated that the effect of radon daughter alpha 
particle exposure was approximately ten times higher in the cigarette 
smokers than in the non-smokers for production of human lung cancer. 

It would take the utmost mayhem with these results to interpret the 
radiation as anything but á a multiplier. These results are very direct


ly relevant since they arise from high LET radiation ( alpha particles) 
which is at issue with respect to plutonium radiation. But there have 
long existed data concerning radiation as a multiplier for low LET 
radiation as well. The studies of Stewart and her colleagues on the 
effect of pre-natal radiation (X-rays) in induction of cancer and 
leukemia in childhood are by now classic. A prime result of those 

studies was the demonstration that cancers and leukemias were induced 
by radiation in proportion to the "spontaneous" occurrence of those 
diseases. 

Among those who fail to understand this problem there seems 
to exist the mystical idea that the relative risk method and the 
absolute risk method give rise to different answers concerning the 
number of cancers per rem of ionizing radiation. Nothing could be 
further from the truth. Both methods must give the same answer or 
one of the methods is simply not correct! The virtue of the relative 
risk method is that it enables predictions in situations where actual 
experimental data are unavailable. Should the results of the relative 
risk method ever predict any result at variance with absolute risks 
as measured, one would have to give up the relative risk methoq. That 
has not yet happened .in any study with reliable,meaningful data. 

A crucial feature of the relative risk method is its prediction 
that the multiplier for radiation is very sensitive to the age at 
irradiation. In CNR-2, Gofman reproduced a table (Table lV from Reference 
10 cited there) showing how the percent increase in cancer 
mortal i ty per rad varies with age. For the 21-30 year age group (and it 
is this age group that CNR-1, CNR-2 and JAMA explicitly address ) the 

value is 2 % per rad. For the 41-50 year age group the valu e drops to 


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0.5 % per rad. Gofman and Tamplin published a report in 1970 
Gofman, J.W . and Tamplin, A.R. "Radiation-Induction of Human Lung 
Cancer", Hearings of the Joint Committee on Atomic Energy, January 
28, 1970) pp. 389-399. 

which presented the doubling dose for radiation induction of human 
lung cancer based upon the Japanese studies of Wanebo et al. That 
doubling dose was estimated to be 79.7 rads and applied to a population 
of Hiroshima~Nagasaki subjects over 35 years of age. A value 
of 79.7 rads as a aoubling dose corresponds to 1.25 % per rad. Just 
recently the extended data from Japan have appeared in a paper by 
Beebe and Kato from which the per cent increase in cancer per rad 

Beebe, G.W. and Kato, H. "Review of Thirty Years Study of Hiroshima 
and Nagasaki Atomic Bomb Survivors II. Biological Effects,E. Cancers 
Other Than Leukemia '',Journal of Radiation Research, Supplement, 
pp. 97-107, 1975. 

for lung cancer can be estimated. The data of Table 1 ( reference just 
cited) give a relative risk of 140 % for the group having received between 
10 rads and 100 rads and a relative ris k of of 2 0-0!%for the 
group having received over 100 rads. The mean dose for the 10-100 
rad group cannot be f ar different from 50 rads. It would be a conservative 
estimate to assign a value of 200 rads for the group over 
100 rads. These data then translate into 0. 8% per rad for the 50 
rad mean, and into 0.5 % per rad for the 200 rad mean. Since there 
i s no overt reason to weight one group more than the other, the final 
best estimate is 0. 65 % per rad. It is virtually certain that this 
value is too low, though we shall not alter i t. The reason it is too 
low is that all cancers developing between 1950 and 1972 are i n cluded. 
This means that part of the observation period was during the latent 
period for lung cancer development. Thus spontaneous cancers occur 
during the latent period, but radiation-induced ones do not, giving a 
f alsely low value for the radiation-induced cancers relati v e to the 
spontaneous ones. The earlier estimate áof Gofman-Tamplin of 1. 25 % per 
rad is probabl y closer to the true v alue, but since it is an estimate 

o f the effect of including part of the latent period , we shall not 
i nsist on it here, and shall accept the 0 . 65% per rad fi gu re that 
comes out of the extensive recent Japanese data. Beebe a n d Kato are 
quite explicit in stat i ng that these data refer to t hose who were 35 
years of age or older at the time of bombing. They do not provide 

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the mean .age at time of bombing for this group, but that mean age 
canno _t possibly have been far away from 45 years .. If we use 45 years 
we shall be conservative. So, for a group of meáan age of 45 years 
we have a mean value of 0.65% increase in cancer per rad, versus 
a value of 0.5% predicted by Gofman and Tamplin through the relative 
risk method. Calculating back to persons 21-30 years of age, the new 
Japanese data would suggest 2.6% per rad rather than the 2 % per rad 
utilized by Gofman in the Gofman-Pu papers. If anything ,therefore, 
Gofman underestimated the cancer hazard of radiation. 

The ERDA lab critiques suggest that Gofman should have used a value 
of 0.2 % per rad ( actually 0.19%) to be found in table f-2 of the 
BEIR report. This suggestion is so absurd on the face of it that it 
shouldn't require explanation, but apparently explain we must. First of 
all the BEIR value is for people~ 35 years of age~ Actually the 
BEIR committee erred in that table because they label the group as 
ha v ing a~ age of 35 years! Beebe and Kato are explicit in pointing 
out that even now they are unable to addres~ the issue of persons 
under 35 years~ The most probable estimate of true mean age for the 
group was 45 years or more. Since the Gofman-Pu papers address the 
risk for persons 21-30 years( and most explicitly so ) , it would be 
appropriate to multiply that 0.2% value by four, giving 0.8% . But 
this is only the beginning of the error that would occur using the 
crude tabulated value from BEIR. The BEIR Committee recognized this 
in a very important paragraph which is here reproduced from p.156 
of the BEIR report; 

"All four of these groups are still under investigation, 
and it is probable that because of the long latent period for 
lung cancer, the rates calculated will rise as further cases 
develop. This is particularly true for the spondylitis patients. 
It is possible , therefore, that in the final analysis the 
absolute risk in these groups will approach 2/ 106 / year / rem 
and the relative risk reach 0.5% or higher. For the three 
groups ( miners and Japanese survivors in which up-to-date 
information is available,)it is significant that many new 
cases have been added in the past few years." 

Note that even the 0.5% figure suggested would have to be corrected 
to convert the value to that appropriate for 21-30 years of age. So, 
the BEIR Committee very explicitly tells us that the value in the 
table is outdated, is contaminated by cases in the latent period, 
and that á hence that value may be serio~sly low. The BEIR Committee 
provides some gu i dance as to how high the value might go. All Gofman 
Values with a star ( *) refer to age at time of bombing. 


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did was to read ~hat the BEIR Committee said about its own values. 
The ERDA lab critiques would suggest that reading is out of st y le. 

There is no rational way that the criticism that Gofman used 
too high a value for relative risk per rad will stand up. If we 
add to this the fact that the most recent extensive Japanese data 
suggest Gofman may have underestimated the value for relative risk 
per rad, it would appear that this ERDA Lab criticism falls of its 
own weight unequivocally. 

Lastly on the issue of estimation of risk per rad, some of the 
ERDA lab critiques have exhumed the Nean .dert h al argument that the 
.linear hypothesis should not have been used b y Gofman in the GofmanPu 
papers . There is every reason to have used t he linear hypothesis 
in estimating the lung cancer hazard of plutonium. First of all, it 
represents public health respo~sibility, instead of irresponsibility 
as has been pointed out by virtually . every serious group concerned 
with radiation protection. That the National Council on Radiation 
Protection and Measurements might not concur is hardly surprising 
for this is the same nuclear industry hack organization that in 1954 
stated that 36000 millirems would be without ph y sical effect on man. 
The Environmental Protection Agenc y , in its 197 6 rule-making on 
radiation standards , has just rejected the NCRP suggestions. But 
public health responsibility is only one reason why the linear hypothesis 
should be used . Let us consider the e v idence abundantly 

available to us . 

1. Referring to the Spiess-Mays studies (Spiess,H, Mays, c.w., 
"Bone Cancers Induced by 224Ra (ThX ) in Children and Adults", Healt h 
Physics, Vol. 19, Dec . 1970 , pp 713-7 29) the BEIR Committee sta t ed 
the following; 
"T h e data for the 224Ra-injected patients are consistent wit h 
the linear nonthreshold dose-response cur v e wit h in t h e limit~ 
of the dose range a v ailable and when the dose is expressed as 
mean dose to bone." 

It is worth noting that these studies are for hi g h LET alpha radiation 
in humans, the same type of radiation as for p lutonium. 


2. The data on Ra22 6 i nduction of bone cancer in man ha ve 
been re-anal y zed b y se v eral workers after Ev ans clai med that those 
data were inconsistent with t h e linear hypot h esis. One such refutation 
is by Gofman,J.W. and Tamplin, A.R. "The Qu estion of Safe Radiat ion 

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Thresholds for Alpha Emitting Bone Seekers in Man", Health Physics, 
Vol. 21, July, 1971, pp 47-51. Again, these are data for high LET 
alpha radiation in humans and they are consistent with the linear 
non-threshold hypothesis. 

3. In an analysis of the induction 0£ lung cancer in the uranium 
miners, Gofman and Ta mplin showed that the doubling dose in workinglevel-
months for radon~daughter induction of lung cancer showed no 
evideace of increasing at the low dose ranges, a fact supportive of 
the linear, non-threshold hypothesis. Indeed, in that analysis what 
variation in doubling dose occurred suggested, if anything, that . the 
radiation effect might be even higher than predicted by linear thesis 
for the low-dose region. (Gofman, J.W. and Tamplin,A.R. , "The Colorado 
Plateau: Joachimstahl ' Revisited: An Analysis of the Lung Cancer 
Problem in Uranium and Hardrock Miners" Testimony presented at the 
Hearing of the Joint Committee on Atomic Energy, 91st Congress of the 
United States, Jan. 28, 1970, and GT-106-70.) 
4. E.E . Pechin, in a very recent paper ( Pechin, E.E , "Radiology 
Now: Malignancies Following Low Radiation Exposures in M~n" British 

Journal of Radiology, Vol.49, No . 583 , 577-579, July 1976) has com


mented that for the low LET radiation (X-ra ys) exposure of infants


in-utero, the r isk of malignancy is linearly related to dose. The 

direct quote of Pechin follows ; 

"The inference that the radiation caused malignancies was, 
however, questioned at first. For example, a sub-group of 
mothers might have been more frequently X-rayed than mothers in 
the control group because of hereditary abnormalities, e.g. of 
the pelvis , and this sub-group might have a preponderance of 
children wh::>developed malignant disease as a result of some 
associated congenital abnormality. 

Such a source of bias now appears to be excluded, however, 
by two considerations. Firstly, Stewart and Kneale(l970) showed 
that the likelihood of subsequent malignancy per examination 
increased about linearly with the number of films used in the 
examination, where this number was known ...... " 

Linearity, for these studies, covers the range of about Oto a few rads, 

and for low LET radiation at that. 

Itappears that the public health problem of radiation protection 
will not indefinitely be burdened by the old crowd of AEC diehards, now 
wearing ERDA gowns . There are, after all, retirement rules and time has 

a way of mar c hing on. 


-13


Conclusions: 

The critiques of the Gofman-Pu papers have been con sidered 
here in detail, with respect to the points deserving serious 
comment and those critiques are rejected in toto. Some very trivial 
criticisms from the five ERDA Lab critiques will be dealt with in 
the Appendix to this testimony. The only reason to deal with them 
at all is to re-assure the reader that major gems do not exist there 
which cannot be answered. 

I therefore suggest that the NRC in its GESMO consider ations 
accept the estimates of plutonium lung cancer hazard precisely 
as they appear in the three Gofman papers which are part of 
this testimony, CNR-1, CNR-2, and JAMA. It is my considered opinion 
the GESMO must deal with the consequences of those estimates if the 
NRC chooses to be responsible in its mission. 

Future evidence may show that the Gofman estimates are 
correct as they stand, are too high, or are . too low, as Gofman has 
clearly and explicitly stated in tho se reports. And if and when such 
evidence ( not wishful thinking) appears, the estimates can be appropriately 
altered, if necessary. There does exist one possible source, 
aside from the issue of T~ of clearance,that could force some down ward 
revision of the lung cancer hazard of plutonium from that estimated 
by Gofman. If some of the energy of alpha particle decay is 
expended in cells other than those at risk for carcinogenesis or is 
expended in mucus , the true dose to the cells at risk would have been 
overestimated. But we simply do not know the physical distribution 
of the plutonium that is retained long-term, so there is no way now 
to estimate whether a correction is needed or how large it might be. 
A correction of the order of two-fold is by no means inconceivable. 
On the other hand there is also the possibility that the RBE factor 

should have been chosen as 20 instead of 10, whic h would introduce 

a factor of two in the opposite direction. Probabl y other minor 

factors will occur to alter the estimates. This is why Gofman suggested 

that the final result might be a factor of t wo or thre e too high or 

too low (JAMA, p285 ) . The key point is to realize t hat any correction 

r equired could go either way , and hence from the public health point 

of view there is no basis for optimism that the result predicts too 

high a carcinogenicity. Until such time that evidence dictates a change 

in estimate, any action based upon hopes the the risk estimates are 


-14


too conservative is clearly irresponsible public health practice. 
GESMOá i .s necessarily a public heal th document in addition to its 
functions in describing other aspects of the use . of mixed oxide fuel. 

In the immediately preceding discussion, possible so.urces of 

correction of the Gofman estimates of the lung cancer hazard of 
inhaled plutonium by a factor of 2. or 3 one way or the other are 
considered. However any such possible corrections turn out will 
not alter the fact of the enormously greater carcinogenicity of 
plutonium as demonstrated by the Gofman analysis versus prior 

analyses of this problem. The plutonium carcinogenesis as estimated 
by Gofman is of the order of 1000 times greater than prior estimates, 

(or of some current "we hope and pray" estimates} So corrections 
of a factor of 2 or 3 will not alter the major revisions in all 
its thinking that NRC will have to do to bring GESMO anywhere near 
the realm of the real world. 


-15


APPENDIX 

Responses by J.W. Gofman to the Minor Issues Raised in the ERDA 
Lab Critiques 

l. Document: "Review of John W. Gofman 1 s Reports on Health Hazards 
from Inhaled Plutonium" Chester R. Richmond, ORNL/TM-5257, February 
1976. 
Point No. l Richmond states, p.2, " It would appear that Gofman 
is completely dismissing the hot particle arguments, yet it is not 
clear until one reads the paper that he leans heavily as he derives 
his risk estimate s upon the argument of a large reduction in the 
mass of the presumed critical target tissues within the lung." 

Answer Gofman had no need whatever to address the hot particle 
arguments in this work, so he had no occasion either to accept or 
dismiss hot particle arguments. A bit of reading would help Dr. Richmond 
on this mis-statement of his. Dr. Richmond also complain s 
that one must read Gofman 1 s papers in order for it to become clear 
what Gofman has done . I hardly think it is unusual to have to read 
a paper to understand it. 

Dr. Richmond is indeed correct that Gofman leaned heavily 
upon the argument of a la r ge reduction in mass of the presumed 
target tissues within the lung. In fact a reduction factor of 570, 
thorough l y justified by the fact that it is the bronchial cells one 
must consider if bronchogenic carcinoma is at issue! I doubt very 
seriously that Dr. Richmond can find any scientific support for 
inclusion of irradiation of blood vessels, nerves, alveolar tissue, 
terminal bronchiolar tissue , or other tissue in determination of 
the radiation effect upon bronchial cells in the production of 
bronchogenic cancer . I believe Dr . Richmond would make as much sense 
to include those extraneous tissues in the critical mass as to in clude 
the mass of the ass. There are some rare instances in carcinogenesis 
where indirect effects of radiation can have effects 
upon carcinogenesis.Thus radiat i on injury to a hormone -producing 
target may increase tropic hormone output of the p ituitary and thus 
have influence . I doubt very much that we are dea l ing wi th any t hing 
like this in eliminating the extraneous lung tissues for the critical 
target assessment here. Second there is the relation of immune 
suppression that may operate to accelerate carcinogenesi ;s. It is 


-16


inordinatel y doubtful that elimination of extraneous lung tissue 
from the mass of critical bronchial cells could possibly lead to 

o v erlooking a significant immune response in the carcinogenesis 
process in the bronchial cells. 
Point No.2 Dr. Richmond states that if Gofman's T~ of 509 days 
in the .damaged bronchial areas were true,the"lungs of many heavy 
smokers would obviously become rapidly filling reservoirs for all 
sorts of atmospheric contaminants and particulates and perhaps, 
mor e important, if large regions (whatever anatomical reference this 
might have) were severely damaged by loss of cilia resulting in 
e x tremely long clearance half-times, the affected indi v iduals would 
most probably d rown in their own fluids." (Direct quote of Richmond) 

Answer: Dr. Richmond has simpl y missed the entire point about what 
is being discussed. The subject, Dr. Richmond, is highly insoluble 
pa~ticulates of Puo 2and possibl y other hig~ly i nsoluble particulates. 
So Dr. Richmond's concern .; about fluids is simply absurd. Equally 
foo lish is c oncern about "all sorts of atmospher i c contaminan t s" , 
a lar ge proportion of which are soluble and hence not even at issue. 

M>reover, it i s still a hig hl y open question as to why Pu02 particulates 
are retained so tenaciously when they are. The . alpha activity 
out .

h a s not been ru l e d/ as a f actor. The densit y of the part i culates, 
ve r y high f or Pu0 2 compared with most atmospheric insoluble particles 
is undoubtedl y i mportant. On a q uantitative basis Dr. Ri c hmond would 
be ex tremel y ha r d -pr e ssed to show that the insoluble, high-dens i t y , 
al pha -particle emitt i ng particulates of atmospheric contam~nants 
would, according to the Gofman thes i s, lead to an y bl ockage of ~he 
ai rwa y , to sa y nothing of such nonsense as "dr owning i n their fluids . " 
Lastl y I would a dvise Dr. Richmond to have a hard look at the Radfo r dMartell 
data d i scussed in the bod y of this testimon y , which data 
suggest order-of-magnitude(at least) agreement with Gofman's T~ 
valu es for the hi ghly insoluble Lead-210-conta ining particulates 
fro m mai nst r eam smoke of c igarettes. 


Point 2a: Here I shall take up an expansio n of Poi nt 2 concerning 
possibl e ai rway blockage si nce in one form or another it oc curs in 
al l f i ve of t he ERDA Lab critiques. The Los Alamos crit i que comments 
on the amount of dust that might accumulat e although there is not a 


claim of air way blockage . The other four crit iques claim, outri ghtly 1 


-17


that airway blockage would occur if Gofman's T~ of 500 days for 
highly insoluble Pu0 2 particles were correct for injured regions 
of bronchial epithelium. This assertion is simply absurd,as will 
now be demonstrated in extenso. 

In the Los Alamos critique, Healy et al state the following; 

"Secondly, using his values for the quantity in the bronchial area 
(2.7%) retained with a long half-life (500 days ) a mechanism of entry 
into the tissue would predict that, for a normal dust concentration 
of 100pg /m 3, the one gram of bronchial epithelium would accumulate 
at equilibrium some 39 mg of dust." 

Let us accept the correctness of the Healy et al calculation 
that the accumulation would be 39 milligrams. Healy et al then go on 
to state the following; 

"Of course , in industrialized communities, the actual concentration 

in the air may be several times the 100 ,ug/m3 assumed above." 

Let us grossly exaggerate the problem by not only crediting 

the air concentration as "several times the 100 .g / m3~ but by assumi ng 
anair concentration of one hundred times the 100 ug / m3, a rash assumption 
indeed. We would,therefore, have to multiply Healy's value of 
39 mg of dust by 100, gi ving an accumulation of 3 .-9 grams of dust. 

I'll accept, for ras hn ess' sake, that Healy's calculation that 

all atmospheric dust will behave like insoluble áPu02 aerosol is 

correct ( rash, indeed, but let us assume it nevertheless). Our 

objective now is to estimate how much airway reduction occurs if the 

accumulation in the c rucial bronchial areas is 2. 7% as assumed by 

Gofman . 

In CNR-l R, p.16, Gofman presented a value of 0 .115 cm . as the 

radius of the relevant intrapulmonary bronchi. On p.17 of that same 

reference he calculated the surface area of such bronchi to total up 

to 361 cm2. 

The cross-sectional area of the lumen of such bronchi is ""TT r2, 

which for a radius of 0.115 cm is 3 . 1416 x (0.115 ) 2 , or 0.0415 cm2. 

Now let us calculate how much cross-sectional area is sacrificed to 

accomodate 3 . 9 grams of dust. Let u s start by assuming a uniform 

distribution of the dust over the surface area of all the relevant 

bronchi, which is 361 cm2. Leth= the height of the layer of dust. 

For mass equality, we have the following relation: 

(Height)x(Area)x(Density ) = Mas s of dust. 


-18


As a reasonable value for the dust we shall use a density of 2 grams/ 
cm3 ( noting that Pu02 is much more dense than this). Substituting, 
(h)X 361 X 2 = 3.9 


h = 3.9 / 722 = 0.0054 cm. 
This value of his, to a close approximation, equal to the radius 
reduction for these bronchi after dust accumulation. The new radius 


(post-dust collection) is 0 . 115-0.0054 = 0.1096 cm. The cross-sectional 
area of the reduced lumen is TT r2, or 3.1416 x (0.1096)2, or 
0.0377 cm2. This means that the reduced lumen area is(0.0377 / 0.0415) 
times 100, or 90 . 8 % of the original lumen area. Expressed otherwise 
the loss in lumen area is only 9.2 %. This is so little reduction, 
even for the extremely unrealistic, rash assumptions used, that it is 

absurd to speak of airway blockage. The variations in lumen diameter 
from smooth muscle contractions in the bronchial wall will be far 
greater. Now the issue can be raised that the dust will only accumulate 
over the injured bronchial regions, so that the layer would be 
raised there. That is true, but irrelevant. Even if the ~dust" is 

irregularly d istributed , the approximate cros s-s ectional area lost is 
still the same. 

The final conclusion that must be drawn is that the co ncerns 
of all the five ERDA Lab critiques concerning airway blo ckage is 
ridiculous indeed, since even makin g rashly worse assumptions than 
they did, the blockage is insignificant. Snipes e t al, in the 
Lovelace Foundation critique ,made a c alculation that if all the 
smoke inhaled with the smoking of 20 ciga rett e s p er day were to 
behave like insoluble Pu02 aerosols ( an assumption that is not i n 
the rash clas s, but rather in the wild blue yonde r ) then there would 
be a bout 6 .4 grams accumulat ed in the relevant bronchi . This is 
fol.lowed by the completely guessstimated opinion that " Thus , ve ntilat 
io n would cease or be seriously impaired in heavy smokers . " 
Had Snipes et al taken the trouble to calculate the airway reduction 
by the methods above , he would have found that the radius reduction 
is(6.4 / 3.9) x 0.0054, or 0.0089 cm, the reduced lumen area is 0.0354 
cm, a nd the final ar ea remaining is 85.2% of the original area 


(0 . 0354 / 0 .04 15) x 100), and this means a loss of 14 . 8 % of the airway 
cro ss-section ----fa r, far from "ventilat ion would cease or be seriously 
impaired". And al l this assumes some reas onableness fo r the assumption 
that all ciga ret te smoke be have s like insoluble Pu02 ae rosol. 

-19


Point 3: Richmond go~s through a long discussion of Gofmah's demonstration 
that Hempelmannoverestimated the body burden of the Manhattan 
Project workers by a factor of 14. I thought he was going to 
show that it was an incorrect critic .ism;instead he finally ended up 
admitting that many sources of new data would suggest that Hempelmann 
was wrong by a factor of ten in using urinary excretion data 
to estimate body burden. A factor of ten frow experimental data 

is an excellent confirmation of Gofman's factor of 14. And as for 
the use Gofman made of the factor of 14, the same gen era l conclusion 
would have been arrived at with a factor of 10 . So this issue needs 
no further elaboration. 

Point 4: In a wild , blatantly false statement on p. 12, Richmond 
states the following; 

"The summary and conclusion section of Gofma:a's paper(CNR-1) 
states that there are 7.83 x 109 " lung cancer doses" per pound of 
plutoniu m. He neglects to point out in this se ction , howeve r, that 
this estimate--if true is per pound of plutonium deposited in 
the lung': 

To show how ridiculously false Richmond's assertion is, I shall 
quote the summary and conclusions section on this subject from CNR-1 
of Gofman: 

" For cigarette -sm okers: 

Pu23~ 

(a) 0 .058 micrograms d epos ited Pu239 represents one 
"lung cancer-dose". . 
(b) 7 , 830,000,000 "lung cancer doses"per pound of Pu239 ." 
It is hard to se e how Gofman could hav e more explicitly indicated 
he wa s referring to DEPOSITED plutonium . He defined the" lung cancer 
dose" in terms of deposited plutonium, and that definition is used 
to give "lung cancer do ses" per pound. What could be~ straightforward? 
Perhaps an opthalmological examination is in order. 

The follow -on to this nonsense is even worse in Richmond 's crit ique. 
He says that the unsuspecting reader might incorrectly calculate 
10 13 

to 1014 lung cancer deaths for the five to seven tons of pluton ium 
produced as weapons fallout . On the very next page of Ric hmond's 
own report he then quotes Gofman's own calculation of 1,00 0 ,0 00 deaths. 
Any reader who calculates 10 13 deaths, with a number of 10 6 deaths 
explicitly stated , would simply be totall y incompetent . 

Summary concerning Richmond's cr i tique; There is absolutely nothing 


-20


that can be taken seriousl y in the Richmond critique. It should 
be totally and unequivocally rejected in its entiret y . 

2. Document: "Comments . Prepared by 
gical and Medical Research, Argonne 
Illinois 60439, October 8, 1975. 
Dr. 
NatiD. Grahn , Di v ision 
onal Laboratory, Aof 
rgoBiolo 
nne, 
Point 
1: Grahn states the 
"Gofman then rederives 
following 
risk in 
on 
terms 
page 
of" 
1 of his critique; 
lung cancers per pound 

of plutonium" . This seems algebraically acceptable and technicall y 
it is a kind of extension of the "man-rem" concept. However, scientificall 
y it is inappropriate because it does not allow for the allimportant 
factors of atmospheric dispersion and dilution . " 

Answer: This is á sheer nonsense . Gofman derived all estimates of risk 
in terms of deposited plutonium, clearly, explicitly , and unequ iv ocally 
. In no way can this be mis-interpreted as risk related to 
released pl u tonium. It should be totally obvious to Grahn that t h e 
factors of dispersion and dilution were clearl y taken into account 
in all uses made by Gofman of the risk of lung cancer. All that can 
be said further to D~. Grahn is,that when all else fails when one 
is criticizing a manuscript,it pays to read the man uscript. 

Point 2: Grahn states the following on page 2 of his criti que; 

" A rather serious misconception is entrained in Gofman's discussion 
of the residence time of particulate matter on the bronchiolar 
epithelium in regions where cilia are absent. The assumption 
that epithelial residence half-time would be 500 da y s in the bronchioles 
, as emplo yed for the alveolar regions , is not supported 
by evidence." 

Answer: Gofman made abundantly clear that, for Plutonium aerosols 
in the bronchi of cigarette smokers, there simply existed no e vi dence, 
and that, as a result, reasonable assumptions were being 
made. Indeed, since that time, the Radford-Martell áe v idence did 
appear concerning long residence half-times ( see main body of t h is 
testimony ) for insoluble particles in the bronc h i o f ci g arette 
smokers. Of one thing we can be certai n ---Dr . Grahn certain l y presented 
no evidence to contradict the Gofman T~ estimates. As h e goes 
on in his discussion he cites the work of Albert et a l in donke y s. 


-21


Several of the critiques cite the work of Albert, either for 
donkeys or humans, as evidence showing áthat a long clearance halftime 
cannot obtain for Pu0 aerosols in the injured bronchial epi


2 
thelium . The Los Alamos critique presents a d etailed l isting of the 
papers by Albert and his colleagues. It can be stated flatl y in 
response to Grahn and all the others who cite Albert et al on this 
subject . that the Albert work simply cannot address the question of 
a few percent long-term retention of insoluble aerosols in the bronchi. 
The very definition of bronchial clearance by Alb ert by his methodology 
would exclude long-term retention from the bronchi. It is to the 
credit of the Los Alamos group's critique that th ey recognized 
clearly that the Albert work cannot bear upon the Gofman thesis at all. 
Th~stated on page 7 of their critique the following: 
" However, on careful examination these experiments would not 
detect the increased retention in the bronchial region postulated by 
Gofman since this fraction would be considered as pulm onary deposition 
and the normal fluctuation among individuals is too great to detect 
the Gofman assumption of 2 .7% deposited in t h e bronchiolar region." 

To this, I can only say "Amen, it is nic e to see that somebody 
understands the literature." Richmond, Bair, Grahn, and Snipes, 
representing 4/ 5 of the ERDA Lab critiques , all grossly misu se the 
Albert data in their efforts to refute the Gofman thesis. I t is 
regrettable that they indicated such a total lack of understanding 
of the problem at hand. Essentially the same can be said for the 
misuse by some of the critiques of related data of Lourenco et al. 

Summary Concerning Dr. Gra hn 's Criticisms: 

Aside from the items mentioned above,Dr. Grahn's comments and 
erroneous calculations are amply covered in the issues discussed in 
the main body of this testimony. I c onclude that no ne of Dr. Grahn's 
points are valid in any way. I reject each and every one of his 
criticisms as erroneous. 



-22


Document 3: Bair, W.J . . " Review of Reports by J.W. Gofman on 
Inhaled Plutonium" BNWL-2067 / UC -41 , October 10,1975, Battelle 
Northwest Laboratories. 

The major points of Bair!s critique are thoroughly refuted 
in the main body of this testimony. Some of the minor points are 
those where Bair erred as did other ERDA laboratories,and they are 
covered with mention of Bair in the discussion of the specific points 
for the other ERDA critiques. 

Point 1: Bair makes the point that it is possible that some of the 
plutonium alpha particle energy is lost in mucus or in metaplastic 
cells other than those which are subject to carcinogenesis. 
Answer: As conceded in the main body of this _testimony, Gofman agrees 
with Bair that it is entirely possible that some correction may have 
to be made for such effects. But neither Bair nor anyone else has 
presented any evidence that such a correction is of consequence or . 
even an order of magnitude of possible size. Only some real data can 
help us here. 

Point 2: Bair . states(on page 9 of his critique)the following: 

"If Gofman's premise that clearance á of plutonium from lungs of 
smokers is greatly impaired is true , human autopsy data should be 
showing much higher lung burdens of plutonium in smokers than in 
non-smokers . This has not been revealed in the results published to 
date. " 

Answer: Patent nonsense! It would be a revelation indeed if Dr. Bair 
could point out a single published study of human autopsy material 
that has been studied in a manner to test whether insoluble Pu0 2 
aerosols are retained in cigarette smokers to the extent of 2.7 % 
versus 0.2 % in non-smokers. This would have required meticulous 
analysis of relevant bronchi versus lung parenchyma. While such data 
~~u ld help resolve the problem, Dr. Bair seems unable to point such 
data out to the world . Moreover, the analysis of autopsy material 
obtained a long time after the exposure( more than a couple of clearance 
half-times) would be unsatisfactory even if a careful dissection 
of bronchial epithelium were made to compare with lung parenchyma . 

¥ 



-23


Summary Concerning Dr. Bair's Criticisms: 

The maj6r points of Bair's criticisms are adequately dismissed 
as erroneous in the main body of this testimony since they deal 
with such issues as the T~ of 500 days, the use of the linear hypothesis, 
and the BEIR Repo rt estimate of the relative ri s k per 
rad ---all of which is disposed of there. The one point concerning 
a pos sible correction of alpha energy absorbed in mucus or non -relevant 
cells is a valid point and has been discussed above . There is 
nothing else in the Bair critique that is valid, and hence aside 
from this one point, all else in the Bair critique is rejected in toto. 

Document 4: Snipes, M.B., Brooks, A.L ., Cuddihy, R. G. , and McCl ellan, 

R. O. "Review of John Gofrnan's Papers on Lung Cancer Hazard From 
Inhaled Pl utonium" , L F-51 / UC-48 , Lovelace Foundation for Medical 
Education and Research, P.O . Box 5890, Albuquerque, NM 87115. 
The major points of this critique have already been dismissed 
either in the main body of this testimony or in the discussion of 
other critiques which share the erroneous anal ysi s of this critique . 
There is one point worth me ntioning , ridiculous as it is . Incredibly, 
the Snipes critique states the following; 

"Gofman states that his . approach does not involve the "hot 
particle" hypothesis which pr2cipit~ted considerable controversy in 
1974. However, hi s approach to this problem i s in fact an extension 
of the hot particle hypothesis." 

Answer : "Incredible" is far too weak a word to describe this absurd 
assertion by the Lo vel ace workers. There are only two po ssibilities . 
First, the Lovelace worker s don't have th<~ foggiest notion of what 
the "hot part.Lele " hypothesis is all about. Second, t.h ey don't under stand 
anything they ostensibly read in the Gofman-Pu paper s. On 
second thought, a third possibility must be entertained, namely, the 
Lovelace workers understand neither the "hot particle" hyp othesis nor 
what they ostensibly read in the Gofman -Pu paper s. See footnote, p . 26 ) 

Summary Concerning the Lovelace Foundation Critique: It is impossible 
to find a single item in this critique that has any v alidity at all. 
Everything in this critique is therefore re jected unequivocally and 
totally. 


-24 


Document 5 : Healy, áJ.W., Anderson, E.C. , Mcinroy, J.F., Thomas, R.G., 
and Thomas, R.L. "A Brief Review of the Plutonium Lung Cancer 
Estimates by John W. Gofman" , LA-UR-75-1779, Los Alamos Scientific 
Laboratory, Los Alamos, New Mexico, October 8, 1975. 


There are a few minor points to address specifically in the Los 
Alamos critique. A generai commentary follows in the Summary concerning 
this critique. 

Point 1: The Los Alamos workers raise the question as to whether the 
Auerbach data can be directly described ih terms of percent of cilia 
lost in cigarette smokers. The Auerbach data give a composite measure, 
namely percent of slides showing two features , loss of cilia plus 
an average of 4 or more cell rows .in epithelial depth. According _ to 
this criterion of scoring slides, a slide with total absence of cilia 
but with fewer than four cell rows in depth would be scored as negative. 
Inasmuch as cilia loss is , in all likelihood, a lesser degree of 
damage than metaplasia or hyperplasia, cilia loss mightoe expected 
to be even more frequent a finding than is indicated in the Auerbach 
tables. Because of this uncertaint y in the appropriate use of the 
Auerbach data, Gofman sought data that are unequivocal on the issue 
of per cent of cilia lost in smokers . Such data are published by 
Ide and co-workers, and are referenced in JAMA by Gofman. The Ide 
publication shows 30 % ciliary loss in cigarette smokers, whereas 
Gofman used a value of 25 % as his interpretation of the Auerbach 
tables. Thus it turns out that any revision of the estimation of 
the lung cancer risk in smokers , using the Ide data,would make 
the plutonium risk somewhat worse than estimated by Gofman. 

Point 2: The Los Alamos workers point out that some data indicate 
very long -term retention on part of the plutonium deposited in the 
lung---much longer than would be suggested by a T~ value of 500 
days for clearance . They suggest, therefore, that Gofman's criticism 
of the Hempelmann estimates of body burdens in the Manhattan Project 
Workers may be somewhat too severe. Unfortunately ; this finding of 
some very long-retained burden in the lung does not allow for such 
a simple interpretation. First of all , there are small lymph nodes 
in the lung, other than the large masses of nodes in the tracheobronchial 
reg i on. It is entirely possible that some, or even most, 
of the residual burden is in lymph at ic tiss ue and not in . true lung 


.. 


-25


.tissue. Second, even if the residual burden is in true lung tissue, 
there would be a world of difference if the burden is in the bronchiolealveolar 
region versus being in the bronchial tissue( that is , the 
bronchial tissue relevant for bronchogenic cancer.) If the burden is 

in the bronchiole-alveolar tissue, the concentration of plutonium 
would be estimated to be 570 times lower there than in the bronchial 
tissue , with its corresponding marked reduction in radiation dose 
due to the factor of mass of tissue. Additionally, t~e intrinsic 
risk of bronchiolo-alveolar cancer, "spontaneously" is very much 
lower than that for bronchogenic cancer. Bair , in his critique, 
referencesDeLaRue et al, (Cancer, 29, 90-97-1972 ) as giving a value 
for bronchiole-alveolar cancer representing only 3-6% of the total 
number of lung cancers both in smokers and non-smokers. Thus , if 
any especially . long-term retention does exist , it is of the utmost 
importance to know precisely where in the lung it is. If it is in 
the parenchyma, the estimated risk by Gofman would hardly be much 
~ncreased, contrasted with an estimated risk elevation á that would be 

required if the long-term retained material is in the bronchi. 

Summary Concerning the Los Alamos Lab Critique: There are a number 
of minor points that could be addressed additionally concerning 
the Los Alamos critique. However, the following quotation from the 
Los Alamos paper indicates it is not even worth going into these 
minor points in deta i l. The final section of the Los Alamos paper 
has the quotation on pages 17-18. I quote, 

"T,ye would recommend that measurements continue with more emph 
asis on the absolute bronchial retention, and that until such 
e vi dence is available, the Gofman predictions be regarded as interesting 
and ima g inative speculations which should serve to stimulate 
i nc reased interest in certain phases of current studies. " 

Let us translate what the Los Alamos group i s say ing to ERDA. 
They are sa ying , in plain English , we don't hav e the ability to say 
whether Gofman's estimates are correct or not correct, and we aren't 
goiI1:ItO know until there are more data. 

The message should be pretty clear for GESMO. The NRC draft of 
GESMO makes all kinds of comments about the radiological hazards 
of mixed oxide fuel use util iz ing a hazard estimate for plutonium 
inductio n of lung cancer that may 1000-fold or so too low. In view 
of the Los Alamos admis s io n on this point, the re is no conclusion to 


., . ~ á. -~ 

-26


be drawn other than that which follows. The NRC draft of GESMO 
is simply incompetent on the issue of plutonium toxicity. If the 

NRC persists in using such an incompetent .estimate of the lung 
cancer hazard of plutonium 1 plus fairy-tale dreams of what the release 
fraction of plutonium will be at reprocessing and fuel fabrication 
facilities, then the NRC will be declaring it has no respect whatever 
for the health and safety of the public. 

----------~ ...


Footnote: In several of the ERDA Lab critiques ,reference has been 
made to the "hot particle" hypothesis of Geesaman-Tamplin-Cochran .. 
Indeed some of the ERDA Lab critiques suggest that Gofman's thesis 
makes use of, or is a variant of,the "hot particle" thesis. Such an 
assertion is blatant nonsense of the very worst kind. Those who make 
such an assertion show a total lack of understanding of the "hot 
particle" thesis and the Gofman hypothesis. 

The ERDA Lab critiques which infer that Gofman made use of the 
"hot particle" hypothesis do so because Gofman calculated the mass 
of the rele v ant bronchial tissue (for carcinogenesis ) to be one gram 
rather than the 570 grams of the whole (bloodless ) lung. In usin g 
one gram Gofman is stating a most simple scientific fact, name ly , 
if the bronchial cells represent the target for carcinogenesxs, one 
calculates the dose to that target , not to miscellaneous and sundr y 
assorted garbage . It is pathetic to find this totally straightforward 
scientific operation misconstrued as use of the "hot particle" 
thesis to which it bears exactly~ relationship. 

The "hot particle" thesis predicts that as the dose to a so-called 
"critical architectural unit" increases, the effecti veness of radiation 
increases far more than one would anticipate from linearit y 
because a new mechanism of carcinogenesis has entered the picture. 
In str i king contrast,the Gofman approach sa y s the situation i s precisel 
y what linear theor y would predict, namely if t he mass of target 
is reduced for a given radiation source, the increase in car c inoge n ic 
effect of radiati on is in the same proportion as is the decrease in 
mass of the target tissue . This is precise use of the linear hypothesis, 
and i s in no way related to the "hot particle" hypothesis. 

In tffe LoS Alamos critique it is stated that,since onl y 25 % of 
the one gram of bronchial epitheli!umis injured, and hence the plutonium 
c oncentrates its radiation there, this constitutes use of the 
"hot particle" thesis. Sheer, unadulterated nonsense! If the plutonium 
concentrates in ~ of the bronchial epithelium and deli v ers its dose 
there, the carcinogenic effect is 4 times as high there as it woul d 
be for the plutonium distributed over the whole g ram o f bronchial 
tissue . Thus, in terms of effect, ~x4 = 1, and lxl ~1 . This shows 
that the plutonium concentrating in~ of the cells gi ves exac t ly as 
much c arcinogeni c effect as that same amount of plutonium distributed 
in all the cells . This is exactl y what lin ear t heor y predicts and -it 
i s l in ear theory that Gofman uses. None of these considerati ons even 
r emot e l y resemble any aspect of the "hot particle" thesis.