ML20005B197

Affidavit Re Health Effects of Low Level Radiation.Prof Qualifications Encl

ML20005B197
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Site:	Summer
Issue date:	05/06/1981
From:	Hamilton L BROOKHAVEN NATIONAL LABORATORY
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UNITED STATES OF AMERICA NUCLEAR REGULATORY COMMISSION In the Matter of:

SOUTH CAROLINA ELECTRIC AND )

GAS COMPANY, ~~et al. -~

)

) Docket No. 50-395-OL (Virgil C. Summer Nuclear )

Station, Unit 1) )

AFFIDAVIT OF LEONARD D. HAMILTON CONCERNING THE HEALTH EFFECTS OF LOW LEVEL, RADIATION My name is Leonard D. Hamilton. A statement of my per-sonal qualifications is attached.

I have reviewed: (a) the contention that:

Contention AlO. The following effects - on a long term basis - have been sufficiently underestimated by the App' . cant and the Staff so as to compromise the validi.y of the favorable Benefit-Cost balance struck at the construction permit phase of this proceeding:

a) The somatic and genetic effects of radiation releases, during normal operation, to restricted and unrestricted areas, said releases being within the guidelines and/or requirements of 10 CFR Part 20, and Appendix I to 10 CFR Part 50; b) The health effects of the uranium fuel cycle, given the release values of the existing Table S-3 of 10 CFR Part 51. (Should the Commission modify Table S-3 prior to the litigation of this con-tention, the Board will entertain motions from i any of the parties respecting modifications to l this contention.)

(b) the NRC Staff's " Draft Environmental Statement related to operation of Virgil C. Summer Nuclear Station Unit No. 1, South Carolina Electric and Gas, Docket No. 50-395, June 1979, NUREG-0534."

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I find that the NRC Staff evaluation of the radiological impacts (sonatic and genetic effects of radiation on man) associated with the operation of the facility (Draft Environ-mental Statement (" DES") Sections 4.5 and 4.7)) to be rea-sonably conservative 'and I concur with it. Specifically, I find that the NRC Staff's evaluation of radiation-induced health impacts on man from routine operation in restricted and unrestricted areas (DES Section 4.5.5) and their evalua-tion of health effects associated with the uranium fuel cycle (DES Section 4.7, especially 4.7.5) to be an upper bound of the health effects. Further, I find the impacts to be de minimus particularly when compared to the dose commit-ments and potential health effects resulting from natural background radiation. The basis for this position is derived from my professional experience, my experience in other NRC licensing proceedings regarding health effects and my familiarity with the health effects models used by NRC Staff to calculate health effects impacts.

I have examined all the material supplied by Intervenor Brett A. Bursey concerning Contention A10. This material is listed below:

a. Cancer and Low Level Ionizing Radiation, Karl Z. Morgan.

b. Hazards of Low-Level Radiation, Karl Z. Morgan.

c. Low-Level Radiation And The General Public, Chapter IV, Karl Z. Morgan.

d. Nuclear Madness, Chapters 2, 3 (the section entitled Nuclear Reactors pp. 30-39), 4, pp.

71-74, Helen Caldicott.

e. Long Term Health Hazards of the Fuel Cycle, Chapter II, Dr. Kaku.

f. Honicher vs. Hendrie, A proceeding before the NRC [ sic] 1978 Docket No. 78-3371 NA-CV [de-scribed as an " additional reference"].

It is important to note that the ' conclusions of these documents are not based on the work of the authors them-selves, but rather, are premised on their interpretation and conclusions drawn from the work of others, notably, Bross 4 Manusco, Stewart and Kneale 5 6 and Najarian . Accordingly, I have focused on those references primarily relied upon by the authors of the documents. The essential point made in is that the commonly employed risk estimates based on the BEIR Committee report (1972)1 ("BEIR I"), as corroborated by UNSCEAR (1977)2 , and the subsequent BEIR Committee report (1980)3 ("BEIR III"), underestimate the risk of radiation at all levels. 1/ The documents emphasize that

~1/ Although the contention addresses genetic as well as so-matic effects, and Dr. Kaku, Dr. Caldicott and Dr. Morgan refer to genetic effects, these documents present no evidence from which one can derive risk estimates for genetic effects in man which ywere not already considered in the gEIR Committee Report as corroborated by.

UNSCEAR and BEIR III3 Thus Russell's work and the UNSCEAR 1972 figures, as referred to by Dr.yMorgan, were already considerei and included in the BEIR genetic risk estimates. There is thus no evidence that the DES underestimates genetic effects.

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the linear theory (that the risk per unit dose as derived from available data at high levels of radiation dose holds all the way down to zero exposure dose) is not sufficiently conservative in estimating risk at low doses but rather underestimates it.

As a physician with extensive experience in health effects and their assessments, there are several corgnents I would like to make. First, calculations of health

• effects must be based on risk estimates. Risk estimates are made by multiplying the estimated delivered dose of radiation by an established damage funcnion. I have made such risk estimates rcr the health effects of the uranium and coal fuel cycles based upon the a'nnual incidence of effects to be expected from operation of standard plants. The damage functions for radiation that I have used were derived from the BEIR I I ,

UNSCEAR and currently the BEIR III reports.3 These are 3

< essentially the same reports relied on by the NRC Staff.

The very low dose and dose rates given by natural background radiation in the environment, and the considerably lower doses that would be given at low dose retes by nuclear power stations, are obviously very much lower than those for which there are data on damage. However, to get a rough idea of risk one assumes that the linear' proportional dose and tumor induction observed at much higher doses and dose rates can be extrapolated down to the lowest dose. The assumption of

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linear proportionality down tx) the lowest doses and dose rates undoubtedly ovarastimates actual risk. Indeed both BEIR committees (1972 and 1980) noted that the lower bounds of risk from exposure to low level and low linear energy transfer ("LET") radiation (the type emitted from light l

'l water reactors) could include zero. This means that the '

actual numbers of cancers and genetic effects induced by

, these very low doses, given at very low dose rates will be ,

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lower than the estimates and may be zero. Nevertheless a s conservative approach, and one I use in making risk esti-mates on the nuclear fuel cycle, is to take the dose-effect i

values obtained at high-dose levels and to extrapolate them down to low-dose levels. i 4 believes he has identified subgroups l- Dr. Bross in the population which are especially sensitive to radi-

! ation damage. His belief derives from his analysis of l

l the Tri-State Leukemia Survey, wherein he studied an assoc-iation between some " indicators of susceptibility" (viral infections, bacterial infections, and allergy) shown by the leukemic child from birth until diagnosis of leukemia. He concluded "the apparently harmful effects of antenatal irradiation are areatly increased in certain susceptible subgroups of ctildren possessing the indicators associated with a slightly higher intrinsic rit < of leukemia." However, reanalysis of his findings shows that children with

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leukemia are simply more prone to viral and bacterial infections and allergies before the clinical onset of the

{ disease, i.e., these indicators characterize the disease l itself and do not relate to the child's inherent suscepti-l bility to leukemia. The incidence of these diseases as part of the pre-leukemia phase of leukemia in children is well known in clinical hematology. Analysis of Bross' data shows that the incidence of these indicator diseases before

- the clinical onset of leukemia is the same in children who had received no irradiation 3.n utero as in those who had .

The hypothesis of Bross, that there is a susceptible portion of the population at higher risk of leukemia, has also been challenged on the grounds that Bross' methods yield no f way to indentify susceptible individuals ahead of time and j so no way to test his thesis . 2/

More recently, Bross has suggested that the relatively small radiation exposures from diagnostic X-rays in adults 9

significantly increases the risk of leukemia . It appears that Bross assumes, in coming to this conclusion, that in the l absence of diagnostic X-rays, the incidence of heart disease l and leukemia is zero9,10 . Were this not the case, the fact i

I 2/ It should be noted that the documents provided by Inter-venor make reference to the need to consider in utero -

exposure. The risk of developing cancer after intra-uterine exposure of the fetus determined from the wgrk of Stewart and MacMahon was reviewed in BEIR (1972) and

[ and included in its models for risk estimates.

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that the " dose-response" curves of adults exposed to diagnostic X-rays are flat below 10 rad exposure would suggest a threshold.

Indeed, a more conventional relative risk analysis il found little or no increase in risk of leukemia from a sma11 number of diagnostic X-rays. Brous also assumes here that relative risks are fixed and that the percentage of the population af fected varies with dose, i.e., the basic response variable is the proportion of the irradiated population affected by radiation. Conventional relative risk analyses assume that everyone is affected and that the relative risks vary with dose. The improvement made by Bross et al.'s approach is unclear. The position taken here by Bross appears to be at odds with his earlier paper, in which he postulated the exist-ence of a sensitive subgroup of fixed size whose relative risk of leukemia increased rapidly with increasing X-ray dose.

Finally, one should note that the leukemia risk of (or " percent affected") does increase dramatically in males (females appear to be unaffected) after large number of diagnostic X-rays. However, the cause-effect relationship is uncertain in that large numbers of diagnostic X-rays --

I 40 or more within 10 years -- implies the presence of a disease state perhaps deriving from heart disease or a preleukemic sensitivity to infections.

The BEIR III Report critically reviewed the contribu-tions of Dr. Bross and his colleagues (BEIR III pp. 556-559)

and concluded: "The applications by Dross et al. have been clearly incorrect, and they provide no evidence that the risk of cancer from low-dose radiation is greater than indicated by conventional estimates." (BEIR III p. 559)

Mancuso, Etewart, and Kneale have reported prelim-inary findings on the work and survival experience of 24,939 male workers with 3,520 certified deaths and of an unspeci-fied number of female workers with 412 certified deaths at the Hanford Works, Richland, Washington between 1943 and 1971. The preliminary report, largely limfted to analysis of data on the 3,520 male deaths for which death certificates were available, claims to demonstrate a radiation-induced excess of cancers, greater than linear models would indicate. Their analysis has been widely criticized. Their report does not state the actual individual doses received by Hanford workers who died of cancer, only mean cumulative radiation doses.

Besides, their study did not take into account the calendar l

year in which the cancer began and made no correction for the fact that the incidence of the cancers they were observing in the Hanford workers also increased during the period of the study in the population at large. Thus, Table 11 in their publication, showing an increase in cancer with increasing dose accumulated over increasing time, fails to take into account 1

i that even in the absence of the in-~ easing dose of radiation, 1

l there is a similar increase in cancers they were finding in the

U.S. as a whole when plotted against increasing time. Other analyses of the same data published by Marks et al.12 and by Hutchinson et al.13 point to the possibility of an associa-tion with the work experience for two cancer types: cancer of the pancreas and multiple myeloma (multiple myeloma in whites is increasing in the U.S. for no known reasons). There is no reported radiation relationship for lymphatic or haemo-poietic cancers other than myeloma, i.e., no excess of leukemias (which previous experience suggests should have been most observable where radiation is a factor).

Since the specified radiation doses were very small, per-haps on the order of a f2w rads, the cancer-doubling estimates found in the Mancuso, Stewart, and Kneale paper have been strongly disputed. If the postulated small dose actually caused a doubling of the spontaneous rate of cancers, then background radiation would produce more than the numbers of cancer obser-i ved in the population. It therefore appears that if these doub-ling doses are correct, something other than radiation was the cause of the observed cancers. In its review of the Mancuso, Stewart and Kneale work and subsequent related papers, BEIR III concluded (p. 556) that "[a]t present, however, there seems to be little reason to abandon the body of epidemologic evidence on radiation-induced cancer that, although based on greater exposures, yields consistent and statistically stable estimates."

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6 Najarian and Colton estimated that since the Ports-mouth Naval Shipyard (Ph3) in New England began to service nuclear-powered sh:1ps in 1959, 20,000 people were employed there, of whom about 20% were exposed to radiation. From a search of death certificates 1959-77, 1,450 former PNS employees who had died below age 80 were identified in New Hampshire, Maine, and Massachusetts. To ascertain whether these er.-employees were radiation-exposed workers, attempts were made to contact near relatives by telephone. This was successful in 525 cases and it was established that 146 were probably exposed to radiation during their working life.

The authors show that, compared with mortality in U.S' .

white males for 1973, the observed numbers of cancers and leukemias were considerably greater than those expected: for example, 56 cancer deaths were found in death certificates of 146 ex-workers exposed to radiation; only 34.5 were expected.

In non-exposed workers there were 88 cancers; 79.7 expected.

For leukemias there were 6 in the former radiatien workers; only 1.1 were expected.

Najarian and Colton listed some inadequacies in their survey. It was an analysis of deaths only; no information was available on the total population at risk. There could Se a bias in the infornation supplied by relatives. They had no information on how long workers worked at the shipyard, how long nuclear workers were expoecd to radiation, and the amounts

of radiation they received. Consideration was not given to other toxic agents, such as asbestos, smoking, industrial solvents which could have acted alone or synergistically with radiation to cause the apparent excess deaths from cancer and leukemia.

There are other inadequacies in this survey. To exclude some of the effects of other carcinogens, one must show that cancer frequencies increase with increasing radiation exposure, but knowledge of the lifetime accumulated doses of the former employees was not available. More importantly, if the radia-tion work at PNS began only in 1959, it is unlikely that changes in overall cancer frequency induced by radiation would appear before at least 10 years after exposure, or after 5 years for leukemia, these being roughly minimum latent periods for can-cer induction. The data given in Najarian and Colton can be divided into deaths during the periods from 1959-69, when radiation effects would not be expected to appear, and 1970-77, when effects might be expected. In 585 death certificates of I

persons who died between 1959-69, 24.6% had cancer listed as the cause of death. Considering the 33 radiation-exposed work-i ers who died during this period, 13 or 39.4% of the deaths were l

recorded as due to cancer. In 865 death certificates 1970-77, l

25.7% had cancer as the cause of death; hence there was no significant difference between the percentage of cancer deaths between the two periods for all workers. For the 113 radiation-

1 exposed wor'kers, 43 or 38.1% of deaths in the later period were due to cancer -- no more than in the earlier period (39.4%) .

The data are tabulated below:

I RADIATION EXPOSED l CANCER  % CANCER CANCER  % CANCER ALL DEATHS D_EATHS DEATHS ALL DEATHS DEATHS DEATHS 1959-69 585 144 24.6 33 13 39.4 1970-77 865 222 25.7 113 43 38.1 1,450 366 The absence of any apparent latent period effect casts doubt on conclusions about the contriba'. ion of radiation to the curiously high numbers of cancer deaths among the radiation 14 .

workers In the meanWhile, NIOSH made available to Drs. Najarian and Colton radiation exposure data supplied by the U.S. Navy.

On February 2, 1979, at a symposium sponsored by the John Hopkins School of Public Health, Baltimore, Maryland, Drs.

Najarian and Colton introduced these radiation exposures into their PNS Study. At this time, they announced that in contrast with the original data, where 6 leukemia deaths were observed instead of 1.1 expected, it was found that two of the cases of leukemia had no history of radiation exposure. One had less than 0.1 rem, Which is what one receives after one year's natural background. One received 15 rem, one 5 rem, and one "not remembered" -- probably less than 5 rem.

The number of leukemias is now 3 instead of 1.1 expected.

For all cancers the new data are:

CANCERS EXPOSURE NUMBER OBSERVED EXPECTED RATIO Less than 0.1 rem 64 17 13.5 1.26 From 0.1 to 0.99 50 16 10.5 1.53 Greater than 1 49 19 10.2 1.58 No exposure 358 92 74.9 1.23 Chi-square test shows no significant difference in the ratio among the exposed levels at p = 0.10. Cochran's chi-square test for a linear regression, which considers that that ratios increase in the expected direction, shows no stat-istical significance at p = 0.05 but ist significant at p = 0.10.

In any event, the final report of the U.S. Department of Health and Human Services, Public Health Service Centers for Disease Control, National Institute for Occupational Safety and Health (NIOSH)'s Epidemiologic Study of Civilian Employees at the Portsmouth Naval Shipyard (PNS) based on a total cohort of 24,545 civilian white males employed at PSN between January 1, 1952 and August 15, 1977 is now available. The report found no excess of deaths due to malignant neoplasms and due specifically to neoplasms of the blood and blood-form-ing tissue in civilian workers at PNS. "This NIOSH ctudy Icd over a 99% probability of detecting the 5-fold increased risk of death due to leukemia reported by Najarian et al.

o among radiation exposed employees at PNS if it had existed.

Furthermore, had the true relative-risk of death from leukemia been 2.2, the likelihood of detecting such a risk would still

' However, when observed leukemia deaths at the have been 80%.

shipyard were compared with expected deaths, derived from the United States white male population rates, no excess was found.

No relationship between exposure to radiation and mortality from any cause was observed among the PNS population when com-pared to the United States white male population. Furthermore, no excess in leukemia mortality was observed in the radiation exposed population when campared to the non-radiation exposed employees of PNS."

The report cautions that an insufficient number of years may have elapsed for most " radiation workers since their initial radiation exposure to permit manifestation of currently latent cancers. In addition, the number of workers with radi-t I ation exposure at PNS was relatively small, making the opportun-1 ity for observing a slight excess in mortality very unlikely."

In addition to the above, material furnished by Intervenor makes reference to the work of Dr. Ernest Sternglass. The work of Dr. Sternglass has been widely criticized in the scientific community. Except for his original article in Science in 1963, all Sternglass's references are to his own presentations made at meetings or in unreferenced publica-tions, so that their citation bears no relation to their

scientific merit. His arguments have been shown to depend on select evidence which supports his case while ignoring the evidence that does not.

Other scientists whom he has cited in support of his hypotheses have disavowed his interpretation of their findings.

' For instance, Dr. Alice Stewart, on whose work Dr. Sternglass has allegedly relied, (e.g., Infant Mortality and Nuclear Power Generation by E.J. Sternglass dated October 18, 1970, and Infant Mortality Changes following the Three Mile Island Accident by E.J. Sternglass, presented at the 5th World Congress of Engineers & Architects, Tel-Aviv, Israel, January 25, 1900) has devastingly criticized Dr. Sternglass. In testi-mony at the hearings on the Long Island Lighting Company (Shoreham Nuclear Power Station Unit No. 1), Docket No. 50-322, Transcript pages 7483-7484 (March 15, 1971), Dr. Stewart stated:

I was once asked to review one of his (Dr.

Sternglass) rather repetitive articles in the New Scientist and I pointed out that I think it does in fact render his approach null and void. He is a physicist and he has done what many people have done before, thev have assumed it is quite easy to be an epidemeologist, and they have fallen into one of the more obvious traps. He is not the first person to have done it.

Roughly speaking his evidence is postulating, '

if I_can put it very frivolously, that by 1971 children will be rising from the grave into which they had fallen as a result of infant mortality.

She continued (Tr. 7540-41a); "First of all it [Dr.

l Sternglass's description of Dr. Stewart's work] is riddled l with mistakes...It is just about his usual exaggeration."

These quotations demonstrate the regard which the scientific community has for the work of Dr. Sternglass.

In sum, although these claims of higher risks from the levels described by Bross, Mancuso, Stewart, Kneale, and Najarian have become the subject of considerable public debate and are relied upon by potential Intervenor witnesses, examin-ation to date of their work does not support these claims.

In this regard, BEIR III, after reviewing all the above, con-cluded that "available data relative to the effects of low-dose or low-dose rate exposures on carcinogenesis in humans and experimental animals do not, in general, support the hypothesis of an increased probability of induction at low dose rates."

For these reasons I concur with the NRC . Staff evaluation of health effects contained in DES.

The foregoing affidavit was prepared by me and I swear that it is true and correct to the best of my knowledge, infor-mation and belief.

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UNITED DISTRICTSTATES OF AMERICA)as OF COLUMBIA Leonard D. Hamilton Subscribed and sworn to before me this 6tfday of May, 1981.

del __ D Y Notary Public My Commission Expires: M ZCommission Expires OctoScr T{T953

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DR. L. D. HM1ILTON PERSONAL QUALIFICATIONS My name is Leonard D. Hamilton. My address is: 6 Childs Lane, Setauket, New York, 11733. I am, among other responsibilities, Read of

'the Biomedical and Environmental Assessment . Division in the National Center for Analysis of Energy Systems at Brookhavsn National Laboratory, Associated Universities, Inc., Upton, New York, 11973. The Biomedical and Environmental Assessment Division is jointly sponsored by the Department of Energy and' Environment and Medical Department at Brookhaven. The Biomedical and Environmental Assessment Division (BEAD) aims at developing a realistic as.sessment of biomedical and environmental effects .of energy production and use. All forms of energy, including electric power generation using fossil fuels, hydro, nuclear, and new technologies, are assessed. The Biomedical Environmental Assessment Division is the lead group in the Office of Health and Environnental Research of the Office of Energy Research, U. S. Department of Energy, assessing the health and environmental effects of energy production and use and among other responsibilities is charged with producing a health and environmental effects assessment of the National Energy Plan.

I have been involved in assessing the risks of radiation for man for 35 years, specifically the health effects of nuclear energy for electric power generation for 20 years, and the assessment of the comparative health effects from various energy sources, for the past 7 years. The Biomedical and Environmental Assessment activity formally began in July, 1973; for the past and present year our level of effort is 204 man-months j annually. .

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I received my Bachelor of Arts in 1943 and qualified in medicina from Oxford University in 1945. I am a registered medical practitioner in the United Kingdom and licensed physician in New York State. After several positions in University hospitals, which included a position as -

Resident Medical Officer at the Radiotherapeutic Centre, Addenbrooke's

! Hospital, Cambridge, during which time I was concerned with the management of cancer patients undergoing treatment with radiation, I proceeded to research at Cambridge University on histological studies of the mechanism of the action of therapeutic doses of ionizing radiation for which I received my Ph.D. in experimental pathology in 1952. In the meanwhile, in 1951, I had received my Doctor of Medicine degree from Oxford; this is a senior medical qualificacion in the United Kingdom, roughly equivalent to Diplomate in Internal Medicine in the United '

States. I am also a Diplomate of the American Board of Pathology (Hematology).

From 1950-1964 I spent 14 years on the research staff of the Sloan-Ketterfng Institute for Cancer Research and on the clinical staff of Memorial Hospital in New York being Associate Member and Head, Isotope Studies Section at the Institute and Assistant Attending Physician, Department of Medicine at Memorial. During this time I was also a member of the faculty of Cornell University Medical College and a Visiting Physician, Cornell Division, Bellevue Hospital. Since then I have maintained a continuing association with the Sloan-Kettering Institute as Associate Scientist. '

At the Institute my laboratory research was on the molecular structure of the genetic material (DNA) and the cells in man concerned with the immune mechanism. I provided the DNA on which the proof of the

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double-halical structure of DNA is based, and was one of the first to l

establish the long life of the immune cells in man. My clinical work in l Memorial Hospital invclved research on the treatment of patients afflicted with cancer and .'.eukemia with new chemical agents and also with new applications of radiation therapy.

In 1964 I joined the scientific staff of Brookhaven National t Laboratory as Senior Scientist and Head, Division of Microbiology, and Attending Physician, Hospital of the Medical Research Center. Since 1973 I have been Head of the Biomelical and Environmental Assessment Group which in 1976 became a Division of the National Center of Analysis of -

Energy Systems.

Brookhaven At I continued cy laboratory research begun at Sloan-Kettering. In addition since my Visiting Fellowship at St.

Catherine's College, Oxford 1972-73, I have been concerned with placing all risks in life in perspective; and since becoming Head of the Biomedical and Environmental Assesscent activity in 1973, particularly with the assessment of the hazards associated with different energy sources and their use. Our group has the lead responsiblity to DOE for the assessment of health and environmental effects from various energy systems, and of coordinating such assessments in national laboratories, universities and research institutes in the United States.

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My interest in the risks of radiation for man began with my Ph.D.

work in Cambridge in 1946 and, since DNA and the immune system are prime targets of radiation damage has continued sthroughout my laboratory research. I was associated informally with the United Nations Scientific Committee on Ef fects' of Atomic Radiation (UNSCEAR) almost since its inception in 1957, served as Consultant, Office of the Under-Secretaries'

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for Special Political Affairs (UNSCEAR), 1960-62, and was responsible for I

the first draf t of the somatic effects of radiation in the 1962 report.

This ~section covers the effects of radiation in inducing leukemia and i cancer in' man. I have reviewed most of the working papers of UNSCEAR since then. I was a member of the National Re. search Council-National L-

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Academy of Sciences (NAS-NAS) Committ'ee on Bilogical Effects of Atomic '

Radiation, Subcommittee on Hematologic Effects, 1960-64, the NRC-NAS Solar Energy Research Institute Workshop,1975, the NRC-NAS Committee on

- Environmental Decision Making, Steering Committee on Environmental Monitoring, Pane. on Effects Monitoring 1975-76, the ERC-NAS Health Effects Resource Group, Risk Impact Panel'of the Committee on Nuclear and Alternative Energy Ssytems (CONAES) 1975-80, the NRC-NAS Panel on the Trace Element Geochemistry.of Coal Resource Development Related to Health 1976-80, and the NAS-NRC Committee on Research Needs on the Health Effects of Fossil Fuel Combustion Products, 1976-80.

I was a member of the Mayor's Technical Advisory Committee on

~ r Radiation, New York City, since 1963 until its end, December, 1977 and have been a member of the Technical Advisory Committee on Radiation to i

the Commissioner of Health of the City of New York since August, 1978.

Since 1972, I was a Consultant to the Environment Directorate, Organization for Economic Co-operation and Development; since 1976 serve /

as DOE (formerly ERDA) Representative in the U. S. Delegation to the Environment Committee and U. S. delegate to the Joint Environment-Energy Steering Group. I was a member of the United Nations Environmental Program (UNEP) International Panels of Experts on the Environmental Impacts of Production, Transportation, and Use of Fossil Fuel 1978, on the Environmental Impacts of Nuclear Energy 1978-79, on Renewable Sources L

of Energy and the Environment ^ 1980, and on the Comparacive Assessment of l l

Environmental Impacts of Different Sources of Energy, 1980. I was a member of the Beijer Institute, UNEP, and USSR Commission for UNEP International Workshop on Environmental Implications and Strategies for Expanded Coal Utilization, ~1980.

I am currently a member of the U. S. Department of Health and Human Services, Public Health Service Centers for Disease Control, National Institute for Occupational Safety & Health overview group, supervising

- the epidemilogical study of the employees at the Portsmouth Naval .

Shipyard where an alleged increase in leukemia was reported by Najarian and Colton in 1978, and a consultant to the Division of Environmental Health, World Health Organization and the United Nations Environmental Program on the comparative h2alth effects of different energy sources.

I have been Professor of Medicine, Department of Medicine, Health Sciences Center, State University of New York at Stony Brook, New York since 1968 and I am currently a member of the American Association for Cancer Research, American Society for Clinical Investigation (emeritus),

American Association of Pathologists, Inc., the Harvey Society, and' the British Medical Association.

I have published more than 100 scientific papers, including cany reports essessing the hazards of various energy sources.

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REFERENCES

1. BEIR, The Effects on Populations of Exposure to Low 1 Levels of Ionizing Radiation, Advisory Committee on the Biological Effects of Ionizing Radiation (BEIR).

Division of Medical Sciences, National Academy of Sciences. National Research Council, Wa shington, D.C.,

November 1972.

2. Sources and Effects of Ionizing Radiation, United Nations Scientific Committee on the Effects of Atomic Radiation 1977 Report to the General Assembly, with Annexes, United Nations, New York, 1977.

3 Committee on the Biological Effects of Ionizing Radiations. The Effects on Populations of Exposure to Low Levels of Ionizing Radiations, National Research Council, National Academy of Sciences, Washington, D.C.,

May 1980.

4. Bross, ILD. and Natarjan, N., Leukemia from Low-Level Radiation: Identification of Susceptible Children, New England Journal of Medicine 287:107-110, 1972.

5. Mancuso, T.F., Stewart, A., and Kneale, G., Radiation Exposures of Hanford Workers Dying from Cancer and Other Causes, Health Physi s 33:369-85, 1977.

6. Najarian, T. and Colton, T., Mortaligy from Leukemia and Cancer in Shipyard Nuclear Workers, The Lancet, May 13, 1978, p. 1018.

7. Smith, P.G., Pike, M.C., and Hamilton, L.D., Mutliple Factors in Leukaemogenesis, Letter to Editor, Brit.

Med. J. 2:482-483, 1973.

8. Rothman, K.J., Review of Dr. Irwin Bross' Presentation on Radiation Exposure and Cancer Risk, prepared for a public meet ing of the low-level ef fects of ionizing radiation sponsored by the U.S. Nuclear Regulatory 4

Commission, W a shington, D.C., April 7, 1978; see also Letters to Editor, Journal of the American Medical Association 238(1):1023-1024, 1977.

9. Bross, I.D.J. and Natarjan, N., Genetic Damage from Diagnostic Radiation, J. Amer. Med. Assoc. 237:2399-2401, 1977.

10. Bross, ILD.J . , Ball, M., Rzepko, T., and Laws, R.E.,

Preliminary Report on Radiation and Health Disease.

J. of Med . , 9:3-15, 1978.

31. Ginevan, M.E., Nonlymphatic Leukemias and Adult Expo-sure to Diagnostic X-rays: The Evidence Reconsidered, Health Physics, in press.

12. Marks, S., Gilbert, E.S., and Breitenstein, B.D.,

Cancer Mortality in Hanford Workers, IAEA Symposium on the Latent Biological Effects of Ionizing Irradiation, Marcy 1978, IAEA SM-224.

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13 . - Hutchinson, G.B., Jablon, S., Land, C.E., and MacMahon, B., Review of Report by Mancuso, Stewart, and Kneale of Radiation Exposure of Hanford Workers, Health Physics, in press.

14. Reissland, J.A. and Dolphoin, G.W., A Review of Mortality from Leukemia and Cancer in Shipy.>.rd Nuclear Workers by T. Janjarian and T. Colton, The Lancet, VI, p. 1018, 1978, National Radiology protection Board (NRPB), Harwell, Didcot, England, May 18, 1978.

15. Rinsky, R.A., Waxweiler, R.J., Bierbaum, PLJ.,

Terpilak, M., Zumwalde, R.D., Murray, W.E., Landrigan, P.J., and Cox, C. Epidemiologic Study of Civilian Employees at the Portsmouth Naval Shipyard, Kittery, Maine, U.S. Department of Health and Human Services, Public Health Service Centers for Disease Control, National Institute for Occupational Safety and Health, Division of Surveillance, Hazard Evaluations, and Field Stuides, Cincinnati, Ohio, December 1980; see also Rinsky, R.A., et al., Cancer Mortality at a Na' val Nuclear Shipyard, The Lancet i: 231-235, 1981.

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