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Submitted by John W. Gofman, M.D., Ph.D., Committee for Nuclear Responsibility, Inc. (CNR) Part 2
   Commenting on behalf of the organisation
Document 2005 ICRP Recommendation
[continues from Part 1 just submitted earlier today]

For example, most of the approximately 100,000 participants in the ABSS not only received one acute exposure to bomb-radiation in 1945, but they also accumulated acute partial-body exposures to medical x-rays both before and after 1945.

Unless it can be established, somehow, that all the compared dose-groups in the ABSS have accumulated equal x-ray doses, the findings of the ABSS are compromised to an unknowable degree. By contrast, across the approximately 100 million participants “enrolled” in the RMP study, none of the dose-groups received any acute exposures to bomb-radiation which could augment in unequal amounts their doses from medical x-rays, because they received no bomb exposure at all.

In 1998, a report on the ABSS acknowledged the problem of medical x-rays among the ABSS participants. In its Chapter 3, Kato, Russell, and Kodama state that by 1982, “The doses from diagnostic x-ray examinations had already become significantly great contaminants of the radiation doses from the atomic bombs” (Kato 1998, p.51). And the x-ray doses keep growing.

They also report analyses indicating that, “Numerous atomic bomb survivors have received medical radiation doses which are comparable with their atomic bomb radiation doses” (Kato 1998, p.67). And Kato’s dose-comparison ignores the well-known findings that medical x-rays are about 4-fold more mutagenic per cGy (rad) than a-bomb radiation (Gofman 1999, Chapter 2, Part 7; ICRP 2005 Recommendations, Section 3.4.1) --- which means that the accumulated medical doses, to the extent that they have been reasonably reconstructed, far exceed the bomb doses in “numerous” cases. This makes it essential to have accurate matching of the ABSS dose-groups for accumulated medical x-ray doses. Please see further discussion in Part 3.

Besides medical radiation, the ABSS incorporates several other potential confounders which are absent from the RMP study. For example, because the RMP study is confined to age-adjusted CAD mortality in 1950, the RMP study is not “muddied” by the full impact of cigarettes, whose use peaked for males in 1963 in the USA (Gofman 1999, Chapter 48). Nor do the RMP study’s 1950 age-adjusted CAD mortality rates incorporate consequences from use of chest radiation for cancer therapy and use of chemotherapy --- another mutagen --- because such practices were almost nonexistent before 1950 (Gofman 1999, Chapter 68).

We recommend that the ICRP and other such groups carefully consider the RMP study before issuing any radiation guidelines in 2005. The consequences of effective doses of radiation up to a few cSv (rems) each year, upon causation of such an important disease, should certainly not be excluded from the estimated “detriment.” The proposed exclusion in the ICRP 2005 Recommendations (p.34) is unacceptable and will surely end up creating a false sense of safety.

# PART THREE: Risk-Values Rendered Untrustworthy by Unevaluated Medical X-rays

Contamination, of virtually all dose-response studies which attempt to identify and quantify causal agents in the etiology of CAD and cancer, has resulted from unevaluated and unmatched accumulated exposures to medical x-rays. With respect to studies of ionizing radiation, such contamination renders the ICRP’s estimates of risk per dose-unit inherently untrustworthy.

If either the accumulated doses or the mutagenic power of medical x-rays were negligible, such contamination could be neglected, as are so many variables in epidemiological studies. But both the accumulated doses and the mutagenic power of medical x-rays are far from negligible. In many radiation studies, the “background” dose of accumulated x-ray doses is probably dominant.

This is impossible to ascertain. In all the developed countries, medical x-rays have been very widely used ever since the year 1900 (Gofman 1996, especially Chapters 31, 32, 33), but entrance doses were not measured, and still are far too rarely measured. In the United States, medical x-rays were very liberally given to children until about 1960 (Gofman 1996 throughout), and even during the 1980s, patients below age 45 received a large share of the total estimated number of x-ray procedures (Gofman 1999, Chapter 2, Part 3f). There is probably not one single person in the United States who knows his or her accumulated lifetime organ doses from medical x-rays. For many organs, such doses will far exceed the lifetime accumulated doses from natural background radiation (Gofman 1999, Appendix K).

For instance, up until the 1970s, prenatal irradiation during the mother’s pelvimetry occurred in approximately one birth in every 14; the retroactively estimated fetal doses ranged between one and three cGy or rads (Gofman 1996, Chapter 12). Medical fluoroscopy was frequently and widely used starting in the 1920s; around 1950, the average fluoroscopy exam delivered an estimated skin dose of 65 Roentgens, or approximately 65 cGy or rads (Moeller 1953, pp.58-59; more context in Gofman 1999, Appendix K); more recent medical practice uses fluoroscopy of various duration and cumulative dose to guide catheters and many types of surgical procedures. CT scans, introduced in the 1970s in Japan as well as the USA, have typically delivered over 2 cGy or rads of dose to internal organs, per exposure; many exams require two exposures --- with and without a contrast medium --- and dose-levels vary from one facility to another.

Part 3-a: Permanent Large Uncertainties about Anyone’s Accumulated X-ray Doses

The A-Bomb Survivor Study (ABSS), on which I (jwg) relied for so many years to calculate risk/cGy estimates, is badly contaminated by accumulated doses from medical x-rays. Somewhat heroic efforts in Japan to “reconstruct” x-ray doses for a subcohort of 15,000 ABSS participants (in the Adult Health Study) are necessarily unreliable. For example, surveys in several nations show that doses used for equivalent films vary by factors of 3 due to variation in film-processing methods, that doses vary in a fluoroscopic examination by factors of 10 or more due to variation in dose delivered per minute and number of minutes consumed, and that doses vary for a many reasons by additional factors of 2 or more for any procedure on patients of equal size (details in Gofman 1985, Chapter 16; Gofman 1996, Chapter 48; UNSCEAR 1993, p.243; and elsewhere).

Most dose-response studies do not even attempt to evaluate accumulated x-rays doses. Those that do make the attempt cannot eliminate the inherent and large uncertainty in the individual estimates assigned to each participant. The result is that the menace, of seriously unmatched accumulated x-ray doses among the compared groups, may be present in most studies, and cannot be ruled out of any study. However, the RMP study was designed to minimize the problem of never-measured x-ray doses.

Part 3-b: How Unmatched X-ray Doses Affect Risk-Estimates by ICRP and Others

What are some of the ways in which serious errors in risk-estimates can result from unmatched accumulated x-ray doses? These ways do not differ from inability to match study samples for non-x-ray variables --- for instance, for cigarette smoking. Some of them are demonstrated and depicted in Gofman 1999, Chapter 5 and Appendix L.

The direction of the error depends on how the unequal accumulated x-ray doses are distributed among the dose-groups, of course.

For instance, mismatched dose-groups can, in the most extreme cases, alter a truly positive dose-response to appear as a negative one. Or vice versa (Gofman 1999, Chapter 5). They can alter a truly positive linear dose-response to appear as a supralinear dose-response, or as a concave upward dose-response, or as a hormetic dose-response (Gofman 1999, Appendix L), or as a threshold dose-response, or as a flat “correlation absent” dose-response.

They can change the slope of a truly positive linear dose-response (change the increase in effect per unit increase in cause). And they can increase the scatter around a dose-response curve and thus lower its statistical significance and reliability.

Part 3-c: Conclusion about Neglect of Accumulated X-ray Doses

There is no doubt that the menace of dose-cohorts, unmatched for accumulated x-ray organ-doses in the ABSS, should warn everyone to reduce the trust commonly placed in quantitative risk-estimates derived from the ABSS --- as are most of the ICRP guidelines.

And this menace is not limited to the ABSS or to other dose-response studies of the effects from just ionizing radiation. For instance, it is a hazard in dose-response studies of any suspected causal co-actor (e.g., any mutagen, or diet, smoking, non-ionizing radiation) in mortality from coronary artery disease or cancer.

# Reference List

Fuster 1994. Valentin Fuster and co-workers, “The Pathogenesis of Coronary Artery Disease and the Acute Coronary Syndrome,” New England Journal of Medicine 1992; 326: 242-250 and 310-318.
Gofman 1949. J.W. Gofman + Frank T. Lindgren + Harold A. Elliott, “Ultracentrifugal Studies of Lipoproteins of Human Serum,” Journal of Biological Chemistry 1949; 179: 973-979.
Gofman 1950-a. J.W. Gofman and co-workers, “The Role of Lipids and Lipoproteins in Atherosclerosis,” Science 1950; 111: 166-171 + 186.
Gofman 1950-b. J.W. Gofman and co-workers, “Blood Lipids and Human Atherosclerosis,” Circulation 1950; 2: 161-178.
Gofman 1954. J.W. Gofman and co-workers, “Lipoproteins, Coronary Heart Disease, and Atherosclerosis,” Physiological Reviews 1954; 34: 589-607.
Gofman 1959. J.W. Gofman, “Coronary Heart Disease.” 353 pages. Library of Congress No.58-14073. Charles C. Thomas Publishers, Springfield, Illinois, USA.
Gofman 1966. J.W. Gofman + Wei Young + Robert Tandy, “Ischemic Heart Disease, Atherosclerosis, and Longevity,” (the George Lyman Duff Memorial Lecture), Circulation 1966; 34: 679-697.
Gofman 1976. J.W. Gofman, “The Plutonium Controversy,” Journal of the American Medical Assn 1976; 236; 284-286.
Gofman 1979. J.W. Gofman, “The Question of Radiation Causation of Cancer in Hanford Workers,” Health Physics 1979; 37; 617-639.
Gofman 1981. J.W. Gofman, “Radiation and Human Health: A Comprehensive Investigation of the Evidence Relating Low-Level Radiation to Cancer and Other Diseases.” 908 pages. ISBN 0871562758. For the Japanese edition, ISBN 4390501852.
Gofman 1985. J.W. Gofman + Egan O’Connor, “X-Rays: Health Effects of Common Exams.” 440 pages. ISBN 0871568381.
Gofman 1988. J.W. Gofman, “A Proposal Concerning ‘the New Dosimetry’ DS86,” Health Physics 1988; 55: 58-581.
Gofman 1990. J.W. Gofman, “Radiation-Induced Cancer from Low-Dose Exposure: An Independent Analysis.” 480 pages. ISBN 0932682898. Available from CNR. Also available online at And a Russian-language edition has ISBN 5885870047.
Gofman 1992. J.W. Gofman, “Radiation-Inducible Chromosome Injuries: Some Recent Evidence on Major Health Consequences.” CNR publication 9204. Also available online at
Gofman 1994. J.W. Gofman, “Chernobyl Accident: Radiation Consequences for This and Future Generations.” 574 pages. Available only in the Russian language. ISBN 533900869X.
Gofman 1996. J.W. Gofman, “Preventing Breast Cancer: The Story of a Major, Proven, Preventable Cause of This Disease,” Second Edition. 422 pages. ISBN 0932682960. Available from CNR. Also available online at
Gofman 1998. J.W. Gofman, “Asleep at the Wheel: The Special Menace of Inherited Afflictions from Ionizing Radiation.” CNR publication 9810. Also available online at
Gofman 1999. J.W. Gofman, “Radiation from Medical Procedures in the Pathogenesis of Cancer and Ischemic Heart Disease: Dose-Response Studies with Physicians per 100,000 Population.” 699 pages. ISBN 0932682979 (hardcover) and ISBN 0932682987 (softcover). Bound copies available from and from CNR. Also partially available online at which links to the text through Chapter 5
Kato 1998. Kazuo Kato + Walter J. Russell + Kazunori Kodama, “Medical Radiation Exposures of Atomic Bomb Survivors,” Chapter 3 (pp.51-72) in “Effects of Ionizing Radiation: Atomic Bomb Survivors and Their Children (1945-1995).” Editors: Leif E. Peterson + Seymour Abrahamson. 370 pages. ISBN 0309064023. (National Academy Press, Washington DC.)
Libby 1995. Peter Libby, “Molecular Bases of the Acute Coronary Syndrome: From Bench to Bedside,” Circulation 1995; 91: 2844-2850.
Moeller 1953. Dade W. Moeller + James G. Terrill + Samuel C. Ingraham, “Radiation Exposure in the United States,” Public Health Reports 1953; 68: 57-65.
Morgan 1996. William F. Morgan and co-workers, “Genomic Instability Induced by Ionizing Radiation,” (review paper), Radiation Research 1996; 146: 247-258.
Nowell 1976. Peter C. Nowell, “The Clonal Evolution of Tumor Cell Populations,” Science 1976; 194: 23-28.
UNSCEAR 1993. United Nations Scientific Committee on the Effects of Atomic Radiation, “Sources and Effects of Ionizing Radiation: UNSCEAR 1993 Report to the General Assembly, with Scientific Annexes.” 922 pages. ISBN 9211422000.

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