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Journal of Radiological Protection Response to James Smith's review of Manual for Survival



Response to James Smith's review of Manual for Survival. The article includes refutation of his critique and corrections to misinformation provided by Smith.
Journal of Radiological Protection
Response to James Smith’s review of
Manual for Survival
To cite this article: Kate Brown 2020 J. Radiol. Prot. 40 928
View the article online for updates and enhancements.
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Journal of Radiological Protection
J. Radiol. Prot. 40 (2020) 928–933 (6pp)
Letter to the Editor
Response to James Smiths review of
Manual for Survival
Kate Brown
Received 19 December 2019; revised 12 March 2020
Accepted for publication 1 May 2020
Published 21 August 2020
Keywords: Chernobyl, low-dose radiation, Japanese Life Span study
Some gures may appear in colour only in the online journal
I object to James Smith’s deeply awed 12-page opinion article on my book Manual for Sur-
vival published in your journal (Smith, 2020). The author, Dr. Smith, is entitled to disagree
with the evidence in my book but his article oversteps the mark and descends into personal,
emotional reactions to my book rather than judging the work on the merits of the 77 pages of
archival and peer-reviewed footnotes in the book.
Smith writes that he was personally offended. He felt I misrepresented him in my book. He
writes, ‘According to Brown, I was a physicist (used almost as a term of abuse in the context)
who did not feel it necessary to go to Chernobyl to draw my pre-formed conclusions about
the accident effects.’ I did not write that Smith did not feel it necessary to go to the Chernobyl
Zone. Rather, I reported that after following two other scientists in the Chernobyl Zone who
regularly visit the Zone twice a year, I wrote to him to see if I could observe him as he worked
in the Zone. I wanted to give his very different views on ‘thriving’ wildlife in the Zone equal
time in my book. He responded that his colleagues would be there, but that he did not have
plans at the time to visit. I continued to follow the other biologists in the Zone. I met up with
Smith at a conference in Florida. I did not state one way or another how many times Smith
had visited the Zone.
Smith writes that I made ‘biased’ ‘omissions, inconsistencies, and errors.’ He has a lot of
feelings. He is shocked, elated, mentally exhausted, astonished. His jaw drops. I am impressed
with the passion of this scientist, but I question whether it belongs in a peer-reviewed journal
dedicated to objective science. Smith doubts he can give the book a fair review. He writes: ‘I
will try to give this book as fair a review as I can.
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J. Radiol. Prot. 40 (2020)
Smith says there was no reason for an historian to use Soviet archives, as I did, to nd
the original reports of dose measurements, measurements of contamination in food, bodies
of exposed persons, and medical records. He writes: ‘… you do not have to dig around in
Soviet archives to nd it: reports and results, have been in the international scientic literature
for more than 20 years.’ But then he contradicts himself, ‘but sadly not all the original data.
Would it not be good to have the original data? The radiation protection community has relied
for decades on dose reconstructions created years after given nuclear events.
The trend to belatedly study nuclear events began with the Japanese Life Span Studies, star-
ted in 1950. The historian Susan Lindee reports that Japanese scientists collected samples and
measured radiation levels in Hiroshima and Nagasaki soon after the bombing. This was the
very best, most immediate data collected. Soon after arriving, U.S. occupation forces seized
the data, which is missing to this day [1]. Five years later, when the Life Span Study began,
scientists had to reconstruct radiation levels and doses to survivors after the fact. This meant
a lot of guesswork. All this made for a very ‘messy’ situation, as James Neel, a leading genet-
icist on bomb survivor studies, recognized. Managing the uncertainties of retrospective dose
reconstruction, scientists revised survivors’ doses many times over the decades [2]. Studies
of exposures to Nevada and Hanford downwinders were also carried out through dose recon-
structions decades after the exposures occurred. The International Chernobyl Project, led by
the IAEA in 1990, took the same approach. We know that dose reconstructions coupled with
epidemiology extrapolated from other, often quite different nuclear events create uncertainties.
Dr. Wakeford, editor of the JRP, has recently pointed out this problem [3].
Smith says I omitted later dosimetry work. He implied in the original online version of
this essay (which Smith sent to sympathetic activists and journalists) that my omissions were
He forgets I am an historian. I wanted to understand how we came to know what we do about
Chernobyl, so I sought to reconstruct the scientic work of Soviet doctors and researchers
closest to the accident in the immediate years after the accident. I also sought to give the
political context that led to the failure of the U.N. General Assembly’s September 1991 pledge
drive to raise $1 billion in today’s funds to carry out, in part, a long-term health study on
Chernobyl exposed persons to nd out the impact of chronic, low doses of radioactivity on
human health.
Scientists repeatedly opine that we know little about low dose effects and have called over
the years for a major Chernobyl study akin to the Life Span studies. I sought to nd out why
we do not have that study.
Smith admits he does not know much about bio-dosimetry, so he checked with one
researcher who asserted that the Soviet methods of estimating doses that I report in Manual
for Survival were not valuable. I am not a scientist, but I do hold to standards of checking
sources and cross- referencing them. At this point in my reading of Smith’s review, I started
to wonder about the anecdotal nature of Smith’s evidence-gathering process. I was even more
dubious when he reported, after talking to one physician in Narodichi, Ukraine, that changes
in the reporting of cancers account for the alarming increase in frequencies of cancers in that
region after the accident. Smith does not elaborate. What changes in reporting? Does he have
any evidential material to back up that claim? Instead, he takes this one doctor’s word for it.
This is exactly the kind of anecdotal reporting on Chernobyl (‘I was there!’ ‘Someone told
me something!’) that I was working against. I did report in my book on anomalies in record-
keeping and the political difculties public health ofcials encountered when they did report
data such as rising cancer rates. Soviet public health ofcials were highly encouraged to pass
on only the good news that the Soviet populace was getting healthier every day. I know this
from archival correspondence cross-referenced against interviews with people who collected
J. Radiol. Prot. 40 (2020)
the data at the time. With two research assistants, I worked through over a dozen archives
in the former Soviet Union. We looked at records starting at the All-Union (federal) level,
moved to republic archives, down to province and nally checked records at the county level.
Indeed, cancer reporting changed after the accident as doctors, especially specialists such as
endocrinologists and oncologists, ed the contaminated territories surrounding the Chernobyl
Zone. Hospitals in those areas were staffed at 50% to 60% by 1989. With few oncologists,
fewer cancers were diagnosed. With few pathologists, ambulance drivers tended to be the ones
writing up death certicates.
Smith is most upset about my reporting on wildlife in the Chernobyl Zone. He again tasks
the reader to believe the testimony of one individual, Sergey Gaschak, who works as a xer
for scientists in the Zone, and has 30 years’ experience. For impressions of eyewitnesses,
we can read newspaper accounts. I was impressed with the hundreds of papers that Timothy
Mousseau and Anders Møller have authored from their 20 years of work that entailed at least
two annual visits to the Zone. Smith is incredulous that I did not mention that Møller was once
found guilty of manipulating data on a project that had nothing to do with Chernobyl. I did
not mention this because the CNRS, where Møller is employed now, exonerated him for these
charges, which developed out of an ofce dispute in Denmark. Smith would like me instead
to cite the work of Ron Chesser and Robert Baker at Texas Tech. Chesser and Baker rst
published in 1996 that they found signicant increases in mutations in voles in the Chernobyl
Zone. They reversed their positions in 2006, the year the Chernobyl Forum report ruled that
Chernobyl damage was minimal. Then again, ten years later, Baker returned to his original
observations. I did cite Baker’s most recent work, which I took to be his last word and which
Smith omits in his review. In Baker’s 2017 paper, he and his colleagues write: ‘The observed
increase in mitochondrial genomic diversity in voles from radioactive sites is consistent with
the possibility that chronic, continuous irradiation resulting from the Chernobyl disaster has
produced an accelerated mutation rate in this species over the last 25 years.’ Gaschak too signed
onto this paper [4]. In other words, after years of disagreeing with Mousseau and Møller’s
ndings, Baker now concurs. A recent article in the JRP about the Kyshtym trace in Siberia,
an explosion in an underground waste storage tank that released 20 million curies, ruled that
70 years later the affected forests have failed to recover to their pre-accident state; that the
numbers of soil animals were 15%–77% of those observed in similar but uncontaminated sites
[5]. Other omissions abound in Smith’s 12-page review. The omissions include researchers
who disagree with his ndings, depressed populations at all but the lowest doses [6], and
similar ndings from Fukushima that concur with Chernobyl data [7]. Does Smith have a
bias? Certainly one would presume that if he can convince people the Chernobyl Zone is safe,
he could sell more of his Atomic Vodka.1
Smith makes other assertions about my omissions, for example, of Angelina Guskova’s
statement that ‘in contrast to the rst group (134 ARS patients), this second group of individu-
als working within the 30 km zone, just as the population exposed to radiation, did not exhibit
any manifestations of radiation sickness.’ I assume that by ‘radiation sickness’ Guskova means
acute radiation sickness. There are some reports of acute radiation sickness among some eye-
witnesses to the disaster: a man in Pripyat who sunned himself on his roof the rst day the
reactor burned and a woman who worked outside all day in her garden. Generally, however, as
I argue in my book, people in contaminated areas were exposed to much lower doses and had
1Victoria Gill, “Chernobyl vodka: First consumer product made in exclusion zone,'' BBC News, 251 471.
J. Radiol. Prot. 40 (2020)
symptoms that Soviet doctors at the time attributed to low-level exposures. This was no small
group of people. Archival records show that in the summer after the accident, 40 000 people
were hospitalised for Chernobyl exposures, a quarter of whom were children. Soviet doc-
tors checked people into hospitals to treat and observe them because of troubling symptoms:
nausea, weakness, nose bleeds, chronic fatigue, enlarged thyroids, problems with pregnancies,
etc. As time went on, radioactive contaminants saturated the food chain, as I show by making
use of the records of the State Committee for Industrial Agriculture. With more contamin-
ated food, people took in more doses. By 1988–89, the records show increasing frequencies
of disease.
Smith insists that in the Japanese Life Span Study, effects were examined before 1950. This
is a critical point and he indicates as evidence the effects on children due to pre-conception
exposure of their parents. Still, Smith can see that mothers who did not survive to 1950 or
who, as in the case with many Chernobyl exposed mothers, were not able to give birth to
viable offspring, or had children who died before 1950, would have been excluded from those
studies. The epidemiologists Alice Stewart and George Kneale made this point in 1978 about
what they called the ‘healthy survivor effect,’ which involved the elimination of those in poor
health before the LSS began after 1950 [8]. Smith omitted this citation in his review. In my
book, I was trying to illuminate the political and historical context of the science that is often
taken at face value by scientists who cite the Life Span Study. Smith shows an ignorance of the
conditions and the nature of the data used in the creation of science that is taken as the ‘gold
As for dose reconstruction, Smith should be aware of the considerable evidence (e.g. CER-
RIE, 2004) that estimates of internal radiation doses from inhaled or ingested nuclides may
be highly uncertain. This means they can be unreliable, especially when ill-health evidence
exists. The editor of the journal was a member of the UK Government’s CERRIE Committee.
My point was not to rehash, as many reports have, the controversy over the health effects that
has been debated for the last 25 years, but to look at what Soviet doctors and researchers were
reporting in the critical ve years after the accident in classied documents. I was focused most
closely not on doctors like Guskova, located far away in Moscow and treating patients with
acute symptoms in her specialised clinic, but rather doctors closest to the accident in populated
territories that were contaminated with Chernobyl exposures. These doctors and researchers
worked in communities that experienced low to high levels of ambient radioactivity. Belarusian
scientists at the Academy of Science of Belarus set up case control studies in 1986 that I
found led in the academy archive. Towns and villages of the Mogilev Province had levels of
radioactivity in the soil from 40 to 140 curies of CS-137 per square kilometre. People lived
in these conditions until that area was almost fully depopulated in 1999. These records are
important because Soviet ofcials, as they led their reports in locked cabinets from 1986
to 1990, thought they were having a private conversation among themselves, one that, given
Soviet history up to that time, they assumed would never be revealed. Given that the Japanese
Life Span Studies started ve years after the bombings, and that the U.S. sponsorship of the
study was highly politicised, the Soviet data is unique and should be given more than a cursory
dismissal. That was what I was trying to do in my book. Smith is ‘highly sceptical,’ but, as he
writes, ‘I am not an epidemiologist.’
Smith recounts that mortality rates across the former USSR increased after 1991 and he
refers to the economic crises, alcohol consumption and smoking as factors. Where is his evid-
ence for this claim as it relates to the Chernobyl territories? Because mortality rates increased
in Siberia too after the collapse of the USSR? I would like to emphasise, again, that most of the
data reported in the archives I cite has to do with (non-smoking, non-drinking) children, not
in Siberia, but in contaminated territory in the years before the collapse of the USSR in 1991.
J. Radiol. Prot. 40 (2020)
Those are the years (1986–1991) that, in the chart Smith presents, show that life expectancy
in the Soviet Union peaked at an all-time high.
In terms of the years after 1991, the assumption that all Soviets and former Soviets abused
alcohol and tobacco to the point that it shortened their lives and caused a host of health prob-
lems is a common stereotype that is rarely substantiated. Working from 2000–2019, Wladimir
Wertelecki has led an on-going study showing a six times higher frequency than the European
average of neural tube birth defects in the northern areas of the Rivni Province of Ukraine
(200 km from Chernobyl). Wertelecki checked to see if foetal alcohol syndrome was a factor.
He found that the villagers of these regions were largely Pentecostals, who do not smoke or
drink for religious reasons. He also found levels of CS-137 in the bodies of family members
that were higher than in other parts of Ukraine [9,10]. This is the kind of careful work that
needs to be done in the Chernobyl-contaminated territories.
Smith repeatedly mischaracterises my arguments. He writes that I imply that eating berries
contaminated by up to 3000 Bq kg1of CS 137 is very dangerous. I make no such claim. I
was pointing out the global quality of the circulation of Chernobyl-contaminated food in order
to assert the need to more carefully curate Chernobyl-contaminated areas, rather than make
claims that nature is thriving and so can take care of itself.
On nuclear weapons testing, Smith refers to collective doses and estimated individual doses.
Again, as an expert in the eld, he glosses over obvious points I was making, such as that global
fallout (like Chernobyl fallout) did not spread uniformly across the northern hemisphere, but
was concentrated in certain areas, such as western Minnesota where in the mid-fties farmers
sued for compensation for their sick and dying sheep at the same time that levels of strontium-
90 in the North American plains were three times higher than at ground zero in Nevada [11].
Finally, and this is perhaps most distressing to hear from a scientist, Smith repeatedly
expresses ‘shock’ and ‘astonishment’ that I question in Manual for Survival the science claims
of the Life Span Study and various U.N. committees. If all scientists were to approach the sci-
entic method as Smith does, we would still believe the Earth is at. I report in my book that
from 1990 to 1996, U.N. consultants actively refuted what today is considered the most vis-
ible health outcome of the Chernobyl accident—a large increase in paediatric thyroid cancers.
I found that as early as 1990, when U.N. consultants were given clear evidence of this outbreak,
these consultants failed to mention in their report they had themselves tested 20 biopsies and
found they ‘checked out.’ Only in 1996 did UNSCEAR reverse itself. The ndings of the Life
Span Study have also had to be corrected and reversed over the decades. That, fortunately, is
the nature of science. We have more evidence as time goes on. Recently, a team of scientists
from the Wellcome Sanger Institute and Cambridge University found that low doses of radi-
ation promote the spread of cancer-capable cells in healthy tissue [12]. This is just one of many
recent reports that indicate the sensitivity of biological organisms to ionising radiation. There
is a scientic dispute here, and Smith appears unable to recognise or accept a difference of
In conclusion, Smith’s disparaging treatment of scientists, dismissal of evidence without
inquiry, vague extrapolations across differing nuclear incidents/environments/populations, and
use of anecdotal evidence should have no part in a book review or fact-checked opinion article
in a scholarly journal. I am grateful that Smith included a statement on his conict of interest:
that he has taken money from the nuclear industry. I can state that I have received no money
from either the nuclear industry or anti-nuclear political groups.
J. Radiol. Prot. 40 (2020)
[1] Lindee M S 2016 Survivors and scientists: Hiroshima, Fukushima, and the Radiation Effects
Research Foundation, 1975–2014 Soc. Stud. Sci. 46 184–209
[2] Lindee M S 1994 Suffering Made Real: American Science and the Survivors at Hiroshima 1st edn
(Chicago, IL: University of Chicago Press) pp 183
[3] Dacey J 9 July 2019 Chernobyl’s legacy and why assessing radiation risk is so difcult Phys. World
[4] Baker R J, Dickins B, Wickliffe J K, Khan F A A, Gaschak S, Makova K D and Phillips C D 2017
Elevated mitochondrial genome variation after 50 generations of radiation exposure in a wild
rodent Evol. Appl. 10 784–91
[5] Fesenko S 2019 Review of radiation effects in non-human species in areas affected by the Kyshtym
accident J. Radiol. Prot. 39 R1–17
[6] Mappes T, Boraty´
nski Z, Kivisaari K, Lavrinienko A, Milinevsky G, Mousseau T A, Møller A P,
Tukalenko E and Watts P C 2019 Ecological mechanisms can modify radiation effects in a key
forest mammal of Chernobyl Ecosphere 10 e02667
[7] Garnier-Laplace J, Beaugelin-Seiller K, Della-Vedova C, M´
etivier J-M, Ritz C, Mousseau T A
and Pape Møller A 16 November 2015 Radiological dose reconstruction for birds reconciles
outcomes of Fukushima with knowledge of dose-effect relationships Sci. Rep. 516594
[8] Alvarez R 1984 Radiation Standards and A-bomb Survivors BAS 40 26–28
[9] Wertelecki W 2017 Chernobyl 30 years later: radiation, pregnancies and developmental anomalies
in Rivne, Ukraine Eur. J. Med. Genet. 60 2–11
[10] Wertelecki W, Yevtushok L, Kuznietsov I, Komov O, Lapchenko S, Akhmedzanova D and
Ostapchuk L 2018 Chernobyl, radiation, neural tube defects, and microcephaly Eur. J. Med.
Genet. 61 556–63
[11] Springer P 1988 Forgotten Fallout: What is the Legacy of Radioactive Rains? Fargo Forum, Sunday
May 1
[12] Fernandez-Antoran D, Piedrata G, Murai K, Ong S H, Herms A, Frezza C and Jones P H 2019
Outcompeting p53-Mutant Cells in the Normal Esophagus by Redox Manipulation Cell Stem
Cell 25 32941
ResearchGate has not been able to resolve any citations for this publication.
Full-text available
As humans age, normal tissues, such as the esophageal epithelium, become a patchwork of mutant clones. Some mutations are under positive selection, conferring a competitive advantage over wild-type cells. We speculated that altering the selective pressure on mutant cell populations may cause them to expand or contract. We tested this hypothesis by examining the effect of oxidative stress from low-dose ionizing radiation (LDIR) on wild-type and p53 mutant cells in the transgenic mouse esophagus. We found that LDIR drives wild-type cells to stop proliferating and differentiate. p53 mutant cells are insensitive to LDIR and outcompete wild-type cells following exposure. Remarkably, combining antioxidant treatment and LDIR reverses this effect, promoting wild-type cell proliferation and p53 mutant differentiation, reducing the p53 mutant population. Thus, p53-mutant cells can be depleted from the normal esophagus by redox manipulation, showing that external interventions may be used to alter the mutational landscape of an aging tissue.
Full-text available
Nuclear accidents underpin the need to quantify the ecological mechanisms which determine injury to ecosystems from chronic low-dose radiation. Here, we tested the hypothesis that ecological mechanisms interact with ionizing radiation to affect natural populations in unexpected ways. We used large-scale replicated experiments and food manipulations in wild populations of the rodent, Myodes glareolus, inhabiting the region near the site of the Chernobyl disaster of 1986. We show linear decreases in breeding success with increasing ambient radiation levels with no evidence of any threshold below which effects are not seen. Food supplementation of experimental populations resulted in increased abundances but only in locations where radioactive contamination was low (i.e., below % 1 lSv/h). In areas with higher contamination , food supplementation showed no detectable effects. These findings suggest that chronic low-dose-rate irradiation can decrease the stability of populations of key forest species, and these effects could potentially scale to broader community changes with concomitant consequences for the ecosystem functioning of forests impacted by nuclear accidents.
Full-text available
Currently, the effects of chronic, continuous low dose environmental irradiation on the mitochondrial genome of resident small mammals are unknown. Using the bank vole (Myodes glareolus) as a model system, we tested the hypothesis that approximately 50 generations of exposure to the Chernobyl environment has significantly altered genetic diversity of the mitochondrial genome. Using deep sequencing, we compared mitochondrial genomes from 131 individuals from reference sites with radioactive contamination comparable to that present in Northern Ukraine before the April 26, 1986 meltdown, to populations where substantial fallout was deposited following the nuclear accident. Population genetic variables revealed significant differences among populations from contaminated and uncontaminated localities. Therefore, we rejected the null hypothesis of no significant genetic effect from 50 generations of exposure to the environment created by the Chernobyl meltdown. Samples from contaminated localities exhibited significantly higher numbers of haplotypes and polymorphic loci, elevated genetic diversity, and a significantly higher average number of substitutions-per-site across mitochondrial gene regions. Observed genetic variation was dominated by synonymous mutations, which may indicate a history of purify selection against nonsynonymous or insertion/deletion mutations. These significant differences were not attributable to sample size artifacts. The observed increase in mitochondrial genomic diversity in voles from radioactive sites is consistent with the possibility that chronic, continuous irradiation resulting from the Chernobyl disaster has produced an accelerated mutation rate in this species over the last 25 years. Our results, being the first to demonstrate this phenomenon in a wild mammalian species, are important for understanding genetic consequences of exposure to low-dose radiation sources. This article is protected by copyright. All rights reserved.
Full-text available
We reconstructed the radiological dose for birds observed at 300 census sites in the 50-km northwest area affected by the accident at the Fukushima Daiichi nuclear power plant over 2011–2014. Substituting the ambient dose rate measured at the census points (from 0.16 to 31 μGy h −1) with the dose rate reconstructed for adult birds of each species (from 0.3 to 97 μGy h −1), we confirmed that the overall bird abundance at Fukushima decreased with increasing total doses. This relationship was directly consistent with exposure levels found in the literature to induce physiological disturbances in birds. Among the 57 species constituting the observed bird community, we found that 90% were likely chronically exposed at a dose rate that could potentially affect their reproductive success. We quantified a loss of 22.6% of the total number of individuals per increment of one unit log 10-tansformed total dose (in Gy), over the four-year post-accident period in the explored area. We estimated that a total dose of 0.55 Gy reduced by 50% the total number of birds in the study area over 2011–2014. The data also suggest a significant positive relationship between total dose and species diversity.
The area affected by the Kyshtym accident in 1957 provided a unique opportunity for long-term studies of radiation effects in the environment. The biological effects observed in the area varied from deterministic lethal effects to an enhanced rate of mutations induced by radiation. This paper provides a comprehensive review of the long-term studies of biological effects in plants and animals inhabiting the Kyshtym affected areas over more than 50 years. Most of the observed effects were induced by the high irradiation during the 'acute' period after the accident. At the same time, some of the radiation effects were also because of long-term chronic exposure over many generations. Some phenomena such as (1) the increase of the mutation rate per unit dose with reduction of dose and dose rate, and (2) the radiodaptation of the affected populations to the chronic exposure were documented for the first time based on the radiobiological research performed in that area.
Pregnant women residing in areas impacted by the Chornobyl ionizing radiation of the Rivne Province in Ukraine have persistent higher levels of incorporated cesium-137. In these areas the neural tube defects and microcephaly rates are significantly higher than in areas with lower maternal cesium-137 incorporated levels. In two Rivne counties with populations proximal to nuclear power plants the rates of neural tube defects and microcephaly are the highest in the province. The neural tube defects rates in Rivne are persistently among the highest in Europe.
In the 30 years since the Chornobyl nuclear power plant disaster, there is evidence of persistent levels of incorporated ionizing radiation in adults, children and pregnant women in the surrounding area. Measured levels of Cesium-137 vary by region, and may be influenced by dietary and water sources as well as proximity to nuclear power plants. Since 2000, comprehensive, population-based birth defects monitoring has been performed in selected regions of Ukraine to evaluate trends and to generate hypotheses regarding potential causes of unexplained variations in defect rates. Significantly higher rates of microcephaly, neural tube defects, and microphthalmia have been identified in selected regions of Ukraine collectively known as Polissia compared to adjacent regions collectively termed non-Polissia, and these significantly higher rates were evident particularly in the years 2000–2009. The Polissia regions have also demonstrated higher mean whole body counts of Cesium-137 compared to values in individuals residing in other non-Polissia regions. The potential causal relationship between persistent ionizing radiation pollution and selected congenital anomaly rates supports the need for a more thorough, targeted investigation of the sources of persistent ionizing radiation and the biological plausibility of a potential teratogenic effect.
In this article, I reflect on the Radiation Effects Research Foundation and its ongoing studies of long-term radiation risk. Originally called the Atomic Bomb Casualty Commission (1947–1975), the Radiation Effects Research Foundation has carried out epidemiological research tracking the biomedical effects of radiation at Hiroshima and Nagasaki for almost 70 years. Radiation Effects Research Foundation scientists also played a key role in the assessment of populations exposed at Chernobyl and are now embarking on studies of workers at the Fukushima Daiichi Nuclear Power Plant. I examine the role of estimating dosimetry in post-disaster epidemiology, highlight how national identity and citizenship have mattered in radiation risk networks, and track how participants interpreted the relationships between nuclear weapons and nuclear energy. Industrial interests in Japan and the United States sought to draw a sharp line between the risks of nuclear war and the risks of nuclear power, but the work of the Radiation Effects Research Foundation (which became the basis of worker protection standards for the industry) and the activism of atomic bomb survivors have drawn these two nuclear domains together. This is so particularly in the wake of the Fukushima disaster, Japan’s ‘third atomic bombing’. The Radiation Effects Research Foundation is therefore a critical node in a complex global network of scientific institutions that adjudicate radiation risk and proclaim when it is present and when absent. Its history, I suggest, can illuminate some properties of modern disasters and the many sciences that engage with them.
For more than 33 years, the US government has supported the Life Span Study of Japanese survivors as a follow-up of the 1945 nuclear bombings of Hiroshima and Nagasaki. Since 1975, the study has been funded jointly by the United States and Japan under the auspices of the Radiation Effects Research Foundation. In the May issue of this bulletin radiation epidemiologists Dr. Alice Stewart and George Kneale raise perhaps the most fundamental question of all: Does the Japanese A-bomb survivor study have any value in deriving risk estimates for low-level radiation. On the basis of data published by the Radiation Effects Research Foundation in 1978, Stewart and Kneale suggest that Foundation analysts have confused long-term effects of tissue-destructive high doses with single-cell low-dose effects. If they are correct, the method of linear extrapolation from high-dose studies for low-level radiation risk estimates is invalid. The author feels the A-bomb survivors study should be opened up to an independent peer review process.
The atomic bombs dropped on Hiroshima and Nagasaki in August of 1945 unleashed a force as mysterious as it was deadly—radioactivity. In 1946, the United States government created the Atomic Bomb Casualty Commission (ABCC) to serve as a permanent agency in Japan with the official mission of studying the medical effects of radiation on the survivors. The next ten years saw the ABCC's most intensive research on the genetic effects of radiation, and up until 1974 the ABCC scientists published papers on the effects of radiation on aging, life span, fertility, and disease. Suffering Made Real is the first comprehensive history of the ABCC's research on how radiation affected the survivors of the atomic bomb. Arguing that Cold War politics and cultural values fundamentally shaped the work of the ABCC, M. Susan Lindee tells the compelling story of a project that raised disturbing questions about the ethical implications of using human subjects in scientific research. How did the politics of the emerging Cold War affect the scientists' biomedical research and findings? How did the ABCC document and publicly present the effects of radiation? Why did the ABCC refuse to provide medical treatment to the survivors? Through a detailed examination of ABCC policies, archival materials, the minutes of committee meetings, newspaper accounts, and interviews with ABCC scientists, Lindee explores how political and cultural interests were reflected in the day-to-day operations of this controversial research program. Set against a period of conflicting views of nuclear weapons and nuclear power, Suffering Made Real follows the course of a politically charged research program and reveals in detail how politics and cultural values can shape the conduct, results, and uses of science.