保健医療科学

2018 Vol.67 No.1 p.115－122

Topics: Lessons learned on public health from the Fukushima Daiichi Nuclear Power Plant accident＜ Review ＞
Lessons learned from radiation biology: Health effectsof low levels of exposure to ionizing radiation onhumans regarding the Fukushima accident
Tsutomu Shimura, Ichiro Yamaguchi, Hiroshi Terada, Naoki Kunugita
Department of Environmental Health, National Institute of Public Health
Abstract
Herein we summarize the important issues for radiation health effects on humans based on the reliable
scientific literature. Radiation effects are categorized “tissue reactions” and “stochastic effects”. The former
are previously called “deterministic effects” which have a threshold below which the effect does not occur.
The tissues and organs-threshold doses of local exposure has been estimated at around 100 mSv for fetal
abnormalities, temporary infertility of the male and 120~200 mSv for severe mental retardation among
the atomic bomb survivors of Hiroshima and Nagasaki who were exposed in utero. Whole body irradiation>1000 mGy causes acute radiation syndrome (ARS), including erythema, nausea, vomit, headache,diarrhea, fever and confusion. On the other hand, stochastic effects consist of cancer and genetic effects.
Cancer risks for human exposure to radiation are estimated by epidemiological study among the atomic
bomb survivors of Hiroshima and Nagasaki. Radiation risks below around 100 mSv are not capable to be
estimated directly from this epidemiological data. Although all the epidemiological data do not support thelinear nonthreshold (LNT) model, the model is useful for the purpose of radiation protection but not for risk
assessment. In order to understand radiation effects on humans, we explain the essential terms relative
biological effectiveness, equivalent dose, effective dose, dose and dose-rate effectiveness factor in thismanuscript.
We hope that this review paper facilitates the knowledge acquisition of the radiation effects on humans
and may help administrative officers and public health nurses to implement public health actions against
future nuclear disasters or radiological accidents.
keywords: low-dose radiation, health effects, cancer risk, Fukushima nuclear accident, radiation biology(accepted for publication, 19th January 2018)

I．Introduction
We have had a severe radiological disaster after the Great
East Japan Earthquake and Tsunami of 2011. A large amountof radioactive materials was released into the environment
from the damaged Fukushima Daiichi Nuclear Power Plant[1]. The health-related hazards for human exposure toionizing radiation (hereafter shortened to ʻradiationʼ) are
estimated by using the Life Span Study Cohort data fromthe atomic bomb survivors of Hiroshima and Nagasaki[2]. According to this epidemiological study, incidence ofleukemia and solid cancer increased among those who
received higher doses. Radiation risks below ~100 mSv are
not able to be determined directly from the epidemiological
data because of the requirement of a very large sample size.
In the Fukushima accident, the World Health Organization(WHO) and the United Nations Scientific Committee on the
Effects of Atomic Radiation (UNSCEAR) reports indicatedthat doses of radiation to the public are at low levels [3, 4].
The public health actions for radiation protection, such as

Corresponding author: Tsutomu Shimura
2-3-6 Minami, Wako, Saitama 351-0197, Japan.
Tel. +81-48-458-6261; Fax +81-48-458-6270; Email: tsimura@niph.go.jp

J. Natl. Inst. Public Health, 67 (1) : 2018115

Tsutomu Shimura, Ichiro Yamaguchi, Hiroshi Terada, Naoki Kunugita
evacuations from the radiation affected areas and control ofthe distribution of various food products, remarkably reduced
external and internal radiation exposures [5]. However, there
are mental health issues such as psychological distress fromfear of radiation exposure, especially in long-term low-dose
rate irradiation [6].
The main biological target for radiation is the DNA
molecule. DNA double-strand breaks (DSBs) cause harmful
effect such as cell death and chromosomal aberrationsin irradiated cells [7, 8]. Radiation biology research has
focused on DNA damage responses and has elucidated themechanisms such as DNA repair, cell cycle checkpoint, andapoptosis in mammalian cells [9]. The effects of long-term
radiation exposure are generally milder than for an acuteexposure under the same total dose by repairing damaged
DNA. The health risks associated with low-dose long-term
radiation remain to be elucidated and are currently being
investigated intensively to understand the Fukushima case[10, 11].
We previously summarize the public health actions
taken to mitigate the public exposures to radiation after
the Fukushima accident in order to provide valuablelessons learned for disaster preparedness [5]. We also
introduced governmental action of several occupational
health interventions for Radiation Workers including the
emergency workers and the decontamination workers in the
Fukushima accident [12]. In this review paper, we described
the reliable scientific knowledge about radiation biology tohelp to understand health effect of radiation exposure in
humans. In addition, we explain the terms relative biologicaleffectiveness, equivalent dose, effective dose, dose anddose-rate effectiveness factor in this manuscript.

II．Methods
The Ministry of the Environment, Government of Japan
published “The universal textbook regarding health effectsof radiation” to provide the basic knowledge of radiation
effects after the Fukushima accident (http://www.env.go.jp/
chemi/rhm/kisoshiryo/pdf_h28/2016tk1whole.pdf). The aimof this text is for the avoidance of confusion when using
various sources for the explanations of the radiation effects.
Therefore, we mainly collect the information from this text
and also use the WHO and UNSCEAR reports. The otherpapers which we reviewed were searched from the PubMedelectronic library databases [13].

III．Results
1. External and internal radiation exposure
A large amounts of Iodine-131 (I-131), Cesium-134 (Cs-

116134), and Cesium-137 (Cs-137) were released into theenvironment during the Fukushima event [14]. There are
two main pathways of exposure to radiation in humans:
radiation is externally exposed from outside the body due
to contaminated soil or internally exposed by consuming
foods containing radioactive materials and inhalation ofcontaminated materials. For external exposure, X- andγ-rays penetrate deeply enough into the body to reachliving tissue. However, alpha particles can be absorbed
within the stratum corneum of the skin and do not reachto basal cells as the radiation target. In contrast, the alphaemitter nuclide with accumulative property and long halflife is the most potent in the case of internal exposure.
Radiation exposure is generated when radioactive nuclides
physically decay in the body. However, some of them areexcreted from the body without physical decay so that it nolonger is a source of radiation exposure to the organism.
Taking into consideration the elimination of a substancefrom a living organism, the biological half-life, is an
important factor for consideration of internal exposure in
addition to the physical half-life.
Insoluble Cs-bearing particles were identified in aerosol
samples following the Fukushima accident [15]. Such Csbearing particles are thought to have persisted for a longtime on the land surface, longer than those of the watersoluble Cs particles. The health effects of these particles
are being investigated based on the particle sizes andinsolubility in water.
2. Radiation effects on humanRadiation effects on humans are usually classified into
two categories: “tissue reactions ” and “stochastic effects”(Figure 1) [16].“Tissue reactions” are previously called“deterministic effects” which have a threshold below which
the effect does not occur. Stochastic effects do not always
occur even if it receives a certain amount of radiation. The
influences are increasing as exposure increases. Stochastic
effects consist of cancer and genetic effects. The effectof radiation on tissues is not severe in low- or moderatedoses of radiation (below threshold), despite the small
amounts of cells which die. Surviving cells maintain thetissue and organ function in this dose range. Radiationinduces transient loss of the tissue and organ function
with an increase in the radiation dose. Proliferation anddifferentiation of tissue stem cells contributes to theirrecovery from radiation injury. In contrast, high dosesof radiation irreversibly damage the tissue stem cells byradiation-induced cell death and they never recover. The
tissues and organs-threshold doses of local exposure has
been estimated at around 100 mSv for fetal abnormalities,
temporary infertility of the male and 120~200 mSv for

J. Natl. Inst. Public Health, 67 (1) : 2018

Lessons learned from radiation biology: Health effects of low levels of exposure to ionizing radiation on humans regarding the Fukushima accident
Threshold

No Threshold

Tissue reactions(Deterministic effects)

Stochastic effects

Acute effects

Local exposure
Erythema
Epilation,
Sterility,
Fetal abnormality

Late effects

Acute effects

Late effects

Cataract

None

Solid Cancer
Leukemia

whole-body exposure
ARS(BM injury, GIT injury,
Cardiovascular injury)
Fever
Vomiting

Figure 1 Tissue reactions and Stochastic effects

severe mental retardation among the atomic bomb survivorsof Hiroshima and Nagasaki who were exposed in utero [17].
Exposure >500 mGy to bone mallow transiently decreases
the number of blood cells with a reduction of hematopoietic
capacity [18]. The radiation exposure threshold forcataracts is initially estimated as 1500 mGy and this value
was recently revised to a lower 500 mGy according to theLife Span Study Cohort from the atomic bomb survivorsof Hiroshima and Nagasaki [18]. There is no evidence ofa significant increase in trans-generational genetic effects
following radiation exposure in the atomic-bomb survivorsof Hiroshima and Nagasaki, and the patients who received
radiotherapy [19, 20].
Whole body irradiation >1000 mGy causes acute radiation
syndrome (ARS). In the Chernobyl accident, ARS was
confirmed in 134 of the emergency workers (28 died within
the first four months) [21]. In JCO accident in 1999, twoworkers died of ARS due to exposure to >6~7 Sv of highdoses of radiation [22, 23]. In the case of local radiation

exposure on the body, high doses of radiation causes
erythema, epilation, and sterility etc. We summarized
characteristic symptoms and treatment modality regarding
ARS according to the radiation doses in Table 1. The
prodromal phase of ARS usually occurs in the first 48
hours and represents erythema, nausea, vomit, headache,diarrhea, fever and confusion [16]. Hematopoietic disorders,gastrointestinal disturbances and cardiovascular disorders
appear after 3 weeks in the latent phase of ARS. No
ARS was reported in the Fukushima accident, because ofradiation exposure due to the Fukushima accident is below
1000 mSv among emergency workers [12].
3. Cancer risks associated with radiation exposure
Radiation is known as a carcinogen that causes leukemia
and solid cancer in humans. There is no threshold forstochastic effects, such as cancer induction and mutations
which are thought to depend on the absorbed dose. There
are major concerns about cancer risks for human exposure

Table 1 Characteristic symptons and treatment modality of ARS
Dose (Gy)

Therapeutic range

Below lethal dose

Lethal range

0～1

1～2

2～6

6～10

10～15

>50

Therapeutic needs

None needed

Clinical observation

Effective therapy

Possible therapy

Main targeted organ-

Therapy
Central nervous
systemCharacteristic
symptoms-

Moderate
Leucopenia

Palliative
Gastrointestinal
tract
Diarrhoea, fever,electrolytic
imbalanceNo

1Gy:5%, 2Gy:50%-3hAppearance ofvomiting
Time of delay ofnausea+vomiting
Therapy
Prognosis

Blood-forming tissue

Psychotherapy,
Psychotherapy
haematologicalobservation
Excellent

Lethality(Time of death)

0

Cause of death-

Heavy leucopenia,
purpura,haemorrhage,infection,
epilation(more than 3Gy)

Cramps, tremor
ataxy, lethargy>3Gy:100%2h

0-80%(2 months)

30min

1h

Transplantation ofTransfusion ofbone marrow isblood, antibiotics
possible and white
Guarded80-100%(2 months)

Haemorrhage-infection

J. Natl. Inst. Public Health, 67 (1) : 2018

Support ofelectrolytic balance

Symptomatic

Poor

Hopeless

90-100%(2weeks)

100%(2 days)Enterocolitis

Irreversible
circulatory collapse,
cerebral oedema

117

Tsutomu Shimura, Ichiro Yamaguchi, Hiroshi Terada, Naoki Kunugita
to radiation after the Fukushima accident [3, 4]. The Life
Span Study Cohort from the atomic bomb survivors ofHiroshima and Nagasaki revealed an increase in incidenceof leukemia a few years after the bombing and peakedat 6~7 years after. Cancer risks for human exposure toradiation are estimated by this epidemiological study
among the atomic bomb survivors of Hiroshima andNagasaki. The radiation-associated excess leukemia risks
are evident even 55 years after the bombings [24]. On theother hand, the solid cancer risks increased in persons
over the age of 40, the so-called cancer-prone age [2]. The
cancer risks associated with internal radiation exposure
was reported in the epidemiological study of Chernobyl
victims. Internal exposure to I-131 from contaminated milkin childhood caused an increased risk of thyroid cancer
after the Chernobyl nuclear crisis [21, 25, 26]. Fortunately,
the absorbed doses to the thyroid of younger people werelimited in the Fukushima accident [4]. Details are describedin other papers in this special issue. Cancer risks fromnatural radiation has been investigated among residents
who live in the high natural background radiation area in
Kerala, India [27] and Yangjiang in Guangdong Province,
China [28]. Increased risk of cancer due to the high natural
background radiation has not been observed in theseareas. The other study of the risk of childhood cancer also
showed no evidence of an association [29]. In contrast, anationwide cohort study of the risk of childhood cancer due
to background radiation in the Swiss National Censuses
suggested a positive association [30]. So far, radiation risks
below around 100 mSv are not capable to be estimateddirectly from these epidemiological data. Internationalorganizations such as World Health Organization (WHO)and the United Nations Scientific Committee on the Effectsof Atomic Radiation (UNSCEAR) reported that increased
risk of disease associated with radiation exposure fromthe Fukushima accident will not be expected besides thepossibility of thyroid cancer because of the limited radiation
exposure among public [31]. Dr. Boice from National
Council on Radiation Protection and Measurementscommented that the linear nonthreshold (LNT) model isused for the purpose of radiation protection but not forrisk assessment in the low-dose range because of all theepidemiological data do not support the model [32]. Some
scientists have been suggested utilizing the beneficial effectof radiation such as hormesis and adaptation to low-dosesof radiation for risk assessment [33]. However, the cancer
risks associated with low-dose radiation are uncertainties
because of insufficient scientific evidence.

118

4. R adiation signatures associated with radiationinduced tumorigenesis
The elucidation of the mechanism of radiation-induced
tumorigenesis is indispensable to clarify the cancer risksof low-dose radiation [34]. Identification of DNA mutations
associated with radiation-related carcinogenesis, socalled radiation signature, may help to understand thecharacteristics of radiation-induced tumorigenesis [35, 36].
The transcriptional factor acute myeloid leukemia 1(AML1)
is indispensable for hematopoiesis. It was reported
that AML1 mutations were found in myelodysplastic
syndrome patients among atomic bomb survivors [37].
Radiation is thought to contribute to the transformationof hematopoietic progenitors via AML1 mutations. RET/
PTC rearrangements are frequently observed in adultonset papillary thyroid cancer (PTC) of A-bomb survivor[38]. RET/PTC is considered as radiation signature for IRinduced thyroid cancer. However, others claim that the
mutation also appears in sporadic PTC [39]. Thus, theradiation signatures are still argued among various cancers.
Epigenetic effects may also be involved in radiation-related
cancer. However, little science is available currently on theepigenetic effects [35, 36].
The biological model of carcinogenesis based on scientificevidence may help people understand their risk fromradiation exposure [34]. For instance, the Amitage andDoll multistage model of carcinogenesis in which several
successive changes in the cell are required before cancer
appears as a clinical manifestation [40]. They further
developed a two-stage theory of carcinogenesis. Healthy
cells have acquired growth advantages by the faster rateof multiplication to form intermediated cells at the firststage. Then, the second discrete event occurs to transform
malignant cells at the second stage [41]. This model isapplied to the understanding of the risk of radiation-related
carcinogenesis by using human epidemiological data.
5. Relative biological effectiveness, equivalent doseand effective dose
Radiation includes diverse particles such as photons,
electrons, protons, and neutrons which produces ionized
and/or excited atoms in irradiated materials. The linear
energy transfer (LET) differs depending on the type andenergy of the incident radiation. Alpha particles consist of
two protons and two neutron (charged helium nuclei), areless penetrating and are classified as high-LET radiation.
The biological target of ionizing radiation is DNA. HighLET causes more severe unrepairable DNA damage in the
nucleus (so-called clustered DNA damage [42]) than otherradiation. On the other hand, X- and γ-rays belonged to lowLET and are less effective to the organelle by the repair

J. Natl. Inst. Public Health, 67 (1) : 2018

Lessons learned from radiation biology: Health effects of low levels of exposure to ionizing radiation on humans regarding the Fukushima accident

IV．Discussionof damaged DNA. Thus, the biological effect of radiation
is influenced by radiation dose, dose rates and radiation
quality. Relative biological effectiveness (RBE) of radiation
is estimated as the ratio by using the X-ray as a standard.
Equation 1: RBE=DX / D
In Equation 1 D X is a reference absorbed dose of
X-rays, and D is the absorbed dose of tested radiationthat causes the same biological effect. The RBEs havebeen estimated as the effectiveness of various endpoints,
such as cell survival, mutation rates and incidence of
apoptosis. The value of RBE varies according to radiationdose, dose rates, division of irradiation and cell type.
Since RBE is so complicated, it cannot simply apply forradiological protection. The radiation weighting factor WR
is conservatively defined to connect with LET on a basis ofacknowledgement of the experimental RBEs. WR is 20 foralpha particles, while it is 1 for X-,γ-and β-ray. Equivalentdose H (Sv) is calculated as the mean absorbed dose to atissue or organ D (Gy) multiplied by the radiation weighting
factor WR.
Tissue weighting factor WT is considered the radiation
sensitivity of each tissue or organ. Bone marrow, lymph
tissue and testis are particularly susceptible to radiation,
whereas brain and bone are shown to be low radiation
sensitivity [16]. This value applies to determine the effectof partial body irradiation or local irradiation. For instance,
the target organ for internal exposure to I-131 is the
thyroid. It is important to estimate absorbed dose to thethyroid to elucidate the effect of I-131. Effective dose E (Sv)is determined by the tissue-weighted sum of the equivalentdoses multiply by WT . Thus, the absorbed dose Gy converts
to Sv in consideration of the RBE.

The aim of this review paper is to learn from the
Fukushima experience and help practitioners to implement
radiation protection actions against future nuclear disasters
or radiological accidents. After the Fukushima accident,
people believed that the exposure exceeding 1 mSv/year
causes increase in cancer risks and genetic effect in theprogeny. However, radiation risks below around 100 mSv
are not capable to be detected from current epidemiological
data. Trans-generational genetic or epi-genetic effects due
to radiation exposure have not been reported in humans.
We have to know that we know what we know, and toknow that we do not know what we do not know. ICRP
recommends 1 mSv/year as the dose limit for the generalpublic based on the fact that the difference level of naturalradiation background between low and high areas in order
to not suffer the disadvantage of radiation exposure among
the public [48].
It is minimally required to know the units of radiationdose to understand the radiation effect on humans.
Radiation absorbed dose and effective dose uses Gy and Sv,
respectively. We mentioned the difference between Gy and
Sv by interpreting the terms of RBE, equivalent dose andeffective dose.
Many researchers are working on various issues
regarding uncertainty for radiation effects, such as theaccuracy of radiation dose estimation, cancer risk of lowdose and low-dose rate radiation and the health effects ofinsoluble Cs particles. These investigations may contributeto obtain more reliable scientific evidences for radiation
protection in the future.

6. Dose and dose-rate effectiveness factor

V．Conclusion

In the case of fractionated radiation and chronic
exposures, the health effects are typically milder than thoseof acute high-dose rate irradiation at the same total dose[43]. Cells can eliminate the DNA damage induced by low
dose rate radiation through protective mechanisms of DNA
repair and show adaptive responses to long-term exposure[44]. The International Commission of RadiologicalProtection (ICRP) proposes that a dose and dose rate
effectiveness factor (DDREF) of 2 accounts for the reduced
effectiveness of low-dose rate radiation [45]. However, theradiobiological studies were the main argument in numericalvalue of DDREF [46, 47]. The German commission onradiological protection (Strahlenschutzkommision:SSK)
recommended not to use of the DDREF in radiologicalprotection due to uncertainty about the value of DDREF. WHO
did not use DDREF in the global report on the Fukushima
nuclear accident regarding health risk assessment [3].

There is the issue of anxiety from radiation exposure
after the Fukushima accident even though radiation
exposure among the public is limited. Continuous support
to overcome this issue, together with the local community,
is important to protect the public health during the recovery
from the nuclear disaster.

Acknowledgements
Sources of support: This research was supported by agrant from the Japanese Ministry of Education and Science
Houga (15K12220, 15K12212, 17K19944), Industrial
Disease Clinical Research Grants from the Japanese
Ministry of Health, Labour, and Welfare and in part by
NIFS Collaborative Research Program (NIFS13KOBA028).
This work was performed at the Joint Usage/Research

J. Natl. Inst. Public Health, 67 (1) : 2018

119

Tsutomu Shimura, Ichiro Yamaguchi, Hiroshi Terada, Naoki Kunugita
Center (Radiation Biology Center), Kyoto University, theProgram of the network-type joint Usage/Research Center
for Radiation Disaster Medical Science of Hiroshima
University, Nagasaki University and Fukushima Medical
University.

Conflict of Interests
The authors declare that there is no conflict of interests
regarding the publication of this article.

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J. Natl. Inst. Public Health, 67 (1) : 2018121

Tsutomu Shimura, Ichiro Yamaguchi, Hiroshi Terada, Naoki Kunugita

放射線生物学から学ぶ低線量放射線による人の健康影響について
志村勉，山口一郎，寺田宙，欅田尚樹
国立保健医療科学院生活環境研究部

抄録
本総説論文では，人の放射線影響研究について，どこまでわかっているのかを科学的根拠を基に紹介する．ヒトの放射線影響は，組織反応と確率的影響に分類される．組織反応は，以前は確定的影響とよばれ，しきい値があり，しきい値以下の線量の被ばくでは影響が観察されない．胎児の異常や男性の一時的不妊のしきい値は100 mSvで，胎児期の被ばくによる精神発達遅延のしきい値は，広島・長崎原爆被爆者の疫学解析から120~200 mSvと報告されている．1000 mGy以上の高線量の全身被ばく
では，急性放射線障害といわれる，紅斑，吐き気，嘔吐，頭痛，下痢，発熱，混乱等の症状がみられる．一方，確率的影響には，がんと遺伝的影響がある．ヒトの放射線による発がんリスクの科学的根
拠には，広島・長崎の原爆被爆者の寿命調査の疫学データが用いられる．もっとも精度が高いと言われるこの調査によっても100 mSv以下の低線量放射線による発がんリスクの増加があるかどうかを評価することはできない．しきい値なしの直線モデルは，全ての人の放射線発がんに関する疫学データの結果を反映しているわけではないが，放射線防護を考える上で有用ではある．しかし，このモデルを使って放射線リスク評価をすることはできない．
本論文では，ヒトの放射線影響を理解する上において重要な生物効果比，等価線量，実行線量，線量・線量効果値について，説明する．本総説論文が，放射線事故の際に，放射線対策に関わる実務者の放射線基礎知識の向上に活用されることを期待する．
キーワード：低線量放射線，健康影響，がんのリスク，福島第一原子力発電所事故，放射線生物学

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J. Natl. Inst. Public Health, 67 (1) : 2018