Radiation damage

Japanese: 放射線障害

Concept: Radiation has various effects on living organisms depending on the dose. In modern society, it is necessary to consider not only the effects of radiation that is widely used in medical treatment, but also the effects of radiation that exists in the environment due to causes such as nuclear disasters.
Classification When exposed to radiation, various symptoms appear in a time-dependent manner depending on the radiation dose, so there are several ways to classify the effects of radiation (Figure 16-1-8). First, radiation damage is broadly divided into physical effects and genetic effects. Physical effects are further classified according to when symptoms appear: early effects, which occur within a few months of exposure, and late effects, which occur later. Furthermore, if a woman is pregnant at the time of exposure, effects on the fetus may also occur. In addition to these classifications, from the perspective of radiation protection, effects can also be classified into deterministic effects, which have a threshold for the appearance of symptoms, and stochastic effects, which have no clear threshold (Figure 16-1-9).
Pathogenesis: In cells exposed to high doses of radiation, DNA damage cannot be repaired, leading to cell death. If this is widespread and stem cells are also damaged, tissue dysfunction can result. This is the cause of serious disorders as an early effect. In contrast, when exposed to low doses of radiation, there is a higher chance of DNA damage being repaired, so cell death occurs less frequently. However, because the repaired genetic information is not necessarily completely identical to the original, abnormal genetic information is generated, inducing abnormal cell function. This is the cause of cancer and genetic effects as late effects.
Early EffectsWhen whole-body exposure to radiation at a dose higher than about 0.5 Gy occurs, there is a prodromal period characterized by symptoms that appear immediately after exposure. After a latent period in which these symptoms improve, the onset period begins, during which symptoms due to damage to organs highly sensitive to radiation appear. If these symptoms do not improve, the patient enters the severe stage, and whole-body exposure to a dose higher than 4 Gy is likely to be fatal in more than half of cases.
1) Prodromal symptoms:
Gastrointestinal symptoms such as nausea, vomiting, and diarrhea, neurological symptoms such as headache and impaired consciousness, and systemic symptoms such as fever appear depending on the radiation dose (Figure 16-1-10). The higher the radiation dose, the higher the frequency of symptoms and the earlier they tend to appear. Parotid gland swelling is also a characteristic symptom.
2) Onset symptoms:
Symptoms begin to appear in organs that are highly sensitive to radiation. Damage to the hematopoietic system becomes evident early on as a decrease in blood cells, with decreases in lymphocytes, neutrophils, platelets, and red blood cells in that order, followed by symptoms of infection, bleeding tendency, and anemia. Mucosal damage occurs frequently in the small intestine, which is highly sensitive to radiation, and bleeding becomes more likely from the damaged area. Skin damage manifests as erythema, alopecia, dry desquamation, moist desquamation, blisters, ulcers, and necrosis as the radiation dose increases.
3) Severe symptoms:
Among infectious diseases, pneumonia and sepsis are likely to cause respiratory and circulatory instability by leading to respiratory failure and shock. If damage to the gastrointestinal mucosa and skin persists, leakage of bodily fluids from the injured site and infection are likely to occur. These also affect unstable circulatory dynamics. Furthermore, if the severe phase continues for a long time, respiratory failure may worsen due to radiation pneumonitis.
4) Treatment:
Immediately after exposure, it is important to keep the patient's overall condition stable and reduce contamination by radioactive materials. In addition to removing clothing and decontaminating the body surface, if radioactive materials are suspected to have been taken into the body, measures to promote their removal from the body are necessary. Ferric ferrocyanide (Prussian blue) is effective against cesium, and the chelating agent diethylenetriaminepentaacetic acid (DTPA) is effective against plutonium and americium. Potassium iodide is also used to prevent radioactive iodine from being taken up by the thyroid gland. Granulocyte colony-stimulating factor (G-CSF) and blood transfusions are often required for cytopenia due to hematopoietic disorders, but in cases of high-dose exposure, hematopoietic stem cell transplantation may also be considered. Infections require treatment according to the cause, such as bacteria, fungi, or viruses. For gastrointestinal mucosal damage, fluid replacement is required to protect the gastrointestinal tract, and mucosal regeneration is promoted by large doses of L-glutamine, and in cases of high-dose exposure, gastrointestinal sterilization is also necessary. In severe cases, strict management of respiratory and circulatory dynamics is required.
Late effects of radiation are effects that appear long after exposure and last a lifetime. The pathological mechanism has not been established, but even if DNA damage is the initial cause, it does not play a direct role. It is assumed that chromosomal instability, chronic inflammation, aging, etc. are involved.
1) Cancer:
Epidemiological studies of atomic bomb survivors have reported that the excess relative risk per 1 Gy for all cancers is 0.5 (Preston et al., 2007). An increased risk is seen for cancers originating from many organs, but the excess relative risk varies depending on the type of cancer. Hematopoietic tumors, bladder cancer, breast cancer, and lung cancer are typical cancers with a high risk. Furthermore, the risk of radiation-induced cancer depends greatly on the age at the time of exposure, with the risk being higher the younger the person is exposed to radiation.
2) Cataract:
It has been reported that cataracts caused by radiation exposure are characterized by the development of subcapsular opacification at the posterior pole of the lens. The threshold for onset of cataracts has been reported to be significantly lower than previously thought, and detailed investigations are currently underway.
3) Infertility:
Low-dose exposure causes temporary infertility in both men and women, but high-dose exposure causes permanent infertility in both men and women, with the threshold varying greatly from person to person.
4)Other:
Known late effects of radiation include hypothyroidism and benign tumors such as uterine fibroids. In addition, a recent study of atomic bomb survivors has reported that radiation exposure increases the risk of cardiovascular disease, including hypertensive heart disease (Yamada et al., 2004).
Effects on the fetus The effects of radiation on the fetus depend greatly on the time of fetal exposure. Radiation exposure from fertilization, which is the pre-implantation stage, up to around day 9 of pregnancy can cause death, with a threshold of around 100 mGy. During the organ formation period, from the second to eighth week of pregnancy, radiation exposure can cause birth defects, with a threshold of around 100 mGy. During the fetal period, from the eighth to 25th week of pregnancy, radiation exposure can cause mental retardation, which is particularly common up to the 15th week of pregnancy, with a threshold of around 300 mGy. The risk of cancer from radiation increases throughout the entire pregnancy period.
Genetic effects: In the studies conducted to date on the children of atomic bomb survivors, the genetic effects have not been clarified due to the limited number of items surveyed, but long-term studies are needed to determine what health effects occur with age. [Kiyoshi Miyagawa]
■ References
Preston DL, Ron E, et al: Solid cancer incidence in atomic bomb survivors: 1958-1998. Radiat Res, 168: 1-64, 2007.
Yamada M, Wong FL, et al: Noncancer disease incidence in atomic bombs survivors, 1958-1998. Radiat Res, 161: 622-632, 2004.

Figure 16-1-7
Table 6, the international standard for the treatment of decompression sickness

Figure 16-1-7

Figure 16-1-8
Classification of Radiation Damage ">

Figure 16-1-8

Figure 16-1-9
Deterministic and stochastic effects ">

Figure 16-1-9

Figure 16-1-10
Pattern of onset of prodromal symptoms immediately after radiation exposure ">

Figure 16-1-10

Radiation damage (iatrogenic disease)

Unlike occupational exposure to medical professionals and public exposure to the general public, there are no dose limits set for medical exposure to patients for diagnosis or treatment. This is because it is assumed that the benefits of diagnosis or treatment using radiation outweigh the risks of exposure and contribute to maintaining health. Therefore, when performing diagnosis or treatment using radiation, it is necessary to always confirm its necessity. It is also essential to adhere to the planned dose and ensure safety so that excessive irradiation is not performed. On the other hand, even though it is the same exposure for medical treatment, care must be taken not to expose patients to more than the dose limit for occupational exposure and public exposure.
Radiation damage in diagnostic radiologyCompared to plain X-rays, CT scans and radioisotope scintigraphy involve higher radiation doses. According to a 2008 report by the United Nations Scientific Committee on the Effects of Atomic Radiation (UNSCEAR), the average effective dose of a CT scan is 7.4 mSv, and in Japan, the average effective doses are 2.4 mSv for the head, 9.1 mSv for the chest, 12.9 mSv for the abdomen, and 10.5 mSv for the pelvis. The average effective dose of a PET scan in Japan is 6.4 mSv, according to the same report. The average effective dose of an upper gastrointestinal series is reported to be 3.4 mSv internationally. According to an epidemiological study of atomic bomb survivors, which provides important data for the formulation of radiation protection standards, the excess relative risk of developing solid cancer at age 70 after exposure at age 30 is 47% per Sv, and approximately 5% for 100 mSv (Preston et al., 2007). For this reason, frequent use of these procedures can increase the risk of cancer. In addition, in interventional radiology (IVR), which involves treatment following diagnosis, localized radiation can cause local symptoms such as skin disorders.
1) Cancer:
Cancers caused by exposure to diagnostic radiology are a concern due to low doses of radiation. Radiation carcinogenesis is classified as a stochastic effect for which no threshold is clear, but it is unclear whether the linear relationship between dose and risk observed in the higher dose range applies to the low dose range (Mullenders et al., 2009).
It is assumed that there are multiple factors that complicate the relationship between dose and risk in the low-dose range, and among these, the molecular mechanisms of individual differences in DNA damage response mechanisms are being elucidated. The DNA damage response mechanisms identified so far were identified through research on high-dose irradiation. Of these, it has been confirmed that the main molecules play an important role in responding to DNA damage even at low doses of irradiation. Therefore, when the function of these molecules is genetically reduced, the patient belongs to a high-risk group for radiation carcinogenesis (radiation hypersensitivity syndrome). A typical example is seen in the high radiation sensitivity and increased risk of carcinogenesis in ataxia telangiectasia, which is caused by genetic mutations in ATM, a DNA damage sensor. In addition, carriers of this disease have increased radiation sensitivity and an increased risk of breast cancer at a young age because the enzyme activity is reduced due to heterozygous mutations in ATM. Thus, individual differences in DNA damage response functions contribute to the complexity of carcinogenesis risk from low-dose radiation exposure. Other factors that contribute to the complexity of radiation effects in the low-dose range are the bystander effect and adaptive response. The former means that the same radiation effects are manifested in non-exposed cells surrounding exposed cells, and the latter means that cells that have been exposed to low doses of radiation in advance are less affected by radiation than cells that have not been exposed to the same dose. As such, due to the existence of multiple factors, the relationship between dose and risk in the low dose range has not yet been established.
2) Skin disorders:
Even in diagnosis or IVR using low-dose-rate irradiation with a low dose per hour, long-term irradiation can cause skin damage, an early effect of radiation. In mild cases, the cause is acute inflammation and is reversible, but in severe cases, irreversible changes occur because cell death due to DNA damage is the main cause of the disease.
Radiation damage in radiation therapy Even if radiation therapy is planned to concentrate the dose on the tumor tissue, which is the treatment target, the surrounding normal tissue is also exposed to radiation, causing damage in that local area. In cancer treatment, the local radiation exposure dose can reach a high dose range, which can cause a variety of early and late damage.
1) Early Obstruction:
When tissues that are highly sensitive to radiation, such as the hematopoietic system, skin, and mucous membranes, are exposed to high doses of radiation, symptoms appear due to acute inflammation and localized loss of tissue caused by cell death.
2) Late effects:
Late-stage disorders such as pulmonary fibrosis, neuropathy, and rectal disorders are caused by chronic inflammation and cell death, which are similar to the causes of early-stage disorders and therefore appear relatively early among the late-stage disorders. In contrast, cancer is characterized by chromosomal abnormalities and base point mutations, and is assumed to be caused by factors such as DNA damage, chronic inflammation, chromosomal instability, and aging, and does not become apparent until a considerable number of years have passed. In this case, it is important to make a differential diagnosis from recurrence or metastasis of the cancer that was the subject of treatment. In addition, when chemotherapy is administered in addition to radiation therapy, the effects of drugs that are likely to cause DNA damage must also be considered, but with the exception of some drugs such as etoposide, which causes characteristic chromosomal abnormalities, it is difficult to distinguish the contribution of radiation and DNA-damaging drugs to carcinogenesis. In addition to these damages caused by local irradiation, total-body irradiation in hematopoietic stem cell transplantation increases the possibility of infertility due to its effects on reproductive cells. [Kiyoshi Miyagawa]
■ References
Mullenders L, Atkinson M, et al: Assessing cancer risks of low-dose radiation. Nature Rev Cancer, 9: 596-604, 2009.
Preston DL, Ron E, et al: Solid cancer incidence in atomic bomb survivors: 1958-1998. Radiat Res, 168: 1-64, 2007.

Source : Internal Medicine, 10th Edition About Internal Medicine, 10th Edition Information

Japanese:

概念
　放射線は，線量に依存して生体に多様な影響を与える．現代社会においては，医療において多用されている放射線のみならず，原子力災害などの原因によって環境中に存在する放射線の影響についても考慮する必要がある．
分類
　放射線に被曝した場合には，被曝線量に応じて多様な症状が時間依存的に発現するために，放射線影響については複数の分類方法が存在する（図16-1-8）．まず，放射線障害は身体的影響と遺伝的影響に大別される．さらに，身体的影響は症状が発現する時期によって，被曝後数カ月以内に発症する早期影響と，それ以降に発症する晩発影響に分類される．また，被曝時に妊娠している場合には，胎児への影響も発生することがある．これらの分類とは別に，放射線防護の観点から，症状の発現に閾値が存在する確定的影響（deterministic effects）と，閾値がはっきりとしない確率的影響（stochastic effects）に分類することもある（図16-1-9）．
病因
　高線量の放射線に被曝した細胞では，DNA損傷は修復されないために細胞死に至り，それが広汎に及びかつ幹細胞も傷害を受けた場合には，組織の機能不全をきたす．これは，早期影響における重篤な障害の原因となる．それに対して，低線量の放射線に被曝した場合には，DNA損傷が修復される可能性が高くなるために，細胞致死の頻度は少なくなるが，修復された遺伝情報が必ずしも元のものと完全に同じであるとは限らないために，異常な遺伝情報が生成されることによって細胞の機能異常が誘導される．これは，晩発影響である癌や遺伝的影響の原因となる．
早期影響
　0.5 Gy程度よりも高い線量の放射線に全身被曝した場合には，被曝直後から発症する症状によって特徴づけられる前駆期が存在し，いったんこれらの症状が軽快する潜伏期を経て，発症期にはいると放射線感受性の高い臓器の障害による症状が出現する．これらが軽快しない場合には重篤期にはいり，4 Gyよりも高い線量の全身被曝では半数以上が致死に至る可能性が高い．
1）前駆期症状：
悪心・嘔吐，下痢の消化器症状，頭痛と意識障害の神経症状，全身症状である発熱が，線量に応じて発現する（図16-1-10）．線量が高いほど，発現頻度は高く，発現時期は早くなる傾向がある．また，耳下腺腫脹も特徴的な症状である．
2）発症期症状：
放射線感受性の高い臓器から症状が発現する．造血器の障害は早期から血球減少によって顕在化するが，リンパ球，好中球，血小板，赤血球の順に減少し，感染症，出血傾向，貧血による症状が発現する．粘膜傷害は，放射線感受性の高い小腸で発現頻度が高く，障害部位から出血しやすくなる．皮膚傷害は，線量が高くなるにしたがって，紅斑，脱毛，乾性落屑，湿性落屑，水疱，潰瘍，壊死が発現する．
3）重篤期症状：
感染症の中でも肺炎や敗血症は，呼吸不全やショックをきたすことによって呼吸・循環動態の不安定化の原因となりやすい．消化管粘膜と皮膚の傷害が遷延すると，傷害部位からの体液の漏出と感染症が発生しやすくなる．これらも不安定な循環動態に影響を及ぼす．さらに，重篤期が長期におよぶ場合には，放射線肺臓炎（radiation pneumonitis）によって呼吸不全が悪化する可能性がある．
4）治療：
被曝直後は，全身状態を安定に保つとともに，放射性物質の汚染を軽減することが重要である．脱衣と体表面の除染に加えて，体内への放射性物質の取り込みが疑われる場合には，それらの体外への除去を促進する対応が必要である．セシウムに対してはフェロシアン化第二鉄（プルシアンブルー）が，プルトニウムやアメリシウムに対してはキレート剤であるジエチレントリアミン五酢酸（DTPA）が有効である．また，放射性ヨウ素の甲状腺への取り込みを予防するために，ヨウ化カリウムが用いられる．造血器障害による血球減少に対しては，顆粒球コロニー刺激因子（G-CSF）や輸血が必要となることが多いが，高線量被曝では造血幹細胞移植の適応も検討される．感染症に対しては，細菌，真菌，ウイルスなどの原因に応じた治療が必要である．消化管粘膜傷害に対しては，補液によって消化管を保護するとともに，L-グルタミン大量投与などによって粘膜再生を促進し，また高線量被曝においては，消化管滅菌も必要となる．重症化した場合には，厳密な呼吸・循環動態の管理が必要である．
晩発影響
　放射線の晩発影響は，被曝後長時間経過してから発現する影響であり，一生涯に及ぶものである．その病態の機序については確立していないが，DNA損傷が最初の原因であったとしても直接的な役割を果たすのではなく，染色体不安定性，慢性炎症，加齢などが関与することが想定されている．
1）癌：
原爆被爆者の疫学調査によって，1 Gyあたりの過剰相対リスクは，全癌では0.5であると報告されている（Prestonら，2007）．多くの臓器由来の癌でリスクの増加がみられるが，癌の種類によって過剰相対リスクには差がある．造血器腫瘍，膀胱癌，乳癌，肺癌などは，リスクの高い代表的な癌である．また，放射線発癌のリスクは，被曝時年齢に大きく依存し，若年期の被曝ほどリスクは高くなる．
2）白内障：
放射線被曝によって発症する白内障は，水晶体の後極の後囊下の混濁から発生することが特徴であると報告されている．発症の閾値は，以前考えられていた値よりもかなり低いことが報告され，現在も詳細な調査が進行中である．
3）不妊：
低線量被曝では男女とも一時的に不妊になるが，高線量被曝では男女とも永久不妊となり，閾値は個人差が大きい．
4）その他：
放射線の晩発障害として，甲状腺機能低下症，子宮筋腫などの良性腫瘍が知られているが，これらに加えて，最近の原爆被爆者の調査では，高血圧性心疾患などの心血管病のリスクが放射線被曝によって増加することが報告されている（Yamadaら，2004）．
胎児への影響
　放射線の胎児への影響は，胎児の被曝時期に大きく依存する．着床前期である受精から妊娠9日程度までの放射線被曝は死亡の原因となり，閾値は100 mGy程度である．器官形成期である妊娠2週から8週までにおいては，放射線被曝は奇形の発生の原因となり，閾値は100 mGy程度である．妊娠8週から25週までの胎児期においては，放射線被曝は精神発達遅滞の原因となり，特に妊娠15週までにおける頻度が高く，閾値は300 mGy程度である．放射線による癌のリスクは，妊娠期間全体において増加する．
遺伝的影響
　これまでの原爆被爆者の子供を対象とした調査においては，限られた調査項目では遺伝的影響は明らかではないが，加齢に伴ってどのような健康影響が発現するのかについては，長期間にわたる調査が必要である．［宮川　清］
■文献
Preston DL, Ron E, et al: Solid cancer incidence in atomic bomb survivors: 1958-1998. Radiat Res, 168: 1-64, 2007.
Yamada M, Wong FL, et al: Noncancer disease incidence in atomic bombs survivors, 1958-1998. Radiat Res, 161: 622-632, 2004.

図16-1-7
国際標準とされる減圧症の治療表，table 6">

図16-1-7

図16-1-8
放射線障害の分類">

図16-1-8

図16-1-9
確定的影響と確率的影響">

図16-1-9

図16-1-10
放射線被曝直後の前駆期の症状の発症パターン">

図16-1-10

放射線障害(医原性疾患)

概念
　診断や治療のために患者が被曝する医療被曝は，医療従事者が被曝する職業被曝や一般人が被曝する公衆被曝とは異なり，線量限度が設定されていない．これは，放射線による診断や治療の便益が，被曝のリスクを上回って健康維持に寄与することを前提としているからである．したがって，放射線を用いた診断や治療を行う際には，その必要性を常に確認する必要がある．また，計画された線量を照射することを遵守するとともに，過剰な照射が行われないよう安全性の確保も不可欠である．一方，同じ医療における被曝であっても，職業被曝と公衆被曝においては，線量限度をこえて被曝しないよう配慮する必要がある．
放射線診断における被曝障害
　単純X線撮影に比べて，CTスキャンや放射性同位元素を用いたシンチグラフィの検査では被曝線量が高い．原子放射線の影響に関する国連科学委員会（UNSCEAR）2008年の報告によれば，CTスキャンの実効線量の平均は7.4 mSvとされ，日本では部位別に，頭部2.4 mSv，胸部9.1 mSv，腹部12.9 mSv，骨盤部10.5 mSvである．日本のPET検査の実効線量の平均は，同報告では6.4 mSvである．また，上部消化管造影の実効線量の平均は，国際的には3.4 mSvと報告されている．放射線防護基準の策定の際に重要なデータを提供している原爆被爆者を対象とした疫学研究によれば，30歳で被爆した場合の70歳での固形癌発症の過剰相対リスクは1 Svあたり47％であり，100 mSvで約5％となる（Prestonら，2007）．そのために，これらを頻回に施行した場合には，発癌リスクの増加が問題となる．また，診断に引き続いて治療も行うinterventional radiology（IVR）では，局所照射によって皮膚障害などの局所症状も発現する可能性がある．
1）癌：
放射線診断による被曝で問題となる発癌は，低線量の放射線によるものである．放射線発癌は，閾値の存在が明らかではない確率的影響に分類されているが，低線量域においては，より高い線量域で観察される線量とリスクの直線関係が適応されるかどうかは不明である（Mullendersら，2009）．
　低線量域における線量とリスクの関係を複雑化する複数の要因が存在することが想定されているが，その中でもDNA損傷応答機構の個人差は分子機構の解明が進んでいる．これまで同定されているDNA損傷応答機構は，高線量照射の研究によって同定されたものである．これらのうち，主要な分子については低線量照射時でも，DNA損傷に対する応答において重要な役割を果たしていることが確認されている．それゆえ，これらの分子の機能が遺伝的に低下している場合には，放射線発癌の高リスク群に属することになる（放射線高感受性症候群）．代表的な例は，DNA損傷のセンサーであるATMの遺伝性変異によって発症する血管拡張性失調症の放射線高感受性と発癌リスクの増加にみられる．また，この疾患のキャリアでは，ATMのヘテロ接合変異によって酵素活性が低下しているために，放射線感受性の亢進と若年発症の乳癌のリスクが増加している．このように，DNA損傷応答機能の個人差は，低線量の放射線被曝の発癌リスクの複雑性に寄与する．　このほかに低線量域の放射線影響の複雑性に寄与する要因としては，バイスタンダー効果と適応応答が知られている．前者は，被曝した細胞の周辺に存在する非被曝細胞においても被曝細胞と同様の放射線影響が発現することであり，後者は，事前に低線量の放射線照射した細胞では，事前照射をしない細胞に比べて，その後に同じ線量の照射をしても，放射線の影響が少なくなることである．このように，複数の要因が存在するために，低線量域における線量とリスクの関係は，いまだに確立していない．
2）皮膚障害：
時間あたりの線量が低い低線量率の照射による診断あるいはIVRであっても，長時間照射する場合には，放射線の早期影響である皮膚障害が発生する．軽症例では，急性炎症が原因となるために可逆性であるが，重症例では，DNA損傷に起因する細胞死が中心的な病因になるために，不可逆的な変化をきたす．
放射線治療における被曝障害
　放射線治療においては，治療の標的となる腫瘍組織に線量を集中するように計画をしていても，その周辺に存在する正常組織も被曝してしまうために，その局所における障害が発生する．癌治療においては，局所の被曝線量は高線量域に及ぶために，多彩な早期障害と晩期障害が発生する可能性がある．
1）早期障害：
放射線感受性の高い組織である造血器，皮膚，粘膜などが高線量の放射線に被曝した場合には，急性炎症や細胞死による組織の局所脱落による症状が発現する．
2）晩期障害：
晩期障害に分類される肺線維症，神経障害，直腸障害などは，慢性炎症や細胞死が病因となり，これらは早期障害の病因とも類似するために，晩期の中でも比較的早い時期に出現する．それに対して，癌は染色体異常や塩基の点突然変異などを特徴とすることから，DNA損傷，慢性炎症，染色体不安定性，加齢などの要因が原因となることが想定され，かなりの年数を経てから顕在化する．この場合に，治療の対象となった癌の再発や転移との鑑別診断が重要である．また，放射線治療に加えて化学療法を施行している場合には，DNA損傷を生成しやすい薬剤の影響も考慮する必要があるが，特徴的な染色体異常の原因となるエトポシドなどの一部の薬剤を除いては，放射線とDNA損傷性薬剤の発癌への寄与を鑑別することは困難である．このような局所照射の障害に加えて，造血幹細胞移植における全身照射では，生殖細胞への影響によって不妊の可能性が高くなる．［宮川　清］
■文献
Mullenders L, Atkinson M, et al: Assessing cancer risks of low-dose radiation. Nature Rev Cancer, 9: 596-604, 2009.
Preston DL, Ron E, et al: Solid cancer incidence in atomic bomb survivors: 1958-1998. Radiat Res, 168: 1-64, 2007.

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