Risks Associated with Low Doses and Low Dose Rates of Ionizing Radiation: Why Linearity May Be (Almost) the Best We Can Do
Risks Associated with Low Doses and Low Dose Rates of Ionizing Radiation: Why Linearity May Be (Almost) the Best We Can Do
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DOI：
10.1148/radiol.2511081686
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发表时间：
2009-04-01
期刊：
影响因子：
19.7
通讯作者：
de Gonzalez, Amy Berrington
中科院分区：
文献类型：
--
作者：
Little, Mark P.;Wakeford, Richard;de Gonzalez, Amy Berrington
与高剂量电离辐射（X 射线）暴露相关的确定性和随机效应几乎与电离辐射本身一样早为人所知 (1-3)。在较低剂量下，辐射风险主要是随机效应，特别是躯体效应（癌症），而不是较高剂量暴露所特有的确定性效应 (4-6)。与确定性效应相反，对于随机效应，科学委员会通常假设在足够低的剂量下，剂量反应存在正线性分量，即不存在阈值 (4-6)。这并不排除剂量响应中存在剂量的高阶（例如，二次）幂，这在较高剂量时可能很重要。正是在此基础上，剂量线性（或线性二次）模型通常用于推断日本原子弹幸存者（他们通常受到高剂量率到中等剂量[平均，0.1 Sv]）的经历，以估计低剂量和低剂量率的风险（4-6）。大多数基于人群的癌症风险评估主要基于日本原子弹幸存者寿命研究 (LSS) 队列数据 (4-6)。然而，大量其他研究也提供了过度风险的证据。在并行社论（7）中，提出了低剂量电离辐射可能的真实（或至少“实用”）阈值或“毒物兴奋”（有益）效应的证据。正如我们在此总结的那样，与 Tubiana 等人 (7) 的论点相反，我们认为几乎没有流行病学或生物学证据证明这些癌症。争论有三种形式：（a）日本原子弹幸存者和其他暴露群体中癌症剂量反应曲率程度的评估（特别是偏离线性或线性二次曲率），（b）日本人和其他中低剂量群体之间风险的一致性，以及（c）机制生物学数据的评估。大多数有关辐射诱发癌症风险的信息来自（a）日本原子弹幸存者，（b）医疗暴露人群，（c）职业暴露群体，以及（d）环境暴露群体（6）。在较高剂量放射治疗研究中，接受的剂量远高于 LSS，有时在发生细胞绝育的范围内，每单位剂量的过量癌症风险往往低于 LSS 的可比子集 (8, 9)。然而，正如我们所表明的，中剂量和低剂量医疗和职业暴露群体的风险通常与 LSS 中的风险一致。
Deterministic and stochastic effects associated with high-dose ionizing radiation (x-ray) exposure have been known for almost as long as ionizing radiation itself (1–3). At lower doses, radiation risks are primarily stochastic effects, in particular, somatic effects (cancer) rather than the deterministic effects characteristic of higherdose exposure (4–6). In contrast to deterministic effects, for stochastic effects, scientific committees generally assume that at sufficiently low doses there is a positive linear component to the dose response—that is, that there is no threshold (4–6). This does not preclude there being higher-order (eg, quadratic) powers of dose in the dose response that may be of importance at higher doses. It is on this basis that models linear (or linear-quadratic) in dose are often used to extrapolate the experience of the Japanese atomic bomb survivors (who were typically exposed at a high dose rate to moderate doses [average, 0.1 Sv]) to estimate risks from low doses and low dose rates (4–6). Most population-based cancer risk estimates are based primarily on the Japanese atomic bomb survivor Life Span Study (LSS) cohort data (4–6). However, evidence of excess risks comes from a large number of other studies as well. In the parallel editorial (7), evidence is presented for possible real (or at least “practical”) thresholds or “hormetic”(beneficial) effects of low doses of ionizing radiation. As we summarize here, and in contrast to the arguments of Tubiana et al (7), we judge that there is little epidemiologic or biologic evidence for these for cancer. The arguments are of three forms:(a) assessment of the degree of curvature in the cancer dose response within the Japanese atomic bomb survivors and other exposed groups (in particular, departure from linear or linear-quadratic curvature),(b) consistency of risks between the Japanese and other moderate-and low-dose cohorts, and (c) assessment of biologic data on mechanisms. Most of the information on radiation-induced cancer risk comes from (a) the Japanese atomic bomb survivors,(b) medically exposed populations,(c) occupationally exposed groups, and (d) environmentally exposed groups (6). In the higher-dose radiation therapy studies, where doses received are very much higher than in the LSS, sometimes in the range at which cell sterilization occurs, excess cancer risks per unit dose tend to be less than in comparable subsets of the LSS (8, 9). However, as we show, risks in moderate-and low-dose medically and occupationally exposed groups are generally consistent with those in the LSS.