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Low doses and non-targeted effects in environmental radiation protection; where are we now and where should we go?

机译:低剂量和对环境的辐射无目标影响;我们现在在哪里,我们应该去哪里?

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摘要

The field of low dose radiobiology has advanced considerably in the last 30 years from small indications in the 1980s that all was not simple, to a paradigm shift which occurred during the 1990's, which severely dented the dose-driven models and DNA centric theories which had dominated until then. However while the science has evolved, the application of that science in environmental health protection has not. A reason for this appears to be the uncertainties regarding the shape of the low dose response curve, which lead regulators to adopt a precautionary approach to radiation protection. Radiation protection models assume a linear relationship between dose (i.e. energy deposition) and effect (in this case probability of an adverse DNA interaction leading to a mutation). This model does not consider non-targeted effects (NTE) such as bystander effects or delayed effects, which occur in progeny cells or offspring not directly receiving energy deposition from the dose. There is huge controversy concerning the role of NTE with some saying they reflect "biology" and that repair and homeostatic mechanisms sort out the apparent damage while others consider them to be a class of damage which increases the size of the target. One thing which has recently become apparent is that NTE may be very critical for modelling long-term effects at the level of the population rather than the individual. The issue is that NTE resulting from an acute high dose such as occurred after the A-bomb or Chernobyl occur in parallel with chronic effects induced by the continuing residual effects due to radiation dose decay. This means that if ambient radiation doses are measured for example 25 years after the Chernobyl accident, they only represent a portion of the dose effect because the contribution of NTE is not included.
机译:在过去的30年中,低剂量放射生物学领域取得了长足的发展,从1980年代的小迹象表明一切都不简单,到1990年代发生的范式转变,严重地改变了剂量驱动模型和以DNA为中心的理论。直到那时都处于主导地位然而,尽管科学发展了,但该科学在环境保护方面的应用却没有。造成这种情况的原因似乎是有关低剂量反应曲线形状的不确定性,这导致监管机构对辐射防护采取了预防措施。辐射防护模型假定剂量(即能量沉积)与效果(在这种情况下,不利的DNA相互作用导致突变的可能性)之间存在线性关系。该模型未考虑非后代效应(NTE),例如旁观者效应或延迟效应,这种效应发生在未直接从剂量中吸收能量沉积的后代细胞或后代中。关于NTE的作用,存在着巨大的争议,有人说它们反映了“生物学”,修复和体内平衡机制可以清除明显的损害,而另一些人则认为它们是一类损害,增加了目标的规模。最近变得显而易见的一件事是,NTE对于在人口而非个人层面上模拟长期效应可能非常关键。问题是,急性高剂量(如在A型炸弹或切尔诺贝利事故发生后)产生的NTE与放射剂量衰减导致的持续残留效应引起的慢性效应并行。这意味着,如果在切尔诺贝利事故发生后的25年内测量环境辐射剂量,则它们仅代表剂量效应的一部分,因为不包括NTE的贡献。

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