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Origin of the linearity no threshold (LNT) dose-response concept

机译：线性无阈值（LNT）剂量反应概念的由来

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This paper identifies the origin of the linearity at low-dose concept [i.e., linear no threshold (LNT)] for ionizing radiation-induced mutation. After the discovery of X-ray-induced mutations, Olson and Lewis (Nature 121(3052):673-674, 1928) proposed that cosmic/terrestrial radiation-induced mutations provide the principal mechanism for the induction of heritable traits, providing the driving force for evolution. For this concept to be general, a LNT dose relationship was assumed, with genetic damage proportional to the energy absorbed. Subsequent studies suggested a linear dose response for ionizing radiation-induced mutations (Hanson and Heys in Am Nat 63(686):201-213, 1929; Oliver in Science 71:44-46, 1930), supporting the evolutionary hypothesis. Based on an evaluation of spontaneous and ionizing radiation-induced mutation with Drosophila, Muller argued that background radiation had a negligible impact on spontaneous mutation, discrediting the ionizing radiation-based evolutionary hypothesis. Nonetheless, an expanded set of mutation dose-response observations provided a basis for collaboration between theoretical physicists (Max Delbruck and Gunter Zimmer) and the radiation geneticist Nicolai Timoféeff-Ressovsky. They developed interrelated physical science-based genetics perspectives including a biophysical model of the gene, a radiation-induced gene mutation target theory and the single-hit hypothesis of radiation-induced mutation, which, when integrated, provided the theoretical mechanism and mathematical basis for the LNT model. The LNT concept became accepted by radiation geneticists and recommended by national/ international advisory committees for risk assessment of ionizing radiation-induced mutational damage/cancer from the mid-1950s to the present. The LNT concept was later generalized to chemical carcinogen risk assessment and used by public health and regulatory agencies worldwide.
机译：本文确定了电离辐射诱发的突变的低剂量概念线性的起源[即，线性无阈值（LNT）]。在发现X射线诱发的突变后，Olson和Lewis（Nature 121（3052）：673-674，1928）提出，宇宙/地面辐射诱发的突变提供了诱导遗传性状的主要机制，并提供了驱动力。进化的力量。为了使这个概念具有普遍性，我们假定了LNT剂量关系，遗传损害与吸收的能量成正比。随后的研究提出了电离辐射诱导的突变的线性剂量反应（Hanson和Heys in Am Nat 63（686）：201-213，1929; Oliver in Science 71：44-46，1930），支持了进化假说。根据对果蝇自发和电离辐射诱发的突变的评估，Muller认为背景辐射对自发突变的影响可忽略不计，从而使基于电离辐射的进化假说不可信。尽管如此，一组扩展的突变剂量反应观察结果为理论物理学家（麦克斯·德尔布吕克和冈特·齐默尔）与放射遗传学家尼古拉·蒂莫费夫·雷索夫斯基之间的合作提供了基础。他们开发了基于物理科学的相互关联的遗传学观点，包括基因的生物物理模型，辐射诱导的基因突变目标理论和辐射诱导的突变的单一命题假说，这些假说结合在一起，为研究提供了理论机制和数学基础。 LNT模型。 LNT概念已被放射遗传学家接受，并被国家/国际咨询委员会推荐，用于从1950年代中期到现在的电离辐射诱发的突变损伤/癌症的风险评估。 LNT概念后来被推广到化学致癌物风险评估中，并被全世界的公共卫生和监管机构所采用。

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