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首页> 外文期刊>Archives of Toxicology >The road to linearity: why linearity at low doses became the basis for carcinogen risk assessment
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The road to linearity: why linearity at low doses became the basis for carcinogen risk assessment

机译：线性之路：为什么低剂量线性成为致癌物风险评估的基础

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This article assesses the historical foundations of how linearity at low dose became accepted by the scientific/regulatory communities. While the threshold model was used in the 1920s/1930s in establishing radiation health standards, its foundations were challenged by the genetics community who argued that radiation induced mutations in reproductive cells followed a linear response, were cumulative and deleterious. Scientific foundations of linearity for gonadal mutations were based on non-conclusive evidence as well as not being conducted at low doses. Following years of debate, leaders in the genetics community participated in the U.S. National Academy of Sciences (NAS) (1956) Biological Effects of Atomic Radiation (BEAR) BEAR I Committee, getting their perspectives accepted, incorporating linearity for radiation-induced mutational effects in risk assessment. Overtime the concept of linearity was generalized to include somatic effects induced by radiation based on a protectionist philosophy. This affected the course of radiation-induced and later chemically-induced carcinogen risk assessment. Acceptance of linearity at low dose from chemical carcinogens was strongly influenced by the NAS Safe Drinking Water Committee report of 1977 which provided the critical guidance to the U.S. EPA to adopt linear at low dose modeling for risk assessment for chemical carcinogens with little supportive data, much of which has been either discredited or seriously weakened over the past 3 decades. Nonetheless, there has been little practical change of regulatory policy concerning carcinogen risk assessment. These observations suggest that while scientific disciplines are self correcting, that regulatory ‘science’ fails to display the same self-correcting mechanism despite contradictory data.
机译：本文评估了科学/法规界如何接受低剂量线性的历史基础。虽然阈值模型在1920年代/ 1930年代用于建立辐射健康标准，但其基础受到遗传学界的挑战，遗传学界认为辐射引起的生殖细胞突变遵循线性响应，具有累积性和有害性。性腺突变的线性线性的科学基础是基于非结论性的证据，并且也不是在低剂量下进行的。经过多年的辩论，遗传学界的领导者参加了美国国家科学院（NAS）（1956）原子辐射的生物效应（BEAR）BEAR I委员会，他们的观点被接受，并纳入了辐射诱发的突变的线性效应。风险评估。随着时间的流逝，线性的概念被概括为包括基于保护主义理念的辐射引起的躯体效应。这影响了辐射诱发的和后来化学诱发的致癌物风险评估的过程。化学致癌物在低剂量条件下对线性的接受受到NAS安全饮用水委员会1977年的报告的强烈影响，该报告为美国EPA提供了关键指导，采用低剂量线性模型对化学致癌物进行风险评估，几乎没有支持性数据，在过去的30年中，其中的一些已经被抹黑或被严重削弱。但是，关于致癌物风险评估的监管政策几乎没有实际变化。这些观察结果表明，尽管科学学科正在自我纠正，但尽管数据相互矛盾，但监管“科学”仍无法显示出相同的自我纠正机制。

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