塞拉菲尔德、海鳞和斯堪的纳维亚:受影响生态系统中放射性污染的遗产及其对基因进化的未来影响

C. Siddoo-Atwal
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引用次数: 0

摘要

核设施和核后处理工厂产生的放射性废物、核事故和核武器试验产生的放射性沉降物构成了子孙后代面临的严重问题。海洋藻类和浮游植物从其周围环境中积累放射性核素,并被用作环境放射性污染的生物指标。在北欧,受影响的海洋系统包括爱尔兰海、波罗的海和北海。这种放射性污染的主要来源是核武器试验的全球沉降物、西伯利亚的河流运输以及塞拉菲尔德和切尔诺贝利的海洋运输。塞拉菲尔德附近的Seascale地区的幼儿白血病发病率有所增加,在靠近海牙角核后处理设施的法国博蒙-海牙州,0-24岁的年轻人白血病发病率也有所上升。在斯堪的纳维亚,科学家们怀疑瑞典部分地区的人们仍在死于切尔诺贝利事故辐射引起的癌症。此外,波罗的海受到核废料再处理过程中产生的人造钚放射性核素的污染。然而,由于基于致癌突变理论对环境排放物辐射剂量的估计存在重要的不确定性,一些专家能够排除上述关系。因此,在可以解释这种差异的凋亡致癌模型的背景下,重新评估目前的辐射暴露癌症风险评估方法似乎是至关重要的。根据这个新模型,基因表达对致癌物反应的细微差异可以启动细胞死亡或凋亡,并作为致癌的触发因素。同时,未来对人类基因进化的影响是不可避免的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Sellafield, Seascale, and Scandinavia: A Legacy of Radioactive Contamination with Future Implications for Gene Evolution in Affected Ecosystems
Radioactive waste from nuclear installations and nuclear reprocessing plants, nuclear accidents, and radioactive fallout from nuclear weapons testing constitute a serious problem facing future generations. Marine algae and phytoplanktons accumu-late radionuclides from their surroundings and are used as bioindicators of radioactive pollution in the environment. In Northern Europe, the affected marine systems include the Irish Sea, the Baltic Sea, and the North Sea. The main sources of this radioactive contamination are global fallout from nuclear weapons tests, river transport from Siberia, and marine transport of discharges from Sellafield and Chernobyl. An increased leukemia incidence has been observed in young children at Seascale near Sellafield, and an elevated incidence of leukemia has been recorded among young people (0–24 years) in the French canton of Beaumont-Hague close to the Cap de la Hague nuclear reprocessing facility. In Scandinavia, scientists suspect that people in parts of Sweden are still dying from cancer caused by radiation from the Chernobyl accident. Moreover, the Baltic Sea is contaminated with man-made plutonium radionuclides from nuclear reprocessing. However, some experts are able to dismiss the above relationships due to important uncertainties over the estimation of radiation doses from environmental discharges based on a mutational theory of carcinogenesis. Consequently, it appears to be of paramount importance to reevaluate the current methods for cancer risk assessment in the case of radiation exposure within the context of an apoptotic model of carcinogenesis that could explain such a discrepancy. According to this new model, subtle differences in gene expression in response to a carcinogen can initiate cell death or apoptosis and act as a trigger for carcinogenesis. Simultaneously, future implications for human gene evolution are unavoidable.
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