Children whose parents had been exposed to radiation from the Chernobyl Nuclear Power Plant accident in 1986 had no excess germline mutations, a new whole-genome sequencing study shows. “This is one of the first studies to systematically evaluate alterations in human mutation rates in response to a man-made disaster, such as accidental radiation exposure,” say the authors. Effects of radiation exposure from the Chernobyl nuclear accident, which occurred at a power plant in Ukraine in April 1986, remain a topic of interest. To date, there have been several studies examining transgenerational risks of radiation exposure from events such as this, but the results have been inconclusive. What’s more, no large comprehensive effort has explored germline de novo mutations genome-wide in children born from parents exposed to moderately high amounts of ionizing radiation, even as possible genetic effects from such events have remained a concern for radiation-exposed populations like the Fukushima evacuees. To examine whether rates of germline de novo mutations are elevated in children born to parents exposed to ionizing radiation, Meredith Yeager et al. analyzed the genomes of 130 children and parents from families where one or both parents had experienced gonadal radiation exposure related to the Chernobyl accident and where the children were conceived after the accident – and born between 1987 and 2002. The authors did not find an increase in new germline mutations in this population. The incidence of germline de novo mutations was comparable to that reported in the general population, they say. “[O]ur study does not provide support for a transgenerational effect of ionizing radiation on germline DNA in humans,” they conclude.
In a second study examining the effects of radioactive fallout on survivors of the Chernobyl nuclear accident, researchers provide more insights into the process of radiation-induced papillary thyroid cancers – one of the most frequent cancers observed after the Chernobyl event. “These findings substantially extend preliminary reports of radiation-related human tumor characteristics by integrating data from multiple platforms with large sample size and detailed radiation dose data,” the authors say. Exposure to radioactive fallout increases the risk of cancer, particularly papillary thyroid carcinoma (PTC). However, a detailed molecular understanding of these tumors is still lacking, and there are no established markers of radiation-induced cancers. Lindsay Morton et al. analyzed thyroid tumors, normal thyroid tissue, and blood from hundreds of survivors of the Chernobyl nuclear accident and compared them to those of unexposed patients. While no unique radiation-related biomarker was identified, the results reveal radiation dose-related increases in DNA double-strand breaks in human thyroid cancers developing after the Chernobyl accident. Radiation-related genomic alterations were more pronounced for those younger at exposure, the authors say. Their results suggest that thyroid tumor development following radiation exposure results from DNA double-strand breaks in the genome. The authors say their results have implications for radiation protection and public health, particularly for low dose exposure.