One new study found that radiation exposure didn’t genetically harm future generations, while another offers insights into how radiation causes thyroid cancer.
On this day in 1986, workers ran a safety test at the Chernobyl Nuclear Power Plant in northern Ukraine. But the test went awry, starting a fire in a reactor and leading to one of the largest nuclear disasters in history. Smoke from the fire and a second explosion launched radioactive elements into the atmosphere, scattering them over the surrounding fields and towns. Now, 35 years later, scientists are still uncovering the extent of the damage and starting to answer questions about the long-term legacy of radiation exposure on power plant workers, the people in the nearby community, and even their family members born years later.
In two papers published Thursday in Science, an international team of researchers took on two very different but important questions. The first paper tracked the effects of radiation on the children of people who were exposed and found that there were no transgenerational mutations that were passed down from those parents. The second focused on thyroid cancercaused by radiation exposure and examined how radiation acts on DNA to cause the growth of cancerous tumors.
“Each of these are very strong examples of what we’ve learned from situations that we never want to visit again,” says Stephen Cranock, an author on both papers and director of the division of cancer, epidemiology, and genetics at the National Cancer Institute. He says this research is an important reminder of the long-term consequences of human decisions, and hopes it can help guide future conversations about nuclear technology. “This adds to our foundational understanding of radiation and society,” he says.
Researchers were able to finally delve into these longstanding questions thanks to the foresight of scientists who, in the aftermath of the disaster, put together cohorts of affected workers and residents who agreed to be studied over the long term. The researchers also stored tissue samples from people’s tumors. At the time, they didn’t have the tools to study some aspects of the event, but they hoped that future advances would allow others to make use of the materials they gathered. “These papers obviously have in common the radiation exposure, but they’re actually addressing very, very different scientific questions,” says Lindsay Morton, lead author on the tumor paper and a senior investigator in radiation epidemiology at the National Cancer Institute. “But both of them are made possible by these advances in genomic technologies and those investments in basic science. It’s illustrative of these new doors that we can open, which I think should be really exciting for people.”
Cancers are caused by mutations in human DNA. A few lines of genetic code get deleted or mixed up and that change allows cells to proliferate and grow in abnormal ways. Sometimes those DNA changes are genetic—people inherit them from their parents—but sometimes they’re caused by environmental factors. Understanding a tumor’s DNA can help create targeted gene therapies to combat it.
For years, epidemiological studies have shown that thyroid cancer is particularly common among people exposed to radioactive iodine, especially for people who were exposed when they were children. At high enough doses, radioactive iodine kills thyroid cells and can actually be used as a treatment for thyroid cancer and other thyroid conditions. But the radiation from Chernobyl wasn’t enough to kill cells. Instead, says Morton, the months-long exposure to lower doses caused changes to the cells that resulted in tumors.
In her paper, Morton and her colleagues were able to take a closer look at the tumors from people who lived near Chernobyl, studying the DNA of over 350 people who developed thyroid cancer after being exposed to radiation as young children. They created a comprehensive molecular picture of these tumors. Then, to see how they differed from thyroid cancers caused by other factors, the researchers compared these tumors against tissue from 81 people who were born near Chernobyl after 1986 and developed thyroid cancer but were never exposed to radiation. They also compared the tumors to data from the Cancer Genome Atlas, which has characterized the genomes of thousands of cancers.
They found that the cancer cases caused by radioactive iodine exposure following the meltdown had mutated genes by rupturing the twin strands of DNA and breaking them apart. By contrast, the thyroid cancers in the Cancer Genome Atlas and in the control group of 81 unexposed people from the area were more likely to be caused by single-point mutations, where just one single base pair of the DNA is changed.
After the disaster, scientists monitored many of the communities near Chernobyl, as well as the workers who were tasked with cleaning up and encasing the radioactive reactor in a steel and concrete sarcophagus. Researchers also did extensive interviews with residents about their indirect exposure. For example, radioactive isotopes from the reactor fell into the surrounding fields and were eaten by grazing cows, transmitting the radiation to their milk and subsequently to the people who drank it. So information about dairy consumption offered clues about how much radiation someone had been exposed to. Physicists and epidemiologists worked together to piece all these direct and indirect measurements into a reconstruction of the radiation doses that the people who donated the tissue samples would have received. “This is a unique circumstance where we know a lot about the exposure,” says Chanock. “Most of the large genome landscape studies have no information on where and what the people were exposed to.”
This gave researchers an opportunity to take a close look at exactly how this cancer process works. They discovered that the more radiation a person was exposed to, and the younger they were at the time of exposure, the more double-strand DNA breaks they would have.
Finally, the team looked at the cancer’s drivers, the specific genes whose mutations were responsible for tumor growth. They found that the molecular characteristics of the radiation-caused cancers weren’t all that different from what has been observed in randomly-occurring thyroid cancers. It was only the cause—those double-strand DNA breaks—that was different. “That’s what really gave us insight into how radiation is causing cancer,” says Morton.
There were no special biomarkers that labeled these cells as having been mutated by radiation, which tells scientists that the effect of the radiation happened early in the carcinogenic process and that the biomarkers—if there were any—were lost or washed out as the cancer grew. That molecular similarity indicates that these cases don’t require a novel treatment. “These cancers really just look, in the end, like typical thyroid cancers, so there are no specific implications for taking a different treatment approach,” she says.
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In the second paper, researchers concentrated on 130 children whose parents were exposed to radiation, either because they lived near Chernobyl or because they were part of a cohort of “liquidators,” workers who came in to clean up after the disaster. It’s normal for there to be some random gene mutations in a parent’s eggs or sperm; these “germline” mutations are how evolution happens over time. But for decades, people have wondered whether exposure to radiation would increase the likelihood of these mutations, passing the effect down to future generations.
The researchers sequenced the entire genomes of children born 46 weeks and 15 years after the disaster. But despite evidence from some animal models that suggested there might be a genetic effect, the researchers found there weren’t any more DNA mutations in the Chernobyl survivors’ children than there are in kids whose parents had never been exposed to radiation. “We were pleasantly surprised,” Chanock says of the results, which will be especially encouraging for these children, some of whom are now in their early twenties and considering starting families of their own. “The result, which is basically a null result, should be reassuring to them,” he says.
This is also important information for other survivors of radiation exposure, including people who lived near the Fukushima Daiichi nuclear power plant, where, in 2011, an earthquake triggered meltdowns in three reactors. There, the radiation doses were lower than the ones documented at Chernobyl. “Studies like this in humans are exceedingly rare,” Eric Grant, associate chief of research at the Radiation Effects Research Foundation (RERF), writes in an email. RERF, a joint research effort between Japan and the United States, has investigated the effects of the atomic bomb on Japan and the Fukushima meltdown. Grant says people affected by both events have been concerned about what their exposure could mean for their children. “The lack of transgenerational effects observed in this study are undoubtedly good news for radiation-exposed populations,” he writes. “Although the results cannot completely rule out inherited mutations, it is clear that if transgenerational mutations did occur, they did not occur at high rates.”
Taken together, these studies not only give researchers new insights into the protracted effects of radiation, but they also illustrate just how important long-term investments in scientific research and data collection are. While this research takes advantage of recent discoveries in genomics and epigenetics, it couldn’t have been conducted without the tissue samples, radiation monitoring, and interview collection that have continued over decades. When these efforts started in the 1980s, scientists had no way of knowing what technologies would come along to help others make use of their work. Charnock says this is important to keep in mind for so much scientific research: What seems unimportant now could play a huge role we can’t predict. “The investments in this pay off later,” he says. “Not tomorrow, but in the future.”
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