Chernobyl 2? Watching the world’s aging power plants

Satellite imagery from May 2013 of the Yongbyon Nuclear Scientific Research Center in North Korea.DigitalGlobe

The Kalinin nuclear power plant in Russia.IAEA

North Korea’s aging Yongbyon nuclear power plant will probably not lead to a nuclear catastrophe, despite an alarming report calling it the next Chernobyl -- but the danger posed by the world’s aging reactors is real nonetheless.

The defense publication Jane’s recently detailed efforts to bring the small Yongbyon reactor back online, saying they could lead to a meltdown like the  Chernobyl incident in 1986. According to the article, Yongbyon uses obsolete technology that was responsible for a 1957 accident in the United Kingdom and “could lead to a disaster worse than the Ukrainian one."

But Joel Wit, a former U.S. State Department official who manages the 38 North blog for the U.S.-Korea Institute at the Johns Hopkins School of Advanced International Studies, told FoxNews.com he disagreed strongly with the Jane’s report. And when Ferenc Dalnoki-Veress, a scientist-in-residence with the James Martin Center for Nonproliferation Studies, ran an analysis, he concluded that the scale of the reactor posed a far smaller threat than Jane’s suggested.

“In the worst case scenario, the accident would release a dose 500,000 times lower than Chernobyl,” Dalnoki-Veress said.

'The Russians are running into this, the French are running into this, the Japanese are running into this. It’s a big issue.'

- Jon B. Wolfsthal, deputy director of California’s James Martin Center

Nonetheless, the average nuclear power plant is more than 20 years old and is anticipated to last no more than 30 or 40 years, leaving the world facing a potential crisis: How safe are aging nuclear power plants?

No country has a greater reliance on nuclear power than the U.S., which had 104 reactors online in 2011. But all of them have been online since 1990, and most since 1980.

“By far the largest problem is here in the U.S.,” said Jon B. Wolfsthal, deputy director of California’s James Martin Center.

“But the Russians are running into this, the French are running into this, the Japanese are running into this. It’s a big issue.”  

France had 58 nuclear reactors connected to the power grid in 2011, according to a 2012 reference work by the International Atomic Energy Agency (IAEA). Fifty-six of them have been operating since 1990, and 43 have been online since 1985, making them around 30 years old. Japan is in a similar situation, with 51 plants online in 2011 (not including the Fukushima plant), nearly all of which were in operation 20 years earlier.

There were 435 nuclear power plants online worldwide as of New Year’s Eve, 2011. As of that date, 138 others had been permanently shut down, though only 11 cited obsolescence as the reason.

Plot construction of nuclear plants on a grid and you’ll see a near perfect bell curve; most of the world’s power plants were built during the ’60s, ’70s and ’80s, peaking between 1974 and 1976, a three-year span that saw construction begin on 118 plants worldwide. By comparison, ground was broken on just 29 plants throughout the ’90s.

But nuclear power is seeing a renaissance. China has 42 power plants planned for construction, according to the IAEA, and Russia has 35. As of Dec. 31, 2011, 114 were planned, and an additional 65 reactors were under construction.

Yet Chris Englefield, a senior manager in radioactive substances regulation for the U.K. Environment Agency, noted in a 2012 paper that there are no nuclear security specialists. He says there is a need to professionalize security and to facilitate minimum standards of competence and regulatory procedures.

The U.N.’s IAEA acts as a nuclear watchdog at times, but it also helps to do just that, aiding member countries in maintaining power plants to tease extra years from them while preventing incidents.

“One of the IAEA’s key missions is to support its member states in their efforts to improve nuclear safety,” said IAEA spokesman Serge Gas. “In that context, the agency does not single out individual nations, but rather encourages all of them to improve all the time.”

Jeremy A. Kaplan is Science and Technology editor at FoxNews.com, where he heads up coverage of gadgets, the online world, space travel, nature, the environment, and more. Prior to joining Fox, he was executive editor of PC Magazine, co-host of the Fastest Geek competition, and a founding editor of GoodCleanTech.

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Protein linked with rare disease plays role in aging

By Julie Steenhuysen

CHICAGO | Mon Jun 13, 2011 7:40pm EDT

CHICAGO (Reuters) - The same mechanism that causes children with a rare genetic disease called progeria to age at seven times the normal rate may play a role in normal aging as well, government researchers said on Monday.

The study led by Dr. Francis Collins, director of the National Institutes of Health, suggests aging may not simply be a gradual wearing out of cells.

Instead, it may be an active biological mechanism -- one that might be tinkered with to address age-related diseases.

"I think a lot of people in the past have assumed that the aging of cells and of individuals was just a matter of everything running down," Collins told Reuters in a telephone interview.

"What we are learning at the cellular level ... is that is not right," said Collins, whose study appears in the Journal of Clinical Investigation.

Scientists for several years have been working to understand the key biological processes that trigger aging in hopes of discovering new drugs that could delay or prevent age-related diseases such as cancer, heart disease and Alzheimer's disease.

Much of that has been focused on studying protective caps on the tips of chromosomes called telomeres, which Collins likens to "the aglets on shoelaces that keep the laces from them from getting ratty."

When telomeres become too short and frayed through cell division, the cell eventually dies. But it has not been entirely clear how this comes about.

Based on the study by Collins and colleagues at the National Human Genome Research Institute, it now appears that the same toxic protein that drives the premature aging disorder progeria plays a key role in normal cell aging, Collins said.

Formally known as known as Hutchinson-Gilford Progeria Syndrome, progeria is an extremely rare disease in which children experience symptoms normally linked with old age -- hair loss, wrinkled skin, clogged arteries and arthritis.

Children with the disease often die by the age of 13.

INSIGHT INTO AGING

In a 2003 study, Collins and colleagues found the disease is caused by mutations in a gene called LMNA that makes the toxic protein progerin.

"What this paper does is show the process that is happening in those children is clearly an important process in normal aging," Collins said.

"That same toxic protein that we call progerin, which is made in large quantities in those kids, is also made in your cells and mine" as the cells start to die.

"And it shows the telomeres and progerin are connected," Collins said. "They have been on parallel scientific pathways and we have now found they are actually linked together."

He said when telomeres become too short and frayed, this triggers the production of progerin, signaling to the body that the cell is at the end of its useful life.

Collins says the study shows that instead of being a passive wearing out of cells, aging is an active biological mechanism that is programed into cells.

And understanding this mechanism could lead to new kinds of treatments. Already, a study is underway in children with progeria to see if researchers could block the excess production of progerin.

Collins says more work is needed to understand the biological mechanism of aging.

"We clearly don't have the whole picture," he said.

But understanding the aging process could lead to new ways to slow normal aging, and it underscores the need to continue funding research on rare diseases.

"It is often the insights that come from the rare diseases that teach us something about more common ones," he said.

(Editing by Eric Beech)

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