The US government still uses floppy disks.


The federal government is a complicated behemoth that takes a long time to change course. With technology changing faster than ever, it’s no surprise that government regulation and human stubbornness are slowing the transition to new methods. In fact, one government agency still requires parts of the government to submit information on floppy disks.

pile of floppy disks

The Federal Register is basically a daily update on the activities of the federal government. It aggregates all the orders, rule changes, and notices issued by various agencies and publishes them online and in paper form. This fulfills a requirement that the information be made available for public inspection, but the way the Federal Register gets all that information is odd.

Agencies are required to submit multiple certified copies of each document, which they can do multiple ways. Some still send over paper documents, but others provide digital files to the Register. However, the Register won’t accept a thumbdrive or SD card — it’s only floppy or CD, and a surprising number of agencies still send over 3.5-inch floppies. Where are they even finding floppy drives anymore?

There is also a much more modern secure email system for providing files, but moving to this platform is a big expensive change that many agencies haven’t made yet. The alternative, apparently, is to continue using technology from the 80s. There is hope that the issues surrounding the healthcare.gov website launch will prompt agencies to modernize, but it might take an act of congress to mandate the use of new tehcnology like the secure email system. So, all we need is for congress to come together and do away with floppy disks in the federal government. If there’s anything that can bring the two sides together, surely it is a disdain for floppy disks.

 

New sensor tracks zinc in cells, could be exploited for early diagnosis of prostate cancer


Zinc, an essential nutrient, is found in every tissue in the body. The vast majority of the metal ion is tightly bound to proteins, helping them to perform biological reactions. Tiny amounts of zinc, however, are only loosely bound, or “mobile,” and thought to be critical for proper function in organs such as the brain, pancreas, and prostate gland. Yet the exact roles the ion plays in biological systems are unknown.

 

 

 

A new optical sensor created at MIT tracks  within cells and should help researchers learn more about its functions. The sensor, which can be targeted to a specific organelle within the cell, fluoresces when it binds to zinc, allowing scientists to determine where the metal is concentrated.

The MIT chemists who designed the sensor have already used it to shed light on why zinc levels, normally high in the prostate, drop dramatically in cancerous prostate cells.

“We can use these tools to study zinc trafficking within prostate cells, both healthy and diseased. By doing so we’re trying to gain insight into how zinc levels within the cell change during the progression of prostate cancer,” says Robert Radford, an MIT postdoc who led the project and who is an author of the paper describing the sensors, which appears in the Dec. 9 issue of theProceedings of the National Academy of Sciences.

Radford works in the lab of Stephen Lippard, the Arthur Amos Noyes Professor of Chemistry and senior author of the paper. The paper’s lead author is Wen Chyan, a 2013 MIT graduate.

Researchers in Lippard’s lab are now working on exploiting similar fluorescent sensors to develop a diagnostic test for early detection of , which is the second leading cause of cancer death in American men, but is considered very treatable if caught early enough.

Pathway to cancer

Among its known roles, zinc helps to stabilize protein structure and catalyzes some cellular reactions. In the prostate, zinc is believed to help with reproductive functions by aiding in the accumulation of citrate, a component of semen. Within mitochondria of epithelial prostate cells, zinc has been shown to inhibit the metabolic enzyme aconitase. By blocking the activity of aconitase, zinc truncates the citric acid cycle, the series of reactions that produce ATP, the cells’ major energy currency.

Scientists have theorized that when prostate cells become cancerous, they banish zinc from mitochondria (the cell structures where most ATP production occurs). This allows the cancer cell to produce the extra energy it needs to grow and divide.

“If a cell is dividing uncontrollably and it needs a lot of chemical energy, then it definitely wouldn’t want zinc interfering with aconitase and preventing production of more ATP,” Radford says.

The new MIT study supports this theory by showing that, although cancerous prostate cells can absorb zinc, the metal does not accumulate in the mitochondria, as it does in normal .

This finding suggests that, in normal cells, zinc is probably transported into mitochondria by a specialized transport protein, but such a protein has not been identified, Radford says. In cancer cells, this protein might be inactivated.

Follow the zinc

The new zinc sensor relies on a molecule that Lippard’s lab first developed more than 10 years ago, known as Zinpyr1 (ZP1). ZP1 is based on a dye known as fluorescein, but it is modified to fluoresce only when it binds to zinc.

The ZP1 sensor can simply be added to a dish of cells grown in the lab, where it will diffuse into the cells. Until now, a major drawback of the sensor was the difficulty in targeting specific structures within a cell. “We have had some success using proteins and peptides to target small molecule zinc sensors,” Radford says, “but most of the time the sensors get captured in acidic vesicles within the cell and become inactive.”

Lippard’s team overcame that obstacle by making two changes: First, they installed a zinc-reactive protecting group, which altered the physical properties of the sensor and made it easier to target. Second, they attached an “address tag” that directs ZP1 into mitochondria. This tag, which is a derivative of triphenylphosphonium, is tailored to enter the mitochondria because it is both positively charged and hydrophobic. The resulting sensor readily entered cells and allowed the researchers to visualize pools of mobile zinc within .

“This is an exciting new concept for sensing using a combination of reaction- and recognition-based approaches, which has potential applications for diagnostics involving zinc misregulation,” says Christopher Chang, a professor of chemistry and molecular and cell biology at the University of California at Berkeley who was not part of the research team.

In future studies, the researchers plan to expand their strategy to create a palette of sensors that target many other organelles in the cell.

“The identification of intracellular targets for mobile zinc is an important step in understanding its true function in biological signaling. The next steps will involve discovery of the specific biochemical pathways that are affected by zinc binding to receptors in the organelles, such as proteins, and elucidating the structural and attendant functional changes that occur in the process,” Lippard says.

The lab’s immediate interest is study of zinc in the brain, where it is believed to act as a neurotransmitter. By understanding mobile zinc in the auditory cortex, optic nerve, and olfactory bulb, the researchers hope to figure out its role in the senses of hearing, sight, and smell.

 

Oldest human DNA found in Spain


 
A drawing shows what the species of Homo heidelbergensis might have looked like 400,000 years ago.
 
A drawing shows what the species of Homo heidelbergensis might have looked like 400,000 years ago.

STORY HIGHLIGHTS
 

There were no genetic tests 400,000 years ago, so our ancient relatives didn’t know as much about themselves as we know about them now.

Scientists have reconstructed a nearly complete mitochondrial genome of an ancient human relative, whose remains were found in Sima de los Huesos (“pit of bones”) in northern Spain. It is the oldest DNA to be recovered from an early humanlike species, authors of a study wrote in the journal Nature.

The ancient species that has revealed some of its genetic secrets, via bone fragments from a femur, is probably not directly linked to your family tree though.

“It’s quite clear that this is not a direct ancestor of people today,” said Svante Paabo, a biologist at the Max Planck Institute for Evolutionary Anthropology and senior author of the study.

Instead, he said, this representative of an early humanlike species, called Homo heidelbergensis, could be an ancestor of both Neanderthals and another group called the De nisovans.

The genetic relationship to Denisovans, discovered through this DNA research, is surprising because the Homo heidelbergensis remains found in the cave have many Neanderthal-like features. The only remnants of Denisovans come from Siberia — a long way from Spain.

“It’s sort of an open question really what this means, and I think further research into the nuclear genome of these hominins will address that,” Paabo said.

How they did it

Paabo and colleagues used a new method for sequencing ancient, degraded genetic material to put together the 400,000-year-old specimen’s mitochondrial genome. It is the oldest DNA ever found outside permafrost conditions — in other words, it was not permanently frozen.

“The retrieval of such ancient human DNA is a major technical achievement, and promises further recovery of such material from other fossils in this time range, both in the Sima and elsewhere, where we would not previously have expected it, or looked for it,” said Chris Stringer, researcher at the Natural History Museum in London, who was not involved in the study.

 

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Mitochondria are structures in cells that convert food energy into usable forms. DNA stored in the mitochondria is passed to children through the maternal line only (i.e., only moms can pass it on), so it’s only a small snapshot of inherited genes.

Genetic material in the cell’s nucleus comes from both parents and gives a fuller picture of genetic heritage.

To study genetics of our ancient predecessors, researchers have an easier time studying mitochondrial DNA because there are hundreds of times more copies of it in each cell.

“It’s a much bigger chance to find some fragments of this preserved,” Paabo said.

A skeleton of a Homo heidelbergensis representative from a cave site in Spain.
A skeleton of a Homo heidelbergensis representative from a cave site in Spain.

The method that researchers used involves separating the two strands of the DNA double helix. They then make a “library” from each of the two strands. If part of one strand is damaged, its analogue on the other strand — which is made of complementary genetic partners — may be intact.

“That is sort of the big trick involved,” Paabo said.

After sequencing the mitochondrial DNA, researchers then compared the result with genetic information about Neanderthals and Denisovans.

Since nuclear DNA encompasses more information about a person’s inheritance, a nuclear genome sequence from Homo heidelbergensis may reveal even more clearly how it is connected to other ancient humanlike species, he said.

But retrieving the nuclear DNA sequence will be challenging, study authors wrote. Just to get the mitochondrial DNA sequence, it took about two grams of bone — less than 0.1 ounce — even though hundreds of copies of this DNA are in every cell.

Still, Paabo said, the sequencing technique his group used “opens a possibility to now do this at many other sites, and really begin to understand earlier human evolution.”

Relationship to other species

Researchers thought initially the mitochondrial DNA of the Homo heidelbergensis specimen would share a common ancestor with Neanderthals. Neanderthals lived in Europe beginning as much as 300,000 years ago, Paabo said. (Homo sapiens, our species, first appeared in Africa between 100,000 and 200,000 years ago.)

Instead, researchers discovered through the DNA that this specimen is closer to the Denisovans, a group related to the Neanderthals.

A likely explanation is that in Eastern Eurasia this species gave rise to Denisovans, and in Western Eurasia they were the ancestors of Neanderthals, Paabo said. But more research needs to be done to verify that theory.

Humans, Neanderthals related to yet another group

Little is known about the Denisovans. Although some of their remains were found in southern Siberia, their genetic signature is only found today on islands in the Pacific.

Paabo was also the senior author on a 2012 study in the journal Science analyzing the Denisovan genome. That research suggested that human ancestors and the Denisovans’ ancestors must have branched off from one another as much as 700,000 years ago — although that number is vague. Still, it seems that the Denisovans must have mated with indigenous people in Papua New Guinea and Australia, Paabo said.

About 3% to 5% of the DNA of people from Melanesia (islands in the southwest Pacific Ocean), Australia and New Guinea as well as aboriginal people from the Philippines comes from the Denisovans.

On the other hand, everyone who lives outside Africa today probably has some Neanderthal DNA in them, Paabo said in 2012.

The bottom line, Paabo said, is that the relationships between these early human relatives — Homo heidelbergensis, Neanderthals and Denisovans — are not clear-cut.

“It’s going to be a more complex history that one will eventually clarify with the help of DNA,” he said.

Researchers film early concussion damage, describe brain’s response to injury.


There is more than meets the eye following even a mild traumatic brain injury. While the brain may appear to be intact, new findings reported in Nature suggest that the brain’s protective coverings may feel the brunt of the impact.

Using a newly developed mouse trauma model, senior author Dorian McGavern, Ph.D., scientist at the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health, watched specific cells mount an  to the injury and try to prevent more widespread damage. Notably, additional findings suggest a similar immune response may occur in patients with mild head injury.

In this study, researchers also discovered that certain molecules, when applied directly to the mouse skull, can bypass the brain’s protective barriers and enter the brain. The findings suggested that, in the mouse trauma model, one of those molecules may reduce effects of .

Although concussions are common, not much is known about the effects of this type of damage. As part of this study, Lawrence Latour, Ph.D., a scientist from NINDS and the Center for Neuroscience and Regenerative Medicine, examined individuals who had recently suffered a concussion but whose initial scans did not reveal any physical damage to brain tissue. After administering a commonly used dye during MRI scans, Latour and his colleagues saw it leaking into the meninges, the outer covers of the brain, in 49 percent of 142 patients with concussion.

To determine what happens following this mild type of injury, researchers in Dr. McGavern’s lab developed a new model of brain trauma in mice.

“In our mice, there was leakage from blood vessels right underneath the skull bone at the site of injury, similar to the type of effect we saw in almost half of our patients who had mild . We are using this mouse model to look at meningeal trauma and how that spreads more deeply into the brain over time,” said Dr. McGavern.

Dr. McGavern and his colleagues also discovered that the intact skull bone was porous enough to allow small molecules to get through to the brain. They showed that smaller molecules reached the brain faster and to a greater extent than larger ones. “It was surprising to discover that all these protective barriers the brain has may not be concrete. You can get something to pass through them,” said Dr. McGavern.

The researchers found that applying glutathione (an antioxidant that is normally found in our cells) directly on the skull surface after brain injury reduced the amount of  by 67 percent. When the researchers applied glutathione three hours after injury, cell death was reduced by 51 percent. “This idea that we have a time window within which to work, potentially up to three hours, is exciting and may be clinically important,” said Dr. McGavern.

Glutathione works by decreasing levels of reactive oxygen species (ROS) molecules that damage cells. In this study, high levels of ROS were observed at the trauma site right after the physical brain injury occurred. The massive flood of ROS set up a sequence of events that led to cell death in the brain, but glutathione was able to prevent many of those effects.

In addition, using a powerful microscopic technique, the researchers filmed what was happening just beneath the skull surface within five minutes of injury. They captured never-before-seen details of how the brain responds to traumatic injury and how it mobilizes to defend itself.

Initially, they saw cell death in the meninges and at the glial limitans (a very thin barrier at the surface of the brain that is the last line of defense against dangerous molecules). Cell death in the underlying brain tissue did not occur until 9-12 hours after injury. “You have death in the lining first and then this penetrates into the brain tissue later. The goal of therapies for brain injury is to protect the ,” said Dr. McGavern.

Almost immediately after head injury, the glial limitans can break down and develop holes, providing a way for potentially harmful molecules to get into the brain. The researchers observed microglia (immune cells that act as first responders in the brain against dangerous substances) quickly moving up to the brain surface, plugging up the holes.

Findings from Dr. McGavern’s lab indicate that microglia do this in two ways. According to Dr. McGavern, “If the astrocytes, the cells that make up the glial limitans, are still there, microglia will come up to ‘caulk’ the barrier and plug up gaps between individual astrocytes. If an astrocyte dies, that results in a larger space in the glial limitans, so the microglia will change shape, expand into a fat jellyfish-like structure and try to plug up that hole. These reactions, which have never been seen before in living brains, help secure the barrier and prevent toxic substances from getting into the brain.”

Studies have suggested that immune responses in the brain can often lead to severe damage. Remarkably, the findings in this study show that the inflammatory response in a model is actually beneficial during the first 9-12 hours after injury.

Mild traumatic brain injuries are a growing public health concern. According to a report from the Centers of Disease Control and Prevention, in 2009 at least 2.4 million people suffered a traumatic injury and 75 percent of those injuries were mild. This study provides insight into the damage that occurs following head trauma and identifies potential therapeutic targets, such as antioxidants, for reducing the damaging effects.

Nelson Mandela: Aids campaigner


Nelson Mandela in October 2003
Like many others, Nelson Mandela did not at first realise the dangers of HIV

Though at first muted in his approach to the issues surrounding HIV/Aids, Nelson Mandela eventually became a dedicated and extremely effective advocate for a more vigorous approach to the disease.

When Mr Mandela was released from prison in February 1990, HIV/Aids had yet to make its full impact on South Africa.

“Start Quote

We are facing a silent and invisible enemy that is threatening the very fabric of our society”

Nelson Mandela

Following his election as president four years later, Mr Mandela faced huge challenges and – like so many other world leaders at the time – failed to fully understand the depth of the problem and did little to help those with Aids.

At the time, the African National Congress (ANC) was gripped by an ongoing debate about both the causes of, and treatment for, Aids.

Some figures, like Thabo Mbeki, Mr Mandela’s successor as president, openly questioned whether Aids was caused by HIV.

After Mr Mandela left office in 1999, he campaigned for more research into HIV/Aids, for education about safe sex and for better treatment for those affected. However, most South Africans still did not mention the disease in public.

Controversy within ANC

According to UN figures, the rate of HIV infection among adult South Africans rose from less than 1% in 1990 to about 17.9% by 2012.

Aids activists demonstrate outside the US consulate in Johannesburg - 17 June 2010South Africa has one of the highest HIV rates in the world

South Africa is currently home to more people with the virus than any other country – 6.1 million of its citizens were infected with HIV in 2012, including 410,000 children (aged 0-14), out of a population of just over 51 million.

The causes of an epidemic on this scale have been many – primarily poverty, but also economic migration, the poor status of women, and unsafe sexual practices, have all contributed to the rapid spread of the disease.

Apart from the human misery caused by Aids, its economic impact has been huge, with South African economic growth rates badly affected.

Having put the issue of Aids on the back burner when in office, Mr Mandela began to make strong pronouncements on the subject after he stepped down in 1999.

HIV/Aids in South Africa

  • People living with HIV: 6.1 million
  • Rate of infection in adults aged 15-49: 17.9%
  • Children aged 0-14 living with HIV: 410,000
  • Deaths due to Aids in 2012: 240,000
  • Orphans due to Aids aged 0-17: 2.5 million

Source: UNAids 2012

On World Aids Day in 2000, he sent out a hard-hitting message, saying: “Our country is facing a disaster of immeasurable proportions from HIV/Aids.

“We are facing a silent and invisible enemy that is threatening the very fabric of our society.

“Be faithful to one partner and use a condom… Give a child love, laughter and peace, not Aids.”

Mr Mandela said his country should promote abstinence, the use of condoms, early treatment, counselling and drugs to reduce mother-to-child transmission.

Urgency

At the time, there was a marked reluctance on the part of the South African government to fund anti-retroviral drugs for those with HIV.

Nelson Mandela with Makgatho (R) in 2003
Mr Mandela’s son, Makgatho (R) died from Aids-related illness in 2005

The then President Mbeki outraged many people when he told a US journalist that “personally, I don’t know anybody who has died of Aids” and that he did not know if he had ever met anyone infected with HIV.

One of his ministers suggested that people with HIV eat garlic and beetroot to combat the infection.

In November 2003, Mr Mandela – and his Nelson Mandela Foundation – stepped up the campaign, launching an HIV/Aids fundraising campaign called 46664, after his prison number on Robben Island.


Nelson Mandela

1918 Born in the Eastern Cape

1943 Joined African National Congress

1956 Charged with high treason, but charges dropped after a four-year trial

1962 Arrested, convicted of incitement and leaving country without a passport, sentenced to five years in prison

1964 Charged with sabotage, sentenced to life

1990 Freed from prison

1993 Wins Nobel Peace Prize

1994 Elected first black president

1999 Steps down as leader

2001 Diagnosed with prostate cancer

2004 Retires from public life

2010 Last major public appearance at football World Cup in Johannesburg

He compared the urgency and drama of his country’s struggle against HIV/Aids to the fight against apartheid.

Pop stars like Beyonce, Youssou N’Dour and Dave Stewart supported the campaign, and a star-studded concert, held in Cape Town in 2003, was seen by a worldwide television audience of two billion.

The money raised by Mr Mandela’s initiatives has been used to fund research projects and provide practical support for South Africans with HIV/Aids.

The campaign received a further boost in 2005, when Mr Mandela shocked the nation by announcing that his son, Makgatho, had died of Aids.

He urged people to talk about HIV/Aids “to make it appear like a normal illness”.

It was a significant move, which had a huge impact, said Michel Sidibe, head of the UN’s Aids agency Unaids.

“The country has become a leader in the Aids response because of Mr Mandela, and is moving towards an Aids-free generation thanks to his campaigning,” he said.

Mr Mandela also became a central figure in the African and global Aids movement, Mr Sidibe said.

“He was instrumental in laying the foundations of the modern Aids response and his influence helped save millions of lives and transformed health in Africa,” he said.

“He was a statesman who had Aids at the top of his agenda and he used his stature and presence on the global stage to persuade world leaders to act decisively on Aids. His legacy will be felt by generations.”

Gene-testing company ‘here to stay’


DNA
The $99 personal DNA test was designed to detect a range of gene variants
Personal-genetics company 23andMe says it is “not going anywhere”, after the Food and Drug Administration ordered it to stop marketing-spit testing kits.

“Our mission is unchanged,” it says.

On Friday, the Californian company stopped giving its health-risk results – based on gene variants – to those who had bought the tests after 22 November.

The FDA feared they would make poor decisions, such as opting for unnecessary surgery on the basis of a risk for a gene linked to cancer.

Founded in 2006 by Linda Avey, Paul Cusenza and Anne Wojcicki, who reportedly separated recently from her husband, Google co-founder Sergey Brin, the company had offered results about a customer’s risk for 254 diseases and conditions, including genes linked to diabetes, heart disease and breast cancer.

But last week, in response to the regulator’s demands, the company, based in Mountain View and backed by wealthy investors, including Google, halted television, radio and online advertising for its $99 (£60) personal genome analysis product.

The health results had marked the company out from many other direct-to-consumer genetics companies, which are largely focused on providing information about ancestry alone.

The company’s former rivals, Navigenics and deCODEme, have since disappeared from the market after being acquired by bigger companies.

But spokeswoman Catherine Afarian told US website Venturebeat: “We are not going anywhere, although we recognise that the FDA process will take time.”

And she told BBC News the company “remains committed” to consumer genetics.

Warning letter

Many of the affected customers will reportedly be able to request a full refund, although they will continue to receive raw data and ancestry information.

Ms Afarian said the company was working hard to resolve the issues with the FDA and implied it might start to reintroduce aspects of its health tests in stages.

In its warning letter, the FDA said 23andMe had not provided assurances about how well the test predicted the presence or absence of a particular genetic variant or how well that genetic variant related to the risk of a specific disease.

The FDA said it was particularly concerned about the potential health consequences of assessments for drug sensitivity and a gene called BRCA linked to breast and ovarian cancer.

“For instance, if the BRCA-related risk assessment for breast or ovarian cancer reports a false positive, it could lead a patient to undergo prophylactic surgery, chemoprevention, intensive screening, or other morbidity-inducing actions, while a false negative could result in a failure to recognise an actual risk that may exist,” the letter said.

Hank Greely, director of the Center for Law and the Biosciences at Stanford University, said the company would have to overhaul its methods for characterising genetic variants.

In a blog written at the time of the FDA order, he said: “The SNP chip method that 23andMe uses was never very good at providing useful genetic information.

“Its advantage has been its low cost. But as sequencing gets cheaper and cheaper, SNP chips have already largely become obsolete for most genetic testing.”

Anne Wojcicki has said she stands by the data, and Ms Afarian said consumers had not been harmed.

Nevertheless, the company is being sued by customers in California, who say there is “no analytical or clinical validation for the [personal genomics service] for its advertised uses”.

EU-approved ‘safe’ air pollution levels causing early deaths.


Published time: December 09, 2013 14:08
Edited time: December 10, 2013 08:37

General view of the Origny sugar factory in Sainte-Benoite near Saint-Quentin. (AFP Photo / Philippe Huguen)General view of the Origny sugar factory in Sainte-Benoite near Saint-Quentin. (AFP Photo / Philippe Huguen)

Air pollution in the European Union is causing premature deaths even when levels meet quality guidelines, a report has shown. Even in areas where pollution was much lower than the limit, scientists found there is a higher-than-normal risk of death.

The study, published the British Medical Association’s journal The Lancet, found that Europeans who have had prolonged exposure to pollution from industrial activities or road traffic have a higher chance of premature death. The increased risk to a person’s health is linked to tiny particles of soot and dust than can get lodged in the lungs and cause respiratory illnesses.

The study, carried out by Utrecht University in the Netherlands, found the particles measure 2.5 microns or 2.5 millionth of a meter. Exposure for “up to a few months” to particles of 2.5 microns can increase the risk of premature death.

“Although this does not seem to be much, you have to keep in mind that everybody is exposed to some level of air pollution and that it is not a voluntary exposure, in contrast to, for example, smoking,” scientist Rob Beelen, who led the study, told AFP.

The findings of the study echo the results of similar investigations carried out in North America and China.

“Our findings support health impact assessments of fine particles in Europe which were previously based almost entirely on North American studies,” Beelen said.

As part of the study the researchers drew on 22 previously published studies that documented the health of 367,000 people in 13 countries in Western Europe over 14 years. Beelen and his team then traveled to the areas where the participants lived and took traffic pollution readings that they used to calculate how much pollution local residents were exposed to.

 

AFP Photo / Frederick FlorinDuring the investigation, 29,000 of the 367,000 participants recruited in 1990 died. In order to increase accuracy, investigations also took into account such factors as physical exercise, body mass, education and smoking habits. 

European Union guidelines set the maximum exposure to particles of 25 micrograms per cubic meter. Beelen says the results of this study are evidence the EU needs to reset its safety limits to 10 micrograms per cubic meter.

“Despite major improvements in air quality in the past 50 years, the data from Beelen and his colleagues’ report draw attention to the continuing effects of air pollution on health,” Jeremy Langrish and Nicholas Mills, of the University of Edinburgh, told the Medical Press.

In China a red alert was issued for poor air quality was issued Thursday after pollution reached hazardous levels. The coastal city of Qingdao recorded PM2.5 Air Quality Index levels of over 300, while Nanjing saw a reading of 354 on Wednesday, according to local news portal news.longhoo.net.

In light of the dangerous levels of pollution the Chinese government is considering the practice of ‘cloud seeding’ to clear toxic fog in the country. According to a document released by the China Meteorological Administration, from 2015 local meteorological authorities will be permitted to use cloud seeding to disperse pollution.

The World Health Organization has classified outdoor pollution as one of the principal causes of cancer and estimates around 3.2 million people die every year globally as a result of prolonged exposure.