Cells inside our body keep dividing regularly, as is the scheme of the nature. However, if the division fails to take place, the cells will eventually die, leading to the chance of developing age-related diseases as well as cancer.
There are stretches of Deoxy Ribonucleic Acid (DNA) called telomeres present at the ends of chromosomes like protective caps. During cell division, these telomeres become shorter which makes the productivity of the protective cap less effective. Hence, the telomeres need to be checked upon regularly and elongated because if these DNA components get too short, the cell will stop dividing and move towards cell aging.
Scientists have studied what helps the telomeres to function properly and have found that a RNA species called TElomeric Repeat-containing RNA (TERRA) helps to work like the maintenance mechanic for telomeres. These get recruited at sites where telomeres need regulation and send a signal indicating that the telomeres need to be elongated or repaired. Which form of a system sends TERRA to the chromosome end is not known.
TERRA are a type of molecules called the non-coding RNAs, which do not get translated into proteins but instead function as chromosomes’ structural components. To study how these were getting assigned to places and remaining there, scientists visualized TERRA molecules under a microscope and found that a short stretch of the ribonucleic acid (RNA) was instrumental to bring it to the telomeres.
Now once TERRA has reached its required location, several proteins regulate its association with telomeres. Here, a protein called RAD51 plays a crucial role. Scientists from Ecole Polytechnique Fédérale de Lausanne and Masaryk University found that RAD51 was helping TERRA stick to telomeric DNA to form a so-called RNA-DNA hybrid molecule.
This sort of hybrid molecule formation has been previously detected only in the case of DNA repair. To witness it taking place during telomere repair is revolutionary.
A bit of seaweed in cattle feed could reduce methane emissions from beef cattle as much as 82 percent, according to new findings from researchers at the University of California, Davis. The results, published today in the journal PLOS ONE, could pave the way for the sustainable production of livestock throughout the world.
“We now have sound evidence that seaweed in cattle diet is effective at reducing greenhouse gases and that the efficacy does not diminish over time,” said Ermias Kebreab, professor and Sesnon Endowed Chair of the Department of Animal Science and director of the World Food Center. Kebreab conducted the study along with his Ph.D. graduate student Breanna Roque.
“This could help farmers sustainably produce the beef and dairy products we need to feed the world,” Roque added.
Over the course of five months last summer, Kebreab and Roque added scant amounts of seaweed to the diet of 21 beef cattle and tracked their weight gain and methane emissions. Cattle that consumed doses of about 80 grams (3 ounces) of seaweed gained as much weight as their herd mates while burping out 82 percent less methane into the atmosphere. Kebreab and Roque are building on their earlier work with dairy cattle, which was the world’s first experiment reported that used seaweed in cattle.
Less gassy, more sustainable
Greenhouse gases are a major cause of climate change, and methane is a potent greenhouse gas. Agriculture is responsible for 10 percent of greenhouse gas emissions in the U.S., and half of those come from cows and other ruminant animals that belch methane and other gases throughout the day as they digest forages like grass and hay.
Since cattle are the top agricultural source of greenhouse gases, many have suggested people eat less meat to help address climate change. Kebreab looks to cattle nutrition instead.
“Only a tiny fraction of the earth is fit for crop production,” Kebreab explained. “Much more land is suitable only for grazing, so livestock plays a vital role in feeding the 10 billion people who will soon inhabit the planet. Since much of livestock’s methane emissions come from the animal itself, nutrition plays a big role in finding solutions.”
In 2018, Kebreab and Roque were able to reduce methane emissions from dairy cows by over 50 percent by supplementing their diet with seaweed for two weeks. The seaweed inhibits an enzyme in the cow’s digestive system that contributes to methane production.
In the new study, Kebreab and Roque tested whether those reductions were sustainable over time by feeding cows a touch of seaweed every day for five months, from the time they were young on the range through their later days on the feed lot.
Four times a day, the cows ate a snack from an open-air contraption that measured the methane in their breath. The results were clear. Cattle that consumed seaweed emitted much less methane, and there was no drop-off in efficacy over time.
Results from a taste-test panel found no differences in the flavor of the beef from seaweed-fed steers compared with a control group. Similar tests with dairy cattle showed that seaweed had no impact on the taste of milk.
Also, scientists are studying ways to farm the type of seaweed—Asparagopsis taxiformis—that Kebreab’s team used in the tests. There is not enough of it in the wild for broad application.
Another challenge: How do ranchers provide seaweed supplements to grazing cattle on the open range? That’s the subject of Kebreab’s next study.
Kebreab and Roque collaborated with a federal scientific agency in Australia called the Commonwealth Scientific and Industrial Research Organization, James Cook University in Australia, Meat and Livestock Australia, and Blue Ocean Barns, a startup company that sources, processes, markets and certifies seaweed-based additives to cattle feed. Kebreab is a scientific adviser to Blue Ocean Barns.
“There is more work to be done, but we are very encouraged by these results,” Roque said. “We now have a clear answer to the question of whether seaweed supplements can sustainably reduce livestock methane emissions and its long term effectiveness.”
With a relatively minor genetic change, a new treatment developed by researchers at the Georgia Institute of Technology and Emory University appears to stop replication of both flu viruses and the virus that causes COVID-19. Best of all, the treatment could be delivered to the lungs via a nebulizer, making it easy for patients to administer themselves at home.
The therapy is based on a type of CRISPR, which normally allows researchers to target and edit specific portions of the genetic code, to target RNA molecules. In this case, the team used mRNA technology to code for a protein called Cas13a that destroys parts of the RNA genetic code that viruses use to replicate in cells in the lungs. It was developed by researchers in Philip Santangelo’s lab in the Wallace H. Coulter Department of Biomedical Engineering.
“In our drug, the only thing you have to change to go from one virus to another is the guide strand—we only have to change one sequence of RNA. That’s it,” Santangelo said. “We went from flu to SARS-CoV-2, the virus that causes COVID-19. They’re incredibly different viruses. And we were able to do that very, very rapidly by just changing a guide.”
The guide strand is a map that basically tells the Cas13a protein where to attach to the viruses’ RNA and begin to destroy it. Working with collaborators at the University of Georgia, Georgia State University, and Kennesaw State University, Santangelo’s team tested its approach against flu in mice and SARS-CoV-2 in hamsters. In both cases, the sick animals recovered.
Their results are reported Feb. 3 in the journal Nature Biotechnology. It’s the first study to show mRNA can be used to express the Cas13a protein and get it to work directly in lung tissue rather than in cells in a dish. It’s also the first to demonstrate the Cas13a protein is effective at stopping replication of SARS-CoV-2.
What’s more, the team’s approach has the potential to work against 99% of flu strains that have circulated over the last century. It also appears it would be effective against the new highly contagious variants of the coronavirus that have begun to circulate.
The key to that broad effectiveness is the sequence of genes the researchers target.
“In flu, we’re attacking the polymerase genes. Those are the enzymes that allow the virus to make more RNA and to replicate,” said Santangelo, the study’s corresponding author.
With help from a collaborator at the Centers for Disease Control and Prevention, they looked at the genetic sequences of prevalent flu strains over the last 100 years and found regions of RNA that are unchanged across nearly all of them.
“We went after those, because they’re far better conserved,” Santangelo said. “We let the biology dictate what our targets would be.”
Likewise, in SARS-CoV-2, the sequences the researchers targeted so far remain unchanged in the new variants.
The approach means the treatment is flexible and adaptable as new viruses emerge, said Daryll Vanover, a research scientist in Santangelo’s lab and the paper’s second author.
“One of the first things that society and the CDC is going to get when a pandemic emerges is the genetic sequence. It’s one of the first tools that the CDC and the surveillance teams are going to use to identify what kind of virus this is and to begin tracking it,” Vanover said. “Once the CDC publishes those sequences—that’s all we need. We can immediately screen across the regions that we’re interested in to target it and knock down the virus.”
Vanover said that can result in lead candidates for clinical trials in a matter of weeks—which is about how long it took them to scan the sequences, design their guide strands, and be ready for testing in this study.
“It’s really quite plug-and-play,” Santangelo said. “If you’re talking about small tweaks versus large tweaks, it’s a big bonus in terms of time. And in pandemics—if we had had a vaccine in a month or two after the pandemic hit, think about what things would look like now. If we had a therapy a month after it hit, what would things look like now? It could make a huge difference, the impact on the economy, the impact on people.”
The project was funded by the Defense Advanced Research Projects Agency’s (DARPA) PReemptive Expression of Protective Alleles and Response Elements (PREPARE) program, with the goal of creating safe, effective, transient, and reversible gene modulators as medical countermeasures that could be adapted and delivered rapidly. That’s why the team decided to try a nebulizer for delivering the treatment, Santangelo said.
“If you’re really trying to think of something that’s going to be a treatment that someone can actually give themselves in their own house, the nebulizer we used is not terribly different from one that you can go buy at a pharmacy,” he said.
The team’s approach also was sped along by their previous work on delivering mRNA to mucosal surfaces like those in the lungs. They knew there was a good chance they could tackle respiratory infections with that approach. They decided to use mRNA to code for the Cas13a protein because it’s an inherently safe technique.
“The mRNA is transient. It doesn’t get into the nucleus, doesn’t affect your DNA,” Santangelo said, “and for these CRISPR proteins, you really don’t want them expressed for long periods of time.”
He and Vanover said additional work remains—especially understanding more about the specific mechanisms that make the treatment effective. It has produced no side effects in the animal models, but they want to take a deeper look at safety as they consider moving closer to a therapy for human patients.
“This project really gave us the opportunity to push our limits in the lab in terms of techniques, in terms of new strategy,” said Chiara Zurla, the team’s project manager and a co-author on the paper. “Especially with the pandemic, we feel an obligation to do as much as we can as well as we can. This first paper is a great example, but many will follow; we’ve done a lot of work, and we have a lot of promising results.”
A recent study by researchers from the University of Bristol has found that many animals fake death to try to escape their predators. With some individuals in prey species remaining motionless, if in danger, for extended lengths of time.
The study was published today in the science journal Biology Letters.
Charles Darwin recorded a beetle that remained stationary for 23 minutes – however, the University of Bristol has documented individual antlion larvae pretending to be dead for an astonishing 61 minutes.
Of equal importance, the amount of time that an individual remains motionless is not only long but unpredictable. This means that a predator will be unable to predict when a potential prey item will move again, attract attention, and become a meal.
Predators are hungry and cannot wait indefinitely. Similarly, prey may be losing opportunities to get on with their lives if they remain motionless for too long. Thus, death-feigning might best be thought of as part of a deadly game of hiding and seek in which prey might gain most by feigning death if alternative victims are readily available.
The study involved evaluating the benefits of death-feigning in terms of a predator visiting small populations of conspicuous prey. Researchers used computer simulations that utilise the marginal value theorem, a classical model in optimization.
The lead author of the paper Professor Nigel R. Franks from the University of Bristol’s School of Biological Sciences said: “Imagine you are in a garden full of identical soft fruit bushes. You go to the first bush. Initially collecting and consuming fruit is fast and easy, but as you strip the bush finding more fruit gets harder and harder and more time-consuming.
“At some stage, you should decide to go to another bush and begin again. You are greedy and you want to eat as many fruits as quickly as possible. The marginal value theorem would tell you how long to spend at each bush given that time will also be lost moving to the next bush.
“We use this approach to consider a small bird visiting patches of conspicuous antlion pits and show that antlion larvae that waste some of the predator’s time, by ‘playing dead’ if they are dropped, change the game significantly. In a sense, they encourage the predator to search elsewhere.”
The modelling suggests that antlion larvae would not gain significantly if they remained motionless for even longer than they actually do. This suggests that in this arms race between predators and prey, death-feigning has been prolonged to such an extent that it can hardly be bettered.
Professor Franks added: “Thus, playing dead is rather like a conjuring trick. Magicians distract an audience from seeing their sleights of hand by encouraging them to look elsewhere. Just so with the antlion larvae playing dead – the predator looks elsewhere. Playing dead seems to be a very good way to stay alive.”
These sperm also take a straight path unlike their zigzagging rivals.
It turns out there’s a difference in competitiveness between sperm swimming towards an egg, and it’s down to genetics and one protein: RAC1.
If you thought it was by sheer luck that sperm make it all the way to the egg to fertilize it, you have just been proven wrong by a team of researchers at the Max Planck Institute for Molecular Genetics (MPIMG) in Berlin, Germany.
The researchers explained in a study, published in the journal PLOS Genetics on February 4, how a genetic factor called “t-haplotype” awards the success of reaching the egg first to sperm that contain it, and it happens 99 percent of the time.
In a first, the researchers pointed out that sperm with the t-haplotype moved faster than their peers without it. It also turned out that these faster-moving sperm were swimming straight, compared with their zigzagging competitors.
And it comes down to RAC1, a protein that transmits signals from the outside of the sperm cell to the inside by activating other proteins. It essentially helps to direct the sperm in the right direction.
On top of having assistance with directions, the t-haplotype sperm manage to poison their “normal” counterparts. These sperm not only produce a poison to stop their competitors, but they also create an antidote so that they themselves are protected from it, as Bernhard Herrmann, Director at the MPIMG and of the Institute of Medical Genetics at Charité – Universitätsmedizin Berlin, explained.
“Imagine a marathon, in which all participants get poisoned drinking water, but some runners also take an antidote,” Herrmann compares.
The team carried out its research on mice, so as to better understand the reasons for infertility in human males. Through their study, the researchers discovered that male mice with two copies of the t-haplotype were sterile because they produced only sperm with the t-haplotype, turning them all immotile. These cells have higher RAC1 levels.
However, having too low RAC1 levels also leads to disadvantages, as the sperm aren’t able to move quickly enough. So the researchers speculate that aberrant RAC1 activity may be the underlying reason for particular forms of male infertility.
Bioprinting is the medical and biotechnology equivalent of 3D printing. By using the same principles, the aim is to rapidly develop living structures resembling human-grown organs and tissue that can be used to heal people or test new drugs.
Medical fields such as cosmetic surgery, tissue engineering, and regenerative medicine operate on the principle that we can precisely manufacture tissue or whole body parts to help the body repair itself. Bioprinting offers the accuracy of precisely measured biology alongside rapid manufacture so we can heal people more quickly and effectively.
Of course, printing biological tissue is much more complex than building a mechanical part. There are intricate layers of cells in living tissue that need growth factors and surrounding structures to develop successfully. To mimic this bioprinters use bioink made from cells, biochemical nutrients and biological scaffolds to support cells in a precise order.
Additional Materials Required
Bioinks have to operate under conditions that are suitable to living, growing tissue, so they cannot really be printed at temperatures that exceed body temperature. They use a binding agent – often a biopolymer gel, or hydrogel – that acts as the molecular scaffold.
Common components of bioinks include collagen and hyaluronic acid, active molecules found in extracellular matrix (ECM) in the body, plus substances like alginate, a vegetable biopolymer refined from seaweed that retains water. Creating the right cell matrix helps the cells to stick together, communicate with each other and turn into the right types of cells to make the target tissue.
The Process is Real
Perhaps the simplest form of bioprinting is inkjet printing. Bioink is sprayed through tiny nozzles so it has to be almost liquid and this limits the biological materials that can be printed. Most 3D printers operate by extruding material through a nozzle and bioprinters can use extrusion too, though care has to be taken not to damage cells through excessive force.
Other techniques such as laser-assisted bioprinting or electrospinning – which use laser and electrical energy to position cells – are incredibly precise and can be used with thicker bioinks, but they are more tricky to use with living cells and not as rapid or able to create large quantities of tissue.
Once the bioprinter has done its work then the post-processing stage begins. Bioreactor systems are often employed to help the tissue to mature. They can be used to mimic the forces and biochemical support that tissue needs to grow and differentiate correctly.
You Have So Much Potential
Bioprinting may be a relatively new field but the results so far are encouraging. Stem cells, which have the potential to turn into several types of cells, are being used to create bone or cartilage to mend fractures and joint injuries.
Australian researchers have used neural cells in a custom-made bioink to create a ‘benchtop brain‘ that allows medics to test brain function, new drugs and study brain disorders like schizophrenia. Meanwhile, regenerative medicine scientists in the US have created a bioprinter able to construct ear, muscle and bone structures with the right size, strength and function for implantation.
One of the primary goals of bioprinting is to create functioning internal organs such as livers, kidneys or hearts. By printing compatible organs using a patient’s own stem cells, the donor waiting list could become a thing of the past. To get to this point there have been some important breakthroughs in printing vascularized tissue in complex 3D
Organ printing can improve the health of society in general by eliminating the problem of diseases caused by organ failure, costly treatments and social care. That promise may be years away from realization but rapid prototyping enabled by bioprinting is pushing medical advances forward at pace.
An international team of researchers led by Michigan State University’s Morteza Mahmoudi has developed a new method to better understand how nanomedicines — emerging diagnostics and therapies that are very small yet very intricate — interact with patients’ biomolecules.
Medicines based on nanoscopic particles have the promise to be more effective than current therapies while reducing side effects. But subtle complexities have confined most of these particles to research labs and out of clinical use, said Mahmoudi, an assistant professor in the Department of Radiology and the Precision Health Program.
“There’s been a considerable investment of taxpayer money in cancer nanomedicine research, but that research hasn’t successfully translated to the clinic,” Mahmoudi said. “The biological effects of nanoparticles, how the body interacts with nanoparticles, remain poorly understood. And they need to be considered in detail.”
Mahmoudi’s team has now introduced a unique combination of microscopy techniques to enable more detailed consideration of those biological effects, which the researchers described in the journal Nature Communications, published online on Jan. 25.
The team’s methods let researchers see important differences between particles exposed to human plasma, the cell-free part of blood that contains biomolecules including proteins, enzymes and antibodies.
These biological bits latch onto a nanoparticle, creating a coating referred to as a corona (not to be confused with the novel coronavirus), the Latin word for crown. This corona contains clues about how nanoparticles interact with a patient’s biology. Now, Mahmoudi and his colleagues have shown how to get an unprecedented view of that corona.
“For the first time, we can image the 3-D structure of the particles coated with biomolecules at the nano level,” Mahmoudi said. “This is a useful approach to get helpful and robust data for nanomedicines, to get the kind of data that can affect scientists’ decisions about the safety and efficacy of nanoparticles.”
Although work like this is ultimately helping move therapeutic nanomedicines into the clinic, Mahmoudi is not optimistic that broad approval will happen any time soon. There’s still much to learn about the particles. Furthermore, one of the things that researchers do understand very well — that minute variations in these diminutive drugs can have outsized impact — was underscored by this study.
The researchers saw that the coronas of nanoparticles from the same batch, exposed to the same human plasma, could provoke a variety of reactions by a patient to a single dose.
Still, Mahmoudi sees an opportunity in this. He believes these particles could shine as diagnostics tools instead of drugs. Rather than trying to treat diseases with nanoscale medicine, he believes that persnickety particles would be well suited for the early detection of disease. For example, Mahmoudi’s group has previously shown this diagnostic potential for cancers and neurodegenerative diseases.
“We could become more proactive if we used nanoparticles as a diagnostic,” he said. “When you can detect disease at the earlier stages, it becomes easier to treat them.”
By 2050, more than half the global population will live downstream from tens of thousands of large dams near or past their intended lifespan, according to a UN report released Friday.
Most of the world’s nearly 59,000 big dams—constructed between 1930 and 1970—were designed to last 50 to 100 years, according to research from the UN University’s Institute for Water, Environment and Health.
“This is an emerging global risk that we are not yet paying attention to,” co-author and Institute director Vladimir Smakhtin told AFP.
“In terms of dams at risk, the number is growing year by year, decade by decade.”
A well-designed, constructed and maintained dam can easily remain functional for a century.
But many of the world’s major dams fail on one or more of these criteria.
Dozens have suffered major damage or outright collapse over the last two decades in the United States, India, Brazil, Afghanistan and other countries, and the number of such failures could increase, the report warned.
Compounding the risk in ways that have yet to be fully measured is global warming.
“Because of climate change, extreme rainfall and flooding events are becoming more frequent,” lead author Duminda Perera, a researcher at the University of Ottawa and McMaster University, said in an interview.
This not only increases the risk of reservoirs overflowing but also accelerates the build up of sediment, which affects dam safety, reduces water storage capacity, and lowers energy production in hydroelectric dams.
In February 2017, the spillways of California’s Oroville Dam—the tallest in the US—were damaged during heavy rainfall, prompting the emergency evacuation of more than 180,000 people downstream.
In 2019, record flooding sparked concern that Mosul Dam, Iraq’s largest, could fail.
Ageing dams not only pose a greater risk to downstream populations, but also become less efficient at generating electricity, and far more expensive to maintain.
Because the number of large dams under construction or planned has dropped sharply since the 1960s and 1970s, these problems will multiply in coming years.
“There won’t be another dam-building revolution, so the average age of dams is getting older,” said Perera.
“Due to new energy sources coming online—solar, wind—a lot of planned hydroelectric dams will probably not ever be built.”
A global fleet of nearly 60,000 ageing dams also highlights the challenge of dismantling—or “decommissioning”—those that are no longer safe or functional.
More than 150 years old
Several dozen have been torn down in the United States, but all of them small, Smakhtin said.
More than 90 percent of large dams—at least 15 metres from foundation to crest, or holding back no less than three million cubic metres of water—are located in only two dozen countries.
China alone is home to 40 percent of them, with another 15 percent in India, Japan and Korea combined. More than half will be older than 50 within a few years.
Another 16 percent of the world’s dams are in the United States, more than 85 percent of them already operating at or past their life expectancy.
It would cost some $64 billion to refurbish them, according to one estimate.
In India, 64 big dams will be at least 150 years old by 2050. In North America and Asia, there are some 2,300 operational dams at least 100 years old.
Worldwide, there is about 7,500 cubic kilometres of water—enough to submerge most of Canada by a metre—stored behind large dams.
Neurobiology of Thirst: Neural Mechanisms that Control Hydration
Scientists at the Tokyo Institute of Technology (Tokyo Tech) provide deeper insights into neural thirst control. Their study published recently in Nature Communications indicates that cholecystokinin-mediated water-intake suppression is controlled by two neuronal ‘thirst-suppressing’ sub-populations in the subfornical organ in the brain; one population is persistently activated by excessive water levels, and the other, transiently after drinking water.
Water sustains life on earth. The first life originated in an ancient sea, and since then, nearly every species that has existed in the past or lives today depends on the exact balance of salt and water (~145 mM; called body-fluid homeostasis or salt homeostasis) for survival. Humans can go weeks without food but will not last more than a few days without water, stressing the importance of this liquid.
The human body has several intricate mechanisms to make sure we consume an appropriate amount of water for maintaining the homeostasis, which is requisite to survival. One of these simple but key “hacks,” is thirst. When the body experiences dehydration on a hot day (noted by the excess of sodium in the body compared to water, a condition called hypernatremia), the brain sends “signals” to the rest of the body, making us crave the tall glass of water. On the other hand, under a condition called hyponatremia, where there is a more water than sodium, we suppress water drinking. The neural mechanisms of how this happens are a subject of great interest.
A team of researchers from Tokyo Institute of Technology, headed by Prof Masaharu Noda, have conducted extensive research into this. In their previous studies, they identified that thirst is driven by the so-called “water neurons” in the subfornical organ (SFO) of the brain, a region just outside the blood-brain barrier. When the body is dehydrated, the plasma levels of a peptide hormone called angiotensin II increase. These levels are detected by special angiotensin II “receptors” of water neurons to stimulate water intake. In turn, under sodium-depleted conditions (where there is more water than sodium), the activity of these water neurons is suppressed by “GABAergic” interneurons. “The latter control appeared to be dependent on the hormone cholecystokinin (CCK) in the SFO. However, the CCK-mediated neural mechanisms underlying the inhibitory control of water intake had not been elucidated so far,” states Prof Noda.
There’s a spat between tech companies trying to develop a new generation of plastics that biodegrade harmlessly without leaving a trace and skeptics worried that such novel substances won’t live up to their promise and will worsen the plastic waste problem.
The companies are calling for more time to perfect their inventions — which they say differ from earlier efforts to make cleaner plastics — while environmental campaigners demand even firmer regulatory action to get rid of plastic garbage. Firms are also battling against the image problem of an earlier generation of innovative biodegradable plastics that experts say haven’t lived up to the hype.
“The popular understanding of biodegradability is based on legacy solutions such as oxodegradable plastic, many of which unfortunately don’t work,” said Niall Dunne, the CEO of British firm Polymateria, adding that the “landscape has moved on significantly yet outdated perceptions remain.”
Polymateriahas developed a process, called biotransformation,to produce plastic products it says decompose harmlessly when littered.
It involves mixing bio-transformation chemicals with normal plastics to create food and drink packaging, bubble wrap, fruit nets, plastic bags and the like. The technology helped to define a new British standard for biodegradability.
“The role of innovation is consistently underestimated when solving complex global issues, including climate change and plastic pollution,” Dunne said.
But potential innovations like that are facing headwinds.
An expert study, published last week, found that a lack of standards and reliable certification schemes for biodegradable plastics — and, in some cases, misleading labeling — confuses consumers and can “exacerbate” environmental pollution.
The biggest problem, according to the report from the Science Advice for Policy by European Academies, is that while biodegradables can break down under ideal conditions they have a much tougher time doing so in a natural environment like deep in a landfill or on a beach.
Polymateria is tackling those issues. Although it can be recycled in the normal way, its new plastic will decompose into a wax or grease-like substance in a matter of months when exposed to sunlight, air and water. Bacteria and fungi will digest the wax, breaking it down into carbon dioxide, water and more microbes. Most importantly, there are no microplastics left behind.
For now the additives only work when added to the most littered type of plastics — polyolefins, which include polyethylene (plastic bags and packaging) and polypropylene (plastic cups and cutlery, bottle caps and containers).
In lab tests that mimic ambient real-world conditions, “there’s nothing left of polyethylene waxes in 226 days and the polypropylene waxes disappear in 336 days,” said Dunne.
The plan is to stamp a “recycle by” date on each piece of plastic to show consumers that they have a deadline to dispose of them responsibly in the recycling system before they start breaking down.
The technology is currently being tested in a handful of countries, including the U.K. and India, but has already helped to define the first standard for measuring biodegradability, published by the U.K.’s national standards body BSI in October.
That European Commission is also busy developing its own policy framework for bio-based plastics and biodegradable or compostable plastics, which it expects to adopt next year.
Not everyone is lyrical about Polymateria.
For one thing, the additive adds roughly 10 to 15 percent to the overall cost of packaging. There’s also the question of whether plastics should be made biodegradable in the first place.
British environmental groups including RECOUP and the Environmental Services Association wrote to the BSI, insisting the standard “will increase the prevalence of litter in all environments.” They fear that the concept of being able to throw away litter and assume it will biodegrade supports the continued use of plastics.
But Dunne said that most of the problem with plastic waste is due to exports to non-EU countries where it’s “not being recycled and is winding up in unmanaged waste systems,” he said, estimating that littering only accounts for 2 percent of the issue.
He argued that the solution is “innovative technologies which permit reuse and recycling” as well as redesigning materials to be biodegradable at the end of their useful life “if we are really serious about actually solving this global problem.”
The European Commission on Tuesday adopted new waste shipment rules going into effect in January that ban the export of plastic waste from the EU to non-OECD countries, except for clean plastic waste sent for recycling.