It’s possible that I shall make an ass of myself. But in that case one can always get out of it with a little dialectic. I have, of course, so worded my proposition as to be right either way (K.Marx, Letter to F.Engels on the Indian Mutiny)
Wednesday, October 04, 2023
New research finds that ancient carbon in rocks releases as much carbon dioxide as the world's volcanoes
New research has overturned the traditional view that natural rock weathering acts as a CO2 sink that removes CO2 from the atmosphere. Instead, this can also act as a large CO2 source, rivalling that of volcanoes.
The results have important implications for modelling climate change scenarios but at the moment, CO2 release from rock weathering is not captured in climate modelling.
Future work will focus on whether human activities may be increasing CO2 release from rock weathering, and how this could be managed.
A new study led by the University of Oxford has overturned the view that natural rock weathering acts as a CO2 sink, indicating instead that this can also act as a large CO2 source, rivalling that of volcanoes. The results, published today in the journal Nature, have important implications for modelling climate change scenarios.
Rocks contain an enormous store of carbon in the ancient remains of plants and animals that lived millions of years ago. This means that the “geological carbon cycle” acts as a thermostat that helps to regulate the Earth’s temperature. For instance, during chemical weathering rocks can suck up CO2 when certain minerals are attacked by the weak acid found in rainwater. This process helps to counteract the continuous CO2 released by volcanoes around the world, and forms part of Earth’s natural carbon cycle that has helped keep the surface habitable to life for a billion years or more.
However, for the first time this new study measured an additional natural process of CO2 release from rocks to the atmosphere, finding that it is as significant as the CO2 released from volcanoes around the world. Currently, this process is not included in most models of the natural carbon cycle.
The process occurs when rocks that formed on ancient seafloors (where plants and animals were buried in sediments) are pushed back up to Earth’s surface, for example when mountains like the Himalayas or Andes form. This exposes the organic carbon in the rocks to oxygen in the air and water, which can react and release CO2. This means that weathering rocks could be a source of CO2, rather than the commonly assumed sink.
Up to now, measuring the release of this CO2 from weathering organic carbon in rocks has proved difficult. In the new study, the researchers used a tracer element (rhenium) which is released into water when rock organic carbon reacts with oxygen. Sampling river water to measure rhenium levels makes it possible to quantify CO2 release. However, sampling all river water in the world to get a global estimate would be a significant challenge.
To upscale over Earth’s surface, the researchers did two things. First, they worked out how much organic carbon is present in rocks near the surface. Second, they worked out where these were being exposed most rapidly, by erosion in steep, mountain locations.
Dr Jesse Zondervan, the researcher who led the study at the Department of Earth Sciences, University of Oxford, said: “The challenge was then how to combine these global maps with the river data, while considering uncertainties. We fed all of our data into a supercomputer at Oxford, simulating the complex interplay of physical, chemical, and hydrological processes. By piecing together this vast planetary jigsaw, we could finally estimate the total carbon dioxide emitted as these rocks weather and exhale their ancient carbon into the air."
Professor Robert Hilton (Department of Earth Sciences, University of Oxford), who leads the ROC-CO2 research project that funded the study, said: “This is about 100 times less than present day human CO2 emissions by burning fossil fuels, but it is similar to how much CO2 is released by volcanoes around the world, meaning it is a key player in Earth’s natural carbon cycle”.
These fluxes could have changed during Earth’s past. For instance, during periods of mountain building that bring up many rocks containing organic matter, the CO2 release may have been higher, influencing global climate in the past.
Ongoing and future work is looking into how changes in erosion due to human activities, alongside the increased warming of rocks due to anthropogenic climate changes, could increase this natural carbon leak. A question the team are now asking is if this natural CO2 release will increase over the coming century. “Currently we don’t know – our methods allow us to provide a robust global estimate, but not yet assess how it could change’’ says Hilton.
“While the carbon dioxide release from rock weathering is small compared to present-day human emissions, the improved understanding of these natural fluxes will help us better predict our carbon budget” concluded Dr. Zondervan.
Notes to editors:
Media contact – Professor Robert Hilton, robert.hilton@earth.ox.ac.uk
The study ‘Rock organic carbon oxidation CO2 release offsets silicate weathering sink’ will be published in Nature at 16:00 BST/ 11:00 ET on Wednesday 04 October 2023 at https://doi.org/10.1038/s41586-023-06581-9
Oxford University has been placed number 1 in the Times Higher Education World University Rankings for the eighth year running, and number 3 in the QS World Rankings 2024. At the heart of this success are the twin-pillars of our ground-breaking research and innovation and our distinctive educational offer.
Oxford is world-famous for research and teaching excellence and home to some of the most talented people from across the globe. Our work helps the lives of millions, solving real-world problems through a huge network of partnerships and collaborations. The breadth and interdisciplinary nature of our research alongside our personalised approach to teaching sparks imaginative and inventive insights and solutions.
Through its research commercialisation arm, Oxford University Innovation, Oxford is the highest university patent filer in the UK and is ranked first in the UK for university spinouts, having created more than 300 new companies since 1988. Over a third of these companies have been created in the past five years. The university is a catalyst for prosperity in Oxfordshire and the United Kingdom, contributing £15.7 billion to the UK economy in 2018/19, and supports more than 28,000 full time jobs.
Shale rocks high up in the remote Mackenzie mountains Canada, which contain lots of rock organic carbon and are hotspots of CO2 release. Image credit: Robert Hilton.
Landslides in the high Andes of Peru, exposing rocks full of organic matter to weathering which can release CO2. Image credit: Robert Hilton.
High erosion in southern France exposes these sedimentary rocks to weathering, releasing CO2 as the ancient organic carbon breaks down. Image credit: Robert Hilton
INSIDE MOUSE MOTHERS’ HEARING CENTER, PARVALBUMIN INTERNEURONS (PVIN, MAGENTA) ARE SURROUNDED BY PERINEURONAL NETS (PNNS, GREEN). UPON HEARING CRYING PUPS, MICE WITH PVIN LACKING THE MECP2 PROTEIN (BOTTOM ROW) EXPERIENCE A DRAMATIC INCREASE IN PNN NUMBER AND INTENSITY, ESPECIALLY ON DAY ONE OF THE EXPERIMENT (MIDDLE COLUMN). THIS MANIFESTS AS PARENTAL NEGLECT.
CREDIT: SHEA LAB/MICROSCOPY CORE FACILITY/COLD SPRING HARBOR LABORATORY
Developing brains become shaped by the sights, sounds, and experiences of early life. The brain’s circuits grow more stable as we age. However, some experiences later in life open up opportunities for these circuits to be rapidly rewired. New research from Cold Spring Harbor Laboratory Associate Professor Stephen Shea helps explain how the brain adapts during a critical period of adulthood: the time when new mothers learn to care for their young.
Shea’s work in mice shows how this learning process is disrupted when a small set of neurons lack a protein called MECP2. In humans, MECP2 dysfunction causes the rare neurodevelopmental disorder Rett syndrome. Shea’s findings could point researchers toward the brain circuits involved in Rett syndrome and potential treatment strategies. His research could also have implications for more common neurological conditions. Shea explains:
“It’s not lost on us that Rett syndrome patients have difficulty interpreting and producing language. Difficulties with communicating are widespread in autism spectrum disorders. One of the reasons we study Rett syndrome is that this may be a valuable model for other forms of autism.”
The Shea lab’s studies of MECP2 began about 10 years ago when he first learned that female mice with mutations in the Mecp2 gene are poor parents. When it comes to parenting, most mother mice are quick learners. But without adequate MECP2 protein, Shea says, “they neglect their children and don’t listen to their cries.”
Shea and his team tested how eliminating MECP2 from specific cells in the mouse brain affected maternal behavior. They found that for pup retrieval to be delayed, the protein only had to go missing from a small subset of cells in a sound-processing part of the brain. The crucial cells are known as parvalbumin (PV) neurons. To efficiently learn to retrieve their pups, mice need MECP2 in those specific brain cells when they first hear the young animals’ cries of distress.
Shea points out that PV neurons also play an essential role in brain circuits earlier in life. These cells normally dampen the signals of other neurons. But they release this inhibition during development, creating conditions that are favorable for change. Shea says:
“We find that some of the same mechanisms engaged in development are actually at play in adults. They can be reactivated and repurposed for rewiring the brain in a new life time point.”
In other words, it’s not just about development or adulthood. This research may provide clues about brain disorders that arise later on, like dementia and Alzheimer’s disease.
New research being presented at the Annual Meeting of the European Association for the Study of Diabetes (EASD) in Hamburg, Germany (2-6 Oct) has found that severe hypoglycaemia is more than twice as common among adults with diabetes who struggle to afford food.
Severe hypoglycaemia occurs when a person’s blood sugar levels fall to such an extent that it can cause loss of consciousness, seizures, coma and, in rare cases, death.
Severe hypoglycaemia is rare in people with diabetes unless they are taking insulin or secretagogues – two commonly prescribed classes of diabetes drug. When people are taking insulin or secretagogues, severe hypoglycaemia occurs primarily as a side-effect of their medication.
The analysis of data from the US revealed that severe hypoglycaemia was 2.2 times more frequent in people who experienced food insecurity.
Food insecurity is known to influence health but there has been little real-world population-based research into its effect on rates of severe hypoglycaemia.
In the first investigation of its kind, Dr Alexandria Ratzki-Leewing, of Western University, London, Ontario, Canada, and colleagues conducted a secondary analysis of data from the US-wide iNPHORM study: a 12-month prospective panel survey of real-world hypoglycaemia risk.1
Their analysis comprised 1,001 adults (49.6% male) with either type 1 diabetes (T1D, 16.1%) or type 2 diabetes (T2D) who were treated, for at least one year, with insulin and/or secretagogues. Participants were on average 51 years old and had a median diabetes duration of 12 years.
Questionnaires at baseline (spring 2020) and over 12 consecutive months captured data on respondents’ characteristics and frequency of severe hypoglycaemia. Based on the American Diabetes Association Standards of Care guidelines, severe hypoglycaemia was defined as a Level 3 low blood glucose concentration, regardless of blood glucose value, causing altered mental and/or physical status requiring professional or non-professional aid for recovery.At baseline, participants were asked this screening question, “Within the past 12 months, did you ever cut the size of your meals or skip meals because there was not enough food?”. Those who answered “yes” were classified as having experienced food insecurity.
Around one in five of the participants said they’d experienced food insecurity; rates were similar in T1D (18.6%) and T2D (20.4%). Among these individuals, over half experienced at least one Level 3 event in the past year.
The authors performed multivariable regression to determine if food insecurity caused higher rates of severe hypoglycaemia. Their analysis revealed that, after adjusting for potential confounders (age, annual gross household income, insurance coverage, living arrangements and diabetes type), those who had experienced food insecurity had just over twice as many severe hypoglycaemia events during the year studied as those not exposed to food insecurity.
Dr Ratzki-Leewing said: “This is the first community-based, prospective study to look at the impact of food insecurity on rates of Level 3 (severe) hypoglycaemia in adults in the US with diabetes on insulin and/or secretagogues.
“We showed that food insecurity is alarmingly common across this population and that it more than doubles the rate of severe hypoglycaemia.
“We recommend clinicians use our screening question and exercise vigilance when managing individuals with food insecurity prescribed insulin or secretagogues. Public health strategies to address food insecurity are also vital to prevent severe hypoglycaemia and its profound consequences.
“In the short term, severe hypoglycaemia can cause dangerous symptoms (such as seizures and coma) and accidents. It can also lead to impaired awareness of hypoglycaemia (the diminished ability to perceive falling blood glucose levels), which in turn, can increase the risk of future hypoglycaemia events.
“Long-term, severe hypoglycaemia has been associated with nerve and heart damage, as well as premature mortality. These effects have substantial direct and indirect economic costs.
“Ultimately, our study uncovers a key opportunity to reduce the burden of diabetes-related severe hypoglycaemia, while improving overall health. The results are timely given the rising cost of living, not only in the US but also globally.”
Note to editors
This press release is based on poster abstract 750 at the annual meeting of the European Association for the Study of Diabetes (EASD). The material has been peer reviewed by the congress selection committee. There is no full paper at this stage.
ARTICLE PUBLICATION DATE
1-Oct-2023
COI STATEMENT
Dr Ratzki-Leewing has declared these conflicts of interest: Sanofi Global: grant, member advisory board, fees paid for presentations; Sanofi Canada: fees paid for presentations; Abbott: consultant, fees paid for presentations; Dexcom, consultant; Eli Lilly: consultant, fees paid for presentations; Novo Nordisk: consultant.
Massive low earth orbit communications satellites could disrupt astronomy
Observations of the BlueWalker 3 prototype satellite show it is one of the brightest objects in the night sky, outshining all but the brightest stars.
Astronomers have raised concerns that without mitigation, groups of large satellites could disrupt our ability to observe the stars from Earth and perform radio astronomy.
Several companies are planning ‘constellations’ of satellites – groups of potentially hundreds of satellites that can deliver mobile or broadband services anywhere in the world.
However, these satellites need to be in ‘low-Earth’ orbit and can be relatively large, so their potential to disrupt night-sky observations is a concern.
Now, an international team of scientists led by astronomers from the IAU Centre for the Protection of the Dark and Quiet Sky from Satellite Constellation Interference (CPS) and including Imperial College London researchers, have published a paper in Nature assessing the detailed impact of the prototype BlueWalker 3 satellite on astronomy.
Dr Dave Clements, from the Department of Physics at Imperial, said: “The night sky is a unique laboratory that allows scientists to conduct experiments that cannot be done in terrestrial laboratories. Astronomical observations have provided insights into fundamental physics and other research at the boundaries of our knowledge and changed humanity’s view of our place in the cosmos. The pristine night sky is also an important part of humanity’s shared cultural heritage and should be protected for society at large and for future generations.”
Bright observations
BlueWalker 3 was launched into low-Earth orbit on 10 September 2022 by AST SpaceMobile, as a prototype for a planned constellation of over a hundred similar satellites intended for use in mobile communications. Observations taken within weeks of the launch showed that the satellite was among the brightest objects in the sky.
However, to better understand its effects on astronomy, the CPS initiated an international observing campaign. As part of this initiative, both professional and amateur observations were contributed from across the world, from sites in Chile, the US, Mexico, Aotearoa New Zealand, the Netherlands, and Morocco.
Documenting BlueWalker 3’s brightness over a period of 130 days, the newly released data show an abrupt increase coinciding with the complete unfolding of the antenna array, which at 64 square meters is the largest commercial antenna system ever deployed into low-Earth orbit.
A subset of the observations were also used to calculate the satellite’s trajectory over time. Comparing the predicted path with the observations collected, the authors were able to evaluate the accuracy of predictions and how this can change due to factors such as atmospheric drag.
Knowing the positions of the satellites is important, so astronomers can try to avoid them or at least know where they will be in the data. However, mitigating against the brightness is difficult beyond masking their position and losing data for that portion of the sky.
Radio interference
Besides visible observations, BlueWalker 3 could also interfere with radio astronomy, since it uses wavelengths close to those that radio telescopes observe in. While some telescopes are located within designated radio quiet zones, the restrictions in place to preserve these areas currently only apply to terrestrial transmitters, so they are not necessarily protected from satellite transmission.
Dr Mike Peel, co-lead of IAU CPS's Sathub and researcher in the Department of Physics at Imperial, said: "BlueWalker 3 actively transmits at radio frequencies that are close to bands reserved for radio astronomy, and existing observatory protections from radio interference may not be sufficient. Further research is therefore required to develop strategies for protecting existing and upcoming telescopes from the numerous satellites planned for launch over the next decade.”
The IAU and CPS partners recognize that the new satellite constellations have an important role in improving worldwide communications. However, their interference with astronomical observations could severely hamper progress in our understanding of the cosmos. Their deployment should therefore be conducted with due consideration of their side effects and with efforts made to minimize their impact on astronomy.
GRAPHENE OXIDE (ORANGE) CAN EFFECTIVELY ENTER YEAST CELLS AND REDUCE THE TOXICITY OF HARMFUL PROTEIN AGGREGATES (LIGHT GREY), BY PROMOTING DISASSEMBLY AND THEN DEGRADATION OF THE AGGREGATES. RESEARCHERS AT CHALMERS UNIVERSITY OF TECHNOLOGY HAVE DEVELOPED A YEAST MODEL, WHICH MIMICS THE NEURONS IN A HUMAN BRAIN AFFECTED BY ALZHEIMER’S DISEASE, TO DEMONSTRATE THIS. MOREOVER (NOT SHOWN BY THE ILLUSTRATION), GRAPHENE OXIDE TREATMENT CAN ALTER THE METABOLISM OF THE CELLS TO INCREASE THEIR CAPACITY TO COPE WITH STRESS.
CREDIT: ILLUSTRATION: CHALMERS UNIVERSITY OF TECHNOLOGY / KATHARINA MERL
A probable early driver of Alzheimer's disease is the accumulation of molecules called amyloid peptides. These cause cell death, and are commonly found in the brains of Alzheimer’s patients. Researchers at Chalmers University of Technology, Sweden, have now shown that yeast cells that accumulate these misfolded amyloid peptides can recover after being treated with graphene oxide nanoflakes.
Alzheimer’s disease is an incurable brain disease, leading to dementia and death, that causes suffering for both the patients and their families. It is estimated that over 40 million people worldwide are living with the disease or a related form of dementia. According to Alzheimer’s News Today, the estimated global cost of these diseases is one percent of the global gross domestic product.
Misfolded amyloid-beta peptides, Aβ peptides, that accumulate and aggregate in the brain, are believed to be the underlying cause of Alzheimer’s disease. They trigger a series of harmful processes in the neurons (brain cells) – causing the loss of many vital cell functions or cell death, and thus a loss of brain function in the affected area. To date, there are no effective strategies to treat amyloid accumulation in the brain.
Researchers at Chalmers University of Technology have now shown that treatment with graphene oxide leads to reduced levels of aggregated amyloid peptides in a yeast cell model.
“This effect of graphene oxide has recently also been shown by other researchers, but not in yeast cells”, says Xin Chen, Researcher in Systems Biology at Chalmers and first author of the study. “Our study also explains the mechanism behind the effect. Graphene oxide affects the metabolism of the cells, in a way that increases their resistance to misfolded proteins and oxidative stress. This has not been previously reported.”
Investigating the mechanisms using baker’s yeast affected by Alzheimer’s disease In Alzheimer’s disease, the amyloid aggregates exert their neurotoxic effects by causing various cellular metabolic disorders, such as stress in the endoplasmic reticulum – a major part of the cell, in which many of its proteins are produced. This can reduce cells’ ability to handle misfolded proteins, and consequently increase the accumulation of these proteins.
The aggregates also affect the function of the mitochondria, the cells’ powerhouses. Therefore, the neurons are exposed to increased oxidative stress (reactive molecules called oxygen radicals, which damage other molecules); something to which brain cells are particularly sensitive.
The Chalmers researchers have conducted the study by a combination of protein analysis (proteomics) and follow-up experiments. They have used baker's yeast, Saccharomyces cerevisiae, as an in vivo model for human cells. Both cell types have very similar systems for controlling protein quality. This yeast cell model was previously established by the research group to mimic human neurons affected by Alzheimer’s disease.
“The yeast cells in our model resemble neurons affected by the accumulation of amyloid-beta42, which is the form of amyloid peptide most prone to aggregate formation”, says Xin Chen. “These cells age faster than normal, show endoplasmic reticulum stress and mitochondrial dysfunction, and have elevated production of harmful reactive oxygen radicals.”
High hopes for graphene oxide nanoflakes Graphene oxide nanoflakes are two-dimensional carbon nanomaterials with unique properties, including outstanding conductivity and high biocompatibility. They are used extensively in various research projects, including the development of cancer treatments, drug delivery systems and biosensors.
The nanoflakes are hydrophilic (water soluble) and interact well with biomolecules such as proteins. When graphene oxide enters living cells, it is able to interfere with the self-assembly processes of proteins.
“As a result, it can hinder the formation of protein aggregates and promote the disintegration of existing aggregates”, says Santosh Pandit, Researcher in Systems Biology at Chalmers and co-author of the study. “We believe that the nanoflakes act via two independent pathways to mitigate the toxic effects of amyloid-beta42 in the yeast cells.”
In one pathway, graphene oxide acts directly to prevent amyloid-beta42 accumulation. In the other, graphene oxide acts indirectly by a (currently unknown) mechanism, in which specific genes for stress response are activated. This increases the cell’s ability to handle misfolded proteins and oxidative stress.
How to treat Alzheimer’s patients is still a question for the future. However, according to the research group at Chalmers, graphene oxide holds great potential for future research in the field of neurodegenerative diseases. The research group has already been able to show that treatment with graphene oxide also reduces the toxic effects of protein aggregates specific to Huntington’s disease in a yeast model.
“The next step is to investigate whether it is possible to develop a drug delivery system based on graphene oxide for Alzheimer’s disease.” says Xin Chen. “We also want to test whether graphene oxide has beneficial effects in additional models of neurodegenerative diseases, such as Parkinson’s disease.”
More about: proteins and peptides Proteins and peptides are fundamentally the same type of molecule and are made up of amino acids. Peptide molecules are smaller – typically containing less than 50 amino acids – and have a less complicated structure. Proteins and peptides can both become deformed if they fold in the wrong way during formation in the cell. When many amyloid-beta peptides accumulate in the brain, the aggregates are classified as proteins.
UVA RESEARCHER JASON PAPIN, PHD, AND COLLEAGUES HAVE CREATED A SOPHISTICATED NEW COMPUTER MODEL OF MALE AND FEMALE LIVERS THAT WILL MAKE FOR SAFER DRUGS WITH FEWER SIDE EFFECTS.
UVA Health researchers have developed a powerful new tool to understand how medications affect men and women differently, and that will help lead to safer, more effective drugs in the future.
Women are known to suffer a disproportionate number of liver problems from medications. At the same time, they are typically underrepresented in drug testing. To address this, the UVA scientists have developed sophisticated computer simulations of male and female livers and used them to reveal sex-specific differences in how the tissues are affected by drugs.
The new model has already provided unprecedented insights into the biological processes that take place in the liver, the organ responsible for detoxifying the body, in both men and women. But the model also represents a powerful new tool for drug development, helping ensure that new medications will not cause harmful side effects.
“There are incredibly complex networks of genes and proteins that control how cells respond to drugs,” said UVA researcher Jason Papin, PhD, one of the model’s creators. “We knew that a computer model would be required to try to answer these important clinical questions, and we’re hopeful these models will continue to provide insights that can improve healthcare.”
Harmful Effects From Drugs
Papin, of UVA’s Department of Biomedical Engineering, developed the model in collaboration with Connor Moore, a PhD student, and Christopher Holstege, MD, a UVA emergency medicine physician and director of UVA Health’s Blue Ridge Poison Center. “It is exceedingly important that both men and women receive the appropriate dose of recommended medications,” Holstege noted. “Drug therapy is complex and toxicity can occur with subtle changes in dose for specific individuals.”
Before developing their model, the researchers first looked at the federal Food and Drug Administration’s Adverse Event Reporing System to evaluate the frequency of reported liver problems in men and women. The scientists found that women consistently reported liver-related adverse events more often than did men.
The researchers then sought to explain why this might be the case. To do that, they developed computer models of the male and female livers that integrated vast amounts of data on gene activity and metabolic processes within cells. These cutting-edge liver simulations provided important insights into how drugs affect the tissue differently in men and women and allowed the researchers to understand why.
“We were surprised how many differences we found, especially in very diverse biochemical pathways,” said Moore, a biomedical engineering student in Papin's lab. “We hope our results emphasize how important it is for future scientists to consider how both men and women are affected by their research.”
The work has already identified a key series of cellular processes that explain sex differences in liver damage, and the scientists are calling for more investigation of it to better understand “hepatotoxicity” – liver toxicity. Ultimately, they hope their model will prove widely useful in developing safer drugs.
“We’re hopeful these approaches will be help address many other questions where men and women have differences in drug responses or disease processes,” Papin said. “Our ability to build predictive computer models of complex systems in biology, like those in this study, is truly opening all kinds of new avenues for tackling some of the most challenging biomedical problems.”
Article Title: High ‘steaks’: Building support for reducing agricultural emissions
Author Countries: Germany, UK
Funding: This work was financially supported by the Robert Bosch foundation (Junior Professorship grant to LM) The funder had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Using a new analysis method for satellite images, an international research team, coordinated by the French Alternative Energies and Atomic Energy Commission (CEA) and INRAE, mapped for the first time annual changes in global forest biomass between 2010 and 2019. Researchers discovered that boreal and temperate forests have become the main global carbon sinks. Tropical forests, which are older and degraded by deforestation, fire and drought, are nearly carbon neutral. The findings, published in Nature Geoscience, highlight the importance of accounting for young forests and forest degradation in predictive carbon‑sink models to develop more effective climate change mitigation strategies.
Increases in plant biomass play an essential role in carbon sequestration to mitigate climate change. The carbon balance of biomass results from gains due to plant growth and increased forest cover and losses due to harvest, deforestation, degradation, background tree mortality and natural disturbances. Monitoring biomass carbon stocks over time is essential to better understand and predict the effects of ongoing and future climate change, as well as the direct impacts of human activities on ecosystems. This is a key issue for climate change mitigation policies.
The vegetation data, obtained from the Soil Moisture and Ocean Salinity (SMOS) satellite using L-band vegetation optical depth (L-VOD) methods, is unique in estimating average above-ground carbon stocks on a global level. However, the widespread application of L-VOD over the entire globe is limited by signal disruption from radio frequency interference from human activities and by L‑VOD sensitivity to vegetative water content. To address these challenges, the researchers developed a double filter that used temporal signal decomposition (seasonal changes, trends, etc.) to offset these effects. Drawing on above-ground biomass data, researchers determined total biomass using a global map, released in 2020, of the ratio between above- and below-ground biomass (such as roots).* They then calculated the spatial and temporal distribution of total live biomass carbon of terrestrial ecosystems from 2010 to 2019, and developed maps of annual biomass carbon change. Researchers used the maps to assess regional carbon budgets (25×25 km plots), attribute carbon losses and gains to forest-cover change caused by fires and land-use change, and investigate how forest age controls terrestrial carbon storage.
Carbon stocks on Earth increased by 500 million tonnes per year over a 10-year period, primarily because of young trees in temperate and boreal forests
Globally, terrestrial biomass carbon stocks increased from 2010 to 2019 by approximately 500 million tonnes of carbon per year. The main contributors to the global carbon sink are boreal and temperate forests, while tropical forests have become small carbon sources because of deforestation and tree mortality following periods of repeated drought. Old-growth tropical forests, where trees average more than 140 years old, are nearly carbon neutral, whereas temperate and boreal forests, where trees are young (less than 50 years) or middle-aged (50–140 years), are the largest carbon sinks. The new findings differ from existing prediction models that show all old-growth forests to be large carbon sinks and do not account for the importance of forest demography or the impact of deforestation and degradation on tropical forests, which are losing biomass.
The findings highlight the importance of accounting for forest degradation and forest age when predicting dynamics of future carbon sinks at global level, and thereby develop better-suited climate change mitigation policies.
