The annual Global Carbon Budget projects fossil carbon dioxide (CO₂ emissions of 36.8 billion tonnes in 2023, up 1.1% from 2022.

Fossil CO₂ emissions are falling in some regions, including Europe and the USA, but rising overall — and the scientists say global action to cut fossil fuels is not happening fast enough to prevent dangerous climate change.

Emissions from land-use change (such as deforestation) are projected to decrease slightly but are still too high to be offset by current levels of reforestation and afforestation (new forests).

The report projects that total global CO₂ emissions (fossil + land-use change) will be 40.9 billion tonnes in 2023.

This is about the same as 2022 levels, and part of a 10-year “plateau” — far from the steep reduction in emissions that is urgently needed to meet global climate targets.

The research team included the University of Exeter, the University of East Anglia (UEA), CICERO Center for International Climate Research, Ludwig-Maximilian-University Munich and 90 other institutions around the world.

“The impacts of climate change are evident all around us, but action to reduce carbon emissions from fossil fuels remains painfully slow,” said Professor Pierre Friedlingstein, of Exeter’s Global Systems Institute, who led the study.

“It now looks inevitable we will overshoot the 1.5°C target of the Paris Agreement, and leaders meeting at COP28 will have to agree rapid cuts in fossil fuel emissions even to keep the 2°C target alive.”

Professor Corinne Le Quéré, Royal Society Research Professor at UEA’s School of Environmental Sciences said: “The latest CO₂ data shows that current efforts are not profound or widespread enough to put global emissions on a downward trajectory towards Net Zero, but some trends in emissions are beginning to budge, showing climate policies can be effective.

“Global emissions at today’s level are rapidly increasing the CO₂ concentration in our atmosphere, causing additional climate change and increasingly serious and growing impacts.”

“All countries need to decarbonise their economies faster than they are at present to avoid the worse impacts of climate change.”

How long until we cross 1.5°C of global warming?

This study also estimates the remaining carbon budget before the 1.5°C target is breached consistently over multiple years, not just for a single year.

At the current emissions level, the Global Carbon Budget team estimates a 50% chance global warming will exceed 1.5°C consistently in about seven years.

This estimate is subject to large uncertainties, primarily due to the uncertainty on the additional warming coming from non-CO₂ agents, especially for the 1.5°C targets which is getting close to the current warming level.

However, it’s clear that the remaining carbon budget — and therefore the time left to meet the 1.5°C target and avoid the worse impacts of climate change — is running out fast.

Other key findings from the 2023 Global Carbon Budget include:

• Regional trends vary dramatically. Emissions in 2023 are projected to increase in India (8.2%) and China (4.0%), and decline in the EU (-7.4%), the USA (-3.0%) and the rest of the world (-0.4%).
• Global emissions from coal (1.1%), oil (1.5%) and gas (0.5%) are all projected to increase.
• Atmospheric CO₂ levels are projected to average 419.3 parts per million in 2023, 51% above pre-industrial levels.
• About half of all CO₂ emitted continues to be absorbed by land and ocean “sinks,” with the rest remaining in the atmosphere where it causes climate change.
• Global CO₂ emissions from fires in 2023 have been larger than the average (based on satellite records since 2003) due to an extreme wildfire season in Canada, where emissions were six to eight times higher than average.
• Current levels of technology-based Carbon Dioxide Removal (ie excluding nature-based means such as reforestation) amount to about 0.01 million tonnes CO₂, more than a million times smaller than current fossil CO₂ emissions.

The Global Carbon Budget report, produced by an international team of more than 120 scientists, provides an annual, peer-reviewed update, building on established methodologies in a fully transparent manner.

The 2023 edition (the 18th annual report) will be published in the journal Earth System Science Data.

There is no cure for the underlying causes of preeclampsia, so physicians focus on managing and monitoring patients’ blood pressure to allow for as close to a full-term gestation as possible. With severe disease, pre-term deliveries are necessary.

“For some patients who can make it to full term, a preeclampsia diagnosis is scary at first but ultimately a bump in the road,” says Jennifer McIntosh, DO, MS, associate professor of obstetrics and gynecology at the Medical College of Wisconsin (MCW). “For those who get it earlier on, it can be terrifying and life-changing, potentially including a long hospital stay before delivery and significant supportive care for the infant in the NICU afterwards.”

More research is needed into what causes preeclampsia to guide the development of potential new ways to diagnose, treat and prevent this common yet cryptic condition.

“The worldwide incidence of preeclampsia is rising, so research grows more important by the day,” Dr. McIntosh says. “Preeclampsia has existed for as long as women have been giving birth, and yet the only cure for it is delivering the baby. I believe we can be innovative and do better for our patients.”

MCW scientists published results on a study of one of the emerging theories for what causes preeclampsia in Science Advances in December 2023. The experiments focus on a particular layer of cells of the placenta called the syncytiotrophoblast (STB), which is a key part of the barrier between the mother and developing fetus. This blockade helps keep a mother’s fully formed immune system from reacting to the fetus and potentially responding as if the fetus was a foreign threat such as a viral or bacterial invader. The barrier also works in reverse to keep the fetus’s growing immune system from reacting to its mother’s cells and tissues. The study’s authors investigated the hypothesis that an abnormal amount of cellular and molecular stresses to the STB can damage the placenta and lead to preeclampsia.

“There is considerable evidence that these stresses accumulate, however, how and why it happens continues to be an open question,” says Justin Grobe, PhD, MCW professor of physiology and biomedical engineering and the co-corresponding author on the Science Advances manuscript with Dr. McIntosh. “We felt it was important to continue to validate the STB stress findings before advancing work on our hypothesis that elevated hormones of pregnancy contribute to the accumulation of stress by overstimulating the STB.”

The research team began by studying placentas donated for research purposes through the MCW Maternal Research Placenta & Cord Blood Bank. By comparing “normal” placentas with placentas from pregnancies where patients suffered from preeclampsia, investigators demonstrated that preeclampsia was associated with higher levels of cellular stresses in the STB layer on the placenta. Additionally, the researchers found a hyperactive level of activity of the G?q protein known to play a role in transmitting signals related to the levels of several hormones present in excessive amounts during preeclampsia.

“The donated human placenta samples were critical to identifying potential mechanisms of STB stress,” says Megan Opichka, PhD ’23, research and development scientist at BioSpyder Technologies and first author on the publication. “Because these samples are collected upon delivery, we then needed to develop an animal model to determine if these sources of stress may actually be causative.”

Based on the findings of hyperactive signaling through G-protein-coupled receptors (GPCRs) in samples from patients with preeclampsia, the scientists developed a new mouse model genetically engineered to enable the precise manipulation of GPCR signals within specific cell types. This allowed the researchers to activate the signaling pathways associated with preeclampsia within the STB layer of the mouse’s placenta. The team demonstrated that even a very brief activation of the identified signaling cascades during the early or middle portions of gestation led to significant consequences during the mouse pregnancy. These mice developed all the signature signs of preeclampsia, including high blood pressure, kidney damage and other anatomical and cellular changes. In some mice exposed to the preeclampsia inducing signals, the scientists tested the effects of a medicine that reduces stress on the mitochondria that generate energy within each cell. The drug provided substantial protection against developing the signs and symptoms of preeclampsia.

“With our unique model, we can study the effects of contributing factors to preeclampsia throughout pregnancy,” Dr. Grobe says. “We can test specific signaling cascades in specific cells and tissues at specific times to observe their effects. We have only scratched the surface on what we can learn.”

“This will absolutely be a springboard for future research,” Dr. McIntosh adds. “Because the drug we tested, MitoQ, is generally known to be safe, we’re working on plans for a clinical pilot study to test appropriate dosage and efficacy in advance of pursuing larger clinical studies of preeclampsia in the future.”

So, can preeclampsia be prevented? While today the answer is no, MCW scientists now are one step closer with these experimental results. And they are continuing to work as a team to achieve this goal through additional studies.

“What drives my research is my frustration about the lack of understanding of what causes preeclampsia,” says Dr. McIntosh. “We need to continue linking the bench and the bedside together so that we can understand the causes and use them to bring a cure to the bedside.”