Michael Le Page, Author at New Scientist Science news and science articles from New Scientist Fri, 10 Jul 2026 10:51:35 +0000 en-US hourly 1 https://wordpress.org/?v=7.0.1 242057827 Global warming already causing crop losses of over $20 billion a year /article/2533593-global-warming-already-causing-crop-losses-of-over-20-billion-a-year/?utm_campaign=RSS|NSNS&utm_content=currents&utm_medium=RSS&utm_source=NSNS Fri, 10 Jul 2026 14:00:51 +0000 /?post_type=article&p=2533593
The economies of countries where many people work in farming will be hit the hardest
Imago/Alamy

Global warming-fuelled heat and drought is already hitting yields of maize, wheat and soybeans to the tune of $20 billion a year, a study has estimated. This could rise eightfold, to more than $160 billion by 2100, unless we slash emissions.

While the financial losses will be greatest for big producers such as the US, the impacts will be felt most in the lowest-income countries, where , at the International Institute for Applied Systems Analysis (IIASA) in Austria. “If you look at the least-developed countries in Africa, the impact is much bigger.” This could lead to social unrest and increased migration, she warns.

There is great uncertainty about these kinds of projections, not least because so much depends on how farmers respond and adapt to a continually changing climate, for instance, by switching to different crops or adopting irrigation where it is possible. In fact, the whole point of this study is to raise awareness and encourage adaptation, to help ensure these projections turn out to be overestimates, says team member , also at IIASA. “This is the entire mission of climate scientists: we make these cases for people to react, so our projections turn out to be wrong.”

The researchers started by gathering data on the yields per country of maize, wheat and soya from the UN Food and Agriculture Organization (FAO). Next, they took past climate data and calculated the drought level, using a standard approach that estimates soil moisture levels from rainfall and evaporation levels.

Past heat extremes and drought levels were then compared with the yields from 1974 to 2004 to estimate the impact of heat and drought. They then used these statistical correlations to estimate crop losses from 2007 to 2019. Their results suggest that increases in heat extremes and drought have caused a 3.5 per cent decline in yields relative to the 1974 to 2004 baseline. “Three per cent or so might not sound like much, but this is a major impact [on] the global food market, which regionally can trigger a severe crisis,” says Kornhuber.

The researchers then calculated the economic losses, based on FAO data showing how much farmers would have been paid for their produce at the time. Finally, they used the same approach to project future losses in several different emissions scenarios, assuming that some adaptation takes place.

In a high-emissions scenario, known as SSP3-7.0, global yields will fall by around 35 per cent by 2100, with annual losses rising to more than $161 billion. “The production losses caused by heat and drought are around 855 million tonnes a year,” says Hwong, who presented the results at a meeting of the European Geosciences Union in Vienna in May. “I think that is equivalent to what around 2 billion people consume over a year.”

This could be an underestimate of the full impact of climate change for a number of reasons: it’s just three crops, and it doesn’t include flood, storm or rain damage, or the possibility that shortages could lead to big price increases, as is already happening with some other crops such as coffee and cacao.

at Columbia University in New York says the study’s reliance on the statistical relationships between yield losses and extreme heat and drought could result in it overestimating the impacts by 2100. “Statistical yield models are great for explaining what’s happening now, and in the near past [or] future, but they are inherently unreliable when pushed into vastly different environmental regimes, such as high-emission climate scenarios by the end of the century.” Computer models of how plants are affected by rising CO2 and temperatures are better for projecting what will happen by the end of the century, he says.

at the University of Queensland, Australia, makes the same point. “Although models are not perfect, they are better suited for this type of extrapolation.” However, her team recently released a , which hasn’t been peer-reviewed, showing that two widely used models for wheat make large errors and are especially poor at forecasting the combined effects of extreme heat and drought.

But Kornhuber has defended his team’s use of statistical methods. “The models are remarkable tools, but some of the validation papers have suggested that they might not be super responsive to extremes,” he says. “In our project, extremes were the main focus, so we decided to establish these relationships directly through statistics.”

Reference:

EGU General Assembly 2026

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The allergy culprit histamine also boosts our memory /article/2533166-the-allergy-culprit-histamine-also-boosts-our-memory/?utm_campaign=RSS|NSNS&utm_content=currents&utm_medium=RSS&utm_source=NSNS Wed, 08 Jul 2026 09:00:02 +0000 /?post_type=article&p=2533166 Polarised light micrograph of crystals of the chemical histamine
Polarised light micrograph of crystals of the chemical histamine
ALFRED PASIEKA/SCIENCE PHOTO LIBRARY
In most of the body, histamine triggers an immune response, as people with hay fever know only too well. But in the brain, it seems to have a completely different role, with a small experiment demonstrating that boosting histamine levels improves the accuracy of our memory by around 10 per cent. “We think it’s changing something called novelty-linked arousal,” says at the University of Oxford. “So, how alert we feel when we see new things in the environment.” It’s long been known that there are receptors in the brain for detecting histamine. “They are densely packed around areas of the brain which are involved in learning and memory,” says Colwell. Animal studies support the idea that . This might explain some of the , says Colwell. “A lot of those older ones got into the brain,” he says. “They would have made people less able to remember things, which you often see when people were taking those antihistamines for a long time.” But what happens if the levels of histamine in the brain increase? There hadn’t been a way of testing this in people, but Colwell and his colleagues realised an existing drug used to treat narcolepsy, called pitolisant, has this effect. It binds to what are known as histamine 3 receptors and raises the molecule’s levels throughout the brain, he says. To put it to the test, his team recruited 60 volunteers and gave half of them pitolisant and half a placebo. They then imaged their brains in an MRI scanner while they did various memory tests. The scans showed that in those given pitolisant, there was greater connectivity between the parts of the brain where histamine is made and the hippocampus, an area involved in memory. These people were also 11 per cent more accurate in retrieving information learned while they were in the scanner.
But it would be a mistake to try to use pitolisant as a “smart drug”, says Colwell. “I would imagine it’s going to really affect sleep, and that’s going to make your memory much worse in the long term.” at Hannover Medical School in Germany says there’s little danger of pistolisant being abused as a smart drug, as it should be very difficult for people to get hold of. He adds that the findings confirm that the results in non-human animals apply to people, too, and that this may boost interest in treating various brain conditions by targeting histamine receptors. People who take pitolisant to help treat narcolepsy or a genetic condition called Prader-Willi syndrome have previously reported improved attention and alertness, says at Heinrich Heine University in Düsseldorf, Germany, who helped create the drug. “A recurring finding has been that pitolisant can help restore impaired cognitive function and improve attention when these are compromised by disease,” he says. “In most cases, however, the effect has been to normalise impaired function rather than to enhance cognition beyond normal levels.” The fact that histamine has two such different effects in the body also shows how evolution repurposes things. “I think the bigger picture is that this shows how economical the human body is,” says Colwell.
Journal reference:

Nature Communications

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June heatwave may have killed around 20,000 people in Europe /article/2532825-june-heatwave-may-have-killed-around-20000-people-in-europe/?utm_campaign=RSS|NSNS&utm_content=currents&utm_medium=RSS&utm_source=NSNS Thu, 02 Jul 2026 16:17:09 +0000 /?post_type=article&p=2532825
The June heatwave is estimated to have killed more than 5000 people in France
Laurent EMMANUEL / AFP via Getty Images

ܰDZ’s most extreme heatwave so far may have killed between 17,000 and 25,000 people, according to an early estimate based on past deaths from heat in the region.

“These numbers are preliminary,” says at Indiana University. “But they highlight the need for rapid adaptation investments to avoid these impacts in the future.”

Callahan’s estimate is based on . “We’re taking data on temperature and mortality across Europe, and we are correlating how high temperatures relate to excess mortality rates,” says Callahan. “We then use that relationship to infer how a given heatwave affects mortality over a region like Europe.”

Callahan’s conclusion is that the heatwave in Europe from 22 to 28 June 2026 killed approximately 20,390 people, including 5210 in France, 4543 in Germany, 3163 in Spain, 2709 in Italy and 862 in the UK. These numbers are much higher than the direct counts announced so far, but this isn’t surprising because it takes time for data on deaths to be collected and analysed.

“This figure is a modelled estimate rather than a final count, and it will be some months before the true toll is confirmed, in part because heat rarely appears on a death certificate,” says at the University of Warwick in the UK.

For instance, on 28 June, the head of the World ҹ1000 Organization, Tedros Adhanom Ghebreyesus, said so far. This number is largely based on reporting around 1000 more deaths in the country than expected from 24 to 26 June.

However, that statement made it clear that this number is based on a computerised death certificate system that is far from complete. It records 80 per cent of hospital deaths, 45 per cent of deaths in long-term care facilities and 25 per cent of deaths at home. “Mortality will consequently be higher than these initial figures suggest,” the statement said.

Even so, other experts think Callahan may have overestimated the numbers. “Twenty-thousand for a single week seems very large,” says at the University of Bristol in the UK. “We’d have to look into details of the modelling to be more sure.”

While Callahan’s method is sound, the main issue is that he used data from 2015 to 2019 to calculate the relationship between heat and deaths, says at Poznań University of Medical Sciences in Poland. People may now be less vulnerable due to ongoing adaptations, such as increased access to air conditioning, . Walkowiak’s back-of-the-envelope calculation is that if this is taken into account, the actual number of deaths would be around 15,000.

Callahan is sticking to his guns. “We don’t have very strong evidence that the relationship between temperature and mortality dramatically changed over time,” he says. “So it’s not obvious it’s different now than it was 10 years ago.”

“In general, we find that our sort of broader statistical estimates give higher numbers than direct reporting on the ground, because that direct reporting can often miss people who die from heat where it’s not obvious that heat was the cause,” he says.

On the flip side, Walkowiak says that Callahan hasn’t taken into account the fact that heatwaves of the same temperature are more deadly in early summer than in late summer. “In late summer, part of the especially vulnerable population is already long gone,” he says.

Mitchell also says the kind of approach used by Callahan also counts only the immediate deaths. There can be longer-term impacts, such as more deaths from domestic violence, suicides and kidney failure. “The impacts of heat on health vary a lot across timescales,” he says.

What matters most is avoiding further deaths as the planet warms further and heat becomes more extreme, says Nunes. “The signal is clear: heat is now the deadliest weather hazard we face, and the majority of these deaths are preventable,” she says. “We can now forecast these events with considerable accuracy; what we have not done is build the systems, across health, housing, social care and transport, for example, that translate an accurate forecast into actual protection. Adaptation is not keeping pace with the risk.”

Reference:

Zenodo

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What is ‘SpudCell’? Arguably the greatest bioengineering feat yet /article/2532689-what-is-spudcell-arguably-the-greatest-bioengineering-feat-yet/?utm_campaign=RSS|NSNS&utm_content=currents&utm_medium=RSS&utm_source=NSNS Wed, 01 Jul 2026 20:08:26 +0000 /?post_type=article&p=2532689 SpudCell, the first synthetic cell system built from non-living components to complete a full cell cycle
SpudCell is the first synthetic cell system built from non-living components to complete a full cell cycle
Orion Venero, Adamala Lab
The “SpudCell” is being proclaimed by its creators as a major advance in synthetic biology. Some of this hype is justified – yes, it’s a cell, but perhaps not quite what you could call a living cell. It has 36 genes that allow it to copy DNA and replicate in a primitive way, but it needs a lot of outside help and fails after five or so divisions. That is, however, much more than any other team has achieved, so it is arguably the greatest feat of bioengineering to date. Created by at the University of Minnesota and her colleagues, the team is now making the SpudCell project open source so it can be developed further and even made capable of dividing indefinitely. Here’s what you need to know:

What is the SpudCell?

It’s a step towards creating a minimal life form whose functions are fully understood. Previous attempts involved deleting genes from bacterial cells whose genomes are small to start with. For instance, in 2016, a bacterium with 901 genes was stripped down so it had just 473 genes. Adamala’s team did things the other way round, starting with just 36 genes. These mostly come from E. coli bacteria, but there are also some from phage viruses that infect bacteria and one for a fluorescent protein from jellyfish to help make the cells visible.

So, is it alive?

No. It can do some of the things that living cells do, such as replicating its genes and dividing, but it doesn’t do them well and it needs a lot of outside help just to do them badly. For instance, the researchers have demonstrated evolution in the sense that when they introduced a beneficial mutation, those cells did better. But the mutation had to be introduced deliberately rather than occurring spontaneously. “I think I would be satisfied with calling it living if it’s replicating indefinitely and if it’s capable of Darwinian evolution,” says Adamala.

Can we really call it a synthetic cell, then?

That depends on how you define things. It is a synthetic cell in the sense that it has been put together in a lab and does some of the things a cell does. But it’s been made using parts of existing cells – mainly those 36 genes – rather than being created entirely from scratch. It could be thought of as an extremely stripped-down E. coli bacterium with a few additions from other viruses, bacteria and jellyfish.

How was it assembled?

The researchers engineered the 36 genes into seven circular pieces of DNA. They made lots of copies of them and put them into a solution containing all the other things the cells need, like the building blocks of DNA and proteins, and fatty molecules that spontaneously form cell-like bubbles. Some of these bubbles ended up with all seven parts of the genome.
The cells are then kept alive by two of the genes coding for proteins that form pores in the membrane, allowing some small molecules to enter. Larger molecules are supplied in the form of small bubbles that fuse with the cells. So the cell is supplied with all the building blocks of life, because it can’t make any itself.

How do the cells divide?

The team added large proteins to the solution that bind to one of the protein pores that protrude from the membrane. These jostle for space and cause the membrane to bend, says Adamala, which can result in part of the SpudCell budding off and forming a separate bubble of its own. It isn’t an equal division into two parts, and the resulting “daughter” cells have a random selection of the circular bits of DNA, so many lack the full sets of genes.

Why not just put all the genes on one piece of DNA?

This would be better to ensure daughter cells get all of the genes, but it is very hard to work with such large pieces of DNA, says Adamala. “Once we have a genome we’re happy with, it definitely has to go on a single large [piece].”
SpudCell, with it's red membrane stained with a lipid dye
SpudCell, with its red membrane stained with a lipid dye
Orion Venero, Adamala Lab

Why do the cells stop doing anything after about five rounds of division?

The team doesn’t know for sure, but the cells aren’t capable of creating their own protein-making factories, or ribosomes. They have to be supplied with them. “We’re speculating that it is because of the failure of the ribosomes [that the cells stop dividing],” says Adamala. So once the cells can make their own ribosomes, they may be able to keep dividing indefinitely. “I think it is achievable very soon,” she says.

This is all very impressive, but why create SpudCell in the first place?

“We want to be able to make all petrochemicals with living biology, so we can basically move away from oil for all the climate and societal benefits,” says Adamala. Virtually all of the chemicals we depend on, from plastics to pesticides, are derived from oil and gas. Many of these chemicals are toxic, she says, and would kill normal cells that made them. But synthetic cells could be designed to tolerate them.

Could it ever be dangerous?

No. It’s a bed-ridden Frankenstein’s monster that has to be spoon-fed. There’s no danger of it running amok. And even if it really can be brought fully to life, it is unlikely to be able to survive outside a lab or factory. Existing bacteria are a far greater threat.]]>
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A type of fibre that stimulates GLP-1 release approved for use in food /article/2532336-a-type-of-fibre-that-stimulates-glp-1-release-approved-for-use-in-food/?utm_campaign=RSS|NSNS&utm_content=currents&utm_medium=RSS&utm_source=NSNS Wed, 01 Jul 2026 13:00:56 +0000 /?post_type=article&p=2532336 2532336 We’ve uncovered a master gene that switches on human development /article/2531950-weve-uncovered-a-master-gene-that-switches-on-human-development/?utm_campaign=RSS|NSNS&utm_content=currents&utm_medium=RSS&utm_source=NSNS Thu, 25 Jun 2026 15:00:21 +0000 /?post_type=article&p=2531950
Understanding embryonic development could improve IVF success
PHILIPPE PLAILLY/SCIENCE PHOTO LIBRARY

We now know the master gene that controls embryonic development in people. Called NANOG, its role has been identified by making precise changes to the DNA of fertilised eggs using a technique called CRISPR base editing.

The discovery might lead to ways to boost the success rate of IVF and help treat non-fertility-related conditions. “The other reason we study these early stages of human development is that it has really profound importance for stem cell biology,” says at the University of Cambridge. “A better understanding will help stem cell research and regenerative medicine, and that could have a transformative impact that can affect all of our lives.”

It’s long been known from animal studies that NANOG plays a role in embryonic development. The gene was named after the Celtic world of the ever-young, Tír na nÓg, because its activation is what makes stem cells immortal. Crucially, though, the team’s work shows that NANOG has a different role in people than in other animals, such as mice.

When a fertilised egg starts developing, the cells take on one of three different roles – forming the placenta, the yolk sac, which is also in mammalian embryos, or the embryo itself. When the team used base editing to disable NANOG in fertilised mouse eggs, none of the resulting cells developed into yolk sac progenitors. Base editing is a modified form of CRISPR that changes a single DNA letter at a time. By contrast, the original form of CRISPR slices through DNA strands, resulting in various kinds of mutations. “The precision of the technique reduces the likelihood of unintended chromosomal abnormalities, which can occur with the original version,” says Niakan.

But when the team disabled NANOG in human eggs donated by women undergoing IVF treatments, none of the cells developed into those that form the embryo. In other words, the activation of NANOG is what initiates the developmental programme that results in cells forming a human body.

These embryos still appeared normal under a microscope, however, and the selection of IVF for implantation is based largely on shape, Niakan says. “One out of two times, even though from the shape it looks like the embryo is developing well, it doesn’t have the potential to implant,” she says. “So perhaps by identifying key markers or genes like NANOG, that knowledge could help improve on these rates.”

Niakan’s team isn’t the first to base-edit human embryos. It was , but using embryos discarded because of abnormalities, so the results might not reflect what happens in healthy embryos. Then last month, at Columbia University in New York and his colleagues released , describing base editing of two-cell embryos.

“What we were trying to achieve was fundamentally different. Our study is about understanding key genes – this is the first time that the technique has been used to study gene function in human embryos,” says Niakan. “Dieter’s study was evaluating the use of the technology in disease-associated mutation correction.”

Egli says Niakan’s study shows that NANOG has an important role in human development that is different to its role in mice.

All three studies suggest that CRISPR base editing of human embryos is much safer than editing them with the original form of CRISPR, as was done with three children. However,  at Monash University in Melbourne, Australia, who was part of Niakan’s team, stresses that we are still far from the point where CRISPR base editing could be used to create gene-edited children, for example, to prevent inherited conditions. “The technology is not ready for that,” says Herbert. “I think there is unanimous agreement on that.”

A major obstacle to this is that, often, only some of the cells in an embryo are successfully gene-edited, known as mosaicism. This means if gene editing was used to correct disease-causing mutations in an embryo, the resulting child might still develop that condition.

For instance, with one edit that Egli’s team tried to make, 80 per cent of embryos were mosaics. Niakan’s team did its editing at a much earlier stage, injecting the gene-editing machinery into eggs along with the sperm used to fertilise them. This reduced mosaicism, but not by much: half of the eggs were still mosaics. “[This] would still be too high a rate of mosaicism in many circumstances if the methods were being used to correct a DNA variant that causes a genetic disorder,” says at the Francis Crick Institute in London.

Niakan says it would be really unethical to try to base-edit children at the moment, but she’s not ruling it out in the future: “I would also hugely advocate for much more basic research that’s publicly available and publicly discussed.”

Journal reference:

Nature

Article amended on 26 June 2026

We have corrected how we described Dieter Egli’s views on the new study.

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If you aren’t terrified by this heatwave, you should be /article/2531853-if-you-arent-terrified-by-this-heatwave-you-should-be/?utm_campaign=RSS|NSNS&utm_content=currents&utm_medium=RSS&utm_source=NSNS Thu, 25 Jun 2026 12:29:55 +0000 /?post_type=article&p=2531853
A red warning for extreme heat was issued for various parts of the UK this week, including London
Brook Mitchell/Getty Images

I’m finding the heatwave hitting Europe really scary. It’s bad enough in itself, with many records being broken, especially for the higher nighttime temperatures that make it so much harder to cope. But I just keep thinking, “If it’s like this now, what’s it going to be like in 10, 20 or 30 years’ time?”

The answer, of course, is hotter and hotter and hotter. In the UK, national weather service the Met Office has just warned that, by 2056, there could be , with some places hitting 45° (113°F). In just 30 years! I’ve seen at least one piece asking “is this the new normal?” about the current heatwave, but we’re never going to have normal in our lifetimes again – just ever more extreme heat.

It’s possible to get through even worse heatwaves than this if all your infrastructure and systems are geared up to cope. But the UK is very much not prepared. The air conditioning in New Scientist’s office, for instance, is failing to keep up with the heat as I write – and lots of people have to endure this hot weather without any air conditioning at all. In a sign of the times, a meeting on adapting to extreme heat – part of London Climate Action Week – got .

Climate scientists are continually warning of the need to prepare for hotter heatwaves, worse droughts, more flooding and rising seas. During heatwaves like this one, they might even get a little media coverage. But then the weather cools, the news agenda moves on and nothing is ever done.

That’s not just my view – it’s the official verdict of the UK’s Climate Change Committee, which advises the UK government. “Adaptation progress is either too slow, has stalled, or is heading in the wrong direction,” it said in last year. Everyone seems to assume this green and pleasant land is going to remain green and pleasant, but it won’t. We’re heading towards catastrophe, but never looking up.

There are many aspects of this that frighten me. Firstly, emissions are still rising, so the fundamental cause of the problem is getting worse. True, it’s not getting worse as fast as it was, but we are currently , and possibly even more.

Even these alarming numbers are a little misleading because the oceans that cover most of the planet don’t warm as fast as the land. Average land temperatures are therefore going to go up by a lot more than the above numbers imply.

And what really matters to us is extreme weather, not the average. The projections for future extremes are already dire, and there are reasons to think that we’re in for extremes even greater than those currently projected for a given level of warming. For starters, heatwaves are already more extreme than projected in some parts of the world. One reason for this is that climate models may not be capturing how the dynamics of the jet streams change in a warmer world. Another is that regional models haven’t accounted for reductions in sunlight-blocking air pollution.

The next level beyond is how bad the knock-on effects of this extreme weather will be. These kinds of things are very difficult to project because so many complex systems are involved, but here, too, there is reason to think we are underestimating the impacts.

For starters, we could see mass deaths even among young people as heatwaves get more extreme. Then there’s our ability to feed people, the basis of civilisation. There’s growing evidence that global warming is already hitting food production, pushing up prices and causing yet more deforestation as farmers try to compensate.

As ever more weather extremes hit the world at the same time, the economic impacts are going to get ever more serious, too. One 2024 study warned that the result could be the worst global financial crisis ever.

And I haven’t even mentioned the wild cards, such as the Amazon drying up or the Atlantic Meridional Overturning Circulation shutting down. One researcher I chatted with at a recent conference thinks a slowdown of this crucial current system around 12,000 years ago triggered extreme seasonality in places like Britain, with sweltering summers, but temperatures plummeting tens of degrees below freezing in winter.

The fact is, the world is changing fast and we need to change just about every aspect of our lives to adapt – our homes and offices, factories and schools, cars and trains, farms and gardens, and so on. But it’s not happening.  That’s why if you’re not scared witless by this heatwave, you should be.

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Screwworm could be the first species targeted by an ‘extinction drive’ /article/2531859-screwworm-could-be-the-first-species-targeted-by-an-extinction-drive/?utm_campaign=RSS|NSNS&utm_content=currents&utm_medium=RSS&utm_source=NSNS Wed, 24 Jun 2026 17:19:04 +0000 /?post_type=article&p=2531859 2531859 You should turn off fans when it’s too hot – but how hot is too hot? /article/2531606-you-should-turn-off-fans-when-its-too-hot-but-how-hot-is-too-hot/?utm_campaign=RSS|NSNS&utm_content=currents&utm_medium=RSS&utm_source=NSNS Tue, 23 Jun 2026 16:50:59 +0000 /?post_type=article&p=2531606 MELBOURNE, AUSTRALIA - JANUARY 16: Tennis fans cool off from the heat in front of mist cooling fans on day one of the 2017 Australian Open at Melbourne Park on January 16, 2017 in Melbourne, Australia. (Photo by Scott Barbour/Getty Images)
Fans don’t always cool you down
Scott Barbour/Getty Images
With Europe in the grip of a mega heatwave and deaths already being reported, staying cool isn’t just about comfort – for many, it is a matter of life and death. Many people will be relying on fans rather than air conditioning, so it is important to be aware that, as it gets hotter, fans can flip from cooling you to warming you. But how hot is too hot? The UK government warns , whereas the World ҹ1000 Organization says . Some studies suggest even lower or . The reality is that there is no simple answer, as several factors are involved. The key thing to know is that you become less good at sweating as you age, so fans will start to warm you at a lower temperature than is the case for younger people. However, you can compensate for this by spraying yourself with water or wetting your clothes. The situation would be very simple if we didn’t sweat. Our skin temperature in the shade is typically between 35° and 37° (99°F). If the air temperature is lower than our skin temperature, heat is transferred to the air, cooling us, but if it is higher, we gain heat from the air. Moving air over our skin with a fan speeds up this heat transfer, whichever way it is going. Because of this, in the past, 35° was often said to be the point at which fans stop cooling us, says in the UK. But this number doesn’t take account of evaporative cooling. The evaporation of water transfers lots of heat from our skin into the air, cooling us even when air temperatures exceed skin temperatures. But blowing air over our skin with a fan doesn’t necessarily cool us more if it’s too dry or too humid.
When it is very dry, our sweat can evaporate as fast as we produce it. In this situation, turning on a fan won’t help, because evaporation cannot increase any further. Instead, the moving air will just transfer more heat to your skin. For instance, modelling and experiments show that at 15 per cent humidity and 45°, turning on a fan will almost certainly . But as the humidity rises, evaporation slows because there’s already lots of moisture in the air. Basically, if you are dripping with sweat, you are producing sweat faster than it can evaporate. In these conditions, a fan does help. For instance, a fan can still cool you at up to 60 per cent humidity and 38°. As the humidity gets even higher, however, evaporation will slow to a point when a fan stops helping. “So it depends on the humidity in the air,” says Havenith. “That’s why people often look at what kind of climate you have in different countries.” The other big factor is age. As we age, our body temperature and skin temperature can fall. It also takes longer for us to start to sweat, and we produce less sweat. This means the temperature at which a fan will start warming us at a given humidity declines as we age. In this situation, wearing wet clothes or spraying ourselves with water can help. This can also reduce sweating and thus reduce the risk of dehydration. Many other factors also play a part, such as clothing and whether your body is adapted to high temperatures. The bottom line, however, is that if you live in a building that gets really hot, temperatures during this heatwave could well exceed the level at which fans will help, even if you’re spraying yourself with water. “At that stage, you probably would have to leave your house and find a cooler place,” says Havenith. “Because it’s a really bad situation.” ]]>
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Most portable air conditioners suck – but there’s an easy fix /article/2530899-most-portable-air-conditioners-suck-but-theres-an-easy-fix/?utm_campaign=RSS|NSNS&utm_content=currents&utm_medium=RSS&utm_source=NSNS Fri, 19 Jun 2026 15:08:41 +0000 /?post_type=article&p=2530899 2530899