Humidity Is the Real Heatwave Threat
By Alex Kirby
When the mercury climbs to extreme levels, it's the dangerous humidity produced by heat reacting with water-sodden air that can spell death, not just the heat alone.
U.S. researchers have warned yet again of the need to beware the risks of this combination. With fierce heat waves expected to become more common as the climate warms, they say humidity can greatly intensify the effects of the heat by itself.
They report in the journal Environmental Research Letters that during this century the drastic effects of high humidity in many areas will increase significantly. At times, they may overtake people's ability to work outdoors or, in some cases, even to survive.
Health and economies would suffer, especially in regions where people work outside and have little access to air conditioning. Potentially affected regions include large swathes of the already muggy Southeastern U.S., the Amazon, Western and Central Africa; Southern areas of the Middle East, including the Arabian peninsula; northern India; and eastern China.
"The conditions we're talking about basically never occur now—people in most places have never experienced them," said lead author Ethan Coffel, a graduate student at Columbia University's Lamont-Doherty Earth Observatory. "But they're projected to occur close to the end of the century."
The warming climate is projected to make many now-dry areas dryer, in part by changing precipitation patterns. But, as global temperatures rise, the atmosphere can hold more water vapor. That means chronically humid areas may only get more humid.
Muggy heat is more oppressive than the "dry" kind, because humans and other mammals cool down by sweating; sweat evaporates off the skin into the air, taking the excess heat with it. That works well in a desert. But when the air is already laden with moisture, evaporation off the skin slows down and eventually becomes impossible.
When this cooling process stops, a creature's core body temperature rises beyond the narrow tolerable range. Without air conditioning, organs strain and then start to fail, leading to lethargy, sickness and possibly death.
Using global climate models, the researchers mapped current and projected future "wet-bulb" temperatures, which reflect the combined effects of heat and humidity (the measurement is made by draping a water-saturated cloth over the bulb of a conventional thermometer; it does not correspond directly to air temperature alone).
The study found that by the 2070s, high wet-bulb readings that now occur perhaps only once a year could stretch to 100 to 250 days annually in some parts of the tropics. In the Southeastern U.S., wet-bulb temperatures now sometimes reach 29 or 30°C; by the 2070s or 2080s, such weather could occur 25 to 40 days each year, say the researchers.
Laboratory experiments have shown wet-bulb readings of 32°C are the threshold beyond which many people would have trouble functioning outside. This level is rarely reached anywhere today.
Risk to India
But the study projects that in 50 or 60 years the limit could be reached one or two days a year in the Southeastern U.S. and three to five days in parts of South America, Africa, India and China. Worldwide, hundreds of millions of people would suffer.
The hardest-hit area in terms of human impact, the researchers say, will probably be densely populated Northeastern India.
"Lots of people would crumble well before you reach wet-bulb temperatures of 32°C, or anything close," said co-author Radley Horton, a climate scientist at Lamont-Doherty. "They'd run into terrible problems."
The study projects that some parts of the southern Middle East and Northern India may even hit 35 wet-bulb degrees Celsius by late this century—equal to the human skin temperature, and the theoretical limit at which people will die within hours without artificial cooling.
Using a related combined heat/humidity measure, the so-called heat index, this would be the equivalent of nearly 170° F of "dry" heat. But the heat index, invented in the 1970s to measure the real feel of moist summer weather, actually ends at 136; anything above that is literally off the chart.
Avoiding the Worst
On the bright side, the paper says that if nations can substantially cut greenhouse gas emissions in the next few decades, the worst effects could be avoided.
Only a few weather events like those projected have ever been recorded. The most recent was in Iran's Bandar Mahshahr in July 2015. That day the "dry" air temperature alone was 115°; saturated with moisture, the air's wet bulb reading neared the 35 °C fatal limit, translating to a heat index of 165°F.
Bandar Mahshahr's infrastructure is good and electricity cheap, so residents adapted by staying in air-conditioned buildings and vehicles, and showering after brief excursions outside. But this is not an option in other vulnerable places, where many people cannot afford such remedies.
"It's not just about the heat, or the number of people. It's about how many people are poor, how many are old, who has to go outside to work, who has air conditioning," said the study co-author Alex deSherbinin of Columbia's Center for International Earth Science Information Network.
He said that even if the weather does not kill people outright or stop all activity, the necessity of working on farms or elsewhere outdoors in such conditions can bring chronic kidney problems and other damaging health effects.
Other researchers have sounded the alarm about the risks dangerous humidity levels can pose. A 2015 study said parts of the Gulf region, where Bandar Mahshahr lies, could, on present trends, become uninhabitable for humans by 2100.
The following year another study extended the warning to include North Africa. Earlier this year sports chiefs even reported that humidity could affect the behaviour of cricket balls.
Climate scientist Steven Sherwood of the University of New South Wales, who proposed the 35°C survivability limit, said he was skeptical that this threshold could be reached as soon as the researchers say. All the same, he said, "the basic point stands."
Unless greenhouse emissions are cut, "we move toward a world where heat stress is a vastly greater problem than it has been in the rest of human history. The effects will fall hardest on hot and humid regions."
Reposted with permission from our media associate Climate News Network.
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From the mythical minotaur to the mule, creatures created from merging two or more distinct organisms – hybrids – have played defining roles in human history and culture. However, not all hybrids are as fantastic as the minotaur or as dependable as the mule; in fact, some of them cause human diseases.
When Looking Through a Microscope Isn’t Close Enough.<p>For the last few years, <a href="http://www.rokaslab.org/" target="_blank">our team at Vanderbilt University</a>, <a href="https://www.researchgate.net/lab/Gustavo-Goldman-Lab" target="_blank">Gustavo Goldman's team at São Paulo University in Brazil</a> and many other collaborators around the world have been collecting samples of fungi from patients infected with different species of <em>Aspergillus</em> molds. One of the species we are particularly interested in is <a href="https://doi.org/10.1006/rwgn.2001.0082" target="_blank"><em>Aspergillus nidulans</em>, a relatively common and generally harmless fungus</a>. Clinical laboratories typically identify the species of <em>Aspergillus</em> causing the infection by examining cultures of the fungi under the microscope. The problem with this approach is that very closely related species of <em>Aspergillus</em> tend to look very similar in their broad morphology or physical appearance when viewing them through a microscope.</p><p>Interested in examining the varying abilities of different <em>A. nidulans</em> strains to cause disease, we decided to analyze their total genetic content, or genomes. What we saw came as a total surprise. We had not collected <em>A. nidulans</em> but <em>Aspergillus latus</em>, a close relative of <em>A. nidulans</em> and, as we were to soon find out, <a href="https://doi.org/10.1016/j.cub.2020.04.071" target="_blank">a hybrid species that evolved through the fusion of the genomes</a> of two other <em>Aspergillus</em> species: <em>Aspergillus spinulosporus</em> and an unknown close relative of <em>Aspergillus quadrilineatus</em>. Thus, we realized not only that these patients harbored infections from an entirely different species than we thought they were, but also that this species was the first ever <em>Aspergillus</em> hybrid known to cause human infections.</p>
Several Different Fungal Hybrids Cause Human Disease.<p>Hybrid fungi that can cause infections in humans are well known to occur in several different lineages of single-celled fungi known as yeasts. Notable examples include multiple different species of <a href="https://doi.org/10.1002/yea.3242" target="_blank">yeast hybrids</a> that cause the human diseases <a href="https://rarediseases.info.nih.gov/diseases/6218/cryptococcosis" target="_blank">cryptococcosis</a> and <a href="https://www.cdc.gov/fungal/diseases/candidiasis/index.html" target="_blank">candidiasis</a>. Although pathogenic yeast hybrids are well known, our discovery that the <em>A. latus</em> pathogen is a hybrid is a first for molds that cause disease in humans.</p>
(Left) Candida yeasts live on parts of the human body. Imbalance of microbes on the body can allow these yeasts, some of which are hybrids, to grow and cause infection. (Right) Cryptococcus yeasts, including ones that are hybrids, can cause life-threatening infections in primarily immunocompromised people. Centers for Disease Control and Prevention<p><a href="https://doi.org/10.1371/journal.ppat.1008315" target="_blank">Why certain <em>Aspergillus</em> species are so deadly</a> while others are harmless remains unknown. This may in part be because <a href="https://doi.org/10.1016/j.fbr.2007.02.007" target="_blank">combinations of traits, rather than individual traits</a>, underlie organisms' ability to cause disease. So why then are hybrids frequently associated with human disease? Hybrids inherit genetic material from both parents, which may result in new combinations of traits. This may make them more similar to one parent in some of their characteristics, reflect both parents in others or may differ from both in the rest. It is precisely this mix and match of traits that hybrids have inherited from their parental species that <a href="https://www.nytimes.com/2010/09/14/science/14creatures.html" target="_blank">facilitates their evolutionary success</a>, including their ability to cause disease.</p>
The Evolutionary Origin of an Aspergillus Hybrid.<p>Multiple evolutionary paths can lead to the emergence of hybrids. One path is through mating, just as the horse and donkey mate to create a mule. Another path is through the merging or fusion of genetic material from cells of different species.</p><p>It is this second path that appears to have been taken by our fungus. <em>A. latus</em> appears to have two of almost everything compared to its parental species: twice the genome size, twice the total number of genes and so on. But unlike other hybrids, which are often sterile like the mule, we found that <em>A. latus</em> is capable of reproducing both asexually and sexually.</p><p>But how distinct were the parents of <em>A. latus</em>? By comparing the parts contributed by each parent in the <em>A. latus</em> genome, we estimate that its parents are approximately 93% genetically similar, which is about as related as we humans are with lemurs. In other words, <em>A. latus</em>, an agent of infectious disease, is the fungal equivalent of a human-lemur hybrid.</p>
How A. Latus Differs From its Parents.<p>Elucidating the identity of closely related fungal pathogens and how they differ from each other in infection-relevant characteristics is a key step toward reducing the burden of fungal disease. For example, we found that <em>A. latus</em> was three times more resistant than <em>A. nidulans</em>, the species it was originally identified as using microscopy-based methods, to one of the most common antifungal drugs, <a href="https://www.drugbank.ca/drugs/DB00520" target="_blank">caspofungin</a>. This result provides a clear example of the potential importance of accurate identification of the <em>Aspergillus</em> pathogen causing an infection.</p><p>We also examined how <em>A. latus</em> and <em>A. nidulans</em> interact with cells from our immune system. We found that immune cells were less efficient at combating <em>A. latus</em> compared to <em>A. nidulans</em>, suggesting the hybrid fungus may be trickier for our immune systems to identify and destroy.</p><p>In the midst of the COVID-19 pandemic, our quest to understand <em>Aspergillus</em> pathogens is becoming more urgent. Growing evidence suggests that <a href="https://doi.org/10.1111/myc.13096" target="_blank">a fraction of COVID-19 patients are also infected with <em>Aspergillus</em>.</a> More worrying is that these <a href="https://doi.org/10.3201/eid2607.201603" target="_blank">secondary <em>Aspergillus</em> infections</a> can worsen the clinical outcomes for those infected with the novel coronavirus. That being said, we stress that little is known about <em>Aspergillus</em> infections in COVID-19 patients due to a lack of systematic testing, and none of the infections identified so far appear to have been caused by hybrids.</p><p>So, when it comes to hybrids, some are fantastic (the minotaur), some are helpful (the mule) and some are dangerous (<em>Aspergillus latus</em>). Understanding more about the biology of <em>Aspergillus latus</em> may help in our understanding of how microbial pathogens arise and how to best prevent and combat their infections.</p>
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