Some bridges could really put a swing in your step.

Crowds walking on a bridge can cause it to sway — sometimes dangerously. Using improved simulations to represent how people walk, scientists have now devised a better way to calculate under what conditions this swaying may arise, researchers report November 10 online in Science Advances.

When a bridge — typically a suspension bridge — is loaded with strolling pedestrians, their gaits can sync, causing the structure to shimmy from side to side. The new study “allows us to better predict the crowd size at which significant wobbling can appear abruptly,” says mathematician Igor Belykh of Georgia State University in Atlanta.
Engineers might eventually use the researchers’ results to avoid debacles like the one that befell the Millennium Bridge in London. This suspension bridge temporarily shut down just days after it opened in 2000 due to the large wobble that occurred when many people tromped across it at once (SN: 11/24/07, p. 331), necessitating costly repairs to fix the problem.

Pedestrians crossing a bridge can cause slight sideways motion of the bridge as they push with their feet. This swaying may lead to the crowd unintentionally falling into lockstep because it’s easier to go with the flow of the swinging bridge than fight it. That synchronization, in turn, creates larger and larger oscillations.
“It’s a dangerous phenomenon that could cause a bridge to collapse if it went unchecked,” says applied mathematician Daniel Abrams of Northwestern University in Evanston, Ill., who was not involved with the research.

Previous mathematical models of the phenomenon “didn’t realistically capture how people exerted force on the bridge,” Abrams says, “but this new model is pretty realistic.” Whereas earlier simulations focused on the timing of footfalls or the amount of force produced with each step, the new work takes both into account.

Tests of the Millennium Bridge showed that the lurching occurred only after a critical number of people — around 165 — entered the bridge. Likewise, in their simulations, Belykh and his colleagues find that oscillations begin abruptly above a certain threshold number of walkers, depending on the properties of the bridge.

The research challenges some previous assumptions. For instance, in the new simulations, the onset of the wobbling began just before the walkers joined in lockstep. This suggests that the synchrony of the crowd might not be a root cause but instead acts as a feedback effect that amplifies preexisting small-scale wobbles. That insight could be relevant for wobbles that occur in certain bridges without pedestrians syncing, Belykh says. Future work will further investigate how the swaying starts.

Cholera strains behind worldwide outbreaks of the deadly disease over the last five decades are jet-setters rather than homebodies.

It had been proposed that these cholera epidemics were homegrown, driven by local strains of Vibrio cholerae living in aquatic ecosystems. But DNA fingerprints of the V. cholerae strains behind recent large outbreaks in Africa and Latin America were more closely related to South Asian strains than local ones, according to two papers published in the Nov. 10 Science.
This evidence that the guilty strains traveled from abroad could guide public health efforts, the researchers say. “If you don’t understand how the bug spreads, then it’s very difficult to try to stop the bug,” says François-Xavier Weill, a clinical microbiologist at the Institut Pasteur in Paris who coauthored both papers.

People are exposed to V. cholerae by consuming water or food contaminated by the bacteria. Poor sanitation and drinking water treatment can fuel an epidemic, as seen in Yemen (SN: 8/19/17, p. 4), where nearly a million people are suspected to have been infected and more than 2,000 have died in the world’s largest recorded cholera outbreak.

A cholera infection can produce mild or no symptoms. But about one in 10 people will rapidly develop severe diarrhea and dehydration that, without treatment, can kill within hours. Although underreported, cholera cases worldwide each year are estimated to range from 1.4 million to four million, and 21,000 to 143,000 people die from the disease, according to the World Health Organization’s Global Health Observatory.
There have been seven cholera pandemics, or global outbreaks, since the 19th century, when the bacteria spread from its original home on the Indian subcontinent. The seventh one, which began in Indonesia in 1961, reached Africa in 1970 and hit Latin America in 1991, is still ongoing. It’s attributed to strains that originated near the Bay of Bengal, where cholera is a seasonal occurrence.

But it was unclear whether the large outbreaks happening around the world were related to each other, or if they had each originated from local strains. Previous methods used to track V. cholerae were unable to distinguish strains with enough detail, Weill says. “It was impossible then, during the last 50 years, to understand the routes of propagation of cholera.”

Weill and an international research team analyzed the genetic information of about 1,700 strains of V. cholera, including those collected during and in between outbreaks over about 40 years from 45 countries in Africa and 14 countries throughout Latin America.

In both Africa and Latin America, the strains responsible for the large epidemics were most closely related to the South Asian strains, rather than strains existing in the local environment. These “epidemic” strains have been introduced 11 times in Africa since 1970 and have caused large outbreaks that lasted as long as 28 years, the researchers found.

In Latin America, there were three main introductions of the South Asian “epidemic” strains. One that came through Africa hit Peru in 1991. Another invaded Mexico around the same time, possibly arriving with coca smugglers using an airstrip near Mexico City. The third introduction, from Nepalese United Nations personnel, devastated Haiti in 2010 (SN: 2/25/12, p. 16).

“We now know what cholera is with much more precision,” says Nicholas Thomson, a genome scientist at the Wellcome Trust Sanger Institute in Cambridge, England, who also coauthored both papers. “You can find V. cholerae in the environment, no doubt about it, but the patterns of spread tell you that that’s not the primary route of transmission.” Rather, he says, it’s transmission between people that allows the bacteria to spread rapidly internationally.

“These studies affirm the primary role that people play in the spread of cholera,” says Yonatan Grad, an infectious diseases clinician at Harvard T.H. Chan School of Public Health in Boston who was not involved with the studies. “The emphasis on infected people as the vectors for spread underscores the importance of vaccination as a strategy to limit cholera.”

PHILADELPHIA — Protein-manufacturing factories within cells are picky about which widgets they construct, new research suggests. These ribosomes may not build all kinds of proteins, instead opting to craft only specialty products.

Some of that specialization may influence the course of embryo development, developmental biologist and geneticist Maria Barna of Stanford University School of Medicine and colleagues discovered. Barna reported the findings December 5 at the joint meeting of the American Society for Cell Biology and European Molecular Biology Organization.
Ribosomes, which are themselves made up of many proteins and RNAs, read genetic instructions copied from DNA into messenger RNAs. The ribosomes then translate those instructions into other proteins that build cells and carry out cellular functions. A typical mammalian cell may carry 10 million ribosomes. “The textbook view of ribosomes is that they are all the same,” Barna said. Even many cell biologists have paid little attention to the structures, viewing them as “backstage players in controlling the genetic code.”

But that view may soon change. Ribosomes actually come in many varieties, incorporating different proteins, Barna and colleagues found. Each variety of ribosome may be responsible for reading a subset of messenger RNAs, recent studies suggest. For instance, ribosomes containing the ribosomal protein RPS25 build all of the proteins involved in processing vitamin B12, Barna and colleagues reported July 6 in Molecular Cell. Vitamin B12 helps red blood cells and nerves work properly, among other functions. Perhaps other biological processes are also controlled, in part, by having specific types of ribosomes build particular proteins, Barna said.

In unpublished work presented at the meeting, Barna and colleagues also found that certain ribosome varieties may be important at different stages of embryonic development. The researchers coaxed embryonic stem cells growing in lab dishes to develop into many types of cells. The team then examined the ribosomal proteins found in each type of cell. Of the 80 ribosomal proteins examined, 31 changed protein levels in at least one cell type, Barna said. The finding may indicate that specialized ribosomes help set a cell’s identity.

Although Barna’s idea of diverse ribosomes goes against the classical textbook view, “the concept is not heretical at all,” says Vassie Ware, a molecular cell biologist at Lehigh University in Bethlehem, Pa., not involved in the work.
These findings may help explain why some people with mutations in certain ribosomal protein genes develop conditions such as Diamond-Blackfan anemia — a blood disorder in which the bone marrow doesn’t make enough red blood cells — but don’t have problems in other body tissues, Ware says.

That disease is caused by mutations in the RPL5 and RPL11 genes, which encode ribosomal building blocks. If all ribosomes were alike, people with mutations in ribosomal components should have malfunctions all over their bodies, or might not ever be born. RPL5 and RPL11 proteins may be part of specialized ribosomes that are important in the bone marrow but not elsewhere in the body.

Despite their name, pelican spiders aren’t massive, fish-eating monstrosities. In fact, the shy spiders in the family Archaeidae are as long as a grain of rice and are a threat only to other spiders.

Discovering a new species of these tiny Madagascar spiders is tough, but Hannah Wood has done just that — 18 times over.

Wood, an arachnologist at the Smithsonian National Museum of Natural History in Washington D.C., analyzed the genes and anatomy of live and museum pelican spider specimens to find these new species. She describes them in a paper published online January 11 in ZooKeys.
Like other pelican spiders, the new species have an elongated “neck” and beaklike pincers, or chelicerae. The way they use those long chelicerae to strike from a distance, earned them another name: assassin spiders. Once impaled, the helpless prey dangles from these meat hooks until the venom does its work (SN: 3/22/14, p. 4).

Probing the spiders’ tiny anatomy under a microscope, Wood looked for hints to distinguish one species from another. Arachnologists often look to spiders’ genitals: Males and females from the same species typically evolved specially shaped organs to mate. If the “lock” doesn’t fit the “key,” the spiders are likely of a different species.

Thanks to Wood, 18 more species of pelican spiders — some of which were previously misclassified — now have names. Eriauchenius rafohy honors an ancient Madagascar queen, and E. wunderlichi, an eminent arachanologist. Wood, one of the foremost experts on pelican spiders, says she expects there are still more species to find. Perhaps an E. woodi?

A teenage girl climbed into an underground cave around 13,000 years ago. Edging through the ink-dark chamber, she accidentally plunged to her death at the bottom of a deep pit.

Rising seas eventually inundated the cave, located on Central America’s Yucatán Peninsula. But that didn’t stop scuba divers from finding and retrieving much of the girl’s skeleton in 2007.

“First Face of America,” a new NOVA documentary airing February 7 on PBS, provides a closeup look at two dangerous underwater expeditions that resulted in the discovery and salvaging of bones from one of the earliest known New World residents, dubbed Naia.
The program describes how studies of Naia’s bones (SN: 6/14/14, p. 6) and of genes from an 11,500-year-old infant recently excavated in Alaska have generated fresh insights into how people populated the Americas. Viewers watch anthropologist and forensic consultant James Chatters, who directed scientific studies of Naia’s remains, as he reconstructs the ancient teen’s face and charts the lower-body injuries that testify to what must have been a rough life.
In one suspenseful scene, cameras record Chatters talking with scuba divers shortly before the divers descend into the submerged cave to collect Naia’s bones. The scientist describes how thousands of years of soaking in seawater have rendered the precious remains fragile. He uses a plaster cast of a human jaw to demonstrate for scuba diver Susan Bird how to handle Naia’s skull so that it stays intact while being placed in a padded box. Bird’s worried expression speaks volumes.

“On the day of the dive, there was so much tension, so many people on the verge of freaking out,” Bird recalls in the show. When the divers return from their successful mission, collective joy breaks out.
The scene then shifts to a lab where Chatters painstakingly re-creates what Naia looked like. Asian-looking facial features raise questions about how the ancient youth ended up in Central America. That’s where University of Alaska Fairbanks anthropologist Ben Potter enters the story. In 2013, Potter and colleagues excavated the remains of two infant girls at an Alaskan site dating nearly to Naia’s time. Analysis of DNA recovered from one of the infants , described in the Jan. 11 Nature , supports a scenario in which a single founding Native American population reached a land bridge that connected northeast Asia to North America around 35,000 years ago. As early as 20,000 years ago, those people had moved into their new continent, North America. Naia’s face reflects her ancestors’ Asian roots.
In tracing back how people ended up in the Americas, NOVA presents an outdated model of ancient humans moving out of Africa along a single path through the Middle East around 80,000 years ago. Evidence increasingly indicates that people started leaving Africa 100,000 years ago or more via multiple paths (SN: 12/24/16, p. 25). That’s a topic for another show, though. In this one, Naia reveals secrets about the peopling of the Americas with a lot of help from intrepid scuba divers and state-of-the-art analyses. It’s fitting that a slight smile creases her reconstructed face.

Bedbugs leave a lasting legacy.

Their poop contains a chemical called histamine, part of the suite of pheromones that the insects excrete to attract others of their kind. Human exposure to histamine can trigger allergy symptoms like itchiness and asthma. (Our bodies also naturally release histamine when confronted with an allergen.) Histamine stays behind long after the bedbugs disappear, scientists report February 12 in PLOS ONE.

Researchers from North Carolina State University in Raleigh collected dust from apartments in a building with a chronic bedbug infestation. After a pest control company treated the apartments by raising the temperature to a toasty 50° Celsius, the researchers sampled the dust again. They compared those two sample groups with a third, from area homes that hadn’t had bedbugs for at least three years.

Dust from the infested apartments had levels of histamine chemical that were 22 times as much as the low amount found in bedbug-free houses, the researchers found. And while the heat treatment got rid of the tiny bloodsuckers, it didn’t lower the histamine levels.

Future pest control treatments might need to account for bedbugs’ long-term effects.

AUSTIN, Texas — An analysis of the metals in dozens of Picasso’s bronze sculptures has traced the birthplace of a handful of the works of art to the outskirts of German-occupied Paris during World War II.

This is the first time that the raw materials of Picasso’s sculptures have been scrutinized in detail, conservation scientist Francesca Casadio of the Art Institute of Chicago said February 17 at the annual meeting of the American Association for the Advancement of Science. And the elemental “fingerprints” help solve a mystery surrounding the sculptures’ origins.
“In collaboration with curators, we can write a richer history of art that is enriched by scientific findings,” Casadio said.

Casadio and colleagues from the Art Institute of Chicago and Northwestern University in Evanston, Ill., studied 39 bronzes in the collection of the Picasso Museum in Paris. The team used a portable X-ray fluorescence spectrometer to record the amount of copper, tin, zinc and lead at several points on each sculpture.
Based on the percentage of tin versus zinc in the bronze, “we found that there are compositional groups that relate to a specific foundry,” Casadio said. Seventeen sculptures had a foundry mark on them, so the researchers could relate metal mixes to specific foundries.
But seven sculptures lack foundry marks. Based on their composition, researchers pegged five to a specific foundry — that of Émile Robecchi, a craftsman whose workshop sat in the southern outskirts of Paris. Original invoices from the foundry surfaced two years ago and revealed when some of the pieces were cast. For instance, the description, weight and size written on one invoice confirmed that the bronze of Tête de femme de profil (Marie­Thérèse) — a portrait of one of Picasso’s mistresses originally sculpted in plaster in 1931 — was cast at the foundry in February 1941.
At that time, the war had been under way for years and the Germans had just occupied Paris. Picasso worried that his fragile plaster sculptures could be easily destroyed and sought to have them cast in bronze.

The team’s analysis also found two distinct mixtures of bronze that came out of the Robbechi foundry. That difference makes sense in the context of 1940s occupied Paris, when the Germans instituted laws requiring that people turn in certain metals to go toward war efforts, Casadio said.

“A lot of [foundries’] archives are incomplete or nonexistent,” Casadio said. The new analysis “reinforces why it’s really important to collaborate and how science adds the missing piece of the puzzle.”

Chile’s Atacama Desert is so dry that some spots see rain only once a decade. Salt turns the sandy soil inhospitable, and ultraviolet radiation scorches the surface. So little can survive there that scientists have wondered whether snippets of DNA found in the soil are just part of the desiccated skeletons of long-dead microbes or traces of hunkered-down but still living colonies.

A rare deluge has solved that mystery. Storms that dumped a few centimeters of rain on the Atacama in March 2015 — a decade’s worth in one day — sparked a microbial superbloom, researchers report February 26 in Proceedings of the National Academy of Sciences.
That storm initially threw a wrench into plans for scientists to get a snapshot of microbial life under normal, hyperarid conditions in the Atacama. “But in the end, it came back as a lucky stroke,” says study coauthor Dirk Schulze-Makuch, an astrobiologist at the Technische Universität Berlin. He and his colleagues drove mining vehicles into the desert to collect soil samples just a few weeks after the storm, and then returned again in 2016 and 2017 to track changes as the moisture dissipated.

The team found microbes — a mix of extremophile archaea, bacteria and fungi — that were tolerant of desiccation, salinity and UV radiation. The kinds of species were fairly consistent across sampling sites, which suggests there’s something of a native microbial community that can survive in this salty sand by going dormant between periods of moisture, says Schulze-Makuch.

Schulze-Makuch and his colleagues also found evidence for enzymes that are by-products of cellular metabolism. And traces of ATP, the molecule that cells use for energy, lingered inside cells. Those markers of life were the most bountiful at the first sampling time, and then declined as the soil dried out again.

Collectively, it’s evidence that microbes aren’t just dying and leaving their DNA behind in the Atacama — they’re laying low to live another day. That’s encouraging to Schulze-Makuch: He’s interested in the Atacama as a proxy for conditions on Mars.
Armando Azua-Bustos, an astrobiologist at the Centro de Astrobiología in Madrid who was not part of this study, agrees. “If we’re finding that, on Earth, truly dry places are still inhabited,” he says. “That opens the door to finding life elsewhere in the universe.”

Mass: About 60 billion suns’ worth.

Location: The galaxy NGC1052–DF2, about 65 million light-years from Earth.

An unusual galaxy is surprisingly lacking in dark matter, scientists report March 28 in Nature.

In typical galaxies, normal matter is swamped by dark matter, an unidentified invisible substance that makes up most of the matter in the universe. The existence of dark matter explains the unexpectedly fast speeds at which stars swirl around galaxies, and how galaxies move within clusters.
But one galaxy, NGC1052–DF2, appears to have less dark matter than normal matter, or potentially none at all. Given its mass — it holds stars with about 200 million times the mass of the sun — it would be expected to have about 300 times as much dark matter as normal matter. That adds up to about 60 billion times the sun’s mass in missing dark matter.

Using observations from several telescopes, Yale University astronomer Pieter van Dokkum and colleagues studied 10 bright clumps of stars within the galaxy, known as globular clusters, and measured their velocities. The more mass there is in the galaxy, the faster the clusters should move around it. So if dark matter were present, the clusters should cruise at a relatively rapid clip. Instead, the clusters were moving slowly, indicating a dark matter–free zone.
In most galaxies, stars move faster than naïvely expected, which suggests dark matter lurks within them, providing an extra source of mass. Most physicists believe dark matter is an undetected type of particle. But some think that the hint of extra matter might be a mirage, caused by an incomplete understanding of the workings of gravity. These researchers favor a theory known as modified Newtonian dynamics, or MOND (SN: 3/31/07, p. 206), which adjusts the rules of gravity to make sense of stars’ motions, without requiring any new, elusive particles.

The new study, says van Dokkum, bolsters the idea that dark matter is real, instead of an illusion. “Until now, whenever we saw a galaxy, we also saw dark matter,” says van Dokkum. “We didn’t know for sure whether dark matter and galaxies were two separable things.”

Because MOND proposes tweaking the laws of physics, then — if correct — its effects should be felt in every galaxy across the cosmos. That makes it hard for MOND to explain the unusually slow speeds of the star clusters in NGC1052–DF2.

“It’s intriguing, but it’s not something I’m going to lose sleep over,” says Stacy McGaugh, an astrophysicist at Case Western Reserve University in Cleveland. He studies MOND and thinks the theory might still be able to explain this galaxy. That’s because NGC1052–DF2 is nestled close to another galaxy. That other galaxy could alter MOND’s predictions, perhaps explaining why the star clusters move slowly. The effect of that proximity needs to be taken into account to determine if MOND can explain the observations, he says.

Still, McGaugh acknowledges that NGC1052–DF2 is problematic for MOND. But it is also problematic for the standard dark matter picture, he says, as it’s not clear how such a galaxy could form in the first place. Most galaxies are thought to form around clumps of dark matter, so a galaxy devoid of the stuff is hard to explain.

NGC1052–DF2 is unusual in other ways. It’s a faint, ghostly blob known as an ultradiffuse galaxy. Although about the same volume as the Milky Way, NGC1052–DF2 contains many fewer stars. Scientists are struggling to understand why such galaxies look so different from most others (SN: 12/10/16, p. 18). Finding an ultradiffuse galaxy without dark matter further complicates the puzzle.

If scientists can explain how the galaxy formed, it might improve understanding of the properties of dark matter. “In physics we always want to find really extreme laboratories to test theories and ideas,” says astrophysicist James Bullock of the University of California, Irvine. This galaxy is extreme indeed.

Some victims were found at home. An 84-year-old woman who’d spent over half her life in the same Sacramento, Calif., apartment died near her front door, gripping her keys. A World War II veteran succumbed in his bedroom. Many died outside, including a hiker who perished on the Pacific Crest Trail, his water bottles empty.

The killer? Heat. Hundreds of others lost their lives when a stifling air mass settled on California in July 2006. And this repeat offender’s rap sheet stretches on. In Chicago, a multiday scorcher in July 1995 killed nearly 700. Elderly, black residents and people in homes without air conditioning were hardest hit. Europe’s 2003 heat wave left more than 70,000 dead, almost 20,000 of them in France. Many elderly Parisians baked to death in upper-floor apartments while younger residents who might have checked in on their neighbors were on August vacation. In 2010, Russia lost at least 10,000 residents to heat. India, in 2015, reported more than 2,500 heat-related deaths.

Year in and year out, heat claims lives. Since 1986, the first year the National Weather Service reported data on heat-related deaths, more people in the United States have died from heat (3,979) than from any other weather-related disaster — more than floods (2,599), tornadoes (2,116) or hurricanes (1,391). Heat’s victim counts would be even higher, but unless the deceased are found with a fatal body temperature or in a hot room, the fact that heat might have been the cause is often left off of the death certificate, says Jonathan Patz, director of the Global Health Institute at the University of Wisconsin–Madison.

As greenhouse gases accumulate in the atmosphere, heat’s toll is expected to rise. Temperatures will probably keep smashing records as carbon dioxide, methane and other gases continue warming the planet. Heat waves (unusually hot weather lasting two or more days) will probably be longer, hotter and more frequent in the future.
Beyond deaths, researchers are beginning to document other losses: Heat appears to rob us of sleep, of smarts and of healthy births. “Heat has the ability to affect so many people,” says Rupa Basu, an epidemiologist with the California Environmental Protection Agency’s Office of Environmental Health Hazard Assessment in Oakland. “Everybody’s vulnerable.”

Many people see heat as more of an annoyance than a threat, but climate change, extreme heat and human health are entwined. “There might not be a huge burden of disease from heat-related illness right now in your community,” says Jeremy Hess, an emergency medicine physician and public health researcher at the University of Washington in Seattle. “But give it another 20 years, and it might be a more significant issue.”
Adaptation has limits
The human body can’t tolerate excessive heat. The biological and chemical processes that keep us alive are best carried out at a core temperature of 36° to 37° Celsius (96.8° to 98.6° Fahrenheit), with slight variation from person to person. Beyond that, “the body’s primary response to heat is to try and get rid of it,” says Jonathan Samet, dean of the Colorado School of Public Health in Aurora. Blood vessels in the skin dilate and heart rate goes up to push blood flow to the skin, where the blood can release heat to cool down. Meanwhile, sweating kicks in to cool the skin.

With repeated exposure to high temperatures, the body can become more efficient at shedding excess heat. That’s why a person can move from cold Minneapolis to steamy Miami and get used to the higher heat and humidity. But there is a limit to how much a person can adjust, which depends on the person’s underlying health and the ambient temperature and humidity. If the outside is hotter than the body, blood at the skin surface won’t release heat. If humidity is high, sweating won’t cool the skin. Two scientists proposed in 2008 that humans cannot effectively dissipate heat with extended exposure to a wet-bulb temperature, which combines heat and humidity, that is greater than 35° C.
Forced to regulate heat without a break, the body gets worn out. Heat exhaustion leads to weakness, dizziness and nausea. If a person doesn’t cool off, heat stroke is likely — and likely fatal. The ability to regulate heat breaks down and core body temperature reaches or exceeds 40° C. A person suffering heat stroke may have seizures, convulsions or go into a coma.

No one is immune to heat, but it hits some groups harder than others. The elderly, considered the most vulnerable, have fewer sweat glands and their bodies respond more slowly to rising temperatures. Children haven’t fully developed the ability to regulate heat, and pregnant women can struggle due to the demands of the fetus. People with chronic diseases like diabetes, cardiovascular disease and obesity can have trouble dissipating heat. And, of course, people living in poverty often lack air conditioning and other resources to withstand sweltering conditions.
Collateral damage
Researchers are discovering more ways that heat can hurt. Take sleep: The onset and duration of sleep is sensitive to temperature. The body cools down as it prepares to sleep; this decrease in core temperature is a signal to bring on the z’s. Body temperature stays low throughout the night, then rises just before awakening. A good night’s rest is a cornerstone of health.

Hot nights make for bad sleep, according to a study combining responses to a U.S. Centers for Disease Control and Prevention sleep survey of 765,000 U.S. residents from 2002 to 2011 with data on nighttime temperatures during that period. The higher the nighttime temperatures, the more nights respondents reported getting too little shut-eye. The effect hit low-income respondents and the elderly hardest, the researchers reported in May 2017 in Science Advances.

The ability to think and calculate may take a beating in the heat, according to a small study presented in January in Austin, Texas, at the American Meteorological Society’s annual meeting. Researchers from Harvard University tested undergraduate students for 12 days — the time before, during and after a heat wave. Twenty-four lived in buildings with air conditioning and 20 in buildings without. The researchers assessed how quickly and accurately students performed an addition and subtraction test and a test that asked for the color of a written word, rather than the word itself. During the heat wave, the students without air conditioning got about 6 percent fewer correct answers on the math problems and 10 percent fewer on the color problems than the students with air conditioning.

Heat may even increase the risk of stillbirth. Researchers with the National Institute of Child Health and Human Development in Bethesda, Md., analyzed weather data and more than 223,000 U.S. births from 2002 to 2008. During the warm months of the year, a 1 degree C increase in temperature during the week before birth was associated with about four additional stillbirths per 10,000 births, the researchers reported in June 2017 in Environmental Health Perspectives.
As heat gets vicious, it threatens to disrupt the fabric of society. Extreme heat — beyond a wet-bulb temperature of 35° C — could become more regular in South Asia and the Persian Gulf, rendering parts of those areas uninhabitable, according to studies in the August 2017 Science Advances (SN: 9/2/17, p. 10) and the February 2016 Nature Climate Change. It’s not hard to imagine that there will be profound societal and political instability “in a world where tens of millions of people have to move and are looking for cooler places to live,” says Howard Frumkin, a physician epidemiologist specializing in environmental health at the University of Washington.

Emerald cities
Fifty-four percent of the world’s population — and around 80 percent of U.S. residents — live in urban areas. Cities are where some action to combat heat can be taken now, says Brian Stone Jr., an environmental planner and member of the Urban Climate Lab at Georgia Tech in Atlanta. “If we’re waiting for the national government to signal it’s time to do this, we’re going to wait too long,” he says. “We are well into a world that’s been altered by climate change.”

Heat thrives in cities. All of the nonreflective roofs, walls, roads and other surfaces absorb and retain heat during the day. Waste heat, emitted from air conditioners and vehicles, concentrates in cities too. Together, these factors contribute to what’s called an urban heat island, an amplification of heat that occurs within cities. On average, a city with at least a million residents can be 1 to 3 degrees C hotter than surrounding areas. At night, the temperature differences widen. Cities may be as much as 12 degrees C hotter than surrounding areas in the evening hours, because cities release built-up heat back out among buildings and avenues.

Hotlanta
These Landsat satellite images show urban Atlanta on September 28, 2000. The core urban area is at the center of the images. The left side shows areas of vegetation (green), bare ground (brown) and roads and dense development (gray). The heat map on the right shows the areas of densest development also have the hottest land surface temperatures (red), near 30 degrees Celsius. The areas of heaviest vegetation are the coolest (yellow) due to evaporation of water and shade.
City planners can rid their locales of some of this heat with several strategies. One is to plant more trees to create shade for residents and structures. Trees also lower the air temperature by transferring water from the soil through the tree to the air. The surrounding air is cooled as the water changes from a liquid to a vapor. The process is “much like the way sweating works for our bodies,” says George Ban-Weiss, an environmental engineer at the University of Southern California in Los Angeles.

Another strategy is to reduce the amount of sunlight that city surfaces absorb by using “cool” materials on exposed surfaces. The best known are cool roofs, which “reflect more sunlight than usual,” says Ronnen Levinson of Lawrence Berkeley National Laboratory in Berkeley, Calif., who studies cool surfaces and urban heat islands. In general, to make a surface cool, you make it lighter, with coatings or other light-colored materials. For example, a white roof that reflects 80 percent of the sun’s light on a typical summer afternoon will stay about 31 degrees C cooler than a gray roof that reflects only 20 percent.
Giving buildings cool-surface makeovers counters the urban heat island effect and reduces the temperature inside a building. “In disadvantaged communities, people simply may not have air conditioning to help them ride out hot summers,” Levinson says. Cooling off the insides of buildings is “where I think the greatest potential benefits are for improving human comfort and health,” he says.

Stone has estimated how many heat-related deaths could be avoided by reducing urban heat island effects. In 2016, he and colleagues produced a report for the city of Louisville, Ky., that analyzed the impact of adding 450,000 trees, converting 168 square kilometers of surfaces to cool materials and more. The researchers estimated that areas of the city could reduce average summertime temperatures by as much as 1.7 degrees C or more. And based on the 53 deaths Stone attributed to the city’s unusually warm summer of 2012, there could be 11 fewer deaths from heat, a reduction of 21 percent. “When we get a big heat wave,” Stone says, “that could really translate into hundreds of lives.”

Many cities in the United States and abroad are working on tempering their urban heat islands with a variety of strategies, including programs to install cool roofs or plant more trees. The city of Los Angeles now requires that new or replaced roofs for homes and other residential buildings meet a solar reflectance index value — a measure of a materials’ ability to stay cool in the sun between zero (black surface) and 100 (white) — of at least 75 for flatter roofs and 16 for steeper ones. Through a provision in California’s building energy efficiency code, cities throughout the state have been converting flat, commercial roofs, like those on big-box stores, to light-colored cool roofs when a new topper is needed.
New York City has planted a million new trees since 2007 and committed additional funds to adding even more to streets and parks. The city also has coated 0.62 square kilometers of roof surfaces white since 2009. The city of Ahmedabad, India, where about 25 percent of the residents live in slum communities, announced a heat action plan in 2017 that includes a cool roofs initiative to paint or otherwise convert at least 500 slum household roofs and to improve the reflectivity of roofs on government buildings and schools.

Measures that tackle the urban heat island effect also make cities more energy efficient (by reducing the cooling needs inside buildings) and more comfortable (by shading city residents). Individual cities need to implement strategies that make sense for their landscapes, their water resources, their usual climate and their populations, Ban-Weiss says.

But ameliorating urban heat can only do so much. There will still need to be a worldwide push to reduce emissions of greenhouse gases. Ban-Weiss and colleagues estimated how much cool roofs could counter warming from climate change in Southern California. Assuming that greenhouse gas emissions continue to increase, the widespread adoption of cool roofs in the Los Angeles metropolitan area would offset some of the warming expected by midcentury, the team reported in 2016 in Environmental Research Letters. But by the end of the century, Ban-Weiss says, the cool roof benefits “become mostly dwarfed by climate change.”