ORLANDO, Fla. — Weight gain may depend on how an individual’s genes react to certain diets, a new study in mice suggests.
Four strains of mice fared differently on four different diets, William Barrington of North Carolina State University in Raleigh reported July 15 at the Allied Genetics Conference.
One strain, the A/J mouse, was nearly impervious to dietary changes. Those mice didn’t gain much weight or have changes in insulin or cholesterol no matter what they ate: a fat-and-carbohydrate-laden Western diet, traditional Mediterranean or Japanese diet (usually considered healthy) or very low-carbohydrate, fat-rich fare known as the ketogenic diet. In contrast, NOD/ShiLtJ mice gained weight on all but the Japanese diet. Those mice’s blood sugar shot up — a hallmark of diabetes — on a Mediterranean diet, but decreased on the Japanese diet.
FVB/NJ mice didn’t get fat on the Western diet, but became obese and developed high cholesterol and other health problems on the ketogenic diet. The opposite was true for C57BL/6J mice. They became obese and developed cholesterol and other problems linked to heart disease and diabetes in people on the Western diet, but not on the ketogenic diet. They also fattened up on the Mediterranean diet.
The results indicate that “there’s no universally healthy diet,” Barrington said. The findings echo results of a human study in which blood sugar rose in some people after eating some foods, even when the same food had no effect on other people (SN: 1/9/16, p. 8). Such individual reactions to food suggest that diets should be personalized.
Barrington and colleagues are working to find the genes that control the mouse strains’ varying responses to what they eat. There is still no way to predict how people will fare on a given diet, he said.
WASHINGTON — When bacteria lose genes needed to make enzymes for important chemical reactions, defeat isn’t inevitable. Sometimes other enzymes will take on new roles to patch together a work-around chain of reactions that does the job, biologist Shelley Copley reported August 4 at the 2nd American Society for Microbiology Conference on Experimental Microbial Evolution.
Bacteria that can adapt in this way are more likely to survive when living conditions change, passing along these new tricks to their descendants. So studying these biochemical gymnastics is helping scientists to understand how evolution works on a molecular level. Working with different strains of Escherichia coli bacteria, Copley and colleagues deleted genes responsible for making crucial enzymes. The team then watched the microbes replicate for many generations to see how they worked around those limitations.
Most enzymes are highly specialized: They only work well to speed up one type of reaction, the way a key fits only one lock. But some enzymes are more like master keys — they can boost multiple reactions, though they tend to specialize in one. These so-called “promiscuous” enzymes can switch away from their specialty if conditions change.
Copley’s team found that new enzymes would sub in to replace the missing ones. For instance, E. coli missing an enzyme needed to make vitamin B6 synthesized the vitamin using a different set of enzymes. But surprisingly, the promiscuous enzymes didn’t end up directly triggering the same reaction as the enzymes they replaced. Instead, the replacement enzymes cobbled together a different (often longer) work-around series of reactions that ultimately achieved the same function.
“We were rerouting metabolism,” said Copley, of the University of Colorado Boulder.
By modifying the bacteria’s genes and forcing the microbes to survive with a more limited chemical toolkit, Copley’s work gives a more detailed look at the biochemistry underlying evolution, says biologist Gavin Sherlock of Stanford University, who was not involved in the research. Betul Kacar, a synthetic biologist at Harvard University, says promiscuity could also be a window into the past, giving hints about enzymes’ previous roles earlier in evolutionary history. The role that an enzyme jumps in to play in a pinch could have once been its main job. “Trying to understand how novel pathways arise, what kind of mechanistic underlying forces shape those trajectories, is quite essential,” she says.
Bacteria can piece together all sorts of alternative routes in response to missing enzymes, depending on specific environmental conditions, Copley said. The ones that are most successful are more efficient —they have fewer steps, or they yield more of the desired reaction product.
Even if you’ve never lived in rattlesnake territory, you know what the sound of a snake’s rattle means: Beware! A shake of its rattle is an effective way for a snake to communicate to a potential predator that an attack could result in a venomous bite.
For more than a century, scientists have posited how that rattle might have evolved. The rattle is composed of segments of keratin (the same stuff that makes up human hair), and specialized muscles in a snake’s tail vibrate those segments rapidly to create the rattling sound. The rattlesnake’s rattle is a trait that evolved only once in the past and is now found in only two closely related genera of snakes that live in North and South America. But plenty of other species of snakes also vibrate their tails as a warning to potential predators.
Bradley Allf and colleagues at the University of North Carolina in Chapel Hill think that the tail vibration and the evolution of the rattle might be connected. They gathered 155 snakes of 56 species — 38 species from the Viperidae family, which includes rattlesnakes, and 18 species from the largest snake family, Colubridae — from museums, zoos and private collectors. Working with captive snakes let them control conditions, such as temperature, that can affect tail vibration. With each snake, one of the researchers tried to get it to behave defensively by waving a stuffed animal in front of it. The team videotaped the snakes as they vibrated their tails, or not.
The researchers plotted the snakes’ tail vibration duration and rate against how closely related a species was to rattlesnakes. One group of snakes that lives in the Americas was taken out of the analysis because its tail vibrations were so similar to those of rattlesnakes; it appears that these species are mimicking the dangerous snakes that live near them (not a bad strategy for survival). Among the rest of the snakes analyzed, those that were more closely related had tail behavior that was more similar to that of rattlesnakes.
“Our results suggest that tail vibration by rattleless ancestors of rattlesnakes may have served as the signal precursor to rattlesnake rattling behavior,” the researchers write in the October issue of the American Naturalist. “If ancestral tail vibration was a reliable cue to predators that a bite was imminent, then this behavior could have become elaborated as a defensive signal.”
Allf and his colleagues propose a couple of ways that this could have happened. Perhaps snakes that made noise with their tails were better at startling predators, and this may have prompted such noise-making tail features to spread and eventually become refined into what is now a rattle. Or maybe snakes that shook their tails longer and faster developed calluses of keratin. If these calluses provided better warning, that may have somehow evolved into a rattle.
“Thus, the rattlesnake rattle might have evolved via elaboration of a simple behavior,” they conclude.
The first time Jessica Cantlon met Kumang at the Seneca Park Zoo, the matriarch orangutan regurgitated her previous meal right into Cantlon’s face. “I was retching,” Cantlon recalls. “It was so gross.” But Cantlon was there to kick off a series of behavioral experiments, and her students, who would be working with Kumang regularly, were watching. “Does anyone have any towels?” she remembers asking, knowing she had to keep her cool.
Cantlon’s deliberate nature and whatever-it-takes attitude have served her well. As a cognitive neuroscientist at the University of Rochester in New York, she investigates numerical thinking with some of the most unpredictable and often difficult study subjects: nonhuman primates, including orangutans, baboons and rhesus macaques, and — most remarkably — children as young as age 3. Both groups participate in cognitive tests that require them, for example, to track relative quantities as researchers sequentially add items to cups and to distinguish between quantities of assorted dots on touch screens. The kids also go into the functional MRI scanner where, in a feat impressive to parents everywhere, they lie completely still for 20 to 30 minutes so Cantlon and colleagues can get pictures of their brains. “She takes steps carefully, and she thinks very hard about where she is going,” says Daniel Ansari, a developmental cognitive neuroscientist at the University of Western Ontario in London, Canada, who is familiar with Cantlon’s work. “She goes for the big questions and big methodological challenges.”
The central question in Cantlon’s research is: How do humans understand numbers and where does that understanding come from? Sub-questions include: What are the most primitive mathematical concepts? What concepts do humans and other primates share? Are these shared concepts the foundation for fancier forms of mathematical reasoning? In addressing these questions, Cantlon draws on a wide range of methods. “Very few people can combine work on cognitive skills — studies from the point of view of behavior — with imaging work in very young children, and very few people do that same combination in nonhuman primates,” says Elissa Newport, who chaired the brain and cognitive sciences department at Rochester for more than a decade and now leads the Center for Brain Plasticity and Recovery at Georgetown University.
As a graduate student, Cantlon determined that neuroimaging studies would add an independent source of data to the cognitive questions under exploration in Elizabeth Brannon’s lab at Duke University. So she identified collaborators and taught herself functional MRI. “By the time she graduated, she had something like four dissertations’ worth of work,” says Brannon, now of the University of Pennsylvania.
In the years since, Cantlon has identified a type of “protocounting” in baboons; they can keep tabs on approximate quantities of peanuts as researchers increase those quantities (SN Online: 5/17/15). In her most attention-grabbing work, Cantlon studied activity in the brains of children while they watched Sesame Street clips that dealt with number concepts — an unexpected success that proved everyday, relatively unaltered stimuli can yield meaningful data. An ongoing study in Cantlon’s lab seeks to find out how monkeys, U.S. kids and adults, and the Tsimané people of Bolivia, who have little formal education, distinguish between quantities. Do they determine the number of dots presented on the computer screen or do they rely on a proxy such as the total area covered by the dots? The work explores how the brain understands everyday concepts, but it could also inform strategies in math education. “If we understand the fundamental nature of the human brain and mind, that might give us a better insight into how to communicate number concepts to kids,” Cantlon says.
Growing up outside of Chicago, Cantlon enjoyed digging deep into a topic and becoming an expert. She and a friend turned themselves into ice skating superfans one summer, reading up on the Olympic skaters and checking videos out of the local library. In another project, Cantlon decided to learn everything possible about the price of gold. When she moved to a school where she could no longer take Latin, she taught and tested herself. Despite the fact that neither of her parents went to college, no one ever questioned that Cantlon would go. She studied anthropology as an undergraduate at Indiana University in Bloomington. “I was interested in the question of where we come from,” Cantlon says. “I was interested in studying people.” During college, she went on an archaeological dig in Belize and studied lemurs in Madagascar. For a year after graduation, she observed mountain gorillas in Rwanda, detailing their behavior every 10 minutes. “What they were thinking was something that was constantly on my mind,” she says. “‘How are we similar? Are you thinking what I’m thinking?’” Though she might have succeeded in any number of careers, she wanted exploration to be a big part of her life: “I don’t think doing a less exotic type of work would have been as satisfying.”
Today, Cantlon, who at age 40 recently earned tenure, doesn’t spend much time in the field. And even in the lab, she leaves much of the data collection to her graduate students and research assistants. “At this point, we are a well-oiled system,” she says, referring to the brain scan studies on kids. To make the kids comfortable, Cantlon’s team does trial runs in a mock scanner, describing it as a spaceship and providing “walkie-talkies” for any necessary communication. To keep them interested, the researchers treat it as a team activity and offer a ton of positive reinforcement, with prizes including Lego sets and a volcano-making kit. The kids receive pictures of their brains, which typically interest the parents most. The older of Cantlon’s two daughters, a 5-year-old extrovert named Cloe, has participated in behavioral tests and will no doubt be excited for her first brain scan.
The Sesame Street study was in part inspired by a paper by Uri Hasson, a neuroscientist at Princeton University who imaged the brains of volunteers while they watched The Good, the Bad and the Ugly. To better understand brain development, Cantlon wanted to see how brain activity compared in kids and adults exposed to math in a natural way. Of particular interest was a region called the intraparietal sulcus, or IPS, thought to play a role in symbolic number processing. The results, reported in PLOS Biology in 2013, showed that kids with IPS activity more closely resembling adults’ activity performed better on mathematical aptitude tests.
“It was the clearest, cleanest — did not have to come out this way — result,” Cantlon says.
Cantlon is notable for her diverse set of tools, says Steve Piantadosi, a computational neuroscientist and colleague at Rochester. “But she has something which is even more powerful than that. If you have different hypotheses and you want to come up with the perfect experiment that distinguishes them, that is something she is very good at thinking about. She is a great combination of critical and creative.”
To add another methodological approach, Cantlon next plans to collaborate with Piantadosi to develop computational models that explain the operations the brain performs as it counts or compares quantities. She would also like to add data analyses from wild primates into the mix. When researchers talk about the evolution of a primitive number sense, they often speak about foraging activity — identifying areas of the forest with more food, for example. But Cantlon wonders whether social interactions also require some basic understanding of quantities.
As for a recent question from a colleague about what risky project she’ll pursue now that she has tenure, Cantlon says nothing in particular comes to mind: “I feel like we’ve been doing the crazy things all along.”
ORLANDO, Fla. — New evidence from separate labs supports the controversial idea that an overlooked and unexpected Culex mosquito might spread Zika virus.
The southern house mosquito, Culex quinquefasciatus, is common in the Americas. Constância Ayres, working with Brazil’s Oswaldo Cruz Foundation in Recife, previously surprised Zika researchers with the disturbing proposal that this mosquito might be a stealth spreader of Zika. But two U.S. research groups tested the basic idea and couldn’t get the virus to infect the species. Now, preliminary results from Ayres’ and two other research groups are renewing the discussion. The data, shared September 26 at the International Congress of Entomology, suggest that Zika can build up in the house mosquito’s salivary glands — a key step in being able to transmit disease. Basic insect physiology is only part of the puzzle, though. Even if the mosquitoes prove competent at passing along Zika, there remain questions of whether their tastes, behavior and ecology will lead them to actually do so.
In the current outbreak, the World Health Organization has focused on mosquitoes in a different genus, Aedes, particularly Ae. aegypti, as the main disease vector. But Ayres had announced months ago the discovery of the virus in Brazil’s free-flying house mosquitoes (SN Online: 7/28/16).
At the congress, Ayres’ foundation colleague Duschinka Guedes reported that captive mosquitoes fed Zika-tainted blood had virus growing in their own guts and salivary glands within days. The virus doesn’t spread every time a mosquito slurping contaminated blood gets virus smeared on its mouthparts, though. To move from the mosquito to what it bites, viruses have to infect the insect midgut, then travel to the salivary glands and build up enough of a population for an infective dose drooling into the next victim. When Guedes offered the infected mosquitoes a special card to bite, they left telltale virus in the salivary traces, a sign of what they could do when biting — and infecting — a real animal.
Researchers from China and Canada who were not originally on the symposium program also stepped up to share their results, some of which are unpublished. Some tasks are still in early stages, but both labs showed Zika virus building up in some kind of Culex mosquitoes.
At the Beijing Institute of Microbiology and Epidemiology, Tong-Yan Zhao found the virus peaking in the house mosquitoes eight days after their first contaminated drink. As a test of the infectious powers of the mosquitoes, researchers let the Zika-carrying insects bite baby lab mice. Later, the virus showed up in the brains of eight out of nine lab mice. The results were reported September 7 in Emerging Microbes & Infections. From Brock University in St. Catharines, Canada, Fiona Hunter has found signs that 11 out of 50 wild-caught Culex pipiens pipiens mosquitoes picked up the virus somewhere on their bodies. So far, she has completely analyzed one mosquito and reports that the virus was indeed in its saliva.
These positive results contradict Culex tests at the University of Texas Medical Branch in Galveston. Those tests, with U.S. mosquitoes, found no evidence that C. quinquefasciatus can pick up and pass along a Zika infection, says study coauthor Scott Weaver. Stephen Higgs of Kansas State University in Manhattan and his colleagues got similar results. “We’re pretty good at infecting mosquitoes,” Higgs says, so he muses over whether certain virus strains won’t infect mosquitoes from particular places.
The main risk from Culex at the moment is distraction, warned Roger Nasci of North Shore Mosquito Abatement District in Northfield, Ill. After the talks, he rose from the audience to say that Ae. aegypti is a known enemy and limited resources should not be diverted from fighting it.
George Peck, who runs mosquito control for Clackamas County in Oregon, isn’t convinced that the high virus concentrations dosing the test mosquitoes are realistic. Yet he’s watching the issue because like much of northern North America, Clackamas doesn’t have the Ae. aegypti vector to worry about. But it does have plenty of Culex mosquitoes.
Using nasal cartilage cells to repair joints is nothing to sniff at.
It has worked in goats. Now, in the first human trial, researchers at the University of Basel in Switzerland have grown cells called chondrocytes, taken from the noses of 10 patients with damaged knee joints, into cartilage grafts. These repair patches were then surgically implanted into the patients’ knee joints.
Two years after surgery, nine patients have seen improvements in knee function, quality of life and pain. (One patient dropped out of the trial because of additional athletic injuries.) MRI scans showed that the grafts looked like normal hyaline cartilage, the hard-to-replicate material that coats the tips of bones, the team reports in the Oct. 22 Lancet. Tests in more people are needed to determine whether the technique is ready for prime time.
Mothers who don’t eat enough during pregnancy could give birth to babies with long-lasting heart problems. The results from a new study in primates add to accumulating evidence that a mother’s nutrition has more bearing on her child’s health than previously thought.
“We pass more biological milestones during development than we will ever pass again in our entire lives,” says Peter Nathanielsz, coauthor of the study published November 6 in the Journal of Physiology. And during those critical nine months, calorie intake at the extremes — too many or too few — appears to have a lifelong influence on newborn weight, future metabolism and chronic health problems (SN: 1/23/16, p. 22). One landmark epidemiological investigation found that people born in the Dutch Hunger Winter during World War II suffered from an elevated risk of heart disease and other health concerns, with some risks even affecting two generations. But studies of human populations are complicated. It’s hard to account for the role of stress, behavior or environmental exposures. So Nathanielsz, of the University of Wyoming in Laramie, and colleagues from the University of Texas Health Science Center at San Antonio studied baboons, close genetic relatives to humans.
Sixteen pregnant baboons were fed their normal amount of chow, while 16 others received 30 percent less during pregnancy, a reduction researchers characterize as “moderate.” All other living conditions were the same. The researchers then compared offspring of the well-fed mothers with the offspring of undernourished mothers.
Infants of the underfed mothers were born small but nonetheless caught up in body weight to the offspring of the well-fed mothers by young adulthood. However, those whose mothers were underfed had more fibrous, abnormally shaped heart muscle, the researchers report. A normal heart is roughly an upside-down pyramid, but underfed offspring had more rounded and less muscular hearts. Evidence showed that these less-muscled hearts were not as efficient at pumping blood, with an average output about 20 percent lower.
Offspring undernourished in the womb also had hearts that appeared to age faster. By age five, the human equivalent of almost 25, many of their heart functions more closely resembled those of hearts of primates about three times as old.
Such experiments can show cause and effect — something that human studies can’t do, says Susan Ozanne, a developmental endocrinologist at the University of Cambridge. As a result, they provide strong evidence about the effects of maternal nutrition. “What this shows us is that certainly maternal diet has an effect on a child’s cardiac health long-term,” she says. Studies in rodents have produced similar findings, but “when you validate those in multiple species, it shows you you’re looking at a fundamentally conserved mechanism.” The next step, she says, is to learn whether diet and exercise after birth can make up for poor nutrition during development. Doctors also don’t know whether there is a window of time during childhood for intervention, or a longer period to counteract any effects, she says.
Much attention on maternal nutrition has focused on the obesity epidemic, Nathanielsz says, but undernutrition remains a public health challenge throughout the world, even in developed countries. The U.S. Department of Agriculture estimates that approximately 13 percent of American households in 2015 reported food insecurity, or uncertainty about having enough money for food. “The number of people with food insecurity is very high,” Nathanielsz says. “It would be sad if we discounted this problem.”
Science’s human side In “The SN 10: Scientists to Watch” (SN: 10/1/16, p. 16), Science News recognized 10 up-and-coming scientists across a range of scientific fields who will be answering big questions in the decades to come.
Barry Maletzky thought that highlighting 10 young scientists may have been unfair and detrimental to other researchers. “By drawing attention to just 10, I wonder if you are thereby discouraging others who may not make the headlines but whose basic research may lead the way toward important discoveries in the future,” Maletzky said. He also pointed out that scientific progress is made “through the tedious and often under-publicized work of a number of investigators working barely noticed through the years.” It’s true that in science journalism, as with all journalism, what you choose to cover can matter as much as how you choose to cover it, says Elizabeth Quill, Science News’ enterprise editor, who led the SN 10 project. Science News editors and writers take this responsibility seriously, which is why Science News avoided terms like “top,” “best” and other superlatives. Whenever possible, the names of mentors and collaborators were also included in the stories. “We recognize the dangers in calling out specific individuals, but we believe the rewards outweigh the risks,” Quill says. “The majority of Science News focuses on the data and the process. But here we see a different side. We are showing science as a human endeavor. We hope this list inspires all young scientists to follow their passion and their curiosity. But we also hope to do what we do best — inform our readers about new and interesting science.”
Kenneth Abate was disappointed by “The SN 10: Scientists to Watch” profiles and questioned how Science News chose the researchers. “The issue is probably a nice piece of advertising for the individuals to further their careers,” Abate said. However, it “is of little value to the scientific community nor does it contribute to the knowledge bank of those scientists or would-be scientist readers.” Choosing is never easy, but thankfully Science News staff didn’t do it alone. Every featured scientist was nominated by a Nobel laureate or recently elected member of the National Academy of Sciences on the basis of the scientist’s contributions to the field and promise for future contributions. As they do with any news or feature story, Science News editors and writers selected the final list of scientists by looking at who was doing novel, interesting and important work. As readers point out, the list could have easily been much, much longer.
Cool it The next big thing in high-tech clothing may be a plastic material similar to kitchen cling wrap that vents body heat, Meghan Rosen reported in “New fabric could make cool clothes” (SN: 10/1/16, p. 9).
Online reader Karl Chwe pointed out one potential drawback to the new material: “It is just a thin plastic film with tiny holes, and the holes aren’t big enough to allow water vapor to escape easily, so it doesn’t allow evaporative cooling,” he wrote. Chwe suggested that it might be better to wear fewer clothes.
Actually, the nanopores are permeable to water vapor, the authors reported. “In this regard, the new fabric is comparable to cotton,” Rosen says. “Without the nanopores, the fabric would be a literal sweat suit; it’s completely nonpermeable.” But even with pores, the fabric doesn’t quite feel like normal clothes just yet. Weaving the fibers into a textile could help. Still, when it comes to evaporative cooling, Rosen says, wearing fewer clothes might be the simplest solution of all.
Correction “A gut check gets personal” (SN: 10/1/16, p. 19) profiles Lawrence David, a computational biologist who studies the human gut microbiome at Duke University. David’s wife is a psychiatrist, not a psychologist as was incorrectly stated in the article.
Iridescent blue leaves on some begonias aren’t just for show — they help the plants harvest energy in low light.
The begonias’ chloroplasts, which use photosynthesis to convert light into fuel, have a repeating structure that allows the plants to efficiently soak up light. This comes in handy for a plant that lives on the shady forest floor. The structure acts as a “photonic crystal” that preferentially reflects blue wavelengths of light and helps the plant better absorb reds and greens for energy production, scientists report October 24 in Nature Plants. Colors in plants and animals typically come from pigments, chemicals that absorb certain wavelengths, or colors, of light. In rare cases, plants and animals derive their hues from microstructures. In begonias, such tiny, regular architectures can be found within certain chloroplasts, known as iridoplasts. As light bounces off these structures within an iridoplast, the reflected waves interfere at certain wavelengths (SN: 6/7/08, p. 26), creating a blue, iridescent shimmer. Those structured chloroplasts also offer a survival benefit, the new research shows: They help the plants collect light. In a hybrid of two species — Begonia grandis and Begonia pavonina — the structures enhance the absorption of green and red wavelengths by concentrating these rays on light-absorbing compartments within the iridoplasts. Importantly, the structures slow the light. The “group velocity,” or the speed of a packet of light waves, is decreased due to interference between incoming and reflected light. The slowdown gives the plant more time to absorb precious sunbeams.
“These iridoplasts can basically photosynthesize at low-light levels where normal chloroplasts just simply could not photosynthesize,” says study coauthor Heather Whitney, a plant biologist at the University of Bristol in England. Iridoplasts, however, can’t hold their own in bright light. So begonias also have standard chloroplasts, which provide energy in plentiful sunshine. Iridoplasts act like “a backup generator” in dim conditions, Whitney says.
Other plants have structured chloroplasts, too, so begonias might not be alone in their feats of light manipulation. “Plants can’t really run away from their problems,” Whitney says. Instead, they have to be crafty enough to survive where they stand.
In a rare bright spot for global environmental news, atmospheric scientists reported in 2016 that the ozone hole that forms annually over Antarctica is beginning to heal. Their data nail the case that the Montreal Protocol, the international treaty drawn up in 1987 to limit the use of ozone-destroying chemicals, is working.
The Antarctic ozone hole forms every Southern Hemisphere spring, when chemical reactions involving chlorine and bromine break apart the oxygen atoms that make up ozone molecules. Less protective ozone means that more ultraviolet radiation reaches Earth, where it can damage DNA and lead to higher rates of skin cancer, among other threats. The Montreal Protocol cut back drastically on the manufacture of ozone-destroying compounds such as chlorofluorocarbons, or CFCs, which had been used in air conditioners, refrigerators and other products. It went into force in 1989 and phased out CFCs by 2010.
Earlier studies had hinted that the ozone hole was on the mend. The new work, reported in Science in June, is the most definitive yet (SN: 7/23/16, p. 6). A team led by Susan Solomon, an atmospheric chemist at MIT, looked not only at the month of October, when Antarctic ozone loss typically peaks, but also at September, when the hole is growing. The healing trend was most obvious in September. Satellite measurements showed that from 2000 to 2015, the average extent of the September ozone hole shrank by about 4.5 million square kilometers, to approximately 18 million square kilometers. Soundings taken by weather balloons over Antarctica confirmed the findings. CFC concentrations peaked above Antarctica in the late 1990s and early 2000s and have been dropping ever since, says Birgit Hassler, an atmospheric chemist at Bodeker Scientific in Alexandra, New Zealand. Each passing year allows scientists to gather more convincing data. The new study, Hassler says, “makes the whole development of the Antarctic ozone hole healing very transparent and understandable.” It is a fitting capstone to Solomon’s career. In the 1980s she led a team that proposed that chlorine compounds were to blame for Antarctic ozone loss. She then traveled to the frozen continent to conduct pioneering experiments that measured the accumulating chemicals there. “It’s very humbling now to be 30 years later and be able to say we have a clear fingerprint that the ozone hole is starting to get better,” she says.
Solomon says that public engagement was key to solving the ozone problem, with people coming together to identify an issue that threatened society and develop new technologies to fix it. In that respect, the most successful environmental treaty in history holds lessons for dealing with a much bigger threat, she says — climate change.
To fix the ozone layer, industry stopped using CFCs and similar compounds and replaced them with hydrofluorocarbons. Those chemicals, however, turned out to be powerful greenhouse gases that accelerated global warming. In October, the nations that ratified the Montreal Protocol agreed to expand it to cover hydrofluorocarbons as well (SN: 11/26/16, p. 13).
