One of the planet’s deadliest viruses makes an annual pass through the United States with little fanfare. It rarely generates flashy headlines or news footage of health workers in hazmat suits. There’s no sudden panic when a sick person shows up coughing and feverish in an emergency room. Yet before next spring, this season’s lethal germ will probably have infected millions of Americans, killing tens of thousands. Still, it’s often referred to as just the flu.

The influenza virus seems so normal to most Americans that only about half of us will heed those “time for your flu shot” banners that pop up at pharmacies and worksites every autumn. Those annual shots remain the best means of protection, but they must be manufactured months before flu season starts, based on a best educated guess of what strains of the virus will be circulating. That means even in a successful year, vaccine performance may not be impressive. During the 2015–2016 season, only about half of those immunized were protected, according to a study in the Aug. 10 New England Journal of Medicine. Some years’ vaccines are duds: For the 2014–2015 season, the vaccine protected only 19 percent of people who received it, based on U.S. Centers for Disease Control and Prevention data.
Scientists have long worked to develop a flu shot that works better and lasts longer. But, unlike the very stable measles virus, influenza is a moving target. While only a few strains of flu virus circulate worldwide in a typical year, dozens more may exist. Each one is highly likely to mutate from year to year, with just enough shape-shifting to be unrecognizable to the body’s defenses.

Now, after years of searching, scientists believe they have better strategies to attack the parts of the virus that stay the same from year to year, offering the hope of protection across multiple seasons. The vaccines being developed in laboratories around the world “offer more promise than we’ve ever had,” says Walter Orenstein, associate director of the Emory Vaccine Center in Atlanta. And there are new creative approaches: One research group is trying to make a kind of super shot by anticipating every possible mutation a circulating virus might undergo.

“I’m optimistic we are going to get to a vaccine,” says Anthony Fauci, head of the National Institute of Allergy and Infectious Diseases, or NIAID, in Bethesda, Md. Then, you may need to heed those “time for your flu shot” messages only once.
Researchers often describe the flu virus as looking like a ball with lollipops sticking out. Tucked inside the ball is RNA, which the virus needs to make copies of itself. The lollipops on the outside are proteins: hemagglutinin and neuraminidase. There are 18 different kinds of hemagglutinin and 11 kinds of neuraminidase. Each kind of flu virus is named for its particular combination of these proteins; the current forms circulating around the world are H1N1 and H3N2. Hemagglutinin attaches to human cells to launch an infection; neuraminidase is more important for spreading the virus once infection has occurred.

Flu viruses involved in human epidemics are divided into types A and B, and A viruses are sliced even further into group 1 and group 2. Influenza A, the most troublesome for vaccine scientists, travels the world among birds, pigs and humans. The bird and pig versions don’t easily infect people, but the virus is constantly mutating and even swapping genes with other influenza viruses it meets along the way. Sometimes these genetic changes create a version that allows a bird or pig flu to move directly into humans. In 2013, one called H7N9 moved into people in China (SN Online: 3/11/15). The virus has since infected more than 1,500 people. Mostly, though, the genetic changes are more subtle, with just enough alterations to evade the human immune system.
Like kids with a sweet tooth, the immune system gets most excited about the top part of the hemagglutinin lollipop, and makes antibodies against it. The top is, after all, the first thing the immune system notices once the virus slips inside the nose, mouth and lungs. Every year, genetic mutations in the virus slightly change the chemical flavor of the lollipop, making it more sweet or sour than last season’s — just different enough so the immune system doesn’t recognize it. That’s why most years there’s a new flu shot.

Sometimes, in the gene shuffling with viruses in birds and pigs, the changes are so great that the flavor changes completely. Those are pandemic years, when there is so little residual immunity that a large portion of the global population falls ill from the new virus. The devastating 1918 flu, which killed an estimated 50 million people globally, was caused by such a drastic genetic shift (SN Online: 4/29/14). The most recent pandemic occurred in 2009, with the appearance of the “swine flu,” so named because the virus was first found in pigs. By one analysis, it caused between 148,000 and 249,000 deaths around the world.

Attack the stem
The 2009 disaster helped provide a blueprint for some of the latest experimental vaccines. Researchers noticed that when people with swine flu developed antibodies to the virus, those antibodies did something odd: They favored the hemagglutinin stem — the stick of the lollipop. And, more important, they appeared to react broadly against two kinds of flu virus. Scientists had known that the hemagglutinin stem, or stalk, isn’t as apt to change as the lollipop top, which theoretically makes the stem a good target for a universal vaccine. But in a usual flu season, the human body isn’t inclined to make infection-fighting antibodies against the stem.

“Unfortunately, the immune system preferentially recognizes the head, and we don’t know why it does that,” says Adrian McDermott, an immunologist at NIAID. So after infection, the biggest share of antibodies flocks to the hemagglutinin head. (Neuraminidase, the bigger player in disease after infection, is a target for influenza treatments but not a major focus for vaccine development.)

But in a study reported in the Journal of Experimental Medicine in 2011, a team of scientists from Emory and elsewhere found that antibodies to the so-called swine flu behaved unexpectedly. “If you have a head that the immune system hasn’t seen, you potentially redirect to a stalk response,” McDermott says. “That was an aha! moment.”
Researchers investigated further. For one study in 2012 in Frontiers in Immunology, scientists from Canada injected these stem-recognizing antibodies into mice to see if the mice were shielded from a different strain of flu. Not only were the mice protected from lethal doses of flu virus, but the protection was also in large part due to the absence of familiar antibodies against the head, the researchers found. Without the distraction of a head it recognized, the immune system seemed to rally against the stem.

Then came the what ifs: What if a vaccine produced just antibodies to the stem? Would that be enough protection? For the last few years, McDermott and others have been trying to develop vaccines made of “headless stalks” — just the sticks of the lollipops. With no head in place to hoard the immune response, the vaccine might coax the body to make enough stem-focused antibodies to protect against flu, the researchers hoped, regardless of the seasonal mutations occurring at the top.

Several groups soon found that headless stalks are difficult to make. Without the top to stabilize it, the molecular assembly tended to break apart. Two teams working independently reported in 2015 their success in keeping the stalk in one piece. NIAID scientists and their partners held the stalks together by anchoring them to the protein ferritin, which can assemble itself into nanoparticles. In a study in Nature Medicine, the team reported that vaccinated mice and ferrets appeared to be protected from dying of the H5N1 bird flu after receiving the vaccine, even when they developed symptoms. Unvaccinated mice and ferrets died.

The second team, from the Janssen Center of Excellence for Immunoprophylaxis in Leiden, the Netherlands, and the Scripps Research Institute in La Jolla, Calif., glued the stalk together by creating a series of genetic mutations at its top. In Science, the researchers reported that the vaccine reduced the symptoms of flu in vaccinated monkeys.

“We realized that the stem has much less variability than the head, and then we developed the capability to use it for a possible vaccine,” says Fauci, commenting on both efforts. “These were two important things that came together.”

Despite progress, these stalk-focused vaccines haven’t yet been put to human tests that would show whether they could protect broadly against many mutations of flu circulating annually, which is the ultimate test. And some stalk-directed antibodies might be better than others. In July in Science Immunology, McDermott and colleagues reported that the stalk antibodies against group 2 of the A viruses appear to be more broadly effective than those against group 1 viruses.

Other researchers have stabilized the stalk by attaching a new hemagglutinin head — a lollipop flavor that the human immune system has never tasted. In this case, researchers from the Icahn School of Medicine at Mount Sinai in New York City took tops from two flu strains that circulate only in birds, and connected each one to a human hemagglutinin stalk. This experimental vaccine consists of two doses. The first dose prompts the immune system to make antibodies against the stalk with the first top, and a second dose produces a second round of antibodies against the stalk with the second top. The idea is that the abundance of stem-focused antibodies — amplified from the two shots of vaccine — will come to the rescue during a natural infection from a virus that possesses a third, totally different head.
“The human immune system will try to find something it has seen before,” says Peter Palese, chairman of microbiology at Mount Sinai. In theory, the only antibodies in play will be the ones responding to the parts of the stalk that the immune system recognizes, known as the “conserved domains.”

“The $64,000 question,” according to Palese: “Will the immune response to these conserved domains be enough to elicit a broad immune system reaction?”

In 2016, Palese and colleagues described a test of the vaccine in the Journal of Virology. Six ferrets given the two doses were housed with six ferrets infected with H1N1 flu. Within 10 days, the vaccinated animals had become infected but had no symptoms or signs of being able to easily spread virus to others. A report in June in the same journal described tests of the vaccine in mice against influenza B viruses; the animals were protected from normally lethal doses of flu.

What’s not known is whether the stem-focused antibodies are enough to protect people from all virus variants. The vaccine from the Mount Sinai researchers is entering the first human safety trials with drugmaker GlaxoSmithKline.

Unhide and seek
Another approach incorporates proteins that don’t tend to mutate like the hemagglutinin head but are hidden from the immune system under normal circumstances. When these proteins are made visible to types of white blood cells called T cells, the immune system wakes up. T cells don’t make antibodies, but certain T cells hold on to a memory of foreign molecules seen before. When these pre-programmed T cells recognize an infection, they destroy the invader.

This work began in the 1990s, when researchers at the Weizmann Institute of Science in Rehovot, Israel, set out to find parts of the virus that remain unchanged from year to year. The team identified stable regions in three proteins — hemagglutinin, plus one from the virus membrane and one from the virus core. In 2003, a company called BiondVax Pharmaceuticals formed to develop and test, in humans, an experimental vaccine that takes these proteins and packages them in a way that the immune system can recognize them.

So far, almost 700 volunteers have participated in six small trials, all of which showed signs of a lasting immune response among most volunteers. Writing in February in Vaccine, the researchers reported that the stored serum of elderly volunteers who received the vaccine in 2011 showed an immune response to new strains of flu that were circulating three years later. The company is starting larger trials to see if the vaccine can actually protect people from getting sick.
Out of many, one
Other experimental vaccines take a different approach. Rather than relying on precision to hit a narrow target, microbiologist Ted Ross and colleagues at the University of Georgia in Athens are attempting to cast a wide net. The researchers are taking hemagglutinin mutations from every flu strain that has ever circulated, dumping them into a kind of scientific blender and attaching them to particles that can form the basis of a vaccine.

“The question we asked is, how can we make a vaccine against a strain we don’t even know exists?” Ross says. The technique he uses is called COBRA for computationally optimized broadly reactive antigen. A computer compiles all seemingly possible genetic iterations of a particular flu type — in this case H1N1 — and then bundles them into one molecule. It’s kind of like taking every novel in your local library and combining them into one giant book.

Last year in the Journal of Virology, Ross and colleagues described a COBRA-derived vaccine that represented almost all forms of H1N1 that have been around for the last 100 years. The vaccine protected mice against infection from strains of H1N1 that the mice had never been exposed to. “We took a bunch of different hemagglutinins and mixed them into one hemagglutinin molecule,” Ross says. “It protected against any strain of H1N1 we could throw at it.”

The study caught the attention of vaccine maker Sanofi Pasteur, which plans to test the vaccine in clinical trials. Ross’ lab is now using the same strategy to develop a vaccine against H3N2 strains, the other dominant kind of flu circulating around the world. Same approach, different library.

Meanwhile, the virus isn’t waiting around. Based on the heavy flu season in the Southern Hemisphere, some experts are predicting this year’s epidemic could be severe. It’s still too early to know whether the current vaccine will provide good protection, but someday, a super shot may remove the guesswork altogether.

Campfire legends of massive, shaggy bipeds called yetis are grounded in a less mysterious truth: bears.

Eight samples of remains such as fur, bones and teeth purportedly from mountain-dwelling yetis actually come from three different kinds of bears that live in the Himalayas, researchers report November 29 in the Proceedings of the Royal Society B. A ninth sample turned out to come from a dog.

Previous analyses of smaller fragments of “yeti” DNA yielded controversial results. The new study looks at bigger chunks of DNA, analyzing the complete mitochondrial genomes from alleged yetis and comparing them with the mitochondrial genomes of various bears, including polar bears and Tibetan brown bears.
The results also give new insight into the genetic relationships between the different bears that call the Tibetan Plateau home, which could guide efforts to protect these rare subspecies. During a period of glaciation about 660,000 years ago, Himalayan brown bears were one of the first groups to branch off and become distinct from other brown bears, the data suggest.

Tibetan brown bears, on the other hand, share a more recent common ancestor with their relatives in Eurasia and North America. They might have migrated to the area around 340,000 years ago, but were probably kept geographically isolated from Himalayan brown bears by the rugged mountain terrain.

COLLEGE PARK, Md. — Campus life typically challenges students with new opportunities for learning, discovery — and intimacy with germs. Lots of germs.

That makes dormitories and their residents an ideal natural experiment to trace the germs’ paths. “You pack a bunch of college kids into a very small environment … we’re not known as being the cleanliest of people,” says sophomore Parker Kleb at the University of Maryland in College Park. Kleb is a research assistant for an ongoing study tracking the spread of respiratory viruses through a student population. The study’s goal is to better understand how these viruses move around, in order to help keep illness at bay — all the more pressing, as the current flu season is on track to be among the worst recorded in the United States.
Called “C.A.T.C.H. the Virus,” which stands for Characterizing and Tracking College Health, the study traces the trajectory of viral infections using blood samples, nasal swabs and breath samples from ailing freshmen and their closest contacts. (Tagline: It’s snot your average research study.)

Donald Milton, an environmental and occupational health physician-scientist, heads the project. On a recent day, he described the study to a classroom of freshmen he hopes to recruit. He ticked off questions this research seeks to answer: What is it that makes people susceptible to getting sick? What makes them contagious? And how do they transmit a virus to others? “Maybe your house, your room has something to do with whether you’re at risk of getting infected,” Milton said.

He had a receptive audience: members of the College Park Scholars’ Global Public Health program. Infection control is right up their alley. “How sick do we have to be?” one student asked. It’s the culprit that matters, she’s told. The study covers acute respiratory infections due to influenza viruses, adenoviruses, coronaviruses or respiratory syncytial virus, known as RSV.

Of most interest, however, is influenza. “Flu is important to everybody,” says Milton. Influenza is thought to spread among humans three ways — touch; coughing and sneezing, which launches droplets containing virus from the lungs onto surfaces; and aerosols, smaller droplets suspended in the air that could be inhaled (SN: 6/29/13, p. 9).
How much each of these modes of transmission contributes to the spread of viruses is a point of fierce debate, Milton says. And that makes infection control difficult, especially in hospitals. “If we don’t understand how [viruses] are transmitted, it’s hard to come up with policies that are really going to work.”
Milton and his colleagues recently reported that people with the flu can shed infectious virus particles just by breathing. Of 134 fine-aerosol samples taken when patients were breathing normally, 52 contained infectious influenza virus — or 39 percent, according to the study, published online January 18 in the Proceedings of the National Academy of Sciences . Those fine-aerosol particles of respiratory tract fluid are 5 microns in diameter or less, small enough to stay suspended in the air and potentially contribute to airborne transmission of the flu, the researchers say.
“This could mean that just having good cough and sneeze etiquette — sneezing or coughing into tissues — may not be enough to limit the spread of influenza,” says virologist Andrew Pekosz at Johns Hopkins University, who was not involved with the study. “Just sitting in your office and breathing could fill the air with infectious influenza.”

The C.A.T.C.H. study aims to find out if what’s in the air is catching. In two University of Maryland dorms, carbon dioxide sensors measure how much of the air comes from people’s exhalations. In addition, laboratory tests measure how much virus sick students are shedding into the air. To get those samples, students sit in a ticket booth‒sized contraption called the Gesundheit-II and breathe into a giant cone. These data can help researchers estimate students’ airborne exposure to viruses, Milton says.

Another key dataset comes from DNA testing of the viruses infecting the students. “The virus mutates reasonably fast,” Milton says, so the more people it’s moved through, the more changes it will have. By combining this molecular chain of transmission with the social chain of transmission, the researchers will try to “establish who infected whom, and where, and how,” Milton says.

The goal is to enroll 130 students in C.A.T.C.H. It’s doubtful they’ll all get sick, but not that many students from this initial group are needed to start the ball rolling, says Jennifer German, a virologist and C.A.T.C.H. student engagement coordinator. “For every index case that has an infection we’re interested in, we’re following four additional contacts,” she says. “And then if any of those contacts becomes sick, we’ll get their contacts and so on.”

The study began in November 2017. As of the end of January, German says, researchers have collected samples from five sick students, but only one was infected with a target virus, influenza. The researchers now are following three contacts from that case.

But timing and the size of the current flu outbreak may be on the researchers’ side. Kleb, the research assistant, says that students are still waiting for this season’s flu to sweep through the dorms. “Once one person gets sick, it goes around to everyone on the floor,” he says. “I’m very interested to see what happens in the next few weeks, and how the study will hopefully benefit.”

The ghost catfish transforms from glassy to glam when white light passes through its mostly transparent body. Now, scientists know why.

The fish’s iridescence comes from light bending as it travels through microscopic striped structures in the animal’s muscles, researchers report March 13 in the Proceedings of the National Academy of Sciences.

Many fishes with iridescent flair have tiny crystals in their skin or scales that reflect light (SN: 4/6/21). But the ghost catfish (Kryptopterus vitreolus) and other transparent aquatic species, like eel larvae and icefishes, lack such structures to explain their luster.

The ghost catfish’s see-through body caught the eye of physicist Qibin Zhao when he was in an aquarium store. The roughly 5-centimeter-long freshwater fish is a popular ornamental species. “I was standing in front of the tank and staring at the fish,” says Zhao, of Shanghai Jiao Tong University. “And then I saw the iridescence.”

To investigate the fish’s colorful properties, Zhao and colleagues first examined the fish under different lighting conditions. The researchers determined its iridescence arose from light passing through the fish rather than reflecting off it. By using a white light laser to illuminate the animal’s muscles and skin separately, the team found that the muscles generated the multicolored sheen.
The researchers then characterized the muscles’ properties by analyzing how X-rays scatter when traveling through the tissue and by looking at it with an electron microscope. The team identified sarcomeres — regularly spaced, banded structures, each roughly 2 micrometers long, that run along the length of muscle fibers — as the source of the iridescence.

The sarcomeres’ repeating bands, comprised of proteins that overlap by varying amounts, bend white light in a way that separates and enhances its different wavelengths. The collective diffraction of light produces an array of colors. When the fish contracts and relaxes its muscles to swim, the sarcomeres slightly change in length, causing a shifting rainbow effect.
The purpose of the ghost catfish’s iridescence is a little unclear, says Heok Hee Ng, an independent ichthyologist in Singapore who was not involved in the new study. Ghost catfish live in murky water and seldom rely on sight, he says. But the iridescence might help them visually coordinate movements when traveling in schools, or it could help them blend in with shimmering water to hide from land predators, like some birds, he adds.

Regardless of function, Ng is excited to see scientists exploring the ghost catfish’s unusual characteristics.

“Fishes actually have quite a number of these interesting structures that serve them in many ways,” he says. “And a lot of these structures are very poorly studied.”

Tiny particles of plastic have been found everywhere — from the deepest place on the planet, the Mariana Trench, to the top of Mount Everest. And now more and more studies are finding that microplastics, defined as plastic pieces less than 5 millimeters across, are also in our bodies.

“What we are looking at is the biggest oil spill ever,” says Maria Westerbos, founder of the Plastic Soup Foundation, an Amsterdam-based nonprofit advocacy organization that works to reduce plastic pollution around the world. Nearly all plastics are made from fossil fuel sources. And microplastics are “everywhere,” she adds, “even in our bodies.”
In recent years, microplastics have been documented in all parts of the human lung, in maternal and fetal placental tissues, in human breast milk and in human blood. Microplastics scientist Heather Leslie, formerly of Vrije Universiteit Amsterdam, and colleagues found microplastics in blood samples from 17 of 22 healthy adult volunteers in the Netherlands. The finding, published last year in Environment International, confirms what many scientists have long suspected: These tiny bits can get absorbed into the human bloodstream.

“We went from expecting plastic particles to be absorbable and present in the human bloodstream to knowing that they are,” Leslie says.
The findings aren’t entirely surprising; plastics are all around us. Durable, versatile and cheap to manufacture, they are in our clothes, cosmetics, electronics, tires, packaging and so many more items of daily use. And the types of plastic materials on the market continues to increase. “There were around 3,000 [plastic materials] when I started researching microplastics over a decade ago,” Leslie says. “Now there are over 9,600. That’s a huge number, each with its own chemical makeup and potential toxicity.”

Though durable, plastics do degrade, by weathering from water, wind, sunlight or heat — as in ocean environments or in landfills — or by friction, in the case of car tires, which releases plastic particles along roadways during motion and braking.

In addition to studying microplastic particles, researchers are also trying to get a handle on nanoplastics, particles which are less than 1 micrometer in length. “The large plastic objects in the environment will break down into micro- and nanoplastics, constantly raising particle numbers,” says toxicologist Dick Vethaak of the Institute for Risk Assessment Sciences at Utrecht University in the Netherlands, who collaborated with Leslie on the study finding microplastics in human blood.

Nearly two decades ago, marine biologists began drawing attention to the accumulation of microplastics in the ocean and their potential to interfere with organism and ecosystem health (SN: 2/20/16, p. 20). But only in recent years have scientists started focusing on microplastics in people’s food and drinking water — as well as in indoor air.

Plastic particles are also intentionally added to cosmetics like lipstick, lip gloss and eye makeup to improve their feel and finish, and to personal care products, such as face scrubs, toothpastes and shower gels, for the cleansing and exfoliating properties. When washed off, these microplastics enter the sewage system. They can end up in the sewage sludge from wastewater treatment plants, which is used to fertilize agricultural lands, or even in treated water released into waterways.

What if any damage microplastics may do when they get into our bodies is not clear, but a growing community of researchers investigating these questions thinks there is reason for concern. Inhaled particles might irritate and damage the lungs, akin to the damage caused by other particulate matter. And although the composition of plastic particles varies, some contain chemicals that are known to interfere with the body’s hormones.

Currently there are huge knowledge gaps in our understanding of how these particles are processed by the human body.

How do microplastics get into our bodies?
Research points to two main entry routes into the human body: We swallow them and we breathe them in.

Evidence is growing that our food and water is contaminated with microplastics. A study in Italy, reported in 2020, found microplastics in everyday fruits and vegetables. Wheat and lettuce plants have been observed taking up microplastic particles in the lab; uptake from soil containing the particles is probably how they get into our produce in the first place.

Sewage sludge can contain microplastics not only from personal care products, but also from washing machines. One study looking at sludge from a wastewater treatment plant in southwest England found that if all the treated sludge produced there were used to fertilize soils, a volume of microplastic particles equivalent to what is found in more than 20,000 plastic credit cards could potentially be released into the environment each month.

On top of that, fertilizers are coated with plastic for controlled release, plastic mulch film is used as a protective layer for crops and water containing microplastics is used for irrigation, says Sophie Vonk, a researcher at the Plastic Soup Foundation.

“Agricultural fields in Europe and North America are estimated to receive far higher quantities of microplastics than global oceans,” Vonk says.
A recent pilot study commissioned by the Plastic Soup Foundation found microplastics in all blood samples collected from pigs and cows on Dutch farms, showing livestock are capable of absorbing some of the plastic particles from their feed, water or air. Of the beef and pork samples collected from farms and supermarkets as part of the same study, 75 percent showed the presence of microplastics. Multiple studies document that microplastic particles are also in fish muscle, not just the gut, and so are likely to be consumed when people eat seafood.

Microplastics are in our drinking water, whether it’s from the tap or bottled. The particles may enter the water at the source, during treatment and distribution, or, in the case of bottled water, from its packaging.

Results from studies attempting to quantify levels of human ingestion vary dramatically, but they suggest people might be consuming on the order of tens of thousands of microplastic particles per person per year. These estimates may change as more data come in, and they will likely vary depending on people’s diets and where they live. Plus, it is not yet clear how these particles are absorbed, distributed, metabolized and excreted by the human body, and if not excreted immediately, how long they might stick around.

Babies might face particularly high exposures. A small study of six infants and 10 adults found that the infants had more microplastic particles in their feces than the adults did. Research suggests microplastics can enter the fetus via the placenta, and babies could also ingest the particles via breast milk. The use of plastic feeding bottles and teething toys adds to children’s microplastics exposure.

Microplastic particles are also floating in the air. Research conducted in Paris to document microplastic levels in indoor air found concentrations ranging from three to 15 particles per cubic meter of air. Outdoor concentrations were much lower.

Airborne particles may turn out to be more of a concern than those in food. One study reported in 2018 compared the amount of microplastics present within mussels harvested off Scotland’s coasts with the amount of microplastics present in indoor air. Exposure to microplastic fibers from the air during the meal was far higher than the risk of ingesting microplastics from the mussels themselves.

Extrapolating from this research, immunologist Nienke Vrisekoop of the University Medical Center Utrecht says, “If I keep a piece of fish on the table for an hour, it has probably gathered more microplastics from the ambient air than it has from the ocean.”
What’s more, a study of human lung tissue reported last year offers solid evidence that we are breathing in plastic particles. Microplastics showed up in 11 of 13 samples, including those from the upper, middle and lower lobes, researchers in England reported.

Perhaps good news: Microplastics seem unable to penetrate the skin. “The epidermis holds off quite a lot of stuff from the outside world, including [nano]particles,” Leslie says. “Particles can go deep into your skin, but so far we haven’t observed them passing the barrier, unless the skin is damaged.”

What do we know about the potential health risks?
Studies in mice suggest microplastics are not benign. Research in these test animals shows that lab exposure to microplastics can disrupt the gut microbiome, lead to inflammation, lower sperm quality and testosterone levels, and negatively affect learning and memory.

But some of these studies used concentrations that may not be relevant to real-world scenarios. Studies on the health effects of exposure in humans are just getting under way, so it could be years before scientists understand the actual impact in people.

Immunologist Barbro Melgert of the University of Groningen in the Netherlands has studied the effects of nylon microfibers on human tissue grown to resemble lungs. Exposure to nylon fibers reduced both the number and size of airways that formed in these tissues by 67 percent and 50 percent, respectively. “We found that the cause was not the microfibers themselves but rather the chemicals released from them,” Melgert says.

“Microplastics could be considered a form of air pollution,” she says. “We know air pollution particles tend to induce stress in our lungs, and it will probably be the same for microplastics.”

Vrisekoop is studying how the human immune system responds to microplastics. Her unpublished lab experiments suggest immune cells don’t recognize microplastic particles unless they have blood proteins, viruses, bacteria or other contaminants attached. But it is likely that such bits will attach to microplastic particles out in the environment and inside the body.

“If the microplastics are not clean … the immune cells [engulf] the particle and die faster because of it,” Vrisekoop says. “More immune cells then rush in.” This marks the start of an immune response to the particle, which could potentially trigger a strong inflammatory reaction or possibly aggravate existing inflammatory diseases of the lungs or gastrointestinal tract.
Some of the chemicals added to make plastic suitable for particular uses are also known to cause problems for humans: Bisphenol A, or BPA, is used to harden plastic and is a known endocrine disruptor that has been linked to developmental effects in children and problems with reproductive systems and metabolism in adults (SN: 7/18/09, p. 5). Phthalates, used to make plastic soft and flexible, are associated with adverse effects on fetal development and reproductive problems in adults along with insulin resistance and obesity. And flame retardants that make electronics less flammable are associated with endocrine, reproductive and behavioral effects.

“Some of these chemical products that I worked on in the past [like the polybrominated diphenyl ethers used as flame retardants] have been phased out or are prohibited to use in new products now [in the European Union and the United States] because of their neurotoxic or disrupting effects,” Leslie says.
What are the open questions?
The first step in determining the risk of microplastics to human health is to better understand and quantify human exposure. Polyrisk — one of five large-scale research projects under CUSP, a multidisciplinary group of researchers and experts from 75 organizations across 21 European countries studying micro- and nanoplastics — is doing exactly that.

Immunotoxicologist Raymond Pieters, of the Institute for Risk Assessment Sciences at Utrecht University and coordinator of Polyrisk, and colleagues are studying people’s inhalation exposure in a number of real-life scenarios: near a traffic light, for example, where cars are likely to be braking, versus a highway, where vehicles are continuously moving. Other scenarios under study include an indoor sports stadium, as well as occupational scenarios like the textile and rubber industry.

Melgert wants to know how much microplastic is in our houses, what the particle sizes are and how much we breathe in. “There are very few studies looking at indoor levels [of microplastics],” she says. “We all have stuff in our houses — carpets, insulation made of plastic materials, curtains, clothes — that all give off fibers.”

Vethaak, who co-coordinates MOMENTUM, a consortium of 27 research and industry partners from the Netherlands and seven other countries studying microplastics’ potential effects on human health, is quick to point out that “any measurement of the degree of exposure to plastic particles is likely an underestimation.” In addition to research on the impact of microplastics, the group is also looking at nanoplastics. Studying and analyzing these smallest of plastics in the environment and in our bodies is extremely challenging. “The analytical tools and techniques required for this are still being developed,” Vethaak says.

Vethaak also wants to understand whether microplastic particles coated with bacteria and viruses found in the environment could spread these pathogens and increase infection rates in people. Studies have suggested that microplastics in the ocean can serve as safe havens for germs.

Alongside knowing people’s level of exposure to microplastics, the second big question scientists want to understand is what if any level of real-world exposure is harmful. “This work is confounded by the multitude of different plastic particle types, given their variations in size, shape and chemical composition, which can affect uptake and toxicity,” Leslie says. “In the case of microplastics, it will take several more years to determine what the threshold dose for toxicity is.”

Several countries have banned the use of microbeads in specific categories of products, including rinse-off cosmetics and toothpastes. But there are no regulations or policies anywhere in the world that address the release or concentrations of other microplastics — and there are very few consistent monitoring efforts. California has recently taken a step toward monitoring by approving the world’s first requirements for testing microplastics in drinking water sources. The testing will happen over the next several years.

Pieters is very pragmatic in his outlook: “We know ‘a’ and ‘b,’” he says. “So we can expect ‘c,’ and ‘c’ would [imply] a risk for human health.”

He is inclined to find ways to protect people now even if there is limited or uncertain scientific knowledge. “Why not take a stand for the precautionary principle?” he asks.

For people who want to follow Pieters’ lead, there are ways to reduce exposure.

“Ventilate, ventilate, ventilate,” Melgert says. She recommends not only proper ventilation, including opening your windows at home, but also regular vacuum cleaning and air purification. That can remove dust, which often contains microplastics, from surfaces and the air.

Consumers can also choose to avoid cosmetics and personal care products containing microbeads. Buying clothes made from natural fabrics like cotton, linen and hemp, instead of from synthetic materials like acrylic and polyester, helps reduce the shedding of microplastics during wear and during the washing process.

Specialized microplastics-removal devices, including laundry balls, laundry bags and filters that attach to washing machines, are designed to reduce the number of microfibers making it into waterways.

Vethaak recommends not heating plastic containers in the microwave, even if they claim to be food grade, and not leaving plastic water bottles in the sun.

Perhaps the biggest thing people can do is rely on plastics less. Reducing overall consumption will reduce plastic pollution, and so reduce microplastics sloughing into the air and water.

Leslie recommends functional substitution: “Before you purchase something, think if you really need it, and if it needs to be plastic.”

Westerbos remains hopeful that researchers and scientists from around the world can come together to find a solution. “We need all the brainpower we have to connect and work together to find a substitute to plastic that is not toxic and doesn’t last [in the environment] as long as plastic does,” she says.

A thick sphere of icy debris known as the Oort cloud shrouds the solar system. Other star systems may harbor similar icy reservoirs, and those clouds may be visible in the universe’s oldest light, researchers report.

Astronomer Eric Baxter of the University of Pennsylvania and colleagues looked for evidence of such exo-Oort clouds in maps of the cosmic microwave background, the cool cosmic glow of the first light released after the Big Bang, roughly 13.8 billion years ago. No exo-Oort clouds have been spotted yet, but the technique looks promising, the team reports November 2 in the Astronomical Journal. Finding exo-Oort clouds could help shed light on how other solar systems — and perhaps even our own — formed and evolved.
The Oort cloud is thought to be a planetary graveyard stretching between about 1,000 and 100,000 times as far from the sun as Earth. Scientist think that this reservoir of trillions of icy objects formed early in the solar system’s history, when violent movements of the giant planets as they took shape tossed smaller objects outward. Every so often, one of those frozen planetary fossils dives back in toward the sun and is visible as a comet (SN: 11/16/13, p. 14).

But it’s difficult to observe the Oort cloud directly from within it. Despite a lot of circumstantial evidence for the Oort cloud’s existence, no one has ever seen it.

Ironically, exo-Oort clouds might be easier to spot, Baxter and colleagues thought. The objects in an exo-Oort cloud wouldn’t reflect enough starlight to be seen directly, but they would absorb starlight and radiate it back out into space as heat. For the sun’s Oort cloud, that heat signal would be smeared evenly across the entire sky from Earth’s perspective. But an exo-Oort cloud’s warmth would be limited to a tiny region around its star.

Baxter and colleagues calculated that the expected temperature of an exo-Oort cloud should be about –265° Celsius, or 10 kelvins. That’s right in range for experiments that detect the cosmic microwave background, or CMB, which is about 3 kelvins.
The team used data from the CMB-mapping Planck satellite to search for areas across the sky with the right temperature (SN Online: 7/24/18). Then, the researchers compared the results with the Gaia space telescope’s ultraprecise stellar map to see if those regions surrounded stars (SN: 5/26/18, p. 5).

Although the astronomers found some intriguing signals around several bright, nearby stars, it wasn’t enough to declare victory. “That’s pretty interesting, but we can’t definitively say that it’s from an Oort cloud or not,” Baxter says.

Other ongoing CMB experiments with higher resolution, like those with the South Pole Telescope and the Atacama Cosmology Telescope in the Chilean Andes, could confirm if those hints of exo-Oort clouds are real.

“It’s a super clever observational idea,” says astronomer Nicolas Cowan of McGill University in Montreal who was not involved in the new work. “Looking for exo-Oort clouds is looking for a signature of these violent histories in other solar systems.”

Cowan has suggested that the cosmic microwave background could also be used to search for a hypothetical Planet Nine in the sun’s Oort cloud (SN: 7/23/16, p. 7). “The very coolest thing would be if we could get measurements of the exo-Oort clouds and find planets in those systems,” he says.

DNA from a 9,000-year-old baby tooth from Alaska, the oldest natural mummy in North America and remains of ancient Brazilians is helping researchers trace the steps of ancient people as they settled the Americas. Two new studies give a more detailed and complicated picture of the peopling of the Americas than ever before presented.

People from North America moved into South America in at least three migration waves, researchers report online November 8 in Cell. The first migrants, who reached South America by at least 11,000 years ago, were genetically related to a 12,600-year-old toddler from Montana known as Anzick-1 (SN: 3/22/14, p. 6). The child’s skeleton was found with artifacts from the Clovis people, who researchers used to think were the first people in the Americas, although that idea has fallen out of favor. Scientists also previously thought these were the only ancient migrants to South America.
But DNA analysis of samples from 49 ancient people suggests a second wave of settlers replaced the Clovis group in South America about 9,000 years ago. And a third group related to ancient people from California’s Channel Islands spread over the Central Andes about 4,200 years ago, geneticist Nathan Nakatsuka of Harvard University and colleagues found.
People who settled the Americas were also much more genetically diverse than previously thought. At least one group of ancient Brazilians shared DNA with modern indigenous Australians, a different group of researchers reports online November 8 in Science.
Early Americans moved into prehistoric South America in at least three migratory waves, a study proposes. Ancestral people who crossed from Siberia into Alaska first gave rise to groups that settled North America (gray arrows). The first wave of North Americans (blue) were related to Clovis people, represented by a 12,600-year-old toddler from Montana called Anzick-1. They moved into South America at least 11,000 years ago, followed by a second wave (green) whose descendants contributed most of the indigenous ancestry among South Americans today. A third migration wave (yellow) from a group that lived near California’s Channel Island moved into the Central Andes about 4,200 years ago. Dotted areas indicate that people there today still have that genetic ancestry.
Genetically related, but distinct groups of people came into the Americas and spread quickly and unevenly across the continents, says Eske Willerslev, a geneticist at the Natural History Museum of Denmark in Copenhagen and a coauthor of the Science study. “People were spreading like a fire across the landscape and very quickly adapted to the different environments they were encountering.”

Both studies offer details that help fill out an oversimplified narrative of the prehistoric Americas, says Jennifer Raff, an anthropological geneticist at the University of Kansas in Lawrence who was not involved in the work. “We’re learning some interesting, surprising things,” she says.

For instance, Willerslev’s group did detailed DNA analysis of 15 ancient Americans different from those analyzed by Nakatsuka and colleagues. A tooth from Trail Creek in Alaska was from a baby related to a group called the ancient Beringians, who occupied the temporary land mass between Alaska and Siberia called Beringia. Sometimes called the Bering land bridge, the land mass was above water before the glaciers receded at the end of the last ice age. The ancient Beringians stayed on the land bridge and were genetically distinct from the people who later gave rise to Native Americans, Willerslev and colleagues found.

The link between Australia and ancient Amazonians also hints that several genetically distinct groups may have come across Beringia into the Americas.

The Australian signature was first found in modern-day indigenous South Americans by Pontus Skoglund and colleagues (SN: 8/22/15, p. 6). No one was sure why indigenous Australians and South Americans shared DNA since the groups didn’t have any recent contact. One possibility, says Skoglund, a geneticist at the Francis Crick Institute in London and a coauthor of the Cell paper, was that the signature was very old and inherited from long-lost ancestors of both groups.

So Skoglund, Nakatsuka and colleagues tested DNA from a group of ancient Brazilians, but didn’t find the signature. Willerslev’s group, however, examined DNA from 10,400-year-old remains from Lagoa Santa, Brazil, and found the signature, supporting the idea that modern people could have inherited it from much older groups. And Skoglund is thrilled. “It’s amazing to see it confirmed,” he says.

How that genetic signature got to Brazil in the first place is still a mystery, though. Researchers don’t think early Australians paddled across the Pacific Ocean to South America. “None of us really think there was some sort of Pacific migration going on here,” Skoglund says.

That leaves an overland route through Beringia. There’s only one problem: Researchers didn’t find the Australian signature in any of the ancient remains tested from North or Central America. And no modern-day indigenous North or Central Americans tested have the signature either.

Still, Raff thinks it likely that an ancestral group of people from Asia split off into two groups, with one heading to Australia and the other crossing the land bridge into the Americas. The group that entered the Americas didn’t leave living descendants in the north. Or, because not many ancient remains have been studied, it’s possible that scientists have just missed finding evidence of this particular migration.

If Raff is right, that could mean that multiple groups of genetically distinct people made the Berigian crossing, or that one group crossed but was far more genetically diverse than researchers have realized.

The studies may also finally help lay to rest a persistent idea that some ancient remains in the Americas are not related to Native Americans today.

The Lagoa Santans from Brazil and a 10,700-year-old mummy from a place called Spirit Cave in Nevada had been grouped as “Paleoamericans” because they both had narrow skulls with low faces and protruding jaw lines, different from other Native American skull shapes. Some researchers have suggested that Paleoamericans — including the so-called Kennewick Man, whose 8,500-year-old remains were found in the state of Washington (SN: 12/26/15, p. 30) — weren’t Native Americans, but a separate group that didn’t have modern descendants.

But previous studies of Paleoamericans and Willerslev’s analysis of the Spirit Cave mummy’s DNA provide evidence that, despite their skull shapes, the Paleoamericans were not different from other Native Americans of their time. And the ancient people are more closely related to present-day Native Americans than any other group.

Willerslev presented the results about the Spirit Cave mummy to the Fallon Paiute-Shoshone tribe when the data became available. Based on the genetic results, the tribe was able to claim the mummy as an ancestor and rebury the remains.

Disinfection of public drinking water is one of the great public health success stories of the 20th century. In 1900, outbreaks of cholera and typhoid, both caused by waterborne bacteria, were common in American cities. In 1908, Jersey City, N.J., became the first U.S. city to routinely disinfect community water. Other cities and towns quickly followed, and by 1920, the typhoid rate in the United States had dropped by 66 percent.

But that battle isn’t over. Around the world, more than 2 billion people lack reliable access to safe water (SN: 8/18/18, p. 14), and half a million people die each year from diarrhea caused by contaminated water, according to the World Health Organization.
And in the United States, challenges remain. The management failures that caused the 2014 lead contamination crisis in Flint, Mich., were a wake-up call (SN: 3/19/16, p. 8), but Flint is hardly alone. Systems in other big cities are also falling short. In October, officials in Newark, N.J., scrambled to hand out home water filters after it became clear that efforts to prevent lead from leaching into drinking water were not getting the job done. In the first six months of 2017, more than 22 percent of water samples in that city exceeded federal limits for lead, according to news reports.

If big cities are struggling, small towns with skimpy budgets as well as the many people who get their water from private wells often have it harder, lacking access to the infrastructure or technology to make water reliably safe. But science can help.

In this issue, Science News staff writer Laurel Hamers digs into the latest research on water treatment technology and finds a focus on efforts to invent affordable, scalable solutions. There’s a lot of engineering and chemistry involved, not surprisingly, and also physics — it’s hard to move water efficiently through a filter while also catching the bad stuff. Her story is a testament to researcher ingenuity, and a helpful primer on how a typical municipal water treatment plant works.

As I read Hamers’ story, I realized that I didn’t know how our water is treated here in Washington, D.C., even though I live barely a mile from one of the city’s two treatment plants. (I at least get credit for knowing the water comes from the Potomac River.) So I Googled it and found a description of how that process works. Plus I found data on potential contaminants such as Giardia and Cryptosporidium, as well as information on how residents can get their water tested for lead, which can leach from pipes or fixtures.
I also learned that each spring, the Washington Aqueduct briefly switches disinfectants from chloramine to chlorine while the agency cleans the water pipes. That might explain the short-lived swimming pool smell in the tap water.

For me, this became a double win; I learned a lot about advances in water treatment technology from Hamers’ reporting, and I was motivated to seek out information about my local water supply.

If other readers feel inspired by our work to learn more, count me as a happy journalist.

A newly designed airplane prototype does away with noisy propellers and turbines.

Instead, it’s powered by ionic wind: charged molecules, or ions, flowing in one direction and pushing the plane in the other. That setup makes the aircraft nearly silent. Such stealth planes could be useful for monitoring environmental conditions or capturing aerial imagery without disturbing natural habitats below.

The aircraft is the first of its kind to be propelled in this way, researchers report in the Nov. 22 Nature. In 10 indoor test flights the small plane, which weighs about as much as a Chihuahua, traveled 40 to 45 meters for almost 10 seconds at a steady height, even gaining about half a meter of altitude over the course of a flight.
Most planes rely on spinning parts to move forward. In some, an engine turns a propeller that pushes the plane forward. Or a turbine sucks in air with a spinning fan, and then shoots out jets of gas that propel the plane forward.

Ionic wind is instead generated by a high-voltage electric field around a positively charged wire, called an emitter. The electricity, often supplied by batteries, makes electrons in the air collide with atoms and molecules, which then release other electrons. That creates a swarm of positively charged air molecules around the emitter, which are drawn to a negatively charged wire. The movement of molecules between the two wires, the ionic wind, can push a plane forward. The current design uses four sets of these wires.
Moving ions have helped other things to fly through the air, such as tiny airborne robots. But conventional wisdom said that using the approach to move something through the air as big as an airplane wasn’t possible, because adding enough battery power to propel a plane this way would make it too heavy to stay aloft. (The ion thrusters that propel spacecraft through the vacuum of space work in a very different way and aren’t functional in air.) Attempts to build ion-propelled aircraft in the 1960s weren’t very successful.
MIT aeronautics researcher Steven Barrett thought differently. With the right aircraft design and light enough batteries, flight might be possible, his initial calculations suggested. So he and his team used mathematical equations to optimize various features of the airplane — its shape, materials, power supply — and to predict how each version would fly. Then the researchers built prototypes of promising designs and tested the planes at the MIT indoor track, launching them via a bungee system.
“The models and the reality of construction don’t always match up perfectly,” Barrett says, so finding the right design took a lot of tries. But in the new study, he and his collaborators report success: 10 flights of the aircraft, which has a 5-meter wingspan and weighs just under 2.5 kilograms.

Barrett’s team isn’t the only one who thought the ionic wind method might take off. Based on calculations done in his lab, “we were confident that this could be done,” says Franck Plouraboue of the Toulouse Fluid Mechanics Institute in France, who wasn’t part of the research. “Here they’ve done it — which is fantastic!”

It’s an example of distributed electric propulsion, says Plouraboue — spreading out the thrust-generating parts of the plane, instead of having one centralized source. That’s a hot area for aircraft research right now. NASA’s X-57 Maxwell plane, for example, bears 14 battery-operated motors along its wings. Increasing the number of propellers makes the plane go farther on the same amount of energy, says Plouraboue, but also increases the drag. With ionic wind propulsion, increasing the number of wires doesn’t increase drag very much.

The plane still needs some upgrades before it’s ready for the real world: Its longest flight was only 12 seconds. And while the aircraft can maintain steady flight for a short time once launched, it can’t actually get off the ground using ionic wind.

Even with improvements, ion-propelled aircraft won’t find their niche as passenger planes, predicts Daniel Drew, an aerodynamics researcher at the University of California, Berkeley, who was not involved in the work. (Drew has designed miniature flying bots that fly using ionic propulsion.) It’s probably not feasible to scale up to something the size of a 747 — there are efficiency trade-offs as planes get bigger, he says. But down the road, the approach might be useful for small, uncrewed planes or drones.

From tales about whales to enthralling scientific histories and the memoir of a frustrated astrophysicist, 2018 was a banner year for science books. Here are Science News’ picks for the titles that should be on any science lover’s bookshelf. Find detailed reviews of many of these books in the links below and in our Editor’s Pick: Favorite books of 2018.

The Truth About Animals
Lucy Cooke

A zoologist debunks myths about bats, pandas, Adélie penguins and many other misunderstood creatures, recounting surprising stories from the animal kingdom (SN: 4/14/18, p. 26). Basic Books, $28

Spying On Whales
Nick Pyenson

In this captivating look at whales, a paleontologist dives into the animals’ past, exploring how some of Earth’s most intelligent species came to be, and their uncertain future (SN: 7/7/18, p. 29). Viking, $27

Eager
Ben Goldfarb

Some people see beavers as pests. But a science writer explains how the dam-building rodents are actually vital ecosystem engineers that can create or expand habitats that benefit the entire wildlife community (SN: 8/4/18, p. 28). Chelsea Green Publishing, $24.95

The Rise and Fall of the Dinosaurs
Steve Brusatte

In this memoir, a paleontologist blends experiences from his career with evolutionary science to take readers on an engrossing journey through time, from the beginnings of the dinosaurs to their ultimate extinction. William Morrow, $29.99

The Big Ones
Lucy Jones

A seismologist examines past catastrophic natural disasters, including volcanic eruptions, earthquakes and floods, and their impact on culture, politics and society (SN: 3/31/18, p. 26). With the past as a guide, the author warns readers to be prepared for when the next disaster strikes. Doubleday, $26.95

Losing the Nobel Prize
Brian Keating

An astrophysicist’s dream of winning a Nobel Prize turned to dust after a promising experiment failed to find the first definitive evidence of cosmic inflation. The experience revealed how the prize can hamper scientific progress (SN: 4/14/18, p. 27). W.W. Norton & Co., $27.95

The Poisoned City
Anna Clark

Weaving together history, science and reporting, a journalist explores the public health crisis that began in Flint, Mich., when lead started leaching into residents’ drinking water (SN: 7/21/18, p. 28). Metropolitan Books, $30

The Poison Squad
Deborah Blum

A Pulitzer Prize–winning journalist tells the story of a government chemist at the turn of the 20th century and his mission to make food safe in the United States. Penguin Press, $28

Aroused
Randi Hutter Epstein

The history of endocrinology makes for a strange and fascinating read, from the scientists who discovered the effects of hormones to the people whose lives have been irrevocably changed by these powerful substances (SN: 7/7/18, p. 28). W.W. Norton & Co., $26.95

Nine Pints
Rose George

Blood, the feared as well as revered substance that flows throughout the human body, has a rich historical and scientific past (SN: 10/27/18, p. 28). Metropolitan Books, $30

She Has Her Mother’s Laugh
Carl Zimmer

This comprehensive history recounts how researchers have come to understand genetic inheritance. Looking to the future, the author considers risks of gene manipulation (SN: 6/9/18, p. 29). Dutton, $30

Genetics in the Madhouse
Theodore M. Porter

Using archival records, a science historian traces the origins of the study of human heredity to insane asylums in the 1800s (SN: 7/7/18, p. 29). Princeton Univ., $35

The Tangled Tree
David Quammen

In chronicling the lives of researchers who made important advances in molecular biology and genetics, this book shows how recent findings shake up our understanding of evolution and the tree of life. Simon & Schuster, $30