concerns Studies

Some studies raise concerns about sunscreen chemicals. But if you dig deeper, evidence is still lacking, experts say. – The Washington Post

It is part of a daily routine for some, and for others, a routine source of doubt and uncertainty: to wear sunscreen or not?

Recent research has deepened the confusion. In a clinical trial published this year, researchers from the Food and Drug Administration reported that six common chemical ingredients in sunscreens permeate the skin and enter the bloodstream in amounts high enough to require extra safety testing by the FDA. Levels of the chemicals, which included oxybenzone and avobenzone, increased with each subsequent day of use.

It can feel like a lose-lose scenario: If you put sunscreen on, you risk damage from chemical ingredients. If you don’t, you risk UV damage from the sun.

Experts say there is still no evidence that chemical sunscreens cause harm, especially if used on limited areas that are most exposed to the sun. There are other ways of protecting yourself from UV rays in addition to sunscreen. And other sunscreen options exist: Studies show that mineral alternatives, including zinc dioxide and titanium dioxide, are both safe and effective.

“There’s really no reason to forgo sunscreen when we have known tested safe alternatives,” says Kanade Shinkai, a dermatologist at the University of California at San Francisco. Despite what can seem like alarming research, she adds, chemical versions are not necessarily dangerous. “The systemic absorption of chemical sunscreen does not necessarily mean that it’s unsafe or unhealthy. And avoiding the risks of UV exposure is still a very important health aim.”

Sunscreen has a decades-long history that gave it a pass onto pharmacy shelves, Shinkai says. Invented before the FDA developed standards for testing over-the-counter products for safety and effectiveness, sunscreen was grandfathered in for sale before its ingredients had been thoroughly studied.

Over time, plenty of evidence has accumulated to show that UV radiation from the sun triggers skin cancers, including melanoma, and that sunscreen helps mitigate those risks.

In one long-running study of more than 1,600 people that began in 1992, Australian researchers randomized people to either wear sunscreen or do what they normally do. After more than a decade of follow-up, results showed that, compared with the group that didn’t get instructions to slather it on, the sunscreen group developed far fewer cases of skin cancer, says Henry Lim, a dermatologist at the Henry Ford Medical Center in Detroit.

In another study published in 2012, one of the same researchers and colleagues estimated that increasing sunscreen use could lead to between 231,000 and 797,000 fewer melanomas for people with white skin in the United States by 2031.

But for decades, evidence has also been accumulating to suggest that the ingredients in sunscreen can get through our skin and into our bodies.

In a 1997 study, researchers instructed nine healthy people to apply sunscreen with a sun protection factor of at least 15 on their forearms, using the amount they would normally use. Twelve hours later, they washed the sunscreen off with soap and water. Urine samples taken before and after application showed that between 1 and 2 percent of the applied amount of oxybenzone seeped through the skin.

Then in 2008, researchers from the Centers for Disease Control and Prevention analyzed more than 2,500 urine samples collected as part of the long-running National Health and Nutrition Examination Survey. They found the sunscreen ingredient benzophenone-3 in nearly 97 percent of samples. The study couldn’t show that sunscreen was the source of the chemical in people’s bodies, Shinkai says: The same chemicals are also used on commercial products, such as outdoor lawn furniture. Still, the results were suggestive.

Testing data from the FDA finally started to come out in 2019, two decades after the agency announced its plans to systematically investigate the safety of sunscreen. The study included 24 people who applied sunscreen four times a day for four days, covering 75 percent of their bodies with each application. Participants were randomized into four groups, who received different combinations of four active ingredients (avobenzone, oxybenzone, octocrylene, and ecamsule) in creams, lotions or sprays.

Results drew plenty of attention: analyses of blood plasma showed, for the first time, concentrations of all four ingredients that exceeded levels at which FDA guidelines require more safety testing.

“It was the first study to really demonstrate that four really common ingredients that are found in the top-selling sunscreens are all absorbed into the bloodstream, and they do so at levels exceeding that safety threshold set by the FDA,” Shinkai says.

The FDA’s follow-up study in 2020 duplicated the results for three of the same ingredients and three others in 48 people. It also found levels exceeding the threshold after a single application.

Shinkai emphasized that the studies don’t show that sunscreen causes harm, and that more research is needed. “We have no idea whether there is actually any negative health impact,” she says. “We need the data.”

One reason not to freak out yet about the new findings is that the amount of sunscreen that participants were instructed to use does not mimic real-world conditions, Lim says.

Multiple studies suggest that, when left to their own whims, people use 80 percent less sunscreen than the 2 milligrams per centimeter of skin enforced in the study. Study participants also covered most of their bodies with sunscreen multiple times a day, whereas typical use is far less extensive.

“Most of us only do that for the three days a year we go to Florida,” Shinkai says.

Even if sunscreen chemicals do get into the bloodstream, it is not clear that they cause harm there, either.

Animal studies have raised concerns about endocrine disruption and reproductive issues. But animals are not people, Lim says. And despite decades of sunscreen use, there has been no population-wide signal that rates of infertility, birth defects or other health problems are higher in people who use more sunscreen or in places where people apply more of it.

So far, safety research has included only healthy adults, leaving a dearth of information about potential risks to pregnant women and children. Because children’s bodies have a relatively larger surface area compared with adults, absorption is theoretically higher, Kanade says. Lim advises his pregnant patients to use mineral sunscreens, which have been studied extensively.

To stay safe from the sun, researchers also recommend looking beyond sunscreen to other strategies. Wear hats, sunglasses and clothing. Concentrate time outdoors during the hours of the day when the sun is not as intense — early in the morning or later in the afternoon. Sit in the shade. And take a vitamin D supplement to avoid inconsistent evidence about how much of the vitamin people manage to get from sun exposure.

“What I tell all my patients is that we do know that excessive sun exposure is not good for your skin, from wrinkling to skin cancer,” Lim says.

Protecting yourself requires a multipronged approach, he adds.

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Coronavirus Studies

Studies of coronavirus evolution stir up a controversy for scientists on social media – Yahoo Money

A graphic generated by Nextstrain shows how different variants of the SARS-CoV-2 coronavirus have spread around the world. Purple streaks show where the virus was transmitted from China, green and yellow-green streaks show transmission from Europe, and red streaks show transmission from the United States. ( Graphic)

Is the coronavirus behind COVID-19 turning into a more insidious pathogen? Or are such claims overblown?

A fast-moving debate over virus evolution illustrates how not-yet-vetted reports about the course of the coronavirus outbreak can go, um, viral — and how important social media channels have become in the global discussion of the science behind the pandemic.

Johns Hopkins University reports nearly 3.7 million confirmed cases around the world, with a global death toll of more than 250,000. The United States accounts for 1.2 million cases and 71,000 deaths so far, and that toll could double before the worst is over.” data-reactid=”25″ type=”text”>The nature of SARS-CoV-2, the virus that causes COVID-19, is of such great interest because the disease is so deadly and disruptive: As of today, Johns Hopkins University reports nearly 3.7 million confirmed cases around the world, with a global death toll of more than 250,000. The United States accounts for 1.2 million cases and 71,000 deaths so far, and that toll could double before the worst is over.

Every day, several hundred new studies about SARS-CoV-2 and COVID-19 — most of which haven’t yet gone through the traditional peer-review process — go online, to face scrutiny by researchers and a wide swath of the general public.

One study got more than the usual traction today: The research project, led by scientists at Los Alamos National Laboratory and the University of Sheffield, looked at the way 14 variants of the virus have spread across the world.

The latest COVID-19 developments in Seattle and the world of tech” data-reactid=”28″ type=”text”>Coronavirus Live Updates: The latest COVID-19 developments in Seattle and the world of tech

The resulting paper was filed to the BioRxiv preprint server last week but has not yet been peer-reviewed. It concluded that one particular variant known as D614G is “of urgent concern.” That variant, a descendant of a form of the virus that started out in China, began spreading in Europe in early February and eventually made the leap to other parts of the world.” data-reactid=”29″ type=”text”>The resulting paper was filed to the BioRxiv preprint server last week but has not yet been peer-reviewed. It concluded that one particular variant known as D614G is “of urgent concern.” That variant, a descendant of a form of the virus that started out in China, began spreading in Europe in early February and eventually made the leap to other parts of the world.

“When introduced to new regions, it repeatedly and rapidly becomes the dominant form,” the researchers noted.

The concern was that the virus had evolved to become more transmissible, and that interventions aimed at curbing the pandemic might not be as successful as hoped. People who survived a bout with one variant of the virus might still fall prey to the increasingly dominant variant, the researchers said.

quoted by the Los Angeles Times. “Please be encouraged by knowing the global scientific community is on this, and we are cooperating with each other in ways I have never seen … in my 30 years as a scientist.”” data-reactid=”32″ type=”text”>“We cannot afford to be blindsided as we move vaccines and antibodies into clinical testing,” lead study author Bette Korber said in a Facebook post quoted by the Los Angeles Times. “Please be encouraged by knowing the global scientific community is on this, and we are cooperating with each other in ways I have never seen … in my 30 years as a scientist.”

It didn’t take long for the scientific community to start assessing the team’s conclusions — and the way they were being reported to the general public. Cornell University virologist Brian Wasik pulled no punches on Twitter:

This LATimes article is INFURIATING. So much misinformation based on just that preprint. They took quotes from the author’s PERSONAL FACEBOOK PAGE. An anonymous quote that this is ‘classic Darwinian evolution.’ Commentary on viral load and pathogenesis from a toxicologist.

— Brian Wasik (@BrianRWasik) May 5, 2020

she tweeted.” data-reactid=”35″ type=”text”>And he wasn’t alone. Columbia University’s Angela Rasmussen said the report made her blood boil. “There is no evidence that the dominant strain is such because it is ‘more contagious,’ ” she tweeted.

Harvard University’s Bill Hanage laid out an alternate explanation in his own Twitter thread, posted way back on Friday. He argued that D614G might have become the dominant variant of the virus simply because of a metaphorical roll of the dice:

This preprint has been getting attention. It claims that the SARS-CoV-2 virus is mutating into a more transmissible form as the pandemic wears on. I think those claims are suspect, to say the least 1/n

— Bill Hanage (@BillHanage) May 2, 2020

Major observation: a specific mutation in the spike protein of the virus has been in a higher fraction of cases as the pandemic has worn on in multiple places. Given the role of the spike protein in entry of the virus to cells this might be reasonable. Now for the cold water 2/n

— Bill Hanage (@BillHanage) May 2, 2020

We need to distinguish between selection, in which a variant becomes more common because it leaves more descendants, and founder effects in which a variant becomes more common because it was fortunate rolling the dice 3/n

— Bill Hanage (@BillHanage) May 2, 2020

by that, I mean this variant might have been lucky and got introduced to places outside Wuhan and different approaches to social distancing early on. It’s not about the virus, it’s the environment and the opportunities for transmission 4/n

— Bill Hanage (@BillHanage) May 2, 2020

how Hanage uses data from Washington state to back up his view. Here’s his bottom line: “Right now there are better ways of fighting the pandemic than worrying about different strains defined by one non-synonymous SNP. … If anyone who does not know what it is already googles ‘non-synonymous SNP,’ I will be delighted.”” data-reactid=”45″ type=”text”>You’ll have to read through the entire 15-tweet thread to find out how Hanage uses data from Washington state to back up his view. Here’s his bottom line: “Right now there are better ways of fighting the pandemic than worrying about different strains defined by one non-synonymous SNP. … If anyone who does not know what it is already googles ‘non-synonymous SNP,’ I will be delighted.”

started tracing coronavirus evolution back in January. Ever since then, he and his colleagues at Nextstrain and the Seattle Flu Study have been comparing genetic fingerprints from viral variants to map how they’re spreading globally.” data-reactid=”46″ type=”text”>But wait … there’s more: This afternoon brought a more ambiguous verdict from Trevor Bedford, the epidemiologist at Seattle’s Fred Hutchinson Cancer Research Center who started tracing coronavirus evolution back in January. Ever since then, he and his colleagues at Nextstrain and the Seattle Flu Study have been comparing genetic fingerprints from viral variants to map how they’re spreading globally.

Bedford said there’s some evidence to back up the claims made by Korber and her colleagues, but that the case is “far from conclusive.” He also stressed that D614G doesn’t appear to be more dangerous than the other variants, even if it’s currently more dominant. Here’s the full thread:

I wanted to address the hypothesis put forward in Korber et al ( that the mutation in spike protein D614G causes an increase in transmissibility of SARS-CoV-2 virus. I find this hypothesis to be plausible, but far from proven. 1/16

— Trevor Bedford (@trvrb) May 6, 2020

I’ve been watching D614G closely as mutations in spike protein deserve added attention due to spike’s role in binding to the human ACE2 receptor. 2/16

— Trevor Bedford (@trvrb) May 6, 2020

This D614G mutation occurred in the transmission chain that initially seeded the European outbreak in ~Jan 2020. Almost all viruses possessing this mutation descend from this initial introduction into Europe. 3/16

— Trevor Bedford (@trvrb) May 6, 2020

European viruses are enriched for D614G because of a founder effect in which the initial introduction included this mutation. If we look at the geographic distribution of D vs G in sequenced viruses we see Europe with G, Asia largely D and a mix in the US and Australia. 4/16

— Trevor Bedford (@trvrb) May 6, 2020

The primary finding of Korber et al is that D614G appears to be increasing in frequency over time in sequenced SARS-CoV-2 genomes. I strongly caution against interpretation of selective effects in the global frequency of D614G. 5/16

— Trevor Bedford (@trvrb) May 6, 2020

Its global frequency is heavily confounded with epidemiological circumstance, ie perhaps G is prevalent because it got lucky in the European introduction. However, regional frequencies should be more robust to this confounding (although not perfectly so). 6/16

— Trevor Bedford (@trvrb) May 6, 2020

This figure recapitulates the Korber et al findings using @nextstrain. Here, I’ve shown states in the US and Australia with more than 70 sequences available and our estimate of frequency of D (green) vs G (yellow) from March 1 to April 15. 7/16

— Trevor Bedford (@trvrb) May 6, 2020

It’s still very possible that this pattern could emerge from repeated introductions from Europe / NYC in the US spreading the G variant and multiple introductions from Europe spreading G in Australia. 9/16

— Trevor Bedford (@trvrb) May 6, 2020

The alternative explanation put forth by Korber et al is that this pattern is due to the G variant being more transmissible. I think this is possible, but it’s difficult to distinguish between these hypotheses with this frequency data alone. 10/16

— Trevor Bedford (@trvrb) May 6, 2020

Additional evidence for the hypothesis of a functional effect of D614G comes from Korber et al’s observation that the G variant has lower cycle threshold (Ct) value in clinical specimens from Sheffield. This indicates a possible higher viral load in these individuals. 11/16

— Trevor Bedford (@trvrb) May 6, 2020

There are confounders to worry about here as well (primarily time from symptom onset to specimen collection), but I believe replication in two study populations is suggestive of an effect of D vs G on Ct value and possibly viral load. 13/16

— Trevor Bedford (@trvrb) May 6, 2020

Both Korber et al and our analysis show no measurable effect on patient outcome. Hence, the hypothesis at this point is entirely in terms of transmissibility rather than severity. 14/16

— Trevor Bedford (@trvrb) May 6, 2020

Overall, I would refer everyone to @edyong209‘s piece on handling uncertainty during the pandemic ( I don’t agree with takes that there is “no evidence” that G is more transmissible. There is some evidence, but it’s far from conclusive. 15/16

— Trevor Bedford (@trvrb) May 6, 2020

We have to live with this uncertainty over the functional impact of D614G while more data is gathered. We need:

1. Cell culture studies to demonstrate effect in vitro

2. Further clinical comparisons between patients with D vs G

3. More careful epidemiological analysis


— Trevor Bedford (@trvrb) May 6, 2020

“Visible Human” figurines provid

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Evidence Studies

New Studies Add to Evidence that Children May Transmit the Coronavirus – The New York Times

Experts said the new data suggest that cases could soar in many U.S. communities if schools reopen soon.

Credit…Eric Gaillard/Reuters

Among the most important unanswered questions about Covid-19 is this: What role do children play in keeping the pandemic going?

Fewer children seem to get infected by the coronavirus than adults, and most of those who do have mild symptoms, if any. But do they pass the virus on to adults and continue the chain of transmission?

The answer is key to deciding whether and when to reopen schools, a step that President Trump urged states to consider before the summer.

Two new studies offer compelling evidence that children can transmit the virus. Neither proved it, but the evidence was strong enough to suggest that schools should be kept closed for now, many epidemiologists who were not involved in the research said.

Many other countries, including Israel, Finland, France, Germany, the Netherlands and the United Kingdom have all either reopened schools or are considering doing so in the next few weeks.

In some of those countries, the rate of community transmission is low enough to take the risk. But in others, including the United States, reopening schools may nudge the epidemic’s reproduction number — the number of new infections estimated to stem from a single case, commonly referred to as R0 — to dangerous levels, epidemiologists warned after reviewing the results from the new studies.

In one study, published last week in the journal Science, a team analyzed data from two cities in China — Wuhan, where the virus first emerged, and Shanghai — and found that children were about a third as susceptible to coronavirus infection as adults were. But when schools were open, they found, children had about three times as many contacts as adults, and three times as many opportunities to become infected, essentially evening out their risk.

Based on their data, the researchers estimated that closing schools is not enough on its own to stop an outbreak, but it can reduce the surge by about 40 to 60 percent and slow the epidemic’s course.

“My simulation shows that yes, if you reopen the schools, you’ll see a big increase in the reproduction number, which is exactly what you don’t want,” said Marco Ajelli, a mathematical epidemiologist who did the work while at the Bruno Kessler Foundation in Trento, Italy.

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The second study, by a group of German researchers, was more straightforward. The team tested children and adults and found that children who test positive harbor just as much virus as adults do — sometimes more — and so, presumably, are just as infectious.

“Are any of these studies definitive? The answer is ‘No, of course not,’” said Jeffrey Shaman, an epidemiologist at Columbia University who was not involved in either study. But, he said, “to open schools because of some uninvestigated notion that children aren’t really involved in this, that would be a very foolish thing.”

The German study was led by Christian Drosten, a virologist who has ascended to something like celebrity status in recent months for his candid and clear commentary on the pandemic. Dr. Drosten leads a large virology lab in Berlin that has tested about 60,000 people for the coronavirus. Consistent with other studies, he and his colleagues found many more infected adults than children.

The team also analyzed a group of 47 infected children between ages 1 and 11. Fifteen of them had an underlying condition or were hospitalized, but the remaining were mostly free of symptoms. The children who were asymptomatic had viral loads that were just as high or higher than the symptomatic children or adults.

“In this cloud of children, there are these few children that have a virus concentration that is sky-high,” Dr. Drosten said.

He noted that there is a significant body of work suggesting that a person’s viral load tracks closely with their infectiousness. “So I’m a bit reluctant to happily recommend to politicians that we can now reopen day cares and schools.”

Dr. Drosten said he posted his study on his lab’s website ahead of its peer review because of the ongoing discussion about schools in Germany.

Many statisticians contacted him via Twitter suggesting one or another more sophisticated analysis. His team applied the suggestions, Dr. Drosten said, and even invited one of the statisticians to collaborate.

“But the message of the paper is really unchanged by any type of more sophisticated statistical analysis,” he said. For the United States to even consider reopening schools, he said, “I think it’s way too early.”

In the China study, the researchers created a contact matrix of 636 people in Wuhan and 557 people in Shanghai. They called each of these people and asked them to recall everyone they’d had contact with the day before the call.

They defined a contact as either an in-person conversation involving three or more words or physical touch such as a handshake, and asked for the age of each contact as well as the relationship to the survey participant.

Comparing the lockdown with a baseline survey from Shanghai in 2018, they found that the number of contacts during the lockdown decreased by about a factor of seven in Wuhan and eight in Shanghai.

“There was a huge decrease in the number of contacts,” Dr. Ajelli said. “In both of those places, that explains why the epidemic came under control.”

The researchers also had access to a rich data set from Hunan province’s Center for Disease Control and Prevention. Officials in the province traced 7,000 contacts of 137 confirmed cases, observed them over 14 days and tested them for coronavirus infection. They had information not just for people who became ill, but for those who became infected and remained asymptomatic, and for anyone who remained virus-free.

Data from hospitals or from households tend to focus only on people who are symptomatic or severely ill, Dr. Ajelli noted. “This kind of data is better.”

The researchers stratified the data from these contacts by age and found that children between the ages of 0 and 14 years are about a third less susceptible to coronavirus infection than those ages 15 to 64, and adults 65 or older are more susceptible by about 50 percent.

They also estimated that closing schools can lower the reproduction number — again, the estimate of the number of infections tied to a single case — by about 0.3; an epidemic starts to grow exponentially once this metric tops 1.

In many parts of the United States, the number is already hovering around 0.8, Dr. Ajelli said. “If you’re so close to the threshold, an addition of 0.3 can be devastating.”

However, some other experts noted that keeping schools closed indefinitely is not just impractical, but may do lasting harm to children.

Jennifer Nuzzo, an epidemiologist at Johns Hopkins University’s Bloomberg School of Public Health, said the decision to reopen schools cannot be made based solely on trying to prevent transmission.

“I think we have to take a holistic view of the impact of school closures on kids and our families,” Dr. Nuzzo said. “I do worry at some point, the accumulated harms from the measures may exceed the harm to the kids from the virus.”

E-learning approaches may temporarily provide children with a routine, “but any parent will tell you it’s not really learning,” she said. Children are known to backslide during the summer months, and adding several more months to that might permanently hurt them, and particularly those who are already struggling.

Children also need the social aspects of school, and for some children, home may not even be a safe place, she said.

“I’m not saying we need to absolutely rip off the Band-aid and reopen schools tomorrow,” she said, “but we have to consider these other endpoints.”

Dr. Nuzzo also pointed to a study in the Netherlands, conducted by the Dutch government, which concluded that “patients under 20 years play a much smaller role in the spread than adults and the elderly.”

But other experts said that study was not well designed because it looked at household transmission. Unless the scientists deliberately tested everyone, they would have noticed and tested only more severe infections — which tend to be among adults, said Bill Hanage, an epidemiologist at the Harvard T.H. Chan School of Public Health.

“Assumptions that children are not involved in the epidemiology, because they do not have severe illness, are exactly the kind of assumption that you really, really need to question in the face of a pandemic,” Dr. Hanage said. “Because if it’s wrong, it has really pretty disastrous consequences.”

A new study by the National Institutes of Health may help provide more information to guide decisions in the United States. The project, called Heros, will follow 6,000 people from 2,000 families and collect information on which children get infected with the virus and whether they pass it on to other family members.

The experts all agreed on one thing: that governments should hold active discussions on what reopening schools looks like. Students could be scheduled to come to school on different days to reduce the number of people in the building at one time, for example; desks could be placed six feet apart; and schools could avoid having students gather in large groups.

Teachers with underlying health conditions or of advanced age should be allowed to opt out and given alternative jobs outside the classroom, if possible, Dr. Nuzzo said, and children with underlying conditions should continue to learn from home.

The leaders of the two new studies, Dr. Drosten and Dr. Ajelli, were both more circumspect, saying their role is merely to provide the data that governments can use to make policies.

“I’m somehow the bringer of the bad news but I can’t change the news,” Dr. Drosten said. “It’s in the data.”

  • Updated April 11, 2020

    • What should I do if I feel sick?

      If you’ve been exposed to the coronavirus or think you have, and have a fever or symptoms like a cough or difficulty breathing, call a doctor. They should give you advice on whether you should be tested, how to get tested, and how to seek medical treatment without potentially infecting or exposing others.

    • When will this end?

      This is a difficult question, because a lot depends on how well the virus is contained. A better question might be: “How will we know when to reopen the country?” In an American Enterprise Institute report, Scott Gottlieb, Caitlin Rivers, Mark B. McClellan, Lauren Silvis and Crystal Watson staked out four goal posts for recovery: Hospitals in the state must be able to safely treat all patients requiring hospitalization, without resorting to crisis standards of care; the state needs to be able to at least test everyone who has symptoms; the state is able to conduct monitoring of confirmed cases and contacts; and there must be a sustained reduction in cases for at least 14 days.

    • Should I wear a mask?

      The C.D.C. has recommended that all Americans wear cloth masks if they go out in public. This is a shift in federal guidance reflecting new concerns that the coronavirus is being spread by infected people who have no symptoms. Until now, the C.D.C., like the W.H.O., has advised that ordinary people don’t need to wear masks unless they are sick and coughing. Part of the reason was to preserve medical-grade masks for health care workers who desperately need them at a time when they are in continuously short supply. Masks don’t replace hand washing and social distancing.

    • How does coronavirus spread?

      It seems to spread very easily from person to person, especially in homes, hospitals and other confined spaces. The pathogen can be carried on tiny respiratory droplets that fall as they are coughed or sneezed out. It may also be transmitted when we touch a contaminated surface and then touch our face.

    • Is there a vaccine yet?

      No. Clinical trials are underway in the United States, China and Europe. But American officials and pharmaceutical executives have said that a vaccine remains at least 12 to 18 months away.

    • What makes this outbreak so different?

      Unlike the flu, there is no known treatment or vaccine, and little is known about this particular virus so far. It seems to be more lethal than the flu, but the numbers are still uncertain. And it hits the elderly and those with underlying conditions — not just those with respiratory diseases — particularly hard.

    • What if somebody in my family gets sick?

      If the family member doesn’t need hospitalization and can be cared for at home, you should help him or her with basic needs and monitor the symptoms, while also keeping as much distance as possible, according to guidelines issued by the C.D.C. If there’s space, the sick family member should stay in a separate room and use a separate bathroom. If masks are available, both the sick person and the caregiver should wear them when the caregiver enters the room. Make sure not to share any dishes or other household items and to regularly clean surfaces like counters, doorknobs, toilets and tables. Don’t forget to wash your hands frequently.

    • Should I stock up on groceries?

      Plan two weeks of meals if possible. But people should not hoard food or supplies. Despite the empty shelves, the supply chain remains strong. And remember to wipe the handle of the grocery cart with a disinfecting wipe and wash your hands as soon as you get home.

    • Should I pull my money from the markets?

      That’s not a good idea. Even if you’re retired, having a balanced portfolio of stocks and bonds so that your money keeps up with inflation, or even grows, makes sense. But retirees may want to think about having enough cash set aside for a year’s worth of living expenses and big payments needed over the next five years.

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