Month: March 2022

At first, Lauren Nichols tried to explain away her symptoms. In early March, the healthy 32-year-old felt an intense burning sensation, like acid reflux, when she breathed. Embarrassed, she didn’t initially seek medical care. When her shortness of breath kept getting worse, her doctor tested her for Covid-19.

Her results came back positive. But for Nichols, that was just the beginning. Over the next eight weeks, she developed wide and varied symptoms, including extreme and chronic fatigue, diarrhea, nausea, tremors, headaches, difficulty concentrating, and short-term memory loss.

“The guidelines that were provided by the CDC [Centers for Disease Control and Prevention] were not appropriately capturing the symptoms that I was experiencing, which in turn meant that the medical community was unable to ‘validate’ my symptoms,” she says. “This became a vicious cycle of doubt, confusion, and loneliness.”

An estimated 40 to 45 percent of people with Covid-19 may be asymptomatic, and others will have a mild illness with no lasting symptoms. But Nichols is one of many Covid-19 patients who are finding their recovery takes far longer than the two weeks the World Health Organization says people with mild cases can expect. (The WHO says those with severe or critical cases can expect three to six weeks of recovery.)

Because Covid-19 is a new disease, there are no studies about its long-term trajectory for those with more severe symptoms; even the earliest patients to recover in China were only infected a few months ago. But doctors say the novel coronavirus can attach to human cells in many parts of the body and penetrate many major organs, including the heart, kidneys, brain, and even blood vessels.

“The difficulty is sorting out long-term consequences,” says Joseph Brennan, a cardiologist at the Yale School of Medicine. While some patients may fully recover, he and other experts worry others will suffer long-term damage, including lung scarring, heart damage, and neurological and mental health effects.

The UK National Health Service assumes that of Covid-19 patients who have required hospitalization, 45 percent will need ongoing medical care, 4 percent will require inpatient rehabilitation, and 1 percent will permanently require acute care. Other preliminary evidence, as well as historical research on other coronaviruses like severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS), suggests that for some people, a full recovery might still be years off. For others, there may be no returning to normal.

There’s a lot we still don’t know, but here are a few of the most notable potential long-term impacts that are already showing up in some Covid-19 patients.

Lung scarring

Melanie Montano, 32, who tested positive for Covid-19 in March, says that more than seven weeks after she first got sick, she still experiences symptoms on and off, including burning in her lungs and a dry cough.

Brennan says symptoms like that occur because “this virus creates an incredibly aggressive immune response, so spaces [in the lungs] are filled with debris and pus, making your lungs less pliable.”

On CT scans, while normal lungs appear black, Covid-19 patients’ lungs frequently have lighter gray patches, called “ground-glass opacities” — which may not heal.

One study from China found that this ground-glass appearance showed up in scans of 77 percent of Covid-19 patients. In another study out of China, published in Radiology, 66 of 70 hospitalized patients had some amount of lung damage in CT scans, and more than half had the kind of lesions that are likely to develop into scars. (A third study from China suggests this is not just for critically ill patients; its authors found that of 58 asymptomatic patients, 95 percent also had evidence of these ground-glass opacities in their lungs. More than a quarter of these individuals went on to develop symptoms within a few days.)

“These kinds of tissue changes can cause permanent damage,” says Ali Gholamrezanezhad, a radiologist at the Keck School of Medicine at the University of Southern California.

Although it’s still too early to know if patients with ongoing lung symptoms like Montano will have permanent lung damage, doctors can learn more about what to expect from looking back to people who have recovered from SARS and MERS, other coronaviruses that resulted in similar lung tissue changes.

One small longitudinal study published in Nature followed 71 SARS patients from 2003 until 2018 and found that more than a third had reduced lung capacity. MERS is a little harder to extrapolate from, since fewer than 2,500 people were infected, and somewhere between 30 and 40 percent died. But one study found that about a third of 36 MERS survivors also had long-term lung damage.

Gholamrezanezhad has recently done a literature review of SARS and MERS and says that for this subset of people, “The pulmonary function never comes back; their ability to do normal activities never goes back to baseline.”

Additionally, Covid-19 scarring rates may end up being higher than SARS and MERS patients because those illnesses often attacked only one lung. But Covid-19 appears to often affect both lungs, which Gholamrezanezhad says escalates the risks of lung scarring.

He has already seen residual scarring in Covid-19 patients and is now designing a study to identify what factors might make some people at higher risk of permanent damage. He suspects having any type of underlying lung disease, like asthma, or other health conditions, like hypertension, might increase the risk of having longer-term lung issues. Additionally, “the older you are, probably the higher your chance of scarring,” he says.

For people with this kind of lung scarring, normal activities may become more challenging. “Routine things, like running up a flight of stairs, would leave these individuals gasping for air,” Brennan says.

Stroke, embolisms, and blood clotting

Many patients hospitalized for Covid-19 are experiencing unexpectedly high rates of blood clots, likely due to inflammatory responses to the infection. These can cause lung blockages, strokes, heart attacks, and other complications with serious, lasting effects.

Blood clots that form in or reach the brain can cause a stroke. Although strokes are more typically seen in older people, strokes are now being reported even in young Covid-19 patients. In Wuhan, China, about 5 percent of hospitalized Covid-19 patients had strokes, and a similar pattern was reported with SARS.

In younger people who have strokes, mortality rates are relatively low compared to those who are older, and many people recover. But studies show only between 42 and 53 percent are able to return to work.

Blood clots can also cut off circulation to part of the lungs, a condition known as a pulmonary embolism, which can be deadly. In France, two studies suggest that between 23 and 30 percent of people with severe Covid-19 are also having pulmonary embolisms.

One analysis found that after a pulmonary embolism, “symptoms and functional limitations are frequently reported by survivors.” These include fatigue, heart palpitations, shortness of breath, marked limitation of physical activity, and inability to do physical activity without discomfort.

Blood clots in other major organs can also cause serious problems. Renal failure has been a common challenge in many severe Covid-19 patients, and patients’ clotted blood has been clogging dialysis machines. Some of these acute kidney injuries may be permanent, requiring ongoing dialysis.

Clots outside organs can be serious, too. Deep vein thrombosis, for example, occurs when a blood clot forms in a vein, often the legs. Nick Cordero, a Tony-nominated Broadway and television actor, recently had to have his right leg amputated after Covid-related blood clots.

Abnormal blood clotting even seems to be happening in people after they’ve appeared to recover. One 32-year-old woman in Chicago, for example, had been discharged from the hospital for a week when she died suddenly with a severely swollen leg, a sign of deep vein thrombosis, according to local broadcaster WGN9. Or take Troy Randle, a 49-year-old cardiologist in New Jersey, who was declared safe to go back to work after recovering from Covid-19 when he developed a vicious headache. A CT scan confirmed he’d had a stroke.

Although there’s still a shortage of data, one study found that as many as 31 percent of ICU patients with Covid-19 infections had these kinds of clotting problems. In the meantime, the International Society on Thrombosis and Haemostasis has issued guidelines that recovered Covid-19 patients should continue taking anticoagulants even after being discharged from the hospital.

Heart damage

Being critically ill, especially with low oxygen levels, puts additional stress on the heart. But doctors now think that in Covid-19 patients, viral particles might also be specifically inflaming the heart muscle. (The heart has many ACE2 receptors, which scientists have identified as an entry point for the SARS-CoV-2 virus.)

“In China, doctors noted some people coming [in] with chest pain,” says Mitchell Elkind, president-elect of the American Heart Association and professor of neurology and epidemiology at Columbia University. “They had a heart attack, and then developed Covid symptoms or tested positive after.”

One study from Wuhan in January found 12 percent of Covid-19 patients had signs of cardiovascular damage. These patients had higher levels of troponin, a protein released in the blood by an injured heart muscle. Since then, other reports suggest the virus may directly cause acute myocarditis and heart failure. (Heart failure was also seen with MERS and is known to be correlated with even the seasonal flu.)

In March, another study looked at 416 hospitalized Covid-19 patients and found 19 percent showed signs of heart damage. University of Texas Health Science Center researchers warn that in survivors, Covid-19 may cause lingering cardiac damage, as well as making existing cardiovascular problems worse, further increasing the risk for heart attack and stroke.

A pulmonary critical care doctor at Mount Sinai Hospital in New York City, for example, recovered from Covid-19, only to learn she had developed cardiomyopathy, a condition in which your heart has trouble delivering blood around your body. Although previously healthy, when she returned to work, she told NBC, “I couldn’t run around like I always do.”

The specific consequences may vary depending on how the heart is affected. For example, Covid-19 has been linked to myocarditis, a condition where inflammation weakens the heart, creates scar tissue, and makes it work harder to circulate the body’s oxygen. The Myocarditis Foundation recommends these patients avoid cigarettes and alcohol, and stay away from rigorous exercise until approved by their doctor.

Neurocognitive and mental health impacts

Covid-19 also seems to affect the central nervous system, with potentially long-lasting consequences. In one study from China, more than a third of 214 people hospitalized with confirmed Covid-19 had neurological symptoms, including dizziness, headaches, impaired consciousness, vision, taste/smell impairment, and nerve pain while they were ill. These symptoms were more common in patients with severe cases, where the incidence increased to 46.5 percent. Another study in France found neurologic features in 58 of 64 critically ill Covid-19 patients.

As the pandemic goes on, Elkind says, “We need to be on the lookout for long-term neurocognitive problems.”

Looking back to SARS and MERS suggests that Covid-19 patients may have slightly delayed onset of neurological impacts. Andrew Josephson, a doctor at the University of California San Francisco, wrote in JAMA, “Although the SARS epidemic was limited to about 8,000 patients worldwide, there were some limited reports of neurologic complications of SARS that appeared in patients 2 to 3 weeks into the course of the illness.” These included muscular weakness, burning or prickling, and numbness, and the breakdown of muscle tissue into the blood. Neurological injuries, including impaired balance and coordination, confusion, and coma, were also found with MERS.

Long-term complications of Covid-19 — whether caused by the virus itself or the inflammation it triggers — could include decreased attention, concentration, and memory, as well as dysfunction in peripheral nerves, “the ones that go to your arms, legs, fingers, and toes,” Elkind says.

There are other cognitive implications for people who receive intensive treatment in hospitals. For example, delirium — an acutely disturbed state of mind that can result in confusion and seeing or hearing things that aren’t there — affects a third or more of ICU patients, and research suggests the presence of delirium during severe illness predicts future long-term cognitive decline.

Previous research on acute respiratory distress syndrome (ARDS) more generally may also provide clues to what neurological issues critically ill Covid-19 patients might see after leaving the hospital.

Research shows one in five ARDS survivors experiences long-term cognitive impairment, even five years after being discharged. Continuing impairments can include short-term memory problems and difficulty with learning and executive function. These can lead to challenges like difficulty working, impaired money management, or struggling to perform daily tasks.

ARDS survivors frequently have increased rates of depression and anxiety, and many experience post-traumatic stress. Although it’s still too early to have much data on Covid-19, during the SARS outbreak, former patients struggled with psychological distress and stress for at least a year after the outbreak.

“I felt imprisoned within my body, imprisoned within my home, and tremendously ignored and misunderstood by the general public, and even those closest to me,” Nichols says about her battle with Covid-19. “I feel incredibly alone.”

Jane, who prefers to use a pseudonym because she fears retribution at the hospital where she works, tested positive for Covid-19 more than a month ago. She’s still struggling with fevers, heart issues, and neurological issues, but the most difficult part, she says, is how tired she is of “being treated like I am a bomb that no one knows how to disarm.” Jane, a nurse who cared for AIDS patients during the ’90s, says, “This is exactly what those people went through. There is a terrible stigma.” In addition to the stigma, uncertainty has added to her mental health burden.

“People need to know this disease can linger and wreck your life and health,” she says. “And no one knows what to do for us.”

Childhood inflammation, male infertility, and other possible lasting effects

The novel coronavirus continues to frustrate scientists and patients alike with its mysteries. One of these is a small but growing number of children who recently began showing up at doctors’ offices in Britain, Italy, and Spain with strange symptoms, including a rash, a high fever, and heart inflammation.

On May 4, the New York City Health Department noted that at least 15 children with these symptoms had been hospitalized there, too. These cases present like a severe immune response called Kawasaki disease, where blood vessels can begin to leak, and fluid builds up in the lungs and other major organs. Although only some of these children have tested positive for Covid-19, Russell Viner, president of the Royal College of Pediatrics and Child Health, told the New York Times, “the working hypothesis is that it’s Covid-related.”

Children who survive Kawasaki-like conditions can suffer myocardial and vascular complications in adulthood. But it’s too early to know how Covid-related cases will develop. Many of the small number of reported cases appear to be responding well to treatment.

Other researchers are suggesting that Covid-19 may pose particular problems for men beyond their disproportionate mortality from the illness. The testicles contain a high number of ACE2 receptors, explained researcher Ali Raba, in a recent letter to the World Journal of Urology. “There is a theoretical possibility of testicular damage and subsequent infertility following COVID-19 infection,” he wrote.

Another study, looking at 38 patients in China who had been severely ill with Covid-19, found that during their illness, 15 had virus RNA in their semen samples, as did two of 23 recovering patients. (The presence of viral RNA doesn’t necessarily indicate infectious capacity.)

Another recent study also showed that in 81 men with Covid-19, male hormone ratios were off, which could signal trouble for fertility down the line. The authors called for more attention to be paid, particularly on “reproductive-aged men.” An April 20 paper published in Nature went so far as to suggest, “After recovery from COVID-19, young men who are interested in having children should receive a consultation regarding their fertility.”

And we are just at the beginning of figuring out what this complex infection means for other organ systems and their recovery. For example, a recent preprint from Chinese doctors looked at 34 Covid-19 survivors’ blood. While they saw a difference between severe and mild cases, the researchers found that regardless of the severity of the disease, after recovered patients were discharged from the hospital, many biological measures “failed to return to normal.” The most concerning measures suggested ongoing impaired liver function.

What all of this means for survivors and researchers

As all this preliminary research shows, we are still in the early days of understanding what this virus might mean for the growing number of Covid-19 survivors — what symptoms they might expect to have, how long it might take them to get back to feeling normal (if they ever will), and what other precautions they might need to be taking.

Many people aren’t even receiving adequate information about when it might be safe for them to stop self-isolating. Nichols and other survivors report feeling better one day and terrible the next.

But in the chaos Covid-19 has caused in the medical systems, survivors say it’s hard to get attention for their ongoing struggles. “The support and awareness is simply lacking,” Nichols says. “It is a true roller coaster of symptoms and severities, with each new day offering many unknowns: I may feel healthier one day but may feel utterly debilitated and in pain the next.”

Lois Parshley is a freelance investigative journalist and the 2019-2020 Snedden Chair of Journalism at the University of Alaska Fairbanks. Follow her Covid-19 reporting on Twitter @loisparshley.

Correction, June 23: This story previously misstated the amount of lung scarring in SARS patients.

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Decades of research paint a clear picture: The No. 1 environmental health risk in the US is soot. Also known as particulate pollution, it is made up of extremely small particles spewed into the air by power generation, industrial processes, and cars and trucks.

There are “coarse particles,” between 2.5 and 10 micrometers in diameter, and “fine particles,” at 2.5 micrometers and smaller. By way of comparison, the average human hair has a diameter of about 70 micrometers.

Research has consistently found that inhaling these particles is incredibly harmful to human physiology, at high concentrations over short periods or low concentrations over extended periods. Particulate pollution is linked to increased asthma, especially among children, along with lung irritation and inflammation, blood clots, heart attacks, weakened immune systems, and, according to a wave of recent research, long-term cognitive impacts (reduced productivity, inability to concentrate, and dementia).

Research is equally consistent on another point: the harms of particulate pollution are not equitably distributed. They fall most heavily on vulnerable populations like children, the elderly, people with preexisting health conditions, low-income people, and, above all, people of color.

A groundbreaking 2019 study from researchers at the Universities of Minnesota and Washington attempted to quantify both sides of particulate pollution, who produces it and who suffers from it. They found that the consumption producing the pollution was concentrated in majority white communities, while exposure to the pollution was concentrated in minority communities.

“On average, non-Hispanic whites experience a ‘pollution advantage’: They experience ∼17% less air pollution exposure than is caused by their consumption,” the study concluded. “Blacks and Hispanics on average bear a ‘pollution burden’ of 56% and 63% excess exposure, respectively, relative to the exposure caused by their consumption.”

To put it more bluntly: People of color are choking on white people’s pollution.

The current regulatory limits on particulate pollution under the Clean Air Act were set in 2012, based on scientific review concluded in 2010. As subsequent science has revealed, they are inadequate to protect public health. That was the strong and unanimous conclusion of the panel of 19 scientists assembled in 2015 to assess the evidence.

Nonetheless, EPA claims the science is not settled and is refusing to tighten the standards, which will mean, on an ongoing basis, well over 10,000 unnecessary deaths in the US every year.

The purported rationale, of this and all the administration’s deregulatory efforts, is to reduce costs to industry. But the costs of pollution don’t disappear when they are removed from industry’s books. They are simply shifted onto the public ledger, in the form of health care costs and lost work days. Lax pollution standards represent an ongoing transfer of costs from industry to the public.

In the case of particulate pollution, the costs are disproportionately borne by black people — who, in part because of the air pollution in their communities, also suffer disproportionately from Covid-19.

Lax particulate pollution standards are, in short, yet another way of devaluing black bodies and black lives, yet another expression of the structural racism that Trump has so effectively flushed to the surface.

How EPA stacked the deck to ignore the science

Particulate pollution is regulated under the Clean Air Act’s National Ambient Air Quality Standards (NAAQS) program. The Act mandates that scientists periodically review the latest evidence on air pollution and recommend updates to NAAQS standards as necessary, so that the program stays abreast of the latest science.

The EPA’s seven-member Clean Air Scientific Advisory Committee (CASAC) reviews the standards, but because it does not have depth of expertise in all the various subject matters, it typically consults with a panel of outside scientists.

When the latest review of particulate standards began in 2015, such a panel was assembled: the 19-member Particulate Matter Review Panel, made up of experts in epidemiology, physiology, and other relevant disciplines. The review was delayed in getting underway, and Trump’s EPA initially talked about moving the deadline for completion to 2022. But in early 2018, then-EPA Administrator Scott Pruitt abruptly announced that the agency would rush to be done by December 2020, the tail end of Trump’s first term.

Later in 2018, to “streamline” the review process, newly appointed EPA Administrator Andrew Wheeler unceremoniously disbanded the PM Review Panel and left the review in the hands of CASAC — which had, over the previous year, been entirely reconstituted with Trump appointees. It was chaired by an industry consultant; just one of the seven members was a scientist.

The disbanded scientific panel later reconvened and rebranded as the Independent Particulate Matter Review Panel. It went on to issue the same assessments and recommendations it would have offered CASAC.

For fine particles (PM2.5), it recommended reducing the annual average concentration limit from 12 micrograms per cubic meter of air to between 10 and 8, though it noted that “even at the lower end of the range, risk is not reduced to zero.” It recommended reducing the daily exposure limit from 35 to between 30 and 25.

Now, the Independent PM Review Panel has penned an extraordinary piece in The New England Journal of Medicine, excoriating the EPA.

“We unequivocally and unanimously concluded that the current PM2.5 standards do not adequately protect public health,” they write. Ignoring that clear conclusion required serial abuses of the review process, as outlined in this somewhat mind-boggling paragraph:

The dismissal of our review panel is just one of numerous recent ad hoc changes to scientific review of the NAAQS since 2017 that undermine the quality, credibility, and integrity of the review process and its outcome. Other changes include imposing nonscientific criteria for appointing the Clean Air Scientific Advisory Committee members related to geographic diversity and affiliation with governments, replacing the entire membership of the chartered committee over a period of 1 year, banning nongovernmental recipients of EPA scientific research grants from committee membership while allowing membership for persons affiliated with regulated industries, ignoring statutory requirements for the need for a thorough and accurate scientific review of the NAAQS in setting a review schedule, disregarding key elements of the committee-approved Integrated Review Plan, reducing the number of drafts of a document for committee review irrespective of whether substantial revision of scientific content is needed, commingling science and policy issues, and creating an ad hoc “pool” of consultants that fails to address the deficiencies caused by dismissing the Clean Air Scientific Advisory Committee PM Review Panel.

That is … a lot. “It’s not surprising [CASAC] would retain the standards,” Gretchen Goldman, research director for the Union of Concerned Scientists, told the Washington Post, “because they broke the process.”

The chair of CASAC, Tony Cox — who has worked as a consultant for energy and chemical industry trade groups — contends that the particulate science doesn’t hold up. In the end, CASAC ignored the panel’s work and recommended that the standards be kept where they are.

The 60-day comment period on the new rule ends on June 29; there is no sign that the vast number of critical comments and submissions to EPA will change Wheeler’s mind.

Once the rule is put into effect, it will immediately face lawsuits. Given how shoddy the process has been and how clearly the results fly in the face of consensus science, it is unlikely to hold up in court. Like many of the Trump administration’s hastily executed regulatory rollbacks, it will likely end up quietly rejected — in the end, less an enduring victory than a flashy nationalist pageant that merely delays inevitable changes.

If it is rejected, it will go back to EPA for another rulemaking process that will take years. In the meantime, tens of thousands of people, disproportionately people of color, will needlessly get sick and die.

Black people are most likely to suffer the effects of soot

It is well known that the harms of pollution are inequitably distributed. Like so many social harms, they fall hardest on the most vulnerable.

That means people with weak or compromised immune systems, like children, the elderly, or people with preexisting respiratory or circulatory problems. And it also means people who happen to live close to the industrial facilities and highways that produce the pollution, typically low-income communities and communities of color. Black people fall disproportionately into both those categories, with high rates of preexisting conditions and high likelihood of living proximate to pollution sources.

A 2018 study by EPA scientists, published in the American Journal of Public Health, attempted to quantify the disparities in pollution exposure down to the county level. It found that, for PM2.5 pollution, “those in poverty had 1.35 times higher burden than did the overall population, and non-Whites had 1.28 times higher burden. Blacks, specifically, had 1.54 times higher burden than did the overall population.” These results held steady across the country.

This illustrates that the impact of pollution on the black population can not be reduced to geography or economic status. It “should be considered in conjunction with existing health disparities,” the study says. “Access to health care has well-documented disparities by race/ethnicity, and the prevalence of certain diseases is notably higher in non-White populations.” In other words, the pollution burden should be considered in the context of systemic racism.

Another recent study, focused on Texas, found that “the percentage of Black population and median household income are positively associated with excess emissions; percentage of college graduate, population density, median housing value, and percentage of owner-occupied housing unit are negatively associated with excess emissions.”

These studies are consonant with a long history of research — see here, here, here, and here — showing that air pollution reflects and reproduces wider income and racial disparities. The poor suffer; minorities suffer; black people suffer most of all.

Trump’s environmental policies reinforce structural racism

Inequitable distribution of pollution is as old as industrial society. The Clean Air Act was meant, in part, to address that injustice, to secure healthy air for every American. And despite its flaws and failings, it has been, among other things, one of the most effective environmental justice policies in US history. Just as pollution hurts people of color most, reducing it helps them most.

Emission of the six big pollutants — particles, ozone, lead, carbon monoxide, nitrogen dioxide, and sulfur dioxide — declined an average of 73 percent between 1970 and 2017. Fine particle concentrations fell by 43 percent between 2000 and 2019.

The Clean Air Act has accomplished this much because it is not a static law but a living, evolving set of policy tools. It has scientific reviews built in every few years, so that the level of public protection keeps up with the latest evidence. Scholars call this “green drift,” as the landmark environmental laws of the 1970s continue updating, even in the face of some hostile administrations.

Trump’s is the most hostile yet, working overtime to gum up the Clean Air Act and blunt its effectiveness. It goes beyond weakened standards for particulates, mercury, methane, and fuel economy.

There’s the “Transparency in Regulatory Science” (or “secret science”) rule, which would prohibit EPA from considering a broad swathe of the epidemiological research that supports particulate rules. There’s the effort to alter EPA cost-benefit analysis to exclude consideration of “cobenefits.” Many rules reducing other pollutants — mercury and CO2, for example — are justified in part by the fact that they also reduce particulates, which substantially adds to their health benefits. Excluding cobenefits is a way to justify weakening a whole range of other air-quality standards.

EPA is doing as much as it can to dismantle, weaken, or delay Clean Air Act protections before the end of Trump’s first term. The typical framing of these moves is that Trump is doing them on behalf of industry and that they are hurting “the environment,” or, worse, “the planet” (ugh).

There’s another way to frame them: They are expressions of structural racism, America’s long history of exploiting people of color for their labor while rewarding them with deprivation, marginalization, and ill health. Just as black people are often denied police protection while subjected to police violence, they are often denied the wealth and consumption that produce pollution while subjected to the health ravages of inhaling it.

Science-based air quality standards are one way to ease the burdens imposed on black bodies. The Trump administration’s staunch opposition to those standards, its attempts to undermine the bureaucratic machinery that produces them, is just one more expression of its disregard for black lives.

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Several states are now seeing a surge in new Covid-19 coronavirus infections and hospitalizations. And the states with more alarming outbreaks — Arizona, North Carolina, South Carolina, Texas, Utah, Arkansas, Florida, and Tennessee — generally saw few cases early in the pandemic.

Many of these states have started to relax the restrictions on movement, businesses, and public gatherings that were meant to control the spread of Covid-19. But with infections rising, there will be more illnesses, deaths, and financial hardships for people who have already suffered immensely from this pandemic.

If cases continue to rise and threaten to overwhelm the health system, officials may be faced with a daunting prospect: another round of shutdowns, requiring businesses that have reopened to close, public gatherings to be banned again, and stay-at-home orders to go back in effect.

Some local officials are already talking about this possibility. The city of Houston, Texas, for instance, is weighing another stay-in-place order. (It may ultimately be prohibited from having stricter rules than the state government.)

Thanks to several studies, including two recent scientific papers in the journal Nature, there’s now more certainty these measures dramatically lower the case count and save lives. However, the shutdowns also drove a massive spike in unemployment and caused huge social strains as people were forced to stay apart.

Asked about the prospect of further lockdowns, Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases, told Science Friday last week it depends on how well other public health strategies are deployed.

“Whether those infections turn into a real resurgence of infections and a rebound will depend on how effectively we’re able to identify, isolate, and contact trace,” Fauci said.

Other public health experts are debating the viability of additional lockdowns, noting it may be harder for leaders to muster the political will for them now, and that citizens may be less likely to comply with them.

What’s clear is that it will be difficult to get quick, satisfying results from shutdowns at this stage of the pandemic. And while there are other ways to protect public health that don’t require such sacrifices from the public, they require investment, coherent public messaging, and political will. Unfortunately, it doesn’t appear every state has these elements in place.

The US is in a much different place than it was at the start of the Covid-19 pandemic

The United States is now the epicenter of Covid-19, with 2.16 million confirmed cases and 118,000 deaths as of June 16.

This growth is evident in states like Arizona, now a hot spot for the virus with daily cases climbing rapidly in the last two weeks. Will Humble, former director of the Arizona Department of Health Services, said the shutdowns worked when they were implemented on March 31. Arizonans largely complied with stay-at-home orders. Businesses closed. People maintained social distance.

But there was little transmission at that point. “The first stay-at-home order was done when we just had a couple hundred cases a day,” Humble said. Then on May 15, Arizona Gov. Doug Ducey allowed the order to expire, replacing it with an executive order that suggested guidelines for how people should behave, but no enforcement. It’s likely that this relaxation contributed to the rise in cases.

“We’re blowing the doors off now with 1,500. … We’d be going into a stay-at-home order under very different circumstance than back in April,” Humble said.

A reimposition of shutdown measures at this point, if they were obeyed, would still reduce the number of new infections. But that reduction would be in proportion to a higher baseline. New cases would drop, but it would take much longer to reach the levels seen after the first round of shutdowns.

When starting from a higher number of cases, there is more transmission baked in. For instance, there will likely be more cases of household spread among family members under a stay-at-home order. And when there are a higher number of overall infections, there are likely to be even more undetected infections that may continue to worsen the pandemic.

And as states saw during their first brush with shutdowns, it can take a while for pandemic control policies to show up in the data. “We can expect those lags and timings would operate in a similar way,” said Joshua Salomon, a professor of medicine at the Stanford University School of Medicine who studies disease models and public health interventions. “It takes a few weeks after you change people’s interactions and contacts for that to translate into a reduction in the number of cases.”

Perhaps the biggest unknown for a second shutdown is how well people will adhere to the orders. Already, people in some parts of the country are gathering en masse, flocking to reopened businesses, and flouting guidance to wear masks in public places.

“We are starting to notice a lot of people across South Carolina are not doing the social distancing or not avoiding group gatherings and wearing masks in public the way, especially, that they were earlier on,” Brannon Traxler, the physician consultant for the South Carolina state health department, told ABC News. Public officials are also facing intense political pressure to ease restrictions.

Hannah Druckenmiller, a doctoral student at the University of California Berkeley, co-authored a recent paper looking at the effectiveness of shutdown measures. She and her team found that across the US, such tactics averted 4.8 million more confirmed cases of Covid-19 and up to 60 million infections in total.

But the results also showed that these policies had different effects in different parts of the world because some governments took the policies more seriously than others.

“This is likely a result of the fact that populations have different cultures and governments enforced the policies to varying degrees,” said Druckenmiller, in an email. “One interpretation of this result is that if a second round of lockdowns was less strictly enforced and had lower levels of compliance, these containment measures may not be as effective as they were in March and April.”

With states taking so many different approaches to the pandemic, however, the US is likely to experience a patchwork of different outcomes from further school closures, public gathering bans, and shelter-in-place orders.

There are alternatives to shutdowns, but the US hasn’t invested in them enough

Economic and social shutdowns are effective, but they’re expensive. They weren’t meant to stay in place indefinitely, but were aimed at slowing the spread of the virus to prevent hospitals from being overwhelmed with patients.

The more targeted strategy for containing Covid-19 is testing, tracing, and isolation. With a robust system of testing, health officials can identify people who are infected and spreading the disease, even before they feel sick. Then they can trace the contacts of the infected to test other people who may have been exposed. And the people who test positive can be directed to isolate themselves. All the while, the general public should maintain social distance and minimize exposure as they take calculated risks in going about their lives.

Such an approach would break the chain of transmission of the virus. It would also only require a handful of people to stay home rather than large swaths of the population. But it demands a lot of infrastructure to deploy tests and trace contacts, and it takes time to set up.

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“Shutdowns really had two goals. One was to stop the uncontrolled spread, which they did,” said Salomon. “The other was to try to buy us time to set up the public health infrastructure to do testing and tracing and isolation at scale. And we really failed to make use of that time.”

Another round of closures and stay-at-home orders could still be availed to build up the testing and tracing capacity. The more testing and tracing is available, the less strict shutdowns need to be. And building a system for testing millions of people would still be cheaper than an indefinite pause of the economy.

At this point in the pandemic, public health officials also have a better understanding of the spectrum of risk for the virus. Rather than issuing blanket orders to stay home, more nuanced guidance about what kinds of public spaces are safe and what precautions are necessary could ease the acceptance of pandemic control measures. But that requires careful and nuanced public messaging, and given the mixed messages the public has received on tactics like wearing masks, health officials would have to rebuild trust.

“What we really want to do is get as much benefit as we can from lockdowns in a way that’s more targeted and doesn’t demand as much sacrifice,” Salomon said. He added that policies like paid sick leave and building up work-from-home capabilities would also be important steps to helping people avoid unnecessary exposure to Covid-19.

As for when states can relax, that remains a fraught question. Some of the guidelines from the federal government for reopening have been confusing, and some states have gone ahead and established their own.

More recently, the Centers for Disease Control and Prevention put out a list of best practices to reduce Covid-19 risk as shutdowns relax. Measures include wearing masks and maintaining distance from other people.

However, with cases spiking in several states, it may still be too soon to think about relaxing, and efforts may still be needed for containment. But with the most blunt yet effective public health tool losing strength, it’s more urgent than ever to fight the pandemic without such drastic measures.

When states had strict stay-at-home orders and lockdowns in place, many decisions about the risk of getting the coronavirus were simple. People didn’t have to think about whether dining in a restaurant is safe if the restaurant was closed.

Now, that states are opening up — with varying degrees of precautions and adherence in place — individuals will need to weigh some risks on their own.

It isn’t easy; information about what’s safe, and what’s not, can be contradictory and confusing. A state may allow restaurants to reopen and concerts to resume, but should you really go? Is it safer if people are only allowed to dine outside?

The hunger for guidance is clear: On May 6, infectious disease expert Erin Bromage posted a blog post summarizing the evidence of coronavirus transmission risks, and 17 million people have since read it, he says. The CDC didn’t post its own updated guidance for individuals and events venturing out into a post-lockdown world until June 12. Perhaps a bit too late, as new cases and hospitalizations are currently rising in several states.

As Bromage conveys, the scientific understanding of how the virus transmits in public is improving. Contact tracing studies around the world have taken a magnifying glass to the “superspreading” events, where one person ends up infecting dozens of others. These studies shine a light on the key risk factors that create dangerous situations.

From these studies, one thing is clear: The main way people are getting sick with SARS-CoV-2 is from respiratory droplets spreading between people in close quarters. The risk of catching the coronavirus, simply put, “is breathing in everybody’s breath,” says Charles Haas, an environmental engineer at Drexel University. Droplets fly from people’s mouths and noses when they breathe, talk, or sneeze. Other people can breathe them in. That’s the main risk, and that’s why face masks are an essential precaution (they help stop the droplets from spewing far from a person’s mouth or nose).

The Centers for Disease Control and Prevention (CDC) emphasizes the risk of close contact over other modes of transmission. “The virus does not spread easily in other ways,” the CDC writes. It’s still possible that a person can catch it from touching a contaminated surface (more on that below.). But it’s “not thought to be the main way the virus spreads,” the CDC states.

As Bromage put it in his piece, “We know most people get infected in their own home,” from housemates or family members who caught the virus in the community.

So how can we assess the risk of going places outside the home?

The story is a little more complicated than the simple “stay 6 feet away” guidelines. Coronavirus risk is simply not one-dimensional. We need to think about risk in four dimensions: distance to other people, environment, activity, and time spent together.

Let’s walk through them.

A simple suggestion: Imagine people are smoking, or farting really bad, and try to avoid breathing it in

It’s easy to get into the weeds talking about the risk of catching and spreading the coronavirus as people reenter communal spaces in society. We can talk about the number of viral-laden droplets expelled by a single breath (a lot, perhaps 100 or more), by a person talking (10 times more than breathing), about how far a sneeze can propel those droplets (much farther than 6 feet), how long those viral droplets linger in the air (around eight to 14 minutes, at least in a controlled indoor lab setting).

But really, what all this means is that the greatest Covid-19 risk is being around breathing, laughing, coughing, sneezing, talking, people.

It’s still hard to visualize the risk, though, as the respiratory droplets are invisible to our eyes.

Perhaps helpful: Imagine everyone is smoking, as Ed Yong reported in the Atlantic, and you’d like to avoid inhaling as much smoke as possible. In a cramped indoor space, that smoke is going to get dense and heavy fast. If the windows are open, some of that smoke will blow away. If fewer people are in the space, less smoke will accumulate, and it might not waft over to you if you’re standing far enough away. But spend a lot of time in an enclosed space with those people, and the smoke grows denser.

The denser the smoke, the more likely it is to affect you. It’s the same with this virus: The more of it you inhale, the more likely you are to get sick.

An alternative image to thinking about this risk: “With my kids, I just sort of joke around that if you can smell their farts, you need to move farther apart,” Bromage says. So if not smoking, imagine everyone is farting. Keep this in mind and surely you’ll realize outdoor activities are better than indoor ones. “This tells you the gradient of risk,” Bromage says. “The closer you are, the more it’s gonna smell, the more dangerous it is.“

At a barbecue, you can still imagine being close enough to people to smell their farts. So even in outdoor spaces, we need to limit our contacts.

A crowded indoor place, then, with poor ventilation, filled with people talking, shouting, or singing for hours on end will be the riskiest scenario. A sparsely populated indoor space with open windows is less risky (but not completely safe). Running quickly past another jogger outside is on the other end of the spectrum; minimal risk.

There are many scenarios in between. “In general, outdoors is lower risk,” Muge Cevik, a physician and virology expert at the University of St. Andrews, says. But “if you have a gathering or a barbecue outside, and you spent all day together with your friends, your risk is still higher.”

What recent contact tracing studies can teach us about risk

Scientists pointed out a few recent contact tracing studies that nicely illustrate the dimensions of Covid-19 risk.

In China, 8,437 shoppers and employees of a supermarket were tracked in late January after one of the employees was confirmed positive with Covid-19 while working in the store.

The risk for infection was much higher for the workers than for the shoppers. Around 9 percent of the supermarket employees (11 out of 120 employees) got sick as a result. But just 0.02 percent of the shoppers (2 out of 8,224 shoppers) got sick.

What does this show?

The employees are at a much larger risk due to the time they spent working in the store. Both the employees and shoppers were in the same physical space, but their risk was not the same. (The study did not note whether the shoppers and customers were wearing masks in the store.) The employees may have interacted more with their colleagues, but they also had a greater chance of breathing in the virus.

What we should learn from this: If we have to spend time with people indoors, try to make it quick.

Another recent study out of China investigated an outbreak that started at a Buddhist temple event.

Two buses brought people to the function. On one of the buses, there was a person who later tested positive for the coronavirus who had not yet started to feel symptoms. The other bus was free of infected people.

Both buses brought people to the same temple, where they mixed and mingled outdoors*. But who was most at risk of getting sick? Those who rode the bus with the infected person. Twenty-four out of 67 people on that bus got sick. No one on the other bus did. The event was attended by another 172 people who arrived by other transportation. Only seven of these people got sick.

The lesson? The confines of a bus are a much riskier environment for viral spread than a larger outdoor space, like at the temple. The risk at the temple was not zero. But it was much reduced compared to the confines of the bus. And it appears those who were exposed at the temple were in close contact with the infected person.

“When you look at public transport, work spaces, restaurants — places where we’re just trying to fit many people in a small confined space — respiratory viruses like those spaces,” Cevik says. It’s “just common sense.”

There’s no set time that’s safe to be in these places. “Generally, for droplet transmission, we say 15 minutes,” Cevik says. “So if you spend 15 minutes face to face with somebody, you’re close contact [and at high risk], but that doesn’t mean if you spend 14 minutes your risk is zero.” And if you have to choose between a big open indoor space and a smaller one, choose the larger one, where people can spread out.

It’s not just the location or the time spent together: The activity people are engaged in matters, too.

In Washington state, a person with the virus attended a choir practice, and more than half of the other singers subsequently got sick. This was labeled a “superspreading” event, as one infection led to 32 others. Why was this so risky?

“The superspreading event is about the behavior of the person involved,” Cevik says. There are many reasons why a person could become a “superspreader”: Some people shed more of the virus than others, and it appears people shed most of it when they are just starting to feel symptoms.

But what made this event so risky was the convergence of many risk factors: the singing activity (during which the infected person released viral particles into the air), the time spent together (the practice was 2.5 hours), and the interaction between the choir members in an enclosed space (not only did they all practice together, they also split up into smaller groups and shared cookies and tea).

In a new paper published by CDC, researchers in Japan identified 61 clusters (five or more cases stemming from a common event) of Covid-19 cases. The researchers found most commonly the clusters originated in health care facilities. But outside of that they note “many Covid-19 clusters were associated with heavy breathing in close proximity, such as singing at karaoke parties, cheering at clubs, having conversations in bars, and exercising in gymnasiums,” the scientists wrote.

Notably, too, were the ages of the people who instigated spread outside of the health care settings. “Half … were 20–39 years of age,” the report finds. Which is a reminder: younger people can catch the virus, survive, but at the same time spread it to others who may die from it.

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What about touching something with infected droplets? Is that still a risk?

According to the CDC, the coronavirus does not often spread from people touching surfaces. That is, if someone with Covid-19 touches a hand railing, does that make that hand railing dangerous for other people to touch? The CDC is now saying that such events are not a huge risk for Covid-19 transmission.

But, there’s a catch: It is still the case that surface transmission is possible. Scientists believe the virus can remain viable on a hard, non-porous surface like plastic or steel for around three days, and a rough surface like cardboard for about a day. You could, conceivably, touch a contaminated surface, and then touch your face, and get sick. (The good news is that even though some virus can remain on a surface for a day or more, the amount of virus on a given surface drops by half after several hours, and then continues dropping.)

Bromage cautions it’s just really hard to study surface transmission. In contact tracing studies, it’s much easier to ask people who they’ve been in contact with than to have them remember every surface they’ve touched.

“I agree with this [CDC] statement,” Cevik says, agreeing that surfaces aren’t the most significant mode of transmission. “But this does not mean it does not happen.” Cevik points me to a contact tracing study that suggests (with a good deal of uncertainty) that some people caught the infection in a mall via the restroom. “Bottom line,” she says, “it’s still important to maintain personal hygiene and wash hands.”

Also consider how scientists recently found live Covid-19 virus in feces. So good bathroom hygiene is still as important as ever.

There are no magic numbers to eliminate risk

It would be great if there were very specific numbers and guidelines we could follow to minimize coronavirus risk to zero.

But there aren’t. While 6 feet away from another person, it’s not like the virus will immediately decide to drop dead. That’s why we need to think of risk in terms of many dimensions: so we can each think critically and not fall back on rules that are too simplified.

“When I first said restaurants were risks, people interpreted that as ‘every restaurant is a risk,’” Bromage says. “Each restaurant has its own unique environment, its own unique challenges that need to be worked out. If you’ve got a large open-seating area, and you can open up the windows and doors … the risk there is much lower than a boutique restaurant with five tables that creates that really intimate atmosphere.”

When we venture out into the world, we need to remember we can reduce risk, but never eliminate it.

“Wearing a mask is not going to completely reduce your risk, hand-washing is not going to completely reduce your risk, and staying a distance away from people in an enclosed space is not going to completely reduce your risk,” Haas, the Drexel professor, says. “But the concurrent use of all those strategies will hopefully reduce your risk down to a lower level. We can never get to zero. There’s no such thing as zero risk.”

And we still need more data, and follow-up on potential exposures. A hair salon in Missouri made headlines when a couple of their hair stylists were reportedly back at work after testing positive for Covid-19. Both hairdressers wore masks, and so did their clients, and a follow-up investigation by their county health department revealed no new infections among the 140 clients they saw.

This data point is a bit anecdotal. “I think they got lucky,” Bromage says. “But it does highlight the importance of masks.” Perhaps more data will reveal that getting a haircut while everyone is wearing a mask is a low-risk activity.

Contact tracing studies have taught us a lot so far. But as of now, most of this work has been done in Asian countries, which may have different expectations around mask-wearing, among other differences.

“Contact tracing, testing, isolating — these are the building blocks to understand where the transmission is occurring,” Cevik says. And the more we learn, the more power we have to stop the spread of this pandemic.

*This piece was updated to clarify the temple event occured outdoors.

The search for life in our solar system got a lot more exciting this week. On Monday, a team of scientists announced its members had detected phosphine gas in the caustic, hot atmosphere of Venus. So what? The gas — which you’d recognize by its fishy odor — is thought to be a byproduct of life.

“We did exhaustively search through all known chemistry … and we didn’t find anything that could produce more than the tiniest amount of phosphine in Venus’s atmosphere,” says MIT planetary scientist Sara Seager, who was one of the co-authors on the discovery published in Nature Astronomy, says. That leaves us two possibilities: The gas was created by life or by some chemical interaction scientists don’t yet know about.

Seager is one of the leading dreamers and thinkers in astronomy, looking for life beyond our planet. She studies planets orbiting stars many light-years away and thinks about how to detect life on them and others closer to home, like Venus.

She’s also thinking creatively about the microscopic life forms that could potentially survive there. This summer, before the phosphine announcement, she and her co-authors published a speculative, hypothetical sketch of what life on Venus could look like. The vision is beautiful: a living rain of microbes floating, cyclically, in the clouds, blooming and desiccating continually for millions of years.

I wanted to hear more about this vision of life in a world so very different from our own, so I called her up.

This conversation has been edited for length and clarity.

Evidence for life on the planet next door
Brian Resnick

To start off: What’s the gist of the discovery that you and the team announced this week?

Sara Seager

We aren’t claiming we found signs of life. We are claiming we have a robust detection of the gas phosphine in the atmosphere.

[After searching] all the known chemistry — volcanoes, photochemistry, lightning — we didn’t find anything that could produce more than the tiniest amount of phosphine in Venus’s atmosphere. So we’re left with two possibilities. One is that there is some kind of unknown chemistry, which seems unlikely. And the other possibility is that there’s some kind of life, which seems even more unlikely. So that’s where we’re at. It took a long time to accept it.

Brian Resnick

Okay, so it’s very unlikely. Has Venus historically been thought of as a place life might exist in the solar system?

Sara Seager

It’s been fringe pretty much the whole time that it’s been a topic. Carl Sagan first proposed there could be life in [Venus’s] clouds. There is a small group [of scientists] that writes about this topic. A lot of people love it. It’s like a closeted love because a lot of people are enthusiastic about it, but they either didn’t want to say so or they never had a reason to say so.

Brian Resnick

What do they love about it?

Sara Seager

I think it’s just the intrigue that there could be life so close to home.

[Venus is closer to Earth than Mars. It’s also the second-brightest object in our night sky, other than the moon.]

Why life would have to exist in Venus’s clouds, not on the surface

Brian Resnick

As I understand it, if life exists on Venus, it wouldn’t be on the surface of the planet, but in its sulfuric acid clouds?

Sara Seager

It’s always been the theory because the surface is too hot for complex molecules.

Brian Resnick

What is too hot? What happens there?

Sara Seager

Molecules break apart. If you took a protein or an amino acid, or anything, and put it in high temperature, it would come apart into smaller fragments and atoms.

Brian Resnick

Why, then, is the atmosphere a better place to look for life?

Sara Seager

It has the things that astrobiologists think life needs. It needs a liquid of some kind. And there is liquid in the atmosphere, although it is liquid sulfuric acid.

Life needs an energy source. So there’s definitely the sun, at least as an energy source. Life needs the right temperature. In the atmosphere, there is the right temperature. And life needs a changing environment to promote Darwinian evolution. So if you want to break it down like that, that’s why. To simplify, it’s mostly the temperature argument. Temperature and liquid.

Brian Resnick

Do we know of any life form on Earth that can exist in liquid sulfuric acid?

Sara Seager

No, we don’t.

Brian Resnick

What makes it seem possible for life to exist in sulfuric acid?

Sara Seager

We simply don’t know. I think your questions are the next decades of research, basically.

Brian Resnick

How do you even begin to imagine life in such a different world — life that has to live in conditions that would be deadly for any life on Earth?

Sara Seager

It has to be made up of different building blocks than our life is made up of. Our building blocks — like proteins, and amino acids, and DNA — wouldn’t survive in sulfuric acid. Or life has to have found a way to have a protective shell, made of materials that are resistant to sulfuric acid.

The dance of (potential) life on Venus

Brian Resnick

Over the summer, you and your colleagues published a paper speculating on what life on Venus could look like. You describe that it could basically dance in the atmosphere, alternating between an active phase up high and a dormant phase down low. I found it to be kind of beautiful. Can you describe how you came up with this?

Sara Seager

I had to help plug a hole in the concept of life in the atmosphere. That’s where it came from. Life has to live inside the liquid droplets, to be protected from the outside.

But in these droplets — where life is living, reproducing, metabolizing — the droplets would collide and grow.

Over time, like four months or a year or so, the droplets get big enough, so they start settling out of the atmosphere, like rain, but really slowly.

And so my colleagues told me I had to figure out how life could survive. If it all just rains out, it couldn’t stay in the atmosphere for billions of years, or hundreds of millions of years.

Brian Resnick

How did you solve this?

Sara Seager

So I came up with this life cycle idea: as the droplets fall, they evaporate, and we’re left with a dried, spore-like life form. Now that’s not very massive; it stops falling and becomes suspended in a haze layer [lower down in the atmosphere]. And this haze layer is known to exist beneath the clouds of Venus. It’s very stable and long-lived. So the concept is that this haze layer is populated by dried-out spores, which can stay there for days, weeks, months years — and eventually they get updrafted back up to the region that has the right temperature for life, where it can attract liquid, hydrate it, and start their life cycle again.

Brian Resnick

It’s like a living rain, of sorts.

Sara Seager

Right.

Brian Resnick

Why wouldn’t the spore die suspended in that lower layer?

Sara Seager

It’s pretty warm there, so some might die. And this is all just a hypothesis, so it’s not a proven theory or anything, but for this to work, some of them have to live. We have examples on Earth of dried-out spore living a long time.

What it would mean to discover life on Venus
Brian Resnick

Why is it important to do this type of exercise, to be so speculative, and imagine life in a world so seemingly hostile to life?

Sara Seager

If we think about it and couldn’t find any possible way for life to be in the atmosphere indefinitely, that would be bad news for the enthusiasts for life on Venus. Does that make sense?

Brian Resnick

Yeah, if you can’t think of any hypothetical that allows life to survive, it’s hard to make a case to go look for it. Does the life you imagined fit in with in the new discovery of the phosphine gas?

Sara Seager

Yes. Well, it was motivated by the phosphine work.

Brian Resnick

What would it mean to find life on Venus?

Sara Seager

I think it would mean that if there’s life there, it has to be so different from Earth, and that we could show that it had a unique origin. It would just give us confidence that life can originate almost anywhere. And that would mean that our galaxy would be teeming with life. All the planets around other stars. It just sort of ups our thinking that there could be life everywhere.

Brian Resnick

Are you talking about a second genesis of life happening separately on Venus? Or would we have to figure out if there’s a common origin of life in our solar system? That something seeded life on both Earth and Venus?

Sara Seager

We’d have to figure it out.

How to find life on Venus, once and for all
Brian Resnick

What are the next steps, ideally?

Sara Seager

Our ideal next step would be to send a spacecraft or spacecrafts, plural, to Venus, that could involve a probe going into the atmosphere and measuring gases confirming phosphine, looking for other gases, looking for complex molecules that might indicate life, and maybe even searching for life itself.

Brian Resnick

Anyone working on that?

Sara Seager

Rocket Lab had mentioned about a month ago that they were planning to send a rocket to Venus. There are two NASA discovery class missions under a phase A competition [meaning they’re just mission proposals and need to be greenlit]. if they get selected for launch, they will get to go. Russia and India are planning to send something there. And I’ve started to lead a privately funded study. It’s not a mission. It’s just a study of what it would really take.

Brian Resnick

Can we answer this question — is there life on Venus — in our lifetimes?

Sara Seager

I think it is answerable in a human lifetime.

Brian Resnick

Is too much time and money spent on finding life on Mars? Venus seems to be neglected in terms of big NASA missions.

Sara Seager

Well, we don’t have infinite resources, unfortunately, but it sure would be nice to see more spent on Venus. We haven’t explored Venus for a very long time. You’d have to look up when the last time the US went to Venus. [It was the Magellan mission that launched in 1989.]

Brian Resnick

What would you love the public to think about and dwell on with this topic?

Sara Seager

Our solar system, our galaxy, our universe is full of mysteries. We’d like to solve them, but some end up being unsolvable and they just leave us in limbo. So hopefully that’s not going to be the case here.

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There’s a lot we still don’t know about President Trump’s Covid-19 case, starting with the basics: Is he having trouble breathing? Is he experiencing side effects, such as delirium or confusion, from the multiple experimental drugs for Covid-19 he’s taking? When was his last negative coronavirus test?

There’s another burning question about Trump’s health that matters more for the people around him, including his family members and staff at the White House who haven’t yet tested positive: Is the president still contagious?

Patients who have been diagnosed with Covid-19 are supposed to — per Centers of Disease Control and Prevention guidelines — isolate for at least 10 days since they first noticed they were sick or tested positive and until their symptoms have improved, including no fevers for at least 24 hours.

In cases like Trump’s that required hospitalization, that isolation period can last even longer. “For patients who had severe or critical illness, we wait up to 20 days to state they are noninfectious,” said Sigal Yawetz, an attending physician at Brigham and Women’s Hospital in Boston who has been caring for Covid-19 patients.

Doctors rely on clinical symptoms because there’s no clinically validated way to check if a patient is still contagious — even when the patient is the president.

But we don’t know exactly when Trump became symptomatic — one of the many basic facts about his case that’s been muddled by confusing reports. If we go by what his doctors and colleagues have suggested, he started experiencing symptoms on Thursday, a day before entering hospital.

That means Trump should probably still be isolating for at least two more days — perhaps longer.

Instead, he rode in a car with others on day four of his symptoms, and on day five, took off his mask as he entered the White House. As of Wednesday, he’d returned to the Oval Office to work — necessitating those around him to don N95 masks, gowns, and gloves.

Safely donning and doffing personal protective equipment requires training and can be challenging for even highly experienced clinicians. Considering the White House’s colossal failure at basic coronavirus prevention measures — such as social distancing, mask-wearing, and contact tracing — it’s hard to imagine they’ll successfully turn the residence and Oval Office into a model of infection control.

But if the White House wants to prevent more coronavirus cases, they’ll have to for this simple fact: Trump may still be contagious.

There’s no clinically validated way to test for Covid-19 contagion

The best research we have so far on Covid-19 transmissibility suggests that people can shed infectious virus for up to nine days after getting sick. In general, they are most contagious two days before symptom onset, and in the first five days after, as the graph in the tweet below, from this Oxford University Press study, shows.

But these are averages — and they hide a lot of the variability among patients. Some people are infectious for a shorter period, while others shed virus for up to 20 days after symptom onset.

That’s why doctors and public health officials ask patients to isolate for at least 10 days after their symptoms appear, or even longer in some cases.

As for Trump, “potentially he passed through the most infectious stage already,” said University of St. Andrew’s virologist Muge Cevik. It’s also possible the medications he’s on, including the antiviral remdesivir, brought down his viral load quickly. “But he may be still contagious depending on his symptom onset.”

Doctors rely on the date symptoms appeared, or the first positive test in cases where people don’t notice symptoms, because there’s actually no proven way to show that a person is no longer infectious. The diagnostics available to check for infection — PCR tests — “can’t distinguish between intact, infectious virus and degraded viral genetic material,” Ilan Schwartz, an infectious disease doctor and professor at the University of Alberta, told Vox.

Doctors could use something called the CT, or cycle threshold, that’s part of the PCR test. It’s a measure of a person’s viral load, and if the number gets higher over time, the viral load in the sample is getting smaller. But the link between a person’s CT number and their transmissibility is still not fully understood, said University of Michigan infectious disease doctor Kevin Gregg.

“There are not completely established guidelines for [using CT values],” he added. So it’s not something doctors typically rely on to determine how long a patient should isolate.

That’s why — as a precaution — “[Trump] should be isolating,” Gregg said, “so as not to infect members of his family, the staff of the White House, and other people.”

“We don’t say, ‘It’s been 10 days, you can take off your mask’”

There is one other, more advanced, way to check on a person’s contagiousness: cell culturing. Scientists used the technique in many of the studies that informed the quarantine period. It involves infecting animal cells in Petri dishes with the SARS-CoV-2 virus, waiting for them to incubate, and seeing whether the virus can still grow in them.

One of Trump’s physicians, Jason Blaylock of Walter Reed National Military Medical Center, mentioned the president’s medical team was working with “various laboratories in the area, state of the art facilities … on obtaining advanced diagnostic testing to really inform the White House medical team of both the status of the president as well as his ability to transmit virus to others.”

He didn’t specify, but perhaps cell culturing was what he was referring to. Yet even that isn’t foolproof for use in patients. “There is a big difference between the virus being culturable in a Petri dish full of cells derived from a monkey’s kidney and being capable of infecting the respiratory epithelium of living people,” Schwartz said. “This test has absolutely not been validated for ruling out SARS-CoV-2 infectiousness in people.”

What’s more, it takes several days to grow the virus and get a reliable result. “So I don’t think they’d have that information yet,” said Gregg.

Even after isolation, patients are still advised to wear a face mask. “If someone had Covid, after the contagious period is over, it doesn’t mean you go out and do things as usual,” said Preeti Malani, an editor at JAMA and infectious disease doctor who treats Covid-19 patients. “We don’t say, ‘It’s been 10 days, you can take off your mask.’ We continue to treat people as if they might be infectious because the truth is we don’t know.”

Instead of mask-wearing, the White House has relied heavily on testing to prevent outbreaks. That, too, is problematic. “Many White House officials have been feeling comfortable after receiving a negative test,” Cevik said, “but maybe they don’t necessarily understand or haven’t been told the negative test doesn’t give you 100 percent clearance.”

As Vox’s Brian Resnick reports, coronavirus tests can fail for a multiplicity of reasons — including improper swabbing or taking the test before someone has enough virus to test positive. This means anyone who encountered Trump, who wasn’t wearing full personal protective equipment while Trump is infectious, could now be carrying the virus, even if they’ve tested negative. According to guidelines, those people should be quarantining for 14 days, too.

If the White House wants to prevent more coronavirus infections, they’ll have to change course. “Testing on its own is not going to prevent onward transmission,” Cevik said. But isolating — in addition to masks, contact tracing, social distancing, and testing — can.

Eliza Barclay contributed reporting to this story.

Correction, October 7: This article originally misattributed a quotation by Ilan Schwartz on the limits of advanced Covid-19 diagnostics to Sigal Yawetz.

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A day after the Food and Drug Administration announced tougher measures for a coronavirus vaccine approval, dashing President Trump’s hope of getting a vaccine out before the election, the president put out a video on Twitter suggesting he had changed course: a promise to bring the American people a Covid-19 “cure.”

Following his admission to the hospital Friday, “within a very short period of time, they gave me Regeneron … and it was, like, unbelievable. I felt good immediately,” Trump said in the video. The president then claimed “hundreds of thousands of doses” of the Regeneron drug were nearly ready, and that Americans could “get ’em and you’re going to get ’em free.”

“I call that a cure,” he added, saying it’s a “blessing from God” that he got infected with the virus, which has killed more than 212,000 Americans.

Before we go any further, Regeneron is the name of a pharmaceutical company that manufactures one of the experimental treatments Trump received, not the name of the drug. The drug itself, REN-COV2, is an experimental “monoclonal antibody cocktail.”

In theory, the synthetic antibodies are supposed help patients mount an immune response early in their illness — slowing the virus from progressing into the cells and preventing it from causing serious disease or death.

But the cocktail is still considered experimental because clinical trials are ongoing and it hasn’t been approved for market by the FDA. Trump was only able to access the treatment through the FDA’s “compassionate use” provision, whereby unapproved drugs are administered to seriously ill patients who have no other treatment options on a case-by-case basis. (Whether Trump should have gotten the antibodies this way is a matter of ethical debate.)

All we know about its effectiveness comes from a September 29 Regeneron press release, as Vox’s Umair Irfan reported, about a multi-phase, randomized, double-blind clinical trial involving only 275 people.

While the company did report promising results — the treatment cut the viral load of Covid-19 patients who were not hospitalized, and it reduced the time it took to resolve symptoms — these are very early, unvetted findings. They say nothing of whether the drug cut the risk of death or “cured” people.

“The sample size is pitiful,” said David Nunan, a senior research fellow at the Center for Evidence-Based Medicine at Oxford University, referring to the 106 participants in the trial who reported the main outcome of symptom alleviation in the interim results. “There’s going to be huge uncertainty, and any of the differences we see in [the treatment group compared to the placebo group] are unlikely to be statistically significant — meaning they could just be chance effects.”

Data from the trial hasn’t yet been peer-reviewed. And, again, the trial isn’t even finished.

It’s the same story for another antibody therapy from the drug company Eli Lilly, which Trump also mentioned in the video. No published data. Just a press release.

There’s no way to evaluate the Regeneron treatment until the company publishes its data

Science by press release is not reliable science. Drug companies are notorious for exaggerating and skewing their early findings in public announcements to grab attention and boost investor interest.

“There’s a natural conflict of interest in people putting out the press release,” Nunan said. “Why wouldn’t they release something favorable [about] their treatment?”

Remember in May, when Moderna — the company with a coronavirus vaccine that’s far along in clinical trials — put out a press release about promising phase 1 results. While it first caused the company’s stock valuation to swell, vaccine researchers pointed out in Stat that the information in the press release was way too preliminary and vague to gauge whether the vaccine was actually working.

Similarly, researchers at Oxford University were also criticized for announcing the results of their trials of dexamethasone via press release instead of a peer-reviewed paper or publishing their data. (Dexamethasone is a corticosteroid treatment being used for Covid-19 that Trump has also been given.)

The infectious disease doctors Vox spoke to about Trump’s treatment with the Regeneron cocktail were also leery of how little firm data there is about the drug.

“There’s a reason we’re not giving this to patients [yet],” said intensive care doctor Lakshman Swamy, who works with the Cambridge Health Alliance. “We don’t know enough about it.”

“This is very, very early data,” said Joshua Barocas, an assistant professor of medicine at Boston University and infectious disease physician at Boston Medical Center.

“The monoclonal antibody is just not tested,” Jen Manne-Goehler, an infectious diseases doctor at Brigham and Women’s Hospital, told Vox.

Plus, even if the experimental drug looks promising in early research, Swamy noted, “people said the same thing about hydroxychloroquine,” the malaria drug — also embraced by Trump — now known to be ineffective for Covid-19.

Trump’s single case is not enough to draw conclusions about the drug

As the Times’s Katie Thomas reports, Regeneron is now seeking FDA approval for its monoclonal antibody therapy, raising fears that Trump may pressure the FDA to approve the treatment in time for the election.

What drug regulators are supposed to do in this situation is wait for more carefully reported data on many patients to evaluate the treatment’s efficacy and safety. (The FDA did not respond to the Times’s request for comment.)

“We need people to be enrolled in trials,” Swamy said. “Whenever a high-profile case gets a therapy or doesn’t, the public is swayed based on what happens in that one case.”

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The issue is that one case, no matter how high-profile, isn’t reliable evidence of a drug’s effects or safety. What’s more, the Trump case is probably not even representative. He got a higher dose of the antibodies than what’s being tested in the clinical trial. And although Trump pointed to the Regeneron treatment as the reason for his apparent turnaround, we can’t be sure the cocktail made a difference in his case. He’s been on at least two other Covid-19 drugs, according to his doctors: One is the antiviral remdesivir, and the other is dexamethasone.

Nunan called it “massive confounding.” “You’ve got no idea as to which of those interventions if any were having an effect,” he said.

Leana Wen, an emergency physician and public health professor at George Washington University, told NPR the president is likely “the only person in the world to have received this combination of treatments.”

For now, Trump is not out of the Covid-19 “red zone.” Around seven to 10 days after symptom onset, even patients who appear to be stable can take a turn for the worse. (Trump reportedly started to experience symptoms last Thursday.) He may also still experience side effects from his multiple therapies.

If the Regeneron cocktail does make it through clinical trials and gets approved, it won’t quite be free for all Americans, said Craig Garthwaite, a health economics professor at Northwestern University’s Kellogg School of Management.

The government — with taxpayer dollars — already invested $450 million in Regeneron to develop and manufacture an undetermined number of doses (between 70,000 and 1.3 million, depending on the final dosing and how the drug is used). So though the company has said the drug will come free of charge, Garthwaite said, “that’s because we already entered into a supply agreement.”

OVER THE WEEKEND, a number of payers were sent-off while others were somewhat fortunate to stay on the field.

Shane McGuigan and Niall Daly were dismissed in controversial circumstances during the Derry-Roscommon tie in Division 2.

In the top flight, Tyrone lost skipper Padraig Hampsey picked up a black card in the opening period against Dublin and was sent-off in the 38th minute when he was booked for shoving Cormac Costello on the concrete in front of the stand.

“Costello threw the ball over the fence wasting a bit of time, I’d say Hampsey saw red and just levelled him,” remarked Marc Ó Sé on the latest episode of The42 GAA Weekly.

“I’d say Costello nearly wanted him to do it because he came out sheepishly. If Costello had left the ball down it would have gone just over the line and Hampsey would have got the ball. I’m not saying it was right, it was bad.

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“He led him straight into the barrel and took the bait. Hampsey shouldn’t have done that. He needs to be more disciplined.”

The All-Ireland champions were fortunate not to finish with 13 men when Michael McKernan’s punch into the midriff of Brian Fenton went unnoticed by the officials.

In the Dr Hyde Park clash between the top two sides in the second tier, 18 cards were issued by Seán Lonergan.

Rossie centre-back Daly looked to be harshly dismissed on a second yellow, and McGuigan’s dismissal arrived after he was hauled to the ground by his marker Brian Stack in the final moments of the game.

Derry won a free but with their free-taker given his marching orders, Emmett Bradley missed a chance to win the game.

“Referees are dishing out yellow cards now for absolutely nothing, if you ask me,” said Ó Sé.

“They’re dishing out yellow cards, some aren’t even free kicks. There are incidents that happened in the game that he did call right but the referee is going to look back on that game…he had an absolute disaster.

“The big thing for me with the referees is there’s no consistency. There’s some referees that leave things go a small bit, there’s others that done leave anything go. The bite is gone out of games in terms of what’s acceptable.

“There was one tackle that particular Niall Daly put in, maybe it was his reputation, but he got a second yellow. That didn’t merit a second yellow. For me, it wasn’t even a free-kick.

“I’ve often found this. I played in the full-back line all my life. The best referees are the ones that are vocal, the ones that will tell you why there’s a free. You see some referees and they’re dogmatic and they just point the hand and give a free-kick, they won’t communicate with you. What happens then is frustration builds up within a player and the player is likely to do something out of pure frustration.

“It’s the good referees that will say, ‘No Marc you pulled him back there.’ It’s the ones that make hand gestures saying why the foul was – that actually calms the player in my view.

“What happens now is referees are not communicating with players and as a result frustration builds up.”

To listen to the full episode, go to members.the42.ie.

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Updated Thu 9:30 PM

SATURDAY’S HURLING SCHEDULE will commence for Tommy Guilfoyle in Dr Hyde Park.

He’s jumped on board as coach to the Roscommon senior hurlers this year, alongside new manager Francis O’Halloran, a pair of Clare natives trying to spread the hurling gospel.

They’re having a puck around at 9am in the Roscommon county ground, to acclimatise themselves to the surroundings before Sunday’s league opener against Tyrone.

Guilfoyle, a long-serving stalwart in Clare hurling forward lines, will be on the sideline for that Division 3A fixture but in between he’ll be back home immersed in local hurling matters.

The plan is hit the road and by Saturday lunchtime be parked up at the Gaelic Grounds in Limerick. He’s on co-commentary duty for Clare FM, this is a game close to his heart. His alma mater St Joseph’s from Tulla partake in a moment of history, their first appearance in a Dr Harty Cup final, the premier Munster hurling colleges competition.

There will be a healthy representation of players from his own club Feakle. The semi-final win over Waterford’s De La Salle took place in Mallow and saw another day of hurling double-jobbing.

After that mid-afternoon game, he was headed to the Connacht GAA Air Dome in Mayo to witness Roscommon win a pre-season provincial league final at the expense of Sligo.

It’s a hectic time but covering so many miles on the road is worth it as he sees the impact in East Clare of this novel hurling journey.

“It’s been building since Christmas really, winning the quarter-final and the semi-final and now this unique occasion.

“The last day, the game was on the Saturday and the lockdown finished on the Friday, so we were back to normal opening. Someone described Tulla on Saturday evening as like Paddy’s weekend, there was a carnival atmosphere around the town.

“The crowd have played a big part in it. They’ve got great support from local clubs and businesses. 

“I’ve been at colleges games own the years but the after the quarter-final, the emotion and joy on the field, I never saw that level before. Parents, past pupils, grandparents, teachers, ex-teachers. There was a big sing-song on the field, I never saw it after a game.

“Just relief and great joy. So many outside people that weren’t parents or pupils to turn up to a game, and for it to take off with a school team. Saturday afternoons, watching St Joseph’s Tulla is the place to be.”

The final hurdle to be surmounted is on Saturday after a campaign filled with milestones. St Joseph’s had never won a game before in the Dr Harty Cup, that was their modest aim at the outset this season. Their team had climbed steadily through the ranks and have flourished in this knockout format, clipping the wings of St Colman’s Fermoy, CBC Cork and De La Salle Waterford.

The victories have been founded on stirring comebacks and the remarkable free-taking expertise of forward Sean Withycombe, who has hit 1-38 in their last three victories.

“Sean’s father is a Kerryman, he’s very proud of that,” says Guilfoyle.

“It’s the sum of the team more so than individuals. In the quarter-final, the corner-back Dara Ryan popped up with a score when all looked lost. The inspiration and the winnings have come from different areas.

“It’s very much player driven. That comes from a great belief amongst themselves where they’re never beaten.

“This is a once in a generation team based on the strength of the clubs around. They wouldn’t have a conveyor belt coming every year. Down the years Tulla would be looking in the road to Flannan’s, the aristocrats of hurling. I suppose Tulla were wondering, ‘Could it be us?’ ”

Feakle and St Joseph’s Tulla player Adam Hogan.

Source: Lorraine O’Sullivan/INPHO

It is a team anchored by three local clubs – Tulla, Feakle and O’Callaghan Mills supply 12 of the starting side between them. There was one player apiece from Clooney-Quin, Crusheen and Broadford in their starting fifteen for the semi-final.

They have been powered by a strong spirit and sense of unity in their playing group. Life off the pitch has illustrated to Guilfoyle how the players look out for each other and the locality is there to provide valuable support.

“What really bonds this group together is Ronan O’Connor and Oisin O’Connor, the brothers from Feakle, they’ve had a double tragedy in the last couple of years. They lost their father Pat to a farming accident and last year they buried their mother Denise, she died of cancer. It was tragic and such a tough blow for them.

“There has been great support from the school, the teachers and all the parents of their team-mates, not alone when it happened but continue to do so. The lads live just up the road from me. Their fellow players and school mates have really stuck together, in its own way it has really bound them together.

“I remember being around the house at the funerals and the most striking was the amount of students that were there for the few days. The school continues to oversee the supply of dinners and stuff like that. Ronan is the captain, he was on the Clare minor team last year.

“It shines through very strongly that they are a very united bunch. The hurling has been a great outlet for them. The support has been brilliant from everyone and continues within the parish and the clubs and more importantly, the school.”

Galway’s Aidan Harte.

Source: James Crombie/INPHO

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On the hurling front they have plenty expertise guiding them. Terence Fahy is the Clare U20 hurling manager. Tomas Kelly steered Inagh-Kilnamona to last year’s county senior showpiece in the Banner county. Aidan Harte has come across the border from Gort, bringing with him a wealth of playing experience in Galway colours which included the highlight of contributing to their 2017 Liam MacCarthy Cup win.

That trio of teachers adds profile to the sideline, opponents Ardscoil Rís have people of similar stature in current Clare senior Paul Flanagan, former Limerick senior Niall Moran and Clonlara’s Cormac O’Donovan, the supplier of a famous match-winner in Clare’s 2009 All-Ireland U21 final glory.

Ardscoil Rís coach Niall Moran.

Source: Ryan Byrne/INPHO

“The Clare connections add to the intrigue,” says Guilfoyle.

“I’d be a past pupil of Tulla, we had great teachers down the line. We won All-Ireland colleges B back in the ’80s. Seanie McMahon that went on to play for Clare centre-back, his father Michael was involved. John Stack was another great man that put in a lot of effort.”

“The lads now have great experience and know-how. The new school was built seven or eight years ago, and there’s an all-weather pitch there, that all helps and this team has that new identity.

“Let’s hope they can do themselves justice on Saturday. Play the game rather than the occasion because Ardscoil have been there before and they have that winning tradition.

“There’s great excitement around. Everyone wants to be a part of this.”

• Dr Harty Cup final: St Joseph’s Tulla v Ardscoil Rís, Gaelic Grounds, 1pm – Saturday 5 February.

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TIPPERARY STAR HURLER Pádraic Maher says that his decision to retire from the sport was made to ensure a greater quality of life going forward.

Paudie Maher on the ball for Tipperary.

Source: Ryan Byrne/INPHO

The three-time All-Ireland winner made the shock announcement during the week, saying that he had received medical advice to step away from contact sport due to a neck injury.

Maher had previously indicated his intentions to return for a 14th season with the Premier County, but will now be bringing the curtain down on his decorated career with both Tipperary and his club Thurles Sarsfields.

Speaking to the media today, the six-time All-Star elaborated on some of the details of his neck injury. He began by explaining how he was prompted to seek medical advice after he mistook some headaches and neck pain for possible having Covid-19 symptoms.

“I still have to meet one or two more lads about it to determine how old it is but at the moment from what I know I only got the symptoms from around the time of the county final when my neck was at me and I was getting a few headaches.

“That’s when it arose but again it could have been an accumulation of things, I don’t know. That’s why I’m hoping to meet one or two more specialists tomorrow and at the start of next week and hopefully they’ll be able to give me a bit more information as regards how old it is, how it happened, but there is a fair chance from what I told it happened in training or something between the county semi-final and final because the symptoms arose a few days before the county final.

“I said I wasn’t feeling great. At the time, I thought ‘am I getting Covid?’, I didn’t know what was going on. But then we got to the root of it recently and thankfully we did because if the doc didn’t send me for a scan I could be in training and could have been making it a lot worse unbeknownst to myself. Very unlucky but very lucky at the same time.

“So there is a fair chance I took a knock at training, noticed it myself. The way we train with Sarsfields is fairly physical so there is a fair chance I got a knock there and whether it ruptured something then or made an old injury worse I don’t know but hopefully I’ll get a lot of answers in the following weeks.”

Maher added that he was reassured by the doctor that eliminating the risk now means he can look forward to a healthy life away from hurling. He’s also clear to continue working for An Garda Síochána.

All forms of contact sport are no longer available to him, but individual pursuits like running, swimming and cycling are still safe options.

He has also recently opened the Heyday coffee house in Thurles with his Tipp team-mate Séamus Callanan, which will give him a new focus.

“He [the doctor] only listed off what the damage could be,” says Maher, “especially when you are working in the head and neck area, he put it to me, do you want your girlfriend lifting you off the couch to put you to bed every night? It was that extreme so when he started talking like that, I said, this is a fairly black and white decision for me.

“Thankfully, the risk has been taken away, please God, and with the bit of guidance from the medics going forward I will have a perfectly healthy life to live.

“It’s going to be some void to fill alright, being gone four or five nights a week and building up to big games at the weekend. So it’s going to be strange.

“I don’t know if I can be twisting or turning or moving my neck too sharply but there’s still loads for me to do between work and the coffee shop.”

Source: James Crombie/INPHO

Maher departs as one of Tipperary’s greatest ever players, who won three senior All-Ireland titles throughout the course of a decade. He also enjoyed success at underage level and was part of an exciting group of emerging talents that broke through to the senior ranks in 2010.

He added that the outpouring of appreciation for his contribution to hurling has been “amazing” and that he didn’t expect the huge volume of messages.

Tipperary will get their Division 1B campaign underway this weekend when they travel to face Laois in Portlaoise. Maher’s brother Ronan is still a key player for the county, and he wants to get started on adjusting to the role of supporter.

“I’m actually thinking this morning I might go down to Portlaoise to get it out of the system. It will be strange alright but get to the first one or two games and I’ll be as much a supporter as anyone.

“Ronan is involved there as well and I need to support him as well and yeah, sure, we’ll see we might go down to Portlaoise on Saturday evening and a few pints on the way home. Life has changed a lot in the last few days, it’s very strange.”

– First published 13.59, 3 February

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