Jack Drennan had tried to quit vaping before, but it took a global pandemic to make him finally follow through.
“I heard you get a lot sicker if you do vape and get coronavirus, so it kind of [pushed me] to quit,” says the Mississippi 20-year-old. Plus, “my mom’s on my ass [about it].”
Speculation about a link between vaping and COVID-19 has grown in recent weeks. News reports have noted that some young, hospitalized COVID-19 patients also vaped, and at a tele-town hall on March 19, a constituent asked New York Rep. Anthony Brindisi about the possibility of a connection. The National Institute on Drug Abuse wrote on its blog that people with substance-use disorders, including those who vape, could be especially hard-hit by COVID-19. In various corners of the internet, fringe theories with little-to-no scientific evidence have popped up making connections between a prior outbreak of vaping-related lung illnesses in the U.S. and COVID-19.
But is there any actual link between vaping and coronavirus? Experts say it’s impossible to say for sure.
Preliminary data show that a fairly high number of U.S. hospitalizations have been among younger adults—the same population known for vaping. At this point, though, that’s just an interesting observation; there is no real data to back up an association between vaping rates and COVID-19 rates in young adults.
The science around vaping is in general evolving. While some studies have shown that vaping can lead to lung damage and other health problems, the products have not been on the market long enough to speak confidently about their long-term effects. The science around COVID-19, which did not exist three months ago, is also still evolving. Putting the two topics together, then, makes for a lot of uncertainty.
Having a preexisting condition—especially one related to respiratory health—increases the chances that someone will experience complications from COVID-19, so it’s reasonable to think vaping could play a part. But since scientists can’t say for sure that vaping leads to lung disease or other chronic conditions, it’s also difficult to say whether it opens people up to more risks associated with COVID-19.
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Combustible cigarette-smoking is a clearer cause for concern during the outbreak, says Dr. Michael Siegel, a professor of community health sciences at the Boston University School of Public Health. Early data suggest men are more susceptible to COVID-19 than women, which could be associated with the fact that more men than women smoke—especially in China. Smoking-related conditions, such as heart and lung disease, put people at risk of more severe illnesses, Siegel says. Smoking also inhibits the body’s ability to heal from infections, he adds.
But “with vaping, we just don’t know,” Siegel says. “We don’t have the evidence.”
Yasmin Thanavala, an immunologist at Roswell Park Comprehensive Cancer Center in Buffalo, New York, says some of her group’s animal research suggests vaping may prevent the body from healing from bacterial infections. COVID-19, of course, is a viral infection, but Thanavala says “on a theoretical basis,” a similar effect could apply. There’s not conclusive evidence to say so definitively, though.
Even assuming vaping does cause some amount of lung damage, it’s unlikely that most people who vape have been using e-cigarettes long enough to see the full brunt of it, says Dr. Steve Schroeder, a professor of medicine at the University of California, San Francisco. The exceptions, of course, are patients who got sick during a vaping-related lung injury outbreak last year, which health authorities traced mainly back to THC vape products spiked with the additive vitamin E acetate.
Daniel Ament, a 17-year-old from Michigan who needed a double lung transplant after vaping, is one such patient. “I definitely am [at higher risk for COVID-19],” he says. “[Doctors] didn’t have to tell me that.” Given his past lung injury and fragile immune system post-transplant, Ament is staying inside, wearing a mask almost constantly and visiting his doctors and therapists virtually. His whole family self-quarantined starting last week, to avoid bringing home germs.
E-cigarette users without a known lung injury should not quit if it means they’ll go back to using combustible tobacco, Siegel says. “Relapsing to smoking is the worst thing they could do.” But for recreational vapers, COVID-19 may be the final push needed to quit—and that’s a silver-lining to the situation, Siegel says.
“It’s always better not to be breathing chemicals into your lungs. I would have said that even without this particular outbreak,” he says. “It would certainly be a potential incentive to get people who are vaping to stop, just as a precautionary measure.”
Christian Fracassi, founder and CEO of Isinnova, an Italian engineering startup, heard the call for help last Friday. The hospital in Chiari, in the Brescia area of northern Italy where the coronavirus pandemic has hit hard, urgently needed valves for its respirators in order to keep patients who required oxygen alive. The manufacturer couldn’t provide them quickly enough and the hospital was desperate.
Fracassi immediately started tinkering with his engineers to reverse-engineer a 3D-printed version of the official part. Called a venturi valve, it connects to a patient’s face mask to deliver oxygen at a fixed concentration. The valves need to be replaced for each patient.
By Saturday evening, Fracassi had a prototype, and, the next day, he brought it to the Chiari hospital for testing. “They told us, ‘It’s good. It works. We need 100,’” says Fracassi, who is 36 and holds a Ph.d. in materials science with a focus on polymers. “We printed 100 of them on Sunday, and we gave all the pieces to the hospital. They are working very well.”
As the coronavirus spreads globally, shortages of medical supplies have become a major problem. Manufacturers simply can’t crank up their production of life-saving medical devices fast enough. The biggest supply crunch is with ventilators, but respirator parts like the ones in Italy and even simple nasopharyngeal swabs for testing are all in short supply. Meanwhile, the technology of 3D printing, which allows digital design of parts and the “printing” of them off a machine that creates them layer by layer, is ideally suited to emergency manufacturing because it is fast, cheap and can be done without a big factory.
But it raises issues, ranging from the quality of the products in a medical situation to the patents held by the original device’s manufacturers. Typically, new 3D-printed parts have to be certified. In Italy, Fracassi says, emergency rules during the coronavirus pandemic allowed that requirement to be waived. “They said, ‘We know the product you will bring will never be the same,’” says Alessandro Romaioli, Isinnova’s engineer, who designed the 3D-printed valves. Isinnova offered the hospital in Chiari the valves for free; Fracassi says the cost to print them is two or three Euros (or $2-3) apiece. Isinnova now has the capacity to produce around 100 parts per day, and is talking with a second hospital in Italy about sending the valves there, too.
Yet potential legal and medical issues have stopped Fracassi from distributing the digital design file more widely, despite receiving hundreds of requests for the 3D-printed valves. There are complexities because hospitals use a wide variety of respirators, each of which has slightly different technical specs and would require slightly different valves. Then, too, there’s the threat of potential patent litigation, as first raised by Techdirt. “We don’t know if something is patented. We just hope the factory can close its eyes because they cannot produce it in time,” Fracassi says. “It’s only for emergencies.”
Still, in the face of the coronavirus pandemic, 3D printing offers a smart stop-gap solution at least. Davide Sher, the 3D printing analyst who wrote the original story about Isinnova for trade publication 3D Printing Media Network, subsequently created an online Emergency AM Forum to help hospitals, 3D printing companies and inventors share ideas in the fight against COVID-19. As he writes there: “While there are both copyright issues and medical issues that need to be taken into account when 3D printing any medical product, and a critical one such as a venturi valve, in particular, this case has shown that a life-and-death situation could warrant using a 3D-printable replica.”
Fracassi says that Isinnova is now working to design other medical products that hospitals need during the coronavirus pandemic. The first is a mask. The startup created a prototype earlier this week, and sent it to the hospital for testing, he says. “We are waiting for a response, and if it works, we are ready,” Fracassi says. “Then every hospital can make their own masks.”
I’m a senior editor at Forbes, where I cover manufacturing, industrial innovation and consumer products. I previously spent two years on the Forbes’ Entrepreneurs team. It’s my second stint here: I learned the ropes of business journalism under Forbes legendary editor Jim Michaels in the 1990s. Before rejoining, I was a senior writer or staff writer at BusinessWeek, Money and the New York Daily News. My work has also appeared in Barron’s, Inc., the New York Times and numerous other publications. I’m based in New York, but my family is from Pittsburgh—and I love stories that get me out into the industrial heartland. Ping me with ideas, or follow me on Twitter @amyfeldman.
A sequel to a movie that you didn’t want to see in the first place is one thing, like Ghost Rider 2 after Ghost Rider. A sequel to having a COVID-19 infection would be something completely different.
You may think that the one “positive” of testing positive for the COVID-19 causing coronavirus (SARS-CoV2) and surviving would be that you won’t get infected by that virus again. At least not during this pandemic. Ah, but is this assumption really true? Will you indeed be immune to the SARS-CoV2 after you’ve recovered from a COVID-19 infection? Some reports out of Japan and China seem to suggest otherwise.
Does this case actually prove that re-infection with the virus is possible? Or was this just a mistake in the testing? Or did the person have a particularly weak immune system so that she couldn’t generate immunity? After all, one case can be an accident, an aberration, an anomaly, an aardvark in a sea of anemone.
Well, oops something like this happened again, according to a more recent NHK-World Japan report. This time it was a man in his 70’s, who first tested positive for SARS-CoV2 on February 14 while on a Diamond Princess cruise ship. After being transferred to a medical facility in Tokyo, he stayed there until testing negative for the virus. On March 2, he left the facility and traveled home via public transportation. However, the man eventually began feeling sick with a fever, which prompted him to go to a hospital on March 13. The following day he tested positive for the virus again.
Then there’s the February 14 article from Caixin, a Beijing, China-based media group, that was entitled “14% of Recovered Covid-19 Patients in Guangdong Tested Positive Again.” Umm, 14% would seem more like an “ooop” than an “ooops.” This CGTN news warned of such reinfection possibilities:
Remember though, these are news reports and not scientific studies yet. While the reappearance of Nicholas Cage with a flaming skull riding a motorcycle may not call for additional scientific studies, all of these cases certainly do. First, scientists need to confirm whether the test results were indeed accurate. Remember, no test is perfect. If people can screw up a drink order, they can certainly mess up a medical test. Even if a test is performed properly, you could still get a positive result when you don’t actually have an infection. On the flip side, just because you test negative doesn’t necessarily mean that there is no way that you are carrying the virus. That’s why a doctor may test you multiple times to be sure of a result.
Secondly, doctors and other scientists need to double-check or triple-check that each of these patients actually got re-infected with the virus rather than had an infection that simply lasted a long time. What if, for example, the cruise passenger and the tour bus guide each had fairly long infections and just happened to have intervening false negative test results? The tests could have simply been like commercial breaks in the middle of a single long episode of a television show.
Third of all, the amount of immunity that you build up after being exposed to any virus depends on not only virus itself but surprise, surprise your immune system and its response. When your immune system sees a particular virus for the first time, it can essentially get caught with its pants down, not ready to defend your body against this new invader. However, exposure to the virus either through a vaccine or getting infected may train your immune system so that, borrowing the words of former President George W. Bush, “fool me once, shame on — shame on you. Fool me — you can’t get fooled again.” If strong enough, your immune system then may be ready with proper defenses next time the virus comes calling. Could the cases of reinfection then be examples of people who happened to have weaker immune systems?
Or are these cases any indication that our immune systems may not be able to consistently build up enough protection against SARS-CoV2? Well, a review article published in January 2020 in the Journal of Medical Virology summarizes much of what is known about your immune system’s response to various types of coronavirus. As you can see, this involves a complex orchestra of different cells and chemicals. Therefore, the immune response to one virus won’t necessarily be the same as to another virus, even if both viruses were different types of coronaviruses. All of this also depends on how strong your immune system may be and how well your immune system recognizes an invader like SARS-CoV2.
Plus, your immune system has got to remember the virus. Over time, immunity may fade, allowing the virus to reinfect you. It’s like when you get back together with an ex after you have forgotten how terrible you are for each other. The question then is how long can your immune system remember SARS-CoV2?
With SARS-CoV2 having emerged so quickly, there just haven’t been enough studies yet on how your immune system may react specifically to SARS-CoV2 and how this may differ from person to person. Therefore, we have to rely on studies of other coronaviruses for now. The closest approximation is probably the even more evil cousin of SARS-CoV2, the original SARS virus that caused the outbreak of 2002-2003.
In a study published in a 2007 issue of Emerging Infectious Diseases, a research team from the Shanxi Provincial Center for Disease Control and Prevention in Taiyuan, China, followed 176 patients who had had severe acute respiratory syndrome (SARS). On average, SARS-specific antibodies remained at the same level in a patient’s blood for about two years. Then, during the third year after infection, antibody levels tended to drop precipitously. This suggests that immunity to the SARS virus may remain for two to three years with reinfection possible after three years.
Keep in mind though that antibody levels do not always correlate with immunity. They can be like selfies on Instagram, only indirect measures of what’s really going on at a deeper level. Some people may have immunity against a virus without detectable antibody levels, and some people may be very susceptible to infection even though antibodies are present. The only way to have determined if the patients actually had immunity against the SARS virus would have been to have re-exposed them to the virus and checked what happened. And that would have been a horrible experiment to do.
The other question is how many different versions of SARS-CoV2 may be running around, or rather spreading around since viruses don’t have little feet and little sneakers. It’s difficult to answer this question for sure without more thorough and widespread testing. According to a study published in the journal National Science Review, an analysis of samples from 103 COVID-19 cases suggests that at least two different versions of SARS-CoV2 are circulating. This doesn’t necessarily mean that these versions are so different that immunity to one version doesn’t mean immunity to another. Regardless, things may evolve in the near future. Viruses can be like the characters in Game of Thrones or an actor in a Broadway show, changing rapidly. Over time, the new coronavirus could possibly mutate to the point that new versions are no longer as recognizable by your immune system as the original version. After all, mutations are probably what allowed the virus to jump from another animal to humans.
Not knowing exactly how immunity against SARS-CoV2 works and how long it may last throws a gigantic wrench into public health planning. Many trying to predict the course of the pandemic have been assuming that once a high enough proportion of the overall population has been infected and has become immune, the pandemic will subside. Herd immunity is the percentage of the overall population that is immune to a given pathogen. When this percentage gets high enough, the virus will struggle to find more susceptible people to infect, sort of like trying to sell Justin Bieber T-shirts in a crowd when most of the people are already wearing such shirts. The belief is that when around 70% of the population is immune to the virus, SARS-CoV2 will struggle to continue transmitting.
However, things could change substantially if people can actually get re-infected with the virus or different enough versions of the virus end up circulating. Such possibilities would be yet more reasons to question the “herd immunity” approach to controlling the pandemic that’s currently being discussed in the U.K. and described by Sarah Boseley for The Guardian. Since there is no vaccine available against SARS-CoV2, there is actually talk of allowing those with stronger immune systems to get infected to achieve the 70% or so herd immunity threshold. Huh?
This strategy would make sense except for the fact that it doesn’t. First of all, those who get infected could end up having serious consequences such as death, which is typically a very serious consequence. This would be reminiscent of the saying that “the operation was successful, but the patient died.” Allowing people to become infected by a potentially deadly virus is always a risky proposition, sort of like playing roulette when your lungs are on the betting table. So far, the COVID-19 case-fatality rate seems to be somewhere between 1% and 3.4%. This isn’t as high as the rate for SARS but nonetheless significantly higher than that of a bad flu season.
Secondly, this herd immunity strategy depends on people not getting re-infected with the virus. But with the aforementioned reports from Japan and China, you have to wonder if the strategy is not a “herd immunity” strategy but rather a “herd immunity maybe” strategy to borrow the words of Carly Rae Jepsen. “Maybe” may work to some degree with flirting and dating but not when lives are at stake.
Third of all, this strategy assumes that people will not leave or enter the U.K. That may work only if you want to completely eliminate travel to and from the country.
Finally, such a strategy would run counter to other mitigation strategies such as social distancing as indicated by the following tweet:
Uh, U.K., would this really be O.K.?
All of this is a reminder that scientists do not yet know enough about this new coronavirus. What percentage of people become immune to the virus if exposed? How strong is the immunity? Will it actually prevent reinfection? How long would this immunity last? Is it two years as the SARS study hints at or could it be much shorter than that? How does all of this vary from person to person? How many different versions of the virus may end up circulating? As the Internet meme goes, I and many other scientists have so many questions.
Therefore, if you do get exposed to the virus and recover, don’t view it as a free pass to start hugging strangers, digging your fingers deep into your nose like you are looking for pocket change, and licking door knobs. Keep doing what everyone else should be doing such as social distancing, washing your hands frequently and thoroughly, keeping your filthy fingers from gravitating towards your gigantic face, and actively disinfecting surfaces, objects, and that enormous BTS statue that you have in your living room. Just because you survived the first infection, doesn’t necessarily mean that future exposures and possible infections will end up OK. As you know, sequels don’t always have the same endings.
I am a writer, journalist, professor, systems modeler, computational and digital health expert, avocado-eater, and entrepreneur, not always in that order. Currently, I am a Professor of Health Policy and Management at the City University of New York (CUNY), Executive Director of PHICOR (@PHICORteam), Associate Professor at the Johns Hopkins Carey Business School, and founder and CEO of Symsilico. My previous positions include serving as Executive Director of the Global Obesity Prevention Center (GOPC) at Johns Hopkins University, Associate Professor of International Health at the Johns Hopkins Bloomberg School of Public Health, Associate Professor of Medicine and Biomedical Informatics at the University of Pittsburgh, and Senior Manager at Quintiles Transnational, working in biotechnology equity research at Montgomery Securities, and co-founding a biotechnology/bioinformatics company. My work involves developing computational approaches, models, and tools to help health and healthcare decision makers in all continents (except for Antarctica) and has been supported by a wide variety of sponsors such as the Bill and Melinda Gates Foundation, the NIH, AHRQ, CDC, UNICEF, USAID and the Global Fund. I have authored over 200 scientific publications and three books. Follow me on Twitter (@bruce_y_lee) but don’t ask me if I know martial arts
Coronaviruses (CoV) are a family of viruses that cause sicknesses like the common cold, as well as more severe diseases, such as Middle East Respiratory Syndrome and Severe Acute Respiratory Syndrome. A novel coronavirus (nCoV) is a new strain – one that hasn’t previously been recognized in humans. Coronaviruses cause diseases in mammals and birds. A zoonotic virus is one that is transmitted between animals and people. When a virus circulating in animal populations infects people, this is termed a “spillover event”. How does CoVID-19 affect the body? The virus is fitted with protein spikes sticking out of the envelope that forms the surface and houses a core of genetic material. Any virus that enters your body looks for cells with compatible receptors – ones that allow it to invade the cell. Once they find the right cell, they enter and use the cell’s replication machinery to create copies of themselves. It is likely that COVID-19 uses the same receptor as SARS – found in both lungs and small intestines. It is thought that CoVID-19 shares many similarities with SARS, which has three phases of attack: viral replication, hyper-reactivity of the immune system, and finally pulmonary destruction. Early on in infection, the coronavirus invades two types of cells in the lungs – mucus and cilia cells. Mucus keeps your lungs from drying out and protects them from pathogens. Cilia beat the mucus towards the exterior of your body, clearing debris – including viruses! – out of your lungs. Cilia cells were the preferred hosts of SARS-CoV, and are likely the preferred hosts of the new coronavirus. When these cells die, they slough off into your airways, filling them with debris and fluid. Symptoms include a fever, cough, and breathing difficulties. Many of those infected get pneumonia in both their lungs. Enter the immune system. Immune cells recognize the virus and flood into the lungs. The lung tissue becomes inflamed. During normal immune function, the inflammatory process is highly regulated and is confined to infected areas. However, sometimes the immune system overreacts, and this results in damage to healthy tissue. More cells die and slough off into the lungs, further clogging them and worsening the pneumonia. As damage to the lungs increases, stage three begins, potentially resulting in respiratory failure. Patients that reach this stage of infection can incur permanent lung damage or even die. We see the same lesions in the lungs of those infected by the novel coronavirus as those with SARS. SARS creates holes in the lungs, so they look honeycomb-like. This is probably due to the aforementioned over-reactive immune response, which affects tissue both infected and healthy and creates scars that stiffen the lungs. As such, some patients may require ventilators to aid breathing. The inflammation also results in more permeable alveoli. This is the location of the thin interface of gas exchange, where your lungs replace carbon dioxide in your blood with fresh oxygen you just inhaled. Increased permeability causes fluid to leak into the lungs. This decreases the lungs’ ability to oxygenate blood, and in severe cases, floods them so that you become unable to breathe. Sometimes, this can be fatal. The immune system’s over-reaction can also cause another kind of damage. Proteins called cytokines are the immune system’s alarm system, recruiting immune cells to the infection site. Over-production of cytokines can result in a cytokine storm, where there is large-scale inflammation in the body. Blood vessels become more permeable and fluid seeps out. This makes it difficult for blood and oxygen to reach the rest of the body and can result in multi-organ failure. This has happened in the most severe cases of CoVid-19. Although there are no specific treatments for coronaviruses, symptoms can be treated through supportive care. Also, vaccines are currently in development. What can you do to protect yourself from CoVid-19? Basic protocol comes down to regular hand washing, avoiding close contact with anyone coughing or sneezing, avoiding unnecessary contact with animals, washing hands after contact with animals, thoroughly cooking meat and eggs prior to consumption, and covering your mouth and nose while coughing or sneezing. Respiratory viruses are typically transmitted via droplets in sneezes or coughs of those infected, so preventing their travel stops the spread of disease. Alveoli model from: https://www.turbosquid.com/3d-models/…