As wildfire smoke growing swathes of the West, scientists are beginning to understand more about how their smoke affects the transmission and severity of COVID-19 and other illnesses, and how it differs from that of other types of air pollution.
Alongside a global pandemic that has killed millions, residents of the American West have for two consecutive summers confronted unprecedented wildfire seasons. So far this year, roughly 43,500 wildfires have charred more than 5 million acres, and fires continue to grow in frequency and intensity. With them come a number of human health concerns, including the risk that bodies worn down by exposure to smoke could more easily succumb to infectious diseases.
Teasing out the effects of wildfire smoke on health is both urgent and difficult. “With wildfires, we’re generally looking in the rearview mirror, looking retroactively,” says Sheryl Magzamen, a respiratory epidemiologist at Colorado State University. While air pollution from cars can be studied in real time by placing sensors near roads, she adds, wildfires are sporadic and unpredictable. “Where they are and when they happen and where the smoke goes is really complex.”
But a burgeoning interest in respiratory diseases born out of the pandemic are bringing together wildfires and human health in new ways. While many effects are ascribed to smoke making lungs more susceptible to diseases such as influenza and COVID-19, early research indicates that in addition, smoke may itself also be a vector for spreading pathogens. “Even though it’s upsetting to think about sometimes, it’s an exciting time to be doing this kind of work,” Magzamen tells The Scientist. “There’s energy and motivation that maybe wasn’t there before.”
How dangerous are hazy skies?
The health effects of air pollution are well-documented, and scientists are beginning to probe wildfire smoke as a particularly damaging subset. Dirty air—full of exhaust from cars and factories, dust, smoke, metals, and pollen—kills an average of 9 million people worldwide each year, and a global study published today (September 8) in The Lancet Planetary Health attributed 33,500 deaths each year directly to wildfire pollution. For decades, scientists have linked exposure to particulate matter in pollution to increased incidences of asthma, allergies, cardiovascular disease, diabetes, dementia, and certain cancers. “There’s really no part of the body it doesn’t touch,” says Mary Prunicki, the director of air pollution and health research at Stanford University’s Sean Parker Center for Asthma and Allergy Research.
Fine particles less than 2.5 micrometers in diameter (PM2.5) are considered to be the most dangerous component in air pollution, including smoke. That’s because the particles are so small that they can pass across the lungs and enter the blood. “There’s localized inflammation in the lung itself, but when the particle size is small enough, that inflammation and other problems can now happen throughout the body,” Prunicki tells The Scientist.
See “Q&A: Pollution Linked to 15 Percent Increase in COVID–19 Deaths”
Inside our lungs, PM2.5 interferes with oxygen exchange and negatively affects lung function, making it hard to breathe deeply and disrupting the ability of cilia in the lungs to clear mucus and the potential irritants it contains, including viruses. Once it passes into the blood, PM2.5 also causes inflammation in the heart and brain and primes our immune system to react aggressively to allergens and bacteria, leaving us more vulnerable to viral pathogens such as influenza.
A study in rural Montana found that periods of dense wildfire smoke were associated with unusually bad influenza seasons in the winters that followed. University of Montana computational ecologist Erin Landguth, who led the study, says she originally expected smoke exposure in the weeks before flu season started to have the strongest association with the number of cases. Instead, PM2.5 levels from months before—during the height of the fire season—correlated most strongly with influenza cases: a small increase in the daily average summer PM2.5 was associated with an increase in the subsequent winter influenza rate of between 16 and 22 percent. “We were not expecting to see that long, long delay, but we threw a bunch of modeling at it and sure enough, it always popped out,” she says.
This and research on fires is leading scientists to a better understanding of the unique risks posed by wildfire smoke, and recent evidence has shown that it may actually be more dangerous than other types of air pollution such as car exhaust. A study published in Nature Communications found that in Southern California, PM2.5 attributed to wildfire smoke was associated with a 10 percent increase in hospitalizations for respiratory events—the highest rise attributed to any source the team studied—and that wildfire-specific PM2.5 appeared to be up to 10 times more harmful to human health than that from other sources.
One reason may be that PM2.5 stemming from wildfires has a different composition than particulate matter from other sources. Wildfires burn wood, which can cause respiratory issues—as in the case of eucalyptus—but they might also burn rubber, metal, plastic, glass, or other synthetic materials, creating smoke that is more toxic when inhaled. Indeed, research in mice has shown that the respiratory toxicity of wildfire PM2.5 is three to four times greater than equal doses of ambient air pollution.
Evidence of the long-lasting damage caused by wildfire smoke in particular exists for people as well. For 50 days in 2017, smoke from across the West blanketed Seeley Lake, Montana, with a daily average air quality index of 221 micrograms per cubic meter (anything over 150 micrograms per cubic meter is considered unhealthy). Researchers at the University of Montana tracked 95 residents of the area over the next two years. Just after being exposed to smoke, roughly 10 percent of the participants had disrupted lung functioning similar to asthma, as measured by a spirometer. One year later, that number jumped to almost 46 percent, dropping only slightly to 34 percent the year after that.
People don’t need to be near fires to be affected by their smoke, either. Because fires produce erratic wind patterns that can transport particles high into the atmosphere, smoke from fires on the West Coast darkened the skies over Manhattan in July. Like other types of air pollution, PM2.5 becomes oxidized and produces more free radicals as it ages, and because wildfire-derived PM2.5 often starts out as more inherently toxic because of what gets burned, it could also cause more damage once it enters the body, although the specifics of this effect are still under investigation. “We don’t yet know whether acute exposure to a less toxic type of smoke is ‘better’ than a smaller quantity of more toxic smoke,” Magzamen tells The Scientist. “But if we keep having these fires, I think we’ll probably find out.”
The wildfire smoke–COVID–19 connection
The increasing frequency and intensity of wildfires has taken place in tandem with another emergency: the COVID-19 pandemic. When the virus first appeared in the US in the spring of 2020, many residents were contending with evacuation orders prompted by wildfires alongside stay-at-home orders.
More than a year later, researchers are now releasing studies that document how that all played out. In Reno, Nevada, residents in 2020 encountered smoke from fires burning across several states, even those that were hundreds of miles away. “Normally, you would have really beautiful views, but even right now I’m looking out and you can’t see the buildings downtown,” says Daniel Kiser, a data scientist at the Desert Research Institute in Nevada who spoke to The Scientist in August, as several fire burned nearby. “It’s just not a fun experience.”
Kiser worked with a local hospital to study whether exposure to wildfire smoke was associated with the rate of positive SARS-CoV-2 tests in Reno. He measured PM2.5 using an array of four sensors and supplemented his readings with data from the EPA. From a local hospital, he received almost 36,000 test results. Between August 16 and October 10, 2020, the time period that year most affected by the smoke, positive cases rose by more than 17 percent (178 additional cases out of a total of 2,881). “I wouldn’t say that we were particularly surprised by what we found,” Kiser says, adding that smoke may make otherwise asymptomatic cases into symptomatic ones, or make symptoms more severe, “which might motivate [patients] in turn to go get tested when they might not otherwise have.”
More recently, Harvard University biostatistician and epidemiologist Francesca Dominici and her colleagues extended those findings, modeling how many COVID-19 cases and deaths could be attributed to wildfire smoke across 92 counties in California, Oregon, and Washington. To estimate the number of “fire days” each county experienced between March and December of 2020, team members used satellite imagery from the National Oceanic and Atmospheric Administration (NOAA) and PM2.5 readings from the EPA. They drew on county health records for numbers of daily cases and deaths.
The team found that fire days had higher levels of PM2.5 compared to nonfire days, and that elevated levels of wildfire-derived PM2.5 corresponded with more hospitalizations and deaths from COVID-19. “The general trend is there,” Dominici tells The Scientist, although the impact was not uniform across counties. In some places, there may have only been a handful of COVID-19 cases or deaths linked to wildfire. But in California’s Sonoma County, one of the hardest hit areas, the authors attributed more than 1,700 additional cases—a 65 percent increase—and 18 additional deaths to wildfire smoke.
That the trend was not consistent does not surprise her, Dominici tells The Scientist. The model doesn’t account for demographics, public health guidelines, or human behavior. There is a possibility, for example, “that wildfires are the cause of increasing numbers of COVID-19 cases even if PM2.5 is not, because others have been hypothesizing that people are spending more time indoors” where they could infect others, she says.
That interpretation contradicts preliminary results presented by Magazamen’s colleagues at the International Society for Environmental Epidemiology conference in August. She and her team found that while deaths in Colorado in 2020 did increase overall, the interplay between wildfire smoke and COVID-19—which cooccurred between March and December of 2020—actually resulted in a reduced risk of death compared to periods in the preceding decade with smoke only. They hypothesized that smoke from local fires drove people indoors, but that this resulted in a decrease in SARS-CoV-2 transmission. Contradictory findings don’t necessarily mean either study is wrong, Magazamen says. Rather, it comes back to a lack of detailed demographic information such as age or occupation that might explain the different trends. “We don’t have that level of community data, because it’s hard to do it in real time. But through sensors and crowdsourcing science, our hope is that we’re going to start to be able to figure that out.”
Getting at mechanisms
In addition to large epidemiological studies that show broad trends in infections, researchers are also beginning to probe for possible cellular-level mechanisms to find out exactly how wildfire smoke might make people more susceptible to COVID-19.
One hypothesis is that when SARS-CoV-2 particles are attached to particulate matter, they’re able to remain viable for longer while traveling farther in the air and penetrating deeper into the respiratory tract. Macrophages in the lung’s alveoli that typically engulf and remove particles sometimes fail to clear the debris when exposed to chronic smoke, instead remaining with their ingested cargo in the alveolar region. In this scenario, the PM2.5 and other, smaller particles do double duty, shuttling the virus while simultaneously increasing oxidative stress and inducing local inflammation, which damages epithelial cells and makes them more susceptible to viral infection. Once SARS-CoV-2 is inside the lungs, that inflammation facilitates viral replication by disrupting normal cell function, while the leaky, damaged epithelial cells let the virus enter circulation and move to other parts of the body.
Another active area of research, Prunicki says, is how smoke and SARS-CoV-2 activate similar inflammatory and viral-recognition pathways, which may not only increase the risk for infection, but also lead to more severe cases of COVID-19. To do this, she adds, scientists are looking more closely at the individual cells and specific genes involved.
In research that hasn’t yet been peer reviewed, scientists exposed cultured human nasal epithelial cells to wood smoke from eucalyptus or red oak and then infected the cells with SARS-CoV-2. Cells that hadn’t been exposed to smoke upregulated antiviral response genes upon encountering the virus, including those involved in recognizing viruses, blocking viral entry, and signaling among cells. But epithelial cells that were bathed in smoke, particularly from red oak, downregulated many of those same genes in the three days following infection. The effect was sex-dependent, with cells from women showing more gene suppression than men, supporting epidemiological data showing that during wildfires in California in 2008, women were more likely than men to visit the hospital for asthma- or hypertension-related reasons.
Nasal epithelial cells are thought to be a primary site for SARS-CoV-2 infection because of their high expression of angiotensin-converting enzyme II, or ACE2, that the virus uses to slip inside cells. But ACE2 is found on many different cell types, and emerging evidence suggests that exposure to wildfire smoke causes epithelial cells in alveoli and pulmonary capillaries to increase production of ACE2 to reduce cytokine-induced lung injury or inflammation and avoid acute respiratory distress syndrome (ARDS). Rats exposed to wood smoke expressed more ACE2 within their alveolar cells, and smokers express more ACE2 in their lower respiratory tract epithelial cells than nonsmokers. “If there is more of that ACE2 receptor, it can make it easier for the virus to enter the cell and reproduce, which could lead to more infections,” Kiser tells The Scientist, and, at least in mice, viral binding to ACE2 also keeps the enzyme from its role in repairing PM2.5-induced lung damage.
Outstanding questions
Even as the nexus of wildfires and human health draws more attention, much remains unknown: how chronic exposure to smoke might differ from acute events, and how the age of the smoke affects that dynamic; the details of how wildfire smoke makes humans susceptible to diseases like COVID-19; how much disease transmission takes place via airborne transport in wildfire smoke; and how to best protect against the double threat of a pandemic and rampant climate change.
It’s increasingly urgent to find out. A 2019 census report stated that roughly a quarter of the US population resides in the West, where wildfires are projected to increase over the next several decades. Indeed, six of the 20 largest fires in California’s history took place in 2020 alone, and the state is expected to emit between 19 and 101 percent more wildfire-derived material, including greenhouse and trace gases as well as particulate matter, through 2100.
In addition, scientists are predicting that COVID-19, too, will continue to be a part of daily life in the future—perhaps as a less potent, seasonal virus like its endemic coronavirus cousins. The current pandemic aside, in the long run, “I think, unfortunately, we are going to be dealing with viruses that continue to attack us and our respiratory system,” Harvard’s Dominici tells The Scientist. Given that the mechanisms behind how wildfires leave people more susceptible to COVID-19 remain largely unknown, she says, “I think this is going to be a really important area of research for my team for quite a while moving forward.”
Originally Published By TheScientist