Smoke Gets In Your Eyes -- Your Lungs and Your Brain

"It's not just a few days in these extreme events that you need to protect  yourself."

"It is also the days when the sky looks OK [while air quality indexes or weather reports warn of the presence of smoke]."

Dr. Kai Chen, associate professor, Yale School of Public Health 

 

The health effects of short-term PM_2.5 exposure, and subsequently smoke, can range from relatively minor (e.g., eye and respiratory tract irritation) to more serious health effects (e.g., exacerbation of asthma and heart failure and premature death). In addition, there is initial evidence that short-term smoke exposure may lead to preterm birth (Picciotto et al. 2024) and impact brain function (i.e., cognitive performance as measured through a brain-training game) (Cleland et al. 2022). Fine particles are respiratory irritants, and exposures to high concentrations can lead to persistent coughing, phlegm, wheezing and difficulty breathing. Exposure to PM_2.5 may affect the body’s ability to remove inhaled foreign materials, such as viruses and bacteria, from the lungs. For example, some studies have reported an increase in the risk of COVID-19 cases and deaths in response to wildfire smoke exposure (Zhou et al. 2021; Meo et al. 2021; Schwarz et al. 2022). Although most healthy people will recover quickly from smoke exposure, some may experience health effects such as pulmonary inflammation and transient reductions in lung function (U.S. EPA 2019).

United States Environment Protection Agency  

Vancouver skyline   Wildfires and smoke have always occurred in British Columbia, but they are becoming more frequent and severe as the climate changes. Wildfire smoke is a form of air pollution that can affect your health.  BC Centre for Disease Control 

 

Evaluation of air pollution from wildfires presents unique challenges, compared to air pollution from other sources, such as traffic or industrial point sources, as smoke exposure is seasonal and episodic in nature (Gould et al., 2023). Also, as the number and size of wildfires impacting an area are variable and as smoke production from wildfires is not constant or steady, the concentration of smoke experienced by populations can vary considerably, and can include high levels of exposure for short time periods or moderate exposure levels lasting for several days or longer. Additionally, to evaluate the health effects of wildfire smoke, it is necessary to distinguish the contribution of wildfire smoke from that of other sources of air pollution within the mixture that people are exposed to. To address this, researchers have employed a variety of methods to assess exposure to wildfire smoke for use in health studies including use of land-based PM monitors, satellite imagery, air quality modelling, comparison of fire versus non-fire periods, proximity to wildfire burn area, and self-reports. In these studies, the most commonly used surrogates for wildfire smoke exposure are PM_2.5 (particles with a diameter of 2.5 micrometres or less) and PM₁₀ (particles with a diameter of 10 micrometres or less). For the primary investigations included in the systematic reviews considered here, the health outcome data were based on administrative sources (for example, mortality registries, health care utilization data), surveys, or self-reports. In addition, most of the primary studies focused on short-term or episodic exposure to wildfire smoke (that is, daily exposure), while some of the studies assessing mental health impacts considered health effects in years following the wildfires, and studies of reproductive or developmental impacts considered wildfire smoke exposure during the gestational period. It is noted that the health effects of PM_2.5, a key pollutant in wildfire smoke, have been extensively studied and Health Canada has evaluated the health risks of ambient PM_2.5 (that is, PM_2.5 from all sources combined) (Health Canada 2022). 

Government of Canada 

People who are exposed to smoke from wildfires, according to more recent scientific investigations, are increasingly assailed by lung-damaging toxins, but new discoveries identify that hearts, brains and other body organs are also being damaged by wildfire smoke. Smoke exposure could sound the death knell of up to 1.9 million people in the United States alone, over three decades, according to one 2025 study. Lungs can be penetrated deeply by the concentration of airborne particles known as PM2.5, from wildfires.

 

PM2.5 is a primary pollutant that air quality indexes measure, but fails to reflect other substances that can be contained in wildfire smoke that include lead, mercury and formaldehyde, cautions Karl Nadeau, dean of the University of California, Los Angeles Fielding School of Public Health. Preliminary research suggests that wildfire smoke may be of greater harm than air pollution from more common sources such as car exhaust. Fire in proximity to urban areas, moreover, may be of particular toxicity, through consuming buildings vehicles and electronics.

 

Smoke and flames from the Palisades Fire fill the sky as seen from the Pacific Palisades neighborhood of Los Angeles. | Getty Images

 

Associations between wildfire smoke and cardiovascular hospitalization, diabetes complications, preterm birth, cancer, impaired cognition and other problems, as well as respiratory effects including  attacks of asthma have been associated through scientific analytical studies. Wildfire smoke was linked in a 2024 study to deaths from cardiovascular, digestive, endocrine and kidney diseases. Asthma attacks and heart attacks can increase within an hour, in the presence of the severity of ambient smoke, pointed out professor Michael Brauer with the University of British Columbia.

 

Cognitive effect research has seen a significant expansion, explains Stephanie Cleland, associate professor at Simon Fraser University in British Columbia. Dr. Cleland was lead author of a 2022 study finding smoke exposure to be associated with lower scores on a 'brain training' game. A link between cumulative exposure throughout a school year and lower standardized test scores was also found through research, while other studies indicate a possible association with dementia. 

 

Less dramatic, lower-level exposures over time have an add-on impact, according to Professor Chen, who suggests the wearing of masks to be avoidance-helpful to exposure to ambient smoke during such events, not necessarily only when the surrounding air is redolent of burning, charred wood, and the atmosphere turns grey in reduced visibility with wildfire smoke. One study published in 2025 linked the risk of death from all causes with three-year exposure to wildfire smoke. Yet another 2025 study concluded that as average wildfire exposure increased, North Americans over age 65 suffered a higher risk of dying from chronic obstructive pulmonary disease.  

 

A woman wears an N95 mask to protect herself from high levels of smoke pollution. Daniiielc, Getty Images

 

"The data pretty clearly say that there is no safe level of exposure to wildfire smoke: the more exposure we get, the worse a range of health outcomes. The data also pretty clearly show that our notion of sensitive groups should probably be greatly expanded. In addition to kids, elderly populations, or anyone else with preexisting conditions, like asthma, we need to think about populations like pregnant people whose birth outcomes can be substantially affected by exposure. Portable indoor filtration is often the best option for many households, and well-fitting N95 masks can help when outside. "

"Climate change, and in particular increasing fuel aridity brought about by hotter temperatures and variable rainfall, is playing a central role in the recent rapid increase in wildfire activity and smoke exposure throughout the US. It is certainly not the only factor, but is substantially amplifying the risk brought about by other factors, which include a century of fire suppression that has left abundant fuels in our wildlands, as well as increased human construction and activity in the wildland-urban interface. We can say with strong confidence that climate change has made these events much more likely and much more severe."

Marshall Burke,  associate professor, Stanford Doerr School of Sustainability 

The Link Between Asthma and Brain Tumours

"Of course, we're not going to start inducing asthma in anyone; asthma can be a lethal disease. But what if we could trick the T cells into thinking they're asthma T cells when they enter the brain, so they no longer support brain tumour formation and growth?"

"These findings open the door to new kinds of therapies targeting T cells and their interactions with cells in the brain."

"The most exciting part of this is that it shows that there is a normal communication between T cells in the body and the cells in the brain that support optic pathway glioma formation and growth."

"The next step for us is to see whether this is also true for other kinds of brain tumours. We're also investigating the role of eczema and early-childhood infections, because they both involve T cells."

David Gutmann, researcher, expert on neurofibromatosis, professor of genetics, of neurosurgery and paediatrics, Washington University School of Medicine, St.Louis 

(bobex73 - stock.adobe.com)

 

Insatiable curiosity teamed with the methodology and collaboration between inquisitive scientific minds often represent the emerging blueprint for discovery of new potential therapies in solving human ills that often threaten lives. Researchers at Washington University School of Medicine in St.Louis discovered that when mice develop asthma, their T cells activate in such a manner that induces inflammation in the lungs, yet prevents growth of tumours in the brain.

In essence, the research team may just have happened upon a new method of designing a response to brain tumors after discovering just why it is that the peculiar and unproven previously-known connection between asthma sufferers being less likely than others to go on to develop this insidious form of cancer. Published in the journal Nature Communications, the study explored the relationship, mysterious as it is, between inflammation diseases and brain tumours.

These two conditions so very different from one another, long puzzled the medical community in a possible connection, despite which new research has led to the discovery that T cells in the body may hold the answer to a question that has long mystified scientists. When mice develop asthma, their T cells activate to induce inflammation in the lungs, an effect that also has the effect of preventing growth of tumours in the brain. 

It was first postulated 15 years ago that inflammatory diseases have a relation to reduced risk of brain tumours, based largely on epidemiologic observations. No obvious link presented, however, linking the two conditions, leaving many researchers in doubt that an association actually was present. Dr. Gutmann, senior scientist in the study, noticed an inverse relationship between the two conditions some five years earlier through study of neurofibromatosis; a set of complex genetic disorders leading to the growth of tumours on nerves in the brain and throughout the body.

Uncertain how to link to a connection, more recent research taking place in his laboratory identified the key role that immune cells play in formation of tumours on the optic pathways of children with type 1 NF (neurofibromatosis). A collaboration resulted with Jit Chatterjee, post-doctoral researcher who was in the process of diagnosing the underlying mechanism at work. Dr.Chatterjee exposed mice that were engineered to carry a mutation in the NF1 genes to result in tumours on their optic nerves.

Glioma

These young mice in their formative period of growth were exposed to irritants known to be the cause of asthma, administering a salt-water solution to a control group of mice. The mice that developed asthma turned out not to experience tumour growth on their optic nerves. Then it was revealed through further study that the T cells of these mice were behaving differently after developing asthma, secreting a protein named decorin, known to act on and irritate the lining of the brain airways.

The protein blocked the activation of immune cells called microglia, that promote tumour growth. "As we understand this communication between T cells and the cells that promote brain tumors better, we’ll start finding more opportunities to develop clever therapeutics to intervene in the process", explained Dr. Gutmann.