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Review

Effects of Wildfire Exposure on the Human Immune System

by
Davide Frumento
1,* and
Ștefan Țãlu
2,*
1
Department of Pharmacy, University of Genoa, Viale Benedetto XV 7, 16132 Genoa, Italy
2
The Directorate of Research, Development and Innovation Management (DMCDI), The Technical University of Cluj-Napoca, Constantin Daicoviciu Street, No. 15, 400020 Cluj-Napoca, Romania
*
Authors to whom correspondence should be addressed.
Fire 2024, 7(12), 469; https://doi.org/10.3390/fire7120469
Submission received: 5 September 2024 / Revised: 15 October 2024 / Accepted: 21 November 2024 / Published: 9 December 2024
Browse Figure
Versions Notes

Abstract

:

Highlights

  • Wildfire smoke contains immuno-toxic components, including fine particles, VOCs, and PAHs.
  • Chronic exposure to wildfire smoke can induce oxidative stress, inflammation, and long-term effects on the immune system.
  • Wildfire smoke poses significant risks to immune health due to the presence of toxic com-ponents.
  • Ongoing exposure to these toxic components may lead to persistent health effects, underlining the need for intervention and protective measures.

Abstract

Wildfires have become a significant environmental and public health concern worldwide, particularly due to their increased frequency and intensity driven by climate change. Wildfire smoke, composed of a complex mixture of particulate matter, gases and chemicals, has been linked to numerous health issues, primarily affecting the respiratory and cardiovascular systems. However, emerging evidence suggests that wildfire smoke exposure also has profound effects on the immune system. This review aims to synthesize current knowledge on how wildfire smoke exposure affects the human immune system, including acute and chronic impacts, underlying mechanisms and potential long-term consequences. The review discusses the role of inflammation, oxidative stress and immune cell modulation in response to wildfire smoke, highlighting the need for further research to fully understand these effects.

1. Introduction

Wildfires, also known as forest fires or bushfires, are uncontrolled fires that spread rapidly across vegetation, whose incidence and severity have been increasing globally due to climate change, inappropriate land management practices and various anthropogenic activities [1]. Such phenomena release large amounts of smoke, i.e., a complex mixture of gases and particulate matter (PM). While smoke’s detrimental effects on both the respiratory and cardiovascular systems are well-documented, its impact on the immune system has been less studied [2]. Short-term exposure can lead to immediate symptoms such as coughing, throat irritation and difficulty in breathing, while long-term exposure can exacerbate chronic conditions like asthma, bronchitis and heart disease [3].
Significant alterations in key immune pathways have been observed in both animals and humans following exposure to wildfire smoke, with effects persisting for days to weeks. Specifically, such exposure has been linked to the activation of the arylhydrocarbon receptor, Toll-like receptor and NF-ĸB signaling pathways, alongside an increase in pro-inflammatory cytokines and reactive oxygen species [4,5,6]. Furthermore, firefighters who have been exposed to wildfires exhibit heightened pulmonary and systemic inflammation; serum samples collected from these individuals 12 h post-exposure reveal elevated levels of IL-6 and IL-12, coupled with a reduction in IL-10 [7,8].
In recent years, there has been growing concern about the impact of wildfire smoke on the immune system. While traditional research has focused on the direct effects of smoke on the respiratory and cardiovascular systems, emerging studies indicate that the immune system may also be adversely affected by prolonged exposure to wildfire smoke. This review examines the growing body of evidence concerning the impact of wildfire smoke on human immune system functionality.

2. Composition of Wildfire Smoke and Immunotoxins

Wildfire smoke contains a variety of immuno-toxic components, including particulate matter (PM), volatile organic compounds (VOCs: benzene, toluene, ethylbenzene, xylenes, isoprene and pinene [9]) and polycyclic aromatic hydrocarbons (PAHs: acenaphtene, acenaphtylene, anthracene, chrysene, fluoranthene, fluorene, phenanthrene and pyrene [10]). A gaseous mixture such as this is likely to contain a significant number of allergens due to the specific conditions of the fire, which often leads to the incomplete combustion of vegetative material [11]. PM, particularly fine particles (PM2.5), can penetrate deep into the lungs and enter the bloodstream, posing a significant risk to human health. Interestingly, they are known to induce oxidative stress and inflammation, which can disrupt immune function [12]. In fact, PM2.5 exposure is associated with increased levels of pro-inflammatory cytokines (e.g., IL-6, TNF-alpha and IL-1alpha), leading to a systemic inflammatory response, which can affect the functionality of various immune cells, such as macrophages, dendritic cells, T cells and B cells [13]. VOCs and PAHs are organic compounds found in wildfire smoke and have both immunosuppressive and pro-inflammatory effects [14]. They are metabolized to produce reactive intermediates able to bind DNA, causing oxidative damage and mutagenesis, leading to immune cell apoptosis or dysregulation [15] VOCs, such as formaldehyde and benzene, are known to modulate immune cell function, including the suppression of lymphocyte proliferation and antibody production [16], while exposure to PAHs has the potential to induce thymus atrophy, as persistent activation of the aryl hydrocarbon receptor (AhR) may influence the proliferation of thymocytes, consequently leading to a reduction in T lymphocyte populations within the thymus [17].

3. Acute Immune Responses to Wildfire Smoke Exposure

Acute exposure to smoke from wildfires can trigger immediate and potentially severe immune reactions, primarily manifested through inflammation and oxidative stress [18,19]. Upon exposure, the immune system starts an inflammatory response to protect from inhaled particles and chemicals [20], elevating the production of pro-inflammatory cytokines and chemokines, such as IL-8 and MCP-1, which facilitates the recruitment of immune cells to areas of inflammation. It must be noted that histamine can be released too, possibly due to allergic reactions [13]. This reaction, while inherently protective, may become maladaptive if it is prolonged or excessive [20]. Inhalation of wildfire smoke has been linked to elevated concentrations of acute-phase proteins, including C-reactive protein (CRP), which suggests the presence of systemic inflammation [21]. Oxidative stress arises from a disparity between the generation of reactive oxygen species (ROS) and the capacity of the body’s antioxidant defenses to neutralize them [22]. The aforementioned chemicals, including PM, have the capacity to produce reactive oxygen species (ROS), which can induce oxidative stress. This oxidative stress may result in the impairment of cellular components such as lipids, proteins and nucleic acids, thereby potentially affecting the functionality of immune cells [23]. Furthermore, oxidative stress has been shown to impair immune cell functions, impacting both macrophages and neutrophils by reducing their ability to internalize and kill pathogens [24]. Acute exposure to wildfire smoke in humans is linked to a rise in respiratory symptoms, which encompasses heightened asthma symptoms (which is an autoimmune process) and an increase in medication usage, as well as exacerbations of chronic obstructive pulmonary disease [25,26,27,28].

4. Chronic Immune Effects of Prolonged Wildfire Smoke Exposure

Chronic exposure to wildfire smoke can have long-term effects on the immune system, such as suppression (induced by PM2.5 and PAHs) and increased susceptibility to both infections and chronic diseases [29,30,31]. Prolonged exposure has been associated with reduced counts and impaired function of lymphocytes, macrophages and natural killer (NK) cells, increasing susceptibility to infections and reducing vaccine efficacy [22]. Long-term effects may result in impaired adaptive immunity, with decreased antibody production and altered T-cell responses [32], potentially exacerbating or contributing to the development of autoimmune and allergic diseases [33]. Interestingly, air pollutants including wildfire smoke, may trigger or exacerbate autoimmune diseases such as rheumatoid arthritis and systemic lupus erythematosus [34], enhancing responses to allergens and increasing the risk of developing allergic disorders such as asthma and allergic rhinitis [35].
Exposure to smoke from wildfires and air pollution stemming from traffic has been linked to the activation of aryl hydrocarbon receptors, toll-like receptors and the signaling pathway of nuclear factor (NF)-ĸB. This exposure also leads to an increase in pro-inflammatory cytokines, including IL-22 [6]. Firefighters exhibit elevated levels of IL-6 and IL-12, alongside a reduction in IL-10, in their serum 12 h following exposure to a wildfire [36]. The correlation between environmental pollutants and the activation of the NLRP3 inflammasome, along with the subsequent induction of pyroptosis, has been linked to a variety of diseases [37,38]. Perfluoroalkyl substance pollutants, for instance, have been demonstrated to stimulate the innate immune response via the absence of melanoma 2 (AIM2) inflammasome [39]. In a separate investigation, it was demonstrated that micro- and nanoplastics, which are becoming more prevalent in the atmosphere, can activate the inflammasome [40].

5. Mechanisms of Immune Modulation by Wildfire Smoke

Several mechanisms have been proposed to explain how wildfire smoke affects the immune system, including oxidative stress, inflammation and epigenetic changes [41]. Interestingly, oxidative stress and inflammation are closely linked and have been proven to be central mechanisms by which exposure impacts the immune system [42]. Inhaled smoke chemicals can activate NADPH oxidase in immune cells, leading to increased ROS production and perpetuating a cycle of oxidative stress and inflammation [43]. Epigenetic changes, such as DNA methylation and histone modifications, which can alter gene expression related to immune responses [44], may lead to altered expression of genes involved in immune function, potentially contributing to immune dysregulation and increased disease susceptibility [45]. The composition of the respiratory and gut microbiome, which can influence immune responses, has been shown to be subject to smoke-exposure-induced variations [46], potentially contributing to immune dysregulation and increased susceptibility to infections and inflammatory diseases [47]. The inhalation of particulate matter (PM) from wildfires triggers an immune and inflammatory response that seems to play a role in the development of disease (Figure 1). Research indicates that exposure to fine PM from diverse origins leads to an elevation in the production of lymphocytes, eosinophils and neutrophils [48,49,50,51].

6. Vulnerable Populations

Certain populations are more vulnerable to the immune effects of wildfire smoke than others, including children, the elderly and individuals with pre-existing medical conditions [52]. The developing immune system of children may be more susceptible to the immuno-toxic effects, potentially leading to long-term health consequences [53], while the aging immune system is characterized by immuno-senescence, making the elderly more vulnerable to the effects of exposure, including increased susceptibility to infections and exacerbation of chronic inflammatory conditions [54]. A notable decline in lung function among adults a decade following exposure to a significant wildfire was found, while no such decline was observed in children. Nevertheless, given that lung development persists into the postnatal phase, children may be theoretically vulnerable to the adverse effects of wildfire smoke on lung function. In an elderly population, wildfire smoke exposure was associated with more respiratory-related hospitalizations in women (10.4%) than in men (3.7%) [52]. Exposure to PM2.5 emissions from wildfires has been associated with reductions in lung function in non-asthmatic children. Some researchers propose that the use of asthma medications in children with asthma may mitigate the deterioration of lung function. Individuals with pre-existing respiratory, cardiovascular, or immune-mediated diseases are at higher risk of adverse immune responses following smoke exposure [55,56,57].

7. Effects on Asthma

As pointed out in a 2019 review by Reid and Maestas [58], the evidence for an association between WFS and respiratory diseases is clearest for acute effects on asthma, compared to the evidence for long-term effects or acute respiratory conditions other than asthma, as illustrated by several population-based studies of hospital admission rates [58,59]. Asthma is primarily characterized by airway obstruction resulting from a decrease in airway diameter. This narrowing is driven by chronic inflammation of the airway walls, which is marked by the infiltration and activation of various immune cells, including dendritic cells (DCs), eosinophils, neutrophils, lymphocytes, innate lymphoid cells (ILCs) and mast cells. The intricate interactions among these immune cell types, along with adjacent structural cells like epithelial cells, contribute to the manifestation of asthma-related features, such as bronchial hyperresponsiveness (BHR), which is typically reversible through the administration of bronchodilators. Being that such conditions are susceptible to being elicited by wildfire chemicals inhalation, this constitutes a relevant topic for the present review [44]. We focused the current review on original research studies referenced in PubMed, for the past 5 years, using the search terms “wildfire smoke AND asthma”. Studies that did not attempt to estimate WFS-specific exposure (as opposed to particulate matter in general) were not reviewed. Highlights of these studies are shown in Table 1 [60,61,62,63,64,65,66,67,68,69,70,71,72,73,74,75]. A variety of specific methods were used to estimate exposure, but most involved combining data from ground-level, fixed monitoring sites for PM2.5 with meteorological data and satellite-based imaging or physicochemical data to model the portion of exposure specific to WFS. Nearly all studies showed a statistically significant, exposure-dose-related increase in risk for diagnosis or exacerbation of asthma after exposure to WFS [76,77]. Many of these studies were conducted in western North America, where seasonal wildfires are common, but it has been pointed out by O’Dell and colleagues [78] that actual asthma morbidity from WFS in the USA may be greater in the east, due to much greater population density.
Reid and Maestas in 2019 [57] highlighted that the association between wildfire smoke (WFS) and respiratory diseases is most evident in the context of acute asthma effects, as opposed to long-term impacts or acute respiratory conditions other than asthma. This conclusion is supported by various population-based studies examining hospital admission rates [58,59]. The present review concentrates on original research published in the last five years, as indexed in PubMed, utilizing the search terms “wildfire smoke AND asthma”. Studies that did not specifically assess WFS exposure, distinguishing it from general particulate matter, were excluded from this review. The key findings from these studies are summarized in Table 1 [60,61,62,63,64,65,66,67,68,69,70,71,72,73,74,75]. A range of methodologies was employed to estimate exposure, predominantly involving the integration of data from ground-level fixed monitoring stations for PM2.5, alongside meteorological data and satellite imagery, to model WFS-specific exposure. Almost all studies reported a statistically significant increase in the risk of asthma diagnosis or exacerbation correlated with WFS exposure, with many of these investigations taking place in western North America, where seasonal wildfires are prevalent. However, O’Dell et al. [78] have noted that the actual burden of asthma morbidity due to WFS in the United States may be higher in the eastern regions, attributed to a significantly denser population.
The data illustrated in Table 1 reveals that a significant number of studies focused on establishing a correlation between wildfire smoke (WFS) exposure estimates and asthma-related health indicators sourced from de-identified population health databases. These papers primarily utilized billing codes and measurable events, such as visits to emergency departments or hospital admissions. Typically, periods of active WFS exposure were contrasted with non-exposure periods within the same demographic, with some investigations employing a time-stratified case-crossover methodology to compare exposure days with adjacent non-exposure days at the individual level. Furthermore, certain studies examined specific lag times related to the impact of WFS. The reported relative risks or odds ratios concerning the short-term effects of WFS on asthma exhibited a notable degree of consistency, generally around 1.10 (with a range from 1.07 to 1.68) for each 10 μg/m3 increase in WFS PM2.5 concentrations (spanning from 1 to 23 μg/m3). An increased risk of new-onset asthma was also observed among firefighters who were exposed to the Fort McMurray fire in Alberta, Canada, as indicated by a rise in asthma consultations following the fire [75,76,77]. The odds ratio for this occupational group, characterized by frequent exposure to WFS, was significantly higher than that reported in the majority of studies listed in Table 1 (OR 2.56). Among the studies examined, only one did not identify a significant association between WFS and risk; this particular study focused on lung function and symptom scores in a relatively small cohort of individuals with asthma [62]. Numerous investigations have examined the association between exposure to WFS and the risk of non-asthmatic respiratory disorders, including pneumonia and chronic obstructive pulmonary disease (COPD), as well as non-respiratory illnesses such as cardiovascular disease. In general, the findings related to the influence of WFS exposure on these health conditions were less consistent compared to those concerning asthma.
Children diagnosed with asthma may exhibit heightened vulnerability to the worsening of symptoms induced by WFS [60]. A recent review highlighted the potential dangers linked to childhood exposure [79], suggesting that long-term consequences for lung function may arise, as evidenced by research conducted on infant rhesus monkeys subjected to ambient WFS [80]. Other research has shown no substantial differences in the likelihood of asthma exacerbation between children and adults after exposure to WFS [81]. Reid et al. [58] observed a heightened risk among individuals from low socioeconomic backgrounds, while multiple studies have reported increased risks for indigenous populations [70,71,72].
Two studies that explored sex-specific effects revealed that the impact of WFS was more significant in women than in men [57,71].
The relative risk and odds ratios reported for the impact of short-term wildfire smoke (WFS) on asthma demonstrated a considerable level of consistency, generally around 1.10 (ranging from 1.07 to 1.68) for each 10 μg/m3 increase in PM2.5 due to WFS, with concentrations varying from 1 to 23 μg/m3. A heightened risk of new-onset asthma was noted, as evidenced by an increase in asthma-related consultations following the Fort McMurray fire in Alberta, Canada, particularly among firefighters exposed to the event. Notably, the odds ratio for this occupational group, which experiences frequent WFS exposure, was significantly elevated (OR 2.56) in comparison to most other studies referenced in Table 1. It is worth mentioning that only one study within the reviewed literature failed to find a significant risk linked to WFS; this study specifically concentrated on lung function and symptom scores within a relatively small group of asthmatics. Furthermore, numerous studies investigated the risk of non-asthmatic respiratory ailments, such as pneumonia and chronic obstructive pulmonary disease (COPD), as well as non-respiratory issues like cardiovascular disease. In general, the evidence concerning the effects of WFS exposure on these latter conditions was less uniform than that observed for asthma.
Reid et al. identified a linear relationship between asthma hospitalizations and exposure to wildfires, reporting a relative risk of 1.07 (95% CI 1.05–1.1) for each 5 μg/m3 increase in PM2.5 levels associated with wildfires [57]. Malig et al. illustrated that PM2.5 resulting from fire incidents is more closely associated with visits to the emergency department for asthma (RR 1.46, 95% CI 1.38–1.55) compared to PM2.5 from non-fire sources (RR 0.77, 95% CI 0.55–1.08) [69]. Heaney et al. reported that “smoke event days”, characterized by daily wildfire PM2.5 exposure exceeding the 98th percentile, correlate with a 3.3% rise in hospital visits for all respiratory ailments and a 10.3% increase in asthma-related hospitalizations [73]. Research by Doubleday’s team in Washington revealed a notable association between wildfires and emergency department visits for asthma, as well as for all respiratory conditions, with this uptick in healthcare utilization lasting for five or more days following initial smoke exposure [82]. A systematic review corroborated a significant rise in emergency department visits for respiratory issues and asthma-related hospitalizations within the first three days following exposure to wildfire smoke [83]. Collectively, the aggregated relative risk for short-term adverse effects of wildfire smoke on asthma is approximately 1.1, with a range of 1.07 to 1.68 reported across various studies for each 10 μg/m3 increase in wildfire PM2.5 levels [84].
Our opinion is that asthma could act as an immune response elicitor in case of wildfire smoke exposure.

8. Long-Term Outcomes

Previous research indicates that animal studies have identified potential long-term effects of wildfire smoke (WFS) exposure on lung function and disease [4]. However, there is a scarcity of published data regarding the prolonged effects of WFS exposure in humans, both with and without asthma. An observational cohort study involving 842 patients at an allergy clinic evaluated peak flow rates one year following the Dismal Swamp peat bog fires in northeastern North Carolina in 2008 and 2011. This study found a correlation between decreased peak flow rates and previous smoke exposure, as determined by wind patterns directing smoke toward the community. Interestingly, a reduction in peak flow was noted one year following the exposure, indicating potential immune involvement and suggesting the possibility of sensitization [11]. Additionally, our research group is currently reviewing a retrospective study that investigates the relationship between exposure to wildfire smoke and the incidence of respiratory diseases in children. This study revealed that exposure to wildfire smoke during the first six months of life was linked to an increased reliance on medications for respiratory issues. In a separate study involving Alberta firefighters, clinical evaluations were conducted up to 46 months after the fire. Among those reporting pulmonary symptoms, there was a higher incidence of positive methacholine challenge tests (28.6% in symptomatic individuals compared to 8.9% in asymptomatic ones), as well as a combination of positive tests and bronchiole wall thickening, both of which correlated with greater estimated exposure during the fire (10.4 ± 1.4 logPM2.5 μg/m3·h) [75]. Collectively, these studies indicate the potential for long-term consequences of WFS exposure, warranting further investigation.

9. Effects on Upper Respiratory Illnesses

Previous epidemiological research has identified a correlation between the rise in sinonasal symptoms and exposure to wildfire or wood smoke, particularly among children and first responders [85,86,87]. For instance, a study conducted during the Southern California wildfires in October 2003 reported an odds ratio (OR) of 1.98 for symptoms such as sneezing or a runny nose, with higher prevalence among asthmatic individuals, probably due to the immune system involvement in the asthmatic process [27]. More recently, a study involving children exposed to a significant wildfire in Spain indicated an OR of 3.11 (1.62, 5.97) for itchy or watery eyes, with a notable impact on asthmatic subjects, being immunologically more prone to such symptoms, as noted above [84]. Numerous recent studies have explored the specific relationship between wildfire smoke (WFS) and symptoms of rhinitis or allergies (being the latter immunologically driven), yielding varied outcomes. Among the asthma-related epidemiological studies previously mentioned, several assessed the link between WFS and acute upper respiratory infections (URI). The findings were mixed, with some studies reporting no significant effect of WFS, one indicating a positive association with a relative risk (RR) of 1.77, and another suggesting that the impact of WFS on URI risk was less than that of non-wildfire PM2.5 [30,32,38,39]. Fadadu et al. [88] reported an RR of 1.49 (1.07, 2.07) for children and 1.15 (1.02, 1.31) for adults regarding clinic visits for atopic dermatitis symptoms during exposure to WFS from the 2018 Camp Fire in the San Francisco region. Although not exclusively focused on WFS exposure, several studies have highlighted that PM2.5 exposure may act as a risk factor for exacerbating chronic rhinosinusitis (CRS) severity, supported by histological evidence of type 2 eosinophilic inflammation [89,90,91,92]. This discussion allowed us to explore the immunological consequences of exposure to wildfire smoke on the upper respiratory tract.

10. Implications for Public Health and Future Research

Understanding the effects of wildfire smoke on the immune system is critical for public health, particularly as wildfires become more frequent and intense due to climate change [52]. Future research should focus on conducting long-term studies to understand the chronic effects of wildfire smoke on the immune system [93], whilst further studies are needed to elucidate the precise biological mechanisms by which wildfire smoke components alter immune function [94]. Last but not least, developing and testing interventions to mitigate the health impacts of wildfire smoke, particularly for vulnerable populations, are highly needed [95].
Data about short-term outcomes indicate a notable presence of inflammation in both the upper and lower respiratory tracts, accompanied by exacerbations in respiratory illnesses. The limited data available on long-term outcomes raise significant concerns, as it implies that the immediate and apparent issues may be succeeded by more insidious yet critical adverse effects. The necessity for further research and enhanced public health communication can be contextualized within the annual rise in population exposures and the potential long-term consequences for vulnerable groups, including children who may develop chronic illnesses, thereby placing a substantial strain on the healthcare system. Individuals with pre-existing chronic health conditions are likely to experience exacerbated effects, as are those with heightened exposure risks, such as outdoor workers and those facing housing instability. A deeper comprehension of the long-term effects of immunomodulation and the potential for heritable changes through DNA methylation is highly needed.
Wildfire smoke exposure has emerged as an escalating public health issue, particularly as the frequency and intensity of megafires and fires at the wildland–urban interface continue to rise. The smoke produced by these fires contains numerous pollutants that adversely affect health and are associated with various health complications and chronic conditions. Therefore, effectively communicating with the public, particularly vulnerable populations, to mitigate their exposure to this environmental hazard has become a critical public health objective. Despite the increase in research on wildfire smoke risk communication over the past ten years, there remains a scarcity of best practice guidelines, and many health communication efforts fail to align with health literacy principles, including readability, accessibility and actionability. This scoping review aims to identify peer-reviewed studies focused on wildfire smoke risk communications, highlighting gaps in the research and evaluation of initiatives designed to inform the public [95].

11. Conclusions

Wildfire smoke exposure poses a significant risk to human health, extending beyond the respiratory and cardiovascular systems to include profound effects on the immune system. Both acute and chronic exposures can lead to immune dysregulation and increased susceptibility to infections, potentially contributing to the development of autoimmune diseases and allergies. Understanding such effects is crucial for developing effective public health strategies to mitigate the adverse health outcomes associated with wildfire smoke exposure.
Additionally, studies indicate that exposure to wildfire smoke may alter cytokine profiles, leading to an inappropriate immune response that can exacerbate pre-existing conditions or trigger new health issues. Vulnerable populations, such as children, the elderly and individuals with pre-existing health conditions, are at even greater risk, as their immune systems may be less capable of handling the stressors introduced by smoke exposure.
Understanding these multifaceted effects is crucial for developing effective public health strategies to mitigate the adverse health outcomes associated with wildfire smoke exposure. This includes implementing timely air quality warnings, promoting community awareness about protective measures and enhancing healthcare resources in affected areas. Moreover, research aimed at elucidating the mechanisms of immune dysregulation caused by wildfire smoke can inform future interventions and policies aimed at protecting public health in the face of increasing wildfire frequency and intensity due to climate change.

Author Contributions

D.F.: conceptualization, methodology, investigation, validation, writing—original draft. Ș.Ț.: Resources, software, funding acquisition, project administration. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Data Availability Statement

The data used to support the findings of this study are available from the corresponding authors upon request.

Conflicts of Interest

The authors declare no conflicts of interest.

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Figure 1. Immune regulation methods.
Figure 1. Immune regulation methods.
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Table 1. Summary of original studies about wildfire-smoke-related asthma published in 2018–2023 and PubMed-indexed. WFS: wildfire smoke [27].
Table 1. Summary of original studies about wildfire-smoke-related asthma published in 2018–2023 and PubMed-indexed. WFS: wildfire smoke [27].
Study [Reference]Population and LocationExposure AssessmentOutcomeComments
Hutchinson et al. [60]October 2007 fire complex, Medi-Cal beneficiaries, San Diego CountySpatiotemporal model using wildland fire emission system and atmospheric dispersionHospital admissions, outpatient visits243% increase in asthma diagnosis for age 0–1 yr
DeFlorio-Barker et al. [61]Hospitalized adults  ≥  65 yr, all US counties within 200 km of large wildfires 2008–2010 (asthma admissions, Medicare database)Fixed monitor data, adjusted for “smoke” days from wildfiresHospital admissionsIncreased asthma risk
Stowell JD et al. [62]Colorado 2011–2014 fire seasons (May–August)Ground PM2.5 from EPA monitors, plus high-resolution satellite optical density data for WFSED and hospital admissionsSimilar asthma results for adults and children
Reid et al. [63]Northern California, zip codes exposed to June–July 2008 wildfiresSpatiotemporal model, fixed monitors, machine learning algorithmED visits and hospital admissionsUnlike PM2.5, O3 effect was not significant in the multivariate model
Lipner et al. [64]Pediatric asthma patients at National Jewish Health (Western U.S.) 2012–2015Retrospective; assessed local WFS-related PM2.5 during clinic visitsAsthma symptom score, PFT during routine (not sick) clinic visitsAssessed non-urgent visits, unlike all other studies
Gan et al. [65]2013 Oregon wildfire season; asthma claims
Time-stratified, case-crossover design		Blended model of in situ monitoring, chemical transport models and satellite-based dataAsthma healthcare utilization (insurance claims)Similar results for office visits and refills of rescue inhalers
Kiser et al. [66]Reno, NV 2013–2018; data from a regional health systemLocal fixed monitors for PM2.5, with dates when WFS was presentED or urgent care visitsSimilar outcome to DeFlorio-Barker [41]
Magzamen et al. [67]Colorado Front Range area, 2012 and 2015
Time-stratified, case-crossover analysis		Surface monitors for Western US, plus satellite-based smoke plume estimatesHospital admissionsThis relationship was seen for “long-range transport” WFS events, but not local wildfires
Tornevi et al. [68]Sweden, 2018 wildfire events in Jamtland Harjedalen regionModeled WFS PM2.5 exposures using MATCH model (complex meteorological and atmospheric chemical data)Clinic visits-
Malig et al. [69]San Francisco Bay area, October 2017 wildfiresCounty-level monitoring avg PM2.5 during wildfire period compared to adjacent periodsED visits and hospital admissions-
Hahn et al. [70]Alaska (3 cities) during 2015–2019 wildfire seasonsGround-based monitors and satellite-based smoke plume estimatesED visitsSimilar for >65 year-olds, Native Alaskans
Howard et al. [71]Northwest Territories (Canada), summer 2014 prolonged, severe wildfire periodCompared WFS period to before and after periodsHospital admissions, ED visits; SABA prescriptionsMedian 24-h mean PM2.5 fivefold higher in the summer of 2014 compared with 2012, 2013 and 2015 (median = 30.8 ìg/m3), with mean peaking at 320.3 ìg/m3. Inuit more affected
Beyene et al. [72]Eastern Australia asthma registry, 2019–2020 bushfires24 h avg PM2.5 at fixed monitoring stations; satellite imagery for bushfire componentSelf-reported symptomsMean PM2.5 exposure 32.5 ìg/m3 on bushfire days
Heaney et al. [73]California, 2004–2009 wildfire seasonsGoddard Earth-Observing System (GEOS-Chem), all-source vs. without wildfire-specific PM2.5Unscheduled hospital visits for asthma and other conditionsLargest effect for 0–5 year-old subjects
Moore et al. [74]Calgary, Canada 2010–2021Ground-level monitors with WFS dates estimated from satellite imagesHealth insurance claims for asthma exacerbation in childrenExacerbations significantly reduced during periods of COVID-19 healthcare precautions
Blando et al. [11]Northeastern North Carolina, patients at allergy clinic, studied before, during and after Dismal Swap peat bog fires in 2008 and 2011Wind blowing from fire area toward community as proxy for exposurePeak flowStudy conducted 1 year after exposures
Cherry et al. [75]Fort McMurray fire in Alberta, Canada 2016, firefighters and controlsExposure to fire-related PM2.5 from Alberta Environment monitoring stations and satellite imagerySpirometry and asthma consultationIndividuals with ongoing symptoms also had a higher occurrence of positive methacholine challenge and bronchial wall thickening (OR 4.35; 95% CI 1.11–17.12. Lower diffusion capacity also related to increased exposure
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