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Review

Wildfire Smoke Implications on Immune Homeostasis

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 2026, 9(2), 77; https://doi.org/10.3390/fire9020077
Submission received: 10 December 2025 / Revised: 26 January 2026 / Accepted: 6 February 2026 / Published: 10 February 2026
(This article belongs to the Special Issue Wildfire Smoke Effects on Public Health)
Versions Notes

Highlights

  • Wildfire smoke disrupts immune balance through complex, multi-pathway effects.
  • NK cells are highly vulnerable to wildfire smoke-induced dysregulation.
  • Acute and chronic smoke exposures impair NK cell number, phenotype, and function.
  • NK cell deficits may raise infection risk and weaken tumor surveillance.

Abstract

Wildfires have emerged as a critical environmental and public health challenge globally, with their rising frequency and severity largely attributed to climate change. Although wildfire smoke is well recognized for its detrimental effects on respiratory and cardiovascular health, a growing body of evidence indicates that its immunological impacts are equally consequential. Composed of a complex mixture of particulate matter, volatile gases, and organic chemicals, wildfire smoke can disrupt immune homeostasis through multiple, interconnected pathways. Recent findings underscore the susceptibility of natural killer (NK) cells—key effectors of the innate immune system—to wildfire smoke-induced dysregulation. This review synthesizes current knowledge on the immunotoxicological effects of wildfire smoke with a specific focus on NK cell biology. It examines how both acute and chronic smoke exposures alter NK cell frequency, phenotype, and cytotoxic function, and explores the mechanistic contributions of inflammation, oxidative stress, and pollutant-mediated receptor modulation. Furthermore, the review considers potential long-term consequences of NK cell impairment, including heightened vulnerability to viral infections, diminished tumor surveillance, and broader disruptions in innate–adaptive immune crosstalk. Collectively, the evidence highlights the need for targeted research to delineate the pathways by which wildfire smoke compromises NK cell-mediated immunity and to inform strategies for mitigating these risks in exposed populations.

1. Introduction

Uncontrolled large-scale fires occurring in natural vegetation—commonly described as wildland, forest or bush fires—have become increasingly prevalent and destructive worldwide. This upward trend is attributed to shifting climatic conditions, ineffective land-use strategies and multiple human-associated influences [1]. Such fire events generate extensive smoke emissions composed of a chemically diverse assemblage of fine particulate matter (PM) and volatile gaseous compounds. While the harmful impacts of wildfire-derived air pollution on pulmonary and cardiovascular health are widely recognized, considerably less is known about its effects on immune function, particularly in relation to innate lymphoid cell populations [2]. Short-duration exposure is frequently associated with airway irritation, persistent coughing and impaired breathing, whereas repeated or long-term exposure contributes to the progression and worsening of chronic disorders such as asthma, bronchitis and cardiovascular disease [3]. Investigations using both clinical and experimental models have revealed pronounced disruptions to immune regulatory networks following inhalation of wildfire smoke, with certain immune changes remaining detectable long after exposure. Mechanistically, these effects have been linked to stimulation of the aryl hydrocarbon receptor (AhR), engagement of Toll-like receptor (TLR) pathways, and activation of nuclear factor κB (NF-κB) signaling cascades, accompanied by increased production of pro-inflammatory mediators and reactive oxygen species (ROS) [4,5,6]. Firefighters acutely exposed to wildfire emissions exhibit pronounced pulmonary and systemic inflammation; serum obtained 12 h post-exposure shows increased levels of interleukin-6 (IL-6) and interleukin-12 (IL-12), concomitant with reduced interleukin-10 (IL-10) [7,8]. This cytokine signature reflects a pro-inflammatory, T helper 1 (Th1)-skewed immune milieu characterized by elevated oxidative stress and enhanced activation of innate immune pathways. Such immune perturbations are particularly relevant for NK cells, whose cytotoxic function, cytokine secretion, and receptor expression are highly responsive to inflammatory and redox-dependent signals. IL-12 and IL-6 directly regulate NK-cell activation, metabolic programming, and interferon-γ (IFN-γ) production, whereas diminished IL-10 signaling alleviates inhibitory constraints on NK-cell effector responses. In parallel, wildfire-associated particulates and reactive oxygen species may alter NK-cell receptor repertoires, collectively reshaping NK-cell effector function following acute exposure. Growing attention in recent years has focused on the vulnerability of immune defenses—particularly NK cells—to disruption caused by exposure to wildfire-derived smoke. Whereas initial investigations largely centered on pulmonary and cardiovascular outcomes, more recent findings indicate that sustained inhalation of smoke can markedly alter NK cell characteristics and impair their functional capacity.

Rationale

This review evaluates the expanding literature on wildfire smoke–associated immune disruption, with a specific emphasis on the consequences for NK cell–mediated immunity. NK cells are frontline innate immune effectors that are highly sensitive to pollutant-induced inflammation and oxidative stress, making their dysfunction a plausible mechanistic link between wildfire smoke exposure and increased susceptibility to infection, impaired tumor surveillance, and dysregulated airway inflammation.

2. Composition of Wildfire Smoke and Immunotoxins

Smoke produced during wildland fires is a complex source of immune-disrupting agents. Its composition includes fine particulate matter (PM), numerous volatile organic chemicals (VOCs such as benzene, toluene, ethylbenzene, xylenes, isoprene and pinene [9]) and a wide range of polycyclic aromatic hydrocarbons (PAHs, including acenaphthene, acenaphthylene, anthracene, chrysene, fluoranthene, fluorene, phenanthrene and pyrene [10]). The partial burning of plant biomass produces an aerosol enriched with allergenic material and biologically active organic substances [11]. Of particular concern is PM2.5, which is capable of reaching the distal regions of the lung and entering the bloodstream, where it promotes oxidative damage and inflammatory signaling that influence immune cell behavior [12]. Exposure to PM2.5 is associated with elevated concentrations of pro-inflammatory cytokines, including IL-6, tumor necrosis factor alpha (TNF-α), and interleukin-1 alpha (IL-1α), driving systemic inflammation and diminishing the functional capacity of diverse immune populations such as macrophages, dendritic cells, T lymphocytes and B lymphocytes [13]. These same pollutants are increasingly implicated in the modulation of NK cell responses. Volatile organic compounds (VOCs) and polycyclic aromatic hydrocarbons (PAHs) exhibit both immunosuppressive and pro-inflammatory properties [14], reflecting dose-, timing-, and context-dependent effects on immune signaling. Their metabolic conversion by cytochrome P450 enzymes generates electrophilic intermediates and reactive oxygen species capable of DNA adduct formation, oxidative injury, and mutagenesis, thereby disrupting immune cell viability, redox balance, and transcriptional regulation [15]. VOCs such as formaldehyde and benzene suppress lymphocyte proliferation and antibody synthesis through interference with cell-cycle progression and induction of oxidative stress responses [16], while PAH-induced activation of the aryl hydrocarbon receptor (AhR) contributes to thymic atrophy and diminished T-cell output by altering thymocyte differentiation and survival [17]. In parallel, AhR activation in innate lymphocytes modulates NK cell receptor expression, including dysregulation of activating receptors and inhibitory checkpoints, and impairs cytotoxic granule release and cytokine production. Together, these pathways position NK cells as central and mechanistically vulnerable targets of smoke-mediated immunotoxicity.

3. Acute Immune Responses to Wildfire Smoke Exposure

Short-term contact with wildfire-derived smoke provokes immediate immune activation marked by pronounced inflammatory signaling and increased oxidative burden [18,19]. Following inhalation, host defense mechanisms are rapidly engaged to respond to inhaled particulates and toxic compounds [20], leading to enhanced secretion of chemotactic mediators and cytokines—such as IL-8 and monocyte chemoattractant protein-1 (MCP-1)—that drive immune cell recruitment to affected tissues. In parallel, exposure to allergen-laden particles can stimulate histamine release [13]. While these early responses serve a defensive role, excessive or sustained activation may shift toward pathological inflammation [20]. Systemic involvement is reflected by elevated concentrations of acute-phase reactants, including C-reactive protein (CRP), after smoke exposure [21]. Disruption of redox homeostasis, defined by an excess of reactive oxygen species (ROS) relative to antioxidant capacity, underlies smoke-induced oxidative stress [22], with fine particulates and co-emitted chemicals acting as strong inducers of ROS generation [23]. Resultant oxidative damage can undermine immune cell viability and performance, including that of NK cells, whose effector functions—granule-mediated cytotoxicity and cytokine release—are particularly sensitive to redox imbalance. Oxidative stress further diminishes microbial clearance by macrophages and neutrophils [24]. Clinically, acute smoke exposure in human populations is associated with worsening respiratory symptoms, increased asthma exacerbations—reflecting immune dysregulation—and higher rates of chronic obstructive pulmonary disease (COPD) flare-ups [25,26,27,28].

4. Chronic Immune Effects of Prolonged Wildfire Smoke Exposure

Repeated or sustained contact with wildfire-derived air pollution produces enduring changes in immune homeostasis, characterized by pollutant-driven immunosuppression—largely attributed to fine particulate matter (PM2.5) and polycyclic aromatic hydrocarbons (PAHs)—and an increased susceptibility to infectious and chronic inflammatory conditions [29,30,31]. Extended exposure has been linked to reductions in both the abundance and functional competence of key immune populations, including lymphocytes, macrophages and NK cells [22]. In the case of NK cells, continuous exposure to airborne toxins diminishes cytolytic capacity, alters the balance of activating versus inhibitory receptors and blunts cytokine-mediated signaling, collectively undermining antiviral and tumor surveillance functions. Persistent smoke inhalation further disrupts adaptive immunity, evidenced by impaired antibody generation and dysregulated T-cell responses [32], changes that may facilitate the onset or progression of autoimmune and allergic pathologies [33]. Components of wildfire smoke have been epidemiologically associated with elevated incidence of autoimmune diseases such as rheumatoid arthritis and systemic lupus erythematosus [34], and with heightened allergic sensitization contributing to conditions including asthma and allergic rhinitis [35]. Pollutants originating from both wildfires and vehicular emissions converge on common molecular pathways, activating the aryl hydrocarbon receptor (AhR), Toll-like receptors and NF-κB signaling while promoting cytokine production, including IL-22 [6]. Occupational exposure studies indicate that firefighters exhibit increased circulating IL-6 and IL-12 alongside suppressed levels of the anti-inflammatory cytokine IL-10 following smoke exposure [36]. In addition, diverse environmental contaminants have been shown to activate the NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasome, leading to pyroptotic cell death [37,38]. Other airborne toxicants, such as perfluoroalkyl substances, activate innate immune pathways via the absent in melanoma 2 (AIM2) inflammasome, whereas micro- and nanoplastic particles—now detected with increasing frequency in atmospheric samples—are similarly capable of triggering inflammasome signaling cascades [39]. The International Agency for Research on Cancer (IARC) has classified occupational exposure among firefighters as carcinogenic to humans. This determination was supported by strong mechanistic evidence demonstrating that exposed firefighters exhibit several key characteristics of carcinogens (KCs), including induction of oxidative stress (KC 5), promotion of chronic inflammation (KC 6), and modulation of receptor-mediated pathways such as aryl hydrocarbon receptor (AhR) signaling (KC 8) [40].
These inflammatory pathways are particularly relevant to NK cells, since cytokine milieus shaped by inflammasome activation can alter NK cell behavior and diminish their capacity to detect and eliminate abnormal cells.

5. Mechanisms of Immune Modulation by Wildfire Smoke

Immune perturbations associated with wildfire smoke arise through several interconnected biological processes, most notably redox imbalance, sustained inflammatory activity and epigenetic reprogramming [41]. Oxidative stress and inflammation reinforce one another and together form a core axis of smoke-related immune toxicity [42]. Upon inhalation, airborne contaminants stimulate nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity, resulting in excessive generation of reactive oxygen species (ROS) and the maintenance of self-amplifying oxidative and inflammatory signaling loops [43]. Such conditions interfere with NK cell performance by disrupting mitochondrial bioenergetics, reshaping cytokine sensitivity and altering the balance of activating and inhibitory surface receptors. Beyond these immediate effects, smoke exposure induces epigenetic alterations—including changes in deoxyribonucleic acid (DNA) methylation patterns and histone modifications—that modulate the transcriptional regulation of immune-related genes [44], thereby promoting durable immune dysfunction [45]. Wildfire-derived pollutants also modify microbial communities in both the respiratory tract and gastrointestinal system [46], with downstream consequences for systemic immune regulation, including NK cell development and activation status [47]. Inhalation of particulate matter (PM) originating from wildfires triggers immune and inflammatory signaling networks linked to disease development. Exposure to fine particulates from diverse sources has been associated with elevated circulating levels of lymphocytes, eosinophils and neutrophils [48,49,50,51], and accumulating data indicate that these hematological shifts may coincide with altered NK cell trafficking and progressive functional exhaustion.

6. Vulnerable Populations

Vulnerability to the immune-disrupting effects of wildfire-derived air pollution is not uniform across populations, with children, older adults and those living with underlying health conditions experiencing disproportionate risk [52]. During childhood, immune development is ongoing, rendering the system particularly responsive to toxic environmental exposures that may permanently alter immune cell differentiation and performance [53]. NK cells, which continue to mature after birth, are therefore likely to be especially sensitive to pollutant-driven oxidative and inflammatory challenges during early life. In later life, age-related immune decline—commonly referred to as immunosenescence—reduces the effectiveness of both innate and adaptive defenses [54], including diminished NK cell cytolytic activity and shifts in receptor expression patterns, potentially intensifying the immunological burden of wildfire smoke exposure. Longitudinal population-based analyses have identified reductions in adult pulmonary function nearly ten years following large-scale wildfire incidents, whereas comparable declines were not detected in children; however, continued lung growth during childhood suggests a persistent susceptibility to delayed respiratory and immune consequences. Among older individuals, wildfire smoke exposure has been associated with increased rates of respiratory-related hospital admissions, with women exhibiting a greater relative increase (10.4%) than men (3.7%) [52]. Fine particulate matter (PM2.5) originating from wildfires has also been linked to measurable reductions in lung function in children without asthma, and some evidence indicates that the use of asthma medications may partially offset these effects. Individuals affected by chronic respiratory, cardiovascular or immune-related disorders face an elevated likelihood of adverse immune outcomes following smoke exposure [21,55,56]. Within these susceptible groups, impairment of NK cell activity—whether existing prior to exposure or induced by pollutants—may further weaken antiviral defenses and tumor surveillance mechanisms.

7. Effects on Asthma

A synthesis published in 2019 by Reid et al. emphasized that the strongest and most consistent evidence linking wildfire smoke (WFS) to respiratory morbidity concerns its immediate effects on asthma [57]. Analyses conducted at the population level repeatedly demonstrate transient surges in asthma-related hospital admissions following episodes of WFS exposure [57,58]. Asthma arises from persistent inflammatory processes within the airways that culminate in airflow limitation and involve a broad array of immune cells, including dendritic cells, eosinophils, neutrophils, T and B lymphocytes, innate lymphoid cells (ILCs) and mast cells. Through dynamic interactions with airway epithelial and stromal compartments, these immune populations generate defining features of the disease, most notably bronchial hyperresponsiveness (BHR), a condition that is generally reversible with bronchodilator treatment. Chemical constituents of wildfire smoke act as strong initiators of the inflammatory signaling networks that underpin asthma pathophysiology, making asthma a central focus of this review [44]. Although disease mechanisms are largely governed by innate and adaptive immune responses, NK cells also participate in shaping disease outcomes. Recent studies indicate that exposure to environmental pollutants can modify NK cell effector functions, including cytokine secretion and cytolytic activity, with potential downstream effects on epithelial communication and type 2-biased inflammatory pathways that influence asthma severity. This review evaluates primary research articles published within the last five years, identified through PubMed searches using the terms “wildfire smoke AND asthma.” Investigations that failed to differentiate WFS-specific exposure from generalized particulate matter exposure were excluded. Despite methodological heterogeneity—spanning direct PM2.5 measurements, atmospheric modeling and satellite-derived exposure estimates—the majority of studies reported statistically significant, dose-responsive increases in asthma incidence or exacerbation following WFS exposure [59,60]. While much of the existing literature originates from western regions of North America, where wildfire activity is most frequent, O’Dell and colleagues [61] suggest that the overall burden of WFS-associated asthma morbidity in the United States may be greater in eastern regions due to substantially higher population density.
The above-discussed association between wildfire smoke (WFS) aligns with numerous population-based studies assessing hospital admissions during WFS events [57,58]. Many epidemiological investigations have linked WFS exposure to asthma outcomes by analyzing de-identified healthcare databases containing diagnostic codes or emergency department records. These studies frequently compared periods with elevated WFS exposure to intervals without exposure in the same populations, and some employed time-stratified case-crossover methodologies. Across these analyses, relative risks (RRs) and odds ratios (ORs) for short-term exposure to WFS PM2.5 typically cluster around 1.10 per 10 μg/m3 increase (range 1.07–1.68), reflecting a reproducible inflammatory response that plausibly involves innate immune mechanisms, including NK cell activation, functional exhaustion, or impaired cytotoxicity. Firefighters exposed to the Fort McMurray wildfire exhibited a markedly increased incidence of new-onset asthma, as reflected by elevated healthcare consultation rates [59,60,62]; the corresponding odds ratio (OR) of 2.56 substantially exceeded population averages, consistent with the intensified and repeated exposures characteristic of occupational settings. This heightened risk aligns with evidence that severe or chronic exposure to airborne pollutants can compromise NK cell cytotoxicity, disrupt cytokine balance, and amplify susceptibility to inflammation-driven airway pathology [63,64,65,66,67]. One study did not identify a clear relationship between WFS and asthma risk; however, it relied on a small cohort of individuals with pre-existing asthma and focused on symptom scores and lung function [62]. Several investigations also examined associations with non-asthmatic respiratory or cardiovascular endpoints, though findings were more variable [68]. Children with asthma appear particularly sensitive to symptom exacerbation following WFS exposure [25,69,70,71]. While some reports indicate age-dependent differences in susceptibility, others observed no significant variation between children and adults [72,73]. Given that NK cell maturation and receptor expression continue to develop throughout childhood, pollutant-induced shifts in NK cell activation thresholds may partly explain age-related differences in asthma severity during smoke events. Socioeconomic factors further influence risk, with Reid et al. [57] highlighting disparities, and several studies reporting elevated vulnerability among Indigenous populations [74,75,76]. Two investigations assessing sex differences found stronger associations in women than men [56,75], potentially reflecting sex-specific variations in baseline NK cell cytokine production. Aggregated metrics indicate that short-term WFS exposure consistently elevates asthma risk, with relative risks (RRs) and odds ratios (ORs) of approximately 1.10 per 10 μg/m3 increase in wildfire-specific PM2.5. Reid et al. reported a RR of 1.07 (95% CI 1.05–1.10) for each 5 μg/m3 increase [57], while Malig et al. demonstrated that wildfire-derived PM2.5 is more strongly linked to asthma-related emergency visits (RR 1.46) than non-fire PM2.5 [77]. Heaney et al. observed a 10.3% rise in asthma hospitalizations on “smoke event days” (PM2.5 > 98th percentile) [78], and Doubleday et al. found that asthma-related emergency visits remained elevated for up to five days post-WFS exposure [79]. A systematic review further confirmed that respiratory emergencies increase within the first three days of smoke exposure [80]. Collectively, these epidemiological patterns, combined with emerging evidence that NK cells rapidly respond to environmental pollutants, support the notion that asthma exacerbation represents one aspect of a broader innate immune reaction triggered by wildfire smoke. The above discussed data were summarized in Table 1.

8. Long-Term Outcomes

Experimental evidence from animal models indicates that exposure to wildfire smoke (WFS) can induce lasting alterations in pulmonary architecture and immune function [4]. Comparable data in humans are relatively sparse. In one observational cohort of 842 patients from an allergy clinic, peak expiratory flow rates were lower one year after the Dismal Swamp peat fires, with exposure estimated using smoke-trajectory modeling [11]. Such delayed reductions in lung function may reflect sustained immune changes, including modifications in NK cell numbers or receptor expression, potentially contributing to chronic airway hyperreactivity or increased allergen sensitivity. A retrospective analysis from our research group similarly suggests that exposure to WFS within the first six months of life correlates with elevated later use of respiratory medications, implying early immune perturbation. Given the critical role of NK cells in antiviral defense during infancy, disruption of their activity by pollutants may underlie these prolonged respiratory susceptibilities. Among Alberta firefighters, clinical follow-up extending up to 46 months post-exposure demonstrated higher rates of positive methacholine challenge tests and radiographic evidence of bronchiolar abnormalities in individuals with higher cumulative WFS exposure (10.4 ± 1.4 logPM2.5 μg/m3·h) [62]. Collectively, these observations support the concept that WFS can trigger long-term immune dysregulation, including persistent alterations in NK cell function, long after the initial exposure event.

9. Effects on Upper Respiratory Illnesses

Epidemiological studies have linked exposure to wildfire or wood smoke with symptoms affecting the sinonasal tract, with children and first responders being particularly susceptible [81,82,83]. For instance, during the 2003 Southern California wildfires, individuals experienced nearly double the odds of sneezing or nasal discharge (OR 1.98), with the effect being most pronounced in people with asthma [27]. More recently, children exposed to a significant wildfire event in Spain demonstrated elevated risk of ocular irritation, including itchy or watery eyes (OR 3.11) [56]. Because NK cells reside in mucosal tissues and play an early role in antiviral defense, disruptions in their activity induced by pollutants may heighten susceptibility to upper respiratory symptoms or infections following smoke exposure. Findings on wildfire smoke and acute upper respiratory infections (URI) are inconsistent: some studies report no association, one observed a strong positive link (RR 1.77), and others found effects weaker than those caused by non-wildfire PM2.5 [30,32,38,39]. Additional research indicates increased healthcare visits for atopic dermatitis during periods of WFS exposure [84], and several studies have connected PM2.5 exposure to worsening chronic rhinosinusitis (CRS), with histological evidence of type 2 eosinophilic inflammation [85,86,87,88]. While these mucosal effects are not solely mediated by NK cells, altered NK cell activation and cytokine secretion are recognized contributors to local inflammatory responses and may partly drive these upper airway manifestations. Recent work further documents wildfire-related immune dysregulation and advances in immune cell monitoring relevant to public health preparedness [89,90,91,92,93,94].

10. Implications for Public Health and Future Research

As climate change drives more frequent and severe wildfires, understanding how WFS affects the immune system has become increasingly important [52]. Longitudinal research is necessary to define the chronic consequences of WFS on immunity [95], while mechanistic studies are required to determine how individual smoke constituents influence immune pathways, including NK cell activation, functional exhaustion, and epigenetic modifications [96]. Developing and testing strategies to protect susceptible populations remains a critical priority [97]. Current evidence documents widespread acute inflammation throughout both upper and lower airways, along with worsening of existing respiratory conditions. Although data on long-term impacts are limited, early findings indicate that immune dysregulation may persist, potentially producing delayed effects such as epigenetic changes that could influence NK cell development. Groups at particular risk include children, individuals with pre-existing health conditions, outdoor laborers, and those living in unstable housing. Strengthening public health communication with clear, practical guidance is essential to minimize exposure and associated risks.

11. Conclusions

Exposure to wildfire smoke poses a major threat to human health, extending well beyond respiratory and cardiovascular effects to include profound impacts on immune function. Both short-term and prolonged exposures can disrupt immune homeostasis, heightening vulnerability to infections and potentially promoting the development of autoimmune and allergic conditions. NK cells, key players in innate immunity, are especially susceptible to smoke-induced dysfunction, including reduced cytotoxic activity, altered cytokine profiles, and possible epigenetic modifications. These complex immunological consequences highlight the importance of comprehensive public health measures, such as early alert systems, community education, and tailored protection strategies for high-risk populations. Advancing mechanistic studies focused on how wildfire smoke perturbs NK cell pathways will be essential for developing interventions to safeguard immune health in the context of increasingly frequent and intense wildfires driven by climate change.

Author Contributions

D.F.: conceptualization, data curation, methodology, investigation, validation, supervision, 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.

Institutional Review Board Statement

Not necessary for observational studies.

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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Table 1. Summary of Recent Evidence on Wildfire Smoke (WFS) Exposure and Asthma Outcomes.
Table 1. Summary of Recent Evidence on Wildfire Smoke (WFS) Exposure and Asthma Outcomes.
CategoryKey FindingsRepresentative DataNotes/Mechanistic Insights
Study Inclusion CriteriaPubMed search: “wildfire smoke AND asthma”; only studies distinguishing WFS-specific PM from other PM sources included.Variable methods (PM2.5 monitoring, meteorology, satellite modeling).Integrated exposure modeling improves WFS attribution accuracy.
OutcomeWFS consistently associated with short-term increases in asthma diagnoses, ED visits and hospitalizations.RRs/ORs ~1.10 per 10 μg/m3 WFS PM2.5 (range 1.07–1.68). +10.3% hospitalizations on smoke-event days.Suggests robust, rapid inflammatory response involving epithelial–immune pathways.
ExposureMarkedly elevated asthma risk with intense or repeated WFS exposure.OR 2.56 for new-onset asthma after Fort McMurray fire.High-dose exposure may impair NK cytotoxicity and enhance airway inflammation.
Age-RelatedChildren with asthma often show greater symptom worsening during WFS events; results mixed on differential risk.Increased vulnerability reported in several studies.NK cell development and activation thresholds may modulate age-dependent responses.
HealthHigher WFS-related asthma risk in lower-SES groups and Indigenous communities.Reid et al. [57] and multiple population-based analyses.Reflects structural disparities in exposure, baseline health, and access to care.
PathwaysWFS triggers inflammation, oxidative stress and type 2 airway responses; NK cells modulate asthma severity.Evidence of pollutant-induced NK cytokine shifts and cytotoxic dysregulation.NK cells may influence epithelial crosstalk and amplify WFS-driven airway dysfunction.
Outlier FindingsOne small cohort study found no association between WFS exposure and asthma symptoms or lung function.Small asthma cohort examining symptoms and spirometry.Likely underpowered; inconsistent with broader evidence base.
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Frumento, D., & Țãlu, Ș. (2026). Wildfire Smoke Implications on Immune Homeostasis. Fire, 9(2), 77. https://doi.org/10.3390/fire9020077

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