Wildfire Exposure and Respiratory Health: A Comprehensive Review of Emerging Evidence

Abstract

In January 2025, a catastrophic wildfire in Los Angeles, California, resulted in extensive economic losses and created a substantial risk to public respiratory health. With the progression of climate change, the increasing frequency and severity of wildfires have become a critical global issue due to their substantial impact on respiratory health. Wildfire smoke comprises elevated levels of ambient air pollutants, such as particulate matter (PM_2.5, PM₁₀), carbon monoxide (CO), nitrogen oxides (NOx), ozone (O₃), and a range of toxic substances. Notably, wildfire-related PM is especially detrimental because it can penetrate deeply into the lower respiratory tract and alveoli, provoking stronger oxidative and inflammatory responses, and leading to both the development and worsening of respiratory conditions, including asthma and chronic obstructive pulmonary disease (COPD). Research indicates that short-term exposure to wildfire smoke is linked to acute exacerbations of asthma, COPD, and pneumonia, contributing to higher mortality rates and increased demands on healthcare utilization. Long-term exposure may increase the risk of developing COPD, accelerate disease progression, and is potentially linked to a heightened risk of lung cancer and mortality. Collectively, these data underscore the substantial threat posed by wildfire smoke, escalating morbidity, mortality, and socioeconomic burdens. This review systematically summarizes recent advances in our understanding of respiratory health impacts linked with wildfire smoke exposure. By aggregating current evidence, the review seeks to guide healthcare practitioners and public health officials, thereby promoting evidence-based interventions for clinical management, health communication, and disaster response amid the escalating risk associated with wildfires.

Key Figure

Introduction

In early January 2025, an outbreak of large-scale wildfires erupted across the greater Los Angeles area, exacerbated by atypically intense Santa Ana winds and long-standing drought conditions (Figure 1) [1,2]. The wildfires first ignited around January 7, with several continuing for weeks. The most consequential events—affecting an estimated 16,000 structures and burning an estimated 40,000 acres—included the Palisades Fire, which devastated Pacific Palisades and Malibu, and the Eaton Fire, which burned areas in Altadena and Pasadena [3]. Together, these incidents accounted for most of the acreage burned and the majority of property destruction within the county [4].

Fig. 1.

Satellite image of wildfire smoke dispersion in Southern California (January 2025). Image was captured by the Copernicus Sentinel-3 mission (European Space Agency) on January 9, 2025, shows the Palisades Fire at lower left and the Eaton Fire at upper right, with smoke seen reaching Catalina Island and the Santa Barbara reserve to the south of the fires (European Space Agency[2]).

Santa Ana winds are intense, seasonally recurring winds that primarily develop from October to January, originating from inland high-pressure areas situated in Western Utah and Eastern Nevada and advancing toward the coastal areas of Southern California [5,6]. As these air masses move down the leeward slopes of the Sierra Nevada, they undergo adiabatic warming and drying processes, which cause a marked increase in temperature and a sharp decline in relative humidity [7]. These atmospheric changes give rise to hot, desiccating winds that significantly elevate the risk of wildfire ignition and rapid spread, especially in coastal regions where vegetation is already affected by low moisture availability [8]. These meteorological phenomena are highly significant in the context of environmental health, as they contribute not only to more frequent wildfires but also to deteriorating air quality and an increased burden of respiratory health issues within impacted communities [9].

Various climatic and meteorological factors have been identified as drivers of the exceptional severity observed in the 2025 Los Angeles wildfires, encompassing the combined effects of strong seasonal wind activity and broader climate fluctuations. A key factor involves the interplay associated with the El Niño–La Niña transition. During the El Niño event of 2023 to 2024, there was an increase in rainfall that stimulated substantial vegetation growth throughout California, particularly in the southern part of the state, thereby increasing the biomass available for subsequent wildfire ignition [10]. However, beginning in mid-2024, a prolonged dry period—identified as the second driest interval from May 2024 to January 2025 since 1877— resulted in widespread dehydration of vegetation [10,11]. The situation was compounded by the emergence of a weak La Niña event in December 2024, persisting into early 2025. This climatic alteration diverted precipitation toward northern regions, heightened drought conditions in Southern California, and substantially raised wildfire susceptibility [11,12]. The synergy of these climate phenomena demonstrates how global climatic oscillations, particularly those related to El Niño Southern Oscillation (ENSO) dynamics, have become a principal influence in intensifying regional wildfire threats in California.

In 2022, South Korea witnessed a series of large-scale wildfires, with the eastern regions being most severely affected. A major wildfire that began in Uljin and spread to Samcheok caused widespread destruction of forest land, while concurrent fires in the Gangneung and Donghae regions led to a combined loss of 24,000 hectares, resulting in pronounced environmental and economic consequences [13]. These fires generated extensive smoke and particulate emissions, leading to critically diminished regional air quality. According to national data, annual PM2.5 emissions increased by 3.7% relative to the preceding year [14], underscoring the significant impact of these wildfires on air pollution (Figure 2) [15].

Fig. 2.

Satellite imagery of wildfire-associated air pollution in Korea (March 2022). 2022 March, GEOKOMPSAT-2A (Korea Aerospace Research Institute) detection of yellow dust, aerosols, and volcanic ash[15].

The Yeongdong region of Gangwon Province, the site of these fire events, is periodically influenced by a local atmospheric phenomenon called Yangganjipung—a hot and dry foehn wind that descends from the Taebaek Mountains during spring [16]. These winds can attain force levels similar to those of typhoons, which dramatically facilitate the rapid spread of fires. Comparable climatic conditions have historically been key factors in the occurrence of previous large-scale wildfires along the East Sea coast, including those in Goseong in 1996, Donghae in 2000, and Yangyang in 2005.

Climate change is increasingly acknowledged as a key factor that exacerbates wildfire risk in South Korea. Over the last century, the country’s mean annual temperature has risen by roughly 1.6°C, with the most pronounced warming recorded during the spring season [17,18]. With spring serving as the primary wildfire season, temperature rise intensifies evapotranspiration processes, promoting reduced soil and vegetation moisture [19,20]. Although human activity predominantly sparks wildfires, the progression to larger, more destructive events is enabled by the interplay of climate change-driven temperature increases, inherent structural weaknesses in forests, and local wind dynamics. The large-scale wildfires that occurred in Uiseong and Andong in March 2025 provide further evidence of this climate-exacerbated pattern. Such environmental conditions not only result in significant forest depletion but also lead to collateral impacts on the environment and public health, including increased air pollution and a greater incidence of illnesses associated with particulate matter (PM).

Air Pollutants Released During Wildfires

Wildfire smoke is comprised of a complex mixture of pollutants. The specific composition of air pollutants in wildfire smoke can vary considerably and is determined by several factors, such as the nature of the burned materials, meteorological conditions during the fire, and proximity to the source of ignition. Key air pollutants with significant health implications include PM (PM₂.₅ and PM₁₀), carbon monoxide (CO), nitrogen oxides (NO₂ and NO), ozone (O₃), and volatile organic compounds (VOCs) [8,17,19,21-23]. Additionally, wildfire smoke contains carcinogenic agents such as benzene, formaldehyde, and trace metals, including lead and mercury, which further increase its toxicological impact [24]. Among these, PM is widely regarded as the most critical component affecting health outcomes during wildfire smoke exposure. Concentrations of PM2.5 in wildfire smoke can quickly rise above 200 μg/m³, which is over ten times greater than average ambient levels and significantly exceeds the World Health Organization’s recommended exposure limits [25,26]. Research indicates that wildfire PM contains higher amounts of oxidative and proinflammatory components—such as oxygenated polycyclic aromatic hydrocarbons (PAHs) and quinones—compared to PM from urban environments, which may result in heightened toxicological responses[27]. Furthermore, wildfire-related PM frequently consists of smaller ultrafine particles, facilitating their longer atmospheric transport and enhancing the potential for adverse health effects across broader regions[28].

Inhalation and Physiological Responses to Wildfire-Related Pollutants

When wildfire smoke is inhaled, fine and ultrafine PM, including PM2.5, can penetrate the lower airways and alveolar spaces, where these particles may initiate a complex series of inflammatory and immune-mediated responses [21]. Laboratory investigations utilizing mouse models demonstrate that wildfire-derived PM provokes cell-type-specific oxidative stress and inflammatory reactions in the lung, with PM2.5 specifically associated with heightened toxicity, evidenced by more severe pulmonary injury and increased systemic inflammation [29-31]. Generally, inhaled PM2.5 stimulates the production of reactive oxygen species (ROS), which in turn activate the NLR family pyrin domain containing 3 (NLRP3) inflammasome, resulting in pyroptotic cell death mediated by proinflammatory cytokines such as interleukin 1β (IL-1β) and IL-18 [32]. Notably, ROS generated from wildfire smoke can inflict DNA damage, disrupt mitochondrial function, and compromise cellular repair mechanisms, which may ultimately contribute to genomic instability and the development of chronic lung injury [33,34]. Additionally, carcinogens such as PAHs present in wildfire smoke can promote mutagenicity and lung toxicity through direct inhalation exposure [35]. Furthermore, toxic gaseous components and PM2.5 compromise epithelial barrier integrity through transient receptor potential cation channel subfamily A member 1 (TRPA1) ion channel activation in epithelial and sensory neurons, resulting in pronounced calcium influx, mitochondrial dysfunction, and neurogenic inflammation[36]. Additionally, wildfire smoke modulates macrophage activity and disrupts human lung epithelial cell function, thereby facilitating the development or worsening of respiratory infections and airway diseases, including asthma and chronic obstructive pulmonary disease (COPD) [37,38].

Health Impacts of Short-Term Wildfire Smoke Exposure

1. Mortality: all-cause and respiratory disease mortality

Exposure to wildfire smoke has been linked to higher mortality rates in the overall population. The PM from wildfires is finer and contains elevated concentrations of oxidative and proinflammatory substances compared to urban pollutants, which increases the risks of both respiratory and cardiovascular deaths. Multiple studies have demonstrated that exposure to wildfire smoke raises the risk of mortality from respiratory illnesses [8,27,39-44]. Recent systematic reviews report that greater exposure to wildfire-derived PM2.5 correlates with increased risk of all-cause and respiratory-specific mortality [24,45,46]. Furthermore, O₃ generated secondarily from wildfires is implicated in additional respiratory disease mortality [40]. The public health risk from wildfire smoke-related mortality is significant, and such events have also been documented to cause notable economic burdens [47].

2. Healthcare utilization: emergency department visits, physician visits, and hospital admissions

1) All-cause respiratory disease healthcare utilization

Wildfires emit substantial amounts of air pollutants in a short period, often persisting for several weeks, which leads to elevated levels of PM and other hazardous components. These exposures play a role in triggering new cases as well as worsening acute exacerbation of respiratory diseases, thereby increasing demand for healthcare services. The impact is particularly pronounced among those with underlying health issues, driving up emergency department visits, outpatient care, and hospital admissions [8,24,27,39,45].

Emergency department visits represent the most sensitive metric for assessing acute exacerbations of respiratory diseases linked to wildfire smoke exposure. Exposure to wildfire-related PM2.5 has been correlated with an elevated risk of emergency department visits for respiratory conditions, especially in individuals with pre-existing asthma or COPD [24,46,48-57]. Additionally, wildfire-related PM2.5 has been shown to significantly increase the risk of physician visits [58] and hospital admissions for respiratory diseases [24,25,54,59-62].

2) Disease specific healthcare utilization

(1) Asthma

Asthma is the respiratory condition most acutely affected by wildfire smoke exposure. This heightened susceptibility is mainly attributed to the specific properties of wildfire smoke, which possesses a substantial fraction of ultrafine PM that can reach the distal airways [31]. The smoke from wildfires is enriched with oxidative and proinflammatory agents that aggravate asthma by compromising epithelial barrier function and triggering immune responses through oxidative stress and cytokine-mediated mechanisms, resulting in increased airway inflammation and hyperresponsiveness [31,63]. Acute exposure to wildfire PM2.5 is significantly associated with acute exacerbation of asthma. Furthermore, data suggest that asthma acute exacerbations triggered by wildfire smoke can increase asthma-related mortality by more than threefold [64]. Moreover, asthma exacerbations following wildfire smoke exposure frequently lead to increased healthcare utilization, such as additional emergency department visits [46,48,50-52,54-57,65] and higher rates of hospital admissions [51,54,59,60,66] (Table 1). Evidence from a meta-analysis indicates that short-term exposure to wildfire smoke PM2.5 is significantly linked to elevated risks for asthma-related hospital admissions (relative risk [RR], 1.06; 95% confidence interval [CI], 1.02 to 1.09) and emergency department visits (RR, 1.07; 95% CI, 1.04 to 1.09), with these risks being especially elevated in older adults and children [63]. Notably, for pediatric asthma, the administration of rescue medications has proven beneficial, lending support to current clinical guidance that recommends providing rescue therapy to children as a particularly at-risk group during wildfire smoke events [67].

Table 1.

Research assessing the impact of wildfire smoke exposure on asthma-related healthcare utilization (emergency department visits and hospital admissions)

Study	Wildfire location	Study participants	Main result (OR/RR, 95% CI) for each outcome
Asthma-related emergency department visit
Rappold et al. (2011) [69]	North Carolina, USA	Records of 111 of 114 civilian North Carolina Eds	1.65 (1.25–2.10) (RR)
Resnick et al. (2015) [46]	New Mexico, USA	0.55 million population	1.08 (0.91–1.29) (RR)
Haikerwal et al. (2016) [65]	Victoria, Australia	5.1 million population	1.02 (1.00–1.04) (RR)
Alman et al. (2016) [50]	Colorado, USA	10,699 ED records	1.04 (1.02–1.06) (OR)
Reid et al. (2016) [51]	California, USA	12.7 million population	1.06 (1.05–1.07) (RR)
Parthum et al. (2017) [52]	Virginia, USA	2 million population	1.65 (1.25–2.17) (RR)
Hutchinson et al. (2018) [48]	California, USA	176,851 Healthcare utilized population	2.12 (1.57–2.86) (RR)
Borchers Arriagada et al. (2019) [63]	Meta-analysis	20 Studies (meta-analysis)	1.07 (1.04–1.09) (RR)
Malig et al. (2021) [54]	California, USA	Bay Area population	1.56 (1.49–1.64) (RR)
Tornevi et al. (2021) [76]	Jämtland Härjedalen Region, Sweden	130,000 Population	1.68 (1.09–2.57) (RR)
Heaney et al. (2022) [62]	California, USA	Total population of California	1.10 (1.02–1.19) (RR)
Duncan et al. (2023) [55]	North Carolina, USA	12,483 ED records	1.10 (1.06–1.14) (OR)
Chen et al. (2023) [56]	California, USA	17,847,917 Population	1.57 (1.45–1.71) (RR)
Schweizer et al. (2023) [77]	California, USA	Total population of California	1.38 (1.21–1.57) (OR)
Doubleday et al. (2023) [57]	Washington, USA	1,864,470 Non-traumatic ED visits	1.13 (1.10–1.17) (OR)
Asthma-related hospital admission
Morgan et al. (2010) [59]	Sydney, Australia	3.5 million population of Sydney	1.05 (1.02–1.08) (RR)
Kollanus et al. (2016) [60]	Helsinki, Finland	1 million population of Helsinki	1.16 (0.98-1.37) (RR)
Reid et al. (2016) [51]	California, USA	12.7 million population of California	1.07 (1.05–1.10) (RR)
Gan et al. (2017) [66]	Washington, USA	26,835 Admissions	1.07 (1.02–1.14) (OR)
Borchers Arriagada et al. (2019) [63]	Meta-analysis	20 Studies (meta-analysis)	1.06 (1.02–1.09) (RR)
Malig et al. (2021) [54]	California, USA	Bay Area population of San Francisco	1.22 (1.06–1.40) (RR)
Magzamen et al. (2021) [64]	Colorado, USA	46,585 Admissions of Colorado	1.46 (1.09–1.94) (OR)

OR: odds ratio; RR: relative risk; CI: confidence interval; ED: emergency department.

(2) Chronic obstructive pulmonary disease

COPD is a highly prevalent respiratory disorder that significantly increases healthcare utilization on a global scale. Exposure to wildfire smoke has been identified as a crucial environmental factor contributing to both the progression and exacerbation of COPD [68]. Wildfire smoke exacerbates COPD by inhibiting autophagic flux and compromising airway epithelial barrier integrity, which results in heightened inflammation and increased epithelial vulnerability [37]. In a case-crossover study conducted in Washington State, exposure to wildfire smoke was significantly correlated with an elevated risk of COPD mortality (odds ratio, 1.14; 95% CI, 1.02 to 1.26) [43]. Exposure to wildfire smoke PM2.5 is consistently associated with COPD exacerbations and increased demand for medical services, such as hospitalization [59,60,64,66], emergency department presentations [49-52,55,69], and outpatient consultations [58] (Table 2).

Table 2.

Research assessing the impact of wildfire smoke exposure on COPD-related healthcare utilization (emergency department visits and hospital admissions)

Study	Wildfire location	Study participants	Main result (OR/RR, 95% CI) for each outcome
COPD-related emergency department visit
Rappold et al. (2011) [69]	North Carolina, USA	Records of 111 of 114 civilian North Carolina EDs	1.73 (1.06–2.83) (RR)
Alman et al. (2016) [50]	Colorado, USA	10,699 ED records	1.05 (1.02–1.08) (OR)
Reid et al. (2016) [51]	California, USA	12.7 million population	1.02 (1.01–1.04) (RR)
Parthum et al. (2017) [52]	Virginia, USA	2 million population	1.73 (1.06–2.83) (RR)
Duncan et al. (2023) [55]	North Carolina, USA	12,483 ED records	2.93 (1.59–5.41) (OR)
COPD-related hospital admission
Morgan et al. (2010) [59]	Sydney, Australia	3.5 million population	1.04 (1.01–1.06) (RR)
Gan et al. (2017) [66]	Washington, USA	26,835 Cardiopulmonary hospital admissions	1.08 (1.03–1.15) (OR)
Magzamen et al. (2021) [64]	Colorado, USA	46,585 Hospital admissions	1.15 (1.00–1.31) (OR)

COPD: chronic obstructive pulmonary disease; OR: odds ratio; RR: relative risk; CI: confidence interval; ED: emergency department.

(3) Miscellaneous diseases: respiratory tract infectious disease (pneumonia) and interstitial lung disease

Exposure to wildfire smoke can disrupt the regulation of the respiratory immune system, thereby increasing vulnerability to respiratory tract infections, such as pneumonia [8,21]. Inhalation of wildfire-related PM2.5 is associated with elevated risk and severity of pneumonia through the promotion of lung inflammation, compromised integrity of the respiratory epithelium and immune function, enhancement of deeper viral penetration, and the amplification of proinflammatory cytokine activity. As a result of these biological effects, short-term exposure to wildfire-related PM2.5 has been linked to significant increases in hospital admissions [66] and emergency department visits [52,69] for pneumonia. Although patients with interstitial lung disease (ILD) are thought to have increased clinical vulnerability to wildfire smoke, as indicated by higher rates of emergency room visits and intensive care unit admissions, epidemiological studies specifically investigating this association are limited.

Health Impacts of Long-Term Wildfire Smoke Exposure

Long-term exposure to wildfire smoke is recognized as a major environmental factor in the development and progression of respiratory diseases. While numerous studies have characterized the short-term effects of wildfire smoke, the evidence regarding its long-term health effects remains scarce. A natural experiment stemming from the 1997 Indonesian wildfires demonstrated that lung capacity was reduced even 10 years post-exposure, with the impact most pronounced among men and older adults, whereas children exhibited near-complete recovery. Despite confounding influences from age and socioeconomic status, air pollution was confirmed as a principal determinant in long-term lung function [70].

Recently, the Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines adopted the classification framework introduced by the ‘Lancet Commission’ on COPD, which categorizes COPD into five etiological subtypes [71,72]. Among these subtypes, COPD-P (pollution-related COPD) was newly defined to represent disease arising from environmental exposures [72]. Greater awareness of the link between environmental factors and COPD pathogenesis has led to increased research focus on the effects of wildfire smoke exposure in COPD [68].

Lung cancer development is heavily influenced by environmental pollutant exposure. In recent years, substantial attention has been directed toward the impacts of air pollution on both lung cancer incidence and mortality, with wildfire smoke recognized as a particularly important emerging factor. Several studies indicate that exposure to wildfire-derived PM2.5 may be associated with higher cancer mortality compared to general PM2.5, showing a notable relationship with lung cancer mortality (hazard ratio [HR], 1.011; 95% CI, 1.004 to 1.018) [73,74]. Evidence suggests that prolonged exposure to wildfire smoke increases the risk of lung cancer. For example, a large Canadian population-based cohort study by Korsiak et al. [75] demonstrated that residents living within 50 km of wildfire events over a 10-year period exhibited a 4.9% higher hazard of developing lung cancer compared to those not exposed (HR, 1.049; 95% CI, 1.028 to 1.071). Collectively, these findings demonstrate that chronic exposure to wildfire smoke contributes to the long-term development of lung cancer.

Conclusion

Climate change induced by global warming is causing significant harm to both ecosystems and public health. Through the expansion of arid areas and intensification of extreme wind conditions, global warming is closely linked to a higher frequency of large-scale wildfire. Such wildfires are likely to pose growing risks to public health, especially in terms of respiratory diseases.

Wildfire smoke contains a complex mixture of hazardous air pollutants, with fine M (PM2.5) recognized as the most significant concern for respiratory health. Wildfire PM2.5 exhibits greater oxidative and proinflammatory properties compared to other sources, resulting in increased respiratory toxicity upon inhalation. Brief exposure is associated with acute worsening of respiratory illnesses such as asthma, COPD, and pneumonia, and is linked to higher rates of emergency department utilization and hospital admissions. Moreover, accumulating evidence indicates long-term adverse effects, including the onset or advancement of COPD and lung cancer, highlighting the ongoing public health risks posed by wildfire smoke exposure.

With wildfires becoming more frequent and severe, the responsibilities of healthcare professionals are expanding. Comprehensive, evidence-based insight into the impacts of wildfire smoke on different respiratory conditions is increasingly essential. Physicians should also take the initiative to educate and prepare at-risk patients for potential wildfire-related hazards. Additionally, significant gaps exist in the current literature regarding the impact of wildfire smoke on rare diseases such as ILD, despite the suspected elevated susceptibility among these groups. Thus, it is essential to conduct focused epidemiological investigations to elucidate the health outcomes associated with wildfire smoke exposure in individuals with ILD and other rare conditions. Improving knowledge of wildfire-related health effects will not only optimize clinical management but also support effective public health strategies and inform policy development in the context of climate change. Wildfires have become an immediate concern for all, necessitating urgent and collective action.