Driven by the climate crisis, ‘megafires’ (or sixth-generation fires) have shifted from anomalies to a global norm. Defined by exceeding 10,000ha, these explosive events release sufficient energy to generate their own weather conditions. Recent history has witnessed their devastation across continents: from the ‘Black Summer’ in Australia and the record-breaking Canadian season that choked North America, to the blackened urban interfaces of California and Chile, and the relentless burning of the Amazon.

In the summer of 2025, this phenomenon struck Southern Europe with unprecedented force. Data from the Copernicus Atmosphere Monitoring Service (CAMS) reveals that in 2025, more than 1 million hectares burned across several EU countries, making it the worst year on record1. In Spain alone, fires consumed over 382,000 hectares, representing >6 times the 2006–2024 average. In this editorial, we address this emerging crisis, which represents not only an environmental catastrophe but poses unprecedented challenges for public health.

Wildfires generate a complex mixture of atmospheric pollutants that dramatically deteriorate air quality. CAMS forecasts showed fine particulate matter (PM2.5) concentrations well above WHO-recommended air quality guidelines across large regions of Spain [1]. Moreover, smoke plumes traveled hundreds of kilometers, reaching France, the United Kingdom, and Scandinavia, demonstrating that the threat extends far beyond fire proximity.

Beyond suspended particles, smoke contains toxic gases including nitrogen oxides, volatile organic compounds, and polycyclic aromatic hydrocarbons derived from biomass combustion. These compounds induce oxidative stress, promote inflammation, and cause cellular injury in the respiratory tract, while also impairing macrophage function and reducing the lungs’ ability to clear pathogens and particulate matter [2]. This chemical composition confers distinctive toxicity to wildfire smoke, potentially exceeding that of conventional urban particles, with direct implications for respiratory health [3].

In clinical practice, immediate smoke exposure effects are well-established: cough, throat irritation, eye irritation, and to a lesser extent, chest pain, dyspnea, or dizziness. While these symptoms are typically mild and transient, multiple systematic reviews and meta-analyses have demonstrated significant increases in emergency department visits and hospitalizations for respiratory problems during wildfire episodes. Each 10μg/m3 increase in wildfire-specific PM2.5 is estimated to increase respiratory hospitalizations by up to 10% [4]. Chronic respiratory patients are the primary at-risk group, with robust evidence showing that wildfire smoke exposure significantly increases the probability of exacerbations in conditions such as asthma or COPD, requiring bailout medication use or hospitalization [5].

While respiratory symptoms typically show within a few hours, cardiovascular effects may be delayed up to 10 days post-exposure. Polluting gases and ultrafine particles penetrating the lungs can enter the bloodstream, triggering systemic inflammation and oxidative stress that promote endothelial dysfunction, hypercoagulability, and atherosclerotic progression. Simultaneously, they alter autonomic regulation (favoring arrhythmias) and, along with gases like NO2 and ozone, worsen myocardial oxygen supply-demand balance [6]. Wildfire smoke exposure is positively associated with cardiovascular events including ischemic heart disease, arrhythmias, heart failure, ischemic stroke, and pulmonary embolism [7].

The combination of respiratory epithelial damage and immune system dysfunction creates favorable conditions for respiratory infections. Short-term wildfire smoke exposure is associated with significant increases in medical consultations and hospitalizations for acute bronchitis and pneumonia [8]. Research during the COVID-19 pandemic linked wildfire PM2.5 peaks with higher SARS-CoV-2 infection and mortality rates in affected areas. Landguth et al. [9] (2020) examined the delayed effects of wildfire-related PM [2,5] exposure and found that summer smoke exposure was associated with a 3–5-fold increase in influenza incidence later in the same year [9]. These episodes have also been associated with substantial increases in active tuberculosis diagnoses in subsequent months. The particles’ capacity to transport live pathogens over long distances may explain increased fungal infections observed in some studies, including those caused by Aspergillus and Coccidioides.

Of particular concern are the potential long-term consequences. Multicenter and cohort studies have demonstrated associations between wildfire smoke exposure and sustained declines in pulmonary function, as well as an increased risk of developing or accelerating chronic respiratory diseases, including asthma and chronic obstructive pulmonary disease [3]. Although evidence is more limited, inhalation of wildfire particles induces activation of profibrotic pathways (e.g., TGF-β), potentially worsening the progression and prognosis of diseases like idiopathic pulmonary fibrosis and hypersensitivity pneumonitis [10]. In the cardiovascular domain, it may accelerate atherosclerosis and heart failure progression, contributing to greater chronic disease burden and mortality persisting years after acute exposure [11]. Most concerning is the possible link between long-term wildfire exposure and a higher incidence rate of lung cancer [12], forcing us to question whether wildfire smoke exposure should be considered a new environmental carcinogenic risk factor.

From an occupational perspective, frontline workers including firefighters, forest brigades, and emergency personnel face repeated and prolonged exposures to these complex pollutant mixtures. Documented effects include pulmonary function decline, bronchial hyperreactivity episodes (including RADS), cardiovascular events, and elevated systemic inflammation markers—effects that may persist beyond immediate exposure periods [13]. Particularly concerning is exposure to multiple occupational carcinogens raising questions about long-term cancer risk. Despite well-documented risks, significant gaps persist in implementing effective protection measures, especially in rural departments where respiratory protection program compliance is inconsistent [14].

Given this scenario, what recommendations can we offer patients and the general population? (Table 1):

Strategies must focus on exposure reduction: remaining indoors with effective filtration (closed windows, recirculation, HEPA purifiers) or relocating if protection is inadequate. Education on interpreting air quality indices is crucial. For necessary outdoor activities, FFP2/N95 masks provide filtration (unlike ineffective surgical masks) though they lack gas protection and may create false security.

Clinicians should document exposure and schedule follow-up to detect sequelae. Patients need individualized action plans specifying rescue treatment escalation, short oral corticosteroid courses, and urgent care criteria. Finally, respiratory vaccination updates (influenza, pneumococcus, SARS-CoV-2) are a priority given the increased infection susceptibility.

Climate change is radically transforming the epidemiological landscape of respiratory diseases. Scientific projections are unequivocal: rising global temperatures, prolonged droughts, and altered precipitation patterns are creating perfect conditions for more intense, longer, and more frequent wildfires, converting previously exceptional episodes into increasingly common events [15]. As respiratory health specialists, we cannot limit ourselves to treating the consequences of this emerging health crisis. We must advocate for environmental health policies, collaborate in community preparedness protocols, and use every patient conversation to teach protection in a world where clean air is becoming an increasingly scarce commodity.