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Background: In the USA, higher forced vital capacity (FVC) is linked with longer survival, and FVC is associated with survival independently of ethnicity. The implications for the low FVC values in parts of Asia and Africa are unknown.

Methods: We used data from 16 sites of the multinational Burden of Obstructive Lung Disease (BOLD) study that completed follow-up of participants between 2019 and 2021 and reported at least five deaths between baseline and follow-up. We assessed the association of mortality with FVC and Forced Expiratory Volume in 1 second (FEV₁)/FVC ratio within each site using Cox proportional hazards models. These models were adjusted for age, smoking, height, and weight. Effect estimates from all sites were combined using meta-analysis. Systematic regional differences were investigated.

Results: Of 9927 study participants with follow-up data, 1120 (11.3%) had died [mean follow-up = 8.7 years, standard deviation (SD) = 3.3 years]. Baseline post-bronchodilator FVC and FEV₁/FVC were inversely associated with mortality. When both FVC and FEV₁/FVC were mutually adjusted for each other, the decreased mortality rates were more pronounced for each SD higher FVC at baseline [44% (95% confidence interval (CI): 25%, 58%) for men and 28% (95% CI: 11%, 41%) for women] than for FEV₁/FVC at baseline [14% (95% CI: 8%, 20%) for men and 7% (95% CI: -10%, 21%) for women]. The probability of true regional differences was low.

Conclusions: People with a higher FVC adjusted for age, sex, and height have a longer survival. Regional adjustments to lung function standards are inappropriate when assessing prognosis.

Asthma is a heterogeneous chronic airway disease in which oxidative stress (OS) plays a central mechanistic role beyond classical immune-mediated inflammation. Reactive oxygen and nitrogen species (ROS/RNS), generated by recruited inflammatory cells and activated airway structural cells, drive epithelial injury, mucus hypersecretion, airway remodeling, and modulate key transcription factors including nuclear factor kappa B (NF-kappa B) and mitogen-activated protein kinase (MAPK) pathways. This review synthesizes current evidence on the multilevel redox-based determinants of asthma severity, spanning from genetic polymorphisms to circulating biomarkers. We examine serum antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), peroxiredoxins (PRDXs), and the thioredoxin (Trx) system as dynamic indicators of systemic redox status and disease severity, alongside oxidative enzymes including NADPH oxidases and dual oxidases (NOX/DUOX), xanthine oxidase (XO), and myeloperoxidase (MPO) that serve as upstream sources of airway oxidant burden. Functional genetic polymorphisms in antioxidant genes (SOD2, CAT, glutathione S-transferase mu 1/glutathione S-transferase theta 1 (GSTM1/GSTT1), heme oxygenase-1 (HO-1), NAD(P)H quinone dehydrogenase 1 (NQO1), nuclear factor erythroid 2-related factor 2/Kelch-like ECH-associated protein 1 (Nrf2/KEAP1)) and oxidative enzyme genes including nitric oxide synthase 1/2/3 (NOS1/2/3), MPO, cytochrome b-245 alpha chain (CYBA), and xanthine dehydrogenase (XDH) are reviewed as modulators of individual redox capacity and asthma susceptibility, with particular attention to gene-environment interactions. We further discuss oxidative damage biomarkers, including malondialdehyde (MDA), 8-isoprostanes, 4-hydroxynonenal, 8-oxo-7, 8-dihydro-2 '-deoxyguanosine, protein carbonyls, 3-nitrotyrosine, and advanced oxidation protein products as indicators of lipid, DNA, and protein oxidation that correlate with disease activity and control. The roles of micronutrient cofactors in modulating antioxidant enzyme function and their potential as contextual biomarkers are also addressed. Additionally, emerging evidence on microRNAs (miRNAs) linked to OS biology in asthma is presented. Finally, we critically evaluate the challenges limiting clinical translation, including biomarker non-specificity, analytical variability, gene-environment complexity, and the absence of standardized reference ranges. This integrated framework supports the development of multilevel redox prognostic panels combining genetic, enzymatic, and oxidative damage readouts for improved asthma phenotyping, severity stratification, and personalized therapeutic approaches.

INTRODUCTION: Although Chronic Obstructive Pulmonary Disease (COPD) is generally considered a progressive condition with limited reversibility, recent data suggests potential for lung function improvement with exercise. Mechanistic insights into exercise-induced benefits remain limited, but in vitro models offer promise for understanding cellular and molecular changes. This study aims to elucidate the mechanisms behind lung tissue regeneration in COPD through adapted exercise training as well as validating advanced lung function tests, such as Impulse Oscillometry (IOS) and Airspace Dimension Assessment (AiDA) for improved detection of early physiological /structural changes and predicting clinical outcomes.

METHODS: This is the protocol of a multicenter, hypothesis-generating, single-arm study exploring the mechanisms for lung regeneration in subjects with COPD induced by exercise. The exercise protocol includes supervised and individually tailored moderate-intensity aerobic- and muscle strengthening exercise, performed three times per week for 12 weeks. Eighty sedentary adults with a clinically stable COPD will be recruited at two study sites. Included participants will be assessed at baseline and at 12 weeks by comprehensive pulmonary function testing (including spirometry, IOS, body plethysmography, diffusing capacity of the lung, single breath nitrogen wash-out, AiDA, questionnaires, physical capacity performance (including 6-minutes walking test (6MWT), one-minute sit-to-stand test, and cardiopulmonary exercise testing (CPET)), and collection of blood and urine samples and bronchoscopy. A mid-intervention assessment at week 6 will include medication use, health status, questionnaires, spirometry, and blood sampling.

DISCUSSION: Understanding the molecular and cellular activities related to lung function induced by exercise provides insights into repair pathways, challenges the notion of irreversible lung damage in COPD, and paves the way for improved management strategies with potential identification of biomarkers and pharmacological interventions.

TRIAL REGISTRATION: ClinicalTrials.gov ID NCT06335992 (Registration date 2024-03-28).

Sleep disorders such as obstructive sleep apnea (OSA) may be influenced by environmental exposures, yet the contribution of indoor microbial communities is not well understood. In this study, we examined whether the composition and load of airborne bacteria in bedrooms were associated with the Multivariable Apnea Prediction (MAP) index, a validated indicator of OSA risk. Bedroom air was sampled using electrostatic dust fall collectors in five Nordic centres participating in ECRHS III. Dust was analysed for bacterial load, endotoxin levels, and microbial composition using qPCR, LAL assay, and 16S rRNA sequencing. Associations between microbial exposures and MAP index were assessed using linear regression and categorical MAP cutoffs (≥0.5 and ≥0.7) adjusting for environmental factors. Bacterial community composition differed significantly between MAP groups, and participants with MAP ≥0.7 showed higher bacterial loads. However, alpha diversity and endotoxin levels did not vary by MAP category. A total of 35 bacterial genera were associated with MAP scores; taxa enriched in individuals with higher MAP values were primarily anaerobic and human-associated, whereas negatively associated genera were mostly aerobic and environmental. These findings suggest that the bedroom microbiome may carry a distinct microbial signature related to elevated OSA risk, potentially reflecting or contributing to sleep-disordered breathing.

BACKGROUND: Allergic sensitization is a hallmark of asthma, linked to increased disease burden. However, its role in chronic obstructive pulmonary disease (COPD) and asthma + COPD remains less understood.

OBJECTIVE: This cross-sectional study evaluates the prevalence of allergic sensitization and its associations with disease severity, lung function, exacerbations and health status across these conditions in the multinational observational NOVELTY cohort.

METHODS: Allergic sensitization was assessed from specific IgE (sIgE) to11 common aeroallergens. Physician-assessed severity, post-bronchodilator FEV1 % predicted, exacerbation history, and health status were evaluated. Mixed-effects multivariable regression models were used to assess associations, adjusted for age, sex, BMI, smoking history, and geographical region.

RESULTS: Baseline sIgE data were available from n = 5389 participants (asthma:2707; asthma + COPD:773; COPD:1909). Allergic sensitization prevalence was 56 % in asthma, 36 % in asthma + COPD, and 19 % in COPD. In asthma, sensitization to any allergen, mites or molds was associated with more severe disease (odds ratios (OR) 1.46 to 2.91) and lower post-BD FEV₁ % predicted (coefficients -1.88 % to -8.94 %). Conversely, in COPD, sensitization was associated with higher FEV₁ and milder severity. Women were less likely than men to be sensitized across all diagnostic groups. Regional differences were evident, with higher sensitization rates in North America and Europe compared to Asia.

CONCLUSION: Allergic sensitization shows divergent clinical associations across asthma and COPD, being linked to more severe disease in asthma but higher lung function and milder severity in COPD.

CLINICAL IMPLICATION: These findings emphasize the phenotypic heterogeneity of allergic sensitization in airway diseases and support its use in guiding personalized diagnostic and therapeutic strategies.

Objective: To investigate associations between short-term fluctuations in urban background air pollution and the incidence of COVID-19 across three Swedish cities using detailed individual-level data.

Methods: A case-crossover analysis was conducted using individual-level data from a prospective cohort of adults across three Swedish cities (Stockholm, Gothenburg and Uppsala), including 3999 confirmed COVID-19 cases. Subjects were classified as cases on the date of their first positive PCR test, which occurred between 7 March 2020 and 26 January 2022. Exposure data for daily levels of PM2.5, PM10 and NO₂ were obtained from urban background monitoring stations. Lag-specific and cumulative associations were examined using distributed lag models and distributed lag non-linear models, adjusting for meteorological variables.

Results: A significant association was observed between elevated PM2.5 levels and testing positive for COVID-19 on the same day (lag 0), with an OR of 1.084 (95% CI 1.011 to 1.162) per IQR (3.3 μg/m³) increase. Similar lag 0 effects were found across the three cities. For PM10, the most consistent associations were observed at lag 3. For NO₂, significant effects at lag 0 emerged only after excluding the final COVID-19 wave. Subgroup analyses showed similar effects among individuals with pre-existing respiratory conditions, though results were less consistent.

Conclusions: Our findings suggest that short-term fluctuations in air pollution, particularly for PM2.5, are associated with the timing of confirmed COVID-19 cases. A possible explanation for the short lag association is that air pollution exacerbates symptoms, prompting individuals to seek testing, rather than directly facilitating new infections.

Background

Occupational exposures are contributors to chronic respiratory diseases, particularly in low- and middle-income countries (LMICs), where regulatory policies are limited. We investigated associations between occupational exposures and respiratory outcomes using longitudinal data from the Burden of Obstructive Lung Disease study.

Methods

We analysed data from 4237 participants across 17 sites, mostly in LMICs. Occupational exposures were assessed by self-report (never vs ever) and the ALOHA+Job Exposure Matrix for vapours, gases, dusts, fumes (VGDF), pesticides, solvents and metals (cumulative exposure). Respiratory outcomes included: forced expiratory volume in 1 s (FEV₁), forced vital capacity (FVC), the FEV₁/FVC and respiratory symptoms. Associations were examined using multilevel linear and logistic regression models adjusted for age, sex, smoking, pack-years, education, body mass index and baseline FVC. We further explored sex differences and non-linear relationships for symptoms.

Results

Over a median 10 years of follow-up, FEV₁/FVC decline was associated with moderate (β=–1.34; 95% CI –2.32 to –0.35) and high (β=–1.79; 95% CI –3.33 to –0.20) exposure to VGDF and low (β=–1.11; 95% CI –2.11 to –0.08) and high (β=–2.16; 95% CI –4.08 to –0.24) exposure to pesticides. Increased risk of wheeze was associated with moderate (Relative Risk (RR) =1.45; 95% CI 1.05 to 2.15) and high (RR=1.89; 95% CI 1.100 to 3.26) exposure to pesticides. Associations did not differ by sex. There was weak evidence of non-linear exposure–response relationships and no associations with solvents or metals.

Conclusions

A significant decline in FEV1/FVC was associated with exposure to VGDF and pesticides. Increased risk of wheeze was also associated with exposure to pesticides. These findings underscore the need for continued monitoring in high-exposure settings, particularly in LMICs.

Background: Identifying biomarkers for different aspects of asthma morbidity is crucial for effective disease monitoring and management. The performance of fractional exhaled nitric oxide (FeNO), blood eosinophil count (BEC), and eosinophil activity markers should be evaluated.

Objective: This study aimed to compare the associations of FeNO, BEC, serum and plasma eosinophil-derived neurotoxin (S- and P-EDN), and serum eosinophilic cationic protein (S-ECP) with important clinical outcomes in asthma.

Methods: In total, 390 individuals aged 10-35 years with physician-diagnosed asthma were included. Asthma control test (ACT), spirometry, and methacholine challenge tests were used to assess asthma morbidity. The biomarkers' associations with asthma outcomes: impaired spirometry (FEV₁ < 80% predicted, FEV1/FVC < lower limit of normal), airway hyperresponsiveness (AHR), uncontrolled asthma (ACT < 20) were analysed with multiple logistic regression models adjusted for body mass index, sex, age, immunoglobulin E sensitisation, smoking, and controller medication. The Akaike information criterion (AIC) was calculated for each model, to compare biomarker performance.

Results: S-EDN had the lowest AIC value of all biomarkers in models assessing the association with reduced lung function, showing better model fit than P-EDN and S-ECP. However, FeNO and BEC had the lowest AIC values for AHR. FeNO was the only biomarker associated with uncontrolled asthma.

Conclusion: S-EDN may serve as an alternative to BEC in research setting and could be relevant in assessing airway obstruction. However, adding S-EDN as a routine biomarker alongside FeNO and BEC may offer limited additional clinical value. Further research in larger cohorts is needed to validate these findings and establish optimal cut-offs.

Introduction

Rapid urbanisation over the past century has led to increased traffic density and higher levels of ambient air pollutants. We aimed to investigate whether the prevalence of respiratory symptoms, asthma, and chronic bronchitis increases with the level of self-reported exposure to traffic and occupational-related pollution.

Material and methods

The study population comprised 25,889 general population subjects ages 16-75 years participating in the Swedish part of the GA2LEN study. Data were collected in the cities of Umeå, Uppsala, Stockholm, and Gothenburg. Self-reported data on disturbance of fumes from traffic in the residential area or occupational exposure to gas, dust, or smoke, as well as on patient demographics, respiratory symptoms, asthma and chronic bronchitis, were obtained from questionnaires.

Results

The prevalence of respiratory symptoms, asthma, and chronic bronchitis was higher both among participants reporting traffic-related exposure and those with a history of occupational exposure to fumes, smoke, and dust than among those unexposed; (wheeze 27 vs 13%), nocturnal cough (35 vs 22%), asthma (11 vs 6%) and chronic bronchitis (22 vs 8%); all p < 0.0001. When combining traffic and occupational exposure, the highest prevalence was found amongst those exposed to both. Associations with occupational exposure were generally stronger in women, and those with traffic exposure were stronger in men.

Conclusion

In this large population-based sample, self-reported residential traffic exposure and occupational exposure to dust, fumes, or smoke were associated with increased prevalence of respiratory symptoms, asthma, and chronic bronchitis. Although causality cannot be inferred, these findings underscore the importance of assessing environmental and occupational exposures in evaluating respiratory health.