Lung cancer (LC) is the leading cause of cancer-related mortality worldwide, primarily due to diagnosis at advanced stages. Although low-dose computed tomography (LDCT) screening reduces lung cancer mortality in high-risk populations, current screening programmes are largely restricted to individuals defined by age and smoking history. This approach excludes never-smokers and individuals with non-smoking-related risk factors, limiting the equity, efficiency and scalability of lung cancer screening. The LUng Cancer risk factors and their Impact Assessment (LUCIA) project aims to overcome these limitations by developing personalised lung cancer risk prediction models and evaluating novel non-invasive technologies for early detection within a risk-adapted screening strategy.

Socio-economic and demographic variables have been identified as determinants of transmission of, and susceptibility to, COVID-19. In this study, we analyse the heterogeneous impacts of non-pharmaceutical interventions on the socio-economic and demographic (SED) variables driving COVID-19 incidence in Toronto during the 2nd, 3rd and 4th waves of the pandemic. Spatial autoregressive models were used to explore associations between COVID-19 incidence and SED variables at neighborhood scale, accounting for vaccination levels. This approach helps clarify how SED factors and vaccine coverage drive COVID-19 incidence and how non-pharmaceutical interventions (NPIs) modulate these factors at neighborhoods' level, while taking into account the pervious nature of boundaries at these scales to disease transmission due to population mobility, although without directly informing on behaviours, exposure, or vulnerability at individual level. Three distinct models were considered for each of the second, third and fourth COVID-19 waves, from late 2020 to late 2021. Associations highlighted by the models were interpreted with reference to the NPIs implemented. Level of scholarity, income, proportion of the population living alone, average number of children in families, and the proportion of the population whose mother tongue is not an official language showed significant relationships with COVID-19 incidence. Model results were different for each wave, reflecting the unequal impacts of NPIs at different time points, and for different population groups, depending on the nature of interventions and the SED determinants considered. Prioritization of population groups for testing, unequal gathering restrictions, selective closure of economic activities or work-from-home policies led to heterogenous impacts on incidence. The results highlight the unequal burden of the pandemic across populations and likely disparities in occupational exposure driven by SED factors, as well as their evolution with the implementation and lifting of NPIs. Populations with the lowest income and scholarity cumulate the highest risks of exposure and the highest risks of severe disease outcomes. Our results support the development of knowledge based public health surveillance programs integrating both non-communicable and infectious diseases cases, beyond their acute occurrences, along with their socio-economic characteristics.

The purpose of this paper is to identify studies of hospital-based occupational stress prior to the COVID-19 pandemic that can offer lessons to nurse leaders in our current post-pandemic environment. A scoping review was conducted based on the Joanna Briggs Institute framework, including key phases and principles identified by Arksey and O'Malley. Evidence from different disciplines and settings has been relatively siloed. Nurses and doctors have tended to be studied separately using different constructs. Progress in developing more effective interventions to mitigate occupational stress in healthcare may require greater cross-disciplinary collaboration in which nurse leaders are well poised to lead.

Background and objectives: Occupational and environmental inhalation exposures, including high-aspect-ratio carbon nanotubes, can trigger pulmonary fibrosis (PF). The relationship between exposure-specific fibrogenic pathways (granulomatous inflammation versus diffuse epithelial injury) and lung microbiome dysbiosis remains incompletely understood. We therefore compared lung microbiome alterations in rat PF models induced by multi-walled carbon nanotubes (MWCNTs) and bleomycin. Materials and Methods: Female Wistar rats received a single intratracheal instillation of vehicle, MWCNTs (750 μg/rat), or bleomycin (1 mg/rat). At day 28, fibrosis and inflammation were evaluated by histopathology and bronchoalveolar lavage fluid (BALF) profiling. Lung microbial communities were characterized by 16S rRNA gene sequencing (V3-V4). Seventeen lung samples passed stringent quality control and were analyzed (control n = 5; bleomycin n = 7; MWCNT n = 5). Results: Both agents induced PF with increased profibrotic signaling, but with distinct pathological signatures: MWCNTs produced localized granulomatous lesions and a robust neutrophilic response (25% of BALF cells), whereas bleomycin caused diffuse interstitial remodeling. Bleomycin increased microbial richness (alpha diversity; p < 0.05) and significantly shifted community structure (beta diversity; p < 0.05), while MWCNT exposure showed comparatively limited changes in global diversity. The relative abundance of Pseudogracilibacillus (including P. marinus) was higher in the bleomycin group than in controls, whereas Facklamia tabacinasalis and Corynebacterium maris were more abundant in the MWCNT group. Across samples, Proteobacteria abundance was inversely correlated with BALF TGF-β, MCP-1, and neutrophil proportion. At the species level, Pseudogracilibacillus marinus was positively correlated with BALF TGF-β, while Facklamia tabacinasalis and Corynebacterium maris were positively correlated with MCP-1, CINC-3, and neutrophil proportion (Spearman; p < 0.05). Conclusions: Mechanistically distinct fibrogenic exposures generate exposure-linked lung microbiome signatures that track with host inflammatory and profibrotic responses. These signatures may support biomarker development for environmentally and occupationally relevant PF and motivate longitudinal and functional studies to clarify causality.

Bronchial asthma (BA) is a major public health problem worldwide and represents a significant health burden in Saudi Arabia. The prevalence and risk factors of asthma vary across regions and are influenced by genetic, environmental, occupational, and lifestyle-related factors. A cross-sectional epidemiological study was conducted among 738 adults residing in the Makkah region of Saudi Arabia. Data were collected using a self-administered questionnaire that included sociodemographic characteristics and potential risk factors for asthma. Crude and adjusted odds ratios were calculated to assess associations between participant characteristics and self-reported BA. Of the 738 participants, 192 (26.0%) reported having BA. Asthma prevalence differed significantly across cities within the Makkah region (Taif, Makkah, and Jeddah) and among individuals who lived or worked near factories (P < .01). Among asthma patients, 76.6% reported using asthma medications. The most frequently reported environmental and lifestyle exposures included the use of chemicals in cleaning, farming, or hair styling (76.6%), use of air conditioners (73.4%), and use of firewood for heating or cooking (70.3%). Passive smoking was reported by 57.3% of patients, while 46.0% were active smokers. The prevalence of BA among adults in the Makkah region was considerable and varied by geographic location and environmental exposure. Living or working near factories and exposure to indoor and occupational risk factors were associated with asthma. These findings underscore the importance of addressing regional environmental and occupational factors in asthma prevention and management strategies in Saudi Arabia.

Chronic respiratory diseases (CRDs) are a growing global health concern. Emerging evidence implicates circulating metabolites in their development and progression, but definitive causal insights into how metabolic patterns influence disease pathways remain limited. We conducted a two-sample Mendelian randomization (MR) analysis to evaluate potential causal effects of 1400 serum metabolites on 5 major CRDs: chronic obstructive pulmonary disease (COPD), asthma, idiopathic pulmonary fibrosis (IPF), sarcoidosis, and pneumoconiosis. Each disease was analyzed separately; no composite CRD outcome was constructed. The inverse-variance weighted method was the primary approach, complemented by MR-Egger, weighted median, and MR-PRESSO for outlier detection and correction. Robustness was examined using sensitivity analyses, including Cochran Q for heterogeneity, MR-Egger intercept for directional pleiotropy, the MR-PRESSO global test, and leave-one-out analyses. MR analyses identified significant causal associations between multiple metabolites/metabolite ratios and the 5 CRDs, revealing distinct metabolic profiles for each disease. For COPD, we found 54 potentially causal metabolites (30 risk, 24 protective). Asthma showed 36 associations (13 risk, 20 protective). IPF had 39 (22 risk, 17 protective). Sarcoidosis exhibited the broadest signature with 69 associations (24 risk, 45 protective). Pneumoconiosis showed 53 (25 risk, 28 protective). Most signals were disease-specific; only a small subset overlapped across at least 2 diseases (e.g., four shared between COPD and sarcoidosis, two between pneumoconiosis and asthma), suggesting partially shared pathways. No metabolite displayed consistent associations across all 5 diseases. Circulating metabolites exhibit protective or detrimental causal effects on COPD, asthma, IPF, sarcoidosis, and pneumoconiosis. Effects are heterogeneous and largely disease-specific, with limited overlap across conditions, indicating predominantly distinct etiologic pathways and offering mechanistic insights that may inform risk stratification and target prioritization. Further validation using integrated multi-omics and experimental models is warranted to refine mechanisms and assess translational potential.

ObjectiveDespite of the tentative role of asbestos in chronic obstructive pulmonary disease (COPD), their lung function variation in relation to air pollution remains unexplored. This cross-sectional study aimed to explore the effects of air pollution on severe airway obstruction (SAO) in asbestos-related COPD.MethodsCOPD subjects were retrospectively recruited, and their asbestos exposure and SAO were verified using the existence of pleural plaque in chest X-ray and the predicted value of forced expiratory volume in 1 second in percentage less than 50%, respectively, followed by examining the association between PM2.5, PM10, SO2, NO2, O3, and CO and SAO stratified by asbestos exposure using regression model.ResultsSAO percentage was 67.2% (41/61) and 65.2% (15/23) in COPD subjects without and with asbestos exposure, respectively. An increased 3-day average concentration of CO and O3 correlated with SAO (odds ratio, 95% confidence interval: 0.06, 0.01-0.41 and 0.09, 0.01-0.64, respectively). Moreover, an increased 5-day average CO concentration also correlated with SAO (0.13, 0.02-0.71) prior to hospital admission of COPD subjects irrespective of asbestos exposure, and SAO failed to be associated with asbestos exposure.ConclusionsCertain gaseous pollution at low concentration might generally exhibit a negative association with SAO in COPD subjects, indicating the negligibly negative impact of air pollution on lung function deterioration in asbestos-related COPD.

ObjectiveOccupational exposure to carcinogens significantly contributes to the global burden of tracheal, bronchial, and lung (TBL) cancers. This study aims to quantify the global, regional, and national burden of TBL cancers attributable to occupational carcinogens using Global Burden of Disease (GBD) 2021 data and project trends to 2050. Additionally, we employ Mendelian Randomization (MR) to explore potential causal relationships between modifiable risk factors and TBL cancers.MethodsWe extracted mortality and Disability-Adjusted Life Year (DALY) data for TBL cancers caused by occupational carcinogens from the GBD 2021 database. Exponential smoothing and autoregressive integrated moving average (ARIMA) models projected the burden to 2050. Two-sample MR analysis utilized genome-wide association study (GWAS) data, primarily from individuals of European ancestry, to investigate causal links.ResultsIn 2021, occupational carcinogens caused 285,628 deaths and 6.12 million DALYs globally. While age-standardized mortality and DALY rates declined in some high-income countries, low- and middle-income countries (LMICs) showed rising trends. Projections indicate a potential shift, with some regions plateauing while others face increasing burdens due to persistent exposure. MR analysis confirmed significant causal relationships, identifying higher BMI, smoking, visceral adiposity, and waist circumference as risk factors, while coffee consumption, dried fruit intake, physical activity, and education were protective.ConclusionDespite progress, the burden of occupational TBL cancers remains substantial, particularly in LMICs. The discordance between declining rates in high-income nations and rising burdens elsewhere highlights the need for targeted interventions and stricter regulations. Integrating genetic evidence supports precision prevention strategies focusing on both occupational safety and modifiable lifestyle factors.