Chronic lung disease of prematurity (CLD) is a common complication of preterm birth with a complex pathology. Recent epidemiologic studies have identified a link between neonatal exposure to di(2-ethylhexyl) phthalate (DEHP), frequently used in medical equipment, and the development of CLD. We hypothesize that DEHP exposure in the early neonatal period contributes to lung injury in newborn rats. Newborn rat pups were raised in one of the following environments: room air (RA), RA + DEHP, hyperoxia (60% oxygen), and hyperoxia + DEHP. Ambient DEHP was inhaled at a dose of 25 mg/m3 for 6 h daily for 14 days. Lung tissue and blood samples were collected on the 14th day of life. Independent exposure to DEHP and hyperoxia resulted in thicker pulmonary septal walls, fewer alveoli, increased pulmonary polymorphonuclear leukocytes and myeloperoxidase (MPO) activity and decreased expression of CD31 on endothelial cells in lung tissue. Additionally, DEHP-exposed rats showed higher serum malondialdehyde (MDA) levels and reduced vascular endothelial growth factor (VEGF) mRNA and protein levels compared to controls. Our experiments demonstrate that inhaled DEHP, with or without hyperoxia, resulted in a similar pattern of morphological lung injury and inflammation characteristic of CLD, suggesting an association with CLD of prematurity.

Street-food grilling is a common occupation in Asia, yet the occupational health risks associated with cooking-generated polycyclic aromatic hydrocarbons (PAHs) exposure, occurring alongside plausible unmeasured co-exposures such as ambient heat and physical workload, remain under-researched. This study investigated the internal dose of PAH exposure and its association with early biological effects and physiological strain among grill restaurant workers. A cross-sectional study was conducted involving grill workers and 20 age/BMI-matched controls. Urinary 1-hydroxypyrene (1-OHP) was utilized as the primary exposure biomarker. The study assessed early biological effects such as oxidative stress (8-OHdG, F2-isoprostanes), lung epithelial integrity (CC16), and genotoxicity (BPDE-DNA adducts) via ELISA. Physiological parameters, including blood pressure and heart rate, were recorded to evaluate acute cardiovascular strain. Workers had significantly elevated urinary 1-OHP levels compared to controls (Hodges-Lehmann ratio = 3.66, 95% CI: 1.68-7.12, representing a 3.7-fold median increase), with exposure levels increasing proportionally to smoke proximity. Notably, workers demonstrated a significantly higher median resting heart rate (HL ratio = 1.13, 95% CI: 1.05-1.23; +12.9%) and systolic blood pressure (HL ratio = 1.09, 95% CI: 1.00-1.18; +8.9%) compared to their office-based peers. Although strong correlations were observed among biological effect biomarkers (rs = 0.42-0.63), there were no significant differences between groups for 8-OHdG, CC16, or BPDE-DNA adducts, suggesting that cardiovascular parameters reflect acute short-term responses, while genomic damage markers may require higher cumulative exposure thresholds to become detectable. The study revealed that grill restaurant workers face substantial internal PAH exposure and significant cardiovascular strain, occurring alongside plausible unmeasured co-exposures including ambient heat and physical workload. The prevalence of chronic cough and elevated heart rate is a critical early warning sign for occupational health. Our findings indicate that current general ventilation is inadequate, highlighting an urgent need for localized engineering controls and comprehensive health surveillance, including cardiovascular monitoring in the service sector.

Pulmonary arterial hypertension (PAH) is a fatal vascular disorder with poor prognosis. 6:2 chloro-polyfluorooctane ether sulfonate (F-53B), a persistent environmental contaminant detected in humans, is known to be vasculotoxic, yet its association with PAH remains unexplored. This study aims to elucidate the mechanisms linking F-53B exposure to PAH by integrating network toxicology, molecular docking and in vitro experiments. Potential F-53B targets were predicted using ChEMBL, PharmMapper, and TargetNet. PAH-related genes were compiled from GeneCards, Online Mendelian Inheritance in Man (OMIM), Therapeutic Target Database (TTD), and GSE254617. We identified 42 key targets of F-53B-related PAH. Functional enrichment revealed terms such as inflammatory response and extracellular matrix. Protein-protein interaction (PPI) analysis identified five hub genes: CCL2, CXCL8, CCL5, CCR2, and CCL11. Molecular docking confirmed strong binding between F-53B and these core targets, with CCR2 showing the strongest affinity (-10 kcal/mol). Molecular dynamics simulations further verified stable binding to CCR2. In vitro experiments demonstrated that F-53B activated the CCL2/CCR2 axis and induced IL-1β, TNF-α, and IL-6 in HUVECs and RAW264.7 cells. This study reveals that F-53B is linked to PAH through dysregulation of chemokine signaling networks and induction of inflammatory cytokines. These findings suggest F-53B as a potential environmental risk factor for PAH and pinpoint potential targets for intervention.

Thin-slice high-resolution computed tomography (CT) has improved the detection of small pulmonary nodules, increasing the demand for minimally invasive diagnostic and therapeutic resection. While lobectomy with lymph node dissection remains the standard surgical approach for many patients with resectable non-small cell lung cancer, accumulating evidence supports sublobar resection for selected small, peripheral, and ground-glass-dominant lesions when sufficient margins are achievable. In thoracoscopic and robotic surgery, localization of nodules ≤10 mm or lesions located >5 mm from the pleural surface can be challenging, and failure to identify the target may lead to conversion, larger resection than intended, or prolonged operative time. Several localization strategies have been developed, including CT-guided percutaneous wire/coil/dye marking, bronchoscopic dye mapping, and virtual-assisted lung mapping (VAL-MAP), robotic-assisted bronchoscopic dye or fiducial localization, radiofrequency identification microtag systems (Surgical Real-Time FInger Navigation and Detection) that provide real-time depth information, and single-stage intraoperative CT-guided marking and resection in hybrid operating rooms. This review synthesizes representative evidence and published outcome ranges, and compares workflows, marker-to-lesion precision metrics, complication profiles, operational burden, and cost structures. We emphasize the practical contrast between two-stage and single-stage workflows, the access-route differences between transthoracic and transbronchial techniques, and the need to report localization-to-incision "time at risk". We also present an expert-consensus decision algorithm aimed at facilitating tailored selection of localization strategies for modern minimally invasive thoracic surgery.

Urban greenspace measured by remote sensing has been linked to population health benefits, yet evidence on cardiopulmonary effects at the microenvironmental street level and related molecular mechanisms in older adults remains limited. We conducted a repeated-measures panel study of 76 healthy older adults in Jinan, China, with five monthly clinical examinations. Pedestrian-level neighborhood greenspace exposure was quantified using AI-based semantic segmentation of street-view videos collected around participants' residences. Pulmonary and cardiovascular function were repeatedly assessed, alongside multiomics profiling of blood and urine samples. Linear mixed-effect models were used to examine associations of greenspace exposure with cardiopulmonary outcomes, while causal inference tests and integrative pathway analyses explored potential biological mechanisms. Higher neighborhood greenspace exposure was significantly associated with improved forced vital capacity (FVC), but not with other pulmonary indices or cardiovascular outcomes. In fully adjusted models, each interquartile range (IQR) increase in greenspace exposure was associated with a 189.9 mL (95% CI: 35.9 to 343.2 mL) increase in FVC. Multiomics analyses identified mediating metabolites, lipids, transcripts, and enriched pathways related to immune activation, nitric oxide metabolism, and DNA repair. These findings suggest that pedestrian-level greenness exposure may enhance pulmonary function in older adults through specific biological pathways, highlighting the importance of microscale urban greening for respiratory health.

Occupational health and safety (OHS) practices witnessed profound changes worldwide during the COVID-19 pandemic. The pandemic exposed critical vulnerabilities in workplace preparedness, particularly among workers in high-exposure and essential service sectors.

Silicosis is a severe occupational lung disease characterized by persistent inflammation and progressive fibrosis with no effective treatment. Glycyrrhetinic acid-3-O-β-D-glucuronide (GAMG), an active metabolite of glycyrrhizin, has anti-inflammatory and anti-fibrotic efficacy in our previous work, but its direct molecular target remains unknown. Through integrated multi-omics and molecular docking, we identified stimulator of interferon genes (STING) as a key pathogenic driver and a potential target of GAMG in silica-induced pulmonary injury. In silicosis patients, levels of dsDNA, STING, HMGB1, and α-SMA were significantly elevated (P < 0.01) and correlated with disease severity. Surface plasmon resonance (SPR) showed that GAMG directly binds to STING (Kd = 11.44 µM). Cellular thermal shift assays (CETSA) further demonstrated that GAMG enhances STING stability. In MH-S macrophages, GAMG inhibited the STING/TBK1/NF-κB pathway and reduced silica-induced release of pro-inflammatory (IL-6 and TNF-α) and pro-fibrotic cytokine TGF-β1. In a murine silicosis model, GAMG (100 mg/kg) treatment reduced dsDNA accumulation and blocked STING activation. Moreover, GAMG alleviated lung inflammation and collagen deposition. Collectively, these findings revealed that GAMG targeted the STING/TBK1/NF-κB pathway to alleviate silicosis, identifying STING as a potential therapeutic target. This work supported GAMG as a promising natural metabolite for treating silica-induced lung injury.