Bronchoalveolar lavage (BAL) is a minimally invasive procedure frequently used in the evaluation of pulmonary diseases. The primary indications for its use include the diagnosis of inflammation, infection, and interstitial lung diseases. Additionally, BAL plays a role in tumor diagnostics, detection of rejection following lung transplantation, and the diagnosis of occupational lung diseases (e.g., berylliosis, asbestosis).Although BAL alone mostly does not enable a definitive diagnosis, analysis of the BAL fluid provides important findings that are essential when interpreted in the clinical context. Successful analysis and interpretation require careful sample collection and rapid processing. Sample preparation is technically straightforward, and routine staining (Giemsa) is uncomplicated. BAL is widely available, cost-effective, and an indispensable tool in the diagnostic workup of pulmonary diseases.

In January 1946, the Journal of Industrial Hygiene and Toxicology published "A Health Survey of Pipe Covering Operations in Constructing Naval Vessels." This cross-sectional epidemiological study is one of the most consequential in the history of industrial hygiene and occupational medicine as it errantly concluded that insulation work on ships using asbestos-containing materials was "…not a dangerous occupation." As a consequence of this innocuous conclusion, the U.S. Navy and others neglected to protect insulators and other employees from asbestos dust for the next 25 years, leading to an epidemic of asbestos-related diseases in active and retired workers. Subsequently, attorneys and expert witnesses used this exculpating conclusion to mount "state of the art/science" defenses for asbestos manufacturers in tort actions, arguing that their clients relied on this publication when they failed to protect their own employees from asbestos or warn their customers of the hazard. Both the industrial hygiene and the medical components of this study were deeply flawed. The successor publisher to the original journal has refused to consider retracting this paper, so this catastrophic blunder may remain a part of the literature, available to asbestos tort defense attorneys and their experts. Publishing industry policies and precedent related to retracting very old articles are reviewed.

Interstitial lung diseases (ILDs) encompass a heterogeneous group of pulmonary disorders whose prevalence is increasing, partly driven by the environmental exposome. Fine particulate matter (PM2.5), air pollutants, bioaerosols, and occupational exposures (such as silica, asbestos, and organic dust) play a major role in the initiation, progression, and exacerbations of ILDs. These agents induce oxidative stress, inflammation, and fibrotic activation. Conditions such as asbestosis, anthracosilicosis, idiopathic pulmonary fibrosis, sarcoidosis, and hypersensitivity pneumonitis illustrate the interaction between individual susceptibility and environmental factors. Infections and the lung microbiome also contribute to pathophysiology and may act as disease triggers in at-risk populations. The exposome concept provides an integrative framework to understand these complex interactions. Despite recent advances, uncertainties remain, particularly regarding the long-term effects of inhaled ultrafine particles.

Asbestos use has been banned in ~ 70 countries due to its health and environmental implications, even though for decades, evidence of its use in causing mesothelioma, lung cancer, and asbestosis has been firmly established. The lack of international governance in dealing with asbestos is complicated by global climatic changes, causing disasters that are dislodging existing asbestos; regional conflicts, which vaporizing asbestos without warning; the fact that the general public does not know how to identify materials containing asbestos, which makes them more vulnerable; and finally, emerging mechanisms for releasing existing asbestos, which are not governed by industrial mechanisms, making the situation worse. This paper, therefore, argues that international leadership, legislative mechanisms, and public education are not optional, but the bare minimum that must be done to stop the use of asbestos and the deaths that result from its use once and for all.

Pleural plaques are the most common manifestation of asbestos-related pleural disease and function primarily as markers of prior exposure rather than as direct causes of clinically significant symptoms, often appearing several decades after initial contact. They are typically asymptomatic and discovered incidentally on imaging studies or at autopsy, and they initially present as small, well-circumscribed lesions along the parietal pleura, most commonly over the rib surfaces while sparing the intercostal spaces. They may progressively enlarge, coalesce, and undergo calcification over time. Although asbestos exposure is the primary etiology, pleural plaques and pleural calcifications may also arise from prior infections such as tuberculosis or empyema, trauma, hemothorax, end-stage renal disease, or chronic inflammatory and autoimmune conditions such as systemic lupus erythematosus and rheumatoid arthritis, and in some instances they may be idiopathic. Additionally, pleural plaques can be associated with mesothelioma. When extensive, pleural plaques may restrict lung expansion, leading to exertional dyspnea that can progress to dyspnea at rest and, in advanced cases, respiratory insufficiency. During routine cadaveric dissections conducted as part of the preclinical medical curriculum at the Geisinger Commonwealth School of Medicine (GCSOM), Scranton, Pennsylvania, extensive bilateral pleural thickening, predominantly involving the diaphragmatic pleura, was observed in an 89-year-old male cadaver. After the opening of the thoracic cage and removal of the lungs and heart, pleural plaques were identified, examined, and measured. The pleural cavities were relatively free, with minimal adhesions involving the bases of both lungs in the diaphragmatic regions, and any evidence of pleural effusion was likely lost during the dissection process. Small, isolated pleural plaques were also noted along the anterior aspect of the right parietal costal pleura. A small, firm mass was palpated within the anterior border of the right upper lobe. Tissue specimens were obtained from the pleural plaques of the anterior chest wall and diaphragmatic pleura, as well as from the pulmonary mass, for histopathological evaluation. Microscopic examination demonstrated abundant fibrocollagenous thickening of the parietal pleura with adjacent fibro-adipose connective tissue and associated inflammation, without evidence of asbestos fibers. Histological analysis of the pulmonary mass was consistent with acute pneumonia. Pleural plaques are frequently encountered as incidental findings on chest radiographs and computed tomography scans in elderly individuals, particularly those with prior asbestos exposure, yet many such findings remain clinically uninvestigated during life. Establishing an etiology in cadaveric cases poses a significant challenge due to the absence of reliable occupational, environmental, and medical histories. While the histopathologic features observed in this case are consistent with previously published descriptions, the gross anatomical documentation of extensive pleural plaques predominantly confined to the diaphragmatic pleura, including detailed measurements, texture, and imaging, has not been previously reported. Dissemination of these findings aims to enrich anatomical and pathological educational resources, support future research, and deepen the understanding of pleural pathology encountered during cadaveric dissection and medical education.

Asbestos is a risk factor for occupational lung cancer. This article reported a case of asbestosis. During regular chest CT scans, an enlargement of nodules in the left lower lobe was observed. After undergoing relevant examinations, the patient underwent left lower lobe resection. Postoperative pathology confirmed the diagnosis as SMARCA4-deficient undifferentiated tumor. The patient was subsequently treated with immunotherapy, radiotherapy and chemotherapy and currently has a good prognosis.

An 83-year-old male patient with pulmonary asbestosis was admitted to our hospital with a subacute onset of arthromyalgia affecting the shoulder girdles. He had a history of moderate asbestos exposure in the earlier part of his occupation and was diagnosed with pulmonary asbestosis at 65 years of age. The patient exhibited recent-onset stiffness and myalgia of the shoulder and finger joints. Joint ultrasound findings showed bilateral long head biceps, resulting in a diagnosis of polymyalgia rheumatica (PMR) according to the European League Against Rheumatism/American College of Rheumatology (EULAR/ACR) classification criteria for PMR. Steroid treatment resolved the musculoskeletal symptoms.

The Rocky Flats (RFs) Plant operated from 1951-1989 as part of the U.S. Department of Energy (DOE) nuclear complex. Its primary mission was weapons component fabrication, whereby workers were potentially exposed to radioactive and non-radioactive hazards. RF worker mortality was compared to the general population, and dose-response relationships between mortality and radiation organ doses were examined. RF workers first employed between 1951 and 1979 for ⩾30 d were identified (n= 9397). Vital status was determined using national and state death records up to 2017. Organ doses from external photons and neutrons irritation and internalised plutonium (Pu), americium (Am), and uranium (U) were modelled as cumulative lagged total doses per year. Beryllium exposure was evaluated as an effect modifier using data from the DOE Nationwide Beryllium Medical Program. Statistical analyses included standardised mortality ratios (SMRs), Cox proportional hazard models, and excess relative risk (ERR) models. Approximately 53.2% of workers were deceased by the end of the study. Nearly 90% were monitored for radiation exposure, with a mean weighted absorbed dose of 59.0 mGy for the lungs. Nearly 45% of workers had intakes of alpha-particle emitting radionuclides, and 46.7% were monitored for neutrons. Leading causes of death included ischemic heart disease (n= 999) and lung cancer (n= 361). The highest SMRs were observed for berylliosis (SMR: 176.9; 95% CI: 76.2, 348.7;n< 10) and asbestosis (SMR: 4.65; 95% CI: 2.23, 8.55;n= 10). Dose-response analyses showed no statistical increase in risk from low-dose radiation including lung cancer (ERR per 100 mGy: -0.02; 95% CI: -0.11, 0.08;n= 361) and Parkinson's disease (ERR per 100 mGy: 0.13; 95% CI: -0.26, 0.31;n= 57). Approximately 45% of workers were monitored for beryllium, with a weak non-significant indication of effect modification for lung cancer risk. The RF cohort showed no evidence of a statistically significant increase in mortality from occupational radiation exposure. However, this study was limited by low statistical power, which inhibits the ability to detect effects. Future pooling of Million Person Study (MPS) cohorts will provide further insights, particularly regarding Pu as a carcinogen.

Home monitoring of physical parameters, symptoms and quality of life in individuals with pulmonary fibrosis (PF) could overcome gaps in clinical care by enabling early detection of disease progression, guiding patient management and improving access to specialised care. However, its global adoption in clinical practice is lacking. The aim of this study is to gain a deeper understanding of healthcare professionals' (HCPs) perspectives on implementing home monitoring for individuals with PF.

This data note describes a structured dataset of lung radiomic features derived from thoracic noncontrast computed tomography examinations of 100 subjects (47 males, 53 females; aged 15-74 years). Participants were selected on the basis of the absence of known lung, pleura, and mediastinum diseases in clinical records and radiology reports, as well as systemic diseases affecting the respiratory system. The included computed tomography studies were performed on a single multidetector CT scanner (Siemens Healthineers SOMATOM go. Now), using a uniform protocol (110 kVp; reconstructed slice thickness 0.8 mm; Br60-type lung kernel). For each case, the target thin-slice DICOM series was converted to the NIfTI format. The lung lobes ("raw" masks), vessels and air pathways were segmented automatically with TotalSegmentator. In addition to "raw" lobe masks, vessel/airway-subtracted (parenchyma) masks were generated. Lobe masks (left lung - 2, right lung - 3) were also combined into the left lung, right lung, and both lungs, resulting in eight ROIs per subject for each mask type - with ("raw") and without vessel/air pathways ("parenchyma"). For each SubjectID×ROI, radiomic features (107 "original" features - shape, first-order, and texture families) were extracted via a PyRadiomics-based pipeline with fixed settings (B-spline interpolation; resampling to 1 × 1 × 1 mm; bin width 25 HU; absolute resegmentation) in two attenuation ranges: -1000 to +200 HU and -950 to 0 HU. The dataset is distributed as (i) a CT protocol table, (ii-iii) two feature tables ("raw" and parenchyma masks), (iv) a JSON file with a computational environment description, (v) a Python extraction script, and (vi) a dictionary file. This dataset can serve as a normative reference for lung radiomics, a benchmark for harmonization and robustness studies, and a control cohort for comparative modelling in diffuse lung diseases, as well as region-specific diseases requiring lobar or single-lung-specific radiomic features (such as emphysema, chronic obstructive pulmonary disease, Swyer-James-MacLeod syndrome, asbestosis, and silicosis).