Genetically predicted susceptibility to dust-induced lung diseases and risk of autoimmune diseases: a two sample Mendelian randomization study.

Silicosis is an incurable occupational lung disease characterized by progressive fibrosis and respiratory failure, imposing a significant global health burden. Surfactant protein A (SP-A) plays a critical role in maintaining pulmonary homeostasis, yet its mechanistic role in silicosis remains unclear. SP-A expression was assessed in lung tissues from patients with silicosis and in silica-exposed mice. Sftpa1 gene knockout (Sftpa1-/-) mice were generated to evaluate the functional role of SP-A in vivo, including lung pathology, collagen deposition, and pulmonary function. RNA sequencing was performed to uncover underlying molecular mechanisms. A549 cells with SP-A silenced by siRNA were employed for in vitro experiments. SP-A levels were notably reduced in the lung tissue of silicosis patients and in experimental silicosis mice, correlating inversely with disease severity. Sftpa1⁻/⁻ mice showed markedly exacerbated silica-induced pulmonary fibrosis, extracellular matrix deposition, and functional decline. RNA-seq analysis highlighted activation of intrinsic apoptosis pathways related to pulmonary fibrosis. Mechanistically, SP-A deficiency disrupted the balance of Bcl-2 and Bax, activated Caspase-3, and promoted epithelial apoptosis. Inhibition of the intrinsic apoptosis pathway mitigated the pro-apoptotic effects of SP-A silencing. These findings demonstrate that SP-A deficiency exacerbates silica-induced pulmonary fibrosis by promoting epithelial apoptosis involving the Bcl-2/Bax/Caspase pathway, highlighting the role of SP-A in fibrogenesis progression and providing a basis for its potential therapeutic target for silicosis.

Furniture industry workers in Sambirembe Village, Sragen, face significant health risks from exposure to wood dust, particularly an increased risk of Chronic Obstructive Pulmonary Disease (COPD). This research is prompted by the low awareness among workers regarding these risks and the minimal use of personal protective equipment (PPE). The objective of this program was to increase workers' and business owners' knowledge of lung health, promote early detection of COPD, and encourage the adoption of safer work practices. The method employed was an intervention that included health education and lung function screening via questionnaires and spirometry. The results revealed a critical knowledge gap, where over 85% of workers had never heard of COPD, even though 70% of them reported experiencing respiratory symptoms. Furthermore, over 90% of workers admitted to rarely using masks. The intervention, which combined education with personalized spirometry data feedback, proved effective in increasing worker awareness of tangible health risks. In conclusion, the education-based and health-screening intervention program successfully raised furniture workers' understanding of COPD risks. An approach that integrates information with personal medical evidence is crucial for promoting behavioural change in high-risk work environments.

Coal workers' pneumoconiosis (CWP) is a preventable, progressive occupational lung disease caused by inhaling respirable coal mine dust, a complex mixture commonly containing coal, crystalline silica, and other silicate minerals. Early pneumoconiosis can be asymptomatic, but advanced disease often leads to disability and premature death. To describe CWP-associated mortality among U.S. residents aged ≥15 years by industry and occupation, CDC conducted an exploratory analysis of National Vital Statistics System multiple cause-of-death data for 2020-2023, the most recent years that include information on decedents' usual industry and occupation. During 2020-2023, CWP was listed on the death certificate of 1,754 decedents (age-adjusted CWP-associated death rate = 1.3 per 1 million). By industry group, the highest number of CWP-associated deaths occurred among workers in the mining industry (1,255). The highest proportionate mortality ratios (PMRs) were among persons employed in the mining industry (PMR=50.0) and the construction and extraction occupations (6.2). Among workers employed in the mining industry, the highest PMR was among underground mining machine operators (164.6). The continuing occurrence of CWP-associated deaths underscores the potential value of a comprehensive prevention program (maintaining efforts to control occupational coal mine dust exposures, combined with early disease detection efforts and medical care) and supports potential benefits of ongoing surveillance.

Introduction. The renin-angiotensin system is considered part of the endocrine system, responsible for regulating blood pressure and fluid and electrolyte balance. However, this system is also present locally in various tissues, including the lungs, where it plays a role in the pathogenesis of inflammatory and fibrotic processes.The study aims to investigate the presence of associations between polymorphisms of the genes encoding proteins of the renin-angiotensin system and the development and severity of occupational lung diseases.Materials and methods. The study included patients with established diagnoses of occupational lung diseases: occupational bronchial asthma (n=136), occupational chronic obstructive pulmonary disease (n=63), silicosis (n=42), a comparison group of 80 workers exposed to industrial aerosols with more than 10 years of work experience without lung diseases. An identification of polymorphic variants of the genes AGT rs699, rs5186, REN rs2368564, ACE rs1799752, AGTR1 rs5186, AGTR2 rs1403543 was conducted.Results. Associations of the studied genetic markers with the development of professional occupational lung diseases were revealed: AGTR2 rs1403543 polymorphism increases the risk of developing occupational asthma (OR=1.929, 95% CI 1.067–3.488), ACE rs1799752 and AGT rs699 polymorphisms — the risk of developing occupational COPD from exposure to welding aerosol (OR=2.844, 95% CI 1.253–6.458 and OR=3.059, 95% CI 1.259–7.433, respectively), ACE rs1799752 polymorphism is associated with earlier development of asthma upon contact with metal allergens, AGTR1 rs5186 polymorphism — with the development of silicosis. Polymorphisms AGT rs699, rs5186, AGTR2 rs1403543 increase the risk of developing emphysema in occupational bronchial asthma.Conclusions. The obtained results demonstrate the significance of genetic polymorphisms of renin-angiotensin system proteins in the development and progression of occupational lung diseases. Promising genetic markers for further study were identified (genetic polymorphisms AGT rs699, rs4762, ACE rs1799752, AGTR1 rs5186, AGTR2 rs1403543), which may contribute to risk assessment, severity prediction, and phenotyping of occupational lung diseases.Limitations. The study is limited to a sample of the surveyed.Ethics. The study was conducted in compliance with ethical standards for conducting medical research involving humans in accordance with the requirements of the Helsinki Declaration of the World Medical Association. The study was approved by the conclusion of the local Ethics committee of the FSBSI IRIOH (protocol of the meeting of the Ethics Committee of the FSBSI IRIOH No. 5 dated 08/02/2023).Contributions:Kuzmina L.P. — concept and design, editing;Khotuleva A.G. — concept and design, collecting and processing data, conducting laboratory tests, text writing, editing;Hermassi O. — collecting data, conducting laboratory tests, text writing;Khokhlova O.V. — collecting and processing data, conducting laboratory tests, text writing.Funding. The study had no funding.Conflict of interest. The authors declare no conflict of interest.Received: 19.11.2025 / Accepted: 20.11.2025 / Published: 10.12.2025

Resistance to silicosis progression in mice with Ch25h downregulation: The involvement of NLRP3 inflammasome.

Silicosis is an occupational lung disease characterized by inflammation and fibrosis. As it is irreversible, early identification of high-risk individuals is clinically important, but biomarkers for progression remain lacking. To determine whether ventilation and perfusion defects quantified by phase-resolved functional lung (PREFUL) MRI can predict silicosis progression. Prospective. Thirty participants with silicosis (29 males and 1 female) and 30 healthy controls (29 males and 1 female). 2D spoiled gradient echo, 3.0 T. All participants underwent baseline PREFUL MRI, pulmonary function tests (PFTs), and chest CT, with quantitative calculation of ventilation defect percentages (VDPRVent and VDPFVL-CM) and perfusion defect percentage (QDP). Silicosis was followed for 1 year with assessments including forced vital capacity percent predicted (FVC% predicted), diffusing capacity of the lungs for carbon monoxide percent predicted (DLco% predicted), symptoms, and CT. Disease progression was defined by any two of: (a) CT evidence of progression, (b) worsening symptoms, or (c) ≥ 10% decline in FVC% predicted or ≥ 15% decline in DLco% predicted. Spearman correlation coefficients were used to evaluate the correlation between ventilation/perfusion metrics and PFT parameters. Receiver operating characteristic (ROC) curves were used to assess the ability of PREFUL MRI parameters to classify disease progression, reporting the area under the curve (AUC), sensitivity, and specificity. Significance was set at p < 0.05. Eight patients progressed and 22 remained stable. Baseline VDPRVent, VDPFVL-CM, and QDP were significantly higher in progressors (36%, 34%, 40%) than in non-progressors (22%, 15%, 22%). QDP showed strong predictive performance with AUC of 0.72 (95% CI: 0.51-0.93) for radiological progression, 0.90 (95% CI: 0.79-1.00) for PFTs decline, and 0.97 (95% CI: 0.92-1.00) for global progression. Increased ventilation and perfusion defects on PREFUL MRI are associated with silicosis progression. 2. Stage 2. NCT06431555.

Silicosis is a progressive occupational lung disease marked by persistent silica-induced inflammation and irreversible pulmonary fibrosis. The NLRP3 inflammasome, an innate immune sensor, has been implicated as a key driver of silica-triggered inflammation and fibrosis in preclinical models. However, the specific role of NLRP3 in immune cells, particularly within myeloid cells (monocytes, macrophages and neutrophils), remains poorly defined. In this study, we investigated the in vivo contribution of myeloid-derived NLRP3 to silica-induced lung pathology using a conditional NLRP3 knockout mouse model (LysMCre Nlrp3fl/fl). These mice exhibited efficient deletion of NLRP3 in both resident and infiltrating lung myeloid cells. Following intranasal delivery of 2 mg of silica, NLRP3 expression was upregulated in myeloid cells by day 3. Despite upregulation of NLRP3 in myeloid cells by day 3, early inflammasome activation in the tissue and BAL, including caspase-1 cleavage and IL-1β and IL-18 secretion, remained intact. During the chronic phase (days 14 and 28), myeloid NLRP3 deletion did not mitigate hallmark features of silicosis, including alveolitis, structural lung damage, airway remodeling or peribronchial alpha-smooth muscle actin expression. Furthermore, the formation and size of silicotic nodules were unaffected. These findings indicate that NLRP3 expression in myeloid cells is not essential for the development of silica-induced pulmonary inflammation, tissue damage or fibrosis. This work highlights the need to explore alternative cellular sources and mechanisms of NLRP3-driven pathology in silicosis.

Introduction: Occupational respiratory diseases represent a global public health issue especially in textile Industry. Exposure to cotton dust is a major contributor, leading to respiratory issues such as coughing, phlegm, wheezing, shortness of breath, chest tightness, chronic bronchitis, and byssinosis, all of which cause severe pulmonary illness. The objective is to assess the pulmonary function of selected textile industry workers of Tirupur, Tamil Nadu. Method: Using Crochan’s Formula 656 textile workers from six textile industries of Tirupur (5) and Coimbatore (1) were selected using purposive sampling. The current paper focuses on 160 workers of both the sex (male 124, female 36) working not less than 5-years in the textile industry. A mixed research design (Qualitative and Quantitative) was used. A Qualitative analysis on perception of occupational Hazard and impact on the respiratory illness among the textile industry worker was done among 38 respondents. As part of quantitative research, the demographic details, anthropometric measurements, nature of work, pulmonary function and lifestyle practices such physical activity, smoking, pan chewing and alcohol consumption of the worker were elicited using a validated interview schedule. Using Flow Measuring Spirometer (Helios_v3.2.56) the pulmonary function was tested for Forced Expiratory Volume in the first second (FEV1), Forced Vital Capacity (FVC), FEV1/FVC ratio according to the guidelines of American Thoracic Society. Result: Sneezing was common symptom experienced followed by allergy, cough and irritation. Among the 160 workers interviewed 33% of the textile workers fell within the age group 20-30 years. The mean BMI was found to be similar for both male (23.39±4.2) and female workers (23.4±4.6). The workers had poor pulmonary function with their FEV1, FVC, and FEV1/FVC ratios lower than the reference value significant at 1% level (p&lt;0.0001). A higher prevalence of early airway obstruction in females (44%) was observed compared to males (10%). Mild restriction (&lt;80) was observed in 13% of males and 14% of females, while moderate restriction (&lt;64) was reported in 7% of males and 14% of females respectively. Conclusion: Prolonged exposure to cotton dust may attribute to respiratory symptoms such as coughing, wheezing, and chest tightness.

SOX18 influences the progression of silicosis through the regulation of lymphangiogenesis.

Silicosis is an occupational lung disease caused by prolonged exposure to silica dust in the workplace. It has a complex pathogenesis and currently lacks effective treatments. Homoharringtonine (HHT) is a natural compound approved for the treatment of acute myeloid leukemia, but its effects on silicosis remain unclear. In the present study, we constructed a mouse model of silica (SiO2)-induced pulmonary fibrosis and evaluated the preventive and therapeutic effects of HHT. The results showed that HHT significantly attenuated the progression of SiO2-induced pulmonary fibrosis in mice. We then used MRC-5, a human lung fibroblast cell line, to explore the mechanisms underlying HHT's inhibitory effects in vitro and found that HHT significantly inhibited the activation and migratory capacity of MRC-5 cells. Mechanistically, these effects were mediated by enhanced ubiquitination and degradation of the CCR1 protein. Furthermore, HHT exhibited favorable biocompatibility in vivo, and its preventive and therapeutic effects were validated in SiO2-treated mice. Collectively, the current study demonstrates that HHT shows significant potential as a therapeutic agent for silicosis by targeting CCR1 and the PI3K/AKT/mTOR signaling pathway, highlighting it as a promising candidate for clinical translation for silicosis treatment.

ABSTRACTSilicosis is an occupational lung disease characterized by diffuse pulmonary fibrosis resulting from inhalation of silica particles. As the disease progresses, lung tissue stiffness continuously increases, driving persistent activation and accumulation of myofibroblasts. However, whether these cells undergo senescence in response to prolonged high matrix stiffness and how such senescence impacts fibrosis progression remain unclear. Here, we established an in vitro model using decellularized lung matrices with varying stiffness to simulate the fibrotic mechanical microenvironment. We found that increased matrix stiffness upregulated mitochondrial fission protein DRP1, inducing excessive mitochondrial fragmentation and accumulation of mitochondrial reactive oxygen species (mtROS), leading to oxidative stress, DNA damage, and myofibroblast senescence. Treatment with the mitochondria‐targeted antioxidant Mitoquinone mesylate (MitoQ10) effectively alleviated these effects. Moreover, senescent myofibroblast‐derived secretions promoted fibroblast activation and collagen deposition via paracrine signaling, exacerbating fibrotic remodeling. These findings identify matrix stiffness‐driven cellular senescence as a critical mechanism in silicosis progression, providing a rationale for targeting senescent cells as an antifibrotic therapeutic strategy.

Efficacy of homeopathic medicines in occupational lung disease

Evaluation of advanced SEM-EDX tools for classification of complex particles in respirable dust.

Silicosis is a preventable occupational lung disease that can present in chronic, accelerated or acute forms. While chronic silicosis is a known risk factor for spontaneous pneumothorax, this complication is rarely reported in acute silicosis and can be life-threatening. We report an autopsy of a 40-year-old male with acute silicosis who died following a recurrent right-sided spontaneous pneumothorax. He had worked in a glass manufacturing facility with intense silica dust exposure for one year and had a prior episode of pneumothorax due to suspected silicosis eight months before his death. Post-mortem examination revealed a right tension pneumothorax with complete collapse of the right lung, extensive fibrosis in both lungs and ruptured subpleural bullae. Histopathology confirmed acute silicosis with classic silicotic nodules. This case underscores that even acute silicosis can lead to fatal spontaneous pneumothorax, although such complications are more typically associated with chronic silicosis. It highlights the importance of early recognition of pneumothorax in silicosis patients and reinforces the need for stringent occupational dust control and health surveillance to prevent silicosis and its severe complications.

Viscose rayon fiber is a semi-synthetic material derived from regenerated cellulose. The cellulose used to make viscose rayon is extracted from natural sources, resulting in fibers that are physically similar to cotton and have characteristics such as softness and high absorbency. The viscose manufacturing process involves chemical modification of cellulose using carbon disulfide (CS2), which is dangerous if exposed to humans. Carbon disulfide residues, along with endotoxin biological agents present on rayon fibers, can be inhaled into the respiratory tract. This causes oxidative protein damage, which then activates the oxidative stress response. This response ultimately results in the release of oxidants that induce inflammatory mediators, triggering acute or chronic inflammatory reactions in the airways and alveoli, resulting in decreased lung function. A systematic approach is essential for gathering and interpreting relevant data. This approach can be organized into seven steps to diagnose occupational lung diseases. The use of personal protective equipment (PPE) represents the final but most important defense. Recommended PPE includes respirator masks with suitable particle filters, protective eyewear to prevent eye irritation, chemical-resistant gloves to protect the skin from direct contact, and full-body work clothing.

BackgroundSilicosis is an occupational lung disease characterized by silicotic nodules and progressive pulmonary fibrosis, caused by long-term excessive inhalation of free silica. So far, no effective methods have been developed to delay or cure silicotic fibrosis. Exosomes derived from human umbilical cord mesenchymal stem cells (hucMSC-Exos), which possess functions of intercellular communication, tissue repair and regeneration, offering a potential strategy for the treatment of silicosis.Methods and resultsIn this study, exosomes were extracted from human umbilical cord mesenchymal stem cells (huc-MSCs) using differential centrifugation and characterized for subsequent experiments. A silica-induced silicosis mouse model was established. Lung CT scans were performed to assess pulmonary lesions, while blood oxygenation status was monitored. Histopathological analysis of lung tissues was conducted, and Western blot was used to evaluate inflammatory and fibrotic markers, aiming to investigate the therapeutic effects of hucMSCs and their exosomes on silicotic mice. High-throughput transcriptome sequencing of lung tissues was employed to screen differentially expressed genes and signaling pathways in the two treatment groups, followed by in vitro validation of the proposed mechanisms.ConclusionOur findings demonstrate that hucMSC-Exos alleviate pulmonary inflammation, slow lung fibrosis, inhibit macrophage pyroptosis, activate the actin cytoskeleton signaling pathway, and maintain plasma membrane integrity in silicotic mice. This study provides possible therapeutic targets and molecular mechanisms for silicosis, establishing a link among silicosis, cytoskeleton, and pyroptosis, while validating the protective effect of hucMSC-Exos on the lungs of silicotic mice.Supplementary InformationThe online version contains supplementary material available at 10.1186/s13287-025-04646-2.

A review of modern approaches to the prevention, treatment and rehabilitation of occupational dust-related lung diseases, including chronic obstructive pulmonary disease, with an emphasis on maintaining working capacity, is realized. The analysis of scientific literature, including articles, guidelines and recommendations of professional associations, with an assessment of the levels of evidence, is carried out. The pathogenetic principles of treatment, medicinal and non-medicinal methods (pulmonary rehabilitation, physiotherapy, balneotherapy), their effectiveness in improving respiratory function, quality of life and reducing disability are described. Prevention includes technical, hygienic and medical measures.Chronic obstructive pulmonary disease of occupational etiology remains a global problem requiring an integrated approach. Existing methods are effective, but new solutions for prevention and rehabilitation are needed.

This research introduces a unique dataset targeting Silicosis, a significant global occupational lung disease, and a member of the Pneumoconiosis family. Addressing the challenges in healthcare data collection and the need for expert annotation, this dataset aims to aid AI algorithms in medical applications. The comprehensive dataset includes not only Silicosis cases but also related conditions, such as tuberculosis and silicotuberculosis, alongside healthy lung images, addressing the diagnostic complexity due to symptom overlap. As the first public dataset of its kind, it offers detailed annotations for lung and disease region segmentation, as well as disease prediction, provided by multiple radiologists. Baseline experiments and findings demonstrate that current AI models have limited predictive accuracy for these disease classes, emphasizing the critical need for dedicated research. It is our assertion that the proposed Silicodata can be a key dataset in designing automated Silicosis detection tools and addressing challenges associated with small sample sizes in medical AI research.

Introduction. Upgrading of nickel production technologies, in this case the transition from electrolytic to more modern electroextractive refining, is not always accompanied by an improvement in the working conditions in the employees involved. The aim of the study. To analyze working conditions and occupational respiratory diseases in workers at electrolytic and electroextractive nickel production. Materials and methods. We studied the data of industrial control at nickel industry enterprises and the Murmansk regional register of occupational diseases for 2004–2023. Results. A comparative analysis of hygienic data revealed a 2.4-3.5-fold decrease in the concentration of nickel hydroaerosols at the electrolytic bath operator workplaces and a 4.4–31.4-fold increase in chlorine concentrations in the workplace air of the hydrometallurgical department during the transition to electroextractive refining. Clinical studies have shown the transition to electroextraction method to be accompanied by a decline in the number and in the proportion of workers with occupational respiratory diseases (p=0.002–0.003), a 24.5% decrease in the level of occupational morbidity (from 56.12 cases to 42.35 cases per 10,000 workers), a decrease in the risk of developing respiratory occupational diseases (OR=1.89; 95% CI 1.31–2.73). Over 10 years, only one case of acute chlorine poisoning was registered. Conclusion. We have no found adverse impact of elevated chlorine concentrations on the development of occupational respiratory diseases in workers engaged in electrowinning nickel refining. However, further improvement of nickel electrowinning technology is necessary to reduce the concentration of nickel and chlorine salt hydroaerosols, as well as more effective personal respiratory protection equipment is needed. The impact of working conditions on workers’ health during electrowinning nickel refining requires a longer study.