This study aims to investigate the anti-inflammatory and anti-fibrotic effects of dimethyl sulfoxide (DMSO) in a mouse model of silicosis, thereby exploring its potential therapeutic value. A mouse model of silicosis was established by intranasal instillation, and DMSO treatment was administered via intraperitoneal injection. The experiment was conducted over a period of 1 month. Lung tissues were collected from all mice; a subset was subjected to transcriptomic analysis, and differentially expressed genes were identified using the limma package. Gene ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) enrichment analyses were conducted using ClusterProfiler to investigate gene functions and associated pathways. The remaining samples were subjected to histopathological assessment by hematoxylin and eosin staining (HE) and Masson's trichrome staining, while Western blot analysis was performed to validate transcriptomic results. This study suggests that DMSO may alleviate the fibrotic process in silicosis by modulating the IL-6/STAT3-MMP12 signaling axis. In the silica-induced silicosis mouse model, DMSO attenuated disease-associated weight loss and reduced collagen deposition. Transcriptomic analysis indicated that DMSO suppressed the activity of multiple fibrosis-related pathways and identified 51 key genes, including MMP12, which was significantly downregulated. Western blot analysis further confirmed reduced MMP12 expression, accompanied by markedly decreased levels of IL-6 and p-STAT3, suggesting the IL-6/STAT3 pathway may play a crucial role in regulating MMP12 expression. DMSO may attenuate inflammatory responses and pulmonary fibrosis in silicosis by inhibiting activation of the IL-6/STAT3 signaling pathway, thereby reducing MMP12 expression.

Silicosis is caused by occupational exposure to respirable crystalline silica (CS) particles and is characterized by chronic inflammation and progressive pulmonary fibrosis. To date, the underlying mechanisms of silicosis remain poorly understood and effective treatment options are limited. Stimulator of interferon genes (STING) has been identified by us and others as a critical initiator of inflammatory responses and lung damage during silicosis. In this study, we investigate the role of STING pathway in regulating programmed death-ligand 1 (PD-L1) expression and epithelial-mesenchymal transition (EMT) during silicosis, and further explore the underlying mechanisms and profibrotic significance of this axis. Our findings demonstrate that STING signaling regulates PD-L1 expression and promotes EMT progression in the silicosis mouse model. Mechanistically, CS-activated macrophage STING signaling induces PD-L1 expression and drives the EMT process in alveolar epithelial cells by the TGF-β1/Smad2/3 signaling pathway. Furthermore, we demonstrate that epithelial PD-L1 mediates CS-induced EMT and fibrogenic activity in alveolar epithelia. Collectively, these findings extend our mechanistic understanding of how STING promotes silicotic fibrosis and identify potential therapeutic targets for silicosis.

Silicosis is the oldest occupational lung disease known to medicine and, at the same time, one of the most contemporary public health emergencies. Described in classical antiquity, given monographic attention by Paracelsus and Agricola, established as the founding example of occupational medicine by Ramazzini in 1700, and named by Visconti in 1870, the disease was widely assumed by the late 20th century to be a controlled relic of heavy industry. Yet over the past two decades it has returned with force as an acute and accelerated disease of the young, through two technology-driven outbreaks: denim sandblasting and the fabrication of engineered (artificial) stone. This article traces silicosis across roughly 2,500 years and argues that its history is best understood less as a story of mineralogy than as one of political economy: of who works, who profits, who is believed, and who is compensated. This article integrates three dimensions usually treated apart: the medical history of recognition and pathophysiology; the social history of class, race and the deliberate manufacture of doubt; and the history of labor mobilization and health policy, from the world's first silicosis compensation statute (South Africa, 1911) and the 1930 Johannesburg conference of the International Labor Office (ILO) to the United States silica standard of 2016 and Australia's world-first prohibition of engineered stone in 2024. As Sisyphus was condemned to roll a boulder uphill only to watch it roll back each time he neared the summit, so each silicosis epidemic that one society defeats tends to reappear in another; we argue that this cyclical recurrence is driven by economic disparity. Each time a wealthy jurisdiction eliminates a hazardous process, that process, and with it the disease, migrates to a poorer country or a less-regulated sector rather than disappearing, and until those underlying inequalities are addressed the boulder will keep rolling back down. This article closes with a forward projection on emerging hazards, diagnostics, the prospects for the World Health Organization-ILO goal of global elimination, and the equity question of who is left behind. Silicosis is wholly preventable; its persistence is therefore a political choice, not a scientific mystery.

Pneumoconiosis complicated with pulmonary tuberculosis is characterized by high prevalence and disability rates, as well as difficulty in early diagnosis, constituting a serious public health problem. The Chinese Society of Tuberculosis (Chinese Medical Association) and the Society of Labor Hygiene and Occupational Diseases (Chinese Preventive Medicine Association) organized multidisciplinary experts in respiratory diseases, occupational diseases, tuberculosis and other related fields to formulate the Chinese expert consensus on the diagnosis and treatment of pneumoconiosis complicated with tuberculosis. This consensus aims to enhance professional practitioners' understanding of the disease, improve the capacity for early clinical diagnosis, and further advance the prevention and treatment of pneumoconiosis complicated with pulmonary tuberculosis in China. It summarizes 12 key clinical issues and proposes 13 targeted recommendations to address difficulties and misconceptions in clinical practice. This consensus was registered on the International Practice Guidelines Registry Platform (PREPARE-2024CN271). It aims to enhance the standardized diagnosis and treatment of pneumoconiosis complicated by pulmonary tuberculosis, improve patient outcomes, and provide practical guidance for the prevention and control of occupational and infectious diseases in China. The main recommendations are as follows.Recommendation 1: Clinicians and pathologists are advised to pay attention to the mixed pathological features of pneumoconiosis complicated with pulmonary tuberculosis. For patients with pneumoconiosis presenting atypical imaging manifestations or poor response to conventional treatment, pathological specimens should be actively obtained to confirm the diagnosis. Combined use of acid-fast staining, Mycobacterium tuberculosis culture or molecular pathological detection is recommended to increase the detection rate (2C).Recommendation 2: When performing chest CT examinations and dynamic follow-up for pneumoconiosis patients, clinicians and radiologists should focus on multifocal and polymorphic lesions, as well as short-term imaging changes suggestive of active tuberculosis (2C).Recommendation 3: For patients with suspected pulmonary tuberculosis complicated with pneumoconiosis: (1) Be aware that sputum bacteriological tests may yield false-negative results due to dust interference. Repeated sampling or combined detection methods are recommended, including bacteriological and molecular tests on bronchoalveolar lavage fluid (BALF) obtained via bronchoscopy. Results of immunological assays such as the interferon-γ release assay (IGRA) and tuberculin skin test (TST)shall also be combined for comprehensive judgment. (2) In cases with atypical imaging findings and clinical symptoms, bronchoscopy-guided pathological sampling (e.g., EBUS-GS [endobronchial ultrasound with guide sheath], ENB [electromagnetic navigation bronchoscopy]) is prioritized. When microbiological evidence is insufficient, percutaneous lung biopsy or pleural biopsy (for patients with pleural effusion) is suggested to clarify the diagnosis (2B).Recommendation 4: The diagnosis of pneumoconiosis complicated with pulmonary tuberculosis shall follow the integrated diagnostic principle. Provided that patients meet the national diagnostic criteria for pneumoconiosis and pulmonary tuberculosis respectively, a comprehensive assessment shall be conducted combining occupational exposure history, dynamic imaging changes and laboratory results. Patients shall be stratified for managementaccording to the activity of tuberculosis (2C).Recommendation 5: For differential diagnosis between pneumoconiosis complicated with pulmonary tuberculosis and non-tuberculous mycobacterial (NTM) lung disease: (1) NTM lung disease commonly involves the apical and anterior segments of the upper lobes, the right middle lobe and the lingular segment of the left upper lobe. Typical imaging manifestations include a combination of centrilobular nodules and bronchiectasis. (2) Multiple thin-walled cavities are frequently seen in silicosis complicated with NTM lung disease. (3) Pathologically, NTM lesions are dominated by epithelioid granulomas with inconspicuous caseous necrosis. (4) Definitive diagnosis relies on mycobacterial culture and species identification, complying with combined clinical, imaging and microbiological criteria (2C).Recommendation 6: For patients with pneumoconiosis complicated with pulmonary tuberculosis who present progressively enlarged cavities or newly developed cavities accompanied by aggravated symptoms after anti-tuberculosis treatment, radiologists shall evaluate imaging signs of pulmonary aspergillosis, such as the early halo sign and the late air crescent sign within cavities (2C).Recommendation 7: For patients with suspected pneumoconiosis complicated with pulmonary aspergillosis: (1) Bronchoscopy is performed to collect BALF or tissue specimens for fungal culture and pathological examination (gold standard). (2) Conduct BALF galactomannan (GM) test, metagenomic next-generation sequencing (mNGS) or other DNA detection assays. (3) Detect serum specific antibodies against Aspergillus fumigatus (e.g., IgE-m3, IgM) (1A).Recommendation 8: For patients with pneumoconiosis complicated with drug-susceptible pulmonary tuberculosis: (1) Adopt the standard first-line four-drug anti-tuberculosis regimen. (2) Ensure a sufficient treatment course (generally ≥6-8 months). (3) Extend the treatment course to≥9-12 months for patients with severe lesions or concomitant tracheal, pleural or extrapulmonary tuberculosis, so as to improve clinical outcomes and reduce recurrence (2A).Recommendation 9: For patients receiving concurrent treatment for pneumoconiosis (including tetrandrine, nintedanib, pirfenidone, glucocorticoids, bronchodilators, etc.) and rifampicin-containing anti-tuberculosis regimens: (1) Be aware that rifampicin, a potent hepatic enzyme inducer, may accelerate the metabolism of concomitant drugs such as glucocorticoids and nintedanib and reduce their efficacy. (2) Adjust the dose of affected drugs accordingly when rifampicin is initiated or discontinued (1B).Recommendation 10: Extracorporeal membrane oxygenation (ECMO) may be used as a bridge to lung transplantation only for end-stage pneumoconiosis patients complicated with pulmonary tuberculosis awaiting transplantation (2D).Recommendation 11: For end-stage patients with pneumoconiosis complicated with pulmonary tuberculosis who have received adequate and standard anti-tuberculosis therapy, the feasibility of lung transplantation shall be evaluated. Pre-transplant precautions: (1) Ensure complete control of active tuberculosis. (2) Optimize the anti-tuberculosis regimen (e.g., replace rifampicin with rifabutin) to maintain the effective concentration of immunosuppressants (2D).Recommendation 12: For patients with severe, end-stage pneumoconiosis complicated with pulmonary tuberculosis who no longer benefit from active treatment, palliative care and hospice care shall be initiated. Clinicians and medical teams shall communicate fully with patients and their families about the condition, prognosis, treatment options and medical burden. The core goals are to relieve symptoms, alleviate suffering and improve quality of life (2D).Recommendation 13: For patients with pneumoconiosis complicated with tuberculosis who meet the indications for surgical or interventional therapy, a multidisciplinary team shall conduct joint decision-making and implement treatment in a timely manner after full assessment of pulmonary function, nutritional status and surgical risks. Surgical treatment is mainly indicated for patients with drug-resistant tuberculosis with localized lesions, persistent cavitary lesions with ongoing mycobacterial excretion, destroyed lung, massive hemoptysis unresponsive to medical treatment, tuberculous empyema and other critical conditions. Interventional therapy can be applied for emergency treatment of massive hemoptysis, as well as palliative treatment for pulmonary artery stenosis secondary to tuberculosis or pneumoconiosis (2C).

Accurate recognition of early-stage pneumoconiosis presents significant challenges due to the irregular morphology, diffuse distribution, and small size of pulmonary lesions. Existing 2D methods struggle to focus on lesion-level 3D characteristics and inter-slice correlations in localized weak lesion regions, resulting in incomplete feature extraction and inaccurate calculation of lesion volume. To obtain complete 3D fine-grained lesion features in the entire lung, this paper proposes an early pneumoconiosis recognition network (EPRNet) to enhance fine-grained feature acquisition abilities and discover inter-slice correlations, thereby improving early pneumoconiosis recognition accuracy in a more structured and flexible manner. Specifically, to obtain the fine-grained 3D features of early pneumoconiosis more comprehensively, a distance-similarity graph encoding module is proposed to construct and encode the relationships of the distributed tiny lesions within CT slices, integrating the spatial positions and the corresponding feature similarities of the lesions to improve the accuracy of pneumoconiosis feature representation. To adaptively preserve accurate graph representations of the correlations of the lesions across inter-CT slices, a hierarchical dynamic-scored adaptive pooling module is proposed to discover the potential long distance correlations between cross-slices, obtaining spatial semantic information of diffused lesions in the entire lung. Experimental results based on multiple datasets demonstrate that EPRNet achieves state-of-the-art performance while exhibiting better generalization. The ablation experiments also prove the effectiveness of each module in EPRNet.

Construction dust is a major source of air pollution and easily causes intractable respiratory diseases such as pneumoconiosis. Dust suppressants are effective for dust control, yet most existing studies only focus on dust suppression performance, lacking systematic toxicological assessments, especially data on extrapulmonary multi-organ toxicity. In this study, SPF male C57BL/6 mice were used to establish three subchronic inhalation exposure groups: dust alone, dust suppressant alone, and co-exposure of dust and suppressant. Indicators including body weight, organ coefficients, blood routine, serum cytokines, and liver, kidney, and heart pathological lesions were detected to investigate the extrapulmonary multi-organ toxicity of an eco-friendly composite dust suppressant. The suppressant had little effect on mouse body weight. At appropriate concentrations (4-20 mg/m[3]), it inhibited dust-induced inflammatory responses and alleviated liver and kidney injuries. When the concentration reached 100 mg/m[3], the suppressant interacted with dust to increase DNA oxidative damage markers, indicating potential genotoxic risks. This study fills the gap in extrapulmonary toxicological research of dust suppressants, provides references for toxicology evaluation and experimental basis for determining safe application concentrations on construction sites.

The potential of pneumoconiosis was only discussed in the pretext of coal mining, but there is a new spectrum of respiratory diseases affecting coal miners termed as coal mine dust lung disease. In this narrative review, an attempt has been made to understand the prevalence of respiratory disorders among coal miners. A narrative synthesis was undertaken, using thematic analysis to synthesize the findings of the studies included within the review. The final narrative synthesis contains 12 studies. The majority of the studies were conducted in the USA. Among the total sample of 35,480 from 4 articles, a cumulative prevalence of 4.5% was found for Coal workers' pneumoconiosis in the studies conducted in mines of USA. Whereas the study in South Africa revealed a prevalence of 2.59%. The review has found a strong association of years of coal dust exposure with the occurrence of respiratory disorders among coal mine workers. Smoking is also found to be strongly associated with increasing the risk of respiratory disorders. So the review recommends an appropriate workplace culture, including respiratory hygiene, protection and avoiding habits like smoking among coal mine workers. The occupational surveillance for respiratory disorders among the workers needs to be strengthened.

Silica dioxide is a widely prevalent hazardous dust in occupational environments, with respiratory exposure serving as the primary pathogenic factor for silicosis. Macrophage damage, chronic inflammation, and abnormal activation of the immune system play pivotal roles in the pathogenesis of silicosis. Numerous domestic and international studies have demonstrated that occupational silica dioxide exposure is associated with an increased risk of connective tissue diseases such as rheumatoid arthritis, systemic lupus erythematosus, and systemic sclerosis. To systematically review the evidence linking occupational silica dioxide exposure to connective tissue diseases and elucidate its underlying pathogenic mechanisms, this article summarizes recent epidemiological research findings worldwide. It delineates the pathogenic pathway through which silica dioxide damages macrophages, induces persistent chronic inflammation, and triggers abnormal autoantibody production, thereby mediating systemic immune dysregulation.

Objective: To investigate the feasibility of computed tomography (CT) quantitative analysis in assessing the degree of silicosis fibrosis induced by silicon dioxide (SiO(2)) . Methods: In March 2024, twenty specific pathogen-free (SPF) male C57BL/6J mice were randomly divided into a control group and a model group (n=10 per group). Each group was further subdivided into 28-day and 56-day subgroups (n=5 per subgroup). The model group received a single intratracheal instillation of 50 μl of sterile SiO? suspension at a concentration of 200 mg/ml via a non-surgical tracheal approach, while the control group received an equal volume of normal saline using the same method. At 28 and 56 days post-modeling, pulmonary function tests were performed, hydroxyproline (HYP) content in lung tissue was measured, and histopathological changes were evaluated by hematoxylin-eosin (HE) and Masson staining. Additionally, micro-CT scanning of lung tissue was conducted. Intergroup comparisons were performed using the t-test or a two-way analysis of variance (ANOVA) followed by post-hoc tests. Spearman rank correlation analysis was used to evaluate the correlation between CT quantitative parameters and Masson staining quantitative results. Results: At 56 days, compared with the control group, the model group showed significantly lower tidal volume (TVb) and significantly higher respiratory frequency (f), expiratory time (Te), and inspiratory time (Ti) (all P<0.001). HYP concentration in lung tissue was also significantly increased (P<0.05). At 28 days, HYP concentration in the model group was significantly higher than that in the control group (P<0.01). The volume percentages of non-normally ventilated lung regions in the control and model groups were 30.54% and 50.99% at 28 days, and 37.40% and 61.60% at 56 days, respectively; all differences were statistically significant (P<0.01). Spearman rank correlation analysis revealed a significant positive correlation between the volume fraction of non-normally ventilated lung regions and Masson staining collagen fiber content in the model group (r(s)=0.68, P=0.035), whereas no statistically significant correlation was observed in the control group (r(s)=0.54, P=0.114) . Conclusion: CT quantitative analysis demonstrates a favorable correlation with the pathological severity of silicosis fibrosis, suggesting that micro-CT may serve as a reliable non-invasive imaging tool for evaluating silicosis fibrosis.

Objective: To analyze the distribution characteristics of body mass index (BMI) and its associated factors among pneumoconiosis patients in China. Methods: A cross-sectional survey was conducted among 12210 pneumoconiosis patients from 27 provinces, autonomous regions, and municipalities directly under the central government of China from March 2017 to December 2021 using stratified sampling combined with purposive sampling. Data were collected on sociodemographic characteristics, dust exposure history, disease severity, complications, economic and employment status, dietary pattern, and social insurance coverage. BMI was calculated and classified (underweight, normal weight, overweight, obesity) according to WS/T 428-2013 Criteria of weight for adults. Comparisons among different BMI groups were conducted using Pearson's χ(2) test. Binary logistic regression (forward method) was used to analyze factors associated with underweight, with underweight as the dependent variable (underweight=1, normal weight=0) . Results: The mean BMI of pneumoconiosis patients was (23.3±3.6) kg/m(2). The proportions of underweight, normal weight, overweight, and obesity were 6.9% (844/12210), 52.6% (6425/12210), 32.7% (3997/12210), and 7.7% (944/12210), respectively. Among respondents with valid data, underweight patients were predominantly distributed in western regions[44.3% (374/844) ] and rural areas [71.9% (605/841) ], and had higher proportions of silicosis [60.5% (506/836) ], stage Ⅲ pneumoconiosis [44.8% (376/839) ], and pulmonary complications (pulmonary tuberculosis 17.1%, pulmonary infection 29.9%, cor pulmonale 23.6%, chronic obstructive pulmonary disease 41.6%, pulmonary bullae or pneumothorax 26.1%). They also had lower personal income (47.5% earning ≤5000 yuan per year), lower coverage of urban employee medical insurance (26.1%), and lower daily egg intake (35.3%). Overweight and obese patients were mostly coal workers' pneumoconiosis and stage I, and had higher proportions of hypertension and diabetes (P<0.05). Multivariate logistic regression analysis showed that stage Ⅲ pneumoconiosis (OR=2.41, 95%CI: 1.94-2.99), silicosis (OR=1.27, 95%CI: 1.07-1.50), pulmonary complications (OR=1.36-1.55), and socioeconomic factors (lack of work-related injury insurance, lack of urban employee medical insurance, low income) were factors associated with underweight (P<0.05) . Conclusion: BMI level of pneumoconiosis patients in China is correlated with geographic region, disease severity, and social security. Individualized intervention strategies are recommended for different BMI strata.