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Ecotoxicology and Environmental Safety Aug 2023Long-term inhalation of silica particles in the workplace causes silicosis, which is incurable and seriously endangers the health of workers. It is believed that...
Long-term inhalation of silica particles in the workplace causes silicosis, which is incurable and seriously endangers the health of workers. It is believed that silicosis is caused by an imbalance of the pulmonary immune microenvironment, in which pulmonary phagocytes play a crucial role. As an emerging immunomodulatory factor, it is unclear whether T cell immunoglobulin and mucin domain-containing protein 3 (TIM3) participate in silicosis by modulating pulmonary phagocytes function. The purpose of this study was to investigate the dynamic changes of the TIM-3 in pulmonary macrophages, dendritic cells (DCs), and monocytes during the development of silicosis in mice. The plasma levels of soluble TIM-3 in silicosis patients were also examined. Flow cytometry was used to identify alveolar macrophages (AMs), interstitial macrophages (IMs), CD11b DC, CD103 DC, Ly6C, and Ly6C monocytes in mouse lung tissues, and further analyses were conducted on the expression of TIM-3. Results showed that soluble TIM-3 was significantly elevated in plasma of silicosis patients, and the level of which was higher in stage II and III patients than that in stage I. In silicosis mice, the protein and mRNA levels of TIM-3 and Galectin9 were significantly upregulated in lung tissues. Specific to pulmonary phagocytes, silica exposure affected TIM-3 expression in a cell-specific and dynamic manner. In macrophages, TIM-3 expression upregulated in AM after 28 days and 56 days of silica instillation, while the expression of TIM-3 in IM decreased at all observation time points. In DCs, silica exposure only caused a decrease of TIM-3 expression in CD11b DCs. In monocytes, TIM-3 dynamics in Ly6C and Ly6C monocytes were generally consistent during silicosis development, which significant decrease after 7 and 28 days of silica exposure. In conclusion, TIM-3 may mediate the development of silicosis by regulating pulmonary phagocytes.
Topics: Mice; Animals; Hepatitis A Virus Cellular Receptor 2; Lung; Silicosis; Phagocytes; Silicon Dioxide
PubMed: 37285680
DOI: 10.1016/j.ecoenv.2023.115087 -
The Journal of International Medical... Sep 2023Superficial siderosis of the central nervous system (SSCNS) is a rare disease characterized by iron deposition on the tissue surface of the middle axis system. We report... (Review)
Review
Superficial siderosis of the central nervous system (SSCNS) is a rare disease characterized by iron deposition on the tissue surface of the middle axis system. We report the case of a man in his late 40 s who was admitted to the hospital with ataxia. A physical examination revealed cerebellar ataxia, sensorineural deafness, and bilateral pyramidal tract injury. Susceptibility-weighted magnetic resonance imaging showed linear hypointense signals on the surface of the cerebral hemispheres, sulcus gyrus, lateral ventricles, and cerebellum. The patient underwent treatment with deferiprone, mecobalamin, and vitamin B1, and the symptoms were not aggravated. The patient's daily living ability was near normal after 1 year of follow-up. A literature review indicated that most SSCNS patients present diverse clinical manifestations. Clinicians may consider SSCNS in patients with hearing impairment and gait ataxia, especially for those receiving anticoagulant therapy and with a history of brain injury or accident.
Topics: Male; Humans; Siderosis; Central Nervous System; Brain Injuries; Hearing Loss, Sensorineural; Cell Membrane
PubMed: 37702555
DOI: 10.1177/03000605231198389 -
International Journal of Molecular... Sep 2023Silicosis is a fatal occupational respiratory disease caused by the prolonged inhalation of respirable silica. The core event of silicosis is the heightened activity of...
Silicosis is a fatal occupational respiratory disease caused by the prolonged inhalation of respirable silica. The core event of silicosis is the heightened activity of fibroblasts, which excessively synthesize extracellular matrix (ECM) proteins. Our previous studies have highlighted that human umbilical cord mesenchymal stem cell-derived extracellular vesicles (hucMSC-EVs) hold promise in mitigating silicosis and the significant role played by microRNAs (miRNAs) in this process. Delving deeper into this mechanism, we found that miR-148a-3p was the most abundant miRNA of the differential miRNAs in hucMSC-EVs, with the gene heat shock protein 90 beta family member 1 (Hsp90b1) as a potential target. Notably, miR-148a-3p's expression was downregulated during the progression of silica-induced pulmonary fibrosis both in vitro and in vivo, but was restored after hucMSC-EVs treatment ( < 0.05). Introducing miR-148a-3p mimics effectively hindered the collagen synthesis and secretion of fibroblasts induced by transforming growth factor-β1 (TGF-β1) ( < 0.05). Confirming our hypothesis, Hsp90b1 was indeed targeted by miR-148a-3p, with significantly reduced collagen activity in TGF-β1-treated fibroblasts upon Hsp90b1 inhibition ( < 0.05). Collectively, our findings provide compelling evidence that links miR-148a-3p present in hucMSC-EVs with the amelioration of silicosis, suggesting its therapeutic potential by specifically targeting Hsp90b1, thereby inhibiting fibroblast collagen activities. This study sheds light on the role of miR-148a-3p in hucMSC-EVs, opening avenues for innovative therapeutic interventions targeting molecular pathways in pulmonary fibrosis.
Topics: Humans; Pulmonary Fibrosis; Transforming Growth Factor beta1; Silicon Dioxide; MicroRNAs; Silicosis; Fibroblasts; Collagen; Extracellular Vesicles
PubMed: 37833927
DOI: 10.3390/ijms241914477 -
BMC Pulmonary Medicine Aug 2023Development of pleural effusion (PE) following CABG is common. Post-CABG PE are divided into early- (within 30 days of surgery) and delayed-onset (30 days-1 year) which...
BACKGROUND
Development of pleural effusion (PE) following CABG is common. Post-CABG PE are divided into early- (within 30 days of surgery) and delayed-onset (30 days-1 year) which are likely due to distinct pathological processes. Some experts suggest asbestos exposure may confer an independent risk for late-onset post-CABG PE, however no large studies have explored this potential association.
RESEARCH QUESTION
To explore possible association between asbestos exposure and post-CABG PE using routine data.
METHODS
All patients who underwent CABG 01/04/2013-31/03/2018 were identified from the Hospital Episode Statistics (HES) Database. This England-wide population was evaluated for evidence of asbestos exposure, pleural plaques or asbestosis and a diagnosis of PE or PE-related procedure from 30 days to 1 year post-CABG. Patients with evidence of PE three months prior to CABG were excluded, as were patients with a new mesothelioma diagnosis.
RESULTS
68,150 patients were identified, of whom 1,003 (1%) were asbestos exposed and 2,377 (3%) developed late-onset PE. After adjusting for demographic data, Index of Multiple Deprivation and Charlson Co-morbidity Index, asbestos exposed patients had increased odds of PE diagnosis or related procedure such as thoracentesis or drainage (OR 1.35, 95% CI 1.03-1.76, p = 0.04). In those with evidence of PE requiring procedure alone, the adjusted OR was 1.66 (95% CI 1.14-2.40, p = 0.01). Additional subgroup analysis of the 518 patients coded for pleural plaques and asbestosis alone revealed an adjusted OR of post-CABG PE requiring a procedure of 2.16 (95% CI 1.38-3.37, p = 0.002).
INTERPRETATION
This large-scale study demonstrates prior asbestos exposure is associated with modestly increased risk of post-CABG PE development. The risk association appears higher in patients with assigned clinical codes indicative of radiological evidence of asbestos exposure (pleural plaques or asbestosis). This association may fit with a possible inflammatory co-pathogenesis, with asbestos exposure 'priming' the pleura resulting in greater propensity for PE evolution following the physiological insult of CABG surgery. Further work, including prospective studies and clinicopathological correlation are suggested to explore this further.
Topics: Humans; Asbestosis; Prospective Studies; Pleural Effusion; Asbestos; Pleural Diseases; Coronary Artery Bypass
PubMed: 37605147
DOI: 10.1186/s12890-023-02555-9 -
Medical Sciences (Basel, Switzerland) Oct 2023There are several risk factors attributed to tuberculosis (TB) mortality and morbidity. There are few studies and systematic reviews showing the association of silicosis...
INTRODUCTION
There are several risk factors attributed to tuberculosis (TB) mortality and morbidity. There are few studies and systematic reviews showing the association of silicosis and tuberculosis at a country level. Very limited studies have been conducted using multi-country data in studying the association of incidence of silicosis with TB mortality and morbidity. Hence, the aim of this research was to explore the association of incidence of silicosis and other important risk factors with TB mortality and morbidity using multi-country data.
METHODS
Data from 217 WHO region countries were utilized, sourcing TB-related statistics from the Institute of Health Metrics and Evaluation and additional risk factors from the Demographic and Health Survey, Global Burden of Disease, and World Bank for 2019. Regression analysis was conducted to examine the association between silicosis incidence and TB outcomes.
RESULTS
The study found an average silicosis incidence of 121.92 per 100,000 population. Additionally, 62.69% of the sample population are exposed to air pollution from solid fuel cooking. Sanitation access stands at an average of 59.67%. Regression outcomes indicate that while alcohol consumption's influence on TB is not statistically significant, a unit increase in silicosis incidence significantly elevates TB deaths (235.9, = 0.005), YLL (9399.3, = 0.011), and YLD (910.8, = 0.002).
CONCLUSION
The burden of silicosis is found to be one of the important determinants of deaths, YLL, and YLD due to tuberculosis. Country-specific strategies to prevent and control silicosis is a need of the hour.
Topics: Humans; Incidence; Tuberculosis; Risk Factors; Regression Analysis; Silicosis
PubMed: 37873748
DOI: 10.3390/medsci11040063 -
Toxicology Letters Jan 2024Silicosis is a common occupational disease caused by the long-term inhalation of large amounts of silica dust. Lipid metabolism plays an important role in the...
Silicosis is a common occupational disease caused by the long-term inhalation of large amounts of silica dust. Lipid metabolism plays an important role in the progression of silicosis, but its contributing mechanism remains unclear. The aim of this study was to investigate the differential lipid metabolites and active metabolic pathways in silicosis rat lung tissue. We first constructed a silicosis rat model, and randomly divided 24 male SD rats into control group (C), silicosis group for 1 week (S1W), silicosis group for 2 weeks (S2W) and silicosis group for 4 weeks (S4W) with 6 rats in each group. 1 mL SiO suspension (50 mg/mL) or normal saline were injected into the trachea, and the rats were killed at 1 week, 2 weeks and 4 weeks, respectively. The lung tissue pathology of the rats was observed by HE staining and VG staining, and the plasma TC and FC levels were detected by the kit. Western blot was used to detect the expression of lipid-related factors CD36, PGC1α and LXR. In addition, lipidomics analysis of lung tissue samples was performed using UPLC-IMS-QTOF mass spectrometer to screen out potential differential metabolites in silicosis models and analyze lipid enrichment, and verified the expression of differential gene CHPT1 in the metabolic pathway. HE and VG staining showed that the number of nodules and fibrosis increased in a time-dependent manner in the silicosis model group, and the levels of TC, FC and CE in silicosis plasma increased. Western blot results showed that PGC1α and LXR decreased in the silicosis model group, while CD36 expression increased. In addition, metabolomics screened out 28 differential metabolites in the S1W group, 32 in the S2W group, and 22 in the S4W group, and found that the differential metabolites were mainly enriched in metabolic pathways such as glycerophospholipid metabolism and ether lipid metabolism, and the expression of differential gene CHPT1 in the metabolic pathway was decreased in the silicosis model group. These results suggest that there are significant changes in lipid metabolites in lung tissue in silicosis rat models, and glycerophospholipid metabolism was significantly enriched, suggesting that glycerophospholipids play an important role in the progression of silicosis. The differential metabolites and pathways reported in this study may provide new ideas for the pathogenesis of silicosis.
Topics: Rats; Male; Animals; Silicon Dioxide; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; Rats, Wistar; Rats, Sprague-Dawley; Silicosis; Lung; Metabolomics; Glycerophospholipids; Lipids
PubMed: 38061438
DOI: 10.1016/j.toxlet.2023.12.002 -
Sangyo Eiseigaku Zasshi = Journal of... Mar 2024To review the historical aspects of compensation system for workers with pneumoconiosis who developed lung cancer.
OBJECTIVE
To review the historical aspects of compensation system for workers with pneumoconiosis who developed lung cancer.
METHODS
Materials and papers published on the compensation system as discussed in administrative meetings were utilized.
RESULTS
Legal claims for compensation for lung cancer among individuals with pneumoconiosis increased during the period of rapid economic growth in Japan. A possible causal relationship between pneumoconiosis and lung cancer in workers has been discussed by committees of specialists. The Expert Committee on Pneumoconiosis and Lung Cancer in 1978 did not find a causal relationship between them. However, a survey of physicians specializing in pneumoconiosis revealed medical disadvantages among individuals diagnosed with pneumoconiosis who developed lung cancer. The Ministry of Labour announced the risk of work-related lung cancer in patients with advanced pneumoconiosis (class IV or equivalent severity). Since then, numerous lung cancer patients with pneumoconiosis have been adjudicated. In 1997, the International Agency for Research on Cancer (IARC) re-evaluated the carcinogenicity of silica and declared it to be a Group I carcinogen in humans. The Expert Committee on Compensation of Lung Cancer Cases Developing from Pneumoconiosis discussed the IARC evaluation but did not accept this classification. However, the Committee of Occupational Exposure Limits in the Japan Society of Occupational Health upheld the IARC evaluation of silica as a Group I carcinogen. Because the Expert Committee of Medical Disadvantage of Lung Cancer Patients with Pneumoconiosis accepted the increased risk of lung cancer in patients with class III or equivalent severity pneumoconiosis, the Ministry of Labour announced worker compensation for such patients. The Expert Committee of Health Control of Pneumoconiosis Complicated with Lung Cancer reported in 2002 that a meta-analysis revealed no increased risk of lung cancer among workers exposed to crystalline silica; however, there was an increased risk of lung cancer in patients with pneumoconiosis. The Ministry of Labour has added lung cancer to the list of complications from pneumoconiosis and, if necessary, regular medical checkups for lung cancer. After Leaving dust work, the Health Care System provides for workers who are diagnosed With class II or higher pneumoconiosis. Therefore, if an individual with pneumoconiosis develops class II or higher lung cancer, that individual becomes eligible for workers' compensation.
CONCLUSIONS
The conclusion of the Expert Committee in 2002 and the decision of the Ministry of Labour to add lung cancer to its list of complications of pneumoconiosis are evaluated to be appropriate.
PubMed: 38538329
DOI: 10.1539/sangyoeisei.2023-025-A -
Ecotoxicology and Environmental Safety Jul 2024Oxidative stress and inflammation play a fundamental role in the beginning and advancement of silicosis. Hence, questing active phytocompounds (APCs) with anti-oxidative...
Oxidative stress and inflammation play a fundamental role in the beginning and advancement of silicosis. Hence, questing active phytocompounds (APCs) with anti-oxidative and anti-inflammatory properties such as diosgenin (DG) and emodin (ED) can be a therapeutic intervention targeting silica-induced pulmonary inflammation and fibrosis. Hydrophobicity and low bioavailability are the barriers that restrict the therapeutic efficacy of DG and ED against pulmonary defects. Encapsulating these APCs in polymeric nanoparticles can overcome this limitation. The present study has thus explored the anti-inflammatory and anti-fibrotic effects of polylactic-co-glycolic acid (PLGA) nanoparticles (NPs) individually loaded with DG (DGn) or ED (EDn) and in combine DG+ED [(DG+ED)n] in respirable silica dust (RSD)-induced pulmonary fibrosis silicosis rat model. Our study found that individual and combined NPs revealed physiochemical characteristics appropriate for IV administration with sustained-drug release purposes. Physiological evaluations of RSD-induced silicosis rats suggested that no treatment could improve the body weight. Still, they reduced the lung coefficient by maintaining lung moisture. Only (DG+ED)n significantly cleared free lung silica. All interventions were found to attribute the increased per cent cell viability in BALF, reduce cytotoxicity via minimizing LDH levels, and balance the oxidant-antioxidant status in silicotic rats. The expression of inflammatory cytokines (TNF-α, IL-1β, IL-6, MCP-1, and TGF-β1) were efficiently down-regulated with NPs interventions compared to pure (DG+ED) treatment. All drug treatments significantly declined, the 8-HdG and HYP productions indicate that RSD-induced oxidative DNA damage and collagen deposition were successfully repaired. Moreover, histopathological investigations proposed that individual or combined drugs NPs interventions could decrease the fibrosis and alveolitis grades in RSD-induced silicosis rats. However, (DG+ED)n intervention significantly inhibited pulmonary fibrosis and alveolitis compared to pure (DG+ED) treatment. In conclusion, the RSD can induce oxidative stress and inflammation in rats, producing reactive oxygen species (ROS)-mediated cytotoxicity to pulmonary cells and leading to silicosis development. The IV administration of combined NP suppressed lung inflammation and collagen formation by maintaining oxidant-antioxidant status and effectively interrupting the fibrosis-silicosis progression. These results may be attributed to the improved bioavailability of DG and ED through their combined nano-encapsulation-mediated targeted drug delivery.
Topics: Animals; Diosgenin; Silicosis; Silicon Dioxide; Pulmonary Fibrosis; Rats; Emodin; Nanoparticles; Male; Dust; Oxidative Stress; Anti-Inflammatory Agents; Rats, Wistar; Lung; Polylactic Acid-Polyglycolic Acid Copolymer
PubMed: 38788565
DOI: 10.1016/j.ecoenv.2024.116483 -
Artificial Intelligence in Medicine Jun 2024Early detection of pneumoconiosis by routine health screening of workers in the mining industry is critical for preventing the progression of this incurable disease....
Early detection of pneumoconiosis by routine health screening of workers in the mining industry is critical for preventing the progression of this incurable disease. Automated pneumoconiosis classification in chest X-ray images is challenging due to the low contrast of opacities, inter-class similarity, intra-class variation and the existence of artifacts. Compared to traditional methods, convolutional neural networks have shown significant improvement in pneumoconiosis classification tasks, however, accurate classification remains challenging due to mainly the inability to focus on semantically meaningful lesion opacities. Most existing networks focus on high level abstract information and ignore low level detailed object information. Different from natural images where an object occupies large space, the classification of pneumoconiosis depends on the density of small opacities inside the lung. To address this issue, we propose a novel two-stage adaptive multi-scale feature pyramid network called AMFP-Net for the diagnosis of pneumoconiosis from chest X-rays. The proposed model consists of 1) an adaptive multi-scale context block to extract rich contextual and discriminative information and 2) a weighted feature fusion module to effectively combine low level detailed and high level global semantic information. This two-stage network first segments the lungs to focus more on relevant regions by excluding irrelevant parts of the image, and then utilises the segmented lungs to classify pneumoconiosis into different categories. Extensive experiments on public and private datasets demonstrate that the proposed approach can outperform state-of-the-art methods for both segmentation and classification.
PubMed: 38917599
DOI: 10.1016/j.artmed.2024.102917 -
Radiology and Oncology Dec 2023Asbestos exposure is associated with different asbestos-related diseases, including malignant mesothelioma (MM). MM diagnosis is confirmed with immunohistochemical...
BACKGROUND
Asbestos exposure is associated with different asbestos-related diseases, including malignant mesothelioma (MM). MM diagnosis is confirmed with immunohistochemical analysis of several markers, including calretinin. Increased circulating calretinin was also observed in MM. The aim of the study was to determine if polymorphisms or polymorphisms in genes that can regulate calretinin expression are associated with serum calretinin levels or MM susceptibility.
SUBJECTS AND METHODS
The study included 288 MM patients and 616 occupationally asbestos-exposed subjects without MM (153 with asbestosis, 380 with pleural plaques and 83 without asbestos-related disease). Subjects were genotyped for seven polymorphisms in , , , and genes using competitive allele-specific polymerase chain reaction (PCR). Serum calretinin was determined with ELISA in 545 subjects. Nonparametric tests, logistic regression and receiver operating characteristic (ROC) curve analysis were used for statistical analysis.
RESULTS
Carriers of at least one polymorphic rs889704 allele had lower calretinin levels (P = 0.036). Carriers of two polymorphic rs3807348 alleles had higher calretinin (P = 0.027), while carriers of at least one polymorphic rs13241028 allele had lower calretinin levels (P = 0.034) in subjects without MM. Carriers of two polymorphic rs2075995 alleles were less likely to develop MM (odds ratio [OR] = 0.64, 95% confidence interval [CI] = 0.43-0.96, P = 0.032), but the association was no longer significant after adjustment for age (P = 0.093). Optimal serum calretinin cut-off values differentiating MM patients from other subjects differed according to , , , and genotypes.
CONCLUSIONS
The results of presented study suggest that genetic variability could influence serum calretinin levels. These findings could contribute to a better understanding of calretinin regulation and potentially to earlier MM diagnosis.
Topics: Humans; Asbestos; Asbestosis; Calbindin 2; Mesothelioma, Malignant
PubMed: 38038422
DOI: 10.2478/raon-2023-0061