[Australia's engineered stone ban. A sound decision]. / La prohibición de los aglomerados de cuarzo en Australia, una decisión modélica.

Australia se convirtió en diciembre de 2023 en el primer país en prohibir el uso de los aglomerados de cuarzo. El consumo de estos materiales sintéticos, que contienen más del 80% de sílice cristalina y que desde los años 90 se han empleado para la fabricación de encimeras de cocina y baños, ha contribuido al resurgimiento en numerosos países de formas aceleradas de silicosis y a una notable incidencia de enfermedades sistémicas. El objeto de este trabajo es analizar los fundamentos que sustentan la decisión australiana. Dichos fundamentos están principalmente recogidos en el informe elaborado en 2023 por la agencia gubernamental Safe Work Australia (SWA), que recomendó la prohibición del producto. SWA llevó a cabo una consulta pública entre todos los actores sociales y científicos interesados en el problema. El informe de SWA señaló la ausencia de evidencia científica sobre un umbral de sílice toxicológicamente seguro cuestionando la estrategia de los fabricantes del material de presentar como productos seguros a los aglomerados con menos del 40% de contenido de sílice. La recomendación de SWA tomó en consideración la evaluación del nivel de cumplimiento de las estrictas medidas de prevención implementadas entre 2019 y 2023, constatando que el incumplimiento siguió siendo generalizado en el sector. Además se realizó un análisis coste-beneficio para valorar el número de casos de silicosis que sería necesario evitar para "compensar" los costes económicos asociados a cada opción de prohibición. Para ello empleó el Valor Estadístico de la Vida (VEV) actualizado en 2023 en Australia y estimó en 4,9 millones de dólares australianos cada vida salvada y silicosis evitada. En nuestra opinión, la prohibición australiana es modélica por la forma en que se ha gestado la decisión, por su sólida fundamentación científica y socio-laboral, y por la aplicación del principio de precaución.

Celastrol Pyrazine Derivative Alleviates Silicosis Progression via Inducing ROS-Mediated Apoptosis in Activated Fibroblasts.

Silicosis is a complex occupational disease without recognized effective treatment. Celastrol, a natural product, has shown antioxidant, anti-inflammatory, and anti-fibrotic activities, but the narrow therapeutic window and high toxicity severely limit its clinical application. Through structural optimization, we have identified a highly efficient and low-toxicity celastrol derivative, CEL-07. In this study, we systematically investigated the therapeutic potential and underlying mechanisms of CEL-07 in silicosis fibrosis. By constructing a silicosis mouse model and analyzing with HE, Masson, Sirius Red, and immunohistochemical staining, CEL-07 significantly prevented the progress of inflammation and fibrosis, and it effectively improved the lung respiratory function of silicosis mice. Additionally, CEL-07 markedly suppressed the expression of inflammatory factors (IL-6, IL-1α, TNF-α, and TNF-ß) and fibrotic factors (α-SMA, collagen I, and collagen III), and promoted apoptosis of fibroblasts by increasing ROS accumulation. Moreover, bioinformatics analysis combined with experimental validation revealed that CEL-07 inhibited the pathways associated with inflammation (PI3K-AKT and JAK2-STAT3) and the expression of apoptosis-related proteins. Overall, these results suggest that CEL-07 may serve as a potential candidate for the treatment of silicosis.

Concept of health surveillance programme for workers exposed to respirable crystalline silica at present and in the past.

In the paper authors present general assumptions of health surveillance programme concept for workers employed in respirable crystalline silica (RCS) exposure at present and in the past. There is no effective treatment for silicosis thus disease prevention is of paramount significance. For decades efforts of World Health Organization (WHO) and International Work Organization (ILO) have been focused on eliminating silicosis globally. Unfortunately silicosis is still one of the most lethal occupational diseases and the preventative programmes have not yet been successful. The authors identify main steps to complete an overview of RCS exposure and suggest lines of actions to be taken before launching the health surveillance programme. Introduction of the health surveillance programme would increase awareness of harmful health effects of the RCS exposure, emphasize the significance of preventive medical check-ups and early diagnostics of occupational diseases as well as the importance of using appropriate protective equipment. The programme development on a national level might be carried out with the cooperation of multiple backgrounds and institutions. This would allow for detailed planning, implementation, monitoring and effective evaluation of its results. Having a better and updated knowledge of silicosis epidemiology, early diagnostics, the possible sources of RCS occupational exposure and evaluation of undertaken preventive actions are crucial factors in disease prevention. The programme introduction would be of educational significance for all the stakeholders and the groups engaged in the project implementation, which would contribute to high effectiveness of the preventive activities and their improvement in the future. Med Pr Work Health Saf. 2023;74(4):341-6.

Analyzing the incidence of silicosis across various industries in Taiwan: a study of occupational disease surveillance by linking national-based workers' and medicoadministrative databases.

OBJECTIVES: This study aimed to establish an occupational disease surveillance system by identifying high-risk industries for silicosis in Taiwan using a national database linkage approach. METHODS: The study was based on a comprehensive analysis of benefit claims from the National Labor Insurance Research Database and medical records from the National Health Insurance Research Database between 2004 and 2020, providing coverage for more than 88.5% of the workforce and 99.9% of citizens. Silicosis was defined as having received compensation for labor insurance benefits or having received a diagnosis of silicosis (International Classification of Diseases, 10th Revision: J62 or International Classification of Diseases, Ninth Revision: 502). The study used the International Standard Industrial Classification of All Economic Activities for industry-specific classification. Cox proportional hazard models were used to compare the silicosis incidence and risk among each industry and identify high-risk industries for silicosis. RESULTS: This study analyzed 1466 cases of silicosis between 2004 and 2020 and found that 28 industries had incidence rates of over 40 cases per 100,000 workers, indicating more than double the risk of developing silicosis. Of these industries, 14 were considered high risk (relative risk of over four times). Among these, this study identified industries rarely mentioned in the past, such as wholesale of brick, sand, cement, and products, artistic creation, landscape construction, and materials recovery. Stratification by years of work experience reveals those industries such as quarrying of stone, sand, clay, and other mining, construction of buildings, landscape construction, site preparation, foundation and structure construction, building completion and finishing, manufacture of ships, boats, and floating structures, and plumbing, heat, and air conditioning installation display higher hazard ratios for individuals with <10 years of work experience. CONCLUSIONS: The current surveillance system has identified certain industries that are at a higher risk of developing silicosis, which could be used for future occupational epidemiological surveys and targeted preventive measures in these sectors.

Silicosis: Emerging Trends and How to Screen for Early Detection.

BACKGROUND: National investigations are finding silicosis in young workers. We developed a silicosis case-finding process and conducted follow-up interviews to identify emerging exposure sources. METHODS: Probable cases were identified through Wisconsin hospital discharge and emergency department data and Wisconsin lung transplant programs. Interviews were attempted with case-patients under age 60. RESULTS: We identified 68 probable silicosis cases and interviewed 4 case-patients. Occupational exposures for cases under age 60 included sandblasting, quarry work, foundry work, coal mining, and stone fabrication. Two stone fabrication workers were diagnosed before age 40. DISCUSSION: Prevention is critically important to eliminate occupational silicosis. Clinicians should obtain the occupational and exposure history to identify cases of occupational lung disease and notify public health to identify and prevent workplace exposures.

Prevention of the Occupational Silicosis Epidemic in Australia: What Do Those Who Assess Workplace Health Risk Think Should Be Done Now?

An Australian National Dust Disease Taskforce was established to address the re-emergence of occupational lung disease, in particular silicosis. Exposure to respirable crystalline silica (RCS) occurs in various industries in Australia. We asked occupational hygienists about their practical experiences and perspectives on RCS exposure and regulatory action. A total of 105 members of the Australian Institute of Occupational Hygienists completed an anonymous questionnaire, which addressed individual characteristics, experience, perceived level of employer awareness, effectiveness of current regulation, and recommendations for improvement, across three main industrial sectors. Based on professional experience, 71% were concerned about the potential for RCS over-exposure. Barriers to adequate exposure control included lack of management commitment and financial resources. The employment of specialist occupational hygiene inspectors was considered to be the most effective regulatory strategy. Given the large number of exposed workers in the construction industry, with only a moderate awareness, there is the potential for significant cost shifting of the burden of occupational lung disease from employers on to individuals and the public health system. A nationally consistent approach to RCS exposure control across all industrial sectors is now recommended, with an increased focus on measuring and controlling exposure.

Inhibition of Galectin-3 attenuates silica particles-induced silicosis via regulating the GSK-3ß/ß-catenin signal pathway-mediated epithelial-mesenchymal transition.

Silica is a very common and important chemical raw material with a wide range of uses. Long-term inhalation of silica particles could cause lung toxicity, of which the most important representative is silicosis. Silicosis is a serious and fatal occupational pulmonary disease, characterized by persistent pulmonary inflammation and fibrosis. Despite intensive research, the toxic mechanism of silicosis caused by silica particles is not completely clear, which deserves further research and exploration. Many studies have indicated that the epithelial cells partially participate in the formation, accumulation, and activation of fibroblasts through epithelial-mesenchymal transition (EMT), which is conducive to the occurrence of fibrosis. Galectin-3 (Gal-3), widely expressed in epithelial cells, was observed to induce EMT in fibrotic diseases and tumors by regulating the GSK-3ß and ß-catenin. Previous studies have demonstrated that silica particles is indeed involved in the silicosis process by inducing EMT. However, it remains to be further studied whether there is a certain relationship between silica particles and Gal-3 expression, and whether Gal-3 also mediates the development of the silica particles-induced silicosis by regulating GSK-3ß/ß-catenin signal pathway-mediated EMT. Our research results showed that silica particles could significantly induce Gal-3 expression to promote the development of EMT through activating the GSK-3ß/ß-catenin signal pathway in mice and in A549 cells, which then significantly exacerbated the pulmonary fibrosis caused by silica particles. And the inhibition of Gal-3 could effectively inhibit the occurrence of EMT, and then effectively alleviate silicosis caused by silica particles. These findings would help us to further clarify the toxicological mechanisms of silicosis caused by silica particles and provide a novel target for prevention and intervention of silicosis.

Elevated exposures to respirable crystalline silica among engineered stone fabrication workers in California, January 2019-February 2020.

BACKGROUND: Workers fabricating engineered stone face high risk for exposure to respirable crystalline silica (RCS) and subsequent development of silicosis. In response, the California Division of Occupational Safety and Health (Cal/OSHA) performed targeted enforcement inspections at engineered stone fabrication worksites. We investigated RCS exposures and employer adherence to Cal/OSHA's RCS and respiratory protection standards from these inspections to assess ongoing risk to stone fabrication workers. METHODS: We extracted employee personal air sampling results from Cal/OSHA inspection files and calculated RCS exposures. Standards require that employers continue monitoring employee RCS exposures and perform medical surveillance when exposures are at or above the action level (AL; 25 µg/m3 ); exposures above the permissible exposure limit (PEL; 50 µg/m3 ) are prohibited. We obtained RCS and respiratory protection standard violation citations from a federal database. RESULTS: We analyzed RCS exposures for 152 employees at 47 workplaces. Thirty-eight (25%) employees had exposures above the PEL (median = 89.7 µg/m3 ; range = 50.7-670.7 µg/m3 ); 17 (11%) had exposures between the AL and PEL. Twenty-four (51%) workplaces had ≥1 exposure above the PEL; 7 (15%) had ≥1 exposure between the AL and PEL. Thirty-four (72%) workplaces were cited for ≥1 RCS standard violation. Twenty-seven (57%) workplaces were cited for ≥1 respiratory protection standard violation. CONCLUSIONS: Our investigation demonstrates widespread RCS overexposure among workers and numerous employer Cal/OSHA standard violation citations. More enforcement and educational efforts could improve employer compliance with Cal/OSHA standards and inform employers and employees of the risks for RCS exposure and strategies for reducing exposure.

Protective effects of intranasal curcumin on silica-induced lung damage.

OBJECTIVE: Being anti-inflammatory and an antioxidant in nature, curcumin has been studied for its anti-asthmatic effects, but its impact on silicosis has not been investigated before. It is a form of occupational lung illness caused by inhaling crystalline silica. It is particularly common among those who work in construction-related sectors. Therefore, present study has been undertaken to investigate impact of intranasal curcumin on silica induced lung damage in mice model of silicosis. MATERIALS AND METHODS: Mice model of silicosis was developed by intranasal silica instillation (2.5 mg/mice) for different durations mainly 7, 14 and 21 days, where the longest duration of silica exposure (21 days) mimics chronic occupational exposure of silica dust leading to silicosis. Curcumin (5 mg/kg,i.n) and /or dexamethasone, a known corticosteroid (10 mg/kg,i.p) was administered an hour prior to silica administration. RESULTS: Present study revealed silica induced lung damage in the mice model of silicosis characterized by airway inflammation, collagen deposition and enhanced expression of fibrosis markers (MMP-9, α-SMA, Hydroxyproline), which were significantly reduced in curcumin treatment groups. Inhibitory effects of curcumin were compared with standard drug, dexamethasone, a corticosteroid and was found better in protecting structural alterations in the lung. Damaged and abnormal mitochondria (enlarged and irregular shapes) were observed in silicosis group which were reduced in curcumin and dexamethasone treatment groups as revealed in transmission electron microscopic studies. CONCLUSIONS: Present study shows protective effects of intranasal curcumin on silica-induced airway inflammation and structural changes thereby lung damage. Hence, it can be considered as an alternative and complementary medication for silicosis.

Trading One Risk for Another: Consequences of the Unauthenticated Treatment and Prevention of Silicosis in Ontario Miners in the McIntyre Powder Aluminum Inhalation Program.

From 1943 to 1979, miners and factory workers in more than two hundred work sites globally were subjected to mandatory medical treatments by their employers as an unproven, and ultimately ineffective, treatment to prevent the lung disease silicosis. The treatments involved inhaling finely ground aluminum dust known as McIntyre Powder, blown into miners' change rooms each shift using compressed air systems. Tens of thousands of industrial laborers were exposed to McIntyre Powder, yet their story is scarcely known, and the possible health impacts of their aluminum treatments were rarely studied. This paper integrates the history of the aluminum prophylaxis program and its control by the northern Ontario mining industry with the lived experience of one of the affected miners, whose daughter created a voluntary registry which documents health issues in exposed miners, and stimulated research that found a link to her father's Parkinson disease.

3-methyadenine inhibits lipopolysaccharides-induced pulmonary inflammation at the early stage of silicosis via blocking NF-κB signaling pathway.

Occupational exposure to silica dust is related to pulmonary inflammation and silicosis. Lipopolysaccharides (LPSs) could aggravate apoptosis in alveolar macrophages (AMs) of human silicosis through autophagy, yet how the reduction of autophagy attenuated LPS-induced lung injury and the related mechanisms need to be investigated. In the study, we aim to understand the role of 3-methyladenine (3-MA), an inhibitor of autophagy, in LPS-mediated inflammatory responses and fibrosis. We collected AMs from observers/silicosis patients. The results showed that LPS induced NF-κB-related pulmonary inflammation in observers and silicosis patients, as confirmed by an increase in the expression of IL-1ß, IL-6, TNF-α, and p65, which could be inhibited by 3-MA treatment. In mice models, at the early stage (7d) of silicosis, but not the late (28d) stage, blocking autophagy reversed the increased levels of IL-1ß, IL-6, TNF-α, and p65 caused by LPS. Mechanism study revealed that LPS triggered the expression of LC3 II, p62, and cleaved caspase-3 at the early stage exposed to silica, which could be restored by 3-MA, while there was no difference in the expression of LAMP1 either at the early or late stage of silicosis in different groups. Similarly, 3-MA treatment did not prevent fibrosis characterized by destroyed alveoli, collagen deposition, and increased expression of α-SMA and Col-1 induced by LPS at the late stage of silicosis. The results suggested that 3-MA has a role in the protection of lung injury at the early stage of silicosis and provided an experimental basis for preventive strategies of pulmonary inflammation and silicosis.

Emodin attenuates silica-induced lung injury by inhibition of inflammation, apoptosis and epithelial-mesenchymal transition.

Silicosis is a fatal pulmonary disease caused by the inhalation of silica dust, and characterized by inflammation and fibrosis of the lung, with no effective treatment to date. Here we investigate the effect of emodin, an anthraquinone derivative isolated from rhubarb using a mouse silicosis model and in vitro cultured human macrophages and alveolar epithelial cells. Results from histological examination indicated that emodin reduced the degree of alveolitis and fibrosis in the lungs of mice exposed to silica particles. We also demonstrated that emodin effectively inhibited the phosphorylation of Smad3 and NF-κB and reduced the levels of inflammatory factors in the lung tissue of mice treated with silica particles. In addition, we found that emodin inhibited apoptosis and demonstrated an anti-fibrotic effect by down-regulating the pro-apoptotic protein Bax and up-regulating the anti-apoptotic protein Bcl-2. Furthermore, emodin increased E-cadherin levels, reduced the expression of Vimentin, α-SMA and Col-I, as well as pro-inflammatory factors TGF-ß1, TNF-α and IL-1ß in vivo and in vitro. These results suggested that emodin can regulate epithelial-mesenchymal transition (EMT) through the inhibition of the TGF-ß1/Smad3 signaling pathway and the NF-κB signaling pathway to prevent alveolar inflammation and apoptotic process. Overall, this study showed that emodin can alleviate pulmonary fibrosis in silicosis through regulating the inflammatory response and fibrotic process at multiple levels.

Respiratory surveillance for coal mine dust and artificial stone exposed workers in Australia and New Zealand: A position statement from the Thoracic Society of Australia and New Zealand.

Coal mine lung dust disease (CMDLD) and artificial stone (AS) silicosis are preventable diseases which have occurred in serious outbreaks in Australia recently. This has prompted a TSANZ review of Australia's approach to respiratory periodic health surveillance. While regulating respirable dust exposure remains the foundation of primary and secondary prevention, identification of workers with early disease assists with control of further exposure, and with the aims of preserving lung function and decreasing respiratory morbidity in those affected. Prompt detection of an abnormality also allows for ongoing respiratory specialist clinical management. This review outlines a medical framework for improvements in respiratory surveillance to detect CMDLD and AS silicosis in Australia. This includes appropriate referral, improved data collection and interpretation, enhanced surveillance, the establishment of a nationwide Occupational Lung Disease Registry and an independent advisory group. These measures are designed to improve health outcomes for workers in the coal mining, AS and other dust-exposed and mining industries.

Intranasal Flunisolide Suppresses Pathological Alterations Caused by Silica Particles in the Lungs of Mice.

Silicosis is an occupational disease triggered by the inhalation of fine particles of crystalline silica and characterized by inflammation and scarring in the form of nodular lesions in the lungs. In spite of the therapeutic arsenal currently available, there is no specific treatment for the disease. Flunisolide is a potent corticosteroid shown to be effective for controlling chronic lung inflammatory diseases. In this study, the effect of flunisolide on silica-induced lung pathological changes in mice was investigated. Swiss-Webster mice were injected intranasally with silica particles and further treated with flunisolide from day 21 to 27 post-silica challenge. Lung function was assessed by whole body invasive plethysmography. Granuloma formation was evaluated morphometrically, collagen deposition by Picrus sirius staining and quantitated by Sircol. Chemokines and cytokines were evaluated using enzyme-linked immunosorbent assay. The sensitivity of lung fibroblasts was also examined in in vitro assays. Silica challenge led to increased leukocyte numbers (mononuclear cells and neutrophils) as well as production of the chemokine KC/CXCL-1 and the cytokines TNF-α and TGF-ß in the bronchoalveolar lavage. These alterations paralleled to progressive granuloma formation, collagen deposition and impairment of lung function. Therapeutic administration of intranasal flunisolide inhibited granuloma and fibrotic responses, noted 28 days after silica challenge. The upregulation of MIP-1α/CCL-3 and MIP-2/CXCL-2 and the cytokines TNF-α and TGF-ß, as well as deposition of collagen and airway hyper-reactivity to methacholine were shown to be clearly sensitive to flunisolide, as compared to silica-challenge untreated mice. Additionally, flunisolide effectively suppressed the responses of proliferation and MCP-1/CCL-2 production from IL-13 stimulated lung fibroblasts from silica- or saline-challenged mice. In conclusion, we report that intranasal treatment with the corticosteroid flunisolide showed protective properties on pathological features triggered by silica particles in mice, suggesting that the compound may constitute a promising strategy for the treatment of silicosis.

MiR-411-3p alleviates Silica-induced pulmonary fibrosis by regulating Smurf2/TGF-ß signaling.

Occupational exposure to silica dust particles was the major cause of pulmonary fibrosis, and many miRNAs have been demonstrated to regulate target mRNAs in silicosis. In the present study, we found that a decreasing level of miR-411-3p in silicosis rats and lung fibroblasts induced by TGF-ß1. Enlargement of miR-411-3p could inhibit the cell proliferation and migration in lung fibroblasts with TGF-ß1 treatment and attenuate lung fibrosis in silicotic mice. In addition, a mechanistic study showed that miR-411-3p exert its inhibitory effect on Smad ubiquitination regulatory factor 2 (Smurf2) expression and decrease ubiquitination degradation of Smad7 regulated by smurf2, result in blocking of TGF-ß/Smad signaling. We proposed that increased expression of miR-411-3p abrogates silicosis by blocking activation of TGF-ß/Smad signaling through decreasing ubiquitination degradation effect of smurf2 on Smad7.