Accelerated silicosis in sandblasters: Pathology, mineralogy, and clinical correlates.

BACKGROUND: With increasing reports of accelerated and acute silicosis, PMF, and autoimmune disease among coal miners and silica-exposed countertop workers, we present previously incompletely-described pulmonary pathology of accelerated silicosis and correlations with mineralogy, radiography, and disease progression in 46 Texas oilfield pipe sandblasters who were biopsied between 1988 and 1995. METHODS: Worker examinations included pulmonary function tests, chest X-ray (CXR), high-resolution computed tomography (HRCT), and Gallium-67 scans. Quantitative mineralogic analysis of pulmonary parenchymal burden of silica, silicates, and metal particles used scanning electron microscopy with energy dispersive x-ray spectroscopy (SEM EDS). RESULTS: Workers had clinical deterioration after <10 years exposure in dusty workplaces. Although initial CXR was normal in 54%, Gallium-67 scans were positive in 68% of those with normal CXR, indicating pulmonary inflammation. The histology of accelerated silicosis is diffuse interstitial infiltration of macrophages filled with weakly birefringent particles with or without silicotic nodules or alveolar proteinosis. Lung silica concentrations were among the highest in our database, showing a dose-response relationship with CXR, HRCT, and pathologic changes (macrophages, fibrosis, and silicotic nodules). Radiographic scores and diffusing capacity worsened during observation. Silica exposure was intensified, patients presented younger, with shorter exposure, more severe clinical abnormalities, higher lung particle burdens, and more rapid progression in a subset of patients exposed to recycled blasting sand. CONCLUSIONS: Accelerated silicosis may present with a normal CXR despite significant histopathology. Multivariable analyses showed silica, and not other particles, is the driver of observed radiologic, physiologic, and histologic outcomes. Eliminating this preventable disease requires higher physician, public health, and societal awareness.

Association between SNPs at IL-17A and IL-17F and susceptibility to accelerated silicosis.

The association between single nucleotide polymorphisms (SNPs) in the interleukin (IL)-17 gene and silicosis has been evaluated in different populations. The aim of the present study was to analyze the association between SNPs at IL-17A (-832A/G) and IL-17F (+7488A/G) and susceptibility to accelerated silicosis in the Iranian Kurdish population. We studied 48 patients with accelerated silicosis and 62 controls. Genomic DNA was isolated using the "salting out" method. PCR-RFLP was performed for all SNPs typing. The frequencies of A/A, A/G, and G/G genotypes at IL-17A (-832A/G) were 4 (8.33%), 23 (47.92%), and 21 (43.75%) in patients and 5 (8.06%), 35 (56.45%), and 22 (35.48%) in controls, respectively. The frequencies of A and G alleles at IL-17 (-832A/G) were 31 (32.29%) and 65 (67.71%) in patients, and 45 (36.29%) and 79 (63.71%) in the controls, respectively. The frequencies of A/A, A/G, and G/G genotypes at IL-17F (+7488A/G) were 1 (2.08%), 47 (97.92%), and 0 (0%) in patients, and 11 (17.74%), 51 (82.26%), and 0 (0%) in the controls, respectively. The frequencies of A and G alleles at IL-17F (+7488A/G) were 49 (51.04%) and 47 (48.96%) in patients, and 73 (58.87%) and 51 (41.13%) in the controls, respectively. IL-17F (+7488A/G) genotype was more frequent among the cases compared with controls (97.92% vs. 82.26%). The frequency of the IL-17F (+7488A/G) genotype was significantly greater in patients with accelerated silicosis (odds ratio = 10.13 95%; confidence interval = 1.2-81.5; p = 0.008). The IL-17F (+7488A/G) genotype revealed a significantly increased risk of accelerated silicosis ( p < 0.05). The IL-17F (+7488 G) allele was associated with an increased risk of accelerated silicosis, but in the case of the IL-17A (-832A/G) polymorphism, a significant association was not observed.

Lipid dysregulation associated with progression of silica-induced pulmonary fibrosis.

Silicosis is an irreversible, progressive, fibrotic lung disease caused by long-term exposure to dust-containing silica particles at the workplace. Despite the precautions enforced, the rising incidence of silicosis continues to occur globally, particularly in developing countries. A better understanding of the disease progression and potential metabolic reprogramming of silicosis is warranted. The low- or high-dose silica-induced pulmonary fibrosis in mice was constructed to mimic chronic or accelerated silicosis. Silica-induced mice lung fibrosis was analyzed by histology, lung function, and computed tomography scans. Non-targeted metabolomics of the lung tissues was conducted by ultra-high-performance liquid chromatography-mass spectrometry to show the temporal metabolic trajectory. The low-dose silica-induced silicosis characterized inflammation for up to 42 days, with the onset of cellular silicon nodules. Conversely, the high-dose silica-induced silicosis characterized inflammation for up to 14 days, after which the disease developed rapidly, with a large volume of collagen deposition, presenting progressive massive fibrosis. Both low- and high silica-induced fibrosis had aberrant lipid metabolism. Combined with the RNA-Seq data, this multiomics study demonstrated alterations in the enzymes involved in sphingolipid metabolism. Time-dependent metabolic reprogramming revealing abnormal glycerophospholipid metabolism was intimately associated with the process of inflammation, whereas sphingolipid metabolism was crucial during lung fibrosis. These findings suggest that lipid dysregulation, especially sphingolipid metabolism, was involved in the process of silicosis.

A cluster onset of acute and accelerated silicosis cases in workers of ramming mass industries in Jharkhand, Eastern India.

Introduction and Methodology: A cross-sectional study was conducted among workers of ramming mass industries in the East Singhbhum district of Jharkhand, eastern India. Workers had occupational exposure to respirable crystalline silica dust of varied duration between 1 and 6 years. A total of 122 subjects participated in it. Relevant epidemiological information was collected from them. All were x-rayed using 300 mA radiation for the detection of the presence of silicotic opacities if any as described by the International Labour Organisation (ILO) for the detection of silicosis. Results: The study revealed that 61.4% (n = 75) of subjects had silicosis. Of them, 19 had acute silicosis (having a duration of silica dust exposure of 2 years or lesser) and 56 had accelerated silicosis (a duration of occupational exposure of > 2 to 6 years). The offending agent was clouds of respirable crystalline silica dust from the ramming mass industries. Epidemiological Interpretation: To the best of our knowledge, this is the first report of an outbreak of acute and accelerated silicosis cases because of occupational inhalational exposure to ramming mass in India with a sizable portion of female workers with silicosis. Regional as well as national authorities need to take appropriate interventional measures in a programmatic mode as soon as possible. Conclusion: An in-depth investigation on the existence and magnitude of the problem of silico-tuberculosis is needed to be performed in them as silicosis increases the vulnerability of pulmonary tuberculosis among the affected workers.

Clinical efficacy of tetrandrine in artificial stone-associated silicosis: A retrospective cohort study.

Background: Outbreaks of silicosis have occurred among workers in the artificial stone (AS) industry, and there is currently no effective antifibrosis treatment for silicosis. Design: A retrospective cohort study. Methods: We retrospectively analyzed the clinical data of 89 artificial stone-associated silicosis patients treated in Shanghai Pulmonary Hospital (China). Patients who agreed to be administered tetrandrine entered the observation group and those who disagreed entered the control group. Changes in chest HRCT, pulmonary function, and clinical symptoms of patients in two groups were compared pre- and post-treatment. Results: After treatment for 3-12 months, 56.5%-65.4% of patients in the observation group showed improvements in HRCT imaging, while there was no improvement in the control group (p < 0.05). Disease progression occurred in 0%-17.4% of patients in the observation group after 3-12 months of treatment compared with 44.4%-92.0% of patients in the control group (p < 0.05). After 3 months of treatment, the forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), and diffusing capacity of the lung for carbon monoxide (DLco) in the observation group increased by 136.7 ± 189.2 mL (p < 0.05), 124.2 ± 169.9 mL (p < 0.05), and 1.4 ± 2.3 mL/min/mmHg (p > 0.05), respectively, while those in the control group decreased (145.8 ± 356.5; 107.5 ± 272.1; 1.9 ± 3.8). After 6 months of treatment, FVC, FEV1, and DLco in the observation group increased by 207.8 ± 372.2 mL (p > 0.05), 107.8 ± 295.2 mL (p > 0.05) and 0.7 ± 6.0 mL/min/mmHg (p > 0.05), respectively, while those of the control group decreased (383.3 ± 536.7; 215.6 ± 228.9; 1.4 ± 1.7). The incidences of clinical symptoms such as cough, expectoration, dyspnea, chest tightness, and chest pain in the observation group were decreased-after treatment (all p < 0.05), while the incidences of these symptoms increased in the control group, although the change was not statistically significant (all p > 0.05). Conclusion: Tetrandrine can control and delay the progression of AS-associated silicosis fibrosis, with improved chest HRCT imaging and pulmonary function.

Accelerated silicosis and silico-tuberculosis: A difficult diagnosis.

It is well established that exposure to respirable crystalline silica is associated with higher mortality. Such exposures are associated with an increased risk of silico-tuberculosis, silicosis, and other respiratory morbidities. We report two cases of accelerated silicosis, complicated with pulmonary tuberculosis and pulmonary infection.

Chylothorax in a Case of Accelerated Silicosis with Pulmonary Silicoproteinosis: A Unique Association.

A 32-year-old gentleman, a worker in a cement-manufacturing facility with suspected silica-induced lung disease presented with acutely worsening Type 1 respiratory failure. With a negative work-up for infectious causes and no further revelations on bronchoalveolar lavage fluid or endobronchial biopsy, it was a transbronchial biopsy that ultimately led us to a diagnosis of silicoproteinosis with accelerated silicosis. Interestingly, the patient had a pleural effusion which on thoracentesis showed chylous fluid-the first reported case of chylothorax in association with silicosis.

Silicosis: An Update and Guide for Clinicians.

This overview provides an update on silicosis epidemiology with review of exposures and emerging trends in acute and accelerated silicosis in the twenty-first century. The silicosis epidemics in mining, denim sandblasting, and engineering stone industries are highlighted. Clinical presentations of silicosis and silica-related conditions such as autoimmune, kidney, and mycobacterial disease, as well as lung cancer, are discussed. Important aspects of the new OSHA 2017 Silica Standard are presented. This review also includes practical guidance for clinicians to address questions that may arise when evaluating silica-exposed patients and to the public health responses needed following a diagnosis of silica-related disease.

Silicosis en trabajadores expuestos aconglomerados de cuarzo / Silicosis in workers exposed to quartz conglomerates

Introducción: la silicosis, enfermedad crónica, causada por la inhalación de polvo de sílice cristalina, sigue siendo un problema de salud laboral vigente. El objetivo de la investigación consistió en estimar el riesgo de silicosis complicada y/o acelerada en trabajadores expuestos a polvo de sílice de conglomerados de cuarzo frente al riesgo de los trabajadores expuestos a roca ornamental. Método: se desarrolló un estudio analítico de casos y controles prevalentes en trabajadores cuya vigilancia de la salud se realizó en el instituto Nacional de Silicosis (España), entre el 1 de enero de 2008 y el 31 de diciembre de 2018 (N = 90). El valor de la significación de todos los contrastes de hipótesis realizados fue α = 0,05. Resultados: se determinó mayor riesgo de silicosis complicada en los trabajadores expuestos a polvo de sílice proveniente del uso de conglomerados de cuarzo mediante el cálculo de Chi cuadrado, con un total de 7 casos (46,67%) de silicosis complicada (p = 0,046). Conclusiones: existe mayor riesgo de silicosis complicada en los trabajadores expuestos a polvo de sílice proveniente del uso de conglomerados de cuarzo frente a los expuestos a polvo de sílice de roca ornamental. No se observó relación entre el riesgo de desarrollar silicosis acelerada y la exposición a conglomerados de cuarzo en la muestra analizada (AU)

Introduction: silicosis, a chronic disease caused by the inhalation of crystalline silica dust, continues to be a current occupational health problem. The objective of the research was to estimate the risk of complicated and/or accelerated silicosis in workers exposed to silica dust from quartz conglomerates compared to the risk of workers exposed to ornamental rock. Method: an analytical study of cases and controls prevalent in workers whose health surveillance was carried out at the National Institute of Silicosis (Spain), between January 1, 2008 and December 31, 2018 was developed (N = 90). The significance value of all the hypotheses tests performed was α = 0.05. Results: a higher risk of complicated silicosis was determined in workers exposed to silica dust from the use of quartz conglomerates by calculating Chi square, with a total of 7 cases (46.67%) of complicated silicosis (p = 0.046). Conclusions: there is a higher risk of complicated silicosis in workers exposed to silica dust from the use of quartz conglomerates compared to those exposed to silica dust from ornamental rock. No relationship was observed between the risk of developing accelerated silicosis and exposure to quartz conglomerates in the analyzed sample (AU)