Silica‐associated lung disease: An old‐world exposure in modern industries

Barnes, Hayley; Goh, Nicole; Leong, Tracy L.; Hoy, Ryan

doi:10.1111/resp.13695

Cited by 203 publications

(166 citation statements)

References 71 publications

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“…Despite the sustained incidence of silicosis, little has been achieved concerning treatment development. Studies aiming to identify an effective therapy for silicosis are occurring, though management of silicosis still consists of supportive therapy including the use of bronchodilators and cough medication, as well as oxygen therapy (25)(26)(27). We demonstrated, herein, the efficacy of the therapeutic administration of flunisolide in reversing granuloma formation and collagen deposition triggered by silica particles.…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2020

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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-β 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-β, 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.

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Section: Discussionmentioning

confidence: 99%

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

et al. 2020

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“…Silicosis continues to be reported from traditional extractive and industrial operations in Brazil [2], China [3], India [4] and Zambia [5], among many others. Severe silicosis has appeared in new industrial settings, specifically the fabrication of engineered stone [6] and denim apparel sandblasting [7].…”

Section: Introductionmentioning

confidence: 99%

Predictors of silicosis and variation in prevalence across mines among employed gold miners in South Africa

et al. 2020

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Background: The stated intention to eliminate silicosis from the South African goldmining industry as well as current programmes to find and compensate ex-miners with silicosis require an understanding of variation in silicosis prevalence across the industry. We aimed to identify the predictors of radiological silicosis in a large sample of working miners across gold mines in South Africa. Methods: Routine surveillance chest radiographs were collected from 15 goldmine "clusters" in a baseline survey undertaken in preparation for a separate tuberculosis isoniazid prophylaxis trial. All images were read for silicosis by a health professional experienced in using the International Labour Organisation (ILO) classification. Profusion thresholds of > 1/0 and > 1/1 were used. Demographic and occupational information was obtained by questionnaire. Predictors of silicosis were examined in a multivariable logistic regression model, including age, gender, racial ascription, country of origin, years since starting mine employment, mine shaft, skill category, underground work status and tuberculosis. Results: The crude silicosis prevalence at ILO > 1/1 was 3.8% [95% confidence interval (CI) 3.5-4.1%]. The range across mine shafts was 0.8-6.9%. After adjustment for covariates, the interquartile range across shafts was reduced from 2.4 to 1.2%. Black miners [adjusted odds ratio (aOR) 2.8; 95% CI 1.1-7.2] and miners in full-time underground work (aOR 2.1; 95% CI 1.3-3.4) had substantially elevated odds of silicosis, while workers from Mozambique had lower odds (aOR 0.54; 95% CI 0.38-0.77). Silicosis odds rose sharply with both age and years since starting in the industry (p for linear trend < 0.005), with 95.5% of affected miners having > 15 years since first exposure and 2.2% < 10 years. Conclusions: In surveillance of silicosis in working gold miners time since first exposure remains a powerful predictor. Age appears to be an independent predictor, while the detection of radiological silicosis in short-service miners requires attention. Public risk reporting by mines should include factors bearing on silicosis prevalence, specifically dust concentrations, with independent verification. Studies of silicosis and tuberculosis in ex-miners are needed, supported by an accessible electronic database of the relevant medical and dust exposure records of all gold miners.

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“…Inhalation of respirable Si dust will be deposited in airways and alveoli, then phagocytized by macrophages (Balakrishnan et al, 2019). This will activate the proinflammatory and profibrotic pathway that leads to cell necrosis, autophagy and release of cytotoxic, inflammatory cytokines and arachidonic metabolites (Barnes, 2019). Subsequently causing alveolar inflammation and fibrosis (Balakrishnan et al, 2019;Barnes et al, 2019).…”

Section: Hazard Quotient (Hq)mentioning

confidence: 99%

“…This will activate the proinflammatory and profibrotic pathway that leads to cell necrosis, autophagy and release of cytotoxic, inflammatory cytokines and arachidonic metabolites (Barnes, 2019). Subsequently causing alveolar inflammation and fibrosis (Balakrishnan et al, 2019;Barnes et al, 2019). After adjusting for various factors, cement manufacturing workers were 2.31 times more likely to get cancer after exposure to respirable Si dust (Cassidy et al, 2007).…”

Section: Hazard Quotient (Hq)mentioning

confidence: 99%

“…This will activate the proinflammatory and profibrotic pathway that leads to cell necrosis, autophagy and release of cytotoxic, inflammatory cytokines and arachidonic metabolites (Barnes et al, 2019). Subsequently causing alveolar inflammation and fibrosis (Barnes et al, 2019;Balakrishnan et al, 2019). The exposure to crystalline Si can bioaccumulate in the lung and cause a build-up connective tissues known as silicosis (Nakladalova et al, 2018).…”

Section: Hazard Quotient (Hq)mentioning

confidence: 99%

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Exposure to Silica, Arsenic, and Chromium (VI) in Cement Workers: A Probability Health Risk Assessment

Kamaludin

Jalaludin

Tamrin

et al. 2020

Aerosol Air Qual. Res.

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Cement mineral dust contains a variety of carcinogenic and non-carcinogenic substances. The study aimed to determine the probability of health risk among cement workers due to respirable silica (Si), arsenic (As), and chromium (Cr) VI dust exposure. A cross-sectional study was carried out among 123 cement workers. A personal air sampling pump was used to assess respirable cement dust exposure. Inductively coupled plasma mass spectrometry (ICP-MS) was used for As, and Cr analysis, and X-ray powder diffraction (XRD) was used for Si analysis. The Fractional Exhaled Nitric Oxide levels and lung function test were obtained by using NIOX MINO and Chestgraph H1-105 spirometer. Risk assessment was calculated by using the incremental lifetime cancer risk (ILCR) and non-cancerous hazard quotient (HQ). The geometric mean and standard deviation of respirable Si and Cr dust concentrations were 5.27 ± 2.36 mg m-3 and 1.53 ± 2.47 mg m-3 , respectively, in manufacturing workers. The mean concentration for As in administrative workers was 0.07 ± 0.02 mg m-3. After controlling for confounders, the abnormalities of FVC% predicted and FEV 1 % predicted were significantly associated with the respirable Si dust among cement workers (OR = 6.913; CI = 1.965-24.322 and OR = 18.320; CI = 3.078-109.027). FENO concentrations in administrative workers were significantly influenced by the exposure to respirable Si dust (R 2 = 0.584, p = 0.006). Manufacturing workers had a high probability of getting cancer due to Si exposure in cement respirable dust at 29.81 × 10-4 times compared to administrative workers at 4.14 × 10-4 times. After reducing for control factors, the probability of manufacturing workers reduced to 0.45 × 10-4 times. As and Cr (VI) dust exposures among cement workers had a probability of cancer risk of 7.49 × 10-4 and 44.09 × 10-4 times, respectively, after reducing for control factors. The non-cancerous disease risk of the workers from exposure to cement mineral dust exceeded the acceptance limit (HQ > 1). Cement workers were at high risk of developing cancerous and non-cancerous diseases due to exposure while working. Cement workers were highly exposed to respirable Si, As, and Cr dust above the permissible exposure limit.

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Silica‐associated lung disease: An old‐world exposure in modern industries

Cited by 203 publications

References 71 publications

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

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

Predictors of silicosis and variation in prevalence across mines among employed gold miners in South Africa

Exposure to Silica, Arsenic, and Chromium (VI) in Cement Workers: A Probability Health Risk Assessment

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