Explore chapters and articles related to this topic
Answers
Published in Ken Addley, MCQs, MEQs and OSPEs in Occupational Medicine, 2023
Silicosis: Soapstone is a natural stone (also known as steatite) that consists primarily of talc. It has become increasingly popular in the manufacture of kitchen countertops. It has a high silica content which produces large amounts of respirable silica when cut/sanded and has been associated with outbreaks of silicosis in workshops with poor ventilation/low-grade personal protective equipment.
Inflammatory, Hypersensitivity and Immune Lung Diseases, including Parasitic Diseases.
Published in Fred W Wright, Radiology of the Chest and Related Conditions, 2022
These are due to the inhalation of dusts (κονο = dust), mainly silicon, which is often combined with other substances, e.g. carbon, iron, tin, etc. Not only may silicosis occur with mining, but also as a complication of the manufacture of various products, boiler cleaning, in iron and steel works, the making of scouring powders, lens polishing, pottery manufacture, sand-blasting; grinding, quarry workers, etc.
Paper 2
Published in Amanda Rabone, Benedict Thomson, Nicky Dineen, Vincent Helyar, Aidan Shaw, The Final FRCR, 2020
Amanda Rabone, Benedict Thomson, Nicky Dineen, Vincent Helyar, Aidan Shaw
The correct underlying diagnosis is silicosis. This is a pneumoconiosis found in those in sandblasting or mining industries, secondary to inhaled silica. The features of tiny calcified pulmonary nodules and calcified hila lymph nodes is indicative of this condition, complicated by progressive massive fibrosis (PMF). PMF occurs when the nodules coalesce and form large opacities in the upper zones with upper zone fibrosis.
Identification of key pathways and genes in the progression of silicosis based on WGCNA
Published in Inhalation Toxicology, 2022
Jiaqi Lv, Jingwei Xiao, Qiang Jia, Xiangjing Meng, Zhifeng Yang, Shuangshuang Pu, Ming Li, Tao Yu, Yi Zhang, Haihua Wang, Li Liu, Zhongsheng Li, Xiao Chen, Haitao Yang, Yulu Li, Mengyun Qiao, Airu Duan, Hua Shao, Bin Li
Although thousands of years have passed since the first case of silicosis was reported, its specific mechanism has remained to be elucidated until now. In general, the progress of silicosis could be divided into two major stages, namely the inflammation and fibrosis stage, which are characterized by aggregation of inflammatory cells and deposition of collagen fibers, respectively (Dong et al. 2016). Unfortunately, although there is no doubt that the general mechanism could provide certain clues for the further exploration of silicosis’s thorough mechanism and its effective treatment, there are many uncertainties and debates on the specific mechanism of silicosis from exposure to silica particles to the advanced silicosis (Palabiyik et al. 2013; Chan et al. 2018; Barnes et al. 2019). Not only that, but the overall research progress in treatment for silicosis is rather slow and limited, especially in the lack of effective radical treatments: lung transplantation seems to be the only lifesaver for silicosis patients, especially those diagnosed with advanced silicosis (Jiao and Chen 2020). As a result, the silicosis mechanism ought to be clarified and proposed from a target-centric drug discovery standpoint, creating a silver lining for silicosis patients.
Genotoxic stress of particulate matter in the electric furnace of an iron casting industry on human lung epithelial cells; an in vitro study
Published in Toxin Reviews, 2021
Zahra Panjali, Behjat Jafari-Tehrani, Nader Maghsoudi, Parviz Abdolmaleki, Rezvan Zendehdel
Crystalline silica is known as a human carcinogen. Chronic exposure to silica induce silicosis (IARC 2012, ATSDR 2019). Darne et al. reported that, silica showed no DNA breaks as well as no chromosome abnormality for V79 cell lines (Darne et al.2016). In this regard, the studied concentrations were 3.3–13.3 µg/cm. Whereas the results of the present study showed that, DNA impairments of silica in the concentration of 4–32 µg/mL were higher than the controls and are statistically significant (p < 0.0001) for the concentration of 32 µg/mL, which can be affected by the presence of other impurities in the ore. In addition, Mu et al. reported that, silica genotoxicity at A549 cells was observed at the >1 µg/mL concentrations (Mu et al.2012). Also, there is limited published data on the co-exposure to crystalline silica and metals. However, Mohmood et al. investigated the genotoxicity effect of co-exposure of mercury band silica-coated iron oxide particles. Accordingly, co-exposure of these components made an additive effect related to genotoxicity in erythrocytes (Mohmood et al.2015). However, the comparison of DNA damage for metal particles in our study and other published reports is shown in Table 2S.
Is individual genetic susceptibility a link between silica exposure and development or severity of silicosis? A systematic review
Published in Inhalation Toxicology, 2020
Kaio Cezar Rodrigues Salum, Marcos Cesar Santos Castro, Ângela Santos Ferreira Nani, Fabiana Barzotto Kohlrausch
Depending on individual biological characteristics and toxicity of the inhaled silica dust (Ziskind et al. 1976; Leung et al. 2012), silicosis can manifest in different clinical forms. Chronic silicosis is the most common form characterized by progressive fibrosis resulting from the inhalation of low levels of dust containing crystalline silica for more than 10 years (Barboza et al. 2008; Barnes et al. 2019). Initially asymptomatic, it shows over the years with the appearance of dyspnea on exertion, which together with the radiological findings and history of occupational exposure to silica characterize the diagnosis of the disease. The accelerated form is clinically similar to the chronic form, differing only by the time of onset of symptoms, from 5 to 10 years, after the initial exposure. This form affects workers who are exposed to high silica concentrations and, in this case, dyspnea on exertion is more limiting when compared to the chronic form. Acute silicosis, the rarest and severest form of silicosis, occurs from a few months to five years after the initial exposure (Wagner 1997; Fernández Álvarez et al. 2015; Barnes et al. 2019).