Silicosis and coal workers' pneumoconiosis.

Abstract

Exposure to coal mine dust and/or crystalline silica results in pneumoconiosis with initiation and progression of pulmonary fibrosis. This review presents characteristics of simple and complicated coal workers' pneumoconiosis (CWP) as well as pathologic indices of acute and chronic silicosis by summarizing results of in vitro, animal, and human investigations. These results support four basic mechanisms in the etiology of CWP and silicosis: a) direct cytotoxicity of coal dust or silica, resulting in lung cell damage, release of lipases and proteases, and eventual lung scarring; b) activation of oxidant production by pulmonary phagocytes, which overwhelms the antioxidant defenses and leads to lipid peroxidation, protein nitrosation, cell injury, and lung scarring; c) activation of mediator release from alveolar macrophages and epithelial cells, which leads to recruitment of polymorphonuclear leukocytes and macrophages, resulting in the production of proinflammatory cytokines and reactive species and in further lung injury and scarring; o) secretion of growth factors from alveolar macrophages and epithelial cells, stimulating fibroblast proliferation and eventual scarring. Results of in vitro and animal studies provide a basis for proposing these mechanisms for the initiation and progression of pneumoconiosis. Data obtained from exposed workers lend support to these mechanisms.

Platelet Indices in Patients with Coal Workers’ Pneumoconiosis

“…CWP results from exposure to coal mine dust [1]. Although the risk of CWP is associated with the intensity of dust exposure and the total dose, the pathogenesis of CWP remains unclear.…”

“…Coal workers' pneumoconiosis (CWP) is caused by the chronic inhalation and deposition of coal particles in the lungs [1]. CWP is divided into two categories according to the severity of the disease: simple pneumoconiosis (SP) and complicated pneumoconiosis with progressive massive fibrosis (PMF) [1].…”

“…CWP is divided into two categories according to the severity of the disease: simple pneumoconiosis (SP) and complicated pneumoconiosis with progressive massive fibrosis (PMF) [1]. Even though the mechanism for the development of CWP remains elusive, reactive oxygen species (ROS) play an important role in the pathogenesis of the disease [2].…”

Ceramics manufacturing contributes to ambient silica air pollution and burden of lung disease

“…Kachuri et al (2014) indicated that an increasing duration of employment at any concentrations of silica dust exposure was associated with a significantly higher lung cancer risk in Canadian males with odds ratio of 1.76 (95 % CI 1.34-2.31) for ≥30 exposure years adjusted for age, residence, cigarette smoking, and passive smoking. Moreover, excessive and prolonged exposure to silica dust could lead to inflammation in the lung, resulting in pneumoconiosis and progression of pulmonary fibrosis and related lung diseases (Castranova and Vallyathan 2000;Dostert et al 2008;Fubini and Hubbard 2003;Kuroda et al 2011).…”

Ceramic Manufacturing Processes

“…As a result, the term silicosis is often inappropriately used in referring to any pneumoconiosis, independently of the actual cause. However, particulates other than silica, such as coal dust, can also produce pneumoconiosis (25).…”