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Inorganic Particulates in Human Lung: Relationship to the Inflammatory Response
Published in William S. Lynn, Inflammatory Cells and Lung Disease, 2019
Victor L. Roggli, J. P. Mastin, John D. Shelburne, Michael Roe, Arnold R. Brody
Coal workers are occupationally exposed to large quantities of inorganic carbon as well as other particulates in coal dust. Inorganic carbon pollutes the environment of both urban and rural areas, deriving from incomplete combustion from automobiles, industry, home heating, and for some individuals, from cigarette smoke.
Occupational and Environmental Lung Diseases
Published in James M. Rippe, Lifestyle Medicine, 2019
Sunkaru Touray, Emil Tigas, Nicholas A. Smyrnios
In the United States, environmental controls are mandated by federal law. Coal dust exposure can be minimized using ventilation systems, water sprays, and other dust capture devices as part of a continuous monitoring program. There is no specific medical therapy that has proven effective in reversing CMDLD. Management involves periodic medical monitoring with periodic chest radiographs and spirometry.42 Patients with CMDLD should be offered vaccinations against viral and bacterial pathogens, and smoking cessation counseling should be offered to patients who smoke.
Tumours of the Larynx
Published in John C Watkinson, Raymond W Clarke, Terry M Jones, Vinidh Paleri, Nicholas White, Tim Woolford, Head & Neck Surgery Plastic Surgery, 2018
Vinidh Paleri, Stuart Winter, Hannah Fox, Nachi Palaniappan
Other known risk factors include occupational toxic agents such as asbestos, polycyclic aromatic hydrocarbons, wood dust, coal dust and cement dust.11, 12 Lower socioeconomic status and manual ‘blue-collar’ occupations also experience a higher risk of developing laryngeal cancer.11
Association between duration of coal dust exposure and respiratory impairment in coal miners of West Bengal, India
Published in International Journal of Occupational Safety and Ergonomics, 2021
Shilpi K. Prasad, Siddhartha Singh, Ananya Bose, Bimlesh Prasad, Oly Banerjee, Ankita Bhattacharjee, Bithin K. Maji, Amalendu Samanta, Sandip Mukherjee
Coal dust produced during mining, crushing or transporting is continuously being inhaled by workers during their working time. In this study, the mean dust concentration at the workface (2.02 mg/m3) was found to be higher than the NIOSH (1 mg/m3) and the MSHA (1.5–2 mg/m3) recommended permissible exposure limits for respirable coal dust [12,19]. Long-term inhalation of coal dust which contains fine carbon-rich suspended particulates, mainly below a diameter of 2.5 µm, can cause chronic health situations like CWP and silicosis [2]. CWP and silicosis are major lung diseases associated with reduced lung volumes and, ultimately, premature death. This study also demonstrates that long-term exposure to coal dust in underground mines significantly decreased the pulmonary function in coal-exposed workers. It was reported earlier that the occurrence of pneumoconiosis is seen in coal dust-exposed employees after an average exposure of 10 years [9]. The findings of the present study also revealed that a significant decrease was observed in the group where the length of service was more than 10 years. Different pulmonary function indices were significantly decreased in the exposed group according to the increasing length of the service, suggesting that with the advancement of service, the continuous inhalation of coal dust hampers pulmonary ventilation. Prolonged exposure to coal dust can disturb normal process of lung ventilation and exchange of air by causing lung nodules and interstitial fibrosis [20,21].
Using categorical data analyses in determination of dust-related occupational diseases in mining
Published in International Journal of Occupational Safety and Ergonomics, 2021
Mustafa Onder, Burcu Demir Iroz, Seyhan Onder
Inhaled coal dust can deposit in the lungs and can lead to the development of several diseases in exposed workers. CWP, a disease defined in terms of coal dust deposition in the lungs, is observed to be highly common in coal miners and is caused by inhalation and retention of coal mine dust [8,9]. A number of studies showed that up to 30 g of total dust may be found in the lungs of coal mine workers, with an accumulation rate of 0.4–1.7 g of dust retained each year [10]. The concentration of respirable coal dust, the period of exposure and the free silica content are important factors associated with pneumoconiosis risks [11]. Diagnosis of CWP is generally based on chest X-ray findings and a history of working in coal mines (usually for 10 years or more) [12]. The incidence of CWP is affected by coal rank. CWP is five times more prevalent in anthracite miners than for miners of lower rank coal. Data indicate a direct relationship between the mass of respirable coal mine dust inhaled and the incidence and severity of CWP [13]. Different categories of workers are exposed to different dust levels depending on many factors like the type of work, activity, period of exposure, etc. [14]. Coal mine workers have high exposure to respirable dust and quartz, especially the development team that creates mining paths for the miners to extract the coal [15].
Associations of HMGB1 gene polymorphisms with risk of coal workers’ pneumoconiosis susceptibility in Chinese Han population
Published in Inhalation Toxicology, 2020
Yijun Tang, Jingzhu Duan, Yun Wang, Leyong Yuan
Coal Worker’s Pneumoconiosis (CWP) is an occupational disease provoked by pulmonary accumulation of silica-containing coal dust, which is the prevalent occupational disease in China (Petsonk et al. 2013; Han et al. 2015; Blackley et al. 2016). Patients with CWP exhibit chronic pulmonary inflammation and fibrotic nodular lesions, predisposing patients to progressive fibrosis (Oyunbileg et al. 2011). As reported in 2016, 88.05% of all the reported occupational cases was pneumoconiosis, among which CWP accounted for over 50% (Wang et al. 2018). Among the Chinese workers exposed to coal mine dust or silica, the incidence and mortality were increasing each year (Castranova and Vallyathan 2000). However, only a proportion of individuals develop CWP, suggesting that the development of CWP may be related to genetic factors, that could be trackable by specific single-nucleotide polymorphisms (SNPs) (Yucesoy and Luster 2007; Ji et al. 2014; Wang et al. 2014; Han et al. 2015; Yang J et al. 2015).