# Research Status of Pathogenesis of Pneumoconiosis and Dust Control Technology in Mine--A Review
## 2 Research Progress of Mine Pneumoconiosis
### Pneumoconiosis Pathogenesis  
In recent years, research reports on the pathogenesis of coal workers' pneumoconiosis have emerged one after another [13; 14; 15; 16; 17; 18; 19]. There are several hypotheses, as shown in Figure 1. First, the direct toxic effect of coal dust on the lungs. Second, the oxidation products of pulmonary phagocytes exceed the role of antioxidants, leading to lipid peroxidation and protein nitrosylation, resulting in cell damage and finally pulmonary fibrosis. Third, alveolar macrophages and epithelial cells release active mediators, which cause the aggregation of leukocytes and phagocytes, aggravate the increase and release of inflammatory factors, and lead to lung injury. Fourth, transforming growth factors released by alveolar macrophages and epithelial cells stimulate fibroblast proliferation, which leads to pulmonary fibrosis. Scholars have found that tumor necrosis factor and transforming growth factor are related to the pathogenesis of coal workers' pneumoconiosis [20; 21; 22; 23; 24; 25; 26; 27]. In addition, the incidence rate of coal worker pneumoconiosis is related to the bioavailability of iron in coal dust [28; 29; 30]. Iron activates epithelial cells, activating proteins and t-nuclear factors, which leads to inflammation and cell proliferation. Other studies have shown that silica can induce macrophages to express FasL, induce apoptosis, produce reactive oxygen species mediators and release a variety of chemical stimulating factors [31; 32; 33; 34; 35; 36]. Some studies have also shown that coal worker pneumoconiosis is an independent disease different from silicosis. Simple coal worker pneumoconiosis is only related to the deposition of coal dust in the lung, while pneumoconiosis with severe pulmonary fibrosis is not only related to the deposition of coal dust in the lung, but also related to immune cells, cytokines and humoral immunity [37; 38; 39; 40; 41; 42; 43].  
The incidence rate of pneumoconiosis is related to the composition of coal. Especially, SiO\({}_{2}\) has a great impact on pneumoconiosis. In addition, with the increase of the content of  
Figure 1: Hypothesis of pathogenesis of coal workers’ pneumoconiosis [10].  
metal and metalloid elements in coal, coal dust toxicity to lung cells and the degree of cell damage increase, which leads to the increase of the prevalence of coal worker pneumoconiosis. Some studies [16; 17; 43] present that the probability of coal workers suffering from pneumoconiosis is also relatively high in workplaces with high lead, cadmium, manganese and copper elements; these elements are suspected carcinogens and have a significant negative impact on the early development of pneumoconiosis [18]. The transition metal ions such as iron and copper on the surface of coal dust are reductive, which can produce free radicals in the suspension, and then lead to the toxic effect of coal dust on lung tissue cells. Trace nickel in coal may cause lung cancer, which is related to nickel compounds inducing excessive reactive oxygen free radicals, and then results in oxidative damage to cells [19]. At present, the study of dust particle exposure and tumor-related genes has become a hot spot in the pathogenesis of pneumoconiosis [44; 45; 46].