[The clinical pathological analysis of 14 autopsy cases of pneumoconiosis].

OBJECTIVE: To investigate the histopathological features, complications, diagnosis, and differential diagnosis of coal workers' pneumoconiosis (CWP). METHODS: The lung tissue sections from 14 autopsy cases of CWP were subjected to HE staining and observed under a light microscope, and a retrospective analysis was performed considering the occupational history and clinical features. RESULTS: The 14 cases were 46-71 years of age (mean, 57.7 years). Two cases were diagnosed as dust reaction, 1 case as simple CWP (stage I anthracosilicosis), and 11 cases as complicated CWP (9 cases of stage II anthracosilicosis, 1 case of stage III anthracosilicosis, and 1 case of stage III silicosis). Twelve cases were complicated by chronic bronchitis and emphysema, 8 cases by pulmonary heart disease, 4 cases by pulmonary tuberculosis, 3 cases by liver cirrhosis and liver cancer with pulmonary metastases, and 2 cases by cerebral hemorrhage. CONCLUSION: Among patients with CWP, the pathological changes of lung tissue become more complex with increasing years of dust exposure. Coal macule is the common pathological feature of CWP, and dust nodules and massive fibrosis are the necessary indices of pathological diagnosis.

[Pathologic observation on animal model of silicosis].

OBJECTIVE: To explore the pathological changes of pulmonary fibrosis induced by SiO2 in rats and pigs. METHODS: The silicosis models in rats and pigs were established by non-exposure method. The pathologic changes in lung tissues of rats and pigs were observed with HE staining under a light microscopy and under a transmission electron microscopy (TEM), the expression of cytokines was detected by immunohistochemistry. RESULTS: (1) The main pathologic changes of silicosis models in rats and pigs included: in 7 ∼ 15 days after treatment, silica dusts, dust cells, a lot of macrophages, lung epithelial cells, a few neutrophils, macrophage alveolar inflammation and nodules of stage I were found in alveolar space; in 30 ∼ 90 days after treatment, many nodules of stage I-III or IV with lymphocytes infiltration were observed in respiratory bronchioles, alveoli, interlobular septa, the subpleural and around blood vessels and bronchi. (2) The expression levels of CK protein, SP-A protein, CD68, b-FGF, TNF-α, IL-6, TGF-ß1, NFKappa/P50, Kappa/P65 and VEGF reduced with exposure time, but still were higher than those of the control. (3) The shed alveolar type I cells, proliferation of alveolar type II cells or macrophages and activated cellular function induced by silica were observed under TEM. CONCLUSION: The development of pulmonary fibrosis in silicosis models corresponded with the process from macrophages alveolar inflammation to pulmonary fibrosis.