1.Biological responses of tin mine particles and their association with adverse effects on health in tin mine.
Wei-hong CHEN ; Karin STEMPELMANN ; Steffeni REHN ; Herbert DIEDERICHS ; Bernd REHN ; Joachim BRUCH
Chinese Journal of Industrial Hygiene and Occupational Diseases 2005;23(5):366-370
OBJECTIVETo evaluate the biological and toxicity of tin mine particles mixed with crystalline silica using an in vitro test, and to compare to the pathogenesis of pneumoconiosis and lung cancer.
METHODSRespirable particle samples were sampled from four tin mines, in which elevated mortality of pneumoconiosis and lung cancer were reported in miners exposed to particles. Alveolar macrophages (AM) are considered as the target cells of primary dust effects. The samples were then measured in 15, 30, 60 and 120 microg particle per 106 AM for cytoxicity with the release of glucuronidase, lactate dehydrogenase, for reactive oxygen damage with H2O2 release, and for ability to induce fibrosis using the secretion of tumor necrosis factor-alpha (TNF-(alpha) in guinea pig and/or rat am. pure quartz (dq12) and corundum were used as controls.
RESULTSThe results showed the samples from tin mines caused a higher cytoxicity when compared to corundum, yet lower when compared to quartz. However, reactive oxygen species release induced by the samples were significantly higher than that induced by quartz and corundum. Beside particle samples induced higher TNF-alpha secretion than corundum, samples from Limu tin mine also induced greatly higher TNF-alpha levels than that induced by pure quartz, even in the lowest concentration. The results from epidemiological research show that high incidence of silicosis among tin miners. And standardize mortality from all cancer (SMR = 1.58, 95% CI: 1.39-1.76) and lung cancer (SMR = 3.17, 95% CI: 2.59-3.76) are higher than national average level.
CONCLUSIONThe results from in vitro test may reasonable interpret high risk of pneumoconiosis and lung cancer in tin miners. The in vitro multidimensional reaction patterns of AM can be used to screen workplace particles for adverse effects to health.
Animals ; Cell Line ; Cohort Studies ; Dust ; Guinea Pigs ; Humans ; Lung Neoplasms ; epidemiology ; Macrophages, Alveolar ; cytology ; metabolism ; Mining ; Occupational Exposure ; Quartz ; Rats ; Tin ; toxicity
2.Changes of tumor necrosis factor, surfactant protein A, and phospholipids in bronchoalveolar lavage fluid in the development and progression of coal workers' pneumoconiosis.
Jing-Cai XING ; Wei-Hong CHEN ; Wen-Hui HAN ; Mei-Feng GUO ; Steffeni REHN ; Joachim BRUCH
Biomedical and Environmental Sciences 2006;19(2):124-129
OBJECTIVETo evaluate the alterations of biomarkers in the development and progression of coal workers' pneumoconiosis (CWP).
METHODSThe type and number of cells, and the levels of tumor necrosis factor-alpha (TNF-alpha), pulmonary surfactant protein, phospholipids and fibronectin in bronchoalveolar lavage fluid were assayed in 14 health active coal miners, 21 coal miners without CWP and 13 miners with CWP of 0/1 to 1/1.
RESULTSCompared to active coal miners without CWP (8.23 microg/mL), TNF-alpha concentration was gradually decreased when dust exposure was stopped (5.90 microg/mL). Elevated surfactant protein A (SP-A) level and phosphatidylglycerol (PG) to phosphatidylinositol (PI) ratio were found in miners actively exposed to coal dust (6528 ng/mL for SP-A and 10. for PG/PI), and both parameters decreased when CWP progressed from CWP (0/1) (3419 microg/mL for SP-A and 5.9 for PG/PI) to CWP (1/1) (1654 microg/mL for SP-A and 5.5 for PG/PI).
CONCLUSIONBiomarkers in bronchoalveolar lavage fluid can be used to screen coal miners at high risk of developing coal workers' pneumoconiosis.
Adult ; Animals ; Biomarkers ; analysis ; Bronchoalveolar Lavage Fluid ; chemistry ; Coal Mining ; Disease Progression ; Humans ; L Cells (Cell Line) ; Mice ; Middle Aged ; Phospholipids ; metabolism ; Pneumoconiosis ; diagnosis ; metabolism ; physiopathology ; Pulmonary Surfactant-Associated Protein A ; metabolism ; Tumor Necrosis Factor-alpha ; metabolism