Production of monoclonal antibody and development of an enzyme-linked immunosorbent assay for the determination of okadaic acid in shellfish from China

cell-free system mimicking the phagolysosomes of ceUs as well as in human lung epithelial type II A549 cells. Levels of BAI in the US Geological Survey (USGS) database of coal quality were calculated using a model taking into account chemical interactions of pyrite, sulfuric acid, calcite, and total iron. Results: The CWP prevalence in the three c0almine regions ofPA, WV, and UT correlated positively with the content of BAI released in the cell-free system (correlation coefficient r=0.94). The UT coals had very little BAI due to the presence of calcite (CaCO3). Two coal samples with different BAI contents were then selected for cell treatment. The coal from the PA coalmine with a high BAI induced activator protein-I, a transcription factor responsive to oxidative stress. In contrast, the coai from the UT coalmine without BAI had no effect. Intedeukin-6 (IL-6), a pro-inflammatory cytokine, was significantly increased and persisted in cells treated with the PA coal. The IL-6 level in cells treated with UT coal was increased but reverted to the control level shortly. Using the linear fit of CWP prevalence and the calculated BAI in the USGS coal database, we have derived and mapped seven thousands coal samples' pneumoconiotic potencies. Conclusions: Our results suggest that a sustainable level of oxidative stress induced by BAI in the PA and WV coals may be responsible for cellular damage, thus leading to the observed high prevalence of lung disease in the PA and WV coal miners. Levels of BAI in the coals may be used for the prediction of coal's toxicity, even before large-scale mining.