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Iron, calcium, and oxidative stress in lung injury.
Huang X; Frenkel K; Chen L
Atlanta, GA: U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, R01-OH-003561, 2003 Dec; :1-39
Coal remains a very significant part of world energy needs. Coal mining causes health problems, such as pneumoconiosis and emphysema. In the present study, we show evidence that bio-available iron (BAI) may be the active component in coal dust-induced cell injury through oxidative stress pathways, and that calcite (CaCO3) plays a protective role by inhibiting solubilization of iron compounds, making iron less bioavailable. Thirty coal samples from Utah (UT), West Virginia (WV) and Pennsylvania (PA) coalmine regions with a low, moderate, and high prevalence of pneumoconiosis, respectively, were tested in a system mimicking the phagolysosomes, a cellular compartment for particle digestion, as well as in intact living human lung epithelial cells and primary rat alveolar macrophages. We found that the prevalence of pneumoconiosis correlated positively with the content of BAI released from the coals, as well as levels of ferritin and lipid peroxidation in the cells. The UT coals had very little BAI due to the presence of CaCO3. We have further shown that coals from the PA coalmine with a high level of BAI induced activator protein-I, a transcription factor responsive to oxidative stress. In contrast, the coal from the UT coalmine without BAI had no effect. Interleukin-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 the UT coal was increased but reverted to the control level shortly. These results suggest that a sustainable level of oxidative stress induced by BAI in the P A and WV coals may be responsible for cellular damage, thus leading to the observed high prevalence of lung disease in the P A and WV coal miners. By adding calcite into the PA coals, levels of BAI as well as IL-6 were diminished as compared to the P A coals without the addition of the calcite. Using characterized coal samples collected by the U.S. Geological Survey's coal quality database, we have developed a model that can predict coal's toxicity in the major coalproducing beds in the US, even before mining. Our study indicates that BAI my be a useful marker for risk assessment of coal mining and the addition of calcite into the water spray when mining may be proposed for pneumoconiosis prevention.
Iron-compounds; Calcium-compounds; Injuries; Coal-miners; Coal-mining; Health-hazards; Pneumoconiosis; Coal-dust; Cell-damage; Lung-cells; Lung-disease; Injury-prevention; Coal-workers-pneumoconiosis; Black-lung
Department of Environmental Medicine, New York University School of Medicine, 550 First Avenue, PHL 802, New York, NY 10019
7439-89-6; 7440-70-2; 471-34-1
Final Grant Report
National Institute for Occupational Safety and Health
New York University Medical Center, New York, New York