Fluidized bed ash and passive treatment reduce the adverse effects of acid mine drainage on aquatic organisms

Elevated concentrations of acidity and metals in acid mine drainage (AMD) may be effectively addressed by active and passive treatment technologies. However, typical evaluations consider only chemical water quality with little if any regard for biological metrics. Robust evaluations including both chemical and biological indicators of water quality improvement are needed. In this study, injection of alkaline fluidized bed ash (FBA) into a flooded underground coal mine was coupled with a five-cell passive treatment system to ameliorate an abandoned AMD discharge in eastern Oklahoma. The passive system included process units promoting both aerobic and anaerobic treatment mechanisms. Resulting water quality changes and biological responses were evaluated. Organisms of two distinct functional groups (the filter-feeding mollusk Corbicula fluminea and the wide-spectrum feeding fish Lepomis macrochirus) were exposed to mine waters in several treatment cells. The combination of treatment technologies was hypothesized to limit potential negative effects on these aquatic organisms. Tissues were harvested and analyzed for concentrations of several metals (Al, Fe, Mn, Mg, Ca, Ni, Cu and Zn) of interest. Organismal responses, such as hepatosomatic index, condition factor, and condition index, did not vary significantly among organisms exposed within different treatment cells when compared to non-AMD impaired waters. Metal tissue accumulation trends, compared to aqueous concentrations, were observed for Fe, Ni and Zn. Exposure experiments with these two organisms indicated that FBA introductions coupled with passive treatment decreased the potential adverse effects of AMD to biological systems.     

Mitochondrial genome damage associated with cigarette smoking

We have investigated the level of mitochondrial DNA (mtDNA) damage and deletions in bronchoalveolar lavage tissues from smokers and nonsmokers using quantitative, extra-long PCR and a "common" mtDNA deletion assay. Smokers had 5.6 times the level of mtDNA damage, 2.6 times the damage at a nuclear locus (beta-globin gene cluster), and almost 7 times the level of a 4.9-kb mtDNA deletion compared to nonsmokers, although the latter increase was not significant. Although both genomes (mitochondrial and nuclear) showed significantly increased levels of DNA damage in smokers (mtDNA P = 0.00072; beta-globin P = 0.0056), the relative differences were greatest in the mtDNA. Damage to the mtDNA may inhibit oxidative phosphorylation and, therefore, potentially cause or contribute to chronic lung disease and cancer. Consequently, the mtDNA may be a sensitive biomarker for environmentally induced genetic damage and mutation.