A study was conducted to investigate the effect of selective catalytic reduction (SCR) catalyst on mercury (Hg) speciation in bituminous and subbituminous coal combustion flue gases. Three different Illinois Basin bituminous coals (from high to low sulfur [S] and chlorine [Cl]) and one Powder River Basin (PRB) subbituminous coal with very low S and very low Cl were tested in a pilot-scale combustor equipped with an SCR reactor for controlling nitrogen oxides (NOx) emissions. The SCR catalyst induced high oxidation of elemental Hg (Hg0), decreasing the percentage of Hg0 at the outlet of the SCR to values <12% for the three Illinois coal tests. The PRB coal test indicated a low oxidation of Hg0 by the SCR catalyst, with the percentage of Hg0 decreasing from approximately 96% at the inlet of the reactor to approximately 80% at the outlet. The low Cl content of the PRB coal and corresponding low level of available flue gas Cl species were believed to be responsible for low SCR Hg oxidation for this coal type. The test results indicated a strong effect of coal type on the extent of Hg oxidation. 相似文献
Mitochondria play a central role in maintaining cellular and metabolic homeostasis during vital development cycles of foetal growth. Optimal mitochondrial functions are important not only to sustain adequate energy production but also for regulated epigenetic programming. However, these organelles are subtle targets of environmental exposures, and any perturbance in the defined mitochondrial machinery during the developmental stage can lead to the re-programming of the foetal epigenetic landscape. As these modifications can be transferred to subsequent generations, we herein performed a cross-sectional study to have an in-depth understanding of this intricate phenomenon. The study was conducted with two arms: whereas the first group consisted of in utero pro-oxidant exposed individuals and the second group included controls. Our results showed higher levels of oxidative mtDNA damage and associated integrated stress response among the exposed individuals. These disturbances were found to be closely related to the observed discrepancies in mitochondrial biogenesis. The exposed group showed mtDNA hypermethylation and changes in allied mitochondrial functioning. Altered expression of mitomiRs and their respective target genes in the exposed group indicated the possibilities of a disturbed mitochondrial-nuclear cross talk. This was further confirmed by the modified activity of the mitochondrial stress regulators and pro-inflammatory mediators among the exposed group. Importantly, the disturbed DNMT functioning, hypermethylation of nuclear DNA, and higher degree of post-translational histone modifications established the existence of aberrant epigenetic modifications in the exposed individuals. Overall, our results demonstrate the first molecular insights of in utero pro-oxidant exposure associated changes in the mitochondrial-epigenetic axis. Although, our study might not cement an exposure-response relationship for any particular environmental pro-oxidant, but suffice to establish a dogma of mito-epigenetic reprogramming at intrauterine milieu with chronic illness, a hitherto unreported interaction.
