Distribution and bioavailability of mercury in size-fractioned atmospheric particles around an ultra-low emission power plant in Southwest China.

Ultra-low emission (ULE) technology retrofits significantly impact the particulate-bound mercury (Hg) emissions from coal-fired power plants (CFPPs); however, the distribution and bioavailability of Hg in size-fractioned particulate matter (PM) around the ULE-retrofitted CFPPs are less understood. Here, total Hg and its chemical speciation in TSP (total suspended particles), PM10 (aerodynamic particle diameter ≤ 10 µm) and PM2.5 (aerodynamic particle diameter ≤ 2.5 µm) around a ULE-retrofitted CFPP in Guizhou Province were quantified. Atmospheric PM2.5 concentration was higher around this ULE-retrofitted CFPP than that in the intra-regional urban cities, and it had higher mass Hg concentration than other size-fractioned PM. Total Hg concentrations in PM had multifarious sources including CFPP, vehicle exhaust and biomass combustion, while they were significantly higher in autumn and winter than those in other seasons (P < 0.05). Regardless of particulate size, atmospheric PM-bound Hg had lower residual fractions (< 21%) while higher HCl-soluble fractions (> 40%). Mass concentrations of exchangeable, HCl-soluble, elemental, and residual Hg in PM2.5 were higher than those in other size-fractioned PM, and were markedly elevated in autumn and winter (P < 0.05). In PM2.5, HCl-soluble Hg presented a significantly positive relationship with elemental Hg (P < 0.05), while residual Hg showed the significantly positive relationships with HCl-soluble Hg and elemental Hg (P < 0.01). Overall, these results suggested that atmospheric PM-bound Hg around the ULE-retrofitted CFPP tends to accumulate in finer PM, and has higher bioavailable fractions, while has potential transformation between chemical speciation.

Evaluation of the effects of Hg/DOC ratios on the reduction of Hg(II) in lake water.

Reduction of mercury (Hg) in natural waters, which releases a substantial amount of gaseous Hg(0) to the atmosphere, has a close relationship to Hg/DOC ratios. However, the role of Hg/DOC ratio on the Hg(II) reduction in natural waters remains poorly understood. In this study, natural water collected from Hongfeng Lake, SW China, was used to study the effects of Hg/DOC ratio on the Hg(II) reduction. The lake water was spiked with variable amounts of Hg to make different Hg/DOC solutions. Through a 72 h Hg(II) reduction process, we demonstrated that the maximum percentage reduction of Hg (29 ± 3%) occurred when Hg/DOC ratio was 1134 ng mg-1. Further increase or decrease of the Hg/DOC ratios would inhibit the reduction of Hg(II). This study clearly demonstrated that Hg/DOC ratio has a dual role in the reduction of Hg(II) from natural waters.

Protective effect of bone morphogenetic protein-6 on neurons from H2O2 injury.

Bone morphogenetic protein-6 (BMP6) is a member of the TGF-beta superfamily. Expression of BMP6 and its receptors are increased when brain tissues of adult rats are injured, suggesting that BMP6 may have a neuroprotective function in the physiologic response to neurological damage. This research investigates the molecular mechanisms supporting a neuroprotective effect of BMP6 in neural cells traumatized by H(2)O(2). We demonstrate that presence of BMP6 either before or after H(2)O(2)-induced injury protects the cultured primary cortical cells from apoptosis. However, molecular mechanisms mediating the protective effects of either pre- or post-treatment with BMP6 are different. Cells pre-treated with BMP6 have attenuated MAPK activity induced by H(2)O(2), whereas the MAPK activity in cells post-treated with BMP6 remains unchanged. Further, pharmacological inhibitors of MAPKs, PD98059 and SB203580, block the protective effect of BMP6 in the cells pre-treated with BMP6 but not in the cells post-treated with BMP6. The protective effect of post-treatment with BMP6 appears to be mediated through regulation of p53 and Bax molecules, evidenced by decreased mRNA levels after BMP6 treatment. Taken together, these data suggest BMP6 protect cortical cells against oxidation stress induced by H(2)O(2) via two different mechanisms, where (1) pre-treatment with BMP6 acts through MAPK pathway and (2) post-treatment with BMP6 works by down-regulating p53 and Bax.