Department of Earth and Environmental Studies, Montclair State University, Montclair, NJ 07043, United States.
Passaic River Institute, Montclair State University, Montclair, NJ 07043, United States; Department of Biology, Montclair State University, Montclair, NJ 07043, United States.
Chemosphere. 2017 Nov;186:757-761. doi: 10.1016/j.chemosphere.2017.08.052. Epub 2017 Aug 11.
Although ferrate(VI) has long been recognized as a multi-purpose treatment agent, previous investigations regarding ferrate(VI) for addressing harmful algal blooms (HABs) impacts in drinking water treatment only focused on a single HAB pollutant (e.g. algal cells or algal toxins). Moreover, the performance of ferrate(VI)-driven coagulation was poorly investigated in comparison with ferrate(VI) oxidation, though it has been widely acknowledged as a major ferrate(VI) treatment mechanism. We herein reported ferrate(VI) as an emerging agent for simultaneous and effective removal of algal cells and toxins in a simulated HAB-impacted water. Ferrate(VI)-driven oxidation enabled algal cell inactivation and toxin decomposition. Subsequently, Fe(III) from ferrate(VI) reduction initiated an in-situ coagulation for cell aggregation. Cell viability (initial 4.26 × 10 cells/mL at pH 5.5 and 5.16 × 10 cells/mL at pH 7.5) decreased to 0.0% at ≥ 7 mg/L Fe(VI) at pH 5.5 and 7.5, respectively. Cell density and turbidity were dramatically decreased at pH 5.5 once ferrate(VI) doses were beyond their respective threshold levels, which are defined as minimum effective iron doses (MEIDs). However, the particulate removal at pH 7.5 was poor, likely because the coagulation was principally driven by charge neutralization and a higher pH could not sufficiently lower the particle surface charge. Meanwhile, algal toxins (i.e., microcystins) of 3.98 μg/L could be substantially decomposed at either pH. And the greater degradation achieved at pH 5.5 was due to the higher reactivity of ferrate(VI) at the lower pH. This study represents the first step toward the ferrate(VI) application as a promising approach for addressing multiple HABs impacts for water treatment.
尽管高铁酸盐（VI）长期以来一直被认为是一种多用途的处理剂，但以前关于高铁酸盐（VI）处理饮用水中有害藻类 bloom（HABs）影响的研究仅集中在单一的 HAB 污染物（如藻类细胞或藻类毒素）上。此外，尽管高铁酸盐（VI）驱动的混凝作用已被广泛认为是高铁酸盐（VI）的主要处理机制，但与高铁酸盐（VI）氧化相比，其性能研究甚少。在此，我们报告了高铁酸盐（VI）作为一种新兴的处理剂，可同时有效去除模拟 HAB 影响水中的藻类细胞和毒素。高铁酸盐（VI）驱动的氧化使藻类细胞失活并分解毒素。随后，高铁酸盐（VI）还原生成的 Fe(III)引发原位混凝以聚集细胞。细胞活力（在 pH 5.5 时初始为 4.26×10 个细胞/mL，在 pH 7.5 时初始为 5.16×10 个细胞/mL）在 pH 5.5 和 7.5 下分别降至≥7 mg/L Fe(VI)时降至 0.0%。一旦高铁酸盐（VI）剂量超过各自的阈值水平（定义为最小有效铁剂量 MEIDs），在 pH 5.5 下细胞密度和浊度会急剧下降。然而，在 pH 7.5 下的颗粒去除效果不佳，可能是因为混凝主要由电荷中和驱动，较高的 pH 值不能充分降低颗粒表面电荷。同时，在两种 pH 值下，3.98μg/L 的藻类毒素（即微囊藻毒素）均可得到有效分解。在 pH 5.5 下实现更高的降解是由于高铁酸盐（VI）在较低 pH 值下具有更高的反应性。本研究是将高铁酸盐（VI）作为一种有前途的处理方法应用于处理多种 HABs 影响的第一步。
