Mobilisation of arsenic from bauxite residue (red mud) affected soils: effect of pH and redox conditions

The tailings dam breach at the Ajka alumina plant, western Hungary in 2010 introduced ~1 million m3 of red mud suspension into the surrounding area. Red mud (fine fraction bauxite residue) has a characteristically alkaline pH and contains several potentially toxic elements, including arsenic. Aerobic and anaerobic batch experiments were prepared using soils from near Ajka in order to investigate the effects of red mud addition on soil biogeochemistry and arsenic mobility in soil–water experiments representative of land affected by the red mud spill. XAS analysis showed that As was present in the red mud as As(V) in the form of arsenate. The remobilisation of red mud associated arsenate was highly pH dependent and the addition of phosphate to red mud suspensions greatly enhanced As release to solution. In aerobic batch experiments, where red mud was mixed with soils, As release to solution was highly dependent on pH. Carbonation of these alkaline solutions by dissolution of atmospheric CO2 reduced pH, which resulted in a decrease of aqueous As concentrations over time. However, this did not result in complete removal of aqueous As in any of the experiments. Carbonation did not occur in anaerobic experiments and pH remained high. Aqueous As concentrations initially increased in all the anaerobic red mud amended experiments, and then remained relatively constant as the systems became more reducing, both XANES and HPLC–ICP-MS showed that no As reduction processes occurred and that only As(V) species were present. These experiments show that there is the potential for increased As mobility in soil–water systems affected by red mud addition under both aerobic and anaerobic conditions

Vascular Remodeling in Health and Disease

The term vascular remodeling is commonly used to define the structural changes in blood vessel geometry that occur in response to long-term physiologic alterations in blood flow or in response to vessel wall injury brought about by trauma or underlying cardiovascular diseases.1, 2, 3, 4 The process of remodeling, which begins as an adaptive response to long-term hemodynamic alterations such as elevated shear stress or increased intravascular pressure, may eventually become maladaptive, leading to impaired vascular function. The vascular endothelium, owing to its location lining the lumen of blood vessels, plays a pivotal role in regulation of all aspects of vascular function and homeostasis.5 Thus, not surprisingly, endothelial dysfunction has been recognized as the harbinger of all major cardiovascular diseases such as hypertension, atherosclerosis, and diabetes.6, 7, 8 The endothelium elaborates a variety of substances that influence vascular tone and protect the vessel wall against inflammatory cell adhesion, thrombus formation, and vascular cell proliferation.8, 9, 10 Among the primary biologic mediators emanating from the endothelium is nitric oxide (NO) and the arachidonic acid metabolite prostacyclin [prostaglandin I2 (PGI2)], which exert powerful vasodilatory, antiadhesive, and antiproliferative effects in the vessel wall

Distinctive Expression of Chemokines and Transforming Growth Factor-β Signaling in Human Arterial Endothelium during Atherosclerosis

Knowledge about the in vivo role of endothelium in chronic human atherosclerosis has mostly been derived by insights from mouse models. Therefore, we set out to establish by microarray analyses the gene expression profiles of endothelium from human large arteries, as isolated by laser microbeam microdissection, having focal atherosclerosis of the early or the advanced stage. Within individual arteries, the endothelial transcriptomes of the lesional and unaffected sides were compared pairwise, thus limiting genetic and environmental confounders. Specific endothelial signature gene sets were identified with changed expression levels in either early (n = 718) or advanced atherosclerosis (n = 403), relative to their paired plaque-free controls. Gene set enrichment analysis identified distinct sets of chemokines and differential enrichments of nuclear factor-κB-, p53-, and transforming growth factor-β-related genes in advanced plaques. Immunohistochemistry validated the discriminative value of corresponding endothelial protein expression between early (fractalkine/CX3CL1, IP10/CCL10, TBX18) or advanced (BAX, NFKB2) stages of atherosclerosis and versus their plaque-free controls. The functional involvement of transforming growth factor-β signaling in directing its downstream gene repertoire was substantiated by a consistent detection of activated SMAD2 in advanced lesions. Thus, we identified truly common, local molecular denominators of pathological changes to vascular endothelium, with a marked distinction of endothelial phenotype between early and advanced plaques