High-carbon wood ash biochar for mine tailings restoration: A field assessment of planted tree performance and metals uptake.

Unique properties of biochar render it appealing for revegetating and decontaminating historic, barren, and chemically complex mine tailings. Bottom ash from bioenergy facilities can contain high levels of charcoal residue, and thus qualify as a type of biochar; the wide availability of this material at low cost makes it of particular interest in the context of tailings remediation. Nevertheless, bottom ash is variable and often contains residual toxic metal/loids that could be phytoabsorbed into plant tissues. We implemented a replicated field trial on historic contaminated metal mine tailings in Northern Ontario (Canada) over a range of high­carbon wood ash biochar (HCWAB) dosages (0-30 t/ha) to evaluate tree and substrate responses. Sapling survivorship and aboveground biomass growth were quantified over a 4-year period; substrate chemical parameters were measured using acid-digestion and ICP-MS, as well as ion exchange resin probes. To assess elemental composition of sapling tissues, we used electron probe microanalysis combined with laser-ablation inductively coupled plasma mass spectrometry (LA-ICP-MS) on intact samples across the range of dosages applied. Survival and growth of saplings peaked at mid-range ash dosages of 3-6 t/ha. Similarly, substrate ion availability of P, K, and Zn were stable at lower dosages, but increased above 6 t/ha. The trace amounts of toxic metal/loids of concern measured in wood ash (As, Cd, Cu, and Pb) did not result in significantly increased sapling tissue concentrations at low to moderate dosages, but in some cases tissue contaminant levels were elevated at the highest dosage examined (30 t/ha). Our findings highlight the potential for high­carbon wood ash biochar to be used for metal mine restoration at low to moderate dosages.

Prehospital and Emergency Management.

Burn care in the prehospital and emergency settings requires rapid assessment of airway, breathing, and circulation. Intubation (if indicated) and fluid resuscitation are most important in emergency burn care. Total body surface area burned and depth of burn are important early assessments that help guide resuscitation and disposition. Burn care in the emergency department further includes carbon monoxide and cyanide toxicity evaluation and management.

Zinc deficiency induces hypertension by promoting renal Na+ reabsorption.

Zn2+ deficiency (ZnD) is a common comorbidity of many chronic diseases. In these settings, ZnD exacerbates hypertension. Whether ZnD alone is sufficient to alter blood pressure (BP) is unknown. To explore the role of Zn2+ in BP regulation, adult mice were fed a Zn2+-adequate (ZnA) or a Zn2+-deficient (ZnD) diet. A subset of ZnD mice were either returned to the ZnA diet or treated with hydrochlorothiazide (HCTZ), a Na+-Cl- cotransporter (NCC) inhibitor. To reduce intracellular Zn2+ in vitro, mouse distal convoluted tubule cells were cultured in N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine (TPEN, a Zn2+ chelator)- or vehicle (DMSO)-containing medium. To replete intracellular Zn2+, TPEN-exposed cells were then cultured in Zn2+-supplemented medium. ZnD promoted a biphasic BP response, characterized by episodes of high BP. BP increases were accompanied by reduced renal Na+ excretion and NCC upregulation. These effects were reversed in Zn2+-replete mice. Likewise, HCTZ stimulated natriuresis and reversed BP increases. In vitro, Zn2+ depletion increased NCC expression. Furthermore, TPEN promoted NCC surface localization and Na+ uptake activity. Zn2+ repletion reversed TPEN effects on NCC. These data indicate that 1) Zn2+ contributes to BP regulation via modulation of renal Na+ transport, 2) renal NCC mediates ZnD-induced hypertension, and 3) NCC is a Zn2+-regulated transporter that is upregulated with ZnD. This study links dysregulated renal Na+ handling to ZnD-induced hypertension. Furthermore, NCC is identified as a novel mechanism by which Zn2+ regulates BP. Understanding the mechanisms of ZnD-induced BP dysregulation may have an important therapeutic impact on hypertension.