High-carbon wood ash biochar enhances native tree survival and growth on sand-capped mine tailings.

Use of waste wood biomass for bioenergy produces wood ash as a by-product; this ash is typically landfilled, but can potentially play an important role in soil improvement and forest restoration. In particular, high-carbon wood ash biochar (HCWAB) could supply nutrients, improve substrate water-holding capacity and pH, and emulate the ecosystem benefits of wildfire residues. Thickened tailings sites at metal mines across Canada are subject to stringent restoration regulations that entail planting of native trees to promote rapid reforestation. While HCWAB may prove beneficial in this context, field trials have been very limited to date. We conducted a large-scale, replicated field trial on sand-capped tailings at an operational gold mine in the Canadian boreal forest to assess the impact of HCWAB (at dosages of 0, 6.4, 12.8, and 19.1 t/ha) on survival and growth of four native tree species, as well as substrate chemical properties and element uptake in tree tissues. After 2 years, the survival of planted, native trees was highest at low to moderate application rates; HCWAB dosages above 13 t/ha presented reduced tree survival to levels comparable to unamended substrates. Tree growth was higher across all HCWAB doses relative to growth in samples planted on untreated substrates; tree species and initial size also had large impacts on final tree survival and aboveground growth. The survival of Betula papyrifera was significantly higher than other species, while smaller transplanted trees in general survived in greater numbers compared to larger size classes. Volunteer herbaceous vegetation significantly increased at the higher HCWAB application dosages and tree performance was negatively correlated with vegetation cover, consistent with a resource competition effect. HCWAB additions to sand-capped mine tailings did not significantly alter tree tissue concentrations or substrate availability of potentially toxic metals (Cd, Cu, Al). We conclude that low to moderate dosages of HCWAB on sand-capped tailings, particularly between 6.4 and 12.8 t/ha, may offer benefits to early tree survival, growth, and substrate nutrient status without causing significant risks of phytotoxicity and recommend future field trials focus on strategies to reduce tree competition with competing vegetation.

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.