Gaseous Mercury Emissions From Soil Following Forest Loss And Land Use Changes: Field Experiments In The United States And Brazil

Forest ecosystems are a sink of atmospheric mercury, trapping the metal in the canopy, and storing it in the forest floor after litter fall. Fire liberates a portion of this mercury; however, little is known about the long-term release of mercury post deforestation. We conducted two large-scale experiments to study this phenomenon. In upstate New York, gaseous mercury emissions from soil were monitored continually using a Teflon dynamic surface flux chamber for two-weeks before and after cutting of the canopy on the edge of a deciduous forest. In Brazil, gaseous mercury emissions from soil were monitored in an intact Ombrophilous Open forest and an adjacent field site both before and after the field site was cleared by burning. In the intact forest, gaseous mercury emissions from soil averaged-0.73±1.84ngm-2h-1 (24-h monitoring) at the New York site, and 0.33±0.09ngm-2h-1 (daytime-only) at the Brazil site. After deforestation, gaseous mercury emissions from soil averaged 9.13±2.08ngm-2h-1 in New York and 21.2±0.35ngm-2h-1 at the Brazil site prior to burning. Gaseous mercury emissions averaged 74.9±0.73ngm-2h-1 after burning of the cut forest in Brazil. Extrapolating our data, measured over several weeks to months, to a full year period, deforested soil is estimated to release an additional 2.30gha-1yr-1 of gaseous mercury to the atmosphere in the Brazilian experiment and 0.41gha-1yr-1 in the New York experiment. In Brazil, this represents an additional 50% of the mercury load released during the fire itself. © 2014 The Authors.96423429Almeida, M.D., Lacerda, L.D., Bastos, W.R., Herrmann, J.C., Mercury loss from soils following conversion from forest to pasture in RondÔnia, Western Amazon, Brazil (2005) Environ. 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COVID-19 in Adults With Congenital Heart Disease.

Adults with congenital heart disease (CHD) have been considered potentially high risk for novel coronavirus disease-19 (COVID-19) mortality or other complications. This study sought to define the impact of COVID-19 in adults with CHD and to identify risk factors associated with adverse outcomes. Adults (age 18 years or older) with CHD and with confirmed or clinically suspected COVID-19 were included from CHD centers worldwide. Data collection included anatomic diagnosis and subsequent interventions, comorbidities, medications, echocardiographic findings, presenting symptoms, course of illness, and outcomes. Predictors of death or severe infection were determined. From 58 adult CHD centers, the study included 1,044 infected patients (age: 35.1 ± 13.0 years; range 18 to 86 years; 51% women), 87% of whom had laboratory-confirmed coronavirus infection. The cohort included 118 (11%) patients with single ventricle and/or Fontan physiology, 87 (8%) patients with cyanosis, and 73 (7%) patients with pulmonary hypertension. There were 24 COVID-related deaths (case/fatality: 2.3%; 95% confidence interval: 1.4% to 3.2%). Factors associated with death included male sex, diabetes, cyanosis, pulmonary hypertension, renal insufficiency, and previous hospital admission for heart failure. Worse physiological stage was associated with mortality (p = 0.001), whereas anatomic complexity or defect group were not. COVID-19 mortality in adults with CHD is commensurate with the general population. The most vulnerable patients are those with worse physiological stage, such as cyanosis and pulmonary hypertension, whereas anatomic complexity does not appear to predict infection severity

COVID-19–Related Thrombotic and Bleeding Events in Adults With Congenital Heart Disease

Background: Altered coagulation is a striking feature of COVID-19. Adult patients with congenital heart disease (ACHD) are prone to thromboembolic (TE) and bleeding complications. Objectives: The purpose of this study was to investigate the prevalence and risk factors for COVID-19 TE/bleeding complications in ACHD patients. Methods: COVID-19-positive ACHD patients were included between May 2020 and November 2021. TE events included ischemic cerebrovascular accident, systemic and pulmonary embolism, deep venous thrombosis, myocardial infarction, and intracardiac thrombosis. Major bleeding included cases with hemoglobin drop >2 g/dl, involvement of critical sites, or fatal bleeding. Severe infection was defined as need for intensive care unit, endotracheal intubation, renal replacement therapy, extracorporeal membrane oxygenation, or death. Patients with TE/bleeding were compared to those without events. Factors associated with TE/bleeding were determined using logistic regression. Results: Of 1,988 patients (age 32 [IQR: 25-42] years, 47% male, 59 ACHD centers), 30 (1.5%) had significant TE/bleeding: 12 TE events, 12 major bleeds, and 6 with both TE and bleeding. Patients with TE/bleeding had higher in-hospital mortality compared to the remainder cohort (33% vs 1.7%; P < 0.0001) and were in more advanced physiological stage (P = 0.032) and NYHA functional class (P = 0.01), had lower baseline oxygen saturation (P = 0.0001), and more frequently had a history of atrial arrhythmia (P < 0.0001), previous hospitalization for heart failure (P < 0.0007), and were more likely hospitalized for COVID-19 (P < 0.0001). By multivariable logistic regression, prior anticoagulation (OR: 4.92; 95% CI: 2-11.76; P = 0.0003), cardiac injury (OR: 5.34; 95% CI: 1.98-14.76; P = 0.0009), and severe COVID-19 (OR: 17.39; 95% CI: 6.67-45.32; P < 0.0001) were independently associated with increased risk of TE/bleeding complications. Conclusions: ACHD patients with TE/bleeding during COVID-19 infection have a higher in-hospital mortality from the illness. Risk of coagulation disorders is related to severe COVID-19, cardiac injury during infection, and use of anticoagulants. © 2023 The AuthorsOpen access journalThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]