We develop an improved treatment of the surface ocean in the GEOS-Chem global 3-D biogeochemical model for mercury (Hg). We replace the globally uniform subsurface ocean Hg concentrations used in the original model with basin-specific values based on measurements. Updated chemical mechanisms for Hg 0 /Hg II redox reactions in the surface ocean include both photochemical and biological processes, and we improved the parametrization of particle-associated Hg scavenging. Modeled aqueous Hg concentrations are consistent with limited surface water observations. Results more accurately reproduce high-observed MBL concentrations over the North Atlantic (NA) and the associated seasonal trends. High seasonal evasion in the NA is driven by inputs from Hg enriched subsurface waters through entrainment and Ekman pumping. Globally, subsurface waters account for 40% of Hg inputs to the ocean mixed layer, and 60% is from atmospheric deposition. Although globally the ocean is a net sink for 3.8 Mmol Hg y -1 , the NA is a net source to the atmosphere, potentially due to enrichment of subsurface waters with legacy Hg from historical anthropogenic sources. IntroductionAnthropogenic mercury (Hg) sources have enriched atmospheric Hg deposition globally by at least a factor of 3 (1).Atmospheric Hg is predominantly the gaseous elemental form (Hg 0 ), and is oxidized to Hg II , which is then rapidly deposited. It is estimated that more than 80% of the Hg deposited to oceans is reemitted to the atmosphere as Hg 0 , driving the cycle of Hg through biogeochemical reservoirs (2). Aqueous reduction of divalent inorganic mercury (Hg II ) and subsequent loss of Hg 0 reduces the potentially bioavailable Hg II pool that may be converted to monomethylmercury, the most toxic species that poses health risks to fish consuming populations and wildlife (3).Previous efforts to model Hg air-sea exchange (2) and atmospheric transport (4-6) have been unable to reproduce high atmospheric concentrations observed in the Northern Hemisphere marine boundary layer (MBL) during ocean cruises (7-9). We hypothesize that this results from subsurface seawater Hg enrichment, reflecting the legacy of past anthropogenic inputs and controlling Northern Hemisphere MBL concentrations. Previous research comparing preindustrial and contemporary Hg budgets for different ocean basins indicates that anthropogenic enrichment of Hg reservoirs in the Atlantic Ocean and Mediterranean Sea is >50% (3). Other regions such as deep waters of the Pacific Ocean have seen negligible anthropogenic impacts while Hg concentrations in intermediate waters of the North Pacific (NP) appear to be increasing (10). These gradients in subsurface Hg across ocean regions (11, 12) have not been represented in models simulating atmospheric Hg. Here we investigate the potential effects of legacy anthropogenic Hg accumulation on oceanic air-sea exchange in the GEOSChem global model (1) by including the effects of variability in subsurface ocean concentrations in our simulation.Most marine surface waters...

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BACKGROUNDIntravenous fluids are recommended for the treatment of patients who are in septic shock, but higher fluid volumes have been associated with harm in patients who are in the intensive care unit (ICU). METHODSIn this international, randomized trial, we assigned patients with septic shock in the ICU who had received at least 1 liter of intravenous fluid to receive restricted intravenous fluid or standard intravenous fluid therapy; patients were included if the onset of shock had been within 12 hours before screening. The primary outcome was death from any cause within 90 days after randomization. RESULTSWe enrolled 1554 patients; 770 were assigned to the restrictive-fluid group and 784 to the standard-fluid group. Primary outcome data were available for 1545 patients (99.4%). In the ICU, the restrictive-fluid group received a median of 1798 ml of intravenous fluid (interquartile range, 500 to 4366); the standard-fluid group received a median of 3811 ml (interquartile range, 1861 to 6762). At 90 days, death had occurred in 323 of 764 patients (42.3%) in the restrictive-fluid group, as compared with 329 of 781 patients (42.1%) in the standard-fluid group (adjusted absolute difference, 0.1 percentage points; 95% confidence interval [CI], −4.7 to 4.9; P = 0.96). In the ICU, serious adverse events occurred at least once in 221 of 751 patients (29.4%) in the restrictive-fluid group and in 238 of 772 patients (30.8%) in the standard-fluid group (adjusted absolute difference, −1.7 percentage points; 99% CI, −7.7 to 4.3). At 90 days after randomization, the numbers of days alive without life support and days alive and out of the hospital were similar in the two groups. CONCLUSIONSAmong adult patients with septic shock in the ICU, intravenous fluid restriction did not result in fewer deaths at 90 days than standard intravenous fluid therapy. (Funded by the Novo Nordisk Foundation and others; CLASSIC ClinicalTrials.gov number, NCT03668236.