Constraining Present-Day Anthropogenic Total Iron Emissions Using Model and Observations

Iron emissions from human activities, such as oil combustion and smelting, affect the Earth's climate and marine ecosystems. These emissions are difficult to quantify accurately due to a lack of observations, particularly in remote ocean regions. In this study, we used long-term, near-source observations in areas with a dominance of anthropogenic iron emissions in various parts of the world to better estimate the total amount of anthropogenic iron emissions. We also used a statistical source apportionment method to identify the anthropogenic components and their sub-sources from bulk aerosol observations in the United States. We find that the estimates of anthropogenic iron emissions are within a factor of 3 in most regions compared to previous inventory estimates. Under- or overestimation varied by region and depended on the number of sites, interannual variability, and the statistical filter choice. Smelting-related iron emissions are overestimated by a factor of 1.5 in East Asia compared to previous estimates. More long-term iron observations and the consideration of the influence of dust and wildfires could help reduce the uncertainty in anthropogenic iron emissions estimates.Human activities, such as smelting and oil combustion, release smoke and particles into the atmosphere. These particles often contain iron, which not only absorbs sunlight, contributing to atmospheric warming, but also serves as a nutrient for phytoplankton in various ocean regions. However, the precise extent of human-induced iron emissions remains uncertain due to a lack of comprehensive monitoring data. In this study, we leverage a global data set of iron observations to refine our estimates of iron emissions attributed to human activities. Additionally, we examine other co-released substances, such as carbon and nickel, to identify specific emission sources of iron. We employ statistical techniques to distinguish human-caused iron emissions from those originating from natural sources like dust and wildfires. Moreover, we utilize iron oxide observations to constrain emissions originating from East Asia and Norway, which are estimated to originate largely from smelting emissions. Through the analysis of long-term data sets, we provide lower and upper bounds to human-caused iron emissions. Furthermore, we investigate the impact of reduced observation numbers and a sparse network on the range of estimated iron emissions. Our findings highlight the critical role of observation quality in accurately assessing iron emissions from human activities.Anthropogenic total iron emissions are constrained to a factor of 3 in most global regions using long-term aerosol observations The number of sites, interannual variability, and site selection filter can affect the model-observation comparison uncertainty by 15%-50% Smelting-related emissions are constrained to a factor of 1.5 using iron oxide observations from East Asi

Effect of angiotensin-converting enzyme inhibitor and angiotensin receptor blocker initiation on organ support-free days in patients hospitalized with COVID-19

IMPORTANCE Overactivation of the renin-angiotensin system (RAS) may contribute to poor clinical outcomes in patients with COVID-19. Objective To determine whether angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) initiation improves outcomes in patients hospitalized for COVID-19. DESIGN, SETTING, AND PARTICIPANTS In an ongoing, adaptive platform randomized clinical trial, 721 critically ill and 58 non–critically ill hospitalized adults were randomized to receive an RAS inhibitor or control between March 16, 2021, and February 25, 2022, at 69 sites in 7 countries (final follow-up on June 1, 2022). INTERVENTIONS Patients were randomized to receive open-label initiation of an ACE inhibitor (n = 257), ARB (n = 248), ARB in combination with DMX-200 (a chemokine receptor-2 inhibitor; n = 10), or no RAS inhibitor (control; n = 264) for up to 10 days. MAIN OUTCOMES AND MEASURES The primary outcome was organ support–free days, a composite of hospital survival and days alive without cardiovascular or respiratory organ support through 21 days. The primary analysis was a bayesian cumulative logistic model. Odds ratios (ORs) greater than 1 represent improved outcomes. RESULTS On February 25, 2022, enrollment was discontinued due to safety concerns. Among 679 critically ill patients with available primary outcome data, the median age was 56 years and 239 participants (35.2%) were women. Median (IQR) organ support–free days among critically ill patients was 10 (–1 to 16) in the ACE inhibitor group (n = 231), 8 (–1 to 17) in the ARB group (n = 217), and 12 (0 to 17) in the control group (n = 231) (median adjusted odds ratios of 0.77 [95% bayesian credible interval, 0.58-1.06] for improvement for ACE inhibitor and 0.76 [95% credible interval, 0.56-1.05] for ARB compared with control). The posterior probabilities that ACE inhibitors and ARBs worsened organ support–free days compared with control were 94.9% and 95.4%, respectively. Hospital survival occurred in 166 of 231 critically ill participants (71.9%) in the ACE inhibitor group, 152 of 217 (70.0%) in the ARB group, and 182 of 231 (78.8%) in the control group (posterior probabilities that ACE inhibitor and ARB worsened hospital survival compared with control were 95.3% and 98.1%, respectively). CONCLUSIONS AND RELEVANCE In this trial, among critically ill adults with COVID-19, initiation of an ACE inhibitor or ARB did not improve, and likely worsened, clinical outcomes. TRIAL REGISTRATION ClinicalTrials.gov Identifier: NCT0273570