The 2019 Raikoke volcanic eruption - Part 1: Dispersion model simulations and satellite retrievals of volcanic sulfur dioxide

Abstract. Volcanic eruptions can cause significant disruption to society, and numerical models are crucial for forecasting the dispersion of erupted material. Here we assess the skill and limitations of the Met Office's Numerical Atmospheric-dispersion Modelling Environment (NAME) in simulating the dispersion of the sulfur dioxide (SO2) cloud from the 21–22 June 2019 eruption of the Raikoke volcano (48.3∘ N, 153.2∘ E). The eruption emitted around 1.5±0.2 Tg of SO2, which represents the largest volcanic emission of SO2 into the stratosphere since the 2011 Nabro eruption. We simulate the temporal evolution of the volcanic SO2 cloud across the Northern Hemisphere (NH) and compare our model simulations to high-resolution SO2 measurements from the TROPOspheric Monitoring Instrument (TROPOMI) and the Infrared Atmospheric Sounding Interferometer (IASI) satellite SO2 products. We show that NAME accurately simulates the observed location and horizontal extent of the SO2 cloud during the first 2–3 weeks after the eruption but is unable, in its standard configuration, to capture the extent and precise location of the highest magnitude vertical column density (VCD) regions within the observed volcanic cloud. Using the structure–amplitude–location (SAL) score and the fractional skill score (FSS) as metrics for model skill, NAME shows skill in simulating the horizontal extent of the cloud for 12–17 d after the eruption where VCDs of SO2 (in Dobson units, DU) are above 1 DU. For SO2 VCDs above 20 DU, which are predominantly observed as small-scale features within the SO2 cloud, the model shows skill on the order of 2–4 d only. The lower skill for these high-SO2-VCD regions is partly explained by the model-simulated SO2 cloud in NAME being too diffuse compared to TROPOMI retrievals. Reducing the standard horizontal diffusion parameters used in NAME by a factor of 4 results in a slightly increased model skill during the first 5 d of the simulation, but on longer timescales the simulated SO2 cloud remains too diffuse when compared to TROPOMI measurements. The skill of NAME to simulate high SO2 VCDs and the temporal evolution of the NH-mean SO2 mass burden is dominated by the fraction of SO2 mass emitted into the lower stratosphere, which is uncertain for the 2019 Raikoke eruption. When emitting 0.9–1.1 Tg of SO2 into the lower stratosphere (11–18 km) and 0.4–0.7 Tg into the upper troposphere (8–11 km), the NAME simulations show a similar peak in SO2 mass burden to that derived from TROPOMI (1.4–1.6 Tg of SO2) with an average SO2 e-folding time of 14–15 d in the NH. Our work illustrates how the synergy between high-resolution satellite retrievals and dispersion models can identify potential limitations of dispersion models like NAME, which will ultimately help to improve dispersion modelling efforts of volcanic SO2 clouds. </jats:p

Satellite detection, long-range transport, and air quality impacts of volcanic sulfur dioxide from the 2014–2015 flood lava eruption at Bárðarbunga (Iceland)

The 2014–2015 Bárðarbunga-Veiðivötn fissure eruption at Holuhraun produced about 1.5 km3 of lava, making it the largest eruption in Iceland in more than 200 years. Over the course of the eruption, daily volcanic sulfur dioxide (SO2) emissions exceeded daily SO2 emissions from all anthropogenic sources in Europe in 2010 by at least a factor of 3. We present surface air quality observations from across Northern Europe together with satellite remote sensing data and model simulations of volcanic SO2 for September 2014. We show that volcanic SO2 was transported in the lowermost troposphere over long distances and detected by air quality monitoring stations up to 2750 km away from the source. Using retrievals from the Ozone Monitoring Instrument (OMI) and the Infrared Atmospheric Sounding Interferometer (IASI), we calculate an average daily SO2 mass burden of 99 ± 49 kilotons (kt) of SO2 from OMI and 61 ± 18 kt of SO2 from IASI for September 2014. This volcanic burden is at least a factor of 2 greater than the average SO2 mass burden between 2007 and 2009 due to anthropogenic emissions from the whole of Europe. Combining the observational data with model simulations using the United Kingdom Met Office's Numerical Atmospheric-dispersion Modelling Environment model, we are able to constrain SO2 emission rates to up to 120 kilotons per day (kt/d) during early September 2014, followed by a decrease to 20–60 kt/d between 6 and 22 September 2014, followed by a renewed increase to 60–120 kt/d until the end of September 2014. Based on these fluxes, we estimate that the eruption emitted a total of 2.0 ± 0.6 Tg of SO2 during September 2014, in good agreement with ground-based remote sensing and petrological estimates. Although satellite-derived and model-simulated vertical column densities of SO2 agree well, the model simulations are biased low by up to a factor of 8 when compared to surface observations of volcanic SO2 on 6–7 September 2014 in Ireland. These biases are mainly due to relatively small horizontal and vertical positional errors in the simulations of the volcanic plume occurring over transport distances of thousands of kilometers. Although the volcanic air pollution episodes were transient and lava-dominated volcanic eruptions are sporadic events, the observations suggest that (i) during an eruption, volcanic SO2 measurements should be assimilated for near real-time air quality forecasting and (ii) existing air quality monitoring networks should be retained or extended to monitor SO2 and other volcanic pollutants

Blockade of IL-33 release and suppression of type 2 innate lymphoid cell responses by helminth secreted products in airway allergy

Helminth parasites such as the nematode Heligmosomoides polygyrus strongly inhibit T helper type 2 (Th2) allergy, as well as colitis and autoimmunity. Here, we show that the soluble excretory/secretory products of H. polygyrus (HES) potently suppress inflammation induced by allergens from the common fungus Alternaria alternata. Alternaria extract, when administered to mice intranasally with ovalbumin (OVA) protein, induces a rapid (1–48 h) innate response while also priming an OVA-specific Th2 response that can be evoked 14 days later by intranasal administration of OVA alone. In this model, HES coadministration with Alternaria/OVA suppressed early IL-33 release, innate lymphoid cell (ILC) production of IL-4, IL-5, and IL-13, and localized eosinophilia. Upon OVA challenge, type 2 ILC (ILC2)/Th2 cytokine production and eosinophilia were diminished in HES-treated mice. HES administration 6 h before Alternaria blocked the allergic response, and its suppressive activity was abolished by heat treatment. Administration of recombinant IL-33 at sensitization with Alternaria/OVA/HES abrogated HES suppression of OVA-specific responses at challenge, indicating that suppression of early Alternaria-induced IL-33 release could be central to the anti-allergic effects of HES. Thus, this helminth parasite targets IL-33 production as part of its armory of suppressive effects, forestalling the development of the type 2 immune response to infection and allergic sensitization

Low-level regulatory T-cell activity is essential for functional type-2 effector immunity to expel gastrointestinal helminths

Helminth infection is frequently associated with the expansion of regulatory T cells (Tregs) and suppression of immune responses to bystander antigens. We show that infection of mice with the chronic gastrointestinal helminth Heligmosomoides polygyrus drives rapid polyclonal expansion of Foxp3(+)Helios(+)CD4(+) thymic (t)Tregs in the lamina propria and mesenteric lymph nodes while Foxp3(+)Helios(-)CD4(+) peripheral (p)Treg expand more slowly. Notably, in partially resistant BALB/c mice parasite survival positively correlates with Foxp3(+)Helios(+)CD4(+) tTreg numbers. Boosting of Foxp3(+)Helios(+)CD4(+) tTreg populations by administration of recombinant interleukin-2 (rIL-2):anti-IL-2 (IL-2C) complex increased worm persistence by diminishing type-2 responsiveness in vivo, including suppression of alternatively activated macrophage and granulomatous responses at the sites of infection. IL-2C also increased innate lymphoid cell (ILC) numbers, indicating that Treg functions dominate over ILC effects in this setting. Surprisingly, complete removal of Tregs in transgenic Foxp3-DTR mice also resulted in increased worm burdens, with "immunological chaos" evident in high levels of the pro-inflammatory cytokines IL-6 and interferon-γ. In contrast, worm clearance could be induced by anti-CD25 antibody-mediated partial depletion of early Treg, alongside increased T helper type 2 responses and without incurring pathology. These findings highlight the overarching importance of the early Treg response to infection and the non-linear association between inflammation and the prevailing Treg frequency

Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990-2015:a systematic analysis for the Global Burden of Disease Study 2015

Background Non-fatal outcomes of disease and injury increasingly detract from the ability of the world's population to live in full health, a trend largely attributable to an epidemiological transition in many countries from causes affecting children, to non-communicable diseases (NCDs) more common in adults. For the Global Burden of Diseases, Injuries, and Risk Factors Study 2015 (GBD 2015), we estimated the incidence, prevalence, and years lived with disability for diseases and injuries at the global, regional, and national scale over the period of 1990 to 2015.Methods We estimated incidence and prevalence by age, sex, cause, year, and geography with a wide range of updated and standardised analytical procedures. Improvements from GBD 2013 included the addition of new data sources, updates to literature reviews for 85 causes, and the identification and inclusion of additional studies published up to November, 2015, to expand the database used for estimation of non-fatal outcomes to 60 900 unique data sources. Prevalence and incidence by cause and sequelae were determined with DisMod-MR 2.1, an improved version of the DisMod-MR Bayesian meta-regression tool first developed for GBD 2010 and GBD 2013. For some causes, we used alternative modelling strategies where the complexity of the disease was not suited to DisMod-MR 2.1 or where incidence and prevalence needed to be determined from other data. For GBD 2015 we created a summary indicator that combines measures of income per capita, educational attainment, and fertility (the Socio-demographic Index [SDI]) and used it to compare observed patterns of health loss to the expected pattern for countries or locations with similar SDI scores.Findings We generated 9.3 billion estimates from the various combinations of prevalence, incidence, and YLDs for causes, sequelae, and impairments by age, sex, geography, and year. In 2015, two causes had acute incidences in excess of 1 billion: upper respiratory infections (17.2 billion, 95% uncertainty interval [UI] 15.4-19.2 billion) and diarrhoeal diseases (2.39 billion, 2.30-2.50 billion). Eight causes of chronic disease and injury each affected more than 10% of the world's population in 2015: permanent caries, tension-type headache, iron-deficiency anaemia, age-related and other hearing loss, migraine, genital herpes, refraction and accommodation disorders, and ascariasis. The impairment that affected the greatest number of people in 2015 was anaemia, with 2.36 billion (2.35-2.37 billion) individuals affected. The second and third leading impairments by number of individuals affected were hearing loss and vision loss, respectively. Between 2005 and 2015, there was little change in the leading causes of years lived with disability (YLDs) on a global basis. NCDs accounted for 18 of the leading 20 causes of age-standardised YLDs on a global scale. Where rates were decreasing, the rate of decrease for YLDs was slower than that of years of life lost (YLLs) for nearly every cause included in our analysis. For low SDI geographies, Group 1 causes typically accounted for 20-30% of total disability, largely attributable to nutritional deficiencies, malaria, neglected tropical diseases, HIV/AIDS, and tuberculosis. Lower back and neck pain was the leading global cause of disability in 2015 in most countries. The leading cause was sense organ disorders in 22 countries in Asia and Africa and one in central Latin America; diabetes in four countries in Oceania; HIV/AIDS in three southern sub-Saharan African countries; collective violence and legal intervention in two north African and Middle Eastern countries; iron-deficiency anaemia in Somalia and Venezuela; depression in Uganda; onchoceriasis in Liberia; and other neglected tropical diseases in the Democratic Republic of the Congo.Interpretation Ageing of the world's population is increasing the number of people living with sequelae of diseases and injuries. Shifts in the epidemiological profile driven by socioeconomic change also contribute to the continued increase in years lived with disability (YLDs) as well as the rate of increase in YLDs. Despite limitations imposed by gaps in data availability and the variable quality of the data available, the standardised and comprehensive approach of the GBD study provides opportunities to examine broad trends, compare those trends between countries or subnational geographies, benchmark against locations at similar stages of development, and gauge the strength or weakness of the estimates available. Copyright (C) The Author(s). Published by Elsevier Ltd.</p

Iron Behaving Badly: Inappropriate Iron Chelation as a Major Contributor to the Aetiology of Vascular and Other Progressive Inflammatory and Degenerative Diseases

The production of peroxide and superoxide is an inevitable consequence of aerobic metabolism, and while these particular "reactive oxygen species" (ROSs) can exhibit a number of biological effects, they are not of themselves excessively reactive and thus they are not especially damaging at physiological concentrations. However, their reactions with poorly liganded iron species can lead to the catalytic production of the very reactive and dangerous hydroxyl radical, which is exceptionally damaging, and a major cause of chronic inflammation. We review the considerable and wide-ranging evidence for the involvement of this combination of (su)peroxide and poorly liganded iron in a large number of physiological and indeed pathological processes and inflammatory disorders, especially those involving the progressive degradation of cellular and organismal performance. These diseases share a great many similarities and thus might be considered to have a common cause (i.e. iron-catalysed free radical and especially hydroxyl radical generation). The studies reviewed include those focused on a series of cardiovascular, metabolic and neurological diseases, where iron can be found at the sites of plaques and lesions, as well as studies showing the significance of iron to aging and longevity. The effective chelation of iron by natural or synthetic ligands is thus of major physiological (and potentially therapeutic) importance. As systems properties, we need to recognise that physiological observables have multiple molecular causes, and studying them in isolation leads to inconsistent patterns of apparent causality when it is the simultaneous combination of multiple factors that is responsible. This explains, for instance, the decidedly mixed effects of antioxidants that have been observed, etc...Comment: 159 pages, including 9 Figs and 2184 reference

Group 2 Innate Lymphoid Cell Proportions Are Diminished in Young Helminth Infected Children and Restored by Curative Anti-helminthic Treatment

BACKGROUND:Group 2 Innate lymphoid cells (ILC2s) are innate cells that produce the TH2 cytokines IL-5 and IL-13. The importance of these cells has recently been demonstrated in experimental models of parasitic diseases but there is a paucity of data on ILC2s in the context of human parasitic infections and in particular of the blood dwelling parasite Schistosoma haematobium. METHODOLOGY/PRINCIPAL FINDINGS:In this case-control study human peripheral blood ILC2s were analysed in relation to infection with the helminth parasite Schistosoma haematobium. Peripheral blood mononuclear cells of 36 S. haematobium infected and 36 age and sex matched uninfected children were analysed for frequencies of ILC2s identified as Lin-CD45+CD127+CD294+CD161+. ILC2s were significantly lower particularly in infected children aged 6-9 years compared to healthy participants. Curative anti-helminthic treatment resulted in an increase in levels of the activating factor TSLP and restoration of ILC2 levels. CONCLUSION:This study demonstrates that ILC2s are diminished in young helminth infected children and restored by removal of the parasites by treatment, indicating a previously undescribed association between a human parasitic infection and ILC2s and suggesting a role of ILC2s before the establishment of protective acquired immunity in human schistosomiasis