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Australian mega-wildfires in the summer of 2019-2020 injected smoke into the stratosphere, causing strong ozone depletion in the lower stratosphere. Here, we model the smoke plume and reproduce its unexpected trajectory toward the middle stratosphere at ~35-kilometer altitude. We show that a smoke-charged vortex (SCV) induced and maintained by absorbing aerosols played a key role in lofting pollutants from the lower stratosphere and nearly doubled the southern hemispheric aerosol burden in the middle stratosphere. The SCV caused a redistribution of stratospheric aerosols, which boosted heterogeneous chemistry in the middle stratosphere and enhanced ozone production, compensating for up to 70% of the ozone depletion in the lower stratosphere. As global warming continues, we expect a growing frequency and importance of SCVs in promoting the impacts of wildfires on stratospheric aerosols and chemistry.
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The ongoing energy transition from conventional fuels to renewable energy sources (RES) has given nations the potential to achieve levels of energy self-sufficiency previously thought unattainable. RES in the form of utility-scale solar and wind energy are currently the leading alternatives to fossil-fuel generation. Precise location siting that factors in efficiency limitations related to current and future climate variables is essential for enabling the green energy transition envisioned for 2050. In this context, understanding and mapping the intermittency of RES provides insights to energy system operators for their seamless integration into the grid. The Eastern Mediterranean and Middle East (EMME) region has the potential to harness vast amounts of RES. The scarcity of observations from weather station networks and the lack of private sector incentives for transitioning to RES mean that relevant, supporting weather and climate studies have been limited. This study employs the Weather Research and Forecasting model with Chemistry (WRF-CHEM) to estimate the RES technical potential of EMME countries and map the hourly generation profiles per source and country, simulated for the reference year 2015 and considering future conditions. The findings indicate that by 2050, seven countries within the region could transform into net energy exporters, while the remaining nine might remain reliant on energy imports or fossil fuels. Egypt emerges as a "powerhouse", potentially enjoying a potential surplus energy generation of 76 GW per hour, whereas the United Arab Emirates may face an annual deficit of 955 TWh. Further, we derived the hourly generation profiles for wind and solar during different seasons. Four dominant patterns were identified. We find a complementary relationship for six countries, and for four countries, a substitute relationship between solar and wind energy generation. Greece stands out with a near-constant wind energy source, which would facilitate its integration into the national grid.
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Rate coefficients (k4) for the reaction of hydroxyl radicals (OH) with methyl nitrate (CH3ONO2) were measured over the temperature range 232-343 K using pulsed laser photolysis to generate OH and pulsed laser-induced fluorescence to detect it in real-time and under pseudo-first-order conditions. In order to optimize the accuracy of the rate coefficients obtained, the concentration of CH3ONO2 (the reactant in excess) was measured on-line by absorption spectroscopy at 213.86 nm for which the absorption cross-section was also measured (σ213.86 = 1.65 ± 0.09 × 10-18 cm2 molecule-1). The temperature-dependent rate coefficient is described by k4(T) = 7.5 × 10-13 exp[(-1034 ± 40)/T] cm3 molecule-1 s-1 with a room temperature rate coefficient of k4(296 ± 2 K) = (2.32 ± 0.12) × 10-14 cm3 molecule-1 s-1 where the uncertainty includes the statistical error of 2σ and an estimation of the potential systematic bias of 5%. This new dataset helps to consolidate the database for this rate coefficient and to reduce uncertainty in the atmospheric lifetime of CH3ONO2. As part of this study, an approximate rate coefficient for the reaction of H-atoms with CH3ONO2 (k9) was also derived at room temperature: k9(298 K) = (1.68 ± 0.45) × 10-13 cm3 molecule-1 s-1.
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Air pollution causes morbidity and excess mortality. In the epithelial lining fluid of the respiratory tract, air pollutants trigger a chemical reaction sequence that causes the formation of noxious hydroxyl radicals that drive oxidative stress. For hitherto unknown reasons, individuals with pre-existing inflammatory disorders are particularly susceptible to air pollution. Through detailed multiphase chemical kinetic analysis, we show that the commonly elevated concentrations of endogenous nitric oxide in diseased individuals can increase the production of hydroxyl radicals via peroxynitrite formation. Our findings offer a molecular rationale of how adverse health effects and oxidative stress caused by air pollutants may be exacerbated by inflammatory disorders.
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Contaminantes Atmosféricos , Contaminación del Aire , Humanos , Contaminantes Atmosféricos/análisis , Óxido Nítrico/análisis , Óxido Nítrico/farmacología , Material Particulado/análisis , Cinética , Estrés Oxidativo , Contaminación del Aire/análisis , Radical Hidroxilo/análisis , Radical Hidroxilo/farmacologíaRESUMEN
Exposure to fine particulate matter (PM2.5) is associated with an increased risk of morbidity and mortality. In Europe, residential fuel combustion and road transport emissions contribute significantly to PM2.5. Toxicological studies indicate that PM2.5 from these sources is relatively more hazardous, owing to its high content of black and organic carbon. Here, we study the contribution of the emissions from these sectors to long-term exposure and excess mortality in Europe. We quantified the impact of anthropogenic carbonaceous aerosols on excess mortality and performed a sensitivity analysis assuming that they are twice as toxic as inorganic particles. We find that total PM2.5 from residential combustion leads to 72,000 (95% confidence interval: 48,000-99,000) excess deaths per year, with about 40% attributed to carbonaceous aerosols. Similarly, road transport leads to about 35,000 (CI 23,000-47,000) excess deaths per year, with 6000 (CI 4000-9000) due to carbonaceous particles. Assuming that carbonaceous aerosols are twice as toxic as other PM2.5 components, they contribute 80% and 37%, respectively, to residential fuel combustion and road transport-related deaths. We uncover robust national variations in the contribution of each sector to excess mortality and emphasize the importance of country-specific emission reduction policies based on national characteristics and sectoral shares.
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Contaminantes Atmosféricos , Contaminación del Aire , Aerosoles/análisis , Aerosoles/toxicidad , Contaminantes Atmosféricos/análisis , Contaminantes Atmosféricos/toxicidad , Contaminación del Aire/efectos adversos , Contaminación del Aire/análisis , Carbono/análisis , Carbono/toxicidad , Monitoreo del Ambiente , Europa (Continente) , Material Particulado/análisis , Material Particulado/toxicidadRESUMEN
OBJECTIVES: To estimate all cause and cause specific deaths that are attributable to fossil fuel related air pollution and to assess potential health benefits from policies that replace fossil fuels with clean, renewable energy sources. DESIGN: Observational and modelling study. METHODS: An updated atmospheric composition model, a newly developed relative risk model, and satellite based data were used to determine exposure to ambient air pollution, estimate all cause and disease specific mortality, and attribute them to emission categories. DATA SOURCES: Data from the global burden of disease 2019 study, observational fine particulate matter and population data from National Aeronautics and Space Administration (NASA) satellites, and atmospheric chemistry, aerosol, and relative risk modelling for 2019. RESULTS: Globally, all cause excess deaths due to fine particulate and ozone air pollution are estimated at 8.34 million (95% confidence interval 5.63 to 11.19) deaths per year. Most (52%) of the mortality burden is related to cardiometabolic conditions, particularly ischaemic heart disease (30%). Stroke and chronic obstructive pulmonary disease both account for 16% of mortality burden. About 20% of all cause mortality is undefined, with arterial hypertension and neurodegenerative diseases possibly implicated. An estimated 5.13 million (3.63 to 6.32) excess deaths per year globally are attributable to ambient air pollution from fossil fuel use and therefore could potentially be avoided by phasing out fossil fuels. This figure corresponds to 82% of the maximum number of air pollution deaths that could be averted by controlling all anthropogenic emissions. Smaller reductions, rather than a complete phase-out, indicate that the responses are not strongly non-linear. Reductions in emission related to fossil fuels at all levels of air pollution can decrease the number of attributable deaths substantially. Estimates of avoidable excess deaths are markedly higher in this study than most previous studies for these reasons: the new relative risk model has implications for high income (largely fossil fuel intensive) countries and for low and middle income countries where the use of fossil fuels is increasing; this study accounts for all cause mortality in addition to disease specific mortality; and the large reduction in air pollution from a fossil fuel phase-out can greatly reduce exposure. CONCLUSION: Phasing out fossil fuels is deemed to be an effective intervention to improve health and save lives as part the United Nations' goal of climate neutrality by 2050. Ambient air pollution would no longer be a leading, environmental health risk factor if the use of fossil fuels were superseded by equitable access to clean sources of renewable energy.
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Contaminantes Atmosféricos , Contaminación del Aire , Ozono , Humanos , Combustibles Fósiles/efectos adversos , Contaminación del Aire/efectos adversos , Contaminación del Aire/análisis , Ozono/efectos adversos , Ozono/análisis , Material Particulado/efectos adversos , Material Particulado/análisis , Renta , Contaminantes Atmosféricos/efectos adversos , Contaminantes Atmosféricos/análisisRESUMEN
The world population is aging rapidly, and by some estimates, the number of people older than 60 will double in the next 30 years. With the increase in life expectancy, adverse effects of environmental exposures start playing a more prominent role in human health. Air pollution is now widely considered the most detrimental of all environmental risk factors, with some studies estimating that almost 20% of all deaths globally could be attributed to poor air quality. Cardiovascular diseases are the leading cause of death worldwide and will continue to account for the most significant percentage of non-communicable disease burden. Cardiovascular aging with defined pathomechanisms is a major trigger of cardiovascular disease in old age. Effects of environmental risk factors on cardiovascular aging should be considered in order to increase the health span and reduce the burden of cardiovascular disease in older populations. In this review, we explore the effects of air pollution on cardiovascular aging, from the molecular mechanisms to cardiovascular manifestations of aging and, finally, the age-related cardiovascular outcomes. We also explore the distinction between the effects of air pollution on healthy aging and disease progression. Future efforts should focus on extending the health span rather than the lifespan.
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Contaminación del Aire , Enfermedades Cardiovasculares , Sistema Cardiovascular , Humanos , Anciano , Envejecimiento , LongevidadRESUMEN
BACKGROUND: Ambient air pollution is a major risk to health and wellbeing in European cities. We aimed to estimate spatial and sector-specific contributions of emissions to ambient air pollution and evaluate the effects of source-specific reductions in pollutants on mortality in European cities to support targeted source-specific actions to address air pollution and promote population health. METHODS: We conducted a health impact assessment of data from 2015 for 857 European cities to estimate source contributions to annual PM2·5 and NO2 concentrations using the Screening for High Emission Reduction Potentials for Air quality tool. We evaluated contributions from transport, industry, energy, residential, agriculture, shipping, and aviation, other, natural, and external sources. For each city and sector, three spatial levels were considered: contributions from the same city, the rest of the country, and transboundary. Mortality effects were estimated for adult populations (ie, ≥20 years) following standard comparative risk assessment methods to calculate the annual mortality preventable on spatial and sector-specific reductions in PM2·5 and NO2. FINDINGS: We observed strong variability in spatial and sectoral contributions among European cities. For PM2·5, the main contributors to mortality were the residential (mean contribution of 22·7% [SD 10·2]) and agricultural (18·0% [7·7]) sectors, followed by industry (13·8% [6·0]), transport (13·5% [5·8]), energy (10·0% [6·4]), and shipping (5·5% [5·7]). For NO2, the main contributor to mortality was transport (48·5% [SD 15·2]), with additional contributions from industry (15·0% [10·8]), energy (14·7% [12·9]), residential (10·3% [5·0]), and shipping (9·7% [12·7]). The mean city contribution to its own air pollution mortality was 13·5% (SD 9·9) for PM2·5 and 34·4% (19·6) for NO2, and contribution increased among cities of largest area (22·3% [12·2] for PM2·5 and 52·2% [19·4] for NO2) and among European capitals (29·9% [12·5] for PM2·5 and 62·7% [14·7] for NO2). INTERPRETATION: We estimated source-specific air pollution health effects at the city level. Our results show strong variability, emphasising the need for local policies and coordinated actions that consider city-level specificities in source contributions. FUNDING: Spanish Ministry of Science and Innovation, State Research Agency, Generalitat de Catalunya, Centro de Investigación Biomédica en red Epidemiología y Salud Pública, and Urban Burden of Disease Estimation for Policy Making 2023-2026 Horizon Europe project.
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Contaminación del Aire , Evaluación del Impacto en la Salud , Adulto , Humanos , Ciudades , Dióxido de Nitrógeno , Contaminación del Aire/efectos adversos , Material ParticuladoRESUMEN
The Asian tiger mosquito, Aedes albopictus, is an important vector of arboviruses that cause diseases such as dengue, chikungunya, and zika. The vector is highly invasive and adapted to survive in temperate northern territories outside its native tropical and sub-tropical range. Climate and socio-economic change are expected to facilitate its range expansion and exacerbate the global vector-borne disease burden. To project shifts in the global habitat suitability of the vector, we developed an ensemble machine learning model, incorporating a combination of a Random Forest and XGBoost binary classifiers, trained with a global collection of vector surveillance data and an extensive set of climate and environmental constraints. We demonstrate the reliable performance and wide applicability of the ensemble model in comparison to the known global presence of the vector, and project that suitable habitats will expand globally, most significantly in the northern hemisphere, putting at least an additional billion people at risk of vector-borne diseases by the middle of the 21st century. We project several highly populated areas of the world will be suitable for Ae. albopictus populations, such as the northern parts of the USA, Europe, and India by the end of the century, which highlights the need for coordinated preventive surveillance efforts of potential entry points by local authorities and stakeholders.
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Most research on the air pollution-related health effects of decarbonization has focused on adults. We assess the potential health benefits that could be achieved in children and young people in a global sample of 16 cities through global decarbonization actions. We modelled annual average concentrations of fine particulate matter (PM2.5) and nitrogen dioxide (NO2) at 1x1 km resolution in the cities using a general circulation/atmospheric chemistry model assuming removal of all global combustion-related emissions from land transport, industries, domestic energy use and power generation. We modelled the impact on childhood asthma incidence and adverse birth outcomes (low birthweight, pre-term births) using published exposure-response relationships. Removal of combustion emissions was estimated to decrease annual average PM2.5 by between 2.9 µg/m3 (8.4%) in Freetown and 45.4 µg/m3 (63.7%) in Dhaka. For NO2, the range was from 0.3 ppb (7.9%) in Freetown to 18.8 ppb (92.3%) in Mexico City. Estimated reductions in asthma incidence ranged from close to zero in Freetown, Tamale and Harare to 149 cases per 100,000 population in Los Angeles. For pre-term birth, modelled impacts ranged from a reduction of 135 per 100,000 births in Dar es Salaam to 2,818 per 100,000 births in Bhubaneswar and, for low birthweight, from 75 per 100,000 births in Dar es Salaam to 2,951 per 100,000 births in Dhaka. The large variations chiefly reflect differences in the magnitudes of air pollution reductions and estimated underlying disease rates. Across the 16 cities, the reduction in childhood asthma incidence represents more than one-fifth of the current burden, and an almost 10% reduction in pre-term and low birthweight births. Decarbonization actions that remove combustion-related emissions contributing to ambient PM2.5 and NO2 would likely lead to substantial but geographically-varied reductions in childhood asthma and adverse birth outcomes, though there are uncertainties in causality and the precision of estimates.
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Contaminantes Atmosféricos , Contaminación del Aire , Asma , Niño , Adulto , Humanos , Adolescente , Contaminantes Atmosféricos/análisis , Ciudades , Peso al Nacer , Dióxido de Nitrógeno/análisis , Salud Infantil , Exposición a Riesgos Ambientales/efectos adversos , Exposición a Riesgos Ambientales/análisis , Tanzanía , Bangladesh , Zimbabwe , Contaminación del Aire/análisis , Asma/etiología , Material Particulado/análisisRESUMEN
Traffic noise and air pollution are 2 major environmental health risk factors in urbanized societies that often occur together. Despite cooccurrence in urban settings, noise and air pollution have generally been studied independently, with many studies reporting a consistent effect on blood pressure for individual exposures. In the present reviews, we will discuss the epidemiology of air pollution and noise effects on arterial hypertension and cardiovascular disease (part I) and the underlying pathophysiology (part II). Both environmental stressors have been found to cause endothelial dysfunction, oxidative stress, vascular inflammation, circadian dysfunction, and activation of the autonomic nervous system, thereby facilitating the development of hypertension. We also discuss the effects of interventions, current gaps in knowledge, and future research tasks. From a societal and policy perspective, the health effects of both air pollution and traffic noise are observed well below the current guideline recommendations. To this end, an important goal for the future is to increase the acceptance of environmental risk factors as important modifiable cardiovascular risk factors, given their substantial impact on the burden of cardiovascular disease.
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Contaminantes Atmosféricos , Contaminación del Aire , Enfermedades Cardiovasculares , Hipertensión , Humanos , Enfermedades Cardiovasculares/etiología , Enfermedades Cardiovasculares/inducido químicamente , Exposición a Riesgos Ambientales/efectos adversos , Hipertensión/etiología , Hipertensión/inducido químicamente , Factores de Riesgo , Contaminación del Aire/efectos adversos , Contaminantes Atmosféricos/efectos adversos , Material Particulado/efectos adversosRESUMEN
Traffic noise and air pollution are environmental stressors found to increase risk for cardiovascular events. The burden of disease attributable to environmental stressors and cardiovascular disease globally is substantial, with a need to better understand the contribution of specific risk factors that may underlie these effects. Epidemiological observations and experimental evidence from animal models and human controlled exposure studies suggest an essential role for common mediating pathways. These include sympathovagal imbalance, endothelial dysfunction, vascular inflammation, increased circulating cytokines, activation of central stress responses, including hypothalamic and limbic pathways, and circadian disruption. Evidence also suggests that cessation of air pollution or noise through directed interventions alleviates increases in blood pressure and intermediate surrogate pathways, supporting a causal link. In the second part of this review, we discuss the current understanding of mechanisms underlying and current gaps in knowledge and opportunities for new research.
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Contaminantes Atmosféricos , Contaminación del Aire , Enfermedades Cardiovasculares , Hipertensión , Animales , Humanos , Exposición a Riesgos Ambientales/efectos adversos , Hipertensión/etiología , Hipertensión/inducido químicamente , Factores de Riesgo , Enfermedades Cardiovasculares/etiología , Enfermedades Cardiovasculares/inducido químicamente , Contaminación del Aire/efectos adversos , Contaminantes Atmosféricos/efectos adversos , Material Particulado/efectos adversosRESUMEN
Atmospheric ozone and oxygen protect the terrestrial biosphere against harmful ultraviolet (UV) radiation. Here, we model atmospheres of Earth-like planets hosted by stars with near-solar effective temperatures (5300 to 6300 K) and a broad range of metallicities covering known exoplanet host stars. We show that paradoxically, although metal-rich stars emit substantially less ultraviolet radiation than metal-poor stars, the surface of their planets is exposed to more intense ultraviolet radiation. For the stellar types considered, metallicity has a larger impact than stellar temperature. During the evolution of the universe, newly formed stars have progressively become more metal-rich, exposing organisms to increasingly intense ultraviolet radiation. Our findings imply that planets hosted by stars with low metallicity are the best targets to search for complex life on land.
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BACKGROUND: The Middle East and North Africa (MENA) is one of the regions that is most vulnerable to the negative effects of climate change, yet the potential public health impacts have been underexplored compared to other regions. We aimed to examine one aspect of these impacts, heat-related mortality, by quantifying the current and future burden in the MENA region and identifying the most vulnerable countries. METHODS: We did a health impact assessment using an ensemble of bias-adjusted statistically downscaled Coupled Model Intercomparison Project phase 6 (CMIP6) data based on four Shared Socioeconomic Pathway (SSP) scenarios (SSP1-2·6 [consistent with a 2°C global warming scenario], SSP2-4·5 [medium pathway scenario], SSP3-7·0 [pessimistic scenario], and SSP5-8·5 [high emissions scenario]) and Bayesian inference methods. Assessments were based on apparent temperature-mortality relationships specific to each climate subregion of MENA based on Koppen-Geiger climate type classification, and unique thresholds were characterised for each 50 km grid cell in the region. Future annual heat-related mortality was estimated for the period 2021-2100. Estimates were also presented with population held constant to quantify the contribution of projected demographic changes to the future heat-mortality burden. FINDINGS: The average annual heat-related death rate across all MENA countries is currently 2·1 per 100â000 people. Under the two high emissions scenarios (SSP3-7·0 and SSP5-8·5), most of the MENA region will have experienced substantial warming by the 2060s. Annual heat-related deaths of 123·4 per 100â000 people are projected for MENA by 2100 under a high emissions scenario (SSP5-8·5), although this rate would be reduced by more than 80% (to 20·3 heat-related deaths per 100â000 people per year) if global warming could be limited to 2°C (ie, under the SSP1-2·6 scenario). Large increases are also expected by 2100 under the SSP3-7·0 scenario (89·8 heat-related deaths per 100â000 people per year) due to the high population growth projected under this pathway. Projections in MENA are far higher than previously observed in other regions, with Iran expected to be the most vulnerable country. INTERPRETATION: Stronger climate change mitigation and adaptation policies are needed to avoid these heat-related mortality impacts. Since much of this increase will be driven by population changes, demographic policies and healthy ageing will also be key to successful adaptation. FUNDING: National Institute for Health Research, EU Horizon 2020.
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Evaluación del Impacto en la Salud , Calor , Humanos , Teorema de Bayes , Medio Oriente , África del NorteRESUMEN
BACKGROUND: A growing body of evidence suggests that air pollution exposure is associated with an increased risk for cardiovascular diseases. Data regarding the impact of long-term air pollution exposure on ischemic stroke mortality are sparse. METHODS: The German nationwide inpatient sample was used to analyse all cases of hospitalized patients with ischemic stroke in Germany 2015-2019, which were stratified according to their residency. Data of the German Federal Environmental Agency regarding average values of air pollutants were assessed from 2015 to 2019 at district-level. Data were combined and the impact of different air pollution parameters on in-hospital case-fatality was analyzed. RESULTS: Overall, 1,505,496 hospitalizations of patients with ischemic stroke (47.7% females; 67.4 % ≥70 years old) were counted in Germany 2015-2019, of whom 8.2 % died during hospitalization. When comparing patients with residency in federal districts with high vs. low long-term air pollution, enhanced levels of benzene (OR 1.082 [95%CI 1.034-1.132],P = 0.001), ozone (O3, OR 1.123 [95%CI 1.070-1.178],P < 0.001), nitric oxide (NO, OR 1.076 [95%CI 1.027-1.127],P = 0.002) and PM2.5 fine particulate matter concentrations (OR 1.126 [95%CI 1.074-1.180],P < 0.001) were significantly associated with increased case-fatality independent from age, sex, cardiovascular risk-factors, comorbidities, and revascularization treatments. Conversely, enhanced carbon monoxide, nitrogen dioxide, PM10, and sulphur dioxide (SO2) concentrations were not significantly associated with stroke mortality. However, SO2-concentrations were significantly associated with stroke-case-fatality rate of >8 % independent of residence area-type and area use (OR 1.518 [95%CI 1.012-2.278],P = 0.044). CONCLUSION: Elevated long-term air pollution levels in residential areas in Germany, notably of benzene, O3, NO, SO2, and PM2.5, were associated with increased stroke mortality of patients. RESEARCH IN CONTEXT: Evidence before this study: Besides typical, established risk factors, increasing evidence suggests that air pollution is an important and growing risk factor for stroke events, estimated to be responsible for approximately 14 % of all stroke-associated deaths. However, real-world data regarding the impact of long-term exposure to air pollution on stroke mortality are sparse. Added value of this study: The present study demonstrates that the long-term exposure to the air pollutants benzene, O3, NO, SO2 and PM2.5 are independently associated with increased case-fatality of hospitalized patients with ischemic stroke in Germany. Implications of all the available evidence: The results of our study support the urgent need to reduce the exposure to air pollution by tightening emission controls to reduce the stroke burden and stroke mortality.
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Contaminantes Atmosféricos , Contaminación del Aire , Accidente Cerebrovascular Isquémico , Femenino , Humanos , Anciano , Masculino , Benceno/análisis , Exposición a Riesgos Ambientales/efectos adversos , Exposición a Riesgos Ambientales/análisis , Contaminación del Aire/efectos adversos , Contaminación del Aire/análisis , Contaminantes Atmosféricos/efectos adversos , Contaminantes Atmosféricos/análisis , Material Particulado/efectos adversos , Material Particulado/análisis , Óxido Nítrico , HospitalesRESUMEN
Meteorological station measurements are an important source of information for understanding the weather and its association with risk, and are vital in quantifying climate change. However, such data tend to lack spatial coverage and are often plagued with flaws such as erroneous outliers and missing values. Alternative meteorological data exist in the form of climate model output that have better spatial coverage, at the expense of bias. We propose a probabilistic framework to integrate temperature measurements with climate model (reanalysis) data, in a way that allows for biases and erroneous outliers, while enabling prediction at any spatial resolution. The approach is Bayesian which facilitates uncertainty quantification and simulation based inference, as illustrated by application to two countries from the Middle East and North Africa region, an important climate change hotspot. We demonstrate the use of the model in: identifying outliers, imputing missing values, non-linear bias correction, downscaling and aggregation to any given spatial configuration.
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Modelos Climáticos , Temperatura , Teorema de Bayes , Simulación por Computador , Análisis EspacialRESUMEN
Worldwide, up to 8.8 million excess deaths/year have been attributed to air pollution, mainly due to the exposure to fine particulate matter (PM). Traffic-related noise is an additional contributor to global mortality and morbidity. Both health risk factors substantially contribute to cardiovascular, metabolic and neuropsychiatric sequelae. Studies on the combined exposure are rare and urgently needed because of frequent co-occurrence of both risk factors in urban and industrial settings. To study the synergistic effects of PM and noise, we used an exposure system equipped with aerosol generator and loud-speakers, where C57BL/6 mice were acutely exposed for 3d to either ambient PM (NIST particles) and/or noise (aircraft landing and take-off events). The combination of both stressors caused endothelial dysfunction, increased blood pressure, oxidative stress and inflammation. An additive impairment of endothelial function was observed in isolated aortic rings and even more pronounced in cerebral and retinal arterioles. The increase in oxidative stress and inflammation markers together with RNA sequencing data indicate that noise particularly affects the brain and PM the lungs. The combination of both stressors has additive adverse effects on the cardiovascular system that are based on PM-induced systemic inflammation and noise-triggered stress hormone signaling. We demonstrate an additive upregulation of ACE-2 in the lung, suggesting that there may be an increased vulnerability to COVID-19 infection. The data warrant further mechanistic studies to characterize the propagation of primary target tissue damage (lung, brain) to remote organs such as aorta and heart by combined noise and PM exposure.
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COVID-19 , Sistema Cardiovascular , Ratones , Animales , Material Particulado/efectos adversos , Ratones Endogámicos C57BL , Inflamación/inducido químicamente , Estrés Oxidativo , AeronavesRESUMEN
High levels of fine particulate matter (PM2.5) pose a severe air pollution challenge in China. Both land use changes and anthropogenic emissions can affect PM2.5 concentrations. Only a few studies have addressed the long-term impact of land surface changes on PM2.5 in China. We conducted a comprehensive analysis of PM2.5 trends over China using the Modern-Era Retrospective Analysis for Research and Applications, version 2 (MERRA-2) during 1980-2020. The monthly mean PM2.5 concentrations of MERRA-2 were evaluated across mainland China against independent surface measurements from 2013 to 2020, showing a good agreement. For the trend analysis, China was subdivided into six regions based on land use and ambient aerosols types. Our results indicate an overall significant PM2.5 increase over China during 1980-2020 with major changes in-between. Notwithstanding continued urbanization and associated anthropogenic activities, the PM2.5 reversed to a downward trend around 2007 over most regions except for the part of China that is most affected by desert dust. Statistical analysis suggests that PM2.5 trends during 1980-2010 were associated with urban expansion and deforestation over eastern and southern China. The trend reversal around 2007 is mainly attributed to Chinese air pollution control measures. A multiple linear regression analysis reveals that PM2.5 variability is linked to soil moisture and vegetation. Our results suggest that land use and land cover changes as well as pollution controls strongly influenced PM2.5 trends and that drought conditions affect PM2.5 particularly over desert and forest regions of China. This work contributes to a better understanding of the changes in PM2.5 over China.
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Contaminantes Atmosféricos , Contaminación del Aire , Material Particulado/análisis , Contaminantes Atmosféricos/análisis , Estudios Retrospectivos , Monitoreo del Ambiente/métodos , Contaminación del Aire/análisis , China , PolíticasRESUMEN
Human health is linked to climatic factors in complex ways, and climate change can have profound direct and indirect impacts on the health status of any given region. Susceptibility to climate change is modulated by biological, ecological and socio-political factors such as age, gender, geographic location, socio-economic status, occupation, health status and housing conditions, among other. In the Eastern Mediterranean and Middle East (EMME), climatic factors known to affect human health include extreme heat, water shortages and air pollution. Furthermore, the epidemiology of vector-borne diseases (VBDs) and the health consequences of population displacement are also influenced by climate change in this region. To inform future policies for adaptation and mitigation measures, and based on an extensive review of the available knowledge, we recommend several research priorities for the region. These include the generation of more empirical evidence on exposure-response functions involving climate change and specific health outcomes, the development of appropriate methodologies to evaluate the physical and psychological effects of climate change on vulnerable populations, determining how climate change alters the ecological determinants of human health, improving our understanding of the effects of long-term exposure to heat stress and air pollution, and evaluating the interactions between adaptation and mitigation strategies. Because national boundaries do not limit most climate-related factors expected to impact human health, we propose that adaptation/mitigation policies must have a regional scope, and therefore require collaborative efforts among EMME nations. Policy suggestions include a decisive region-wide decarbonisation, the integration of environmentally driven morbidity and mortality data throughout the region, advancing the development and widespread use of affordable technologies for the production and management of drinking water by non-traditional means, the development of comprehensive strategies to improve the health status of displaced populations, and fostering regional networks for monitoring and controlling the spread of infectious diseases and disease vectors.