Endogenous Nitric Oxide Can Enhance Oxidative Stress Caused by Air Pollutants and Explain Higher Susceptibility of Individuals with Inflammatory Disorders.

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.

Kinetics of the reaction of OH with methyl nitrate (223-343 K).

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.

Climate change and human health in the Eastern Mediterranean and Middle East: Literature review, research priorities and policy suggestions.

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.

COVID-19 lockdowns cause global air pollution declines.

The lockdown response to coronavirus disease 2019 (COVID-19) has caused an unprecedented reduction in global economic and transport activity. We test the hypothesis that this has reduced tropospheric and ground-level air pollution concentrations, using satellite data and a network of >10,000 air quality stations. After accounting for the effects of meteorological variability, we find declines in the population-weighted concentration of ground-level nitrogen dioxide (NO2: 60% with 95% CI 48 to 72%), and fine particulate matter (PM2.5: 31%; 95% CI: 17 to 45%), with marginal increases in ozone (O3: 4%; 95% CI: -2 to 10%) in 34 countries during lockdown dates up until 15 May. Except for ozone, satellite measurements of the troposphere indicate much smaller reductions, highlighting the spatial variability of pollutant anomalies attributable to complex NOx chemistry and long-distance transport of fine particulate matter with a diameter less than 2.5 µm (PM2.5). By leveraging Google and Apple mobility data, we find empirical evidence for a link between global vehicle transportation declines and the reduction of ambient NO2 exposure. While the state of global lockdown is not sustainable, these findings allude to the potential for mitigating public health risk by reducing "business as usual" air pollutant emissions from economic activities. Explore trends here: https://nina.earthengine.app/view/lockdown-pollution.

Natural gas shortages during the "coal-to-gas" transition in China have caused a large redistribution of air pollution in 2017.

The Chinese "coal-to-gas" and "coal-to-electricity" strategies aim at reducing dispersed coal consumption and related air pollution by promoting the use of clean and low-carbon fuels in northern China. Here, we show that on top of meteorological influences, the effective emission mitigation measures achieved an average decrease of fine particulate matter (PM2.5) concentrations of ∼14% in Beijing and surrounding areas (the "2+26" pilot cities) in winter 2017 compared to the same period of 2016, where the dispersed coal control measures contributed ∼60% of the total PM2.5 reductions. However, the localized air quality improvement was accompanied by a contemporaneous ∼15% upsurge of PM2.5 concentrations over large areas in southern China. We find that the pollution transfer that resulted from a shift in emissions was of a high likelihood caused by a natural gas shortage in the south due to the coal-to-gas transition in the north. The overall shortage of natural gas greatly jeopardized the air quality benefits of the coal-to-gas strategy in winter 2017 and reflects structural challenges and potential threats in China's clean-energy transition.

Fine particulate matter (PM2.5) trends from land surface changes and air pollution policies in China during 1980-2020.

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.

Rate Coefficients for OH + NO (+N2) in the Fall-off Regime and the Impact of Water Vapor.

The termolecular, association reaction between OH and NO is a source of nitrous acid (HONO), an important atmospheric trace gas. Rate coefficients for the title reaction as recommended by evaluation panels differ substantially at the temperatures and pressures that prevail in the Earth's boundary layer where the reaction is in the fall-off regime between low- and high-pressure limiting rate coefficients. Using pulsed laser methods for generation and detection of OH, we have reinvestigated the kinetics of the title reaction at pressures of 22-743 Torr (1 Torr = 1.333 hPa) and temperatures (273, 298, and 333 K) in pure N2 and in N2-H2O bath gases. In situ optical absorption measurements were used to rule out any bias due to NO2 or HONO impurities. Our rate coefficients (k1) in N2 bath gas are parametrized in terms of low-pressure (k0) and high-pressure (k∞) rate coefficients and a fall-off parameter (FC) with k1,0N2 = 7.24 × 10-31 (T/300 K)-2.17 cm6 molecule-2 s-1, k1,∞ = 3.3 × 10-12 (T/300 K)-0.3 cm3 molecule-1 s-1, and FC = 0.53. Used with the "Troe" expression for termolecular reactions, these parameters accurately reproduce the current data in the fall-off regime and also capture literature rate coefficients at extrapolated temperatures. The presence of water vapor was found to enhance the rate coefficients of the title reaction significantly. The low-pressure limiting rate coefficient in H2O bath gas is a factor 5-6 larger than in N2, at room temperature (k1,0H2O = 4.55 × 10-30 (T/300 K)-4.85 cm6 molecule-2 s-1) indicating that H2O is much more efficient in quenching the association complex HONO* through collisional energy transfer. Based on measurements in N2-H2O mixtures, a parametrization of k1 including both N2 and H2O as third-body quenchers was derived. Neglecting the effect of H2O results, e.g., in an underestimation of k1 by >10% in the tropical boundary layer.

Heart healthy cities: genetics loads the gun but the environment pulls the trigger.

The world's population is estimated to reach 10 billion by 2050 and 75% of this population will live in cities. Two-third of the European population already live in urban areas and this proportion continues to grow. Between 60% and 80% of the global energy use is consumed by urban areas, with 70% of the greenhouse gas emissions produced within urban areas. The World Health Organization states that city planning is now recognized as a critical part of a comprehensive solution to tackle adverse health outcomes. In the present review, we address non-communicable diseases with a focus on cardiovascular disease and the urbanization process in relation to environmental risk exposures including noise, air pollution, temperature, and outdoor light. The present review reports why heat islands develop in urban areas, and how greening of cities can improve public health, and address climate concerns, sustainability, and liveability. In addition, we discuss urban planning, transport interventions, and novel technologies to assess external environmental exposures, e.g. using digital technologies, to promote heart healthy cities in the future. Lastly, we highlight new paradigms of integrative thinking such as the exposome and planetary health, challenging the one-exposure-one-health-outcome association and expand our understanding of the totality of human environmental exposures.

Air pollution declines during COVID-19 lockdowns mitigate the global health burden.

The lockdown response to COVID-19 has resulted in an unprecedented reduction in global economic activity and associated air pollutant levels, especially from a decline in land transportation. We utilized a network of >10,000 air quality stations distributed over 34 countries during lockdown dates up until 15 May 2020 to obtain lockdown related anomalies for nitrogen dioxide, ozone and particulate matter smaller than 2.5 µm in diameter (PM2.5). Pollutant anomalies were related to short-term health outcomes using empirical exposure-response functions. We estimate that there were a net total of 49,900 (11,000 to 90,000; 95% confidence interval) excess deaths and 89,000 (64,700 to 107,000) pediatric asthma emergency room visits avoided during lockdowns. In China and India alone, the PM2.5-related avoided excess mortality was 19,600 (15,300 to 24,000) and 30,500 (5700 to 68,000), respectively. While the state of COVID-19 imposed lockdown is not sustainable, these findings illustrate the potential health benefits gained by reducing "business as usual" air pollutant emissions from economic activities primarily through finding alternative transportation solutions.

[Air pollution and cardiovascular diseases]. / Luftverschmutzung und Herz-Kreislauf-Erkrankungen.

Air pollution in the environment and in households is responsible worldwide for almost 9 million preventable premature deaths per year and almost 800,000 such deaths within Europe. Air pollution therefore shortens life expectancy worldwide by almost 3 years. Smoking, a proven cardiovascular risk factor, shortens the mean life expectancy by 2.2 years. Epidemiological studies have shown that air pollution from fine and coarse particulate matter is associated with increased cardiovascular morbidity and mortality. Responsible for this are mainly cardiovascular diseases, such as coronary heart disease, heart attack, heart failure, stroke, hypertension and also diabetes, which are mainly caused or aggravated by fine particulate matter. After inhalation fine particulate matter can reach the brain directly and also reach the bloodstream via a transition process. There, the particles are absorbed by the blood vessels where they stimulate the formation of reactive oxygen species (ROS) in the vascular wall. They therefore promote the formation of atherosclerotic changes and in this way increase the cardiovascular risks, especially an increase in chronic ischemic heart disease and stroke. Recent studies also reported that in coronavirus disease 2019 (COVID-19) patients a high degree of air pollution is correlated with severe disease courses with cardiovascular complications and pulmonary diseases. This necessitates preventive measures, such as lowering of the upper limits for air pollutants. Individual measures to mitigate the health consequences of fine particulate matter are also discussed.

Perspective: cardiovascular disease and the Covid-19 pandemic.

We summarize the cardiovascular risks associated with Covid-19 pandemic, discussing the risks for both infected and non-infected patients.

Cardiovascular disease burden from ambient air pollution in Europe reassessed using novel hazard ratio functions.

AIMS: Ambient air pollution is a major health risk, leading to respiratory and cardiovascular mortality. A recent Global Exposure Mortality Model, based on an unmatched number of cohort studies in many countries, provides new hazard ratio functions, calling for re-evaluation of the disease burden. Accordingly, we estimated excess cardiovascular mortality attributed to air pollution in Europe. METHODS AND RESULTS: The new hazard ratio functions have been combined with ambient air pollution exposure data to estimate the impacts in Europe and the 28 countries of the European Union (EU-28). The annual excess mortality rate from ambient air pollution in Europe is 790 000 [95% confidence interval (95% CI) 645 000-934 000], and 659 000 (95% CI 537 000-775 000) in the EU-28. Between 40% and 80% are due to cardiovascular events, which dominate health outcomes. The upper limit includes events attributed to other non-communicable diseases, which are currently not specified. These estimates exceed recent analyses, such as the Global Burden of Disease for 2015, by more than a factor of two. We estimate that air pollution reduces the mean life expectancy in Europe by about 2.2 years with an annual, attributable per capita mortality rate in Europe of 133/100 000 per year. CONCLUSION: We provide new data based on novel hazard ratio functions suggesting that the health impacts attributable to ambient air pollution in Europe are substantially higher than previously assumed, though subject to considerable uncertainty. Our results imply that replacing fossil fuels by clean, renewable energy sources could substantially reduce the loss of life expectancy from air pollution.

Ambient Air Pollution Increases the Risk of Cerebrovascular and Neuropsychiatric Disorders through Induction of Inflammation and Oxidative Stress.

Exposure to ambient air pollution is a well-established determinant of health and disease. The Lancet Commission on pollution and health concludes that air pollution is the leading environmental cause of global disease and premature death. Indeed, there is a growing body of evidence that links air pollution not only to adverse cardiorespiratory effects but also to increased risk of cerebrovascular and neuropsychiatric disorders. Despite being a relatively new area of investigation, overall, there is mounting recent evidence showing that exposure to multiple air pollutants, in particular to fine particles, may affect the central nervous system (CNS) and brain health, thereby contributing to increased risk of stroke, dementia, Parkinson's disease, cognitive dysfunction, neurodevelopmental disorders, depression and other related conditions. The underlying molecular mechanisms of susceptibility and disease remain largely elusive. However, emerging evidence suggests inflammation and oxidative stress to be crucial factors in the pathogenesis of air pollution-induced disorders, driven by the enhanced production of proinflammatory mediators and reactive oxygen species in response to exposure to various air pollutants. From a public health perspective, mitigation measures are urgent to reduce the burden of disease and premature mortality from ambient air pollution.

Effects of gaseous and solid constituents of air pollution on endothelial function.

Ambient air pollution is a leading cause of non-communicable disease globally. The largest proportion of deaths and morbidity due to air pollution is now known to be due to cardiovascular disorders. Several particulate and gaseous air pollutants can trigger acute events (e.g. myocardial infarction, stroke, heart failure). While the mechanisms by which air pollutants cause cardiovascular events is undergoing continual refinement, the preponderant evidence support rapid effects of a diversity of pollutants including all particulate pollutants (e.g. course, fine, ultrafine particles) and gaseous pollutants such as ozone, on vascular function. Indeed alterations in endothelial function seem to be critically important in transducing signals and eventually promoting cardiovascular disorders such as hypertension, diabetes, and atherosclerosis. Here, we provide an updated overview of the impact of particulate and gaseous pollutants on endothelial function from human and animal studies. The evidence for causal mechanistic pathways from both animal and human studies that support various hypothesized general pathways and their individual and collective impact on vascular function is highlighted. We also discuss current gaps in knowledge and evidence from trials evaluating the impact of personal-level strategies to reduce exposure to fine particulate matter (PM2.5) and impact on vascular function, given the current lack of definitive randomized evidence using hard endpoints. We conclude by an exhortation for formal inclusion of air pollution as a major risk factor in societal guidelines and provision of formal recommendations to prevent adverse cardiovascular effects attributable to air pollution.

Clean air in the Anthropocene.

In atmospheric chemistry, interactions between air pollution, the biosphere and human health, often through reaction mixtures from both natural and anthropogenic sources, are of growing interest. Massive pollution emissions in the Anthropocene have transformed atmospheric composition to the extent that biogeochemical cycles, air quality and climate have changed globally and partly profoundly. It is estimated that mortality attributable to outdoor air pollution amounts to 4.33 million individuals per year, associated with 123 million years of life lost. Worldwide, air pollution is the major environmental risk factor to human health, and strict air quality standards have the potential to strongly reduce morbidity and mortality. Preserving clean air should be considered a human right, and is fundamental to many sustainable development goals of the United Nations, such as good health, climate action, sustainable cities, clean energy, and protecting life on land and in the water. It would be appropriate to adopt "clean air" as a sustainable development goal.

Aerosol Health Effects from Molecular to Global Scales.

Poor air quality is globally the largest environmental health risk. Epidemiological studies have uncovered clear relationships of gaseous pollutants and particulate matter (PM) with adverse health outcomes, including mortality by cardiovascular and respiratory diseases. Studies of health impacts by aerosols are highly multidisciplinary with a broad range of scales in space and time. We assess recent advances and future challenges regarding aerosol effects on health from molecular to global scales through epidemiological studies, field measurements, health-related properties of PM, and multiphase interactions of oxidants and PM upon respiratory deposition. Global modeling combined with epidemiological exposure-response functions indicates that ambient air pollution causes more than four million premature deaths per year. Epidemiological studies usually refer to PM mass concentrations, but some health effects may relate to specific constituents such as bioaerosols, polycyclic aromatic compounds, and transition metals. Various analytical techniques and cellular and molecular assays are applied to assess the redox activity of PM and the formation of reactive oxygen species. Multiphase chemical interactions of lung antioxidants with atmospheric pollutants are crucial to the mechanistic and molecular understanding of oxidative stress upon respiratory deposition. The role of distinct PM components in health impacts and mortality needs to be clarified by integrated research on various spatiotemporal scales for better evaluation and mitigation of aerosol effects on public health in the Anthropocene.

Implementing the US air quality standard for PM2.5 worldwide can prevent millions of premature deaths per year.

BACKGROUND: Air pollution by fine aerosol particles is among the leading causes of poor health and premature mortality worldwide. The growing awareness of this issue has led several countries to implement air pollution legislation. However, populations in large parts of the world are still exposed to high levels of ambient particulate pollution. The main aim of this work is to evaluate the potential impact of implementing current air quality standards for fine particulate matter (PM2.5) in the European Union (EU), United States (US) and other countries where PM2.5 levels are high. METHODS: We use a high-resolution global atmospheric chemistry model combined with epidemiological concentration response functions to investigate premature mortality attributable to PM2.5 in adults ≥30 years and children <5 years. We perform sensitivity studies to estimate the reductions in mortality that could be achieved if the PM2.5 air quality standards of the EU and US and other national standards would be implemented worldwide. RESULTS: We estimate the global premature mortality by PM2.5 at 3.15 million/year in 2010. China is the leading country with about 1.33 million, followed by India with 575 thousand and Pakistan with 105 thousand per year. For the 28 EU member states we estimate 173 thousand and for the United States 52 thousand premature deaths in 2010. Based on sensitivity analysis, applying worldwide the EU annual mean standard of 25 µg/m(3) for PM2.5 could reduce global premature mortality due to PM2.5 exposure by 17 %; while within the EU the effect is negligible. With the 2012 revised US standard of 12 µg/m(3) premature mortality by PM2.5 could drop by 46 % worldwide; 4 % in the US and 20 % in the EU, 69 % in China, 49 % in India and 36 % in Pakistan. These estimates take into consideration that about 22 % of the global PM2.5 related mortality cannot be avoided due to the contribution of natural PM2.5 sources, mainly airborne desert dust and PM2.5 from wild fires. CONCLUSIONS: Our results reflect the need to adopt stricter limits for annual mean PM2.5 levels globally, like the US standard of 12 µg/m(3) or an even lower limit to substantially reduce premature mortality in most of the world.