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.
COVID-19 lockdowns cause global air pollution declines Venter, Zander S.; Aunan, Kristin; Chowdhury, Sourangsu ...
Proceedings of the National Academy of Sciences - PNAS,
08/2020, Volume:
117, Issue:
32
Journal Article
Peer reviewed
Open access
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.
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BFBNIB, NMLJ, NUK, PNG, SAZU, UL, UM, UPUK
The self-cleaning or oxidation capacity of the atmosphere is principally controlled by hydroxyl (OH) radicals in the troposphere. Hydroxyl has primary (P) and secondary (S) sources, the former mainly ...through the photodissociation of ozone, the latter through OH recycling in radical reaction chains. We used the recent Mainz Organics Mechanism (MOM) to advance volatile organic carbon (VOC) chemistry in the general circulation model EMAC (ECHAM/MESSy Atmospheric Chemistry) and show that S is larger than previously assumed. By including emissions of a large number of primary VOC, and accounting for their complete breakdown and intermediate products, MOM is mass-conserving and calculates substantially higher OH reactivity from VOC oxidation compared to predecessor models. Whereas previously P and S were found to be of similar magnitude, the present work indicates that S may be twice as large, mostly due to OH recycling in the free troposphere. Further, we find that nighttime OH formation may be significant in the polluted subtropical boundary layer in summer. With a mean OH recycling probability of about 67 %, global OH is buffered and not sensitive to perturbations by natural or anthropogenic emission changes. Complementary primary and secondary OH formation mechanisms in pristine and polluted environments in the continental and marine troposphere, connected through long-range transport of O3, can maintain stable global OH levels.
Abstract
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.
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.
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IZUM, KILJ, NUK, PILJ, PNG, SAZU, UL, UM, UPUK
Abstract
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.
Non-communicable diseases (NCDs) are fatal for more than 38 million people each year and are thus the main contributors to the global burden of disease accounting for 70% of mortality. The majority ...of these deaths are caused by cardiovascular disease (CVD). The risk of NCDs is strongly associated with exposure to environmental stressors such as pollutants in the air, noise exposure, artificial light at night, and climate change, including heat extremes, desert storms, and wildfires. In addition to the traditional risk factors for CVD such as diabetes, arterial hypertension, smoking, hypercholesterolaemia, and genetic predisposition, there is a growing body of evidence showing that physicochemical factors in the environment contribute significantly to the high NCD numbers. Furthermore, urbanization is associated with accumulation and intensification of these stressors. This comprehensive expert review will summarize the epidemiology and pathophysiology of environmental stressors with a focus on cardiovascular NCDs. We will also discuss solutions and mitigation measures to lower the impact of environmental risk factors with focus on CVD.
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Chronic exposure to fine particulate matter (PM2.5) poses a major global health risk, commonly assessed by assuming equivalent toxicity for different PM2.5 constituents. We used a ...data-informed global atmospheric model and recent exposure–response functions to calculate the health burden of ambient PM2.5 from ten source categories. We estimate 4.23 (95% confidence interval 3.0–6.14) million excess deaths annually from the exposure to ambient PM2.5. We distinguished contributions and major sources of black carbon (BC), primary organic aerosols (POA) and anthropogenic secondary organic aerosols (aSOA). These components make up to ∼20% of the total PM2.5 in South and East Asia and East Africa. We find that domestic energy use by the burning of solid biofuels is the largest contributor to ambient BC, POA and aSOA globally. Epidemiological and toxicological studies indicate that these compounds may be relatively more hazardous than other PM2.5 compounds such as soluble salts, related to their high potential to inflict oxidative stress. We performed sensitivity analyses by considering these species to be more harmful compared to other compounds in PM2.5, as suggested by their oxidative potential using a range of potential relative risks. These analyses show that domestic energy use emerges as the leading cause of excess mortality attributable to ambient PM2.5, notably in Asia and Africa. We acknowledge the uncertainties inherent in our assumed enhanced toxicity of the anthropogenic organic and BC aerosol components, which suggest the need to better understand the mechanisms and magnitude of the associated health risks and the consequences for regulatory policies. However our assessment of the importance of emissions from domestic energy use as a cause of premature mortality is robust to a range of assumptions about the magnitude of the excess risk.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
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