Health effects of carbonaceous PM2.5 compounds from residential fuel combustion and road transport in Europe.

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.

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.

Air pollution deaths attributable to fossil fuels: observational and modelling study.

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.

Global organic and inorganic aerosol hygroscopicity and its effect on radiative forcing.

The climate effects of atmospheric aerosol particles serving as cloud condensation nuclei (CCN) depend on chemical composition and hygroscopicity, which are highly variable on spatial and temporal scales. Here we present global CCN measurements, covering diverse environments from pristine to highly polluted conditions. We show that the effective aerosol hygroscopicity, κ, can be derived accurately from the fine aerosol mass fractions of organic particulate matter (ϵorg) and inorganic ions (ϵinorg) through a linear combination, κ = ϵorg ⋅ κorg + ϵinorg ⋅ κinorg. In spite of the chemical complexity of organic matter, its hygroscopicity is well captured and represented by a global average value of κorg = 0.12 ± 0.02 with κinorg = 0.63 ± 0.01 as the corresponding value for inorganic ions. By showing that the sensitivity of global climate forcing to changes in κorg and κinorg is small, we constrain a critically important aspect of global climate modelling.

A global review of the state of the evidence of household air pollution's contribution to ambient fine particulate matter and their related health impacts.

Direct exposure to household fine particulate air pollution (HAP) associated with inefficient combustion of fuels (wood, charcoal, coal, crop residues, kerosene, etc.) for cooking, space-heating, and lighting is estimated to result in 2.3 (1.6-3.1) million premature yearly deaths globally. HAP emitted indoors escapes outdoors and is a leading source of outdoor ambient fine particulate air pollution (AAP) in low- and middle-income countries, often being a larger contributor than well-recognized sources including road transport, industry, coal-fired power plants, brick kilns, and construction dust. We review published scientific studies that model the contribution of HAP to AAP at global and major sub-regional scales. We describe strengths and limitations of the current state of knowledge on HAP's contribution to AAP and the related impact on public health and provide recommendations to improve these estimates. We find that HAP is a dominant source of ambient fine particulate matter (PM2.5) globally - regardless of variations in model types, configurations, and emission inventories used - that contributes approximately 20 % of total global PM2.5 exposure. There are large regional variations: in South Asia, HAP contributes âˆ¼ 30 % of ambient PM2.5, while in high-income North America the fraction is âˆ¼ 7 %. The median estimate indicates that the household contribution to ambient air pollution results in a substantial premature mortality burden globally of about 0.77(0.54-1) million excess deaths, in addition to the 2.3 (1.6-3.1) million deaths from direct HAP exposure. Coordinated global action is required to avert this burden.

Synergistic HNO3-H2SO4-NH3 upper tropospheric particle formation.

New particle formation in the upper free troposphere is a major global source of cloud condensation nuclei (CCN)1-4. However, the precursor vapours that drive the process are not well understood. With experiments performed under upper tropospheric conditions in the CERN CLOUD chamber, we show that nitric acid, sulfuric acid and ammonia form particles synergistically, at rates that are orders of magnitude faster than those from any two of the three components. The importance of this mechanism depends on the availability of ammonia, which was previously thought to be efficiently scavenged by cloud droplets during convection. However, surprisingly high concentrations of ammonia and ammonium nitrate have recently been observed in the upper troposphere over the Asian monsoon region5,6. Once particles have formed, co-condensation of ammonia and abundant nitric acid alone is sufficient to drive rapid growth to CCN sizes with only trace sulfate. Moreover, our measurements show that these CCN are also highly efficient ice nucleating particles-comparable to desert dust. Our model simulations confirm that ammonia is efficiently convected aloft during the Asian monsoon, driving rapid, multi-acid HNO3-H2SO4-NH3 nucleation in the upper troposphere and producing ice nucleating particles that spread across the mid-latitude Northern Hemisphere.

Global health burden of ambient PM2.5 and the contribution of anthropogenic black carbon and organic aerosols.

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.

Spatial Distribution of PM2.5-Related Premature Mortality in China.

PM2.5 is a major component of air pollution in China and has a serious threat to public health. It is very important to quantify spatial characteristics of the health effects caused by outdoor PM2.5 exposure. This study analyzed the spatial distribution of PM2.5 concentration (45.9 µg/m3 national average in 2016) and premature mortality attributed to PM2.5 in cities at the prefectural level and above in China in 2016. Using the Global Exposure Mortality Model (GEMM), the total premature mortality in China was estimated to be 1.55 million persons, and the per capita mortality was 11.2 per 10,000 persons in the year 2016, resulting in higher estimates compared to the integrated exposure-response model. We assessed the premature mortality attributed to PM2.5 through common diseases, including ischemic heart disease (IHD), cerebrovascular disease (CEV), chronic obstructive pulmonary disease (COPD), lung cancer (LC), and lower respiratory infections (LRI). The premature mortality due to IHD and CEV accounted for 68.5% of the total mortality, and the per capita mortality (per 10,000 persons) for all ages due to IHD was 3.86, the highest among diseases. For the spatial distribution of disease-specific premature mortality, the top two highest absolute numbers of premature mortality associated with IHD, CEV, LC, and LRI, respectively, were found in Chongqing and Beijing. In 338 cities of China, we have found a significant positive spatial autocorrelation of per capita premature mortality, indicating the necessity of coordinated regional governance for an efficient control of PM2.5.

Regional and global contributions of air pollution to risk of death from COVID-19.

AIMS: The risk of mortality from the coronavirus disease that emerged in 2019 (COVID-19) is increased by comorbidity from cardiovascular and pulmonary diseases. Air pollution also causes excess mortality from these conditions. Analysis of the first severe acute respiratory syndrome coronavirus (SARS-CoV-1) outcomes in 2003, and preliminary investigations of those for SARS-CoV-2 since 2019, provide evidence that the incidence and severity are related to ambient air pollution. We estimated the fraction of COVID-19 mortality that is attributable to the long-term exposure to ambient fine particulate air pollution. METHODS AND RESULTS: We characterized global exposure to fine particulates based on satellite data, and calculated the anthropogenic fraction with an atmospheric chemistry model. The degree to which air pollution influences COVID-19 mortality was derived from epidemiological data in the USA and China. We estimate that particulate air pollution contributed ∼15% (95% confidence interval 7-33%) to COVID-19 mortality worldwide, 27% (13 - 46%) in East Asia, 19% (8-41%) in Europe, and 17% (6-39%) in North America. Globally, ∼50-60% of the attributable, anthropogenic fraction is related to fossil fuel use, up to 70-80% in Europe, West Asia, and North America. CONCLUSION: Our results suggest that air pollution is an important cofactor increasing the risk of mortality from COVID-19. This provides extra motivation for combining ambitious policies to reduce air pollution with measures to control the transmission of COVID-19.

Impact of U.S. Oil and Natural Gas Emission Increases on Surface Ozone Is Most Pronounced in the Central United States.

Observations of volatile organic compounds (VOCs) from a surface sampling network and simulation results from the EMAC (ECHAM5/MESSy for Atmospheric Chemistry) model were analyzed to assess the impact of increased emissions of VOCs and nitrogen oxides from U.S. oil and natural gas (O&NG) sources on air quality. In the first step, the VOC observations were used to optimize the magnitude and distribution of atmospheric ethane and higher-alkane VOC emissions in the model inventory for the base year 2009. Observation-based increases of the emissions of VOCs and NOx stemming from U.S. oil and natural gas (O&NG) sources during 2009-2014 were then added to the model, and a set of sensitivity runs was conducted for assessing the influence of the increased emissions on summer surface ozone levels. For the year 2014, the added O&NG emissions are predicted to affect surface ozone across a large geographical scale in the United States. These emissions are responsible for an increased number of days when the averaged 8-h ozone values exceed 70 ppb, with the highest sensitivity being in the central and midwestern United States, where most of the O&NG growth has occurred. These findings demonstrate that O&NG emissions significantly affect the air quality across most of the United States, can regionally offset reductions of ozone precursor emissions made in other sectors, and can have a determining influence on a region's ability to meet National Ambient Air Quality Standard (NAAQS) obligations for ozone.

On the widespread enhancement in fine particulate matter across the Indo-Gangetic Plain towards winter.

Fine particulate matter (PM2.5, aerodynamic diameter ≤2.5 µm) impacts the climate, reduces visibility and severely influences human health. The Indo-Gangetic Plain (IGP), home to about one-seventh of the world's total population and a hotspot of aerosol loading, observes strong enhancements in the PM2.5 concentrations towards winter. We performed high-resolution (12 km × 12 km) atmospheric chemical transport modeling (WRF-Chem) for the post-monsoon to winter transition to unravel the underlying dynamics and influences of regional emissions over the region. Model, capturing the observed variations to an extent, reveals that the spatial distribution of PM2.5 having patches of enhanced concentrations (≥100 µgm-3) during post-monsoon, evolves dramatically into a widespread enhancement across the IGP region during winter. A sensitivity simulation, supported by satellite observations of fires, shows that biomass-burning emissions over the northwest IGP play a crucial role during post-monsoon. Whereas, in contrast, towards winter, a large-scale decline in the air temperature, significantly shallower atmospheric boundary layer, and weaker winds lead to stagnant conditions (ventilation coefficient lower by a factor of ~4) thereby confining the anthropogenic influences closer to the surface. Such changes in the controlling processes from post-monsoon to winter transition profoundly affect the composition of the fine aerosols over the IGP region. The study highlights the need to critically consider the distinct meteorological processes of west-to-east IGP and changes in dominant sources from post-monsoon to winter in the formulation of future pollution mitigation policies.

Loss of life expectancy from air pollution compared to other risk factors: a worldwide perspective.

AIMS: Long-term exposure of humans to air pollution enhances the risk of cardiovascular and respiratory diseases. A novel Global Exposure Mortality Model (GEMM) has been derived from many cohort studies, providing much-improved coverage of the exposure to fine particulate matter (PM2.5). We applied the GEMM to assess excess mortality attributable to ambient air pollution on a global scale and compare to other risk factors. METHODS AND RESULTS: We used a data-informed atmospheric model to calculate worldwide exposure to PM2.5 and ozone pollution, which was combined with the GEMM to estimate disease-specific excess mortality and loss of life expectancy (LLE) in 2015. Using this model, we investigated the effects of different pollution sources, distinguishing between natural (wildfires, aeolian dust) and anthropogenic emissions, including fossil fuel use. Global excess mortality from all ambient air pollution is estimated at 8.8 (7.11-10.41) million/year, with an LLE of 2.9 (2.3-3.5) years, being a factor of two higher than earlier estimates, and exceeding that of tobacco smoking. The global mean mortality rate of about 120 per 100 000 people/year is much exceeded in East Asia (196 per 100 000/year) and Europe (133 per 100 000/year). Without fossil fuel emissions, the global mean life expectancy would increase by 1.1 (0.9-1.2) years and 1.7 (1.4-2.0) years by removing all potentially controllable anthropogenic emissions. Because aeolian dust and wildfire emission control is impracticable, significant LLE is unavoidable. CONCLUSION: Ambient air pollution is one of the main global health risks, causing significant excess mortality and LLE, especially through cardiovascular diseases. It causes an LLE that rivals that of tobacco smoking. The global mean LLE from air pollution strongly exceeds that by violence (all forms together), i.e. by an order of magnitude (LLE being 2.9 and 0.3 years, respectively).

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.

Global tropospheric effects of aromatic chemistry with the SAPRC-11 mechanism implemented in GEOS-Chem version 9-02.

The Goddard Earth Observing System with chemistry (GEOS-Chem) model has been updated with the Statewide Air Pollution Research Center version 11 (SAPRC-11) aromatics chemical mechanism, with the purpose of evaluating global and regional effects of the most abundant aromatics (benzene, toluene, xylenes) on the chemical species important for tropospheric oxidation capacity. The model evaluation based on surface and aircraft observations indicates good agreement for aromatics and ozone. A comparison between scenarios in GEOS-Chem with simplified aromatic chemistry (as in the standard setup, with no ozone formation from related peroxy radicals or recycling of NOx) and with the SAPRC-11 scheme reveals relatively slight changes in ozone, the hydroxyl radical, and nitrogen oxides on a global mean basis (1 %-4 %), although remarkable regional differences (5 %-20 %) exist near the source regions. NO x decreases over the source regions and increases in the remote troposphere, due mainly to more efficient transport of peroxyacetyl nitrate (PAN), which is increased with the SAPRC aromatic chemistry. Model ozone mixing ratios with the updated aromatic chemistry increase by up to 5 ppb (more than 10 %), especially in industrially polluted regions. The ozone change is partly due to the direct influence of aromatic oxidation products on ozone production rates, and in part to the altered spatial distribution of NOx that enhances the tropospheric ozone production efficiency. Improved representation of aromatics is important to simulate the tropospheric oxidation.

Age-dependent health risk from ambient air pollution: a modelling and data analysis of childhood mortality in middle-income and low-income countries.

BACKGROUND: WHO estimates that, in 2015, nearly 1 million children younger than 5 years died from lower respiratory tract infections (LRIs). Ambient air pollution has a major impact on mortality from LRIs, especially in combination with undernutrition and inadequate health care. We aimed to estimate mortality due to ambient air pollution in 2015, particularly in children younger than 5 years, to investigate to what extent exposure to this risk factor affects life expectancy in different parts of the world. METHODS: Applying results from a recent atmospheric chemistry-general circulation model and health statistics from the WHO Global Health Observatory, combined in integrated exposure-response functions, we updated our estimates of mortality from ambient (outdoor) air pollution. We estimated excess deaths attributable to air pollution by disease category and age group, particularly those due to ambient air pollution-induced LRIs (AAP-LRIs) in childhood. Estimates are presented as excess mortality attributable to ambient air pollution and years of life lost (YLLs). To study recent developments, we calculated our estimates for the years 2010 and 2015. FINDINGS: Overall, 4·55 million deaths (95% CI 3·41 million to 5·56 million) were attributable to air pollution in 2015, of which 727 000 deaths (573 000-865 000) were due to AAP-LRIs. We estimated that AAP-LRIs caused about 237 000 (192 000-277 000) excess child deaths in 2015. Although childhood AAP-LRIs contributed about 5% of air pollution-attributable deaths worldwide, they accounted for 18% of losses in life expectancy, equivalent to 21·5 million (17 million to 25 million) of the total 122 million YLLs due to ambient air pollution in 2015. The mortality rate from ambient air pollution was highest in Asia, whereas the per capita YLLs were highest in Africa. We estimated that in sub-Saharan Africa, ambient air pollution reduces the average life expectancy of children by 4-5 years. In Asia, all-age mortality increased by about 10% between 2010 and 2015, whereas childhood mortality from AAP-LRIs declined by nearly 30% in the same period. INTERPRETATION: Most child deaths due to AAP-LRIs occur in low-income countries in Africa and Asia. A three-pronged strategy is needed to reduce the health effects of ambient air pollution in children: aggressive reduction of air pollution levels, improvements in nutrition, and enhanced treatment of air pollution-related health outcomes. FUNDING: None.

Estimating health and economic benefits of reductions in air pollution from agriculture.

Agricultural ammonia emissions strongly contribute to fine particulate air pollution (PM2.5) with significant impacts on human health, contributing to mortality. We used model calculated emission scenarios to examine the health and economic benefits accrued by reducing agricultural emissions. We applied the "value of statistical life" metric to monetize the associated health outcomes. Our analysis indicates that a 50% reduction in agricultural emissions could prevent >200 thousand deaths per year in the 59 countries included in our study, notably in Europe, Russia, Turkey, the US, Canada and China, accompanied with economic benefits of many billions US$. In the European Union (EU) mortality could be reduced by 18% with an annual economic benefit of 89 billion US$. A theoretical complete phase-out of agricultural emissions could lead to a reduction in PM2.5 related mortality of >50% plus associated economic costs in 42 out of the 59 countries studied. Within the EU, 140 thousand deaths could be prevented per year with an associated economic benefit of about 407billionUS$/year. A cost-benefit assessment of ammonia emission abatement options for the EU indicates that the reduction of agricultural emissions generates net financial and social benefits. The monetization of the health benefits of air pollution abatement policies and the costs of implementation can help devise cost-effective air quality management strategies.

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.