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Air pollution modeling, and problem areas in air pollution dispersion modeling were surveyed. Emission source inventory, meteorological data, and turbulent diffusion are discussed in terms of developing a dispersion model. Existing mathematical models of urban air pollution, and highway and airport models are discussed along with their limitations. Recommendations for improving modeling capabilities are included.
This Candidate Solution is based on using NASA Earth science research on atmospheric ozone and aerosols data as a means to predict and evaluate the effectiveness of photocatalytically created surfaces (building materials like glass, tile and cement) for air pollution mitigation purposes. When these surfaces are exposed to near UV light, organic molecules, like air pollutants and smog precursors, will degrade into environmentally friendly compounds. U.S. EPA (Environmental Protection Agency) is responsible for forecasting daily air quality by using the Air Quality Index (AQI) that is provided by AIRNow. EPA is partnered with AIRNow and is responsible for calculating the AQI for five major air pollutants that are regulated by the Clean Air Act. In this Solution, UV irradiance data acquired from the satellite mission Aura and the OMI Surface UV algorithm will be used to help understand both the efficacy and efficiency of the photocatalytic decomposition process these surfaces facilitate, and their ability to reduce air pollutants. Prediction models that estimate photocatalytic function do not exist. NASA UV irradiance data will enable this capability, so that air quality agencies that are run by state and local officials can develop and implement programs that utilize photocatalysis for urban air pollution control and, enable them to make effective decisions about air pollution protection programs.
An overview of our methods, findings, and takeaways for how we used Earth observations to monitor wildfire smoke and air pollution for enhanced air quality management.
Abstract According to the hypothesis of aerosol invigoration, the higher concentration of aerosols in polluted air intensifies storms. A leading theory for explaining such a relationship is warm‐phase invigoration, in which cloudy updrafts that are more polluted more readily condense water vapor onto liquid drops, thereby releasing latent heat faster, leading to higher buoyancies and higher updraft speeds. For this mechanism to work, water‐vapor supersaturations well in excess of 1% must be typical of relatively unpolluted cloudy updrafts. Here, the supersaturation is calculated from in situ observations of warm‐phase cloudy updrafts over the Amazon. Instead of values well in excess of 1%, the typical values are found to be around 0.2%. These observations imply that cleaner preindustrial air might have generated supersaturations around 1%, but those are still too low for warm‐phase invigoration to have any practically significant impact on cloud buoyancy and updraft speeds.
Fetal development is a crucial window of susceptibility in which exposure-related alterations can be induced on the molecular level, leading to potential changes in metabolism and development. The placenta serves as a gatekeeper between mother and fetus, and is in contact with environmental stressors throughout pregnancy. This makes the placenta as a temporary organ an informative non-invasive matrix suitable to investigate omics-related aberrations in association with in utero exposures such as ambient air pollution.
Highlights: • Heavy sandstorms are a major pollution source in China. • Trans-Pacific air pollution from sandstorms in China affect health in California. • Policymakers could plan for worsened air quality in California following sandstorms. China is among the greatest emitters of air pollution in the world and one concern is the effects of intercontinental air pollution traveling across the Pacific Ocean from China to the U.S. We exploit a natural experiment by observing the effects of changes in intercontinental air pollution associated with Chinese New Year, a 7-day national holiday, and sandstorms from China on air quality and morbidity in California. The timing of these events are unlikely correlated to other factors affecting air quality and health in California. Chinese New Year follows the Lunar New Year which varies each traditional calendar year while sandstorms are a naturally occurring phenomenon. We examine effects on morbidity using restricted emergency department and inpatient hospitalization data for the universe of patients with respiratory and heart disease between 2005 and 2012 in California. This is the first study to use patient-level data to examine the effects of trans-Pacific air pollution from China on morbidity in the U.S. We show that heavy sandstorms are associated with a modest increase in acute respiratory disease per capita, representing 0.5–4.6% of average weekly hospitalizations. However, we find no significant effect on morbidity in California from Chinese New Year. Results suggest that policymakers could prepare for changes in air quality following major sandstorms in China.
Poor air quality is currently responsible for large impacts on human health across the world. In addition, the air pollutants ozone (O3) and particulate matter less than 2.5 µm in diameter (PM2.5) are also radiatively active in the atmosphere and can influence Earth's climate. It is important to understand the effect of air quality and climate mitigation measures over the historical period and in different future scenarios to ascertain any impacts from air pollutants on both climate and human health. The Coupled Model Intercomparison Project Phase 6 (CMIP6) presents an opportunity to analyse the change in air pollutants simulated by the current generation of climate and Earth system models that include a representation of chemistry and aerosols (particulate matter). The shared socio-economic pathways (SSPs) used within CMIP6 encompass a wide range of trajectories in precursor emissions and climate change, allowing for an improved analysis of future changes to air pollutants. Firstly, we conduct an evaluation of the available CMIP6 models against surface observations of O3 and PM2.5. CMIP6 models consistently overestimate observed surface O3 concentrations across most regions and in most seasons by up to 16 ppb, with a large diversity in simulated values over Northern Hemisphere continental regions. Conversely, observed surface PM2.5 concentrations are consistently underestimated in CMIP6 models by up to 10 µg m−3, particularly for the Northern Hemisphere winter months, with the largest model diversity near natural emission source regions. The biases in CMIP6 models when compared to observations of O3 and PM2.5 are similar to those found in previous studies. Over the historical period (1850–2014) large increases in both surface O3 and PM2.5 are simulated by the CMIP6 models across all regions, particularly over the mid to late 20th century, when anthropogenic emissions increase markedly. Large regional historical changes are simulated for both pollutants across East and South Asia with an annual mean increase of up to 40 ppb for O3 and 12 µg m−3 for PM2.5. In future scenarios containing strong air quality and climate mitigation measures (ssp126), annual mean concentrations of air pollutants are substantially reduced across all regions by up to 15 ppb for O3 and 12 µg m−3 for PM2.5. However, for scenarios that encompass weak action on mitigating climate and reducing air pollutant emissions (ssp370), annual mean increases in both surface O3 (up 10 ppb) and PM2.5 (up to 8 µg m−3) are simulated across most regions, although, for regions like North America and Europe small reductions in PM2.5 are simulated due to the regional reduction in precursor emissions in this scenario. A comparison of simulated regional changes in both surface O3 and PM2.5 from individual CMIP6 models highlights important regional differences due to the simulated interaction of aerosols, chemistry, climate and natural emission sources within models. The projection of regional air pollutant concentrations from the latest climate and Earth system models used within CMIP6 shows that the particular future trajectory of climate and air quality mitigation measures could have important consequences for regional air quality, human health and near-term climate. Differences between individual models emphasise the importance of understanding how future Earth system feedbacks influence natural emission sources, e.g. response of biogenic emissions under climate change.
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Background: Exposure to air pollution is associated with elevated cardiovascular risk. Evidence shows that omega-3 polyunsaturated fatty acids (omega-3 PUFA) may attenuate the adverse cardiovascular effects of exposure to fine particulate matter (PM 2.5 ). However, it is unclear whether habitual dietary intake of omega-3 PUFA protects against the cardiovascular effects of short-term exposure to low-level ambient air pollution in healthy participants. In the present study, sixty-two adults with low or high dietary omega-3 PUFA intake were enrolled. Blood lipids, markers of vascular inflammation, coagulation and fibrinolysis, and heart rate variability (HRV) and repolarization were repeatedly assessed in 5 sessions separated by at least 7 days. This study was carried out in the Research Triangle area of North Carolina, USA between October 2016 and September 2019. Daily PM 2.5 and maximum 8-h ozone (O 3 ) concentrations were obtained from nearby air quality monitoring stations. Linear mixed-effects models were used to assess the associations between air pollutant concentrations and cardiovascular responses stratified by the omega-3 intake levels. Results: The average concentrations of ambient PM 2.5 and O 3 were well below the U.S. National Ambient Air Quality Standards during the study period. Significant associations between exposure to PM 2.5 and changes in total cholesterol, von Willebrand factor (vWF), tissue plasminogen activator, D-dimer, and very-low frequency HRV were observed in the low omega-3 group, but not in the high group. Similarly, O 3 -associated adverse changes in cardiovascular biomarkers (total cholesterol, high-density lipoprotein, serum amyloid A, soluable intracellular adhesion molecule 1, and vWF) were mainly observed in the low omega-3 group. Lag-time-dependent biphasic changes were observed for some biomarkers. Conclusions: This study demonstrates associations between short-term exposure to PM 2.5 and O 3 , at concentrations below regulatory standard, and subclinical cardiovascular responses, and that dietary omega-3 PUFA consumption may provide protection against such cardiovascular effects in healthy adults.
Household air pollution (HAP) is of public health concern, with ~3 billion people worldwide (including >15 million in the US) exposed. HAP from coal use is a human lung carcinogen, yet the epidemiological evidence on carcinogenicity of HAP from biomass use, primarily wood, is not conclusive. To robustly assess biomass’s carcinogenic potential, prospective studies of individuals experiencing a variety of HAP exposures are needed. We have built a global consortium of 13 prospective cohorts (HAPCO: Household Air Pollution Consortium) that have site- and disease-specific mortality and solid fuel use data, for a combined sample size of 587,257 participants and 57,483 deaths. HAPCO provides a novel opportunity to assess the association of HAP with lung cancer death while controlling for important confounders such as tobacco and outdoor air pollution exposures. HAPCO is also uniquely positioned to determine the risks associated with cancers other than lung as well as nonmalignant respiratory and cardiometabolic outcomes, for which prospective epidemiologic research is limited. HAPCO will facilitate research to address public health concerns associated with HAP-attributed exposures by enabling investigators to evaluate sex-specific and smoking status-specific effects under various exposure scenarios.
Maintaining indoor air pollutants under acceptable levels is significant to protect occupants from exposure to excessive air pollutants in natural ventilation. In this paper, using the representative air pollutant concentration data, we present the natural ventilation usability with associated cooling energy saving potentials in different location settings (urban and city center, suburban and rural) of the US under the influence of local weather conditions and major outdoor air pollutants, i.e. PM2.5, PM10 and ozone. It is found that the impacts of air pollutants on natural ventilation are usually higher in urban/suburban areas than rural areas (up to 25% difference) with the PM2.5 being the most significant outdoor air pollutant affecting natural ventilation usage. Furthermore, ozone could become increasingly influential on natural ventilation as moving from urban to suburban/rural areas. As to the cooling energy saving considering the impacts of outdoor air pollutants, natural ventilation is estimated to save approximately 10%–40% cooling energy (800–2600 kWh per small commercial building) annually in different location settings of investigated areas across the US. The following economic analysis demonstrates that these electricity savings lead to approximately 80–540 dollars annual savings of building operation cost per building. If the time of use rate is adopted, these cost savings could further increase by approximately 20% (Los Angeles) to more than 50% (Albuquerque) depending on different rate structures, which further demonstrates the potential of adopting natural ventilation as a sustainability measurement with benefits for building owners without compromising occupants health.
Ambient air pollution from ground-level ozone and fine particulate matter (PM(sub 2.5)) is associated with premature mortality. Future concentrations of these air pollutants will be driven by natural and anthropogenic emissions and by climate change. Using anthropogenic and biomass burning emissions projected in the four Representative Concentration Pathway scenarios (RCPs), the ACCMIP ensemble of chemistry climate models simulated future concentrations of ozone and PM(sub 2.5) at selected decades between 2000 and 2100. We use output from the ACCMIP ensemble, together with projections of future population and baseline mortality rates, to quantify the human premature mortality impacts of future ambient air pollution. Future air-pollution-related premature mortality in 2030, 2050 and 2100 is estimated for each scenario and for each model using a health impact function based on changes in concentrations of ozone and PM(sub 2.5) relative to 2000 and projected future population and baseline mortality rates. Additionally, the global mortality burden of ozone and PM(sub 2.5) in 2000 and each future period is estimated relative to 1850 concentrations, using present-day and future population and baseline mortality rates. The change in future ozone concentrations relative to 2000 is associated with excess global premature mortality in some scenarios/periods, particularly in RCP8.5 in 2100 (316 thousand deaths per year), likely driven by the large increase in methane emissions and by the net effect of climate change projected in this scenario, but it leads to considerable avoided premature mortality for the three other RCPs. However, the global mortality burden of ozone markedly increases from 382000 (121000 to 728000) deaths per year in 2000 to between 1.09 and 2.36 million deaths per year in 2100, across RCPs, mostly due to the effect of increases in population and baseline mortality rates. PM(sub 2.5) concentrations decrease relative to 2000 in all scenarios, due to projected reductions in emissions, and are associated with avoided premature mortality, particularly in 2100: between 2.39 and 1.31 million deaths per year for the four RCPs. The global mortality burden of PM(sub 2.5) is estimated to decrease from 1.70 (1.30 to 2.10) million deaths per year in 2000 to between 0.95 and 1.55 million deaths per year in 2100 for the four RCPs due to the combined effect of decreases in PM(sub 2.5) concentrations and changes in population and baseline mortality rates. Trends in future air-pollution-related mortality vary regionally across scenarios, reflecting assumptions for economic growth and air pollution control specific to each RCP and region. Mortality estimates differ among chemistry climate models due to differences in simulated pollutant concentrations, which is the greatest contributor to overall mortality uncertainty for most cases assessed here, supporting the use of model ensembles to characterize uncertainty. Increases in exposed population and baseline mortality rates of respiratory diseases magnify the impact on premature mortality of changes in future air pollutant concentrations and explain why the future global mortality burden of air pollution can exceed the current burden, even where air pollutant concentrations decrease.
Highlights: • Associations of ambient air pollution with metabolic syndrome were scarcely studied. • Data from 15,477 Chinese adults were analyzed. • Long-term exposure to air pollution was associated with metabolic syndrome. • Demographic and lifestyle factors modified the association between metabolic syndrome and air pollution. Little evidence exists about the effects of long-term exposure to ambient air pollution on metabolic syndrome (MetS). This study aimed to determine the association between long-term ambient air pollution and MetS in China. A total of 15,477 adults who participated in the 33 Communities Chinese Health Study (33CCHS) in 2009 were evaluated. MetS was defined based on the recommendation by the Joint Interim Societies. Exposure to air pollutants was assessed using data from monitoring stations and a spatial statistical model (including particles with diameters ≤ 1.0 µm (PM{sub 1}), ≤ 2.5 µm (PM{sub 2.5}), and ≤ 10 µm (PM{sub 10}), sulfur dioxide (SO{sub 2}), nitrogen dioxide (NO{sub 2}), and ozone (O{sub 3})). Two-level logistic regression analyses were utilized to assess the associations between air pollutants and MetS. The prevalence of MetS was 30.37%. The adjusted odds ratio of MetS per 10 µg/m{sup 3} increase in PM{sub 1}, PM{sub 2.5}, PM{sub 10}, SO{sub 2}, NO{sub 2}, and O{sub 3} were 1.12 (95% CI = 1.00–1.24), 1.09 (95% CI = 1.00–1.18), 1.13 (95% CI = 1.08–1.19), 1.10 (95% CI = 1.02–1.18), 1.33 (95% CI = 1.12–1.57), and 1.10 (95% CI = 1.01–1.18), respectively. Stratified analyses indicated that the above associations were stronger in participants with the demographic variables of males, < 50 years of age, and higher income, as well as with the behavioral characteristics of smoking, drinking, and consuming sugar-sweetened soft drinks frequently. This study indicates that long-term exposure to ambient air pollutants may increase the risk of MetS, especially among males, the young to middle aged, those of low income, and those with unhealthy lifestyles.
Highlights: • Daily exposure to ozone may vary across air pollution models, considerably. • The exposure model influenced disparity of exposure across socio-economic strata. • The air pollution model does not affect disparity of susceptibility. • Multiple air pollution models should be used to assess socio-economic disparities. Studies assessing socio-economic disparities in air pollution exposure and susceptibility are usually based on a single air pollution model. A time stratified case-crossover study was designed to assess the impact of the type of model on differential exposure and on the differential susceptibility in the relationship between ozone exposure and daily mortality by socio-economic strata (SES) in Montreal. Non-accidental deaths along with deaths from cardiovascular and respiratory causes on the island of Montreal for the period 1991–2002 were included as cases. Daily ozone concentration estimates at partictaipants’ residence were obtained from the five following air pollution models: Average value (AV), Nearest station model (NS), Inverse-distance weighting interpolation (IDW), Land-use regression model with back-extrapolation (LUR-BE) and Bayesian maximum entropy model combined with a land-use regression (BME-LUR). The prevalence of a low household income (< 20,000/year) was used as socio-economic variable, divided into two categories as a proxy for deprivation. Multivariable conditional logistic regressions were used considering 3-day average concentrations. Multiplicative and additive interactions (using Relative Excess Risk due to Interaction) as well as Cochran's tests were calculated and results were compared across the different air pollution models. Heterogeneity of susceptibility and exposure according to socio-economic status (SES) were found. Ratio of exposure across SES groups means ranged from 0.75 [0.74–0.76] to 1.01 [1.00–1.02], respectively for the LUR-BE and the BME-LUR models. Ratio of mortality odds ratios ranged from 1.01 [0.96–1.05] to 1.02 [0.97–1.08], respectively for the IDW and LUR-BE models. Cochran's test of heterogeneity between the air pollution models showed important heterogeneity regarding the differential exposure by SES, but the air pollution model was not found to influence heterogeneity regarding the differential susceptibility. The study showed air pollution models can influence the assessment of disparities in exposure according to SES in Montreal but not that of disparities in susceptibility.
Air pollution and climate change are a deadly duo for Africa, and must be tackled together. Air pollutants and greenhouse gases often share the same sources and can be even more dangerous when combined. Africa is particularly vulnerable to climate change, and currently, an estimated 1 million people per year die prematurely from air pollution on the continent. But there is a way to improve the situation: preventing emissions from short-lived climate pollutants, like methane and black carbon, is crucial for the world to stay below 1.5°C. Reducing SLCPs will help both save lives and protect the environment. Africa has a huge opportunity to continue developing sustainably, improve human well-being, and protect nature by investing in solutions to fight climate change and air pollution together. A new Integrated Assessment of Air Pollution and Climate Change for Sustainable Development in Africa from the African Union Commission, the Climate and Clean Air Coalition, and the UN Environment Programme, developed by African scientists in a process led by the Stockholm Environment Institute, shows how African leaders can act quickly across 5 key areas—transport, residential, energy, agriculture, and waste—to fight climate change, prevent air pollution, and protect human health.
Highlights: • Little is known about the effect of stress-pollution interaction on childhood asthma. • We examined associations of parental stress and air pollution with childhood asthma in China. • Association of air pollution with asthma is significant in children exposed to high parental stress. • Association of parental stress with asthma is significant in children exposed to high air pollution. • Interactive effect of stress and air pollution on asthma indicates a common biological pathway. Although air pollution and social stress may independently increase childhood asthma, little is known on their synergistic effect on asthma, particularly in China with high levels of stress and air pollution.
Carbon dioxide and non-greenhouse gas air pollutants are emitted from many of the same sources. Decarbonization actions thus typically yield air pollutant emission reductions, resulting in significant air quality benefits. Although several studies have highlighted this connection, including in the context of net zero carbon emission targets, substantial uncertainty remains regarding how alternative technological pathways to this goal will affect the spatial distribution and magnitude of air pollutants. Comprehensive multi-model and multi-scenario analyzes are needed to explore the relative impacts of alternative pathways. Here, our study begins to address this gap by leveraging the results from the recent Energy Modeling Forum 37 inter-model comparison exercise on U.S. decarbonization pathways. Comparing the results of the six teams who submitted air pollutant emissions suggests that strategies that target net zero U.S. carbon emissions would yield significant reductions in many air pollutants, and that this finding is generally robust across pathways. However, some energy sources, such as biomass and fossil fuels with carbon capture, will emit air pollutants and can potentially influence the magnitude, spatial distribution, and even sign of localized air pollutant emission changes. In the second part of this analysis, a simplified air quality and health impacts screening model is used to evaluate the air quality impacts in 2035 of sectoral emission changes from the three models that provided sectoral detail. Relative to a reference scenario, a net zero pathway is estimated to reduce fine particulate matter concentrations across the contiguous U.S., with health benefits from reduced mortality ranging from $\$$65 billion to $\$$250 billion in 2035 alone (2023$\$$s). These benefits would be expected to grow over time as the net zero trajectory becomes more stringent. Both the magnitude of potential benefits and the substantial variation of the projections across models underscore the need for an EMF-like inter-model comparison exercise focused on air quality.
Highlights: • Burden of ischemic heart disease related to PM{sub 2.5}, SO{sub 2} and NO{sub 2} were estimated. • Stronger impacts of gaseous pollutants versus particulate matter were found. • SO{sub 2} exposure was positively associated with YLL in widowed group. Air pollution is considered one of the most important risk factors for ischemic heart disease (IHD), which is a major public health concern. The disease burden of IHD has continued to rise in China in the past two decades. However, epidemiological studies examining the associations between air pollution and IHD have been scarce in China, and the only studies were conducted in severe air pollution areas, where air pollution levels seriously exceed the World Health Organization Air Quality Guidelines. Whether the influence of air pollution on IHD in areas with relatively low levels of air pollution differs from the influence of high pollution levels in heavily studied areas was unknown until now. Furthermore, the estimation of the disease burden of IHD related to air pollution has been very limited.