The Quick Urban and Industrial Complex (QUIC) plume modeling system is used to explore how the transport and dispersion of vehicle emissions in cities are impacted by the presence of buildings. Using downtown Philadelphia as a test case, notional vehicle emissions of gases and particles are specified as line source releases on a subset of the east–west and north–south streets. Cases were run in flat terrain and with 3D buildings present in order to show the differences in the model-computed outdoor concentration fields with and without buildings present. The QUIC calculations show that buildings result in regions with much higher concentrations and other areas with much lower concentrations when compared to the flat-earth case. On the roads with vehicle emissions, street-level concentrations were up to a factor of 10 higher when buildings were on either side of the street as compared to the flat-earth case due to trapping of pollutants between buildings. However, on roads without vehicle emissions and in other open areas, the concentrations were up to a factor of 100 times smaller as compared to the flat earth case because of vertical mixing of the vehicle emissions to building height in the cavity circulation that develops on the downwind side of unsheltered buildings. QUIC was also used to calculate infiltration of the contaminant into the buildings. Indoor concentration levels were found to be much lower than outdoor concentrations because of deposition onto indoor surfaces and particulate capture for buildings with filtration systems. Large differences in indoor concentrations from building to building resulted from differences in leakiness, air handling unit volume exchange rates, and filter type and for naturally ventilated buildings, whether or not the building was sheltered from the prevailing wind by a building immediately upwind.

With the increasing awareness of health impacts of particulate matter, there is a growing need to comprehend the spatial and temporal variations of the global abundance of ground-level airborne particulate matter (PM_2.5). Here we use a suite of remote sensing and meteorological data products together with ground based observations of PM_2.5 from 8,329 measurement sites in 55 countries taken between 1997 and 2014 to train a machine learning algorithm to estimate the daily distributions of PM_2.5 from 1997 to the present. We demonstrate that the new PM_2.5 data product can reliably represent global observations of PM_2.5 for epidemiological studies. An analysis of Baltimore schizophrenia emergency room admissions is presented in terms of the levels of ambient pollution. PM_2.5 appears to have an impact on some aspects of mental health.

An understanding of human health implications from atmosphere exposure is a priority in both the geographic and the public health domains. The unique properties of geographic tools for remote sensing of the atmosphere offer a distinct ability to characterize and model aerosols in the urban atmosphere for evaluation of impacts on health. Asthma, as a manifestation of upper respiratory disease prevalence, is a good example of the potential interface of geographic and public health interests. The current study focused on Athens, Greece during the year of 2004 and (1) demonstrates a systemized process for aligning data obtained from satellite aerosol optical depth (AOD) with geographic location and time, (2) evaluates the ability to apply imputation methods to censored data, and (3) explores whether AOD data can be used satisfactorily to investigate the association between AOD and health impacts using an example of hospital admission for childhood asthma. This work demonstrates the ability to apply remote sensing data in the evaluation of health outcomes, that the alignment process for remote sensing data is readily feasible, and that missing data can be imputed with a sufficient degree of reliability to develop complete datasets. Individual variables demonstrated small but significant effect levels on hospital admission of children for AOD, nitrogen oxides (NO_x), relative humidity (rH), temperature, smoke, and inversely for ozone. However, when applying a multivari-able model, an association with asthma hospital admissions and air quality could not be demonstrated. This work is promising and will be expanded to include additional years.

Carbon disulfide (CS₂) has been historically associated with the production of rayon, cellophane, and carbon tetrachloride. This study identifies multiple mechanisms by which CS₂ contributes to the formation of CO₂ in the atmosphere. CS₂ and other associated sulfide compounds were found by this study to be present in emissions from unconventional shale gas extraction and processing (E&P) operations. The breakdown products of CS₂; carbonyl sulfide (COS), carbon monoxide (CO), and sulfur dioxide (SO₂) are indirect greenhouse gases (GHGs) that contribute to CO₂ levels in the atmosphere. The heat-trapping nature of CO₂ has been found to increase the surface temperature, resulting in regional and global climate change. The purpose of this study is to identify five mechanisms by which CS₂ and the breakdown products of CS₂ contribute to atmospheric concentrations of CO₂. The five mechanisms of CO₂ formation are as follows:

1. Chemical Interaction of CS₂ and hydrogen sulfide (H₂S) present in natural gas at high temperatures, resulting in CO₂ formation;

2. Combustion of CS₂ in the presence of oxygen producing SO₂ and CO₂;

3. Photolysis of CS₂ leading to the formation of COS, CO, and SO₂, which are indirect contributors to CO₂ formation;

4. One-step hydrolysis of CS₂, producing reactive intermediates and ultimately forming H₂S and CO₂;

5. Two-step hydrolysis of CS₂ forming the reactive COS intermediate that reacts with an additional water molecule, ultimately forming H₂S and CO₂. CS₂ and COS additionally are implicated in the formation of SO₂ in the stratosphere and/or troposphere. SO₂ is an indirect contributor to CO₂ formation and is implicated in global climate change.

Although ambient concentrations have declined steadily over the past 30 years, Houston has recorded some of the highest levels of hazardous air pollutants in the United States. Nevertheless, federal and state regulatory efforts historically have emphasized compliance with the National Ambient Air Quality Standard for ozone, treating “air toxics” in Houston as a residual problem to be solved through application of technology-based standards. Between 2004 and 2009, Mayor Bill White and his administration challenged the well-established hierarchy of air quality management spelled out in the Clean Air Act, whereby federal and state authorities are assigned primacy over local municipalities for the purpose of designing and implementing air pollution control strategies. The White Administration believed that existing regulations were not sufficient to protect the health of Houstonians and took a diversity of both collaborative and combative policy actions to mitigate air toxic emissions from stationary sources. Opposition was substantial from a local coalition of entrenched interests satisfied with the status quo, which hindered the city's attempts to take unilateral policy actions. In the short term, the White Administration successfully raised the profile of the air toxics issue, pushed federal and state regulators to pay more attention, and induced a few polluting facilities to reduce emissions. But since White left office in 2010, air quality management in Houston has returned to the way it was before, and today there is scant evidence that his policies have had any lasting impact.

Sulfur dioxide (SO₂) is a problematic inhalable air pollutant in areas of widespread industrialization, not only in the United States but also in countries undergoing rapid industrialization, such as China, and it can be a potential trigger factor for asthma exacerbations. It is known that asthmatics are sensitive to the effects of SO₂; however, the basis of this enhanced sensitivity remains incompletely understood. A PubMed search was performed over the course of 2014, encompassing the following terms: asthma, airway inflammation, sulfur dioxide, IL-10, mouse studies, and human studies. This search indicated that biomarkers of SO₂ exposure, SO₂ effects on airway epithelial cell function, and animal model data are useful in our understanding of the body's response to SO₂, as are SO₂-associated amplification of allergic inflammation, and potential promotion of neurogenic inflammation due to chemical irritant properties. While definitive answers are still being sought, these areas comprise important foci of consideration regarding asthmatic responses to inhaled SO₂. Furthermore, IL-10 deficiency associated with asthma may be another important factor associated with an inability to resolve inflammation and mitigate oxidative stress resulting from SO₂ inhalation, supporting the idea that asthmatics are predisposed to SO₂ sensitivity, leading to asthma exacerbations and airway dysfunction.