Current National Ambient Air Quality Research Articles

Impacts of anthropogenic emissions and meteorology on spring ozone differences in San Antonio, Texas between 2017 and 2021

San Antonio has been designated as ozone nonattainment under the current National Ambient Air Quality Standards (NAAQS). Ozone events in the city typically occur in two peaks, characterized by a pronounced spring peak followed by a late summer peak. Despite higher ozone levels, the spring peak has received less attention than the summer peak. To address this research gap, we used the Weather Research and Forecasting (WRF)-driven GEOS-Chem (WRF-GC) model to simulate San Antonio's ozone changes in the spring month of May from 2017 to 2021 and quantified the respective contributions from changes in anthropogenic emissions and meteorology. In addition to modeling, observations from the San Antonio Field Studies (SAFS), the Texas Commission on Environmental Quality (TCEQ) Continuous Ambient Monitoring Stations (CAMS), and the spaceborne TROPOspheric Monitoring Instrument (TROPOMI) are used to examine and validate changes in ozone and precursors. Results show that the simulated daytime mean surface ozone in May 2021 is 3.8 ± 0.6 ppbv lower than in May 2017, which is slightly less than the observed average differences of −5.3 ppbv at CAMS sites. The model predicted that the anthropogenic emission-induced changes contribute to a 1.4 ± 0.5 ppbv reduction in daytime ozone levels, while the meteorology-induced changes account for a 2.4 ± 0.6 ppbv reduction over 2017–2021. This suggests that meteorology plays a relatively more important role than anthropogenic emissions in explaining the spring ozone differences between the two years. We additionally identified (1) reduced NO2 and HCHO concentrations as chemical reasons, and (2) lower temperature, higher humidity, increased wind speed, and a stronger Bermuda High as meteorological reasons for lower ozone levels in 2021 compared to 2017. The quantification of the different roles of meteorology and ozone precursor concentrations helps understand the cause and variation of ozone changes in San Antonio over recent years.

Air Pollution and Acute Kidney Injury in the U.S. Medicare Population: A Longitudinal Cohort Study.

Recent studies have reported the association between air pollution exposure and reduced kidney function. However, it is unclear whether air pollution is associated with an increased risk of acute kidney injury (AKI). To address this gap in knowledge, we investigated the effect estimates of long-term exposures to fine particulate matter [PM in aerodynamic diameter ()], nitrogen dioxide (), and ozone () on the risk of first hospital admission for AKI using nationwide Medicare data. This nationwide population-based longitudinal cohort study included 61,300,754 beneficiaries enrolled in Medicare Part A fee-for-service (FFS) who were years of age and resided in the continental United States from the years 2000 through 2016. We applied Cox-equivalent Poisson models to estimate the association between air pollution and first hospital admission for AKI. Exposure to , , and was associated with increased risk for first hospital admission for AKI, with hazard ratios (HRs) of 1.17 (95% CI: 1.16, 1.19) for a increase in , 1.12 (95% CI: 1.11, 1.13) for a increase in , and 1.03 (95% CI: 1.02, 1.04) for a increase in summer-period (June to September). The associations persisted at annual exposures lower than the current National Ambient Air Quality Standard. This study found an association between exposures to air pollution and the risk of the first hospital admission with AKI, and this association persisted even at low concentrations of air pollution. Our findings provide beneficial implications for public health policies and air pollution guidelines to alleviate health care expenditures and the disease burden attributable to AKI. https://doi.org/10.1289/EHP10729.

Emissions, meteorological and climate impacts on PM2.5 levels in Southern California using a generalized additive model: Historic trends and future estimates

Annual fine particulate matter (PM2.5) mass concentrations in the South Coast Air Basin (SoCAB) of California decreased from around 30 μg/m3 to 11 μg/m3 between 2000 and 2013 but rose from 11 μg/m3 to 13 μg/m3 between 2014 and 2018, raising important questions about the effectiveness of ongoing emission control policies. A two-step generalized additive model (GAM)-least squares approach was developed to explore the effects of emissions, large-scale climate events and meteorological factors on daily PM2.5 mass concentrations from 2000 to 2019 to quantitatively link impacts of emissions and meteorological on PM2.5 and to assess factors leading to the increase. The GAM had an R2 = 0.99 and root mean square error (RMSE) = 0.7 μg/m3 for the annual average PM2.5 concentrations. The two-step method had an R2 = 0.93 and RMSE = 4.07 μg/m3 for the 98th percentile 24-hr average PM2.5 concentrations. Variations in both emissions and relative humidity were of high importance compared with other included factors. Interactions of NH3 emissions with NOx and SO2 emissions, which lead to ammonium nitrate and sulfate aerosol formation, were the most important factors. Meteorological effects on PM2.5 explained the majority of the daily PM2.5 fluctuations. Emission changes (increases in SO2 and PM2.5) led to increases in predicted PM2.5 between 2014 and 2018. Predicted future PM2.5, using projected emissions and meteorological data from model simulations of representative concentration pathway (RCP) scenarios, are around 12 μg/m3 (annual) and 30 μg/m3 (98th percentile daily), which are both close to the current National Ambient Air Quality Standards (NAAQS) for PM2.5. Meteorological impacts on the predicted PM2.5 in future years lead to variations of ±2 μg/m3 for the annual average and ±5 μg/m3 for the 98th percentile daily level. Future climate changes lead to a probable year-to-year variation that will let PM2.5 levels in some years exceed the standard.

Association of Long-term Exposure to Particulate Air Pollution With Cardiovascular Events in California

Long-term exposure to fine particulate air pollution (PM2.5) is a known risk factor for cardiovascular events, but controversy remains as to whether the current National Ambient Air Quality Standard (12 μg/m3 for 1-year mean PM2.5) is sufficiently protective. To evaluate the associations between long-term fine particulate air pollution and cardiovascular events using electronic health record and geocoded address data. This retrospective cohort study included adults in the Kaiser Permanente Northern California integrated health care system during 2007 to 2016 and followed for up to 10 years. Study participants had no prior stroke or acute myocardial infarction (AMI), and lived in Northern California for at least 1 year. Analyses were conducted January 2020 to December 2022. Long-term exposure to PM2.5. Individual-level time-varying 1-year mean PM2.5 exposures for every study participant were updated monthly from baseline through the end of follow-up, accounting for address changes. Incident AMI, ischemic heart disease (IHD) mortality, and cardiovascular disease (CVD) mortality. Cox proportional hazards models were fit with age as time scale, adjusted for sex, race and ethnicity, socioeconomic status, smoking, body mass index, baseline comorbidities, and baseline medication use. Associations below the current regulation limit were also examined. The study cohort included 3.7 million adults (mean [SD] age: 41.1 [17.2] years; 1 992 058 [52.5%] female, 20 205 [0.5%] American Indian or Alaskan Native, 714 043 [18.8%] Asian, 287 980 [7.6%] Black, 696 796 [18.4%] Hispanic, 174 261 [4.6%] multiracial, 1 904 793 [50.2%] White). There was a 12% (95% CI, 7%-18%) increased risk of incident AMI, a 21% (95% CI, 13%-30%) increased risk of IHD mortality, and an 8% (95% CI, 3%-13%) increased risk of CVD mortality associated with a 10 μg/m3 increase in 1-year mean PM2.5. PM2.5 exposure at moderate concentrations (10.0 to 11.9 μg/m3) was associated with increased risks of incident AMI (6% [95% CI, 3%-10%]) and IHD mortality (7% [95% CI, 2%-12%]) compared with low concentrations (less than 8 μg/m3). In this study, long-term PM2.5 exposure at moderate concentrations was associated with increased risks of incident AMI, IHD mortality, and CVD mortality. This study's findings add to the evidence that the current regulatory standard is not sufficiently protective.

Time-lagged relationships between a decade of air pollution exposure and first hospitalization with Alzheimer's disease and related dementias

Alzheimer's disease and related dementias (ADRD) poses substantial health challenges among an aging population. One of the primary challenges in studying ADRD is that biological processes underlying these ailments begin decades prior to diagnosis. Previous studies indicate a relationship between ADRD and air pollution exposure to both fine particulate matter (PM2.5) and nitrogen dioxide (NO2) but are limited in their interpretation because they consider exposure measurements at a single time point. Our retrospective cohort study considered 27 + million Medicare enrollees in the United States followed up to 17 years and matched with highly accurate annual air pollution exposure measurements for PM2.5, NO2, and summer ozone. We applied distributed lag models and estimated the lagged associations between air pollution and odds of first hospitalization with ADRD. We found significantly increased odds due to overall PM2.5 and NO2 exposure and time-lagged exposure 10 and 8 years prior to admission, respectively. Furthermore, we found the connection between air pollution exposure and increased odds of first hospitalization with ADRD exists at air pollution levels below current National Ambient Air Quality Standards set by the US Environmental Protection Agency, with the steepest increase in odds occurring at low concentrations of PM2.5. Our findings are the first to show that air pollution exposures from as many as 10 years prior to the admission are related to increased odds of hospitalizations with ADRD. As there are no clear treatments available for ADRD, identifying modifiable risk factors such as air pollution exposure may make significant contributions towards prevention or delayed disease progression.

Systematic Review of Ozone Effects on Human Lung Function, 2013 Through 2020

BackgroundOzone effects on lung function are particularly important to understand in the context of the air pollution-health outcomes epidemiologic literature, given the complex relationships between ozone and other air pollutants with known lung function effects.Research QuestionWhat has been learned about the association between ozone exposures and lung function from epidemiology studies published from 2013 through 2020?Study Design and MethodsOn March 18, 2018, and September 8, 2020, PubMed was searched using the terms health AND ozone, filtering to articles in English and about humans, from 2013 or later. An additional focused review searching for ozone AND (lung function OR FEV1OR FVC) was performed June 26, 2021. Articles were selected for this review if they reported a specific relationship between a lung function outcome and ozone exposure.ResultsOf 3,271 articles screened, 53 ultimately met criteria for inclusion. A systematic review with assessment of potential for bias was conducted, but a meta-analysis was not carried out because of differences in exposure duration and outcome quantification. Consistent evidence exists of small decreases in children’s lung function, even associated with very low levels of short-term ozone exposure. The effects on adult lung function from exposure to low-level, short-term ozone are less clear, although ozone-associated decrements may occur in the elderly. Finally, long-term ozone exposure decreases both lung function and lung function growth in children, although few new studies have examined long-term ozone and lung function in adults.InterpretationMuch of this literature involves concentrations below the current US Environmental Protection Agency’s National Ambient Air Quality Standard of 70 parts per billion over an 8-h averaging time, suggesting that this current standard may not protect children adequately from ozone-related decrements in lung function.

How protective is China’s National Ambient Air Quality Standards on short-term PM2.5? Findings from blood pressure measurements of 1 million adults

Although short-term exposure to fine particulate matter (PM2.5) air pollution has been shown to induce elevated blood pressure (BP), limited evidence is available regarding the association between ambient PM2.5 and BP levels in nationwide China and how the association may change. This study sought to explore acute BP changes with exposure to PM2.5 at levels below China’s current National Ambient Air Quality Standards (NAAQS). Based on a spatiotemporal study of over 1 million adults, we linked BP measurements to daily estimates of PM2.5 from multiple sources (i.e. in situ observations, satellite measurements of aerosol and numeric simulations of air quality model) after adjusting for several individual-level covariates and further conduced the below-criteria models by restricting the analyses within subsets of individuals with short-term PM2.5 exposure below 75 μg m−3 (i.e. NAAQS of 24 h PM2.5 in China). We further explored variations in BP-PM2.5 associations by pollution level and for different demographic groups. With full adjustments, a 10 μg m−3 increase in PM2.5 was statistically significantly associated with a 0.049 mmHg (95% confidence interval, CI: 0.041, 0.057) increase in systolic BP, a 0.022 mmHg (95% CI: 0.017, 0.027) increase in diastolic BP and a 0.77% (95% CI: 0.62%, 0.92%) increased risk of hypertension (HPN). For both BP and HPN, the exposure-response curves were linear, with no threshold effects, at the low-concentration ends and sublinear at the high-concentration ends. Below the current NAAQS, the associations in population level remained statistically significant and were even stronger. A 10 μg m−3 increase in below-NAAQS PM2.5 was associated with a 1.95% (95% CI: 1.44%, 2.47%) increased risk of HPN. Specific subpopulations were more susceptible to PM2.5 exposure. These findings can help support decisions by policymakers to revise related environmental regulations to protect public health.

Ambient PM2.5 exposure and rapid spread of COVID-19 in the United States

It has been posited that populations being exposed to long-term air pollution are more susceptible to COVID-19. Evidence is emerging that long-term exposure to ambient PM2.5 (particulate matter with aerodynamic diameter 2.5 μm or less) associates with higher COVID-19 mortality rates, but whether it also associates with the speed at which the disease is capable of spreading in a population is unknown. Here, we establish the association between long-term exposure to ambient PM2.5 in the United States (US) and COVID-19 basic reproduction ratio R0– a dimensionless epidemic measure of the rapidity of disease spread through a population. We inferred state-level R0 values using a state-of-the-art susceptible, exposed, infected, and recovered (SEIR) model initialized with COVID-19 epidemiological data corresponding to the period March 2–April 30. This period was characterized by a rapid surge in COVID-19 cases across the US states, implementation of strict social distancing measures, and a significant drop in outdoor air pollution. We find that an increase of 1 μg/m3 in PM2.5 levels below current national ambient air quality standards associates with an increase of 0.25 in R0 (95% CI: 0.048–0.447). A 10% increase in secondary inorganic composition, sulfate-nitrate-ammonium, in PM2.5 associates with ≈10% increase in R0 by 0.22 (95% CI: 0.083–0.352), and presence of black carbon (soot) in the ambient environment moderates this relationship. We considered several potential confounding factors in our analysis, including gaseous air pollutants and socio-economical and meteorological conditions. Our results underscore two policy implications – first, regulatory standards need to be better guided by exploring the concentration-response relationships near the lower end of the PM2.5 air quality distribution; and second, pollution regulations need to be continually enforced for combustion emissions that largely determine secondary inorganic aerosol formation.

Causal effects of air pollution on mortality in Massachusetts

Background: Epidemiologic studies of air pollution and mortality have primarily investigated long- and short-term exposures separately, have used multiplicative models, and have been associational studies.Methods: We analyzed 1.5 million Medicare beneficiaries living in Massachusetts with 3.9 billion person-days of follow-up during 2000-2012. We implemented a generalized propensity score adjustment approach, which accounted for joint confounding by the concurrent exposures, individual- and area-level covariates, meteorological covariates, seasonal variations, and long-term time trend, to evaluate causal effects of long- (one-year moving average) and short-term (two-day moving average) exposures to PM2.5, O3, and NO2 on all-cause mortality. By modeling the binary outcome of death with linear probability model, we estimated the potential number of deaths that would occur per unit increase in each air pollutant exposure.Results: We found that long- and short-term PM2.5, O3, and NO2 were all associated with an increased risk of mortality. Specifically, per 10 million person-days, each 1 µg·m-3 increase in long- and short-term PM2.5 were associated with 35.4 (95% confidence interval [CI], 33.4-37.6) and 3.04 (95% CI, 2.17-3.94) excess deaths, respectively; each 1 ppb increase in long- and short-term O3 were associated with 2.35 (95% CI, 1.08-3.61) and 2.41 (95% CI, 1.81-2.91) excess deaths, respectively; and each 1 ppb increase in long- and short-term NO2 were associated with 3.24 (95% CI, 2.75-3.77) and 5.60 (95% CI, 5.24-5.98) excess deaths, respectively. Importantly, risk differences associated with long-term effects of PM2.5 and O3 increased substantially when the exposure levels went below the increasingly stringent thresholds, including those well below the current National Ambient Air Quality Standards (NAAQS).Conclusions: The findings suggest that air pollution exposures were causally associated with mortality, even at levels below NAAQS. The estimates on additive probability scale provide clearer insights into the relative magnitude of air pollution effects.

The impact of emissions and climate change on future ozone concentrations in the USA

The potential impacts of climate change and future anthropogenic emissions on ozone levels in the USA are examined by linking global climate models to regional meteorological and air quality models during 3-year summer periods over the nine climate regions of the continental United States for three cases: (1) using 2016 meteorology and emissions (CTRL), (2) using 2050 meteorology and 2016 emissions (CASE1), and (3) using 2050 meteorology and 2050 emissions (CASE2). As climate change alone is expected to worsen ozone pollution and emission reductions are expected to reduce ozone concentrations, in this paper, the non-linear response of future ozone levels to both meteorological conditions and emissions was studied. The results show the well-known positive ozone correlation with surface temperature and negative ozone correlation with humidity in all regions. Climate change alone will increase future MDA8 ozone in the USA by 3.6 ppb. With climate change and policy intervention based on RCP 8.5, ozone levels will decrease 7.2 ppb on average for all climate regions in the USA. Furthermore, while climate change alone will double the number of stations violating the current National Ambient Air Quality Standard (NAAQS) for ozone in 2050, when policies are in effect, this number was reduced to 21 stations. The number of high-ozone days will also increase in climate change only case in all regions with an average of 5.7 extra high-ozone days which confirms previous studies. The results show that even with high-ozone precursor reductions, the ozone levels will still violate the current national ozone standard. Therefore, in order to meet the current ozone standard by 2050, more stringent climate and air pollution control policies for most regions in the USA are needed.

Impact of Long-Term Exposures to Ambient PM2.5 and Ozone on ARDS Risk for Older Adults in the United States

Chronic exposures to particulate matter with an aerodynamic diameter< 2.5 μm (PM2.5) and ozone pollution can affect respiratory function. ARDS, an often lethal respiratory failure, is most common among older adults. However, few epidemiology studies have investigated an association between air pollution and the risk of ARDS. This observational study was conducted to estimate air pollution exposures at theZIP code level and hospital admissions with ARDS among US Medicare beneficiaries aged≥ 65 years from 2000 to 2012. A two-pollutant generalized linear mixed model, adjusting for sex, age, race, median household income, smoking, and weather, was applied. There were a total of 1,164,784 hospital admissions with ARDS in the cohort. Increases of 1 µg/m3 in annual average PM2.5 and of 1 parts per billion in annual average ozone were associated with increases in annual hospital admission rates for ARDS of 0.72%(95%CI, 0.62-0.82) and 0.15%(95%CI, 0.08-0.22), respectively. In low-pollution regions (annual average PM2.5 level< 12 µg/m3 and annual average ozone level< 45 parts per billion), the same annual increase in PM2.5 and ozone were associated with increases in annual hospital admission rates for ARDS of 1.50%(95%CI, 1.27-1.72) and 0.27%(95%CI, 0.16-0.38). Long-term exposures to PM2.5 and ozone were associated with increased risk of ARDS among older adults in the United States, including exposures below current annual US National Ambient Air Quality Standards.

Long-term exposure to traffic-related air pollution and systemic lupus erythematosus in Taiwan: A cohort study

Systemic lupus erythematosus (SLE) is a multi-systemic chronic autoimmune disease, the etiology of SLE is still unclear. Only a few studies evaluated the associations between air pollution and SLE. We conducted a population-based cohort study in Taiwan to examine the associations of air pollution with SLE. A total of 682,208 individuals aged 18–70 years were retrieved from National Health Insurance Research Database. We applied 1-km resolution land use regression and satellite-based models to estimate air pollutant concentrations during 2001–2010. The mixed effect Cox models with time-dependent variables were performed to estimate the associations between air pollution and SLE, as hazard ratios (HRs) with 95% confidence interval (CI). We identified 1292 newly diagnosed SLE patients with average age of 43.26 ± 13.64 years, most of them were female. There were positive associations of SLE with exposure to a 9.76 ppb increase in nitrogen dioxide (NO2), a 0.20 ppm increase in carbon monoxide (CO), and a 10.2 μg/m3 increase in fine particles (PM2.5) (HR = 1.21, 95% CI: 1.08–1.36, HR = 1.44, 95% CI: 1.31–1.59, and HR = 1.12, 95% CI: 1.02–1.23, respectively). Additionally, we observed negative associations with ozone (O3) and sulfur dioxide (SO2). According to the exposure-response relationships, exposure to NO2 between 28 and 38 ppb, exposure to CO above 0.6 ppm, and exposure to PM2.5 between 18 and 46 μg/m3 were positively associated with SLE. The results suggested that long-term exposure to traffic-related gaseous air pollutants (NO2 and CO) less than current National Ambient Air Quality Standards and PM2.5 are significantly associated with the risk of SLE.

8 - Supplementation with omega-3 fatty acids potentiates glutathione oxidation in human airway epithelial cells exposed to ozone

The health benefits of dietary fish oil consumption have been widely reported. Eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids, two omega-3 fatty acids found in fish oil, have been associated with anti-inflammatory and pro-resolving effects through their metabolism to specialized pro-resolving mediators (SPMs) and displacement of arachidonic acid (AA). However, the 5 and 6 double bonds in EPA and DHA respectively are targets for lipid peroxidation by ozone (O3), a major photochemical pollutant to which millions of Americans are exposed. Products of unsaturated fatty acid peroxidation by O3 have been proposed to mediate functional and inflammatory effects of O3 exposure. Thus, cellular supplementation with omega-3s has the potential to both promote and help resolve inflammation during O3 exposure. To investigate this paradox, we supplemented 16-HBE human airway epithelial cells (HAEC) expressing the fluorogenic glutathione redox potential (EGSH) sensor roGFP overnight with EPA, DHA, the monounsaturated fatty acid oleic acid (OA), or the saturated fatty acid stearic acid (SA). Alterations in EGSH were monitored in real time using live-cell microscopy during exposure to O3. We found that supplementation with EPA and DHA, but not OA or SA, caused a marked potentiation of the O3-induced increases in EGSH, evident as both an accelerated response time and increase in the magnitude of response. Notably, the potentiation of GSH oxidation occurred at O3 concentrations as low as 0.08 ppm, the current National Ambient Air Quality Standard level. These results suggest that membrane fatty acid saturation is a determinant of the oxidative responses to O3 in HAEC. These findings may have implications for dietary recommendations for populations exposed to O3. This abstract does not necessarily reflect EPA policy.

Estimating Fine-Scale Temporal and Spatial Characteristics of SO2 Exposures Using U.S. EPA's Air Pollutants Exposure (APEX) Model

The U.S. EPA Air Pollutants Exposure Model (APEX) is a stochastic model simulating inhalation exposure using fine-scale population demographics, human activity and physiology, time series of ambient chemical concentrations, and parameterizations of chemical infiltration into microenvironments. For a recent high-resolution population-based exposure assessment of three U.S. urban areas (Tulsa, OK; Indianapolis, IN; Fall River, MA), we used APEX to estimate the percent of the study population experiencing 5-minute SO2 exposures at or above selected benchmark levels (100&amp;#8211;400 ppb, 100-ppb increments) and the resultant lung-function decrements. We generated complete time series of 5-minute ambient SO2 concentrations at thousands of receptors in each study area, combining modeled hourly concentrations with continuous 5-minute ambient measurements for 2011&amp;#8211;2013, then adjusted to just meet the current national ambient air quality standard. We developed new model input data and algorithms as a function of sex and age to support the high resolution of this assessment, including data on demographics, commuting patterns, and asthma prevalence at the level of U.S. Census blocks, and algorithms to estimate short-term breathing rates and energy expenditure. Results showed notable differences in SO2 exposure by location, with fewer elevated exposures and health risks estimated in Tulsa, OK relative to the other study areas. An important factor in these results is the lower numbers of people estimated to live or work in areas of higher SO2 concentrations in the Tulsa scenario relative to the other scenarios. These results indicate the importance of the accuracy and spatiotemporal resolution of the air concentration and population data in estimating population exposures and health risks to inform policy decisions.

Exposure to indoor radon can be a concern in studies on the role of short-term exposure to air pollution and mortality.

Abstract Recent studies show that short-term exposure to ambient particulate matter is associated with more emergency department visits and hospitalizations for pneumonia as well as increased mortality and increased health care costs among older adults. Moreover, exposure to ambient particulate matter is shown to be connected with an increased rate of daily mortality and hospitalizations due to cardiovascular diseases (CVDs). The association between short-term exposures to particulate matter with a diameter less than 2.5 µm (PM2.5) and ozone [at levels below the current daily National Ambient Air Quality Standards (NAAQS)] and mortality in the continental United States has been recently addressed by some researchers. Although exposure to radon is usually known to cause late health effects such as lung cancer, some studies show a significant association between radon exposure and cerebrovascular disease (CeVD) mortality. In some residential areas with high levels of radon, it has been found that the incidences of respiratory, nervous system and cardiovascular system diseases exceed the average. Studies that calculated the radiation dose to blood and the walls of coronary arteries from radon and progeny also indicate that exposure to radon can increase the incidence of CVDs. Based on the evidence provided in this short communication, it can be concluded that ignoring the key role of radon in non-cancer mortality can easily affect the validity of the studies aimed at investigating the association between exposure to ambient fine particulate matter and mortality.

Baseline Air Quality Assessment of Goods Movement Activities before the Port of Charleston Expansion: A Community-University Collaborative.

As the demand for goods continues to increase, a collective network of transportation systems is required to facilitate goods movement activities. This study examines air quality near the Port of Charleston before its expansion and briefly describes the establishment and structure of a community-university partnership used to monitor existing pollution. Particulate matter (PM) concentrations (PM2.5 and PM10) were measured using the Thermo Fisher Scientific Partisol 2000i-D Dichotomous Air Sampler, Thermo Scientific Dichotomous Sequential Air Sampler Partisol-Plus 2025-D, and Rupprecht & Patashnick TEOM Series 1400 Sampler at neighborhood (Union Heights, Rosemont, and Accabee) and reference (FAA2.5 and Jenkins Street) sites. Descriptive statistics were performed and an ANOVA (analysis of variance) was calculated to find the difference in overall mean 24-hour PM average concentrations in communities impacted by environmental injustice. PM2.5 (15.2 μg/m3) and PM10 (27.2 μg/m3) maximum concentrations were highest in neighborhoods such as Union Heights neighborhoods due to more goods movement activities. Nevertheless, there was no statistically significant difference in mean concentrations of PM2.5 and PM10 across neighborhood sites. In contrast, mean PM10 neighborhood concentrations were significantly lower than mean PM10 reference concentrations for Union Heights (p = 0.00), Accabee (p ≤ 0.0001), and Rosemont (p = 0.01). Although PM concentrations were lower than current National Ambient Air Quality Standards, this study demonstrated how community-university partners can work collectively to document baseline PM concentrations that will be used to examine changes in air quality after the port expansion brings additional goods movement activities to the area.

Different effects of long-term exposures to SO2 and NO2 air pollutants on asthma severity in young adults

ABSTRACTNumerous studies demonstrated that exposure to ambient air pollutants contributes to severity and frequency of asthma exacerbations. However, whether common air pollutants, such as nitrogen dioxide (NO2) and sulfur dioxide (SO2), exert differential effects on asthma occurrence and severity is unclear. The aim of this investigation was to determine whether exposure to NO2 and/or SO2 may initiate different long-term effects on prevalence and severity of asthma in young adults. Medical records of 137,040 males, 17 years old, who underwent standard premilitary service health examinations during 1999–2008 were examined. Air-pollution data for NO2 and SO2 were linked to the place of residence of each subject. The influence of specific air pollutants on asthma prevalence and severity was evaluated using bivariate logistic regression, controlling for individuals’ sociodemographic attributes. For both ambient air pollutants, there was a significant dose-response effect on severity of asthma at ambient concentrations below the current National Ambient Air Quality Standards. However, in residential areas with high levels of SO2 (13.3–592.7µg/m3) and high levels of NO2 (27.2–43.2µg/m3) the risk of asthma occurrence was significantly higher than that in residential areas with high levels of NO2 (27.2–43.2 µg/m3) and intermediate levels (6.7–13.3 µg/m3) of SO2 pollution. The effects of exposure to SO2 and NO2 air pollutants on the respiratory airways system appear to differ, with possible implications regarding medical management, even in cases of exposure to mixtures of these pollutants.

Future year ozone source attribution modeling studies for the eastern and western United States

Three modeling approaches, the U.S. Environmental Protection Agency’s (EPA) Community Multiscale Air Quality (CMAQ) zero-out, the Comprehensive Air quality Model with extensions (CAMx) zero-out, and the CAMx probing tools ozone source apportionment tool (OSAT), were used to project the contributions of various source categories to future year design values for summer 8-hr average ozone concentrations at selected U.S. monitors. The CMAQ and CAMx zero-out or brute-force approaches predicted generally similar contributions for most of the source categories, with some small differences. One of the important findings from this study was that both the CMAQ and CAMx zero-out approaches tended to apportion a larger contribution to the “other” category than the OSAT approach. For the OSAT approach, this category is the difference between the total emissions and the sum of the tracked emissions and consists of non-U.S. emissions. For the zero-out approach, it also includes the effects of nonlinearities in the system because the sum of the sensitivities of all sources is not necessarily equal to the sum of their contributions in a nonperturbed environment. The study illustrates the strengths and weaknesses of source apportionment approaches, such as OSAT, and source sensitivity approaches, such as zero-out. The OSAT approach is suitable for studying source contributions, whereas the zero-out approach is suitable for studying response to emission changes. Future year design values of summer 8-hr average ozone concentrations were projected to decrease at all the selected monitors for all the simulations in each city, except at the downtown Los Angeles monitor. Both the CMAQ and CAMx results showed all modeled locations project attainment in 2018 and 2030 to the current National Ambient Air Quality Standards (NAAQS) level of 75 ppb, except the selected Los Angeles monitor in 2018 and the selected San Bernardino monitor in 2018 and 2030.Implications:This study illustrates the strengths and weaknesses of three modeling approaches, CMAQ zero-out, CAMx zero-out, and OSAT to project contributions of various source categories to future year design values for summer 8-hr average ozone concentrations at selected U.S. monitors. The OSAT approach is suitable for studying source contributions, whereas the zero-out approach is suitable for studying response to emission changes. Future year design values of summer 8-hr average ozone concentrations were projected to decrease, except at the downtown Los Angeles monitor. Comparing projections with the current NAAQS (75 ppb) show attainment everywhere, except two locations in 2018 and one location in 2030.

Ozone in remote areas of the Southern Rocky Mountains

Ozone (O3) data are sparse for remote, non-urban mountain areas of the western U.S. Ozone was monitored 2007–2011 at high elevation sites in national forests in Colorado and northeastern Utah using a portable battery-powered O3 monitor. The data suggest that many of these remote locations already have O3 concentrations that would contribute to exceedance of the current National Ambient Air Quality Standard (NAAQS) for O3 and most could exceed a proposed more stringent secondary standard. There were significant year-to-year differences in O3 concentration. Ozone was primarily in the mid-concentration range, rarely exceeding 100 ppb or dropping below 30 ppb. The small diel changes in concentration indicate mixing ratios of NOx, VOCs, and O3 that favor stable O3 concentrations. The large number of mid-level O3 concentrations contributed to high W126 O3 values, the metric proposed as a possible new secondary standard. Higher O3 concentrations in springtime and at night suggest that stratospheric intrusion may be contributing to ambient O3 at these sites. Highest nighttime O3 concentrations occurred at the highest elevations, while daytime O3 concentrations did not have a relationship with elevation. These factors favor O3 concentrations at many of our remote locations that may exceed the O3 NAAQS, and suggest that exceedances are likely to occur at other western rural locations.

Evaluation of adverse human lung function effects in controlled ozone exposure studies

The US EPA is evaluating controlled human ozone exposure studies to determine the adequacy of the current ozone National Ambient Air Quality Standard of 75 ppb. These studies have shown that ozone exposures of 80 ppb and greater are associated with lung function decrements. Here, we critically review studies with exposures below 80 ppb to determine the lowest ozone concentration at which decrements are causally associated with ozone exposure and could be considered adverse using the Adverse Effects/Causation Framework. Regarding causation, the framework includes consideration of whether exposure-related effects are primary or secondary, statistically significant, isolated or independent, or due to study limitations. Regarding adversity, the framework indicates one should consider whether effects are adaptive, compensatory, precursors to an apical effect, severe, transient and/or reversible. We found that, at exposures below 72 ppb ozone, lung function effects are primary effects, but are isolated, independent and not statistically different compared to effects observed during filtered air exposure, indicating a lack of causation. Up to 72 ppb, lung function effects may be precursors to an apical effect, but are not likely adverse because they are transient, reversible, of low severity, do not interfere with normal activity and do not result in permanent respiratory injury or progressive respiratory dysfunction. Overall, these studies do not demonstrate a causal association between ozone concentrations in the range of the current National Ambient Air Quality Standard and adverse effects on lung function.