Jongbae Heo

Source apportionment of PM2.5 at the coastal area in Korea

In this study, we analyzed the chemical composition of fine particulate matter 2.5 μm or less (PM) collected at Incheon, the coastal area in Seoul, Korea every third day from June 2009 to May 2010. Based on the analyzed chemical species in the PM samples, the sources of PM were identified using a positive matrix factorization (PMF). Nine sources of PM were determined from PMF analysis. The major sources of PM were secondary nitrate (25.4%), secondary sulfate (19.0%), motor vehicle 1 (14.8%) with a lesser contribution from industry (8.5%), motor vehicle 2 (8.2%), biomass burning (6.1%), soil (6.1%), combustion and copper production emissions (6.1%), and sea salt (5.9%). From a paired t-test, it was found that yellow sand samples were characterized as having higher contribution from soil sources (p<0.05). Furthermore, the likely source areas of PM emissions were determined using the conditional probability function (CPF) and the potential source contribution function (PSCF). CPF analysis identified the likely local sources of PM as motor vehicles and sea salt. PSCF analysis indicated that the likely source areas for secondary particles (sulfate and nitrate) were the major industrial areas in China. Finally, using the source contribution of PM and associated organic composition data, principal component analysis (PCA) was conducted to evaluate the accuracy of the PM source apportionments by PMF. The PCA analysis confirmed eight of the nine PM sources. Our result implies that the chemical composition analysis of PM data and various modeling techniques can effectively identify the potential contributing sources.

Fine particle air pollution and mortality: importance of specific sources and chemical species.

Background: While exposure to ambient fine particles <2.5 &mgr;m in aerodynamic diameter (PM2.5) has well-established health effects, there is limited quantitative evidence that links specific sources of PM2.5 with those effects. This study was designed to examine the risks of exposure to chemical species and source-specific PM2.5 mass on mortality in Seoul, Korea, a highly populated city. Methods: We compare daily mortality counts with PM2.5 chemical speciation data collected every 3 days, as well as nine sources of PM2.5 mass resolved by a positive matrix factorization receptor model, from March 2003 through November 2007. A Poisson generalized linear model incorporating natural splines was used to evaluate associations of PM2.5 chemical species and sources with mortality. Results: PM2.5 mass and several chemical species were associated with mortality. Organic carbon, elemental carbon, and lead were associated with mortality outcomes when using multipollutant models adjusted for other chemical species levels. Source-apportioned PM2.5 derived from mobile sources (ie, gasoline and diesel emissions) and biomass burning was associated with respiratory mortality and cardiovascular mortality, respectively. There were moderate associations of industry and of roadway emissions with cardiovascular mortality. Conclusions: Local combustion sources may be particularly important contributors to PM2.5, leading to adverse health effects.

Ambient air pollution and out-of-hospital cardiac arrest

BACKGROUND Sudden cardiac arrest is a leading cause of cardiovascular death. This study aimed at investigating the impact of short-term exposure to air pollutants on the incidence of OHCA. METHODS We identified OHCA cases that occurred in Seoul between 2006 and 2013 from the nationwide emergency medical service database. The association of the daily incidence of OHCA with air pollutants including PM2.5 (particles ≤ 2.5 μm in aerodynamic diameter), PM10, CO, O3, NO2, and SO2 was analyzed with the use of time-series and case-crossover analyses. RESULTS A total of 21,509 OHCAs of presumed cardiac origin were identified. An elevation in PM2.5 by 10 μg/m(3) at a moving average of lag 1 and 2 days was shown to increase the risk of OHCA by 1.30% (95% confidence intervals, 0.20-2.41%). An exposure-response relationship was present: the risk of OHCA increased significantly with even a mild elevation of PM2.5 (10-15 μg/m(3)) and further increased with higher levels. While PM10, NO2, CO, and SO2 also showed significant associations with OHCA in single-pollutant models, only PM2.5 remained significant after adjustment for other pollutants. Subgroup analyses showed male sex, advanced age, hypertension, diabetes, heart disease, and history of stroke were risk factors for OHCA in response to elevations in PM2.5. CONCLUSIONS This study showed that increased ambient levels of PM2.5 were significantly associated with increased risk of OHCA within 1 to 2 days of exposure, which had a dose-response relationship. Subjects with conventional cardiovascular risk factors were more susceptible to harm of PM2.5.

An in vitro alveolar macrophage assay for the assessment of inflammatory cytokine expression induced by atmospheric particulate matter.

Exposures to air pollution in the form of particulate matter (PM) can result in excess production of reactive oxygen species (ROS) in the respiratory system, potentially causing both localized cellular injury and triggering a systemic inflammatory response. PM‐induced inflammation in the lung is modulated in large part by alveolar macrophages and their biochemical signaling, including production of inflammatory cytokines, the primary mechanism via which inflammation is initiated and sustained. We developed a robust, relevant, and flexible method employing a rat alveolar macrophage cell line (NR8383) which can be applied to routine samples of PM from air quality monitoring sites to gain insight into the drivers of PM toxicity that lead to oxidative stress and inflammation. Method performance was characterized using extracts of ambient and vehicular engine exhaust PM samples. Our results indicate that the reproducibility and the sensitivity of the method are satisfactory and comparisons between PM samples can be made with good precision. The average relative percent difference for all genes detected during 10 different exposures was 17.1%. Our analysis demonstrated that 71% of genes had an average signal to noise ratio (SNR) ≥ 3. Our time course study suggests that 4 h may be an optimal in vitro exposure time for observing short‐term effects of PM and capturing the initial steps of inflammatory signaling. The 4 h exposure resulted in the detection of 57 genes (out of 84 total), of which 86% had altered expression. Similarities and conserved gene signaling regulation among the PM samples were demonstrated through hierarchical clustering and other analyses. Overlying the core congruent patterns were differentially regulated genes that resulted in distinct sample‐specific gene expression “fingerprints.” Consistent upregulation of Il1f5 and downregulation of Ccr7 was observed across all samples, while TNFα was upregulated in half of the samples and downregulated in the other half. Overall, this PM‐induced cytokine expression assay could be effectively integrated into health studies and air quality monitoring programs to better understand relationships between specific PM components, oxidative stress activity and inflammatory signaling potential.

Assessing the role of chemical components in cellular responses to atmospheric particle matter (PM) through chemical fractionation of PM extracts

In order to further our understanding of the influence of chemical components and ultimately specific sources of atmospheric particulate matter (PM) on pro-inflammatory and other adverse cellular responses, we promulgate and apply a suite of chemical fractionation tools to aqueous aerosol extracts of PM samples for analysis in toxicity assays. We illustrate the approach with a study that used water extracts of quasi-ultrafine PM (PM0.25) collected in the Los Angeles Basin. Filtered PM extracts were fractionated using Chelex, a weak anion exchanger diethylaminoethyl (DEAE), a strong anion exchanger (SAX), and a hydrophobic C18 resin, as well as by desferrioxamine (DFO) complexation that binds iron. The fractionated extracts were then analyzed using high-resolution sector field inductively coupled plasma mass spectrometry (SF-ICPMS) to determine elemental composition. Cellular responses to the fractionated extracts were probed in an in vitro rat alveolar macrophages model with measurement of reactive oxygen species (ROS) production and the cytokine tumor necrosis factor-α (TNF-α). The DFO treatment that chelates iron was very effective at reducing the cellular ROS activity but had only a small impact on the TNF-α production. In contrast, the hydrophobic C18 resin treatment had a small impact on the cellular ROS activity but significantly reduced the TNF-α production. The use of statistical methods to integrate the results across all treatments led to the conclusion that sufficient iron must be present to participate in the chemistry needed for ROS activity, but the amount of ROS activity is not proportional to the iron solution concentration. ROS activity was found to be most related to cationic mono- and divalent metals (i.e., Mn and Ni) and oxyanions (i.e., Mo and V). Although the TNF-α production was not significantly affected by the chelexation of iron, it was greatly impacted by the removal of organics with the C18 resin and all other metal removal methods, suggesting that iron is not a critical pathway leading to TNF-α production, but a wide range of soluble metals and organic compounds in particulate matter play a role. Although the results are specific to the Los Angeles Basin, where the samples used in the study were collected, the method employed in the study can be widely employed to study the role of components of particulate matter in in vitro or in vivo assays.

Spatial and Temporal Variation in Fine Particulate Matter Mass and Chemical Composition: The Middle East Consortium for Aerosol Research Study

Ambient fine particulate matter (PM2.5) samples were collected from January to December 2007 to investigate the sources and chemical speciation in Palestine, Jordan, and Israel. The 24-h PM2.5 samples were collected on 6-day intervals at eleven urban and rural sites simultaneously. Major chemical components including metals, ions, and organic and elemental carbon were analyzed. The mass concentrations of PM2.5 across the 11 sites varied from 20.6 to 40.3 μg/m3, with an average of 28.7 μg/m3. Seasonal variation of PM2.5 concentrations was substantial, with higher average concentrations (37.3 μg/m3) in the summer (April–June) months compared to winter (October–December) months (26.0 μg/m3) due mainly to high contributions of sulfate and crustal components. PM2.5 concentrations in the spring were greatly impacted by regional dust storms. Carbonaceous mass was the most abundant component, contributing 40% to the total PM2.5 mass averaged across the eleven sites. Crustal components averaged 19.1% of the PM2.5 mass and sulfate, ammonium, and nitrate accounted for 16.2%, 6.4%, and 3.7%, respectively, of the total PM2.5 mass. The results of this study demonstrate the need to better protect the health and welfare of the residents on both sides of the Jordan River in the Middle East.

Understanding the sources and composition of the incremental excess of fine particles across multiple sampling locations in one air shed

Well-designed health studies and the development of effective regulatory policies need to rely on an understanding of the incremental differences in particulate matter concentrations and their sources. Although only a limited number of studies have been conducted to examine spatial differences in sources to particulate matter within an air shed, routine monitoring data can be used to better understand these differences. Measurements from the US EPA Chemical Speciation Network (CSN) collected between 2002-2008 were analyzed to demonstrate the utility of regulatory data across three sites located within 100 km of each other. Trends in concentrations, source contribution, and incremental excesses across three sites were investigated using the Positive Matrix Factorization model. Similar yearly trends in chemical composition were observed across all sites, however, excesses of organic matter and elemental carbon were observed in the urban center that originated from local emissions of mobile sources and biomass burning. Secondary sulfate and secondary nitrate constituted over half of the PM2.5 with no spatial differences observed across sites. For these components, the excess of emissions from industrial sources could be directly quantified. This study demonstrates that CSN data from multiple sites can be successfully used to derive consistent source profiles and source contributions for regional pollution, and that CSN data can be used to quantify incremental differences in source contributions of across these sites. The analysis strategy can be used in other regions of the world to take advantage of existing ambient particulate matter monitoring data to better the understanding of spatial differences in source contributions within a given air shed.

Cardiovascular Effects of Long‐Term Exposure to Air Pollution: A Population‐Based Study With 900 845 Person‐Years of Follow‐up

Background Studies have shown that long‐term exposure to air pollution such as fine particulate matter (≤2.5 μm in aerodynamic diameter [PM 2.5]) increases the risk of all‐cause and cardiovascular mortality. To date, however, there are limited data on the impact of air pollution on specific cardiovascular diseases. This study aimed to evaluate cardiovascular effects of long‐term exposure to air pollution among residents of Seoul, Korea. Methods and Results Healthy participants with no previous history of cardiovascular disease were evaluated between 2007 and 2013. Exposure to air pollutants was estimated by linking the location of outdoor monitors to the ZIP code of each participants residence. Crude and adjusted analyses were performed using Cox regression models to evaluate the risk for composite cardiovascular events including cardiovascular mortality, acute myocardial infarction, congestive heart failure, and stroke. A total of 136 094 participants were followed for a median of 7.0 years (900 845 person‐years). The risk of major cardiovascular events increased with higher mean concentrations of PM 2.5 in a linear relationship, with a hazard ratio of 1.36 (95% confidence interval, 1.29–1.43) per 1 μg/m3 PM 2.5. Other pollutants including PM 2.5–10 of CO, SO 2, and NO 2, but not O3, were significantly associated with increased risk of cardiovascular events. The burden from air pollution was comparable to that from hypertension and diabetes mellitus. Conclusions This large‐scale population‐based study demonstrated that long‐term exposure to air pollution including PM 2.5 increases the risk of major cardiovascular disease and mortality. Air pollution should be considered an important modifiable environmental cardiovascular risk factor.

Source apportionments of ambient fine particulate matter in Israeli, Jordanian, and Palestinian cities ☆

This manuscript evaluates spatial and temporal variations of source contributions to ambient fine particulate matter (PM2.5) in Israeli, Jordanian, and Palestinian cities. Twenty-four hour integrated PM2.5 samples were collected every six days over a 1-year period (January to December 2007) in four cities in Israel (West Jerusalem, Eilat, Tel Aviv, and Haifa), four cities in Jordan (Amman, Aqaba, Rahma, and Zarka), and three cities in Palestine (Nablus, East Jerusalem, and Hebron). The PM2.5 samples were analyzed for major chemical components, including organic carbon and elemental carbon, ions, and metals, and the results were used in a positive matrix factorization (PMF) model to estimate source contributions to PM2.5 mass. Nine sources, including secondary sulfate, secondary nitrate, mobile, industrial lead sources, dust, construction dust, biomass burning, fuel oil combustion and sea salt, were identified across the sampling sites. Secondary sulfate was the dominant source, contributing 35% of the total PM2.5 mass, and it showed relatively homogeneous temporal trends of daily source contribution in the study area. Mobile sources were found to be the second greatest contributor to PM2.5 mass in the large metropolitan cities, such as Tel Aviv, Hebron, and West and East Jerusalem. Other sources (i.e. industrial lead sources, construction dust, and fuel oil combustion) were closely related to local emissions within individual cities. This study demonstrates how international cooperation can facilitate air pollution studies that address regional air pollution issues and the incremental differences across cities in a common airshed. It also provides a model to study air pollution in regions with limited air quality monitoring capacity that have persistent and emerging air quality problems, such as Africa, South Asia and Central America.

Heat, heat waves, and out-of-hospital cardiac arrest

OBJECTIVE Cardiac arrest is one of the common presentations of cardiovascular disorders and a leading cause of death. There are limited data on the relationship between out-of-hospital cardiac arrest (OHCA) and ambient temperatures, specifically extreme heat. This study investigated how heat and heat waves affect the occurrence of OHCA. METHODS Seven major cities in Korea with more than 1 million residents were included in this study. A heat wave was defined as a daily mean temperature above the 98th percentile of the yearly distribution for at least two consecutive days. RESULTS A total of 50,318 OHCAs of presumed cardiac origin were identified from the nationwide emergency medical service database between 2006 and 2013. Ambient temperature and OHCA had a J-shaped relationship with a trough at 28°C. Heat waves were shown to be associated with a 14-% increase in the risk of OHCA. Adverse effects were apparent from the beginning of each heat wave period and slightly increased during its continuation. Excess OHCA events during heat waves occurred between 3PM and 5PM. Subgroup analysis showed that those 65years or older were significantly more susceptible to heat waves. CONCLUSIONS Ambient temperature and OHCA had a J-shaped relationship. The risk of OHCA was significantly increased with heat waves. Excess OHCA events primarily occurred during the afternoon when the temperature was high. We found that the elderly were more susceptible to the deleterious effects of heat waves.