Optimizing an airborne mass-balance methodology for accurate emission rate quantification of industrial facilities: A case study of industrial facilities in South Korea.

Accurate estimation of emissions from industrial point sources is crucial in understanding the effectiveness of reduction efforts and establishing reliable emission inventories. In this study, we employ an airborne Chemical Ionization Mass Spectrometry (CIMS) instrument to quantify sulfur dioxide (SO2) emissions from prominent industrial facilities in South Korea, including power plants, a steel mill, and a petrochemical facility. Our analysis utilizes the box mass balance technique to derive SO2 emissions and associated uncertainty. We evaluate the interpolation methods between 2D kriging and 3D radial basis function. The results demonstrate that the total uncertainty of the box mass balance technique ranges from 5 % to 28 %, with an average of 20 %. Mixing ratio ground extrapolation from the lowest altitude of the airborne sampling to the ground emerges as the dominant source of uncertainty, followed by the determination of the boundary layer height. Adequate sampling at multiple altitudes is found to be essential in reducing the overall uncertainty by capturing the full extent of the plume. Furthermore, we assess the uncertainty of the single-height transect mass balance method commonly employed in previous studies. Our findings reveal an average precision of 47 % for this method, with the potential for overestimating emissions by up to 206 %. Samplings at fewer altitudes or with larger altitude gaps increase the risk of under-sampling and elevate method uncertainties. Therefore, this study provides a quantitative basis to evaluate previously airborne observational emission constraints.

Sulfur isotope-based source apportionment and control mechanisms of PM2.5 sulfate in Seoul, South Korea during winter and early spring (2017-2020).

High level of particulate matter (PM) concentrations are a major environmental concern in Seoul, South Korea, especially during winter and early spring. Sulfate is a major component of PM and induces severe environmental pollution, such as acid precipitation. Previous studies have used numerical models to constrain the relative contributions of domestic and trans-boundary sources to PM2.5 sulfate concentration in South Korea. Because of the scarce measurement result of δ34S for PM2.5 sulfate in South Korea, poorly defined δ34S value of domestic sulfur sources, and no application of sulfur isotope fractionation during sulfate formation in previous observation-based studies, source apportionment results conducted by model studies have not been corroborated from independent chemical observations. Here, we examined the δ34S of PM2.5 in Seoul and domestic sulfur sources, and considered the sulfur isotope fractionation for accurate source apportionment constraint. Accordingly, domestic and trans-boundary sulfur sources accounted for approximately (16-32) % and (68-84) % of the sulfate aerosols in Seoul, respectively, throughout the winter and early spring of 2017-2020. Air masses passing through north-eastern China had relatively low sulfate concentrations, enriched δ34S, and a low domestic source contribution. Those passing through south-eastern China had relatively a high sulfate concentrations, depleted δ34S, and high domestic source contribution. Furthermore, elevated PM2.5 sulfate concentrations (>10 µg m-3) were exclusively associated with a weak westerly wind speed of <3 m s-1. From December 2019 to March 2020, Seoul experienced relatively low levels of PM2.5 sulfate, which might be attributed to favorable weather conditions rather than the effects of COVID-19 containment measures. Our results demonstrate the potential use of δ34S for accurate source apportionment and for identifying the crucial role of regional air mass transport and meteorological conditions in PM2.5 sulfate concentration. Furthermore, the data provided can be essential for relevant studies and policy-making in East Asia.

The Korea-United States Air Quality (KORUS-AQ) field study.

The Korea-United States Air Quality (KORUS-AQ) field study was conducted during May-June 2016. The effort was jointly sponsored by the National Institute of Environmental Research of South Korea and the National Aeronautics and Space Administration of the United States. KORUS-AQ offered an unprecedented, multi-perspective view of air quality conditions in South Korea by employing observations from three aircraft, an extensive ground-based network, and three ships along with an array of air quality forecast models. Information gathered during the study is contributing to an improved understanding of the factors controlling air quality in South Korea. The study also provided a valuable test bed for future air quality-observing strategies involving geostationary satellite instruments being launched by both countries to examine air quality throughout the day over Asia and North America. This article presents details on the KORUS-AQ observational assets, study execution, data products, and air quality conditions observed during the study. High-level findings from companion papers in this special issue are also summarized and discussed in relation to the factors controlling fine particle and ozone pollution, current emissions and source apportionment, and expectations for the role of satellite observations in the future. Resulting policy recommendations and advice regarding plans going forward are summarized. These results provide an important update to early feedback previously provided in a Rapid Science Synthesis Report produced for South Korean policy makers in 2017 and form the basis for the Final Science Synthesis Report delivered in 2020.

The role of a suburban forest in controlling vertical trace gas and OH reactivity distributions - a case study for the Seoul metropolitan area.

We present trace gas vertical profiles observed by instruments on the NASA DC-8 and at a ground site during the Korea-US air quality study (KORUS) field campaign in May to June 2016. We focus on the region near the Seoul metropolitan area and its surroundings where both anthropogenic and natural emission sources play an important role in local photochemistry. Integrating ground and airborne observations is the major research goal of many atmospheric chemistry field campaigns. Although airborne platforms typically aim to sample from near surface to the free troposphere, it is difficult to fly very close to the surface especially in environments with complex terrain or a populated area. A detailed analysis integrating ground and airborne observations associated with specific concentration footprints indicates that reactive trace gases are quickly oxidized below an altitude of 700 m. The total OH reactivity profile has a rapid decay in the lower part of troposphere from surface to the lowest altitude (700 m) sampled by the NASA DC-8. The decay rate is close to that of very reactive biogenic volatile organic compounds such as monoterpenes. Therefore, we argue that photochemical processes in the bottom of the boundary layer, below the typical altitude of aircraft sampling, should be thoroughly investigated to properly assess ozone and secondary aerosol formation.

Characterizing isotopic compositions of TC-C, NO3--N, and NH4+-N in PM2.5 in South Korea: Impact of China's winter heating.

The origin of PM2.5 has long been the subject of debate and stable isotopic tools have been applied to decipher. In this study, weekly PM2.5 samples were simultaneously collected at an urban (Seoul) and rural (Baengnyeong Island) site in Korea from January 2014 through February 2016. The seasonal variation of isotopic species showed significant seasonal differences with sinusoidal variation. The isotopic results implied that isotope species from Baengnyeong were mostly originated from coal combustion during China's winter heating seasons, whereas in summer, the isotopic patterns observed that were more likely to be from marine. In Seoul, coal combustion related isotopic patterns increased during China's winter heating period while vehicle related isotopic patterns were dominated whole seasons by default. Therefore, aerosol formation was originated from long-range transported coal combustion-related NOx by vehicle-related NH3 in Seoul. δN-NH4+ in Seoul showed highly enriched 15N compositions in all seasons, indicating that NH3 from vehicle emission is the important source of NH4+ in PM2.5 in Seoul. In addition, Baengnyeong should be consistently considered as a key region for observing the changes of isotopic features depend on the contribution of individual emissions to the atmospheric as a result of the reduction of coal consumption in China.

REV1 and polymerase ζ facilitate homologous recombination repair.

REV1 and DNA Polymerase ζ (REV3 and REV7) play important roles in translesion DNA synthesis (TLS) in which DNA replication bypasses blocking lesions. REV1 and Polζ have also been implicated in promoting repair of DNA double-stranded breaks (DSBs). However, the mechanism by which these two TLS polymerases increase tolerance to DSBs is poorly understood. Here we demonstrate that full-length human REV1, REV3 and REV7 interact in vivo (as determined by co-immunoprecipitation studies) and together, promote homologous recombination repair. Cells lacking REV3 were hypersensitive to agents that cause DSBs including the PARP inhibitor, olaparib. REV1, REV3 or REV7-depleted cells displayed increased chromosomal aberrations, residual DSBs and sites of HR repair following exposure to ionizing radiation. Notably, cells depleted of DNA polymerase η (Polη) or the E3 ubiquitin ligase RAD18 were proficient in DSB repair following exposure to IR indicating that Polη-dependent lesion bypass or RAD18-dependent monoubiquitination of PCNA are not necessary to promote REV1 and Polζ-dependent DNA repair. Thus, the REV1/Polζ complex maintains genomic stability by directly participating in DSB repair in addition to the canonical TLS pathway.

Mre11-Rad50-Nbs1 complex is activated by hypertonicity.

When exposed to hypertonic conditions, cells accumulate double-strand DNA breaks (DSBs) like they are exposed to ionizing radiation. It has been proposed that inactivation of the Mre11-Rad50-Nbs1 (MRN) complex due to nuclear exit is responsible for the accumulation of DSBs as cells fail to repair DSBs produced during normal cellular activity. In this study, we examined the MRN complex in cells switched to hypertonicity. Surprisingly, we found that the MRN complex stayed in the nucleus and remained intact in response to hypertonicity. In fact, the MRN complex was dramatically activated after 4 h of switch to hypertonicity in a dose-dependent manner as shown by formation of foci. Activation of ATM and the MRN complex by hypertonicity and bleomycin was additive as was activation of their downstream targets including gammaH2AX and Chk2 indicating that the cellular response to DSB was intact in hypertonic conditions. Activation of Chk2 in response to hypertonicity was not observed in mutant cells with functionally impaired MRN complex confirming that they are in the same pathway. After 20 h of a switch to hypertonicity, MRN foci and gammaH2AX returned to a control level, suggesting that cells adapted to hypertonicity by repairing DNA. We conclude that cells respond normally to DSB and repair the DNA damages induced by hypertonicity.

Pim-1 is up-regulated by constitutively activated FLT3 and plays a role in FLT3-mediated cell survival.

Constitutively activating internal tandem duplication (ITD) mutations of the receptor tyrosine kinase FLT3 (Fms-like tyrosine kinase 3) play an important role in leukemogenesis, and their presence is associated with poor prognosis in acute myeloid leukemia (AML). To better understand FLT3 signaling in leukemogenesis, we have examined the changes in gene expression induced by FLT3/ITD or constitutively activated wild-type FLT3 expression. Microarrays were used with RNA harvested before and after inhibition of FLT3 signaling. Pim-1 was found to be one of the most significantly down-regulated genes upon FLT3 inhibition. Pim-1 is a proto-oncogene and is known to be up-regulated by signal transducer and activator of transcription 5 (STAT5), which itself is a downstream target of FLT3 signaling. Quantitative polymerase chain reaction (QPCR) confirmed the microarray results and demonstrated approximately 10-fold decreases in Pim-1 expression in response to FLT3 inhibition. Pim-1 protein also decreased rapidly in parallel with decreasing autophosphorylation activity of FLT3. Enforced expression of either the 44-kDa or 33-kDa Pim-1 isotypes resulted in increased resistance to FLT3 inhibition-mediated cytotoxicity and apoptosis. In contrast, expression of a dominant-negative Pim-1 construct accelerated cytotoxicity in response to FLT3 inhibition and inhibited colony growth of FLT3/ITD-transformed BaF3 cells. These findings demonstrate that constitutively activated FLT3 signaling up-regulates Pim-1 expression in leukemia cells. This up-regulation contributes to the proliferative and antiapoptotic pathways induced by FLT3 signaling.

Phosphorylation of threonine 68 promotes oligomerization and autophosphorylation of the Chk2 protein kinase via the forkhead-associated domain.

Phosphorylation of Thr-68 by the ataxia telangiectasia-mutated is necessary for efficient activation of Chk2 when cells are exposed to ionizing radiation. By an unknown mechanism, this initial event promotes additional autophosphorylation events including modifications of Thr-383 and Thr-387, two amino acid residues located within the activation loop segment within the Chk2 catalytic domain. Chk2 and related kinases possess one or more Forkhead-associated (FHA) domains that are phosphopeptide-binding modules believed to be crucial for their checkpoint control activities. We show that the Chk2 FHA domain is dispensable for Thr-68 phosphorylation but necessary for efficient autophosphorylation in response to ionizing radiation. Phosphorylation of Thr-68 promotes oligomerization of Chk2 by serving as a specific ligand for the FHA domain of another Chk2 molecule. In addition, Chk2 phosphorylates its own FHA domain, and this modification reduces its affinity for Thr-68-phosphorylated Chk2. Thus, activation of Chk2 in irradiated cells may occur through oligomerization of Chk2 via binding of the Thr-68-phosphorylated region of one Chk2 to the FHA domain of another. Oligomerization of Chk2 may therefore increase the efficiency of trans-autophosphorylation resulting in the release of active Chk2 monomers that proceed to enforce checkpoint control in irradiated cells.