Interpretation of the effects of anthropogenic chlorine on nitrate formation over northeast Asia during KORUS-AQ 2016.

The Weather Research and Forecasting-Community Multiscale Air Quality (WRF-CMAQ) model, implemented with anthropogenic chlorine (Cl) emissions, was evaluated against ground and NASA DC-8 aircraft measurements during the Korea-United States Air Quality (KORUS-AQ) 2016 campaign. The latest anthropogenic Cl emissions, including gaseous HCl and particulate chloride (pCl-) emissions from the Anthropogenic Chlorine Emissions Inventory of China (ACEIC-2014) (over China) and a global emissions inventory (Zhang et al., 2022) (over outer China), were used to examine the impacts of Cl emissions and the role of nitryl chloride (ClNO2) chemistry in N2O5 heterogeneous reactions on secondary nitrate (NO3-) formation across the Korean Peninsula. The model results against aircraft measurements clearly showed significant Cl- underestimations due mainly to the high gas-particle (G/P) partitioning ratios at aircraft measurement altitudes such as 700-850 hPa, but the ClNO2 simulations were reasonable. Several simulations of CMAQ-based sensitivity experiments against ground measurements indicated that although addition of Cl emission did not significantly alter NO3- formation, the activated ClNO2 chemistry with Cl emissions showed the best model performance with the reduced normalized mean bias (NMB) of 18.7 % compared to a value of 21.1 % for the Cl emissions-free case. In our model evaluation, ClNO2 accumulated during the night but quickly produced Cl radical due to ClNO2 photolysis at sunrise, which modulated other oxidation radicals (e.g., ozone [O3] and hydrogen oxide radicals [HOx]) in the early morning. In the morning hours (0800-1000 LST), the HOx were the dominant oxidants, contributing 86.6 % of the total oxidation capacity (sum of major oxidants such as O3 and HOx species), while oxidability was enhanced by up to ∼6.4 % (increase in 1 h HOx average of 2.89 × 106 molecules·cm-3) in the early morning mainly due to the changes in OH (+7.2 %), hydroperoxyl radical (HO2)(+10.0 %), and O3 (+4.2 %) over the Seoul Metropolitan Area, during the KORUS-AQ campaign. Our results improve understanding of the atmospheric changes in the PM2.5 formation pathway caused by ClNO2 chemistry and Cl emissions over northeast Asia.

Quantifying the premature mortality and economic loss from wildfire-induced PM2.5 in the contiguous U.S.

Emissions from wildfires worsen air quality and can adversely impact human health. This study utilized the fire inventory from NCAR (FINN) as wildfire emissions, and performed air quality modeling of April-October 2012, 2013, and 2014 using the U.S. Environmental Protection Agency CMAQ model under two cases: with and without wildfire emissions. This study then assessed the health impacts and economic values attributable to PM2.5 from fires. Results indicated that wildfires could lead annually to 4000 cases of premature mortality in the U.S., corresponding to $36 billion losses. Regions with high concentrations of fire-induced PM2.5 were in the west (e.g., Idaho, Montana, and northern California) and Southeast (e.g., Alabama, Georgia). Metropolitan areas located near fire sources, exhibited large health burdens, such as Los Angeles (119 premature deaths, corresponding to $1.07 billion), Atlanta (76, $0.69 billion), and Houston (65, $0.58 billion). Regions in the downwind of western fires, although experiencing relatively low values of fire-induced PM2.5, showed notable health burdens due to their large population, such as metropolitan areas of New York (86, $0.78 billion), Chicago (60, $0.54 billion), and Pittsburgh (32, $0.29 billion). Results suggest that impacts from wildfires are substantial, and to mitigate these impacts, better forest management and more resilient infrastructure would be needed.

Transboundary aerosol transport process and its impact on aerosol-radiation-cloud feedbacks in springtime over Northeast Asia.

Northeast Asia has been suffering from dramatic increases of particulate matter (PM) since the late 1990s, and it still continues to undergo haze despite various abating regulations. In this study, we investigated aerosol-cloud-precipitation (ACP) interactions with the varied PM, and the impact of long-range transport (LRT) process on ACP in springtime was assessed in Northeast Asia. Our long-term (1995-2019) analysis of PM10 exhibited the correlation with decreases of both sunshine duration and drizzle occurrences that can be interpreted as direct and indirect aerosol effects, while cloud cover induced by the varied PM10 was found only in more than 90% cloud cover (9/10-10/10 category). The online WRF-Chem with wind-blown dust simulation indicated that cloud water was affected by secondary inorganic aerosol (SIA) formation near the surface in upwind areas dominantly, whereas, along the LRT pathway, cloud water perturbation altitudes were increased quasi-linearly toward downward between 1 and 3 km. The gas-to-particle conversion ratios of sulfur ([SO42-]/[SO2 + SO42-]) and nitrogen ([NO3-]/[NO2 + NO3-]) both remain aloft long at the same vertical levels of most perturbed cloud altitude enough to be transported over long distance in springtime. Formations of sulfate and nitrate showed different ACP interaction timing; distinctive shifts in the ratios observed at the exit (Shanghai-Yellow Sea) by nitrate, and entrance areas (Seoul-Tokyo) by sulfate along the LRT pathway, respectively, with higher ratios of 0.8 or more in springtime. Our results indicate that ACP processes have been enhanced at a LRT-related altitude with different SIA production timings that can be considered in species-specific springtime PM abatements over Northeast Asia.

Lin28a ameliorates glucotoxicity-induced ß-cell dysfunction and apoptosis.

An excessive and prolonged increase in glucose levels causes ß-cell dysregulation, which is accompanied by impaired insulin synthesis and secretion, a condition known as glucotoxicity. Although it is known that both Lin28a and Lin28b regulate glucose metabolism, other molecular mechanisms that may protect against glucotoxicity are poorly understood. We investigated whether Lin28a overexpression can improve glucotoxicityinduced ß-cell dysregulation in INS-1 and primary rat islet cells. INS-1, a rat insulinoma cell line was cultured and primary rat islet cells were isolated from SD-rats. To define the effect of Lin28a in chronic high glucose-induced ß-cell dysregulation, we performed several in vitro and ex-vivo experiments. Chronic exposure to high glucose led to a downregulation of Lin28a mRNA and protein expression, followed by a decrease in insulin mRNA expression and secretion in ß-cells. The mRNA and protein expression levels of PDX-1 and BETA2, were reduced; The levels of apoptotic factors, including c-caspase3 and the Bax/Bcl-2 ratio, were increased due to glucotoxicity. Adenovirusmediated Lin28a overexpression in ß-cells reversed the glucotoxicity- induced reduction of insulin secretion and insulin mRNA expression via regulation of ß-cell-enriched transcription factors such as PDX-1 and BETA2. Adenovirus-mediated overexpression of Lin28a downregulated the glucotoxicity-induced upregulation of c-caspase3 levels and the Bax/Bcl-2 ratio, while inhibition of endogenous Lin28a by small interfering RNA resulted in their up-regulation. Lin28a counteracted glucotoxicity-induced downregulation of p-Akt and p-mTOR. Our results suggest that Lin28a protects pancreatic ß-cells from glucotoxicity through inhibition of apoptotic factors via the PI3 kinase/Akt/mTOR pathway. [BMB Reports 2021; 54(4): 215-220].

The impact of the direct effect of aerosols on meteorology and air quality using aerosol optical depth assimilation during the KORUS-AQ campaign.

To quantify the impact of the direct aerosol effect accurately, this study incorporated the Geostationary Ocean Color Imager (GOCI) aerosol optical depth (AOD) into a coupled meteorology-chemistry model. We designed three model simulations to observe the impact of AOD assimilation and aerosol feedback during the KORUS-AQ campaign (May - June 2016). By assimilating the GOCI AOD with high temporal and spatial resolutions, we improve the statistics from the comparison AOD and AERONET data (RMSE: 0.12, R: 0.77, IOA: 0.69, MAE: 0.08). The inclusion of the direct effect of aerosols produces the best model performance (RMSE: 0.10, R: 0.86, IOA: 0.72, MAE: 0.07). AOD values were increased as much as 0.15, which is associated with an average reduction in solar radiation of -31.39 W/m2, a planetary boundary layer height (-104.70 m), an air temperature (-0.58 °C), and a surface wind speed (-0.07 m/s) over land. In addition, concentrations of major gaseous and particulate pollutants at the surface (SO2, NO2, NH3, SO 4 2 - , NO 3 - , NH 4 + , PM2.5) increase by 7.87 - 34% while OH concentration decreases by -4.58 %. Changes in meteorology and air quality appear to be more significant in high-aerosol loading areas. The integrated process rate analysis shows decelerated vertical transport, resulting in an accumulation of air pollutants near the surface and the amount of nitrate, which is higher than that of sulfate because of its response to reduced temperature. We conclude that constraining aerosol concentrations using geostationary satellite data is a prerequisite for quantifying the impact of aerosols on meteorology and air quality.

Identification of chemical fingerprints in long-range transport of burning induced upper tropospheric ozone from Colorado to the North Atlantic Ocean.

This study investigates a significant biomass burning (BB) event occurred in Colorado of the United States in 2012 using the Community Multi-scale Air Quality (CMAQ) model. The simulation reasonably reproduced the significantly high upper tropospheric O3 concentrations (up to 145ppb) caused by BB emissions. We find the BB-induced O3 was primarily affected by chemical reactions and dispersion during its transport. In the early period of transport, high NOx and VOCs emissions caused O3 production due to reactions with the peroxide and hydroxyl radicals, HO2 and OH. Here, NOx played a key role in O3 formation in the BB plume. The results indicated that HO2 in the BB plume primarily came from formaldehyde (HCHO+hv=2HO2+CO), a secondary alkoxy radical (ROR=HO2). CO played an important role in the production of recycled HO2 (OH+CO=HO2) because of its abundance in the BB plume. The chemically produced HO2 was largely converted to OH by the reactions with NO (HO2+NO=OH+NO2) from BB emissions. This is in contrast to the surface, where HO2 and OH are strongly affected by VOC and HONO, respectively. In the late stages of transport, the O3 concentration was primarily controlled by dispersion. It stayed longer in the upper troposphere compared to the surface due to sustained depletion of NOx. Sensitivity analysis results support that O3 in the BB plume is significantly more sensitive to NOx than VOCs.

Inhibitory effect of luteolin on osteoclast differentiation and function.

Osteoclasts are multinucleated cells that play a crucial role in bone resorption, and are formed by the fusion of mononuclear osteoclasts derived from osteoclast precursors of the macrophage lineage. Compounds that specifically target functional osteoclasts would be ideal candidates for anti-resorptive agents for clinical applications. In the present study, we investigated the effects of luteolin, a flavonoid, on the regulation of receptor activator of nuclear factor-kappaB ligand (RANKL)-induced osteoclastogenesis, functions and signaling pathway. Addition of luteolin to a coculture system of mouse bone marrow cells and ST2 cells in the presence of 10(-8) M 1alpha,25(OH)(2)D(3) caused significant inhibition of osteoclastogenesis. Luteolin had no effects on the 1alpha,25(OH)(2)D(3)-induced expressions of RANKL, osteoprotegerin and macrophage colony-stimulating factor mRNAs. Next, we examined the direct effects of luteolin on osteoclast precursors using bone marrow macrophages and RAW264.7 cells. Luteolin completely inhibited RANKL-induced osteoclast formation. Moreover, luteolin inhibited the bone resorption by mature osteoclasts accompanied by the disruption of their actin rings, and these effects were reversely induced by the disruption of the actin rings in mature osteoclasts. Finally, we found that luteolin inhibited RANKL-induced osteoclastogenesis through the suppression of ATF2, downstream of p38 MAPK and nuclear factor of activated T-cells, cytoplasmic, calcineurin-dependent 1 (NFATc1) expression, respectively. Taken together, the present results indicate that naturally occurring luteolin has inhibitory activities toward both osteoclast differentiation and functions through inhibition of RANKL-induced signaling pathway as well as actin ring disruption, respectively.