Fossil and Nonfossil Sources of Organic and Elemental Carbon Aerosols in the Outflow from Northeast China

Source quantification of carbonaceous aerosols in the Chinese outflow regions still remains uncertain despite their high mass concentrations. Here, we unambiguously quantified fossil and nonfossil contributions to elemental carbon (EC) and organic carbon (OC) of total suspended particles (TSP) from a regional receptor site in the outflow of Northeast China using radiocarbon measurement. OC and EC concentrations were lower in summer, representing mainly marine air, than in other seasons, when air masses mostly traveled over continental regions in Mongolia and northeast China. The annual-mean contribution from fossil-fuel combustion to EC was 76 ± 11% (0.1–1.3 μg m^–3). The remaining 24 ± 11% (0.03–0.42 μg m^–3) was attributed to biomass burning, with slightly higher contribution in the cold period (∼31%) compared to the warm period (∼21%) because of enhanced emissions from regional biomass combustion sources in China. OC was generally dominated by nonfossil sources, with an annual average of 66 ± 11% (0.5–2.8 μg m^–3), approximately half of which was apportioned to primary biomass-burning sources (34 ± 6%). In winter, OC almost equally originated from primary OC (POC) emissions and secondary OC (SOC) formation from fossil fuel and biomass-burning sources. In contrast, summertime OC was dominated by primary biogenic emissions as well as secondary production from biogenic and biomass-burning sources, but fossil-derived SOC was the smallest contributor. Distinction of POC and SOC was performed using primary POC-to-EC emission ratios separated for fossil and nonfossil emissions

Effect of rapamycin on LOX-1 expression in HUVECs.

<p>(A, B) Knocking down LOX-1 significantly reduced the rate of Dil-ox-LDL uptake in HUVECs. ***P < 0.001 versus control; ###P < 0.001 versus ox-LDL group. Data are expressed as mean ± SEM, n = 3. (C, D) The expression of LOX-1 protein assessed by western blotting after treatment of HUVECs with ox-LDL by time and concentration course. (E) The q-PCR showed that at least 20 nM rapamycin reduced the increase in LOX-1 mRNA expression induced by ox-LDL. ***P < 0.001 versus control; ###P < 0.001 versus Dil-ox-LDL group; NS = not significant compared with the Dil-ox-LDL group. Data are expressed as mean ± SEM, n = 3. (F) Western blotting indicated that rapamycin dose-dependently reduced the increase in production of LOX-1 protein triggered by ox-LDL. GAPDH was used as the loading control. ***P < 0.001 versus control; #P < 0.05 versus ox-LDL group; ###P < 0.001 versus ox-LDL group; NS = not significant compared with the ox-LDL group. Data are expressed as mean ± SEM, n = 3. (G) Western blotting indicated that 20 nM rapamycin time-dependently reduced the production of LOX-1 protein. *P < 0.05 versus control; ***P < 0.001 versus control; NS = not significant compared with the control group. Data are expressed as mean ± SEM, n = 3.</p

Effect of the P65/NF-κB signaling pathway on ox-LDL uptake in HUVECs.

<p>(A, B) Phosphorylation and degradation of IκBα analyzed by western blotting. *P < 0.05 versus control; **P < 0.01 versus control; ***P < 0.001 versus control; ##P < 0.01 versus ox-LDL group; NS = not significant compared with the control group. Data are expressed as mean ± SEM, n = 3–4. (C) Western blotting indicated that rapamycin time-dependently inhibited the phosphorylation of IκBα. *P < 0.05 versus control; ***P < 0.001 versus control; NS = not significant compared with the control group. Data are expressed as mean ± SEM, n = 3. (D) Translocation of NF-κB p65 was observed after ox-LDL treatment for 30 h under a fluorescence microscope. The experiment was repeated independently three times. (E-G) Flow cytometry showed that inhibition of NF-κB significantly reduced Dil-ox-LDL uptake in HUVECs. ***P < 0.001 versus control; ##P < 0.01 versus Dil-ox-LDL group; ###P < 0.001 versus Dil-ox-LDL group. Data are expressed as mean ± SEM, n = 3.</p

Upstream and downstream relationship between mTOR, NF-κB, LOX-1 and ox-LDL uptake in HUVECs.

<p>(A, B) Western blotting showed that inhibition of mTOR significantly reduced the increase in the expression of LOX-1 protein expression induced by ox-LDL. ***P < 0.001 versus control; ###P < 0.001 versus ox-LDL; NS = not significant. Data are expressed as mean ± SEM, n = 3. (C-E) Western blotting showed that inhibition of NF-κB significantly reduced the increase in the expression of LOX-1 protein expression induced by ox-LDL. ***P < 0.001 versus control; ###P < 0.001 versus ox-LDL; NS = not significant. Data are expressed as mean ± SEM, n = 3. (F) q-PCR indicated that mTOR and NF-κB knockdown reduced the upregulated expression of LOX-1 mRNA induced by ox-LDL. **P < 0.01 versus control; ###P < 0.001 versus ox-LDL. Data are expressed as mean ± SEM, n = 3. (G, H) IκBα phosphorylation and (I-K) mTOR phosphorylation were analyzed by western blotting, which showed that mTOR deficiency significantly reduced the IκBα phosphorylation triggered by ox-LDL, whereas inhibition of NF-κB did not reduce mTOR phosphorylation induced by ox-LDL. **P < 0.01 versus control; ***P < 0.001 versus control; ##P < 0.01 versus ox-LDL group; NS = not significant. Data are expressed as mean ± SEM, n = 3.</p

Effect of rapamycin on Dil-ox-LDL uptake in HUVECs.

<p>(A) MTT assay for cell viability after treatment with rapamycin by concentration course. NS = not significant. Data are expressed as mean ± SEM, n = 3. (B) Flow cytometry showed that pretreatment with at least 20 nM rapamycin for 1h significantly reduced Dil-ox-LDL accumulation in HUVECs. ***P < 0.001 versus control; ###P < 0.001 versus Dil-ox-LDL group; NS = not significant compared with the Dil-ox-LDL group. Data are expressed as mean ± SEM, n = 3. (C) Continuous images obtained from live cell imaging after 30 μg/mL Dil-ox-LDL treatment for 6 h. (D) Continuous images obtained from live cell imaging after 30 μg/mL Dil-ox-LDL treatment for 6 h following pretreatment with 20 nM rapamycin for 1 h. The experiment was repeated independently three times. (E)Western blot indicated that p62 was increased by bafilomycin A1, and was not reduced by simultaneous treatment with ox-LDL. NS = not significant. **P < 0.01 versus bafilomycin A1 group. Data are expressed as mean ± SEM, n = 3. (F)Flow cytometry indicated that after pretreatment with bafilomycin A1, rapamycin could still inhibit Dil-ox-LDL uptake in HUVECs. ***P < 0.001 versus control; #P < 0.05 versus Dil-ox-LDL group; ###P < 0.001 versus Dil-ox-LDL group; ##P < 0.01 versus Dil-ox-LDL group. Data are expressed as mean ± SEM, n = 3.</p

Radiocarbon-Based Source Apportionment of Carbonaceous Aerosols at a Regional Background Site on Hainan Island, South China

To assign fossil and nonfossil contributions to carbonaceous particles, radiocarbon (¹⁴C) measurements were performed on organic carbon (OC), elemental carbon (EC), and water-insoluble OC (WINSOC) of aerosol samples from a regional background site in South China under different seasonal conditions. The average contributions of fossil sources to EC, OC and WINSOC were 38 ± 11%, 19 ± 10%, and 17 ± 10%, respectively, indicating generally a dominance of nonfossil emissions. A higher contribution from fossil sources to EC (∼51%) and OC (∼30%) was observed for air-masses transported from Southeast China in fall, associated with large fossil-fuel combustion and vehicle emissions in highly urbanized regions of China. In contrast, an increase of the nonfossil contribution by 5–10% was observed during the periods with enhanced open biomass-burning activities in Southeast Asia or Southeast China. A modified EC tracer method was used to estimate the secondary organic carbon from fossil emissions by determining ¹⁴C-derived fossil WINSOC and fossil EC. This approach indicates a dominating secondary component (70 ± 7%) of fossil OC. Furthermore, contributions of biogenic and biomass-burning emissions to contemporary OC were estimated to be 56 ± 16% and 44 ± 14%, respectively