Probing the occurrence, sources and cancer risk assessment of polycyclic aromatic hydrocarbons in PM2.5 in a humid metropolitan city in China.

Fifty-two consecutive PM2.5 samples from December 2021 to February 2022 (the whole winter) were collected in the center of Chongqing, a humid metropolitan city in China. These samples were analysed for the 16 USEPA priority polycyclic aromatic hydrocarbons (16 PAHs) to explore their composition and sources, and to assess their cancer risks to humans. The total concentrations of the 16 PAHs (ng m-3) ranged from 16.45 to 174.15, with an average of 59.35 ± 21.45. Positive matrix factorization (PMF) indicated that traffic emissions were the major source (42.4%), followed by coal combustion/industrial emission (31.3%) and petroleum leakage/evaporation (26.3%). The contribution from traffic emission to the 16 PAHs increased from 40.0% in the non-episode days to as high as 46.2% in the air quality episode during the sampling period. The population attributable fraction (PAF) indicates that when the unit relative risk (URR) is 4.49, the number of lung cancer cases per million individuals under PAH exposure is 27 for adults and 38 for seniors, respectively. It was 5 for adults and 7 for seniors, when the URR is 1.3. The average incremental lifetime cancer risk (ILCR) for children, adolescents, adults and seniors was 0.25 × 10-6, 0.23 × 10-6, 0.71 × 10-6, and 1.26 × 10-6, respectively. The results of these two models complemented each other well, and both implied acceptable PAH exposure levels. Individual genetic susceptibility and exposure time were identified as the most sensitive parameters. The selection and use of parameters in risk assessment should be further deepened in subsequent studies to enhance the reliability of the assessment results.

A comprehensive exploration of characteristics and source attribution of carbonaceous aerosols in PM2.5 in an East China megacity.

A total of 84 PM2.5 (fine particulate matter) aerosol samples were collected between October 2020 and August 2021 within an urban site in Hangzhou, an East China megacity. Chemical species, such as organic carbon (OC), elemental carbon (EC), as well as char, soot, and n-alkanes, were analyzed to determine their pollution characteristics and source contributions. The mean yearly concentrations of OC, EC, char, soot, and total n-alkanes (∑n-alkane) were 8.76 ± 3.61 µg/m3, 1.44 ± 0.76 µg/m3, 1.21 ± 0.69 µg/m3, 0.3 ± 0.1 µg/m3, and 24.2 ± 10.6 ng/m3. The OC, EC, and ∑n-alkanes were found in the highest levels during winter and lowest during summer. There were strong correlations between OC and EC in both winter and spring, suggesting similar potential sources for these carbonaceous components in both seasons. There were poor correlations among the target pollutants due to summertime secondary organic carbon formation. Potential source contribution functions analysis showed that local pollution levels in winter and autumn were likely influenced by long-range transportation from the Plain of North China. Source index and positive matrix factorization models provided insights into the complex sources of n-alkanes in Hangzhou. Their major contributors were identified as terrestrial plant releases (32.7%), traffic emissions (28.8%), coal combustion (27.3%), and microbial activity (11.2%). Thus, controlling vehicular emissions and coal burning could be key measures to alleviate n-alkane concentrations in the atmosphere of Hangzhou, as well as other Chinese urban centers.

Astaxanthin inhibits homocysteine­induced endothelial cell dysfunction via the regulation of the reactive oxygen species­dependent VEGF­VEGFR2­FAK signaling pathway.

Increased plasma levels of homocysteine (Hcy) can cause severe damage to vascular endothelial cells. Hcy­induced endothelial cell dysfunction contributes to the occurrence and development of human cerebrovascular diseases (CVDs). Our previous studies have revealed that astaxanthin (ATX) exhibits novel cardioprotective activity against Hcy­induced cardiotoxicity in vitro and in vivo. However, the protective effect and mechanism of ATX against Hcy­induced endothelial cell dysfunction requires further investigation. In the present study, treatment of human umbilical vascular endothelial cells (HUVECs) with Hcy inhibited the migration, invasive and tube formation potentials of these cells in a dose­dependent manner. Hcy treatment further induced a time­dependent increase in the production of reactive oxygen species (ROS), and downregulated the expression of vascular endothelial growth factor (VEGF), phosphorylated (p)­Tyr­VEGF receptor 2 (VEGFR2) and p­Tyr397­focal adhesion kinase (FAK). On the contrary, ATX pre­treatment significantly inhibited Hcy­induced cytotoxicity and increased HUVEC migration, invasion and tube formation following Hcy treatment. The mechanism of action may involve the effective inhibition of Hcy­induced ROS generation and the recovery of FAK phosphorylation. Collectively, our findings suggested that ATX could inhibit Hcy­induced endothelial dysfunction by suppressing Hcy­induced activation of the VEGF­VEGFR2­FAK signaling axis, which indicates the novel therapeutic potential of ATX in treating Hcy­mediated CVD.

Sources and dry deposition of carbonaceous aerosols over the coastal East China Sea: Implications for anthropogenic pollutant pathways and deposition.

75 paired TSP and PM2.5 samples were collected over four seasons on Huaniao Island (HNI), an island that lies downwind of continental pollutants emitted from mainland China to the East China Sea (ECS). These samples were analyzed for organic carbon (OC) and elemental carbon (EC), with a special focus on char-EC (char) and soot-EC (soot), to understand their sources, and the scale and extent of pollution and dry deposition over the coastal ECS. The results showed that char concentrations in PM2.5 and TSP averaged from 0.13 to 1.01 and 0.31-1.44 µg m-3; while for soot, they were from 0.03 to 0.21 and 0.16-0.56 µg m-3, respectively. 69.0% of the char and 36.4% of the soot were present in PM2.5. The char showed apparent seasonal variations, with highest concentrations in winter and lowest in summer; while soot displayed maximum concentrations in fall and minimum in summer. The char/soot ratios in PM2.5 averaged from 3.29 to 17.22; while for TSP, they were from 1.20 to 7.07. Both of the ratios in PM2.5 and TSP were highest in winter and lowest in fall. Comparisons of seasonal variations in OC/EC and char/soot ratios confirmed that char/soot may be a more effective indicator of carbonaceous aerosol source identification than OC/EC. Annual average atmospheric dry deposition fluxes of OC and EC into ECS were estimated to be 229 and 107 µg m-2 d-1, respectively, and their deposition fluxes significantly increased during episodes. It was estimated that the loadings of OC + EC and EC accounted for 1.3% and 4.1% of the total organic carbon and EC in ECS surface sediments, respectively, implying a relatively small contribution of OC and EC dry deposition to organic carbon burial. This finding also indicates a possibly more important contribution of wet deposition to organic carbon burial in sediments of ECS, and this factor should be considered for future study.

Silencing the receptor of activated C-kinase 1 (RACK1) suppresses tumorigenicity in epithelial ovarian cancer in vitro and in vivo.

Epithelial ovarian cancer (EOC) is a fatal disease for women due to lack of effective diagnostic biomarkers and therapeutic targets. Thus, it is important to identify and develop specific markers to formulate novel therapeutic methods for advanced and recurrent ovarian cancer. We found that the receptor of activated C-kinase 1 (RACK1) was elevated in most EOCs compared to normal ovarian tissue, and its expression levels correlated with key pathological characteristics including clinical stage and metastasis by quantitative PCR and immunohistochemistry. In addition, we found that downregulation of RACK1 expression using an RNA silencing approach in SKVO3 tumor cells significantly suppressed the proliferation, migration and invasion in vitro and tumor growth in vivo. Furthermore, it is found that RACK1 silencing was able to significantly suppress constitutive phosphorylation of Akt and MAPK, which may contribute to the inhibition of tumor growth. These results suggest that RACK1 can act as a new promising diagnostic biomarker and a potential anticancer therapeutic target for EOC.