Groundwater is an important natural resource of drinking water in rural areas in Inner Mongolia, China. In this study, 4438 drinking groundwater samples were collected from the rural areas of 81 counties in Inner Mongolia, and were analyzed for 16 parameters, including pH, total hardness (TH), chemical oxygen demand (COD), total dissolved solids (TDS), sulfate (SO₄^2-), chloride (Cl^-), fluoride (F^-), iron (Fe), manganese (Mn), arsenic (As), cadmium (Cd), hexavalent chromium (Cr), lead (Pb), aluminum (Al), cuprum (Cu), zinc (Zn). The groundwater quality was evaluated with water quality index (WQI) and human health risk assessment (HRA). Monte Carlo simulation were applied for the uncertainty and sensitivity analysis in the health risk assessment. The spatial map was employed based on the inverse distance weighted (IDW) interpolation technique. The results reveal that while the hazard quotient (HQ) suggests that the risk of single element contamination is feeble, the hazard index (HI) indicates a potential health risk for the local population. The observed cumulative carcinogenic risk (CCR) indicates a probable risks of carcinogenic health hazards in the study area. The sensitivity analysis revealed that daily ingestion rate (IR), exposure frequency (EF), and the concentrations of As, Mn, F^-, and Cr are the most influential parameters for health hazards. The highly polluted areas are mainly distributed in the central and western regions of Inner Mongolia, including Xianghuangqi, New Barag Zuoqi, and Togtoh. It is observed that the groundwater may cause a potential health risk after long-term ingestion. The results of this study will contribute to groundwater management and protection in Inner Mongolia.

Rare earth elements (REEs) have been broad application in a range of industries, including the electronics industry, advanced materials, and medicine. However, health risks associated with REEs received increasing attention. 31 residents (16 males and 15 females) from Bayan Obo mining in Inner Mongolia, China, were enrolled in this study. In total, 677 food samples, the major human exposure matrices (drinking water and duplicate diets), and bio-samples (urine and blood) of 31 participants were obtained. The concentrations of REEs were measured to characterize their external and internal exposures, and the potential health risk of exposure to REE through the ingestion route was analyzed. The results revealed that the detection rate in blood samples (100%) is higher than in urine (32.86%), and only a few REEs were detected in water samples (8.06%), the urine concentrations were considerably lower than in blood. Exposure to REEs through drinking water was considered negligible compared to food intake. Lanthanum and cerium were the most concentrated REEs in food samples. Health risks were calculated based on a dose-response model, the total hazard quotients (THQ) values for all food groups were within normal levels, and the Monte Carlo simulation results show that the 5th, the 50th, and the 95th percentile values of HI were found as 1.45 × 10^-2, 3.52 × 10^-2, and 9.13 × 10^-2, respectively, neither exceeds the threshold, indicating low health risks associated with food intake exposure for this area. The sensitivity results suggest that underweight people are at higher risk, cerium, lanthanum, and yttrium concentrations, and food intake contributes more to health risks. The use of probability distribution methods can improve the accuracy of the results. The cumulative health risk through food intake is negligible, and further attention should be paid to the health risk induced by other routes of exposure to REEs by the local residents.

The objective of this study was to investigate the effect of sodium acetate on the viability of the human gastric adenocarcinoma (AGS) epithelial cell line. AGS cells were exposed to a range of concentrations of sodium acetate for different periods of time, and the sodium acetate-induced cytotoxic effects, including cell viability, DNA fragmentation, apoptotic gene expression, and caspase activity, were assessed. The changes in these phenotypes were quantified by performing a lactate dehydrogenase cell viability assay, annexin V staining, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL), and several caspase activity assays. In vitro studies demonstrated that the cytotoxicity of sodium acetate on the AGS cell line were dose- and time-dependent manners. No differences were found between the negative control and sodium acetate-treated cells stained with annexin V and subjected to the TUNEL assay. However, caspase-3 activity was increased in AGS cells exposed to sodium acetate. Overall, it was concluded that sodium acetate exerted an apoptotic effect in AGS cells via a caspase-dependent apoptotic pathway.

The contamination of soils surrounding rare earth tailings (SRET) with potentially toxic trace elements (PTEs), including Ni, Cd, Cr, As, Pb, Mn, Cu, Zn, and Hg, has garnered increasing scientific concern. However, existing studies predominantly focused on localized regions, limiting insights into nationwide pollution patterns associated with SRET. To address this gap, we systematically compiled and analyzed PTE concentration data from SRET across China using peer-reviewed studies published between 2012 and 2023. The index of geo-accumulation (I_geo) was applied to quantify contamination levels, while Monte Carlo simulation (MCS) was employed to assess uncertainty and sensitivity in health risks posed by ingestion, inhalation, and dermal exposure pathways. Results revealed that average concentrations of Cd, As, Pb, Mn, Zn, and Hg exceeded Chinese soil background values by up to 11.16-fold. I_geo revealed significant Cd contamination in SRET in Inner Mongolia (I_geo = 1.77), Fujian (I_geo = 5.64), and Sichuan (I_geo = 3.89). Moderate Mn contamination was identified in Guangdong (I_geo = 1.80) and Inner Mongolia (I_geo = 1.63). Adults exhibited elevated health risks via oral ingestion of PTEs-contaminated SRET. MCS demonstrated that the median hazard index (HI) and carcinogenic risk (CR) values in five provinces surpassed safety thresholds (CR > 1.00 ×10^-6, HI > 1.00). Sensitivity analyses identified daily soil intake and exposure duration were positively linked to health risks, with As, Ni, Cd, Cr, and Mn concentrations contributing substantially to cumulative risks. This study provides actionable insights for optimizing cost-effective PTE remediation strategies in SRET-affected regions.

Background: This study aims to investigate the effects of water soluble particulate matter (WSPM) on the viability and protein expression profile of human lung adenocarcinoma cell A549 in the Bayou Obo rare earth mining area, and explore the influence of WSPM on the A549 cell cycle.Results: It was found that WSPM can inhibit the viability of A549 cells and induce cell arrest in the G2/M phase. Compared with controls, exposure to WSPM10 and WSPM2.5 induced 134 and 116 proteins to be differentially expressed in A549 cells, respectively. In addition, 33 and 31 differentially expressed proteins were further confirmed, and was consistent with the proteomic analysis. The most prominent enrichment in ribosome-associated proteins were presented. WhenRPL6,RPL13, orRPL18Agene expression was inhibited, A549 cells were arrested in the G1 phase, affecting the expression ofCyclin D1,p21,RB1,Cyclin A2,Cyclin B1,CDC25A,CDK2,CHEK2andE₂F₁. Furthermore, the La³⁺, Ce³⁺, Nd³⁺and F^-in WSPM also inhibited the viability of A549 cells. After 24 h of exposure to 2 mM of NaF, A549 cells were also arrested in the G2/M phase, while the other three compounds did not have this effect. These four compounds affected the cell cycle regulatory factors in A549 cells, mainly focusing on effecting the expression ofCDK2,CDK4,RB1,ATM,TP53andMDM2genes. These results are consistent with the those from WSPM exposure.Conclusions: These results revealed that WSPM from rare earth mines decreased the viability of A549 cells, and induced cell cycle G2/M phase arrest, and even apoptosis, which may be independent of the NF-κB/MYD88 pathway, and be perceived by the TLR4 receptor. The dysfunction of the cell cycle is correlated to the down-expression of ribosomal proteins (RPs). However, it is not the direct reason for the A549 cell arrest in the G2/M phase. La³⁺, Ce³⁺, and F^-are probably the main toxic substances in WSPM, and may be regulate the A549 cell cycle by affecting the expression of genes, such asMDM2, RB1, ATM, TP53, E₂F₁,CDK2andCDK4. These results indicate the importance for further research into the relationship between APM and lung cancer.

Background: The association between low-density lipoprotein cholesterol (LDL-C) levels and the risk of hemorrhagic stroke (HS) detected through different blood pressure statuses remains unclear. Hence, we systematically evaluated the association between LDL-C and HS in populations with and without hypertension. Methods: We searched PubMed, Cochrane Library, and Embase databases for articles written in English. Only prospective design or randomized controlled trials (RCTs) reporting effect estimates with 95% confidence intervals (CIs) for the relationship between LDL-C and HS were included. We pooled risk ratios (RRs) stratified by blood pressure status and dose–response analyses with a two-stage generalized least squares for trend estimation (GLST) model. Finally, we compared the lower and optimal groups to find the effect of very low LDL-C levels on the risk of HS. Results: We included seven randomized controlled trials and 9 prospective cohort studies involving 304,763 participants with 2125 (0.70%) HS events. The non-linear trend suggested that LDL-C levels of approximately 80 mg/dL among hypertensive patients and 115 mg/dL among non-hypertensive patients had the lowest risk of HS. Meanwhile, continually lowering LDL-C levels under the optimal (80 mg/dL for hypertensive patients and 115 mg/dL for non- hypertensive patients) LDL-C level would increase the risk of HS in the hypertensive population (RR = 1.84, 95% CI: 1.36–2.50) but not in the non-hypertensive population (RR = 1.15, 95% CI: 0.97–1.36). Conclusions: The risk of HS can be effectively reduced by controlling LDL-C levels to 60–80 mg/dL in the hypertensive population and 115 mg/dL in the non-hypertensive population. The safety range of controlling LDL-C levels to protect against HS among hypertensive patients is narrower than that among the non-hypertensive population. Additionally, controlling blood pressure might play a positive role in safeguarding against HS by lowering LDL-C levels.