The Genesis Mechanism and Health Risk Assessment of High Boron Water in the Zhaxikang Geothermal Area, South Tibet

The natural discharge of geothermal water containing harmful components affects the water quality of the surrounding environment and brings security risks to drinking water safety. The geothermal water in Tibet is characterized by high boron content, but the water pollution caused by the discharge of this high boron geothermal water is not clear. In this study, we collected geothermal water and surface water from the Zhaxikang geothermal system in southern Tibet to investigate the causes of high boron geothermal water and the water pollution of water quality by its discharge. The results indicate that the hydrochemical type of geothermal water was HCO3-Cl-Na, while that of cold spring water, mine water, river water, and lake water was SO4-HCO3-Ca-Mg. Hydrogen and oxygen isotopes show that the recharge source of cold groundwater was mainly snow-melting water and meteoric water, while in addition to that, there is magmatic water for hot springs. The boron content of geothermal water in the study area is as high as 42.36 mg/L, far exceeding the World Health Organization limit for drinking water (0.5 mg/L). The analysis of ion components and PHREEQC modeling indicated that the dissolution of silicate minerals and cation exchange controlled the composition of groundwater, and the boron in groundwater mainly came from the volatilization of magmatic components and the leaching of shallow sediments. The entropy weight water quality index was used to evaluate the water quality of the study area; about 42.9% of the groundwater samples are of good quality and can be used for drinking, mainly cold water that has not been mixed with geothermal water in the upstream. With the discharge of geothermal water into the river (with a mix ratio of ~20%), the downstream water quality gradually deteriorated. The health risk assessment of drinking water in the study area showed that the hazard index (HI) of drinking water in the mixed area was higher than 1 (with an average of 1.594 for children and 1.366 for adults), indicating that children are at a higher health risk than adults. Geothermal water with high boron content has been found all over the world, and the adverse effects of its natural drainage cannot be ignored

Impacts of event-specific air quality improvements on total hospital admissions and reduced systemic inflammation in COPD patients.

There is limited evidence linking the impacts of reduced air pollution on hospital admissions. The potential biological mechanisms are still not completely understood. This study examined the effects of mitigated ambient pollution on hospital admissions and inflammatory biomarker levels in chronic obstructive pulmonary disease (COPD) COPD patients. Daily hospital admissions were compared over 51 days associated with the Asian Games period (Nov 1-Dec 21, 2010) with the identical calendar dates of baseline years (2004-2009 and 2011-2013). A three-year cohort study was conducted with 36 COPD patient participants. The daily particulate matter (PM10) decreased from 65.86 μg/m3 during the baseline period to 62.63 μg/m3 during the Asian Games period; the daily NO2 level decreased from 51.33 μg/m3 to 42.63 μg/m3. Between the baseline period and the Asian Games, daily hospital admissions from non-accidental diseases decreased from 116 to 93, respectively; respiratory diseases decreased from 20 to 17, respectively; and cardiovascular diseases decreased from 11 to 9 during the Asian Games period, respectively. No statistically significant reductions were seen in the remaining months of 2010 in Guangzhou, during the the Asian Games period in the control city, and two other control diseases. Furthermore, we identified significant improvement in CRP and fibrinogen by -20.4% and -15.4% from a pre-Asian game period to a during-Asian game period, respectively. For CRP, we found significant increases in NO2 at lag1-3 days after-Asian game period and significant increases in PM10 at lag1-2 days. Similar effects were also seen with fibrinogen. This discovery provides support for efforts to diminish air pollution and improve public health through human air pollutants intervention. Improved air pollution during the 2010 Asian games was correlated with decreases in biomarkers associated with systemic inflammation in COPD patient participants

Escin Increases the Survival Rate of LPS-Induced Septic Mice Through Inhibition of HMGB1 Release from Macrophages

Background: Previous studies have described the effects of Escin on improving the survival rate of endotoxemic animals. The purpose of this study was to explore the molecular mechanisms of this potentially beneficial treatment. Methods: First, the survival rate of endotoxemic mice was monitored for up to 2 weeks after Escin pretreatment, Escin post-treatment, or Escin post-treatment + rHMGB1. The effects of Escin on the release of pro-inflammatory cytokines such as TNF-a, IL-1ß, IL-6 and HMGB1 in the serum of endotoxemic mice and LPS-induced macrophages were evaluated by ELISA. Furthermore, the mRNA and protein levels of HMGB1 in LPS-induced macrophages were measured by qRT-PCR and Western blot, respectively. Additionally, the release of pro-inflammatory cytokines such as TNF-a, IL-1ß, IL-6 was evaluated by ELISA in rHMGB1-induced macrophages. Finally, the protein levels and the activity of NF-κB in macrophages were checked by Western blot and ELISA, respectively. Results: Both pretreatment and post-treatment with Escin could improve the survival rate of endotoxemic mice, while exogenous rHMGB1 reversed this effect. In addition, Escin decreased the level of the pro-inflammatory cytokines TNF-a, IL-1ß, IL-6 and HMGB1 in endotoxemic mice and in LPS-induced macrophages. Escin could also inhibit the mRNA levels and activity of HMGB1. The release of the pro-inflammatory cytokines TNF-a, IL-1ß, IL-6 could be suppressed in rHMGB1-induced macrophages by Escin. Finally, Escin could suppress the activation of NF-κB in LPS-induced macrophages. Conclusion: Escin could improve the survival of mice with LPS-induced endotoxemia. This effect maybe meditated by reducing the release of HMGB1, resulting in the suppression of the release of pro-inflammatory cytokines