Arsenic (As) is a ubiquitous environmental and industrial toxin with known correlates of oxidative stress and cognitive deficits in the brain. Nuclear factor erythroid 2-related factor 2 (Nrf2) is a transcriptional factor that represents a central cellular antioxidant defense mechanism and transcribes many antioxidant genes. Peroxisome proliferator-activated receptor-gamma (PPARγ) is a well-known nuclear receptor to regulate lipid metabolism in many tissues, and it has been also associated with the control of oxidative stress, neuronal death, neurogenesis and differentiation. The role of Nrf2 and PPARγ in As-induced neurotoxicity is still debated. The present study was designed to investigate the neurobehavioral toxic effect of sub-chronic and middle-dose sodium arsenite exposure in mice hippocampus, as well as the response of Nrf2/PPARγ expression and influence on protein expression levels of their downstream antioxidant genes. Our results showed that mice treated with intraperitoneal injection of sodium arsenite (50 mg/kg body wt.) twice a week for 7 weeks resulted in increased generation of reactive oxygen species and impairment of spatial cognitive function. The present study also found a positive association between Nrf2/PPARγ expression in hippocampus of mice, and activation of antioxidant defenses by the evidently upregulated expression of their downstream genes, including superoxide dismutase, heme oxygenase-1 and glutathione peroxidase-3. Therefore, our findings were helpful for further understanding the role of Nrf2/PPARγ feedback loop in As-induced neurobehavioral toxicity.

OBJECTIVE To evaluate the relationship between ambient air pollutants and chronic obstructive pulmonary disease in relatively low-polluted areas in China. METHODS Atmospheric pollutants levels and meteorological data were obtained from January 2016 to December 2020. The medical database including daily hospital admissions for chronic obstructive pulmonary disease (ICD10: J44) was derived from the First Affiliated Hospital of Gannan Medical University. The generalized additive model was used to analyze the percentage change with 95% confidence interval in daily hospital admissions for chronic obstructive pulmonary disease associated with a 10 µg/m3 increase in atmospheric pollutants levels. RESULTS In total, occurred 4,980 chronic obstructive pulmonary disease hospital admissions (not including emergency department visits) during 2016–2020. The mean concentrations of daily PM2.5, PM10, SO2, NO2, O3, and CO were 37.5 μg/m3, 60.1 μg/m3, 18.7 μg/m3, 23.5 μg/m3, 70.0 μg/m3, and 1.2 mg/m3 in Ganzhou. Each 10 µg/m3 increment of PM2.5, PM10, NO2, and O3 were significantly associated with 2.8% (95%CI: 1.0–4.7), 1.3% (95%CI: 0.3–2.4), 2.8% (95%CI: 0.4–5.4), and 1.5% (95%CI: 0.2–2.7) elevation in daily chronic obstructive pulmonary disease hospital admissions. The estimates of delayed effects of PM2.5, PM10, NO2, and O3 were observed at lag6, lag6, lag8, lag1, respectively. The health effects of particulate pollutants (PM2.5 and PM10) may be independent of other pollutants. The adverse effects of air pollutants were more evident in the warm season (May–Oct) than in the cold season (Nov–Apr). CONCLUSION Our study demonstrated that elevated concentrations of atmospheric pollutant (PM2.5, PM10, NO2, and O3), especially particulate pollutants, can be associated with increased daily count of hospital admissions for chronic obstructive pulmonary disease , which may promote further understanding of the potential hazards of relatively low levels of air pollution on chronic obstructive pulmonary disease and other respiratory disorders.

Fine particulate matter (PM_2.5) and respirable particulate matter (PM₁₀) are two major air pollutants with toxic effects on the cardiovascular system. Hypertension, as a chronic noncommunicable cardiovascular disease, is also a risk factor for several diseases. We applied generalized linear models with a quasi-Poisson link to assess the effect of air pollution exposure on the number of daily admissions for patients with hypertension. In addition, we established a two-pollutant model to evaluate PM_2.5 and PM₁₀ hazard effect stability by adjusting the other gaseous pollutants. Results showed that during the study period, 24h mean concentrations of ambient PM_2.5 and PM₁₀ at 38.17 and 59.84μg/m³, respectively, and a total of 2,611 hypertension hospital admissions were recorded. Air pollution concentrations significantly affected the number of hospitalizations for hypertension approximately 2months after exposure. For each 10μg/m³ increase in PM_2.5 and PM₁₀ in single-pollutant models, the number of hospitalizations for hypertension increased by 7.92 (95 CI: 5.48 to 10.42) and 4.46 (95 CI: 2.86 to 5.65), respectively, at the lag day with the strongest effect. NO₂, O₃, CO, and SO₂ had different significant effects on the number of hospitalizations over the same time period, and PM_2.5 and PM₁₀ still showed robust significant effects after adjustment of gas pollutants through a two-pollutant model. These findings may contribute to a better understanding of the health effects of ambient particulate matter.

Hypertension is a prevalent condition that contributes significantly to the global disease burden. Recent research endeavors have been investigating the potential causal link between metal exposure and the development of hypertension, yet consensus remains elusive. Nevertheless, studies examining the interplay among metal exposure, hypertension, and oxidative stress are relatively limited. This study utilized data from a cross-sectional survey conducted in southern Jiangxi Province, China. We evaluated urinary concentrations of 19 metals, including aluminum and manganese, in conjunction with measurements of systolic and diastolic blood pressures, as well as three oxidative stress biomarkers: glutathione peroxidase (GSH), superoxide dismutase (SOD), and malondialdehyde (MDA). In the monometallic model, chromium, iron, manganese, and molybdenum exhibited positive correlations with blood pressure. These findings were consistent in the mixed exposure model. Conversely, all the aforementioned metals exhibited a negative correlation with GSH and SOD, while demonstrating a positive correlation with MDA. Mediation effect analysis revealed that GSH and SOD mediated the relationships between urinary concentrations of aluminum, iron, manganese, and antimony and blood pressure. In contrast, MDA mediated the associations between urinary silver and antimony and blood pressure. Furthermore, GSH and SOD were identified as mediators in part of the relationship between mixed metal exposure and blood pressure, with mediation rates of 19.09% for GSH and 27.36% for SOD. The results of this study suggest that exposure to both individual and combined metals effects blood pressure levels, which are further associated with changes in oxidative stress levels. Moreover, oxidative stress levels may modulate the changes in blood pressure related to metal exposure, providing a basis for further investigation into the health risks associated with these metal exposures.

Dyslipidemia is a known risk factor for cardiovascular disease. While the health effects of rare earth elements have garnered interest, there is a lack of epidemiological evidence of associations between REEs and oxidative stress, inflammation, and dyslipidemia. This study quantified 15 urinary REEs, blood lipid profiles, oxidative stress biomarkers (glutathione, superoxide dismutase, and malondialdehyde), and the inflammatory marker C-reactive protein in a community population from southern Jiangxi Province, China. The analyses of both the single-element and mixed-element models revealed negative associations between yttrium, gadolinium, and terbium and high-density lipoprotein cholesterol. Yttrium, praseodymium, neodymium, europium, gadolinium, terbium, erbium, ytterbium, and lutetium were positively associated with remnant cholesterol. All these elements were positively associated with C-reactive protein, malondialdehyde, and glutathione. Mediation analysis indicated that oxidative stress and inflammation played mediating roles in the relationships between REEs and blood lipids. These findings suggest that exposure to REEs may influence blood lipid profiles. Additionally, oxidative stress and inflammation might mediate REEs-related blood lipid changes Further research is warranted to explore the health risks of REEs.