Accumulated oxidative stress risk in HUVECs by chronic exposure to non-observable acute effect levels of PM2.5

Nan, Bingru; Sun, Xia; Zhang, Jie; Huang, Qingyu; Zhang, Xi; Li, Yanbo; Duan, Junchao; Chen, Rui; Sun, Zhiwei; Shen, Heqing

doi:10.1016/j.tiv.2022.105376

Cited by 3 publications

(1 citation statement)

References 67 publications

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“…The design of the long‐term cell culture, NOAEL PM 2.5 treatments, and sample collection were shown in Figure S1 and Supplementary Information 2. In this study, the long‐term exposure strategy of the low‐dose PM 2.5 was the same as our previous studies (Nan et al, 2022). In brief, the logarithmic growth AC16 was treated with freshly prepared PM 2.5 with two doses of 5 and 50 μg/mL, respectively.…”

Section: Methodsmentioning

confidence: 99%

Integrative proteomics and metabolomics analysis of non‐observable acute effect level PM_2.5 induced accumulative effects in AC16 cells

Nan

Sun

Yang

et al. 2023

J of Applied Toxicology

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Chronic exposure to very low ambient PM2.5 has been linked to cardiovascular risks in epidemiological observation, which also brought doubts on its safety threshold. In this study, we approached this question by chronic exposure of AC16 to the non‐observable acute effect level (NOAEL) PM2.5 5 μg/mL and its positive reference 50 μg/mL, respectively. The doses were respectively defined on the cell viabilities >95% (p = 0.354) and >90% (p = 0.004) when treated acutely (24 h). To mimic the long‐term exposure, AC16 was cultured from the 1st to 30th generations and treated with PM2.5 24 h in every three generations. The integration of proteomic and metabolomic analysis was applied, and 212 proteins and 172 metabolites were significantly altered during the experiments. The NOAEL PM2.5 induced both dose‐ and time‐dependent disruption, which showed the dynamic cellular proteomic response and oxidation accumulation, the main metabolomics changes were ribonucleotide, amino acid, and lipid metabolism that have involved in stressed gene expression, and starving for energy metabolism and lipid oxidation. In summary, these pathways interacted with the monotonically increasing oxidative stress and led to the accumulated damage in AC16 and implied that the safe threshold of PM2.5 may be non‐existent when a long‐term exposure occurred.

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Section: Methodsmentioning

confidence: 99%

Integrative proteomics and metabolomics analysis of non‐observable acute effect level PM_2.5 induced accumulative effects in AC16 cells

Nan

Sun

Yang

et al. 2023

J of Applied Toxicology

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Ambient Air Pollution and Hospitalizations for Schizophrenia in China

Bai,

Jiang,

Wang

et al. 2024

JAMA Netw Open

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ImportanceSchizophrenia episodes may be triggered by short-term environmental stimuli. Short-term increases in ambient air pollution levels may elevate the risk of schizophrenia episodes, yet few epidemiologic studies have examined this association.ObjectiveTo investigate whether short-term increases in air pollution levels are associated with an additional risk of schizophrenia episodes, independent of absolute air pollution concentrations, and whether sustained increases in air pollution levels for several days are associated with more pronounced risks of schizophrenia episodes.Design, Setting, and ParticipantsThis nationwide, population-based, time-stratified case-crossover study was performed based on hospitalization records for schizophrenia across 295 administrative divisions of prefecture-level or above cities in China. Records were extracted from 2 major health insurance systems from January 1, 2013, to December 31, 2017. Thirty-six cities with a small number of schizophrenia hospitalizations (n &lt; 50) were excluded. Data analysis for this study was performed from January to March 2024.ExposureDaily absolute concentrations of fine particulate matter (PM2.5), inhalable particulate matter (PM10), nitrogen dioxide, sulfur dioxide, ozone, and carbon monoxide were collected. Air pollution increases between neighboring days (APINs) were generated as the differences in absolute air pollution concentrations on the current day minus that on the previous day. Sustained increases (APIN ≥5 μg/m3 for PM2.5 and PM10, APIN ≥1 μg/m3 for nitrogen dioxide and sulfur dioxide, and APIN ≥0.05 mg/m3 for carbon monoxide) lasting for 1 or more to 4 or more days were defined for different air pollutants.Main Outcome and MeasurePatients with schizophrenia episodes were identified by principal discharge diagnoses of schizophrenia. A conditional logistic regression model was used to capture the associations of absolute concentrations, APINs, and sustained increase events for different air pollutants with risks of schizophrenia hospitalizations.ResultsThe study included 817 296 hospitalization records for schizophrenia across 259 Chinese cities (30.6% aged 0-39 years, 56.4% aged 40-64 years, and 13.0% aged ≥65 years; 55.04% male). After adjusting for the absolute concentrations of respective air pollutants, per-IQR increases in 6-day moving average (lag0-5) APINs of PM2.5, PM10, nitrogen dioxide, sulfur dioxide, and carbon monoxide were associated with increases of 2.37% (95% CI, 0.88%-3.88%), 2.95% (95% CI, 1.46%-4.47%), 4.61% (95% CI, 2.93%-6.32%), 2.16% (95% CI, 0.59%-3.76%), and 2.02% (95% CI, 0.39%-3.68%) in schizophrenia hospitalizations, respectively. Greater risks of schizophrenia hospitalizations were associated with sustained increases in air pollutants lasting for longer durations up to 4 or more days.Conclusions and RelevanceThis case-crossover study of the association between ambient air pollution increases and schizophrenia hospitalizations provides novel evidence that short-term increases in ambient air pollution levels were positively associated with an elevated risk of schizophrenia episodes. Future schizophrenia prevention practices should pay additional attention to APINs, especially sustained increases in air pollution levels for longer durations, besides the absolute air pollution concentrations.

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MIR-107/HMGB1/FGF-2 axis responds to excessive mechanical stretch to promote rapid repair of vascular endothelial cells

Wang

Sun

et al. 2023

Archives of Biochemistry and Biophysics

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Accumulated oxidative stress risk in HUVECs by chronic exposure to non-observable acute effect levels of PM2.5

Cited by 3 publications

References 67 publications

Integrative proteomics and metabolomics analysis of non‐observable acute effect level PM_2.5 induced accumulative effects in AC16 cells

Integrative proteomics and metabolomics analysis of non‐observable acute effect level PM_2.5 induced accumulative effects in AC16 cells

Ambient Air Pollution and Hospitalizations for Schizophrenia in China

MIR-107/HMGB1/FGF-2 axis responds to excessive mechanical stretch to promote rapid repair of vascular endothelial cells

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Accumulated oxidative stress risk in HUVECs by chronic exposure to non-observable acute effect levels of PM2.5

Cited by 3 publications

References 67 publications

Integrative proteomics and metabolomics analysis of non‐observable acute effect level PM2.5 induced accumulative effects in AC16 cells

Integrative proteomics and metabolomics analysis of non‐observable acute effect level PM2.5 induced accumulative effects in AC16 cells

Ambient Air Pollution and Hospitalizations for Schizophrenia in China

MIR-107/HMGB1/FGF-2 axis responds to excessive mechanical stretch to promote rapid repair of vascular endothelial cells

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Product

Resources

About

Integrative proteomics and metabolomics analysis of non‐observable acute effect level PM_2.5 induced accumulative effects in AC16 cells

Integrative proteomics and metabolomics analysis of non‐observable acute effect level PM_2.5 induced accumulative effects in AC16 cells