Long-Term Exposure to Fine Particulate Matter and the Risk of Chronic Liver Diseases: A Meta-Analysis of Observational Studies

Sui, Jing; Xia, Hui; Zhao, Qun; Sun, Guiju; Cai, Yinyin

doi:10.3390/ijerph191610305

Cited by 12 publications

(7 citation statements)

References 67 publications

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“…The liver is an active organ central to metabolism and detoxification for exogenous chemicals. Many research studies indicate that PM 2.5 has toxic effects on the liver [7,8], including triggering liver cancer and NAFLD. The toxicological mechanisms involve liver pathology injury, inflammation, oxidative stress, liver fibrosis and abnormal lipid metabolism induced by prolonged exposure to PM 2.5 [4,6,21].…”

Section: Discussionmentioning

confidence: 99%

“…Empirical research has revealed that PM 2.5 infiltrates the liver via the bloodstream, instigating a cascade of pathological alterations, including hepatic inflammation, oxidative stress, steatosis, and liver fibrosis [4][5][6], exerting profound impacts on liver function. A meta-analysis indicated that long-term exposure to PM 2.5 was associated with an increased risk of chronic liver disease [7]. Studies have also pointed to a significant relationship between exposure to PM 2.5 and the incidence of non-alcoholic fatty liver disease (NAFLD) [8].…”

Section: Introductionmentioning

confidence: 99%

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Protective Effects of Resveratrol on Cytotoxicity of Mouse Hepatic Stellate Cells Induced by PM2.5

Zhang,

Chen,

Bai

et al. 2024

Atmosphere

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The atmosphere’s fine particulate matter (PM2.5) can enter the liver through the circulatory system, leading to hepatic inflammation and fibrosis. As a non-flavonoid polyphenolic compound, resveratrol (RES) has anti-oxidant, anti-inflammatory and hepatoprotective effects, but the molecular mechanisms of liver fibrosis induced by PM2.5 exposure are still limited. In this study, we established an in vitro cell model to investigate the intervention effect of RES with different concentrations (5 and 20 μmol/mL) on mouse hepatic stellate cells (mHSCs) injury induced by PM2.5 (100 μg/mL). We determined the cell viability in mHSCs after treatment with PM2.5 or/and RES for 24 h. We investigated the intracellular oxidative stress by detecting the changes in reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD) and lactate dehydrogenase (LDH) levels. We also measured the protein expressions of fibrosis-related genes (α-SMA, Collagen I and Collagen III) and key genes (SIRT1, NF-κB, NLRP3, Cleaved-Caspase1, IL-1β) in the NLRP3 pathway in mHSCs exposed to PM2.5 with or without RES. The results showed that (1) PM2.5 has cytotoxic effects on mHSCs, whereas RES (5 μmol/L and 20 μmol/L) inhibited PM2.5-induced cytotoxicity and LDH leakage; (2) RES effectively reduces ROS and MDA production caused by PM2.5 while concurrently enhancing SOD levels, thereby improving cellular anti-oxidant capacity; (3) the expression of α-SMA, Collagen I and Collagen III were notably downregulated in the PM2.5 plus RES treatment group compared to the PM2.5-exposed group; (4) RES significantly increased SIRT1 expression and decreased the expression of NF-κB, NLRP3, Cleaved-Caspase1 and IL-1β in mHSCs exposure to PM2.5 compared to the PM2.5 group. These results demonstrate that RES can up-regulate SIRT1 and mitigate PM2.5-induced fibrosis by suppressing oxidative stress in mHSCs and the SIRT1/NF–κB/NLRP3 pathway activated by PM2.5.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Protective Effects of Resveratrol on Cytotoxicity of Mouse Hepatic Stellate Cells Induced by PM2.5

Zhang,

Chen,

Bai

et al. 2024

Atmosphere

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“…Studies have shown that air pollution is associated with an increased risk of chronic liver disease [82][83][84]. In a cross-sectional study involving 90,086 participants, Guo et al found that when the 3-year average concentrations of PM 1 , PM 2.5 , PM 10 , and NO 2 increased by 10 µg/m 3 , the risk of metabolic dysfunction-associated fatty liver disease (MAFLD) increased by 13% (95% CI: 10-17%), 29% (1.25-1.34%), 11% (9-14%), and 15% (12-17%), respectively [82].…”

Section: Metabolic Dysfunction Diseasesmentioning

confidence: 99%

“…In a cross-sectional study involving 90,086 participants, Guo et al found that when the 3-year average concentrations of PM 1 , PM 2.5 , PM 10 , and NO 2 increased by 10 µg/m 3 , the risk of metabolic dysfunction-associated fatty liver disease (MAFLD) increased by 13% (95% CI: 10-17%), 29% (1.25-1.34%), 11% (9-14%), and 15% (12-17%), respectively [82]. A meta-analysis of 16 studies showed that when PM 2.5 increased by 10 µg/m 3 , the risk of liver cancer, liver cirrhosis, and fatty liver disease increased by 23 (95% CI: 14-33%), 17 (6-29%), and 51% (9-108%), respectively [84]. The increased risk of these diseases suggests that air pollution may lead to abnormal liver lipid metabolism, which has also been confirmed in some animal experiments [85][86][87].…”

Section: Metabolic Dysfunction Diseasesmentioning

confidence: 99%

Association between Air Pollution and Lipid Profiles

Zhang,

Shi,

et al. 2023

Toxics

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Dyslipidemia is a critical factor in the development of atherosclerosis and consequent cardiovascular disease. Numerous pieces of evidence demonstrate the association between air pollution and abnormal blood lipids. Although the results of epidemiological studies on the link between air pollution and blood lipids are unsettled due to different research methods and conditions, most of them corroborate the harmful effects of air pollution on blood lipids. Mechanism studies have revealed that air pollution may affect blood lipids via oxidative stress, inflammation, insulin resistance, mitochondrial dysfunction, and hypothalamic hormone and epigenetic changes. Moreover, there is a risk of metabolic diseases associated with air pollution, including fatty liver disease, diabetes mellitus, and obesity, which are often accompanied by dyslipidemia. Therefore, it is biologically plausible that air pollution affects blood lipids. The overall evidence supports that air pollution has a deleterious effect on blood lipid health. However, further research into susceptibility, indoor air pollution, and gaseous pollutants is required, and the issue of assessing the effects of mixtures of air pollutants remains an obstacle for the future.

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“…We evaluated the quality of eligible literature works and scored all publications from 0 to 9 on the Newcastle-Ottawa Scale (NOS) [23]. Studies awarded higher scores than the mean score were considered as high-quality studies.…”

Section: Literature Quality Assessmentmentioning

confidence: 99%

Effect of Fine Particulate Matter Exposure on Liver Enzymes: A Systematic Review and Meta-Analysis

Pan

Sui

et al. 2023

IJERPH

Self Cite

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Although previous studies have presented that fine particulate matter (PM2.5) regulates liver enzyme levels in the development of liver diseases, the evidence regarding the relationship between PM2.5 exposure and liver enzyme is not robust. We further aimed to conduct a systematic review and meta-analysis of observational studies to summarize the recent evidence on the effects of PM2.5 on liver enzyme in humans. In the meta-analysis, we retrieved online databases including PubMed and Web of Science database from 1982 up to 2022. A random-effects model was applied to evaluate the correlation between PM2.5 and liver enzyme level. A total of 10 studies fulfilled the inclusion criteria, including five prospective cohort studies, two cross-sectional studies, two longitudinal studies, and one time-series analysis. Each 10 μg/m3 increase in PM2.5 concentration was significantly correlated with a 4.45% increase in alanine aminotransferase (ALT) level (95% CI: 0.51–8.38%, p = 0.03), a 3.99% increase in aspartate transferase (AST) level (95% CI: 0.88–7.10%, p = 0.01), and a 2.91% increase in gamma-glutamyl transferase (GGT) level (95% CI: 1.18–4.64%, p < 0.001), but this significant association was not observed in alkaline phosphatase (ALP). Subgroup analysis revealed that PM2.5 has a significant correlation with ALT (5.07%, 95% CI: 0.81–9.33%), AST (4.11%, 95% CI: 0.74–7.48%), and GGT (2.74%, 95% CI: 1.09–4.38%) in Asia. Our meta-analysis showed that increments in PM2.5 exposure were significantly associated with a higher level of ALT, AST, and GGT. In addition, investigations into liver enzyme subtypes and specific chemical components of PM2.5 are important directions for future research.

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Long-Term Exposure to Fine Particulate Matter and the Risk of Chronic Liver Diseases: A Meta-Analysis of Observational Studies

Cited by 12 publications

References 67 publications

Protective Effects of Resveratrol on Cytotoxicity of Mouse Hepatic Stellate Cells Induced by PM2.5

Protective Effects of Resveratrol on Cytotoxicity of Mouse Hepatic Stellate Cells Induced by PM2.5

Association between Air Pollution and Lipid Profiles

Effect of Fine Particulate Matter Exposure on Liver Enzymes: A Systematic Review and Meta-Analysis

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