Diesel exhaust particles exposure induces liver dysfunction: Exploring predictive potential of human circulating microRNAs signature relevant to liver injury risk

Xu, Lin; Li, Yanting; Ma, Wanli; Sun, Xueying; Fan, Rongrong; Yuan, Jing; Chen, Ningning; Zhu, Xiaoxiao; Guo, Huan; Zhao, Kunming; Luo, Jiao; Li, Chuanhai; Zheng, Yuxin; Yu, Dianke

doi:10.1016/j.jhazmat.2023.132060

Cited by 3 publications

(1 citation statement)

References 77 publications

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“…Bond et al [ 62 ] suggested that the liver might serve as the primary site for the metabolism of carcinogens, such as 1-nitropyrene (1-NP), carried by diesel exhaust. Consistent with our findings, a cohort study conducted by Lin Xu et al [ 63 ] on young adult males around the age of 35 found that exposure to diesel engine exhaust particles led to a significant increase in ALT and AST levels in participants, thereby increasing the risk of liver damage. Another study investigating the impact of nanoparticle rich-diesel exhaust (NR-DE) on the livers of 8-week-old male F344 rats revealed that NR-DE exposure led to increased AST and ALT activity in rats, and high concentrations of NR-DE further activated hepatic inflammatory signaling [ 64 ].…”

Section: Discussionsupporting

confidence: 92%

Lipid Dysregulation Induced by Gasoline and Diesel Exhaust Exposure and the Interaction with Age

Gao,

Zhang,

et al. 2024

Toxics

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Limited knowledge exists regarding gasoline and diesel exhaust effects on lipid metabolism. This study collected gasoline and diesel exhaust under actual driving conditions and conducted inhalation exposure on male young and middle-aged C57BL/6J mice for 4 h/day for 5 days to simulate commuting exposure intensity. Additionally, PM2.5 from actual roadways, representing gasoline and diesel vehicles, was generated for exposure to human umbilical vein endothelial cells (HUVECs) and normal liver cells (LO2) for 24, 48, and 72 h to further investigate exhaust particle toxicity. Results showed that diesel exhaust reduced total cholesterol and low-density lipoprotein cholesterol levels in young mice, indicating disrupted lipid metabolism. Aspartate aminotransferase and alanine aminotransferase levels increased by 53.7% and 21.7%, respectively, suggesting potential liver injury. Diesel exhaust exposure decreased superoxide dismutase and increased glutathione peroxidase levels. Cell viability decreased, and reactive oxygen species levels increased in HUVECs and LO2 following exposure to exhaust particles, with dose- and time-dependent effects. Diesel exhaust particles exhibited more severe inhibition of cell proliferation and oxidative damage compared to gasoline exhaust particles. These findings provide novel evidence of the risk of disrupted lipid metabolism due to gasoline and diesel exhaust, emphasizing the toxicity of diesel exhaust.

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Section: Discussionsupporting

confidence: 92%

Lipid Dysregulation Induced by Gasoline and Diesel Exhaust Exposure and the Interaction with Age

Gao,

Zhang,

et al. 2024

Toxics

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Functional polymorphisms in Benzo(a)Pyrene-induced toxicity pathways associated with the risk on laryngeal squamous cell carcinoma

Xu,

Sun,

Wang

et al. 2023

Food and Chemical Toxicology

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Numerical study on the effect of smoke emitted from the vents on the roof of a diesel train on the intake of downstream air-conditioning units

Chen,

Zhang,

et al. 2024

Physics of Fluids

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Constrained by economic development and geographical features, numerous railway lines remain unelectrified, underscoring the expansive potential of diesel trains. Diesel engine emissions discharged from the roof of trains pose a challenge as some of the smoke infiltrates the cabin through the intake of roof-mounted air-conditioning units (ACUs). This intrusion diminishes the indoor air quality, posing health risks to passengers and potentially jeopardizing their safety. This study employs the shear stress transport k-omega turbulence model to formulate a multiphase flow model for simulating smoke diffusion in diesel trains. Additionally, we conducted an optimization design to minimize smoke entry into the ACUs. This study defined six cases based on variations in the shape and height of the cover and the spacing of the smoke vents. The results show that the effect of the diffusion characteristics decreased with the cover height. With the progression of airflow diffusion, the effect of the smoke vent structure on the concentration diminished farther from the vents. The minimum smoke mass flow rate into the intake occurred with the vent spacing of 2.14 m and without a cover, resulting in a 57.0% decrease compared with the maximum. Thus, a smoke vent spacing of 2.14 m without a cover was deemed to be the optimal configuration. The research results provide certain engineering guidance significance for the design and operation of train-smoke vent structures.

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Diesel exhaust particles exposure induces liver dysfunction: Exploring predictive potential of human circulating microRNAs signature relevant to liver injury risk

Cited by 3 publications

References 77 publications

Lipid Dysregulation Induced by Gasoline and Diesel Exhaust Exposure and the Interaction with Age

Lipid Dysregulation Induced by Gasoline and Diesel Exhaust Exposure and the Interaction with Age

Functional polymorphisms in Benzo(a)Pyrene-induced toxicity pathways associated with the risk on laryngeal squamous cell carcinoma

Numerical study on the effect of smoke emitted from the vents on the roof of a diesel train on the intake of downstream air-conditioning units

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