Acute exposure to seasonal PM2.5 induces toxicological responses in A549 cells cultured at the air-liquid interface mediated by oxidative stress and endoplasmic reticulum stress

Wankang Chen; Pengxiang Ge; Zhenyu Lu; Xiaoming Liu; Maoyu Cao; Zhansheng Yan; Mindong Chen

doi:10.1016/j.envres.2024.118283

Acute exposure to seasonal PM_2.5 induces toxicological responses in A549 cells cultured at the air-liquid interface mediated by oxidative stress and endoplasmic reticulum stress

Environ Res. 2024 May 1:248:118283. doi: 10.1016/j.envres.2024.118283. Epub 2024 Jan 20.

Authors

Wankang Chen¹, Pengxiang Ge¹, Zhenyu Lu¹, Xiaoming Liu¹, Maoyu Cao², Zhansheng Yan¹, Mindong Chen³

Affiliations

¹ Jiangsu Key Laboratory of Atmospheric Environment Monitoring and Pollution Control, Collaborative Innovation Center of Atmospheric Environment and Equipment Technology, School of Environmental Science and Engineering, Nanjing University of Information Science & Technology, Nanjing, 210044, China.
² School of Atmospheric Sciences, Nanjing University, Nanjing, 210023, China.
³ Jiangsu Key Laboratory of Atmospheric Environment Monitoring and Pollution Control, Collaborative Innovation Center of Atmospheric Environment and Equipment Technology, School of Environmental Science and Engineering, Nanjing University of Information Science & Technology, Nanjing, 210044, China. Electronic address: chenmd@nuist.edu.cn.

PMID: 38253190
DOI: 10.1016/j.envres.2024.118283

Abstract

Atmospheric fine particulate matter (PM_2.5) enters the human body through respiration and poses a threat to human health. This is not only dependent on its mass concentration in the atmosphere, but also related to seasonal variations in its chemical components, which makes it important to study the cytotoxicity of PM_2.5 in different seasons. Traditional immersion exposure cannot simulate the living environment of human epithelial cells in the human body, making this method unsuitable for evaluating the inhalation toxicity of PM_2.5. In this study, a novel air-liquid interface (ALI) particulate matter exposure device (VITROCELL Cloud 12 system) was used to evaluate the toxic effects and potential mechanisms of human lung epithelial cells (A549) after exposure to seasonal PM_2.5. PM_2.5 samples from four seasons were collected and analyzed for chemical components. After 6 h of exposure to seasonal PM_2.5, winter PM_2.5 exhibited the highest cytotoxicity among most toxicity indicators, especially apoptosis rate, reactive oxygen species (ROS), inflammatory responses and DNA damage (γ-H2AX). The effect of autumn PM_2.5 on apoptosis rate was significantly higher than that in spring, and there was no significant difference in other toxicity indicators between spring and autumn. The cytotoxicity of summer PM_2.5 was the lowest among the four seasons. It should be noted that even exposure to low doses of summer PM_2.5 leads to significant DNA damage in A459 cells. Correlation analysis results showed that water-soluble ions, metallic elements, and polycyclic aromatic hydrocarbons (PAHs) were associated with most toxicological endpoints. Inhibitors of oxidative stress and endoplasmic reticulum (ER) stress significantly inhibited cellular damage, indicating that PM_2.5-induced cytotoxicity may be related to the generation of ROS and ER stress. In addition, PM_2.5 can induce ER stress through oxidative stress, which ultimately leads to apoptosis.

Keywords: Air-liquid interface; Cytotoxicity; DNA damage; Endoplasmic reticulum stress; Oxidative stress; Seasonal PM(2.5).

MeSH terms

A549 Cells
Air Pollutants* / toxicity
China
Endoplasmic Reticulum Stress
Environmental Monitoring / methods
Humans
Oxidative Stress
Particulate Matter / analysis
Polycyclic Aromatic Hydrocarbons* / analysis
Reactive Oxygen Species / analysis
Seasons

Substances

Air Pollutants
Reactive Oxygen Species
Particulate Matter
Polycyclic Aromatic Hydrocarbons