Toxicological responses of A549 and HCE-T cells exposed to fine particulate matter at the air-liquid interface.

Fine particulate matter (PM2.5) can enter the human body in various ways and have adverse effects on human health. Human lungs and eyes are exposed to the air for a long time and are the first to be exposed to PM2.5. The "liquid immersion exposure method" has some limitations that prevent it from fully reflecting the toxic effects of particulate matter on the human body. In this study, the collected PM2.5 samples were chemically analyzed. An air-liquid interface (ALI) model with a high correlation to the in vivo environment was established based on human lung epithelial cells (A549) and immortalized human corneal epithelial cells (HCE-T). The VITROCELL Cloud 12 system was used to distribute PM2.5 on the cells evenly. After exposure for 6 h and 24 h, cell viability, apoptosis rate, reactive oxygen species (ROS) level, expression of inflammatory factors, and deoxyribonucleic acid (DNA) damage were measured. The results demonstrated significant dose- and time-dependent effects of PM2.5 on cell viability, cell apoptosis, ROS generation, and DNA damage at the ALI, while the inflammatory factors showed dose-dependent effects only. It should be noted that even short exposure to low doses of PM2.5 can cause cell DNA double-strand breaks and increased expression of γ-H2AX, indicating significant genotoxicity of PM2.5. Increased abundance of ROS in cells plays a crucial role in the cytotoxicity induced by PM2.5 exposure These findings emphasize the significant cellular damage and genotoxicity that may result from short-term exposure to low levels of PM2.5.

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.

Atmospheric fine particulate matter (PM2.5) 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 PM2.5 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 PM2.5. 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 PM2.5. PM2.5 samples from four seasons were collected and analyzed for chemical components. After 6 h of exposure to seasonal PM2.5, winter PM2.5 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 PM2.5 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 PM2.5 was the lowest among the four seasons. It should be noted that even exposure to low doses of summer PM2.5 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 PM2.5-induced cytotoxicity may be related to the generation of ROS and ER stress. In addition, PM2.5 can induce ER stress through oxidative stress, which ultimately leads to apoptosis.

Chemical Composition and Transgenerational Effects on Caenorhabditis elegans of Seasonal Fine Particulate Matter.

While numerous studies have demonstrated the adverse effects of fine particulate matter (PM) on human health, little attention has been paid to its impact on offspring health. The multigenerational toxic effects on Caenorhabditis elegans (C. elegans) were investigated by acute exposure. PM2.5 and PM1 samples were collected and analysed for their chemical composition (inorganic ions, metals, OM, PAHs) in different seasons from April 2019 to January 2020 in Lin'an, China. A higher proportion of organic carbon components (34.3%, 35.9%) and PAHs (0.0144%, 0.0200%) occupied the PM2.5 and PM1 samples in winter, respectively. PM1 in summer was enriched with some metal elements (2.7%). Exposure to fine PM caused developmental slowing and increased germ cell apoptosis, as well as inducing intestinal autofluorescence and reactive oxygen species (ROS) production. PM1 caused stronger toxic effects than PM2.5. The correlation between PM component and F0 generation toxicity index was analysed. Body length, germ cell apoptosis and intestinal autofluorescence were all highly correlated with Cu, As, Pb, OC and PAHs, most strongly with PAHs. The highest correlation coefficients between ROS and each component are SO42- (R = 0.743), Cd (R = 0.816) and OC (R = 0.716). The results imply that OC, PAHs and some transition metals play an important role in the toxicity of fine PM to C. elegans, where the organic fraction may be the key toxicogenic component. The multigenerational studies show that PM toxicity can be passed from parent to offspring, and gradually returns to control levels in the F3-F4 generation with germ cell apoptosis being restored in the F4 generation. Therefore, the adverse effects of PM on reproductive damage are more profound.

Ecotoxicity induced by total, water soluble and insoluble components of atmospheric fine particulate matter exposure in Caenorhabditis elegans.

Although PM2.5 could cause toxicity in environmental organisms, the toxicity difference of PM2.5 under different solubilities is still poorly understood. To acquire a better knowledge of the ecotoxicity of PM2.5 under different solubilities, the model animal Caenorhabditis elegans (C. elegans) was exposed to Total-PM2.5, water insoluble components of PM2.5 (WIS-PM2.5) and water soluble components of PM2.5 (WS-PM2.5). The physiological (growth, locomotion behavior, and reproduction), biochemical (germline apoptosis, and reactive oxygen species (ROS) production) indices, and the related gene expression were examined. According to the findings, acute exposure to these three components caused adverse physiological effects on growth and locomotion behavior, and significantly induced germline apoptosis or ROS production. In contrast, prolonged exposure showed stronger adverse effects than acute exposure. Additionally, the results of multiple toxicological endpoints showed that the toxicity effects of WIS-PM2.5 are more intense than WS-PM2.5, which means that insoluble components contributed more to the toxicity of PM2.5. Prolonged exposure to 1000 mg/L WS-PM2.5, WIS-PM2.5, and Total-PM2.5 dramatically altered the expression of stress-related genes, which further indicated that apoptosis, DNA damage and oxidative stress play a crucial part in toxicity induced by PM2.5.

The Cytotoxic Effects of Fine Particulate Matter (PM2.5) from Different Sources at the Air-Liquid Interface Exposure on A549 Cells.

The health of humans has been negatively impacted by PM2.5 exposure, but the chemical composition and toxicity of PM2.5 might vary depending on its source. To investigate the toxic effects of particulate matter from different sources on lung epithelial cells (A549), PM2.5 samples were collected from residential, industrial, and transportation areas in Nanjing, China. The chemical composition of PM2.5 was analyzed, and toxicological experiments were conducted. The A549 cells were exposed using an air-liquid interface (ALI) exposure system, and the cytotoxic indicators of the cells were detected. The research results indicated that acute exposure to different sources of particulate matter at the air-liquid interface caused damage to the cells, induced the production of ROS, caused apoptosis, inflammatory damage, and DNA damage, with a dose-effect relationship. The content of heavy metals and PAHs in PM2.5 from the traffic source was relatively high, and the toxic effect of the traffic-source samples on the cells was higher than that of the industrial- and residential-source samples. The cytotoxicity of particulate matter was mostly associated with water-soluble ions, carbon components, heavy metals, PAHs, and endotoxin, based on the analysis of the Pearson correlation. Oxidative stress played an important role in PM2.5-induced biological toxicity.