Water soluble and insoluble components of urban PM2.5 and their cytotoxic effects on epithelial cells (A549) in vitro

Zou, Yajuan; Jin, Chengyu; Su, Yue; Li, Jiaru; Zhu, Bingquan

doi:10.1016/j.envpol.2016.03.022

Cited by 144 publications

(68 citation statements)

References 43 publications

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“…A 2 cm × 18 cm strip was cut from each filter (33 samples for summer, 32 samples for winter), immersed in 150 mL of ultrapure water, and ultrasonicated for 20 min in an ice bath (repeated three times). The solution was filtered, and then the collected solution was freeze-dried in vacuum to obtain the extracted particles [27]. We thought the substance obtained by ultrasonic extraction was only PM 2.5 , regardless of the decomposition of quartz filter membrane.…”

Section: Pm 25 Preparation and Cell Culturementioning

confidence: 99%

Chemical Characterization of Two Seasonal PM2.5 Samples in Nanjing and Its Toxicological Properties in Three Human Cell Lines

et al. 2019

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PM2.5 pollution is of great concern in China due to its adverse health effects. Many diseases have been proven to be associated with PM2.5 components, but the effects of chemical characteristics of PM2.5 on toxicological properties, especially in different human organs, are poorly understood. In this study, two seasonal PM2.5 samples (summer and winter) were collected in Nanjing, and their chemical compositions (heavy metals, water-soluble ions, organic carbon (OC), and elemental carbon (EC)) were analyzed. Human lung epithelial carcinoma cells (A549), human hepatocellular liver carcinoma cells (HepG2), and human neuroblastoma cells (Sh-Sy5y) were employed to evaluate the toxicological properties of the collected PM2.5. The results showed that the average mass concentrations of PM2.5 were lower in summer (51.3 ± 21.4 μg/m3) than those in winter (62.1 ± 21.5 μg/m3). However, the mass fractions of heavy metals, OC, and EC exhibited an opposite seasonal difference. Among all tested fractions, water-soluble ions were the major compositions of particles in both summer and winter, especially the secondary ions (SO42−, NO3− and NH4+). Besides, the ratio of OC/EC in PM2.5 was greater than two, indicating serious secondary pollution in this area. The NO3–/SO42− ratio (< 1) suggested that fixed sources made important contributions. The toxicological results showed that PM2.5 in the summer and winter significantly inhibited cell viability (p < 0.01) and induced intracellular reactive oxygen species (ROS) production (p < 0.01). Moreover, the viability inhibition in A549, Sh-Sy5y, and HepG2 cells was more prominent in summer, especially at high PM2.5 (400 μg/mL) (p < 0.05), and the induction of reactive oxygen species (ROS) in A549 and Sh-Sy5y cells was also more evident in summer. Such seasonal differences might be related to the variations of PM2.5 components.

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Section: Pm 25 Preparation and Cell Culturementioning

confidence: 99%

Chemical Characterization of Two Seasonal PM2.5 Samples in Nanjing and Its Toxicological Properties in Three Human Cell Lines

et al. 2019

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“…Elevated plasma ROS production has been observed in healthy male volunteers [61], animals [64], and epithelial cells [65] after increased PM 2.5 inhalation. ROS production initiates a series of cellular reactions including damage to cellular macromolecules (e.g., functional and constitutive proteins, DNA, and membranes), cytotoxicity, and release of inflammatory cytokines, all of which have been reviewed by Ghio et al [66].…”

Section: Potential Cellular and Molecular Biology Mechanismsmentioning

confidence: 99%

Potential Harmful Effects of PM2.5 on Occurrence and Progression of Acute Coronary Syndrome: Epidemiology, Mechanisms, and Prevention Measures

Meng

Zhang

Yang

et al. 2016

IJERPH

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The harmful effects of particulate matter with an aerodynamic diameter of <2.5 µm (PM2.5) and its association with acute coronary syndrome (ACS) has gained increased attention in recent years. Significant associations between PM2.5 and ACS have been found in most studies, although sometimes only observed in specific subgroups. PM2.5-induced detrimental effects and ACS arise through multiple mechanisms, including endothelial injury, an enhanced inflammatory response, oxidative stress, autonomic dysfunction, and mitochondria damage as well as genotoxic effects. These effects can lead to a series of physiopathological changes including coronary artery atherosclerosis, hypertension, an imbalance between energy supply and demand to heart tissue, and a systemic hypercoagulable state. Effective strategies to prevent the harmful effects of PM2.5 include reducing pollution sources of PM2.5 and population exposure to PM2.5, and governments and organizations publicizing the harmful effects of PM2.5 and establishing air quality standards for PM2.5. PM2.5 exposure is a significant risk factor for ACS, and effective strategies with which to prevent both susceptible and healthy populations from an increased risk for ACS have important clinical significance in the prevention and treatment of ACS.

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“…Following exposure to specific concentrations of NPM-protein corona, it was expected that the growth and proliferation of 3D-cultured HLFs would be accelerated. However, PM2.5 has been thought to be toxic, which would effectively inhibit cell growth 40 , 41 . Our results differ from those of previous studies of PM2.5.…”

Section: Discussionmentioning

confidence: 99%

Protein corona of airborne nanoscale PM2.5 induces aberrant proliferation of human lung fibroblasts based on a 3D organotypic culture

Wang

et al. 2018

Sci Rep

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Exposure to PM2.5 has become one of the most important factors affecting public health in the world. Both clinical and research studies have suggested that PM2.5 inhalation is associated with impaired lung function. In this study, material characterization identified the existence of nanoscale particulate matter (NPM) in airborne PM2.5 samples. When coming into contact with protein-rich fluids, the NPM becomes covered by a protein layer that forms a “protein corona”. Based on a 3D organotypic cell culture, the protein corona was shown to mitigate NPM cytotoxicity and further stimulate the proliferation of human lung fibroblasts (HLFs). ROS-activated alpha-smooth muscle actin (α-SMA) is considered to be one of the proliferation pathways. In this research, 3D cell cultures exhibited more tissue-like properties compared with the growth in 2D models. Animal models have been widely used in toxicological research. However, species differences make it impossible to directly translate discoveries from animals to humans. In this research, the 3D HLF model could partly simulate the biological responses of NPM-protein corona-induced aberrant HLF proliferation in the human lung. Our 3D cellular results provide auxiliary support for an animal model in research on PM2.5-induced impaired lung function, particularly in lung fibrosis.

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Water soluble and insoluble components of urban PM2.5 and their cytotoxic effects on epithelial cells (A549) in vitro

Cited by 144 publications

References 43 publications

Chemical Characterization of Two Seasonal PM2.5 Samples in Nanjing and Its Toxicological Properties in Three Human Cell Lines

Chemical Characterization of Two Seasonal PM2.5 Samples in Nanjing and Its Toxicological Properties in Three Human Cell Lines

Potential Harmful Effects of PM2.5 on Occurrence and Progression of Acute Coronary Syndrome: Epidemiology, Mechanisms, and Prevention Measures

Protein corona of airborne nanoscale PM2.5 induces aberrant proliferation of human lung fibroblasts based on a 3D organotypic culture

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