Epidemiological studies have associated high levels of airborne particulate matter (PM) with increased respiratory diseases. In order to investigate the mechanisms of air pollution-induced lung toxicity in humans, human bronchial epithelial cells (16HBE) were exposed to various concentrations of particles smaller than 2.5 μm (PM2.5) collected from Beijing, China. After observing that PM2.5 decreased cell viability in a dose-dependent manner, we first used Illumina RNA-seq to identify genes and pathways that may contribute to PM2.5-induced toxicity to 16HBE cells. A total of 539 genes, 283 up-regulated and 256 down-regulated, were identified to be significantly differentially expressed after exposure to 25 μg/cm² PM2.5. PM2.5 induced a large number of genes involved in responses to xenobtiotic stimuli, metabolic response, and inflammatory and immune response pathways such as MAPK signaling and cytokine-cytokine receptor interaction, which might contribute to PM2.5-related pulmonary diseases. We then confirmed our RNA-seq results by qPCR and by analysis of IL-6, CYP1A1, and IL-8 protein expression. Finally, ELISA assay demonstrated a significant association between exposure to PM2.5 and secretion of IL-6. This research provides a new insight into the mechanisms underlying PM2.5-induced respiratory diseases in Beijing.

Epidemiological studies have corroborated that respiratory diseases, including lung cancer, are related to fine particulate matter (<2.5 μm) (PM_2.5) exposure. The toxic responses of PM_2.5 are greatly influenced by the source of PM_2.5. However, the effects of PM_2.5 from Beijing on bronchial genotoxicity are scarce. In the present study, PM_2.5 from Beijing was sampled and applied in vitro to investigate its genotoxicity and the mechanisms behind it. Human bronchial epithelial cells 16HBE were used as a model for exposure. Low (67.5 μg/mL), medium (116.9 μg/mL), and high (202.5 μg/mL) doses of PM_2.5 were used for cell exposure. After PM_2.5 exposure, cell viability, oxidative stress markers, DNA (deoxyribonucleic acid) strand breaks, 8-OH-dG levels, micronuclei formation, and DNA repair gene expression were measured. The results showed that PM_2.5 significantly induced cytotoxicity in 16HBE. Moreover, the levels of reactive oxygen species (ROS), malondialdehyde (MDA), and cellular heme oxygenase (HO-1) were increased, and the level of glutathione (GSH) was decreased, which represented the occurrence of severe oxidative stress in 16HBE. The micronucleus rate was elevated, and DNA damage occurred as indicators of the comet assay, γ-H2AX and 8-OH-dG, were markedly enhanced by PM_2.5, accompanied by the influence of 8-oxoguanine DNA glycosylase (OGG1), X-ray repair cross-complementing gene 1 (XRCC1), and poly (ADP-ribose) polymerase-1 (PARP1) expression. These results support the significant role of PM_2.5 genotoxicity in 16HBE cells, which may occur through the combined effect on oxidative stress and the influence of DNA repair genes.

PM2.5 is an important factor to affect the patients with respiratory and cardiovascular diseases. Clinical studies have found that the morbidity and mortality of patients with heart failure (HF) have a close relationship with the movement and deposition state of PM2.5. One reason is that the breathing pattern of patients with HF has obvious difference with healthy people, however the effect caused by these differences on the distribution regularity of PM2.5 in the respiratory tract is still unclear. Hence, a computational fluid dynamics simulation was conducted to clarify the aerodynamic effect of breathing pattern of patients with HF on respiratory system. Ideal upper respiratory tract geometric model was established based on standardized aerosol research laboratory of Alberta and Weibel A dimension. The discrete phase method is used to calculate the movement of the airflow and particles. The flow rate were chosen as the inlet boundary conditions, and the outlets are set at a constant pressure. The rate of particle deposition, distribution location, wall pressure, flow velocity and wall shear stress are obtained, and compared to the normal control. The results demonstrated that the rate of escaped particles in every bronchial outlet of the patients with HF was more than the normal controls, meanwhile the trapped was less (1024 < 1160). There was higher by 12.9% possibility that the PM2.5 entered the lungs than the normal control. The aerodynamic performances of HF patients are different from normal control. Compared to the normal control, under similar environment, there is higher possibility of PM2.5 moving into lungs, and these particles could affect the function of the respiratory system, resulting in the deterioration of the state of cardiovascular system. In short, it’s necessary to pay more attention to the living environment of HF patients, to reduce the content of PM2.5 particles in the air, and reduce the damage of PM2.5 particles caused by breathing patterns.