Effects of DNA Damage and Oxidative Stress in Human Bronchial Epithelial Cells Exposed to PM2.5 from Beijing, China, in Winter

Abstract

<jats:p>Epidemiological studies have corroborated that respiratory diseases, including lung cancer, are related to fine particulate matter (&lt;2.5 μm) (PM2.5) exposure. The toxic responses of PM2.5 are greatly influenced by the source of PM2.5. However, the effects of PM2.5 from Beijing on bronchial genotoxicity are scarce. In the present study, PM2.5 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 PM2.5 were used for cell exposure. After PM2.5 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 PM2.5 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 PM2.5, 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 PM2.5 genotoxicity in 16HBE cells, which may occur through the combined effect on oxidative stress and the influence of DNA repair genes.</jats:p>

Calling Attention to the Role of Race-Driven Societal Determinants of Health on Aggressive Tumor Biology: A Focus on Black Americans

“…[15][16][17] PM 2.5 exposure is also associated with increased risk of chronic obstructive pulmonary disease, heart disease, asthma, stroke, preterm labor, and death, [18][19][20][21][22][23] and is known to promote oxidative stress. 24 Similarly, lung, breast, and prostate incidence has been linked to nitrogen dioxide and other measures of traffic exposure, [25][26][27] and cancer mortality has been linked to traffic proximity. 28 Thus, exposure to these air toxins results in a 16% higher cancer risk among individuals living in Black-dominant areas than those in European American-dominant areas (P , .01).…”

SARS-CoV-2 test positivity rate in Reno, Nevada: association with PM2.5 during the 2020 wildfire smoke events in the western United States

“…However, in vitro studies suggest that relatively short exposure to PM2.5 may induce cellular changes and inflammation (ref. [33,34]).…”

Narrative review: association between lung cancer development and ambient particulate matter in never-smokers

“…Recent studies have reported new aspects of PMrelated oxidative stress in the lung tissue. A study by Niu et al (43), using human bronchial epithelial (HBE) cells, showed increased levels of ROS, malondialdehyde, and cellular heme oxygenase and decreased levels of GSH, after exposure to PM 2.5 , reflecting the occurrence of oxidative stress in a dose-dependent manner. Quantitative analysis indicated that PM 2.5 caused a significant increase in malondialdehyde in a dose-dependent manner, while GSH was greatly reduced after exposure (P<0.05).…”