Airborne Fine Particulate Matter Induces Oxidative Stress and Inflammation in Human Nasal Epithelial Cells

Abstract

Airborne fine particulate matter with an aerodynamic diameter equal to or smaller than 2.5 μ m is abbreviated as PM 2.5 , which is one of the main components in air pollution. Exposure to PM 2.5 is associated with increased risk of many human diseases, including chronic and allergic rhinitis, but the underlying molecular mechanism for its toxicity has not been fully elucidated. We have hypothesized that PM 2.5 may cause oxidative stress and enhance inflammatory responses in nasal epithelial cells. Accordingly, we used human RPMI 2650 cells, derived from squamous cell carcinoma of the nasal septum, as a model of nasal epithelial cells, and exposed them to PM 2.5 that was collected at Fudan University (31.3°N, 121.5°E) in Shanghai, China. PM 2.5 exposure decreased the viability of RPMI 2650 cells, suggesting that PM 2.5 may impair the barrier function of nasal epithelial cells. Moreover, PM 2.5 increased the levels of intracellular reactive oxygen species (ROS) and the nuclear translocation of NF-E2-related factor-2 (Nrf2). Importantly, PM 2.5 also decreased the activities of superoxide dismutase, catalase and glutathione peroxidase. Pretreatment with N-Acetyl-L-cysteine (an anti-oxidant) reduced the degree of the PM 2.5 -induced oxidative stress in RPMI 2650 cells. In addition, PM 2.5 increased the production of granulocyte-macrophage colonystimulating factor, tumor necrosis factor-α, interleukin-13 and eotaxin (C-C motif chemokine ligand 11), each of which initiates and/or augments local inflammation. These results suggest that PM 2.5 may induce oxidative stress and inflammatory responses in human nasal epithelial cells, thereby leading to nasal inflammatory diseases. The present study provides insights into cellular injury induced by PM 2.5 .

PM2.5-Induced Oxidative Stress and Mitochondrial Damage in the Nasal Mucosa of Rats

“…The chemical characteristics of the PM 2.5 used in this study were previously described [6]. The mean levels of NO 3− , SO 4 2− , and NH 4+ ions in the PM 2.5 samples reached 386.32, 209.34, and 199.14 μg/mg, respectively.…”

“…To explore whether the nasal mucosa injury induced by PM 2.5 was related to increased inflammatory activity, we detected the levels of proinflammatory cytokines, such as IL-6, IL-8, and TNF-α, which are known to be higher in the inflammatory response in nasal epithelial cells exposed to PM 2.5 in vitro [6]. Moreover, PM 2.5 can increase ROS levels and reduce intracellular antioxidant enzymatic activity accompanied with altered morphology and decreased viability of nasal epithelial cells.…”

“…PM 2.5 was collected as previously described [6]. Briefly, the PM 2.5 was collected using Whatman 41 filters (Whatman, Maidstone, UK) with TSP/PM 10 /PM 2.5 -2 samplers (Dickel, Beijing, China) at a flow rate of 77.59 L/min.…”

“…Ten inorganic ions (F − , CH 3 COO − , HCOO − , Cl − , NO 3 − , SO 4 2− , PO 4 3− , Na + , NH 4 + , and K + ) in PM 2.5 samples were analyzed with ICS 3000 ion chromatography (Dionex, Sunnyvale, CA, USA). Poly aromatic hydrocarbons (PAHs) in PM 2.5 were measured with a gas chromatography-mass spectrometer (GC-MS; Agilent, Alpharetta, GA, USA), as previously described [6]. Concentrated PM 2.5 was diluted with sterile 0.9% saline according to experimental concentrations.…”

“…Recent data have indicated that oxidative stress and the inflammatory response may play an important role in the nasal epithelium and contribute to the impairment of nasal epithelial barrier dysfunction following PM 2.5 exposure in vitro [6]. Mitochondria are unique double-membrane subcellular organelles that provide energy through oxidative phosphorylation and participate in metabolic and genetic functions.…”