Abstract
BackgroundExposure to indoor air pollution from solid fuel combustion is associated with lung diseases and cancer. This study investigated the cytotoxicity and molecular mechanisms of biomass combustion-derived particles in human pulmonary alveolar epithelial cells (HPAEpiC) using a platform that combines air–liquid interface (ALI) and dynamic culture (DC) systems.MethodsHPAEpiC were cultured on the surface of polycarbonate (PC) membranes on the ALI–DC platform. The cells were sprayed with an aerosolized solution of biomass combustion soluble constituents (BCSCs) and simultaneously nourished with culture medium flowing beneath the permeable PC membranes. The ALI–DC method was compared with the traditional submerged culture approach. BCSC particle morphology and dosages deposited on the chip were determined for particle characterization. Flow cytometry, scanning electron microscopy, and transmission electron microscopy were used to investigate the apoptosis rate of HPAEpiC and changes in the cell ultrastructure induced by BCSCs. Additionally, the underlying apoptotic pathway was examined by determining the protein expression levels by western blotting.ResultsScanning electron microscope images demonstrated that the sample processing and delivering approach of the ALI–DC platform were suitable for pollutant exposure. Compared with the submerged culture method, a significant decline in cell viability and increase in apoptosis rate was observed after BCSC exposure on the ALI–DC platform, indicating that the ALI–DC platform is a more sensitive system for investigating cytotoxicity of indoor air pollutants in lung cells. The morphology and ultrastructure of the cells were damaged after exposure to BCSCs, and the p53 pathway was activated. The Bcl-2/Bax ratio was reduced, upregulating caspase-9 and caspase-3 expression and subsequently inducing apoptosis of HPAEpiC. The addition of N-acetyl cysteine antioxidant significantly alleviated the cytotoxicity induced by BCSCs.ConclusionA novel ALI–DC platform was developed to study the cytotoxicity of air pollutants on lung cells. Using the platform, we demonstrated that BCSCs could damage the mitochondria, produce reactive oxygen species, and activate p53 in HPAEpiC, ultimately inducing apoptosis.
Highlights
Exposure to indoor air pollution from solid fuel combustion is associated with lung diseases and cancer
A novel air–liquid interface (ALI)–dynamic culture (DC) platform was developed to study the cytotoxicity of air pollutants on lung cells
We demonstrated that biomass combustion soluble constituents (BCSCs) could damage the mitochondria, produce reactive oxygen species, and activate p53 in human pulmonary alveolar epithelial cells (HPAEpiC), inducing apoptosis
Summary
Exposure to indoor air pollution from solid fuel combustion is associated with lung diseases and cancer. Long-term exposure to indoor air pollution from solid fuel combustion has been shown to increase the occurrence and development of lung diseases [8]. A study has shown that 35.7% of respiratory diseases, 22% of chronic lung diseases, and 15% of bronchial diseases are associated with indoor air pollution [9]. Epidemiological statistics have demonstrated a higher incidence of lung cancer among women in China than among those in several European countries with a higher prevalence of female smokers [10, 11] This discrepancy may be related to the more widespread use of solid fuel stoves in China. Investigating the effects of indoor air pollution from solid fuel combustion on lung health is essential for improving health outcomes
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