Cooking Oil Fume-Induced Cytokine Expression and Oxidative Stress in Human Lung Epithelial Cells

Abstract

Epidemiological studies have shown an association between exposure to indoor air pollution from Chinese-style cooking and risk of lung cancer among Chinese females. Several toxic substances have been identified in cooking oil fumes (COF) collected from heated rapeseed oil. In this study, we examined the biological effects of COF on CL3 human lung epithelial cells. Exposure to 200 μg/ml COF significantly reduced cell growth within 4 days. In addition, we examined the effect of COF on TGFβ1, TGFβ2, IL-6, IL-8, and IFN-γ gene expressions with the RT-PCR method. We found that TGFβ1 mRNA levels increased after exposure to 200 μg/ml COF for 24 h. Similarly, exposure to 10 μM benzo[a]pyrene or 100 nM 12-O-tetradecanoylphorbol-13-acetate increased TGFβ1 mRNA levels at 24 h. The mRNA levels of TGFβ2, IL-6, IL-8, and IFN-γ did not increase after treatment with COF, benzo[a]pyrene, or 12-O-tetradecanoylphorbol-13-acetate. COF-induced TGFβ1 production was confirmed by quantification of TGFβ1 in conditioned medium with enzyme-linked immunosorbent assay. Exposure to 200 μg/ml COF significantly increased TGFβ1 secretion in a time-dependent and dose-dependent manner. It has been demonstrated that reactive oxygen intermediates induce TGFβ1 gene expression. When CL3 cells were exposed to 200 μg/ml COF for 15 min, there was an increase in intracellular peroxide formation with the dichlorofluorescein method. Furthermore, treatment with 200 μg/ml COF for 12 h also significantly induced lipid peroxidation in CL3 cells. Our results show that exposure to COF inhibits cell growth, increases TGFβ1 secretion, and induces oxidative stress in CL3 lung epithelial cells. This suggests that TGFβ1 and oxidative stress play a role in the biological effects of COF on lung epithelial cells.