Cooking Oil Fume Exposure Research Articles

Reduction of cooking oil fume exposure following an engineering intervention in Chinese restaurants

BackgroundA new engineering intervention measure, an embracing air curtain device (EACD), was used to increase the capture efficiency of cooker hoods and reduce cooking oil fume (COF) exposure in Chinese...

Association of cooking oil fumes exposure and oxidative DNA damage among occupational exposed populations

Previous investigations indicate that cooks are exposed to polycyclic aromatic hydrocarbons (PAH) from cooking oil fumes (COF). However, Emission of PAH and their carcinogenic potencies from cooking oil fumes sources have not been investigated among cooks. To investigate the urinary excretion of a marker for oxidative DNA damage, 8-hydroxydeoxyguanosine (8-OHdG), in different groups of cooks and different exposure groups, and to study the association between 8-OHdG and 1-hydroxypyrene (1-OHP), a biological marker for PAH exposure. Urine samples were collected from different groups of cooks (n = 86) and from unexposed controls (n = 36), all are male with similar age and smoking habits. The health status, occupational history, smoking, and alcohol consumption 24 hours prior to sampling was estimated from questionnaires. The urinary samples were frozen for later analyses of 8-OHdG and 1-OHP by high performance liquid chromatography. Excretion in urine of 8-OHdG were similar for controls (mean 1.2 µmol/mol creatinine, n = 36), and for those who had been in the kitchen room with exhaust hood operation (mean 1.5 µmol/mol creatinine, n = 45). COF exposed cooks without exhaust hood operation had increased excretion of 8-OHdG (mean 2.3 µmol/mol creatinine, n = 18). The difference between this group and the unexposed controls was significant. The urinary levels of ln 1-OHP and ln 8-OHdG were still significantly correlated in a multiple regression analysis. Results indicate that exposure to PAH or possibly other compounds in COF may cause oxidative DNA damage.

Urinary 1-hydroxypyrene and malondialdehyde in male workers in Chinese restaurants

Objectives: To assess internal dose and oxidative stress in male restaurant workers exposed to polycyclic aromatic hydrocarbons (PAHs) from cooking oil fumes (COFs) in Chinese restaurants. Methods: The study participants...

The Association Between Cooking Oil Fume Exposure and Heart Rate Variability in Chinese Cooks

The Association Between Cooking Oil Fume Exposure and Heart Rate Variability in Chinese Cooks

Association of cooking oil fumes exposure with lung cancer: Involvement of inhibitor of apoptosis proteins in cell survival and proliferation in vitro

Cooking oil fumes (COF) have been shown to be associated with lung cancer incidence in Chinese women. Our recent report indicates that inhibitor of apoptosis protein 2 (IAP2) induced by COF may contribute to the survival and proliferation of A549 lung cancer cells. In this study, to further verify whether other antiapoptosis proteins including IAP1, X-linked IAP (XIAP), and survivin, were linked with lung cancer cell survival and proliferation, these IAPs expressions in A549 cells after treatment with COF and its two major components, benzo[ a]pyrene (BaP) and 2,4-decadienal (2,4-DDE) were evaluated by Western blotting. Our data showed that IAP2 was significantly induced by COF, BaP, and 2,4-DDE, but XIAP was decreased by COF and 2,4-DDE, but not by BaP. Even though different effects of COF and 2,4-DDE on IAP2 and XIAP protein expressions were observed, the caspase-3 expression was diminished by COF and 2,4-DDE. In addition, induction of IAP2 and phosphorylated Akt proteins by COF and 2,4-DDE were simultaneously abolished by LY294002. Flow cytometry and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) analysis showed that the proportion of A549 cells at the S-phase was increased significantly after treatment with COF or 2,4-DDE. The cell proliferation induced by COF is associated with the attenuation of p21 Cip/Waf1 expression. Therefore, increases of IAP1, IAP2, survivin, and cyclin D1 expressions and decreases of XIAP, caspase-3, and p21 expressions might partly contribute to the survival and proliferation of lung cancer cells after exposure to 2,4-DDE and COF. In conclusion, the lung cancer cell growth promoted by COF might support previous epidemiological reports indicating that exposure of COF was associated with lung cancer development among Chinese women.

Cooking Oil Fumes Improve Lung Adenocarcinoma Cell Survival Through c-IAP2 Induction

Cooking oil fumes (COF) exposure was demonstrated to be associated with lung cancer development in Taiwanese nonsmoking women. Previous studies identified Cox-2 overexpression and oxidative DNA damage in lung adenocarcinoma cells after exposure to COF. Involvement of COF in lung tumorigenesis may be associated with cell survival, as well as proliferation of lung adenocarcinoma. To test this hypothesis, A549, a lung adenocarcinoma cell line, was used, and MTT assay data showed that the cell viability of A549 was significantly increased in a concentration-dependent manner by COF treatment for 48h. Flow cytometery results indicated that the proportion of A549 cell at S-phase was markedly increased after exposure of COF. To elucidate whether the antiapoptotic c-IAP2 (IAP2) was involved in COF-improved cell survival, IAP2 protein levels was determined by Western blot, and the results showed it was significantly induced by COF in a concentration-dependent manner. Moreover, the suppression of BAY, a nuclear factor (NF)-κB binding inhibitor, or the COF-induced IAP2 protein levels indicated that NF-κB activation by COF may partly be involved in IAP2 induction. These results showed that the positive impact of COF on cell survival and proliferation of A549 lung tumor cells may be through an induction of IAP2 overexpression.