Genotoxicity of Fumes from Heated Cooking Oils Produced in Taiwan

Wu, Pei Fen; Chiang, Tai An; Ko, Ying Chin; Lee, Huei

doi:10.1006/enrs.1997.3798

Cited by 35 publications

(19 citation statements)

References 24 publications

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“…COFs routinely [Hinds et al, 1981;Koo et al, 1985;Wu et al, 1999]. The possible mechanisms for COFs to cause the adverse human health effects remain unclear.…”

Section: Discussionmentioning

confidence: 98%

Enhanced sensitivity to DNA damage induced by cooking oil fumes in human OGG1 deficient cells

Che

Zhang

2008

Environ and Mol Mutagen

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Cooking oil fumes (COFs) have been implicated as an important nonsmoking risk factor of lung cancer in Chinese women. However, the molecular mechanism of COFs-induced carcinogenicity remains unknown. To understand the molecular basis underlying COFs-induced cytotoxicity and genotoxicity as well as the roles of hOGG1 in the repair of COFs-induced DNA damage, a human lung cancer cell line with hOGG1 deficiency, A549-R was established by using a ribozyme gene targeting technique that specifically knockdowned hOGG1 in A549 lung adenocarcinoma cells. MTT and comet assays were employed to examine cell viability and DNA damage/repair, respectively, in A549-R and A549 cell lines treated with COF condensate (COFC). RT-PCR and Western blot results showed that the expression of hOGG1 in A549-R cell line was significantly decreased compared with that in A549 cell line. The concentration of COFC that inhibited cell growth by 50% (the IC50) in the A549-R cell line was much lower than that in the A549 cell line, and more COFC-induced DNA damage was detected in the A549-R cell line. The time course study of DNA repair demonstrated delayed repair kinetics in the A549-R cell line, suggesting a decreased cellular damage repair capacity. Our results showed that hOGG1 deficiency enhanced cellular sensitivity to DNA damage caused by COFC. The results further indicate that hOGG1 plays an important role in repairing COF-induced DNA damage. Our study suggests that COFs may lead to DNA damage that is subjected to hOGG1-mediated repair pathways, and oxidative DNA damage may be involved in COF-induced carcinogenesis.

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“…COFs routinely [Hinds et al, 1981;Koo et al, 1985;Wu et al, 1999]. The possible mechanisms for COFs to cause the adverse human health effects remain unclear.…”

Section: Discussionmentioning

confidence: 98%

Enhanced sensitivity to DNA damage induced by cooking oil fumes in human OGG1 deficient cells

Che

Zhang

2008

Environ and Mol Mutagen

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“…Over 50 volatile organic compounds have been identified from heated oil as well as cooked foods, and some of these agents in emissions of cooking oils are mutagens and human carcinogens, such as 1,3-butadiene, benzene, benzo(a)pyrene, dibenzo(a,h)anthracene, acrolein, and formaldehyde (29)(30)(31)(32)(33)(34). It has been found in experimental studies that temperature is the most important factor for mutagen formation (35,36).…”

Section: Discussionmentioning

confidence: 99%

Dose-Response Relationship between Cooking Fumes Exposures and Lung Cancer among Chinese Nonsmoking Women

et al. 2006

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The high incidence of lung cancer among Chinese females, despite a low smoking prevalence, remains poorly explained. Cooking fume exposure during frying could be an important risk factor. We carried out a population-based case-control study in Hong Kong. Cases were Chinese female nonsmokers with newly diagnosed primary lung cancer. Controls were female nonsmokers randomly sampled from the community, frequency matched by age groups. Face-to-face interviews were conducted using a standardized questionnaire. The ''total cooking dish-years,'' categorized by increments of 50, was used as a surrogate of cooking fumes exposure. Multiple unconditional logistic regression was used to estimate the odds ratios (OR) for different levels of exposure after adjusting for various potential confounding factors. We interviewed 200 cases and 285 controls. The ORs of lung cancer across increasing levels of cooking dish-years were 1, 1.17, 1.92, 2.26, and 6.15. After adjusting for age and other potential confounding factors, the increasing trend of ORs with increasing exposure categories became clearer, being 1, 1.31, 4.12, 4.68, and 34. The OR of lung cancer was highest for deep-frying (2.56 per 10 dish-years) followed by that of frying (1.47), and stir-frying had the lowest OR (1.12) among the three methods. Cumulative exposure to cooking by means of any form of frying could increase the risk of lung cancer in Hong Kong nonsmoking women. Practical means to reduce exposures to cooking fumes should be given top priority in future research. (Cancer Res 2006; 66(9): 4961-7)

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“…Several studies have shown aerosols from cooking oils to be mutagenic42 43 and genotoxic,44 possibly contributing to the raised incidence of lung cancer found among Taiwanese and Chinese women, not entirely explicable by exposure to cigarette smoke 4546 Recently, Ko et al 47 published details on cooking conditions and habits of 131 non-smoking incident cases of newly diagnosed lung cancer in women and found that the risk of lung cancer increased with the number of meals cooked each day, with not using a fume extractor, and with waiting until fumes were emitted from the oil before they began cooking.…”

Section: Discussionmentioning

confidence: 99%

Ultrafine particles and nitrogen oxides generated by gas and electric cooking

2001

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Objectives-To measure the concentrations of particles less than 100 nm diameter and of oxides of nitrogen generated by cooking with gas and electricity, to comment on possible hazards to health in poorly ventilated kitchens. Methods-Experiments with gas and electric rings, grills, and ovens were used to compare diVerent cooking procedures. Nitrogen oxides (NO x ) were measured by a chemiluminescent ML9841A NO x analyser. A TSI 3934 scanning mobility particle sizer was used to measure average number concentration and size distribution of aerosols in the size range 10-500 nm.Results-High concentrations of particles are generated by gas combustion, by frying, and by cooking of fatty foods. Electric rings and grills may also generate particles from their surfaces. In experiments where gas burning was the most important source of particles, most particles were in the size range 15-40 nm. When bacon was fried on the gas or electric rings the particles were of larger diameter, in the size range 50-100 nm. The smaller particles generated during experiments grew in size with time because of coagulation. Substantial concentrations of NO X were generated during cooking on gas; four rings for 15 minutes produced 5 minute peaks of about 1000 ppb nitrogen dioxide and about 2000 ppb nitric oxide. Conclusions-Cooking in a poorly ventilated kitchen may give rise to potentially toxic concentrations of numbers of particles. Very high concentrations of oxides of nitrogen may also be generated by gas cooking, and with no extraction and poor ventilation, may reach concentrations at which adverse health eVects may be expected. Although respiratory eVects of exposure to NO x might be anticipated, recent epidemiology suggests that cardiac eVects cannot be excluded, and further investigation of this is desirable. (Occup Environ Med 2001;58:511-516)

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Genotoxicity of Fumes from Heated Cooking Oils Produced in Taiwan

Cited by 35 publications

References 24 publications

Enhanced sensitivity to DNA damage induced by cooking oil fumes in human OGG1 deficient cells

Enhanced sensitivity to DNA damage induced by cooking oil fumes in human OGG1 deficient cells

Dose-Response Relationship between Cooking Fumes Exposures and Lung Cancer among Chinese Nonsmoking Women

Ultrafine particles and nitrogen oxides generated by gas and electric cooking

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