Yuebin Ke1, Lihua Huang2, Junjie Xia2, Xinyun Xu2, Honghe Liu2, Y Robert Li3. 1. Key Laboratory of Genetics and Molecular Medicine of Shenzhen, Shenzhen Center for Disease Control and Prevention, Shenzhen 518055, China. Electronic address: keyke@szu.edu.cn. 2. Key Laboratory of Genetics and Molecular Medicine of Shenzhen, Shenzhen Center for Disease Control and Prevention, Shenzhen 518055, China. 3. Department of Pharmacology, Campbell University School of Medicine, Buies Creek, NC 27546, USA; Department of Biomedical Sciences and Pathobiology, Virginia Polytechnic Institute and State University, and Virginia Tech-Wake Forest University School of Biomedical Engineering and Sciences, Blacksburg, VA 24061, USA.
Abstract
OBJECTIVES: To evaluate how exposure to deep-frying oils, repeated frying oil (RFO) and restaurant waste oil (RWO) affects emission of polycyclic aromatic hydrocarbons (PAHs) and oxidative stress in male restaurant workers. METHODS: The study participants included 236 male restaurant workers in 12 restaurants in Shenzhen. Airborne particulate PAHs were measured over 12h on each of two consecutive work days. Urinary 1-hydroxypyrene (1-OHP) measurements were used to indicate cooking oil fumes (COF) exposure, and urinary malondialdehyde (MDA) and 8-hydroxy-2'-deoxyguanosine (8-OHdG) were adopted as oxidative stress markers. RESULTS: The production and emission rates of ultrafine particles (UFPs) and PM2.5 were higher in the exposed groups than in the control group. The concentrations of summed PAHs were in the order of RFO-frying group>RWO-frying group>deep-frying group>unexposed control group. Urinary 1-OHP was found to be a significant predictor of elevated urinary MDA and 8-OHdG concentrations (all, P<0.05). UFPs were a significant predictor of elevated urinary 8-OHdG for restaurant workers (P<0.05). The RFO- and RWO-frying groups had higher mean urinary concentrations of 1-OHP, MDA and 8-OHdG than the control group (P<0.05). RFO exposure was found to be a significant risk factor for elevated urinary 8-OHdG and RWO exposure was found to be a significant risk factor for elevated urinary MDA (both, P<0.001). CONCLUSIONS: Concentrations of urinary 1-OHP, MDA and 8-OHdG reflect occupational exposure to PAHs from COFs and oxidative stress in restaurants workers. Exposure to RFO may cause increased oxidative DNA damage, and exposure to RWO might cause increased lipid peroxidation.
OBJECTIVES: To evaluate how exposure to deep-frying oils, repeated frying oil (RFO) and restaurant waste oil (RWO) affects emission of polycyclic aromatic hydrocarbons (PAHs) and oxidative stress in male restaurant workers. METHODS: The study participants included 236 male restaurant workers in 12 restaurants in Shenzhen. Airborne particulate PAHs were measured over 12h on each of two consecutive work days. Urinary 1-hydroxypyrene (1-OHP) measurements were used to indicate cooking oil fumes (COF) exposure, and urinary malondialdehyde (MDA) and 8-hydroxy-2'-deoxyguanosine (8-OHdG) were adopted as oxidative stress markers. RESULTS: The production and emission rates of ultrafine particles (UFPs) and PM2.5 were higher in the exposed groups than in the control group. The concentrations of summed PAHs were in the order of RFO-frying group>RWO-frying group>deep-frying group>unexposed control group. Urinary 1-OHP was found to be a significant predictor of elevated urinary MDA and 8-OHdG concentrations (all, P<0.05). UFPs were a significant predictor of elevated urinary 8-OHdG for restaurant workers (P<0.05). The RFO- and RWO-frying groups had higher mean urinary concentrations of 1-OHP, MDA and 8-OHdG than the control group (P<0.05). RFO exposure was found to be a significant risk factor for elevated urinary 8-OHdG and RWO exposure was found to be a significant risk factor for elevated urinary MDA (both, P<0.001). CONCLUSIONS: Concentrations of urinary 1-OHP, MDA and 8-OHdG reflect occupational exposure to PAHs from COFs and oxidative stress in restaurants workers. Exposure to RFO may cause increased oxidative DNA damage, and exposure to RWO might cause increased lipid peroxidation.
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