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1.
China Occupational Medicine ; (6): 309-312, 2017.
Article in Chinese | WPRIM | ID: wpr-881613

ABSTRACT

OBJECTIVE: To compare and analyze the risk of formaldehyde hazards in a plywood manufacturing factory using two risk assessment methods,and to evaluate the occupational health risk. METHODS: Occupational health investigation and formaldehyde detection for workplaces were carried out in a plywood manufacturing factory in Shandong province. The risk ratings of different posts were assessed by US Environmental Protection Agency( EPA) inhalation risk( EPA assessment model) and Singapore Semi-quantitative Assessment Model( MOM assessment model). The risk classification results of the 2 risk assessment methods were compared and analyzed. RESULTS: The concentration of airborne formaldehyde on the positions of shaving,woods feeding,gluing,hot milling,hot pressing,sanding and reprocessing were 0. 25,0. 13,1. 47,0. 72,0. 92 and 0. 58 mg/m~3,respectively. By the EPA assessment model,all of the positions were evaluated as high carcinogenic risk. Through the MOM assessment model,the feeding position was evaluated as medium risk,the positions of shaving,hot milling,hot pressing sanding and reprocessing were high risk,and the position of gluing was higher risk. CONCLUSION: It suggests that there is a high formaldehyde exposure in several posts in the plywood production processing. EPA assessment model is a suitable for occupational health risk assessment for formaldehyde exposure.

2.
China Occupational Medicine ; (6): 14-19, 2017.
Article in Chinese | WPRIM | ID: wpr-881572

ABSTRACT

OBJECTIVE: To establish the cell model using human leukemia cell line HL-60 for exposure of coke oven emissions( COE) in vitro and to explore the mechanism of COE-induced acute toxicity in HL-60 cells. METHODS: HL-60 cells were collected in their logarithmic growth phase and cultured in medium that had final concentrations of COE in 2. 5,5. 0,10. 0 and 20. 0 mg / L for 24 hours. Cell survival rate was examined by CCK-8 assay. The cytotoxicity was evaluated using lactate dehydrogenase release assay. Reactive oxygen species( ROS) production was determined by the 2',7'-dichlorofluorescein diacetate and nitroblue tetrazolium method. The activation of nuclear factor-κB( NF-κB) pathway was evaluated by western blot. RESULTS: With the increasing exposure concentrations of COE,the cytotoxicity of HL-60 cells increased( P < 0. 01),the cell survival rate decreased( P < 0. 01),intracellular ROS decreased( P < 0. 01),whereas extracellular ROS increased( P < 0. 01). These changes had a dose-effect relationship. The levels of phospho-nuclear factor-kappa B p65 and phospho-inhibitor of kappa Bα were higher in all the COE-treated cells compared with untreated cells( P < 0. 05),with no dose-effect relationship. CONCLUSION: COE could cause acute toxicity in HL-60 cells in a doseeffect relationship. The mechanism may be related to the COE-induced in-balanced ROS release and removal,leading to the activation of NF-κB pathway. HL-60 cells can be used as a common cell line for COE hematotoxicity analysis.

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