• Safety and Health at Work
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• 제9권2호
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• pp.149-158
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• 2018

Background: Work comfort studies have been extensively conducted, especially in the underground and meteorological fields resulting in an avalanche of recommendations for their evaluation. Nevertheless, no known or universally accepted model for comprehensively assessing the thermal work condition of the underground mine environment is currently available. Current literature presents several methods and techniques, but none of these can expansively assess the underground mine environment since most methods consider only one or a few defined factors and neglect others. Some are specifically formulated for the built and meteorological climates, thus making them unsuitable to accurately assess the climatic conditions in underground development and production workings. Methods: This paper presents a series of sensitivity analyses to assess the impact of environmental parameters and metabolic rate on the thermal comfort for underground mining applications. An approach was developed in the form of a "comfort model" which applied comfort parameters to extensively assess the climatic conditions in the deep, hot, and humid underground mines. Results: Simulation analysis predicted comfort limits in the form of required sweat rate and maximum skin wettedness. Tolerable worker exposure times to minimize thermal strain due to dehydration are predicted. Conclusion: The analysis determined the optimal air velocity for thermal comfort to be 1.5 m/s. The results also identified humidity to contribute more to deviations from thermal comfort than other comfort parameters. It is expected that this new approach will significantly help in managing heat stress issues in underground mines and thus improve productivity, safety, and health.

• Molecular & Cellular Toxicology
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• 제1권2호
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• pp.73-77
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• 2005

Nickel is the one of potent environmental, the occupational pollutants and the classified human carcinogens. It is a serious hazard to human health, when the metal exposure. To prevent human diseases from the heavy metals, it is seemingly important that understanding of how nickel exerts their toxicity and carcinogenic effect at a molecular and a genomic level. The process of nickel absorption has been demonstrated as phagocytosis, iron channel and diffusion. Uptaked nickel has been suggested to induce carcinogenesis via two pathways, a direct DNA damaging pathway and an indirect DNA damaging pathway. The former was originated from the ability of metal to generate Reactive Oxygen Species (ROS) and the reactive intermediates to interact with DNA directly. Ni-generated ROS or Nickel itself, interacts with DNAs and histones to cause DNA damage and chromosomal abnormality. The latter was originated from an indirect DNA damage via inhibition of DNA repair, or condensation and methylation of DNA. Cells have ability to protect from the genotoxic stresses by changing gene expression. Microarray analysis of the cells treated with nickel or nickel compounds, show the specific altered gene expression profile. For example, HIF-I (Hypoxia-Inducible Factor I) and p53 were well known as transcription factors, which are upregulated in response to stress and activated by both soluble and insoluble nickel compounds. The induction of these important transcription factors exert potent selective pressure and leading to cell transformation. Genes of metallothionein and family of heat shock proteins which have been known to play role in protection and damage control, were also induced by nickel treatment. These gene expressions may give us a clue to understand of the carcinogenesis mechanism of nickel. Further discussions on molecular and genomic, are need in order to understand the specific mechanism of nickel toxicity and carcinogenicity.