Toxicological Research

Korean Society of Toxicology & Korea Environmental Mutagen Society (한국독성학회)
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The Effects of Hazardous Chemical Exposure on Cardiovascular Disease in Chemical Products Manufacturing Workers

  • Kim, Ki-Woong (Occupational Safety and Health Research Institute, KOSHA) ;
  • Won, Yong Lim (Occupational Safety and Health Research Institute, KOSHA) ;
  • Ko, Kyung Sun (Occupational Safety and Health Research Institute, KOSHA) ;
  • Heo, Kyung-Hwa (Occupational Safety and health Training Institute, KOSHA) ;
  • Chung, Yong Hyun (Occupational Safety and Health Research Institute, KOSHA)
  • Received : 2012.10.12
  • Accepted : 2012.12.03
  • Published : 2012.12.31
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Abstract

The purpose of this study was to understand the mechanism of cardiovascular disease (CVD) caused by exposure to hazardous chemicals. We investigated changes in the symptoms of metabolic syndrome, which is strongly related to CVD, and in levels of other CVD risk factors, with a special emphasis on the roles of catecholamines and oxidative stress. The results revealed that neither body mass index (BMI) nor waist and hip circumferences were associated with exposure to hazardous chemicals. Among metabolic syndrome criteria, only HDL-cholesterol level increased on exposure to hazardous chemicals. Levels of epinephrine (EP) and norepinephrine (NEP) were not influenced by exposure to hazardous chemicals; however, the total antioxidative capacity (TAC) reduced because of increased oxidative stress. Both hazardous chemical exposure level and metabolite excretion were related to EP, NEP, and the oxidative stress index (OSI). Logistic regression analysis with these factors as independent variables and metabolic syndrome criteria as dependent variables revealed that EP was associated with blood pressure, and NEP with metabolic syndrome in the chemical-exposed group. In conclusion, the results suggest that reactive oxygen species generated and oxidative stress due to exposure to hazardous chemicals act as mediators and cause changes in the physiological levels of EP and NEP to increase blood pressure. This ultimately leads to the development of CVD through increase in cholesterol, triglyceride, and blood glucose levels by lipid peroxidation.

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References

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