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The Effects of Hazardous Chemical Exposure on Cardiovascular Disease in Chemical Products Manufacturing Workers
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 th...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Korean Society of Toxicology
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3834428/ https://www.ncbi.nlm.nih.gov/pubmed/24278620 http://dx.doi.org/10.5487/TR.2012.28.4.269 |
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author | Kim, Ki-Woong Won, Yong Lim Ko, Kyung Sun Heo, Kyung-Hwa Chung, Yong Hyun |
author_facet | Kim, Ki-Woong Won, Yong Lim Ko, Kyung Sun Heo, Kyung-Hwa Chung, Yong Hyun |
author_sort | Kim, Ki-Woong |
collection | PubMed |
description | 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 chemicalexposed 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. |
format | Online Article Text |
id | pubmed-3834428 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | The Korean Society of Toxicology |
record_format | MEDLINE/PubMed |
spelling | pubmed-38344282013-11-25 The Effects of Hazardous Chemical Exposure on Cardiovascular Disease in Chemical Products Manufacturing Workers Kim, Ki-Woong Won, Yong Lim Ko, Kyung Sun Heo, Kyung-Hwa Chung, Yong Hyun Toxicol Res Articles 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 chemicalexposed 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. The Korean Society of Toxicology 2012-12 /pmc/articles/PMC3834428/ /pubmed/24278620 http://dx.doi.org/10.5487/TR.2012.28.4.269 Text en Copyright ©2012, The Korean Society of Toxicology http://creativecommons.org/licenses/by-nc/3.0/ This is an Open-Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Articles Kim, Ki-Woong Won, Yong Lim Ko, Kyung Sun Heo, Kyung-Hwa Chung, Yong Hyun The Effects of Hazardous Chemical Exposure on Cardiovascular Disease in Chemical Products Manufacturing Workers |
title | The Effects of Hazardous Chemical Exposure on Cardiovascular Disease in Chemical Products Manufacturing Workers |
title_full | The Effects of Hazardous Chemical Exposure on Cardiovascular Disease in Chemical Products Manufacturing Workers |
title_fullStr | The Effects of Hazardous Chemical Exposure on Cardiovascular Disease in Chemical Products Manufacturing Workers |
title_full_unstemmed | The Effects of Hazardous Chemical Exposure on Cardiovascular Disease in Chemical Products Manufacturing Workers |
title_short | The Effects of Hazardous Chemical Exposure on Cardiovascular Disease in Chemical Products Manufacturing Workers |
title_sort | effects of hazardous chemical exposure on cardiovascular disease in chemical products manufacturing workers |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3834428/ https://www.ncbi.nlm.nih.gov/pubmed/24278620 http://dx.doi.org/10.5487/TR.2012.28.4.269 |
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