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 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 Effects of Long-Term, Low-Level Exposure to Monocyclic Aromatic Hydrocarbons on Worker's Insulin Resistance.

OBJECTIVES: This study was designed to investigate whether long-term, low-level exposure to monocyclic aromatic hydrocarbons (MAHs) induced insulin resistance. METHODS: The subjects were 110 male workers who were occupationally exposed to styrene, toluene, and xylene. One hundred and ten age-matched male workers who had never been occupationally exposed to organic solvents were selected as a control group. Cytokines, which have played a key role in the pathogenesis of insulin resistance, and oxidative stress indices were measured. Assessment of exposure to MAHs was performed by measuring their ambient levels and their urinary metabolites in exposed workers, and the resulting parameters between the exposed group and non-exposed control groups were compared. RESULTS: There was no significant difference in general characteristics and anthropometric parameters between the two groups; however, total cholesterol, fasting glucose, fasting insulin, and homeostasis model assessment of insulin resistance levels were significantly higher in the exposed group. Phenylglyoxylic acid levels showed significant association with tumor necrosis factor-α, total oxidative status, and oxidative stress index via multiple linear regression analysis. Further, there was a negative correlation between methylhippuric acid levels and total anti-oxidative capacity, and there was a significant relationship between MAHs exposure and fasting glucose levels, as found by multiple logistic regression analysis (odds ratio = 3.95, 95% confidence interval = 1.074-14.530). CONCLUSION: This study indicated that MAHs increase fasting glucose level and insulin resistance. Furthermore, these results suggested that absorbing the organic solvent itself and active metabolic intermediates can increase oxidative stress and cytokine levels, resulting in the changes in glucose metabolism and the induction of insulin resistance.