The Relationship between Duration of Benzene Exposure with Liver Enzymes in Car Painting Workshop Workers

Introduction: Benzene is a carcinogenic compound that can be found in a car painting workshop in Surabaya. The source of benzene in the car painting workshop comes from thinners. Inhalation is the main route for benzene to enter the body. The duration of benzene exposure can affect the accumulation of benzene concentrations. If work safety is not considered, the benzene compound can cause the liver disease. Furthermore, SGOT and SGPT are basic parameters of liver function. The study aims to determine the relationship between the duration of benzene exposure with SGOT and SGPT levels in car painting workshop workers. Method: observational research with a cross-sectional approach was applied as the method of this study. The research was conducted in a car painting workshop in 2019 with 20 workers. The variables were the duration of benzene exposure (hours/day) and levels of SGOT and SGPT. Data analysis used the Fisher's Exact Test and Coefficient Contingency test. Results: Workers worked with a duration of benzene exposure ≤ 8 hours/day by 70% and > 8 hours/day by 30%. The measurement results exceeded the normal limit with the value of SGOT of 15% and the SGPT of 30%. Furthermore, the Sstatistical test show p-values between the duration of benzene exposure and SGOT (0.202) and SGPT (0.303), body weight with SGOT (1.000) and SGPT (1.000), education with SGOT (0.199) and SGPT (0.182) and alcohol consumption with SGOT (1.000) and SGPT (1.000). Conclusion: There was no relationship between the duration of benzene exposure with SGOT and SGPT levels in car painting workshop workers in Surabaya with a p-value >0.05.Keywords: car painting workers, duration of benzene exposure, SGOT, SGPT

Benzene Exposure on Rig X from Drilling Fluid and Effectiveness of Local Exhaust Ventilation

Introduction: Benzene is a carcinogenic compound commonly found in drilling fluid, a chemical used in oil and gas drilling operations. Benzene exposure to workers is known to cause acute and/or chronic disease. Adequate control measures shall be identified and implemented to prevent the adverse health effects of benzene from the utilization of drilling fluid. Methods: This study measured benzene concentrations at several locations, above the drilling rig, which has the potential risk of benzene vapor exposure. From the measurement results, if the threshold limit value was exceeded, LEV was proposed to be installed and the effectiveness of LEV at each location would be assessed. A two-tailed t-test was used with a confidence level of 95% (α=0.05) to measure the effectiveness of LEV. Results: In several areas, benzene concentration exceeded TLV-TWA, and LEV was installed in those areas as control measures. In this study, it was found that LEV was not always effective in reducing the concentration of benzene in some areas. Conclusion: Drilling fluid was essential for drilling activity, and this could cause benzene vapor to contaminate the working area. The installation of the LEV shall consider the type of containment through which the drilling fluid flows to ensure the mitigation measures are effective to reduce the concentration of benzene in the air that may be exposed to workers.Keywords: benzene, drilling fluid, exhaust ventilation

Factors Affecting Adverse Health Effects of Gasoline Station Workers

This cross-sectional study examined the risk factors affecting adverse health effects from benzene exposure among gasoline station workers in Khon Kean province, Thailand. An interview questionnaire of adverse symptoms relating to benzene toxicity was administered to 151 workers. Area samplings for benzene concentration and spot urine for tt-muconic acid (tt-MA), a biomarker of benzene exposure, were collected. The factors associated with adverse symptoms were analysed by using multiple logistic regression. It was found that these symptoms mostly affected fuelling workers (77.5%), and the detected air benzene reached an action level or higher than 50% of NIOSH REL (>50 ppb). The top five adverse symptoms, i.e., fatigue, headache, dizziness, nasal congestion, and runny nose, were reported among workers exposed to benzene. More specific symptoms of benzene toxicity were chest pain, bleeding/epistaxis, and anaemia. The detected tt-MA of workers was 506.7 ug/g Cr (IQR), which was a value above the BEI and higher than that of asymptomatic workers. Risk factors significantly associated with adverse symptoms, included having no safety training experience (ORadj = 5.22; 95% CI: 2.16–12.58) and eating during work hours (ORadj = 16.08; 95% CI: 1.96–131.74). This study urges the tightening of health and safety standards at gasoline stations to include training and eating restrictions while working in hazardous areas.

Chronic Benzene Exposure Aggravates Pressure Overload-Induced Cardiac Dysfunction

Benzene is a ubiquitous environmental pollutant abundant in household products, petrochemicals and cigarette smoke. Benzene is a well-known carcinogen in humans and experimental animals; however, little is known about the cardiovascular toxicity of benzene. Recent population-based studies indicate that benzene exposure is associated with an increased risk for heart failure. Nonetheless, it is unclear whether benzene exposure is sufficient to induce and/or exacerbate heart failure. We examined the effects of benzene (50 ppm, 6 h/day, 5 days/week, 6 weeks) or HEPA-filtered air exposure on transverse aortic constriction (TAC)-induced pressure overload in male C57BL/6J mice. Our data show that benzene exposure had no effect on cardiac function in the Sham group; however, it significantly compromised cardiac function as depicted by a significant decrease in fractional shortening and ejection fraction, as compared with TAC/Air-exposed mice. RNA-seq analysis of the cardiac tissue from the TAC/benzene-exposed mice showed a significant increase in several genes associated with adhesion molecules, cell-cell adhesion, inflammation, and stress response. In particular, neutrophils were implicated in our unbiased analyses. Indeed, immunofluorescence studies showed that TAC/benzene exposure promotes infiltration of CD11b+/S100A8+/myeloperoxidase+-positive neutrophils in the hearts by 3-fold. In vitro, the benzene metabolites, hydroquinone and catechol, induced the expression of P-selectin in cardiac microvascular endothelial cells by 5-fold and increased the adhesion of neutrophils to these endothelial cells by 1.5-2.0-fold. Benzene metabolite-induced adhesion of neutrophils to the endothelial cells was attenuated by anti-P-selectin antibody. Together, these data suggest that benzene exacerbates heart failure by promoting endothelial activation and neutrophil recruitment.

Biomarkers of Cardiovascular Toxicity of Benzene Inhalation in Mice

ABSTRACTBenzene is a ubiquitous environmental pollutant. Recent population-based studies suggest that benzene exposure is associated with an increased risk for cardiovascular disease. However, it is unclear whether benzene exposure is sufficient to induce cardiovascular toxicity. We examined the effects of benzene inhalation (50 ppm, 6 h/day, 5 days/week, 6 weeks) or HEPA-filtered air exposure on the biomarkers of cardiovascular toxicity in male C57BL/6J mice. Benzene inhalation significantly increased the biomarkers of endothelial activation and injury including endothelial microparticles, activated endothelial microparticles, endothelial progenitor cell microparticles, lung endothelial microparticles, and activated lung and endothelial microparticles while having no effect on circulating levels of endothelial adhesion molecules, endothelial selectins, and biomarkers of angiogenesis. To understand how benzene may induce endothelial injury, we exposed human aortic endothelial cells to benzene metabolites. Of metabolites tested, trans,trans-mucondialdehyde (10 μM, 18h) was most toxic. It induced caspases-3, −7 and −9 (intrinsic pathway) activation, and enhanced microparticle formation by 2.4-fold. Levels of plateletleukocyte aggregates, platelet macroparticles, and proportion of CD4+ and CD8+ T-cells were also significantly elevated in the blood of the benzene-exposed mice. We also found that benzene exposure increased the transcription of genes associated with endothelial cell and platelet activation in the liver; and induced inflammatory genes and suppressed cytochrome P450s in the lungs and the liver. Together, these data suggest that benzene exposure induces endothelial injury, enhances platelet activation and inflammatory processes; and circulatory levels of endothelial cell and platelet-derived microparticles and platelet-leukocyte aggregates are excellent biomarkers of cardiovascular toxicity of benzene.HighlightsInhaled benzene exposure increases the levels of blood endothelial microparticles.In vitro, benzene metabolite trans, trans-mucondialdehyde induces endothelial cell apoptosis and microparticles formation.Inhaled benzene exposure decreases the levels of hematopoietic progenitor cells in the bone marrow.Inhaled benzene exposure augments the circulating levels of platelet-leukocyte adducts.