Assessment of potential cardiovascular risk in trichloroethylene exposure by serum methylated arginine levels.

Trichloroethylene (TCE) is a widely used solvent in industrial applications and has toxic effects on various systems. Methylated arginine amino acids (eg asymmetric dimethyl arginine (ADMA), symmetric dimethyl arginine (SDMA)) cause the development of cardiovascular disease by inhibiting NO synthesis, which is considered to be heart-protector. The aim of this study is to determine the risk of cardiovascular diseases in TCE exposure by methylated arginine biomarkers. About 98 controls and 100 TCE-exposed male subjects were included in the study. Trichloroacetic acid (urinary metabolite of TCE), arginine, homoarginine, citrulline ADMA, SDMA, and N-monomethyl L-arginine (L-NMMA) levels were found significantly higher than control group (p < 0.001). The strongest correlation was found between ADMA and Trichloroacetic acid (TCA) level (r = 0.453, p < 0.01). Long-term TCE exposure, may be an important risk factor for cardiovascular diseases by increasing methylated arginine levels.

The relationship between impaired lung functions and cytokine levels in formaldehyde exposure.

Exposure to formaldehyde (FA) causes detrimental effects on respiratory system. Inflammation is one of the mechanisms responsible for these effects. Our aim is to demonstrate the possible effect of formaldehyde on inflammation biomarkers and pulmonary function tests. One hundred ninety-eight male workers in a fiber production factory are included. Eighty two of them were not exposed to FA. Thirty nine workers were exposed to FA for 4 h or more in a work shift and 77 workers were exposed less than 4 h. Statistically significant differences were found for FA, TNF-α, and IL-6 levels and pulmonary function test parameters (FEV1 and FVC) between no exposure and exposure groups. The results revealed a correlation between decrement in pulmonary function tests and an increase in cytokine levels concordant with the duration of FA exposure. The results may emphasize that FA exposure shows its effect on pulmonary system via inflammatory pathways.

Assessment of Endothelial Dysfunction with Methylated Arginines and L-arginine in Cadmium-Exposed People: a Pilot Study.

BACKGROUND: Workers can be exposed to cadmium (Cd) in various industries. On the other hand, another potential source for Cd exposure is the food chain and smoking. Environmental pollution to Cd plays an important role in the development of atherosclerosis. Asymmetric dimethyl arginine (ADMA) levels promote the development of endothelial dysfunction and atherosclerosis-related diseases such as hypertension, acute coronary syndrome, congestive heart failure, and peripheral vascular diseases. The aim of this study is to evaluate the cardiovascular risks of non-symptomatic cadmium-exposed workers and to promote the value of methylated arginines in screening of toxic exposures. METHODS: A total 176 participants were included in the study which has been separated as control group (n = 79) and Cd-exposed group (n = 94). Inductively Coupled Plasma Mass Spectrometry (ICP-MS) was used for toxicological analysis of Cd levels. Also, liquid Chromatography-Mass Spectrometry (LC-MS/MS) was used for levels of methylated arginines such as ADMA, symmetric dimethylarginine (SDMA), NG-monomethyl-L-arginine (L-NM-MA), homoarginine, and citrulline. RESULTS: Statistically significant differences were observed for control and Cd-exposed groups, respectively as follows: Cd levels (0.25 ± 0.13 µg/L and 1.33 ± 0.61 µg/L), ADMA (0.16 ± 0.04 µmol/L and 0.22 ± 0.11 µmol/L), SDMA (0.21 ± 0.06 µmol/L and 0.27 ± 0.07 µmol/L), L-NMMA(0.02 ± 0.01 µmol/L and 0.03 ± 0.01µmol/L), and arginine/ADMA levels (695.82 ± 620.63 and 478.30 ± 432.61). CONCLUSIONS: Our results suggest that workers chronically exposed to Cd showed imbalances in endothelial parameters.

Changing levels of selenium and zinc in cadmium-exposed workers: probable association with the intensity of inflammation.

Inflammation is a response mediated by multiple cytokines, such as IL-6, IL-10 and TNF-α. Cadmium (Cd) has been involved in the etiopathogenesis of many diseases via inflammation. Selenium (Se) and zinc (Zn) play a pivotal role in maintaining many physiological functions of cells as well as inhibiting Cd-induced cytotoxicity. This study investigated the anti-inflammatory effects of Se and Zn in cadmium-exposed workers by measuring the levels of IL-6, IL-10 and TNF-α cytokines in 68 control and 91 Cd-exposed subjects. Blood samples were obtained from each participant for immunological, toxicological and routine analysis. All samples were digested by microwave oven and analysed by inductively coupled plasma mass spectrometry (ICP-MS). IL-6, IL-10 and TNF-α cytokine levels were found to be statistically different (p < 0.001) between the control and Cd-exposed groups (23.50 ± 7.70 pg/mL vs. 69.05 ± 19.06 pg/mL; 28.61 ± 9.83 pg/mL vs. 51.79 ± 11.77 pg/mL; 3.44 ± 1.14 pg/mL vs. 5.79 ± 1.04 pg/mL, respectively). High positive correlations were found between Cd levels of participants and IL-6, IL-10, TNF-α and CRP levels (r = 0.568, r = 0.615, r = 0.614 and r = 0.296, respectively, p < 0.01). In terms of the regression analysis results, there were significant effects of Cd on IL-6, IL-10 and TNF-α levels (p < 0.05). The Cd, Zn and Se levels between control and exposed group were significantly different [0.26 ± 0.15 µg/L vs. 3.36 ± 1.80 µg/L; 143.91 ± 71.13 µg/dL vs. 121.09 ± 59.88 µg/dL; 92.98 ± 17.03 µg/L vs. 82.72 ± 34.46 µg/L (p < 0.001, p < 0.03, p < 0.015), respectively]. In conclusion, increasing levels of Se and Zn decreases the intensity of inflammation as measured by IL-6, IL-10 and TNF-α levels.

TNF-α and IL-6 as Biomarkers of Impaired Lung Functions in Dimethylacetamide Exposure.

BACKGROUND: Tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) are well-known biomarkers of systemic inflammation that have been associated with many diseases in the past. In this study, we aimed to determine the relationship between impaired lung functions and the levels of these biomarkers in DMAc exposed people. METHODS: 101 non-exposed control subjects (Group 1) and 109 DMAc-exposed workers from the polyvinyl chloride (PVC) industry were included in the study. In the next step, the exposed group was divided into two groups according to the level of exposure (Group 2 and 3). DMAc, TNF-α, IL-6, creatinine, ALT, AST, GFR and standard spirometry measurements were carried out in all subjects. RESULTS: When compared to the control group, TNF-α and IL-6 levels were significantly high compatible with the increase of DMAc levels, in the exposed groups. Urinary DMAc Levels were 0.06 mg/L in the control group. This level is significantly low when compared to exposed and severely exposed group (2.43 mg/L and 3.17 mg/L). TNF-α levels were 56.86 pg/mL, 145.52 pg/mL and 230.52 pg/mL in control, exposed and severely exposed groups. IL-6 levels were found to be 38.08 pg/mL, 89.19 pg/mL and 116 pg/mL for control, exposed and severely exposed groups, respectively. Similarly, the FEV1/FVC ratio decreased especially in the severely exposed group (p 0.001). CONCLUSIONS: In our study, results have revealed that TNF-and IL-6 levels are promising biomarkers in the early diagnosis of lung function impairment in inhalational DMAc exposure.

The effects of occupational lead exposure on selected inflammatory biomarkers.

In exposure to toxic metals such as lead, determining lead and cytokine levels (IL-6, IL-10, and TNF-α) is essential for early detection of diseases. The aim of this study was to develop an model for early detection of inflammation and onset of atherosclerosis in the absence of clinical findings in young workers, which could help physicians take timely an action and start treatment. This study included 49 metal workers exposed to lead occupationally and 50 unexposed administrative workers (controls) who underwent immunological analysis for cytokines (IL-6, IL-10, and TNF-α) and atherosclerosis markers (h-FABP and VCAM-1), toxicological analysis for lead, and routine biochemical analysis (ALT, AST, creatinine) at the Ankara Occupational and Environmental Diseases Hospital in 2017. Lead levels correlated with IL-6, IL-10, and TNF-α (r=0.469, r=0.521 and r=0.279, respectively, p<0.01) but did not significantly affect h-FABP and VCAM-1 levels.

Arsenic-induced inflammation in workers.

Occupational and environmental exposures to metal and metalloids can result in neurotoxicity and immunotoxicity. Selenium (Se) is essential for the proper functioning of neutrophils, macrophages, natural killer (NK) cells, T-lymphocytes and other immune mechanisms, while zinc (Zn) is a trace element essential for basic cell activities, including cell growth and differentiation. Arsenic (As) may lead to different types of immunosuppressive effects. This study consisted of 62 male workers, who had been exposed to arsenic for different durations and 73 non-exposed male workers (control group) with no history of occupational toxic metal exposure. Whole blood and serum samples were taken from each participant for immunological, toxicological and routine analysis during their annual periodical examination. Arsenic, selenium and zinc levels were determined by the ICP-MS and cytokines, IL-6, IL-10, TNF-α, sE-selectin and VCAM-1, were measured by ELISA. There were statistically significant differences (p < 0.001) between control and As-exposed group in As (1.37 ± 0.42 vs. 4.27 ± 1.54 µg/L) and Se levels (106.37 ± 48.04 vs. 74.70 ± 30.45 µg/L). The changing levels of As, Zn and Se seems to affect the severity of inflammatory reactions based on IL-6, IL-10 and TNF-α levels (r = 0.755, r = 0.679 and r = 0.617, respectively, for all p < 0.01). Selenium was found to have a suppressive effect on cytokines, as evidenced by Pearson correlations and regression analysis. These findings support the need to closely monitor Se levels in individuals exposed to arsenic and benefits for Se supplementation in the case of arsenic exposure, occupationally or environmentally.

Serum endocan level and diastolic functions in the case of lead exposure

Background/aim: Lead can cause morphological and functional changes in heart, and inflammation and endothelial dysfunction in vasculature. Endocan, as a novel indicator of endothelial dysfunction, has been used for cardiovascular diseases. This study investigated the relationship between lead exposure, endocan levels, and diastolic functions. Materials and methods: A total of 51 lead-exposed workers without a known cardiovascular disease or risk factors and 54 healthy controls were enrolled. All participants underwent transthoracic echocardiography. Blood lead and serum endocan levels were analyzed. Results: Baseline demographic and clinical characteristics were found to be similar between groups. Median blood lead (32 vs 1.5 µg/dL, P < 0.001) and serum endocan levels (67 vs 57.1 pg/mL, P = 0.02) were significantly higher in the lead-exposed group. Serum endocan level showed a positive correlation with blood lead levels (r = 0.404, P = 0.003) in lead-exposed workers. Serum endocan level was an independent risk factor for increased E/E' ratio (ß = 0.704, P = 0.002) and left atrial volume index (ß = 1.158, P = 0.011) and higher level of lead in blood was an independent risk factor for increased E wave (ß = 8.004, P = 0.022) in lead-exposed workers. Conclusion: Worsened diastolic functions may be seen in the course of lead exposure. Due to sharing a similar mechanism, a higher serum level of endocan may be a valuable laboratory clue for impaired diastolic function in this population.

A new potential biomarker in early diagnosis of firefighter lung function impairment: dynamic thiol/disulphide homeostasis.

OBJECTIVES: The aim of this study was to investigate the associations between urinary arsenic, oxidative stress, assessed by thiol/disulphide homeostasis, and lung diseases in firefighters. METHODS: The study conducted among the municipality-based male firefighters (n = 100) who were admitted to occupational diseases clinic for periodic medical examination. The control group consisted of non-exposed male office workers (n = 50). Urinary arsenic levels, thiol/disulphide homeostasis parameters of participants were determined. Also, lung diseases were assessed by chest X-ray and pulmonary function tests. RESULTS: The mean age and work year did not differ in the study and control group. The median urinary arsenic concentration of firefighters was significantly higher than in the control group: 15.65 (2.5-246) µg/L and 3 (0.10-6) µg/L, respectively (p < 0.001). The parameters of pulmonary function tests (PFT) FVC (%), FEV1 (%), FEV1/FVC ratio and FEF 25-75 (%) were all significantly lower in firefighters compared to controls. A significant increase in mean serum disulphide concentration (17.10 ± 8.31 µmol/L vs. 7.48 ± 5.91) (Fig. 1) and disulphide/native thiol % ratio: 3.63 (0.53-11.43) vs. 1.51 (0.03-7.65) (p < 0.001) were found between exposed group and controls. The Spearman's correlation analysis revealed a positive correlation between urinary arsenic and disulphide (r = 0.422, p < 0.001), disulphide/native thiol % ratio (r = 0.409, p < 0.001). Nevertheless, urinary arsenic correlated negatively with all PFT parameters including FVC (%), FEV1 (%), FEV1/FVC and FEF 25-75 (%) (p < 0.001). CONCLUSION: We showed the arsenic-induced oxidative stress in firefighters with impairments of several lung functions determined by thiol/disulphide homeostasis using a novel method.

Occupational exposure to asphalt fume can cause oxidative DNA damage among road paving workers.

OBJECTIVES: We designed the present study to determine the effect of occupational exposure to asphalt fumes on oxidative status and DNA damage in road paving workers. METHODS: Sixty road paving workers exposed to asphalt fumes and forty non-exposed control subjects were recruited. Occupational exposure to PAHs was assessed by urinary 1-hydroxypyrene (1-OHP) excretion. Serum thiol disulfide homeostasis (TDH), total oxidant status (TOS) and total antioxidant status (TAS) and urinary 8-hydro-deoxyguanosine (8-OH-dG) level were evaluated by automated colourimetric method. RESULTS: The urinary concentrations of 1-OHP and 8-OH-dG were significantly higher in the exposed group than in the control group (P < 0.001). Disulfide/thiol ratio, TOS, and TAS were also significantly higher for the asphalt workers. A positive correlation existed between urinary 1-OHP and 8-OH-dG, TOS and TAS. CONCLUSION: Study results indicate that exposure to PAHs induces oxidative stress and causes genotoxic effects in asphalt workers.

C-Reactive Protein Concentrations Among Crop and Dairy Farmers with Stable Chronic Obstructive Pulmonary Disease.

AIM: To assess the mean serum C-reactive protein concentrations among farmers and office controls, and further examined its relation to exposure duration, smoking habit, as well as presence or absence of COPD. METHODS: A cross-sectional survey was performed including examined group (EG), composed of agricultural workers (87 crop - EG1 and 83 dairy farmers - EG2), and control group (CG) composed by 80 office workers. Evaluation of subjects included a questionnaire on chronic respiratory symptoms, lung function tests, COPD diagnostics, and measurement of CRP serum concentrations. RESULTS: Serum CRP concentrations were raised in stable COPD patients independent of smoking habit or exposure duration. The mean CRP serum concentrations were higher in the subjects of EG1 and EG2 compared with those in CG, but without statistical significance. This count for mean CRP serum concentrations in subjects of EG1 and EG2 exposed more than 20 years and for those in smokers in all three groups as well. The mean CRP serum concentrations were significantly higher in subjects with COPD within EG1 (P=0.049) and EG2 (P=0.040), while those in CG were not. CONCLUSION: Data obtained suggest that systemic inflammation is present in farmers with COPD and CRP is an important biomarker in COPD in means of reflecting disease severity and prognosis of exposed farmers.

Thiol/disulfide homeostasis in asphalt workers.

The aim of this study was to investigate thiol/disulfide homeostasis in asphalt workers who are exposed to polycyclic aromatic hydrocarbons occupationally. The study was carried out in 34 nonsmoker asphalt workers. Additionally, 35 healthy nonsmoker volunteers were recruited as control group. Thiol and disulfide concentrations were determined using the novel automated measurement method. Levels of urinary 1-OH-pyrene were analyzed by liquid chromatography. Disulfide/thiol ratio was significantly higher in exposed group (p = .034). Also, a positive correlation was detected between disulfide/thiol ratio and 1-OH-pyrene values (r = .249, p = .036). Thiol/disulfide homeostasis was found to be disturbed in asphalt workers. The novel test used in this study may be useful for evaluating the oxidative status in polycyclic aromatic hydrocarbon (PAH) exposure.