Dynamic thiol disulfide homeostasis in painters as indices of oxidative stress.

This study was designed to determine thiol-disulfide homeostasis as indices of oxidative stress in painters by using a novel and automated colorimetric measurement method. Male painters (n = 117) were separated into three groups according to duration of work; group 1 (<5 years), group 2 (5-14 years) and group 3 (≥15 years). Hippuric acid, trichloroacetic acid (TCA), and phenol in urine was determined. Catalase activity and ischemia-modified albumin (IMA) levels were also assessed. Disulfide/Native Thiol and Disulfide/Total Thiol of group 2 and group 3 were significantly higher than those of group 1 (p < 0.001). A positive correlation was observed between urinary phenol and disulfide/native thiol (r = 0.214, p = 0.035), IMA (r = 0.305, p = 0.002), disulfide (r = 0.209, p = 0.040), and duration of work (r = 0.341, p < 0.001). The newly developed automated colorimetric method used in our study proposes a promising, practical and daily applicable test for evaluating oxidative status of painters.

Alteration of thiol disulfide homeostasis and ischemia-modified albumin levels as indicators of oxidative status in patients with silicosis.

The aim of this study was to evaluate the oxidative status in patients with silicosis by detecting dynamic thiol disulfide homeostasis (TDH), ischemia-modified albumin level (IMA) catalase (CAT) activity, and the correlation of these markers with pulmonary function tests. Male ceramic workers with silicosis (n = 91) and healthy individuals (n = 47) were recruited for the study. Radiographic abnormalities of pneumoconiosis were classified into three profusion categories (categories 1, 2, and 3), and patients with silicosis, those with category 1, were defined as group 1 and those with category 2 or 3 were defined as group 2. Plasma levels of native thiol (NT), total thiol (TT), disulfide (Ds), IMA, and CAT activities were determined. Pulmonary function tests of groups were compared. NT, TT, and NT/TT ratios were significantly lower in groups 1 and 2 than the control group (p < 0.05). These did not differ between patients with silicosis (groups 1 and 2) and control group (p = 0.421). Ds/NT and Ds/TT ratios were significantly higher in group 2 than the control group (p < 0.05). NT, TT, and Ds did not differ significantly between groups 1 and 2. The oxidant biomarker IMA was higher (p < 0.001), and the antioxidant parameters albumin and CAT were lower in groups 1 and 2 (p < 0.001) compared with the control group. The mean FEV1act, FVCact, forced expiratory volume in 1 second/forced vital capacity (%), and value of 25-75 percent maximum expiratory flow were significantly lower in groups 1 and 2 than control group. We have used a novel colorimetric method to assess TDH in patients with silicosis. Alteration of plasma thiol/disulfide homeostasis and IMA levels might be novel indicators of oxidative stress in silicosis.

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.

Assessment of Diastolic Function and Thiol-Disulphide Homeostasis in Arsenic-Exposed Workers.

OBJECTIVES: Exposure to arsenic is associated with various cardiovascular diseases. The imbalance between antioxidant and oxidant homeostasis plays a crucial role in the cardiovascular effects of arsenic. The aim of this study was to investigate the effect of arsenic exposure on diastolic function by measuring thiol and disulphide in arsenic-exposed workers. METHODS AND RESULTS: A total of 107 male arsenic-exposed workers and 36 healthy subjects were enrolled. Mitral inflow velocity and parameters of diastolic function were measured. As oxidative stress indicators, total thiol, native thiol, disulphide, and their percent ratios were determined. The mean age was 39.1 ± 9.5 years in the arsenic-exposed group and 37.4 ± 9.6 years in the controls. The median blood arsenic level was 42 µg/dL in the arsenic-exposed group and 3.75 µg/dL in the controls. E-wave, E/A ratio, and e' wave were lower and left atrial diameter, A-wave, average E/e' ratio, and tricuspid regurgitation velocity were higher in the arsenic-exposed group. Native and total thiol concentrations were lower, and disulphide/native and disulphide/total thiol ratios were higher in the arsenic-exposed group. Fourteen (13.1%) workers had diastolic dysfunction, 26 (24.3%) had indeterminate, and 67 (62.6%) had normal diastolic function, compared to 1 (2.8%), 2 (5.6%), and 33 (97.7%) in the control group, respectively. In regression analysis, disulphide/native thiol ratio (p < 0.001) and blood arsenic level (p < 0.001) predicted increased average E/e' ratio in the arsenic-exposed group. CONCLUSIONS: This study showed strong associations among arsenic exposure, oxidative stress, and diastolic function, and revealed the influence of arsenic exposure on diastolic dysfunction through oxidative stress.

Dynamic thiol/disulphide homeostasis as indicator of oxidative stress in automotive workers.

Purpose: To examine thiol-disulphide homeostasis auto painters.Materials and methods: A total of 115 male workers, including 60 auto painters workers and 55 reference group, of the painting and assembly line units respectively, were included in the study. Thiol-disulphide parameters and ischaemia-modified albumin (IMA) of groups were determined. Urinary hippuric acid, (HA) phenol, hexanedione, trichloroacetic acid, arsenic and blood lead and manganese were analysed.Results: The median urinary HA level was significantly higher in auto painters when compared to the reference group [(2461 (1212) vs. 520 (513) µgr/L), (p < 0.001)] . The mean disulphide level [19.7 (4.3) vs 0.15.1(4.1) µmol/L, (p < 0.001)], the disulphide/native thiol ratio [4.72 (1.47) vs. 3.13 (1.21, (p < 0.001)] and the disulphide/total thiol ratio [4.31 (1.23) vs. 2.94 (1.06), (p < 0.001)] were higher in auto painters when compared to the reference group. There was a statistically significant positive correlation between urinary HA and disulphide concentrations (r = 0.536 and p < 0.001), disulphide/native thiol ratio (r = 0.564 and p < 0.001) and the disulphide/total thiol ratio (r = 0.564 and p < 0.001) and IMA (r = 0.396 and p < 0.001).Conclusion: The results presented in this study showed that oxidative stress can be associated with occupational exposure to toluene denoted by alteration of thiol disulphide homeostasis and ischaemia-modified albumin levels.

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.

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.

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.

Radiological progression and lung function decrements among silica-exposed ceramic workers: a longitudinal study.

Objectives: This follow-up study set out to evaluate the natural course and radiographic progression of silicosis among ceramic workers and describe the risk factors related with disease progression. Materials and methods: We retrospectively analyzed the data of ceramic workers with silicosis who were referred to our hospital between February 2010 and March 2018. A total of 165 ceramic workers followed at least 24 months and with at least two chest radiographs were included in the study. Results: The duration of silica exposure ranged from 5.5 to 27 (median 13.6) years. The numbers of patients according to follow-up time were as follows: 38 (2-2.9) years, 77 (3-3.9) years, 26 (4-4.9) years, 17 (5-5.9) years, and 7 (≥6) years. Overall 62 of 165 (37.5%) cases showed radiologic evidences of progression ranging from 2 to 8.9 years (mean 3.7 years). Pulmonary function loss rate among silicosis patients was 36.9% (61/165). Multiple logistic regression analysis showed a significant relation between radiographic progression and age (OR, 1.079: 95% CI, 1.011-1.152), follow-up time (OR, 1.557: 95% CI, 1.144-2.118), and the ILO category (category 2 or 3) at first visit (OR, 3.507: 95% CI, 1.505-8.170). Conclusions: Our findings suggest that one-third of Turkish ceramic workers with silicosis who were followed up to 8.9 years showed progression that was related to increasing age greater ILO category at time of initial visit and follow-up duration.

Predictive risk factors for development of silicosis in Turkish ceramic workers.

INTRODUCTION: Silicosis is still one of the the most common occupational disease in the world. The ceramic industry is one of the main sectors where silicosis patients are increasingly reported. The aim of this study was to evaluate the differences in demographic characteristics, radiological findings and pulmonary function test results of the ceramic workers with silicosis and those did not develop the disease. MATERIALS AND METHODS: A total of 626 workers, 459 with silicosis and 167 without silicosis, working in the ceramics industry those admitted to Ankara Occupational and Environmental Diseases Hospital between 2009 and 2018 were included in the study. The cases were evaluated retrospectively. RESULT: The median age and duration of work of the workers with silicosis were significantly higher (p< 0.001) compared to workers without silicosis. The risk of silicosis was found to be 22.5 times higher in 50 years or older age. Working 11-20 years and more than 20 years increased the risk of silicosis by 3.1 fold and 3.9 fold respectively. Smoking more than 10 package-years was found to increase the risk of silicosis 2 fold. The workers who had worked in clay processing, sanding, glazing or smelting were found to have 5.2-fold, 3.8-fold 2.5 and 2.4 fold higher silicosis risk, respectively. CONCLUSIONS: In this study, it has been shown that older age, longer duration of work, smoking, working in clay processing, sanding, glazing or smelting sections increase the risk of silicosis in ceramic workers.

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.

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.

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.

Comprehensive Electrocardiographic Analysis of Lead Exposed Workers: An Arrhythmic Risk Assessment Study.

BACKGROUND: To evaluate electrocardiographic parameters which are related with atrial and ventricular arrhythmias measured from 12-lead surface electrocardiogram (ECG) in workers occupationally exposed to lead. METHODS: Sixty lead-exposed workers and 60 healthy controls were enrolled. Twelve-lead surface ECG was recorded and measurements of P wave durations (Pmax, Pmin) and P wave dispersion (PWD), QT durations and dispersion (QTd), corrected QT (QTc), Tp-e interval, and Tp-e/QT ratio were analyzed. RESULTS: The lead-exposed and control groups were similar with respect to baseline demographic, laboratory, and transthoracic echocardiographic indices. PWD (26.3 ± 9.7 vs 22.0 ± 9.0 ms, P = 0.014), Pmin (89.9 ± 13.8 vs 79.2 ± 10.1 ms, P < 0.001), and Pmax (116.2 ± 15.0 vs 101.2 ± 14.2 ms, P < 0.001), QT maximum (377.0 ± 27.6 vs 364.9 ± 28.5 ms, P = 0.02), QTd (38.4 ± 16.5 vs 30.5 ± 12.4 ms, P = 0.004), Tp-e interval (78.9 ± 16.5 vs 70.3 ± 14.5 ms, P = 0.003), and Tp-e/QT ratio (0.22 ± 0.04 vs 0.20 ± 0.04, P = 0.013) were significantly higher in lead-exposed workers. QT minimum and QTc values did not differ significantly. QT maximum, QTd, and Tp-e/QT ratio were correlated with urine lead level and Tp-e interval was correlated with both blood and urine lead levels. CONCLUSIONS: Lead-exposed workers have a higher risk for atrial and ventricular arrhythmias even without overt cardiac diseases compared with healthy subjects. These workers should be followed closely for adverse cardiovascular outcomes especially arrhythmias.

Assessment of heart rate response to exercise and recovery during treadmill testing in arsenic-exposed workers.

BACKGROUND: Arsenic exposure is associated with various cardiovascular diseases. The aim of the present study was to assess cardiac autonomic function via heart rate response to exercise and recovery period of treadmill testing in arsenic-exposed workers. METHODS: Sixty-five (65) occupationally arsenic-exposed workers and 35 healthy controls were enrolled. Blood and urinary arsenic levels were analyzed and symptom limited maximal treadmill exercise test were performed. Chronotropic response to exercise including age-predicted maximal heart rate (APMHR), heart rate reserve (HRreserve ), age-predicted HRreserve (APHRreserve ) and adjusted HRreserve and 1st-, 2nd-and 3rd-min heart rate recovery (HRR) indices were calculated. RESULTS: Baseline clinical and echocardiographic parameters, exercise test duration, resting and maximal heart rate, peak exercise capacity, HRreserve , APMHR, APHRreserve , and adjusted HRreserve were found to be similar between groups. HRR1 (22.0 ± 4.3 vs. 24.3 ± 3.1 bpm, p = .003) and HRR2 (43.2 ± 6.2 vs. 46.7 ± 6.4 bpm, p = .012) were significantly lower in arsenic-exposed workers compared to controls. Blood and urinary arsenic levels negatively correlated with HRR1 (r = -.477, p < .001 and r = -.438, p < .001, respectively) and HRR2 (r = -.507, p < .001 and r = -.412, p < .001 respectively). CONCLUSIONS: Arsenic-exposed workers had lower HRR indices than normal subjects but chronotropic response were similar. Cardiac autonomic dysregulation may be one of the cardiovascular consequences of arsenic exposure.

Dynamic disulfide/thiol homeostasis in lead exposure denoted by a novel method.

Lead is a toxic heavy metal, and prevention of human exposure to lead has not been accomplished yet. The toxicity of lead is continually being investigated, and the molecular mechanisms of its toxicity are still being revealed. In this study, we used a novel method to examine thiol (SH)/disulfide homeostasis in workers who were occupationally exposed to lead. A total of 80 such workers and 70 control subjects were evaluated, and their native and total SH values were measured in serum using a novel method; their blood lead levels were also assessed. The novel method used for SH measurements was based on the principle of measuring native SH, after which disulfide bonds were reduced and total SHs were measured. These measurements allowed us to calculate disulfide amounts, disulfide/total SH percent ratios, disulfide/native SH percent ratios, and native SH /total SH percent ratios. We found that disulfide levels were significantly higher in workers who were exposed to lead (21.08(11.1-53.6) vs. 17.9(1.7-25), p < 0.001). Additionally, the disulfide/native SH and disulfide/total SH percent ratios were higher in exposed workers, while the native SH/total SH percent ratios were higher in the control subjects. Furthermore, the lead and disulfide levels showed a positive correlation, with p < 0.001 and a correlation coefficient of 0.378. Finally, the novel method used in this study successfully showed a switch from SH to disulfide after lead exposure, and the method is fully automated, easy, cheap, reliable, and reproducible. Use of this method in future cases may provide valuable insights into the management of lead exposure.

Assessment of the Cardiac Autonomic Nervous System in Mercury-Exposed Individuals via Post-Exercise Heart Rate Recovery.

OBJECTIVE: The aim of this study was to assess exercise heart rate recovery (HRR) indices in mercury-exposed individuals when evaluating their cardiac autonomic function. SUBJECTS AND METHODS: Twenty-eight mercury-exposed individuals and 28 healthy controls were enrolled. All the subjects underwent exercise testing and transthoracic echocardiography. The HRR indices were calculated by subtracting the first- (HRR1), second- (HRR2) and third-minute (HRR3) heart rates from the maximal heart rate. The two groups were evaluated in terms of exercise test parameters, especially HRR, and a correlation analysis was performed between blood, 24-hour urine and hair mercury levels and the test parameters. RESULTS: The mercury-exposed and control groups were similar in age (37.2 ± 6.6 vs. 36.9 ± 9.0 years), had an identical gender distribution (16 females and 12 males) and similar left ventricular ejection fractions (65.5 ± 3.1 vs. 65.4 ± 3.1%). The mean HRR1 [25.6 ± 6.5 vs. 30.3 ± 8.2 beats per min (bpm); p = 0.009], HRR2 (43.5 ± 5.3 vs. 47.8 ± 5.5 bpm; p = 0.010) and HRR3 (56.8 ± 5.1 vs. 59.4 ± 6.3 bpm; p = 0.016) values were significantly lower in the mercury-exposed group than in the healthy controls. However, there were no significant correlations between blood, urine and hair mercury levels and exercise test parameters. CONCLUSIONS: Mercury-exposed individuals had lower HRR indices than normal subjects. In these individuals, mercury exposure measurements did not show correlations with the exercise test parameters, but age did show a negative correlation with these parameters. Therefore, cardiac autonomic functions might be involved in cases of mercury exposure.

Prolactin levels in manganese-exposed male welders.

PURPOSE: Early studies on manganese (Mn) exposure have demonstrated that this transition metal affects dopamine neurotransmission. Dopamine serves as a tonic inhibitor of prolactin release in the anterior hypophysis. Our aim was to determine the relation between serum prolactin levels and manganese-exposure. METHODS: Whole blood was collected from 95 non-exposed control subjects and 179 manganese-exposed male welders. Whole blood manganese was analyzed by Inductively Coupled Plasma--Mass Spectrometer on Agilent 7700 (Agilent Technologies, USA). Serum prolactin levels (PRL), aspartate transaminase (AST), alanine transaminase (ALT), urea, creatinine, soduim (Na), potassium (K) were analyzed by immunological and spectrophotometric methods on Roche E170 Modular System (Roche Diagnostics, Mannheim, Germany). RESULTS: The mean ages for control and manganese-exposed group were 40.5 ± 7.8 and 39.5 ± 8.7, respectively (p = 0.258). The mean working period (years) for control and manganese-exposed group were 17.4 ± 9.8 and 18.2 ± 7.7 years, respectively (p = 0.581). Serum AST and potassium levels were significantly higher in control group than manganese-exposed group (p = 0.002 and p = 0.048, respectively) and body-mass index (BMI) was significantly lower in control group than manganese-exposed group (p = 0.033). There was a significantly positive correlation between whole blood manganese levels and serum prolactin (r = 0.860, p < 0.001). Serum ALT levels were positively correlated with serum AST, urea and sodium (r = 0.315, p < 0.001; r = 0.121, p = 0.046; r = 0.130, p = 0.031). CONCLUSIONS: Serum prolactin level is a diagnostic marker for determining the effect of manganese-exposure.

Effect of chelation therapy on arrhythmogenic and basal ECG parameters of lead exposed workers.

Lead exposure has etiological role on cardiovascular system diseases as hypertension, atherosclerosis, stroke, and arrhythmic events. In this study, we aimed to compare the basal and arrhythmogenic ECG parameters of lead exposed workers before and after chelation therapy and to evaluate the effect of acute change of blood lead levels on ECG. Fourty consecutive occupationally lead exposed workers were enrolled, demographic, blood, echocardiographic, and electrocardiographic data's were analyzed before and after chelation therapy. Pmax, P min, P Wave Dispersion, and QT Dispersion values which are arrhythmia predictors were significantly lower after chelation therapy compared to values before chelation therapy. Lead exposed workers are under the risk of ventricular and atrial arrythmias and chelation treatment has a positive effect on these parameters.

Neutrophil-to-Lymphocyte Ratio and Platelet-to-Lymphocyte Ratio as Inflammatory Markers in Patients With Welders' Lung Disease.

OBJECTIVE: To investigate neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) in patients with welders' lung disease (PWLD) and its relation with pulmonary function parameters. METHODS: One hundred sixteen male PWLD and 118 healthy non-exposed individuals were recruited. Pulmonary function tests (PFTs), complete blood count, erythrocyte sedimentation rate (SED), c-reactive protein (CRP), NLR and PLR of both groups were retrospectively analyzed. RESULTS: NLR, PLR, WBC, ESR, and CRP were significantly higher in PWLD compared to controls (all P < 0.001). All PFTs, except for FEV1/FVC, significantly decreased in PWLD compared to controls as. NLR correlated positively with ESR (r = 0.241 and P < 0.001). CONCLUSION: Our results show that NLR and PLR can be considered as new inflammatory markers in PWLD with their cheap, fast and easily measurable feature with routine blood count analysis.