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• The study was carried out in metal industry plants under real working conditions. • Welding fumes and airborne metals were collected in the welders' breathing zone. • Chromium, nickel and manganese were determined in biological samples. • Effectiveness of biological monitoring was confirmed. The aim of the study was to determine the concentration of hexavalent and trivalent chromium, nickel, manganese, and iron in welding fumes (WFs) and to evaluate the significant association between the concentration of metals in the biological material of welders. The studies were conducted in welders (n = 67) and controls (n = 52). Stainless steel WFs were continuously collected in the workers' breathing zone during a shift. The serum and urine concentrations of Cr and Ni were determined by ICP-MS. The content of Mn in the whole blood was determined using ET-AAS. The content of Cr in the erythrocytes was determined using ICP-MS. The Cr concentration in the welders' urine positively correlated with a work environment concentration of Cr (R = 0.59, p < 0.0001), Cr(VI) (R = 0.58, p < 0.0001), and Cr(III) (R = 0.64, p < 0.0001) in the inhalable fraction. The Ni concentration in the welders' urine positively correlated with the Ni concentration in the inhalable and respirable fraction (R = 0.34, p < 0.005 and R = 0.44, p < 0.002). The correlation between the Mn concentration in the work environment air and the Mn concentration in the welders' whole blood (R = 0.46, p < 0.0001) was observed. [ABSTRACT FROM AUTHOR]

Anita Liput-Sikora,1 Anna Maria Cybulska,2 Wiesława Fabian,1 Marzanna Stanisławska,2 Magdalena Sylwia Kamińska,3 Elżbieta Grochans,2 Anna Jurczak4 1Primary Care Center (NZOZ Przychodnia Medycyny Rodzinnej SJ), Szczecin 71-521, Poland; 2Department of Nursing, Faculty of Health Sciences, Pomeranian Medical University in Szczecin, Szczecin 71-210, Poland; 3Subdepartment of Long-Term Care, Department of Social Medicine, Faculty of Health Sciences, Pomeranian Medical University in Szczecin, Szczecin 71-210, Poland; 4Department of Specialized Nursing, Faculty of Health Sciences, Pomeranian Medical University in Szczecin, Szczecin 71-210, PolandCorrespondence: Anna Maria CybulskaPomeranian Medical University in Szczecin, Faculty of Health Sciences, Żołnierska 48, Szczecin 71-210, PolandTel +48 91 48 00 910Fax +48 91 48 00 905Email anna.cybulska@pum.edu.plPurpose: The aim of this study was to analyze the severity of changes in cardiovascular risk factors (hypertension, overweight and obesity, carbohydrate metabolism disorders, burdened family history) and to assess the risk of a cardiovascular incident according to the Systematic Coronary Risk Evaluation (SCORE) algorithm in the same group of patients over a five-year interval.Patients and Methods: The research method was analysis of medical records of patients from the area of West Pomeranian Province, Poland, included in the Cardiovascular Disease Prevention Program of the National Health Fund five years after the first examination (2012/2013 vs 2017/2018). We collected data on changes in the levels of selected cardiovascular risk factors over five years and calculated the SCORE values.Results: In the second measurement (after five years), the odds of obesity were about 2.5 times higher. The repeated BMI measurement showed that after five years more respondents were classified as overweight and obese compared with the first measurement (p = 0.000; η2 = 0.056). The repeated SCORE measurement indicated that after five years the SCORE values significantly increased compared with the first measurement (p = 0.000; η2 = 0.588). Statistically significant differences (p < 0.05) were also found between the first and the second measurements of arm circumference, waist circumference, BMI, diastolic blood pressure, heart rate, and triglycerides. The risk of visceral obesity was statistically significantly higher for men than for women (RHM = 1.47).Conclusion: In the group of patients examined twice over five years, the incidence of obesity, including abdominal obesity, significantly increased. Furthermore, five years after the last examination, the risk of a cardiovascular incident significantly increased. The participants had higher values of such parameters as: arm circumference, waist circumference, BMI, diastolic blood pressure, heart rate, and triglycerides.Keywords: cardiovascular disease, risk factors, prevention, SCORE

Mercury (Hg) is a potent toxicant. In the field of public health a chronic-low-level environmental Hg exposure resulting from fish consumption in general population is still being discussed. The objective of the study was to assess the influence of real Hg exposure on biomarkers of selenium (Se) status and selected biomarkers of pro-oxidant/anti-oxidant effects in healthy men (n = 67) who participated in the short-term intervention study consisting in daily fish consumption for two weeks. The analysis included Se level, Se-associated antioxidants at molecular (profile of 7 genes encoding selected proteins related to antioxidant defense) and biochemical levels (Se-dependent glutathione peroxidases activities and plasma selenoprotein P concentration). A pro-oxidant/anti-oxidant balance was explored using a biomarker of plasma lipid peroxidation and total antioxidant activity. The study revealed significant correlations (p < 0.05) between the biomarkers of exposure to Hg, Se level and Se-dependent antioxidants. Even though the risk of adverse effects of Hg for volunteers was substantially low, biomarkers of Hg altered levels of circulation selenoproteins and their genes expression. Changes in genes expression during study differed between the main enzymes involved in two systems: downregulation of thioredoxin reductase1 and upregulation of glutathione peroxidases. Hg exposure caused imbalance between the biomarkers of pro-oxidant/anti-oxidant effects., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

Arsenic (As) is a known toxic element and carcinogen. Transcription factor nuclear factor-erythroid 2-related factor 2 (NRF2) controls cellular adaptation to oxidants and electrophiles by inducing antioxidant genes in response to redox stress. To explore associations between As level and NRF2-regulated cytoprotective genes expression, an observational study was conducted in a population of 61 occupationally exposed men with median (Me) age 50 years (interquartile range (IQR) 42-54) and in a control group of 52 men aged 40 (IQR 31-51.5) without occupational exposure. NRF2, KEAP1, GSTP1, HMOX1, NQO1, PRDX1, and TXNRD1 transcript levels were determined by means of quantitative real-time PCR along with the gene expression, methylation of NRF2 and KEAP1, as well as global DNA methylation were assessed. The median urine As tot. level in the exposed and control group was found to be 21.8 μg/g creat. (IQR 15.5-39.8 μg/g creat.) and 3.8 μg/g creat. (IQR 2.5-9.3) (p < 0.001). Global DNA methylation was significantly higher in occupationally exposed workers than in controls (Me 14.1 (IQR 9.5-18.1) vs Me 8.5 (IQR 5.9-12.6) p < 0.0001). NRF2 mRNA level was positively correlated with expression of all investigated NRF2-target genes in both groups (0.37 > R < 0.76, all p values < 0.0001). The multivariate linear regression adjusting for global methylation showed that As(III) level was significantly associated with expression of TXNRD1, GSTP1, HMOX1, and PRDX1. The results of this study indicate that arsenic occupational exposure is positively associated with global DNA methylation. The findings provide evidence for rather inactivation of NRF2-KEAP1 pathway in response to chronic arsenic exposure.

The present observation based research was designed to evaluate the influence of occupational human exposure to metallic mercury (Hg°) vapor on the biomarkers of selenium status involved in the antioxidant defense system. For this purpose we determined Hg and selenium (Se) concentrations in body fluids, the markers of antioxidant effect measured as an activity of Se-dependent enzymes (red blood cell and plasma glutathione peroxidase: GPx1-RBC and GPx3-P), concentration of selenoprotein P in the plasma (SeP-P) and total antioxidant activity in the plasma (TAA-P) in 131 male workers from a chloralkali plant exposed to Hg° and 67 non-exposed males (control group). The mRNA expression levels of glutathione peroxidases (GPX1, GPX3), selenoprotein P (SEPP1), thioredoxin reductase 1 (TRXR1), thioredoxin 1 (TRX1), peroxiredoxins (PRDX1, PRDX2) were also examined in the leukocytes of peripheral blood. Hg concentration in the blood (Hg-B) and urine (Hg-U) samples was determined using the thermal decomposition amalgamation/atomic absorption spectrometry (TDA-AAS) method and Se concentrations in plasma (Se-P) and urine (Se-U) using the inductively coupled plasma mass spectrometry (ICP-MS) method. Activities of GPx1-RBC, GPx3-P and TAA-P were determined using the kinetic and spectrophotometric method, respectively. Gene expression analysis was performed using the quantitative Real-Time PCR. The results showed significant higher Hg levels among the Hg°-exposed workers in comparison to control group (12-times higher median for Hg-B and almost 74-times higher median for Hg-U concentration in chloralkali workers). Se-P was also significantly higher (Me (median): 82.85 μg/L (IQR (interquartile range) 72.03-90.28 μg/L) for chloralkali workers vs. Me: 72.74 μg/L (IQR 66.25-80.14 μg/L) for control group; p = 0.0001) but interestingly correlated inversely with Hg-U in chloralkali workers suggesting depletion of the Se protection among the workers with the highest Hg-U concentration. The mRNA level for GPX1, PRXD1 were markedly but significantly higher in the workers compared to the control group. Moreover, concentrations of Hg-B and Hg-U among the workers were significantly positively correlated with the levels of selenoprotein P at both the mRNA and selenoprotein levels. In the multivariate model, after adjusting to cofounders (dental amalgam fillings, age, BMI, job seniority time, smoking), we confirmed that Hg-U concentration was inversely correlated with genes expression of TRXR1. This is the first comprehensive assessment of the impact of occupational exposure of workers to Hg° at both the mRNA and selenoprotein levels, with investigation of fish intake obtained by means of a questionnaire. These findings suggest that exposure to Hg° alters gene expression of the antioxidant enzymes and the level of Se-containing selenoproteins., (Copyright © 2018 Elsevier GmbH. All rights reserved.)

The paper's objective was to estimate weekly Hg intake from fish meals based on intervention research. Total Hg (THg) concentrations in blood and hair samples collected from men (n = 67) from an intervention study as well as muscular tissues of fresh and after heat-treating fish were determined using the thermal decomposition amalgamation atomic absorption spectrometry method (TDA-AAS) using direct mercury analyzer (DMA-80). The mean of the estimated weekly intake (EWI) was estimated at 0.62 μg/kg bw/week in the range 0.36-0.96 μg/kg body weight (bw) /week through the consumption of 4 edible marine fish species every day (for 10 days) by the participants from the intervention research in Lodz, Poland. The Hg intake in the volunteers in our intervention study accounted for 38.6% of the provisional tolerable weekly intake (PTWI) (1.6 μg/kg bw, weekly) value. The average Hg concentration in the analyzed fish ranged from 0.018 ± 0.006 mg/kg wet weight (Gadus chalcogrammus) to 0.105 ± 0.015 mg/kg wet weight (Macruronus magellanicus). The results for the average consumers were within PTWI of methylmercury (MeHg). Moreover, the average concentration of Hg in the selected fish after heat treatment did not exceed the maximum permitted concentrations for MeHg (MPCs = 0.5 mg/kg wet weight) in food set by the European Commission Regulation (EC/1881/2006). Hence, the risk of adverse effects of MeHg for the participants is substantially low.

The interaction between arsenic (As) and selenium (Se) has been one of the most extensively studied. The antagonism between As and Se suggests that low Se status plays an important role in aggravating arsenic toxicity in diseases development. The objective of this study was to assess the Se contents in biological samples of inorganic As exposed workers (n=61) and in non-exposed subjects (n=52). Median (Me) total arsenic concentration in urine of exposed workers was 21.83μg/g creat. (interquartile range (IQR) 15.49-39.77) and was significantly higher than in the control group - (Me 3.75μg/g creat. (IQR 2.52-9.26), p<0.0001). The median serum Se concentrations in the study group and the control were: 54.20μg/l (IQR 44.2-73.10μg/l) and 55.45μg/l (IQR 38.5-69.60μg/l) respectively and did not differ significantly between the groups. In the exposed group we observed significantly higher urine concentrations of selenosugar 1 (SeSug 1) and selenosugar 3 (SeSug3) than in the control group Me: 1.68μg/g creat. (IQR 1.25-2.97 vs Me: 1.07μg/g creat. (IQR 0.86-1.29μg/g), p<0.0001 for SeSug1; Me: 0.45μg/g creat. (IQR 0.26-0.69) vs Me: 0.28μg/g creat. (IQR 0.17-0.45μg/g), p=0.0021). In the multivariate model, after adjusting to cofounders (age, BMI, job seniority time, consumption of fish and seafood and smoking habits) the high rate of arsenic urine wash out (measured as a sum of iAs+MMA+DMA) was significantly associated with the high total selenium urine excretion (B=0.14 (95%CI (confidence interval) 0.05-0.23)). Combination of both arsenic and selenium status to assess the risk of arsenic-induced diseases requires more studies with regard to both the analysis of speciation, genetics and the influence of factors such as nutritional status., (Copyright © 2017 Elsevier GmbH. All rights reserved.)

Welding processes that generate fumes containing toxic metals, such as hexavalent chromium (Cr(VI)), manganese (Mn), and nickel (Ni), have been implicated in lung injury, inflammation, and lung tumor promotion in animal models. The principal objective of this study was to determine the dynamics of toxic effects of inhalation exposure to morphologically rated welding dust from stainless steel welding and its soluble form in TSE System with a dynamic airflow. We assessed the pulmonary toxicity of welding dust in Wistar rats exposed to 60.0 mg/m 3 of respirable-size welding dust (mean diameter 1.17 µm) for 2 weeks (6 h/day, 5 days/week); the aerosols were generated in the nose-only exposure chambers (NOEC). An additional aim included the study of the effect of betaine supplementation on oxidative deterioration in rat lung during 2 weeks of exposure to welding dust or water-soluble dust form. The animals were divided into eight groups (n = 8 per group): control, dust, betaine, betaine + dust, soluble-form dust, soluble-form dust + betaine, saline and saline + betaine groups. Rats were euthanized 1 or 2 weeks after the last exposure for assessment of pulmonary toxicity. Differential cell counts, total protein concentrations and cellular enzyme (lactate dehydrogenase-LDH) activities were determined in bronchoalveolar lavage (BAL) fluid, and corticosterone and thiobarbituric acid reactive substances (TBARS) concentrations were assessed in serum. The increase in polymorphonuclear (PMN) leukocytes in BAL fluid (a cytological index of inflammatory responses of the lung) is believed to reflect pulmonary toxicity of heavy metals. Biomarkers of toxicity assessed in bronchoalveolar fluids indicate that the level of the toxic effect depends mainly on the solubility of studied metal compounds; biomarkers that showed treatment effects included: total cell, neutrophil and lymphocyte counts, total protein concentrations, and cellular enzyme (lactate dehydrogenase) activity. Betaine supplementation at 250 mg/kg/day in all study rats groups attenuated stress indices, and corticosterone and TBARS serum levels, and simultaneously stimulated increase of polymorphonuclear cells in BALF of rats. The study confirmed deleterious effect of transitory metals and particles during experimental inhalation exposure to welding dusts, evidenced in the lungs and brain by increased levels of total protein, higher cellular influx, rise of LDH in BALF, elevated TBARS and increased corticosterone in serum of rats. Our result confirm also the hypothesis about the effect of the welding dusts on the oxidative stress responsible for disturbed systemic homeostasis and impairment of calcium regulation.

Purpose: To examine the differences in urinary arsenic metabolism patterns in men affected by occupational exposure, we performed a study on 149 participants—workers of a copper mill and 52 healthy controls without occupational exposure. To elucidate the role of genetic factors in arsenic (As) metabolism, we studied the associations of six polymorphisms: As3MT Met287Thr (T>C) in exon 9; As3MT A>G in 5'UTR; As3MT C>G in intron 6; As3MT T>G in intron 1; GSTP1 Ile105Val and GSTO2 T>C., Methods: Air samples were collected using individual samplers during work shift. Urine samples were analyzed for total arsenic and arsenic chemical forms (As(III); As(V), MMA, DMA, AsB) using HPLC-ICP-MS. A specific polymerase chain reaction was done for the amplification of exons and flanking regions of As3MT and GSTs., Results: The geometric mean arsenic concentrations in the air were 27.6 ± 4.9 µg/m(3). A significant correlation (p < 0.05) was observed between arsenic in air and sum of iAs +MMA and iAs. As3MT (rs3740400) GG homozygotes showed significantly (p < 0.05) higher %iAs (21.8 ± 2.0) in urine than GC+CC heterozygotes (16.0 ± 2.1). A strong association between the gene variants and As species in urine was observed for GSTO2 (rs156697) polymorphism., Conclusions: The findings of the study point out that the concentration of iAs or the sum of iAs + MMA in urine can be a reliable biological indicator of occupational exposure to arsenic. This study demonstrates that As3MT and/or GSTs genotype may influence As metabolism. Nevertheless, further studies investigating genetic polymorphism in occupational conditions are required.

The toxicity and bioavailability of chromium species are highly dependable on the form or species, therefore determination of total chromium is insufficient for a complete toxicological evaluation and risk assessment. An analytical method for determination of soluble and insoluble Cr (III) and Cr (VI) compounds in welding fume at workplace air has been developed. The total chromium (Cr) was determined by using quadruple inductively coupled plasma mass spectrometry (ICP-MS) equipped with a dynamic reaction cell (DRC(®)). Soluble trivalent and hexavalent chromium compounds were determined by high performance liquid chromatography with inductively coupled plasma mass spectrometry (HPLC-ICP-MS). A high-speed, reversed-phase CR C8 column (PerkinElmer, Inc., Shelton, CT, USA) was used for the speciation of soluble Cr (III) and soluble Cr (VI). The separation was accomplished by interaction of the chromium species with the different components of the mobile phase. Cr (III) formed a complex with EDTA, i.e. retained on the column, while Cr (VI) existed in the solutions as dichromate. Alkaline extraction (2% KOH and 3% Na2CO3) and anion exchange column (PRP-X100, PEEK, Hamilton) were used for the separation of the total Cr (VI). The results of the determination of Cr (VI) were confirmed by the analysis of the certified reference material BCR CRM 545 (Cr (VI) in welding dust). The results obtained for the certified material (40.2±0.6 g kg(-1)) and the values recorded in the examined samples (40.7±0.6 g kg(-1)) were highly consistent. This analytical method was applied for the determination of chromium in the samples in the workplace air collected onto glass (Whatman, Ø 37 mm) and membrane filters (Sartorius, 0.8 μm, Ø 37 mm). High performance liquid chromatography with inductively coupled plasma mass spectrometry is a remarkably powerful and versatile technique for determination of chromium species in welding fume at workplace air., (Crown Copyright © 2013 Published by Elsevier B.V. All rights reserved.)

The effect of reperfusion following hemorrhagic shock on splanchnic prostanoid release was studied. Anesthetized male rats were bled to a mean arterial blood pressure of 30 mmHg for 30 minutes and either killed or treated with shed blood for 60 minutes and then killed. The superior mesenteric arterial bed was cannulated and perfused in vitro with oxygenated Krebs. Collected venous effluent (up to 180 minutes) was analyzed for 6-keto-PGF1 alpha (PGI2 metabolite), PGE2, PGF2 alpha, and thromboxane B2 by radioimmunoassay in shock, shock plus reperfusion, and sham groups. The major prostanoid released was 6-keto-PGF1 alpha and was three times higher in the shock group compared to the sham group (p less than 0.05). Reperfusion of shed blood abolished the increase in 6-keto-PGF1 alpha found in the shock group (p less than 0.05). These data show that the attempt of the rat splanchnic bed to compensate for hemorrhagic shock by increasing release of PGI2 (potent vasodilator) was abolished during reperfusion of blood.