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.
One of the major complications of arsenic on human health is hypertension. Arsenic-related hypertension and negative effects of arsenic on arterial system such as oxidative stress and vasoconstriction/vasorelaxation imbalance may lead to impair aortic elasticity. The aim of this study was to evaluate the effects of arsenic on aortic elasticity parameters including aortic strain and distensibility. One hundred twelve (112) workers were occupationally exposed to arsenic and 60 healthy control subjects were enroled. All patients underwent transthoracic echocardiography for detecting aortic strain and aortic distensibility. There were no differences in baseline demographic and echocardiographic characteristics between the groups. Aortic strain (10.3±3.9 vs 12.1±2.7%, P=0.001) and aortic distensibility (0.45±0.17 vs 0.54±0.15 cm per dyn, P=0.001) were decreased in arsenic-exposure group compared with controls. Urinary arsenic level was found to be negatively and significantly correlated with aortic strain (r=-0.306, P=0.001) and aortic distensibility (r=-0.259, P=0.006). Duration of arsenic exposure was also found to be negatively and significantly correlated with aortic strain (r=-0.386, P<0.001) and aortic distensibility (r=-0.333, P<0.001). This study suggests that arsenic exposure is related to impairment of aortic elasticity parameters even in subjects without overt cardiovascular disease.
Background:Oxidative stress is implicated as one of the main molecular mechanism underlying silicosis.Aims:In this study, our aim was to asses the redox status in occupationally silica-exposed workers, by evaluating the dynamic thiol-disulphide homeostasis.Study Design:Case-control study.Methods:Thirty-six male workers occupationally exposed to silica particles and 30 healthy volunteers, working as office workers were included to the study. Posteroanterior chest radiographs and pulmonary function tests of both groups were evaluated. Also serum thiol disulphide levels were measured using the spectrophotometric method described by Erel and Neşelioğlu.Results:Among the 36 workers that underwent pulmonary function tests 6 (17%) had obstructive, 7 (19%) had restrictive, 6 (17%) had obstructive and restrictive signs whereas 17 (47%) had no signs. The mean PFTs results of silica-exposed workers were significantly lower than control subjects. The serum disulphide levels of silica-exposed workers were significantly higher than control subjects (23.84±5.89 μmol/L and 21.18±3.44 μmol/L, respectively p=0.02).Conclusion:The serum disulphide levels, a biomarker of oxidative stress, are found to be higher in silica-exposed workers.
Introduction Occupational exposure to crystalline silica over time may result in silicosis: a fatal, irreversible occupational disease leading to lung function impairment. A complex inflammatory process, excessive accumulation of mesenchymal cells and collagen production are the primary mechanisms underlying silicosis. Neutrophil to lymphocyte ratio (NLR) and the platelet to lymphocyte ratio (PLR) have emerged as representative indices of systemic inflammation. Objectives The purpose of the present study was to investigate the relationship between NLR, PLR and silicosis. Methods We retrospectively analysed the demographic and laboratory data of ceramic workers who were referred to our Hospital between 2010 and 2018. Five hundred and seventy‐three patients with silicosis and 222 ceramic workers without silicosis (controls) were included in the study. Results The radiographic ILO classification of silicosis patients was as follows: category 1 (71.5%), category 2 (19.2%), category 3 (7.5%). NLR and PLR in categories 2 and 3 were significantly higher when compared with the control group (P < .005). FEV1, FEV1%, FVC, FVC % and PEF were significantly lower in all silicosis patients and also in patients with subcategories (all P < .005). NLR showed a poor positive correlation with CRP (r = 0.095, P < .05) and ESR (r = 0.207, P = .000) while PLR only with ESR (r = 0.317, P = .000) in patients with silicosis. NLR and PLR showed negative correlations with FEV1, FVC and PEF (all P < .005). Conclusion We conclude that NLR and PLR have significant but poor correlations with pulmonary functions and severity of silicosis, especially in late radiographic profusion categories.
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.
Study results indicate that exposure to PAHs induces oxidative stress and causes genotoxic effects in asphalt workers.
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