6 research outputs found
Učinci profesionalne izloženosti olovu na izabrane upalne biomarkere
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.Pri izloženosti toksičnim metalima poput olova, utvrđivanje razina olova i upalnih citokina (IL-6, IL-10 i TNF-α) ključno je za rano otkrivanje bolesti. Cilj je ovoga ispitivanja bio osmisliti model za rano otkrivanje upala i ateroskleroze u mladih radnika profesionalno izloženih olovu dok se još nisu pojavili klinički znakovi i simptomi. Zahvaljujući tomu, liječnici bi mogli pravovremeno započeti liječenje. Ispitivanje je obuhvatilo 49 metalskih radnika izloženih olovu i 50 neizloženih administrativnih radnika (kontrolna skupina) koji su bili podvrgnuti imunološkim testovima na citokine (IL-6, IL-10, i TNF-α) i na markere ateroskleroze (h-FABP i VCAM-1), toksikološkomu testu na olovo te rutinskim biokemijskim testovima (ALT, AST, kreatinin) u Bolnici za profesionalne i okolišne bolesti u Ankari 2017. Razine olova u krvi korelirale su s razinama IL-6, IL-10 odnosno TNF-α (r=0,469, r=0,521, odnosno r=0,279, p<0,01), ali nisu značajno utjecale na razine h-FABP odnosno VCAM-1
The effect of manganese exposure on erythropoietic and reproductive system parameters
The aim of this study is determining the effect of manganese (Mn) exposure on erythropoietic and reproductive system. A study group consisting of 51 non-smoking welders older than 18 years old with Mn exposure, who visited Ankara Occupational and Environmental Diseases Hospital, and a control group consisting of 79 healthy office employees without Mn exposure, were chosen as study group. Blood Mn level, total testosterone (TT), freetestosterone (FT), alanine aminotransferase (ALT), aspartate aminotransferase(AST), thyroid stimulant hormone (TSH), triiodothyronine (T3), thyroxine (T4), uric acid, creatinine, complete blood count (CBC), prolactin, follicle stimulating hormone (FSH), luteinizing hormone (LH) levels were analysed along with the demographic data of the patient. The study and control groups consisting of a total of 130 persons were all male, 39.2% (n=51) of which represented the study group with manganese exposure and 60.8% (n=79) of which represented the healthy control group. A significant difference was identified statistically between Mn (t= 4,501, p= 0,000), FT (t= -6.959, p=0.000), TT (t= -2.835, p=0.005) values of those with and without manganese exposure. AST and ALT levels were not found significant although they were higher in the exposed group. When the values are examined according to uric acid, creatinine, TSH, T3, T4and complete blood count, it was observed that the values of exposure group and control group were almost identical. Although FHS, LH and PRL values were high in the study group, the differences were not found significant. Consequently, although Mn is a trace element, it was concluded that, in high levels,it might reduce the testosterone synthesis with direct toxic effect on the testicle in the long-term exposures leading. [Med-Science 2018; 7(4.000): 817-20
The relation between lead exposure and inflammation / endothelial dysfunction
Pb exposure is a well-known risk factor for inflammation including vessels. In our study, we aimed to investigate the relationship between Pb levels of exposed workers and the severity of inflammation/endothelial dysfunction. We analyzed the correlation between blood lead level and the markers of endothelial damage. There was a significant correlation between blood lead levels and vascular cell adhesion molecule-1 (VCAM-1). Elevated levels of blood lead also show correlation with soluble CD40 ligand (sCD40L). The strongest correlation was with sE-selectin. Association between lead exposure and markers of cardiovascular injury may help to predict cardiovascular effects of lead earlier and to protect workers who are exposed to lead. [Med-Science 2020; 9(2.000): 468-72
Pro-inflammatory cytokine and vascular adhesion molecule levels in manganese and lead-exposed workers
Objectives: This study aimed to develop a model of the relationship between inflammatory cytokine and/or vascular adhesion molecule levels and clinical symptoms in individuals exposed to lead (Pb), manganese (Mn) or both (Pb+Mn).Methods: The study included 104 male workers exposed to metals for different durations in a factory setting (Mn-, Pb- and Pb+Mn-exposed groups) and 76 non-exposed male workers (control group). Interleukin (IL)-6, IL-10, Tumor Necrosis Factor (TNF)-α, soluble (s)E-selectin, and Vascular Cell Adhesion protein (VCAM)-1 levels were analyzed using enzyme-linked immunosorbent assays. Mn and Pb levels were determined using inductively coupled plasma mass spectrometry.Results: Significant intergroup differences were observed in the levels of IL-6, IL-10, TNF-α, and sE-selectin (p<0.01 for all), but not VCAM-1 (p=0.298). Fatigue was the most frequent symptom in all groups (25.7%, 37.1%, and 44.1%, respectively). Other symptoms included tremor and anxiety in the Mn-exposed group (5.7%), and tremor and paresthesia in the Pb-exposed (14.7%) and Pb+Mn-exposed groups (20.6%).Conclusions: The correlation between increased biomarker levels and clinical symptoms suggests a close relationship between inflammation and neurotoxicity. This relationship not only explains the effect of the former on the latter but also provides a clinical model for the early diagnosis of neuroinflammation.</p