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Objectives: The assessment of the neurotoxic effect of arsenic (As) and its inorganic compounds is still the subject of interest due to a growing As application in a large array of technologies and the need to constantly verify the principles of prevention and technological parameters. The aim of this study was to determine the status of the nervous system (NS) in workers exposed to As at concentrations exceeding hygiene standards (Threshold Limit Values (TLV) – 10 μg/m³, Biological Exposure Index (BEI) – 35 μg/l) and to analyze the relationship between the NS functional state, species of As in urine and As levels in the workplace air. Material and Methods: The study group comprised 21 men (mean age: 47.43±7.59) employed in a copper smelting factory (mean duration of employment: 22.29±11.09). The control group comprised 16 men, matched by age and work shifts. Arsenic levels in the workplace air (As-A) ranged from 0.7 to 92.3 μg/m³; (M = 25.18±28.83). The concentration of total arsenic in urine (Astot-U) ranged from 17.35 to 434.68 μg/l (M = 86.82±86.6). Results: Syndrome of peripheral nervous system (PNS) was manifested by extremity fatigue (28.6%), extremity pain (33.3%) and paresthesia in the lower extremities (33.3%), as well as by neuropathy-type mini-symptoms (23.8%). Electroneurographic (ENeG) tests of peroneal nerves showed significantly decreased response amplitude with normal values of motor conduction velocity (MCV). Stimulation of sural nerves revealed a significantly slowed sensory conduction velocity (SCV) and decreased sensory potential amplitude. Neurophysiological parameters and the results of biological and environmental monitoring showed a relationship between $\text{As}^\text{tot}$, $\text{As}^\text{III}$ (trivalent arsenic), the sum of iAs ($\text{As}^\text{III}+\text{As}^\text{V}$ (pentavalent arsenic))+MMA (monomethylarsonic acid) concentration in urine and As levels in the air. Conclusions: The results of the study demonstrate that occupational exposure to inorganic arsenic levels exceeding hygiene standards (TLV, BEI) generates disorders typical of peripheral neuropathy.
EN
Background: Benzalkonium chloride (BAC) is a quaternary ammonium compound (QAC) toxic to microorganisms. Inhalation is one of the major possible routes of human exposure to BAC. Materials and Methods: Experiments were performed on female Wistar rats. The rats were exposed to aerosol of BAC water solution at the target concentration of 0 (control group) and 35 mg/m³ for 5 days (6 h/day) and, after a 2-week interval, the animals were challenged (day 21) with BAC aerosol at the target concentration of 0 (control group) and 35 mg/m³ for 6 h. Results: Compared to the controls, the animals exposed to BAC aerosol were characterized by lower food intake and their body weight was significantly smaller. As regards BAC-exposed group, a significant increase was noted in relative lung mass, total protein concentration, and MIP-2 in BALF both directly after the termination of the exposure and 18 h afterwards. Significantly higher IL-6 and IgE concentrations in BALF and a decrease in the CC16 concentration in BALF were found in the exposed group immediately after the exposure. The leukocyte count in BALF was significantly higher in the animals exposed to BAC aerosol compared to the controls. In the lungs of rats exposed to BAC the following effects were observed: minimal perivascular, interstitial edema, focal aggregates of alveolar macrophages, interstitial mononuclear cell infiltrations, thickened alveolar septa and marginal lipoproteinosis. Conclusion: Inhalation of BAC induced a strong inflammatory response and a damage to the blood-air barrier. Reduced concentrations of CC16, which is an immunosuppressive and anti-inflammatory protein, in combination with increased IgE concentrations in BALF may be indicative of the immuno-inflammatory response in the animals exposed to BAC aerosol by inhalation. Histopathological examinations of tissue samples from the BAC-exposed rats revealed a number of pathological changes found only in the lungs.
EN
Objectives Welding processes that generate fumes containing toxic metals, such as hexavalent chromium (Cr(VI)), manganese, and nickel (Ni), have been implicated in lung injury, inflammation, and lung tumor promotion in animal models. Bronchiolar epithelium Clara cells/club cells, coordinate these inflammatory responses. Clara cells secretory protein (CC16) with ant-inflammatory role. Material and Methods The pulmonary toxicity of welding dust (WD) was assessed for Wistar rats exposed to 60 mg/m³ of respirable-size welding dust (mean diameter 1.17 μm for 1 and 2 weeks (6 h/day, 5 days/week)) or the aerosols of soluble form (SWD) in the nose-only exposure chambers. Additionally the effect of antiinflammatory betaine supplementation was assessed. Clara cells secretory protein, differential cell counts, total protein concentrations and cellular enzyme (lactate dehydrogenase – LDH) activities were determined in bronchoalveolar lavage fluid, and corticosterone and thiobarbituric acid reactive substances (TBARS) and prolactin concentrations were assessed in serum. Histopathology examination of lung, brain, liver, kidney, spleen was done. Additionally slices of brain and lung were exanimated in laser ablation inductively coupled plasma mass spectrometry. Results Both WD and SWD exposure evoked large bronchiolar infiltration shoved in histopathology examination. In this study, TBARS inversely correlated with a significant decrease of CC16 concentration that occurred after instillation of both WD and SWD indicating decreased anti- inflammatory potential in the lung. In WD exposed rats prolactin correlated with nuclear factor-kappa B (NF-κB), LDH, TBARS and serum levels Cr, Ni and inversely with c-Jun. In SWD exposed rats prolactin correlated with CC16 indicated effect of prolactin on the population of epithelial cells. Conclusions In the current study, deleterious effects of repeated inhalation stainless steel welding dust form on club (Clara) cell secretory protein (CC16) were demonstrated. Clara cells secretory protein relation with prolactin in exposed rats to welding dust were shown and explored whether the NF-κB and c-Jun/activator protein 1 related pathway was involved. Int J Occup Med Environ Health 2018;31(5):613–632
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