Search Results (8)

Background: There is growing interest in the potential role of manganese (Mn) in the development of Alzheimer’s Disease and related dementias (ADRD). Methods: In this nested pilot study of a ferroalloy worker cohort, we investigated the impact of chronic occupational Mn exposure on cognitive function through β-amyloid (Aβ) deposition and multi-omics profiling. We evaluated six male Mn-exposed workers (median age 63, exposure duration 31 years) and five historical controls (median age: 60 years), all of whom had undergone brain PET scans. Exposed individuals showed significantly higher Aβ deposition in exposed individuals (p < 0.05). The average annual cumulative respirable Mn was 329.23 ± 516.39 µg/m³ (geometric mean 118.59), and plasma Mn levels were significantly elevated in the exposed group (0.704 ± 0.2 ng/mL) compared to controls (0.397 ± 0.18 in controls). Results: LC-MS/MS-based pathway analyses revealed disruptions in olfactory signaling, mitochondrial fatty acid β-oxidation, biogenic amine synthesis, transmembrane transport, and choline metabolism. Simoa analysis showed notable alterations in ADRD-related plasma biomarkers. Protein microarray revealed significant differences (p < 0.05) in antibodies targeting neuronal and autoimmune proteins, including Aβ (25–35), GFAP, serotonin, NOVA1, and Siglec-1/CD169. Conclusion: These findings suggest Mn exposure is associated with neurodegenerative biomarker alterations and disrupted biological pathways relevant to cognitive decline. Full article

Manganese (Mn) is an essential trace element and a cofactor for several key enzymes, such as mitochondrial superoxide dismutase. Consequently, it plays an important defense role against reactive oxygen species. Despite this, Mn chronic overexposure can result in a neurological disorder referred to as manganism, which shares some similarities with Parkinson’s disease. Mn levels seem regulated by many transporters responsible for its uptake and efflux. These transporters play an established role in many inherited disorders of Mn metabolism and neurotoxicity. Some inherited Mn metabolism disorders, caused by mutations of SLC30A10 and SLC39A14, assume crucial importance since earlier treatment results in a better prognosis. Physicians should be familiar with the clinical presentation of these disorders as the underlying cause of dystonia/parkinsonism and look for other accompanying features, such as liver disease and polycythemia, which are typically associated with SLC30A10 mutations. This review aims to highlight the currently known Mn transporters, Mn-related neurotoxicity, and its consequences, and it provides an overview of inherited and acquired disorders of Mn metabolism. Currently available treatments are also discussed, focusing on the most frequently encountered presentations. Full article

In recent years, a series of articles has been published concerning magnetic resonance imaging (MRI) studies in a group of patients exposed to manganism, specifically factory workers, welders, and individuals with liver diseases, as well as those abusing home-produced ephedrone. Some potential symptoms of manganese toxicity include motor disturbances, neurocognitive problems, sleep disorders, and psychosocial changes. Despite various publications on MRI research in individuals with an elevated risk of manganism, there is a noticeable absence of a comprehensive review in this field. The detection of the accumulation of manganese in the brain through MRI can confirm the diagnosis and guide appropriate treatment. Due to the high cost of determining manganese ion levels in biological material, an additional aim of the manuscript was to identify simple medical laboratory parameters that, when performed concurrently with MRI, could assist in the diagnosis of manganism. Among these types of parameters are the levels of bilirubin, magnesium, liver enzymes, creatinine, hemoglobin, and hematocrit. Full article

Exposure to metals poses potential health risks, including insulin resistance (IR), to those exposed to them in excess. Limited studies have examined such risks in occupational workers, including welders, and these have yielded inconsistent results. Thus, we examined the associations between exposure to welding metals and IR in welders. We recruited 78 welders and 75 administrative staff from a shipyard located in northern Taiwan. Personal exposure to heavy metals, including chromium (Cr), manganese (Mn), iron (Fe), nickel (Ni), copper (Cu), zinc (Zn), and cadmium (Cd), was monitored through particulate matter with an aerodynamic diameter of less than 2.5 μm (PM_2.5) and urine analysis by inductively coupled plasma mass spectrometry (ICP–MS). After each participant fasted overnight, blood samples were collected and analyzed for IR assessment through updated homeostasis model assessment (HOMA2) modeling. Air sampling in the personal breathing zone was performed during a Monday shift prior to the blood and urine sample collection the following morning. The welders’ median personal Cr, Mn, Fe, Ni, Cu, and Zn airborne PM_2.5 levels and urinary Cd levels were significantly higher than those of the administrative staff. After adjustment for covariates, logarithmic PM_2.5-Mn, PM_2.5-Fe, PM_2.5-Cu, and PM_2.5-Zn levels were positively correlated with logarithmic fasting plasma glucose (P-FGAC) levels (PM_2.5-Mn: β = 0.0105, 95% C.I.: 0.0027–0.0183; PM_2.5-Fe: β = 0.0127, 95% C.I.: 0.0027–0.0227; PM_2.5-Cu: β = 0.0193, 95% C.I.: 0.0032–0.0355; PM_2.5-Zn: β = 0.0132, 95% C.I.: 0.0005–0.0260). Logarithmic urinary Zn was positively correlated with logarithmic serum insulin and HOMA2-IR levels and negatively correlated with logarithmic HOMA2-insulin sensitivity (%S; β_insulin = 0.2171, 95% C.I.: 0.0025–0.4318; β_IR = 0.2179, 95% C.I.: 0.0027–0.4330; β_%S = −0.2180, 95% C.I.: −0.4334 to −0.0026). We observed that glucose homeostasis was disrupted by Mn, Fe, Cu, and Zn exposure through increasing P-FGAC and IR levels in shipyard welders. Full article

In this study, the urinary concentrations of selected metals in workers from an electric steel foundry in Tunisia were assessed and compared with existing biological limit values and general population reference values. Moreover, the association between oxidative DNA damage, measured as urinary 8-oxo-7,8-dihydro-2’deoxyguanosine (8-oxodG) and co-exposure to metals and polycyclic aromatic hydrocarbons (PAHs) was evaluated. Urinary levels of 12 metals were determined by inductively coupled plasma-mass spectrometry (ICP-MS) in end-shift spot samples from 89 workers. The urinary levels of phenanthrene (U-PHE), as marker of exposure to PAHs, and 8-oxodG were also available. Median levels ranged from 0.4 µg/L (cobalt, Co, and thallium, Tl) to 895 µg/L (zinc, Zn). Only 1% of samples was above the biological limit values for Co, and up to 13.5% of samples were above limit values for Cd. From 3.4% (Co) to 72% (lead, Pb) of samples were above the reference values for the general population. Multiple linear regression models, showed that manganese (Mn), Zn, arsenic (As), barium (Ba), Tl, and Pb were significant predictors of 8-oxodG (0.012 ≤ p ≤ 0.048); U-PHE was also a significant predictor (0.003 ≤ p ≤ 0.059). The variance explained by models was low (0.11 ≤ R² ≤ 0.17, p < 0.005), showing that metals and PAHs were minor contributors to 8-oxodG. Overall, the comparison with biological limit values showed that the study subjects were occupationally exposed to metals, with levels exceeding biological limit values only for Cd. Full article

Exposure to fine particulate matter 2.5 (PM_2.5) is associated with adverse health effects, varying by its components. The health-related effects of PM_2.5 exposure from ore mining may be different from those of environment pollution. The aim of this study was to investigate the effects of different concentrations of PM_2.5 exposure on the cardio-pulmonary function of manganese mining workers. A total of 280 dust-exposed workers who were involved in different types of work in an open-pit manganese mine were randomly selected. According to the different concentrations of PM_2.5 in the working environment, the workers were divided into an exposed group and a control group. The electrocardiogram, blood pressure, and multiple lung function parameters of the two groups were measured and analyzed. The PM_2.5 exposed group had significantly lower values in the pulmonary function indexes of forced expiratory volume in one second (FEV1.0), maximum mid expiratory flow (MMEF), peak expiratory flow rate (PEFR), percentage of peak expiratory flow out of the overall expiratory flow volume (PEFR%), forced expiratory flow at 25% and 75% of forced vital capacity (FEF 25, FEF75), forced expiratory flow when 25%, 50%, and 75% of forced vital capacity has been exhaled (FEF25%,FEF50%, FEF75%), and FEV1.0/FVC% (the percentage of the predicted value of forced vital capacity) than the control group (all p < 0.05). Both groups had mild or moderate lung injury, most of which was restrictive ventilatory disorder, and there was significant difference in the prevalence rate of restrictive respiratory dysfunction between the two groups (41.4% vs. 23.6%, p = 0.016). Electrocardiogram (ECG) abnormalities, especially sinus bradycardia, were shown in both groups, but there was no statistical difference of the prevalence rate between the two groups (p > 0.05). Also, no significant difference of the prevalence rate of hypertension was observed between the PM2.5 exposure and control groups (p > 0.05). PM_2.5 exposure was associated with pulmonary function damage of the workers in the open-pit manganese mine, and the major injury was restrictive ventilatory disorder. The early effect of PM_2.5 exposure on the cardiovascular system was uncertain at current exposure levels and exposure time. Full article

Background: Workers chronically exposed to manganese in welding fumes may develop an extra-pyramidal syndrome with postural and action tremors. Objectives: To determine the utility of tremor analysis in distinguishing tremors among workers exposed to welding fumes, patients with Idiopathic Parkinson’s Disease (IPD) and Essential Tremor (ET). Methods: Retrospective study of recorded tremor in subjects from academic Movement Disorders Clinics and Welders. Quantitative tremor analysis was performed and associated with clinical status. Results: Postural tremor intensity was increased in Welders and ET and was associated with visibly greater amplitude of tremor with arms extended. Mean center frequencies (Cf) of welders and patients with ET were significantly higher than the mean Cf of PD subjects. Although both the welders and the ET group exhibited a higher Cf with arms extended, welders could be distinguished from the ET subjects by a significantly lower Cf of the rest tremor than that measured in ET subjects. Conclusions: In the context of an appropriate exposure history and neurological examination, tremor analysis may be useful in the diagnosis of manganese-related extra-pyramidal manifestations. Full article

Welding is a major industrial process used for joining metals. Occupational exposure to welding fumes is a serious occupational health problem all over the world. The degree of risk to welder’s health from fumes depends on composition, concentration, and the length of exposure. The aim of this study was to investigate workers’ welding fume exposure levels in some industries in Jeddah, Saudi Arabia. In each factory, the air in the breathing zone within 0.5 m from welders was sampled during 8-hour shifts. Total particulates, manganese, copper, and molybdenum concentrations of welding fumes were determined. Mean values of eight-hour average particulate concentrations measured during welding at the welders breathing zone were 6.3 mg/m³ (Factory 1), 5.3 mg/m³ (Factory 2), 11.3 mg/m³ (Factory 3), 6.8 mg/m³ (Factory 4), 4.7 mg/m³ (Factory 5), and 3.0 mg/m³ (Factory 6). Mean values of airborne manganese, copper, and molybdenum levels measured during welding were in the range of 0.010 mg/m³–0.477 mg/m³, 0.001 mg/m³–0.080 mg/m³ and 0.001 mg/m³–0.058 mg/m³ respectively. Mean values of calculated equivalent exposure values were: 1.50 (Factory 1), 1.56 (Factory 2), 5.14 (Factory 3), 2.21 (Factory 4), 2.89 (Factory 5), and 1.20 (Factory 6). The welders in factories 1, 2, 3, and 4 were exposed to welding fume concentration above the SASO limit value, which may increase the risk of respiratory health problems. Full article