High-level occupational manganese (Mn) exposure has been reported to induce irreversible brain alterations determining a Parkinson-like disease. This study aimed to assess subclinical neurophysiological alterations in welding workers. They were employed in a machine building factory with an average Mn exposure <200 mg/m3. Sixty-eight workers (mean age: 34 years; mean Mn exposure duration: 16 years) and 42 flour factory workers (control group) with similar age and smoking habit were recruited. Autonomic nervous function test battery (ANSFT), composed of Valsalva maneuvre-induced heart rate variation (HR-V), heart rate variation following deep breathing (HR-DB) and heart rate variation following immediate standing up (HR-IS) was assessed. Electroencephalogram (EEG), brain electricity activity mapping (BEAM) were also performed. HR-V, HR-DB, and HR-IS were significantly lower in Mn-exposed subjects showing altered autonomic nervous system activity, parasympathetic-sympathetic imbalance and, and consequently, altered cardiovascular regulation and reactivity. The EEG of the Mn-exposed workers evidenced beta-wave rhythms significantly reduced, theta-waves markedly increased and abnormal wave activities of either localized or diffusive type. In the same workers BEAM revealed higher theta, delta and beta power values in the F7 area, lower d power values in the FP1, FP2 and C4 areas as well as dissymmetry in the central area, parietal region and occipital region. This study suggests that Mn impairs neuron activity within central nervous system. In this context, brainstem parasympathetic and sympathetic centers receiving axon projections from cortical and diencephalic areas, may reflect Mn effects on upper pathways. However, direct actions of Mn on these centers cannot be excluded.

Adult↗

PubMedDate not supplied

Neurobehavioral functions, serum prolactin and plasma renin activity of manganese-exposed workers.

Objective of this study was to assess effects of manganese (Mn) exposure on 56 workers employed in a Mn welding workshop of a machine building factory in Taiyuan (Shanxi Province, P.R. China) for a mean period of 16.1 years. The mean air Mn level in the workshop was 138.4 microg/m3. Neurobehavioral Core Test Battery (NCTB), including the Profile fo Mood States, (POMS), was performed. Blood pressure (BP) increase following immediate stand-up (BP-IS), serum prolactin (PRL) and plasma renin activity (PRA) in supine position were also determine. Most of the NCTB scores of the Mn-exposed workers were lower than those of controls, while the POMS scores were higher, indicating a Mn-induced impairment of neurophysiological functions and a deflection of mood towards negative emotion states. PRL values of the Mn-exposed workers were higher than those of the controls. BP-IS of Mn-exposed workers was significantly lower than that of the controls. PRA of the same workers was augmented more that 200%. In the Mn-exposed workers, the higher PRL values are possibly due to a reduced inhibitory effect on pituitary lactotrope cells by the tubero-infundibular dopamine system; the decreased BP-IS was referred to imbalance between the sympathetic and parasympathetic activities, whereas the higher basal PRA was thought to depend on neuroendocrine changes (including increased central sympathetic tone) and/or on a direct effect of Mn on renal juxta-glomerular cells. On the whole, this study demonstrates that occupational Mn exposure is responsible for neurobehavioral changes coexisting with alterations of neuroendocrine and humoral systems.

Adult↗

PubMedDate not supplied

Clastogenic but not apoptotic effects on human artery endothelial cells by concentrations of inorganic lead inhibiting their nitric oxide production.

Human coronary artery endothelial cells (HCAEC 5156) were cultured as monolayers and exposed to concentrations of lead (as acetate, Pb) in the culture medium similar or lower than those commonly found in the blood of human beings occupationally or environmentally exposed to this element. Only at the concentration of 200 ng/mL, Pb reduced growth rate of HCAEC 5156 cells starting from the 3rd day and up too the 5th day of incubation. On the other hand, Pb (0.2, 2 and 200 ng/mL) increased concentration-dependently micronuclei formation in binucleated HCAEC 5156 cells, as it was shown by the cytokinesis-blocked micronucleus assay (CMBN assay) carried out after 48 hours of exposure to the metal. However Pb was unable, at all the above concentrations to induce apoptosis in the HCAEC 5156 cells following a 48 hour-exposure, as shown by an electorphoretic apoptotic DNA fragmentation test. Moreover, Pb (2 and 200 ng/mL) reduced significantly the concentration of nitric oxide (NO, determined analytically as L-citrulline) in both culture medium and cytosol of HCAEC 5156 cells following a 7 day-exposure to the element. Results were discussed also in relation so evidences of other studies reporting genotoxic and/or apoptotic effects of Pb on various cell types at very elevated dosages of concentrations. The observed clastogenic effects of Pb were explained through a series of mechanisms involving interactions between oxygen reactive species and NO and/or reduced NO synthesis in the endothelium, thus leading to a depressed NO bioavailability. This research first shows that Pb is provided with clastogenic but not apoptotic effects on cultured human endothelial cells. It was emphasized that such effects are induced by Pb concentrations similar to those commonly found in blood and tissues of laboratory animals showing Pb induced cardiovascular and/or neuropsychological alterations.

Apoptosis↗

PubMedDate not supplied

Aluminum impairs rat neural cell mitochondria in vitro.

Exposure to aluminum has been reported to lead to neurotoxicity. Mitochondria are important organelles involved in maintaining cell function. This study investigates the effect of aluminum on mitochondria in rat neural cells. The ultrastructure of mitochondria was observed, and the cell death rate (CDR), reactive oxygen species (ROS), mitochondrial membrane potential (MMP) and 3-[4,5demethyl-2-thiazalyl]-2,-5diphenyl-2H-tetrazolium bromide (MTT) were measured to investigate the effect of aluminum on the mitochondrial structure and its function in neural cells. Results observed from the mitochondrial ultrastructure show that aluminum may impair the mitochondrial membrane and cristae. Increased CDR, enhanced ROS, decreased MMP, and decreased enzyme activity in mitochondria were observed in the Al-exposed neurons (100 500 microM). The present study demonstrates that alteration in the mitochondrial structure and function plays an important role in neurotoxic mechanisms induced by aluminum.

Aluminum↗

PubMedDate not supplied

A comprehensive neurobehavioral and neurophysiological study for low level lead-exposed workers.

UNLABELLED: A comprehensive neurobehavioral and neurophysiological study was performed to evaluate the adverse effect of low level lead-exposure, and to compare the sensibility, easiness of the test methods utilized. The tests were: WHO recommended Neurobehavioral Core Test Battery (NCTB), Autonomic Nouvers System Function (ANS) Test Battery, Brain Electricity Active Mapping (BEAM), and Nerve Conduction Velocity. 44 lead-exposed workers were selected, with 34 age, education degree, family economic level, smoking and drinking matched referents. RESULT: The mean blood lead concentration of lead-exposed workers was 1.3870 mumol/L, whereas that of referents was 0.6080 mumol/L, the difference was very significant. The negative Profile of Mood State (POMS) score of lead-expose workers was higher than that of referents, whereas the positive POMS score of the referents was higher than that of lead-exposed group, with a covariance analysis. The lead-exposure affected some NCTB test items, such as simple reaction time (SRT), digital symbol (DSY), correct dots (PAC) and total dots (PA). The heart-rate response to Valsalva manoeuvre (HR-V), heart-rate response to deep breathing (HR-DB), and blood-pressure response to immediate standing (BP-IS) were lowered in lead-exposed workers significantly. Some abnormal brain electric waves (dominant beta frequency, semetry-diffuse abnormal and non semetry-diffuse abnormal wave distribution, dominant low wave amplitude) appeared in lead-exposed workers. Left ulnar nerve maximal conduction velocity was significantly lowered in lead-exposed group. CONCLUSION: The NCTB (including POMS), and ANS function test should be the regular screening battery for low level lead-exposed workers. The threshold blood lead concentration for health surveillance should be 30 micrograms/dL, or 1.4 mumol/L.

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