Objectives: A number of metals, especially heavy metals, exhibit neurotoxic properties. Neurological and neurophysiological studies indicate that the functions of the central (CNS) and peripheral nervous system (PNS) may be impaired under conditions of exposure to arsenic (As). The aim of the present study was to assess the effects of inorganic arsenic on the central and peripheral nervous system. Materials and Methods: The study covered a group of 21 male workers (mean age: 41.9 yr; SD: 7.6; range: 31-55 yr) employed in a copper smelting factory. Their employment duration ranged from 5 to 33 years (mean: 18.1 yr; SD: 7.8). Arsenic concentrations in workplace air amounted to 0.01003 mg/m 3 on average (SD: 0.00866). Urine arsenic concentrations ranged from 3.48 to 23.63 μg/l (mean: 11.91 μg/l; SD: 9.5). The control group consisted of 16 males non-occupationally exposed to As, matched for gender, age and work shift pattern. The evaluation of neurological effects was based on the findings of neurological examination, electroencephalography (EEG), visual evoked potentials (VEPs) and electroneurography (ENeG). Results: Clinical symptoms, such as sleeplessness or sleepiness, irritability, headache, painful spasms in extremity muscles, extremity paresthesia and pain, and muscular fatigue prevailed among functional disorders of the nervous system in workers chronically exposed to As. Neurological examination did not reveal any organic lesions in the CNS or PNS. In EEG records classified as abnormal, generalized changes were most common. VEP examinations revealed abnormalities in evoked response latency. Stimulation of the motor fibers of the peroneal and medial nerves resulted in a decreased amplitude of the motor potential. Stimulation of the sensory fibers of medial nerves brought about a decreased amplitude of the sensory potential and a lower conduction velocity of the sural nerves. Conclusion: The findings of the study indicate that exposure to As concentrations within the threshold limit values (TLV) can induce subclinical effects on the nervous system, especially subclinical neuropathy.
Background: Benzalkonium chloride (BAC) is a quaternary ammonium compound (QAC) with a C 8 to C 18 chain length of alkyl groups. Since BAC exerts toxic effects on microorganisms, it has been used as an effective germicide and preservative, mostly in cosmetic industry and medicine. However, the toxic potential of BAC may be hazardous to humans, due to the common use of preparations containing BAC as a preservative. Material and Methods: To assess the possible toxic effects of BAC, two-stage experiments were performed on female Wistar rats. At first, LC 50 after a single exposure to BAC aerosol was determined. Then, the animals were exposed to BAC aerosol at 30 mg/m 3 for 6 h, and for 3 days (6 h/day). The controls were unexposed rats. Directly after BAC exposure and 18 h afterwards,, BALF concentrations were measured of total protein, Clara cell protein, matrix metalloproteinase-9 (MMP-9), hyaluronic acid (HA), immunoglobulin E (IgE) and cytokines (TF-α, IL-6 and MIP-20), lactate dehydrogenase (LDH) and GSH-S-transferase (GST). Results: The LC 50 value for exposed rats was ca. 53 mg BAC in m 3 air for 4 h. All the rats survived single and repeated inhalation exposure to 30 mg/m 3 BAC. After single and repeated exposure, lung weight, total protein, HA and LDH activity in BALF of exposed rats were higher than in controls while CC16 levels were decreased. A significantly higher BALF concentration of IL-6 and IgE was noted in animals exposed to single and repeated doses. BALF concentrations of MMP-9, TNF-α, and MIP-2 in exposed rats were similar to those in control animals. Conclusion: BAC may be classified to class I acute inhalation toxicity. It showed a strong inflammatory and irritant activity on the lungs after 6h inhalation and stimulated dynamic patterns of IL-6 and IgE production and protein infiltration from blood vessels to BALF. Continued exposure resulted in cellular destruction, a statistically significant increase in LDH activity and a continuous decrease in CC16 concentration in BALF.
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