Toxicology and Industrial Health最新文献

Occupational exposure to volatile organic solvents has been reported to lead to hazardous effects. Ethyl acetate is a volatile organic compound used commonly in industry and found in many commercial products. The present study aimed to investigate the acute behavioural effects of ethyl acetate exposure in rats. The mechanism of its effects was further investigated by focusing on the possible involvement of L-type calcium channels. For this purpose, ethyl acetate (0.3 g/kg, i.p.) alone or concurrently with nimodipine (3 and 5 mg/kg, i.p.), a dihydropyridine calcium channel antagonist selective to L-type calcium channels, was administered to male Wistar albino rats. When compared to the saline control group, ethyl acetate significantly decreased the number of square-crossing, rearing, and sniffing in the open-field and impaired the reference memory performance in the three-panel runway. However, administration of nimodipine at the given doses did not block these effects of ethyl acetate. The findings suggest that L-type calcium channels may not contribute to the mechanism(s) responsible for the acute toxicity of ethyl acetate in rats regarding their central nervous system depression and memory disturbances although it should be more thoroughly investigated in further studies.

Cadmium (Cd) is a toxic environmental heavy metal with a long biological half-life and a high affinity for renal accumulation, posing serious health risks in both humans and animals. Ursodeoxycholic acid (UDCA), a bile acid primarily used for liver disorders, has gained attention for its antioxidant properties and potential protective effects in various toxicological settings. This study investigated the protective role of UDCA against cadmium-induced renal injury in rats. Twenty-eight male Wistar Albino rats (180-220 g) were divided into four groups: control (C, n = 6), cadmium (Cd, n = 8), UDCA (n = 6), and cadmium + UDCA (Cd + UDCA, n = 8). Cd was administered intraperitoneally (3 mg/kg) from days 8 to 15. UDCA was given intragastrically (60 mg/kg) from days 1 to 15. The Cd + UDCA group received both treatments concurrently. Biochemical analysis showed that Cd exposure significantly elevated serum BUN, creatinine, KIM-1, and MDA levels while decreasing GSH concentrations, indicating oxidative stress and renal injury. Conversely, the Cd + UDCA group demonstrated marked attenuation of these changes, with significantly lower BUN, creatinine, KIM-1, and MDA levels, and partially preserved GSH levels. Histopathological examination confirmed extensive renal damage in the Cd group, including cortical necrosis, tubular debris, vascular damage, glomerular alterations, and interstitial inflammation. These alterations were less severe in the Cd + UDCA group, supporting the biochemical findings. In conclusion, UDCA partially mitigated cadmium-induced oxidative stress and nephrotoxicity, reducing renal injury and supporting its potential as a protective agent against heavy metal-induced kidney damage.

Potassium bromate (KBrO₃), a strong oxidizing agent, is widely used in various industrial settings, thereby increasing the risk of oxidative damage and subsequent tissue toxicity in individuals who are exposed to it. Additionally, KBrO₃ has been used as a maturing agent and is also generated as a by-product during water disinfection process. Previously, we have demonstrated that KBrO₃ causes oxidative damage to human erythrocytes. The present work shows the protective effects of taurine (2-aminoethane sulfonic acid) against oxidative stress induced by KBrO₃ in human erythrocytes. Erythrocytes from healthy donors were incubated with either KBrO₃ alone or taurine alone and KBrO₃ plus varying concentrations of taurine. The treatment of erythrocytes with KBrO₃ caused disruption in the oxidative-reductive homeostasis as evidenced by severe alterations in antioxidant enzyme functions and a marked depletion in total sulfhydryl content. Exposure of erythrocytes to KBrO₃ also caused the elevation in methemoglobin levels, protein carbonyls, hydrogen peroxide levels, protein oxidation, and lipid peroxidation. However, the KBrO₃-induced cellular/biochemical alterations were greatly protected by taurine. These results suggest that taurine significantly decreases the toxic effects of KBrO₃ in human erythrocytes.

Hydrogen peroxide (H₂O₂) is a well-known irritant that affects the eyes, respiratory tract, and skin, and long-term exposure may lead to chronic respiratory conditions such as bronchitis, pulmonary fibrosis, and an increased risk of lung cancer, particularly in occupational settings. The objective of this study was to evaluate occupational exposure to H₂O₂ among dairy processing plant workers and to characterize the associated semi-quantitative risks using the methodology of the Singapore Occupational Health Department. This research was conducted in the sterilization units of three dairy processing plants located in Neyshabur, Iran. The semi-quantitative risk assessment in this study adhered to the methodology recommended by the Singapore Occupational Health Department. The findings revealed that the average occupational exposure to H₂O₂ for 29 workers across three dairy processing plants was 0.91 ± 0.54 ppm, with individual exposure levels ranging from 0.10 to 2.12 ppm. The mean exposure level exceeded the adjusted threshold limit value (TLV) for H₂O₂ (0.78 ppm). The evaluation of health risks associated with H₂O₂ exposure revealed that all participants fell within the medium-risk category. This classification underscores the potential for adverse health effects among dairy workers and highlights the need for targeted interventions to mitigate exposure risks and enhance workplace safety.

Chlorpyrifos (CPF) is an insecticide that humans are exposed to when used for agricultural and domestic purposes. Many studies have shown that CPF has adverse effects on human health and causes toxicity in various cells and tissues. Since there are few studies in the literature examining the effects of CPF on the male reproductive system, Sertoli cells, which are crucial to the continuation of spermatogenesis, were chosen as a model in our study. The objective of this study was to investigate the cytotoxic, oxidative stress-related, apoptotic, and genotoxic effects of chlorpyrifos in TM4 Sertoli cells. In this study, Sertoli cells were exposed to two concentrations of CPF (100 and 500 μM) for 24 h. The cytotoxic and genotoxic potential of CPF in Sertoli cells was evaluated by measuring metabolic activity, malondialdehyde content, antioxidant enzyme levels, apoptosis rates, and DNA damage. According to the findings, applied CPF concentrations increased oxidative stress and decreased antioxidant enzyme levels in Sertoli cells. The results indicated that cell viability and the nuclear division index decreased in a concentration-dependent manner, while apoptotic cells, the micronucleus, and comet formation increased. Consequently, the results suggest that DNA damage and apoptosis play a major role in the mechanisms underlying the cytotoxic effects of CPF in Sertoli cells, establishing CPF as a strong genotoxic agent.

Workers involved in paint production or application are extensively exposed to various hazardous substances like organic solvents, lead-based pigments, adhesives, and residual plastic monomers. Therefore, workers in the paint industry are at high risk of suffering adverse health effects. Studies of the lymphocytes of paint workers have demonstrated that industrial paint induces DNA damage and cellular changes. The aim of the present study was to assess DNA damage in 54 paint workers from paint production and application areas and 54 age-gender matched control subjects using a non-invasive buccal micronucleus (MN) assay. Buccal MN frequencies were significantly increased in workers compared to controls. MN frequencies significantly increased among workers from paint production areas compared with workers from paint application areas. MN frequencies in long-term workers (>10 years) were found to be significantly higher than those of short-term workers (≤10 years), which indicates that the duration of exposure to paints causes cytogenetic damage. MN frequencies increased with increasing age, while smoking status and the use of protective masks had no additional effect on MN frequencies within groups. In conclusion, it appears that long-term exposure to complex chemical mixtures during paint production may increase DNA damage in the workers. Understanding the possible causes of occupational exposure-induced genotoxicity in paint industry workers is of great importance for the protection of public health. Monitoring variables related to genotoxic damage in the paint workers using non-invasive methods will facilitate and improve risk assessment in the paint production sector.

Air pollution caused by pesticide drift poses a significant environmental health risk. The lungs are directly targeted by airborne pesticide exposure via inhalation; however, their inhalation toxicological data are poorly understood. In the present study, we evaluated the combined toxicity and interactions of lambda-cyhalothrin and its binary mixtures with eight insecticides at a concentration ratio of 1:1 in the non-small-cell lung cancer A549 line cells. Cytotoxicity tests showed that the selected pesticide binary mixtures reduced cell viability in a concentration-dependent manner. The combination index (CI) model indicated that the mixtures of lambda-cyhalothrin with acetamiprid, thiamethoxam, or clothianidin exhibited antagonistic effects, while other combinations shifted from antagonism to synergy at a toxicity level of 40%-60%. A synergistic toxicity occurred between lambda-cyhalothrin and emamectin benzoate with CI values of 0.58-0.95, and the obtained benchmark dose limits (BMDLs) value of their binary mixture was greater than 1.5 times more toxic than that of these pesticides individually. Moreover, combined exposure to the binary mixtures produced greater amounts (1.30- to 2.93-fold increase) of reactive oxygen species, malondialdehyde, and lactate dehydrogenase compared with exposure to these pesticides individually. This result suggested that the synergistic cytotoxicity of lambda-cyhalothrin and emamectin benzoate may be driven by excessive oxidative stress. Our findings serve to better understand the complex toxic pesticide interactions that humans face in the environment.

This study aimed to investigate the effect of alpha-lipoic acid (ALA) on liver damage caused by extremely low-frequency magnetic fields (ELF-MFs) in rats. Thirty-two male rats were arbitrarily assigned into four groups: Group 1 (control group), Group 2 (ELF-MF exposure group), Group 3 (ELF-MF exposure + ALA administration), and Group 4 (sham group). Groups 2 and 3 were exposed to ELF-MF at 2 mT intensity emitted by two Helmholtz coils for 4 hours/day throughout 30 days. Group 3 received ALA intraperitoneally (100 mg/kg/day) 1 hour prior to each exposure for 30 days. Group 4 was placed inside the coils, but the generator was turned off. Histopathological analysis of the liver revealed statistically significant increases in hyperemia, inflammation, fibrosis, vacuolization, multiple nuclei, and biliary proliferation in Group 2 compared to all other groups. Immunohistochemical evaluation showed that Group 2 had statistically significantly higher TUNEL and caspase-3 levels than all other groups. ELF-MF-induced alterations, including hyperemia, inflammation, vacuolization, and multiple nuclei, were significantly reduced in Group 3 compared with Group 2. However, no significant difference was observed between Group 2 and Group 3 regarding bile duct proliferation or fibrosis. No pathological changes were observed in Groups 1 and 4. ALA administration effectively reduced some histopathological changes caused by ELF-MF, particularly hyperemia, inflammation, vacuolization, and multiple nuclei, but did not improve fibrosis or biliary proliferation. Additionally, it reduced TUNEL and caspase-3 expression. Our findings suggest that ALA exhibits anti-apoptotic and anti-inflammatory effects against ELF-MF-induced liver damage.

Non-alcoholic fatty liver disease (NAFLD) is an escalating global health threat that has been linked to environmental pollutants such as the highly toxic dioxin-like congener 3,3',4,4',5-pentachlorobiphenyl (PCB 126). Although PCB 126 is known to impair hepatic function, the precise mechanisms-particularly the contribution of ferroptosis, an iron-dependent, lipid-peroxidation-mediated form of cell death-remain elusive. Here, we tested the hypothesis that ferroptosis underlies PCB 126-induced NAFLD and delineated the key molecular pathways involved. Balb/c mice were intraperitoneally injected with PCB 126 (1, 5, or 10 μM/kg) for 14 days. Hepatic injury was assessed through serum biomarkers (ALT, AST, ALP), histopathology (H&E and Oil Red O staining), and mitochondrial ultrastructure via transmission electron microscopy. Ferroptosis markers (GPX4, 4-HNE, Tf receptor), lipid peroxidation (MDA, GSH, SOD), iron homeostasis, and inflammatory cytokines (IL-1β, IL-6, TNF-α) were evaluated using qPCR, Western blotting, and ELISA. Results demonstrated that PCB 126 exposure induced NAFLD, evidenced by elevated liver-to-body weight ratios, serum liver enzymes, and steatosis. Ferroptosis was implicated through reduced mitochondrial cristae, suppressed GPX4 and SLC7A11 expression, increased lipid peroxidation, and iron accumulation. Additionally, PCB 126 activated the NF-κB pathway, elevating pro-inflammatory cytokines and myeloperoxidase (MPO) activity, while oxidative stress was marked by NRF2/KEAP1/HO-1 axis disruption. In conclusion, PCB 126 promotes NAFLD in mice by triggering ferroptosis, inflammation, and oxidative stress. These findings highlight ferroptosis as a pivotal mechanistic link in PCB 126-induced NAFLD, suggesting potential therapeutic targets for mitigating pollutant-driven liver injury.