Toxicology and Industrial Health最新文献

Co-exposure to noise and nanomaterials, such as silver nanoparticles (Silver-NPs), is a common occurrence in today's industries. This study aimed to investigate the effects of exposure to noise and the administration of silver-NPs on the liver tissue of rats. Thirty-six adult male albino Wistar rats were randomly divided into six groups: a control group (administered saline intraperitoneally), two groups administered different doses of Silver-NPs (50 mg/kg and 100 mg/kg, 5 days a week for 28 days), two groups exposed to noise in addition to Silver-NPs (at the same doses as mentioned before), and a group exposed only to noise (104 dB, 6 hours a day, 5 days a week for 4 weeks). Blood samples were taken to assess hepatic-functional alterations, such as serum ALP, ALT, and AST levels. Additionally, biochemical parameters (MDA, GPX, and CAT) and the silver concentration in the liver were measured. Histopathological analysis, mRNA expression (P53 and NF-κB), protein expression (CYP450), and liver weight changes in rats were also documented. The study found that the administration of Silver-NPs and exposure to noise resulted in elevated levels of ALP, ALT, AST, and MDA (p < .01). Conversely, GPX and CAT levels decreased in all groups compared with the control group (p < .0001). There was a significant increase (p < .05) in liver weight and silver concentration in the liver tissues of groups administered Silver-NPs (50 mg/kg) plus noise exposure, Silver-NPs (100 mg/kg), and Silver-NPs (100 mg/kg) plus noise exposure, respectively. The expression rate of P53, NF-κB, and cytochromes P450 (CYPs-450) was increased in the experimental groups (p < .05). These findings were further confirmed by histopathological changes. In conclusion, this study demonstrated that exposure to noise and the administration of Silver-NPs exacerbated liver damage by increasing protein and gene expression, causing hepatic necrosis, altering biochemical parameters, and affecting liver weight.

Bisphenol P (BPP) is a structural analog of bisphenol A (BPA) and is increasingly used as a substitute of BPA in commercial and household applications. In recent years, BPP has been frequently detected in terrestrial and aquatic ecosystems. Very little epidemiological and experimental information are available on the toxicity potential of BPP in human and animal systems, which is very concerning in view of its increasing use. The current study evaluated the biochemical and histopathological effects of BPP in rats. The seven experimental groups (n = 5 rats/group) included BPA5 (5 mg), BPA50 (50 mg), BPA100 (100 mg), BPP5 (5 mg), BPP50 (50 mg), and BPP100 (100 mg) while the remaining one group served as untreated control. At the end of treatment, the organs (liver, kidney, heart, and lung) of rats were harvested for oxidative stress and histopathological analyses. A significant (p < .05) decrease was observed in the weight of the liver, lungs, and kidneys in the BPP100 group similar to the BPA100 group compared with the control group. Further, a significant (p < .05) decrease was also observed for concentrations of antioxidant enzymes (catalase, peroxidase, superoxide dismutase, and glutathione peroxidase) in the liver, lungs, kidneys, and heart at the highest two doses of BPP similar to the respective BPA groups compared with the control group. The two highest doses of BPP induced histopathological changes in the liver such as nuclei distortion, excessive necrosis of hepatocytes, nuclei shrinkage and pyknosis of cells with disrupted cell structure (BPP100), and cellular congestion and degeneration of hepatocytes (BPP50) similar to the two respective doses of BPA. The BPP treated groups also showed varying histopathological changes in kidney tissue, heart tissue, and lung tissue similar to BPA treated rats. In conclusion, the present study indicated that BPP has the potential to induce oxidative stress and alter the histomorphological architecture of different organs and is as deleterious as BPA.

Phthalates (PAEs), a group of environmental endocrine disruptors, are associated with oxidative stress and have adverse effects on female ovarian reserves. However, this association has been poorly investigated, particularly with respect to clinical evidence. In this study, we provided clinical evidence of a relationship between exposure levels of PAEs, oxidative stress and decreased ovarian reserve (DOR). Firstly, the urinary concentrations of metabolites of PAEs were measured by high performance liquid chromatography coupled with tandem mass spectrometry (HPLC-MS/MS). The serum concentrations of follicle-stimulating hormone (FSH), luteinizing hormone (LH), and anti-Mullerian hormone (AMH), and the biomarkers of oxidative stress, malondialdehyde (MDA), superoxide dismutase (SOD), and total antioxidant capacity (T-AOC), were determined. Finally, statistical analyses were conducted to describe the relationship between the PAEs exposure, oxidative stress and DOR. We found that the levels of monomethyl phthalate (MMP), monoisobutyl phthalate (MiBP), mono-(2-ethylhexyl) phthalate (MEHP), and mono-(2-ethyl-5-hydroxypentyl) phthalate (MECPP) in the DOR group were significantly higher than those in the control group. There was a significant negative association between AMH and MMP, MiBP levels. and a significant positive association between FSH and MMP levels. PAEs exposure was also associated with a significant increase in MDA levels and decrease in SOD levels. In conclusion, the exposure of PAEs was closely associated with DOR, potentially mediated by oxidative stress pathways; however, small sample size was a limitation in this study.

A rapid and sensitive assessment of the toxicity of oxygenated polycyclic aromatic hydrocarbons (OPAHs), widely distributed persistent organic pollutants in the environment, is crucial for human health. In this study, using high-performance liquid chromatography, the separation and detection of four purines, xanthine (X), guanine (G), adenine (A), and hypoxanthine (HX) in cells were performed. The aim was to evaluate the cytotoxicity of three OPAHs, namely 1,4-benzoquinone (1,4-BQ), 1,2-naphthoquinone (1,2-NQ) and 9,10-phenanthrenequinone (9,10-PQ), with higher environmental concentrations, from the perspective of purine nucleotide metabolism in human skin fibroblast cells (HFF-1). The results revealed that the levels of G and A were low in HFF-1 cells, while the levels of HX and X showed a dose-response relationship with persistent organic pollutants concentration. With increased concentration of the three persistent organic pollutants, the purine metabolism in HFF-1 cells weakened, and the impact of the three persistent organic pollutants on purine metabolism in cells was in the order of 9,10-PQ > 1,4-BQ > 1,2-NQ. This study provided valuable insights into the toxic mechanisms of 1,4-BQ, 1,2-NQ and 9,10-PQ, contributing to the formulation of relevant protective measures and the safeguarding of human health.

During recent decades, the application of zirconium dioxide nanoparticles (ZrO₂-NP) has been expanded in various fields ranging from medicine to industry. It has been shown that ZrO₂-NP has the potential to cross the blood-brain barrier (BBB) and induce neurotoxicity. In the current study, we investigated the in vivo neurotoxicity, as well as, the cellular mechanism of ZrO₂-NP toxicity on two neuronal-like cell lines, PC12 and N2a. PC12 and N2a cells were exposed to increasing concentrations of ZrO₂-NP (0-2000 µg/ml) for 48 h. The apoptotic effect of ZrO₂-NP was determined using annexin V/propidium iodide double staining (by flow cytometry), and western blot analysis of relative apoptotic proteins, including caspase-3, caspase-9, bax, and bcl2. Based on our results, ZrO₂-NP at concentrations of 250-2000 μg/mL increased both early and late-stage apoptosis in a concentration-dependent manner. Moreover, the expressions of cleaved-caspase-3 and -9 proteins and the bax/bcl2 ratio were significantly increased. In addition, oral administration of ZrO₂-NP (50 mg/kg) to male Wistar rats for 28 days led to the loss of neuronal cells in the cerebral cortex. Taken together, our findings highlighted the role of apoptosis on cytotoxicity induced by ZrO₂-NP.

Phthalic acid esters (PAEs) and carbon nanotubes (CNTs) are common environmental pollutants and may degrade differently with different resulting biotoxicity, when present together. This study investigated the toxicological effects of singular or combined exposure to dibutyl phthalate (DBP) and multi-walled carbon nanotubes (MWCNTs) in KM mice. Results indicated that combined exposure led to slower weight gain and an increased leukocyte count in the blood, as well as liver tissue lesions and downregulation of organ coefficients. Additionally, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were elevated in the liver, and glucose, pyruvate, triglyceride (TG), and total cholesterol (T-CHO) were significantly reduced, suggesting compromised liver function. Furthermore, mRNA levels of genes related to hepatic glucose and lipid metabolism were significantly altered. These findings suggest that combined exposure to DBP and MWCNTs can have severe impacts on liver function in mice, highlighting the importance of considering interactions between multiple contaminants in environmental risk assessments.

Dust pollution is common in Indian roads and several industrial settings (including mines) that affects human health. Identification and characterization of the dust particles in the mining area is essential for knowing the properties of the dust that effectively causes ailments to humans, particularly among workers those who are working in unorganized industrial settings. The present study aimed to determine the level of dust pollution and to know the size and characterize the dust particles in the Pachami-Hatgacha stone mine areas of Birbhum district, West Bengal, India. Dust samples were collected and analysed for Dynamic Light Scattering (DLS) to determine the size and shape of the particles, Fourier Transform Infrared Spectroscopy (FT-IR) to determine the free silica content, and X-ray Florence (XRF) analysis for quantitative estimation of components in the sample. All the analyses were done following standard instrumentation and techniques. The size of the dust particles was much less (ranges 101-298 nm) than the size of respirable particles (2500 nm). Those were mostly generated as well as precipitated during peak working hours of the day. Presence of considerable amounts of silica was confirmed by the FT-IR (strong and broad band at 1000 cm^-1) and XRF analysis (76.85% SiO₂). Exposure to these dust particles may cause severe health impairments. Therefore, interventions like wet drilling and blasting, sprinkling of water during peak working hours, and awareness of use of personal protective devices among workers are required to reduce the risk and hazards associated with dust pollution to the health of miners and inhabitants around the mines.

Contaminated water and food are the main sources of documented per- and polyfluoroalkyl substances (PFAS) exposure in humans. However, other sources may contribute to the overall PFAS intake. While several studies documented the presence of PFAS in consumer products, PFAS evaluation in dental products has been limited to floss and tape to date. This study estimated PFAS exposures from a convenience sample of leave-in dental products (night guards and whitening trays), which remain in contact with the mouth for longer durations than previously evaluated dental products. This analysis evaluated whether consumer usage of these dental products meaningfully contributes to oral exposure of PFAS. Leaching of PFAS upon disposal of products was also considered. Out of 24 PFAS measured, perfluorobutanoic acid (PFBA; 3.24-4.17 ng/product or 0.67-0.83 ng/g) and perfluorooctanesulfonic acid (PFOS; 7.25-16.45 ng/product or 1.2-2.3 ng/g) were detected in night guards, and no PFAS were detected in whitening trays. Non-targeted analysis showed additional possible PFAS, which could not be characterized. The findings showed that PFOS and/or PFBA present in night guards were unlikely to pose a health concern. From an ecological perspective, the dental products examined were shown to constitute a negligible contribution to environmental PFAS. In conclusion, the examined dental products do not represent a significant source of exposure to PFAS for humans or the environment. The study demonstrates how risk assessment can be integrated by the industry into product stewardship programs to evaluate the potential health and environmental impacts of chemicals in consumer products.

Electret technology was widely used to prevent the airborne transmission of bioaerosols during the COVID-19 pandemic and improve the filtration efficiency of masks and high-efficiency particulate air (HEPA) filters. As alcohol disinfectants are widely used in medical and welfare institutions, concerns about alcohol exposure inactivating electret exist. However, comprehensive alcohol exposure tests have not been conducted on masks and HEPA filters distributed in Japan. Twenty-five types of masks and five types of HEPA filters were subjected to a discharging process according to ISO 16890 to quantitatively elucidate the resistance to alcohol exposure. Measurements of changes in filtration efficiency and pressure drop before and after discharge show that 17 masks (68%) and four HEPA filters (80%) exhibited a significant decrease in filtration efficiency, confirming their vulnerability to alcohol. In addition, a survey (n = 500 Japanese adults, including 30 healthcare professionals) revealed that ∼90% of the general public were unaware that alcohol exposure could degrade masks and air purifiers. Furthermore, 36% of the surveyed healthcare professionals had sprayed alcohol directly onto their masks. The effectiveness of user warnings through product labels and instructions was investigated from the perspective of ensuring the safety of patients and healthcare professionals. Results revealed that the best approach was to describe the extent and duration of the adverse effects caused by disregarding precautions. Increase in awareness of healthcare professionals and general public by authorities and manufacturers through guidelines and warning labels would reduce the risk of inhaling bioaerosols caused by unintentional electret inactivation.

Increasing applications of silver nanoparticles (AgNPs) in multiple products like cosmetics, medicines, drugs, paints, and other new materials have raised concern for their toxic effects on living beings and the surrounding environment. In the present study, cytotoxicity and genotoxicity of AgNPs synthesized using plant flavonoid (Naringin) as a reducing agent were investigated on human promyelocytic leukemic (HL-60) cells and human blood as an in vitro model. The LC₅₀ of AgNPs was found to be 4.85 µM. Dose-dependent increase in cell death and caspase activity was observed in the presence of AgNPs. The comet assay showed a 60%-70% (p < .05) increase in tail DNA at 0.48 and 0.96 µM AgNPs. CBMN in PBMCs also confirmed the genotoxic potential of AgNPs-induced DNA damage. AgNPs resulted in 1.5-1.54 fold (p < .05) increase in the level of ROS in HL-60 cells after 12 h of exposure. AgNP showed toxicity in human cells through ROS generation and cellular damage through membrane dysfunction, caspase activation, apoptosis, and DNA damage.