Toxicology and Industrial Health最新文献

The Globally Harmonized System (GHS) is a crucial framework for chemical hazard communication, especially in protecting workers from skin sensitizers. A critical assessment of the principles, issues, and challenges around classification of skin sensitization in GHS is warranted. Classification of dermal sensitizers relies on a weight of evidence (WoE) approach that incorporates human, animal, and non-test data. However, current testing methods have limitations in sensitivity, specificity, and predictive accuracy. Current test methods take into account the issue of potency and thresholds for sensitization. However, the focus on induction thresholds rather than induction and elicitation thresholds may create a gap in protecting already sensitized individuals since elicitation thresholds are in some cases lower than induction thresholds. While the sensitization process may take weeks or years, current test methods are largely acute in nature, potentially incapable of identifying all (chronic) sensitizers. Moreover, current methods used for classification of skin sensitizers only take into account the dermal route, whereas some chemicals may cause dermal sensitization through other routes, which presents a significant limitation, especially when considering non-animal testing methods. Finally, lack of UV irradiation in current methods may inadvertently miss potential photosensitizers, which may result in misclassification. Continuous refinement of testing methods and integrating novel approaches are essential to improve GHS classifications for skin sensitizers.

Lead is one of the main environment pollutants, which has strong inhibitory effects on the functioning of the CNS. Exposure to high amounts of lead, even shortly, stimulates glial cells and activates inflammatory pathways in brain. Lead can also increase the amount of oxidative stress. In this study, the effect of hydrogen sulfide (H₂S) donors on lead-induced neurotoxicity was investigated. The protective effects of H₂S have been proven in various neurological diseases. Lead and H₂S were administered for 2 weeks. The animals' cognitive performance, exploratory behavior, and anxiety were evaluated using the shuttle box, open field, and elevated plus maze tests. The level of malondialdehyde (MDA), tumour necrosis factor alpha (TNFα), and interleukin 10 (IL-10); the total antioxidant capacity of the hippocampus; and blood lead levels were measured. Lead increased the level of TNFα and MDA and decreased the level of IL-10 in the hippocampus. H₂S was able to moderate the inflammatory and oxidative factors and tissue damage caused by lead in the hippocampus, which led to better cognitive and behavioral functions. The results of this study indicated that H₂S reduced the damage caused by lead through its well-known antioxidant and anti-inflammatory activity, which ultimately resulted in improved behavioral and cognitive functions in lead-poisoned animals. .

This study endeavored to elucidate the association between exposure to individual and combined volatile organic compounds (VOCs) and the occurrence of periodontitis in adults. Data were derived from the 2009-2012 National Health and Nutrition Examination Survey (NHANES). Weighted logistic regression and restricted cubic spline (RCS) analyses were employed to assess the relationship between blood VOC concentrations and periodontitis. Significant positive associations were observed for benzene, furan, 2,5-dimethylfuran, ethylbenzene, m-/p-xylene, and o-xylene, with adjusted odds ratios (ORs) ranging from 1.44 to 2.31. RCS analyses demonstrated linear associations for benzene, furan, 2,5-dimethylfuran, m-/p-xylene, and 1,4-dichlorobenzene, whereas ethylbenzene and o-xylene exhibited nonlinear associations. In addition, weighted quantile sum regression revealed that cumulative VOC exposure was positively associated with periodontitis, with 2,5-dimethylfuran, ethylbenzene, benzene, and furan identified as the most influential contributors. Collectively, these findings suggested that VOC exposure possibly plays a substantive role in the pathogenesis and progression of periodontitis, underscoring the need for strategies aimed at reducing environmental VOC exposure as part of comprehensive preventive and therapeutic public health measures.

Methylparaben and propylparaben are widely used as preservatives in consumer products, including cosmetics, personal care items, and pharmaceuticals. Concerns have been raised regarding their potential for systemic absorption and estrogenic activity, which may contribute to endocrine disruption. This review evaluates current evidence on dermal absorption, metabolism, and systemic distribution of methylparaben and propylparaben, emphasizing factors influencing their bioavailability. Additionally, the estrogenic potential of these compounds in experimental studies is examined, assessing receptor binding affinity and biological effects. Overall, while parabens exhibit weak estrogenic activity compared to endogenous hormones, repeated exposure and cumulative effects warrant further investigation. The toxicokinetic data combined with estrogenic activity assessments provide critical insight into the risk of endocrine disruption associated with paraben exposure. This assessment provides an understanding of methylparaben and propylparaben safety, supporting informed regulatory decisions and consumer awareness.

Formaldehyde (FA) is a critical industrial compound implicated in leukemogenesis via the induction of oxidative stress. Our previous studies observed aberrant expression of peroxiredoxin II (PrxII), phosphatase and tensin homologue (PTEN), phosphoinositide 3-kinase (PI3K), and protein kinase B (Akt) in FA-exposed bone marrow cells (BMCs) under conditions of oxidative stress. We speculate that the PrxII gene may be functionally linked to the PI3K pathway in formaldehyde-induced oxidative damage. Therefore, in the current study, we first used a specific PI3K inhibitor (LY294002, 10 μM) to suppress the PI3K pathway at 100 μM FA, and co-treated mouse bone marrow cells for 24 hours to investigate their potential interactions. We then evaluated the expression levels of PrxII, PTEN, PI3K, and Akt (via qRT-PCR and Western blot analysis), as well as the BMC's viability (CCK-8 assay), ROS levels (DCFH-DA), and cell apoptosis (Annexin V/PI staining). Additionally, to explore the potential regulatory role of PrxⅡ in the PI3K pathway, we employed siRNA-mediated PrxⅡ gene silencing through a small interfering RNA and subsequently measured PTEN, PI3K, and Akt mRNA and protein levels using qRT-PCR and Western blot analysis. We observed that inhibition of the PI3K pathway with 10 μM LY294002 mitigated FA-induced oxidative damage in BMCs, as evidenced by improved cell viability, reduced ROS levels, and decreased apoptosis rates. Moreover, PrxII silencing led to downregulation of PTEN expression while concurrently activating the PI3K/Akt signaling cascade. This study provides evidence that PrxII silencing may trigger the PI3K pathway mediated by PTEN gene, thereby exacerbating FA-induced oxidative injury.

Endosulfan is a broad-spectrum organochlorine pesticide widely used in many developing countries despite its high toxicity potential. Endosulfan, listed as potent endocrine-disrupting chemical and xenoestrogen, gains importance for its potential to cause reproductive and developmental dysfunction. In females, endosulfan disrupts ovarian and uterine development, leading to infertility, miscarriage, and developmental toxicity. It acts by mimicking estrogen and interferes with estrogen and androgen pathways, impacting hormone regulation and gene expression, including estrogen receptor α (ERα) and progesterone receptors. Endosulfan triggers oxidative stress in ovaries, reduces follicle count, and impairs uterine differentiation, affecting embryo implantation. Additionally, it alters gene expression and causes epigenetic modifications, contributing to reproductive dysfunctions. In males, endosulfan affects spermatogenesis by causing oxidative stress, mitochondrial dysfunction, and lipid peroxidation. It reduces sperm quality, motility, and quantity, with effects on testicular tissues, sperm chromatin condensation, and enzymatic activity. Oxidative damage, increased reactive oxygen species (ROS), and disrupted energy metabolism are central to its toxicity. Epidemiological studies also link pesticide exposure to reduced sperm counts, higher DNA fragmentation, and infertility. Moreover, endosulfan can cross the placental barrier, leading to fetal resorption, malformations, and maternal toxicity. This review provides a comprehensive overview of the reproductive toxicity of endosulfan in males and females. We also highlight the various possible mechanisms of reproductive toxicity of endosulfan and its potential to impart deleterious effects over HPG axis, gonads, and uterine differentiation and development and implantation.

Radiation exposures, whether planned or unexpected, can have harmful consequences on biological systems. To avoid these radiotoxic consequences, a variety of natural and synthetic radioprotectors are given prior to radiation exposure. The present study aimed to investigate the radioprotective potential of Aloe vera gel extract against damage induced by whole-body X-ray exposure in male balb/c mice. The animals were divided into four groups: Control, Aloe vera (50 mg/kg body weight orally on alternate days for 30 days), X-ray (cumulative dose of 2 Gy) (i.e., 0.258 Gy twice a day for four consecutive days) in the last week of the experimental protocol, and Aloe vera + X-ray. Following irradiation, Fourier transform infrared spectroscopy (FTIR) analysis showed structural changes in molecules by altering the ratios of CH₃/lipid, CH₂/lipid, lipid/protein, Amide I/II, and nucleic acid in liver and testes. X-ray exposure led to an increase in DNA strand breaks in the liver, spleen, kidney, and testes of mice, as indicated by comet assay. Bcl-2 levels were shown to be up-regulated in the kidney and testes following irradiation. In liver, kidney, and spleen, caspase 3 was also found to be up-regulated. Furthermore, after being exposed to X-rays, the expression of caspase 9 and bax was up-regulated in all the tissues examined. Administration of Aloe vera to the X-ray-exposed group exhibited decline in DNA strand breaks in all tissues investigated. Moreover, protein expressions of these genes were found to be down-regulated in the Aloe vera + X-ray-exposed group. These observations illustrate the potential of Aloe vera in providing radioprotection for rodents, possibly DNA protection, through its anti-apoptotic properties.

This study examined ingredient disclosure and concealment patterns in cosmetic products reported under California's Safe Cosmetics Program (CSCP), with particular attention to trade secret designations and their implications for public health transparency. Drawing on a dataset from CSCP filings, descriptive analyses and logistic regressions were calculated to identify category predictors of ingredient non-disclosure, including product type, manufacturer characteristics, and chemical hazard profiles. Limitations in standard statistical models, such as rare outcomes and complete separation, required a pivot to stratified descriptive summaries and sensitivity checks. The study also documented inconsistencies in ingredient naming conventions and reporting formats that hinder public access and regulatory oversight. The results highlight the need for stronger disclosure standards, improved data coordination, and stronger labeling enforcement to enable meaningful assessment of chemical risks in personal care products. The analysis provides a framework for translating legal disclosure mandates into empirical research and policy evaluation.

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.