Journal of Environmental Science and Health Part C-Toxicology and Carcinogenesis最新文献

The changes in dietary habit around the world have led to an increased use of additives in the food. The safety of food additives has been a main focus of research for many years due to the ongoing debate on their potential effects on health. In this study, the in vitro genotoxic effects of mannitol and lactitol, polyols used as sweetener food additives, were evaluated using chromosomal aberrations (CAs) and micronucleus (MN) assays in human peripheral lymphocytes. Additionally, the effects of these sweeteners on the mitotic index (MI) and nuclear division index (NDI) were investigated. Concentrations of 500, 1000, 2000, 4000, and 8000 μg/mL for mannitol and 250, 500, 1000, 2000, and 4000 μg/mL for lactitol were used. The results indicated that both polyols did not affect CA and MN frequency, and did not cause a significant change in NDI at all treatment concentratoins. However, mannitol (except at concentrations of 500 and 1000 μg/mL) and lactitol (except at 250 μg/mL) significantly decreased the MI compared to the control at almost all concentrations and treatment times. In conclusion, it was observed that mannitol and lactitol did not have a significant genotoxic effect at the concentrations used in human lymphocytes in vitro.

Caffeine is a widely consumed substance, and there is a discussion about its effects when ingested by women during pregnancy and lactation. We aimed to identify the genotoxic effects of caffeine in female mice that consumed it during pregnancy and lactation periods and its consequences in their offspring. Thirty-six couples of Swiss mice received water or caffeine (0.3 and 1.0 mg/mL) treatment during pregnancy and lactation. The male and female offspring were divided into 12 groups according to the treatment administered to the female mice. Genotoxicity was assessed using the comet assay and the micronucleus test. Both doses of caffeine showed genotoxic effects in pregnant and lactating mice groups compared to groups not administered caffeine. In relation to offspring, it can be observed that females and males of the offspring had low weight in early life. In both female and male offspring, genotoxicity was detected in the blood, liver, and kidney tissues. Thus, from the present study, we can suggest that the caffeine consumed by female mice during the periods of pregnancy and lactation led to genotoxic effects in their offspring.

This study aimed to assess the triclosan (TCS) health risk in an Iranian pregnant women sample by Monte Carlo simulation (MCS). The urinary TCS of 99 women after the 28^th week of pregnancy was detected by gas chromatography/mass spectrometry detector (GC/MS), and the MCS model implemented a health risk assessment. The corresponding hazard quotient (HQ) and the sensitivity analysis were calculated. TCS was measured in 100% of the urine samples with a median concentration of 2.89 µg/L. The median of HQ was obtained at 1.93 × 10^-4. The TCS exposure risk in the studied population was lower than the allowable limit. A comparison between HQ values in the two weight subgroups of pregnant women showed that the risk level is almost equal, and there was minimal health risk in pregnant women from exposure to TCS.

Climate change and air pollution are two interconnected global challenges that have profound impacts on human health. In Africa, a continent known for its rich biodiversity and diverse ecosystems, the adverse effects of climate change and air pollution are particularly concerning. This review study examines the implications of air pollution and climate change for human health and well-being in Africa. It explores the intersection of these two factors and their impact on various health outcomes, including cardiovascular disease, respiratory disorders, mental health, and vulnerable populations such as children and the elderly. The study highlights the disproportionate effects of air pollution on vulnerable groups and emphasizes the need for targeted interventions and policies to protect their health. Furthermore, it discusses the role of climate change in exacerbating air pollution and the potential long-term consequences for public health in Africa. The review also addresses the importance of considering temperature and precipitation changes as modifiers of the health effects of air pollution. By synthesizing existing research, this study aims to shed light on complex relationships and highlight the key findings, knowledge gaps, and potential solutions for mitigating the impacts of climate change and air pollution on human health in the region. The insights gained from this review can inform evidence-based policies and interventions to mitigate the adverse effects on human health and promote sustainable development in Africa.

In vitro genotoxicity testing plays an important role in chemical risk assessment. The human B-lymphoblastoid cell line TK6 is widely used as a standard cell line for regulatory safety evaluations. Like many other mammalian cell lines, TK6 cells have limited metabolic capacity; therefore, usually require a source of exogenous metabolic activation for use in genotoxicity testing. Previously, we developed a set of TK6-derived cell lines that individually express one of fourteen cytochrome P450s (CYPs). In the present study, we surveyed a panel of major Phase II drug-metabolizing enzymes to characterize their baseline expression in TK6 cells. These results may serve as a reference enzymatic profile of this commonly used cell line.

Ultraviolet (UV) irradiated cells release factors that result in varied responses by non-irradiated cells via bystander effects (BE). The UV-BE is dependent on the cell types involved and on the wavelength of the radiation. Using conditioned medium from UVA-irradiated A375 human melanoma cells (UVA-CM), UVA-bystander response was evaluated on the viability of naïve A375 cells. UVA-CM treatment itself did not alter cell viability; however, UVA-CM treated bystander cells were more resistant to the lethal action of UVA, UVB, UVC or H₂O₂. Effects of UVA-CM on cell proliferation, mechanism of cell death, DNA damage, malondialdehyde formation, generation of reactive oxygen species (ROS) and antioxidant status were studied in A375 cells. We observed that UVA-CM triggered antioxidant defenses to elicit protective responses through elevation of antioxidant enzyme activities in cells, which persisted until 5 h after exposure to UVA-CM. This was possibly responsible for decreased generation of ROS and diminished DNA and membrane damage in cells. These bystander cells were resistant to killing when exposed to different genotoxic agents. Damaged nuclei, induction of apoptosis and autophagic death were also lowered in these cells. The influence of UVA-CM on cancer stem cells side population was assessed.Highlights:UVA radiation induced bystander effects in A375 cellsDamage by genotoxicants is suppressed due to lower ROS generation on UVA-CM treatmentUVA-CM exposure enhanced higher activities of CAT and GPxResistance to genotoxic agents in such cells was due to elevated antioxidant defenceUVA-bystander phenomenon was a protective response.

Pharmaceutical compounds released into the aquatic environment are known to cause toxic effects on the environment. Isoniazid is widely used in the treatment of tuberculosis and is, therefore, frequently encountered in environmental waters. In this study, the degradation of isoniazid was investigated by anodic oxidation and subcritical water oxidation method which are members of Advanced Oxidation Processes. The Box-Behnken Design was used to determine the effects of current, initial concentration, and electrolysis time on mineralization in the anodic oxidation process, which carried out a cell with a Pt cathode and boron-doped diamond anode. The highest mineralization value of 78.14% was achieved at optimal conditions of 300 mA, 3 h, and 100 mg/L initial concentration. The degradation of Isoniazid was also investigated under subcritical water conditions using an ecological oxidizing agent, H₂O₂. The maximum mineralization rate of 72.23% was obtained when 100 mM H₂O₂ was used for a 90 min treatment at 125 °C for 100 mg/L Isoniazid solution in the subcritical water oxidation process. The LC-MS results showed that the degradation products obtained by AO and SWO methods were different from each other. Finally, possible degradation mechanisms are proposed according to the degradation products obtained for both processes.

Lead exposure during childhood has been associated with a variety of negative outcomes, including antisocial/aggressive behavior. However, different subtypes of antisocial behavior have been found to have different neurobiological correlates, and it is unclear whether lead exposure is related to specific subtypes of aggressive behavior. The objective of the study was to examine relationships between childhood blood lead levels (BLL) and proactive and reactive aggression. Further, given prior findings of sex differences in the effects of lead exposure, we examine whether there are sex differences in these relationships. In a sample of 818 youth (47.2% girls) ages 10-13 in China, we assessed BLL and administered the Reactive Proactive Aggression Questionnaire. Results show that BLLs were associated with reactive, but not proactive aggression. There was a significant interaction between BLL and sex in predicting aggression; boys with higher BLL scored higher in both proactive and reactive aggression than boys with lower BLL, but these differences were not present for girls. These findings suggest that lead exposure may have broad effects on antisocial behavior, but that boys may be more susceptible than girls. These findings may provide insights to identifying protective factors that could be potential targets for intervention.

Polychlorinated biphenyls (PCBs) are a class of environmental pollutants with a long half-life that sequester in fat. Women with polycystic ovarian syndrome (PCOS) may represent a sensitive subgroup to endogenous exposure to PCBs because of associated weight gain. Seven PCB congeners were compared in age, ethnicity, and BMI matched women with (n = 29) and without (n = 30) PCOS and related to metabolic outcomes, and steroid and thyroid hormone levels. PCB118, PCB138, PCB153, and PCB180 were detected in all serum samples but geometric mean did not differ between cases and controls. PCBs correlated with increasing concentrations of each other (p < .01), increasing age (p < .01) and decreasing lneGFR (p < .05). lnPCB118 correlated with increasing Free-T4 (p = .028). lnPCB158, lnPCB180, and ln∑PCB correlated with increasing lnSHBG (p = .044). In regression modeling, although not significant, PCB118 positively associated with lnSHBG in controls (p = .0504) but not in cases; estradiol inversely associated with PCB138 in controls (p = .055) and ∑PCB in cases (p = .051). No significant associations were observed between metabolic endpoints, and steroid and thyroid hormone levels. The results presented do not suggest the PCOS cases in this cohort are at adverse risk compared to age, ethnicity, and BMI matched controls.

Chronic exposure to polycyclic aromatic hydrocarbons (PAHs) leads to a high incidence of cardiovascular diseases. To assess the effects of PAHs exposure on vascular damages in occupationally exposed populations, 196 sanitation workers were recruited. According to the differences of occupation or operation, they were divided into exposure group (n = 115) and control group (n = 81). Sixteen serum PAHs were determined by gas chromatography-tandem mass spectrometery. Tumor necrosis factor ɑ (TNF-ɑ) and angiotensin II (ANG-II) in serum, blood lipids and blood pressure were also measured. Results showed that, except for indeno(1,2,3-cd)pyrene, dibenzo(a,h)anthracene and benzo(g,h,i)perylene, the detection frequencies of other PAHs were above 85%, showing that subjects are generally exposed to PAHs. The top three compounds in serum concentrations of PAHs were phenanthrene, acenaphthylene and anthracene. Moreover, the concentrations of total serum PAHs in the exposure group were significantly higher than those in the control (p < 0.05), suggesting a higher PAHs exposure in the former. Though there was no significant difference in blood lipids and blood pressure between groups (p > 0.05), TNF-ɑ and ANG-II levels in the exposure group were significantly higher than those in the control group (p < 0.05), suggesting that PAHs exposure may be related to pro-inflammatory effects and vascular endothelial damages.