This systematic review aims to discover the plausible mechanism of Ozone in A.D., to boost translational research. The main focus of our review lies in understanding the effects of ozone pollution on the human brain and causing degenerative disease. Owing to the number of works carried out as preclinical evidence in association with oxidative stress and Alzheimer's disease and the lack of systematic review or meta-analysis prompted us to initiate a study on Alzheimer's risk due to ground-level ozone. We found relevant studies from PubMed, ScienceDirect, Proquest, DOAJ, and Scopus, narrowing to animal studies and the English language without any time limit. The searches will be re-run before the final analysis. This work was registered in Prospero with Reg ID CRD42022319360, followed the PRISMA-P framework, and followed the PICO approach involving Population, Intervention/Exposure, Comparison, and Outcomes data. Bibliographic details of 16 included studies were studied for Exposure dose of ozone, duration, exposure, and frequency with control and exposure groups. Primary and secondary outcomes were assessed based on pathology significance, and results were significant in inducing Alzheimer-like pathology by ozone. In conclusion, ozone altered oxidative stress, metabolic pathway, and amyloid plaque accumulation besides endothelial stress response involving mitochondria as the critical factor in ATP degeneration, caspase pathway, and neuronal damage. Thus, ozone is a criteria pollutant to be focused on in mitigating Alzheimer's Disease pathology.

Long-term exposure to PM₂.₅ has been linked to lung cancer incidence and mortality, but limited evidence existed for other cancers. This study aimed to assess the association between PM₂.₅ on cancer specific mortality. An ecological study based on the cancer mortality data collected from 5,565 Brazilian cities during 2010–2018 using a difference-in-differences approach with quasi-Poisson regression, was applied to examine PM₂.₅-cancer mortality associations. Globally gridded annual average surface PM₂.₅ concentration was extracted and linked with the residential municipality of participants in this study. Sex, age stratified and exposure-response estimations were also conducted. Totalling 1,768,668 adult cancer deaths records of about 208 million population living across 5,565 municipalities were included in this study. The average PM₂.₅ concentration was 7.63 μg/m³ (standard deviation 3.32) with range from 2.95 μg/m³ to 28.5 μg/m³. With each 10 μg/m³ increase in three-year-average (current year and previous two years) concentrations of PM₂.₅, the relative risks (RR) of cancer mortality were 1.16 (95% confidence interval [CI]: 1.11–1.20) for all-site cancers. The PM₂.₅ exposure was significantly associated with several cancer-specific mortalities including oral, nasopharynx, oesophagus, and stomach, colon rectum, liver, gallbladder, larynx, lung, bone, skin, female breast, cervix, prostate, brain and leukaemia. No safe level of PM₂.₅ exposure was observed in the exposure-response curve for all types of cancer. In conclusion, with nationwide cancer death records in Brazil, we found that long-term exposure to ambient PM₂.₅ increased risks of mortality for many cancer types. Even low level PM₂.₅ concentrations had significant impacts on cancer mortality.

Due to their small dimensions, airborne particles are able to penetrate through inhalation into many human organs, from the lungs to the cardiovascular system and the brain, which can threaten our health. This work establishes a novel approach of collecting quantitative data regarding the fraction, the composition and the size distribution of combustion-emitted particulate matter through the magnetic characterization and analysis of samples received by common air pollution monitoring. To this end, SQUID magnetometry measurements were carried out for samples from urban and suburban areas in Thessaloniki, the second largest city of Greece, taking into consideration the seasonal and weekly variation of airborne particles levels as determined by occurring traffic and meteorological conditions. The level of estimated magnetically-responding atmospheric particulate matter was at least 0.5 % wt. of the collected samples, mostly being present in the form of ultrafine particles with nuclei sizes of approximately 14 nm and their aggregates. The estimated quantities of magnetic particulate matter show maximum values during autumn months (0.8 % wt.) when increased commuting takes place, appearing higher in the city center by up to 50% than those in suburban areas. In combination with high-resolution transmission electron imaging and elemental analysis, it was found that Fe₃O₄ and similar ferrites, some of them attached to heavy metals (Co, Cr), are the dominant magnetic contributors arising from anthropogenic high-temperature processes, e.g. due to traffic emissions. Importantly, nasal cytologic samples collected from residents of both central and suburban areas showed same pattern in what concerns magnetic behavior, thus verifying the critical role of nanosized magnetic particles in the assessment of air pollution threats. Despite the inherent statistical limitations of our study, such findings also indicate the potential transmission of infectious pathogens by means of pollution-derived nanoparticles into the respiratory system of the human body.

Hydrogen peroxide (H₂O₂), as a common disinfectant, has been extensively used in aquaculture. The toxicity of high ambient H₂O₂ for gills and liver of fish has received attention from many researchers. However, whether H₂O₂ exposure induced brain injury and neurotoxicity has not been reported in fish. Therefore, this study aimed to explore the potential mechanism of H₂O₂ toxicity in brain of common carp via transcriptome analysis and biochemical parameter detection. The fish were exposed to 0 (control) and 1 mM of H₂O₂ for 1 h per day lasting 14 days. The results showed that H₂O₂ exposure caused oxidative damage in brain evidenced by decreased glutathione (GSH), total antioxidant capacity (T-AOC) and nicotinamide adenine dinucleotide (NAD⁺) levels, and increased formation of malondialdehyde (MDA) and 8-hydroxy-2′-deoxyguanosine (8-OHdG). Meanwhile, H₂O₂ exposure reduced 5-hydroxytryptamine (5-HT) level, and down-regulated tryptophan hydroxylase 1 (tph1a), tph2, 5-hydroxytryptamine receptor 1A-beta (htr1ab) and htr2b expression in brain. Transcriptome analysis showed that H₂O₂ exposure up-regulated 604 genes and down-regulated 1209 genes in brain. Go enrichment displayed that the differently expressed genes (DEGs) were enriched mainly in cellular process, single-organism process, metabolic process, and biological regulation in the biological process category. Further, KEGG enrichment indicated that H₂O₂ exposure led to dysregulation of neurotransmitter signals including depression of glutamatergic synapse, GABAergic synapse and endocannabinoid signaling. Also, we found the alteration of three key pathways including calcium, cAMP and HIF-1 in brain after H₂O₂ exposure. In conclusion, our data indicated that H₂O₂ exposure induced oxidative damage and neurotoxicity, possibly related to dysregulation of neurotransmitters and calcium, cAMP and HIF-1 signaling pathways, which may adversely affect learning, memory and social responses of common carp. This study provided novel insight into biological effects and underlying mechanism of H₂O₂ toxicity in aquatic animal, and contributed to proper application of H₂O₂ in aquaculture.

Fuel additive methylcyclopentadienyl manganese tricarbonyl (MMT) is counted as an organic manganese (Mn)-derived compound. The toxic effects of Mn (alone and complexed) on dopaminergic (DA) neurotransmission have been investigated in both cellular and animal models. However, the impact of environmentally relevant Mn exposure on DA neurodevelopment is rather poorly understood. In the present study, the MMT dose of 100 μM (about 5 mg Mn/L) caused up-regulation of DA-related genes in association with cell body swelling and increase in the number of DA neurons of the ventral diencephalon subpopulation DC2. Furthermore, our analysis identified significant brain Mn bioaccumulation and enhancement of total dopamine levels in association with locomotor hyperactivity. Although DA levels were restored at adulthood, we observed a deficit in the acquisition and consolidation of memory. Collectively, these findings suggest that developmental exposure to low-level MMT-derived Mn is responsible for the selective alteration of diencephalic DA neurons and with long-lasting effects on fish explorative behaviour in adulthood.

Hypoxia (low oxygen) often occurs in aquatic ecosystems that receive effluent from municipal wastewater treatment plants (WWTP). The combination of hypoxia and WWTP effluent could impair fish health, because WWTP effluent contains multiple contaminants that could disrupt the physiological pathways fish use to cope with hypoxia, but the interactive effects of these stressors on fish physiology are poorly understood. We have examined this issue by exposing mummichog killifish (Fundulus heteroclitus) to hypoxia (5 and 2 kPa O₂) and/or 100% WWTP effluent for 21 days in a full factorial design. We then measured hypoxia tolerance, whole-animal metabolism, gill morphology, haematology, and tissue metabolites. In clean water, killifish responded to chronic hypoxia with improvements in hypoxia tolerance, as reflected by increases in time to loss of equilibrium at 0.5 kPa (tLOE). These improvements occurred in association with increases in the exposed surface of gill lamellae that resulted from a regression of interlamellar cell mass (ILCM). Concurrent exposure to wastewater attenuated the increases in tLOE and gill remodeling in chronic hypoxia, and nearly depleted brain glycogen stores. Therefore, exposure to WWTP effluent can disrupt the physiological mechanisms fish use to cope with chronic hypoxia and impair hypoxia tolerance. Our research suggests that the combination of stressors near WWTPs can have interactive effects on the physiology and health of fish.

Although concerns have been raised about the adverse effects of triphenyl phosphate (TPhP) on female fertility, its risk to ovarian functioning remains unknown. In this study, female C57BL/6 mice at postnatal day 21 were exposed on a daily basis to TPhP dose of 2, 10, and 50 mg/kg for 40 days. A significant delay in pubertal timing was observed in the mice exposed to 50 mg/kg of TPhP. An estrogen-responsive reporter transgenic mice assay demonstrated that TPhP significantly downregulated the estrogen receptor (ER) signaling by 45.1% in the whole body in the 50 mg/kg group, and by 14.7–43.7% in the uterus for all exposure groups compared with the control. This strong antagonistic activity of TPhP toward ER explained the delay in pubertal timing. A significant reduction in the number of follicles in all stages was observed in mice after being exposed to TPhP for 40 days at concentrations of 10 and 50 mg/kg, resulting in a decline of the ovarian reserve. The elevation of the follicle-stimulating hormone concentration may have contributed to this phenomenon, as controlled by the antagonistic activity of TPhP toward ER in the brain. The toxic effects of TPhP on ovarian functioning highlight this chemical as a potential risk factor for female fertility.

Global climate change (GCC) significantly affects aquatic ecosystems. Continual use of pyrethroid insecticides results in contamination of these ecosystems and concurrent GCC raises the potential for synergistic effects. Resistance to pyrethroids has been documented in Hyalella azteca, a common epibenthic amphipod and model organism. Resistant H. azteca can bioconcentrate elevated amounts of pyrethroids and represent a threat to consumers via trophic transfer. In the present study, a predator of H. azteca, the inland silverside (Menidia beryllina), was used to examine the impacts of GCC on pyrethroid bioaccumulation via trophic transfer from resistant prey organisms. M. beryllina were fed ¹⁴C-permethrin dosed pyrethroid-resistant H. azteca for 14 days at three salinities (6, 13 and 20 practical salinity units (PSU)) and two temperatures (18 and 23 °C). Fish were analyzed for total body residues, percent parent compound and percent metabolites. Gene expression in liver and brain tissue were evaluated to assess whether dietary bioaccumulation of permethrin would impact detoxification processes, metabolism, and general stress responses. M. beryllina bioaccumulated significant amounts of permethrin across all treatments, ranging from 39 to 557 ng g⁻¹ lipid. No statistically significant effect of temperature was found on total bioaccumulation. Salinity had a significant effect on total bioaccumulation, owing to greater bioaccumulation at 6 PSU compared to 13 and 20 PSU, which may be due to alterations to xenobiotic elimination. Permethrin bioaccumulation and the interaction with temperature and salinity elicited significant transcriptional responses in genes relating to detoxification, growth, development, and immune response. Given the increased prevalence of pesticide-resistant aquatic invertebrates, GCC-induced alterations to temperature and salinity, and the predicted increase in pesticide usage, these findings suggest trophic transfer may play an important role in pesticide bioaccumulation and effects in predatory fish.

Dichlorvos is a common crop insecticide widely used by people which causes extensive and serious environmental pollution. However, it has been shown that organophosphorus poisoning causes energy metabolism and neural disorders. The overall purpose of this study was to investigate the damage to brain tissue and the changes in AMPK signaling pathway-related gene expression after dichlorvos poisoning in chickens. White-feathered broiler chickens, as the research subjects of this experiment, were divided into three groups: control group, low-dose group (77.5% dichlorvos at 1.13 mg/kg dose) and high-dose group (77.5% dichlorvos at 10.2 mg/kg dose). Clinical symptoms were observed after modeling, and an integrative analysis was conducted using HE staining microscopy, immune-histochemical microscopy, electron microscopy and PCR arrays. The results showed that the high-dose group had more obvious dyspnea, salivation, convulsion and other neurological phenomena. Pathological sections showed that nuclear disintegration of neurons was most obvious in the low-dose group, and apoptosis of brain cells was most obvious in the high-dose group, and the mitochondrial structure was destroyed in the two poisoned group, i.e. low-dose group and high-dose group. PCR arrays showed that AMPK signaling pathway was inhibited and the expressions of genes involved in energy metabolism (ACACA and PRKAA1) were significantly changed. Furthermore, genes associated with protein synthesis (EIF4EBP1) were significantly upregulated. FASN and HMGCR expressions were significantly increased. There were significant changes in the expressions of cell cycle-related genes (STK11, TP53 and FOXO3). Organophosphate poisoning can cause a lot of nuclear disintegration of brain neurons, increases cell apoptosis, disrupts the energy metabolism of mitochondrial structure, and inhibits the AMPK signaling pathway. These results provide a certain idea and basis for studying the mechanism of AMPK signaling after organophosphorus poisoning and provide a research basis for the prevention and treatment of organophosphorus poisoning.