The short-term alteration of peripheral cytokines may be an early adverse health effect of PM₂.₅ exposure and may be further associated with cardiovascular disease. We conducted a randomized, double-blind crossover trial using true or sham air filtration among 54 healthy college students in Beijing to investigate the potential benefits of short-term indoor air filtration and the adverse health effects of time-weighted personal PM₂.₅ exposure through inflammatory cytokines. The participants randomly received true or sham air filtration intervention for a week, and the treatment was changed after a two-week washout period. Peripheral blood samples were collected after each intervention period to measure 38 inflammatory cytokines. A linear mixed-effects model was applied to estimate the impacts of air purification or a 10 μg/m³ PM₂.₅ exposure increase on cytokines. Lag effects of PM₂.₅ exposure were analyzed using single-day and moving average lag models. Air filtration reduced indoor and time-weighted average personal PM₂.₅ concentrations by 69.0% (from 33.6 to 10.4 μg/m³) and 40.3% (from 40.6 to 24.3 μg/m³), respectively. We observed a significant association of PM₂.₅ exposure with growth-regulated alpha protein (GRO-α) of −11.3% (95%CI: 17.0%, −5.4%). In the lag models, significant associations between personal PM₂.₅ exposure and interleukin-1 receptor antagonist (IL-1Ra), monocyte chemotactic protein (MCP-1), and eotaxin were obtained at lag0, while associations with cytokines including vascular endothelial growth factor (VEGF), epidermal growth factor (EGF), fibroblast growth factor-2 (FGF-2), granulocyte colony-stimulating factor (G-CSF), macrophage inflammatory protein-1β (MIP-1β), IL-4, tumor necrosis factor-α (TNF-α), and interferon-γ (IFN-γ) were noted at relatively long lagged exposure windows (lag5-lag6). No significant alteration in cytokines was observed under true air filtration intervention. Our study indicates the effectiveness of air filtration on indoor PM₂.₅ reduction. PM₂.₅ exposure may decrease GRO-α levels and change different cytokine levels time-varyingly. Further study is still needed to explore the mechanisms of PM₂.₅ exposure on the inflammatory response.

Ciprofloxacin (Cipro) is commonly detected in water worldwide, however, the ecotoxicological effects to aquatic biota is still not fully understood. In this study, using multiple biomarkers, it was investigated sublethal effects of short-term exposure to Cipro concentrations (1, 10 and 100 μg.L⁻¹) in the Neotropical catfish Rhamdia quelen compared to non-exposure treatment (Control). After 96 h of exposure, the fishes were anesthetized for blood collection to hematological and genotoxicity biomarkers analysis. After euthanasia, the brain and muscle were sampled for biochemical biomarkers analyses. Gills, liver and posterior kidney for genotoxicity, biochemical and histopathological biomarkers analysis and anterior intestine for histopathological biomarkers analysis. Genotoxicity was observed in all tissues, regardless of the Cipro concentrations. Hematological alterations, such as reduction of the number of erythrocytes and leucocytes, as well as in hematocrit concentration and histopathological damages, such as reduction of microridges in gill epithelium and necrosis in liver and posterior kidney, occurred mainly at 100 μg.L⁻¹. In addition, at 100 μg.L⁻¹, Cipro increased antioxidant system activity (Catalase in liver and posterior kidney). These results demonstrated that under short-term exposure, Cipro causes toxic effects in R. quelen that demands attention and surveillance of environmental aquatic concentrations of this antibiotic.

PM₂.₅ (particulate matter ≤2.5 μm in aerodynamic diameter) is a major urban air pollutant worldwide. Its effects on the respiratory system of the susceptible population have been less characterized. This study aimed to estimate the association of short-term PM₂.₅ exposure with respiratory outcomes of the retired adults, and to examine whether these associations were stronger among the subjects with GSTT-null genotype. 32 healthy subjects (55–77 years) were recruited for five follow-up examinations. Ambient concentrations of PM₂.₅ were monitored consecutively for 7 days prior to physical examination. Pulmonary outcomes including forced vital capacity (FVC), forced expiratory volume in 1 s (FEV₁), peak expiratory flow (PEF), and fractional exhaled nitric oxide (FeNO), and nasal fluid concentrations of 8-epi-prostaglandin F2 alpha (8-epi-PGF2α), tumor necrosis factor-α (TNF-α), interleukin-8 (IL-8) and IL-1β were measured. A linear mixed-effect model was introduced to evaluate the associations of PM₂.₅ concentrations with respiratory outcomes. Additionally, GSTT1 genotype-based stratification was performed to characterize modification on PM₂.₅-related respiratory outcomes. We found that a 10 μg/m³ increase in PM₂.₅ was associated with decreases of 0.52 L (95% confidence interval [CI]: -1.04, -0.002), 0.64 L (95% CI: -1.13, -0.16), 0.1 (95% CI: -0.23, 0.04) and 2.87 L/s (95% CI: -5.09, -0.64) in FVC, FEV₁, FEV₁/FVC ratio and PEF at lag 2, respectively. Meanwhile, marked increases of 80.82% (95% CI: 5.13%, 156.50%) in IL-8, 77.14% (95% CI: 1.88%, 152.40%) in IL-1β and 67.87% (95% CI: 14.85%, 120.88%) in 8-epi-PGF2α were observed as PM₂.₅ concentration increased by 10 μg/m³ at lag 2. Notably, PM₂.₅-associated decreases in FVC and PEF and increase in FeNO were stronger among the subjects with GSTT1-null genotype. In summary, short-term exposure to PM₂.₅ is associated with nasal inflammation, oxidative stress and lung function reduction in the retired subjects. Lung function reduction and inflammation are stronger among the subjects with GSTT1-null genotype.

Freshwater salinization is a rapidly emerging ecological issue and is correlated with significant declines in aquatic biodiversity. It remains unclear how changing salinity regimes affect the physiology of sensitive aquatic insects. We used the parthenogenetic mayfly, Neocloeon triangulifer, to ask how ionic exposure history alters physiological processes and responses to subsequent major ion exposures. Using radiotracers (²²Na, ³⁵SO₄, and ⁴⁵Ca), we observed that mayflies chronically reared in elevated sodium or sulfate (157 mg L⁻¹ Na or 667 mg L⁻¹ SO₄) had 2-fold (p < 0.0001) and 8-fold (p < 0.0001) lower ion uptake rates than mayflies reared in dilute control water (16 mg L⁻¹ Na and 23 mg L⁻¹ SO₄) and subsequently transferred to elevated salinities, respectively. These acclimatory ion transport changes provided protection in 96-h toxicity bioassays for sodium, but not sulfate. Interestingly, calcium uptake was uniformly much lower and minimally influenced by exposure history, but was poorly tolerated in the toxicity bioassays. With qRT-PCR, we observed that the expression of many ion transporter genes in mayflies was influenced by elevated salinity in an ion-specific manner (general upregulation in response to sulfate, downregulation in response to calcium). Elevated sodium exposure had minimal influence on the same genes. Finally, we provide novel light microscopic evidence of histomorphological changes within the epithelium of the Malpighian tubules (insect primary excretory system) that undergoes cellular degeneration and necrosis secondary to calcium toxicity. We conclude that physiological plasticity to salinity stress is ion-specific and provide evidence for ion-specific toxicity mechanisms in N. triangulifer.

Fumonisins (FBs) are mycotoxins that are widely distributed in crops and feed, and ingestion of FBs -contaminated crops is harmful to animal health. Furthermore, it is unknown if Fumonisins B1 (FB1) can cause intestinal toxicity. To investigate FB1-induced intestinal toxicity, mice were treated with 0 or 5 mg/kg FB1 by gavage administration for 42 days. Histopathology indicated that FB1 exposure caused proliferation of intestinal epithelial cells, intestinal villi and epithelial layer shedding, intestinal gland atrophy, and necrosis. Notably, FB1 interfered with nuclear xenobiotic receptors (NXR) homeostasis by regulating the level of aryl hydrocarbon receptor (AHR), constitutive androstane receptor (CAR), pregnane X receptor (PXR) and downstream target genes (CYP450s). Moreover, abnormal expression of inflammatory cytokines (IL-1β, IL-2, IL-4, IL-10, and TNF-α) indicated the occurrence of inflammation. The present study provides new insights regarding the mechanism of FB1-induced intestinal toxicity through activating the NXR system and by triggering inflammatory responses in the intestinal tract in mice.

Interactions between the intestine and the liver, the so-called ‘gut-liver axis’, play a crucial role in the onset of hepatic steatosis and non-alcoholic fatty liver disease. However, not much is known about the impact of environmental pollutants on the gut-liver axis and consequent hepatic steatosis. Bisphenol A (BPA), a widely used plasticiser, is an important environmental contaminant that affects gut microbiota. We hypothesised that BPA induces hepatic steatosis by promoting gut microbiota dysbiosis and activating the gut-liver axis. In this study, male CD-1 mice were fed with diet containing BPA (50 μg/kg body weight/day) for 24 weeks. Dietary exposure to BPA increased lipid contents and fat accumulation in the liver. Analysis of 16 S rRNA gene sequencing revealed that the diversity of gut microbiota reduced and the composition of gut microbiota was altered in the BPA-fed mice. Further, the abundance of Proteobacteria, a marker of dysbacteria, increased, whereas the abundance of Akkermansia, a gut microbe associated with increased gut barrier function and reduced inflammation, markedly decreased. Expression levels of intestinal tight junction proteins (zona occludens-1 and occludin) also decreased drastically, leading to increased intestinal permeability and elevated levels of endotoxins. Furthermore, BPA up-regulated the expression of Toll-like receptor 4 (TLR4) and phosphorylation of nuclear factor-kappa B (NF-κB) in the liver and increased the production of inflammatory cytokines, including interleukin-1β, interleukin-18, tumour necrosis factor-α, and interleukin-6. Take together, our work indicated that dietary intake of BPA induced hepatic steatosis, and this was closely related to dysbiosis of gut microbiota, elevated endotoxin levels, and increased liver inflammation through the TLR4/NF-κB pathway.

Pyrazole derivatives display diverse biological and pharmacological activities. The aim of this study is to investigate the antioxidant properties of a novel pyrazolecarboxamide derivative (4-amino-N-[(4-chlorophenyl)]-3-methyl-1-phenyl-1H-thieno [2, 3-c] pyrazole-5-carboxamide) in African catfish, Clarias gariepinus, exposed to 1 mg/L PbNO₃. Fish were intramuscularly injected with pyrazole-5-carboxamidederivative according to the following groupings: Group 1 (control), Group 2 (1 mg/L lead nitrate), Group 3 (1 mg/L lead nitrate + 5 mg pyrazole derivative/kg body weight), and Group 4 (1 mg/L lead nitrate + 10 mg pyrazole derivative/kg body weight) for two weeks and four weeks. Lead nitrate (1 mg/L) caused significant elevation of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), creatinine, uric acid, cholesterol, and glucose-6-phosphate dehydrogenase (G6PDH) compared to the control group after two and four weeks of exposure, while serum total lipids, alkaline phosphatase (ALP), and lactate dehydrogenase (LDH) were significantly reduced compared to the control group. Furthermore, levels of antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) and total antioxidant capacity (TAC) were reduced in group 2 compared to the control group. However, in group 2, hepatic lipid peroxidation (LPO) and DNA fragmentation percentage were significantly increased compared to the control group. Histopathological changes in the liver of lead-exposed groups included marked disturbance of hepatic tissue organization, degeneration of hepatocytes, dilation of blood sinusoids and the central vein as well as necrosis. Injection of pyrazole derivative for two weeks and four weeks reversed alterations in biochemical parameters, antioxidant biomarkers, lipid peroxidation, hepatic DNA damage, and histopathological changes in liver tissue induced by 1 mg/L lead nitrate. This amelioration was higher in response to high-dose pyrazole derivative (10 mg) at the fourth week of exposure, showing concentration-and time-dependency. Overall, the sensitized derivative pyrazolecarboxamide is likely a useful tool to minimize the effects of lead toxicity due to its potent antioxidant activity.

Pollution of marine environments with microplastic particles (i.e. plastic fragments <5 mm) has increased rapidly during the last decades. As these particles are mainly of terrestrial origin, coastal ecosystems such as coral reefs are particularly threatened. Recent studies revealed that microplastic ingestion can have adverse effects on marine invertebrates. However, little is known about its effects on small-polyp stony corals that are the main framework builders in coral reefs. The goal of this study is to characterise how different coral species I) respond to microplastic particles and whether the exposure might II) lead to health effects. Therefore, six small-polyp stony coral species belonging to the genera Acropora, Pocillopora, and Porites were exposed to microplastics (polyethylene, size 37–163 μm, concentration ca. 4000 particles L−1) over four weeks, and responses and effects on health were documented.The study showed that the corals responded differentially to microplastics. Cleaning mechanisms (direct interaction, mucus production) but also feeding interactions (i.e. interaction with mesenterial filaments, ingestion, and egestion) were observed. Additionally, passive contact through overgrowth was documented. In five of the six studied species, negative effects on health (i.e. bleaching and tissue necrosis) were reported.We here provide preliminary knowledge about coral-microplastic-interactions. The results call for further investigations of the effects of realistic microplastic concentrations on growth, reproduction, and survival of stony corals. This might lead to a better understanding of resilience capacities in coral reef ecosystems.