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.

Microbiota associated with airborne particulate matter (PM) is an important indicator of indoor pollution as they can be pathogenic and cause serious health threats to the exposed occupants. Present study aimed to investigate the level of culturable microbes associated with PM and their toxicological characterization in urban and rural houses of Pune city. Highest concentration of bacterial aerosols observed to be associated with PM₁₀ size fraction in urban site (2136 ± 285 CFU/m³) whereas maximum fungal concentration has been measured in rural houses (1521 ± 302 CFU/m³). Predominantly found bacterial species were Bacillus sp., S. aureus, and Pseudomonas aeruginosa and fungal species were Aspergillus sp., Cladosporium sp., and Penicillium sp. in both urban and rural residential premises. Concentration of endotoxin measured using the kinetic Limulus Amebocyte Lysate assay exhibited that the level of endotoxin in both urban and rural sites are associated with household characteristics and the activities performed in indoor as well as outdoor. Cell free DTT assay confirmed the ability of these airborne microbes to induce the production of reactive oxygen species (ROS) varying along with the types of microorganisms. On exposure of A549 cells to airborne microbes, a significant decrease in cell viability was observed in terms of both necrosis and apoptosis pathway. Elevated production of nitric oxide (NO) and proinflammatory cytokines in epithelial cells and macrophages clearly suggest the inflammatory nature of these airborne microbes. Results derived from the present study demonstrated that the indoor air of urban and rural houses of Pune is contaminated in terms of microbial load. Therefore, attention should be paid to control the factors favoring the microbial growth in order to safeguard the health of exposed inhabitants.

Heavy metals (HMs) in an aquatic environment mainly affects fish, and thus, fish are convenient pollution bio-indicators. In this study, the toxic effects of HM mixture (chromium (Cr), cadmium (Cd), copper (Cu)) in 0 mg/L to 3.2 mg/L concentration range was investigated in Cyprinus carpio (28 days). HM accumulation, histopathology, oxidative stress, and gut microbial changes were evaluated. HMs accumulated in the order of Cr > Cu > Cd, primarily in the kidneys and finally scales. Reactive oxygen species generation increased in all exposure groups up to day 14, with maximum generation at 3.2 mg/L mixture, which later decreased on day 28 in all. Malondialdehydeand and superoxide dismutase levels increased from day 7 to 28 with increased HM concentrations, while total protein showed an inverse trend. Gill histopathology showed major changes such as uplifted and disintegrated primary lamella, and secondary lamella shortening. The kidneys were characterized by glomerular necrosis, Bowman’s capsule expansion, and tubular space dilatation. Proteobacteria and Firmicutes abundance increased up to 59.4% and 99.16% in 0.8 mg/L and 3.2 mg/L treatment groups, respectively. This study provided a better understanding on the physiology and gut microbiota alteration in C. carpio under multiple HM stress.

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.

Previous aquaria-based experiments have shown dissolution and leaching of metals, especially copper (Cu), from the simulated sediment plumes generated during mining activities resulting in a pronounced increase of Cu contamination in the surrounding seawater. Metals are bioavailable to corals with food, through ingestion (particulate phase) and through tissue-facilitated transport (passive diffusion). With corals being particularly vulnerable to metal contamination, resuspension of metal-bearing sediments during mining activities represents an important ecological threat. This study was undertaken to evaluate the impact of acute copper exposure (LC50;96 h) on the survival of the cold-water octocoral Dentomuricea aff. meteor. The experimental design was divided in two stages. In stage one, a Cu range-finding toxicity test was performed using Cu dilutions in filtered seawater with concentrations of 0 (control); 60; 150; 250; 450; 600 μg/L. Coral mortality was investigated visually based on the percent surface area of tissue changing from natural yellow colour to black colour indicative of tissue necrosis and death. In stage two, we used the results obtained in the range-finding experiment, to define sub-lethal Cu exposure treatments and exposed D. meteor to Cu concentration of 0 (control); 50; 100; 150; 200; 250 μg/L for 96 h. The corals physical conditions were inspected daily and seawater conditions recorded. Corals were considered dead when all of their tissue turned black. The LC50 value was calculated with regression analysis following Probits methodology. Our results indicate that Cu LC50;96 h for the octocoral D. meteor is 137 μg/L.

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.

Studies have linked gaseous air pollutants to multiple health effects via inflammatory pathways. Several major inflammatory biomarkers, including C-reactive protein (CRP), fibrinogen, interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) have also been considered as predictors of cardiovascular disease. However, there has been no meta-analysis to evaluate the associations between gaseous air pollutants and these typical biomarkers of inflammation to date. To evaluate the overall associations between short-term and long-term exposures to ambient ozone (O₃), nitrogen dioxide (NO₂), sulfur dioxide (SO₂), carbon dioxide (CO) and major inflammatory biomarkers including CRP, fibrinogen, IL-6 and TNF-α. A meta-analysis was conducted for publications from PubMed, Web of Science, Scopus and EMBASE databases up to Feb 1st, 2021. The meta-analysis included 38 studies conducted among 210,438 participants. Generally, we only observed significant positive associations between short-term exposures to gaseous air pollutants and inflammatory biomarkers. For a 10 μg/m³ increase in short-term exposure to O₃, NO₂, and SO₂, there were significant increases of 1.05% (95%CI: 0.09%, 2.02%), 1.60% (95%CI: 0.49%, 2.72%), and 10.44% (95%CI: 4.20%, 17.05%) in CRP, respectively. Meanwhile, a 10 μg/m³ increase in NO₂ was also associated with a 4.85% (95%CI: 1.10%, 8.73%) increase in TNF-α. Long-term exposures to gaseous air pollutants were not statistically associated with these biomarkers, but the study numbers were relatively small. Subgroup analyses found more apparent associations in studies with better study design, higher quality, and smaller sample size. Meanwhile, the associations also varied across studies conducted in different geographical regions. Short-term exposure to gaseous air pollutants is associated with increased levels of circulating inflammatory biomarkers, suggesting that a systemic inflammatory state is activated upon exposure. More studies on long-term exposure to gaseous air pollutants and inflammatory biomarkers are warranted to verify the associations.

The wetland ecosystem (WE) is subject to pollution by many anthropogenic activities, including domestic and industrial effluents. These effluents may contain toxic heavy metals that can interact within the aquatic ecosystem and have a capacity to disturb the metabolic activities, histological profile, and genetic structure and functions in aquatic species inhabiting the environment. The present study observed the karyological and histological alterations in gills of the freshwater fish, Mozambique tilapia, Oreochromis mossambicus in two different sublethal concentrations (1% and 3%) of heavy metals in 7, 15, and 30 days of experimental periods. The heavy metals induced various structural damages such as ring chromosome, sister chromatid exchange, acrocentric association region, condensed chromosomal morphology, heterochromatin region, and nucleolar organizer region in the chromosomes of O. mossambicus treated with 1% and 3% sublethal concentrations of water sample collected from Pallikaranai wetland ecosystem. Gills exposed to 1% and 3% effluent exhibited several variations in the respiratory surfaces of gill arches or lamellae in the light and scanning microscopical study. The gills exposed to 1% concentration for 30 days showed marked necrosis, and the secondary lamellae showed the lamellar membrane's dissolution. Exposure of gills to raw effluent in the field condition was observed in the presence of Cd, Pb, Cr, Cu, and Zn. Thus, this present study shows the environmental deterioration by heavy metal pollution on the structure of the gills in tilapia.