Microplastics (MPs) are a global environmental concern and pose a serious threat to marine ecosystems. This study aimed to determine the abundance and distribution of MPs in beach sediments (12 beaches), marine biota (6 beaches) and the influence of microbes on MPs degradation in eco-sensitive Palk Bay and Gulf of Mannar coast. The mean MP abundance 65.4 ± 39.8 particles/m² in beach sediments; 0.19 ± 1.3 particles/individual fish and 0.22 ± 0.11 particles g⁻¹ wet weight in barnacles. Polyethylene fragments (33.4%) and fibres (48%) were the most abundant MPs identified in sediments and finfish, respectively. Histopathological examination of fish has revealed health consequences such as respiratory system damage, epithelial degradation and enterocyte vacuolization. In addition, eight bacterial and seventeen fungal strains were isolated from the beached MPs. The results also indicated weathering of MPs due to microbial interactions. Model simulations helped in tracking the fate and transboundary landfall of spilled MPs across the Indian Ocean coastline after the X-Press Pearl disaster. Due to regional circulations induced by the monsoonal wind fields, a potential dispersal of pellets has occurred along the coast of Sri Lanka, but no landfall and ecological damage are predicted along the coast of India.

Air pollution exposure is a public health emergency, which attributes globally to an estimated seven million deaths on a yearly basis We are all exposed to air pollutants, varying from ambient air pollution hanging over cities to dust inside the home. It is a mixture of airborne particulate matter and gases that can be subdivided into three categories based on particle diameter. The smallest category called PM₀.₁ is the most abundant. A fraction of the particles included in this category might enter the blood stream spreading to other parts of the body. As air pollutants can enter the body via the lungs and gut, growing evidence links its exposure to gastrointestinal and respiratory impairments and diseases, like asthma, rhinitis, respiratory tract infections, Crohn's disease, ulcerative colitis, and abdominal pain. It has become evident that there exists a crosstalk between the respiratory and gastrointestinal tracts, commonly referred to as the gut-lung axis. Via microbial secretions, metabolites, immune mediators and lipid profiles, these two separate organ systems can influence each other. Well-known immunomodulators and gut health stimulators are probiotics, prebiotics, together called synbiotics. They might combat air pollution-induced systemic inflammation and oxidative stress by optimizing the microbiota composition and microbial metabolites, thereby stimulating anti-inflammatory pathways and strengthening mucosal and epithelial barriers. Although clinical studies investigating the role of probiotics, prebiotics, and synbiotics in an air pollution setting are lacking, these interventions show promising health promoting effects by affecting the gastrointestinal- and respiratory tract. This review summarizes the current data on how air pollution can affect the gut-lung axis and might impact gut and lung health. It will further elaborate on the potential role of probiotics, prebiotics and synbiotics on the gut-lung axis, and gut and lung health.

Across the planet, winter de-icing practices have caused secondary salinization of freshwater habitats. Many amphibians are vulnerable because of permeable skin and reliance on small ponds, where salinity can be high. Early developmental stages of amphibians are especially sensitive to salt, and larvae developing in salt-polluted environments must osmoregulate through ion exchange in gills. Though ionoregulation in amphibian gills is generally understood, the role of gill morphology remains poorly described. Yet gill structure should affect ionoregulatory capacity, for instance in terms of available surface area. As larval amphibian gills also play critical roles in gas exchange and foraging, changes in gill morphology from salt pollution potentially affect not only osmoregulation, but also respiration and feeding. Here, we used an exposure experiment to quantify salinity effects on larval gill morphology in wood frogs (Rana sylvatica). We measured a suite of morphological traits on gill tufts—where ionoregulation and gas exchange occur—and on gill filters used in feeding. Larvae raised in elevated salinity developed larger gill tufts but with lower surface area to volume ratio. Epithelial cells on these tufts were less circular but occurred at higher densities. Gill filters showed increased spacing, likely reducing feeding efficiency. Many morphological gill traits responded quadratically, suggesting that salinity might induce plasticity in gills at intermediate concentrations until energetic demands exceed plasticity. Together, these changes likely diminish ionoregulatory and respiratory functionality of gill tufts, and compromise feeding functionality of gill filters. Thus, a singular change in aquatic environment from a widespread pollutant appears to generate a suite of consequences via changes in gill morphology. Critically, these changes in traits likely compound the severity of fitness impacts in populations dwelling in salinized environments, whereby ionoregulatory energetic demands should increase respiratory and foraging demands, but in individuals who possess structures poorly adapted for these functions.

The use of biomass for cooking and heating is considered an important factor associated with chronic obstructive pulmonary disease (COPD), but few studies have previously addressed its underlying mechanisms. Therefore, this research aimed to evaluate the effects of biomass-related PM₂.₅ (BRPM₂.₅) exposure on 16HBE human airway epithelial cells and in mice with regard to mitochondrial dysfunction. Our study indicated that BRPM₂.₅ exposure of 16HBE cells resulted in mitochondrial dysfunction, including decreased mitochondrial membrane potential, increased expression of fission proteins-phospho-DRP1, increased mitochondrial ROS (mtROS), and decreased levels of ATP. BRPM₂.₅ altered the mitochondrial metabolism of 16HBE cells by decreasing mitochondrial oxygen consumption and glycolysis. However, Mitochondria targeted peptide SS-31 eliminated mitochondrial ROS and alleviated the ATP deficiency and proinflammatory cytokines release. BRPM2.5 exposure resulted in abnormal mitochondrial morphological alterations both in 16HBE and in lung tissue. Taken together, these results suggest that BRPM₂.₅ has detrimental effects on human airway epithelial cells, leading to mitochondrial dysfunction, abnormal mitochondrial metabolism and altered mitochondrial dynamics. The present study provides the first evidence that disruption of mitochondrial structure and mitochondrial metabolism may be one of the mechanisms of BRPM₂.₅-induced respiratory dysfunction.

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.

When the total ambient PM₂.₅ levels are several-fold higher than the recommended limit, it may be important to study the distributions of different sizes of particulate matter (PM). Here, we assess the distributions of various sizes of total PM₂.₅ for 12 months (on a monthly basis) in New Delhi, India. Importantly, we found that ultrafine particles (i.e., particles <0.5 μm) contribute significantly to total PM₂.₅. PM<₀.₂₅ were the most cytotoxic particles to human lung epithelial cells in all the 12 months. In addition, PM<₀.₂₅ were associated with significantly higher cytotoxicity per unit mass compared to other size fractions constituting PM₂.₅. For any given size of PM, the amount of reactive oxygen species (ROS) generated per unit mass is higher for the month of March as compared to that for the rest of the months in the year. The higher ROS generations for all sizes of PM collected in the month of March was not explained by differences in their metal content values. Our data suggests the lack of correlation between total PM₂.₅ levels and the highly cytotoxic PM<₀.₂₅. In summary, this work establishes the need for policy changes to routinely monitor PM<₀.₂₅ and the necessity to establish exposure limits for PM<₀.₂₅, especially when the total PM₂.₅ levels are breached.

The mosquito Aedes aegypti is a primary vector for major arboviruses, and its control is mainly based on the use of insecticides. Caffeine and spent coffee grounds (CG) are potential agents in controlling Ae. aegypti by reducing survival and blocking larval development. In this study, we analyzed the effects of treatment with common CG (CCG: with caffeine), decaffeinated CG (DCG: with low caffeine), and pure caffeine on the survival, behavior, and morphology of the midgut of Ae. aegypti under laboratory conditions. Third instar larvae (L3) were exposed to different concentrations of CCG, DCG, and caffeine. All compounds significantly affected larval survival, and sublethal concentrations reduced larval locomotor activity, delayed development, and reduced adult life span. Damage to the midgut of treated larvae included changes in epithelial morphology, increased number of peroxidase-positive cells (more abundant in DCG-treated larvae), and caspase 3-positive cells (more abundant in CCG-treated larvae), suggesting that the treatments triggered cell damage, leading to activation of cell death. In addition, the treatments reduced the FMRFamide-positive enteroendocrine cells and dividing cells compared to the control. CG and caffeine have larvicidal effects on Ae. aegypti that warrant field testing for their potential to control mosquitoes.

Inhalation represents the most prevalent route of exposure with Thorium-232 compounds (Th-nitrate/Th-dioxide)/Th-containing dust in real occupational scenario. The present study investigated the mechanism of Th response in normal human alveolar epithelial cells (WI26), exposed to Th-nitrate or colloidal Th-dioxide (1–100 μg/ml, 24–72 h). Assessment in terms of changes in cell morphology, cell proliferation (cell count), plasma membrane integrity (lactate dehydrogenase leakage) and mitochondrial metabolic activity (MTT reduction) showed that Th-dioxide was quantitatively more deleterious than Th-nitrate to WI26 cells. TEM and immunofluorescence analysis suggested that Th-dioxide followed a clathrin/caveolin-mediated endocytosis, however, membrane perforation/non-endocytosis seemed to be the mode of Th internalization in cells exposed to Th-nitrate. Th-estimation by ICP-MS showed significantly higher uptake of Th in cells treated with Th-dioxide than with Th-nitrate at a given concentration. Both Th-dioxide and nitrate were found to increase the level of reactive oxygen species, which seemed to be responsible for lipid peroxidation, alteration in mitochondrial membrane potential and DNA-damage. Amongst HSPs, the protein levels of HSP70 and HSP90 were affected differentially by Th-nitrate/dioxide. Specific inhibitors of ATM (KU55933) or HSP90 (17AAG) were found to increase the Th- cytotoxicity suggesting prosurvival role of these signaling molecules in rescuing the cells from Th-toxicity.

Copper (Cu) is a vital micronutrient required for numerous fundamental biological processes, but excessive Cu poses potential detrimental effects on public and ecosystem health. However, the molecular details linking endoplasmic reticulum (ER) stress and apoptosis in duck renal tubular epithelial cells have not been fully elucidated. In this study, duck renal tubular epithelial cells exposed to Cu sulfate (CuSO₄) (0, 100 and 200 μM) and a PERK inhibitor (GSK2606414, GSK, 1 μM) for 12 h were used to investigate the crosstalk between ER stress and apoptosis under Cu exposure. Cell and ER morphological and functional characteristics, intracellular calcium (Ca²⁺) levels, apoptotic rates, ER stress and apoptosis-related mRNA and protein levels were examined. The results showed that excessive Cu could cause ER expansion and swelling, increase the expression levels of ER stress-associated genes (PERK, eIF2α, ATF4 and CHOP) and proteins (p-PERK and CHOP), induce intracellular Ca²⁺ overload, upregulate the expression levels of apoptosis-associated genes (Bax, Bak1, Caspase9 and Caspase3) and the cleaved-Caspase3 protein, downregulate Bcl-xl and Bcl2 mRNA levels and trigger apoptosis. PERK inhibitor treatment could ameliorate the above changed factors caused by Cu. In conclusion, these findings indicate that excessive Cu could trigger ER stress via activation of the PERK/ATF4/CHOP signaling pathway and that ER stress might aggravate Cu-induced apoptosis in duck renal tubular epithelial cells.

Inter-alpha-trypsin inhibitor heavy chain 4 (ITIH4) is a type II acute-phase protein; however, the role of pulmonary ITIH4 after exposure to air pollution remains unclear. In this study, we investigated the role of ITIH4 in the lungs in response to air pollution. ITIH4 expression in bronchoalveolar lavage fluid (BAL) of 47 healthy human subjects and of Sprague-Dawley rats whole-body exposed to air pollution was determined, and the underlying antiapoptotic and matrix-stabilizing pathways in alveolar epithelial A549 cells induced by diesel exhaust particles (DEPs) as well as ITIH4-knockdown were investigated. We found that an interquartile range (IQR) increase in PM₂.₅ was associated with a decrease of 2.673 ng/mL in ITIH4, an increase of 1.104 pg/mL of 8-isoprostane, and an increase of 6.918 pg/mL of interleukin (IL)-6 in human BAL. In rats, increases in 8-isoprostane, IL-6, and p53 and a decrease in sirtuin-1 (Sirt1) in the lungs and decreases in ITIH4 in the BAL, lungs, and serum were observed after PM₂.₅ and gaseous exposure. ITIH4 levels in lung lysates were correlated with levels in BAL samples (r = 0.377, p < 0.01), whereas ITIH4 levels in BAL were correlated with IL-6 levels (r = −0.420, p < 0.01). ITIH4 expression was significantly reduced in alveolar epithelial A549 cells by DEP in a dose-dependent manner. A decrease in Sirt1 and increases in phosphorylated extracellular signal-regulated kinase (p-ERK) and caspase-3 were observed after DEP exposure and ITIH4-knockdown. In conclusion, air pollution decreased ITIH4 expression in the lungs, which was associated with alveolar epithelial cell senescence and apoptosis. ITIH4 could be a vital protein in regulating alveolar cell destruction and its inhibition after exposure to air pollution.