The gut microbiota is important for maintaining homeostasis of the host. Gut microbes represent the initial site for toxicant processing following dietary exposures to environmental contaminants. The diet is the primary route of exposure to polychlorinated biphenyls (PCBs), which are absorbed via the gut, and subsequently interfere with neurodevelopment and behavior. Developmental exposures to PCBs have been linked to increased risk of neurodevelopmental disorders (NDD), including autism spectrum disorder (ASD), which are also associated with a high prevalence of gastrointestinal (GI) distress and intestinal dysbiosis. We hypothesized that developmental PCB exposure impacts colonization of the gut microbiota, resulting in GI pathophysiology, in a genetically susceptible host. Mouse dams expressing two heritable human mutations (double mutants [DM]) that result in abnormal Ca²⁺ dynamics and produce behavioral deficits (gain of function mutation in the ryanodine receptor 1 [T4826I-RYR1] and a human CGG repeat expansion [170–200 CGG repeats] in the fragile X mental retardation gene 1 [FMR1 premutation]). DM and congenic wild type (WT) controls were exposed to PCBs (0–6 mg/kg/d) in the diet starting 2 weeks before gestation and continuing through postnatal day 21 (P21). Intestinal physiology (Ussing chambers), inflammation (qPCR) and gut microbiome (16S sequencing) studies were performed in offspring mice (P28–P30). Developmental exposure to PCBs in the maternal diet caused significant mucosal barrier defects in ileum and colon (increased secretory state and tight junction permeability) of juvenile DM mice. Furthermore, PCB exposure increased the intestinal inflammatory profile (Il6, Il1β, and Il22), and resulted in dysbiosis of the gut microbiota, including altered β-diversity, in juvenile DM mice developmentally exposed to 1 mg/kg/d PCBs when compared to WT controls. Collectively, these findings demonstrate a novel interaction between PCB exposure and the gut microbiota in a genetically susceptible host that provide novel insight into environmental risk factors for neurodevelopmental disorders.

The interrelationships among long-term ambient air pollution exposure, emotional distress and cognitive decline in older adulthood remain unclear. Long-term exposure may impact cognitive performance and subsequently impact emotional health. Conversely, exposure may initially be associated with emotional distress followed by declines in cognitive performance. Here we tested the inter-relationship between global cognitive ability, emotional distress, and exposure to PM₂.₅ (particulate matter with aerodynamic diameter <2.5 μm) and NO₂ (nitrogen dioxide) in 6118 older women (aged 70.6 ± 3.8 years) from the Women’s Health Initiative Memory Study. Annual exposure to PM₂.₅ (interquartile range [IQR] = 3.37 μg/m³) and NO₂ (IQR = 9.00 ppb) was estimated at the participant’s residence using regionalized national universal kriging models and averaged over the 3-year period before the baseline assessment. Using structural equation mediation models, a latent factor capturing emotional distress was constructed using item-level data from the 6-item Center for Epidemiological Studies Depression Scale and the Short Form Health Survey Emotional Well-Being scale at baseline and one-year follow-up. Trajectories of global cognitive performance, assessed by the Modified-Mini Mental State Examination (3MS) annually up to 12 years, were estimated. All effects reported were adjusted for important confounders. Increases in PM₂.₅ (β = -0.144 per IQR; 95% CI = −0.261; −0.028) and NO₂ (β = −0.157 per IQR; 95% CI = −0.291; −0.022) were associated with lower initial 3MS performance. Lower 3MS performance was associated with increased emotional distress (β = −0.008; 95% CI = −0.015; −0.002) over the subsequent year. Significant indirect effect of both exposures on increases in emotional distress mediated by exposure effects on worse global cognitive performance were present. No statistically significant indirect associations were found between exposures and 3MS trajectories putatively mediated by baseline emotional distress. Our study findings support cognitive aging processes as a mediator of the association between PM₂.₅ and NO₂ exposure and emotional distress in later-life.

In February 2014, the coalmine adjacent to the Hazelwood Power Station in the Latrobe Valley of Victoria, Australia, caught fire, with residents from the nearby town of Morwell and the wider area exposed to smoke for six weeks. Although there was evidence linking the mine-fire event with psychological distress, no studies have evaluated the degree of distress in relation to the level of smoke exposure. We aimed to investigate the exposure-response relationship between particulate matter 2.5 μm or less in diameter (PM₂.₅) released during the Hazelwood mine fire event and long-term symptoms of posttraumatic distress in the affected community, including the consideration of other key factors. A total of 3096 Morwell residents, and 960 residents from the largely unexposed comparison community of Sale, were assessed for symptoms of posttraumatic distress 2.5 years after the Hazelwood incident using the Impact of Events Scale-Revised (IES-R). Individual-level PM₂.₅ exposure was estimated by mapping participants’ self-reported location data on modelled PM₂.₅ concentrations related to the mine fire. Multivariate linear regression was used to evaluate the exposure-response relationship. Both mean and peak exposure to mine fire-related PM₂.₅ were found to be associated with participant IES-R scores with an interaction effect between age and mean PM₂.₅ exposure also identified. Each 10 μg/m³ increase in mean PM₂.₅ exposure corresponded to a 0.98 increase in IES-R score (95% CI: 0.36 to 1.61), and each 100 μg/m³ increase in peak PM₂.₅ exposure corresponded to a 0.36 increase (95% CI: 0.06 to 0.67). An age-effect was observed, with the exposure-response association found to be stronger for younger adults. The results suggest that increased exposure to PM₂.₅ emissions from the Hazelwood mine fire event was associated with higher levels of psychological distress associated with the mine fire and the most pronounced effect was on younger adults living in the affected community.

A critical comparison of studies that have investigated tissue accumulation and toxicity of TiO2-NPs in fish is necessary to resolve inconsistencies. The present study used identical TiO2-NPs, toxicological endpoints, and fish (juvenile rainbow trout Oncorhynchus mykiss) as previous studies that investigated waterborne and dietary toxicity of TiO2-NPs, and conducted a critical comparison of results after intravenous caudal-vein injection of 50 μg of TiO2-NPs and bulk TiO2. Injected TiO2-NPs accumulated only in kidney (94% of measured Ti) and to a lesser extent in spleen; and injected bulk TiO2 was found only in kidney. No toxicity of TiO2 was observed in kidney, spleen, or other tissues. Critical comparison of these data with previous studies indicates that dietary and waterborne exposures to TiO2-NPs do not lead to Ti accumulation in internal tissues, and previous reports of minor toxicity are inconsistent or attributable to respiratory distress resulting from gill occlusion during waterborne exposure.

The harmful alga Chattonella marina has caused massive fish kills and economic losses worldwide. However, the fish kill mechanisms by C. marina have not been identified. The present study has confirmed that a significant elevation of blood osmolality is the universal response in moribund fish exposed to C. marina and the possible reasons leading to contradictory reports were identified. Both osmotic distress and respiratory impairment are important mechanisms leading to fish kill by C. marina. The susceptibility of marine fish to C. marina appears to be inversely related to their tolerance to hypoxia, with the hypoxia intolerant goldlined seabream being the most susceptible, and the hypoxia tolerant green grouper being the most tolerant to C. marina. Further studies in the marine medaka (Oryzias melastigma) showed that fish susceptibility to C. marina is directly related to susceptibility of the fish to hypoxia, but not related to its tolerance to hypersalinity stress.

Rural communities inhabited on riverbank areas are frequently facing the ever-increasing psychological, social and economic distress due to negative effects of riverbank erosion. This study focused to investigate the impact of climate-based hazards particularly riverbank erosion on human displacement, food security and livelihood of rural riverine households and how vulnerable households act in response. The survey data of 398 households of erosion-prone riverbank area were collected, and group discussions connecting household heads from this area were also used for this study. In human displacement scenario of the last ten years due to riverbank erosion, almost 60% households lost their homestead once while 38% more than three times and forced to displaced. Empirical estimates of households’ food security status indicated the value of Food Security Index 2.11, highlighting households face issue of food security all over the year. Food security issue of vulnerable households is highly related with migration because these households have insufficient employment chances, and coupled with limited or no farming land, they are highly prone to migration. In conclusion, this study estimated that riverbank erosion risk is a co-exist reason of population displacement, increasing rural environmental vulnerability and obstacles to psychological, cultural and socioeconomic development. Implications of local-based proper policy interventions such as developing advance research regarding infusion of agro-based technology packages for emerging Bait areas for developing resilience, human capital development, credit access and institution service are necessary for improving livelihood and food security of these riverbank erosion households. State-based institutions and local community mutually need to focus increasing forestry specifically in riverbank areas to save fertile land from riverbank erosion and reducing environmental pollution. Convalescing livelihood and food security for erosion riverbank households, more employment opportunity needs to provided, investing more in training and education programmes to promoting income-generating activities that subsequently will develop livelihood and food security of households.

In vulnerable subjects, the increase in air pollution worsens the signs of myocardial ischemia. Lockdown during COVID-19 pandemics substantially cleaned the air. The objective of this is to assess the effects of air cleaning due to lockdown on stress echocardiography (SE) results. We enrolled 19 patients with chronic coronary artery disease and/or heart failure referred to SE (semi-supine bicycle exercise, n = 8, or dipyridamole, n = 11). Before and soon after lockdown, we assessed regional wall motion abnormalities (abnormal value: worsening of ≥ 2 segments), B-lines (a sign of pulmonary congestion, 4-site simplified scan, abnormal value ≥ 2), and coronary flow velocity reserve in left anterior descending artery (CFVR, abnormal value < 2.0). Local air quality indicators (same day of SE) of fine particulate matter (PM₂.₅) and nitrogen dioxide (NO₂) were obtained from publicly available data sets of the regional authority of environmental protection. After lockdown, NO₂ concentration decreased from 19 ± 10 to 10 ± 4 μg/m³ (p = 0.006). After lockdown, abnormal responses remained unchanged for ischemia (21% vs 16%, p = ns) and decreased for B-lines (42% vs 5%, p = 0.008) and CFVR (84 vs 42%, p = 0.007). Changes in coronary flow velocity reserve (CFVR) were correlated to same-day variations in NO₂ (r = −0.578, p = 0.010) and preceding 30-day changes in PM₂.₅ (r = −0.518, p = 0.023). After lockdown, air cleaning was associated with a beneficial effect on coronary small vessel dysfunction and alveolar-capillary barrier distress mirrored by improvement of CFVR and B-lines during SE in vulnerable patients. ClinicalTrials.gov Identifier: NCT 030.49995

Two nonionic POEA surfactants (CAS No. 61791-26-2), TA15 and TH30, were tested to establish their acute pathological effects and lethal concentrations (LC₅₀) in Piaractus brachypomus. Both compounds are nonionic surfactants produced by the alkoxylation of ethylene oxide with tallow amine, and they are used in variety of industries such as textiles, paints, metal working, agriculture, and polish manufacture. Fish were exposed to six concentrations of TA15 (0.2–4.0 mg/L) or TH30 (8–140 mg/L) for 96 h. The LC₅₀ for TA15 was 2.08 mg/L and for TH30 47.32 mg/L. The main clinical signs observed in fish exposed to 4 mg/L of TA15 and 32 to 140 mg/L of TH30, were lethargy, loss of shoaling behavior, respiratory distress, changes in swimming pattern, such as, loss of balance and abnormal buoyancy, prolapse of the lower lip and superior location in the water column. The highest concentrations of these compounds induced nervous signs and collapse. The relevant macroscopic lesions were skin and fins erosions with necrotic lysis of the caudal peduncle. In addition, hemorrhages in mouth, branchial arches, and petechial hemorrhages in skin were observed. An increased fluid in the celomic cavity and meningeal hemorrhages were also evident. Organs as gills, liver, brain, and anterior kidney presented severe lesions at the highest concentrations of each compound. For the first time, it is reported lesions in interrenal tissues and choroidal bodies, as well as severe telencephalic lesions associated with the POEA toxicity. These last lesions were more severe in fish exposed to TA15 than to TH30, although the pattern of injuries was similar with both substances. According to the Global Harmonized System of Classification and Labelling of Chemical (GHS) by the United Nations, we reported that TA15 is classified as Acute Category 2 and TH30 is Acute Category 3 for white cachama. Due to the low LC₅₀ and the highly toxic effects of both POEA compounds for neotropical fish, a revision of the regulation of the use of herbicide mixtures by Colombian legislation is necessary.

Concrete is usually the preferred material for construction of structures in contact with water during their service life. Early age exposure to water is beneficial for curing of concrete structures. However, the pollution of water from freshly cast concrete in contact with water has not been investigated in detail. A significant increase in the alkalinity has recently been observed in a stream in contact with freshly installed concrete culverts. High alkalinity has caused distress to fresh water fish in the stream. A preliminary laboratory study was commenced to explore the effect of leaching of alkali into water from freshly placed concrete. Freshly cast concrete specimens were exposed to fresh water, covering a range of conditions observed in the field such as volume of concrete/volume of water, age of exposure and cement content. Analysis of the results indicated that early age contact with fresh concrete can lead to an increase in the pH levels of water up to 11, similar to the levels of pH observed in pore water inside freshly cast concrete. It was noted that until an age of 4 days from casting of concrete, the age of exposure does not significantly affect the changes in the peak pH levels of water. Continuous monitoring of water in contact with concrete also indicated that the pH levels diminish with time, which is attributed to the possible reaction of calcium hydroxide with atmospheric carbon. The paper will present the experimental study, the results, analysis and outcomes as well as planning of a more comprehensive study to observe possible ways of reducing the leaching of alkali from freshly placed concrete.

ABSTRACT: Achieving environmental sustainability has become a core policy agenda of the Moroccan government. The nation’s monotonic dependence on fossil fuels for meeting the local energy demand has been acknowledged as the major cause of environmental distress. Besides, Morocco has traditionally been a major importer of fossil fuels whereby the nation’s fossil fuel dependency could not be phased out to a large extent. Consequently, the greenhouse gas emission figures of Morocco have persistently surged over the years. Moreover, Morocco has large reserves of untapped renewable energy sources which can be employed for producing power without significantly degrading the environment. Against this backdrop, this study explores the renewable energy consumption-carbon dioxide emissions nexus, controlling for economic growth, financial development, and foreign direct investment inflows, in the context of Morocco over the period between 1980 and 2017. In addition, along with the direct impacts, the indirect environmental impacts associated with renewable energy consumption are also scrutinized in this study. The empirical strategy involves the application of econometric methods that are robust to handling structural break issues in the data. Overall, the results reveal that renewable energy consumption curbs carbon dioxide emissions both in the short and long run. In contrast, financial development and foreign direct investment inflows boost carbon dioxide emissions in Morocco. However, these adverse environmental impacts are partially neutralized by facilitating greater renewable energy use within Morocco. The results indicate that renewable energy consumption interacts with financial development and foreign direct investment inflows to jointly reduce the carbon dioxide emission figures of Morocco in the long run. Furthermore, the findings also validate the environmental Kuznets curve hypothesis in the long run only. In line with these key findings, it is recommended that the Moroccan government should adopt relevant policies that can help the nation overcome the existing barriers faced in transitioning from non-renewable to renewable energy use. Simultaneously, it is also necessary for Morocco to achieve environmentally sustainable economic growth by greening its financial sector and revisiting its financial globalization policies.