Detection of morphological and eco-physiological traits of ornamental woody species to assess their potential Net O3 uptake.

Urban greening can improve cities' air quality by filtering the main gaseous pollutants such as tropospheric ozone (O3). However, the pollutant removal capacity offered by woody species strongly depends on eco-physiological and morphological traits. Woody species with higher stomatal conductance (gs) can remove more gases from the atmosphere, but other species can worsen air quality due to high O3 forming potential (OFP), based on their emitting rates of biogenic volatile organic compounds (bVOCs) and Leaf Mass per Area (LMA). Presently, there is a lack of data on eco-physiological (gs, bVOCs emissions) and foliar traits (LMA) for several ornamental species used in urban greening programs, which does not allow assessment of their O3 removal capacity and OFP. This study aimed to (i) parameterize gs, assess bVOCs emissions and LMA of 14 ornamental woody species commonly used in Mediterranean urban greening, and (ii) model their Net O3 uptake. The gs Jarvis model was parameterized considering various environmental conditions alongside isoprene and monoterpene foliar bVOCs emission rates trapped in the field and quantified by gas chromatography-mass spectrometry. The results are helpful for urban planning and landscaping; suggesting that Catalpa bignonioides and Gleditsia triacanthos have excellent O3 removal capacity due to their high maximum gs (gmax) equal to 0.657 and 0.597 mol H2O m-2 s-1. Regarding bVOCs, high isoprene (16.75 µg gdw-1 h-1) and monoterpene (13.12 µg gdw-1 h-1) emission rates were found for Rhamnus alaternus and Cornus mas. In contrast, no bVOCs emissions were detected for Camellia sasanqua and Paulownia tomentosa. In conclusion, 11 species showed a positive Net O3 uptake, while the use of large numbers of R. alaternus, C. mas, and Chamaerops humilis for urban afforestation planning are not recommended due to their potential to induce a deterioration of outdoor air quality.

Dual-Hit: Glyphosate exposure at NOAEL level negatively impacts birth and glia-behavioural measures in heterozygous shank3 mutants.

The omnipresence of environmental contaminants represents a health danger with ramifications for adverse neurological trajectories. Here, we tested the dual-hit hypothesis that continuous exposure to non-observable adverse effect level (NOAEL) glyphosate from pre-natal to adulthood represents a risk factor for neurological-associated adaptations when in the presence of the heterozygote or homozygote mutation of the Shank3 synaptic gene. Ultrasound analysis of pregnant dams revealed patterns of pre-natal mortality with effects dependent on wild-type, Shank3ΔC/+, or Shank3ΔC/ΔC genotypes exposed to NOAEL glyphosate (GLY) compared to unexposed conditions. The postnatal survival rate was negatively impacted, specifically in Shank3ΔC/+ exposed to GLY. Next, the resulting six groups of pups were tracked into adulthood and analyzed for signs of neuroinflammation and neurological adaptions. Sholl's analysis revealed cortical microgliosis across groups exposed to GLY, with Shank3ΔC/+ mice presenting the most significant modifications. Brain tissues were devoid of astrocytosis, except for the perivascular compartment in the cortex in response to GLY. Distinct behavioral adaptations accompanied these cellular modifications, as locomotion and social preference were decreased in Shank3ΔC/+ mice exposed to GLY. Notably, GLY exposure from weaning did not elicit glial or neurological adaptations across groups, indicating the importance of pre-natal contaminant exposure. These results unveil the intersection between continuous pre-natal to adulthood environmental input and a pre-existing synaptic mutation. In an animal model, NOAEL GLY predominantly impacted Shank3ΔC/+ mice, compounding an otherwise mild phenotype compared to Shank3ΔC/ΔC. The possible relevance of these findings to neurodevelopmental risk is critically discussed, along with avenues for future research.

Sublethal chemical stimulation of arthropod parasitoids and parasites of agricultural and environmental importance.

An increasing number of studies have reported stimulation of various organisms in the presence of environmental contaminants. This has created a need to critically evaluate sublethal stimulation and hormetic responses of arthropod parasitoids and parasites following exposure to pesticides and other contaminants. Examining this phenomenon with a focus on arthropods of agricultural and environmental importance serves as the framework for this literature review. This review shows that several pesticides, with diverse chemical structures and different modes of action, applied individually or in combination at sublethal doses, commonly stimulate an array of arthropod parasitoids and parasites. Exposure at sublethal doses can enhance responses related to physiology (e.g., respiration, total lipid content, and total protein content), behavior (e.g., locomotor activity, antennal drumming frequency, host location, and parasitization), and fitness (longevity, growth, fecundity, population net and gross reproduction). Concordantly, the parasitic potential (e.g., infestation efficacy, parasitization rate, and parasitoid/parasite emergence) can be increased, and as a result host activities inhibited. There is some evidence illustrating hormetic dose-responses, but the relevant literature commonly included a limited number and range of doses, precluding a robust differentiation between sub- and superNOAEL (no-observed-adverse-effect level) stimulation. These results reveal a potentially significant threat to ecological health, through stimulation of harmful parasitic organisms by environmental contaminants, and highlight the need to include sublethal stimulation and hormetic responses in relevant ecological pesticide risk assessments. Curiously, considering a more utilitarian view, hormesis may also assist in optimizing mass rearing of biological control agents for field use, a possibility that also remains neglected.

Surface ozone risk to human health and vegetation in tropical region: The case of Thailand.

Tropospheric ozone (O3) is a threat to vegetation and human health over the world, in particular in Asia. Knowledge on O3 impacts on tropical ecosystems is still very limited. An O3 risk assessment to crops, forests, and people from 25 monitoring stations across the tropical and subtropical Thailand during 2005-2018 showed that 44% of sites exceeded the critical levels (CLs) of SOMO35 (i.e., the annual Sum Of daily maximum 8-h Means Over 35 ppb) for human health protection. The concentration-based AOT40 CL (i.e., sum of the hourly exceedances above 40 ppb for daylight hours during the assumed growing season) was exceeded at 52% and 48% of the sites where the main crops rice and maize are present, respectively, and at 88% and 12% of the sites where evergreen or deciduous forests are present, respectively. The flux-based metric PODY (i.e., Phytotoxic Ozone Dose above a threshold Y of uptake) was calculated and was found to exceed the CLs at 1.0%, 1.5%, 20.0%, 1.5%, 0% and 68.0% of the sites where early rice, late rice, early maize, late maize, evergreen forests, and deciduous forests can grow, respectively. Trend analysis indicated that AOT40 increased over the study period (+5.9% year-1), while POD1 decreased (- 5.3% year-1), suggesting that the role of climate change in affecting the environmental factors that control stomatal uptake cannot be neglected. These results contribute novel knowledge on O3 threat to human health, forest productivity, and food security in tropical and subtropical areas.

Natural Extracts Mitigate the Deleterious Effects of Prolonged Intense Physical Exercise on the Cardiovascular and Muscular Systems.

Muscle fatigue is a common symptom induced by exercise. A reversible loss of muscle force is observed with variable rates of recovery depending on the causes or underlying mechanisms. It can not only affect locomotion muscles, but can also affect the heart, in particular after intense prolonged exercise such as marathons and ultra-triathlons. The goal of our study was to explore the effect of four different natural extracts with recognized antioxidant properties on the contractile function of skeletal (locomotion) and cardiac muscles after a prolonged exhausting exercise. Male Wistar rats performed a bout of exhausting exercise on a treadmill for about 2.5 h and were compared to sedentary animals. Some rats received oral treatment of a natural extract (rosemary, buckwheat, Powergrape®, or rapeseed) or the placebo 24 h and 1 h before exercise. Experiments were performed 30 min after the race and after 7 days of recovery. All natural extracts had protective effects both in cardiac and skeletal muscles. The extent of protection was different depending on muscle type and the duration post-exercise (just after and after one-week recovery), including antiarrhythmic effect and anti-diastolic dysfunction for the heart, and faster recovery of contractility for the skeletal muscles. Moreover, the muscular protective effect varied between natural extracts. Our study shows that an acute antioxidant supplementation can protect against acute abnormal endogenous ROS toxicity, induced here by prolonged exhausting exercise.

Nkx2-5 Loss of Function in the His-Purkinje System Hampers Its Maturation and Leads to Mechanical Dysfunction.

The ventricular conduction or His-Purkinje system (VCS) mediates the rapid propagation and precise delivery of electrical activity essential for the synchronization of heartbeats. Mutations in the transcription factor Nkx2-5 have been implicated in a high prevalence of developing ventricular conduction defects or arrhythmias with age. Nkx2-5 heterozygous mutant mice reproduce human phenotypes associated with a hypoplastic His-Purkinje system resulting from defective patterning of the Purkinje fiber network during development. Here, we investigated the role of Nkx2-5 in the mature VCS and the consequences of its loss on cardiac function. Neonatal deletion of Nkx2-5 in the VCS using a Cx40-CreERT2 mouse line provoked apical hypoplasia and maturation defects of the Purkinje fiber network. Genetic tracing analysis demonstrated that neonatal Cx40-positive cells fail to maintain a conductive phenotype after Nkx2-5 deletion. Moreover, we observed a progressive loss of expression of fast-conduction markers in persistent Purkinje fibers. Consequently, Nkx2-5-deleted mice developed conduction defects with progressively reduced QRS amplitude and RSR' complex associated with higher duration. Cardiac function recorded by MRI revealed a reduction in the ejection fraction in the absence of morphological changes. With age, these mice develop a ventricular diastolic dysfunction associated with dyssynchrony and wall-motion abnormalities without indication of fibrosis. These results highlight the requirement of postnatal expression of Nkx2-5 in the maturation and maintenance of a functional Purkinje fiber network to preserve contraction synchrony and cardiac function.

Neurovascular Hypoxia Trajectories Assessed by Photoacoustic Imaging in a Murine Model of Cardiac Arrest and Resuscitation.

Cardiac arrest is a common cause of death annually mainly due to postcardiac arrest syndrome that leads to multiple organ global hypoxia and dysfunction after resuscitation. The ability to quantify vasculature changes and tissue oxygenation is crucial to adapt patient treatment in order to minimize major outcomes after resuscitation. For the first time, we applied high-resolution ultrasound associated with photoacoustic imaging (PAI) to track neurovascular oxygenation and cardiac function trajectories in a murine model of cardiac arrest and resuscitation. We report the preservation of brain oxygenation is greater compared to that in peripheral tissues during the arrest. Furthermore, distinct patterns of cerebral oxygen decay may relate to the support of vital brain functions. In addition, we followed trajectories of cerebral perfusion and cardiac function longitudinally after induced cardiac arrest and resuscitation. Volumetric cerebral oxygen saturation (sO2) decreased 24 h postarrest, but these levels rebounded at one week. However, systolic and diastolic cardiac dysfunction persisted throughout and correlated with cerebral hypoxia. Pathophysiologic biomarker trends, identified via cerebral PAI in preclinical models, could provide new insights into understanding the pathophysiology of cardiac arrest and resuscitation.

Stomatal responses of terrestrial plants to global change.

Quantifying the stomatal responses of plants to global change factors is crucial for modeling terrestrial carbon and water cycles. Here we synthesize worldwide experimental data to show that stomatal conductance (gs) decreases with elevated carbon dioxide (CO2), warming, decreased precipitation, and tropospheric ozone pollution, but increases with increased precipitation and nitrogen (N) deposition. These responses vary with treatment magnitude, plant attributes (ambient gs, vegetation biomes, and plant functional types), and climate. All two-factor combinations (except warming + N deposition) significantly reduce gs, and their individual effects are commonly additive but tend to be antagonistic as the effect sizes increased. We further show that rising CO2 and warming would dominate the future change of plant gs across biomes. The results of our meta-analysis provide a foundation for understanding and predicting plant gs across biomes and guiding manipulative experiment designs in a real world where global change factors do not occur in isolation.

Tocotrienols-enriched Self-nanoemulsifying Drug Delivery System Enhances the Antileukemic Activity of All-trans Retinoic Acid but not Electrocardiogram Alterations Evoked by Its Combination with Arsenic Trioxide.

All-trans retinoic acid and arsenic trioxide are the leading choices for the treatment of acute promyelocytic leukemia. Notwithstanding the impressive differentiative properties of all-trans retinoic acid and the apoptotic properties of arsenic trioxide, some problems still occur in acute promyelocytic leukemia treatment. These problems are due to patients' relapses, mainly related to changes in the ligand-binding domain of RARα (retinoic acid receptor α) and the cardiotoxic effects caused by arsenic trioxide. We previously developed a self-nanoemulsifying drug delivery system enriched with tocotrienols to deliver all-trans retinoic acid (SNEDDS-TRF-ATRA). Herein, we have evaluated if tocotrienols can help revert ATRA resistance in an APL cell line (NB4-R2 compared to sensitive NB4 cells) and mitigate the cardiotoxic effects of arsenic trioxide in a murine model. SNEDDS-TRF-ATRA enhanced all-trans retinoic acid cytotoxicity in NB4-R2 (resistant) cells but not in NB4 (sensitive) cells. Moreover, SNEDDS-TRF-ATRA did not significantly change the differentiative properties of all-trans retinoic acid in both NB4 and NB4-R2 cells. Combined administration of SNEDDS-TRF-ATRA and arsenic trioxide could revert QTc interval prolongation caused by ATO but evoked other electrocardiogram alterations in mice, such as T wave flattening. Therefore, SNEDDS-TRF-ATRA may enhance the antileukemic properties of all-trans retinoic acid but may influence ECG changes caused by arsenic trioxide administration. SNEDDS-TRF-ATRA presents cytotoxicity in resistant APL cells (NB4-R2). Combined administration of ATO and SNEDDS-TRF-ATRA in mice prevented the prolongation of the QTc interval caused by ATO but evoked ECG abnormalities such as T wave flattening.

Transfer of Cardiac Mitochondria Improves the Therapeutic Efficacy of Mesenchymal Stem Cells in a Preclinical Model of Ischemic Heart Disease.

BACKGROUND: The use of mesenchymal stem cells (MSCs) appears to be a promising therapeutic approach for cardiac repair after myocardial infarction. However, clinical trials have revealed the need to improve their therapeutic efficacy. Recent evidence demonstrated that mitochondria undergo spontaneous transfer from damaged cells to MSCs, resulting in the activation of the cytoprotective and pro-angiogenic functions of recipient MSCs. Based on these observations, we investigated whether the preconditioning of MSCs with mitochondria could optimize their therapeutic potential for ischemic heart disease. METHODS: Human MSCs were exposed to mitochondria isolated from human fetal cardiomyocytes. After 24 h, the effects of mitochondria preconditioning on the MSCs' function were analyzed both in vitro and in vivo. RESULTS: We found that cardiac mitochondria-preconditioning improved the proliferation and repair properties of MSCs in vitro. Mechanistically, cardiac mitochondria mediate their stimulatory effects through the production of reactive oxygen species, which trigger their own degradation in recipient MSCs. These effects were further confirmed in vivo, as the mitochondria preconditioning of MSCs potentiated their therapeutic efficacy on cardiac function following their engraftment into infarcted mouse hearts. CONCLUSIONS: The preconditioning of MSCs with the artificial transfer of cardiac mitochondria appears to be promising strategy to improve the efficacy of MSC-based cell therapy in ischemic heart disease.

Ephrin-B1 regulates the adult diastolic function through a late postnatal maturation of cardiomyocyte surface crests.

The rod-shaped adult cardiomyocyte (CM) harbors a unique architecture of its lateral surface with periodic crests, relying on the presence of subsarcolemmal mitochondria (SSM) with unknown role. Here, we investigated the development and functional role of CM crests during the postnatal period. We found in rodents that CM crest maturation occurs late between postnatal day 20 (P20) and P60 through both SSM biogenesis, swelling and crest-crest lateral interactions between adjacent CM, promoting tissue compaction. At the functional level, we showed that the P20-P60 period is dedicated to the improvement of relaxation. Interestingly, crest maturation specifically contributes to an atypical CM hypertrophy of its short axis, without myofibril addition, but relying on CM lateral stretching. Mechanistically, using constitutive and conditional CM-specific knock-out mice, we identified ephrin-B1, a lateral membrane stabilizer, as a molecular determinant of P20-P60 crest maturation, governing both the CM lateral stretch and the diastolic function, thus highly suggesting a link between crest maturity and diastole. Remarkably, while young adult CM-specific Efnb1 KO mice essentially exhibit an impairment of the ventricular diastole with preserved ejection fraction and exercise intolerance, they progressively switch toward systolic heart failure with 100% KO mice dying after 13 months, indicative of a critical role of CM-ephrin-B1 in the adult heart function. This study highlights the molecular determinants and the biological implication of a new late P20-P60 postnatal developmental stage of the heart in rodents during which, in part, ephrin-B1 specifically regulates the maturation of the CM surface crests and of the diastolic function.

Neurovascular hypoxia after mild traumatic brain injury in juvenile mice correlates with heart-brain dysfunctions in adulthood.

AIM: Retrospective studies suggest that mild traumatic brain injury (mTBI) in pediatric patients may lead to an increased risk of cardiac events. However, the exact functional and temporal dynamics and the associations between heart and brain pathophysiological trajectories are not understood. METHODS: A single impact to the left somatosensory cortical area of the intact skull was performed on juvenile mice (17 days postnatal). Cerebral 3D photoacoustic imaging was used to measure the oxygen saturation (sO2 ) in the impacted area 4 h after mTBI followed by 2D and 4D echocardiography at days 7, 30, 90, and 190 post-impact. At 8 months, we performed a dobutamine stress test to evaluate cardiac function. Lastly, behavioral analyses were conducted 1 year after initial injury. RESULTS: We report a rapid and transient decrease in cerebrovascular sO2 and increased hemoglobin in the impacted left brain cortex. Cardiac analyses showed long-term diastolic dysfunction and a diminished systolic strain response under stress in the mTBI group. At the molecular level, cardiac T-p38MAPK and troponin I expression was pathologic modified post-mTBI. We found linear correlations between brain sO2 measured immediately post-mTBI and long-term cardiac strain after 8 months. We report that initial cerebrovascular hypoxia and chronic cardiac dysfunction correlated with long-term behavioral changes hinting at anxiety-like and memory maladaptation. CONCLUSION: Experimental juvenile mTBI induces time-dependent cardiac dysfunction that corresponds to the initial neurovascular sO2 dip and is associated with long-term behavioral modifications. These imaging biomarkers of the heart-brain axis could be applied to improve clinical pediatric mTBI management.

Involvement of Vasopressin in Tissue Hypoperfusion during Cardiogenic Shock Complicating Acute Myocardial Infarction in Rats.

Acute heart failure (AHF) due to acute myocardial infarction (AMI) is likely to involve cardiogenic shock (CS), with neuro-hormonal activation. A relationship between AHF, CS and vasopressin response is suspected. This study aimed to investigate the implication of vasopressin on hemodynamic parameters and tissue perfusion at the early phase of CS complicating AMI. Experiments were performed on male Wistar rats submitted or not to left coronary artery ligation (AMI and Sham). Six groups were studied Sham and AMI treated or not with either a vasopressin antagonist SR-49059 (Sham-SR, AMI-SR) or agonist terlipressin (Sham-TLP, AMI-TLP). Animals were sacrificed one day after surgery (D1) and after hemodynamic parameters determination. Vascular responses to vasopressin were evaluated, ex vivo, on aorta. AHF was defined by a left ventricular ejection fraction below 40%. CS was defined by AHF plus tissue hypoperfusion evidenced by elevated serum lactate level or low mesenteric oxygen saturation (SmO2) at D1. Mortality rates were 40% in AMI, 0% in AMI-SR and 33% in AMI-TLP. Immediately after surgery, a sharp decrease in SmO2 was observed in all groups. At D1, SmO2 recovered in Sham and in SR-treated animals while it remained low in AMI and further decreased in TLP-treated groups. The incidence of CS among AHF animals was 72% in AMI or AMI-TLP while it was reduced to 25% in AMI-SR. Plasma copeptin level was increased by AMI. Maximal contractile response to vasopressin was decreased in AMI (32%) as in TLP- and SR- treated groups regardless of ligation. Increased vasopressin secretion occurring in the early phase of AMI may be responsible of mesenteric hypoperfusion resulting in tissue hypoxia. Treatment with a vasopressin antagonist enhanced mesenteric perfusion and improve survival. This could be an interesting therapeutic strategy to prevent progression to cardiogenic shock.

Assessing the effect of COVID-19 pandemic on air quality change and human health outcomes in a capital city, southwestern Iran.

The aimsof this study were to assess the spatial variation of PM2.5, NO2, and O3 between 2019 (before) and 2020 (during COVID-19 pandemic); and calculation the health outcomes of exposure to these pollutants. The daily PM2.5, NO2, and O3 concentrations were applied to assess health effects by relative risk, and baseline incidence. The annual PM2.5 and NO2 mean concentrations exceeded the WHO guideline values, while O3 did not exceed. The restrictive measures associated to COVID-19 led to reduction at the annual means of PM2.5 and NO2 by -25.5% and -23.1%, respectively, while the annual mean of O3 increased by +7.9%. The number of M-CVD and M-RD (-25.6%, -26.1%) related to PM2.5 exposure, and HA-COPD and HA-RD >65 years old (-21% and -3.84%) related to NO2 exposure were reduced in 2020, and O3 exposure-related M-CVD (+30.1%) and HA-RD >65 years old (+23.4%) increased compared to the previous year 2019.

Spatiotemporal variations of ozone exposure and its risks to vegetation and human health in Cyprus: an analysis across a gradient of altitudes.

Ground-level ozone (O3) affects vegetation and threatens environmental health when levels exceed critical values, above which adverse effects are expected. Cyprus is expected to be a hotspot for O3 concentrations due to its unique position in the eastern Mediterranean, receiving air masses from Europe, African, and Asian continents, and experiencing a warm Mediterranean climate. In Cyprus, the spatiotemporal features of O3 are poorly understood and the potential risks for forest health have not been explored. We evaluated O3 and nitrogen oxides (NO and NO2) at four regional background stations at different altitudes over 2014-2016. O3 risks to vegetation and human health were estimated by calculating accumulated O3 exposure over a threshold of 40 nmol mol-1 (AOT40) and cumulative exposure to mixing ratios above 35 nmol mol-1 (SOMO35) indices. The data reveal that mean O3 concentrations follow a seasonal pattern, with higher levels in spring (51.8 nmol mol-1) and summer (53.2 nmol mol-1) and lower levels in autumn (46.9 nmol mol-1) and winter (43.3 nmol mol-1). The highest mean O3 exposure (59.5 nmol mol-1) in summer occurred at the high elevation station Mt. Troodos (1819 m a.s.l.). Increasing (decreasing) altitudinal gradients were found for O3 (NOx), driven by summer-winter differences. The diurnal patterns of O3 showed little variation. Only at the lowest altitude O3 displayed a typical O3 diurnal pattern, with hourly differences smaller than 15 nmol mol-1. Accumulated O3 exposures at all stations and in all years exceeded the European Union's limits for the protection of vegetation, with average values of 3-month (limit: 3000 nmol mol-1 h) and 6-month (limit: 5000 nmol mol-1 h) AOT40 for crops and forests of 16,564 and 31,836 nmol mol-1 h, respectively. O3 exposures were considerably high for human health, with an average SOMO35 value of 7270 nmol mol-1 days across stations and years. The results indicate that O3 is a major environmental and public health issue in Cyprus, and policies must be adopted to mitigate O3 precursor emissions at local and regional scales.

Ambient PM2.5 and O3 pollution and health impacts in Iranian megacity.

The main objectives of this study were to (i) assess variation within fine particles (PM2.5) and tropospheric ozone (O3) time series in Khorramabad (Iran) between 2019 (before) and 2020 (during COVID-19 pandemic); (ii) assess relationship between PM2.5 and O3, the PM2.5/O3 ratio, and energy consumption; and (iii) estimate the health effects of exposure to ambient PM2.5 and O3. From hourly PM2.5 and O3 concentrations, we applied both linear-log and integrated exposure-response functions, city-specific relative risk, and baseline incidence values to estimate the health effects over time. A significant correlation was found between PM2.5 and O3 (r =-0.46 in 2019, r =-0.55 in 2020, p < 0.05). The number of premature deaths for all non-accidental causes (27.5 and 24.6), ischemic heart disease (7.3 and 6.3), chronic obstructive pulmonary disease (17 and 19.2), and lung cancer (9.2 and 6.25) attributed to ambient PM2.5 exposure and for respiratory diseases (4.7 and 5.4) for exposure to O3 above 10 µg m-3 for people older than 30-year-old were obtained in 2019 and 2020. The number of years of life lost declined by 11.6% in 2020 and exposure to PM2.5 reduced the life expectancy by 0.58 and 0.45 years, respectively in 2019 and 2020. Compared to 2019, the restrictive measures associated to COVID-19 pandemic led to reduction in PM2.5 (-25.5%) and an increase of O3 concentration (+ 8.0%) in Khorramabad.

Trends in urban air pollution over the last two decades: A global perspective.

Ground-level ozone (O3), fine particles (PM2.5), and nitrogen dioxide (NO2) are the most harmful urban air pollutants regarding human health effects. Here, we aimed at assessing trends in concurrent exposure of global urban population to O3, PM2.5, and NO2 between 2000 and 2019. PM2.5, NO2, and O3 mean concentrations and summertime mean of the daily maximum 8-h values (O3 MDA8) were analyzed (Mann-Kendall test) using data from a global reanalysis, covering 13,160 urban areas, and a ground-based monitoring network (Tropospheric Ozone Assessment Report), collating surface O3 observations at nearly 10,000 stations worldwide. At global scale, PM2.5 exposures declined slightly from 2000 to 2019 (on average, - 0.2 % year-1), with 65 % of cities showing rising levels. Improvements were observed in the Eastern US, Europe, Southeast China, and Japan, while the Middle East, sub-Saharan Africa, and South Asia experienced increases. The annual NO2 mean concentrations increased globally at 71 % of cities (on average, +0.4 % year-1), with improvements in North America and Europe, and increases in exposures in sub-Saharan Africa, Middle East, and South Asia regions, in line with socioeconomic development. Global exposure of urban population to O3 increased (on average, +0.8 % year-1 at 89 % of stations), due to lower O3 titration by NO. The summertime O3 MDA8 rose at 74 % of cities worldwide (on average, +0.6 % year-1), while a decline was observed in North America, Northern Europe, and Southeast China, due to the reduction in precursor emissions. The highest O3 MDA8 increases (>3 % year-1) occurred in Equatorial Africa, South Korea, and India. To reach air quality standards and mitigate outdoor air pollution effects, actions are urgently needed at all governance levels. More air quality monitors should be installed in cities, particularly in Africa, for improving risk and exposure assessments, concurrently with implementation of effective emission control policies that will consider regional socioeconomic imbalances.

Increased tropospheric ozone levels as a public health issue during COVID-19 lockdown and estimation the related pulmonary diseases.

The aims of this study were to i) investigate the variation of tropospheric ozone (O3) levels during the COVID-19 lockdown; ii) determine the relationships between O3 concentrations with the number of COVID-19 cases; and iii) estimate the O3-related health effects in Southwestern Iran (Khorramabad) over the time period 2019-2021. The hourly O3 data were collected from ground monitoring stations, as well as retrieved from Sentinel-5 satellite data for showing the changes in O3 levels pre, during, and after lockdown period. The concentration-response function model was applied using relative risk (RR) values and baseline incidence (BI) to assess the O3-related health effects. Compared to 2019, the annual O3 mean concentrations increased by 12.2% in 2020 and declined by 3.9% in 2021. The spatiotemporal changes showed a significant O3 increase during COVID-19 lockdown, and a negative correlation between O3 levels and the number of COVID-19 cases was found (r = - 0.59, p < 0.05). In 2020, the number of hospital admissions for cardiovascular diseases increased by 4.0 per 105 cases, the mortality for respiratory diseases increased by 0.7 per 105 cases, and the long-term mortality for respiratory diseases increased by 0.9 per 105 cases. Policy decisions are now required to reduce the surface O3 concentrations and O3-related health effects in Iran.

Loss of function of the maternal membrane oestrogen receptor ERα alters expansion of trophoblast cells and impacts mouse fertility.

The binding of 17ß-oestradiol to oestrogen receptor alpha (ERα) plays a crucial role in the control of reproduction, acting through both nuclear and membrane-initiated signalling. To study the physiological role of membrane ERα in the reproductive system, we used the C451A-ERα mouse model with selective loss of function of membrane ERα. Despite C451A-ERα mice being described as sterile, daily weighing and ultrasound imaging revealed that homozygous females do become pregnant, allowing the investigation of the role of ERα during pregnancy for the first time. All neonatal deaths of the mutant offspring mice resulted from delayed parturition associated with failure in pre-term progesterone withdrawal. Moreover, pregnant C451A-ERα females exhibited partial intrauterine embryo arrest at about E9.5. The observed embryonic lethality resulted from altered expansion of Tpbpa-positive spiral artery-associated trophoblast giant cells into the utero-placental unit, which is associated with an imbalance in expression of angiogenic factors. Together, these processes control the trophoblast-mediated spiral arterial remodelling. Hence, loss of membrane ERα within maternal tissues clearly alters the activity of invasive trophoblast cells during placentogenesis. This previously unreported function of membrane ERα could open new avenues towards a better understanding of human pregnancy-associated pathologies.