Heterojunction photocatalysts for degradation of the tetracycline antibiotic: a review.

Antibiotic pollution is a major health issue inducing antibiotic resistance and the inefficiency of actual drugs, thus calling for improved methods to clean water and wastewater. Here we review the recent development of heterojunction photocatalysis and application in degrading tetracycline. We discuss mechanisms for separating photogenerated electron-hole pairs in different heterojunction systems such as traditional, p-n, direct Z-scheme, step-scheme, Schottky, and surface heterojunction. Degradation pathways of tetracycline during photocatalysis are presented. We compare the efficiency of tetracycline removal by various heterojunctions using quantum efficiency, space time yield, and figures of merit. Implications for the treatment of antibiotic-contaminated wastewater are discussed.

Maternal preconceptional and prenatal exposure to El Niño Southern Oscillation levels and child mortality: a multi-country study.

El Niño Southern Oscillation (ENSO) has been shown to relate to the epidemiology of childhood infectious diseases, but evidence for whether they increase child deaths is limited. Here, we investigate the impact of mothers' ENSO exposure during and prior to delivery on child mortality by constructing a retrospective cohort study in 38 low- and middle-income countries. We find that high levels of ENSO indices cumulated over 0-12 lagged months before delivery are associated with significant increases in risks of under-five mortality; with the hazard ratio ranging from 1.33 (95% confidence interval [CI], 1.26, 1.40) to 1.89 (95% CI, 1.78, 2.00). Child mortality risks are particularly related to maternal exposure to El Niño-like conditions in the 0th-1st and 6th-12th lagged months. The El Niño effects are larger in rural populations and those with unsafe sources of drinking water and less education. Thus, preventive interventions are particularly warranted for the socio-economically disadvantaged.

Low-level ambient ozone exposure associated with neutrophil extracellular traps and pro-atherothrombotic biomarkers in healthy adults.

BACKGROUND AND AIMS: Uncertainty of the causality determinations for ambient ozone (O3) on cardiovascular events is heightened by the limited understanding of the mechanisms involved in humans. We aimed to examine the pro-atherothrombotic impacts of O3 exposure and to explore the potential mediating roles of dysfunctional neutrophils, focusing on neutrophil extracellular traps (NETs). METHODS: A longitudinal panel study of 152 healthy adults was conducted in the cool to cold months with relatively low levels of O3 between September 2019 and January 2020 in Beijing, China. Four repeated measurements of indicators reflecting atherothrombotic balance and NETs were performed for each participant. RESULTS: Daily average exposure levels of ambient O3 were 16.6 µg/m3 throughout the study period. Per interquartile range increase in average concentrations of O3 exposure at prior up to 7 days, we observed elevations of 200.1-276.3% in D-dimer, 27.2-36.8% in thrombin-antithrombin complex, 10.8-60.3% in plasminogen activator inhibitor 1, 13.9-21.8% in soluble P-selectin, 16.5-45.1% in matrix metalloproteinase-8, and 2.4-12.4% in lipoprotein-associated phospholipase A2. These pro-atherothrombotic changes were accompanied by endothelial activation, lung injury, and immune inflammation. O3 exposure was also positively associated with circulating NETs indicators, including citrullinated histone H3, neutrophil elastase, myeloperoxidase, and double-stranded DNA. Mediation analyses indicated that NETs could mediate O3-associated pro-atherothrombotic responses. The observational associations remained significant and robust after controlling for other pollutants, and were generally greater in participants with low levels of physical activity. CONCLUSIONS: Ambient O3 exposure was associated with significant increases in NETs and pro-atherothrombotic potential, even at exposure levels well below current air quality guidelines of the World Health Organization.

Short-Term Effects of Primary and Secondary Particulate Matter on Ceramide Metabolism, Pro-Inflammatory Response, and Blood Coagulation.

Evidence of the precise biological pathway responsible for acute cardiovascular events triggered by particulate matter (PM) exposure from anthropogenic emissions is sparse. We investigated the associations of biomarkers relevant to the pathophysiology of atherothrombosis (ceramide metabolism, pro-inflammatory response, and blood coagulation) with primary and secondary components in particulate matter with aerodynamic diameters less than 2.5 µm (PM2.5). A total of 152 healthy participants were followed with four repeated clinical visits between September 2019 and January 2020 in Beijing. Exposure to ambient inorganic aerosols (sulfate, nitrate, ammonium, and chloride), as well as organic aerosols (OA) in PM2.5, was measured by a real-time aerosol chemical speciation monitor, and sources of OA were performed by positive matrix factorization. We found significant increases of 101.9-397.9% in ceramide indicators associated with interquartile-range increases in inorganic aerosols and OA prior to 72 h of exposure. Higher levels of organic and inorganic aerosols in PM2.5 were associated with increases of 3.1-6.0% in normal T cells regulated upon activation and expressed and secreted relevant to the pro-inflammatory response; increases of 276.9-541.5% were observed in D-dimers relevant to coagulation. Detrimental effects were further observed following OA exposure from fossil fuel combustion. Mediation analyses indicated that ceramide metabolism could mediate the associations of PM2.5 components with pro-inflammatory responses. Our findings expand upon the current understanding of potential pathophysiological pathways of cardiovascular events posed by ambient particulates and highlight the importance of reducing primary and secondary PM from anthropogenic combustions.

Association between short-term air pollution exposure and perturbation in thyrotropin levels in 1.38 million Chinese women: A national longitudinal analysis, 2014-2019.

Prevalence of subclinical hypothyroidism substantially increased during the last decade in China, which has been commonly/clinically diagnosed as elevation in thyrotropin (thyroid-stimulating hormone [TSH]). Tobacco smoke containing toxic substances has been linked to thyroid dysfunction; however, data on perturbation of TSH following air pollution exposure in human has not been assessed at nationwide population level. We investigated the longitudinal impact of daily ambient air pollution estimated at residential level on serum TSH in 1.38 million women from China's 29 mainland provinces between 2014 and 2019. We observed that particulate matter with aerodynamic diameter ≤ 10 and ≤ 2.5 µm (PM10, PM2.5) and nitrogen dioxide (NO2) at cumulative lag 0-7 days of exposure were associated with percent elevations in TSH (0.88% [95% CI: 0.71, 1.05] per [interquartile range, IQR: 54.8 µg/m3] of PM10; 0.89% [95% CI, 0.71, 1.07] per IQR [40.3 µg/m3] of PM2.5; 2.01% [95% CI: 1.81, 2.22] per IQR [27.4 µg/m3] of NO2). Greater associations were observed in participants living in areas with ≥adequate iodine intake and those with low BMI levels and high inflammation status. Our results suggest that increased concentrations of recent ambient air pollutants at exposure ranges commonly encountered in Asia were associated with increases in TSH, supporting disturbing role of short-term air pollution exposure on the regulation of thyroid hormone homeostasis.

Pro-inflammation and pro-atherosclerotic responses to short-term air pollution exposure associated with alterations in sphingolipid ceramides and neutrophil extracellular traps.

Air pollution has been associated with the development of atherosclerosis; however, the pathophysiological mechanisms underlying pro-atherosclerotic effects of air pollution exposure remain unclear. We conducted a prospective panel study in Beijing and recruited 152 participants with four monthly visits from September 2019 to January 2020. Linear mixed-effect models were applied to estimate the associations linking short-term air pollution exposure to biomarkers relevant to ceramide metabolism, pro-inflammation (neutrophil extracellular traps formation and systemic inflammation) and pro-atherosclerotic responses (endothelial stimulation, plaque instability, coagulation activation, and elevated blood pressure). We further explored whether ceramides and inflammatory indicators could mediate the alterations in the profiles of pro-atherosclerotic responses. We found that significant increases in levels of circulating ceramides of 9.7% (95% CIs: 0.7, 19.5) to 96.9% (95% CIs: 23.1, 214.9) were associated with interquartile range increases in moving averages of ambient air pollutant metrics, including fine particulate matter (PM2.5), black carbon, particles in size fractions of 100-560 nm, nitrogen dioxide, carbon monoxide and sulfur dioxide at prior up to 7 days. Higher air pollution levels were also associated with activated neutrophils (increases in citrullinated histone H3, neutrophil elastase, double-stranded DNA, and myeloperoxidase) and exacerbation of pro-atherosclerotic responses (e.g., increases in vascular endothelial growth factor, lipoprotein-associated phospholipase A2, matrix metalloproteinase-8, P-selectin, and blood pressure). Mediation analyses further showed that dysregulated ceramide metabolism and potentiated inflammation could mediate PM2.5-associated pro-atherosclerotic responses. Our findings extend the understanding on potential mechanisms of air pollution-associated atherosclerosis, and suggest the significance of reducing air pollution as priority in urban environments.

Exposure to ambient oxidant pollution associated with ceramide changes and cardiometabolic responses.

Evidence of impact of ambient oxidant pollution on cardiometabolic responses remains limited. We aimed to examine associations of oxidant pollutants with cardiometabolic responses, and effect modification by ceramides. During 2019-2020, 152 healthy adults were visited 4 times in Beijing, China, and indicators of ceramides, glucose homeostasis, and vascular function were measured. We found significant increases in ceramides of 13.9% (p = 0.020) to 110.1% (p = 0.005) associated with an interquartile increase in oxidant pollutants at prior 1-7 days. Exposure to oxidant pollutants was also related to elevations in insulin and reductions in adiponectin, and elevations in systolic and diastolic blood pressure. Further, stratified analyses revealed larger changes in oxidant pollutant related cardiometabolic responses among participants with higher ceramide levels compared to those with lower levels. Our findings suggested cardiometabolic effects associated with exposure to oxidant pollutants, which may be modified by ceramide levels.

Ambient Anthropogenic Carbons and Pediatric Respiratory Infections: A Case-Crossover Analysis in the Megacity Beijing.

Carbon loading in airway cells has shown to worsen function of antimicrobial peptides, permitting increased survival of pathogens in the respiratory tract; however, data on the impacts of carbon particles on childhood acute respiratory infection (ARI) is limited. We assembled daily health data on outpatient visits for ARI (bronchitis, pneumonia, and total upper respiratory infection [TURI]) in children aged 0-14 years between 2015 and 2019 in Beijing, China. Anthropogenic carbons, including black carbon (BC) and its emission sources, and wood smoke particles (delta carbon, ultra-violet absorbing particulate matter, and brown carbon) were continuously monitored. Using a time-stratified case-crossover approach, conditional logistic regression was performed to derive risk estimates for each outcome. A total of 856,899 children were included, and a wide range of daily carbon particle concentrations was observed, with large variations for BC (0.36-20.44) and delta carbon (0.48-57.66 µg/m3). Exposure to these particles were independently associated with ARI, with nearly linear exposure-response relationships. Interquartile range increases in concentrations of BC and delta carbon over prior 0-8 days, we observed elevation of the odd ratio of bronchitis by 1.201 (95% confidence interval, 1.180, 1.221) and 1.048 (95% CI, 1.039, 1.057), respectively. Stronger association was observed for BC from traffic sources, which increased the odd ratio of bronchitis by 1.298 (95% CI, 1.273, 1.324). Carbon particles were also associated with elevated risks of pneumonia and TURI, and subgroup analyses indicated greater risks among children older than 6 years. Our findings suggested that anthropogenic carbons in metropolitan areas may pose a significant threat to clinical manifestations of respiratory infections in vulnerable populations.

Associations of climate variability driven by El Niño-southern oscillation with excess mortality and related medical costs in Chinese elderly.

Climate variability driven by El Niño-Southern Oscillation (ENSO) is a significant public health concern in parallel with global population aging; however, its role in healthy aging is less studied. We examined the longitudinal impacts of ENSO exposure on excess mortality and related medical costs in the elderly from 23 provinces of China. A total of 27,533 non-accidental all-cause deaths were recorded in 30,763 participants during 1998-2018. We found that both low and high levels of ENSO metrics over lags of 0-12 months were associated with increased mortality risks. Specifically, comparing the 10th percentile (-1.8) and 90th percentile (2.0) multivariate El Niño index (MEI) levels to the reference level with the minimum effect of MEI exposure, the risk of mortality was 1.87 (95 % confidence interval [CI], 1.75, 2.00) and 4.89 (95 % CI, 4.36, 5.49), respectively. ENSO exposure was also positively related to medical costs. Further, the associations were stronger among drinkers, lower-income participants, and those with higher blood pressure and heart rate measured at the most recent follow-ups. Our results suggested that ENSO exposure was capable of heightening mortality risks and medical burden among older elderly adults, highlighting that climate variability driven by ENSO could be a crucial determinant of healthy aging.

Short-term exposure to traffic-related air pollution and STEMI events: Insights into STEMI onset and related cardiac impairment.

AIMS: Evidence on the impacts of traffic-related air pollution (TRAP) on ST-segment elevation myocardial infarction (STEMI) events is limited. We aimed to assess the acute effects of TRAP exposure on the clinical onset of STEMI and related cardiac impairments. METHODS AND RESULTS: We recruited patients who were admitted for STEMI and underwent primary percutaneous coronary intervention at Peking University Third Hospital between 2014 and 2020. Indicators relevant to cardiac impairments were measured. Concomitantly, hourly concentrations of traffic pollutants were monitored throughout the study period, including fine particulate matter, black carbon (BC), particles in size ranges of 5-560 nm, oxides of nitrogen (NOX), nitrogen dioxide, and carbon monoxide. The mean (SD) age of participants was 62.4 (12.5) years. Daily average (range) concentrations of ambient BC and NOX were 3.9 (0.1-25.0) µg/m3 and 90.8 (16.6-371.7) µg/m3. Significant increases in STEMI risks of 5.9% (95% CI: 0.1, 12.0) to 21.9% (95% CI: 6.0, 40.2) were associated with interquartile range increases in exposure to TRAP within a few hours. These changes were accompanied by significant elevations in cardiac troponin T levels of 6.9% (95% CI: 0.2, 14.1) to 41.7% (95% CI: 21.2, 65.6), as well as reductions in left ventricular ejection fraction of 1.5% (95% CI: 0.1, 2.9) to 3.7% (95% CI: 0.8, 6.4). Furthermore, the associations were attenuated in participants living in areas with higher residential greenness levels. CONCLUSIONS: Our findings extend current understanding that short-term exposure to higher levels of traffic pollution was associated with increased STEMI risks and exacerbated cardiac impairments, and provide evidence on traffic pollution control priority for protecting vulnerable populations who are at greater risks of cardiovascular events.

Photocatalytic degradation of microcystin-LR by modified TiO2 photocatalysis: A review.

Microcystin-LR (MC-LR), the most toxic and commonly encountered cyanotoxin, is produced by harmful cyanobacterial blooms and potentially threatens human and ecosystems health. Titanium dioxide (TiO2) photocatalysis is attracting growing attention and has been considered as an efficient, environmentally friendly and promising solution to eliminate MC-LR in the aquatic ecosystems. Over recent decades, scientific efforts have been directed towards the understanding of fundamentals, modification strategies, and application potentials of TiO2 photocatalysis in degrading MC-LR. In this article, recent reports have been reviewed and progress has been summarized in the development of heterogeneous TiO2-based photocatalysts for MC-LR photodegradation under visible, UV, or solar light. The proposed photocatalytic principles of TiO2 and destruction of MC-LR have been thoroughly discussed. Specifically, some main modification methods for improving the drawbacks and performance of TiO2 nanoparticle were highlighted, including element doping, semiconductor coupling, immobilization, floatability amelioration and magnetic separation. Moreover, the performance evaluation metrics quantum yield (QY) and figure of merit (FOM) were used to compare different photocatalysts in MC-LR degradation. The best performance was seen in N-TiO2 with QY and FOM values of 2.20E-07 molecules/photon and 1.00E-11 mol·L/(g·J·h). N-TiO2 or N-TiO2-based materials may be excellent options for photocatalyst design in terms of MC-LR degradation. Finally, a summary of the remaining challenges and perspectives on new tendencies in this exciting frontier and still an emerging area of research were addressed accordingly. Overall, the present review will offer a deep insight for understanding the photodegradation of MC-LR with modified TiO2 to further inspire researchers that work in associated fields.

Biodegradation of microcystin-RR and nutrient pollutants using Sphingopyxis sp. YF1 immobilized activated carbon fibers-sodium alginate.

A novel biological material named activated carbon fibers-sodium alginate@Sphingopyxis sp. YF1 (ACF-SA@YF1) was synthesized for microcystin-RR (MC-RR) and nutrient pollutant degradation in eutrophic water. The synthesized biomaterial was characterized by scanning electron microscopy (SEM). Box-Behnken design and response surface methodology (RSM) were utilized for the optimization of conditions during the MC-RR degradation. The degradation of MC-RR and nutrient pollutants was dynamically detected. The results revealed that the optimal conditions were temperature 32.51 °C, pH 6.860, and inoculum 14.97%. The removal efficiency of MC-RR, nitrogen, phosphorus, and chemical oxygen demand were 0.76 µg/mL/h, 32.45%, 94.57%, and 64.07%, respectively. In addition, ACF-SA@YF1 also performed satisfactory cyclic stability, while the MC-RR removal efficiency was 70.38% after seven cycles and 78.54% of initial activity after 20 days of storage. Therefore, it is reasonable to believe that ACF-SA@YF1 is an effective material which has a great prospect in removing MC-RR and nutrients from freshwater ecosystems.