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Approaches to investigate crop responses to ozone pollution: from O3 -FACE to satellite-enabled modeling.
Montes, CM, Demler, HJ, Li, S, Martin, DG, Ainsworth, EA
The Plant journal : for cell and molecular biology. 2022;(2):432-446
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Abstract
Ozone (O3 ) is a damaging air pollutant to crops. As one of the most reactive oxidants known, O3 rapidly forms other reactive oxygen species (ROS) once it enters leaves through stomata. Those ROS in turn can cause oxidative stress, reduce photosynthesis, accelerate senescence, and decrease crop yield. To improve and adapt our feed, fuel, and food supply to rising O3 pollution, a number of Free Air Concentration Enrichment (O3 -FACE) facilities have been developed around the world and have studied key staple crops. In this review, we provide an overview of the FACE facilities and highlight some of the lessons learned from the last two decades of research. We discuss the differences between C3 and C4 crop responses to elevated O3 , the possible trade-off between productivity and protection, genetic variation in O3 response within and across species, and how we might leverage this observed variation for crop improvement. We also highlight the need to improve understanding of the interaction between rising O3 pollution and other aspects of climate change, notably drought. Finally, we propose the use of globally modeled O3 data that are available at increasing spatial and temporal resolutions to expand upon the research conducted at the limited number of global O3 -FACE facilities.
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Air Pollution Exposure Impairs Airway Epithelium IFN-β Expression in Pre-School Children.
Bonato, M, Gallo, E, Turrin, M, Bazzan, E, Baraldi, F, Saetta, M, Gregori, D, Papi, A, Contoli, M, Baraldo, S
Frontiers in immunology. 2021;:731968
Abstract
INTRODUCTION Air pollution is a risk factor for respiratory infections and asthma exacerbations. We previously reported impaired Type-I and Type-III interferons (IFN-β/λ) from airway epithelial cells of preschool children with asthma and/or atopy. In this study we analyzed the association between rhinovirus-induced IFN-β/λ epithelial expression and acute exposure to the principal outdoor air pollutants in the same cohort. METHODS We studied 34 children (17asthmatics/17non-asthmatics) undergoing fiberoptic bronchoscopy for clinical indications. Bronchial epithelial cells were harvested by brushing, cultured and experimentally infected with Rhinovirus Type 16 (RV16). RV16-induced IFN-β and λ expression was measured by quantitative real time PCR, as was RV16vRNA. The association between IFNs and the mean exposure to PM10, SO2 and NO2 in the day preceding bronchoscopy was evaluated using a Generalized Linear Model (GLM) with Gamma distribution. RESULTS Acute exposure to PM10 and NO2 was negatively associated to RV16-induced IFNβ mRNA. For each increase of 1ug/m3 of NO2 we found a significative decrease of 2.3x103 IFN-β mRNA copies and for each increase of 1ug/m3 of PM10 a significative decrease of 1x103 IFN-β mRNA copies. No significant associations were detected between IFN-λ mRNA and NO2 nor PM10. Increasing levels of NO2 (but not PM10) were found to be associated to increased RV16 replication. CONCLUSIONS Short-term exposure to high levels of NO2 and PM10 is associated to a reduced IFN-β expression by the airway epithelium, which may lead to increased viral replication. These findings suggest a potential mechanism underlying the link between air pollution, viral infections and asthma exacerbations.
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Air pollution and pre-eclampsia; associations and potential mechanisms.
Bearblock, E, Aiken, CE, Burton, GJ
Placenta. 2021;:188-194
Abstract
INTRODUCTION Air pollution has significant negative health impacts, particularly on the cardiovascular system. The aims of this narrative review were to identify whether there is an association between air pollution and the incidence of pre-eclampsia, and the potential mechanisms by which any effects may be mediated. METHODS We undertook a literature search using Google Scholar, PubMed, the Cochrane Library and NICE Evidence. The primary eligibility criterion was articles correlating exposure to air pollution with incidence of pre-eclampsia. RESULTS Meta-analyses currently show a positive association between pre-eclampsia and exposure to both particulate matter PM2.5 and nitrogen dioxide, but no significant associations with ambient ozone or carbon monoxide exposure. No meta-analysis has been performed for exposure to sulfur dioxide. Variability in terms of quantification of exposure, the exposure period and co-founders among the studies makes comparisons complex. Adverse effects on trophoblast invasion and placental vascularisation, and increases in oxidative stress and anti-angiogenic factors, such as sFlt-1, in response to air pollution provide pathways by which exposure may contribute to the pathophysiology of pre-eclampsia. So far, studies have not discriminated between the early- and late-onset forms of the syndrome. DISCUSSION Future prospective studies using personal air pollution monitors and blood biomarkers of pre-eclampsia would strengthen the associations. Interactions between pollutants are poorly documented, and at present there is minimal informed advice available to women on the need to avoid exposure to air pollutants during pregnancy.
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Air Pollution and Asthma: Mechanisms of Harm and Considerations for Clinical Interventions.
Pfeffer, PE, Mudway, IS, Grigg, J
Chest. 2021;(4):1346-1355
Abstract
There is global concern regarding the harmful impact of polluted air on the respiratory health of patients with asthma. Multiple epidemiologic studies have shown ongoing associations between high levels of air pollution and poor early life lung growth, development of allergic sensitization, development of asthma, airway inflammation, acutely impaired lung function, respiratory tract infections, and asthma exacerbations. However, studies have often yielded inconsistent findings, and not all studies have found significant associations; this may be related to both variations in statistical, measurement, and modeling methodologies between studies as well as differences in the concentrations and composition of air pollution globally. Overall, this variation in findings suggests we still do not fully understand the effects of ambient pollution on the lungs and on the evolution and exacerbation of airway diseases. There is clearly a need to augment epidemiologic studies with experimental studies to clarify the underlying mechanistic basis for the adverse responses reported and to identify the key gaseous and particle-related components within the complex air pollution mixture driving these outcomes. Some progress toward these aims has been made. This article reviews studies providing an improved understanding of causal pathways linking air pollution to asthma development and exacerbation. The article also considers potential strategies to reduce asthma morbidity and mortality through regulation and behavioral/pharmacologic interventions, including a consideration of pollutant avoidance strategies and antioxidant and/or vitamin D supplementation.
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Association between exposure to ambient air pollution and hospital admission, incidence, and mortality of stroke: an updated systematic review and meta-analysis of more than 23 million participants.
Niu, Z, Liu, F, Yu, H, Wu, S, Xiang, H
Environmental health and preventive medicine. 2021;(1):15
Abstract
BACKGROUND Previous studies have suggested that exposure to air pollution may increase stroke risk, but the results remain inconsistent. Evidence of more recent studies is highly warranted, especially gas air pollutants. METHODS We searched PubMed, Embase, and Web of Science to identify studies till February 2020 and conducted a meta-analysis on the association between air pollution (PM2.5, particulate matter with aerodynamic diameter less than 2.5 μm; PM10, particulate matter with aerodynamic diameter less than 10 μm; NO2, nitrogen dioxide; SO2, sulfur dioxide; CO, carbon monoxide; O3, ozone) and stroke (hospital admission, incidence, and mortality). Fixed- or random-effects model was used to calculate pooled odds ratios (OR)/hazard ratio (HR) and their 95% confidence intervals (CI) for a 10 μg/m3 increase in air pollutant concentration. RESULTS A total of 68 studies conducted from more than 23 million participants were included in our meta-analysis. Meta-analyses showed significant associations of all six air pollutants and stroke hospital admission (e.g., PM2.5: OR = 1.008 (95% CI 1.005, 1.011); NO2: OR = 1.023 (95% CI 1.015, 1.030), per 10 μg/m3 increases in air pollutant concentration). Exposure to PM2.5, SO2, and NO2 was associated with increased risks of stroke incidence (PM2.5: HR = 1.048 (95% CI 1.020, 1.076); SO2: HR = 1.002 (95% CI 1.000, 1.003); NO2: HR = 1.002 (95% CI 1.000, 1.003), respectively). However, no significant differences were found in associations of PM10, CO, O3, and stroke incidence. Except for CO and O3, we found that higher level of air pollution (PM2.5, PM10, SO2, and NO2) exposure was associated with higher stroke mortality (e.g., PM10: OR = 1.006 (95% CI 1.003, 1.010), SO2: OR = 1.006 (95% CI 1.005, 1.008). CONCLUSIONS Exposure to air pollution was positively associated with an increased risk of stroke hospital admission (PM2.5, PM10, SO2, NO2, CO, and O3), incidence (PM2.5, SO2, and NO2), and mortality (PM2.5, PM10, SO2, and NO2). Our study would provide a more comprehensive evidence of air pollution and stroke, especially SO2 and NO2.
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The Association Between Ambient Air Pollution and Atrial Fibrillation.
Chen, M, Zhao, J, Zhuo, C, Zheng, L
International heart journal. 2021;(2):290-297
Abstract
Atrial fibrillation (AF) is the most common cardiac arrhythmia; it has been known to increase the risk of stroke and heart failure. The association between air pollutants and AF has remained to be controversial. Thus, in this study, we sought to undertake a systematic review and meta-analysis in order to assess the short- and long-term effects of ambient air pollution on AF.We searched PubMed, Web of Science, Embase, and Ovid for all related studies up to October 2019. We used the random-effects model to estimate the excess risk percentage (ER%) and confidence intervals (CI) for particulate matter with diameter ≤ 2.5 (PM2.5) and ≤ 10 μm (PM10), sulfur dioxide (SO2), nitrogen dioxide (NO2), ozone (O3), and carbon monoxide (CO). Results were further analyzed by subgroups according to location, age, outcome, and gender.In total, 18 studies were included in our meta-analysis: 5 evaluated for long-term effects, 12 for short-term effects, and 1 for both long- and short-term effects. For the short term, ER per 10 μg/m3 increase of pollutants was 1.8% (0%-3.7%) for PM2.5 and 1.1% (-0.2%-2.4%) for PM10; per 10 parts per billion (ppb) increment of gaseous pollutions was 3.2% (0.6%-5.8%) for NO2, 2.9% (0.3%-5.7%) for SO2, 0.5% (-3.4%-4.7%) for O3, and 2.0% (-1.3%-5.4%) for CO per 1000 ppb change. The subgroup analysis showed the short-term effect was significantly different by region, gender, outcome, and age. Meanwhile, in the long term, except for O3, a statistically significant association was noted between AF incidence and all pollutants.Our meta-analysis suggests that short-term exposure to part of pollutants (PM2.5, SO2, and NO2) increases AF attack. Further, long-term exposure to air pollution can significantly contribute to the incidence of AF in a healthy population.
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Acute and chronic exposure to air pollution in relation with incidence, prevalence, severity and mortality of COVID-19: a rapid systematic review.
Katoto, PDMC, Brand, AS, Bakan, B, Obadia, PM, Kuhangana, C, Kayembe-Kitenge, T, Kitenge, JP, Nkulu, CBL, Vanoirbeek, J, Nawrot, TS, et al
Environmental health : a global access science source. 2021;(1):41
Abstract
BACKGROUND Air pollution is one of the world's leading mortality risk factors contributing to seven million deaths annually. COVID-19 pandemic has claimed about one million deaths in less than a year. However, it is unclear whether exposure to acute and chronic air pollution influences the COVID-19 epidemiologic curve. METHODS We searched for relevant studies listed in six electronic databases between December 2019 and September 2020. We applied no language or publication status limits. Studies presented as original articles, studies that assessed risk, incidence, prevalence, or lethality of COVID-19 in relation with exposure to either short-term or long-term exposure to ambient air pollution were included. All patients regardless of age, sex and location diagnosed as having COVID-19 of any severity were taken into consideration. We synthesised results using harvest plots based on effect direction. RESULTS Included studies were cross-sectional (n = 10), retrospective cohorts (n = 9), ecological (n = 6 of which two were time-series) and hypothesis (n = 1). Of these studies, 52 and 48% assessed the effect of short-term and long-term pollutant exposure, respectively and one evaluated both. Pollutants mostly studied were PM2.5 (64%), NO2 (50%), PM10 (43%) and O3 (29%) for acute effects and PM2.5 (85%), NO2 (39%) and O3 (23%) then PM10 (15%) for chronic effects. Most assessed COVID-19 outcomes were incidence and mortality rate. Acutely, pollutants independently associated with COVID-19 incidence and mortality were first PM2.5 then PM10, NO2 and O3 (only for incident cases). Chronically, similar relationships were found for PM2.5 and NO2. High overall risk of bias judgments (86 and 39% in short-term and long-term exposure studies, respectively) was predominantly due to a failure to adjust aggregated data for important confounders, and to a lesser extent because of a lack of comparative analysis. CONCLUSION The body of evidence indicates that both acute and chronic exposure to air pollution can affect COVID-19 epidemiology. The evidence is unclear for acute exposure due to a higher level of bias in existing studies as compared to moderate evidence with chronic exposure. Public health interventions that help minimize anthropogenic pollutant source and socio-economic injustice/disparities may reduce the planetary threat posed by both COVID-19 and air pollution pandemics.
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Effects of ambient particulate matter on fasting blood glucose: A systematic review and meta-analysis.
Ma, R, Zhang, Y, Sun, Z, Xu, D, Li, T
Environmental pollution (Barking, Essex : 1987). 2020;:113589
Abstract
Studies have found that ambient particulate matter (PM) affects fasting blood glucose. However, the results are not consistent. We conducted a systematic review and meta-analysis to determine the relationship between PM with an aerodynamic diameter of 10 μm or less (PM10) and PM with an aerodynamic diameter of 2.5 μm or less (PM2.5) and fasting blood glucose. We searched PubMed, Web of Science, the Wanfang Database and the China National Knowledge Infrastructure up to April 1, 2019. A total of 24 papers were included in the review, and 17 studies with complete or convertible quantitative information were included in the meta-analysis. The studies were divided into groups by PM size fractions (PM10 and PM2.5) and length of exposure. Long-term exposures were based on annual average concentrations, and short-term exposures were those lasting less than 28 days. In the long-term exposure group, fasting blood glucose increased 0.10 mmol/L (95% CI: 0.02, 0.17) per 10 μg/m3 of increased PM10 and 0.23 mmol/L (95% CI: 0.01, 0.45) per 10 μg/m3 of increased PM2.5. In the short-term exposure group, fasting blood glucose increased 0.02 mmol/L (95% CI: -0.01, 0.04) per 10 μg/m3 of increased PM10 and 0.08 mmol/L (95% CI: 0.04, 0.11) per 10 μg/m3 of increased PM2.5. Further prospective studies are needed to explore the relationship between ambient PM exposure and fasting blood glucose.
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Food chemoprevention and air pollution: the health comes with eating.
Visalli, G, Facciolà, A, Laganà, P, Di Pietro, A
Reviews on environmental health. 2020;(4):471-479
Abstract
Ambient air pollution is known to be an important causative agent of many non-communicable diseases, mainly due to fine particulate matter (PM2.5). According to Global Burden Disease study in 2015, the estimated premature deaths caused by PM2.5 were 4.2 million. Besides deaths, airborne pollution's effect on human health also has dramatic economic and social costs, contributing greatly to disability-adjusted life-year (DALY). To reduce the health impact is necessary a double approach, which includes the improvement of air quality and food chemoprevention, aimed at enhancing the homeostatic abilities of exposed subjects. The scavenging, antioxidant, and anti-inflammatory properties of nutraceuticals effectively counteract the pathogenic mechanisms common in almost all non-communicable diseases associated with air pollutants. Moreover, several bioactive compounds of food modulate, by epigenetic mechanisms, the metabolism of xenobiotics, favouring conjugation reactions and promoting excretion. This narrative review summarize the numerous pieces of evidence collected in the last decades by observational and experimental studies which underline the chemopreventive role of flavonoids, contained in several fruits and consumer beverages (wine, tea, etc.), and isothiocyanate sulforaphane, contained in the cruciferous vegetables belonging to the genus Brassica. These bioactive compounds, enhancing the individual homeostatic abilities, reduce the harmful effects of airborne pollution.
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The impact of air pollution to obesity.
Simkova, S, Veleminsky, M, Sram, RJ
Neuro endocrinology letters. 2020;(3):146-153
Abstract
BACKGROUD Air pollution in ambient air could affect the increase of obesity in children. METHOD Review analyze papers about the effect of polycyclic aromatic hydrocarbons (PAHs), fine particles (particulate matter < 2.5 μm, PM2.5), and traffic air pollution (NO2, NOx, PM2.5). RESULTS Prenatal exposure to concentrations 1.73-3.07 ng/m3 PAHs significantly increased obesity at age 5 and 7 years, up to 11 years. All studies indicate the significance of prenatal exposure with concentration > 0.3 ng/m3 of B[a]P (benzo[a]pyrene). Prenatal exposure to PM2.5 above concentrations 10.6-11.9 μg/m3 increased obesity in children up to the age of 9 years. Traffic air pollution was evaluated according to exposure to NO2 and PM2.5. Concentrations NO2 higher 30 μg/m3 affect adiponectin levels in cord blood, cholesterol metabolism, and therefore increase later the risk of overweight or obesity. PM2.5 9.2-11.6 μg/m3 during pregnancy affect adiponectin. These concentrations from the traffic air pollution can affect the metabolism in newborns later related to obesity. CONCLUSION All these studies indicate that contemporary concentrations of PAHs, PM2.5 and NO2 in ambient air, especially during prenatal period, affect overweight and obesity in children.