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1.
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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2.
Aerosol microphysics and chemistry reveal the COVID19 lockdown impact on urban air quality.
Eleftheriadis, K, Gini, MI, Diapouli, E, Vratolis, S, Vasilatou, V, Fetfatzis, P, Manousakas, MI
Scientific reports. 2021;(1):14477
Abstract
Air quality in urban areas and megacities is dependent on emissions, physicochemical process and atmospheric conditions in a complex manner. The impact on air quality metrics of the COVID-19 lockdown measures was evaluated during two periods in Athens, Greece. The first period involved stoppage of educational and recreational activities and the second severe restrictions to all but necessary transport and workplace activities. Fresh traffic emissions and their aerosol products in terms of ultrafine nuclei particles and nitrates showed the most significant reduction especially during the 2nd period (40-50%). Carbonaceous aerosol both from fossil fuel emissions and biomass burning, as well as aging ultrafine and accumulation mode particles showed an increase of 10-20% of average before showing a decline (5 to 30%). It is found that removal of small nuclei and Aitken modes increased growth rates and migration of condensable species to larger particles maintaining aerosol volume.
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3.
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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4.
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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5.
Air pollution and IgE sensitization in 4 European birth cohorts-the MeDALL project.
Melén, E, Standl, M, Gehring, U, Altug, H, Antó, JM, Berdel, D, Bergström, A, Bousquet, J, Heinrich, J, Koppelman, GH, et al
The Journal of allergy and clinical immunology. 2021;(2):713-722
Abstract
BACKGROUND Whether long-term exposure air to pollution has effects on allergic sensitization is controversial. OBJECTIVE Our aim was to investigate associations of air pollution exposure at birth and at the time of later biosampling with IgE sensitization against common food and inhalant allergens, or specific allergen molecules, in children aged up to 16 years. METHODS A total of 6163 children from 4 European birth cohorts participating in the Mechanisms of the Development of ALLergy [MeDALL] consortium were included in this meta-analysis of the following studies: Children, Allergy, Milieu, Stockholm, Epidemiology (BAMSE) (Sweden), Influences of Lifestyle-Related Factors on the Human Immune System and Development of Allergies in Childhood (LISA)/German Infant Study on the Influence of Nutrition Intervention PLUS Environmental and Genetic Influences on Allergy Development (GINIplus) (Germany), and Prevention and Incidence of Asthma and Mite Allergy (PIAMA) (The Netherlands). The following indicators were modeled by land use regression: individual residential outdoor levels of particulate matter with aerodynamic diameters less than 2.5 μm, less than 10 μm, and between 2.5 and 10 μm; PM2.5 absorbance (a measurement of the blackness of PM2.5 filters); and nitrogen oxides levels. Blood samples drawn at ages 4 to 6 (n = 5989), 8 to 10 (n = 6603), and 15 to 16 (n = 5825) years were analyzed for IgE sensitization to allergen extracts by ImmunoCAP. Additionally, IgE against 132 allergen molecules was measured by using the MedALL microarray chip (n = 1021). RESULTS Air pollution was not consistently associated with IgE sensitization to any common allergen extract up to age 16 years. However, allergen-specific analyses suggested increased risks of sensitization to birch (odds ratio [OR] = 1.12 [95% CI = 1.01-1.25] per 10-μg/m3 increase in NO2 exposure). In a subpopulation with microarray data, IgE to the major timothy grass allergen Phleum pratense 1 (Phl p 1) and the cat allergen Felis domesticus 1 (Fel d 1) greater than 3.5 Immuno Solid-phase Allergen Chip standardized units for detection of IgE antibodies were related to PM2.5 exposure at birth (OR = 3.33 [95% CI = 1.40-7.94] and OR = 4.98 [95% CI = 1.59-15.60], respectively, per 5-μg/m3 increase in exposure). CONCLUSION Air pollution exposure does not seem to increase the overall risk of allergic sensitization; however, sensitization to birch as well as grass pollen Phl p 1 and cat Fel d 1 allergen molecules may be related to specific pollutants.
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6.
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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7.
Blood Plasma's Protective Ability against the Degradation of S-Nitrosoglutathione under the Influence of Air-Pollution-Derived Metal Ions in Patients with Exacerbation of Heart Failure and Coronary Artery Disease.
Wądołek, A, Drwiła, D, Oszajca, M, Stochel, G, Konduracka, E, Brindell, M
International journal of molecular sciences. 2021;(19)
Abstract
One of the consequences of long-term exposure to air pollutants is increased mortality and deterioration of life parameters, especially among people diagnosed with cardiovascular diseases (CVD) or impaired respiratory system. Aqueous soluble inorganic components of airborne particulate matter containing redox-active transition metal ions affect the stability of S-nitrosothiols and disrupt the balance in the homeostasis of nitric oxide. Blood plasma's protective ability against the decomposition of S-nitrosoglutathione (GSNO) under the influence of aqueous PM extract among patients with exacerbation of heart failure and coronary artery disease was studied and compared with a group of healthy volunteers. In the environment of CVD patients' plasma, NO release from GSNO was facilitated compared to the plasma of healthy controls, and the addition of ascorbic acid boosted this process. Model studies with albumin revealed that the amount of free thiol groups is one of the crucial factors in GSNO decomposition. The correlation between the concentration of NO released and -SH level in blood plasma supports this conclusion. Complementary studies on gamma-glutamyltranspeptidase activity and ICP-MS multielement analysis of CVD patients' plasma samples in comparison to a healthy control group provide broader insights into the mechanism of cardiovascular risk development induced by air pollution.
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8.
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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9.
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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10.
Physical activity in an air-polluted environment: behavioral, psychological and neuroimaging protocol for a prospective cohort study (Healthy Aging in Industrial Environment study - Program 4).
Elavsky, S, Jandačková, V, Knapová, L, Vašendová, V, Sebera, M, Kaštovská, B, Blaschová, D, Kühnová, J, Cimler, R, Vilímek, D, et al
BMC public health. 2021;(1):126
Abstract
BACKGROUND Air pollution has been linked to increased mortality and morbidity. The Program 4 of the Healthy Aging in Industrial Environment study investigates whether the health and wellbeing benefits of physical activity (PA) can be fully realized in individuals living in highly polluted environments. Herein, we introduce the behavioral, psychological and neuroimaging protocol of the study. METHODS This is a prospective cohort study of N = 1500 individuals aged 18-65 years comparing: (1) individuals living in the highly polluted, industrial region surrounding the city of Ostrava (n = 750), and (2) controls from the comparison region with relative low pollution levels in Southern Bohemia (n = 750). Quota sampling is used to obtain samples balanced on age, gender, PA status (60% active runners vs. 40% insufficiently active). Participants are screened and complete baseline assessments through online questionnaires and in-person lab-based assessments of physiological, biomechanical, neuroimaging and cognitive function parameters. Prospective 12-month intensive monitoring of air pollution and behavioral parameters (PA, inactivity, and sleep) follows, with a focus on PA-related injuries and psychological factors through fitness trackers, smartphones, and mobile apps. Subsequently, there will be a 5-year follow-up of the study cohort. DISCUSSION The design of the study will allow for (1) the assessment of both short-term variation and long-term change in behavioral parameters, (2) evaluation of the incidence of musculoskeletal injuries and psychological factors impacting behavior and injury recovery, and (3) the impact that air pollution status (and change) has on behavior, psychological resilience, and injury recovery. Furthermore, the integration of MRI techniques and cognitive assessment in combination with data on behavioral, biological and environmental variables will provide an opportunity to examine brain structure and cognitive function in relation to health behavior and air pollution, as well as other factors affecting resilience against and vulnerability to adverse changes in brain structure and cognitive aging. This study will help inform individuals about personal risk factors and decision-makers about the impact of environmental factors on negative health outcomes and potential underlying biological, behavioral and psychological mechanisms. Challenges and opportunities stemming from the timing of the study that coincided with the COVID-19 pandemic are also discussed.