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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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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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Association between Outdoor Air Pollution and Childhood Leukemia: A Systematic Review and Dose-Response Meta-Analysis.
Filippini, T, Hatch, EE, Rothman, KJ, Heck, JE, Park, AS, Crippa, A, Orsini, N, Vinceti, M
Environmental health perspectives. 2019;(4):46002
Abstract
BACKGROUND A causal link between outdoor air pollution and childhood leukemia has been proposed, but some older studies suffer from methodological drawbacks. To the best of our knowledge, no systematic reviews have summarized the most recently published evidence and no analyses have examined the dose-response relation. OBJECTIVE We investigated the extent to which outdoor air pollution, especially as resulting from traffic-related contaminants, affects the risk of childhood leukemia. METHODS We searched all case-control and cohort studies that have investigated the risk of childhood leukemia in relation to exposure either to motorized traffic and related contaminants, based on various traffic-related metrics (number of vehicles in the closest roads, road density, and distance from major roads), or to measured or modeled levels of air contaminants such as benzene, nitrogen dioxide, 1,3-butadiene, and particulate matter. We carried out a meta-analysis of all eligible studies, including nine studies published since the last systematic review and, when possible, we fit a dose-response curve using a restricted cubic spline regression model. RESULTS We found 29 studies eligible to be included in our review. In the dose-response analysis, we found little association between disease risk and traffic indicators near the child's residence for most of the exposure range, with an indication of a possible excess risk only at the highest levels. In contrast, benzene exposure was positively and approximately linearly associated with risk of childhood leukemia, particularly for acute myeloid leukemia, among children under 6 y of age, and when exposure assessment at the time of diagnosis was used. Exposure to nitrogen dioxide showed little association with leukemia risk except at the highest levels. DISCUSSION Overall, the epidemiologic literature appears to support an association between benzene and childhood leukemia risk, with no indication of any threshold effect. A role for other measured and unmeasured pollutants from motorized traffic is also possible. https://doi.org/10.1289/EHP4381.
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Meta-Prediction of MTHFR Gene Polymorphism and Air Pollution on the Risks of Congenital Heart Defects Worldwide: A Transgenerational Analysis.
Yang, HL, Yang, YL, Yu, CH, Shiao, SPK
International journal of environmental research and public health. 2018;(8)
Abstract
Congenital heart disease (CHD) is the leading cause of death in children, and is affected by genetic and environmental factors. To investigate the association of air pollution with methylene-tetrahydrofolate reductase (MTHFR) polymorphisms and the risk of CHD, we included 58 study groups of children and parents, with 12,347 cases and 18,106 controls worldwide. Both MTHFR C677T (rs 1801133) and A1298C (rs 1801131) gene polymorphisms were risks for CHD in children with transgenerational effects from their parents. Countries with greater risks of CHD with a pooled risk ratio (RR) > 2 from MTHFR 677 polymorphisms included Germany, Portugal, China, and Egypt for children; and Brazil, Puerto Rico, Mexico, China, and Egypt for mothers. Whereas, countries with greater risk of CHD with RR > 2 from MTHFR 1298 polymorphisms included Taiwan, Turkey, and Egypt for children; and Brazil, China, and Egypt for mothers. Additionally, meta-prediction analysis revealed that the percentages of MTHFR 677TT and TT plus CT polymorphisms together were increased in countries with higher levels of air pollution, with a trend of increased CHD risks with higher levels of air pollution for children (p = 0.07). Our findings may have significant implications for inflammatory pathways in association with MTHFR polymorphisms and future intervention studies to correct for folate-related enzyme deficits resultied from MTHFR polymorphisms to prevent CHDs for future generations.
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Cardiorespiratory health effects of gaseous ambient air pollution exposure in low and middle income countries: a systematic review and meta-analysis.
Newell, K, Kartsonaki, C, Lam, KBH, Kurmi, O
Environmental health : a global access science source. 2018;(1):41
Abstract
BACKGROUND Lack of research on the effects of gaseous pollutants (nitrogen oxides [NOx], sulfur dioxide [SO2], carbon monoxide [CO] and ozone [O3]) in the ambient environment on health outcomes from within low and middle income countries (LMICs) is leading to reliance on results from studies performed within high income countries (HICs). This systematic review and meta-analysis examines the cardiorespiratory health effects of gaseous pollutants in LMICs exclusively. METHODS Systematic searching was carried out and estimates pooled by pollutant, lag and outcome, and presented as excess relative risk per 10 μg/m3 (NOx, SO2, O3) or 1 ppm (CO) increase pollutant. Sub-group analysis was performed examining estimates by specific outcomes, city and co-pollutant adjustment. RESULTS Sixty studies met the inclusion criteria, most (44) from the East Asia and Pacific region. A 10 μg/m3 increase in same day NOx was associated with 0.92% (95% CI: 0.44, 1.39), and 0.70% (0.01, 1.40) increases in cardiovascular and respiratory mortality respectively, same day NOx was not associated with morbidity. Same day sulfur dioxide was associated with 0.73% (0.04, 1.42) and 0.50% (0.01, 1.00) increases in respiratory morbidity and in cardiovascular mortality respectively. CONCLUSIONS Acute exposure to gaseous ambient air pollution (AAP) is associated with increases in morbidity and mortality in LMICs, with greatest associations observed for cardiorespiratory mortality.
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Global Association of Air Pollution and Cardiorespiratory Diseases: A Systematic Review, Meta-Analysis, and Investigation of Modifier Variables.
Requia, WJ, Adams, MD, Arain, A, Papatheodorou, S, Koutrakis, P, Mahmoud, M
American journal of public health. 2018;(S2):S123-S130
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Abstract
BACKGROUND Little is known about the health risks of air pollution and cardiorespiratory diseases, globally, across regions and populations, which may differ because of external factors. OBJECTIVES We systematically reviewed the evidence on the association between air pollution and cardiorespiratory diseases (hospital admissions and mortality), including variability by energy, transportation, socioeconomic status, and air quality. SEARCH METHODS We conducted a literature search (PubMed and Web of Science) for studies published between 2006 and May 11, 2016. SELECTION CRITERIA We included studies if they met all of the following criteria: (1) considered at least 1 of these air pollutants: carbon monoxide, sulfur dioxide, nitrogen dioxide, ozone, or particulate matter (PM2.5 or PM10); (2) reported risk for hospital admissions, mortality, or both; (3) presented individual results for respiratory diseases, cardiovascular diseases, or both; (4) considered the age groups younger than 5 years, older than 65 years, or all ages; and (5) did not segregate the analysis by gender. DATA COLLECTION AND ANALYSIS We extracted data from each study, including location, health outcome, and risk estimates. We performed a meta-analysis to estimate the overall effect and to account for both within- and between-study heterogeneity. Then, we applied a model selection (least absolute shrinkage and selection operator) to assess the modifier variables, and, lastly, we performed meta-regression analyses to evaluate the modifier variables contributing to heterogeneity among studies. MAIN RESULTS We assessed 2183 studies, of which we selected 529 for in-depth review, and 70 articles fulfilled our study inclusion criteria. The 70 studies selected for meta-analysis encompass more than 30 million events across 28 countries. We found positive associations between cardiorespiratory diseases and different air pollutants. For example, when we considered only the association between PM2.5 and respiratory diseases ( Figure 1 , we observed a risk equal to 2.7% (95% confidence interval = 0.9%, 7.7%). Our results showed statistical significance in the test of moderators for all pollutants, suggesting that the modifier variables influence the average cardiorespiratory disease risk and may explain the varying effects of air pollution. CONCLUSIONS Variables related to aspects of energy, transportation, and socioeconomic status may explain the varying effect size of the association between air pollution and cardiorespiratory diseases. Public Health Implications. Our study provides a transferable model to estimate the health effects of air pollutants to support the creation of environmental health public policies for national and international intervention.
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A Meta-Prediction of Methylenetetrahydrofolate-Reductase Polymorphisms and Air Pollution Increased the Risk of Ischemic Heart Diseases Worldwide.
Chen, ZF, Young, L, Yu, CH, Shiao, SPK
International journal of environmental research and public health. 2018;(7)
Abstract
Ischemic heart disease (IHD) is among the leading causes of death worldwide. Methylenetetrahydrofolate reductase (MTHFR) polymorphisms have been associated with IHD risk, but the findings presented with heterogeneity. The purpose of the present meta-analysis was to provide an updated evaluation by integrating machine-learning based analytics to examine the potential source of heterogeneity on the associations between MTHFR polymorphisms and the risk of various subtypes of IHD, as well as the possible impact of air pollution on MTHFR polymorphisms and IHD risks. A comprehensive search of various databases was conducted to locate 123 studies (29,697 cases and 31,028 controls) for MTHFR C677T, and 18 studies (7158 cases and 5482 controls) for MTHFR A1298C. Overall, MTHFR 677 polymorphisms were risks for IHD (TT: Risk ratio (RR) = 1.23, p < 0.0001; CT: RR = 1.04, p = 0.0028, and TT plus CT: RR = 1.09, p < 0.0001). In contrast, MTHFR 677 CC wildtype was protective against IHD (RR = 0.91, p < 0.00001) for overall populations. Three countries with elevated IHD risks from MTHFR C677T polymorphism with RR >2 included India, Turkey, and Tunisia. Meta-predictive analysis revealed that increased air pollution was associated with increased MTHFR 677 TT and CT polymorphisms in both the case and control group (p < 0.05), with the trend of increased IHD risk resulting from increased air pollution. These results associate the potential inflammatory pathway with air pollution and the folate pathway with MTHFR polymorphism. Future intervention studies can be designed to mitigate MTHFR enzyme deficiencies resulting from gene polymorphisms to prevent IHDs for at-risk populations.
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Outdoor Air Pollution and COPD-Related Emergency Department Visits, Hospital Admissions, and Mortality: A Meta-Analysis.
DeVries, R, Kriebel, D, Sama, S
COPD. 2017;(1):113-121
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Abstract
A systematic literature review was performed to identify all peer-reviewed literature quantifying the association between short-term exposures of particulate matter <2.5 microns (PM2.5), nitrogen dioxide (NO2), and sulfur dioxide (SO2) and COPD-related emergency department (ED) visits, hospital admissions (HA), and mortality. These results were then pooled for each pollutant through meta-analyses with a random effects model. Subgroup meta-analyses were explored to study the effects of selected lag/averaging times and health outcomes. A total of 37 studies satisfied our inclusion criteria, contributing to a total of approximately 1,115,000 COPD-related acute events (950,000 HAs, 80,000 EDs, and 130,000 deaths) to our meta-estimates. An increase in PM2.5 of 10 ug/m3 was associated with a 2.5% (95% CI: 1.6-3.4%) increased risk of COPD-related ED and HA, an increase of 10 ug/m3 in NO2 was associated with a 4.2% (2.5-6.0%) increase, and an increase of 10 ug/m3 in SO2 was associated with a 2.1% (0.7-3.5%) increase. The strength of these pooled effect estimates, however, varied depending on the selected lag/averaging time between exposure and outcome. Similar pooled effects were estimated for each pollutant and COPD-related mortality. These results suggest an ongoing threat to the health of COPD patients from both outdoor particulates and gaseous pollutants. Ambient outdoor concentrations of PM2.5, NO2, and SO2 were significantly and positively associated with both COPD-related morbidity and mortality.
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Air pollution and venous thrombosis: a meta-analysis.
Tang, L, Wang, QY, Cheng, ZP, Hu, B, Liu, JD, Hu, Y
Scientific reports. 2016;:32794
Abstract
Exposure to air pollution has been linked to cardiovascular and respiratory disorders. However, the effect of air pollution on venous thrombotic disorders is uncertain. We performed a meta-analysis to assess the association between air pollution and venous thrombosis. PubMed, Embase, EBM Reviews, Healthstar, Global Health, Nursing Database, and Web of Science were searched for citations on air pollutants (carbon monoxide, sulfur dioxide, nitrogen dioxide, ozone, and particulate matters) and venous thrombosis. Using a random-effects model, overall risk estimates were derived for each increment of 10 μg/m(3) of pollutant concentration. Of the 485 in-depth reviewed studies, 8 citations, involving approximately 700,000 events, fulfilled the inclusion criteria. All the main air pollutants analyzed were not associated with an increased risk of venous thrombosis (OR = 1.005, 95% CI = 0.998-1.012 for PM2.5; OR = 0.995, 95% CI = 0.984-1.007 for PM10; OR = 1.006, 95% CI = 0.994-1.019 for NO2). Based on exposure period and thrombosis location, additional subgroup analyses provided results comparable with those of the overall analyses. There was no evidence of publication bias. Therefore, this meta analysis does not suggest the possible role of air pollution as risk factor for venous thrombosis in general population.