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1.
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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2.
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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3.
Ambient air pollution and body weight status in adults: A systematic review and meta-analysis.
Huang, S, Zhang, X, Huang, J, Lu, X, Liu, F, Gu, D
Environmental pollution (Barking, Essex : 1987). 2020;(Pt A):114999
Abstract
Overweight and obesity have become a global epidemic and concern, and contributed to at least 4.0 million deaths each year worldwide. However, current evidence regarding the impact of air pollution on body weight status remains inconsistent. We therefore conducted a systematic review and meta-analysis to evaluate the effect of long-term exposure to ambient air pollutants on body weight status in adults. Three databases were searched up to Dec 31, 2019 for articles investigating the association of gaseous (sulfur dioxide, nitrogen dioxide, ozone) and particulate (diameter ≤ 10 μm or ≤ 2.5 μm) air pollutants with body weight status. Random effect models were used to estimate the pooled odds ratios (ORs), regression coefficients (β) and their 95% confidence intervals (95% CIs) associated with air pollution. Among twelve studies that were eligible in the systematic review, ten were used to estimate the pooled effect size, and most of them were cross-sectional studies. We identified that ambient air pollution had adverse effects on body weight status. For example, elevated PM2.5 and O3 were associated with higher level of body mass index, with the pooled β (95% CIs) of 0.34 (0.30-0.38) and 0.21 (0.17-0.24) per 10 μg/m3 increment, respectively. In addition, increased NO2, SO2 and O3 were associated with higher risk of having overweight/obesity, with the corresponding pooled OR (95% CI) of 1.13 (1.01-1.26), 1.04 (1.01-1.06) and 1.07 (1.02-1.13) per 10 μg/m3 increment. Overall, air pollution is a potential risk factor for body weight status in adults, and more high-quality studies, especially prospective studies from severely polluted regions, are warranted for comprehensive understanding of its health effects.
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4.
The association between short-term exposure to ambient air pollution and fractional exhaled nitric oxide level: A systematic review and meta-analysis of panel studies.
Chen, X, Liu, F, Niu, Z, Mao, S, Tang, H, Li, N, Chen, G, Liu, S, Lu, Y, Xiang, H
Environmental pollution (Barking, Essex : 1987). 2020;(Pt A):114833
Abstract
Several epidemiological studies have evaluated the fractional exhaled nitric oxide (FeNO) of ambient air pollution but the results were controversial. We therefore conducted a systematic review and meta-analysis to investigate the associations between short-term exposure to air pollutants and FeNO level. We searched PubMed and Web of Science and included a total of 27 articles which focused on associations between ambient air pollutants (PM10, PM2.5, black carbon (BC), nitrogen dioxide (NO2), sulfur dioxide (SO2), ozone (O3)) exposure and the change of FeNO. Random effect model was used to calculate the percent change of FeNO in association with a 10 or 1 μg/m3 increase in air pollutants exposure concentrations. A 10 μg/m3 increase in short-term PM10, PM2.5, NO2, and SO2 exposure was associated with a 3.20% (95% confidence interval (95%CI): 1.11%, 5.29%), 2.25% (95%CI: 1.51%, 2.99%),4.90% (95%CI: 1.98%, 7.81%), and 8.28% (95%CI: 3.61%, 12.59%) change in FeNO, respectively. A 1 μg/m3 increase in short-term exposure to BC was associated with 3.42% (95%CI: 1.34%, 5.50%) change in FeNO. The association between short-term exposure to O3 and FeNO level was insignificant (P>0.05). Future studies are warranted to investigate the effect of multiple pollutants, different sources and composition of air pollutants on airway inflammation.
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5.
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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6.
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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7.
Prenatal Particulate Air Pollution and DNA Methylation in Newborns: An Epigenome-Wide Meta-Analysis.
Gruzieva, O, Xu, CJ, Yousefi, P, Relton, C, Merid, SK, Breton, CV, Gao, L, Volk, HE, Feinberg, JI, Ladd-Acosta, C, et al
Environmental health perspectives. 2019;(5):57012
Abstract
BACKGROUND Prenatal exposure to air pollution has been associated with childhood respiratory disease and other adverse outcomes. Epigenetics is a suggested link between exposures and health outcomes. OBJECTIVES We aimed to investigate associations between prenatal exposure to particulate matter (PM) with diameter [Formula: see text] ([Formula: see text]) or [Formula: see text] ([Formula: see text]) and DNA methylation in newborns and children. METHODS We meta-analyzed associations between exposure to [Formula: see text] ([Formula: see text]) and [Formula: see text] ([Formula: see text]) at maternal home addresses during pregnancy and newborn DNA methylation assessed by Illumina Infinium HumanMethylation450K BeadChip in nine European and American studies, with replication in 688 independent newborns and look-up analyses in 2,118 older children. We used two approaches, one focusing on single cytosine-phosphate-guanine (CpG) sites and another on differentially methylated regions (DMRs). We also related PM exposures to blood mRNA expression. RESULTS Six CpGs were significantly associated [false discovery rate (FDR) [Formula: see text]] with prenatal [Formula: see text] and 14 with [Formula: see text] exposure. Two of the [Formula: see text] CpGs mapped to FAM13A (cg00905156) and NOTCH4 (cg06849931) previously associated with lung function and asthma. Although these associations did not replicate in the smaller newborn sample, both CpGs were significant ([Formula: see text]) in 7- to 9-y-olds. For cg06849931, however, the direction of the association was inconsistent. Concurrent [Formula: see text] exposure was associated with a significantly higher NOTCH4 expression at age 16 y. We also identified several DMRs associated with either prenatal [Formula: see text] and or [Formula: see text] exposure, of which two [Formula: see text] DMRs, including H19 and MARCH11, replicated in newborns. CONCLUSIONS Several differentially methylated CpGs and DMRs associated with prenatal PM exposure were identified in newborns, with annotation to genes previously implicated in lung-related outcomes. https://doi.org/10.1289/EHP4522.
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8.
Impact of ambient air pollution on physical activity among adults: a systematic review and meta-analysis.
An, R, Zhang, S, Ji, M, Guan, C
Perspectives in public health. 2018;(2):111-121
Abstract
AIMS: This study systematically reviewed literature regarding the impact of ambient air pollution on physical activity among children and adults. METHODS Keyword and reference search was conducted in PubMed and Web of Science to systematically identify articles meeting all of the following criteria - study designs: interventions or experiments, retrospective or prospective cohort studies, cross-sectional studies, and case-control studies; subjects: adults; exposures: specific air pollutants and overall air quality; outcomes: physical activity and sedentary behaviour; article types: peer-reviewed publications; and language: articles written in English. Meta-analysis was performed to estimate the pooled effect size of ambient PM2.5 air pollution on physical inactivity. RESULTS Seven studies met the inclusion criteria. Among them, six were conducted in the United States, and one was conducted in the United Kingdom. Six adopted a cross-sectional study design, and one used a prospective cohort design. Six had a sample size larger than 10,000. Specific air pollutants assessed included PM2.5, PM10, O3, and NOx, whereas two studies focused on overall air quality. All studies found air pollution level to be negatively associated with physical activity and positively associated with leisure-time physical inactivity. Study participants, and particularly those with respiratory disease, self-reported a reduction in outdoor activities to mitigate the detrimental impact of air pollution. Meta-analysis revealed a one unit (μg/m3) increase in ambient PM2.5 concentration to be associated with an increase in the odds of physical inactivity by 1.1% (odds ratio = 1.011; 95% confidence interval = 1.001, 1.021; p-value < .001) among US adults. CONCLUSIONS Existing literature in general suggested that air pollution discouraged physical activity. Current literature predominantly adopted a cross-sectional design and focused on the United States. Future studies are warranted to implement a longitudinal study design and evaluate the impact of air pollution on physical activity in heavily polluted developing countries.
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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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10.
Modeling vascular inflammation and atherogenicity after inhalation of ambient levels of ozone: exploratory lessons from transcriptomics.
Tham, A, Lullo, D, Dalton, S, Zeng, S, van Koeverden, I, Arjomandi, M
Inhalation toxicology. 2017;(3):96-105
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Abstract
BACKGROUND Epidemiologic studies have linked inhalation of air pollutants such as ozone to cardiovascular mortality. Human exposure studies have shown that inhalation of ambient levels of ozone causes airway and systemic inflammation and an imbalance in sympathetic/parasympathetic tone. METHODS To explore molecular mechanisms through which ozone inhalation contributes to cardiovascular mortality, we compared transcriptomics data previously obtained from bronchoalveolar lavage (BAL) cells obtained from healthy subjects after inhalational exposure to ozone (200 ppb for 4 h) to those of various cell samples from 11 published studies of patients with atherosclerotic disease using the Nextbio genomic data platform. Overlapping gene ontologies that may be involved in the transition from pulmonary to systemic vascular inflammation after ozone inhalation were explored. Local and systemic enzymatic activity of an overlapping upregulated gene, matrix metalloproteinase-9 (MMP-9), was measured by zymography after ozone exposure. RESULTS A set of differentially expressed genes involved in response to stimulus, stress, and wounding were in common between the ozone and most of the atherosclerosis studies. Many of these genes contribute to biological processes such as cholesterol metabolism dysfunction, increased monocyte adherence, endothelial cell lesions, and matrix remodeling, and to diseases such as heart failure, ischemia, and atherosclerotic occlusive disease. Inhalation of ozone increased MMP-9 enzymatic activity in both BAL fluid and serum. CONCLUSIONS Comparison of transcriptomics between BAL cells after ozone exposure and various cell types from patients with atherosclerotic disease reveals commonly regulated processes and potential mechanisms by which ozone inhalation may contribute to progression of pre-existent atherosclerotic lesions.