-
1.
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.
-
2.
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.
-
3.
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.
-
4.
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.
-
5.
Ambient air pollution and depression: A systematic review with meta-analysis up to 2019.
Fan, SJ, Heinrich, J, Bloom, MS, Zhao, TY, Shi, TX, Feng, WR, Sun, Y, Shen, JC, Yang, ZC, Yang, BY, et al
The Science of the total environment. 2020;:134721
Abstract
Although epidemiological studies have evaluated the associations of ambient air pollution with depression, the results remained mixed. To clarify the nature of the association, we performed a comprehensive systematic review and meta-analysis with the Inverse Variance Heterogeneity (IVhet) model to estimate the effect of ambient air pollution on depression. Three English and four Chinese databases were searched for epidemiologic studies investigating associations of ambient particulate (diameter ≤ 2.5 μm (PM2.5), ≤10 μm (PM10)) and gaseous (nitric oxide (NO), nitrogen dioxide (NO2), carbon monoxide (CO), sulfur dioxide (SO2) and ozone (O3)) air pollutants with depression. Odds ratios (OR) and corresponding 95% confidence intervals (CI) were calculated to evaluate the strength of the associations. We identified 22 eligible studies from 10 countries of the world. Under the IVhet model, per 10 µg/m3 increase in long-term exposure to PM2.5 (OR: 1.12, 95% CI: 0.97-1.29, I2: 51.6), PM10 (OR: 1.04, 95% CI: 0.88-1.25, I2: 85.7), and NO2 (OR: 1.05, 95% CI: 0.83-1.34, I2: 83.6), as well as short-term exposure to PM2.5 (OR: 1.01, 95% CI: 0.99-1.04, I2: 51.6), PM10 (OR: 1.01, 95% CI: 0.98-1.04, I2: 86.7), SO2 (OR: 1.03, 95% CI: 0.99-1.07, I2: 71.2), and O3 (OR: 1.01, 95% CI: 0.99-1.03, I2: 82.2) was not significantly associated with depression. However, we observed significant association between short-term NO2 exposure (per 10 µg/m3 increase) and depression (OR: 1.02, 95% CI: 1.00-1.04, I2: 65.4). However, the heterogeneity was high for all of the pooled estimates, which reduced credibility of the cumulative evidence. Additionally, publication bias was detected for six of eight meta-estimates. In conclusion, short-term exposure to NO2, but not other air pollutants, was significantly associated with depression. Given the limitations, a larger meta-analysis incorporating future well-designed longitudinal studies, and investigations into potential biologic mechanisms, will be necessary for a more definitive result.
-
6.
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.
-
7.
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.
-
8.
Association between ambient air pollution and Parkinson's disease: Systematic review and meta-analysis.
Hu, CY, Fang, Y, Li, FL, Dong, B, Hua, XG, Jiang, W, Zhang, H, Lyu, Y, Zhang, XJ
Environmental research. 2019;:448-459
Abstract
Air pollution has been evaluated as a possible risk factor for Parkinson's disease (PD), but, the present results are inconsistent and have not been combined. We performed a systematic review and meta-analysis to estimate the association between long-term exposure to ambient air pollution and PD, given the nature of disease etiology. A total of 10 studies were identified by searching Web of Science, Science Direct, and PubMed before October 2017. We found a significantly increased risk of PD with 10 parts per billion (ppb) increase in nitrogen oxides (NOx) exposure (relative risk (RR) = 1.06; 95% confidence interval (CI): 1.04, 1.09). The pooled RR for the association between carbon monoxide (CO) exposure, 1 parts per million (ppm) increment, and the risk of PD was 1.65 (95% CI: 1.10, 2.48). The pooled RRs for the association between nitrogen dioxide (NO2) and ozone (O3) exposure per 1 ppb increment, and the risk of PD were 1.01 (95% CI: 1.00, 1.03) and 1.01 (95% CI: 1.00, 1.02), respectively. There was a significant heterogeneity in the meta-analysis for fine particulate matter (PM2.5), NO2, sulfur dioxide (SO2), and CO. We concluded that NO2, NOx, CO and O3 exposure were associated with an increased risk of PD, although there is high risk of bias. The dose-response effects evaluated by high-quality studies are needed. Researches should be expanded to low- and/or middle- income countries where indoor and outdoor air pollution are high. CAPSULE Long-term exposure to ambient NO2, NOx, CO and O3 can increase the risk of Parkinson's disease.
-
9.
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.
-
10.
Evaluation of a meta-analysis of air quality and heart attacks, a case study.
Stanley Young, S, Kindzierski, WB
Critical reviews in toxicology. 2019;(1):85-94
Abstract
It is generally acknowledged that claims from observational studies often fail to replicate. An exploratory study was undertaken to assess the reliability of base studies used in meta-analysis of short-term air quality-myocardial infarction risk and to judge the reliability of statistical evidence from meta-analysis that uses data from observational studies. A highly cited meta-analysis paper examining whether short-term air quality exposure triggers myocardial infarction was evaluated as a case study. The paper considered six air quality components - carbon monoxide, nitrogen dioxide, sulphur dioxide, particulate matter 10 μm and 2.5 μm in diameter (PM10 and PM2.5), and ozone. The number of possible questions and statistical models at issue in each of 34 base papers used were estimated and p-value plots for each of the air components were constructed to evaluate the effect heterogeneity of p-values used from the base papers. Analysis search spaces (number of statistical tests possible) in the base papers were large, median = 12,288 (interquartile range = 2496 - 58,368), in comparison to actual statistical test results presented. Statistical test results taken from the base papers may not provide unbiased measures of effect for meta-analysis. Shapes of p-value plots for the six air components were consistent with the possibility of analysis manipulation to obtain small p-values in several base papers. Results suggest the appearance of heterogeneous, researcher-generated p-values used in the meta-analysis rather than unbiased evidence of real effects for air quality. We conclude that this meta-analysis does not provide reliable evidence for an association of air quality components with myocardial risk.