Ambient air pollution and COVID-19 risk: Evidence from 35 observational studies.
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ABSTRACT: Background and aims
The coronavirus disease 2019 (COVID-19) pandemic is severely threatening and challenging public health worldwide. Epidemiological studies focused on the influence of outdoor air pollution (AP) on COVID-19 risk have produced inconsistent conclusions. We aimed to quantitatively explore this association using a meta-analysis.Methods
We searched for studies related to outdoor AP and COVID-19 risk in the Embase, PubMed, and Web of Science databases. No language restriction was utilized. The search date entries were up to August 13, 2021. Pooled estimates and 95% confidence intervals (CIs) were obtained with random-/fixed-effects models. PROSPERO registration number: CRD42021244656.Results
A total of 35 articles were eligible for the meta-analysis. For long-term exposure to AP, COVID-19 incidence was positively associated with 1 μg/m3 increase in nitrogen dioxide (NO2; effect size = 1.042, 95% CI 1.017-1.068), particulate matter with diameter <2.5 μm (PM2.5; effect size = 1.056, 95% CI 1.039-1.072), and sulfur dioxide (SO2; effect size = 1.071, 95% CI 1.002-1.145). The COVID-19 mortality was positively associated with 1 μg/m3 increase in nitrogen dioxide (NO2; effect size = 1.034, 95% CI 1.006-1.063), PM2.5 (effect size = 1.047, 95% CI 1.025-1.1071). For short-term exposure to air pollutants, COVID-19 incidence was positively associated with 1 unit increase in air quality index (effect size = 1.001, 95% CI 1.001-1.002), 1 μg/m3 increase NO2 (effect size = 1.014, 95% CI 1.011-1.016), particulate matter with diameter <10 μm (PM10; effect size = 1.005, 95% CI 1.003-1.008), PM2.5 (effect size = 1.003, 95% CI 1.002-1.004), and SO2 (effect size = 1.015, 95% CI 1.007-1.023).Conclusions
Outdoor air pollutants are detrimental factors to COVID-19 outcomes. Measurements beneficial to reducing pollutant levels might also reduce the burden of the pandemic.
SUBMITTER: Zang ST
PROVIDER: S-EPMC8440008 | biostudies-literature |
REPOSITORIES: biostudies-literature
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| S-EPMC9243647 | biostudies-literature
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| S-EPMC8040542 | biostudies-literature
Project description:IntroductionAir pollution is speculated to increase the risk of Coronavirus disease-2019 (COVID-19). Nevertheless, the results remain inconsistent and inconclusive. This study aimed to explore the association between ambient air pollution (AAP) and COVID-19 risks using a meta-analysis with meta-regression modelling.MethodsThe inclusion criteria were: original studies quantifying the association using effect sizes and 95 % confidence intervals (CIs); time-series, cohort, ecological or case-crossover peer-reviewed studies in English. Exclusion criteria encompassed non-original studies, animal studies, and data with common errors. PubMed, Web of Science, Embase and Google Scholar electronic databases were systemically searched for eligible literature, up to 31, March 2023. The risk of bias (ROB) was assessed following the Agency for Healthcare Research and Quality parameters. A random-effects model was used to calculate pooled risk ratios (RRs) and their 95 % CIs.ResultsA total of 58 studies, between 2020 and 2023, met the inclusion criteria. The global representation was skewed, with major contributions from the USA (24.1 %) and China (22.4 %). The distribution included studies on short-term (43.1 %) and long-term (56.9 %) air pollution exposure. Ecological studies constituted 51.7 %, time-series-27.6 %, cohorts-17.2 %, and case crossover-3.4 %. ROB assessment showed low (86.2 %) and moderate (13.8 %) risk. The COVID-19 incidences increased with a 10 μg/m3 increase in PM2.5 [RR = 4.9045; 95 % CI (4.1548-5.7895)], PM10 [RR = 2.9427: (2.2290-3.8850)], NO2 [RR = 3.2750: (3.1420-3.4136)], SO2 [RR = 3.3400: (2.7931-3.9940)], CO [RR = 2.6244: (2.5208-2.7322)] and O3 [RR = 2.4008: (2.1859-2.6368)] concentrations. A 10 μg/m3 increase in concentrations of PM2.5 [RR = 3.0418: (2.7344-3.3838)], PM10 [RR = 2.6202: (2.1602-3.1781)], NO2 [RR = 3.2226: (2.1411-4.8504)], CO [RR = 1.8021 (0.8045-4.0370)] and O3 [RR = 2.3270 (1.5906-3.4045)] was significantly associated with COVID-19 mortality. Stratified analysis showed that study design, exposure period, and country influenced exposure-response associations. Meta-regression model indicated significant predictors for air pollution-COVID-19 incidence associations.ConclusionThe study, while robust, lacks causality demonstration and focuses only on the USA and China, limiting its generalizability. Regardless, the study provides a strong evidence base for air pollution-COVID-19-risks associations, offering valuable insights for intervention measures for COVID-19.
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Project description:BACKGROUND:Air pollution alters small pulmonary vessels in animal models. We hypothesised that long-term ambient air pollution exposure would be associated with differences in pulmonary vascular volumes in a population-based study. METHODS:The Multi-Ethnic Study of Atherosclerosis recruited adults in six US cities. Personalised long-term exposures to ambient black carbon, nitrogen dioxide (NO2), oxides of nitrogen (NO x ), particulate matter with a 50% cut-off aerodynamic diameter of <2.5??m (PM2.5) and ozone were estimated using spatiotemporal models. In 2010-2012, total pulmonary vascular volume was measured as the volume of detectable pulmonary arteries and veins, including vessel walls and luminal blood volume, on noncontrast chest computed tomography (TPVVCT). Peripheral TPVVCT was limited to the peripheral 2?cm to isolate smaller vessels. Linear regression adjusted for demographics, anthropometrics, smoking, second-hand smoke, renal function and scanner manufacturer. RESULTS:The mean±sd age of the 3023 participants was 69.3±9.3?years; 46% were never-smokers. Mean exposures were 0.80??g·m-3 black carbon, 14.6?ppb NO2 and 11.0??g·m-3 ambient PM2.5. Mean±sd peripheral TPVVCT was 79.2±18.2?cm3 and TPVVCT was 129.3±35.1?cm3. Greater black carbon exposure was associated with a larger peripheral TPVVCT, including after adjustment for city (mean difference 0.41 (95% CI 0.03-0.79)?cm3 per interquartile range; p=0.036). Associations for peripheral TPVVCT with NO2 were similar but nonsignificant after city adjustment, while those for PM2.5 were of similar magnitude but nonsignificant after full adjustment. There were no associations for NO x or ozone, or between any pollutant and TPVVCT. CONCLUSIONS:Long-term black carbon exposure was associated with a larger peripheral TPVVCT, suggesting diesel exhaust may contribute to remodelling of small pulmonary vessels in the general population.
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Project description: Not available
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