Dataset Information

Association between Short-Term Exposure to Air Pollution and COVID-19 Mortality: A Population-Based Case-Crossover Study Using Individual-Level Mortality Registry Confirmed by Medical Examiners.

ABSTRACT:

Background

Studies have suggested links between ambient air pollution and coronavirus 2019 (COVID-19) mortality, yet confirmation by well-designed epidemiological studies with individual data is needed.

Objectives

We aimed to examine whether short-term exposure to air pollution is associated with risk of mortality from COVID-19 for those infected with COVID-19.

Methods

The Cook County Medical Examiner's Office reports individual-level data for deaths from COVID-19 that occur in its jurisdiction, which includes all confirmed COVID-19 deaths in Cook County, Illinois. Case-crossover analysis was conducted to estimate the associations of estimated short-term exposures to particulate matter (PM) with aerodynamic diameter ≤2.5μm (PM2.5) and ozone (O3) on the day of death and up to 21 d before death at location of death with COVID-19. A total of 7,462 deaths from COVID-19 that occurred up to 28 February 2021 were included in the final analysis. We adjusted for potential confounders by time-stratified case-crossover design and by covariate adjustments (i.e., time-invariant factors, meteorological factors, viral transmission, seasonality, and time trend).

Results

Of the 7,462 case and 25,457 self-control days, almost all were days with exposure levels below the PM2.5 24-h National Ambient Air Quality Standard (NAAQS) (35 μg/m3); 98.9% had O3 levels below the maximum 8-h NAAQS (35.7 μg/m3 or 70 parts per billion). An interquartile range (IQR) increase (5.2 μg/m3) in cumulative 3-wk PM2.5 exposure was associated with a 69.6% [95% confidence interval (CI): 34.6, 113.8] increase in risk of COVID-19 mortality. An IQR increase (8.2 μg/m3) in 3-d O3 exposure was associated with a 29.0% (95% CI: 9.9, 51.5) increase in risk of COVID-19 mortality. The associations differed by demographics or race/ethnicity. There was indication of modification of the associations by some comorbid conditions.

Discussion

Short-term exposure to air pollution below the NAAQS may increase the mortality burden from COVID-19. https://doi.org/10.1289/EHP10836.

SUBMITTER: Kim H

PROVIDER: S-EPMC9651183 | biostudies-literature | 2022 Nov

REPOSITORIES: biostudies-literature

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Publications

Association between Short-Term Exposure to Air Pollution and COVID-19 Mortality: A Population-Based Case-Crossover Study Using Individual-Level Mortality Registry Confirmed by Medical Examiners.

Kim Honghyok H Samet Jonathan M JM Bell Michelle L ML

Environmental health perspectives 20221111 11

<h4>Background</h4>Studies have suggested links between ambient air pollution and coronavirus 2019 (COVID-19) mortality, yet confirmation by well-designed epidemiological studies with individual data is needed.<h4>Objectives</h4>We aimed to examine whether short-term exposure to air pollution is associated with risk of mortality from COVID-19 for those infected with COVID-19.<h4>Methods</h4>The Cook County Medical Examiner's Office reports individual-level data for deaths from COVID-19 that occu ...[more]

PMID: 36367781

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Project description:BackgroundInfluenza imposes a heavy burden on public health. Little is known, however, of the associations between detailed measures of exposure to ambient air pollution and influenza at an individual level.ObjectiveWe examined individual-level associations between six criteria air pollutants and influenza using case-crossover design.MethodsIn this individual-level time-stratified case-crossover study, we linked influenza cases collected by the Guangzhou Center for Disease Control and Prevention from 1 January 2013 to 31 December 2019 with individual residence-level exposure to particulate matter (PM2.5 and PM10), sulfur dioxide (SO2), nitrogen dioxide (NO2), ozone (O3) and carbon monoxide (CO). The exposures were estimated for the day of onset of influenza symptoms (lag 0), 1-7 d before the onset (lags 1-7), as well as an 8-d moving average (lag07), using a random forest model and linked to study participants' home addresses. Conditional logistic regression was developed to investigate the associations between short-term exposure to air pollution and influenza, adjusting for mean temperature, relative humidity, public holidays, population mobility, and community influenza susceptibility.ResultsN=108,479 eligible cases were identified in our study. Every 10-μg/m3 increase in exposure to PM2.5, PM10, NO2, and CO and every 5-μg/m3 increase in SO2 over 8-d moving average (lag07) was associated with higher risk of influenza with a relative risk (RR) of 1.028 (95% CI: 1.018, 1.038), 1.041 (95% CI: 1.032, 1.049), 1.169 (95% CI: 1.151, 1.188), 1.004 (95% CI: 1.003, 1.006), and 1.134 (95% CI: 1.107, 1.163), respectively. There was a negative association between O3 and influenza with a RR of 0.878 (95% CI: 0.866, 0.890).ConclusionsOur findings suggest that short-term exposure to air pollution, except for O3, is associated with greater risk for influenza. Further studies are necessary to decipher underlying mechanisms and design preventive interventions and policies. https://doi.org/10.1289/EHP12145.

Project description:BackgroundAmbient pollution and non-optimal temperature are major risk factors for respiratory health. However, the relationships between short-term exposure to these factors and bronchiectasis mortality remain unknown.MethodsA nationwide, time-stratified case-crossover study across Mainland China was conducted from 2013 to 2019. Records of bronchiectasis deaths were extracted from the National Death Registration Reporting Information System. Daily concentrations of fine particulate matter (PM2.5), coarse particulate matter (PM2.5-10), nitrogen dioxide (NO2), ozone (O3), and daily temperature were obtained from high-resolution prediction models. We utilized conditional logistic regression model and distributed lag nonlinear model to explore the associations of these exposures with bronchiectasis mortality.FindingsWe included a total of 19,320 bronchiectasis deaths. Air pollutant was associated with bronchiectasis mortality within the first 3 days after exposure and the exposure-response relationships were almost linear. An interquartile range increase in PM2.5, PM2.5-10, and O3 was associated with increments of 3.18%, 4.14%, and 4.36% in bronchiectasis mortality at lag 02 d, respectively. Additionally, lower temperature was associated with higher odds of bronchiectasis mortality. Compared to referent temperature (23.6 °C), the odds ratio for bronchiectasis mortality associated with extremely low temperature (P1: -13.4 °C) was 1.54 (95% CI: 1.05, 2.25).InterpretationThis national study provides compelling evidence, and highlights the necessity and importance of reducing air pollution exposures and keeping warm for susceptible populations.FundingNational Natural Science Foundation of China (81925001; 82330070); Innovation Program of Shanghai Municipal Education Commission (202101070007-E00097); Program of Shanghai Municipal Science and Technology Commission (21DZ2201800); Program of Shanghai Shenkang Development Center (SHDC12023110); and Major Project of National Health Commission of China.

Project description:BackgroundThe adverse effect of air pollution on mortality is well documented worldwide but the identification of more vulnerable populations at higher risk of death is still limited. The aim of this study was to evaluate the association between natural mortality (overall and cause-specific) and short-term exposure to five air pollutants (PM2.5, PM10, NO2, O3 and black carbon) and identify potential vulnerable populations in Belgium.MethodsWe used a time-stratified case-crossover design with conditional logistic regressions to assess the relationship between mortality and air pollution in the nine largest Belgian agglomerations. Then, we performed a random-effect meta-analysis of the pooled results and described the global air pollution-mortality association. We carried out stratified analyses by individual characteristics (sex, age, employment, hospitalization days and chronic preexisting health conditions), living environment (levels of population density, built-up areas) and season of death to identify effect modifiers of the association.ResultsThe study included 304,754 natural deaths registered between 2010 and 2015. We found percentage increases for overall natural mortality associated with 10 μg/m3 increases of air pollution levels of 0.6% (95% CI: 0.2%, 1.0%) for PM2.5, 0.4% (0.1%, 0.8%) for PM10, 0.5% (-0.2%, 1.1%) for O3, 1.0% (0.3%, 1.7%) for NO2 and 7.1% (-0.1%, 14.8%) for black carbon. There was also evidence for increases of cardiovascular and respiratory mortality. We did not find effect modification by individual characteristics (sex, age, employment, hospitalization days). However, this study suggested differences in risk of death for people with preexisting conditions (thrombosis, cardiovascular diseases, asthma, diabetes and thyroid affections), season of death (May-September vs October-April) and levels of built-up area in the neighborhood (for NO2).ConclusionsThis work provided evidence for the adverse health effects of air pollution and contributed to the identification of specific population groups. These findings can help to better define public-health interventions and prevention strategies.

Project description:ImportanceThe US Environmental Protection Agency is required to reexamine its National Ambient Air Quality Standards (NAAQS) every 5 years, but evidence of mortality risk is lacking at air pollution levels below the current daily NAAQS in unmonitored areas and for sensitive subgroups.ObjectiveTo estimate the association between short-term exposures to ambient fine particulate matter (PM2.5) and ozone, and at levels below the current daily NAAQS, and mortality in the continental United States.Design, setting, and participantsCase-crossover design and conditional logistic regression to estimate the association between short-term exposures to PM2.5 and ozone (mean of daily exposure on the same day of death and 1 day prior) and mortality in 2-pollutant models. The study included the entire Medicare population from January 1, 2000, to December 31, 2012, residing in 39 182 zip codes.ExposuresDaily PM2.5 and ozone levels in a 1-km × 1-km grid were estimated using published and validated air pollution prediction models based on land use, chemical transport modeling, and satellite remote sensing data. From these gridded exposures, daily exposures were calculated for every zip code in the United States. Warm-season ozone was defined as ozone levels for the months April to September of each year.Main outcomes and measuresAll-cause mortality in the entire Medicare population from 2000 to 2012.ResultsDuring the study period, there were 22 433 862 million case days and 76 143 209 control days. Of all case and control days, 93.6% had PM2.5 levels below 25 μg/m3, during which 95.2% of deaths occurred (21 353 817 of 22 433 862), and 91.1% of days had ozone levels below 60 parts per billion, during which 93.4% of deaths occurred (20 955 387 of 22 433 862). The baseline daily mortality rates were 137.33 and 129.44 (per 1 million persons at risk per day) for the entire year and for the warm season, respectively. Each short-term increase of 10 μg/m3 in PM2.5 (adjusted by ozone) and 10 parts per billion (10-9) in warm-season ozone (adjusted by PM2.5) were statistically significantly associated with a relative increase of 1.05% (95% CI, 0.95%-1.15%) and 0.51% (95% CI, 0.41%-0.61%) in daily mortality rate, respectively. Absolute risk differences in daily mortality rate were 1.42 (95% CI, 1.29-1.56) and 0.66 (95% CI, 0.53-0.78) per 1 million persons at risk per day. There was no evidence of a threshold in the exposure-response relationship.Conclusions and relevanceIn the US Medicare population from 2000 to 2012, short-term exposures to PM2.5 and warm-season ozone were significantly associated with increased risk of mortality. This risk occurred at levels below current national air quality standards, suggesting that these standards may need to be reevaluated.

Project description:Zinc (Zn) is a major elemental component of respirable ambient particulate matter (PM) detected often at alarming levels in urban air. Exposure to PM has been widely associated with increased cardiovascular morbidity and mortality, however, it is not known what components or sources of PM are causative. We recently demonstrated that long-term episodic inhalation of combustion PM, having similar amount of Zn found in urban PM, caused myocardial lesions in rats. We further demonstrated that a single pulmonary exposure to Zn at high concentration is associated with disturbances in cardiac mitochondrial function, ion channel regulation, calcium homeostasis, and cell signaling. Therefore, in this study we investigated the role of PM-associated Zn in cardiac injury using multiple exposure scenarios. Male Wistar-Kyoto (WKY) rats of 12-14 wks age were intratracheally exposed (once per wk x 8 or16 wks) to either (1) saline (control); (2) PM having no soluble Zn; (3) combustion PM suspension containing 14.5 ug/mg water-soluble Zn at high and (4) low dose levels, (5) the aqueous fraction of this suspension devoid of solid insoluble particulate fraction (14.5 ug/mg soluble Zn), or (6) Zn sulfate. Zn concentrations were identical in groups 3, 5 and 6. Pulmonary toxicity was apparent in all exposure groups when compared to saline as determined by recovery of cells in bronchoalveolar lavage fluid. Long-term exposure to PM with or without soluble Zn, or Zn sulfate caused distinct myocardial lesions characterized by subepicardial and randomly distributed myocardial inflammation, degeneration, and fibrosis. The lesion severity was higher in those groups receiving Zn PM. Because cardiac mitochondria are likely the primary target of inhaled metal or other absorbed PM components, we analyzed mitochondrial DNA damage using QPCR and found that all exposure groups except those exposed to PM without Zn caused variable degree of damage. Aconitase activity, sensitive to inhibition by oxidative stress was inhibited slightly but significantly in rats receiving zinc sulfate. Although modest, microarray (Affymetrix) analysis revealed expression changes in the heart reflective of effects on cell signaling, inflammation/oxidative stress, mitochondrial fatty acid metabolisms and cell cycle regulation in rats exposed to zinc sulfate. However, these changes were minimal following exposure to PM devoid of soluble metals. We demonstrate that episodic subchronic pulmonary exposure to zinc sulfate causes cardiac injury and mitochondrial DNA damage. Thus, water-soluble PM-associated zinc may be one of the PM components responsible for cardiovascular morbidity. Experiment Overall Design: Group 1 received Saline to serve as a control. Group 2 received Mount St. Helenâs ash, which does not contain any water-soluble zinc or other metals such that we can delineate any cardiac effect secondary to pulmonary deposition of these particles as these fine mode particles themselves are not likely to translocate to the heart. Group 3 received whole saline suspension of the same fugitive oil combustion particle sample used in the previous study, which contained insoluble components plus water-soluble zinc (Kodavanti et al., 2003; 14.5 ug/mg zinc) and also a small amount of water-soluble nickel (3.0 Âµg/mg). Elemental composition of this PM is comparable to Ottawa urban PM (Kodavanti et al., 2003). Group 4 also received same particle sample but at half the dose than group 3. Group 5 received saline-soluble or leachable fraction of PM-HD devoid of any solid material but contained soluble components including zinc and nickel. And, group 6 received zinc sulfate at concentration that was present in groups 3 or 5. This design allowed us to test if cardiac injury in rats was due to leached of zinc or solid particles. There were 4 replicates per treatment group.

Project description:Zinc (Zn) is a major elemental component of respirable ambient particulate matter (PM) detected often at alarming levels in urban air. Exposure to PM has been widely associated with increased cardiovascular morbidity and mortality, however, it is not known what components or sources of PM are causative. We recently demonstrated that long-term episodic inhalation of combustion PM, having similar amount of Zn found in urban PM, caused myocardial lesions in rats. We further demonstrated that a single pulmonary exposure to Zn at high concentration is associated with disturbances in cardiac mitochondrial function, ion channel regulation, calcium homeostasis, and cell signaling. Therefore, in this study we investigated the role of PM-associated Zn in cardiac injury using multiple exposure scenarios. Male Wistar-Kyoto (WKY) rats of 12-14 wks age were intratracheally exposed (once per wk x 8 or16 wks) to either (1) saline (control); (2) PM having no soluble Zn; (3) combustion PM suspension containing 14.5 ug/mg water-soluble Zn at high and (4) low dose levels, (5) the aqueous fraction of this suspension devoid of solid insoluble particulate fraction (14.5 ug/mg soluble Zn), or (6) Zn sulfate. Zn concentrations were identical in groups 3, 5 and 6. Pulmonary toxicity was apparent in all exposure groups when compared to saline as determined by recovery of cells in bronchoalveolar lavage fluid. Long-term exposure to PM with or without soluble Zn, or Zn sulfate caused distinct myocardial lesions characterized by subepicardial and randomly distributed myocardial inflammation, degeneration, and fibrosis. The lesion severity was higher in those groups receiving Zn PM. Because cardiac mitochondria are likely the primary target of inhaled metal or other absorbed PM components, we analyzed mitochondrial DNA damage using QPCR and found that all exposure groups except those exposed to PM without Zn caused variable degree of damage. Aconitase activity, sensitive to inhibition by oxidative stress was inhibited slightly but significantly in rats receiving zinc sulfate. Although modest, microarray (Affymetrix) analysis revealed expression changes in the heart reflective of effects on cell signaling, inflammation/oxidative stress, mitochondrial fatty acid metabolisms and cell cycle regulation in rats exposed to zinc sulfate. However, these changes were minimal following exposure to PM devoid of soluble metals. We demonstrate that episodic subchronic pulmonary exposure to zinc sulfate causes cardiac injury and mitochondrial DNA damage. Thus, water-soluble PM-associated zinc may be one of the PM components responsible for cardiovascular morbidity. Keywords: Pulmonary exposure, Cardiac gene expression

Project description:Background and aimInfant mortality is a widely reported indicator of population health and a leading public health concern. In this systematic review and meta-analysis, we review the available literature for epidemiologic evidence of the association between short-term air pollution exposure and infant mortality.MethodsRelevant publications were identified through PubMed and Web of Science databases using comprehensive search terms and screened using predefined inclusion/exclusion criteria. We extracted data from included studies and applied a systematic rubric for evaluating study quality across domains including participant selection, outcome, exposure, confounding, analysis, selective reporting, sensitivity, and overall quality. We performed meta-analyses, using both fixed and random-effect methods, and estimated pooled odds ratios (ORs) and 95 % confidence intervals (95%CI) for pollutants (nitrogen dioxide (NO2), sulfur dioxide (SO2), coarse particulate matter (PM10), fine particulate matter (PM2.5), ozone (O3), carbon monoxide (CO)) and infant mortality, neonatal mortality, or postneonatal mortality.ResultsOur search returned 549 studies. We excluded 490 studies in the abstract screening phase and an additional 37 studies in the full text screening phase, leaving 22 studies for inclusion. Among these 22 studies, 14 included effect estimates for PM10, 13 for O3, 11 for both NO2 and CO, 8 for SO2, and 3 for PM2.5. We did not calculate a pooled OR for PM2.5 due to the limited number of studies available and demonstrated heterogeneity in the effect estimates. The pooled ORs (95%CI) with the greatest magnitudes were for a 10-ppb increase in SO2 or NO2 concentration in the days before death (1.07 [95%CI: 1.02, 1.12], 1.04 [95%CI: 1.01, 1.08], respectively). The pooled OR for PM10 was 1.02 (95%CI: 1.00, 1.03), and the pooled ORs for CO and O3 were 1.01 (95%CI: 1.00, 1.02) and 0.99 (95%CI: 0.97, 1.01).ConclusionsIncreased exposure to SO2, NO2, PM10, or CO is associated with infant mortality across studies.

Dataset Information

Association between Short-Term Exposure to Air Pollution and COVID-19 Mortality: A Population-Based Case-Crossover Study Using Individual-Level Mortality Registry Confirmed by Medical Examiners.

Background

Objectives

Methods

Results

Discussion

Publications

Association between Short-Term Exposure to Air Pollution and COVID-19 Mortality: A Population-Based Case-Crossover Study Using Individual-Level Mortality Registry Confirmed by Medical Examiners.

Similar Datasets

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