Dataset Information

Systematic review and meta-analysis of cohort studies of long term outdoor nitrogen dioxide exposure and mortality.

ABSTRACT:

Objective

To determine whether long term exposure to outdoor nitrogen dioxide (NO2) is associated with all-cause or cause-specific mortality.

Methods

MEDLINE, Embase, CENTRAL, Global Health and Toxline databases were searched using terms developed by a librarian. Screening, data extraction and risk of bias assessment were completed independently by two reviewers. Conflicts were resolved through consensus and/or involvement of a third reviewer. Pooling of results across studies was conducted using random effects models, heterogeneity among included studies was assessed using Cochran's Q and I2 measures, and sources of heterogeneity were evaluated using meta-regression. Sensitivity of pooled estimates to individual studies was examined and publication bias was evaluated using Funnel plots, Begg's and Egger's tests, and trim and fill.

Results

Seventy-nine studies based on 47 cohorts, plus one set of pooled analyses of multiple European cohorts, met inclusion criteria. There was a consistently high degree of heterogeneity. After excluding studies with probably high or high risk of bias in the confounding domain (n = 12), pooled hazard ratios (HR) indicated that long term exposure to NO2 was significantly associated with mortality from all/ natural causes (pooled HR 1.047, 95% confidence interval (CI), 1.023-1.072 per 10 ppb), cardiovascular disease (pooled HR 1.058, 95%CI 1.026-1.091), lung cancer (pooled HR 1.083, 95%CI 1.041-1.126), respiratory disease (pooled HR 1.062, 95%CI1.035-1.089), and ischemic heart disease (pooled HR 1.111, 95%CI 1.079-1.144). Pooled estimates based on multi-pollutant models were consistently smaller than those from single pollutant models and mostly non-significant.

Conclusions

For all causes of death other than cerebrovascular disease, the overall quality of the evidence is moderate, and the strength of evidence is limited, while for cerebrovascular disease, overall quality is low and strength of evidence is inadequate. Important uncertainties remain, including potential confounding by co-pollutants or other concomitant exposures, and limited supporting mechanistic evidence. (PROSPERO registration number CRD42018084497).

SUBMITTER: Stieb DM

PROVIDER: S-EPMC7861378 | biostudies-literature | 2021

REPOSITORIES: biostudies-literature

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Publications

Systematic review and meta-analysis of cohort studies of long term outdoor nitrogen dioxide exposure and mortality.

Stieb David M DM Berjawi Rania R Emode Monica M Zheng Carine C Salama Dina D Hocking Robyn R Lyrette Ninon N Matz Carlyn C Lavigne Eric E Shin Hwashin H HH

PloS one 20210204 2

<h4>Objective</h4>To determine whether long term exposure to outdoor nitrogen dioxide (NO2) is associated with all-cause or cause-specific mortality.<h4>Methods</h4>MEDLINE, Embase, CENTRAL, Global Health and Toxline databases were searched using terms developed by a librarian. Screening, data extraction and risk of bias assessment were completed independently by two reviewers. Conflicts were resolved through consensus and/or involvement of a third reviewer. Pooling of results across studies was ...[more]

PMID: 33539450

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Project description:BackgroundAmbient air pollution is among the greatest environmental risks to human health. However, little is known about the health effects of nitrogen dioxide (NO2), a traffic-related air pollutant. Herein, we aimed to conduct a meta-analysis to investigate the long-term effects of NO2 on mortality.MethodsWe conducted a systematic search for studies that were published up to February 2020 and performed a meta-analysis of all available epidemiologic studies evaluating the associations between long-term exposure to NO2 with all-cause, cardiovascular, and respiratory mortality. Overall pooled effect estimates as well as subgroup-specific pooled estimates (e.g. location, exposure assessment method, exposure metric, study population, age at recruitment, and key confounder adjustment) and 95% confidence intervals were calculated using random-effects models. Risk of bias assessment was accessed by following WHO global air quality guidelines. Publication bias was accessed by visually inspecting funnel plot and Egger's liner regression was used to test of asymmetry.ResultsOur search initially retrieved 1349 unique studies, of which 34 studies met the inclusion criteria. The pooled hazard ratio (HR) for all-cause mortality was 1.06 (95%CI: 1.04-1.08, n = 28 studies, I2 = 98.6%) per 10 ppb increase in annual NO2 concentrations. The pooled HRs for cardiovascular and respiratory mortality per 10 ppb increment were 1.11 (95%CI: 1.07-1.16, n = 20 studies, I2 = 99.2%) and 1.05 (95%CI: 1.02-1.08, n = 17 studies, I2 = 94.6%), respectively. The sensitivity analysis pooling estimates from multi-pollutant models suggest an independent effect of NO2 on mortality. Funnel plots indicate that there is no evidence for publication bias in our study.ConclusionWe provide robust epidemiological evidence that long-term exposure to NO2, a proxy for traffic-sourced air pollutants, is associated with a higher risk of all-cause, cardiovascular, and respiratory mortality that might be independent of other common air pollutants.

Project description:BACKGROUND:Nitrogen dioxide (NO2) is a pervasive urban pollutant originating primarily from vehicle emissions. Ischemic heart disease (IHD) is associated with a considerable public health burden worldwide, but whether NO2 exposure is causally related to IHD morbidity remains in question. Our objective was to determine whether short term exposure to outdoor NO2 is causally associated with IHD-related morbidity based on a synthesis of findings from case-crossover and time-series studies. METHODS:MEDLINE, Embase, CENTRAL, Global Health and Toxline databases were searched using terms developed by a librarian. Screening, data extraction and risk of bias assessment were completed independently by two reviewers. Conflicts between reviewers were resolved through consensus and/or involvement of a third reviewer. Pooling of results across studies was conducted using random effects models, heterogeneity among included studies was assessed using Cochran's Q and I2 measures, and sources of heterogeneity were evaluated using meta-regression. Sensitivity of pooled estimates to individual studies was examined using Leave One Out analysis and publication bias was evaluated using Funnel plots, Begg's and Egger's tests, and trim and fill. RESULTS:Thirty-eight case-crossover studies and 48 time-series studies were included in our analysis. NO2 was significantly associated with IHD morbidity (pooled odds ratio from case-crossover studies: 1.074 95% CI 1.052-1.097; pooled relative risk from time-series studies: 1.022 95% CI 1.016-1.029 per 10?ppb). Pooled estimates for case-crossover studies from Europe and North America were significantly lower than for studies conducted elsewhere. The high degree of heterogeneity among studies was only partially accounted for in meta-regression. There was evidence of publication bias, particularly for case-crossover studies. For both case-crossover and time-series studies, pooled estimates based on multi-pollutant models were smaller than those from single pollutant models, and those based on older populations were larger than those based on younger populations, but these differences were not statistically significant. CONCLUSIONS:We concluded that there is a likely causal relationship between short term NO2 exposure and IHD-related morbidity, but important uncertainties remain, particularly related to the contribution of co-pollutants or other concomitant exposures, and the lack of supporting evidence from toxicological and controlled human studies.

Project description:ImportanceThe association between short-term exposure to air pollution and mortality has been widely documented worldwide; however, few studies have applied causal modeling approaches to account for unmeasured confounders that vary across time and space.ObjectiveTo estimate the association between short-term changes in fine particulate matter (PM2.5) and nitrogen dioxide (NO2) concentrations and changes in daily all-cause mortality rates using a causal modeling approach.Design, setting, and participantsThis cross-sectional study used air pollution and mortality data from Jiangsu, China; California; central-southern Italy; and Germany with interactive fixed-effects models to control for both measured and unmeasured spatiotemporal confounders. A total of 8 963 352 deaths in these 4 regions from January 1, 2015, to December 31, 2019, were included in the study. Data were analyzed from June 1, 2021, to October 30, 2023.ExposureDay-to-day changes in county- or municipality-level mean PM2.5 and NO2 concentrations.Main outcomes and measuresDay-to-day changes in county- or municipality-level all-cause mortality rates.ResultsAmong the 8 963 352 deaths in the 4 study regions, a 10-μg/m3 increase in daily PM2.5 concentration was associated with an increase in daily all-cause deaths per 100 000 people of 0.01 (95% CI, 0.001-0.01) in Jiangsu, 0.03 (95% CI, 0.004-0.05) in California, 0.10 (95% CI, 0.07-0.14) in central-southern Italy, and 0.04 (95% CI, 0.02- 0.05) in Germany. The corresponding increases in mortality rates for a 10-μg/m3 increase in NO2 concentration were 0.04 (95% CI, 0.03-0.05) in Jiangsu, 0.03 (95% CI, 0.01-0.04) in California, 0.10 (95% CI, 0.05-0.15) in central-southern Italy, and 0.05 (95% CI, 0.04-0.06) in Germany. Significant effect modifications by age were observed in all regions, by sex in Germany (eg, 0.05 [95% CI, 0.03-0.06] for females in the single-pollutant model of PM2.5), and by urbanicity in Jiangsu (0.07 [95% CI, 0.04-0.10] for rural counties in the 2-pollutant model of NO2).Conclusions and relevanceThe findings of this cross-sectional study contribute to the growing body of evidence that increases in short-term exposures to PM2.5 and NO2 may be associated with increases in all-cause mortality rates. The interactive fixed-effects model, which controls for unmeasured spatial and temporal confounders, including unmeasured time-varying confounders in different spatial units, can be used to estimate associations between changes in short-term exposure to air pollution and changes in health outcomes.

Project description:Although many studies have linked elevations in tropospheric ozone to adverse health outcomes, the effect of long-term exposure to ozone on air pollution-related mortality remains uncertain. We examined the potential contribution of exposure to ozone to the risk of death from cardiopulmonary causes and specifically to death from respiratory causes.Data from the study cohort of the American Cancer Society Cancer Prevention Study II were correlated with air-pollution data from 96 metropolitan statistical areas in the United States. Data were analyzed from 448,850 subjects, with 118,777 deaths in an 18-year follow-up period. Data on daily maximum ozone concentrations were obtained from April 1 to September 30 for the years 1977 through 2000. Data on concentrations of fine particulate matter (particles that are < or = 2.5 microm in aerodynamic diameter [PM(2.5)]) were obtained for the years 1999 and 2000. Associations between ozone concentrations and the risk of death were evaluated with the use of standard and multilevel Cox regression models.In single-pollutant models, increased concentrations of either PM(2.5) or ozone were significantly associated with an increased risk of death from cardiopulmonary causes. In two-pollutant models, PM(2.5) was associated with the risk of death from cardiovascular causes, whereas ozone was associated with the risk of death from respiratory causes. The estimated relative risk of death from respiratory causes that was associated with an increment in ozone concentration of 10 ppb was 1.040 (95% confidence interval, 1.010 to 1.067). The association of ozone with the risk of death from respiratory causes was insensitive to adjustment for confounders and to the type of statistical model used.In this large study, we were not able to detect an effect of ozone on the risk of death from cardiovascular causes when the concentration of PM(2.5) was taken into account. We did, however, demonstrate a significant increase in the risk of death from respiratory causes in association with an increase in ozone concentration.

Dataset Information

Systematic review and meta-analysis of cohort studies of long term outdoor nitrogen dioxide exposure and mortality.

Objective

Methods

Results

Conclusions

Publications

Systematic review and meta-analysis of cohort studies of long term outdoor nitrogen dioxide exposure and mortality.

Similar Datasets

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