Long-term exposure to NO2 and O3 and all-cause and respiratory mortality: A systematic review and meta-analysis.
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ABSTRACT:
SUBMITTER: Huangfu P
PROVIDER: S-EPMC7549128 | biostudies-literature | 2020 Nov
REPOSITORIES: biostudies-literature
Publications
Long-term exposure to NO<sub>2</sub> and O<sub>3</sub> and all-cause and respiratory mortality: A systematic review and meta-analysis.
Huangfu Peijue P Atkinson Richard R
Environment international 20201005
<h4>Background</h4>WHO has published several volumes of Global Air Quality Guidelines to provide guidance on the health risks associated with exposure to outdoor air pollution. As new scientific evidence is generated, air quality guidelines need to be periodically revised and, where necessary, updated.<h4>Objectives</h4>The aims of the study were 1) to summarise the available evidence on the effect of long-term exposure to ozone (O<sub>3</sub>) and nitrogen dioxide (NO<sub>2</sub>) on mortality; ...[more]
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Project description:BackgroundMany studies have assessed the harmful effects of ambient air pollution on human mortality, but the evidence needs further exploration, analysis, and refinement, given the large number of studies that have been published in recent years. The objective of this study was to evaluate all the available evidence of the effect of short-term exposure to ambient sulphur dioxide (SO2) on all-cause and respiratory mortality.MethodsArticles reporting observational epidemiological studies were included, comprising time-series and case-crossover designs. A broad search and wide inclusion criteria were considered, encompassing international and regional databases, with no geographical or language restrictions. A random effect meta-analysis was conducted, and pooled relative risk for an increment of 10 µg/m3 in SO2 concentrations were calculated for each outcome. We analysed the risk of bias (RoB) in individual studies for specific domains using a new domain-based RoB assessment tool, and the certainty of evidence across studies with an adaptation of the Grading of Recommendations Assessment, Development and Evaluation approach. The certainty of evidence was judged separately for each exposure-outcome combination. A number of subgroup and sensitivity analyses were carried out, as well as assessments of heterogeneity and potential publication bias. The protocol for this review was registered with PROSPERO (CRD42019120738).ResultsOur search retrieved 1,128 articles, from which 67 were included in quantitative analysis. The RoB was low or moderate in the majority of articles and domains. An increment of 10 µg/m3 in SO2 (24-hour average) was associated with all-cause mortality (RR: 1.0059; 95% CI: 1.0046-1.0071; p-value: <0.01), and respiratory mortality (RR: 1.0067; 95% CI: 1.0025-1.0109; p-value: <0.01), while the same increment in SO2 (1-hour max.) was associated with respiratory mortality (RR:1.0052; 95% CI: 1.0013-1.0091; p-value: 0.03). Similarly, the association was positive but non-significant for SO2 (1-hour max.) and all-cause mortality (RR: 1.0016; 95% CI: 0.9930-1.0102; p-value: 0.60). These associations were still significant after the adjustment for particulate matter, but not for other pollutants, according to the results from 13 articles that evaluated co-pollutant models. In general, linear concentration-response functions with no thresholds were found for the two outcomes, although this was only evaluated in a small number of studies. We found signs of heterogeneity for SO2 (24-hour average) - respiratory mortality and SO2 (1-hour max.) - all-cause mortality, and funnel plot asymmetry for SO2 (24-hour average) - all-cause mortality. The certainty of evidence was high in two combinations, i.e. SO2 (24-hour average) - all-cause mortality and SO2 (1-hour max.) - respiratory mortality, moderate in one combination, i.e. SO2 (24-hour average) - respiratory mortality, and low in the remaining one combination.ConclusionsPositive associations were found between short-term exposure to ambient SO2 and all-cause and respiratory mortality. These associations were robust against several sensitivity analyses, and were judged to be of moderate or high certainty in three of the four exposure-outcome combinations.
| S-EPMC7937788 | biostudies-literature
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.
| S-EPMC8499020 | biostudies-literature
Project description:While there is good evidence for associations between short-term exposure to ozone and a range of adverse health outcomes, the evidence from narrative reviews for long-term exposure is suggestive of associations with respiratory mortality only. We conducted a systematic, quantitative evaluation of the evidence from cohort studies, reporting associations between long-term exposure to ozone and mortality.Cohort studies published in peer-reviewed journals indexed in EMBASE and MEDLINE to September 2015 and PubMed to October 2015 and cited in reviews/key publications were identified via search strings using terms relating to study design, pollutant and health outcome. Study details and estimate information were extracted and used to calculate standardised effect estimates expressed as HRs per 10 ppb increment in long-term ozone concentrations.14 publications from 8 cohorts presented results for ozone and all-cause and cause-specific mortality. We found no evidence of associations between long-term annual O3 concentrations and the risk of death from all causes, cardiovascular or respiratory diseases, or lung cancer. 4 cohorts assessed ozone concentrations measured during the warm season. Summary HRs for cardiovascular and respiratory causes of death derived from 3 cohorts were 1.01 (95% CI 1.00 to 1.02) and 1.03 (95% CI 1.01 to 1.05) per 10 ppb, respectively.Our quantitative review revealed a paucity of independent studies regarding the associations between long-term exposure to ozone and mortality. The potential impact of climate change and increasing anthropogenic emissions of ozone precursors on ozone levels worldwide suggests further studies of the long-term effects of exposure to high ozone levels are warranted.
| S-EPMC4769417 | biostudies-other
Project description:An increasing number of studies examined the potential effects of PM1 (submicronic particulate matter with an aerodynamic diameter ≤ 1 μm) on the risk of respiratory diseases; however, the results have been inconclusive. This study aimed to determine the overall association between PM1 with total and cause-specific respiratory diseases. A systematic review and meta-analysis was conducted with 68 related articles retrieved, and six articles met the full inclusion criteria for the final analysis. For a 10 μg/m3 increase in PM1, the pooled odds ratio (OR) was 1.05 (95% CI 0.98-1.12) for total respiratory diseases, 1.25 (95% CI 1.00-1.56) for asthma, and 1.07 (95% CI 1.04-1.10) for pneumonia with the I2 value of 87%, 70%, and 0%, respectively. Subgroup analyses showed that long-term exposure to PM1 was associated with increased risk of asthma (OR 1.47, 95% CI 1.33-1.63) with an I2 value of 0%, while short-term exposure to PM1 was not associated with asthma (OR 1.07, 95% CI 0.89-1.27) with the I2 value of 0%. Egger's test showed that publication bias existed (P = 0.041); however, the funnel plot was symmetrical with the inclusion of the moderator. In conclusion, elevated levels of PM1 may increase morbidity in total and cause-specific respiratory diseases in the population.
| S-EPMC8810454 | biostudies-literature
Project description:ObjectiveTo determine whether long term exposure to outdoor nitrogen dioxide (NO2) is associated with all-cause or cause-specific mortality.MethodsMEDLINE, 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.ResultsSeventy-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.ConclusionsFor 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).
| S-EPMC7861378 | biostudies-literature
Project description:Long-term ozone (O3) exposure may lead to non-communicable diseases and increase mortality risk. However, cohort-based studies are relatively rare, and inconsistent exposure metrics impair the credibility of epidemiological evidence synthetization. To provide more accurate meta-estimations, this study updates existing systematic reviews by including recent studies and summarizing the quantitative associations between O3 exposure and cause-specific mortality risks, based on unified exposure metrics. Cross-metric conversion factors were estimated linearly by decadal observations during 1990-2019. The Hunter-Schmidt random-effects estimator was applied to pool the relative risks. A total of 25 studies involving 226,453,067 participants (14 unique cohorts covering 99,855,611 participants) were included in the systematic review. After linearly unifying the inconsistent O3 exposure metrics , the pooled relative risks associated with every 10 nmol mol-1 (ppbV) incremental O3 exposure, by mean of the warm-season daily maximum 8-h average metric, were as follows: 1.014 with 95% confidence interval (CI) ranging 1.009-1.019 for all-cause mortality; 1.025 (95% CI: 1.010-1.040) for respiratory mortality; 1.056 (95% CI: 1.029-1.084) for COPD mortality; 1.019 (95% CI: 1.004-1.035) for cardiovascular mortality; and 1.074 (95% CI: 1.054-1.093) for congestive heart failure mortality. Insignificant mortality risk associations were found for ischemic heart disease, cerebrovascular diseases, and lung cancer. Adjustment for exposure metrics laid a solid foundation for multi-study meta-analysis, and widening coverage of surface O3 observations is expected to strengthen the cross-metric conversion in the future. Ever-growing numbers of epidemiological studies supported the evidence for considerable cardiopulmonary hazards and all-cause mortality risks from long-term O3 exposure. However, evidence of long-term O3 exposure-associated health effects was still scarce, so more relevant studies are needed to cover more populations with regional diversity.
| S-EPMC9065904 | biostudies-literature
Project description:Associations between long-term exposure to nitrogen oxides (NOx) and cause-specific mortality remain insufficiently explored. This study utilizes data from 502,040 participants registered in the UK Biobank. Time-varying Cox regression is used to estimate mortality risks associated with NOx. Cause-specific mortality risks, including non-accidental, accidental and 15 major disease categories across 103 subcategories, are assessed for each 10 μg/m3 increase in NOx. Positive associations are observed between NOx and mortality from all-cause (HR: 1.036; 95% CI: 1.024, 1.049) and non-accidental diseases (HR: 1.032; 95% CI: 1.019, 1.045). We further identify 20 specific diseases related to NOx, notably respiratory diseases, mental and behavioral disorders, and circulatory diseases, with generally linear exposure-response relationships. Sex and residential areas are potential modifiers of the observed associations. Our findings suggest long-term exposure to NOx may increase mortality risks from a range of diseases, emphasizing the urgent need for clean air policies to alleviate the health burden.
| S-EPMC11836065 | biostudies-literature
Project description:BackgroundThe link between particulate matter (PM) exposure and adverse health outcomes has been widely evaluated using large cohort studies. However, the possibility of residual confounding and lack of information about the health effects of PM in rural and suburban areas are unsolved issues.ObjectiveOur aim was to estimate the effect of annual PM≤10µg (PM10) exposure on cause-specific mortality in the Latium region (central Italy, of which Rome is the main city) during 2006-2012 using a difference-in-differences approach.MethodsWe estimated daily PM10 concentrations for each 1 km2 of the region from 2006 to 2012 by use of satellite data, land-use predictors, and meteorological parameters. For each of the 378 regional municipalities and each year, we averaged daily PM10 values to obtain annual mean PM10 exposures. We applied a variant of the difference-in-differences approach to estimate the association between PM10 and cause-specific mortality by focusing on within-municipality fluctuations of mortality rates and annual PM exposures around municipality means, therefore controlling by design for confounding from all spatial and temporal potential confounders. Analyses were also stratified by population size of the municipalities to obtain effect estimates in rural and suburban areas of the region.ResultsIn the period 2006-2012, we observed deaths due to three causes: 347,699 nonaccidental; 92,787 cardiovascular; and 16,509 respiratory causes. The annual average (standard deviation, SD) PM10 concentration was 21.9 (±4.9) µg/km3 in Latium. For each 1-µg/m3 increase in annual PM10 we estimated increases of 0.8% (95% confidence intervals (CIs): 0.2%, 1.3%), 0.9% (0.0%, 1.8%), and 1.4% (-0.4%, 3.3%) in nonaccidental, cardiovascular, and respiratory mortality, respectively. Similar results were found when we excluded the metropolitan area of Rome from the analysis. Higher effects were estimated in the smaller municipalities, e.g., those with population < 5,000 inhabitants.ConclusionOur study suggests a significant association of annual PM10 exposure with nonaccidental and cardiorespiratory mortality in the Latium region, even outside Rome and in suburban and rural areas. https://doi.org/10.1289/EHP3759.
| S-EPMC6792372 | biostudies-literature
Project description:BackgroundAmbient air pollution has been characterized as a leading cause of mortality worldwide and has been associated with cardiovascular and respiratory diseases. There is increasing evidence that short-term exposure to nitrogen dioxide (NO2), is related to adverse health effects and mortality.MethodsWe conducted a systematic review of short-term NO2 and daily mortality, which were indexed in PubMed and Embase up to June 2021. We calculated random-effects estimates by different continents and globally, and tested for heterogeneity and publication bias.ResultsWe included 87 articles in our quantitative analysis. NO2 and all-cause as well as cause-specific mortality were positively associated in the main analysis. For all-cause mortality, a 10 ppb increase in NO2 was associated with a 1.58% (95%CI 1.28%-1.88%, I2 = 96.3%, Eggers' test p < 0.01, N = 57) increase in the risk of death. For cause-specific mortality, a 10 ppb increase in NO2 was associated with a 1.72% (95%CI 1.41%-2.04%, I2 = 87.4%, Eggers' test p < 0.01, N = 42) increase in cardiovascular mortality and a 2.05% (95%CI 1.52%-2.59%, I2 = 78.5%, Eggers' test p < 0.01, N = 38) increase in respiratory mortality. In the sensitivity analysis, the meta-estimates for all-cause mortality, cardiovascular and respiratory mortality were nearly identical. The heterogeneity would decline to varying degrees through regional and study-design stratification.ConclusionsThis study provides evidence of an association between short-term exposure to NO2, a proxy for traffic-sourced air pollutants, and all-cause, cardiovascular and respiratory mortality.
| S-EPMC8578359 | biostudies-literature
Project description:BackgroundEstablished evidence suggests risks of developing cardiovascular disease are different by sex. However, it remains unclear whether associations of PM2.5 with cardiovascular risk are comparable between women and men. The meta-analysis aimed to examine sex differences in associations of ischemic heart disease (IHD) and stroke with long-term PM2.5 exposure.MethodsPubMed, EMBASE and Cochrane Library were searched until May 2, 2021. We included cohort studies reporting sex-specific associations of long-term PM2.5 exposure (e.g., ≥1 year) with IHD and stroke. The primary analysis was to estimate relative risk (RR) of PM2.5-outcome in women and men separately, and the additional women-to-men ratio of RR (RRR) was explored to compare sex differences, using random-effect models.ResultsWe identified 25 eligible studies with 3.6 million IHD and 1.3 million stroke cases among 63.7 million participants. A higher level of PM2.5 exposure was significantly associated with increased risk of IHD in both women (RR = 1.21; 95% CI, 1.15-1.27) and men (RR = 1.12; 95% CI, 1.07-1.17). The women-to-men RRR of IHD was 1.05 (95% CI, 1.02-1.08) per 10 μg/m3 increment in PM2.5 exposure, indicating significant excess risk of IHD in women. The significant risks of stroke associated with PM2.5 were obtained in both women (RR = 1.11; 95% CI, 1.08-1.13) and men (RR = 1.11; 95% CI, 1.07-1.14), but no significant women-to-men RRR was observed in stroke (RRR = 1.00; 95% CI, 0.96-1.04).ConclusionsThe study identified excess risk of IHD associated with long-term PM2.5 exposure in women. The findings would not only have repercussions on efforts to precisely evaluate the burden of IHD attributable to PM2.5, but would also provide novel clues for cardiovascular risk prevention accounting for sex-based differences.
| S-EPMC8847390 | biostudies-literature