Ambient Air Pollution and All-Cause and Cause-Specific Mortality in an Analysis of Asian Cohorts
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PROVIDER: S-EPMC10330956 | biostudies-literature | 2023 Jan
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Project description:BackgroundAmbient air pollution is a modifiable risk factor for cardiovascular disease, yet uncertainty remains about the size of risks at lower levels of fine particulate matter (PM2.5) exposure which now occur in the USA and elsewhere.MethodsWe investigated the relationship of ambient PM2.5 exposure with cause-specific cardiovascular disease mortality in 565 477 men and women, aged 50 to 71 years, from the National Institutes of Health-AARP Diet and Health Study. During 7.5 x 106 person-years of follow up, 41 286 cardiovascular disease deaths, including 23 328 ischaemic heart disease (IHD) and 5894 stroke deaths, were ascertained using the National Death Index. PM2.5 was estimated using a hybrid land use regression (LUR) geostatistical model. Multivariate Cox regression models were used to estimate relative risks (RRs) and 95% confidence intervals (CI).ResultsEach increase of 10 μg/m3 PM2.5 (overall range, 2.9-28.0 μg/m3) was associated, in fully adjusted models, with a 16% increase in mortality from ischaemic heart disease [hazard ratio (HR) 1.16; 95% CI 1.09-1.22] and a 14% increase in mortality from stroke (HR 1.14; CI 1.02-1.27). Compared with PM2.5 exposure <8 μg/m3 (referent), risks for CVD were increased in relation to PM2.5 exposures in the range of 8-12 μg/m3 (CVD: HR 1.04; 95% CI 1.00-1.08), in the range 12-20 μg/m3 (CVD: HR 1.08; 95% CI 1.03-1.13) and in the range 20+ μg/m3 (CVD: HR 1.19; 95% CI 1.10-1.28). Results were robust to alternative approaches to PM2.5 exposure assessment and statistical analysis.ConclusionsLong-term exposure to fine particulate air pollution is associated with ischaemic heart disease and stroke mortality, with excess risks occurring in the range of and below the present US long-term standard for ambient exposure to PM2.5 (12 µg/m3), indicating the need for continued improvements in air pollution abatement for CVD prevention.
| S-EPMC7124502 | biostudies-literature
Project description:Short-term exposure to air pollution has adverse effects among patients with asthma, but whether long-term exposure to air pollution is a cause of adult-onset asthma is unclear.We aimed to investigate the association between air pollution and adult onset asthma.Asthma incidence was prospectively assessed in six European cohorts. Exposures studied were annual average concentrations at home addresses for nitrogen oxides assessed for 23,704 participants (including 1,257 incident cases) and particulate matter (PM) assessed for 17,909 participants through ESCAPE land-use regression models and traffic exposure indicators. Meta-analyses of cohort-specific logistic regression on asthma incidence were performed. Models were adjusted for age, sex, overweight, education, and smoking and included city/area within each cohort as a random effect.In this longitudinal analysis, asthma incidence was positively, but not significantly, associated with all exposure metrics, except for PMcoarse. Positive associations of borderline significance were observed for nitrogen dioxide [adjusted odds ratio (OR) = 1.10; 95% CI: 0.99, 1.21 per 10 ?g/m3; p = 0.10] and nitrogen oxides (adjusted OR = 1.04; 95% CI: 0.99, 1.08 per 20 ?g/m3; p = 0.08). Nonsignificant positive associations were estimated for PM10 (adjusted OR = 1.04; 95% CI: 0.88, 1.23 per 10 ?g/m3), PM2.5 (adjusted OR = 1.04; 95% CI: 0.88, 1.23 per 5 ?g/m3), PM2.5absorbance (adjusted OR = 1.06; 95% CI: 0.95, 1.19 per 10-5/m), traffic load (adjusted OR = 1.10; 95% CI: 0.93, 1.30 per 4 million vehicles × meters/day on major roads in a 100-m buffer), and traffic intensity (adjusted OR = 1.10; 95% CI: 0.93, 1.30 per 5,000 vehicles/day on the nearest road). A nonsignificant negative association was estimated for PMcoarse (adjusted OR = 0.98; 95% CI: 0.87, 1.14 per 5 ?g/m3).Results suggest a deleterious effect of ambient air pollution on asthma incidence in adults. Further research with improved personal-level exposure assessment (vs. residential exposure assessment only) and phenotypic characterization is needed.
| S-EPMC4455584 | biostudies-literature
Project description:Long-term exposure to air pollution has been associated with several adverse health effects including cardiovascular, respiratory diseases and cancers. However, underlying molecular alterations remain to be further investigated. The aim of this study is to investigate the effects of long-term exposure to air pollutants on (a) average DNA methylation at functional regions and, (b) individual differentially methylated CpG sites. An assumption is that omic measurements, including the methylome, are more sensitive to low doses than hard health outcomes. This study included blood-derived DNA methylation (Illumina-HM450 methylation) for 454 Italian and 159 Dutch participants from the European Prospective Investigation into Cancer and Nutrition (EPIC). Long-term air pollution exposure levels, including NO2, NOx, PM2.5, PMcoarse, PM10, PM2.5 absorbance (soot) were estimated using models developed within the ESCAPE project, and back-extrapolated to the time of sampling when possible. We meta-analysed the associations between the air pollutants and global DNA methylation, methylation in functional regions and epigenome-wide methylation. CpG sites found differentially methylated with air pollution were further investigated for functional interpretation in an independent population (EnviroGenoMarkers project), where (N=613) participants had both methylation and gene expression data available. Exposure to NO2 was associated with a significant global somatic hypomethylation (p-value=0.014). Hypomethylation of CpG island's shores and shelves and gene bodies was significantly associated with higher exposures to NO2 and NOx. Meta-analysing the epigenome-wide findings of the 2 cohorts did not show genome-wide significant associations at single CpG site level. However, several significant CpG were found if the analyses were separated by countries. By regressing gene expression levels against methylation levels of the exposure-related CpG sites, we identified several significant CpG-transcript pairs and highlighted 5 enriched pathways for NO2 and 9 for NOx mainly related to the immune system and its regulation. Our findings support results on global hypomethylation associated with air pollution, and suggest that the shores and shelves of CpG islands and gene bodies are mostly affected by higher exposure to NO2 and NOx. Functional differences in the immune system were suggested by transcriptome analyses.
| S-EPMC6139298 | biostudies-literature
Project description:BackgroundAmbient air pollution is leading risk factor for health burden in China. Few studies in China have investigated the economic loss related to short-term exposure to ambient PM2.5, which could trigger acute onset of cardiorespiratory diseases within a few days.MethodsDaily ambient air pollutants data are obtained for each city from the National Air Quality Monitoring System and daily hospitalization data are obtained from the urban employee-based basic medical insurance scheme database in 74 Chinese cities with an average coverage of 88.5 million urban employees during 2016-2017. A three-stage time-series analytic approach is used in this study to investigate the impact of short-term exposure to ambient fine particulate (PM2.5) air pollution on hospital admissions, expenses and hospital stays of three cause-specific cardiorespiratory diseases, including lower respiratory infections (LRI), coronary heart disease (CHD) and stroke in the included cities.FindingsBased on the time-series analysis using daily hospitalization data, 28,560 LRI cases, 54,600 CHD cases, and 23,989 stroke cases are attributable to ambient PM2.5 in the 74 cities during the study period, and the related attributable expenses are 220 million CNY (US$ 32.9 million) for LRI, 458 million CNY (US$ 68.5 million) for CHD, and 410 million CNY (US$ 65.8 million) for stroke, respectively. These attributable numbers account for 1.45% to 2.05% of total hospital admissions and 1.10% to 1.51% of total expenses for the three diseases during 2016-2017, respectively. The attributable numbers for the three cause-specific cardiorespiratory diseases would increase to 362,007 hospital admission cases and 3.68 billion CNY expenses ($US550 million) in the entire urban employee population (299 million) in China during 2016-2017, and the related direct economic loss of absence from work would be 798 million CNY (US$ 119.3 million).InterpretationOur results support that short-term exposure to ambient PM2.5 pollution could lead to significant health and economic impacts in China. Reducing levels of ambient PM2.5 can avoid substantial health damage and expenditures, and generate appreciable economic benefits from decreasing absence from work.FundingNatural Science Foundation of China (82073509, 71903010, 71903011), and the National Key Research and Development Program of China (2017YFC0211600, 2017YFC0211601).
| S-EPMC8342975 | biostudies-literature
Project description:BackgroundThe systematic evaluation of the results of time-series studies of air pollution is challenged by differences in model specification and publication bias.MethodsWe evaluated the associations of inhalable particulate matter (PM) with an aerodynamic diameter of 10 μm or less (PM10) and fine PM with an aerodynamic diameter of 2.5 μm or less (PM2.5) with daily all-cause, cardiovascular, and respiratory mortality across multiple countries or regions. Daily data on mortality and air pollution were collected from 652 cities in 24 countries or regions. We used overdispersed generalized additive models with random-effects meta-analysis to investigate the associations. Two-pollutant models were fitted to test the robustness of the associations. Concentration-response curves from each city were pooled to allow global estimates to be derived.ResultsOn average, an increase of 10 μg per cubic meter in the 2-day moving average of PM10 concentration, which represents the average over the current and previous day, was associated with increases of 0.44% (95% confidence interval [CI], 0.39 to 0.50) in daily all-cause mortality, 0.36% (95% CI, 0.30 to 0.43) in daily cardiovascular mortality, and 0.47% (95% CI, 0.35 to 0.58) in daily respiratory mortality. The corresponding increases in daily mortality for the same change in PM2.5 concentration were 0.68% (95% CI, 0.59 to 0.77), 0.55% (95% CI, 0.45 to 0.66), and 0.74% (95% CI, 0.53 to 0.95). These associations remained significant after adjustment for gaseous pollutants. Associations were stronger in locations with lower annual mean PM concentrations and higher annual mean temperatures. The pooled concentration-response curves showed a consistent increase in daily mortality with increasing PM concentration, with steeper slopes at lower PM concentrations.ConclusionsOur data show independent associations between short-term exposure to PM10 and PM2.5 and daily all-cause, cardiovascular, and respiratory mortality in more than 600 cities across the globe. These data reinforce the evidence of a link between mortality and PM concentration established in regional and local studies. (Funded by the National Natural Science Foundation of China and others.).
| S-EPMC7891185 | biostudies-literature
Project description:BackgroundThere is a vast body of literature covering the association between air pollution exposure and nonaccidental mortality. However, the role of socioeconomic status (SES) in this relationship is still not fully understood.ObjectivesWe investigated if individual and contextual SES modified the relationship between short-term exposure to ozone (O3), nitrogen dioxide (NO2), and particulate matter with aerodynamic diameter <10 µm (PM10) on cardiovascular, respiratory, and all nonaccidental mortality.MethodsWe conducted a time-stratified case-crossover study. Analyses were based on information on 280,685 deaths from 2011 to 2015 in the city of São Paulo. Education was used as an individual SES, and information on the district of residence was used to build a contextual SES. Exposure to PM10, NO2, and O3 was accessed from monitoring stations and linked to each case based on the date of death. Conditional logistic regression models were used to estimate the effects of air pollutants, and interaction terms were added to access the effect modification of SES.ResultsIndividuals with lower education had an increased chance of dying for all nonaccidental outcomes (1.54% [0.91%, 2.14%]) associated with exposure to PM10. Individuals living in lower SES areas had an increased chance of dying for nonaccidental (0.52% [0.16%, 0.88%]), cardiovascular (1.17% [0.88%, 1.46%]), and respiratory (1.70% [0.47%, 2.93%]) causes owing to NO2 exposure.ConclusionExposure to air pollutants increases the chance of dying by nonaccidental, cardiovascular, and respiratory causes. Lower educational levels and living on lower contextual SES increased the risk of mortality associated with air pollution exposure.
| S-EPMC11008627 | biostudies-literature
Project description:BackgroundThe impacts of air pollution on circulatory and respiratory systems have been extensively studied. However, the associations between air pollution exposure and the risk of noncommunicable diseases of other organ systems, including diseases of the digestive, musculoskeletal, and genitourinary systems, remain unclear or inconclusive. We aimed to systematically assess the associations between short-term exposure to main air pollutants (fine particulate matter [PM2.5] and ozone) and cause-specific risk of hospital admission in China over a wide spectrum of human diseases.Methods and findingsDaily data on hospital admissions for primary diagnosis of 14 major and 188 minor disease categories in 252 Chinese cities (107 cities in North China and 145 cities in South China) from January 1, 2013, to December 31, 2017, were obtained from the Hospital Quality Monitoring System of China (covering 387 hospitals in North China and 614 hospitals in South China). We applied a 2-stage analytic approach to assess the associations between air pollution and daily hospital admissions. City-specific associations were estimated with quasi-Poisson regression models and then pooled by random-effects meta-analyses. Each disease category was analyzed separately, and the P values were adjusted for multiple comparisons. A total of 117,338,867 hospital admissions were recorded in the study period. Overall, 51.7% of the hospitalized cases were male, and 71.3% were aged <65 years. Robust positive associations were found between short-term PM2.5 exposure and hospital admissions for 7 major disease categories: (1) endocrine, nutritional, and metabolic diseases; (2) nervous diseases; (3) circulatory diseases; (4) respiratory diseases; (5) digestive diseases; (6) musculoskeletal and connective tissue diseases; and (7) genitourinary diseases. For example, a 10-μg/m3 increase in PM2.5 was associated with a 0.21% (95% CI 0.15% to 0.27%; adjusted P < 0.001) increase in hospital admissions for diseases of the digestive system on the same day in 2-pollutant models (adjusting for ozone). There were 35 minor disease categories significantly positively associated with same-day PM2.5 in both single- and 2-pollutant models, including diabetes mellitus, anemia, intestinal infection, liver diseases, gastrointestinal hemorrhage, renal failure, urinary tract calculus, chronic ulcer of skin, and back problems. The association between short-term ozone exposure and respiratory diseases was robust. No safety threshold in the exposure-response relationships between PM2.5 and hospital admissions was observed. The main limitations of the present study included the unavailability of data on personal air pollution exposures.ConclusionsIn the Chinese population during 2013-2017, short-term exposure to air pollution, especially PM2.5, was associated with increased risk of hospitalization for diseases of multiple organ systems, including certain diseases of the digestive, musculoskeletal, and genitourinary systems; many of these associations are important but still not fully recognized. The effect estimates and exposure-response relationships can inform policy making aimed at protecting public health from air pollution in China.
| S-EPMC7410211 | biostudies-literature
Project description:BackgroundExtensive evidence indicates that both lifestyle factors and air pollution are strongly associated with all-cause mortality. However, little studies in this field have integrated these two factors in order to examine their relationship with mortality and explore potential interactions.MethodsA cohort of 271,075 participants from the UK Biobank underwent analysis. Lifestyles in terms of five modifiable factors, namely smoking, alcohol consumption, physical activity, diet, and sleep quality, were classified as unhealthy (0-1 score), general (2-3 score), and healthy (4-5 score). Air pollution, including particle matter with a diameter ≤ 2.5 μm (PM2.5), particulate matter with a diameter ≤ 10 μm (PM10), particulate matter with a diameter 2.5-10 μm (PM2.5-10), nitrogen dioxide (NO2), and nitrogen oxides (NOx), was divided into three levels (high, moderate, and low) using Latent Profile Analysis (LPA). Cox proportional hazard regression analysis was performed to examine the links between lifestyle, air pollution, and all-cause mortality before and after adjustment for potential confounders. Restricted cubic spline curves featuring three knots were incorporated to determine nonlinear relationships. The robustness of the findings was assessed via subgroup and sensitivity analyses.ResultsWith unhealthy lifestyles have a significantly enhanced risk of death compared to people with general lifestyles (HR = 1.315, 95% CI, 1.277-1.355), while people with healthy lifestyles have a significantly lower risk of death (HR = 0.821, 95% CI, 0.785-0.858). Notably, the difference in risk between moderate air pollution and mortality risk remained insignificant (HR = 0.993, 95% CI, 0.945-1.044). High air pollution, on the other hand, was independently linked to increased mortality risk as compared to low air pollution (HR = 1.162, 95% CI, 1.124-1.201). The relationship between NOx, PM10, and PM2.5-10 and all-cause mortality was found to be nonlinear (p for nonlinearity < 0.05). Furthermore, no significant interaction was identified between lifestyle and air pollution with respect to all-cause mortality.ConclusionsExposure to ambient air pollution elevated the likelihood of mortality from any cause, which was impacted by individual lifestyles. To alleviate this hazard, it is crucial for authorities to escalate environmental interventions, while individuals should proactively embrace and sustain healthy lifestyles.
| S-EPMC11202323 | biostudies-literature
Project description:ImportanceAmbient fine particulate matter (PM2.5) air pollution is associated with increased risk of several causes of death. However, epidemiologic evidence suggests that current knowledge does not comprehensively capture all causes of death associated with PM2.5 exposure.ObjectiveTo systematically identify causes of death associated with PM2.5 pollution and estimate the burden of death for each cause in the United States.Design, setting, and participantsIn a cohort study of US veterans followed up between 2006 and 2016, ensemble modeling was used to identify and characterize morphology of the association between PM2.5 and causes of death. Burden of death associated with PM2.5 exposure in the contiguous United States and for each state was then estimated by application of estimated risk functions to county-level PM2.5 estimates from the US Environmental Protection Agency and cause-specific death rate data from the Centers for Disease Control and Prevention.Main outcomes and measuresNonlinear exposure-response functions of the association between PM2.5 and causes of death and burden of death associated with PM2.5.ExposuresAnnual mean PM2.5 levels.ResultsA cohort of 4 522 160 US veterans (4 243 462 [93.8%] male; median [interquartile range] age, 64.1 [55.7-75.5] years; 3 702 942 [82.0%] white, 667 550 [14.8%] black, and 145 593 [3.2%] other race) was followed up for a median (interquartile range) of 10.0 (6.8-10.2) years. In the contiguous United States, PM2.5 exposure was associated with excess burden of death due to cardiovascular disease (56 070.1 deaths [95% uncertainty interval {UI}, 51 940.2-60 318.3 deaths]), cerebrovascular disease (40 466.1 deaths [95% UI, 21 770.1-46 487.9 deaths]), chronic kidney disease (7175.2 deaths [95% UI, 5910.2-8371.9 deaths]), chronic obstructive pulmonary disease (645.7 deaths [95% UI, 300.2-2490.9 deaths]), dementia (19 851.5 deaths [95% UI, 14 420.6-31 621.4 deaths]), type 2 diabetes (501.3 deaths [95% UI, 447.5-561.1 deaths]), hypertension (30 696.9 deaths [95% UI, 27 518.1-33 881.9 deaths]), lung cancer (17 545.3 deaths [95% UI, 15 055.3-20 464.5 deaths]), and pneumonia (8854.9 deaths [95% UI, 7696.2-10 710.6 deaths]). Burden exhibited substantial geographic variation. Estimated burden of death due to nonaccidental causes was 197 905.1 deaths (95% UI, 183 463.3-213 644.9 deaths); mean age-standardized death rates (per 100 000) due to nonaccidental causes were higher among black individuals (55.2 [95% UI, 50.5-60.6]) than nonblack individuals (51.0 [95% UI, 46.4-56.1]) and higher among those living in counties with high (65.3 [95% UI, 56.2-75.4]) vs low (46.1 [95% UI, 42.3-50.4]) socioeconomic deprivation; 99.0% of the burden of death due to nonaccidental causes was associated with PM2.5 levels below standards set by the US Environmental Protection Agency.Conclusions and relevanceIn this study, 9 causes of death were associated with PM2.5 exposure. The burden of death associated with PM2.5 was disproportionally borne by black individuals and socioeconomically disadvantaged communities. Effort toward cleaner air might reduce the burden of PM2.5-associated deaths.
| S-EPMC6902821 | biostudies-literature
Project description:BackgroundCoarse particulate matter with aerodynamic diameter between 2.5 and [Formula: see text] ([Formula: see text]) air pollution is a severe environmental problem in developing countries, but its challenges to public health were rarely evaluated.ObjectiveWe aimed to investigate the associations between day-to-day changes in [Formula: see text] and cause-specific mortality in China.MethodsWe conducted a nationwide daily time-series analysis in 272 main Chinese cities from 2013 to 2015. The associations between [Formula: see text] concentrations and mortality were analyzed in each city using overdispersed generalized additive models. Two-stage Bayesian hierarchical models were used to estimate national and regional average associations, and random-effect models were used to pool city-specific concentration-response curves. Two-pollutant models were adjusted for fine particles with aerodynamic diameter [Formula: see text] ([Formula: see text]) or gaseous pollutants.ResultsOverall, we observed positive and approximately linear concentration-response associations between [Formula: see text] and daily mortality. A [Formula: see text] increase in [Formula: see text] was associated with higher mortality due to nonaccidental causes [0.23%; 95% posterior interval (PI): 0.13, 0.33], cardiovascular diseases (CVDs; 0.25%; 95% PI: 0.13, 0.37), coronary heart disease (CHD; 0.21%; 95% PI: 0.05, 0.36), stroke (0.21%; 95% PI: 0.08, 0.35), respiratory diseases (0.26%; 95% PI: 0.07, 0.46), and chronic obstructive pulmonary disease (COPD; 0.34%; 95% PI: 0.12, 0.57). Associations were stronger for cities in southern vs. northern China, with significant differences for total and cardiovascular mortality. Associations with [Formula: see text] were of similar magnitude to those for [Formula: see text] in both single- and two-pollutant models with mutual adjustment. Associations were robust to adjustment for gaseous pollutants other than nitrogen dioxide and sulfur dioxide. Meta-regression indicated that a larger positive correlation between [Formula: see text] and [Formula: see text] predicted stronger city-specific associations between [Formula: see text] and total mortality.ConclusionsThis analysis showed significant associations between short-term [Formula: see text] exposure and daily nonaccidental and cardiopulmonary mortality based on data from 272 cities located throughout China. Associations appeared to be independent of exposure to [Formula: see text], carbon monoxide, and ozone. https://doi.org/10.1289/EHP2711.
| S-EPMC6378682 | biostudies-literature