Stroke Mortality Attributable to Ambient Particulate Matter Pollution from 1990 to 2015 in China: An Age-Period-Cohort and Spatial Autocorrelation Analysis.
Ontology highlight
ABSTRACT:
SUBMITTER: Luo L
PROVIDER: S-EPMC5551210 | biostudies-other | 2017 Jul
REPOSITORIES: biostudies-other
Similar Datasets
Project description:BackgroundParticularly fine particulate matter (PM2.5) has become a significant public health concern in China due to its harmful effects on human health. This study aimed to examine the trends in all causes and cause specific morality burden attributable to PM2.5 pollution in China.MethodsWe extracted data on all causes and cause specific mortality data attributable to PM2.5 exposure for the period 1990-2019 in China from the Global Burden of Disease 2019. The average annual percent change (AAPC) in age-standardized mortality rates (ASMR) and years of life lost (YLLs) due to PM2.5 exposure were calculated using the Joinpoint Regression Program. Using Pearson's correlation, we estimated association between burden trends, urban green space area, and higher education proportions.ResultsDuring the period 1990-1999, there were increases in mortality rates for All causes (1.6%, 95% CI: 1.5% to 1.8%), Diabetes mellitus (5.2%, 95% CI: 4.9% to 5.5%), Encephalitis (3.1%, 95% CI: 2.6% to 3.5%), Ischemic heart disease (3.3%, 95% CI: 3% to 3.6%), and Tracheal, bronchus and lung cancer (5%, 95% CI: 4.7% to 5.2%). In the period 2010-2019, Diabetes mellitus still showed an increase in mortality rates, but at a lower rate with an AAPC of 1.2% (95% CI: 1% to 1.4%). Tracheal bronchus and lung cancer showed a smaller increase in this period, with an AAPC of 0.5% (95% CI: 0.3% to 0.6%). In terms of YLLs, the trends appear to be similar.ConclusionOur findings highlight increasing trends in disease burden attributable to PM2.5 in China, particularly for diabetes mellitus, tracheal, bronchus, and lung cancer.
| S-EPMC10490985 | biostudies-literature
Project description:ObjectiveTo quantitate the 2016 global and national burden of chronic kidney disease (CKD) attributable to ambient fine particulate matter air pollution ≤ 2.5 μm in aerodynamic diameter (PM2.5).DesignWe used the Global Burden of Disease (GBD) study data and methodologies to estimate the 2016 burden of CKD attributable to PM2.5 in 194 countries and territories. Population-weighted PM2.5 levels and incident rates of CKD for each country were curated from the GBD study publicly available data sources.SettingGBD global and national data on PM2.5 and CKD.Participants194 countries and territories.Main outcome measuresWe estimated the attributable burden of disease (ABD), years living with disability (YLD), years of life lost (YLL) and disability-adjusted life-years (DALYs).ResultsThe 2016 global burden of incident CKD attributable to PM2.5 was 6 950 514 (95% uncertainty interval: 5 061 533-8 914 745). Global YLD, YLL and DALYs of CKD attributable to PM2.5 were 2 849 311 (1 875 219-3 983 941), 8 587 735 (6 355 784-10 772 239) and 11 445 397 (8 380 246-14 554 091), respectively. Age-standardised ABD, YLL, YLD and DALY rates varied substantially among geographies. Populations in Mesoamerica, Northern Africa, several countries in the Eastern Mediterranean region, Afghanistan, Pakistan, India and several countries in Southeast Asia were among those with highest age-standardised DALY rates. For example, age-standardised DALYs per 100 000 were 543.35 (391.16-707.96) in El Salvador, 455.29 (332.51-577.97) in Mexico, 408.41 (283.82-551.84) in Guatemala, 238.25 (173.90-303.98) in India and 178.26 (125.31-238.47) in Sri Lanka, compared with 5.52 (0.82-11.48) in Sweden, 6.46 (0.00-14.49) in Australia and 12.13 (4.95-21.82) in Canada. Frontier analyses showed that Mesoamerican countries had significantly higher CKD DALY rates relative to other countries with comparable sociodemographic development.ConclusionsOur results demonstrate that the global toll of CKD attributable to ambient air pollution is significant and identify several endemic geographies where air pollution may be a significant driver of CKD burden. Air pollution may need to be considered in the discussion of the global epidemiology of CKD.
| S-EPMC6528010 | biostudies-literature
Project description:Aim:We aimed to assess and compare secular trends in type 2 diabetes mortality attributable to particulate matter pollution in China and U.S. Methods:We performed an age-period-cohort (APC) analysis to estimate the independent effects of age, period, and cohort on mortality of type 2 diabetes attributable to particulate matter pollution. We collected age-standardized and age-specific mortality rates (1990-2017) from the Global Burden of Disease 2017 Study for China and the U.S. Results:During the period 1990-2017, the age-standardized mortality rates of type 2 diabetes attributable to particulate matter pollution in China showed a general increasing trend, while that in U.S. showed an increase before 2002 and subsequently a decrease. The age effect increased markedly in China compared with the U.S. The period effect showed a substantially increase in China while that in the U.S. increased during 1990-2007 and tended to be stable during 2007-2017. The cohort effect peaked in birth cohort born in 1902-1906 in both China and U.S. and declined consistently in the cohort born in 1992-1996. Conclusions:The age-standardized mortality rates of type 2 diabetes attributable to particulate matter pollution, the age, and period effect in China have been increasing in both sexes from 1990 to 2017. The overall mortality in the U.S. began to decrease since 2003, and the period effect showed a tendency to stabilize. Consequently, it is necessary to educate the nation with the correct knowledge and adopting policies on pollutant emission and techniques to reduce air pollution in China.
| S-EPMC7306083 | biostudies-literature
Project description:Background: Exposure to ambient particulate matter pollution (APMP) is a global health issue that directly affects the human respiratory system. Thus, we estimated the spatiotemporal trends in the burden of APMP-related respiratory diseases from 1990 to 2019. Methods: Based on the Global Burden of Disease Study 2019, data on the burden of APMP-related respiratory diseases were analyzed by age, sex, cause, and location. Joinpoint regression analysis was used to analyze the temporal trends in the burden of different respiratory diseases over the 30 years. Results: Globally, in 2019, APMP contributed the most to chronic obstructive pulmonary disease (COPD), with 695.1 thousand deaths and 15.4 million disability-adjusted life years (DALYs); however, the corresponding age-standardized death and DALY rates declined from 1990 to 2019. Similarly, although age-standardized death and DALY rates since 1990 decreased by 24% and 40%, respectively, lower respiratory infections (LRIs) still had the second highest number of deaths and DALYs attributable to APMP. This was followed by tracheal, bronchus, and lung (TBL) cancer, which showed increased age-standardized death and DALY rates during the past 30 years and reached 3.78 deaths per 100,000 persons and 84.22 DALYs per 100,000 persons in 2019. Among children aged < 5 years, LRIs had a huge burden attributable to APMP, whereas for older people, COPD was the leading cause of death and DALYs attributable to APMP. The APMP-related burdens of LRIs and COPD were relatively higher among countries with low and low-middle socio-demographic index (SDI), while countries with high-middle SDI showed the highest burden of TBL cancer attributable to APMP. Conclusions: APMP contributed substantially to the global burden of respiratory diseases, posing a significant threat to human health. Effective actions aimed at air pollution can potentially avoid an increase in the PM2.5-associated disease burden, especially in highly polluted areas.
| S-EPMC8650086 | biostudies-literature
Project description:Background: Ambient particulate matter is a public health concern in East Asia as it contributes to a growing number of all-cause and cancer deaths. This study aimed to estimate lung cancer death attributable to ambient particulate matter (PM) < 2.5 μm (PM2.5) in East Asia countries. Methods: The attributable death rates of lung cancer were estimated based on the calculation of population attributable fraction. We performed joinpoint regression analysis and age-period-cohort (APC) model to estimate temporal trends of the attributable death to PM2.5. Results: In 2019, PM2.5 was estimated to have caused 42.2% (nearly 0.13 million) of lung cancer deaths in East Asia men. During 1990-2019, the increase in age-standardized death rates of lung cancer attributable to PM2.5 was highest in China, which increased by 3.50% in males and 3.71% in females. The death rate caused by PM2.5 also significantly increased in the Democratic People's Republic of Korea (2.16% in males; 3.06% in females). Joinpoint analysis showed that the rates generally increased in younger and older people in both the Democratic People's Republic of Korea and Mongolia, while it only increased in elderly people in other countries'. Age effect from APC analysis demonstrated the risk of lung cancer death attributable to PM2.5 generally increased from young to old age. Period effect indicated that from 1994-1998 to 2019-2023 period risk continuously increased by 1.77, 1.68, and 1.72 times in China, the Democratic People's Republic of Korea, and Japan, respectively. The period risk decreased from 1999 to 2009 and subsequently increased from 2009 to 2019 in both the Republic of Korea and Mongolia. Conclusions: The death rate of lung cancer attributable to PM2.5 is increasing in the Democratic People's Republic of Korea, Mongolia, and China. In East Asia, China is facing the highest attributable death rate in recent decades. The period effect suggested a remarkably increased risk of lung cancer death caused by PM2.5 in China, the Democratic People's Republic of Korea, and Japan during the long-term period. It is recommended that the governments of these countries should continuously concentrate on particulate matter pollution governance and improvement.
| S-EPMC8553966 | biostudies-literature
Project description:Particulate matter (PM) in the atmosphere and deposited on solar photovoltaic (PV) panels reduce PV energy generation. Reducing anthropogenic PM sources will therefore increase carbon-free energy generation and as a cobenefit will improve surface air quality. However, we lack a global understanding of the sectors that would be the most effective at achieving the necessary reductions in PM sources. Here we combine well-evaluated models of solar PV performance and atmospheric composition to show that deep cuts in air pollutant emissions from the residential, on-road, and energy sectors are the most effective approaches to mitigate PM-induced PV energy losses over East and South Asia, and the Tibetan Plateau, Central Asia, and the Arabian Peninsula, and Western Siberia, respectively. Using 2019 PV capacities as a baseline, we find that a 50% reduction in residential emissions would lead to an additional 10.3 TWh yr-1 (US$878 million yr-1) and 2.5 TWh yr-1 (US$196 million yr-1) produced in China and India, respectively.
| S-EPMC9228073 | biostudies-literature
Project description:Elevated ambient pollution exposure is potentially linked to thromboembolism. However, the mechanisms by which particulate matter (PM) interferes with the balance of hemostatic system remain unclear. This study investigates PM-mediated hemostatic changes in individuals across unique seasonal variations of ambient pollution. This prospective study was conducted between February and July 2020 during alterations in ambient pollution in Chiang Mai, Thailand. Blood tests from 30 healthy subjects were assessed at four-week intervals, four times in total. Various coagulation tests, including prothrombin time (PT), activated partial thromboplastin time (aPTT), von Willebrand factor (vWF), platelet count, and platelet functions, were evaluated. A mixed-effects model was used to analyze the impact of high PM2.5 and PM10 on hemostatic parameters. Thirty male subjects with mean age of 38.9 ± 8.2 years, were included. High levels of PM2.5 and PM10 were significantly associated with PT shortening, with no such effect observed in aPTT. PM2.5 and PM10 values also positively correlated with vWF function, while vWF antigen levels remained unchanged. Soluble P-selectin showed a strong positive association with PM2.5 and PM10 levels. Platelet function analysis revealed no correlation with PM values. Short-term exposure to elevated PM2.5 and PM10 concentrations was linked to shortened PT and enhanced vWF function in healthy individuals. Exploring the impact of these changes on clinically relevant thrombosis is crucial. Additional studies on the pathogenesis of pollution-related thrombosis are warranted for maintaining good health.
| S-EPMC11292950 | biostudies-literature
Project description:ImportanceIncreased levels of ambient fine particulate matter (PM2.5) air pollution are associated with increased risks for detrimental health outcomes, but risks for patients with kidney transplants (KTs) remain unknown.ObjectiveTo investigate the association of PM2.5 exposure with KT outcomes.Design, setting, and participantsThis retrospective cohort study was conducted using data on patients who received KTs from 2004 to 2016 who were identified in the national US transplant registry and followed up through March 2021. Multiple databases were linked to obtain data on PM2.5 concentration, KT outcomes, and patient clinical, transplant, and contextual factors. Data were analyzed from April 2020 through July 2021.ExposuresExposures included post-KT time-dependent annual mean PM2.5 level (in 10 μg/m3) and mean PM2.5 level in the year before KT (ie, baseline levels) in quartiles, as well as baseline annual mean PM2.5 level (in 10 μg/m3).Main outcomes and measuresAcute kidney rejection (ie, rejection within 1 year after KT), time to death-censored graft failure, and time to all-cause death. Multivariable logistic regression for kidney rejection and Cox analyses with nonlinear assessment of exposure-response for death-censored graft failure and all-cause death were performed. The national burden of graft failure associated with PM2.5 levels greater than the Environmental Protection Agency recommended level of 12 μg/m3 was estimated.ResultsAmong 112 098 patients with KTs, 70 522 individuals (62.9%) were older than age 50 years at the time of KT, 68 117 (60.8%) were men, and the median (IQR) follow-up was 6.0 (3.9-8.9) years. There were 37 265 Black patients (33.2%), 17 047 Hispanic patients (15.2%), 48 581 White patients [43.3%]), and 9205 patients (8.2%) of other race or ethnicity. The median (IQR) baseline PM2.5 level was 9.8 (8.3-11.9) μg/m3. Increased baseline PM2.5 level, compared with quartile 1 baseline PM2.5 level, was not associated with higher odds of acute kidney rejection for quartile 2 (adjusted odds ratio [aOR], 0.99; 95% CI, 0.92-1.06) but was associated with increased odds for quartile 3 (aOR, 1.11; 95% CI, 1.04-1.20) and quartile 4 (aOR, 1.13; 95% CI, 1.05-1.23). Nonlinear assessment of exposure-response for graft failure and death showed no evidence for nonlinearity. Increased PM2.5 levels were associated with increased risk of death-censored graft failure (adjusted hazard ratio [aHR] per 10 μg/m3 increase, 1.17; 95% CI, 1.09-1.25) and all-cause death (aHR per 10 μg/m3 increase, 1.21; 95% CI, 1.14-1.28). The national burden of death-censored graft failure associated with PM2.5 above 12 μg/m3 was 57 failures (95% uncertainty interval, 48-67 failures) per year among patients with KTs.Conclusions and relevanceThis cohort study found that PM2.5 level was an independent risk factor associated with acute rejection, graft failure, and death among patients with KTs. These findings suggest that efforts toward decreasing levels of PM2.5 concentration may be associated with improved outcomes after KT.
| S-EPMC8498852 | biostudies-literature
Project description:IntroductionAssociation has been reported between ambient fine particulate matter (PM) and adverse outcomes of cerebrovascular events. However, it remains unclear that whether short-term exposure to PM relates to stroke and the lag of health effects. This triggers us to examine the relationship between PM and population stroke morbidity in Chengdu.MethodsThe daily average concentration of atmospheric pollutants and meteorological factors and daily morbidity of stroke in Chengdu (2013-2015) were collected. Based on time series analysis-generalized additive models (GAM), single-pollutant, two-pollutant and multi-pollutant model were established. The effects of atmospheric PM2.5 (defined as PM less than 2.5μm in aerodynamic diameter), PMc(defined as PM less than 10μm and more than 2.5μm in aerodynamic diameter) and PM10 (defined as PM less than 10μm in aerodynamic diameter) concentration on the daily mortality of stroke were analyzed, respectively.ResultsThe three-year mean concentrations of PM2.5, PMc and PM10 for air pollutants were 75.9, 43.9 and 119.7 μg/m3, respectively. PM2.5 on the current day (lag0) and with a moving average of 0-1 days were significantly associated with the increasing risk of stroke morbidity, and PM2.5 with a lag of 0-1 days had greater association, whereas for PMc and PM10 there were no significant association observed. In our study, every 10μg/m3 increase of PM2.5 was associated with 0.69% percent change in stroke morbidity (95%CI: 0.01~1.38). For females, every 10μg/m3 increase of PM2.5 contributes to 0.80% percent change of onset. And for the group of age less than 65, we observed 0.78% higher risk every 10μg/m3 increase of PM2.5.ConclusionsThese findings suggest that short-term exposure to PM2.5 within 1 day is associated with the onset of stroke, and the younger people (age<65) and females are more sensitive than older people and males.
| S-EPMC6219788 | biostudies-literature
Project description:Murine Pulmonary Responses to Ambient Baltimore Particulate Matter: Genomic Analysis and Contribution to Airway Hyperresponsiveness Asthma is a complex disease characterized by airway hyperresponsiveness (AHR) and chronic airway inflammation. Environmental factors such as ambient particulate matter (PM), a major air pollutant, has been demonstrated in epidemiological studies to contribute to asthma exacerbation and increased asthma prevalence. OBJECTIVE: We investigated the genomic and pathophysiological effects of Baltimore PM (median diameter 1.78 µm) in a murine model of asthma to identify potential biomarkers. METHODS: A/J mice with ovalbumin (OVA) –induced AHR were exposed to PM (20 mg/kg, intratracheal), and both AHR and bronchoalveolar lavage (BAL) were assayed on days 1, 4, and 7 post exposure. Lung gene expression profiling (Affymetrix Mouse430_ 2.0) by PM (20 mg/kg, intratracheal) were assayed on OVA- and / or PM--challenged mice. RESULTS: Significant increases of airway responsiveness in OVA-treated mice were observed, indicating an asthmatic phenotype. Ambient PM exposure induced significant changes in AHR in both naive mice and OVA-induced asthmatic mice. In both naive and OVA challenged asthmatic mice, PM induced eosinophil and neutrophil infiltration into airways, elevated BAL protein content, and stimulated secretion of TH1 cytokines (IFN-g, IL-6, and TNF-a) and TH2 cytokines (IL-4, IL-5, and eotaxin) into BAL. Consistent with these results, PM induced expression of genes of innate immune response, chemotaxis and complementary system. CONCLUSION: These studies, consistent with epidemiological data, indicate that PM increases AHR and lung inflammation in naïve mice and exacerbates the asthma phenotype of increased AHR and gene expression pattern changes correlated with acute lung inflammation and airway damage. We used microarrays to detail the global programme of gene expression induced by rhPBEF treatment and VALI. Keywords: gene expression
2007-12-01 | GSE9465 | GEO