scholarly journals Burden of cardiovascular diseases associated with fine particulate matter in Beijing, China: an economic modelling study

2020 ◽  
Vol 5 (10) ◽  
pp. e003160
Author(s):  
Yawen Jiang ◽  
Shan Jiang ◽  
Weiyi Ni
Keyword(s):  
Particulate Matter ◽  
Cardiovascular Diseases ◽  
Fine Particulate Matter ◽  
Ambient Air ◽  
Medical Costs ◽  
Economic Modelling ◽  
Annual Average ◽  
Fine Particulate ◽  
Life Years ◽  
Qaly Loss

ObjectiveTo evaluate the economic and humanistic burden associated with cardiovascular diseases that were attributable to fine particulate matter (≤ 2.5 μg/m3 in aerodynamic diameter; PM2.5) in Beijing.MethodsThis study used a health economic modelling approach to compare the actual annual average PM2.5 concentration with the PM2.5 concentration limit (35 µg/m3) as defined by the Chinese Ambient Air Quality Standard in terms of cardiovascular disease outcomes in Beijing adult population. The outcomes included medical costs, quality-adjusted life-years (QALYs) and net monetary loss (NML). Beijing annual average PM2.5 concentration was around 105 µg/m3 during 2013–2015. Therefore, we estimated the differences in cardiovascular outcomes of Beijing adults between exposure to the PM2.5 concentration of 105 µg/m3 and exposure to the concentration of 35 µg/m3. According to WHO estimates, the hazard ratios of coronary heart disease and stroke associated with the increase of PM2.5 concentration from 35 to 105 µg/m3 were 1.15 and 1.29, respectively.ResultsThe total 1-year excess medical costs of cardiovascular diseases associated with PM2.5 pollution in Beijing was US$147.9 million and the total 1-year QALY loss was 92 574 in 2015, amounting to an NML of US$2281.8 million. The expected lifetime incremental costs for a male Beijing adult and a female Beijing adult were US$237 and US$163, the corresponding QALY loss was 0.14 and 0.12, and the corresponding NML was US$3514 and US$2935.ConclusionsPM2.5-related cardiovascular diseases imposed high economic and QALY burden on Beijing society. Continuous and intensive investment on reducing PM2.5 concentration is warranted even when only cardiovascular benefits are considered.

scholarly journals Estimates of the 2016 global burden of kidney disease attributable to ambient fine particulate matter air pollution

BMJ Open ◽  
2019 ◽  
Vol 9 (5) ◽  
pp. e022450 ◽  
Author(s):  
Benjamin Bowe ◽  
Yan Xie ◽  
Tingting Li ◽  
Yan Yan ◽  
Hong Xian ◽  
...  
Keyword(s):  
Air Pollution ◽  
Particulate Matter ◽  
Kidney Disease ◽  
Burden Of Disease ◽  
Fine Particulate Matter ◽  
Ambient Air ◽  
Global Burden ◽  
Years Of Life Lost ◽  
Fine Particulate ◽  
Life Years

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 PM2.5in 194 countries and territories. Population-weighted PM2.5levels and incident rates of CKD for each country were curated from the GBD study publicly available data sources.SettingGBD global and national data on PM2.5and 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 PM2.5was 6 950 514 (95% uncertainty interval: 5 061 533–8 914 745). Global YLD, YLL and DALYs of CKD attributable to PM2.5were 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.

scholarly journals Effect of Short-Term Exposure to Fine Particulate Matter and Temperature on Acute Myocardial Infarction in Korea

2021 ◽  
Vol 18 (9) ◽  
pp. 4822
Author(s):  
Jiyoung Shin ◽  
Jongmin Oh ◽  
In Sook Kang ◽  
Eunhee Ha ◽  
Wook Bum Pyun
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Particulate Matter ◽  
Fine Particulate Matter ◽  
Ambient Air ◽  
Cold Season ◽  
Short Term ◽  
Fine Particulate ◽  
Short Term Exposure ◽  
The Impact

Background/Aim: Previous studies have suggested that the short-term ambient air pollution and temperature are associated with myocardial infarction. In this study, we aimed to conduct a time-series analysis to assess the impact of fine particulate matter (PM2.5) and temperature on acute myocardial infarction (AMI) among adults over 20 years of age in Korea by using the data from the Korean National Health Information Database (KNHID). Methods: The daily data of 192,567 AMI cases in Seoul were collected from the nationwide, population-based KNHID from 2005 to 2014. The monitoring data of ambient PM2.5 from the Seoul Research Institute of Public Health and Environment were also collected. A generalized additive model (GAM) that allowed for a quasi-Poisson distribution was used to analyze the effects of PM2.5 and temperature on the incidence of AMI. Results: The models with PM2.5 lag structures of lag 0 and 2-day averages of lag 0 and 1 (lag 01) showed significant associations with AMI (Relative risk [RR]: 1.011, CI: 1.003–1.020 for lag 0, RR: 1.010, CI: 1.000–1.020 for lag 01) after adjusting the covariates. Stratification analysis conducted in the cold season (October–April) and the warm season (May–September) showed a significant lag 0 effect for AMI cases in the cold season only. Conclusions: In conclusion, acute exposure to PM2.5 was significantly associated with AMI morbidity at lag 0 in Seoul, Korea. This increased risk was also observed at low temperatures.

scholarly journals On the contribution of nocturnal heterogeneous reactive nitrogen chemistry to particulate matter formation during wintertime pollution events in Northern Utah

2019 ◽  
Vol 19 (14) ◽  
pp. 9287-9308 ◽  
Author(s):  
Erin E. McDuffie ◽  
Caroline C. Womack ◽  
Dorothy L. Fibiger ◽  
William P. Dube ◽  
Alessandro Franchin ◽  
...  
Keyword(s):  
Particulate Matter ◽  
Salt Lake ◽  
Fine Particulate Matter ◽  
Ambient Air ◽  
Atmospheric Conditions ◽  
Mixing Processes ◽  
Salt Lake Valley ◽  
Fine Particulate ◽  
Northern Utah ◽  
Pollution Events

Abstract. Mountain basins in Northern Utah, including the Salt Lake Valley (SLV), suffer from wintertime air pollution events associated with stagnant atmospheric conditions. During these events, fine particulate matter concentrations (PM2.5) can exceed national ambient air quality standards. Previous studies in the SLV have found that PM2.5 is primarily composed of ammonium nitrate (NH4NO3), formed from the condensation of gas-phase ammonia (NH3) and nitric acid (HNO3). Additional studies in several western basins, including the SLV, have suggested that production of HNO3 from nocturnal heterogeneous N2O5 uptake is the dominant source of NH4NO3 during winter. The rate of this process, however, remains poorly quantified, in part due to limited vertical measurements above the surface, where this chemistry is most active. The 2017 Utah Winter Fine Particulate Study (UWFPS) provided the first aircraft measurements of detailed chemical composition during wintertime pollution events in the SLV. Coupled with ground-based observations, analyses of day- and nighttime research flights confirm that PM2.5 during wintertime pollution events is principally composed of NH4NO3, limited by HNO3. Here, observations and box model analyses assess the contribution of N2O5 uptake to nitrate aerosol during pollution events using the NO3- production rate, N2O5 heterogeneous uptake coefficient (γ(N2O5)), and production yield of ClNO2 (φ(ClNO2)), which had medians of 1.6 µg m−3 h−1, 0.076, and 0.220, respectively. While fit values of γ(N2O5) may be biased high by a potential under-measurement in aerosol surface area, other fit quantities are unaffected. Lastly, additional model simulations suggest nocturnal N2O5 uptake produces between 2.4 and 3.9 µg m−3 of nitrate per day when considering the possible effects of dilution. This nocturnal production is sufficient to account for 52 %–85 % of the daily observed surface-level buildup of aerosol nitrate, though accurate quantification is dependent on modeled dilution, mixing processes, and photochemistry.

scholarly journals The global and national burden of chronic kidney disease attributable to ambient fine particulate matter air pollution: a modelling study

2020 ◽  
Vol 5 (3) ◽  
pp. e002063 ◽  
Author(s):  
Benjamin Bowe ◽  
Elena Artimovich ◽  
Yan Xie ◽  
Yan Yan ◽  
Miao Cai ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Particulate Matter ◽  
Kidney Disease ◽  
Fine Particulate Matter ◽  
Yield Reduction ◽  
Global Burden ◽  
Exposure Response ◽  
Fine Particulate ◽  
Life Years ◽  
National Burden

IntroductionWe aimed to integrate all available epidemiological evidence to characterise an exposure–response model of ambient fine particulate matter (PM2.5) and the risk of chronic kidney disease (CKD) across the spectrum of PM2.5 concentrations experienced by humans. We then estimated the global and national burden of CKD attributable to PM2.5.MethodsWe collected data from prior studies on the association of PM2.5 with CKD and used an integrative meta-regression approach to build non-linear exposure–response models of the risk of CKD associated with PM2.5 exposure. We then estimated the 2017 global and national incidence, prevalence, disability-adjusted life-years (DALYs) and deaths due to CKD attributable to PM2.5 in 194 countries and territories. Burden estimates were generated by linkage of risk estimates to Global Burden of Disease study datasets.ResultsThe exposure–response function exhibited evidence of an increase in risk with increasing PM2.5 concentrations, where the rate of risk increase gradually attenuated at higher PM2.5 concentrations. Globally, in 2017, there were 3 284 358.2 (95% UI 2 800 710.5 to 3 747 046.1) incident and 122 409 460.2 (108 142 312.2 to 136 424 137.9) prevalent cases of CKD attributable to PM2.5, and 6 593 134.6 (5 705 180.4 to 7 479 818.4) DALYs and 211 019.2 (184 292.5 to 236 520.4) deaths due to CKD attributable to PM2.5. The burden was disproportionately borne by low income and lower middle income countries and exhibited substantial geographic variability, even among countries with similar levels of sociodemographic development. Globally, 72.8% of prevalent cases of CKD attributable to PM2.5 and 74.2% of DALYs due to CKD attributable to PM2.5 were due to concentrations above 10 µg/m3, the WHO air quality guidelines.ConclusionThe global burden of CKD attributable to PM2.5 is substantial, varies by geography and is disproportionally borne by disadvantaged countries. Most of the burden is associated with PM2.5 levels above the WHO guidelines, suggesting that achieving those targets may yield reduction in CKD burden.

scholarly journals Spatial and temporal variability of sources of ambient fine particulate matter (PM<sub>2.5</sub>) in California

2014 ◽  
Vol 14 (22) ◽  
pp. 12085-12097 ◽  
Author(s):  
S. Hasheminassab ◽  
N. Daher ◽  
A. Saffari ◽  
D. Wang ◽  
B. D. Ostro ◽  
...  
Keyword(s):  
Particulate Matter ◽  
Biomass Burning ◽  
Total Mass ◽  
Fine Particulate Matter ◽  
The State ◽  
Vehicular Emissions ◽  
San Jose ◽  
Annual Average ◽  
Fine Particulate ◽  
Sampling Locations

Abstract. To identify major sources of ambient fine particulate matter (PM2.5, dp < 2.5 μm) and quantify their contributions in the state of California, a positive matrix factorization (PMF) receptor model was applied on Speciation Trends Network (STN) data, collected between 2002 and 2007 at eight distinct sampling locations, including El Cajon, Rubidoux, Los Angeles, Simi Valley, Bakersfield, Fresno, San Jose, and Sacramento. Between five to nine sources of fine PM were identified at each sampling site, several of which were common among multiple locations. Secondary aerosols, including secondary ammonium nitrate and ammonium sulfate, were the most abundant contributor to ambient PM2.5 mass at all sampling sites, except for San Jose, with an annual average cumulative contribution of 26 to 63%, across the state. On an annual average basis, vehicular emissions (including both diesel and gasoline vehicles) were the largest primary source of fine PM at all sampling sites in southern California (17–18% of total mass), whereas in Fresno and San Jose, biomass burning was the most dominant primary contributor to ambient PM2.5 (27 and 35% of total mass, respectively), in general agreement with the results of previous source apportionment studies in California. In Bakersfield and Sacramento, vehicular emissions and biomass burning displayed relatively equal annual contributions to ambient PM2.5 mass (12 and 25%, respectively). Other commonly identified sources at all sites included aged and fresh sea salt and soil, which contributed to 0.5–13%, 2–27%, and 1–19% of the total mass, respectively, across all sites and seasons. In addition, a few minor sources were identified exclusively at some of the sites (e.g., chlorine sources, sulfate-bearing road dust, and different types of industrial emissions). These sources overall accounted for a small fraction of the total PM mass across the sampling locations (1 to 15%, on an annual average basis).

scholarly journals Low levels of fine particulate matter increase vascular damage and reduce pulmonary function in young healthy adults

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Lauren H. Wyatt ◽  
Robert B. Devlin ◽  
Ana G. Rappold ◽  
Martin W. Case ◽  
David Diaz-Sanchez
Keyword(s):  
Particulate Matter ◽  
Pulmonary Function ◽  
Adhesion Molecule ◽  
Human Exposure ◽  
Fine Particulate Matter ◽  
Ambient Air ◽  
P Wave ◽  
Low Level ◽  
Link Type ◽  
Fine Particulate

Abstract Background Fine particulate matter (PM2.5) related mild inflammation, altered autonomic control of cardiovascular function, and changes to cell function have been observed in controlled human exposure studies. Methods To measure the systemic and cardiopulmonary impacts of low-level PM exposure, we exposed 20 healthy, young volunteers to PM2.5, in the form of concentrated ambient particles (mean: 37.8 μg/m3, SD 6.5), and filtered air (mean: 2.1 μg/m3, SD 2.6). In this double-blind, crossover study the exposure order was randomized. During the 4 h exposure, volunteers (7 females and 13 males) underwent light intensity exercise to regulate ventilation rate. We measured pulmonary, cardiac, and hematologic end points before exposure, 1 h after exposure, and again 20 h after exposure. Results Low-level PM2.5 resulted in both pulmonary and extra-pulmonary changes characterized by alterations in systematic inflammation markers, cardiac repolarization, and decreased pulmonary function. A mean increase in PM2.5 concentration (37.8 μg/m3) significantly increased serum amyloid A (SAA), C-reactive protein (CRP), soluble intercellular adhesion molecule-1 (sICAM-1), and soluble vascular cell adhesion molecule-1 (sVCAM-1), 1 h after exposure by 8.7, 9.1, 10.7, and 6.6%, respectively, relative to the filtered air control. SAA remained significantly elevated (34.6%) 20 h after PM2.5 exposure which was accompanied by a 5.7% decrease in percent neutrophils. Decreased pulmonary function was observed 1 h after exposure through a 0.8 and 1.2% decrease in forced expiratory volume in 1 s (FEV1) and FEV1/ forced vital capacity (FEV1/FVC) respectively. Additionally, sex specific changes were observed in repolarization outcomes following PM2.5 exposure. In males, P-wave and QRS complex were increased by 15.4 and 5.4% 1 h after exposure. Conclusions This study is the first controlled human exposure study to demonstrate biological effects in response to exposure to concentrated ambient air PM2.5 particles at levels near the PM2.5 US NAAQS standard. Clinical trial registration information clinicaltrials.gov; Identifier: NCT03232086. The study was registered retrospectively on July 25, 2017, prior to final data collection on October 25, 2017 and data analysis.

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