scholarly journals Estimation of Particulate Matter Impact on Human Health within the Urban Environment of Athens City, Greece

Author(s):  
Konstantinos P. Moustris ◽  
Kleopatra Ntourou ◽  
Panagiotis Nastos

The main objective of this work is the assessment of the annual number of hospital admissions for respiratory disease (HARD) due to the exposure to in-healable particulate matter (PM10), within the greater Athens area (GAA), Greece. Towards this aim, the time series of the particulate matter with aerodynamic diameter less than 10μm (PM10) recorded in six monitoring stations located in the GAA, for a 13-year period 2001-2013, is used. Initially, a descriptive statistical treatment of PM10 concentrations took place. Furthermore, the AirQ2.2.3 software developed by the WHO was used to evaluate adverse health effects by PM10 in the GAA during the examined period. The results show that, during the examined period PM10 concentrations present a significant decreasing trend. Also, the mean annual HARD cases per 100,000 inhabitants ranged between 20 (suburban location) and 40 (city centre location). Approximately 70% of the annual HARD cases are due to city centre residents. In all examined locations, a declining trend in the annual number of HARD cases is appeared. Moreover, a strong relation between the annual number of HARD cases and the annual number of days exceeding the European Union daily PM10 threshold value was found.

2015 ◽  
Vol 15 (5) ◽  
pp. 2327-2340 ◽  
Author(s):  
J. G. Charrier ◽  
N. K. Richards-Henderson ◽  
K. J. Bein ◽  
A. S. McFall ◽  
A. S. Wexler ◽  
...  

Abstract. Recent epidemiological evidence supports the hypothesis that health effects from inhalation of ambient particulate matter (PM) are governed by more than just the mass of PM inhaled. Both specific chemical components and sources have been identified as important contributors to mortality and hospital admissions, even when these end points are unrelated to PM mass. Sources may cause adverse health effects via their ability to produce reactive oxygen species in the body, possibly due to the transition metal content of the PM. Our goal is to quantify the oxidative potential of ambient particle sources collected during two seasons in Fresno, CA, using the dithiothreitol (DTT) assay. We collected PM from different sources or source combinations into different ChemVol (CV) samplers in real time using a novel source-oriented sampling technique based on single-particle mass spectrometry. We segregated the particles from each source-oriented mixture into two size fractions – ultrafine Dp ≤ 0.17 μm) and submicron fine (0.17 μm ≤ Dp ≤ 1.0 μm) – and measured metals and the rate of DTT loss in each PM extract. We find that the mass-normalized oxidative potential of different sources varies by up to a factor of 8 and that submicron fine PM typically has a larger mass-normalized oxidative potential than ultrafine PM from the same source. Vehicular emissions, regional source mix, commute hours, daytime mixed layer, and nighttime inversion sources exhibit the highest mass-normalized oxidative potential. When we apportion DTT activity for total PM sampled to specific chemical compounds, soluble copper accounts for roughly 50% of total air-volume-normalized oxidative potential, soluble manganese accounts for 20%, and other unknown species, likely including quinones and other organics, account for 30%. During nighttime, soluble copper and manganese largely explain the oxidative potential of PM, while daytime has a larger contribution from unknown (likely organic) species.


2014 ◽  
Vol 14 (17) ◽  
pp. 24149-24181 ◽  
Author(s):  
J. G. Charrier ◽  
N. K. Richards-Henderson ◽  
K. J. Bein ◽  
A. S. McFall ◽  
A. S. Wexler ◽  
...  

Abstract. Recent epidemiological evidence supports the hypothesis that health effects from inhalation of ambient particulate matter (PM) are governed by more than just the mass of PM inhaled. Both specific chemical components and sources have been identified as important contributors to mortality and hospital admissions, even when these endpoints are unrelated to PM mass. Sources may cause adverse health effects via their ability to produce reactive oxygen species, possibly due to the transition metal content of the PM. Our goal is to quantify the oxidative potential of ambient particle sources collected during two seasons in Fresno, CA using the dithiothreitol (DTT) assay. We collected PM from different sources or source combinations into different ChemVol (CV) samplers in real time using a novel source-oriented sampling technique based on single particle mass spectrometry. We segregated the particles from each source-oriented mixture into two size fractions – ultrafine (Dp ≤ 0.17 μm) and submicron fine (0.17 μm ≤ Dp ≤ 1.0 μm) – and measured metals and the rate of DTT loss in each PM extract. We find that the mass-normalized oxidative potential of different sources varies by up to a actor of 8 and that submicron fine PM typically has a larger mass-normalized oxidative potential than ultrafine PM from the same source. Vehicular Emissions, Regional Source Mix, Commute Hours, Daytime Mixed Layer and Nighttime Inversion sources exhibit the highest mass-normalized oxidative potential. When we apportion the volume-normalized oxidative potential, which also accounts for the source's prevalence, cooking sources account for 18–29% of the total DTT loss while mobile (traffic) sources account for 16–28%. When we apportion DTT activity for total PM sampled to specific chemical compounds, soluble copper accounts for roughly 50% of total air-volume-normalized oxidative potential, soluble manganese accounts for 20%, and other unknown species, likely including quinones and other organics, account for 30%. During nighttime, soluble copper and manganese largely explain the oxidative potential of PM, while daytime has a larger contribution from unknown (likely organic) species.


2021 ◽  
Vol 129 (Suppl_1) ◽  
Author(s):  
Mariana Argenziano ◽  
jiajia yang ◽  
Mariana Burgos Angulo ◽  
Thomas V McDonald

Introduction: Air particulate matter (PM) represents one of the most critical environmental issues worldwide, causing more than 3 million deaths a year. In the US, hospital admissions due to heart failure (HF) increase by 0.8% for every 10 μg/m3 elevation in PM. However, the biological mechanisms behind the effects of PM on cardiovascular disease (CVD) remain poorly defined. Recent studies showed that PM 2.5 can translocate into the circulation, causing cumulative toxicity. With air pollution increasing due to human activity and the growing prevalence of HF, there is a critical need to understand PM's contributions to CVD to develop preventive treatments and novel therapeutic approaches. Hypothesis: We hypothesize that PM can exert its toxic effect by increasing oxidative stress and apoptosis and affecting cardiac electrophysiology. Methods: Three independent induced pluripotent stem cell lines (IPSC) were differentiated into cardiomyocytes (iCMs) and cultured for 30 days before treatment with 100 μg/ml of PM 2.5 for 48h. Experiments including immunostaining, qPCR, RNAseq and Multielectrode Array (MEA) were performed in control (CT) and PM-treated iCMs (PM). Results: Treatment with PM increased ROS and decreased ATP production (CT 9.9±1.2pmol vs PM 6.6±0.8pmol, p<0.01, n=20). Immunostaining showed mitochondrial fragmentation and increased expression of cleaved caspase3 without structural changes. Moreover, PM caused upregulation of the apoptotic markers P53 , PARP1 and CASP3, oxidative stress markers CYP1A1, CYP1B1 and MT2A, and cardiac markers CACNA1C together with downregulation of GJA1 . RNAseq analysis showed upregulation of Gene Ontology terms related to detoxification, response to toxic substances and oxidative stress. Upregulated KEGG pathways included oxidative phosphorylation, hypertrophic cardiomyopathy and dilated cardiomyopathy. MEA experiments revealed a decrease in the spike amplitude and conduction velocity, along with shortening of the action potential (APD90: CT 577±20ms vs. PM 489±16ms, p<0.05, n=20) and increased beat period irregularity (CT 3.2±0.7% vs. PM 13.1±1.6%, p<0.001, n=20). These electrophysiological changes were reversed by treatment with the antioxidant N-acetylcysteine. Conclusions: We conclude that PM plays a direct role in the development of CVD, causing an increase in oxidative stress and affecting the electrophysiology of the heart. Further functional studies in iCMs from HF patients will provide evidence of the effects of these changes on the phenotype of the disease.


PLoS ONE ◽  
2021 ◽  
Vol 16 (7) ◽  
pp. e0253253
Author(s):  
Sung Han Rhew ◽  
Julia Kravchenko ◽  
H. Kim Lyerly

Alzheimer’s disease (AD), non-AD dementia, and Parkinson’s disease (PD) are increasingly common in older adults, yet all risk factors for their onset are not fully understood. Consequently, environmental exposures, including air pollution, have been hypothesized to contribute to the etiology of neurodegeneration. Because persistently elevated rates of AD mortality in the southern Piedmont area of North Carolina (NC) have been documented, we studied mortality and hospital admissions for AD, non-AD dementia, and PD in residential populations aged 65+ with long-term exposures to elevated levels of ambient air particulate matter 2.5 (PM2.5) exceeding the World Health Organization (WHO) air quality standards (≥10μg/m3). Health data were obtained from the State Center for Health Statistics and the Healthcare Cost and Utilization Project. PM2.5 levels were obtained from the MODIS/MISR and SeaWiFS datafiles. Residents in the Study group of elevated air particulate matter (87 zip codes with PM2.5≥10μg/m3) were compared to the residents in the Control group with low levels of air particulate matter (81 zip codes with PM2.5≤7.61μg/m3), and were found to have higher age-adjusted rates of mortality and hospital admissions for AD, non-AD dementia, and PD, including a most pronounced increase in AD mortality (323/100,000 vs. 257/100,000, respectively). After adjustment for multiple co-factors, the risk of death (odds ratio, or OR) from AD in the Study group (OR = 1.35, 95%CI[1.24–1.48]) was significantly higher than ORs of non-AD dementia or PD (OR = 0.97, 95%CI[0.90–1.04] and OR = 1.13, 95%CI[0.92–1.31]). The OR of hospital admissions was significantly increased only for AD as a primary case of hospitalization (OR = 1.54, 95%CI[1.31–1.82]). Conclusion: NC residents aged 65+ with long-term exposures to ambient PM2.5 levels exceeding the WHO standard had significantly increased risks of death and hospital admissions for AD. The effects for non-AD dementia and PD were less pronounced.


2021 ◽  
Author(s):  
Olga von Beckerath ◽  
Knut Kröger ◽  
Frans Santosa ◽  
Ayat Nasef ◽  
Bernd Kowall ◽  
...  

Abstract Objectives This article aimed to compare nationwide time trends of oral anticoagulant prescriptions with the time trend of hospitalization for tooth extraction (TE) in Germany from 2006 through 2017. Patients and Methods We derived the annual number of hospital admissions for TE from the Nationwide Hospital Referral File of the Federal Bureau of Statistics and defined daily doses (DDD) of prescribed anticoagulants in outpatients from reports of the drug information system of the statutory health insurance. Results From 2005 to 2017, annual oral anticoagulation (OAC) treatment rates increased by 143.7%. In 2017, direct oral anticoagulants (DOACs) represented 57.1% of all OAC treatments. The number of cases hospitalized for TE increased by 28.0 only. From all the cases hospitalized for TE in Germany in 2006, 14.2% had a documented history of long-term use of OACs. This proportion increased to 19.6% in 2017. Age-standardized hospitalization rates for all TE cases with long-term use of OACs increased from 6.6 in 2006 to 10.5 cases per 100,000 person-years in 2014 and remained almost unchanged thereafter. Conclusion Our comparison showed that the large increase in OAC treatment rates in general from 2006 to 2017 had only a small impact on hospitalized TE cases with long-term use of OAC which flattens since 2014.


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