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      Estimation of Fine Particulate Matter in Taipei Using Landuse Regression and Bayesian Maximum Entropy Methods

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          Abstract

          Fine airborne particulate matter (PM 2.5) has adverse effects on human health. Assessing the long-term effects of PM 2.5 exposure on human health and ecology is often limited by a lack of reliable PM 2.5 measurements. In Taipei, PM 2.5 levels were not systematically measured until August, 2005. Due to the popularity of geographic information systems (GIS), the landuse regression method has been widely used in the spatial estimation of PM concentrations. This method accounts for the potential contributing factors of the local environment, such as traffic volume. Geostatistical methods, on other hand, account for the spatiotemporal dependence among the observations of ambient pollutants. This study assesses the performance of the landuse regression model for the spatiotemporal estimation of PM 2.5 in the Taipei area. Specifically, this study integrates the landuse regression model with the geostatistical approach within the framework of the Bayesian maximum entropy (BME) method. The resulting epistemic framework can assimilate knowledge bases including: (a) empirical-based spatial trends of PM concentration based on landuse regression, (b) the spatio-temporal dependence among PM observation information, and (c) site-specific PM observations. The proposed approach performs the spatiotemporal estimation of PM 2.5 levels in the Taipei area (Taiwan) from 2005–2007.

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          Most cited references65

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          Epidemiology of fine particulate air pollution and human health: biologic mechanisms and who's at risk?

          C Pope (2000)
          This article briefly summarizes the epidemiology of the health effects of fine particulate air pollution, provides an early, somewhat speculative, discussion of the contribution of epidemiology to evaluating biologic mechanisms, and evaluates who's at risk or is susceptible to adverse health effects. Based on preliminary epidemiologic evidence, it is speculated that a systemic response to fine particle-induced pulmonary inflammation, including cytokine release and altered cardiac autonomic function, may be part of the pathophysiologic mechanisms or pathways linking particulate pollution with cardiopulmonary disease. The elderly, infants, and persons with chronic cardiopulmonary disease, influenza, or asthma are most susceptible to mortality and serious morbidity effects from short-term acutely elevated exposures. Others are susceptible to less serious health effects such as transient increases in respiratory symptoms, decreased lung function, or other physiologic changes. Chronic exposure studies suggest relatively broad susceptibility to cumulative effects of long-term repeated exposure to fine particulate pollution, resulting in substantive estimates of population average loss of life expectancy in highly polluted environments. Additional knowledge is needed about the specific pollutants or mix of pollutants responsible for the adverse health effects and the biologic mechanisms involved.
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            Spatial analysis of air pollution and mortality in Los Angeles.

            The assessment of air pollution exposure using only community average concentrations may lead to measurement error that lowers estimates of the health burden attributable to poor air quality. To test this hypothesis, we modeled the association between air pollution and mortality using small-area exposure measures in Los Angeles, California. Data on 22,905 subjects were extracted from the American Cancer Society cohort for the period 1982-2000 (5,856 deaths). Pollution exposures were interpolated from 23 fine particle (PM2.5) and 42 ozone (O3) fixed-site monitors. Proximity to expressways was tested as a measure of traffic pollution. We assessed associations in standard and spatial multilevel Cox regression models. After controlling for 44 individual covariates, all-cause mortality had a relative risk (RR) of 1.17 (95% confidence interval=1.05-1.30) for an increase of 10 mug/m PM2.5 and a RR of 1.11 (0.99-1.25) with maximal control for both individual and contextual confounders. The RRs for mortality resulting from ischemic heart disease and lung cancer deaths were elevated, in the range of 1.24-1.6, depending on the model used. These PM results were robust to adjustments for O3 and expressway exposure. Our results suggest the chronic health effects associated with within-city gradients in exposure to PM2.5 may be even larger than previously reported across metropolitan areas. We observed effects nearly 3 times greater than in models relying on comparisons between communities. We also found specificity in cause of death, with PM2.5 associated more strongly with ischemic heart disease than with cardiopulmonary or all-cause mortality.
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              Ambient particulate air pollution, heart rate variability, and blood markers of inflammation in a panel of elderly subjects.

              Epidemiologic studies report associations between particulate air pollution and cardiopulmonary morbidity and mortality. Although the underlying pathophysiologic mechanisms remain unclear, it has been hypothesized that altered autonomic function and pulmonary/systemic inflammation may play a role. In this study we explored the effects of air pollution on autonomic function measured by changes in heart rate variability (HRV) and blood markers of inflammation in a panel of 88 elderly subjects from three communities along the Wasatch Front in Utah. Subjects participated in multiple sessions of 24-hr ambulatory electrocardiographic monitoring and blood tests. Regression analysis was used to evaluate associations between fine particulate matter [aerodynamic diameter less than or equal to 2.5 microm (PM2.5)] and HRV, C-reactive protein (CRP), blood cell counts, and whole blood viscosity. A 100- microg/m3 increase in PM2.5 was associated with approximately a 35 (SE = 8)-msec decline in standard deviation of all normal R-R intervals (SDNN, a measure of overall HRV); a 42 (SE = 11)-msec decline in square root of the mean of the squared differences between adjacent normal R-R intervals (r-MSSD, an estimate of short-term components of HRV); and a 0.81 (SE = 0.17)-mg/dL increase in CRP. The PM2.5-HRV associations were reasonably consistent and statistically robust, but the CRP association dropped to 0.19 (SE = 0.10) after excluding the most influential subject. PM2.5 was not significantly associated with white or red blood cell counts, platelets, or whole-blood viscosity. Most short-term variability in temporal deviations of HRV and CRP was not explained by PM2.5; however, the small statistically significant associations that were observed suggest that exposure to PM2.5 may be one of multiple factors that influence HRV and CRP.
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                Author and article information

                Journal
                Int J Environ Res Public Health
                101238455
                International Journal of Environmental Research and Public Health
                Molecular Diversity Preservation International (MDPI)
                1661-7827
                1660-4601
                June 2011
                14 June 2011
                : 8
                : 6
                : 2153-2169
                Affiliations
                [1 ] Department of Bioenvironmental Systems Engineering, National Taiwan University, Taipei 10617, Taiwan; E-Mails: hlyu@ 123456ntu.edu.tw (H.-L.Y.); r96622049@ 123456ntu.edu.tw (C.-H.W.); mingche_liu@ 123456mail.fcu.edu.tw (M.-C.L.)
                [2 ] Department of Design for Sustainable Environment, Ming Dao University, 369 Wen-Hua Rd., Peetow, Chang-Hua 52345, Taiwan
                Author notes
                [* ]Author to whom correspondence should be addressed; E-Mail: airkuo@ 123456ntu.edu.tw ; Tel.: +886-2-33553454.
                Article
                ijerph-08-02153
                10.3390/ijerph8062153
                3138018
                21776223
                a78aabd9-cb90-4016-8981-0ed3853ac383
                © 2011 by the authors; licensee MDPI, Basel, Switzerland.

                This article is an open-access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/3.0/).

                History
                : 7 March 2011
                : 26 May 2011
                : 7 June 2011
                Categories
                Article

                Public health
                particulate matter,bayesian maximum entropy,landuse regression
                Public health
                particulate matter, bayesian maximum entropy, landuse regression

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