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      Characterization of Source-Specific Air Pollution Exposure for a Large Population-Based Swiss Cohort (SAPALDIA)

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          Abstract

          Background

          Although the dispersion model approach has been used in some epidemiologic studies to examine health effects of traffic-specific air pollution, no study has evaluated the model predictions vigorously.

          Methods

          We evaluated total and traffic-specific particulate matter < 10 and < 2.5 μm in aero-dynamic diameter (PM 10, PM 2.5), nitrogren dioxide, and nitrogen oxide concentrations predicted by Gaussian dispersion models against fixed-site measurements at different locations, including traffic-impacted, urban-background, and alpine settings between and across cities. The model predictions were then used to estimate individual subjects’ historical and cumulative exposures with a temporal trend model.

          Results

          Modeled PM 10 and NO 2 predicted at least 55% and 72% of the variability of the measured PM 10 and NO 2, respectively. Traffic-specific pollution estimates correlated with the NO x measurements ( R 2 ≥0.77) for background sites but not for traffic sites. Regional background PM 10 accounted for most PM 10 mass in all cities. Whereas traffic PM 10 accounted for < 20% of the total PM 10, it varied significantly within cities. The modeling error for PM 10 was similar within and between cities. Traffic NO x accounted for the majority of NO x mass in urban areas, whereas background NO x accounted for the majority of NO x in rural areas. The within-city NO 2 modeling error was larger than that between cities.

          Conclusions

          The dispersion model predicted well the total PM 10, NO x, and NO 2 and traffic-specific pollution at background sites. However, the model underpredicted traffic NO x and NO 2 at traffic sites and needs refinement to reflect local conditions. The dispersion model predictions for PM 10 are suitable for examining individual exposures and health effects within and between cities.

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          Most cited references48

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          Fine particulate air pollution and mortality in 20 U.S. cities, 1987-1994.

          Air pollution in cities has been linked to increased rates of mortality and morbidity in developed and developing countries. Although these findings have helped lead to a tightening of air-quality standards, their validity with respect to public health has been questioned. We assessed the effects of five major outdoor-air pollutants on daily mortality rates in 20 of the largest cities and metropolitan areas in the United States from 1987 to 1994. The pollutants were particulate matter that is less than 10 microm in aerodynamic diameter (PM10), ozone, carbon monoxide, sulfur dioxide, and nitrogen dioxide. We used a two-stage analytic approach that pooled data from multiple locations. After taking into account potential confounding by other pollutants, we found consistent evidence that the level of PM10 is associated with the rate of death from all causes and from cardiovascular and respiratory illnesses. The estimated increase in the relative rate of death from all causes was 0.51 percent (95 percent posterior interval, 0.07 to 0.93 percent) for each increase in the PM10 level of 10 microg per cubic meter. The estimated increase in the relative rate of death from cardiovascular and respiratory causes was 0.68 percent (95 percent posterior interval, 0.20 to 1.16 percent) for each increase in the PM10 level of 10 microg per cubic meter. There was weaker evidence that increases in ozone levels increased the relative rates of death during the summer, when ozone levels are highest, but not during the winter. Levels of the other pollutants were not significantly related to the mortality rate. There is consistent evidence that the levels of fine particulate matter in the air are associated with the risk of death from all causes and from cardiovascular and respiratory illnesses. These findings strengthen the rationale for controlling the levels of respirable particles in outdoor air.
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            Association of fine particulate matter from different sources with daily mortality in six U.S. cities.

            Previously we reported that fine particle mass (particulate matter [less than and equal to] 2.5 microm; PM(2.5)), which is primarily from combustion sources, but not coarse particle mass, which is primarily from crustal sources, was associated with daily mortality in six eastern U.S. cities (1). In this study, we used the elemental composition of size-fractionated particles to identify several distinct source-related fractions of fine particles and examined the association of these fractions with daily mortality in each of the six cities. Using specific rotation factor analysis for each city, we identified a silicon factor classified as soil and crustal material, a lead factor classified as motor vehicle exhaust, a selenium factor representing coal combustion, and up to two additional factors. We extracted daily counts of deaths from National Center for Health Statistics records and estimated city-specific associations of mortality with each source factor by Poisson regression, adjusting for time trends, weather, and the other source factors. Combined effect estimates were calculated as the inverse variance weighted mean of the city-specific estimates. In the combined analysis, a 10 microg/m(3) increase in PM(2.5) from mobile sources accounted for a 3.4% increase in daily mortality [95% confidence interval (CI), 1.7-5.2%], and the equivalent increase in fine particles from coal combustion sources accounted for a 1.1% increase [CI, 0.3-2.0%). PM(2.5) crustal particles were not associated with daily mortality. These results indicate that combustion particles in the fine fraction from mobile and coal combustion sources, but not fine crustal particles, are associated with increased mortality.
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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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                Author and article information

                Journal
                Environ Health Perspect
                Environmental Health Perspectives
                National Institute of Environmental Health Sciences
                0091-6765
                November 2007
                14 August 2007
                : 115
                : 11
                : 1638-1645
                Affiliations
                [1 ] Institute of Social and Preventive Medicine, University of Basel, Basel, Switzerland
                [2 ] Department of Environmental and Occupational Health Sciences, University of Washington, Seattle, Washington, USA
                [3 ] Infras, Zürich, Switzerland
                [4 ] ICREA (Institució Catalana de Recerca i Estudis Avançats) and Center for Research in Environmental Epidemiology (CREAL) at Institut Municipal d’Investigació Mèdica (IMIM), Barcelona, Spain
                Author notes
                Address correspondence to L.-J.S. Liu, Institute of Social and Preventive Medicine, University of Basel, Steinengraben 49, CH-4051 Basel, Switzerland. Telephone: 41 61 267 6500. Fax: 41 61 267 6190. E-mail: sally.liu@ 123456unibas.ch

                The authors declare they have no competing financial interests.

                Article
                ehp0115-001638
                10.1289/ehp.10177
                2072852
                18007997
                465e5007-5446-4d70-8f50-2f5af5ff9a44
                This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original DOI.
                History
                : 16 February 2007
                : 14 August 2007
                Categories
                Research

                Public health
                long-term exposure,exposure assessment,dispersion model,cumulative exposure,cohort study

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