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      Acute Effects of Ambient Particulate Matter on Mortality in Europe and North America: Results from the APHENA Study

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          Abstract

          Background

          The APHENA (Air Pollution and Health: A Combined European and North American Approach) study is a collaborative analysis of multicity time-series data on the effect of air pollution on population health, bringing together data from the European APHEA (Air Pollution and Health: A European Approach) and U.S. NMMAPS (National Morbidity, Mortality and Air Pollution Study) projects, along with Canadian data.

          Objectives

          The main objective of APHENA was to assess the coherence of the findings of the multicity studies carried out in Europe and North America, when analyzed with a common protocol, and to explore sources of possible heterogeneity. We present APHENA results on the effects of particulate matter (PM) ≤ 10 μm in aerodynamic diameter (PM 10) on the daily number of deaths for all ages and for those < 75 and ≥ 75 years of age. We explored the impact of potential environmental and socioeconomic factors that may modify this association.

          Methods

          In the first stage of a two-stage analysis, we used Poisson regression models, with natural and penalized splines, to adjust for seasonality, with various degrees of freedom. In the second stage, we used meta-regression approaches to combine time-series results across cites and to assess effect modification by selected ecologic covariates.

          Results

          Air pollution risk estimates were relatively robust to different modeling approaches. Risk estimates from Europe and United States were similar, but those from Canada were substantially higher. The combined effect of PM 10 on all-cause mortality across all ages for cities with daily air pollution data ranged from 0.2% to 0.6% for a 10-μg/m 3 increase in ambient PM 10 concentration. Effect modification by other pollutants and climatic variables differed in Europe and the United States. In both of these regions, a higher proportion of older people and higher unemployment were associated with increased air pollution risk.

          Conclusions

          Estimates of the increased mortality associated with PM air pollution based on the APHENA study were generally comparable with results of previous reports. Overall, risk estimates were similar in Europe and in the United States but higher in Canada. However, PM 10 effect modification patterns were somewhat different in Europe and the United States.

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          Most cited references49

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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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            Ozone and short-term mortality in 95 US urban communities, 1987-2000.

            Ozone has been associated with various adverse health effects, including increased rates of hospital admissions and exacerbation of respiratory illnesses. Although numerous time-series studies have estimated associations between day-to-day variation in ozone levels and mortality counts, results have been inconclusive. To investigate whether short-term (daily and weekly) exposure to ambient ozone is associated with mortality in the United States. Using analytical methods and databases developed for the National Morbidity, Mortality, and Air Pollution Study, we estimated a national average relative rate of mortality associated with short-term exposure to ambient ozone for 95 large US urban communities from 1987-2000. We used distributed-lag models for estimating community-specific relative rates of mortality adjusted for time-varying confounders (particulate matter, weather, seasonality, and long-term trends) and hierarchical models for combining relative rates across communities to estimate a national average relative rate, taking into account spatial heterogeneity. Daily counts of total non-injury-related mortality and cardiovascular and respiratory mortality in 95 large US communities during a 14-year period. A 10-ppb increase in the previous week's ozone was associated with a 0.52% increase in daily mortality (95% posterior interval [PI], 0.27%-0.77%) and a 0.64% increase in cardiovascular and respiratory mortality (95% PI, 0.31%-0.98%). Effect estimates for aggregate ozone during the previous week were larger than for models considering only a single day's exposure. Results were robust to adjustment for particulate matter, weather, seasonality, and long-term trends. These results indicate a statistically significant association between short-term changes in ozone and mortality on average for 95 large US urban communities, which include about 40% of the total US population. The findings indicate that this widespread pollutant adversely affects public health.
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              Health effects of fine particulate air pollution: lines that connect.

              Efforts to understand and mitigate thehealth effects of particulate matter (PM) air pollutionhave a rich and interesting history. This review focuseson six substantial lines of research that have been pursued since 1997 that have helped elucidate our understanding about the effects of PM on human health. There hasbeen substantial progress in the evaluation of PM health effects at different time-scales of exposure and in the exploration of the shape of the concentration-response function. There has also been emerging evidence of PM-related cardiovascular health effects and growing knowledge regarding interconnected general pathophysiological pathways that link PM exposure with cardiopulmonary morbidiity and mortality. Despite important gaps in scientific knowledge and continued reasons for some skepticism, a comprehensive evaluation of the research findings provides persuasive evidence that exposure to fine particulate air pollution has adverse effects on cardiopulmonaryhealth. Although much of this research has been motivated by environmental public health policy, these results have important scientific, medical, and public health implications that are broader than debates over legally mandated air quality standards.
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                Author and article information

                Journal
                Environ Health Perspect
                Environmental Health Perspectives
                National Institute of Environmental Health Sciences
                0091-6765
                1552-9924
                November 2008
                26 June 2008
                : 116
                : 11
                : 1480-1486
                Affiliations
                [1 ] Department of Hygiene and Epidemiology, University of Athens Medical School, Athens, Greece
                [2 ] Department of Biostatistics, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, USA
                [3 ] McLaughlin Centre for Population Health Risk Assessment, University of Ottawa, Ottawa, Ontario, Canada
                [4 ] Environmental Health and Consumer Products Branch, Health Canada, Ottawa, Ontario, Canada
                [5 ] Health Effects Institute, Boston, Massachusetts, USA
                [6 ] Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, USA
                Author notes
                Address correspondence to E. Samoli, Department of Hygiene and Epidemiology, University of Athens Medical School, 75 Mikras Asias St., 115 27 Athens, Greece. Telephone: 30-210-7462085. Fax: 30-210-7462205. E-mail: esamoli@ 123456med.uoa.gr

                The authors declare they have no competing financial interests.

                Article
                ehp-116-1480
                10.1289/ehp.11345
                2592267
                19057700
                e8f80985-f363-41f2-ba16-51dbbe4b3e63
                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
                : 8 February 2008
                : 26 June 2008
                Categories
                Research

                Public health
                heterogeneity,air pollution,meta-regression,mortality,effect modification,particulate matter,penalized splines,natural splines,time-series analysis

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