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      An Estimate of the Global Burden of Anthropogenic Ozone and Fine Particulate Matter on Premature Human Mortality Using Atmospheric Modeling

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          Abstract

          Background

          Ground-level concentrations of ozone (O 3) and fine particulate matter [≤ 2.5 μm in aerodynamic diameter (PM 2.5)] have increased since preindustrial times in urban and rural regions and are associated with cardiovascular and respiratory mortality.

          Objectives

          We estimated the global burden of mortality due to O 3 and PM 2.5 from anthropogenic emissions using global atmospheric chemical transport model simulations of preindustrial and present-day (2000) concentrations to derive exposure estimates.

          Methods

          Attributable mortalities were estimated using health impact functions based on long-term relative risk estimates for O 3 and PM 2.5 from the epidemiology literature. Using simulated concentrations rather than previous methods based on measurements allows the inclusion of rural areas where measurements are often unavailable and avoids making assumptions for background air pollution.

          Results

          Anthropogenic O 3 was associated with an estimated 0.7 ± 0.3 million respiratory mortalities (6.3 ± 3.0 million years of life lost) annually. Anthropogenic PM 2.5 was associated with 3.5 ± 0.9 million cardiopulmonary and 220,000 ± 80,000 lung cancer mortalities (30 ± 7.6 million years of life lost) annually. Mortality estimates were reduced approximately 30% when we assumed low-concentration thresholds of 33.3 ppb for O 3 and 5.8 μg/m 3 for PM 2.5. These estimates were sensitive to concentration thresholds and concentration–mortality relationships, often by > 50%.

          Conclusions

          Anthropogenic O 3 and PM 2.5 contribute substantially to global premature mortality. PM 2.5 mortality estimates are about 50% higher than previous measurement-based estimates based on common assumptions, mainly because of methodologic differences. Specifically, we included rural populations, suggesting higher estimates; however, the coarse resolution of the global atmospheric model may underestimate urban PM 2.5 exposures.

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          Most cited references14

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          Long-term ozone exposure and mortality.

          Although many studies have linked elevations in tropospheric ozone to adverse health outcomes, the effect of long-term exposure to ozone on air pollution-related mortality remains uncertain. We examined the potential contribution of exposure to ozone to the risk of death from cardiopulmonary causes and specifically to death from respiratory causes. Data from the study cohort of the American Cancer Society Cancer Prevention Study II were correlated with air-pollution data from 96 metropolitan statistical areas in the United States. Data were analyzed from 448,850 subjects, with 118,777 deaths in an 18-year follow-up period. Data on daily maximum ozone concentrations were obtained from April 1 to September 30 for the years 1977 through 2000. Data on concentrations of fine particulate matter (particles that are < or = 2.5 microm in aerodynamic diameter [PM(2.5)]) were obtained for the years 1999 and 2000. Associations between ozone concentrations and the risk of death were evaluated with the use of standard and multilevel Cox regression models. In single-pollutant models, increased concentrations of either PM(2.5) or ozone were significantly associated with an increased risk of death from cardiopulmonary causes. In two-pollutant models, PM(2.5) was associated with the risk of death from cardiovascular causes, whereas ozone was associated with the risk of death from respiratory causes. The estimated relative risk of death from respiratory causes that was associated with an increment in ozone concentration of 10 ppb was 1.040 (95% confidence interval, 1.010 to 1.067). The association of ozone with the risk of death from respiratory causes was insensitive to adjustment for confounders and to the type of statistical model used. In this large study, we were not able to detect an effect of ozone on the risk of death from cardiovascular causes when the concentration of PM(2.5) was taken into account. We did, however, demonstrate a significant increase in the risk of death from respiratory causes in association with an increase in ozone concentration. 2009 Massachusetts Medical Society
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            Association between mortality and indicators of traffic-related air pollution in the Netherlands: a cohort study.

            Long-term exposure to particulate matter air pollution has been associated with increased cardiopulmonary mortality in the USA. We aimed to assess the relation between traffic-related air pollution and mortality in participants of the Netherlands Cohort study on Diet and Cancer (NLCS), an ongoing study. We investigated a random sample of 5000 people from the full cohort of the NLCS study (age 55-69 years) from 1986 to 1994. Long-term exposure to traffic-related air pollutants (black smoke and nitrogen dioxide) was estimated for the 1986 home address. Exposure was characterised with the measured regional and urban background concentration and an indicator variable for living near major roads. The association between exposure to air pollution and (cause specific) mortality was assessed with Cox's proportional hazards models, with adjustment for potential confounders. 489 (11%) of 4492 people with data died during the follow-up period. Cardiopulmonary mortality was associated with living near a major road (relative risk 1.95, 95% CI 1.09-3.52) and, less consistently, with the estimated ambient background concentration (1.34, 0.68-2.64). The relative risk for living near a major road was 1.41 (0.94-2.12) for total deaths. Non-cardiopulmonary, non-lung cancer deaths were unrelated to air pollution (1.03, 0.54-1.96 for living near a major road). Long-term exposure to traffic-related air pollution may shorten life expectancy.
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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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                Author and article information

                Journal
                Environ Health Perspect
                Environmental Health Perspectives
                National Institute of Environmental Health Sciences
                0091-6765
                1552-9924
                September 2010
                9 April 2010
                : 118
                : 9
                : 1189-1195
                Affiliations
                [1 ] University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA
                [2 ] Geophysical Fluid Dynamics Laboratory, National Oceanic and Atmospheric Administration, Princeton, New Jersey, USA
                [3 ] Science and Technology Corporation, Silver Spring, Maryland, USA
                Author notes
                Address correspondence to J.J. West, 146B Rosenau Hall, CB #7431, Chapel Hill, NC 27599 USA. Telephone: (919) 843-3928. Fax: (919) 966-7911. E-mail: jjwest@ 123456email.unc.edu
                [*]

                Current address: NOAA Air Resources Laboratory, Silver Spring, MD.

                S.C.A. and J.J.W. received unrestricted funding from the Merck Foundation to support a related project, and the Merck Foundation was unaware of this research. D.Q.T. is an employee of Science and Technology Corporation, working at National Oceanic and Atmospheric Administration facilities. L.W.H. declares he has no actual or potential competing financial interests.

                Article
                ehp-118-1189
                10.1289/ehp.0901220
                2944076
                20382579
                099f7ef7-7f6c-4daa-aef8-bbceb3ed3426
                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
                : 19 July 2009
                : 8 April 2010
                Categories
                Research

                Public health
                air pollution,ozone,particulate matter,health effects of air pollution,health impact analysis,atmospheric chemistry model

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