Background:Fine particulate matter (PM2.5) air pollution exposure has been identified as a global health threat. However, the types and sources of particles most responsible are not yet known.Objectives:We sought to identify the causal characteristics and sources of air pollution underlying past associations between long-term PM2.5 exposure and ischemic heart disease (IHD) mortality, as established in the American Cancer Society’s Cancer Prevention Study-II cohort.Methods:Individual risk factor data were evaluated for 445,860 adults in 100 U.S. metropolitan areas followed from 1982 through 2004 for vital status and cause of death. Using Cox proportional hazard models, we estimated IHD mortality hazard ratios (HRs) for PM2.5, trace constituents, and pollution source–associated PM2.5, as derived from air monitoring at central stations throughout the nation during 2000–2005.Results:Associations with IHD mortality varied by PM2.5 mass constituent and source. A coal combustion PM2.5 IHD HR = 1.05 (95% CI: 1.02, 1.08) per microgram/cubic meter, versus an IHD HR = 1.01 (95% CI: 1.00, 1.02) per microgram/cubic meter PM2.5 mass, indicated a risk roughly five times higher for coal combustion PM2.5 than for PM2.5 mass in general, on a per microgram/cubic meter PM2.5 basis. Diesel traffic–related elemental carbon (EC) soot was also associated with IHD mortality (HR = 1.03; 95% CI: 1.00, 1.06 per 0.26-μg/m3 EC increase). However, PM2.5 from both wind-blown soil and biomass combustion was not associated with IHD mortality.Conclusions:Long-term PM2.5 exposures from fossil fuel combustion, especially coal burning but also from diesel traffic, were associated with increases in IHD mortality in this nationwide population. Results suggest that PM2.5–mortality associations can vary greatly by source, and that the largest IHD health benefits per microgram/cubic meter from PM2.5 air pollution control may be achieved via reductions of fossil fuel combustion exposures, especially from coal-burning sources.Citation:Thurston GD, Burnett RT, Turner MC, Shi Y, Krewski D, Lall R, Ito K, Jerrett M, Gapstur SM, Diver WR, Pope CA III. 2016. Ischemic heart disease mortality and long-term exposure to source-related components of U.S. fine particle air pollution. Environ Health Perspect 124:785–794; http://dx.doi.org/10.1289/ehp.1509777

Using daily fine particulate matter (PM2.5) composition data from the 2000–2005 U.S. EPA Chemical Speciation Network (CSN) for over 200 sites, we applied multivariate methods to identify and quantify the major fine particulate matter (PM2.5) source components in the U.S. Novel aspects of this work were: (1) the application of factor analysis (FA) to multi-city daily data, drawing upon both spatial and temporal variations of chemical species; and, (2) the exclusion of secondary components (sulfates, nitrates and organic carbon) from the source identification FA to more clearly discern and apportion the PM2.5 mass to primary emission source categories. For the quantification of source-related mass, we considered two approaches based upon the FA results: 1) using single key tracers for sources identified by FA in a mass regression; and, 2) applying Absolute Principal Component Analysis (APCA). In each case, we followed a two-stage mass regression approach, in which secondary components were first apportioned among the identified sources, and then mass was apportioned to the sources and to other secondary mass not explained by the individual sources. The major U.S. PM2.5 source categories identified via FA (and their key elements) were: Metals Industry (Pb, Zn); Crustal/Soil Particles (Ca, Si); Motor Vehicle Traffic (EC, NO2); Steel Industry (Fe, Mn); Coal Combustion (As, Se); Oil Combustion (V, Ni); Salt Particles (Na, Cl) and Biomass Burning (K). Nationwide spatial plots of the source-related PM2.5 impacts were confirmatory of the factor interpretations: ubiquitous sources, such as Traffic and Soil, were found to be spread across the nation, more unique sources (such as Steel and Metals Processing) being highest in select industrialized cities, Biomass Burning was highest in the U.S. Northwest, while Residual Oil combustion was highest in cities in the Northeastern U.S. and in cities with major seaports. The sum of these source contributions and the secondary PM2.5 components agreed well with the U.S. PM2.5 observed during the study period (mean=14.3 ug/m3; R2= 0.91). Apportionment regression analyses using single-element tracers for each source category gave results consistent with the APCA estimates. Comparisons of nearby sites indicated that the PM2.5 mass and the secondary aerosols were most homogenous spatially, while traffic PM2.5 and its tracer, EC, were among the most spatially representative of the source-related components. Comparison of apportionment results to a previous analysis of the 1979–1982 IP Network revealed similar and correlated major U.S. source category factors, albeit at lower levels than in the earlier period, suggesting a consistency in the U.S. spatial patterns of these source-related exposures over time, as well. These results indicate that applying source apportionment methods to the nationwide CSN can be an informative avenue for identifying and quantifying source components for the subsequent estimation of source-specific health effects, potentially contributing to more efficient re...

During the past three decades, receptor models have been used to identify and apportion ambient concentrations to sources. A number of groups are employing these methods to provide input into air quality management planning. A workshop has explored the use of resolved source contributions in health effects models. Multiple groups have analyzed particulate composition data sets from Washington, DC and Phoenix, AZ. Similar source profiles were extracted from these data sets by the investigators using different factor analysis methods. There was good agreement among the major resolved source types. Crustal (soil), sulfate, oil, and salt were the sources that were most unambiguously identified (generally highest correlation across the sites). Traffic and vegetative burning showed considerable variability among the results with variability in the ability of the methods to partition the motor vehicle contributions between gasoline and diesel vehicles. However, if the total motor vehicle contributions are estimated, good correspondence was obtained among the results. The source impacts were especially similar across various analyses for the larger mass contributors (e.g., in Washington, secondary sulfate SE ¼ 7% and 11% for traffic; in Phoenix, secondary sulfate SE ¼ 17% and 7% for traffic). Especially important for time-series health effects assessment, the source-specific impacts were found to be highly correlated across analysis methods/researchers for the major components (e.g., mean analysis to analysis correlation, r40.9 for traffic and secondary sulfates in Phoenix and for traffic and secondary nitrates in Washington. The sulfate mean r value is 40.75 in Washington.). Overall, although these intercomparisons suggest areas where further research is needed (e.g., better division of traffic emissions between diesel and gasoline vehicles), they provide support the contention that PM 2.5 mass source apportionment results are consistent across users and methods, and that today's source apportionment methods are robust enough for application to PM 2.5 health effects assessments.

BackgroundMany types of tree pollen trigger seasonal allergic illness, but their population-level impacts on allergy and asthma morbidity are not well established, likely due to the paucity of long records of daily pollen data that allow analysis of multi-day effects. Our objective in this study was therefore to determine the impacts of individual spring tree pollen types on over-the-counter allergy medication sales and asthma emergency department (ED) visits.MethodsNine clinically-relevant spring tree pollen genera (elm, poplar, maple, birch, beech, ash, sycamore/London planetree, oak, and hickory) measured in Armonk, NY, were analyzed for their associations with over-the-counter allergy medication sales and daily asthma syndrome ED visits from patients’ chief complaints or diagnosis codes in New York City during March 1st through June 10th, 2002-2012. Multi-day impacts of pollen on the outcomes (0-3 days and 0-7 days for the medication sales and ED visits, respectively) were estimated using a distributed lag Poisson time-series model adjusting for temporal trends, day-of-week, weather, and air pollution. For asthma syndrome ED visits, age groups were also analyzed. Year-to-year variation in the average peak dates and the 10th-to-90th percentile duration between pollen and the outcomes were also examined with Spearman’s rank correlation.ResultsMid-spring pollen types (maple, birch, beech, ash, oak, and sycamore/London planetree) showed the strongest significant associations with both outcomes, with cumulative rate ratios up to 2.0 per 0-to-98th percentile pollen increase (e.g., 1.9 [95 % CI: 1.7, 2.1] and 1.7 [95 % CI: 1.5, 1.9] for the medication sales and ED visits, respectively, for ash). Lagged associations were longer for asthma syndrome ED visits than for the medication sales. Associations were strongest in children (ages 5-17; e.g., a cumulative rate ratio of 2.6 [95 % CI: 2.1, 3.1] per 0-to-98th percentile increase in ash). The average peak dates and durations of some of these mid-spring pollen types were also associated with those of the outcomes.ConclusionsTree pollen peaking in mid-spring exhibit substantive impacts on allergy, and asthma exacerbations, particularly in children. Given the narrow time window of these pollen peak occurrences, public health and clinical approaches to anticipate and reduce allergy/asthma exacerbation should be developed.Electronic supplementary materialThe online version of this article (doi:10.1186/s12940-015-0057-0) contains supplementary material, which is available to authorized users.

BackgroundRecent toxicological and epidemiological studies have shown associations between particulate matter (PM) and adverse health effects, but which PM components are most influential is less well known.ObjectivesIn this study, we used time-series analyses to determine the associations between daily fine PM [PM ≤ 2.5 μm in aerodynamic diameter (PM2.5)] concentrations and daily mortality in two U.S. cities—Seattle, Washington, and Detroit, Michigan.MethodsWe obtained daily PM2.5 filters for the years of 2002–2004 and analyzed trace elements using X-ray fluorescence and black carbon using light reflectance as a surrogate measure of elemental carbon. We used Poisson regression and distributed lag models to estimate excess deaths for all causes and for cardiovascular and respiratory diseases adjusting for time-varying covariates. We computed the excess risks for interquartile range increases of each pollutant at lags of 0 through 3 days for both warm and cold seasons.ResultsThe cardiovascular and respiratory mortality series exhibited different source and seasonal patterns in each city. The PM2.5 components and gaseous pollutants associated with mortality in Detroit were most associated with warm season secondary aerosols and traffic markers. In Seattle, the component species most closely associated with mortality included those for cold season traffic and other combustion sources, such as residual oil and wood burning.ConclusionsThe effects of PM2.5 on daily mortality vary with source, season, and locale, consistent with the hypothesis that PM composition has an appreciable influence on the health effects attributable to PM.