Janet Burke

A population exposure model for particulate matter: case study results for PM 2.5 in Philadelphia, PA

A population exposure model for particulate matter (PM), called the Stochastic Human Exposure and Dose Simulation (SHEDS-PM) model, has been developed and applied in a case study of daily PM2.5 exposures for the population living in Philadelphia, PA. SHEDS-PM is a probabilistic model that estimates the population distribution of total PM exposures by randomly sampling from various input distributions. A mass balance equation is used to calculate indoor PM concentrations for the residential microenvironment from ambient outdoor PM concentrations and physical factor data (e.g., air exchange, penetration, deposition), as well as emission strengths for indoor PM sources (e.g., smoking, cooking). PM concentrations in nonresidential microenvironments are calculated using equations developed from regression analysis of available indoor and outdoor measurement data for vehicles, offices, schools, stores, and restaurants/bars. Additional model inputs include demographic data for the population being modeled and human activity pattern data from EPAs Consolidated Human Activity Database (CHAD). Model outputs include distributions of daily total PM exposures in various microenvironments (indoors, in vehicles, outdoors), and the contribution from PM of ambient origin to daily total PM exposures in these microenvironments. SHEDS-PM has been applied to the population of Philadelphia using spatially and temporally interpolated ambient PM2.5 measurements from 1992–1993 and 1990 US Census data for each census tract in Philadelphia. The resulting distributions showed substantial variability in daily total PM2.5 exposures for the population of Philadelphia (median=20 μg/m3; 90th percentile=59 μg/m3). Variability in human activities, and the presence of indoor-residential sources in particular, contributed to the observed variability in total PM2.5 exposures. The uncertainty in the estimated population distribution for total PM2.5 exposures was highest at the upper end of the distribution and revealed the importance of including estimates of input uncertainty in population exposure models. The distributions of daily microenvironmental PM2.5 exposures (exposures due to time spent in various microenvironments) indicated that indoor-residential PM2.5 exposures (median=13 μg/m3) had the greatest influence on total PM2.5 exposures compared to the other microenvironments. The distribution of daily exposures to PM2.5 of ambient origin was less variable across the population than the distribution of daily total PM2.5 exposures (median=7 μg/m3; 90th percentile=18 μg/m3) and similar to the distribution of ambient outdoor PM2.5 concentrations. This result suggests that human activity patterns did not have as strong an influence on ambient PM2.5 exposures as was observed for exposure to other PM2.5 sources. For most of the simulated population, exposure to PM2.5 of ambient origin contributed a significant percent of the daily total PM2.5 exposures (median=37.5%), especially for the segment of the population without exposure to environmental tobacco smoke in the residence (median=46.4%). Development of the SHEDS-PM model using the Philadelphia PM2.5 case study also provided useful insights into the limitations of currently available data for use in population exposure models. In addition, data needs for improving inputs to the SHEDS-PM model, reducing uncertainty and further refinement of the model structure, were identified.

Air pollution exposure prediction approaches used in air pollution epidemiology studies.

Epidemiological studies of the health effects of outdoor air pollution have traditionally relied upon surrogates of personal exposures, most commonly ambient concentration measurements from central-site monitors. However, this approach may introduce exposure prediction errors and misclassification of exposures for pollutants that are spatially heterogeneous, such as those associated with traffic emissions (e.g., carbon monoxide, elemental carbon, nitrogen oxides, and particulate matter). We review alternative air quality and human exposure metrics applied in recent air pollution health effect studies discussed during the International Society of Exposure Science 2011 conference in Baltimore, MD. Symposium presenters considered various alternative exposure metrics, including: central site or interpolated monitoring data, regional pollution levels predicted using the national scale Community Multiscale Air Quality model or from measurements combined with local-scale (AERMOD) air quality models, hybrid models that include satellite data, statistically blended modeling and measurement data, concentrations adjusted by home infiltration rates, and population-based human exposure model (Stochastic Human Exposure and Dose Simulation, and Air Pollutants Exposure models) predictions. These alternative exposure metrics were applied in epidemiological applications to health outcomes, including daily mortality and respiratory hospital admissions, daily hospital emergency department visits, daily myocardial infarctions, and daily adverse birth outcomes. This paper summarizes the research projects presented during the symposium, with full details of the work presented in individual papers in this journal issue.

Combining Regional-and Local-Scale Air Quality Models with Exposure Models for Use in Environmental Health Studies

Abstract Population-based human exposure models predict the distribution of personal exposures to pollutants of outdoor origin using a variety of inputs, including air pollution concentrations; human activity patterns, such as the amount of time spent outdoors versus indoors, commuting, walking, and indoors at home; microenvironmental infiltration rates; and pollutant removal rates in indoor environments. Typically, exposure models rely upon ambient air concentration inputs from a sparse network of monitoring stations. Here we present a unique methodology for combining multiple types of air quality models (the Community Multi-Scale Air Quality [CMAQ] chemical transport model added to the AERMOD dispersion model) and linking the resulting hourly concentrations to population exposure models (the Hazardous Air Pollutant Exposure Model [HAPEM] or the Stochastic Human Exposure and Dose Simulation [SHEDS] model) to enhance estimates of air pollution exposures that vary temporally (annual and seasonal) and spatially (at census-block-group resolution) in an urban area. The results indicate that there is a strong spatial gradient in the predicted mean exposure concentrations near roadways and industrial facilities that can vary by almost a factor of 2 across the urban area studied. At the high end of the exposure distribution (95th percentile), exposures are higher in the central district than in the suburbs. This is mostly due to the importance of personal mobility factors whereby individuals living in the central area often move between microenvironments with high concentrations, as opposed to individuals residing at the outskirts of the city. Also, our results indicate 20–30% differences due to commuting patterns and almost a factor of 2 difference because of near-roadway effects. These differences are smaller for the median exposures, indicating the highly variable nature of the reflected ambient concentrations. In conjunction with local data on emission sources, microenvironmental factors, and behavioral and socioeconomic characteristics, the combined source-to-exposure modeling methodology presented in this paper can improve the assessment of exposures in future community air pollution health studies.

A source-to-dose assessment of population exposures to fine PM and ozone in Philadelphia, PA, during a summer 1999 episode

A novel source-to-dose modeling study of population exposures to fine particulate matter (PM2.5) and ozone (O3) was conducted for urban Philadelphia. The study focused on a 2-week episode, 11–24 July 1999, and employed the new integrated and mechanistically consistent source-to-dose modeling framework of MENTOR/SHEDS (Modeling Environment for Total Risk studies/Stochastic Human Exposure and Dose Simulation). The MENTOR/SHEDS application presented here consists of four components involved in estimating population exposure/dose: (1) calculation of ambient outdoor concentrations using emission-based photochemical modeling, (2) spatiotemporal interpolation for developing census-tract level outdoor concentration fields, (3) calculation of microenvironmental concentrations that match activity patterns of the individuals in the population of each census tract in the study area, and (4) population-based dosimetry modeling. It was found that the 50th percentiles of calculated microenvironmental concentrations of PM2.5 and O3 were significantly correlated with census-tract level outdoor concentrations, respectively. However, while the 95th percentiles of O3 microenvironmental concentrations were strongly correlated with outdoor concentrations, this was not the case for PM2.5. By further examining the modeled estimates of the 24-h aggregated PM2.5 and O3 doses, it was found that indoor PM2.5 sources dominated the contributions to the total PM2.5 doses for the upper 5 percentiles, Environmental Tobacco Smoking (ETS) being the most significant source while O3 doses due to time spent outdoors dominated the contributions to the total O3 doses for the upper 5 percentiles. The MENTOR/SHEDS system presented in this study is capable of estimating intake dose based on activity level and inhalation rate, thus completing the source-to-dose modeling sequence. The MENTOR/SHEDS system also utilizes a consistent basis of source characterization, exposure factors, and human activity patterns in conducting population exposure assessment of multiple co-occurring air pollutants, and this constitutes a primary distinction from previous studies of population exposure assessment, where different exposure factors and activity patterns would be used for different pollutants. Future work will focus on incorporating the effects of commuting patterns on population exposure/dose assessments as well as on extending the MENTOR/SHEDS applications to seasonal/annual studies and to other areas in the U.S.

Exposure prediction approaches used in air pollution epidemiology studies: key findings and future recommendations.

Many epidemiologic studies of the health effects of exposure to ambient air pollution use measurements from central-site monitors as their exposure estimate. However, measurements from central-site monitors may lack the spatial and temporal resolution required to capture exposure variability in a study population, thus resulting in exposure error and biased estimates. Articles in this dedicated issue examine various approaches to predict or assign exposures to ambient pollutants. These methods include combining existing central-site pollution measurements with local- and/or regional-scale air quality models to create new or “hybrid” models for pollutant exposure estimates and using exposure models to account for factors such as infiltration of pollutants indoors and human activity patterns. Key findings from these articles are summarized to provide lessons learned and recommendations for additional research on improving exposure estimation approaches for future epidemiological studies. In summary, when compared with use of central-site monitoring data, the enhanced spatial resolution of air quality or exposure models can have an impact on resultant health effect estimates, especially for pollutants derived from local sources such as traffic (e.g., EC, CO, and NOx). In addition, the optimal exposure estimation approach also depends upon the epidemiological study design. We recommend that future research develops pollutant-specific infiltration data (including for PM species) and improves existing data on human time-activity patterns and exposure to local source (e.g., traffic), in order to enhance human exposure modeling estimates. We also recommend comparing how various approaches to exposure estimation characterize relationships between multiple pollutants in time and space and investigating the impact of improved exposure estimates in chronic health studies.

The challenge of assessing children's residential exposure to pesticides

In implementing the Food Quality Protection Act (FQPA) the U.S. Environmental Protection Agency (USEPA) has adopted a policy that the exposure factors and models used to assess and predict exposure to pesticides should generally be conservative. Some elements of exposure assessments for FQPA are screening level — they are both uncertain and conservative. If more realistic assessments are to be conducted, then research is required to reduce uncertainty associated with the factors and models used in the exposure assessments. To develop the strategy for conducting this research, critical exposure pathways and factors were identified, and the quality and quantity of data associated with default assumptions for exposure factors were evaluated. Then, based on our current understanding of the pathways that are potentially most important and most uncertain, significant research requirements were identified and prioritized to improve the data available and assumptions used to assess childrens aggregate exposure to pesticides. Based on the results of these efforts, four priority research areas were identified: (1) pesticide use patterns in microenvironments where children spend time, (2) temporal and spatial distribution of pesticides following application in a residential setting, (3) dermal and nondietary ingestion exposure assessment methods and exposure factors, (4) dietary exposure assessment methods and exposure factors for infants and young children. The National Exposure Research Laboratory (NERL) research strategy in support of FQPA is designed to address these priority research needs.

Influence of human activity patterns, particle composition, and residential air exchange rates on modeled distributions of PM 2.5 exposure compared with central-site monitoring data

Central-site monitors do not account for factors such as outdoor-to-indoor transport and human activity patterns that influence personal exposures to ambient fine-particulate matter (PM2.5). We describe and compare different ambient PM2.5 exposure estimation approaches that incorporate human activity patterns and time-resolved location-specific particle penetration and persistence indoors. Four approaches were used to estimate exposures to ambient PM2.5 for application to the New Jersey Triggering of Myocardial Infarction Study. These include: Tier 1, central-site PM2.5 mass; Tier 2A, the Stochastic Human Exposure and Dose Simulation (SHEDS) model using literature-based air exchange rates (AERs); Tier 2B, the Lawrence Berkeley National Laboratory (LBNL) Aerosol Penetration and Persistence (APP) and Infiltration models; and Tier 3, the SHEDS model where AERs were estimated using the LBNL Infiltration model. Mean exposure estimates from Tier 2A, 2B, and 3 exposure modeling approaches were lower than Tier 1 central-site PM2.5 mass. Tier 2A estimates differed by season but not across the seven monitoring areas. Tier 2B and 3 geographical patterns appeared to be driven by AERs, while seasonal patterns appeared to be due to variations in PM composition and time activity patterns. These model results demonstrate heterogeneity in exposures that are not captured by the central-site monitor.

A Comparison of Exposure Metrics for Traffic-Related Air Pollutants: Application to Epidemiology Studies in Detroit, Michigan

Vehicles are major sources of air pollutant emissions, and individuals living near large roads endure high exposures and health risks associated with traffic-related air pollutants. Air pollution epidemiology, health risk, environmental justice, and transportation planning studies would all benefit from an improved understanding of the key information and metrics needed to assess exposures, as well as the strengths and limitations of alternate exposure metrics. This study develops and evaluates several metrics for characterizing exposure to traffic-related air pollutants for the 218 residential locations of participants in the NEXUS epidemiology study conducted in Detroit (MI, USA). Exposure metrics included proximity to major roads, traffic volume, vehicle mix, traffic density, vehicle exhaust emissions density, and pollutant concentrations predicted by dispersion models. Results presented for each metric include comparisons of exposure distributions, spatial variability, intraclass correlation, concordance and discordance rates, and overall strengths and limitations. While showing some agreement, the simple categorical and proximity classifications (e.g., high diesel/low diesel traffic roads and distance from major roads) do not reflect the range and overlap of exposures seen in the other metrics. Information provided by the traffic density metric, defined as the number of kilometers traveled (VKT) per day within a 300 m buffer around each home, was reasonably consistent with the more sophisticated metrics. Dispersion modeling provided spatially- and temporally-resolved concentrations, along with apportionments that separated concentrations due to traffic emissions and other sources. While several of the exposure metrics showed broad agreement, including traffic density, emissions density and modeled concentrations, these alternatives still produced exposure classifications that differed for a substantial fraction of study participants, e.g., from 20% to 50% of homes, depending on the metric, would be incorrectly classified into “low”, “medium” or “high” traffic exposure classes. These and other results suggest the potential for exposure misclassification and the need for refined and validated exposure metrics. While data and computational demands for dispersion modeling of traffic emissions are non-trivial concerns, once established, dispersion modeling systems can provide exposure information for both on- and near-road environments that would benefit future traffic-related assessments.

Development and evaluation of alternative approaches for exposure assessment of multiple air pollutants in Atlanta, Georgia

Measurements from central site (CS) monitors are often used as estimates of exposure in air pollution epidemiological studies. As these measurements are typically limited in their spatiotemporal resolution, true exposure variability within a population is often obscured, leading to potential measurement errors. To fully examine this limitation, we developed a set of alternative daily exposure metrics for each of the 169 ZIP codes in the Atlanta, GA, metropolitan area, from 1999 to 2002, for PM2.5 and its components (elemental carbon (EC), SO4), O3, carbon monoxide (CO), and nitrogen oxides (NOx). Metrics were applied in a study investigating the respiratory health effects of these pollutants. The metrics included: (i) CS measurements (one CS per pollutant); (ii) air quality model results for regional background pollution; (iii) local-scale AERMOD air quality model results; (iv) hybrid air quality model estimates (a combination of (ii) and (iii)); and (iv) population exposure model predictions (SHEDS and APEX). Differences in estimated spatial and temporal variability were compared by exposure metric and pollutant. Comparisons showed that: (i) both hybrid and exposure model estimates exhibited high spatial variability for traffic-related pollutants (CO, NOx, and EC), but little spatial variability among ZIP code centroids for regional pollutants (PM2.5, SO4, and O3); (ii) for all pollutants except NOx, temporal variability was consistent across metrics; (iii) daily hybrid-to-exposure model correlations were strong (r>0.82) for all pollutants, suggesting that when temporal variability of pollutant concentrations is of main interest in an epidemiological application, the use of estimates from either model may yield similar results; (iv) exposure models incorporating infiltration parameters, time-location-activity budgets, and other exposure factors affect the magnitude and spatiotemporal distribution of exposure, especially for local pollutants. The results of this analysis can inform the development of more appropriate exposure metrics for future epidemiological studies of the short-term effects of particulate and gaseous ambient pollutant exposure in a community.

The Triggering of Myocardial Infarction by Fine Particles Is Enhanced When Particles Are Enriched in Secondary Species

Previous studies have reported an increased risk of myocardial infarction (MI) associated with acute increases in PM concentration. Recently, we reported that MI/fine particle (PM2.5) associations may be limited to transmural infarctions. In this study, we retained data on hospital discharges with a primary diagnosis of acute myocardial infarction (using International Classification of Diseases ninth Revision [ICD-9] codes), for those admitted January 1, 2004 to December 31, 2006, who were ≥ 18 years of age, and were residents of New Jersey at the time of their MI. We excluded MI with a diagnosis of a previous MI and MI coded as a subendocardial infarction, leaving n = 1563 transmural infarctions available for analysis. We coupled these health data with PM2.5 species concentrations predicted by the Community Multiscale Air Quality chemical transport model, ambient PM2.5 concentrations, and used the same case-crossover methods to evaluate whether the relative odds of transmural MI associated with increased PM2.5 concentration is modified by the PM2.5 composition/mixture (i.e., mass fractions of sulfate, nitrate, elemental carbon, organic carbon, and ammonium). We found the largest relative odds estimates on the days with the highest tertile of sulfate mass fraction (OR = 1.13; 95% CI = 1.00, 1.27), nitrate mass fraction (OR = 1.18; 95% CI = 0.98, 1.35), and ammonium mass fraction (OR = 1.13; 95% CI = 1.00 1.28), and the lowest tertile of EC mass fraction (OR = 1.17; 95% CI = 1.03, 1.34). Air pollution mixtures on these days were enhanced in pollutants formed through atmospheric chemistry (i.e., secondary PM2.5) and depleted in primary pollutants (e.g., EC). When mixtures were laden with secondary PM species (sulfate, nitrate, and/or organics), we observed larger relative odds of myocardial infarction associated with increased PM2.5 concentrations. Further work is needed to confirm these findings and examine which secondary PM2.5 component(s) is/are responsible for an acute MI response.