An investigation of 24 buildings in the Greater Boston Area revealed that one-third (8 of 24) contained caulking materials with polychlorinated biphenyl (PCB) content exceeding 50 ppm by weight, which is the U.S. Environmental Protection Agency (U.S. EPA) specified limit above which this material is considered to be PCB bulk product waste. These buildings included schools and other public buildings. In a university building where similar levels of PCB were found in caulking material, PCB levels in indoor air ranged from 111 to 393 ng/m3; and in dust taken from the building ventilation system, < 1 ppm to 81 ppm. In this building, the U.S. EPA mandated requirements for the removal and disposal of the PCB bulk product waste as well as for confirmatory sampling to ensure that the interior and exterior of the building were decontaminated. Although U.S. EPA regulations under the Toxic Substances Control Act stipulate procedures by which PCB-contaminated materials must be handled and disposed, the regulations apparently do not require that materials such as caulking be tested to determine its PCB content. This limited investigation strongly suggests that were this testing done, many buildings would be found to contain high levels of PCBs in the building materials and potentially in the building environment. The presence of PCBs in schools is of particular concern given evidence suggesting that PCBs are developmental toxins.
Air pollution exposure patterns may contribute to known spatial patterning of asthma morbidity within urban areas. While studies have evaluated the relationship between traffic and outdoor concentrations, few have considered indoor exposure patterns within low socioeconomic status (SES) urban communities. In this study, part of a prospective birth cohort study assessing asthma etiology in urban Boston, we collected indoor and outdoor 3-4 day samples of nitrogen dioxide (NO 2 ) and fine particulate matter (PM 2.5 ) in 43 residences across multiple seasons from 2003 to 2005. Homes were chosen to represent low SES households, including both cohort and non-cohort residences in similar neighborhoods, and consisted almost entirely of multiunit residences. Reflectance analysis and X-ray fluorescence spectroscopy were performed on the particle filters to determine elemental carbon (EC) and trace element concentrations, respectively. Additionally, information on home characteristics (e.g. type, age, stove fuel) and occupant behaviors (e.g. smoking, cooking, cleaning) were collected via a standardized questionnaire. The contributions of outdoor and indoor sources to indoor concentrations were quantified with regression analyses using mass balance principles. For NO 2 and most particle constituents (except outdoor-dominated constituents like sulfur and vanadium), the addition of selected indoor source terms improved the model's predictive power. Cooking time, gas stove usage, occupant density, and humidifiers were identified as important contributors to indoor levels of various pollutants. A comparison between cohort and non-cohort participants provided another means to determine the influence of occupant activity patterns on indoor-outdoor ratios. Although the groups had similar housing characteristics and were located in similar neighborhoods, cohort members had significantly higher indoor concentrations of PM 2.5 and NO 2 , associated with indoor activities. We conclude that the effect of indoor sources may be more pronounced in high-density multiunit dwellings, and that future epidemiological studies in these populations should explicitly consider these sources in assigning exposures.
The health-related damages associated with emissions from coal-fired power plants can vary greatly across facilities as a function of plant, site, and population characteristics, but the degree of variability and the contributing factors have not been formally evaluated. In this study, we modeled the monetized damages associated with 407 coal-fired power plants in the United States, focusing on premature mortality from fine particulate matter (PM(2.5)). We applied a reduced-form chemistry-transport model accounting for primary PM(2.5) emissions and the influence of sulfur dioxide (SO(2)) and nitrogen oxide (NO(x)) emissions on secondary particulate formation. Outputs were linked with a concentration-response function for PM(2.5)-related mortality that incorporated nonlinearities and model uncertainty. We valued mortality with a value of statistical life approach, characterizing and propagating uncertainties in all model elements. At the median of the plant-specific uncertainty distributions, damages across plants ranged from $30,000 to $500,000 per ton of PM(2.5), $6,000 to $50,000 per ton of SO(2), $500 to $15,000 per ton of NO(x), and $0.02 to $1.57 per kilowatt-hour of electricity generated. Variability in damages per ton of emissions was almost entirely explained by population exposure per unit emissions (intake fraction), which itself was related to atmospheric conditions and the population size at various distances from the power plant. Variability in damages per kilowatt-hour was highly correlated with SO(2) emissions, related to fuel and control technology characteristics, but was also correlated with atmospheric conditions and population size at various distances. Our findings emphasize that control strategies that consider variability in damages across facilities would yield more efficient outcomes.
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.
Background: There is a growing body of literature linking GIS-based measures of traffic density to asthma and other respiratory outcomes. However, no consensus exists on which traffic indicators best capture variability in different pollutants or within different settings. As part of a study on childhood asthma etiology, we examined variability in outdoor concentrations of multiple traffic-related air pollutants within urban communities, using a range of GIS-based predictors and land use regression techniques.
a b s t r a c t a r t i c l e i n f oBackground: Health effects associated with air pollution are typically evaluated using a single pollutant approach, yet people are exposed to mixtures consisting of multiple pollutants that may have independent or combined effects on human health. Development of exposure metrics that represent the multipollutant environment is important to understand the impact of ambient air pollution on human health. Objectives: We reviewed existing multipollutant exposure metrics to evaluate how they can be applied to understand associations between air pollution and health effects. Methods: We conducted a literature search using both targeted search terms and a relational search in Web of Science and PubMed in April and December 2013. We focused on exposure metrics that are constructed from ambient pollutant concentrations and can be broadly applied to evaluate air pollution health effects. Results: Multipollutant exposure metrics were identified in 57 eligible studies. Metrics reviewed can be categorized into broad pollutant grouping paradigms based on: 1) source emissions and atmospheric processes or 2) common health outcomes. Discussion: When comparing metrics, it is apparent that no universal exposure metric exists; each type of metric addresses different research questions and provides unique information on human health effects. Key limitations of these metrics include the balance between complexity and simplicity as well as the lack of an existing "gold standard" for multipollutant health effects and exposure. Conclusions: Future work on characterizing multipollutant exposure error and joint effects will inform development of improved multipollutant metrics to advance air pollution health effects research and human health risk assessment.
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 to 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 develop pollutant-specific infiltration data (including for PM species), and improve 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.
BackgroundMulti-city population-based epidemiological studies have observed heterogeneity between city-specific fine particulate matter (PM2.5)-mortality effect estimates. These studies typically use ambient monitoring data as a surrogate for exposure leading to potential exposure misclassification. The level of exposure misclassification can differ by city affecting the observed health effect estimate.MethodsThe objective of this analysis is to evaluate whether previously developed residential infiltration-based city clusters can explain city-to-city heterogeneity in PM2.5 mortality risk estimates. In a prior paper 94 cities were clustered based on residential infiltration factors (e.g. home age/size, prevalence of air conditioning (AC)), resulting in 5 clusters. For this analysis, the association between PM2.5 and all-cause mortality was first determined in 77 cities across the United States for 2001–2005. Next, a second stage analysis was conducted evaluating the influence of cluster assignment on heterogeneity in the risk estimates.ResultsAssociations between a 2-day (lag 0–1 days) moving average of PM2.5 concentrations and non-accidental mortality were determined for each city. Estimated effects ranged from −3.2 to 5.1% with a pooled estimate of 0.33% (95% CI: 0.13, 0.53) increase in mortality per 10 μg/m3 increase in PM2.5. The second stage analysis determined that cluster assignment was marginally significant in explaining the city-to-city heterogeneity. The health effects estimates in cities with older, smaller homes with less AC (Cluster 1) and cities with newer, smaller homes with a large prevalence of AC (Cluster 3) were significantly lower than the cluster consisting of cities with older, larger homes with a small percentage of AC.ConclusionsThis is the first study that attempted to examine whether multiple exposure factors could explain the heterogeneity in PM2.5-mortality associations. The results of this study were found to explain a small portion (6%) of this heterogeneity.Electronic supplementary materialThe online version of this article (doi:10.1186/s12940-016-0208-y) contains supplementary material, which is available to authorized users.
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