Timothy Gould

Source Apportionment of Indoor, Outdoor, and Personal PM2.5 in Seattle, Washington, Using Positive Matrix Factorization

Abstract As part of a large exposure assessment and health-effects panel study, 33 trace elements and light-absorbing carbon were measured on 24-hr fixed-site filter samples for particulate matter with an aerodynamic diameter <2.5 μm (PM2.5) collected between September 26, 2000, and May 25, 2001, at a central outdoor site, immediately outside each subjects residence, inside each residence, and on each subject (personal sample). Both two-way (PMF2) and three-way (PMF3) positive matrix factorization were used to deduce the sources contributing to PM2.5. Five sources contributing to the indoor and outdoor samples were identified: vegetative burning, mobile emissions, secondary sulfate, a source rich in chlorine, and a source of crustal-derived material. Vegetative burning contributed more PM2.5 mass on average than any other source in all microenvironments, with average values estimated by PMF2 and PMF3, respectively, of 7.6 and 8.7 μg/m3 for the outdoor samples, 4 and 5.3 μg/m3 for the indoor samples, and 3.8 and 3.4 μg/m3 for the personal samples. Personal exposure to the combustion-related particles was correlated with outdoor sources, whereas exposure to the crustal and chlorine-rich particles was not. Personal exposures to crustal sources were strongly associated with personal activities, especially time spent at school among the child subjects.

Infant exposure to fine particulate matter and traffic and risk of hospitalization for RSV bronchiolitis in a region with lower ambient air pollution

Few studies investigate the impact of air pollution on the leading cause of infant morbidity, acute bronchiolitis. We investigated the influence of PM(2.5) and other metrics of traffic-derived air pollution exposure using a matched case-control dataset derived from 1997 to 2003 birth and infant hospitalization records from the Puget Sound Region, Washington State. Mean daily PM(2.5) exposure for 7, 30, 60 and lifetime days before case bronchiolitis hospitalization date were derived from community monitors. A regional land use regression model of NO(2) was applied to characterize subjects exposure in the month prior to case hospitalization and lifetime average before hospitalization. Subjects residential proximity within 150 m of highways, major roadways, and truck routes was also assigned. We evaluated 2604 (83%) cases and 23,354 (85%) controls with information allowing adjustment for mothers education, mothers smoking during pregnancy, and infant race/ethnicity. Effect estimates derived from conditional logistic regression revealed very modest increased risk and were not statistically significant for any of the exposure metrics in fully adjusted models. Overall, risk estimates were stronger when restricted to bronchiolitis cases attributed to respiratory syncytial virus (RSV) versus unspecified and for longer exposure windows. The adjusted odds ratio (OR(adj)) and 95% confidence interval per 10 mcg/m(3) increase in lifetime PM(2.5) was 1.14, 0.88-1.46 for RSV bronchiolitis hospitalization. This risk was also elevated for infants who resided within 150 m of a highway (OR(adj) 1.17, 0.95-1.44). This study supports a developing hypothesis that there may be a modest increased risk of bronchiolitis attributable to chronic traffic-derived particulate matter exposure particularly for infants born just before or during peak RSV season. Future studies are needed that can investigate threshold effects and capture larger variability in spatial contrasts among populations of infants.

Intercity transferability of land use regression models for estimating ambient concentrations of nitrogen dioxide

Land use regression (LUR) is a method for predicting the spatial distribution of traffic-related air pollution. To facilitate risk and exposure assessment, and the design of future monitoring networks and sampling campaigns, we sought to determine the extent to which LUR can be used to predict spatial patterns in air pollution in the absence of dedicated measurements. We evaluate the transferability of one LUR model to two other geographically comparable areas with similar climates and pollution types. The source model, developed in 2003 to estimate ambient nitrogen dioxide (NO2) concentrations in Vancouver (BC, Canada) was applied to Victoria (BC, Canada) and Seattle (WA, USA). Model estimates were compared with measurements made with Ogawa® passive samplers in both cities. As part of this study, 42 locations were sampled in Victoria for a 2-week period in June 2006. Data obtained for Seattle were collected for a different project at 26 locations in March 2005. We used simple linear regression to evaluate the fit of the source model under three scenarios: (1) using the same variables and coefficients as the source model; (2) using the same variables as the source model, but calculating new coefficients for local calibration; and (3) developing site-specific equations with new variables and coefficients. In Scenario 1, we found that the source model had a better fit in Victoria (R2=0.51) than in Seattle (R2=0.33). Scenario 2 produced improved R2-values in both cities (Victoria=0.58, Seattle=0.65), with further improvement achieved under Scenario 3 (Victoria=0.61, Seattle=0.72). Although it is possible to transfer LUR models between geographically similar cities, success may depend on the between-city consistency of the input data. Modest field sampling campaigns for location-specific model calibration can help to produce transfer models that are equally as predictive as their sources.

Changes in Lung Function and Airway Inflammation Among Asthmatic Children Residing in a Woodsmoke-Impacted Urban Area

Fine particulate matter (PM2.5) is associated with respiratory effects, and asthmatic children are especially sensitive. Preliminary evidence suggests that combustion-derived particles play an important role. Our objective was to evaluate effect estimates from different PM2.5 exposure metrics in relation to airway inflammation and lung function among children residing in woodsmoke-impacted areas of Seattle. Nineteen children (ages 6–13 yr) with asthma were monitored during the heating season. We measured 24-h outdoor and personal concentrations of PM2.5 and light-absorbing carbon (LAC). Levoglucosan (LG), a marker of woodsmoke, was also measured outdoors. We partitioned PM2.5 exposure into its ambient-generated (Eag) and nonambient (Ena) components. These exposure metrics were evaluated in relation to daily changes in exhaled nitric oxide (FENO), a marker of airway inflammation, and four lung function measures: midexpiratory flow (MEF), peak expiratory flow (PEF), forced expiratory volume in the first second (FEV1), and forced vital capacity (FVC). Eag, but not Ena, was correlated with combustion markers. Significant associations with respiratory health were seen only among participants not using inhaled corticosteroids. Increases in FENO were associated with personal PM2.5, personal LAC, and Eag but not with ambient PM2.5 or its combustion markers. In contrast, MEF and PEF decrements were associated with ambient PM2.5, its combustion markers, and Eag, but not with personal PM2.5 or personal LAC. FEV1 was associated only with ambient LG. Our results suggest that lung function may be especially sensitive to the combustion-generated component of ambient PM2.5, whereas airway inflammation may be more closely related to some other constituent of the ambient PM2.5 mixture.

Emissions from an International Airport Increase Particle Number Concentrations 4-fold at 10 km Downwind

We measured the spatial pattern of particle number (PN) concentrations downwind from the Los Angeles International Airport (LAX) with an instrumented vehicle that enabled us to cover larger areas than allowed by traditional stationary measurements. LAX emissions adversely impacted air quality much farther than reported in previous airport studies. We measured at least a 2-fold increase in PN concentrations over unimpacted baseline PN concentrations during most hours of the day in an area of about 60 km2 that extended to 16 km (10 miles) downwind and a 4- to 5-fold increase to 8–10 km (5–6 miles) downwind. Locations of maximum PN concentrations were aligned to eastern, downwind jet trajectories during prevailing westerly winds and to 8 km downwind concentrations exceeded 75 000 particles/cm3, more than the average freeway PN concentration in Los Angeles. During infrequent northerly winds, the impact area remained large but shifted to south of the airport. The freeway length that would cause an impact equivalent to that measured in this study (i.e., PN concentration increases weighted by the area impacted) was estimated to be 280–790 km. The total freeway length in Los Angeles is 1500 km. These results suggest that airport emissions are a major source of PN in Los Angeles that are of the same general magnitude as the entire urban freeway network. They also indicate that the air quality impact areas of major airports may have been seriously underestimated.

A Controlled Inhalation Diesel Exhaust Exposure Facility with Dynamic Feedback Control of PM Concentration

A facility has been assembled that provides a controlled inhalation exposure to freshly diluted and mixed diesel exhaust using a diesel engine under load and a two-stage exhaust dilution system with dynamic feedback control. The concentrations of particulate matter less than 2.5 μ m in diameter (PM2.5), particulate carbon, and gaseous pollutants including carbon monoxide and oxides of nitrogen (NOx) have been characterized and the exposure conditions have been found to be both stable and reproducible. Control of the PM2.5 concentration at intended levels relies on the relatively linear relationship between particle light scattering and exhaust particle mass concentration. While the exposure system does not entirely replicate diesel exhaust conditions in the atmosphere due to the relatively low ratio of nitrogen dioxide to total NOx, the fine particulate matter size distributions are quite similar to those of aged diesel exhaust. The facility enables study of the relationship between diesel exhaust and cardiovascular and respiratory health effects in human and animal models.

Effects of select PM-associated metals on alveolar macrophage phosphorylated ERK1 and -2 and iNOS expression during ongoing alteration in iron homeostasis.

It was hypothesized that relative mass relationships among select constituent metals and iron (Fe3+) govern the pulmonary immunotoxic potential of any PM2.5 sample, as these determine the extent to which Fe3+ binding by transferrin is affected (resulting in altered alveolar macrophage [AM] Fe status and subsequent antibacterial function). Iron response protein (IRP) binding activity is a useful indirect measurement of changes in Fe status, as reductions in cell Fe levels lead to increases in IRP binding. However, AM IRP activity can be affected by an increased presence of nitric oxide generated by inducible nitric oxide synthase (iNOS). This study sought to determine if any changes in AM IRP activity induced by PM2.5 constituents V, Mn, or Al were independent from effects of the metals on cell NO formation. NR8383 rat AM were exposed to Fe3+ alone or combined with V, Mn, or Al at metal:Fe ratios representative of those in PM2.5 collected in New York City, Los Angeles, and Seattle during fall 2001. Cells were then assessed for changes in IRP activity and iNOS expression. Phosphorylated extracellular signal-regulated kinase (ERK) 1 and 2 levels were also measured since activated ERKs are involved in signaling pathways that lead to increased iNOS expression. The results indicate that V and Al, and to a lesser extent Mn, altered IRP activity, though the effects were not consistently concentration dependent. Furthermore, while V and Mn treatments did not induce iNOS expression, Al did. These results confirmed our hypothesis that certain metals associated with PM2.5 might alter the pulmonary immunocompetence of exposed hosts by affecting the Fe status of AM, a major class of deep lung defense cells. This study was supported by funds from the USEPA/PM Center Grant R82735101. The authors are also grateful to services/assistance provided, in part, by the Center Program in the NYU Department of Environmental Medicine that is supported by NIEHS (grant ES00260). The authors also acknowledge the support provided from the U.S. EPA/PM Center Grant R82735501 at the Northwest Center for Particulate Matter and Health in Seattle, WA, and by U.S. EPA grants R82735201 and CR8280260-01-0 at the Southern California Particle Center and Supersite in Los Angeles.

The Air Pollution Exposure Laboratory (APEL) for controlled human exposure to diesel exhaust and other inhalants: characterization and comparison to existing facilities.

Objective: The Air Pollution Exposure Laboratory (APEL) was designed for the controlled inhalation of human subjects to aged and diluted diesel exhaust (DE) to mimic “real-world” occupational and environmental conditions. Methods: An EPA Tier 3-compliant, 6.0 kW diesel generator is operated under discrete cyclic loads to simulate diesel on-road emissions. The engine accepts standard ultra-low sulfur diesel or a variety of alternative fuels (such as biodiesel) via a partitioned tank. A portion of raw exhaust is drawn into the primary dilution system and is diluted 9:1 with compressed air at standard temperature (20°C) and humidity (40%) levels. The exhaust is further diluted approximately 25:1 by high efficiency particulate air (HEPA)-filtered air (FA) and then aged for 4 min before entering the 4 × 6 × 7-foot exposure booth. An optional HEPA filter path immediately proximal to the booth can generate a particle-reduced (gas-enriched) exposure. In-booth particulate is read by a nephelometer to provide an instantaneous light scattering coefficient for closed-loop system control. A Scanning Mobility Particle Sizer and multi-stage impactor measures particle size distribution. Filter sampling allows determination of sessional average concentrations of size-fractionated and unfractionated particulate oxidative potential, elemental carbon, organic carbon and trace elements. Results: Approximately 300 μg/m3 PM2.5 is routinely achievable at APEL and is well characterized in terms of oxidative potential and elemental components. Conclusion: APEL efficiently creates fresh DE, appropriately aged and diluted for human experimentation at safe yet realistic concentrations. Description of exposure characteristics allows comparison to other international efforts to deepen the current evidence base regarding the health effects of DE.

Loading effect correction for real-time aethalometer measurements of fresh diesel soot

Abstract In this study, a correction was developed for the aethalometer to measure real-time black carbon (BC) concentrations in an environment dominated by fresh diesel soot. The relationship between the actual mass-specific absorption coefficient for BC and the BC-dependent attenuation coefficients was determined from experiments conducted in a diesel exposure chamber that provided constant concentrations of fine particulate matter (PM; PM2.5; PM <2.5 µm in aerodynamic diameter) from diesel exhaust. The aethalometer reported BC concentrations decreasing with time from 48.1 to 31.5 µg m−3when exposed to constant PM2.5concentrations of 55 ± 1 µg m−3and bscat= 95 ± 3 Mm−1from diesel exhaust. This apparent decrease in reported light-absorbing PM concentration was used to derive a correction K(ATN) for loading of strong light-absorbing particles onto or into the aethalometer filter tape, which was a function of attenuation of light at 880 nm by the embedded particles.

Particulate matter components and subclinical atherosclerosis: common approaches to estimating exposure in a Multi-Ethnic Study of Atherosclerosis cross-sectional study

BackgroundConcentrations of outdoor fine particulate matter (PM2.5) have been associated with cardiovascular disease. PM2.5 chemical composition may be responsible for effects of exposure to PM2.5.MethodsUsing data from the Multi-Ethnic Study of Atherosclerosis (MESA) collected in 2000–2002 on 6,256 US adults without clinical cardiovascular disease in six U.S. metropolitan areas, we investigated cross-sectional associations of estimated long-term exposure to total PM2.5 mass and PM2.5 components (elemental carbon [EC], organic carbon [OC], silicon and sulfur) with measures of subclinical atherosclerosis (coronary artery calcium [CAC] and right common carotid intima-media thickness [CIMT]). Community monitors deployed for this study from 2007 to 2008 were used to estimate exposures at baseline addresses using three commonly-used approaches: (1) nearest monitor (the primary approach), (2) inverse-distance monitor weighting and (3) city-wide average.ResultsUsing the exposure estimate based on nearest monitor, in single-pollutant models, increased OC (effect estimate [95% CI] per IQR: 35.1 μm [26.8, 43.3]), EC (9.6 μm [3.6,15.7]), sulfur (22.7 μm [15.0,30.4]) and total PM2.5 (14.7 μm [9.0,20.5]) but not silicon (5.2 μm [−9.8,20.1]), were associated with increased CIMT; in two-pollutant models, only the association with OC was robust to control for the other pollutants. Findings were generally consistent across the three exposure estimation approaches. None of the PM measures were positively associated with either the presence or extent of CAC. In sensitivity analyses, effect estimates for OC and silicon were particularly sensitive to control for metropolitan area.ConclusionEmploying commonly-used exposure estimation approaches, all of the PM2.5 components considered, except silicon, were associated with increased CIMT, with the evidence being strongest for OC; no component was associated with increased CAC. PM2.5 chemical components, or other features of the sources that produced them, may be important in determining the effect of PM exposure on atherosclerosis. These cross-sectional findings await confirmation in future work employing longitudinal outcome measures and using more sophisticated approaches to estimating exposure.