Personal exposures to traffic-related air pollution and acute respiratory health among Bronx schoolchildren with asthma

Background

Previous studies have reported relationships between adverse respiratory health outcomes and residential proximity to traffic pollution, but have not shown this at a personal exposure level.

Objective

We compared, among inner-city children with asthma, the associations of adverse asthma outcome incidences with increased personal exposure to particulate matter mass ≤ 2.5 μm in aerodynamic diameter (PM_2.5) air pollution versus the diesel-related carbonaceous fraction of PM_2.5.

Methods

Daily 24-hr personal samples of PM_2.5, including the elemental carbon (EC) fraction, were collected for 40 fifth-grade children with asthma at four South Bronx schools (10 children per school) during approximately 1 month each. Spirometry and symptom scores were recorded several times daily during weekdays.

Results

We found elevated same-day relative risks of wheeze [1.45; 95% confidence interval (CI), 1.03–2.04)], shortness of breath (1.41; 95% CI, 1.01–1.99), and total symptoms (1.30; 95% CI, 1.04–1.62) with an increase in personal EC, but not with personal PM_2.5 mass. We found increased risk of cough, wheeze, and total symptoms with increased 1-day lag and 2-day average personal and school-site EC. We found no significant associations with school-site PM_2.5 mass or sulfur. The EC effect estimate was robust to addition of gaseous pollutants.

Conclusion

Adverse health associations were strongest with personal measures of EC exposure, suggesting that the diesel “soot” fraction of PM_2.5 is most responsible for pollution-related asthma exacerbations among children living near roadways. Studies that rely on exposure to PM mass may underestimate PM health impacts.     

Associations between PM2.5 and Heart Rate Variability Are Modified by Particle Composition and Beta-Blocker Use in Patients with Coronary Heart Disease

Background

It has been hypothesized that ambient particulate air pollution is able to modify the autonomic nervous control of the heart, measured as heart rate variability (HRV). Previously we reported heterogeneous associations between particulate matter with aerodynamic diameter < 2.5 μm (PM_2.5) and HRV across three study centers.

Objectives

We evaluated whether exposure misclassification, effect modification by medication, or differences in particle composition could explain the inconsistencies.

Methods

Subjects with coronary heart disease visited clinics biweekly in Amsterdam, the Netherlands; Erfurt, Germany; and Helsinki, Finland for 6–8 months. The standard deviation (SD) of NN intervals on an electrocardiogram (ECG; SDNN) and high frequency (HF) power of HRV was measured with ambulatory ECG during paced breathing. Outdoor levels of PM_2.5 were measured at a central site. In Amsterdam and Helsinki, indoor and personal PM_2.5 were measured during the 24 hr preceding the clinic visit. PM_2.5 was apportioned between sources using principal component analyses. We analyzed associations of indoor/personal PM_2.5, elements of PM_2.5, and source-specific PM_2.5 with HRV using linear regression.

Results

Indoor and personal PM_2.5 were not associated with HRV. Increased outdoor PM_2.5 was associated with decreased SDNN and HF at lags of 2 and 3 days only among persons not using beta-blocker medication. Traffic-related PM_2.5 was associated with decreased SDNN, and long-range transported PM_2.5 with decreased SDNN and HF, most strongly among persons not using beta blockers. Indicators for PM_2.5 from traffic and long-range transport were also associated with decreased HRV.

Conclusions

Our results suggest that differences in the composition of particles, beta-blocker use, and obesity of study subjects may explain some inconsistencies among previous studies on HRV.     

Distributed lag analyses of daily hospital admissions and source-apportioned fine particle air pollution

Background

Past time-series studies of the health effects of fine particulate matter [aerodynamic diameter ≤ 2.5 μm (PM_2.5)] have used chemically nonspecific PM_2.5 mass. However, PM_2.5 is known to vary in chemical composition with source, and health impacts may vary accordingly.

Objective

We tested the association between source-specific daily PM_2.5 mass and hospital admissions in a time-series investigation that considered both single-lag and distributed-lag models.

Methods

Daily PM_2.5 speciation measurements collected in midtown Manhattan were analyzed via positive matrix factorization source apportionment. Daily and distributed-lag generalized linear models of Medicare respiratory and cardiovascular hospital admissions during 2001–2002 considered PM_2.5 mass and PM_2.5 from five sources: transported sulfate, residual oil, traffic, steel metal works, and soil.

Results

Source-related PM_2.5 (specifically steel and traffic) was significantly associated with hospital admissions but not with total PM_2.5 mass. Steel metal works–related PM_2.5 was associated with respiratory admissions for multiple-lag days, especially during the cleanup efforts at the World Trade Center. Traffic-related PM_2.5 was consistently associated with same-day cardiovascular admissions across disease-specific subcategories. PM_2.5 constituents associated with each source (e.g., elemental carbon with traffic) were likewise associated with admissions in a consistent manner. Mean effects of distributed-lag models were significantly greater than were maximum single-day effect models for both steel- and traffic-related PM_2.5.

Conclusions

Past analyses that have considered only PM_2.5 mass or only maximum single-day lag effects have likely underestimated PM_2.5 health effects by not considering source-specific and distributed-lag effects. Differing lag structures and disease specificity observed for steel-related versus traffic-related PM_2.5 raise the possibility of distinct mechanistic pathways of health effects for particles of differing chemical composition.     

Time-series analysis of mortality effects of fine particulate matter components in Detroit and Seattle

Background

Recent 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.

Objectives

In this study, we used time-series analyses to determine the associations between daily fine PM [PM ≤ 2.5 μm in aerodynamic diameter (PM_2.5)] concentrations and daily mortality in two U.S. cities—Seattle, Washington, and Detroit, Michigan.

Methods

We obtained daily PM_2.5 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.

Results

The cardiovascular and respiratory mortality series exhibited different source and seasonal patterns in each city. The PM_2.5 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.

Conclusions

The effects of PM_2.5 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.     

Risk-Based Prioritization among Air Pollution Control Strategies in the Yangtze River Delta,China

Background

The Yangtze River Delta (YRD) in China is a densely populated region with recent dramatic increases in energy consumption and atmospheric emissions.

Objectives

We studied how different emission sectors influence population exposures and the corresponding health risks, to inform air pollution control strategy design.

Methods

We applied the Community Multiscale Air Quality (CMAQ) Modeling System to model the marginal contribution to baseline concentrations from different sectors. We focused on nitrogen oxide (NO_x) control while considering other pollutants that affect fine particulate matter [aerodynamic diameter ≤ 2.5 μm (PM_2.5)] and ozone concentrations. We developed concentration–response (C-R) functions for PM_2.5 and ozone mortality for China to evaluate the anticipated health benefits.

Results

In the YRD, health benefits per ton of emission reductions varied significantly across pollutants, with reductions of primary PM_2.5 from the industry sector and mobile sources showing the greatest benefits of 0.1 fewer deaths per year per ton of emission reduction. Combining estimates of health benefits per ton with potential emission reductions, the greatest mortality reduction of 12,000 fewer deaths per year [95% confidence interval (CI), 1,200–24,000] was associated with controlling primary PM_2.5 emissions from the industry sector and reducing sulfur dioxide (SO₂) from the power sector, respectively. Benefits were lower for reducing NO_x emissions given lower consequent reductions in the formation of secondary PM_2.5 (compared with SO₂) and increases in ozone concentrations that would result in the YRD.

Conclusions

Although uncertainties related to C-R functions are significant, the estimated health benefits of emission reductions in the YRD are substantial, especially for sectors and pollutants with both higher health benefits per unit emission reductions and large potential for emission reductions.     

California Wildfires of 2008: Coarse and Fine Particulate Matter Toxicity

Background

During the last week of June 2008, central and northern California experienced thousands of forest and brush fires, giving rise to a week of severe fire-related particulate air pollution throughout the region. California experienced PM_10–2.5 (particulate matter with mass median aerodynamic diameter > 2.5 μm to < 10 μm; coarse ) and PM_2.5 (particulate matter with mass median aerodynamic diameter < 2.5 μm; fine) concentrations greatly in excess of the air quality standards and among the highest values reported at these stations since data have been collected.

Objectives

These observations prompt a number of questions about the health impact of exposure to elevated levels of PM_10–2.5 and PM_2.5 and about the specific toxicity of PM arising from wildfires in this region.

Methods

Toxicity of PM_10–2.5 and PM_2.5 obtained during the time of peak concentrations of smoke in the air was determined with a mouse bioassay and compared with PM samples collected under normal conditions from the region during the month of June 2007.

Results

Concentrations of PM were not only higher during the wildfire episodes, but the PM was much more toxic to the lung on an equal weight basis than was PM collected from normal ambient air in the region. Toxicity was manifested as increased neutrophils and protein in lung lavage and by histologic indicators of increased cell influx and edema in the lung.

Conclusions

We conclude that the wildfire PM contains chemical components toxic to the lung, especially to alveolar macrophages, and they are more toxic to the lung than equal doses of PM collected from ambient air from the same region during a comparable season.     

Emergency Admissions for Cardiovascular and Respiratory Diseases and the Chemical Composition of Fine Particle Air Pollution

Background

Population-based studies have estimated health risks of short-term exposure to fine particles using mass of PM_2.5 (particulate matter ≤ 2.5 μm in aerodynamic diameter) as the indicator. Evidence regarding the toxicity of the chemical components of the PM_2.5 mixture is limited.

Objective

In this study we investigated the association between hospital admission for cardiovascular disease (CVD) and respiratory disease and the chemical components of PM_2.5 in the United States.

Methods

We used a national database comprising daily data for 2000–2006 on emergency hospital admissions for cardiovascular and respiratory outcomes, ambient levels of major PM_2.5 chemical components [sulfate, nitrate, silicon, elemental carbon (EC), organic carbon matter (OCM), and sodium and ammonium ions], and weather. Using Bayesian hierarchical statistical models, we estimated the associations between daily levels of PM_2.5 components and risk of hospital admissions in 119 U.S. urban communities for 12 million Medicare enrollees (≥ 65 years of age).

Results

In multiple-pollutant models that adjust for the levels of other pollutants, an interquartile range (IQR) increase in EC was associated with a 0.80% [95% posterior interval (PI), 0.34–1.27%] increase in risk of same-day cardiovascular admissions, and an IQR increase in OCM was associated with a 1.01% (95% PI, 0.04–1.98%) increase in risk of respiratory admissions on the same day. Other components were not associated with cardiovascular or respiratory hospital admissions in multiple-pollutant models.

Conclusions

Ambient levels of EC and OCM, which are generated primarily from vehicle emissions, diesel, and wood burning, were associated with the largest risks of emergency hospitalization across the major chemical constituents of PM_2.5.     

Traffic-Related Particulate Matter and Acute Respiratory Symptoms among New York City Area Adolescents

Background

Exposure to traffic-related particulate matter (PM) has been associated with adverse respiratory health outcomes in children. Diesel exhaust particles (DEPs) are a local driver of urban fine PM [aerodynamic diameter ≤ 2.5 μm (PM_2.5)]; however, evidence linking ambient DEP exposure to acute respiratory symptoms is relatively sparse, and susceptibilities of urban and asthmatic children are inadequately characterized.

Objectives

We examined associations of daily ambient black carbon (BC) concentrations, a DEP indicator, with daily respiratory symptoms among asthmatic and nonasthmatic adolescents in New York City (NYC) and a nearby suburban community.

Methods

BC and PM_2.5 were monitored continuously outside three NYC high schools and one suburban high school for 4–6 weeks, and daily symptom data were obtained from 249 subjects (57 asthmatics, 192 nonasthmatics) using diaries. Associations between pollutants and symptoms were characterized using multilevel generalized linear mixed models, and modification by urban residence and asthma status were examined.

Results

Increases in BC were associated with increased wheeze, shortness of breath, and chest tightness. Multiple lags of nitrogen dioxide (NO₂) exposure were associated with symptoms. For several symptoms, associations with BC and NO₂ were significantly larger in magnitude among urban subjects and asthmatics compared with suburban subjects and nonasthmatics, respectively. PM_2.5 was not consistently associated with increases in symptoms.

Conclusions

Acute exposures to traffic-related pollutants such as DEPs and/or NO₂ may contribute to increased respiratory morbidity among adolescents, and urban residents and asthmatics may be at increased risk. The findings provide support for developing additional strategies to reduce diesel emissions further, especially in populations susceptible because of environment or underlying respiratory disease.     

Long-term exposure to traffic-related air pollution and the risk of coronary heart disease hospitalization and mortality

Background

Epidemiologic studies have demonstrated that exposure to road traffic is associated with adverse cardiovascular outcomes.

Objectives

We aimed to identify specific traffic-related air pollutants that are associated with the risk of coronary heart disease (CHD) morbidity and mortality to support evidence-based environmental policy making.

Methods

This population-based cohort study included a 5-year exposure period and a 4-year follow-up period. All residents 45–85 years of age who resided in Metropolitan Vancouver during the exposure period and without known CHD at baseline were included in this study (n = 452,735). Individual exposures to traffic-related air pollutants including black carbon, fine particles [aerodynamic diameter ≤ 2.5 μm (PM_2.5)], nitrogen dioxide (NO₂), and nitric oxide were estimated at residences of the subjects using land-use regression models and integrating changes in residences during the exposure period. CHD hospitalizations and deaths during the follow-up period were identified from provincial hospitalization and death registration records.

Results

An interquartile range elevation in the average concentration of black carbon (0.94 × 10⁻⁵/m filter absorbance, equivalent to approximately 0.8 μg/m³ elemental carbon) was associated with a 3% increase in CHD hospitalization (95% confidence interval, 1–5%) and a 6% increase in CHD mortality (3–9%) after adjusting for age, sex, preexisting comorbidity, neighborhood socioeconomic status, and copollutants (PM_2.5 and NO₂). There were clear linear exposure–response relationships between black carbon and coronary events.

Conclusions

Long-term exposure to traffic-related fine particulate air pollution, indicated by black carbon, may partly explain the observed associations between exposure to road traffic and adverse cardiovascular outcomes.     

Estimating Regional Spatial and Temporal Variability of PM2.5 Concentrations Using Satellite Data,Meteorology, and Land Use Information

Background

Studies of chronic health effects due to exposures to particulate matter with aerodynamic diameters ≤ 2.5 μm (PM_2.5) are often limited by sparse measurements. Satellite aerosol remote sensing data may be used to extend PM_2.5 ground networks to cover a much larger area.

Objectives

In this study we examined the benefits of using aerosol optical depth (AOD) retrieved by the Geostationary Operational Environmental Satellite (GOES) in conjunction with land use and meteorologic information to estimate ground-level PM_2.5 concentrations.

Methods

We developed a two-stage generalized additive model (GAM) for U.S. Environmental Protection Agency PM_2.5 concentrations in a domain centered in Massachusetts. The AOD model represents conditions when AOD retrieval is successful; the non-AOD model represents conditions when AOD is missing in the domain.

Results

The AOD model has a higher predicting power judged by adjusted R² (0.79) than does the non-AOD model (0.48). The predicted PM_2.5 concentrations by the AOD model are, on average, 0.8–0.9 μg/m³ higher than the non-AOD model predictions, with a more smooth spatial distribution, higher concentrations in rural areas, and the highest concentrations in areas other than major urban centers. Although AOD is a highly significant predictor of PM_2.5, meteorologic parameters are major contributors to the better performance of the AOD model.

Conclusions

GOES aerosol/smoke product (GASP) AOD is able to summarize a set of weather and land use conditions that stratify PM_2.5 concentrations into two different spatial patterns. Even if land use regression models do not include AOD as a predictor variable, two separate models should be fitted to account for different PM_2.5 spatial patterns related to AOD availability.     

Limitations of Remotely Sensed Aerosol as a Spatial Proxy for Fine Particulate Matter

Background

Recent research highlights the promise of remotely sensed aerosol optical depth (AOD) as a proxy for ground-level particulate matter with aerodynamic diameter ≤ 2.5 μm (PM_2.5). Particular interest lies in estimating spatial heterogeneity using AOD, with important application to estimating pollution exposure for public health purposes. Given the correlations reported between AOD and PM_2.5, it is tempting to interpret the spatial patterns in AOD as reflecting patterns in PM_2.5.

Objectives

We evaluated the degree to which AOD can help predict long-term average PM_2.5 concentrations for use in chronic health studies.

Methods

We calculated correlations of AOD and PM_2.5 at various temporal aggregations in the eastern United States in 2004 and used statistical models to assess the relationship between AOD and PM_2.5 and the potential for improving predictions of PM_2.5 in a subregion, the mid-Atlantic.

Results

We found only limited spatial associations of AOD from three satellite retrievals with daily and yearly PM_2.5. The statistical modeling shows that monthly average AOD poorly reflects spatial patterns in PM_2.5 because of systematic, spatially correlated discrepancies between AOD and PM_2.5. Furthermore, when we included AOD as a predictor of monthly PM_2.5 in a statistical prediction model, AOD provided little additional information in a model that already accounts for land use, emission sources, meteorology, and regional variability.

Conclusions

These results suggest caution in using spatial variation in currently available AOD to stand in for spatial variation in ground-level PM_2.5 in epidemiologic analyses and indicate that when PM_2.5 monitoring is available, careful statistical modeling outperforms the use of AOD.     

Association of Heart Rate Variability in Taxi Drivers with Marked Changes in Particulate Air Pollution in Beijing in 2008

Background

Heart rate variability (HRV), a marker of cardiac autonomic function, has been associated with particulate matter (PM) air pollution, especially in older patients and those with cardiovascular diseases. However, the effect of PM exposure on cardiac autonomic function in young, healthy adults has received less attention.

Objectives

We evaluated the relationship between exposure to traffic-related PM with an aerodynamic diameter ≤ 2.5 μm (PM_2.5) and HRV in a highly exposed panel of taxi drivers.

Methods

Continuous measurements of personal exposure to PM_2.5 and ambulatory electrocardiogram monitoring were conducted on 11 young healthy taxi drivers for a 12-hr work shift during their work time (0900–2100 hr) before, during, and after the Beijing 2008 Olympic Games. Mixed-effects regression models were used to estimate associations between PM_2.5 exposure and percent changes in 5-min HRV indices after combining data from the three time periods and controlling for potentially confounding variables.

Results

Personal exposures of taxi drivers to PM_2.5 changed markedly across the three time periods. The standard deviation of normal-to-normal (SDNN) intervals decreased by 2.2% [95% confidence interval (CI), −3.8% to −0.6%] with an interquartile range (IQR; 69.5 μg/m³) increase in the 30-min PM_2.5 moving average, whereas the low-frequency and high-frequency powers decreased by 4.2% (95% CI, −9.0% to 0.8%) and 6.2% (95% CI, −10.7% to −1.5%), respectively, in association with an IQR increase in the 2-hr PM_2.5 moving average.

Conclusions

Marked changes in traffic-related PM_2.5 exposure were associated with altered cardiac autonomic function in young healthy adults.     

Black Carbon Exposure,Oxidative Stress Genes,and Blood Pressure in a Repeated-Measures Study

Background

Particulate matter (PM) air pollution has been associated with cardiovascular morbidity and mortality, and elevated blood pressure (BP) is a known risk factor for cardiovascular disease. A small number of studies have investigated the relationship between PM and BP and found mixed results. Evidence suggests that traffic-related air pollution contributes significantly to PM-related cardiovascular effects.

Objectives

We hypothesized that black carbon (BC), a traffic-related combustion by-product, would be more strongly associated with BP than would fine PM [aerodynamic diameter ≤ 2.5 μm (PM_2.5)], a heterogeneous PM mixture, and that these effects would be larger among participants with genetic variants associated with impaired antioxidative defense.

Methods

We performed a repeated-measures analysis in elderly men to analyze associations between PM_2.5 and BC exposure and BP using mixed-effects models with random intercepts, adjusting for potential confounders. We also examined statistical interaction between BC and genetic variants related to oxidative stress defense: GSTM1, GSTP1, GSTT1, NQO1, catalase, and HMOX-1.

Results

A 1-SD increase in BC concentration was associated with a 1.5-mmHg increase in systolic BP [95% confidence interval (CI), 0.1–2.8] and a 0.9-mmHg increase in diastolic BP (95% CI, 0.2–1.6). We observed no evidence of statistical interaction between BC and any of the genetic variants examined and found no association between PM_2.5 and BP.

Conclusions

We observed positive associations between BP and BC, but not between BP and PM_2.5, and found no evidence of effect modification of the association between BC and BP by gene variants related to antioxidative defense.     

Long-Term Traffic-Related Exposures and Asthma Onset in Schoolchildren in Oslo,Norway

Background

Whether there is a causal relation between long-term exposure to traffic and asthma development is so far not clear. This may be explained by inaccurate exposure assessment.

Objective

We investigated the associations of long-term traffic-related exposures with asthma onset assessed retrospectively and respiratory symptoms in 9- to 10-year-old children.

Methods

We collected information on respiratory outcomes and potential confounding variables by parental questionnaire in 2,871 children in Oslo. Nitrogen dioxide exposure was assessed by the EPISODE dispersion model and assigned at updated individual addresses during lifetime. Distance to major road was assigned at birth address and address by date of questionnaire. Cox proportional hazard regression and logistic regression were used.

Results

We did not find positive associations between any long-term traffic-related exposure and onset of doctor-diagnosed asthma. An interquartile range (IQR) increase of NO₂ exposure before asthma onset was associated with an adjusted risk ratio of 0.82 [95% confidence interval (CI), 0.67–1.02]. Handling early asthma cases (children < 4 years of age) with recovery during follow-up as noncases gave a less negative association. The associations for late asthma onset (≥ 4 years of age) were positive but not statistically significant. For current symptoms, an IQR increase of previous year’s NO₂ exposure was associated with adjusted odds ratios of 1.01 (95% CI, 0.83–1.23) for wheeze, 1.10 (95% CI, 0.79–1.51) for severe wheeze, and 1.01 (95% CI, 0.84–1.21) for dry cough.

Conclusions

We were not able to find positive associations of long-term traffic-related exposures with asthma onset or with current respiratory symptoms in 9- to 10-year-old children in Oslo.     

The Effect of Ambient Air Pollution on Sperm Quality

Background

Research has suggested an association with ambient air pollution and sperm quality.

Objectives

We investigated the effect of exposure to ozone (O₃) and particulate matter < 2.5 μm in aerodynamic diameter (PM_2.5) on sperm quality.

Methods

We reexamined a previous cohort study of water disinfection by-products to evaluate sperm quality in 228 presumed fertile men with different air pollution profiles. Outcomes included sperm concentration, total sperm per ejaculate (count), and morphology, as well as DNA integrity and chromatin maturity. Exposures to O₃ and PM_2.5 were evaluated for the 90–day period before sampling. We used multivariable linear regression, which included different levels of adjustment (i.e., without and with season and temperature) to assess the relationship between exposure to air pollutants during key periods of sperm development and adverse sperm outcomes.

Results

Sperm concentration and count were not associated with exposure to PM_2.5, but there was evidence of an association (but not statistically significant) with O₃ concentration and decreased sperm concentration and count. Additionally, a significant increase in the percentage of sperm cells with cytoplasmic drop [β = 2.64; 95% confidence interval (CI), 0.21–5.06] and abnormal head (β = 0.47; 95% CI, 0.03–0.92) was associated with PM_2.5 concentration in the base model. However, these associations, along with all other sperm outcomes, were not significantly associated with either pollutant after controlling for season and temperature. Overall, although we found both protective and adverse effects, there was generally no consistent pattern of increased abnormal sperm quality with elevated exposure to O₃ or PM_2.5.

Conclusions

Exposures to O₃ or PM_2.5 at levels below the current National Ambient Air Quality Standards were not associated with statistically significant decrements in sperm outcomes in this cohort of fertile men. However, some results suggested effects on sperm concentration, count, and morphology.     

Mortality in the Medicare Population and Chronic Exposure to Fine Particulate Air Pollution in Urban Centers (2000–2005)

Background

Prospective cohort studies constitute the major source of evidence about the mortality effects of chronic exposure to particulate air pollution. Additional studies are needed to provide evidence on the health effects of chronic exposure to particulate matter ≤ 2.5 μm in aerodynamic diameter (PM_2.5) because few studies have been carried out and the cohorts have not been representative.

Objectives

This study was designed to estimate the relative risk of death associated with long-term exposure to PM_2.5 by region and age groups in a U.S. population of elderly, for the period 2000–2005.

Methods

By linking PM_2.5 monitoring data to the Medicare billing claims by ZIP code of residence of the enrollees, we have developed a new retrospective cohort study, the Medicare Cohort Air Pollution Study. The study population comprises 13.2 million participants living in 4,568 ZIP codes having centroids within 6 miles of a PM_2.5 monitor. We estimated relative risks adjusted by socioeconomic status and smoking by fitting log-linear regression models.

Results

In the eastern and central regions, a 10-μg/m³ increase in 6-year average of PM_2.5 is associated with 6.8% [95% confidence interval (CI), 4.9–8.7%] and 13.2% (95% CI, 9.5–16.9) increases in mortality, respectively. We found no evidence of an association in the western region or for persons ≥ 85 years of age.

Conclusions

We established a cohort of Medicare participants for investigating air pollution and mortality on longer-term time frames. Chronic exposure to PM_2.5 was associated with mortality in the eastern and central regions, but not in the western United States.     

Fine particulate matter constituents associated with cardiovascular hospitalizations and mortality in New York City

Background

Recent time-series studies have indicated that both cardiovascular disease (CVD)mortality and hospitalizations are associated with particulate matter (PM). However, seasonal patterns of PM associations with these outcomes are not consistent, and PM components responsible for these associations have not been determined. We investigated this issue in New York City (NYC), where PM originates from regional and local combustion sources.

Objective

In this study, we examined the role of particulate matter with aerodynamic diameter ≤ 2.5 μm (PM_2.5) and its key chemical components on both CVD hospitalizations and on mortality in NYC.

Methods

We analyzed daily deaths and emergency hospitalizations for CVDs among persons ≥ 40 years of age for associations with PM_2.5, its chemical components, nitrogen dioxide (NO₂), carbon monoxide, and sulfur dioxide for the years 2000–2006 using a Poisson time-series model adjusting for temporal and seasonal trends, temperature effects, and day of the week. We estimated excess risks per interquartile-range increases at lags 0 through 3 days for warm (April through September) and cold (October through March) seasons.

Results

The CVD mortality series exhibit strong seasonal trends, whereas the CVD hospitalization series show a strong day-of-week pattern. These outcome series were not correlated with each other but were individually associated with a number of PM_2.5 chemical components from regional and local sources, each with different seasonal patterns and lags. Coal-combustion–related components (e.g., selenium) were associated with CVD mortality in summer and CVD hospitalizations in winter, whereas elemental carbon and NO₂ showed associations with these outcomes in both seasons.

Conclusion

Local combustion sources, including traffic and residual oil burning, may play a year-round role in the associations between air pollution and CVD outcomes, but transported aerosols may explain the seasonal variation in associations shown by PM_2.5 mass.     

Global Estimates of Ambient Fine Particulate Matter Concentrations from Satellite-Based Aerosol Optical Depth: Development and Application

Background

Epidemiologic and health impact studies of fine particulate matter with diameter < 2.5 μm (PM_2.5) are limited by the lack of monitoring data, especially in developing countries. Satellite observations offer valuable global information about PM_2.5 concentrations.

Objective

In this study, we developed a technique for estimating surface PM_2.5 concentrations from satellite observations.

Methods

We mapped global ground-level PM_2.5 concentrations using total column aerosol optical depth (AOD) from the MODIS (Moderate Resolution Imaging Spectroradiometer) and MISR (Multiangle Imaging Spectroradiometer) satellite instruments and coincident aerosol vertical profiles from the GEOS-Chem global chemical transport model.

Results

We determined that global estimates of long-term average (1 January 2001 to 31 December 2006) PM_2.5 concentrations at approximately 10 km × 10 km resolution indicate a global population-weighted geometric mean PM_2.5 concentration of 20 μg/m³. The World Health Organization Air Quality PM_2.5 Interim Target-1 (35 μg/m³ annual average) is exceeded over central and eastern Asia for 38% and for 50% of the population, respectively. Annual mean PM_2.5 concentrations exceed 80 μg/m³ over eastern China. Our evaluation of the satellite-derived estimate with ground-based in situ measurements indicates significant spatial agreement with North American measurements (r = 0.77; slope = 1.07; n = 1057) and with noncoincident measurements elsewhere (r = 0.83; slope = 0.86; n = 244). The 1 SD of uncertainty in the satellite-derived PM_2.5 is 25%, which is inferred from the AOD retrieval and from aerosol vertical profile errors and sampling. The global population-weighted mean uncertainty is 6.7 μg/m³.

Conclusions

Satellite-derived total-column AOD, when combined with a chemical transport model, provides estimates of global long-term average PM_2.5 concentrations.     

Ambient air pollution and birth weight in full-term infants in Atlanta, 1994-2004

Background

An emerging body of evidence suggests that ambient levels of air pollution during pregnancy are associated with fetal growth.

Objectives

We examined relationships between birth weight and temporal variation in ambient levels of carbon monoxide, nitrogen dioxide (NO₂), sulfur dioxide (SO₂), ozone, particulate matter ≤ 10 μm in diameter (PM₁₀), ≤ 2.5 μm (PM_2.5), 2.5 to 10 μm (PM_2.5–10), and PM_2.5 chemical component measurements for 406,627 full-term births occurring between 1994 and 2004 in five central counties of metropolitan Atlanta.

Methods

We assessed relationships between birth weight and pollutant concentrations during each infant’s first month of gestation and third trimester, as well as in each month of pregnancy using distributed lag models. We also conducted capture-area analyses limited to mothers residing within 4 miles (6.4 km) of each air quality monitoring station.

Results

In the five-county analysis, ambient levels of NO₂, SO₂, PM_2.5 elemental carbon, and PM_2.5 water-soluble metals during the third trimester were significantly associated with small reductions in birth weight (−4 to −16 g per interquartile range increase in pollutant concentrations). Third-trimester estimates were generally higher in Hispanic and non-Hispanic black infants relative to non-Hispanic white infants. Distributed lag models were also suggestive of associations between air pollutant concentrations in late pregnancy and reduced birth weight. The capture-area analyses provided little support for the associations observed in the five-county analysis.

Conclusions

Results provide some support for an effect of ambient air pollution in late pregnancy on birth weight in full-term infants.     

Survival analysis of long-term exposure to different sizes of airborne particulate matter and risk of infant mortality using a birth cohort in Seoul, Korea

Background

Several studies suggest that airborne particulate matter (PM) is associated with infant mortality; however, most focused on short-term exposure to larger particles.

Objectives

We evaluated associations between long-term exposure to different sizes of particles [total suspended particles (TSP), PM ≤ 10 μm in aerodynamic diameter (PM₁₀), ≤ 10–2.5 μm (PM_10–2.5), and ≤ 2.5 μm (PM_2.5)] and infant mortality in a cohort in Seoul, Korea, 2004–2007.

Methods

The study includes 359,459 births with 225 deaths. We applied extended Cox proportional hazards modeling with time-dependent covariates to three mortality categories: all causes, respiratory, and sudden infant death syndrome (SIDS). We calculated exposures from birth to death (or end of eligibility for outcome at 1 year of age) and pregnancy (gestation and each trimester) and treated exposures as time-dependent variables for subjects’ exposure for each pollutant. We adjusted by sex, gestational length, season of birth, maternal age and educational level, and heat index. Each cause of death and exposure time frame was analyzed separately.

Results

We found a relationship between gestational exposures to PM and infant mortality from all causes or respiratory causes for normal-birth-weight infants. For total mortality (all causes), risks were 1.44 (95% confidence interval, 1.06–1.97), 1.65 (1.18–2.31), 1.53 (1.22–1.90), and 1.19 (0.83–1.70) per interquartile range increase in TSP, PM₁₀, PM_2.5, and PM_10–2.5, respectively; for respiratory mortality, risks were 3.78 (1.18–12.13), 6.20 (1.50–25.66), 3.15 (1.26–7.85), and 2.86 (0.76–10.85). For SIDS, risks were 0.92 (0.33–2.58), 1.15 (0.38–3.48), 1.42 (0.71–2.87), and 0.57 (0.16–1.96), respectively.

Conclusions

Our findings provide supportive evidence of an association of long-term exposure to PM air pollution with infant mortality.