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Background: Studies of chronic health effects due to exposures to particulate matter with aerodynamic diameters ≤ 2.5 μm (PM2.5) are often limited by sparse measurements. Satellite aerosol remote sensing data may be used to extend PM2.5 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 PM2.5 concentrations.
Methods: We developed a two-stage generalized additive model (GAM) for U.S. Environmental Protection Agency PM2.5 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 R (0.79) than does the non-AOD model (0.48). The predicted PM2.5 concentrations by the AOD model are, on average, 0.8–0.9 μg/m 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 PM2.5, 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 PM2.5 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 PM2.5 spatial patterns related to AOD availability.
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 PM10–2.5 (particulate matter with mass median aerodynamic diameter > 2.5 μm to < 10 μm; coarse ) and PM2.5 (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 PM10–2.5 and PM2.5 and about the specific toxicity of PM arising from wildfires in this region.
Methods: Toxicity of PM10–2.5 and PM2.5 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.
Background: Population-based studies have estimated health risks of short-term exposure to fine particles using mass of PM2.5 (particulate matter ≤ 2.5 μm in aerodynamic diameter) as the indicator. Evidence regarding the toxicity of the chemical components of the PM2.5 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 PM2.5 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 PM2.5 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 PM2.5 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 PM2.5.
Background: Exposure to ambient fine particles [particulate matter ≤ 2.5 μm diameter (PM2.5)] is a potential factor in the exacerbation of asthma. National air quality particle standards consider total mass, not composition or sources, and may not protect against health impacts related to specific components.
Objective: We examined associations between daily exposure to fine particle components and sources, and symptoms and medication use in children with asthma.
Methods: Children with asthma (n = 149) 4–12 years of age were enrolled in a year-long study. We analyzed particle samples for trace elements (X-ray fluorescence) and elemental carbon (light reflectance). Using factor analysis/source apportionment, we identified particle sources (e.g., motor vehicle emissions) and quantified daily contributions. Symptoms and medication use were recorded on study diaries. Repeated measures logistic regression models examined associations between health outcomes and particle exposures as elemental concentrations and source contributions.
Results: More than half of mean PM2.5 was attributed to traffic-related sources motor vehicles (42%) and road dust (12%). Increased likelihood of symptoms and inhaler use was largest for 3-day averaged exposures to traffic-related sources or their elemental constituents and ranged from a 10% increased likelihood of wheeze for each 5-μg/m increase in particles from motor vehicles to a 28% increased likelihood of shortness of breath for increases in road dust. Neither the other sources identified nor PM2.5 alone was associated with increased health outcome risks.
Conclusions: Linking respiratory health effects to specific particle pollution composition or sources is critical to efforts to protect public health. We associated increased risk of symptoms and inhaler use in children with asthma with exposure to traffic-related fine particles.
Background: Studies examining the health effects of particulate matter ≤ 2.5 μm in aerodynamic diameter (PM2.5) commonly use ambient PM2.5 concentrations measured at distal monitoring sites as proxies for personal exposure and assume spatial homogeneity of ambient PM2.5. An alternative proxy—the residential outdoor PM2.5 concentration measured adjacent to participant homes—has few advantages under this assumption.
Objectives: We systematically reviewed the correlation between residential outdoor PM2.5 and personal PM2.5 (r̄j) as a means of comparing the magnitude and sources of measurement error associated with their use as exposure surrogates.
Methods: We searched seven electronic reference databases for studies of the within-participant residential outdoor-personal PM2.5 correlation.
Results: The search identified 567 candidate studies, nine of which were abstracted in duplicate, that were published between 1996 and 2008. They represented 329 nonsmoking participants 6–93 years of age in eight U.S. cities, among whom r̄j was estimated (median, 0.53; range, 0.25–0.79) based on a median of seven residential outdoor-personal PM2.5 pairs per participant. We found modest evidence of publication bias (symmetric funnel plot; pBegg = 0.4; pEgger = 0.2); however, we identified evidence of heterogeneity (Cochran’s Q-test p = 0.05). Of the 20 characteristics examined, earlier study midpoints, eastern longitudes, older mean age, higher outdoor temperatures, and lower personal-residential outdoor PM2.5 differences were associated with increased within-participant residential outdoor-personal PM2.5 correlations.
Conclusions: These findings were similar to those from a contemporaneous meta-analysis that examined ambient-personal PM2.5 correlations (r̄j = median, 0.54; range, 0.09–0.83). Collectively, the meta-analyses suggest that residential outdoor-personal and ambient-personal PM2.5 correlations merit greater consideration when evaluating the potential for bias in studies of PM2.5-mediated health effects.
Background: Several studies have reported associations between long-term exposure to ambient fine particulate matter (PM) and cardiovascular mortality. However, the health impacts of long-term exposure to specific constituents of PM2.5 (PM with aerodynamic diameter ≤ 2.5 μm) have not been explored.
Methods: We used data from the California Teachers Study, a prospective cohort of active and former female public school professionals. We developed estimates of long-term exposures to PM2.5 and several of its constituents, including elemental carbon, organic carbon (OC), sulfates, nitrates, iron, potassium, silicon, and zinc. Monthly averages of exposure were created using pollution data from June 2002 through July 2007. We included participants whose residential addresses were within 8 and 30 km of a monitor collecting PM2.5 constituent data. Hazard ratios (HRs) were estimated for long-term exposure for mortality from all nontraumatic causes, cardiopulmonary disease, ischemic heart disease (IHD), and pulmonary disease.
Results: Approximately 45,000 women with 2,600 deaths lived within 30 km of a monitor. We observed associations of all-cause, cardiopulmonary, and IHD mortality with PM2.5 mass and each of its measured constituents, and between pulmonary mortality and several constituents. For example, for cardiopulmonary mortality, HRs for interquartile ranges of PM2.5, OC, and sulfates were 1.55 [95% confidence interval (CI), 1.43–1.69], 1.80 (95% CI, 1.68–1.93), and 1.79 (95% CI, 1.58–2.03), respectively. Subsequent analyses indicated that, of the constituents analyzed, OC and sulfates had the strongest associations with all four outcomes.
Conclusions: Long-term exposures to PM2.5 and several of its constituents were associated with increased risks of all-cause and cardiopulmonary mortality in this cohort. Constituents derived from combustion of fossil fuel (including diesel), as well as those of crustal origin, were associated with some of the greatest risks. These results provide additional evidence that reduction of ambient PM2.5 may provide significant public health benefits.
Background: Epidemiologic and health impact studies of fine particulate matter with diameter < 2.5 μm (PM2.5) are limited by the lack of monitoring data, especially in developing countries. Satellite observations offer valuable global information about PM2.5 concentrations.
Objective: In this study, we developed a technique for estimating surface PM2.5 concentrations from satellite observations.
Methods: We mapped global ground-level PM2.5 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) PM2.5 concentrations at approximately 10 km × 10 km resolution indicate a global population-weighted geometric mean PM2.5 concentration of 20 μg/m. The World Health Organization Air Quality PM2.5 Interim Target-1 (35 μg/m annual average) is exceeded over central and eastern Asia for 38% and for 50% of the population, respectively. Annual mean PM2.5 concentrations exceed 80 μg/m 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 PM2.5 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/m.
Conclusions: Satellite-derived total-column AOD, when combined with a chemical transport model, provides estimates of global long-term average PM2.5 concentrations.
Background: Cardiac autonomic dysfunction has been suggested as a possible biologic pathway for the association between fine particulate matter ≤ 2.5 μm in diameter (PM2.5) and cardiovascular disease (CVD). We examined the associations of PM2.5 with heart rate variability, a marker of autonomic function, and whether metabolic syndrome (MetS) modified these associations.
Methods: We used data from the Multi-Ethnic Study of Atherosclerosis to measure the standard deviation of normal-to-normal intervals (SDNN) and the root mean square of successive differences (rMSSD) of 5,465 participants 45–84 years old who were free of CVD at the baseline examination (2000–2002). Data from the U.S. regulatory monitor network were used to estimate ambient PM2.5 concentrations at the participants’ residences. MetS was defined as having three or more of the following criteria: abdominal obesity, hypertriglyceridemia, low high-density lipoprotein cholesterol, high blood pressure, and high fasting glucose.
Results: After controlling for confounders, we found that an interquartile range (IQR) increase in 2-day average PM2.5 (10.2 μg/m) was associated with a 2.1% decrease in rMSSD [95% confidence interval (CI), −4.2 to 0.0] and nonsignificantly associated with a 1.8% decrease in SDNN (95% CI, −3.7 to 0.1). Associations were stronger among individuals with MetS than among those without MetS: an IQR elevation in 2-day PM2.5 was associated with a 6.2% decrease in rMSSD (95% CI, −9.4 to −2.9) among participants with MetS, whereas almost no change was found among participants without MetS (p-interaction = 0.005). Similar effect modification was observed in SDNN (p-interaction = 0.011).
Conclusion: These findings suggest that autonomic dysfunction may be a mechanism through which PM exposure affects cardiovascular risk, especially among persons with MetS.
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 (NOx) control while considering other pollutants that affect fine particulate matter [aerodynamic diameter ≤ 2.5 μm (PM2.5)] and ozone concentrations. We developed concentration–response (C-R) functions for PM2.5 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 PM2.5 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 PM2.5 emissions from the industry sector and reducing sulfur dioxide (SO2) from the power sector, respectively. Benefits were lower for reducing NOx emissions given lower consequent reductions in the formation of secondary PM2.5 (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.
Background: Systemic lupus erythematosus (SLE) is a chronic disease of unclear etiology, characterized by an overactive immune system and the production of antibodies that may target normal tissues of many organ systems, including the kidneys. It can arise at any age and occurs mainly in women.
Objective: Our aim was to evaluate the potential influence of particulate matter (PM) air pollution on clinical aspects of SLE.
Methods: We studied a clinic cohort of SLE patients living on the island of Montreal, followed annually with a structured clinical assessment. We assessed the association between ambient levels of fine PM [median aerodynamic diameter ≤ 2.5 μm (PM2.5)] measured at fixed-site monitoring stations and SLE disease activity measured with the SLE Disease Activity Index, version 2000 (SLEDAI-2K), which includes anti–double-stranded DNA (anti-dsDNA) serum-specific autoantibodies and renal tubule cellular casts in urine, which reflects serious renal inflammation. We used mixed effects regression models that we adjusted for daily ambient temperatures and ozone levels.
Results: We assessed 237 patients (223 women) who together had 1,083 clinic visits from 2000 through 2007 (mean age at time of first visit, 41.2 years). PM2.5 levels were associated with anti-dsDNA and cellular casts. The crude and adjusted odds ratios (reflecting a 10-μg/m increase in PM2.5 averaged over the 48 hr prior to clinical assessment) were 1.26 [95% confidence interval (CI), 0.96–1.65] and 1.34 (95% CI, 1.02–1.77) for anti-dsDNA antibodies and 1.43 (95% CI, 1.05–1.95) and 1.28 (0.92–1.80) for cellular casts. The total SLEDAI-2K scores were not associated with PM2.5 levels.
Conclusions: We provide novel data that suggest that short-term variations in air pollution may influence disease activity in established autoimmune rheumatic disease in humans. Our results add weight to concerns that pollution may be an important trigger of inflammation and autoimmunity.
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 (PM10–2.5), and ≤ 2.5 μm (PM2.5)] 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, PM2.5, and PM10–2.5, 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.
Background: Recent analysis has demonstrated a remarkably consistent, nonlinear relationship between estimated inhaled dose of combustion particles measured as PM2.5 (particulate matter with aerodynamic diameter ≤ 2.5 μm) and cardiovascular disease mortality over several orders of magnitude of dose—from cigarette smoking, environmental tobacco smoke (ETS) exposure, and ambient air pollution exposure.
Objectives: Here we discuss the implications of this relationship and point out the gaps in our knowledge that it reveals.
Discussion: The nonlinear exposure–response relationship that is revealed—much steeper at lower than at higher doses—explains the seemingly inconsistent risks observed from ambient air pollution and cigarette smoking but also raises important questions about the relative benefits of control at different points along the curve. This analysis also reveals a gap in the evidence base along the dose–response curve between ETS and active smoking, which is the dose range experienced by half the world’s population from indoor biomass and coal burning for cooking and heating.
Conclusions: The shape of the exposure–response relationship implies much larger public health benefits of reductions at the lower end of the dose spectrum (e.g., from reductions in outdoor air pollution) than from reducing the rate of active smoking, which seems counterintuitive and deserving of further study because of its importance for control policies. In addition, given the potential risks and consequent global disease burden, epidemiologic studies are urgently needed to quantify the cardiovascular risks of particulate matter exposures from indoor biomass burning in developing countries, which lie in the dose gap of current evidence.
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 (PM2.5)] concentrations and daily mortality in two U.S. cities—Seattle, Washington, and Detroit, Michigan.
Methods: We obtained daily PM2.5 filters for the years of 2002–2004 and analyzed trace elements using X-ray fluorescence and black carbon using light reflectance as a surrogate measure of elemental carbon. We used Poisson regression and distributed lag models to estimate excess deaths for all causes and for cardiovascular and respiratory diseases adjusting for time-varying covariates. We computed the excess risks for interquartile range increases of each pollutant at lags of 0 through 3 days for both warm and cold seasons.
Results: The cardiovascular and respiratory mortality series exhibited different source and seasonal patterns in each city. The PM2.5 components and gaseous pollutants associated with mortality in Detroit were most associated with warm season secondary aerosols and traffic markers. In Seattle, the component species most closely associated with mortality included those for cold season traffic and other combustion sources, such as residual oil and wood burning.
Conclusions: The effects of PM2.5 on daily mortality vary with source, season, and locale, consistent with the hypothesis that PM composition has an appreciable influence on the health effects attributable to PM.
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 (PM2.5) air pollution versus the diesel-related carbonaceous fraction of PM2.5.
Methods: Daily 24-hr personal samples of PM2.5, 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 PM2.5 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 PM2.5 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 PM2.5 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.
Background: The 2008 Beijing Olympic Games provided a unique case study to investigate the effect of source control measures on the reduction in air pollution, and associated inhalation cancer risk, in a Chinese megacity.
Objectives: We measured 17 carcinogenic polycyclic aromatic hydrocarbons (PAHs) and estimated the lifetime excess inhalation cancer risk during different periods of the Beijing Olympic Games, to assess the effectiveness of source control measures in reducing PAH-induced inhalation cancer risks.
Methods: PAH concentrations were measured in samples of particulate matter ≤ 2.5 μm in aerodynamic diameter (PM2.5) collected during the Beijing Olympic Games, and the associated inhalation cancer risks were estimated using a point-estimate approach based on relative potency factors.
Results: We estimated the number of lifetime excess cancer cases due to exposure to the 17 carcinogenic PAHs [12 priority pollutant PAHs and five high-molecular-weight (302 Da) PAHs (MW 302 PAHs)] to range from 6.5 to 518 per million people for the source control period concentrations and from 12.2 to 964 per million people for the nonsource control period concentrations. This would correspond to a 46% reduction in estimated inhalation cancer risk due to source control measures, if these measures were sustained over time. Benzo[b]fluoranthene, dibenz[a,h]anthracene, benzo[a]pyrene, and dibenzo[a,l]pyrene were the most carcinogenic PAH species evaluated. Total excess inhalation cancer risk would be underestimated by 23% if we did not include the five MW 302 PAHs in the risk calculation.
Conclusions: Source control measures, such as those imposed during the 2008 Beijing Olympics, can significantly reduce the inhalation cancer risk associated with PAH exposure in Chinese megacities similar to Beijing. MW 302 PAHs are a significant contributor to the estimated overall inhalation cancer risk.
Background: Few studies have examined the acute health effects of air pollution exposures experienced while cycling in traffic.
Objectives: We conducted a crossover study to examine the relationship between traffic pollution and acute changes in heart rate variability. We also collected spirometry and exhaled nitric oxide measures.
Methods: Forty-two healthy adults cycled for 1 hr on high- and low-traffic routes as well as indoors. Health measures were collected before cycling and 1–4 hr after the start of cycling. Ultrafine particles (UFPs; ≤ 0.1 μm in aerodynamic diameter), particulate matter ≤ 2.5 μm in aerodynamic diameter (PM2.5), black carbon, and volatile organic compounds were measured along each cycling route, and ambient nitrogen dioxide (NO2) and ozone (O3) levels were recorded from a fixed-site monitor. Mixed-effects models were used to estimate associations between air pollutants and changes in health outcome measures relative to precycling baseline values.
Results: An interquartile range increase in UFP levels (18,200/cm) was associated with a significant decrease in high-frequency power 4 hr after the start of cycling [β = –224 msec; 95% confidence interval (CI), –386 to –63 msec]. Ambient NO2 levels were inversely associated with the standard deviation of normal-to-normal (NN) intervals (β = –10 msec; 95% CI, –20 to –0.34 msec) and positively associated with the ratio of low-frequency to high-frequency power (β = 1.4; 95% CI, 0.35 to 2.5) 2 hr after the start of cycling. We also observed significant inverse associations between ambient O3 levels and the root mean square of successive differences in adjacent NN intervals 3 hr after the start of cycling.
Conclusions: Short-term exposures to traffic pollution may contribute to altered autonomic modulation of the heart in the hours immediately after cycling.
Background: A critical question regarding the association between short-term exposure to ozone and mortality is the extent to which this relationship is confounded by ambient exposure to particles.
Objectives: We investigated whether particulate matter < 10 and < 2.5 μm in aerodynamic diameter (PM10 and PM2.5) is a confounder of the ozone and mortality association using data for 98 U.S. urban communities from 1987 to 2000.
Methods: We a) estimated correlations between daily ozone and daily PM concentrations stratified by ozone or PM levels; b) included PM as a covariate in time-series models; and c) included PM as a covariate as in d), but within a subset approach considering only days with ozone below a specified value.
Results: Analysis was hindered by data availability. In the 93 communities with PM10 data, only 25.0% of study days had data on both ozone and PM10. In the 91 communities with PM2.5 data, only 9.2% of days in the study period had data on ozone and PM2.5. Neither PM measure was highly correlated with ozone at any level of ozone or PM. National and community-specific effect estimates of the short-term effects of ozone on mortality were robust to inclusion of PM10 or PM2.5 in time-series models. The robustness remains even at low ozone levels (< 10 ppb) using a subset approach.
Conclusions: Results provide evidence that neither PM10 nor PM2.5 is a likely confounder of observed ozone and mortality relationships. Further investigation is needed to investigate potential confounding of the short-term effects of ozone on mortality by PM chemical composition.
Background and objectives: We have previously shown that reduced defenses against oxidative stress due to glutathione S-transferase M1 (GSTM1) deletion modify the effects of PM2.5 (fine-particulate air pollution of < 2.5 μm in aerodynamic diameter) on heart rate variability (HRV) in a cross-sectional analysis of the Normative Aging Study, an elderly cohort. We have extended this to include a longitudinal analysis with more subjects and examination of the GT short tandem repeat polymorphism in the heme oxygenase-1 (HMOX-1) promoter.
Methods: HRV measurements were taken on 539 subjects. Linear mixed effects models were fit for the logarithm of HRV metrics—including standard deviation of normal-to-normal intervals (SDNN), high frequency (HF), and low frequency (LF)—and PM2.5 concentrations in the 48 hr preceding HRV measurement, controlling for confounders and a random subject effect.
Results: PM2.5 was significantly associated with SDNN (p = 0.04) and HF (p = 0.03) in all subjects. There was no association in subjects with GSTM1, whereas there was a significant association with SDNN, HF, and LF in subjects with the deletion. Similarly, there was no association with any HRV measure in subjects with the short repeat variant of HMOX-1, and significant associations in subjects with any long repeat. We found a significant three-way interaction of PM2.5 with GSTM1 and HMOX-1 determining SDNN (p = 0.008), HF (p = 0.01) and LF (p = 0.04). In subjects with the GSTM1 deletion and the HMOX-1 long repeat, SDNN decreased by 13% [95% confidence interval (CI), −21% to −4%], HF decreased by 28% (95% CI, −43% to −9%), and LF decreased by 20% (95% CI, −35% to −3%) per 10 μg/m increase in PM.
Conclusions: Oxidative stress is an important pathway for the autonomic effects of particles.
Background: The mechanisms of particulate matter (PM)-induced health effects are believed to involve inflammation and oxidative stress. Increased intake of omega-3 polyunsaturated fatty acids (n-3 PUFA) appears to have anti-inflammatory effects.
Objective: As part of a trial to evaluate whether n-3 PUFA supplementation could protect against the cardiac alterations linked to PM exposure, we measured biomarkers of response to oxidative stimuli [copper/zinc (Cu/Zn) superoxide dismutase (SOD) activity, lipoperoxidation (LPO) products, and reduced glutathione (GSH)] and evaluated the impact of supplementation on plasma levels.
Methods: We recruited residents from a nursing home in Mexico City chronically exposed to PM ≤2.5 μm in aerodynamic diameter (PM2.5) and followed them from 26 September 2001 to 10 April 2002. We randomly assigned subjects in a double-blind fashion to receive either fish oil (n-3 PUFA) or soy oil. We measured PM2.5 levels indoors at the nursing home, and measured Cu/Zn SOD activity, LPO products, and GSH at different times during presupplementation and supplementation phases.
Results: Supplementation with either fish or soy oil was related to an increase of Cu/Zn SOD activity and an increase in GSH plasma levels, whereas exposure to indoor PM2.5 levels was related to a decrease in Cu/Zn SOD activity and GSH plasma levels.
Conclusion: Supplementation with n-3 PUFA appeared to modulate the adverse effects of PM2.5 on these biomarkers, particularly in the fish oil group. Supplementation with n-3 PUFA could modulate oxidative response to PM2.5 exposure.
Background: Biomass fuel is the primary source of domestic fuel in much of rural China. Previous studies have not characterized particle exposure through time–activity diaries or personal monitoring in mainland China.
Objectives: In this study we characterized indoor and personal particle exposure in six households in northeastern China (three urban, three rural) and explored differences by location, cooking status, activity, and fuel type. Rural homes used biomass. Urban homes used a combination of electricity and natural gas.
Methods: Stationary monitors measured hourly indoor particulate matter (PM) with an aerodynamic diameter ≤ 10 μm (PM10) for rural and urban kitchens, urban sitting rooms, and outdoors. Personal monitors for PM with an aerodynamic diameter ≤ 2.5 μm (PM2.5) were employed for 10 participants. Time–activity patterns in 30-min intervals were recorded by researchers for each participant.
Results: Stationary monitoring results indicate that rural kitchen PM10 levels are three times higher than those in urban kitchens during cooking. PM10 was 6.1 times higher during cooking periods than during noncooking periods for rural kitchens. Personal PM2.5 levels for rural cooks were 2.8–3.6 times higher than for all other participant categories. The highest PM2.5 exposures occurred during cooking periods for urban and rural cooks. However, rural cooks had 5.4 times higher PM2.5 levels during cooking than did urban cooks. Rural cooks spent 2.5 times more hours per day cooking than did their urban counterparts.
Conclusions: These findings indicate that biomass burning for cooking contributes substantially to indoor particulate levels and that this exposure is particularly elevated for cooks. Second-by-second personal PM2.5 exposures revealed differences in exposures by population group and strong temporal heterogeneity that would be obscured by aggregate metrics.