Exploration of the rapid effects of personal fine particulate matter exposure on arterial hemodynamics and vascular function during the same day

Background

Levels of fine particulate matter [≤ 2.5 μm in aerodynamic diameter (PM_2.5)] are associated with alterations in arterial hemodynamics and vascular function. However, the characteristics of the same-day exposure–response relationships remain unclear.

Objectives

We aimed to explore the effects of personal PM_2.5 exposures within the preceding 24 hr on blood pressure (BP), heart rate (HR), brachial artery diameter (BAD), endothelial function [flow-mediated dilatation (FMD)], and nitroglycerin-mediated dilatation (NMD).

Methods

Fifty-one nonsmoking subjects had up to 5 consecutive days of 24-hr personal PM_2.5 monitoring and daily cardiovascular (CV) measurements during summer and/or winter periods. The associations between integrated hour-long total personal PM_2.5 exposure (TPE) levels (continuous nephelometry among compliant subjects with low secondhand tobacco smoke exposures; n = 30) with the CV outcomes were assessed over a 24-hr period by linear mixed models.

Results

We observed the strongest associations (and smallest estimation errors) between HR and TPE recorded 1–10 hr before CV measurements. The associations were not pronounced for the other time lags (11–24 hr). The associations between TPE and FMD or BAD did not show as clear a temporal pattern. However, we found some suggestion of a negative association with FMD and a positive association with BAD related to TPE just before measurement (0–2 hr).

Conclusions

Brief elevations in ambient TPE levels encountered during routine daily activity were associated with small increases in HR and trends toward conduit arterial vasodilatation and endothelial dysfunction within a few hours of exposure. These responses could reflect acute PM_2.5-induced autonomic imbalance and may factor in the associated rapid increase in CV risk among susceptible individuals.     

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.     

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.     

Are Particulate Matter Exposures Associated with Risk of Type 2 Diabetes?

Background

Although studies have found that diabetes mellitus (DM) modifies the impact of exposures from air pollution on cardiovascular outcomes, information is limited regarding DM as an air pollution-associated outcome.

Objectives

Using two prospective cohorts, the Nurses’ Health Study (NHS) and the Health Professionals Follow-Up Study (HPFS), we investigated the relationship of incident type 2 DM with exposures to particulate matter (PM) <2.5 μm (PM_2.5), PM <10 μm (PM₁₀), and PM between 2.5 and 10 μm in aerodynamic diameter (PM_10–2.5) in the previous 12 months and the distance to roadways.

Methods

Cases were reported and confirmed through biennial and supplemental questionnaires of diagnosis and treatment information. During follow-up from 1989 to 2002, questionnaires provided information on time-varying covariates and updated addresses. Addresses were geocoded and used to assign air pollution exposures from spatiotemporal statistical models.

Results

Among participants living in metropolitan areas of the northeastern and midwestern United States, there were 3,784 incident cases of DM in the NHS, and 688 cases in the HPFS. Pooled results from random effects meta-analysis of cohort-specific models adjusted for body mass index and other known risk factors produced hazard ratios (HRs) for incident DM with interquartile range (IQR) increases in average PM during the 12 months before diagnosis of 1.03 [95% confidence interval (CI), 0.96–1.10] for PM_2.5, 1.04 (95% CI, 0.99–1.09) for PM₁₀, and 1.04 (95% CI, 0.99–1.09) for PM_10–2.5. Among women, the fully adjusted HR for living < 50 m versus ≥ 200 m from a roadway was 1.14 (95% CI, 1.03–1.27).

Conclusions

Overall, results did not provide strong evidence of an association between exposure to PM in the previous 12 months and incident DM; however, an association with distance to road (a proxy marker of exposure to traffic-related pollution) was shown among women.     

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.     

Ambient carbon monoxide and fine particulate matter in relation to preeclampsia and preterm delivery in western Washington State

Background

Preterm delivery and preeclampsia are common adverse pregnancy outcomes that have been inconsistently associated with ambient air pollutant exposures.

Objectives

We aimed to prospectively examine relations between exposures to ambient carbon monoxide (CO) and fine particulate matter [≤ 2.5 μm in aerodynamic diameter (PM_2.5)] and risks of preeclampsia and preterm delivery.

Methods

We used data from 3,509 western Washington women who delivered infants between 1996 and 2006. We predicted ambient CO and PM_2.5 exposures using regression models based on regional air pollutant monitoring data. Models contained predictor terms for year, month, weather, and land use characteristics. We evaluated several exposure windows, including prepregnancy, early pregnancy, the first two trimesters, the last month, and the last 3 months of pregnancy. Outcomes were identified using abstracted maternal medical record data. Covariate information was obtained from maternal interviews.

Results

Predicted periconceptional CO exposure was significantly associated with preeclampsia after adjustment for maternal characteristics and season of conception [adjusted odds ratio (OR) per 0.1 ppm = 1.07; 95% confidence interval (CI), 1.02–1.13]. However, further adjustment for year of conception essentially nullified the association (adjusted OR = 0.98; 95% CI, 0.91–1.06). Associations between PM_2.5 and preeclampsia were nonsignificant and weaker than associations estimated for CO, and neither air pollutant was strongly associated with preterm delivery. Patterns were similar across all exposure windows.

Conclusions

Because both CO concentrations and preeclampsia incidence declined during the study period, secular changes in another preeclampsia risk factor may explain the association observed here. We saw little evidence of other associations with preeclampsia or preterm delivery in this setting.     

Ozone and other air pollutants and the risk of oral clefts

Background

Air pollution influences the development of oral clefts in animals. There are few epidemiologic data on the relation of prenatal air pollution exposure and the risk of oral clefts.

Objectives

Our goal in this study was to assess the relations between exposure to ambient air pollution and the risk of cleft lip with or without cleft palate (CL/P).

Methods

We conducted a population-based case–control study of all 653 cases of CL/P and a random sample of 6,530 control subjects from 721,289 Taiwanese newborns in 2001–2003. We used geographic information systems to form exposure parameters for sulfur dioxide, nitrogen oxides, ozone, carbon monoxide, and particulate matter with an aerodynamic diameter ≤ 10 μm (PM₁₀) during the first 3 months of pregnancy using inverse distance weighting method. We present the effect estimates as odds ratios (ORs) per 10-ppb change for SO₂, NO_x, and O₃, 100-ppb change for CO, and 10-μg/m³ change for PM₁₀.

Results

The risk of CL/P was increased in relation to O₃ levels in the first gestational month [adjusted OR = 1.20; 95% confidence interval (CI), 1.02–1.39] and second gestational month (adjusted OR = 1.25; 95% CI, 1.03–1.52) in the range from 16.7 ppb to 45.1 ppb, but was not related to CO, NO_x, SO₂, or PM₁₀.

Conclusions

The study provides new evidence that exposure to outdoor air O₃ during the first and second month of pregnancy may increase the risk of CL/P. Similar levels of O₃ are encountered globally by large numbers of pregnant women.     

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.     

Ambient particulate matter air pollution and venous thromboembolism in the Women's Health Initiative Hormone Therapy trials

Background

The putative effects of postmenopausal hormone therapy on the association between particulate matter (PM) air pollution and venous thromboembolism (VTE) have not been assessed in a randomized trial of hormone therapy, despite its widespread use among postmenopausal women.

Objective

In this study, we examined whether hormone therapy modifies the association of PM with VTE risk.

Methods

Postmenopausal women 50–79 years of age (n = 26,450) who did not have a history of VTE and who were not taking anticoagulants were enrolled in the Women’s Health Initiative Hormone Therapy trials at 40 geographically diverse U.S. clinical centers. The women were randomized to treatment with estrogen versus placebo (E trial) or to estrogen plus progestin versus placebo (E + P trial). We used age-stratified Cox proportional hazard models to examine the association between time to incident, centrally adjudicated VTE, and daily mean PM concentrations spatially interpolated at geocoded addresses of the participants and averaged over 1, 7, 30, and 365 days.

Results

During the follow-up period (mean, 7.7 years), 508 participants (2.0%) had VTEs at a rate of 2.6 events per 1,000 person-years. Unadjusted and covariate-adjusted VTE risk was not associated with concentrations of PM < 2.5 μm (PM_2.5) or < 10 μm (PM₁₀)] in aerodynamic diameter and PM × active treatment interactions were not statistically significant (p > 0.05) regardless of PM averaging period, either before or after combining data from both trials [e.g., combined trial-adjusted hazard ratios (95% confidence intervals) per 10 μg/m³ increase in annual mean PM_2.5 and PM₁₀, were 0.93 (0.54–1.60) and 1.05 (0.72–1.53), respectively]. Findings were insensitive to alternative exposure metrics, outcome definitions, time scales, analytic methods, and censoring dates.

Conclusions

In contrast to prior research, our findings provide little evidence of an association between short-term or long-term PM exposure and VTE, or clinically important modification by randomized exposure to exogenous estrogens among postmenopausal women.     

Examining the joint effect of multiple risk factors using exposure risk profiles: lung cancer in nonsmokers

Background

Profile regression is a Bayesian statistical approach designed for investigating the joint effect of multiple risk factors. It reduces dimensionality by using as its main unit of inference the exposure profiles of the subjects that is, the sequence of covariate values that correspond to each subject.

Objectives

We applied profile regression to a case–control study of lung cancer in nonsmokers, nested within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort, to estimate the combined effect of environmental carcinogens and to explore possible gene–environment interactions.

Methods

We tailored and extended the profile regression approach to the analysis of case–control studies, allowing for the analysis of ordinal data and the computation of posterior odds ratios. We compared and contrasted our results with those obtained using standard logistic regression and classification tree methods, including multifactor dimensionality reduction.

Results

Profile regression strengthened previous observations in other study populations on the role of air pollutants, particularly particulate matter ≤ 10 μm in aerodynamic diameter (PM₁₀), in lung cancer for nonsmokers. Covariates including living on a main road, exposure to PM₁₀ and nitrogen dioxide, and carrying out manual work characterized high-risk subject profiles. Such combinations of risk factors were consistent with a priori expectations. In contrast, other methods gave less interpretable results.

Conclusions

We conclude that profile regression is a powerful tool for identifying risk profiles that express the joint effect of etiologically relevant variables in multifactorial diseases.     

Chronic Fine and Coarse Particulate Exposure,Mortality, and Coronary Heart Disease in the Nurses’ Health Study

Background

The relationship of fine particulate matter < 2.5 μm in diameter (PM_2.5) air pollution with mortality and cardiovascular disease is well established, with more recent long-term studies reporting larger effect sizes than earlier long-term studies. Some studies have suggested the coarse fraction, particles between 2.5 and 10 μm (PM_10–2.5), may also be important. With respect to mortality and cardiovascular events, questions remain regarding the relative strength of effect sizes for chronic exposure to fine and coarse particles.

Objectives

We examined the relationship of chronic PM_2.5 and PM_10–2.5 exposures with all-cause mortality and fatal and nonfatal incident coronary heart disease (CHD), adjusting for time-varying covariates.

Methods

The current study included women from the Nurses’ Health Study living in metropolitan areas of the northeastern and midwestern United States. Follow-up was from 1992 to 2002. We used geographic information systems–based spatial smoothing models to estimate monthly exposures at each participant’s residence.

Results

We found increased risk of all-cause mortality [hazard ratio (HR), 1.26; 95% confidence interval (CI), 1.02–1.54] and fatal CHD (HR = 2.02; 95% CI, 1.07–3.78) associated with each 10-μg/m³ increase in annual PM_2.5 exposure. The association between fatal CHD and PM_10–2.5 was weaker.

Conclusions

Our findings contribute to growing evidence that chronic PM_2.5 exposure is associated with risk of all-cause and cardiovascular mortality.     

Electrocardiographic ST-segment depression and exposure to traffic-related aerosols in elderly subjects with coronary artery disease

Background

Air pollutants have not been associated with ambulatory electrocardiographic evidence of ST-segment depression ≥ 1 mm (probable cardiac ischemia). We previously found that markers of primary (combustion-related) organic aerosols and gases were positively associated with circulating biomarkers of inflammation and ambulatory blood pressure in the present cohort panel study of elderly subjects with coronary artery disease.

Objectives

We specifically aimed to evaluate whether exposure markers of primary organic aerosols and ultrafine particles were more strongly associated with ST-segment depression of ≥ 1 mm than were secondary organic aerosols or PM_2.5 (particulate matter with aerodynamic diameter ≤ 2.5 μm) mass.

Methods

We evaluated relations of air pollutants to ambulatory electrocardiographic evidence of cardiac ischemia over 10 days in 38 subjects without ST depression on baseline electrocardiographs. Exposures were measured outdoors in retirement communities in the Los Angeles basin, including daily size-fractionated particle mass and hourly markers of primary and secondary organic aerosols and gases. Generalized estimating equations were used to estimate odds of hourly ST-segment depression (≥ 1 mm) from hourly air pollution exposures and to estimate relative rates of daily counts of ST-segment depression from daily average exposures, controlling for potential confounders.

Results

We found significant positive associations of hourly ST-segment depression with markers of combustion-related aerosols and gases averaged 1-hr through 3–4 days, but not secondary (photochemically aged) organic aerosols or ozone. The odds ratio per interquartile increase in 2-day average primary organic carbon (5.2 μg/m³) was 15.4 (95% confidence interval, 3.5–68.2). Daily counts of ST-segment depression were consistently associated with primary combustion markers and 2-day average quasi-ultrafine particles < 0.25 μm.

Conclusions

Results suggest that exposure to quasi-ultrafine particles and combustion-related pollutants (predominantly from traffic) increase the risk of myocardial ischemia, coherent with our previous findings for systemic inflammation and blood pressure.     

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.     

Ambient PM2.5 exposure up-regulates the expression of costimulatory receptors on circulating monocytes in diabetic individuals

Background

Exposure of humans to air pollutants such as ozone and particulate matter (PM) may result in airway and systemic inflammation and altered immune function. One putative mechanism may be through modification of cell-surface costimulatory molecules.

Objectives

We examined whether changes in expression of costimulatory molecules on circulating cells are associated with ambient levels of fine PM [aerodynamic diameter ≤ 2.5 μm (PM_2.5)] in a susceptible population of diabetic individuals.

Methods

Twenty subjects were studied for 4 consecutive days. Daily measurements of PM_2.5 and meteorologic data were acquired on the rooftop of the exam site. Circulating cell-surface markers that mediate innate immune and inflammatory responses were assessed by flow cytometry on each day. Sensitivity analysis was conducted on glutathione S-transferase M1 (GSTM1) genotype, body mass index, and glycosylated hemoglobin A1c (HbA1c) levels to determine their role as effect modifiers. Data were analyzed using random effects models adjusting for season, weekday, and meteorology.

Results

We found significantly increased monocyte expression (mean fluorescent intensity) of CD80, CD40, CD86, HLA-DR, and CD23 per 10-μg/m³ increase in PM_2.5 at 2- to 4-day lag times after exposure. These findings were significantly higher in obese individuals, in individuals with HbA1c > 7%, and in participants who were GSTM1 null.

Conclusions

Exposure to PM_2.5 can enhance antigen-presenting cell phenotypes on circulating cells, which may have consequences in the development of allergic or autoimmune diseases. These effects are amplified in diabetic individuals with characteristics that are associated with insulin resistance or with oxidative stress.     

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.     

Public Health and Air Pollution in Asia (PAPA): a multicity study of short-term effects of air pollution on mortality

Background and objectives

Although the deleterious effects of air pollution from fossil fuel combustion have been demonstrated in many Western nations, fewer studies have been conducted in Asia. The Public Health and Air Pollution in Asia (PAPA) project assessed the effects of short-term exposure to air pollution on daily mortality in Bangkok, Thailand, and in three cities in China: Hong Kong, Shanghai, and Wuhan.

Methods

Poisson regression models incorporating natural spline smoothing functions were used to adjust for seasonality and other time-varying covariates that might confound the association between air pollution and mortality. Effect estimates were determined for each city and then for the cities combined using a random effects method.

Results

In individual cities, associations were detected between most of the pollutants [nitrogen dioxide, sulfur dioxide, particulate matter ≤ 10 μm in aerodynamic diameter (PM₁₀), and ozone] and most health outcomes under study (i.e., all natural-cause, cardiovascular, and respiratory mortality). The city-combined effects of the four pollutants tended to be equal or greater than those identified in studies conducted in Western industrial nations. In addition, residents of Asian cities are likely to have higher exposures to air pollution than those in Western industrial nations because they spend more time outdoors and less time in air conditioning.

Conclusions

Although the social and environmental conditions may be quite different, it is reasonable to apply estimates derived from previous health effect of air pollution studies in the West to Asia.     

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.     

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.