Acute Adverse Effects of Fine Particulate Air Pollution on Ventricular Repolarization

Background

The mechanisms for the relationship between particulate pollution and cardiac disease are not fully understood.

Objective

We examined the effects and time course of exposure to fine particulate matter ≤ 2.5 μm in aerodynamic diameter (PM_2.5) on ventricular repolarization of 106 nonsmoking adults who were living in communities in central Pennsylvania.

Methods

The 24-hr beat-to-beat electrocardiogram (ECG) data were obtained using a high-resolution 12-lead Holter system. After visually identifying and removing artifacts and arrhythmic beats, we summarized normal beat-to-beat QTs from each 30-min segment as heart rate (HR)-corrected QT measures: QT prolongation index (QTI), Bazett’s HR-corrected QT (QTcB), and Fridericia’s HR-corrected QT (QTcF). A personal PM_2.5 monitor was used to measure individual-level real-time PM_2.5 exposures for 24 hr. We averaged these data and used 30-min time-specific average PM_2.5 exposures.

Results

The mean age of the participants was 56 ± 8 years, with 41% male and 74% white. The means ± SDs for QTI, QTcB, and QTcF were 111 ± 6.6, 438 ± 23 msec, and 422 ± 22 msec, respectively; and for PM_2.5, the mean ± SD was 14 ± 22 μg/m³. We used distributed lag models under a framework of linear mixed-effects models to assess the autocorrelation-corrected regression coefficients (β) between 30-min PM_2.5 and the HR-corrected QT measures. Most of the adverse ventricular repolarization effects from PM_2.5 exposure occurred within 3–4 hr. The multivariable adjusted β (SE, p-value) due to a 10-μg/m³ increase in lag 7 PM_2.5 on QTI, QTcB, and QTcF were 0.08 (0.04, p < 0.05), 0.22 (0.08, p < 0.01), and 0.09 (0.05, p < 0.05), respectively.

Conclusions

Our results suggest a significant adverse effect of PM_2.5 on ventricular repolarization. The time course of the effect is within 3–4 hr of elevated PM_2.5.     

Short-Term Effects of Air Pollution on Wheeze in Asthmatic Children in Fresno,California

Background

Although studies have demonstrated that air pollution is associated with exacerbation of asthma symptoms in children with asthma, little is known about the susceptibility of subgroups, particularly those with atopy.

Objective

This study was designed to evaluate our a priori hypothesis that identifiable subgroups of asthmatic children are more likely to wheeze with exposure to ambient air pollution.

Methods

A cohort of 315 children with asthma, 6–11 years of age, was recruited for longitudinal follow-up in Fresno, California (USA). During the baseline visit, children were administered a respiratory symptom questionnaire and allergen skin-prick test. Three times a year, participants completed 14-day panels during which they answered symptom questions twice daily. Ambient air quality data from a central monitoring station were used to assign exposures to the following pollutants: particulate matter ≤ 2.5 μm in aerodynamic diameter, particulate matter between 2.5 and 10 μm in aerodynamic diameter (PM_10–2.5), elemental carbon, nitrogen dioxide (NO₂), nitrate, and O₃.

Results

For the group as a whole, wheeze was significantly associated with short-term exposures to NO₂ [odds ratio (OR) = 1.10 for 8.7-ppb increase; 95% confidence interval (CI), 1.02–1.20] and PM_10–2.5 (OR = 1.11 for 14.7-μg/m³ increase; 95% CI, 1.01–1.22). The association with wheeze was stronger for these two pollutants in children who were skin-test positive to cat or common fungi and in boys with mild intermittent asthma.

Conclusion

A pollutant associated with traffic emissions, NO₂, and a pollutant with bioactive constituents, PM_10–2.5, were associated with increased risk of wheeze in asthmatic children living in Fresno, California. Children with atopy to cat or common fungi and boys with mild intermittent asthma were the subgroups for which we observed the largest associations.     

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.     

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.     

Particulate Air Pollution,Metabolic Syndrome,and Heart Rate Variability: The Multi-Ethnic Study of Atherosclerosis (MESA)

Background

Cardiac autonomic dysfunction has been suggested as a possible biologic pathway for the association between fine particulate matter ≤ 2.5 μm in diameter (PM_2.5) and cardiovascular disease (CVD). We examined the associations of PM_2.5 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 PM_2.5 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 PM_2.5 (10.2 μg/m³) 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 PM_2.5 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.     

Air Pollution Exposures and Circulating Biomarkers of Effect in a Susceptible Population: Clues to Potential Causal Component mixtures and mechanisms

Background

Mechanisms involving oxidative stress and inflammation have been proposed to explain associations of ambient air pollution with cardiovascular morbidity and mortality. Experimental evidence suggests that organic components and ultrafine particles (UFP) are important.

Methods

We conducted a panel study of 60 elderly subjects with coronary artery disease living in retirement communities within the Los Angeles, California, air basin. Weekly biomarkers of inflammation included plasma interleukin-6, tumor necrosis factor-α soluble receptor II (sTNF-RII), soluble platelet selectin (sP-selectin), and C-reactive protein (CRP). Biomarkers of erythrocyte antioxidant activity included glutathione peroxidase-1 and superoxide dismutase. Exposures included outdoor home daily particle mass [particulate matter < 0.25, 0.25–2.5, and 2.5–10 μm in aerodynamic diameter (PM_0.25, PM_0.25–2.5, PM_2.5–10)], and hourly elemental and black carbon (EC–BC), estimated primary and secondary organic carbon (OC_pri, SOC), particle number (PN), carbon monoxide (CO), and nitrogen oxides–nitrogen dioxide (NO_x–NO₂). We analyzed the relation of biomarkers to exposures with mixed effects models adjusted for potential confounders.

Results

Primary combustion markers (EC–BC, OC_pri, CO, NO_x–NO₂), but not SOC, were positively associated with inflammatory biomarkers and inversely associated with erythrocyte anti-oxidant enzymes (n = 578). PN and PM_0.25 were more strongly associated with biomarkers than PM_0.25–2.5. Associations for all exposures were stronger during cooler periods when only OC_pri, PN, and NO_x were higher. We found weaker associations with statin (sTNF-RII, CRP) and clopidogrel use (sP-selectin).

Conclusions

Traffic-related air pollutants are associated with increased systemic inflammation, increased platelet activation, and decreased erythrocyte antioxidant enzyme activity, which may be partly behind air pollutant–related increases in systemic inflammation. Differences in association by particle size, OC fraction, and seasonal period suggest components carried by UFP are important.     

Long-Term Air Pollution Exposure and Blood Pressure in the Sister Study

Background

Exposure to air pollution has been consistently associated with cardiovascular morbidity and mortality, but mechanisms remain uncertain. Associations with blood pressure (BP) may help to explain the cardiovascular effects of air pollution.

Objective

We examined the cross-sectional relationship between long-term (annual average) residential air pollution exposure and BP in the National Institute of Environmental Health Sciences’ Sister Study, a large U.S. cohort study investigating risk factors for breast cancer and other outcomes.

Methods

This analysis included 43,629 women 35–76 years of age, enrolled 2003–2009, who had a sister with breast cancer. Geographic information systems contributed to satellite-based nitrogen dioxide (NO₂) and fine particulate matter (≤ 2.5 μm; PM_2.5) predictions at participant residences at study entry. Generalized additive models were used to examine the relationship between pollutants and measured BP at study entry, adjusting for cardiovascular disease risk factors and including thin plate splines for potential spatial confounding.

Results

A 10-μg/m³ increase in PM_2.5 was associated with 1.4-mmHg higher systolic BP (95% CI: 0.6, 2.3; p < 0.001), 1.0-mmHg higher pulse pressure (95% CI: 0.4, 1.7; p = 0.001), 0.8-mmHg higher mean arterial pressure (95% CI: 0.2, 1.4; p = 0.01), and no significant association with diastolic BP. A 10-ppb increase in NO₂ was associated with a 0.4-mmHg (95% CI: 0.2, 0.6; p < 0.001) higher pulse pressure.

Conclusions

Long-term PM_2.5 and NO₂ exposures were associated with higher blood pressure. On a population scale, such air pollution–related increases in blood pressure could, in part, account for the increases in cardiovascular disease morbidity and mortality seen in prior studies.

Citation

Chan SH, Van Hee VC, Bergen S, Szpiro AA, DeRoo LA, London SJ, Marshall JD, Kaufman JD, Sandler DP. 2015. Long-term air pollution exposure and blood pressure in the Sister Study. Environ Health Perspect 123:951–958; http://dx.doi.org/10.1289/ehp.1408125     

The Effect of Fine and Coarse Particulate Air Pollution on Mortality: A National Analysis

Background

Although many studies have examined the effects of air pollution on mortality, data limitations have resulted in fewer studies of both particulate matter with an aerodynamic diameter of ≤ 2.5 μm (PM_2.5; fine particles) and of coarse particles (particles with an aerodynamic diameter > 2.5 and < 10 μm; PM coarse). We conducted a national, multicity time-series study of the acute effect of PM_2.5 and PM coarse on the increased risk of death for all causes, cardiovascular disease (CVD), myocardial infarction (MI), stroke, and respiratory mortality for the years 1999–2005.

Method

We applied a city- and season-specific Poisson regression in 112 U.S. cities to examine the association of mean (day of death and previous day) PM_2.5 and PM coarse with daily deaths. We combined the city-specific estimates using a random effects approach, in total, by season and by region.

Results

We found a 0.98% increase [95% confidence interval (CI), 0.75–1.22] in total mortality, a 0.85% increase (95% CI, 0.46–1.24) in CVD, a 1.18% increase (95% CI, 0.48–1.89) in MI, a 1.78% increase (95% CI, 0.96–2.62) in stroke, and a 1.68% increase (95% CI, 1.04–2.33) in respiratory deaths for a 10-μg/m³ increase in 2-day averaged PM_2.5. The effects were higher in spring. For PM coarse, we found significant but smaller increases for all causes analyzed.

Conclusions

We conclude that our analysis showed an increased risk of mortality for all and specific causes associated with PM_2.5, and the risks are higher than what was previously observed for PM₁₀. In addition, coarse particles are also associated with more deaths.     

Chronic Residential Exposure to Particulate Matter Air Pollution and Systemic Inflammatory Markers

Background

Long-term exposure to urban air pollution may accelerate atherogenesis, but mechanisms are still unclear. The induction of a low-grade systemic inflammatory state is a plausible mechanistic pathway. Objectives: We analyzed the association of residential long-term exposure to particulate matter (PM) and high traffic with systemic inflammatory markers.

Methods

We used baseline data from the German Heinz Nixdorf Recall Study, a population-based, prospective cohort study of 4,814 participants that started in 2000. Fine PM [aerodynamic diameter ≤ 2.5 μm (PM_2.5)] exposure based on a small-scale dispersion and chemistry transport model was assigned to each home address. We calculated distances between residences and major roads. Long-term exposure to air pollution (annual PM_2.5 and distance to high traffic) and concentration of inflammatory markers [high-sensitivity C-reactive protein (hs-CRP) and fibrinogen] on the day of the baseline visit were analyzed with sex-stratified multiple linear regression, controlling for individual-level risk factors.

Results

In the adjusted analysis, a cross-sectional exposure difference of 3.91 μg/m³ in PM_2.5 (interdecile range) was associated with increases in hs-CRP of 23.9% [95% confidence interval (CI), 4.1 to 47.4%] and fibrinogen of 3.9% (95% CI, 0.3 to 7.7%) in men, whereas we found no association in women. Chronic traffic exposure was not associated with inflammatory markers. Short-term exposures to air pollutants and temperature did not influence the results markedly.

Conclusions

Our study indicates that long-term residential exposure to high levels of PM_2.5 is associated with systemic inflammatory markers in men. This might provide a link between air pollution and coronary atherosclerosis.     

Effect of Early Life Exposure to Air Pollution on Development of Childhood Asthma

Background

There is increasing recognition of the importance of early environmental exposures in the development of childhood asthma. Outdoor air pollution is a recognized asthma trigger, but it is unclear whether exposure influences incident disease. We investigated the effect of exposure to ambient air pollution in utero and during the first year of life on risk of subsequent asthma diagnosis in a population-based nested case–control study.

Methods

We assessed all children born in southwestern British Columbia in 1999 and 2000 (n = 37,401) for incidence of asthma diagnosis up to 3–4 years of age using outpatient and hospitalization records. Asthma cases were age- and sex-matched to five randomly chosen controls from the eligible cohort. We estimated each individual’s exposure to ambient air pollution for the gestational period and first year of life using high-resolution pollution surfaces derived from regulatory monitoring data as well as land use regression models adjusted for temporal variation. We used logistic regression analyses to estimate effects of carbon monoxide, nitric oxide, nitrogen dioxide, particulate matter ≤ 10 μm and ≤ 2.5 μm in aerodynamic diameter (PM₁₀ and PM_2.5), ozone, sulfur dioxide, black carbon, woodsmoke, and proximity to roads and point sources on asthma diagnosis.

Results

A total of 3,482 children (9%) were classified as asthma cases. We observed a statistically significantly increased risk of asthma diagnosis with increased early life exposure to CO, NO, NO₂, PM₁₀, SO₂, and black carbon and proximity to point sources. Traffic-related pollutants were associated with the highest risks: adjusted odds ratio = 1.08 (95% confidence interval, 1.04–1.12) for a 10-μg/m³ increase of NO, 1.12 (1.07–1.17) for a 10-μg/m³ increase in NO₂, and 1.10 (1.06–1.13) for a 100-μg/m³ increase in CO. These data support the hypothesis that early childhood exposure to air pollutants plays a role in development of asthma.     

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.     

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.     

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.     

Triggering of Transmural Infarctions,but Not Nontransmural Infarctions,by Ambient Fine Particles

Background

Previous studies have reported increased risk of myocardial infarction (MI) after increases in ambient particulate matter (PM) air pollution concentrations in the hours and days before MI onset.

Objectives

We hypothesized that acute increases in fine PM with aerodynamic diameter ≤ 2.5 μm (PM_2.5) may be associated with increased risk of MI and that chronic obstructive pulmonary disease (COPD) and diabetes may increase susceptibility to PM_2.5. We also explored whether both transmural and nontransmural infarctions were acutely associated with ambient PM_2.5 concentrations.

Methods

We studied all hospital admissions from 2004 through 2006 for first acute MI of adult residents of New Jersey who lived within 10 km of a PM_2.5 monitoring site (n = 5,864), as well as ambient measurements of PM_2.5, nitrogen dioxide, sulfur dioxide, carbon monoxide, and ozone.

Results

Using a time-stratified case-crossover design and conditional logistic regression showed that each interquartile-range increase in PM_2.5 concentration (10.8 μg/m³) in the 24 hr before arriving at the emergency department for MI was not associated with an increased risk of MI overall but was associated with an increased risk of a transmural infarction. We found no association between the same increase in PM_2.5 and risk of a nontransmural infarction. Further, subjects with COPD appeared to be particularly susceptible, but those with diabetes were not.

Conclusions

This PM–transmural infarction association is consistent with earlier studies of PM and MI. The lack of association with nontransmural infarction suggests that future studies that investigate the triggering of MI by ambient PM_2.5 concentrations should be stratified by infarction type.     

Air Pollution and Childhood Respiratory Allergies in the United States

Background

Childhood respiratory allergies, which contribute to missed school days and other activity limitations, have increased in recent years, possibly due to environmental factors.

Objective

In this study we examined whether air pollutants are associated with childhood respiratory allergies in the United States.

Methods

For the approximately 70,000 children from the 1999–2005 National Health Interview Survey eligible for this study, we assigned between 40,000 and 60,000 ambient pollution monitoring data from the U.S. Environmental Protection Agency, depending on the pollutant. We used monitors within 20 miles of the child’s residential block group. We used logistic regression models, fit with methods for complex surveys, to examine the associations between the reporting of respiratory allergy or hay fever and annual average exposure to particulate matter ≤ 2.5 μm in diameter (PM_2.5), PM ≤ 10 μm in diameter, sulfur dioxide, and nitrogen dioxide and summer exposure to ozone, controlling for demographic and geographic factors.

Results

Increased respiratory allergy/hay fever was associated with increased summer O₃ levels [adjusted odds ratio (AOR) per 10 ppb = 1.20; 95% confidence interval (CI), 1.15–1.26] and increased PM_2.5 (AOR per 10 μg/m³ = 1.23; 95% CI, 1.10–1.38). These associations persisted after stratification by urban–rural status, inclusion of multiple pollutants, and definition of exposures by differing exposure radii. No associations between the other pollutants and the reporting respiratory allergy/hay fever were apparent.

Conclusions

These results provide evidence of adverse health for children living in areas with chronic exposure to higher levels of O₃ and PM_2.5 compared with children with lower exposures.     

Postural Changes in Blood Pressure Associated with Interactions between Candidate Genes for Chronic Respiratory Diseases and Exposure to Particulate Matter

Background

Fine particulate matter [aerodynamic diameter ≤ 2.5 μm (PM_2.5)] has been associated with autonomic dysregulation.

Objective

We hypothesized that PM_2.5 influences postural changes in systolic blood pressure (ΔSBP) and in diastolic blood pressure (ΔDBP) and that this effect is modified by genes thought to be related to chronic lung disease.

Methods

We measured blood pressure in participants every 3–5 years. ΔSBP and ΔDBP were calculated as sitting minus standing SBP and DBP. We averaged PM_2.5 over 48 hr before study visits and analyzed 202 single nucleotide polymorphisms (SNPs) in 25 genes. To address multiple comparisons, data were stratified into a split sample. In the discovery cohort, the effects of SNP × PM_2.5 interactions on ΔSBP and ΔDBP were analyzed using mixed models with subject-specific random intercepts. We defined positive outcomes as p < 0.1 for the interaction; we analyzed only these SNPs in the replicate cohort and confirmed them if p < 0.025 with the same sign. Confirmed associations were analyzed within the full cohort in models adjusted for anthropometric and lifestyle factors.

Results

Nine hundred forty-five participants were included in our analysis. One interaction with rs9568232 in PHD finger protein 11 (PHF11) was associated with greater ΔDBP. Interactions with rs1144393 in matrix metalloprotease 1 (MMP1) and rs16930692, rs7955200, and rs10771283 in inositol 1,4,5-triphosphate receptor, type 2 (ITPR2) were associated with significantly greater ΔSBP. Because SNPs associated with ΔSBP in our analysis are in genes along the renin–angiotensin pathway, we then examined medications affecting that pathway and observed significant interactions for angiotensin receptor blockers but not angiotensin-converting enzyme inhibitors with PM_2.5.

Conclusions

PM_2.5 influences blood pressure and autonomic function. This effect is modified by genes and drugs that also act along this pathway.     

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.     

Baseline Repeated Measures from Controlled Human Exposure Studies: Associations between Ambient Air Pollution Exposure and the Systemic Inflammatory Biomarkers IL-6 and Fibrinogen

Introduction

Systemic inflammation may be one of the mechanisms mediating the association between ambient air pollution and cardiovascular morbidity and mortality. Interleukin-6 (IL-6) and fibrinogen are biomarkers of systemic inflammation that are independent risk factors for cardiovascular disease.

Objective

We investigated the association between ambient air pollution and systemic inflammation using baseline measurements of IL-6 and fibrinogen from controlled human exposure studies.

Methods

In this retrospective analysis we used repeated-measures data in 45 nonsmoking subjects. Hourly and daily moving averages were calculated for ozone, nitrogen dioxide, sulfur dioxide, and particulate matter ≤ 2.5 μm in aerodynamic diameter (PM_2.5). Linear mixed-model regression determined the effects of the pollutants on systemic IL-6 and fibrinogen. Effect modification by season was considered.

Results

We observed a positive association between IL-6 and O₃ [0.31 SD per O₃ interquartile range (IQR); 95% confidence interval (CI), 0.08–0.54] and between IL-6 and SO₂ (0.25 SD per SO₂ IQR; 95% CI, 0.06–0.43). We observed the strongest effects using 4-day moving averages. Responses to pollutants varied by season and tended to be higher in the summer, particularly for O₃ and PM_2.5. Fibrinogen was not associated with pollution.

Conclusions

This study demonstrates a significant association between ambient pollutant levels and baseline levels of systemic IL-6. These findings have potential implications for controlled human exposure studies. Future research should consider whether ambient pollution exposure before chamber exposure modifies IL-6 response.     

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.