The influence of air pollution on cardiovascular and pulmonary function and exercise capacity: Canadian Health Measures Survey (CHMS)

Background

Air pollution has been associated with adverse cardiovascular effects.

Objective

To measure the association between air pollution, spirometry, blood pressure, and exercise capacity.

Methods

We used data from 5604 subjects collected during the Canada Health Measures Survey to test the association between air pollution measured on the day of the survey and spirometry (n=5011 subjects), blood pressure, and exercise capacity (n=3789 subjects).

Results

An interquartile range (IQR) increase in ozone (17.0 ppb) was significantly associated with a 0.883% higher resting heart rate, a 0.718% higher systolic and 0.407% higher diastolic blood pressure, a 0.393% lower FEV₁/FVC expressed as a percentage of predicted, and a 1.52% reduction in the aerobic fitness score (p<0.05). Resting systolic and diastolic blood pressure were approximately 0.5 mmHg higher for an (IQR 4.5 μg/m³) increase in PM_2.5 (IQR 4.5 μg/m³) and 1 mmHg higher for a 12.6 ppb increase in NO₂ (IQR 12.6 ppb). An increase in PM_2.5 was also associated with an approximate 0.4% decrease in percent predicted FEV₁ and FVC (p<0.05).

Conclusion

Exposure to higher concentrations of air pollution was associated with higher resting blood pressure and lower ventilatory function. Ozone was associated with reduced exercise capacity.     

Traffic-related air pollution, preterm birth and term birth weight in the PIAMA birth cohort study

Background

Maternal exposure to air pollution has been associated with adverse pregnancy outcomes. Few studies took into account the spatial and temporal variation of air pollution levels.

Objectives

To evaluate the impact of maternal exposure to traffic-related air pollution during pregnancy on preterm birth and term birth weight using a spatio-temporal exposure model.

Methods

We estimated maternal residential exposure to nitrogen dioxide (NO₂), particulate matter (PM_2.5) and soot during pregnancy (entire pregnancy, 1st trimester, and last month) for 3853 singleton births within the Dutch PIAMA prospective birth cohort study by means of temporally adjusted land-use regression models. Associations between air pollution concentrations and preterm birth and term birth weight were analyzed by means of logistic and linear regression models with and without adjustment for maternal physical, lifestyle, and socio-demographic characteristics.

Results

We found positive, statistically non-significant associations between exposure to soot during entire pregnancy and during the last month of pregnancy and preterm birth [adj. OR (95% CI) per interquartile range increase in exposure 1.08 (0.88–1.34) and 1.09 (0.93–1.27), respectively]. There was no indication of an adverse effect of air pollution exposure on term birth weight.

Conclusions

In this study, maternal exposure to traffic-related air pollution during pregnancy was not associated with term birth weight. There was a tendency towards an increased risk of preterm birth with increasing air pollution exposure, but statistical power was low.     

Extreme air pollution events from bushfires and dust storms and their association with mortality in Sydney, Australia 1994-2007

Introduction

Extreme air pollution events due to bushfire smoke and dust storms are expected to increase as a consequence of climate change, yet little has been published about their population health impacts. We examined the association between air pollution events and mortality in Sydney from 1997 to 2004.

Methods

Events were defined as days for which the 24 h city-wide concentration of PM₁₀ exceeded the 99th percentile. All events were researched and categorised as being caused by either smoke or dust. We used a time-stratified case-crossover design with conditional logistic regression modelling adjusted for influenza epidemics, same day and lagged temperature and humidity. Reported odds ratios (OR) and 95% confidence intervals are for mortality on event days compared with non-event days. The contribution of elevated average temperatures to mortality during smoke events was explored.

Results

There were 52 event days, 48 attributable to bushfire smoke, six to dust and two affected by both. Smoke events were associated with a 5% increase in non-accidental mortality at a lag of 1 day OR (95% confidence interval (CI)) 1.05 (95%CI: 1.00–1.10). When same day temperature was removed from the model, additional same day associations were observed with non-accidental mortality OR 1.05 (95%CI: 1.00–1.09), and with cardiovascular mortality OR (95%CI) 1.10 (95%CI: 1.00–1.20). Dust events were associated with a 15% increase in non-accidental mortality at a lag of 3 days, OR (95%CI) 1.16 (95%CI: 1.03–1.30).

Conclusions

The magnitude and temporal patterns of association with mortality were different for smoke and dust events. Public health advisories during bushfire smoke pollution episodes should include advice about hot weather in addition to air pollution.     

Comparing exposure assessment methods for traffic-related air pollution in an adverse pregnancy outcome study

Background

Previous studies reported adverse impacts of traffic-related air pollution exposure on pregnancy outcomes. Yet, little information exists on how effect estimates are impacted by the different exposure assessment methods employed in these studies.

Objectives

To compare effect estimates for traffic-related air pollution exposure and preeclampsia, preterm birth (gestational age less than 37 weeks), and very preterm birth (gestational age less than 30 weeks) based on four commonly used exposure assessment methods.

Methods

We identified 81,186 singleton births during 1997–2006 at four hospitals in Los Angeles and Orange Counties, California. Exposures were assigned to individual subjects based on residential address at delivery using the nearest ambient monitoring station data [carbon monoxide (CO), nitrogen dioxide (NO₂), nitric oxide (NO), nitrogen oxides (NO_x), ozone (O₃), and particulate matter less than 2.5 (PM_2.5) or less than 10 (PM₁₀) μm in aerodynamic diameter], both unadjusted and temporally adjusted land-use regression (LUR) model estimates (NO, NO₂, and NO_x), CALINE4 line-source air dispersion model estimates (NO_x and PM_2.5), and a simple traffic-density measure. We employed unconditional logistic regression to analyze preeclampsia in our birth cohort, while for gestational age-matched risk sets with preterm and very preterm birth we employed conditional logistic regression.

Results

We observed elevated risks for preeclampsia, preterm birth, and very preterm birth from maternal exposures to traffic air pollutants measured at ambient stations (CO, NO, NO₂, and NO_x) and modeled through CALINE4 (NO_x and PM_2.5) and LUR (NO₂ and NO_x). Increased risk of preterm birth and very preterm birth were also positively associated with PM₁₀ and PM_2.5 air pollution measured at ambient stations. For LUR-modeled NO₂ and NO_x exposures, elevated risks for all the outcomes were observed in Los Angeles only—the region for which the LUR models were initially developed. Unadjusted LUR models often produced odds ratios somewhat larger in size than temporally adjusted models. The size of effect estimates was smaller for exposures based on simpler traffic density measures than the other exposure assessment methods.

Conclusion

We generally confirmed that traffic-related air pollution was associated with adverse reproductive outcomes regardless of the exposure assessment method employed, yet the size of the estimated effect depended on how both temporal and spatial variations were incorporated into exposure assessment. The LUR model was not transferable even between two contiguous areas within the same large metropolitan area in Southern California.     

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.     

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.     

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.     

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 Mortality in Seven Million Adults: The Dutch Environmental Longitudinal Study (DUELS)

Background

Long-term exposure to air pollution has been associated with mortality in urban cohort studies. Few studies have investigated this association in large-scale population registries, including non-urban populations.

Objectives

The aim of the study was to evaluate the associations between long-term exposure to air pollution and nonaccidental and cause-specific mortality in the Netherlands based on existing national databases.

Methods

We used existing Dutch national databases on mortality, individual characteristics, residence history, neighborhood characteristics, and national air pollution maps based on land use regression (LUR) techniques for particulates with an aerodynamic diameter ≤ 10 μm (PM₁₀) and nitrogen dioxide (NO₂). Using these databases, we established a cohort of 7.1 million individuals ≥ 30 years of age. We followed the cohort for 7 years (2004–2011). We applied Cox proportional hazard models adjusting for potential individual and area-specific confounders.

Results

After adjustment for individual and area-specific confounders, for each 10-μg/m³ increase, PM₁₀ and NO₂ were associated with nonaccidental mortality [hazard ratio (HR) = 1.08; 95% CI: 1.07, 1.09 and HR = 1.03; 95% CI: 1.02, 1.03, respectively], respiratory mortality (HR = 1.13; 95% CI: 1.10, 1.17 and HR = 1.02; 95% CI: 1.01, 1.03, respectively), and lung cancer mortality (HR = 1.26; 95% CI: 1.21, 1.30 and HR = 1.10 95% CI: 1.09, 1.11, respectively). Furthermore, PM₁₀ was associated with circulatory disease mortality (HR = 1.06; 95% CI: 1.04, 1.08), but NO₂ was not (HR = 1.00; 95% CI: 0.99, 1.01). PM₁₀ associations were robust to adjustment for NO₂; NO₂ associations remained for nonaccidental mortality and lung cancer mortality after adjustment for PM₁₀.

Conclusions

Long-term exposure to PM₁₀ and NO₂ was associated with nonaccidental and cause-specific mortality in the Dutch population of ≥ 30 years of age.

Citation

Fischer PH, Marra M, Ameling CB, Hoek G, Beelen R, de Hoogh K, Breugelmans O, Kruize H, Janssen NA, Houthuijs D. 2015. Air pollution and mortality in seven million adults: the Dutch Environmental Longitudinal Study (DUELS). Environ Health Perspect 123:697–704; http://dx.doi.org/10.1289/ehp.1408254     

Is physical activity a modifier of the association between air pollution and arterial stiffness in older adults: The SAPALDIA cohort study

Introduction and objectives

Air pollution and insufficient physical activity have been associated with inflammation and oxidative stress, molecular mechanisms linked to arterial stiffness and cardiovascular disease. There are no studies on how physical activity modifies the association between air pollution and arterial stiffness. We examined whether the adverse cardiovascular effects of air pollution were modified by individual physical activity levels in 2823 adults aged 50–81 years from the well-characterized Swiss Cohort Study on Air Pollution and Lung and Heart Diseases (SAPALDIA).

Well-being and environmental quality: Does pollution affect life satisfaction?

Purpose

We aimed to explore the effect of ambient air pollution on individual persons’ levels of subjective well-being. Our research question was: to what extent is an individual’s life satisfaction shaped by exposure to PM₁₀?

Methods

We used regression models to analyse data on subjective well-being indicators from the last two waves of the European social survey (ESS) and detailed information on local levels of the air pollutant PM₁₀.

Results

An increase in PM₁₀ annual concentrations by 1 μg/m³ was associated with a significant reduction in life satisfaction of .017 points on the ESS 10-point life satisfaction scale.

Conclusions

Our findings suggest that even in cases of relatively low levels of PM₁₀ air pollution (mean annual concentration of 8.3 ± 3.9 μg/m³), in addition to the effects on physical health, exposure negatively affects subjective assessments of well-being.

     

Association between Local Traffic-Generated Air Pollution and Preeclampsia and Preterm Delivery in the South Coast Air Basin of California

Background

Preeclampsia is a major complication of pregnancy that can lead to substantial maternal and perinatal morbidity, mortality, and preterm birth. Increasing evidence suggests that air pollution adversely affects pregnancy outcomes. Yet few studies have examined how local traffic-generated emissions affect preeclampsia in addition to preterm birth.

Objectives

We examined effects of residential exposure to local traffic-generated air pollution on preeclampsia and preterm delivery (PTD).

Methods

We identified 81,186 singleton birth records from four hospitals (1997–2006) in Los Angeles and Orange Counties, California (USA). We used a line-source dispersion model (CALINE4) to estimate individual exposure to local traffic-generated nitrogen oxides (NO_x) and particulate matter < 2.5 μm in aerodynamic diameter (PM_2.5) across the entire pregnancy. We used logistic regression to estimate effects of air pollution exposures on preeclampsia, PTD (gestational age < 37 weeks), moderate PTD (MPTD; gestational age < 35 weeks), and very PTD (VPTD; gestational age < 30 weeks).

Results

We observed elevated risks for preeclampsia and preterm birth from maternal exposure to local traffic-generated NO_x and PM_2.5. The risk of preeclampsia increased 33% [odds ratio (OR) = 1.33; 95% confidence interval (CI), 1.18–1.49] and 42% (OR = 1.42; 95% CI, 1.26–1.59) for the highest NO_x and PM_2.5 exposure quartiles, respectively. The risk of VPTD increased 128% (OR = 2.28; 95% CI, 2.15–2.42) and 81% (OR = 1.81; 95% CI, 1.71–1.92) for women in the highest NO_x and PM_2.5 exposure quartiles, respectively.

Conclusion

Exposure to local traffic-generated air pollution during pregnancy increases the risk of preeclampsia and preterm birth in Southern California women. These results provide further evidence that air pollution is associated with adverse reproductive outcomes.     

Cumulative exposure to particulate matter air pollution and long-term post-myocardial infarction outcomes

Introduction

Chronic environmental exposure to particulate matter < 2.5 μm in diameter (PM_2.5) has been associated with cardiovascular disease; however, the effect of air pollution on myocardial infarction (MI) survivors is not clear. We studied the association of chronic exposure to PM_2.5 with death and recurrent cardiovascular events in MI survivors.

Methods

Consecutive patients aged ≤ 65 years admitted to all medical centers in central Israel after first-MI in 1992–1993 were followed through 2005 for cardiovascular events and 2011 for survival. Data on sociodemographic and prognostic factors were collected at baseline and during follow-up. Residential exposure to PM_2.5 was estimated for each patient based on data recorded at air quality monitoring stations. Cox and Andersen–Gill proportional hazards models were used to study the pollution-outcome association.

Results

Among the 1120 patients, 469 (41.9%) died and 541 (48.3%) experienced one or more recurrent cardiovascular event. The adjusted hazard ratios associated with a 10 μg/m³ increase in PM_2.5 exposure were 1.3 (95% CI 0.8–2.1) for death and 1.5 (95% CI 1.1–1.9) for multiple recurrences of cardiovascular events (MI, heart failure and stroke).

Conclusion

When adjustment for socio-demographic factors is performed, cumulative chronic exposure to PM_2.5 is positively associated with recurrence of cardiovascular events in patients after a first MI.     

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     

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.     

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.     

An Estimate of the Global Burden of Anthropogenic Ozone and Fine Particulate Matter on Premature Human Mortality Using Atmospheric Modeling

Background

Ground-level concentrations of ozone (O₃) and fine particulate matter [≤ 2.5 μm in aerodynamic diameter (PM_2.5)] have increased since preindustrial times in urban and rural regions and are associated with cardiovascular and respiratory mortality.

Objectives

We estimated the global burden of mortality due to O₃ and PM_2.5 from anthropogenic emissions using global atmospheric chemical transport model simulations of preindustrial and present-day (2000) concentrations to derive exposure estimates.

Methods

Attributable mortalities were estimated using health impact functions based on long-term relative risk estimates for O₃ and PM_2.5 from the epidemiology literature. Using simulated concentrations rather than previous methods based on measurements allows the inclusion of rural areas where measurements are often unavailable and avoids making assumptions for background air pollution.

Results

Anthropogenic O₃ was associated with an estimated 0.7 ± 0.3 million respiratory mortalities (6.3 ± 3.0 million years of life lost) annually. Anthropogenic PM_2.5 was associated with 3.5 ± 0.9 million cardiopulmonary and 220,000 ± 80,000 lung cancer mortalities (30 ± 7.6 million years of life lost) annually. Mortality estimates were reduced approximately 30% when we assumed low-concentration thresholds of 33.3 ppb for O₃ and 5.8 μg/m³ for PM_2.5. These estimates were sensitive to concentration thresholds and concentration–mortality relationships, often by > 50%.

Conclusions

Anthropogenic O₃ and PM_2.5 contribute substantially to global premature mortality. PM_2.5 mortality estimates are about 50% higher than previous measurement-based estimates based on common assumptions, mainly because of methodologic differences. Specifically, we included rural populations, suggesting higher estimates; however, the coarse resolution of the global atmospheric model may underestimate urban PM_2.5 exposures.     

Air Pollution and Lung Function in Dutch Children: A Comparison of Exposure Estimates and Associations Based on Land Use Regression and Dispersion Exposure Modeling Approaches

Background

There is limited knowledge about the extent to which estimates of air pollution effects on health are affected by the choice for a specific exposure model.

Objectives

We aimed to evaluate the correlation between long-term air pollution exposure estimates using two commonly used exposure modeling techniques [dispersion and land use regression (LUR) models] and, in addition, to compare the estimates of the association between long-term exposure to air pollution and lung function in children using these exposure modeling techniques.

Methods

We used data of 1,058 participants of a Dutch birth cohort study with measured forced expiratory volume in 1 sec (FEV₁), forced vital capacity (FVC), and peak expiratory flow (PEF) measurements at 8 years of age. For each child, annual average outdoor air pollution exposure [nitrogen dioxide (NO₂), mass concentration of particulate matter with diameters ≤ 2.5 and ≤ 10 μm (PM_2.5, PM₁₀), and PM_2.5 soot] was estimated for the current addresses of the participants by a dispersion and a LUR model. Associations between exposures to air pollution and lung function parameters were estimated using linear regression analysis with confounder adjustment.

Results

Correlations between LUR- and dispersion-modeled pollution concentrations were high for NO₂, PM_2.5, and PM_2.5 soot (R = 0.86–0.90) but low for PM₁₀ (R = 0.57). Associations with lung function were similar for air pollutant exposures estimated using LUR and dispersion modeling, except for associations of PM_2.5 with FEV₁ and FVC, which were stronger but less precise for exposures based on LUR compared with dispersion model.

Conclusions

Predictions from LUR and dispersion models correlated very well for PM_2.5, NO₂, and PM_2.5 soot but not for PM₁₀. Health effect estimates did not depend on the type of model used to estimate exposure in a population of Dutch children.

Citation

Wang M, Gehring U, Hoek G, Keuken M, Jonkers S, Beelen R, Eeftens M, Postma DS, Brunekreef B. 2015. Air pollution and lung function in Dutch children: a comparison of exposure estimates and associations based on land use regression and dispersion exposure modeling approaches. Environ Health Perspect 123:847–851; http://dx.doi.org/10.1289/ehp.1408541     

Effect of the interaction between outdoor air pollution and extreme temperature on daily mortality in Shanghai, China

Background

Both outdoor air pollution and extreme temperature have been associated with daily mortality; however, the effect of their interaction is not known.

Methods

This time-series analysis examined the effect of the interaction between outdoor air pollutants and extreme temperature on daily mortality in Shanghai, China. A generalized additive model (GAM) with penalized splines was used to analyze mortality, air pollution, temperature, and covariate data. The effects of air pollutants were stratified by temperature stratum to examine the interaction effect of air pollutants and extreme temperature.

Results

We found a statistically significant interaction between PM₁₀/O₃ and extreme low temperatures for both total nonaccidental and cause-specific mortality. On days with “normal” temperatures (15th–85th percentile), a 10-µg/m³ increment in PM₁₀ corresponded to a 0.17% (95% CI: 0.03%, 0.32%) increase in total mortality, a 0.23% (0.02%, 0.44%) increase in cardiovascular mortality, and a 0.26% (−0.07%, 0.60%) increase in respiratory mortality. On low-temperature days (<15th percentile), the estimates changed to 0.40% (0.21%, 0.58%) for total mortality, 0.49% (0.13%, 0.86%) for cardiovascular mortality, and 0.24% (−0.33%, 0.82%) for respiratory mortality. The interaction pattern of O₃ with lower temperature was similar. The interaction between PM₁₀/O₃ and lower temperature remained robust when alternative cut-points were used for temperature strata.

Conclusions

The acute health effects of air pollution might vary by temperature level.Key words: air pollution, climate change, extreme temperature, interaction, time-series