Opposing effects of particle pollution, ozone, and ambient temperature on arterial blood pressure

Background: Diabetes increases the risk of hypertension and orthostatic hypotension and raises the risk of cardiovascular death during heat waves and high pollution episodes.Objective: We examined whether short-term exposures to air pollution (fine particles, ozone) and heat resulted in perturbation of arterial blood pressure (BP) in persons with type 2 diabetes mellitus (T2DM).Methods: We conducted a panel study in 70 subjects with T2DM, measuring BP by automated oscillometric sphygmomanometer and pulse wave analysis every 2 weeks on up to five occasions (355 repeated measures). Hourly central site measurements of fine particles, ozone, and meteorology were conducted. We applied linear mixed models with random participant intercepts to investigate the association of fine particles, ozone, and ambient temperature with systolic, diastolic, and mean arterial BP in a multipollutant model, controlling for season, meteorological variables, and subject characteristics.Results: An interquartile increase in ambient fine particle mass [particulate matter (PM) with an aerodynamic diameter of ≤ 2.5 μm (PM_2.5)] and in the traffic component black carbon in the previous 5 days (3.54 and 0.25 μg/m³, respectively) predicted increases of 1.4 mmHg [95% confidence interval (CI): 0.0, 2.9 mmHg] and 2.2 mmHg (95% CI: 0.4, 4.0 mmHg) in systolic BP (SBP) at the population geometric mean, respectively. In contrast, an interquartile increase in the 5-day mean of ozone (13.3 ppb) was associated with a 5.2 mmHg (95% CI: –8.6, –1.8 mmHg) decrease in SBP. Higher temperatures were associated with a marginal decrease in BP.Conclusions: In subjects with T2DM, PM was associated with increased BP, and ozone was associated with decreased BP. These effects may be clinically important in patients with already compromised autoregulatory function.     

Estimated short-term effects of coarse particles on daily mortality in Stockholm, Sweden

Background: Although serious health effects associated with particulate matter (PM) with aerodynamic diameter ≤ 10 μm (PM₁₀) and ≤ 2.5 μm (PM_2.5; fine fraction) are documented in many studies, the effects of coarse PM (PM_2.5–10) are still under debate.Objective: In this study, we estimated the effects of short-term exposure of PM_2.5–10 on daily mortality in Stockholm, Sweden.Method: We collected data on daily mortality for the years 2000 through 2008. Concentrations of PM₁₀, PM_2.5, ozone, and carbon monoxide were measured simultaneously in central Stockholm. We used additive Poisson regression models to examine the association between daily mortality and PM_2.5–10 on the day of death and the day before. Effect estimates were adjusted for other pollutants (two-pollutant models) during different seasons.Results: We estimated a 1.68% increase [95% confidence interval (CI): 0.20%, 3.15%] in daily mortality per 10-μg/m³ increase in PM_2.5–10 (single-pollutant model). The association with PM_2.5–10 was stronger for November through May, when road dust is most important (1.69% increase; 95% CI: 0.21%, 3.17%), compared with the rest of the year (1.31% increase; 95% CI: –2.08%, 4.70%), although the difference was not statistically significant. When adjusted for other pollutants, particularly PM_2.5, the effect estimates per 10 μg/m³ for PM_2.5–10 decreased slightly but were still higher than corresponding effect estimates for PM_2.5.Conclusions: Our analysis shows an increase in daily mortality associated with elevated urban background levels of PM_2.5–10. Regulation of PM_2.5–10 should be considered, along with actions to specifically reduce PM_2.5–10 emissions, especially road dust suspension, in cities.     

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.     

Black carbon as an additional indicator of the adverse health effects of airborne particles compared with PM10 and PM2.5

Background: Current air quality standards for particulate matter (PM) use the PM mass concentration [PM with aerodynamic diameters ≤ 10 μm (PM₁₀) or ≤ 2.5 μm (PM_2.5)] as a metric. It has been suggested that particles from combustion sources are more relevant to human health than are particles from other sources, but the impact of policies directed at reducing PM from combustion processes is usually relatively small when effects are estimated for a reduction in the total mass concentration.Objectives: We evaluated the value of black carbon particles (BCP) as an additional indicator in air quality management.Methods: We performed a systematic review and meta-analysis of health effects of BCP compared with PM mass based on data from time-series studies and cohort studies that measured both exposures. We compared the potential health benefits of a hypothetical traffic abatement measure, using near-roadway concentration increments of BCP and PM_2.5 based on data from prior studies.Results: Estimated health effects of a 1-μg/m³ increase in exposure were greater for BCP than for PM₁₀ or PM_2.5, but estimated effects of an interquartile range increase were similar. Two-pollutant models in time-series studies suggested that the effect of BCP was more robust than the effect of PM mass. The estimated increase in life expectancy associated with a hypothetical traffic abatement measure was four to nine times higher when expressed in BCP compared with an equivalent change in PM_2.5 mass.Conclusion: BCP is a valuable additional air quality indicator to evaluate the health risks of air quality dominated by primary combustion particles.     

Saharan dust and associations between particulate matter and daily mortality in Rome, Italy

Background: Outbreaks of Saharan-Sahel dust over Euro-Mediterranean areas frequently induce exceedances of the Europen Union''s 24-hr standard of 50 μg/m³ for particulate matter (PM) with aerodynamic diameter ≤ than 10 μm (PM₁₀).Objectives: We evaluated the effect of Saharan dust on the association between different PM fractions and daily mortality in Rome, Italy.Methods: In a study of 80,423 adult residents who died in Rome between 2001 and 2004, we performed a time-series analysis to explore the effects of PM_2.5, PM_2.5–10, and PM₁₀ on natural, cardiac, cerebrovascular, and respiratory mortality. We defined Saharan dust days by combining light detection and ranging (LIDAR) observations and analyses from operational models. We tested a Saharan dust–PM interaction term to evaluate the hypothesis that the effects of PM, especially coarse PM (PM_2.5–10), on mortality would be enhanced on dust days.Results: Interquartile range increases in PM_2.5–10 (10.8 μg/m³) and PM₁₀ (19.8 μg/m³) were associated with increased mortality due to natural, cardiac, cerebrovascular, and respiratory causes, with estimated effects ranging from 2.64% to 12.65% [95% confidence interval (CI), 1.18–25.42%] for the association between PM_2.5–10 and respiratory mortality (0- to 5-day lag). Associations of PM_2.5–10 with cardiac mortality were stronger on Saharan dust days (9.73%; 95% CI, 4.25–15.49%) than on dust-free days (0.86%; 95% CI, –2.47% to 4.31%; p = 0.005). Saharan dust days also modified associations between PM₁₀ and cardiac mortality (9.55% increase; 95% CI, 3.81–15.61%; vs. dust-free days: 2.09%; 95% CI, –0.76% to 5.02%; p = 0.02).Conclusions: We found evidence of effects of PM_2.5–10 and PM₁₀ on natural and cause-specific mortality, with stronger estimated effects on cardiac mortality during Saharan dust outbreaks. Toxicological and biological effects of particles from desert sources need to be further investigated and taken into account in air quality standards.     

Acute effects of fine particulate air pollution on cardiac arrhythmia: the APACR study

Background: The mechanisms underlying the relationship between particulate matter (PM) air pollution and cardiac disease are not fully understood.Objectives: We examined the effects and time course of exposure to fine PM [aerodynamic diameter ≤ 2.5 μm (PM_2.5)] on cardiac arrhythmia in 105 middle-age community-dwelling healthy nonsmokers in central Pennsylvania.Methods: The 24-hr beat-to-beat electrocardiography data were obtained using a high-resolution Holter system. After visually identifying and removing artifacts, we summarized the total number of premature ventricular contractions (PVCs) and premature atrial contractions (PACs) for each 30-min segment. A personal PM_2.5 nephelometer was used to measure individual-level real-time PM_2.5 exposures for 24 hr. We averaged these data to obtain 30-min average time–specific PM_2.5 exposures. Distributed lag models under the framework of negative binomial regression and generalized estimating equations were used to estimate the rate ratio between 10-μg/m³ increases in average PM_2.5 over 30-min intervals and ectopy counts.Results: The mean ± SD age of participants was 56 ± 8 years, with 40% male and 73% non-Hispanic white. The 30-min mean ± SD for PM_2.5 exposure was 13 ± 22 μg/m³, and PAC and PVC counts were 0.92 ± 4.94 and 1.22 ± 7.18. Increases of 10 μg/m³ in average PM_2.5 concentrations during the same 30 min or the previous 30 min were associated with 8% and 3% increases in average PVC counts, respectively. PM_2.5 was not significantly associated with PAC count.Conclusion: PM_2.5 exposure within approximately 60 min was associated with increased PVC counts in healthy individuals.     

The effects of particulate matter sources on daily mortality: a case-crossover study of Barcelona, Spain

Background: Dozens of studies link acute exposure to particulate matter (PM) air pollution with premature mortality and morbidity, but questions remain about which species and sources in the vast PM mixture are responsible for the observed health effects. Although a few studies exist on the effects of species and sources in U.S. cities, European cities—which have a higher proportion of diesel engines and denser urban populations—have not been well characterized. Information on the effects of specific sources could aid in targeting pollution control and in articulating the biological mechanisms of PM.Objectives: Our study examined the effects of various PM sources on daily mortality for 2003 through 2007 in Barcelona, a densely populated city in the northeast corner of Spain.Methods: Source apportionment for PM ≤ 2.5 μm and ≤ 10 µm in aerodynamic diameter (PM_2.5 and PM₁₀) using positive matrix factorization identified eight different factors. Case-crossover regression analysis was used to estimate the effects of each factor.Results: Several sources of PM_2.5, including vehicle exhaust, fuel oil combustion, secondary nitrate/organics, minerals, secondary sulfate/organics, and road dust, had statistically significant associations (p < 0.05) with all-cause and cardiovascular mortality. Also, in some cases relative risks for a respective interquartile range increase in concentration were higher for specific sources than for total PM_2.5 mass.Conclusions: These results along with those from our multisource models suggest that traffic, sulfate from shipping and long-range transport, and construction dust are important contributors to the adverse health effects linked to PM.     

Risk of nonaccidental and cardiovascular mortality in relation to long-term exposure to low concentrations of fine particulate matter: a Canadian national-level cohort study

Background: Few cohort studies have evaluated the risk of mortality associated with long-term exposure to fine particulate matter [≤ 2.5 μm in aerodynamic diameter (PM_2.5)]. This is the first national-level cohort study to investigate these risks in Canada.Objective: We investigated the association between long-term exposure to ambient PM_2.5 and cardiovascular mortality in nonimmigrant Canadian adults.Methods: We assigned estimates of exposure to ambient PM_2.5 derived from satellite observations to a cohort of 2.1 million Canadian adults who in 1991 were among the 20% of the population mandated to provide detailed census data. We identified deaths occurring between 1991 and 2001 through record linkage. We calculated hazard ratios (HRs) and 95% confidence intervals (CIs) adjusted for available individual-level and contextual covariates using both standard Cox proportional survival models and nested, spatial random-effects survival models.Results: Using standard Cox models, we calculated HRs of 1.15 (95% CI: 1.13, 1.16) from nonaccidental causes and 1.31 (95% CI: 1.27, 1.35) from ischemic heart disease for each 10-μg/m³ increase in concentrations of PM_2.5. Using spatial random-effects models controlling for the same variables, we calculated HRs of 1.10 (95% CI: 1.05, 1.15) and 1.30 (95% CI: 1.18, 1.43), respectively. We found similar associations between nonaccidental mortality and PM_2.5 based on satellite-derived estimates and ground-based measurements in a subanalysis of subjects in 11 cities.Conclusions: In this large national cohort of nonimmigrant Canadians, mortality was associated with long-term exposure to PM_2.5. Associations were observed with exposures to PM_2.5 at concentrations that were predominantly lower (mean, 8.7 μg/m³; interquartile range, 6.2 μg/m³) than those reported previously.     

Contrasts in oxidative potential and other particulate matter characteristics collected near major streets and background locations

Background: Measuring the oxidative potential of airborne particulate matter (PM) may provide a more health-based exposure measure by integrating various biologically relevant properties of PM into a single predictor of biological activity.Objectives: We aimed to assess the contrast in oxidative potential of PM collected at major urban streets and background locations, the associaton of oxidative potential with other PM characteristics, and the oxidative potential in different PM size fractions.Methods: Measurements of PM with aerodynamic diameter ≤ 10 μm (PM₁₀), PM with aerodynamic diameter ≤ 2.5 μm (PM_2.5), soot, elemental composition, and oxidative potential of PM were conducted simultaneously in samples from 8 major streets and 10 urban and suburban background locations in the Netherlands. Six 1-week measurements were performed at each location over a 6-month period in 2008. Oxidative potential was measured as the ability to generate hydroxyl radicals in the presence of hydrogen peroxide in all PM₁₀ samples and a subset of PM_2.5 samples.Results: The PM₁₀ oxidative potential of samples from major streets was 3.6 times higher than at urban background locations, exceeding the contrast for PM mass, soot, and all measured chemical PM characteristics. The contrast between major streets and suburban background locations was even higher (factor of 6.5). Oxidative potential was highly correlated with soot, barium, chromium, copper, iron, and manganese. Oxidative potential of PM₁₀ was 4.6 times higher than the oxidative potential of PM_2.5 when expressed per volume unit and 3.1 times higher when expressed per mass unit.Conclusions: The oxidative potential of PM near major urban roads was highly elevated compared with urban and suburban background locations, and the contrast was greater than that for any other measured PM characteristic.     

Long-term Exposure to PM2.5 and Incidence of Acute Myocardial Infarction

Background: A number of studies have shown associations between chronic exposure to particulate air pollution and increased mortality, particularly from cardiovascular disease, but fewer studies have examined the association between long-term exposure to fine particulate air pollution and specific cardiovascular events, such as acute myocardial infarction (AMI).Objective: We examined how long-term exposure to area particulate matter affects the onset of AMI, and we distinguished between area and local pollutants.Methods: Building on the Worcester Heart Attack Study, an ongoing community-wide investigation examining changes over time in myocardial infarction incidence in greater Worcester, Massachusetts, we conducted a case–control study of 4,467 confirmed cases of AMI diagnosed between 1995 and 2003 and 9,072 matched controls selected from Massachusetts resident lists. We used a prediction model based on satellite aerosol optical depth (AOD) measurements to generate both exposure to particulate matter ≤ 2.5 μm in diameter (PM_2.5) at the area level (10 × 10 km) and the local level (100 m) based on local land use variables. We then examined the association between area and local particulate pollution and occurrence of AMI.Results: An interquartile range (IQR) increase in area PM_2.5 (0.59 μg/m³) was associated with a 16% increase in the odds of AMI (95% CI: 1.04, 1.29). An IQR increase in total PM_2.5 (area + local, 1.05 μg/m³) was weakly associated with a 4% increase in the odds of AMI (95% CI: 0.96, 1.11).Conclusions: Residential exposure to PM_2.5 may best be represented by a combination of area and local PM_2.5, and it is important to consider spatial gradients within a single metropolitan area when examining the relationship between particulate matter exposure and cardiovascular events.     

Effects of coarse particulate matter on emergency hospital admissions for respiratory diseases: a time-series analysis in Hong Kong

Background: Many epidemiological studies have linked daily counts of hospital admissions to particulate matter (PM) with an aerodynamic diameter ≤ 10 μm (PM₁₀) and ≤ 2.5 μm (PM_2.5), but relatively few have investigated the relationship of hospital admissions with coarse PM (PM_c; 2.5–10 μm aerodynamic diameter).Objectives: We conducted this study to estimate the health effects of PM_c on emergency hospital admissions for respiratory diseases in Hong Kong after controlling for PM_2.5 and gaseous pollutants.Methods: We conducted a time-series analysis of associations between daily emergency hospital admissions for respiratory diseases in Hong Kong from January 2000 to December 2005 and daily PM_2.5 and PM_c concentrations. We estimated PM_c concentrations by subtracting PM_2.5 from PM₁₀ measurements. We used generalized additive models to examine the relationship between PM_c (single- and multiday lagged exposures) and hospital admissions adjusted for time trends, weather conditions, influenza outbreaks, PM_2.5, and gaseous pollutants (nitrogen dioxide, sulfur dioxide, and ozone).Results: A 10.9-μg/m³ (interquartile range) increase in the 4-day moving average concentration of PM_c was associated with a 1.94% (95% confidence interval: 1.24%, 2.64%) increase in emergency hospital admissions for respiratory diseases that was attenuated but still significant after controlling for PM_2.5. Adjusting for gaseous pollutants and altering models assumptions had little influence on PM_c effect estimates.Conclusion: PM_c was associated with emergency hospital admissions for respiratory diseases in Hong Kong independent of PM_2.5 and gaseous pollutants. Further research is needed to evaluate health effects of different components of PM_c.     

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.     

Associations between Long-Term Air Pollutant Exposures and Blood Pressure in Elderly Residents of Taipei City: A Cross-Sectional Study

Background

Limited information is available regarding long-term effects of air pollution on blood pressure (BP) and hypertension.

Objective

We studied whether 1-year exposures to particulate matter (PM) and nitrogen oxides (NO_x) were correlated with BP and hypertension in the elderly.

Methods

We analyzed cross-sectional data from 27,752 Taipei City residents > 65 years of age who participated in a health examination program in 2009. Land-use regression models were used to estimate participants’ 1-year exposures to particulate matter with aerodynamic diameter ≤ 10 μm (PM₁₀), coarse particles (PM_2.5–10), fine particles (≤ 2.5 μm; PM_2.5), PM_2.5 absorbance, NO_x, and nitrogen dioxide (NO₂). Generalized linear regressions and logistic regressions were used to examine the association between air pollution and BP and hypertension, respectively.

Results

Diastolic BP was associated with 1-year exposures to air pollution, with estimates of 0.73 [95% confidence interval (CI): 0.44, 1.03], 0.46 (95% CI: 0.30, 0.63), 0.62 (95% CI: 0.24, 0.99), 0.34 (95% CI: 0.19, 0.50), and 0.65 (95% CI: 0.44, 0.85) mmHg for PM₁₀ (10 μg/m³), PM_2.5–10 (5 μg/m³), PM_2.5 absorbance (10^–5/m), NO_x (20 μg/m³), and NO₂ (10 μg/m³), respectively. PM_2.5 was not associated with diastolic BP, and none of the air pollutants was associated with systolic BP. Associations of diastolic BP with PM₁₀ and PM_2.5 absorbance were stronger among participants with hypertension, diabetes, or a body mass index ≥ 25 kg/m² than among participants without these conditions. One-year air pollution exposures were not associated with hypertension.

Conclusions

One-year exposures to PM₁₀, PM_2.5–10, PM_2.5 absorbance, and NO_x were associated with higher diastolic BP in elderly residents of Taipei.

Citation

Chen SY, Wu CF, Lee JH, Hoffmann B, Peters A, Brunekreef B, Chu DC, Chan CC. 2015. Associations between long-term air pollutant exposures and blood pressure in elderly residents of Taipei City: a cross-sectional study. Environ Health Perspect 123:779–784; http://dx.doi.org/10.1289/ehp.1408771     

Long-Term Exposure to Ambient Air Pollution and Incidence of Cerebrovascular Events: Results from 11 European Cohorts within the ESCAPE Project

Background: Few studies have investigated effects of air pollution on the incidence of cerebrovascular events.Objectives: We assessed the association between long-term exposure to multiple air pollutants and the incidence of stroke in European cohorts.Methods: Data from 11 cohorts were collected, and occurrence of a first stroke was evaluated. Individual air pollution exposures were predicted from land-use regression models developed within the European Study of Cohorts for Air Pollution Effects (ESCAPE). The exposures were: PM_2.5 [particulate matter (PM) ≤ 2.5 μm in diameter], coarse PM (PM between 2.5 and 10 μm), PM₁₀ (PM ≤ 10 μm), PM_2.5 absorbance, nitrogen oxides, and two traffic indicators. Cohort-specific analyses were conducted using Cox proportional hazards models. Random-effects meta-analysis was used for pooled effect estimation.Results: A total of 99,446 study participants were included, 3,086 of whom developed stroke. A 5-μg/m³ increase in annual PM_2.5 exposure was associated with 19% increased risk of incident stroke [hazard ratio (HR) = 1.19, 95% CI: 0.88, 1.62]. Similar findings were obtained for PM₁₀. The results were robust to adjustment for an extensive list of cardiovascular risk factors and noise coexposure. The association with PM_2.5 was apparent among those ≥ 60 years of age (HR = 1.40, 95% CI: 1.05, 1.87), among never-smokers (HR = 1.74, 95% CI: 1.06, 2.88), and among participants with PM_2.5 exposure < 25 μg/m³ (HR = 1.33, 95% CI: 1.01, 1.77).Conclusions: We found suggestive evidence of an association between fine particles and incidence of cerebrovascular events in Europe, even at lower concentrations than set by the current air quality limit value.Citation: Stafoggia M, Cesaroni G, Peters A, Andersen ZJ, Badaloni C, Beelen R, Caracciolo B, Cyrys J, de Faire U, de Hoogh K, Eriksen KT, Fratiglioni L, Galassi C, Gigante B, Havulinna AS, Hennig F, Hilding A, Hoek G, Hoffmann B, Houthuijs D, Korek M, Lanki T, Leander K, Magnusson PK, Meisinger C, Migliore E, Overvad K, Östenson CG, Pedersen NL, Pekkanen J, Penell J, Pershagen G, Pundt N, Pyko A, Raaschou-Nielsen O, Ranzi A, Ricceri F, Sacerdote C, Swart WJ, Turunen AW, Vineis P, Weimar C, Weinmayr G, Wolf K, Brunekreef B, Forastiere F. 2014. Long-term exposure to ambient air pollution and incidence of cerebrovascular events: results from 11 European cohorts within the ESCAPE project. Environ Health Perspect 122:919–925; http://dx.doi.org/10.1289/ehp.1307301     

Long-term exposure to airborne particles and arterial stiffness: the Multi-Ethnic Study of Atherosclerosis (MESA)

Background

Increased arterial stiffness could represent an intermediate subclinical outcome in the mechanistic pathway underlying associations between average long-term pollution exposure and cardiovascular events.

Objective

We hypothesized that 20 years of exposure to particulate matter (PM) ≤ 2.5 and 10 μm in aerodynamic diameter (PM_2.5 and PM₁₀, respectively) would be positively associated with arterial stiffness in 3,996 participants from the Multi-Ethnic Study of Atherosclerosis (MESA) who were seen at six U.S. study sites.

Methods

We assigned pollution exposure during two decades preceding a clinical exam (2000–2002) using observed PM₁₀ from monitors nearest participants’ residences and PM₁₀ and PM_2.5 imputed from a space-time model. We examined three log-transformed arterial stiffness outcome measures: Young’s modulus (YM) from carotid artery ultrasound and large (C₁) and small (C₂) artery vessel compliance from the radial artery pulse wave. All associations are expressed per 10 μg/m³ increment in PM and were adjusted for weather, age, sex, race, glucose, triglycerides, diabetes, waist:hip ratio, seated mean arterial pressure, smoking status, pack-years, cigarettes per day, environmental tobacco smoke, and physical activity. C₁ and C₂ models were further adjusted for heart rate, weight, and height.

Results

Long-term average particle exposure was not associated with greater arterial stiffness measured by YM, C₁, or C₂, and the few associations observed were not robust across metrics and adjustment schemes.

Conclusions

Long-term particle mass exposure did not appear to be associated with greater arterial stiffness in this study sample.     

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.     

Estimated global mortality attributable to smoke from landscape fires

Background: Forest, grass, and peat fires release approximately 2 petagrams of carbon into the atmosphere each year, influencing weather, climate, and air quality.Objective: We estimated the annual global mortality attributable to landscape fire smoke (LFS).Methods: Daily and annual exposure to particulate matter ≤ 2.5 μm in aerodynamic diameter (PM_2.5) from fire emissions was estimated globally for 1997 through 2006 by combining outputs from a chemical transport model with satellite-based observations of aerosol optical depth. In World Health Organization (WHO) subregions classified as sporadically affected, the daily burden of mortality was estimated using previously published concentration–response coefficients for the association between short-term elevations in PM_2.5 from LFS (contrasted with 0 μg/m³ from LFS) and all-cause mortality. In subregions classified as chronically affected, the annual burden of mortality was estimated using the American Cancer Society study coefficient for the association between long-term PM_2.5 exposure and all-cause mortality. The annual average PM_2.5 estimates were contrasted with theoretical minimum (counterfactual) concentrations in each chronically affected subregion. Sensitivity of mortality estimates to different exposure assessments, counterfactual estimates, and concentration–response functions was evaluated. Strong La Niña and El Niño years were compared to assess the influence of interannual climatic variability.Results: Our principal estimate for the average mortality attributable to LFS exposure was 339,000 deaths annually. In sensitivity analyses the interquartile range of all tested estimates was 260,000–600,000. The regions most affected were sub-Saharan Africa (157,000) and Southeast Asia (110,000). Estimated annual mortality during La Niña was 262,000, compared with 532,000 during El Niño.Conclusions: Fire emissions are an important contributor to global mortality. Adverse health outcomes associated with LFS could be substantially reduced by curtailing burning of tropical rainforests, which rarely burn naturally. The large estimated influence of El Niño suggests a relationship between climate and the burden of mortality attributable to LFS.     

Acute respiratory inflammation in children and black carbon in ambient air before and during the 2008 Beijing Olympics

Background: Epidemiologic evidence for a causative association between black carbon (BC) and health outcomes is limited.Objectives: We estimated associations and exposure–response relationships between acute respiratory inflammation in schoolchildren and concentrations of BC and particulate matter with an aerodynamic diameter of ≤ 2.5 μm (PM_2.5) in ambient air before and during the air pollution intervention for the 2008 Beijing Olympics.Methods: We measured exhaled nitric oxide (eNO) as an acute respiratory inflammation biomarker and hourly mean air pollutant concentrations to estimate BC and PM_2.5 exposure. We used 1,581 valid observations of 36 subjects over five visits in 2 years to estimate associations of eNO with BC and PM_2.5 according to generalized estimating equations with polynomial distributed-lag models, controlling for body mass index, asthma, temperature, and relative humidity. We also assessed the relative importance of BC and PM_2.5 with two-pollutant models.Results: Air pollution concentrations and eNO were clearly lower during the 2008 Olympics. BC and PM_2.5 concentrations averaged over 0–24 hr were strongly associated with eNO, which increased by 16.6% [95% confidence interval (CI), 14.1–19.2%] and 18.7% (95% CI, 15.0–22.5%) per interquartile range (IQR) increase in BC (4.0 μg/m³) and PM_2.5 (149 μg/m³), respectively. In the two-pollutant model, estimated effects of BC were robust, but associations between PM_2.5 and eNO decreased with adjustment for BC. We found that eNO was associated with IQR increases in hourly BC concentrations up to 10 hr after exposure, consistent with effects primarily in the first hours after exposure.Conclusions: Recent exposure to BC was associated with acute respiratory inflammation in schoolchildren in Beijing. Lower air pollution levels during the 2008 Olympics also were associated with reduced eNO.     

Short-term Associations between Fine and Coarse Particulate Matter and Hospitalizations in Southern Europe: Results from the MED-PARTICLES Project

Background: Evidence on the short-term effects of fine and coarse particles on morbidity in Europe is scarce and inconsistent.Objectives: We aimed to estimate the association between daily concentrations of fine and coarse particles with hospitalizations for cardiovascular and respiratory conditions in eight Southern European cities, within the MED-PARTICLES project.Methods: City-specific Poisson models were fitted to estimate associations of daily concentrations of particulate matter with aerodynamic diameter ≤ 2.5 μm (PM_2.5), ≤ 10 μm (PM₁₀), and their difference (PM_2.5–10) with daily counts of emergency hospitalizations for cardiovascular and respiratory diseases. We derived pooled estimates from random-effects meta-analysis and evaluated the robustness of results to co-pollutant exposure adjustment and model specification. Pooled concentration–response curves were estimated using a meta-smoothing approach.Results: We found significant associations between all PM fractions and cardiovascular admissions. Increases of 10 μg/m³ in PM_2.5, 6.3 μg/m³ in PM_2.5–10, and 14.4 μg/m³ in PM₁₀ (lag 0–1 days) were associated with increases in cardiovascular admissions of 0.51% (95% CI: 0.12, 0.90%), 0.46% (95% CI: 0.10, 0.82%), and 0.53% (95% CI: 0.06, 1.00%), respectively. Stronger associations were estimated for respiratory hospitalizations, ranging from 1.15% (95% CI: 0.21, 2.11%) for PM₁₀ to 1.36% (95% CI: 0.23, 2.49) for PM_2.5 (lag 0–5 days).Conclusions: PM_2.5 and PM_2.5–10 were positively associated with cardiovascular and respiratory admissions in eight Mediterranean cities. Information on the short-term effects of different PM fractions on morbidity in Southern Europe will be useful to inform European policies on air quality standards.Citation: Stafoggia M, Samoli E, Alessandrini E, Cadum E, Ostro B, Berti G, Faustini A, Jacquemin B, Linares C, Pascal M, Randi G, Ranzi A, Stivanello E, Forastiere F, the MED-PARTICLES Study Group. 2013. Short-term associations between fine and coarse particulate matter and hospitalizations in Southern Europe: results from the MED-PARTICLES project. Environ Health Perspect 121:1026–1033; http://dx.doi.org/10.1289/ehp.1206151     

Associations between Traffic Noise,Particulate Air Pollution,Hypertension, and Isolated Systolic Hypertension in Adults: The KORA Study

Background: Studies on the association between traffic noise and cardiovascular diseases have rarely considered air pollution as a covariate in the analyses. Isolated systolic hypertension has not yet been in the focus of epidemiological noise research.Methods: The association between traffic noise (road and rail) and the prevalence of hypertension was assessed in two study populations with a total of 4,166 participants 25–74 years of age. Traffic noise (weighted day–night average noise level; L_DN) at the facade of the dwellings was derived from noise maps. Annual average PM_2.5 mass concentrations at residential addresses were estimated by land-use regression. Hypertension was assessed by blood pressure readings, self-reported doctor-diagnosed hypertension, and antihypertensive drug intake.Results: In the Greater Augsburg, Germany, study population, traffic noise and air pollution were not associated with hypertension. In the City of Augsburg population (n = 1,893), where the exposure assessment was more detailed, the adjusted odds ratio (OR) for a 10-dB(A) increase in noise was 1.16 (95% CI: 1.00, 1.35), and 1.11 (95% CI: 0.94, 1.30) after additional adjustment for PM_2.5. The adjusted OR for a 1-μg/m³ increase in PM_2.5 was 1.15 (95% CI: 1.02, 1.30), and 1.11 (95% CI: 0.98, 1.27) after additional adjustment for noise. For isolated systolic hypertension, the fully adjusted OR for noise was 1.43 (95% CI: 1.10, 1.86) and for PM_2.5 was 1.08 (95% CI: 0.87, 1.34).Conclusions: Traffic noise and PM_2.5 were both associated with a higher prevalence of hypertension. Mutually adjusted associations with hypertension were positive but no longer statistically significant.Citation: Babisch W, Wolf K, Petz M, Heinrich J, Cyrys J, Peters A. 2014. Associations between traffic noise, particulate air pollution, hypertension, and isolated systolic hypertension in adults: the KORA Study. Environ Health Perspect 122:492–498; http://dx.doi.org/10.1289/ehp.1306981