65 research outputs found
Particulate Air Pollution, Progression, and Survival after Myocardial Infarction
OBJECTIVE: Several studies have examined the effect of particulate pollution (PM) on survival in general populations, but less is known about susceptible groups. Moreover, previous cohort studies have been cross-sectional and subject to confounding by uncontrolled differences between cities. DESIGN: We investigated whether PM was associated with progression of disease or reduced survival in a study of 196,000 persons from 21 U.S. cities discharged alive following an acute myocardial infarction (MI), using within-city between-year exposure to PM. We constructed city-specific cohorts of survivors of acute MI using Medicare data between 1985 and 1999, and defined three outcomes on follow-up: death, subsequent MI, and a first admission for congestive heart failure (CHF). Yearly averages of PM(10) (particulate matter with aerodynamic diameter < 10 Ī¼m) were merged to the individual annual follow-up in each city. We applied Coxās proportional hazard regression model in each city, with adjustment for individual risk factors. In the second stage of the analysis, the city-specific results were combined using a meta-regression. RESULTS: We found significant associations with a hazard ratio for the sum of the distributed lags of 1.3 [95% confidence interval (CI), 1.2ā1.5] for mortality, a hazard ratio of 1.4 (95% CI, 1.2ā1.7) for a hospitalization for CHF, and a hazard ratio of 1.4 (95% CI, 1.1ā1.8) for a new hospitalization for MI per 10 Ī¼g/m(3) PM(10). CONCLUSIONS: This is the first long-term study showing a significant association between particle exposure and adverse post-MI outcomes in persons who survived an MI
Potential Role of Ultrafine Particles in Associations between Airborne Particle Mass and Cardiovascular Health
Numerous epidemiologic time-series studies have shown generally consistent associations of cardiovascular hospital admissions and mortality with outdoor air pollution, particularly mass concentrations of particulate matter (PM) ā¤2.5 or ā¤10 Ī¼m in diameter (PM(2.5), PM(10)). Panel studies with repeated measures have supported the time-series results showing associations between PM and risk of cardiac ischemia and arrhythmias, increased blood pressure, decreased heart rate variability, and increased circulating markers of inflammation and thrombosis. The causal components driving the PM associations remain to be identified. Epidemiologic data using pollutant gases and particle characteristics such as particle number concentration and elemental carbon have provided indirect evidence that products of fossil fuel combustion are important. Ultrafine particles < 0.1 Ī¼m (UFPs) dominate particle number concentrations and surface area and are therefore capable of carrying large concentrations of adsorbed or condensed toxic air pollutants. It is likely that redox-active components in UFPs from fossil fuel combustion reach cardiovascular target sites. High UFP exposures may lead to systemic inflammation through oxidative stress responses to reactive oxygen species and thereby promote the progression of atherosclerosis and precipitate acute cardiovascular responses ranging from increased blood pressure to myocardial infarction. The next steps in epidemiologic research are to identify more clearly the putative PM casual components and size fractions linked to their sources. To advance this, we discuss in a companion article (Sioutas C, Delfino RJ, Singh M. 2005. Environ Health Perspect 113:947ā955) the need for and methods of UFP exposure assessment
Effects of Air Pollution on Heart Rate Variability: The VA Normative Aging Study
Reduced heart rate variability (HRV), a marker of poor cardiac autonomic function, has been associated with air pollution, especially fine particulate matter [< 2.5 Ī¼m in aerodynamic diameter (PM(2.5))]. We examined the relationship between HRV [standard deviation of normal-to-normal intervals (SDNN), power in high frequency (HF) and low frequency (LF), and LF:HF ratio] and ambient air pollutants in 497 men from the Normative Aging Study in greater Boston, Massachusetts, seen between November 2000 and October 2003. We examined 4-hr, 24-hr, and 48-hr moving averages of air pollution (PM(2.5), particle number concentration, black carbon, ozone, nitrogen dioxide, sulfur dioxide, carbon monoxide). Controlling for potential confounders, HF decreased 20.8% [95% confidence interval (CI), 4.6ā34.2%] and LF:HF ratio increased 18.6% (95% CI, 4.1ā35.2%) per SD (8 Ī¼g/m(3)) increase in 48-hr PM(2.5). LF was reduced by 11.5% (95% CI, 0.4ā21.3%) per SD (13 ppb) increment in 4-hr O(3). The associations between HRV and PM(2.5) and O(3) were stronger in people with ischemic heart disease (IHD) and hypertension. The associations observed between SDNN and LF and PM(2.5) were stronger in people with diabetes. People using calcium-channel blockers and beta-blockers had lower associations between O(3) and PM(2.5) with LF. No effect modification by other cardiac medications was found. Exposures to PM(2.5) and O(3) are associated with decreased HRV, and history of IHD, hypertension, and diabetes may confer susceptibility to autonomic dysfunction by air pollution
Interaction Effects of Ultrafine Carbon Black with Iron and Nickel on Heart Rate Variability in Spontaneously Hypertensive Rats
Mechanisms of Inhaled Fine Particulate Air PollutionāInduced Arterial Blood Pressure Changes
Background: Epidemiologic studies suggest a positive association between fine particulate matter and arterial blood pressure, but the results have been inconsistent. Objectives: We investigated the effect of ambient particles on systemic hemodynamics during a 5-hr exposure to concentrated ambient air particles (CAPs) or filtered air (FA) in conscious canines. Methods: Thirteen dogs were repeatedly exposed via permanent tracheostomy to CAPs (358.1 Ā± 306.7 Ī¼g/m, mean Ā± SD) or FA in a crossover protocol (55 CAPs days, 63 FA days). Femoral artery blood pressure was monitored continuously via implanted telemetry devices. We measured baroreceptor reflex sensitivity before and after exposure in a subset of these experiments (n = 10 dogs, 19 CAPs days, 20 FA days). In additional experiments, we administered Ī±-adrenergic blockade before exposure (n = 8 dogs, 16 CAPs days, 15 FA days). Blood pressure, heart rate, rateāpressure product, and baroreceptor reflex sensitivity responses were compared using linear mixed-effects models. Results: CAPs exposure increased systolic blood pressure (2.7 Ā± 1.0 mmHg, p = 0.006), diastolic blood pressure (4.1 Ā± 0.8 mmHg; p < 0.001), mean arterial pressure (3.7 Ā± 0.8 mmHg; p < 0.001), heart rate (1.6 Ā± 0.5 bpm; p < 0.001), and rateāpressure product (539 Ā± 110 bpm Ć mmHg; p < 0.001), and decreased pulse pressure (ā1.7 Ā± 0.7 mmHg, p = 0.02). These changes were accompanied by a 20 Ā± 6 msec/mmHg (p = 0.005) increase in baroreceptor reflex sensitivity after CAPs versus FA. After Ī±-adrenergic blockade, responses to CAPs and FA no longer differed significantly. Conclusions: Controlled exposure to ambient particles elevates arterial blood pressure. Increased peripheral vascular resistance may mediate these changes, whereas increased baroreceptor reflex sensitivity may compensate for particle-induced alterations in blood pressure
Autonomic Effects of Controlled Fine Particulate Exposure in Young Healthy Adults: Effect Modification by Ozone
Background: Human controlled-exposure studies have assessed the impact of ambient fine particulate matter on cardiac autonomic function measured by heart rate variability (HRV), but whether these effects are modified by concomitant ozone exposure remains unknown. Objective: In this study we assessed the impact of O and particulate matter exposure on HRV in humans. Methods: In a crossover design, 50 subjects (19ā48 years of age) were randomized to 2-hr controlled exposures to filtered air (FA), concentrated ambient particles (CAPs), O, or combined CAPs and ozone (CAPs + O). The primary end point was change in HRV between the start and end of exposure. Secondary analyses included blood pressure (BP) responses, and effect modification by asthmatic status. Results: Achieved mean CAPs and O exposure concentrations were 121.6 Ā± 48.0 Ī¼g/m and 113.9 Ā± 6.6 ppb, respectively. In a categorical analysis, exposure had no consistent effect on HRV indices. However, the doseāresponse relationship between CAPs mass concentration and HRV indices seemed to vary depending on the presence of O. This heterogeneity was statistically significant for the low-frequency component of HRV (p = 0.02) and approached significance for the high-frequency component and time-domain measures of HRV. Exposure to CAPs + O increased diastolic BP by 2.0 mmHg (SE, 1.2; p = 0.02). No other statistically significant changes in BP were observed. Asthmatic status did not modify these effects. Conclusion: The potentiation by O of CAPs effects on diastolic BP and possibly HRV is of small magnitude in young adults. Further studies are needed to assess potential effects in more vulnerable populations
Particulate Matter (PM) Research Centers (1999ā2005) and the Role of Interdisciplinary Center-Based Research
Objective: The U.S. Environmental Protection Agency funded five academic centers in 1999 to address the uncertainties in exposure, toxicity, and health effects of airborne particulate matter (PM) identified in the āResearch Priorities for Airborne Particulate Matterā of the National Research Council (NRC). The centers were structured to promote interdisciplinary approaches to address research priorities of the NRC. In this report, we present selected accomplishments from the first 6 years of the PM Centers, with a focus on the advantages afforded by the interdisciplinary, center-based research approach. The review highlights advances in the area of ultrafine particles and traffic-related health effects as well as cardiovascular and respiratory effects, mechanisms, susceptibility, and PM exposure and characterization issues. Data sources and synthesis: The collective publications of the centers served as the data source. To provide a concise synthesis of overall findings, authors representing each of the five centers identified a limited number of topic areas that serve to illustrate the key accomplishments of the PM Centers program, and a consensus statement was developed. Conclusions: The PM Centers program has effectively applied interdisciplinary research approaches to advance PM science
TRPA1 and Sympathetic Activation Contribute to Increased Risk of Triggered Cardiac Arrhythmias in Hypertensive Rats Exposed to Diesel Exhaust
Background: Diesel exhaust (DE), which is emitted from on- and off-road sources, is a complex mixture of toxic gaseous and particulate components that leads to triggered adverse cardiovascular effects such as arrhythmias
Repolarization Changes Induced by Air Pollution in Ischemic Heart Disease Patients
Epidemiologic studies report associations between particulate air pollution and cardiovascular morbidity and mortality, but the underlying pathophysiologic mechanisms are still unclear. We tested the hypothesis that patients with preexisting coronary heart disease experience changes in the repolarization parameters in association with rising concentrations of air pollution. A prospective panel study was conducted in Erfurt, East Germany, with 12 repeated electrocardiogram (ECG) recordings in 56 males with ischemic heart disease. Hourly particulate and gaseous air pollution and meteorologic data were acquired. The following ECG parameters reflecting myocardial substrate and vulnerability were measured: QT duration, T-wave amplitude, T-wave complexity, and variability of T-wave complexity. Fixed effect regression analysis was used adjusting for subject, trend, weekday, and meteorology. The analysis showed a significant increase in QT duration in response to exposure to organic carbon; a significant decrease in T-wave amplitude with exposure to ultrafine, accumulation mode, and PM(2.5) particles (particles < 2.5 Ī¼m in aerodynamic diameter); and a corresponding significant increase of T-wave complexity in association with PM(2.5) particles for the 24 hr before ECG recordings. Variability of T-wave complexity showed a significant increase with organic and elemental carbon in the same time interval. This study provides evidence suggesting an immediate effect of air pollution on repolarization duration, morphology, and variability representing myocardial substrate and vulnerability, key factors in the mechanisms of cardiac death
Ambient Fine Particulate Matter Exposure and Myocardial Ischemia in the Environmental Epidemiology of Arrhythmogenesis in the Womenās Health Initiative (EEAWHI) Study
BackgroundAmbient particulate matter (PM) air pollution is associated with coronary heart disease, but the pathways underlying the association remain to be elucidated.MethodsWe studied the association between PM and ischemia among 57,908 Womenās Health Initiative clinical trial participants from 1999ā2003. We used the Minnesota Code criteria to identify ST-segment and T-wave abnormalities, and estimated T amplitude (microvolt) from resting, standard 12-lead electrocardiogram (ECG). We used U.S. Environmental Protection Agencyās monitor data to estimate concentrations of PM < 2.5 Ī¼m (PM2.5) at geocoded participant addresses over 6 days before the ECGs (lag0 through lag5). We excluded 2,379 women with ECG QRS duration ā„ 120 msec.ResultsOverall, 6% of the remaining 55,529 women (52ā90 years of age; 83% non-Hispanic white) had ST abnormalities and 16% had T abnormalities. Lead-specific T amplitude was normally distributed (range of means from ā14 to 349 Ī¼V). PM2.5 (mean Ā± SD) averaged over lag0ā2 was 14 Ā± 7 Ī¼g/m3. In logistic and linear regression models adjusted for demographic, clinical, temporal, and climatic factors, a 10-Ī¼g/m3 increase in lag0ā2 PM2.5 was associated with a 4% [95% confidence interval (CI), ā3%, to 10%] increase in the odds of ST abnormality and a 5% (95% CI, 0% to 9%) increase in the odds of T abnormality. We observed corresponding decreases in T amplitude in all exam sites and leads except lead V1, reaching a minimum of ā2 Ī¼V (95% CI, ā5 to 0 Ī¼V) in lead V3.ConclusionsShort-term PM2.5 exposure is associated with ECG evidence of myocardial ischemia among postmenopausal women. The principal manifestations include subclinical but potentially arrhythmogenic STāT abnormalities and decreases in T amplitude
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