Cardiac arrhythmia emergency room visits and environmental air pollution in Sao Paulo, Brazil.
ABSTRACT Air-pollution exposure has been associated with increased cardiovascular hospital admissions and mortality in time-series studies. We evaluated the relation between air pollutants and emergency room (ER) visits because of cardiac arrhythmia in a cardiology hospital.
In a time-series study, we evaluated the association between the emergency room visits as a result of cardiac arrhythmia and daily variations in SO(2), CO, NO(2), O(3) and PM(10), from January 1998 to August 1999. The cases of arrhythmia were modelled using generalised linear Poisson regression models, controlling for seasonality (short-term and long-term trend), and weather.
Interquartile range increases in CO (1.5 ppm), NO(2) (49,5 microg/m(3)) and PM(10) (22.2 microg/m(3)) on the concurrent day were associated with increases of 12.3% (95% CI: 7.6% to 17.2%), 10.4% (95% CI: 5.2% to 15.9%) and 6.7% (95% CI: 1.2% to 12.4%) in arrhythmia ER visits, respectively. PM(10), CO and NO(2) effects were dose-dependent and gaseous pollutants had thresholds. Only CO effect resisted estimates in models with more than one pollutant.
Our results showed that air pollutant effects on arrhythmia are predominantly acute starting at concentrations below air quality standards, and the association with CO and NO(2) suggests a relevant role for pollution caused by cars.
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ABSTRACT: Epidemiologic evidence has demonstrated that air pollution may impair cardiovascular health, leading to potentially life-threatening arrhythmias. Efforts have been made, with the use of epidemiologic data and controlled exposures in diverse animal and human populations, to verify the relationship between air pollution and arrhythmias. The purpose of this review is to examine and contrast the epidemiologic and toxicologic evidence to date that relates airborne pollutants with cardiac arrhythmia. We have explored the potential biological mechanisms driving this association. Using the PubMed database, we conducted a literature search that included the terms "air pollution" and "arrhythmia" and eventually divergent synonyms such as "particulate matter," "bradycardia," and "atrial fibrillation." We reviewed epidemiologic studies and controlled human and animal exposures independently to determine whether observational conclusions were corroborated by toxicologic results. Numerous pollutants have demonstrated some arrhythmic capacity among healthy and health-compromised populations. However, some exposure studies have shown no significant correlation of air pollutants with arrhythmia, which suggests some uncertainty about the arrhythmogenic potential of air pollution and the mechanisms involved in arrhythmogenesis. While data from an increasing number of controlled exposures with human volunteers suggest a potential mechanistic link between air pollution and altered cardiac electrophysiology, definite conclusions regarding air pollution and arrhythmia are elusive as the direct arrhythmic effects of air pollutants are not entirely consistent across all studies.The Canadian journal of cardiology 12/2012; · 3.12 Impact Factor
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ABSTRACT: Panel studies show a consistent association between increase in the cardiovascular hospitalizations with air pollutants in economically developed regions, but little evidence in less developed inland areas. In this study, a time-series analysis was used to examine the specific effects of major air pollutants [particulate matter less than 10 microns in diameter (PM(10)), sulfur dioxide (SO(2)), and nitrogen dioxides (NO(2))] on daily hospital admissions for cardio-cerebrovascular diseases in Lanzhou, a heavily polluted city in China. We examined the effects of air pollutants for stratified groups by age and gender, and conducted the modifying effect of seasons on air pollutants to test the possible interaction. The significant associations were found between PM(10), SO(2) and NO(2) and cardiac disease admissions, SO(2) and NO(2) were found to be associated with the cerebrovascular disease admissions. The elderly was associated more strongly with gaseous pollutants than younger. The modifying effect of seasons on air pollutants also existed. The significant effect of gaseous pollutants (SO(2) and NO(2)) was found on daily hospital admissions even after adjustment for other pollutants except for SO(2) on cardiac diseases. In a word, this study provides the evidence for the detrimental short-term health effects of urban gaseous pollutants on cardio-cerebrovascular diseases in Lanzhou.International Journal of Environmental Research and Public Health 01/2013; 10(2):462-77. · 2.00 Impact Factor
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ABSTRACT: Background: Epidemiological studies have assessed T-wave alternans (TWA) as a possible mechanism of cardiac arrhythmias related to air pollution in high-risk subjects and have reported associations with increased TWA magnitude.Objective: In this controlled human exposure study, we assessed the impact of exposure to concentrated ambient particulate matter (CAP) and ozone (O3) on T-wave alternans in resting volunteers without preexisting cardiovascular disease.Methods: Seventeen participants without preexisting cardiovascular disease were randomized to filtered air (FA), CAP (150 μg/m3), O3 (120 ppb), or combined CAP + O3 exposures for 2 hr. Continuous electrocardiograms (ECGs) were recorded at rest and T-wave alternans (TWA) was computed by modified moving average analysis with QRS alignment for the artifact-free intervals of 20 beats along the V2 and V5 leads. Exposure-induced changes in the highest TWA magnitude (TWAMax) were estimated for the first and last 5 min of each exposure (TWAMax_Early and TWAMax_Late respectively). ΔTWAMax (Late-Early) were compared among exposure groups using analysis of variance.Results: Mean ± SD values for ΔTWAMax were -2.1 ± 0.4, -2.7 ± 1.1, -1.9 ± 1.5, and -1.2 ± 1.5 in FA, CAP, O3, and CAP + O3 exposure groups, respectively. No significant differences were observed between pollutant exposures and FA.Conclusion: In our study of 17 volunteers who had no preexisting cardiovascular disease, we did not observe significant changes in T-wave alternans after 2-hr exposures to CAP, O3, or combined CAP + O3. This finding, however, does not preclude the possibility of pollution-related effects on TWA at elevated heart rates, such as during exercise, or the possibility of delayed responses.Environmental Health Perspectives 05/2012; 120(8):1157-61. · 7.26 Impact Factor