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      Increased Risk of Paroxysmal Atrial Fibrillation Episodes Associated with Acute Increases in Ambient Air Pollution

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          Abstract

          O bjectives: We reported previously that 24-hr moving average ambient air pollution concentrations were positively associated with ventricular arrhythmias detected by implantable cardioverter defibrillators (ICDs). ICDs also detect paroxysmal atrial fibrillation episodes (PAF) that result in rapid ventricular rates. In this same cohort of ICD patients, we assessed the association between ambient air pollution and episodes of PAF.

          D esign: We performed a case–crossover study.

          P articipants: Patients who lived in the Boston, Massachusetts, metropolitan area and who had ICDs implanted between June 1995 and December 1999 ( n = 203) were followed until July 2002.

          E valuations/M easurements: We used conditional logistic regression to explore the association between community air pollution and 91 electrophysiologist-confirmed episodes of PAF among 29 subjects.

          R esults: We found a statistically significant positive association between episodes of PAF and increased ozone concentration (22 ppb) in the hour before the arrhythmia (odds ratio = 2.08; 95% confidence interval = 1.22, 3.54; p = 0.001). The risk estimate for a longer (24-hr) moving average was smaller, thus suggesting an immediate effect. Positive but not statistically significant risks were associated with fine particles, nitrogen dioxide, and black carbon.

          C onclusions: Increased ambient O 3 pollution was associated with increased risk of episodes of rapid ventricular response due to PAF, thereby suggesting that community air pollution may be a precipitant of these events.

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          Most cited references19

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          Prevalence of diagnosed atrial fibrillation in adults: national implications for rhythm management and stroke prevention: the AnTicoagulation and Risk Factors in Atrial Fibrillation (ATRIA) Study.

          Atrial fibrillation is the most common arrhythmia in elderly persons and a potent risk factor for stroke. However, recent prevalence and projected future numbers of persons with atrial fibrillation are not well described. To estimate prevalence of atrial fibrillation and US national projections of the numbers of persons with atrial fibrillation through the year 2050. Cross-sectional study of adults aged 20 years or older who were enrolled in a large health maintenance organization in California and who had atrial fibrillation diagnosed between July 1, 1996, and December 31, 1997. Prevalence of atrial fibrillation in the study population of 1.89 million; projected number of persons in the United States with atrial fibrillation between 1995-2050. A total of 17 974 adults with diagnosed atrial fibrillation were identified during the study period; 45% were aged 75 years or older. The prevalence of atrial fibrillation was 0.95% (95% confidence interval, 0.94%-0.96%). Atrial fibrillation was more common in men than in women (1.1% vs 0.8%; P<.001). Prevalence increased from 0.1% among adults younger than 55 years to 9.0% in persons aged 80 years or older. Among persons aged 50 years or older, prevalence of atrial fibrillation was higher in whites than in blacks (2.2% vs 1.5%; P<.001). We estimate approximately 2.3 million US adults currently have atrial fibrillation. We project that this will increase to more than 5.6 million (lower bound, 5.0; upper bound, 6.3) by the year 2050, with more than 50% of affected individuals aged 80 years or older. Our study confirms that atrial fibrillation is common among older adults and provides a contemporary basis for estimates of prevalence in the United States. The number of patients with atrial fibrillation is likely to increase 2.5-fold during the next 50 years, reflecting the growing proportion of elderly individuals. Coordinated efforts are needed to face the increasing challenge of optimal stroke prevention and rhythm management in patients with atrial fibrillation.
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            The distributed lag between air pollution and daily deaths.

            Many studies have reported associations between air pollution and daily deaths. Those studies have not consistently specified the lag between exposure and response, although most have found associations that persisted for more than 1 day. A systematic approach to specifying the lag association would allow better comparison across sites and give insight into the nature of the relation. To examine this question, I fit unconstrained and constrained distributed lag relations to the association between daily deaths of persons 65 years of age and older with PM10 in 10 U.S. cities (New Haven, Birmingham, Pittsburgh, Canton, Detroit, Chicago, Minneapolis, Colorado Springs, Spokane, and Seattle) that had daily monitoring for PM10. After control for temperature, humidity, barometric pressure, day of the week, and seasonal patterns, I found evidence in each city that the effect of a single day's exposure to PM10 was manifested across several days. Averaging over the 10 cities, the overall effect of an increase in exposure of 10 microg/m3 on a single day was a 1.4% increase in deaths (95% confidence intervals (CI) = 1.15-1.68) using a quadratic distributed lag model, and a 1.3% increase (95% CI = 1.04-1.56) using an unconstrained distributed lag model. In contrast, constraining the model to assume the effect all occurs in one day resulted in an estimate of only 0.65% (95% CI = 0.49-0.81), indicating that this constraint leads to a substantial underestimate of effect. Combining the estimated effect at each day's lag across the 10 cities showed that the effect was spread over several days and did not reach zero until 5 days after the exposure. Given the distribution of sensitivities likely in the general population, this result is biologically plausible. I also found a protective effect of barometric pressure in all 10 locations.
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              Triggering of sudden death from cardiac causes by vigorous exertion.

              Retrospective and cross-sectional data suggest that vigorous exertion can trigger cardiac arrest or sudden death and that habitual exercise may diminish this risk. However, the role of physical activity in precipitating or preventing sudden death has not been assessed prospectively in a large number of subjects. We used a prospective, nested case-crossover design within the Physicians' Health Study to compare the risk of sudden death during and up to 30 minutes after an episode of vigorous exertion with that during periods of lighter exertion or none. We then evaluated whether habitual vigorous exercise modified the risk of sudden death that was associated with vigorous exertion. In addition, the relation of vigorous exercise to the overall risk of sudden death and nonsudden death from coronary heart disease was assessed. During 12 years of follow-up, 122 sudden deaths were confirmed among the 21,481 male physicians who were initially free of self-reported cardiovascular disease and who provided information on their habitual level of exercise at base line. The relative risk of-sudden death during and up to 30 minutes after vigorous exertion was 16.9 (95 percent confidence interval, 10.5 to 27.0; P<0.001). However, the absolute risk of sudden death during any particular episode of vigorous exertion was extremely low (1 sudden death per 1.51 million episodes of exertion). Habitual vigorous exercise attenuated the relative risk of sudden death that was associated with an episode of vigorous exertion (P value for trend=0.006). The base-line level of exercise was not associated with the overall risk of subsequent sudden death. These prospective data from a study of U.S. male physicians suggest that habitual vigorous exercise diminishes the risk of sudden death during vigorous exertion.
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                Author and article information

                Journal
                Environ Health Perspect
                Environmental Health Perspectives
                National Institute of Environmental Health Sciences
                0091-6765
                January 2006
                20 September 2005
                : 114
                : 1
                : 120-123
                Affiliations
                [1 ]Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, USA
                [2 ]Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA
                [3 ]Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts, USA
                [4 ]New England Medical Center, Tufts University, Boston, Massachusetts, USA
                [5 ]Channing Laboratory, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA
                [6 ]Department of Biostatistics, Harvard School of Public Health, Boston, Massachusetts, USA
                [7 ]Department of Biostatistical Science, Dana-Farber Cancer Institute, Boston, Massachusetts, USA
                Author notes
                Address correspondence to D.W. Dockery, Harvard School of Public Health, Department of Environmental Health, Landmark Suite 415 West; 401 Park Dr., Boston, MA 02115 USA. Telephone: (617) 384-8741. Fax: (617) 384-8745. E-mail: ddockery@hsph.harvard.edu

                The authors declare they have no competing financial interests.

                Article
                ehp0114-000120
                10.1289/ehp.8371
                1332666
                16393668
                10363c9a-0cdb-4d48-abb9-ab248a50d816
                This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original DOI.
                History
                : 1 June 2005
                : 19 September 2005
                Categories
                Research
                Environmental Medicine

                Public health
                air pollution,epidemiology,arrhythmias,case—crossover,ozone,fibrillation
                Public health
                air pollution, epidemiology, arrhythmias, case—crossover, ozone, fibrillation

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