Abstract:Environmental tobacco smoke (ETS) has been associated with cardiovascular mortality. Pathophysiologic pathways leading from ETS exposure to cardiopulmonary disease are still being explored. Reduced cardiac autonomic function, as measured by heart rate variability (HRV), has been associated with cardiac vulnerability and may represent an important pathophysiologic mechanism linking ETS and risk of cardiac mortality. In this study we evaluated acute ETS exposure in a commercial airport with changes in HRV in 16 … Show more
“…Previous studies have reported HRV associations with ambient PM air pollution exposure (Gold et al 2000;Liao et al 1999;, occupational PM exposure (Magari et al 2001), and PM exposure from secondhand cigarette smoking in an airport smoking lounge (Pope et al 2001). A previous study that used 24-hr ambulatory ECG monitoring was also conducted along the Wasatch Front in Utah , but it had only seven participants with a total of 39 observations and had air pollution monitoring only for PM ≤ 10 µm in aerodynamic diameter (PM 10 ).…”
Epidemiologic studies report associations between particulate air pollution and cardiopulmonary morbidity and mortality. Although the underlying pathophysiologic mechanisms remain unclear, it has been hypothesized that altered autonomic function and pulmonary/systemic inflammation may play a role. In this study we explored the effects of air pollution on autonomic function measured by changes in heart rate variability (HRV) and blood markers of inflammation in a panel of 88 elderly subjects from three communities along the Wasatch Front in Utah. Subjects participated in multiple sessions of 24-hr ambulatory electrocardiographic monitoring and blood tests. Regression analysis was used to evaluate associations between fine particulate matter [aerodynamic diameter ≤ 2.5 µm (PM 2.5 )] and HRV, C-reactive protein (CRP), blood cell counts, and whole blood viscosity. A 100-µg/m 3 increase in PM 2.5 was associated with approximately a 35 (SE = 8)-msec decline in standard deviation of all normal R-R intervals (SDNN, a measure of overall HRV); a 42 (SE = 11)-msec decline in square root of the mean of the squared differences between adjacent normal R-R intervals (r-MSSD, an estimate of short-term components of HRV); and a 0.81 (SE = 0.17)-mg/dL increase in CRP. The PM 2.5 -HRV associations were reasonably consistent and statistically robust, but the CRP association dropped to 0.19 (SE = 0.10) after excluding the most influential subject. PM 2.5 was not significantly associated with white or red blood cell counts, platelets, or whole-blood viscosity. Most short-term variability in temporal deviations of HRV and CRP was not explained by PM 2.5 ; however, the small statistically significant associations that were observed suggest that exposure to PM 2.5 may be one of multiple factors that influence HRV and CRP.
“…Previous studies have reported HRV associations with ambient PM air pollution exposure (Gold et al 2000;Liao et al 1999;, occupational PM exposure (Magari et al 2001), and PM exposure from secondhand cigarette smoking in an airport smoking lounge (Pope et al 2001). A previous study that used 24-hr ambulatory ECG monitoring was also conducted along the Wasatch Front in Utah , but it had only seven participants with a total of 39 observations and had air pollution monitoring only for PM ≤ 10 µm in aerodynamic diameter (PM 10 ).…”
Epidemiologic studies report associations between particulate air pollution and cardiopulmonary morbidity and mortality. Although the underlying pathophysiologic mechanisms remain unclear, it has been hypothesized that altered autonomic function and pulmonary/systemic inflammation may play a role. In this study we explored the effects of air pollution on autonomic function measured by changes in heart rate variability (HRV) and blood markers of inflammation in a panel of 88 elderly subjects from three communities along the Wasatch Front in Utah. Subjects participated in multiple sessions of 24-hr ambulatory electrocardiographic monitoring and blood tests. Regression analysis was used to evaluate associations between fine particulate matter [aerodynamic diameter ≤ 2.5 µm (PM 2.5 )] and HRV, C-reactive protein (CRP), blood cell counts, and whole blood viscosity. A 100-µg/m 3 increase in PM 2.5 was associated with approximately a 35 (SE = 8)-msec decline in standard deviation of all normal R-R intervals (SDNN, a measure of overall HRV); a 42 (SE = 11)-msec decline in square root of the mean of the squared differences between adjacent normal R-R intervals (r-MSSD, an estimate of short-term components of HRV); and a 0.81 (SE = 0.17)-mg/dL increase in CRP. The PM 2.5 -HRV associations were reasonably consistent and statistically robust, but the CRP association dropped to 0.19 (SE = 0.10) after excluding the most influential subject. PM 2.5 was not significantly associated with white or red blood cell counts, platelets, or whole-blood viscosity. Most short-term variability in temporal deviations of HRV and CRP was not explained by PM 2.5 ; however, the small statistically significant associations that were observed suggest that exposure to PM 2.5 may be one of multiple factors that influence HRV and CRP.
“…4,28 Our observations are in agreement with the findings of Pope, who described a short-term decrease in all HRV domains after acute exposure to ETS, but with relatively high standard errors in HF. 12 LF, which is considered to represent both sympathetic and parasympathetic activities, 29 was lower in subjects with higher ETS exposure. We also observed ETS-associated increases in heart rate and, more weakly, in DBP, consistent with increases in sympathetic stimulation.…”
Section: Discussionmentioning
confidence: 94%
“…Short-term effects have been described by Pope, who found a reduction in HRV in 16 never smoking subjects equipped with Holter monitors, who were moved from the non-smoking section of an airport to the smoking lounge. 12 Reports from the 1991 SAPALDIA (Swiss Cohort Study on Air Pollution and Lung Diseases in Adults) study 13 describe the effects of ETS on respiratory symptoms in never smokers 14 and on lung function in asthmatics. 15 In the follow-up study (SAPALDIA 2), we also show a higher probability of the development of asthma in subjects exposed to ETS.…”
Background Exposure to environmental tobacco smoke (ETS) has been shown to increase the risk for cardiovascular diseases and death, and autonomic dysfunction (specifically, reduced heart rate variability (HRV)) is a predictor of increased cardiac risk. This study tests the hypothesis that ETS exposure reduces HRV in the general population and discusses possible pathways.
Methods
This cross-sectional study was conducted between 2001 and 2003 and is part of the SAPALDIA (Swiss CohortStudy on Air Pollution and Lung Diseases in Adults) study. The analysis included 1218 randomly selected non-smokers aged 50 and above who participated in 24-h electrocardiogram recordings. Other examinations included an interview, investigating health status (especially respiratory and cardiovascular health and health relevant behaviours and exposure to ETS) and measurements of blood pressure, body height and weight.
ResultsSubjects exposed to ETS at home or at work for more than 2 h/day had a difference of À15% in total power (95%CI: À26 to À3%), low frequency power (À28 to À1%), low/high frequency ratio (À26 to À3%) and À18% (À29 to À4%) in ultralow frequency power of HRV compared with subjects not exposed to ETS at home or work. We also found a 2.7% (À0.01 to 5.34%) higher heart rate during the recording in exposed subjects.Conclusions Exposure to ETS at home and work is associated with lower HRV and with higher heart rate in an ageing population. Our findings suggest that exposure to ETS increases cardiac risk through disturbances in the autonomic nervous system.
“…HRV measurement was performed between 0600 and 1300 at room temperature between 201C and 301C using a twochannel (five-lead) electrocardiogram (ECG) monitor (Trillium 3000; Forest Medical, East Syracuse, NY, USA) according to published protocol (Pope et al, 2001). The ECG was recorded for approximately 7 min with the subject seated after a 5-min rest (sampling rate of 256 Hz per channel).…”
Although many studies report that exposure to air pollution harms health, few have examined associations between pollution sources and health outcomes. We hypothesized that pollution originating in different locations has different associations with heart rate variability (HRV) among 497 men from the Normative Aging Study in Boston, Massachusetts. We identified the paths that air masses traveled ('back-trajectories') before arriving in Boston on the days the men were examined. Next, we classified these trajectories into six clusters. We examined whether the association of measured air pollutants with HRV (standard deviation of normal-to-normal intervals, high-frequency power (HF) and low-frequency power (LF), and LF/HF ratio) differed by cluster. We also examined whether the clusters alone (not considering air pollution measurements) showed different associations with HRV. The effects of black carbon (BC) on all HRV measures were strongest on days with southwest trajectories. Subjects who were examined on days where air parcels came from west had the strongest associations with ozone. All particle pollutants (particulate matter o2.5 mm in aerodynamic diameter (PM 2.5 ), BC, and sulfates) were associated with increased LF/HF ratio on days with relatively short trajectories, which are related to local, slow-moving air masses. We also observed significant increases in LF/HF in days where air came from the northwest and west, compared to north trajectory days. Health effects associated with exposure to air pollution can be evaluated using pollutant concentrations as well as aspects of the pollution mixture captured by identifying locations where air masses originate. Independent effects of both these indicators of pollution exposure were seen on cardiac autonomic function.
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