The Relationship between Ambient Air Pollution and Heart Rate Variability Differs for Individuals with Heart and Pulmonary Disease

• Published in: Environmental health perspectives 2006-04, Vol.114 (4), p.560-566
• Main Authors: Wheeler, Amanda, Zanobetti, Antonella, Gold, Diane R., Schwartz, Joel, Stone, Peter, Suh, Helen H.
• Format: Article
• Language: English
• Subjects: Adrenergic beta-Antagonists - therapeutic use; Air Pollution; Bronchodilator Agents - therapeutic use; Chronic obstructive pulmonary disease; Disease models; Environmental health; Environmental pollution; Forced Expiratory Volume; Heart attack; Heart Rate; Humans; Lung diseases; Lung diseases, Obstructive; Medications; Myocardial Infarction - drug therapy; Myocardial Infarction - physiopathology; Particulate pollution; Pulmonary Disease, Chronic Obstructive - drug therapy; Pulmonary Disease, Chronic Obstructive - physiopathology; Pulmonary functions; Submarine boats
• ISSN: 0091-6765; 1552-9924
• DOI: 10.1289/ehp.8337

Associations between concentrations of ambient fine particles [$paniculate matter < 2.5 \mu m$ aero-dynamic diameter (PM2.5)] and heart rate variability (HRV) have differed by study population. We examined the effects of ambient pollution on HRV for 18 individuals with chronic obstructive pulmonary disease (COPD) and 12 individuals with recent myocardial infarction (MI) living in Atlanta, Georgia. HRV, baseline pulmonary function, and medication data were collected for each participant on 7 days in fall 1999 and/or spring 2000. Hourly ambient pollution concentrations were obtained from monitoring sites in Atlanta. The association between ambient pollution and HRV was examined using linear mixed-effect models. Ambient pollution had opposing effects on HRV in our COPD and MI participants, resulting in no significant effect of ambient pollution on HRV in the entire population for 1-, 4-, or 24-hr moving averages. For individuals with COPD, interquartile range (IQR) increases in 4-hr ambient PM2.5 ($11.65 \mu g/m^3$) and nitrogen dioxide (11.97 ppb) were associated with 8.3% [95% confidence interval (CI), 1.7-15.3%] and 7.7% (95% CI, 0.1-15.9%) increase in the SD of normal R-R intervals (SDNN), respectively. For individuals with MI, IQR increases in 4-hr PM2.5 ($8.54 \mu g/m^3$) and NO2 (9.25 ppb) were associated with a nonsignificant 2.9% (95% CI, -7.8 to 2.3) and significant 12.1 (95% CI, -19.5 to -4.0) decrease in SDNN. Beta-blocker and bronchodilator intake and baseline forced expiratory volume in 1 sec modified the PM-SDNN association significantly, with effects consistent with those by disease group. Results indicate heterogeneity in the autonomic response to air pollution due to differences in baseline health, with significant associations for ambient NO2 suggesting an important role for traffic-related pollution.