Objectives Short-term elevation of ambient particulate air pollution has been associated with autonomic dysfunction and increased systemic inflammation, but the interconnections between these pathways are not well understood. We examined the association between inflammation and autonomic dysfunction and effect modification of inflammation on the association between air pollution and heart rate variability (HRV) in elderly subjects.
Methods 25 elderly subjects in Steubenville, Ohio, were followed up to 24 times with repeated 30-min ECG Holter monitoring (545 observations). C-reactive protein (CRP), fibrinogen, interleukin-6 (IL-6), soluble inter-cellular adhesion molecule 1 (sICAM-1), and white blood cell and platelet counts were measured in peripheral blood samples collected in the first month of the study. Increased systemic inflammation was defined for subjects within the upper 20% of the distribution for each marker. A central ambient monitoring station provided daily fine particle (PM2.5) and sulphate (SO42−) data. Linear mixed models were used to identify associations between inflammatory markers and HRV and to assess effect modification of the association between air pollution and HRV due to inflammatory status.
Results A 5.8 mg/l elevation in CRP was associated with decreases of between −8% and –33% for time and frequency domain HRV outcomes. A 5.1 μg/m3 increase in SO42− on the day before the health assessment was associated with a decrease of −6.7% in the SD of normal RR intervals (SDNN) (95% CI −11.8% to −1.3%) in subjects with elevated CRP, but not in subjects with lower CRP (p value interaction=0.04), with similar findings for PM2.5.
Conclusions Increased systemic inflammation is associated with autonomic dysfunction in the elderly. Air pollution effects on reduced SDNN are stronger in subjects with elevated systemic inflammation.
- Systemic inflammation
- inflammatory markers
- air pollution
- heart rate variability
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Any opinions, findings, conclusions, or recommendations expressed herein are those of the authors and do not necessarily reflect the views of the U.S. Department of Energy.
Funding This work is supported by funding from the National Institute of Environmental Health Sciences (ES-09825 and ES-00002), the U.S. Environmental Protection Agency (R826780-01-0, R827353-01-0), the Ohio Coal Development Office (CDO/D-98-2) and the U.S. Department of Energy's National Energy Technology Laboratory Award No. DE-FC26-00NT40771.
Competing interests None.
Patient consent Obtained.
Ethics approval This study was conducted with the approval of the Human Subjects Committees of the Brigham and Women's Hospital and the Harvard School of Public Health.
Provenance and peer review Not commissioned; externally peer reviewed.
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