Acute effects of personal day-time noise exposure on heart rate variability

Background: Epidemiological studies have demonstrated that exposure to chronic aircraft and road traffic noise is associated with cardiovascular risk including endpoints like blood pressure, hypertension and ischemic heart disease. However, only little is known about acute effects of personal noise exposure. Objective: We examined the association of personal day-time noise exposure and heart rate variability (HRV) as a marker for cardiac rhythm. Methods: Between March 2007 and December 2008 a panel study consisting of individuals having type 2 diabetes or impaired glucose tolerance or being healthy was conducted in Augsburg, Germany. Each of the 110 participants had up to four repeated electrocardiogram (ECG) recordings. In total, 325 ECGs with an average measurement duration of 5.9 hours were available, 5-min averages of heart rate (HR), root-mean square of successive differences (RMSSD), standard deviation of NN-intervals (SDNN), high frequency (HF) and low frequency (LF) power were determined. Participants were equipped with a noise dosimeter which measured the personal noise exposure as A-weighted equivalent continuous sound pressure levels (Leq). 5-min averages of Leq were calculated. Associations were analysed using additive mixed models adjusting for personal measurements of particle number count and time-trend variables. Results: The median of 5-min averages of Leq was 71 dB(A). An increase of 3 dB(A) in noise exposure was associated with a concurrent increase in HR (percent change of mean: 0.56%, 95%-confidence interval: [0.52; 0.61%]) and with a concurrent decrease in RMSSD (–0.38% [–0.59; –0.17%]), HF power (–5.6% [–6.3; –5.0%]) and LF power (–3.0% [–3.6; –2.3%]). These associations persisted up to 15–20 minutes. SDNN increased concurrent to the noise exposure (1.5% [1.3; 1.7%]), but decreased with a delay of five up to 60 minutes. Conclusion: Our results suggest an association between personal day-time noise exposure and acute changes in HRV, a possible precursor of cardiac adverse events.