Erica D Walker1, Anthony Brammer2, Martin G Cherniack2, Francine Laden1, Jennifer M Cavallari3. 1. Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA. 2. Department of Medicine, UConn Health, 263 Farmington Avenue, Farmington, CT 06030, USA. 3. Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA; Department of Community Medicine, UConn Health, 263 Farmington Avenue, Outpatient Pavilion, S7313, Farmington, CT 06030, USA. Electronic address: cavallari@uchc.edu.
Abstract
BACKGROUND: While previous epidemiological studies report adverse effects of long-term noise exposure on cardiovascular health, the mechanisms responsible for these effects are unclear. We sought to elucidate the cardiovascular and stress response to short-term, low (31.5-125Hz) and high (500-2000Hz) frequency noise exposures. METHODS: Healthy male (n=10) participants were monitored on multiple visits during no noise, low- or high-frequency noise exposure scenarios lasting 40min. Participants were fitted with an ambulatory electrocardiogram (ECG) and blood pressure measures and saliva samples were taken before, during and after noise exposures. ECGs were processed for measures of heart rate variability (HRV): high-frequency power (HF), low-frequency power (LF), the root of the mean squared difference between adjacent normal heart beats (N-N) intervals (RMSSD), and the standard deviation of N-N intervals (SDNN). Systolic blood pressure (SBP), diastolic blood pressure (DPB), and pulse were reported and saliva was analyzed for salivary cortisol and amylase. Multivariate mixed-effects linear regression models adjusted for age were used to identify statistically significant difference in outcomes by no noise, during noise or after noise exposure periods and whether this differed by noise frequency. RESULTS: A total of 658, 205, and 122, HRV, saliva, and blood pressure measurements were performed over 41 person days. Reductions in HRV (LF and RMSSD) were observed during noise exposure (a reduction of 19% (-35,-3.5) and 9.1% (-17,-1.1), respectively). After adjusting for noise frequency, during low frequency noise exposure, HF, LF, and SDNN were reduced (a reduction of 32% (-57,-6.2), 34% (-52,-15), and 16% (-26,-6.1), respectively) and during high frequency noise exposure, a 21% (-39,-2.3) reduction in LF, as compared to during no noise exposure, was found. No significant (p<0.05) changes in blood pressure, salivary cortisol, or amylase were observed. CONCLUSIONS: These results suggest that exposure to noise, and in particular, to low-frequency noise, negatively impacts HRV. The frequencies of noise should be considered when evaluating the cardiovascular health impacts of exposure.
BACKGROUND: While previous epidemiological studies report adverse effects of long-term noise exposure on cardiovascular health, the mechanisms responsible for these effects are unclear. We sought to elucidate the cardiovascular and stress response to short-term, low (31.5-125Hz) and high (500-2000Hz) frequency noise exposures. METHODS: Healthy male (n=10) participants were monitored on multiple visits during no noise, low- or high-frequency noise exposure scenarios lasting 40min. Participants were fitted with an ambulatory electrocardiogram (ECG) and blood pressure measures and saliva samples were taken before, during and after noise exposures. ECGs were processed for measures of heart rate variability (HRV): high-frequency power (HF), low-frequency power (LF), the root of the mean squared difference between adjacent normal heart beats (N-N) intervals (RMSSD), and the standard deviation of N-N intervals (SDNN). Systolic blood pressure (SBP), diastolic blood pressure (DPB), and pulse were reported and saliva was analyzed for salivary cortisol and amylase. Multivariate mixed-effects linear regression models adjusted for age were used to identify statistically significant difference in outcomes by no noise, during noise or after noise exposure periods and whether this differed by noise frequency. RESULTS: A total of 658, 205, and 122, HRV, saliva, and blood pressure measurements were performed over 41 person days. Reductions in HRV (LF and RMSSD) were observed during noise exposure (a reduction of 19% (-35,-3.5) and 9.1% (-17,-1.1), respectively). After adjusting for noise frequency, during low frequency noise exposure, HF, LF, and SDNN were reduced (a reduction of 32% (-57,-6.2), 34% (-52,-15), and 16% (-26,-6.1), respectively) and during high frequency noise exposure, a 21% (-39,-2.3) reduction in LF, as compared to during no noise exposure, was found. No significant (p<0.05) changes in blood pressure, salivary cortisol, or amylase were observed. CONCLUSIONS: These results suggest that exposure to noise, and in particular, to low-frequency noise, negatively impacts HRV. The frequencies of noise should be considered when evaluating the cardiovascular health impacts of exposure.
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