Short-term effects of nocturnal transportation noise on cardio-metabolic outcomes and its association to sleep

Transportation noise is one of the most important environmental risk factors for cardio-metabolic diseases. It is assumed that short-term noise exposure activates a physiological stress response, which in a chronic state can cascade to long-term critical health problems. Sleep disturbances are regarded as the main mediator of transportation noise induced cardio-metabolic diseases. However, no study so far investigated short-term effects of nocturnal transportation noise exposure on glucose regulation and stress markers in association with alterations in sleep macro- and microstructure. This thesis aimed at investigating the following main questions: does short-term nocturnal transportation noise exposure impair glucose regulation and activate stress responses, and are they both related to sleep changes? Do individual covariates such as age and sex modulate the observed noise effects?
Twenty-six (12 women) young (19-33 years) and 16 (8 women) older (52-70 years) volunteers participated in a six day controlled laboratory study. The experiment started and ended respectively with a noise-free baseline and a noise-free recovery night; in-between four different transportation noise scenarios (low/medium/high intermittent road or rail scenarios with an identical equivalent continuous sound level of 45dB) were presented in a randomized order to the volunteers. Sleep was recorded polysomnographically, glucose tolerance and insulin sensitivity were assessed during an oral glucose tolerance test (OGTT) in the morning of the baseline, the last noise night and the recovery night, nocturnal catecholamine was assessed in the urine, daytime cortisol in the saliva and morning inflammatory markers in the fasting blood samples of the OGTT. Blood pressure as well as heart rate variability (HRV) and autonomic arousals were also recorded during the six experimental nights.
Sleep macrostructure and the number of cortical arousals were not significantly altered by nocturnal transportation noise exposure. However, cumulative autonomic arousals duration increased during the highly intermittent road noise scenario night for the young group and during the highly intermittent railway noise scenario night for the entire experimental group compared to baseline night. Four nights of nocturnal transportation noise exposure reduced glucose tolerance and insulin sensitivity in both age groups. Moreover, the reduction in glucose tolerance was associated with the increase in cumulative autonomic arousals duration. Additionally, highly intermittent noise had a stronger deleterious effect on glucose regulation than lower intermittent noise. Highly intermittent road noise increased next evening cortisol levels only in the young subgroup. This increase was associated with the increase in cumulative autonomic arousal duration during the previous sleep episode. Nocturnal blood pressure, HRV spectral analysis and catecholamine as well as morning inflammatory markers were not significantly changed by the noise exposure.
Taken together, even if the effect observed on glucose regulation was not clinically significant, these results underline the harmful effect of nocturnal transportation noise on subcortical activation during sleep and its repercussions on the stress and metabolic system. In a chronic state these effects may lead on long-term to cardio-metabolic diseases.