AimsAircraft noise disturbs sleep, and long-term exposure has been shown to be associated with increases in the prevalence of hypertension and an overall increased risk for myocardial infarction. The exact mechanisms responsible for these cardiovascular effects remain unclear.Methods and resultsWe performed a blinded field study in 75 healthy volunteers (mean age 26 years), who were exposed at home, in random order, to one control pattern (no noise) and two different noise scenarios [30 or 60 aircraft noise events per night with an average maximum sound pressure level (SPL) of 60 dB(A)] for one night each. We performed polygraphy during each study night. Noise caused a worsening in sleep quality (P < 0.0001). Noise60, corresponding to equivalent continuous SPLs of 46.3 dB (Leq) and representing environmental noise levels associated with increased cardiovascular events, caused a blunting in FMD (P = 0.016). As well, although a direct comparison among the FMD values in the noise groups (control: 10.4 ± 3.8%; Noise30: 9.7 ± 4.1%; Noise60: 9.5 ± 4.3%, P = 0.052) did not reach significance, a monotone dose-dependent effect of noise level on FMD was shown (P = 0.020). Finally, there was a priming effect of noise, i.e. the blunting in FMD was particularly evident when subjects were exposed first to 30 and then to 60 noise events (P = 0.006). Noise-induced endothelial dysfunction (ED) was reversed by the administration of Vitamin C (P = 0.0171). Morning adrenaline concentration increased from 28.3 ± 10.9 to 33.2 ± 16.6 and 34.1 ± 19.3 ng/L (P = 0.0099). Pulse transit time, reflecting arterial stiffness, was also shorter after exposure to noise (P = 0.003).ConclusionIn healthy adults, acute nighttime aircraft noise exposure dose-dependently impairs endothelial function and stimulates adrenaline release. Noise-induced ED may be in part due to increased production in reactive oxygen species and may thus be one mechanism contributing to the observed association of chronic noise exposure with cardiovascular disease.

This study adds some important considerations for the use of pressure algometers. It was found that during pressure pain thresholds readings distinct peak pressure profiles could arise, which may influence the perception of pain. Peak pressure could be another contributing factor, which may explain some of the high variability in pressure pain readings.

Pain thresholds are widely used in behavioral research, but unlike other pain modalities, a standardized assessment of pressure pain remains a challenge. In this research, we describe the application of an automatic pressure algometer with a linear increase in force. Ergonomically designed fixation devices were developed to increase the accuracy and to shorten the time of each measurement. Ten healthy volunteers were included in a pilot study to test the algometry method. Pressure pain thresholds (PPTs) were investigated over 2 experimental days in three nonconsecutive runs at 29 measurement sites. During the experiment, subjects reported their subjective sleepiness, level of state-anxiety, psychological status and the perceived pain intensity of each measurement. Pain intensity ratings indicate that instructions were followed. State-anxiety and subjective sleepiness levels were low throughout the experiment. The method has proven to be suitable for standardized PPT measurements across the body in an ergonomic, safe, and user-friendly fashion.

Self-assessment of olfaction is only a reliable indicator in smell-impaired patients, not in healthy controls. For an accurate assessment of olfaction, reliable, standardised tests are needed.

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The CST is an easy-to-handle reliable tool to investigate retronasal olfaction suited for clinical determination of normosmia, hyposmia, and ansomia. In addition, it can be used for investigation where self-application is necessary such as in large survey studies.

This study gives further evidence that even mixtures of organic solvents at concentrations below the threshold-limit values may impair color vision.

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