[Chronic noise exposure and the cardiovascular system in aircraft pilots]

The aim of this study was to assess whether pilots are exposed to any risk of effects on the cardiovascular apparatus, whether chronic exposure to noise can be a risk factor for this occupation, the importance of intensity, length and type of exposure to noise, and if any relationship exists between audiometric deficits and cardiovascular effects. The study comprised 416 pilots subdivided into two groups according to the different levels of chronic exposure to noise, and a group of 150 control subjects not exposed to noise. The results showed: a) a higher prevalence of hypertension, nearly always diastolic, and of ECG abnormalities in the group of pilots of turboprop aircraft compared to jet plane pilots and to controls (p < 0.005 and p < 0.01 respectively); b) a higher prevalence of orthostatic hypotension in the two groups of pilots than in the controls (p < 0.05); c) a higher prevalence of hypertension with audiometric deficit compared to hypertension without audiometric deficit both in the more heavily and in the less heavily exposed to noise (p < 0.05), and a higher prevalence of hypertension with audiometric deficit in subjects exposed to higher levels of noise compared to hypertension with deficit but in subjects with lower levels of exposure (p < 0.05); d) a higher prevalence of abnormalities of basal, maximum effort and recovery ECG in pilots exposed to higher noise intensity (p < 0.05); e) improved hypertensive response to ergometric test in pilots with basal hypertension; f) subjects with a maximal load up to 120 W belonged prevalently to the group exposed to more intense noise (p < 0.001), while those with maximal load up to 210 W (p < 0.001) belonged to the group exposed to less intense noise. Considering that pilots are comparable for traditional cardiovascular risk factors, including age, both within the group and with the controls, the results confirm 1) that pilots could be exposed to the risk of effects on the cardiovascular apparatus, 2) that noise could be one of the risk factors and that cardiovascular effects could be related to intensity, type and length of exposure, age being the same, 3) that vascular damage is often accompanied by hearing loss even if the response of the auditory apparatus is different from the response of the cardiovascular apparatus, 4) that the postural diminution of arterial blood pressure might be a sign of a cardiovascular effect of noise. Lastly, a higher hypertensive response in hypertensive pilots suggests that basal hypertension is not reversible. Also a longer exposure to noise seems to influence the cardiovascular apparatus, causing a decrease in the response to work loads due to a lower sympathetic adaptability. The altered response of sympathetic activity to the postural modifications in the more exposed subjects and the response to lower work loads in pilots exposed to more intense noise, suggests a hypothesis of catecholamine depletion and alteration of baroceptor sensitivity as a consequence of chronic sympathetic activation due to chronic exposure to noise.