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398 Occupational noise exposure and the cortisol awakening response: the impact of exposure level and hearing protection
  1. Z A S Stokholm1,
  2. Hansen2,
  3. Bonde3,
  4. Christensen4,
  5. Frederiksen1,
  6. Kristiansen5,
  7. Lund5,
  8. Vestergaard1,
  9. Wetke6,
  10. Kolstad7
  1. 1Aarhus University Hospital, Aarhus C, Denmark
  2. 2Faculty of Health, University of Copenhagen, Copenhagen, Denmark
  3. 3Department of Occupational and Environmental Medicine, Bispebjerg Hospital, Copenhagen, Denmark
  4. 4Department of Internal Medicine and Cardiology A, Aarhus University Hospital, Aarhus, Denmark
  5. 5National Research Centre for the Working Environment, Copenhagen, Denmark
  6. 6Department of Audiology, University of Southern Denmark, Odense, Denmark
  7. 7Department of Occupational Medicine, Aarhus University Hospital, Aarhus, Denmark

Abstract

Objectives Environmental and occupational noise exposure have in some studies been related to increased risk of cardiovascular disease, hypothetically by activation of the hypothalamic-pituitary-adrenal (HPA) axis. The objective of this study was to investigate the relation between occupational noise exposure and the cortisol awakening response (CAR) as a measure of HPA activity.

Methods This cross-sectional study included 398 industrial workers and as a reference 63 financial workers. Noise exposure levels were recorded every 5 seconds at the dominant shoulder by personal dosimeters for 24 hours and we calculated the LAeq value for work hours. For 310 workers who kept a diary on the use of hearing protection devices (HPD), we subtracted 10 dB from every noise recording obtained during HPD use and estimated the LAEq value at the ear. The next day salivary cortisol level was measured at awakening and after 10–60 min and the CAR was defined as the difference between the two.

Results The mean measured noise exposure level was 79.7 dB(A) [range: 55.0–94.2] and the mean estimated level at the ear 77.6 dB(A) [range: 55.0–94.2]. In a linear regression model that adjusted for sex, age, calendar month, income, body mass index, sampling time and duration since occupational noise exposure, we observed no statistically significant exposure response relation between noise exposure level and CAR. This was neither the case in analyses of the effect of noise level estimated at the ear nor in internal analyses restricted to the industrial workers.

Conclusions Neither measured nor estimated occupational noise exposure level was associated with the cortisol awakening response the following day. Thus, we found no indication that the glucocorticoid part of the HPA axis, measured through CAR, is involved in the causal pathway between occupational and environmental noise exposure and cardiovascular disease.

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