Recent and long-term occupational noise exposure and salivary cortisol level
Research output: Contribution to journal › Journal article › Research › peer-review
Environmental and occupational noise exposure have been related to increased risk of cardiovascular disease, hypothetically mediated by stress-activation of the hypothalamic-pituitary-adrenal (HPA) axis. The objective of this study was to investigate the relation between recent and long-term occupational noise exposure and cortisol level measured off work to assess a possible sustained HPA-axis effect. We included 501 industrial, finance, and service workers who were followed for 24h during work, leisure, and sleep. Ambient occupational noise exposure levels were recorded every 5s by personal dosimeters and we calculated the full-shift LAEq value and estimated duration and cumulative exposure based on their work histories since 1980. For 332 workers who kept a log-book on the use of hearing protection devices (HPD), we subtracted 10dB from every noise recording obtained during HPD use and estimated the noise level at the ear. Salivary cortisol concentration was measured at 20.00h, the following day at awakening, and 30min after awakening on average 5, 14 and 14.5h after finishing work. The mean ambient noise exposure level was 79.9dB(A) [range: 55.0-98.9] and the mean estimated level at the ear 77.7dB(A) [range: 55.0-94.2]. In linear and mixed regression models that adjusted for age, sex, current smoking, heavy alcohol consumption, personal income, BMI, leisure-time noise exposure level, time since occupational noise exposure ceased, awakening time, and time of saliva sampling, we observed no statistically significant exposure response relation between recent, or long-term ambient occupational noise exposure level and any cortisol parameter off work. This was neither the case for recent noise level at the ear. To conclude, neither recent nor long-term occupational noise exposure levels were associated with increased cortisol level off work. Thus, our results do not indicate that a sustained activation of the HPA axis, as measured by cortisol, is involved in the causal pathway between occupational noise exposure and cardiovascular disease.
|Number of pages||12|
|Publication status||Published - Jan 2014|