Background: Airway flow limitation is has been identified in nonsmoker aeronautical technicians who are exposed to long term (> or =10 yr) large pressure amplitude and low frequency (LPALF) noise (> or =90 dB, < or =500 Hz). Considering this work environment, some kind of pulmonary impairment would be expected, given the probable, but not de facto, existence of fuel exhausts and vapors. In the course of morphofunctional studies of rat pleura exposed to LPALF noise environments, intense subpleural fibrosis was identified. Thus, we decided to study the deep lung parenchyma of these noise-exposed rodents.
Methods: One group of five Wistar rats was exposed to LPALF noise for a cumulative 4000 h, and another of five rats were exposed for a cumulative of 5000 h. The control group consisted of 10, age-matched, Wistar rats that were kept in the same conditions, but in silence. Fragments of lung parenchyma were extracted after sacrifice, and processed for light microscopy, and for scanning and transmission electron microscopy.
Results: Focal interstitial fibrosis of the deep lung parenchyma were identified as well as changes in the small bronchial cilia. The amount of brush cells was increased in the locations where microvilli were abnormal. An obvious increase of alveolar type II pneumocyte cells was observed with numerous, large and confluent lamellar bodies.
Discussion: In contrast with the normal lung morphology observed in the control group, changes in the extra-cellular matrix and epithelial cells were identified in the exposed rats. No fuel exhaust, vapors or dust were present in the environment of the noise-exposed rats. These results, linked with the respiratory disorders identified in noise-exposed humans, strongly suggest that LPALF noise is an agent of pulmonary fibrosis.