Grande N R, Aguas A P, De Sousa Pereira A, Monteiro E, Castelo Branco N A
Abel Salazar Institute for the Biomedical Sciences, University of Porto, Portugal.
Aviat Space Environ Med. 1999 Mar;70(3 Pt 2):A70-7.
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.
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.
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.
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.
在长期（≥10年）暴露于大压力振幅和低频（LPALF）噪声（≥90分贝，≤500赫兹）的非吸烟航空技术人员中已发现气道气流受限。考虑到这种工作环境，鉴于可能存在但实际并非一定存在的燃油废气和蒸汽，预计会出现某种肺损伤。在对暴露于LPALF噪声环境的大鼠胸膜进行形态功能研究的过程中，发现了严重的胸膜下纤维化。因此，我们决定研究这些暴露于噪声的啮齿动物的深部肺实质。
一组5只Wistar大鼠累计暴露于LPALF噪声4000小时，另一组5只大鼠累计暴露5000小时。对照组由10只年龄匹配的Wistar大鼠组成，它们在相同条件下饲养，但处于安静环境中。处死大鼠后提取肺实质碎片，进行光镜、扫描电镜和透射电镜检查。
发现深部肺实质有局灶性间质纤维化以及小支气管纤毛的变化。在微绒毛异常的部位，刷细胞数量增加。观察到肺泡II型上皮细胞明显增多，有大量、大且融合的板层小体。
与对照组观察到的正常肺形态相比，暴露大鼠的细胞外基质和上皮细胞出现了变化。暴露于噪声的大鼠环境中不存在燃油废气、蒸汽或灰尘。这些结果与在暴露于噪声的人类中发现的呼吸障碍相关，强烈表明LPALF噪声是肺纤维化的一个致病因素。
