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Abstract: Poster Presentations |

Morphological Changes in the Respiratory System of Vibroacoustic Disease Patients FREE TO VIEW

Carla P. Mendes, MD; José Reis Ferreira, MD, FCCP; Ana P. Martins, MD; Emanuel Monteiro, BSc; Mariana Alves-Pereira, PhD Candidate; Nuno Castelo Branco, MD
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Portuguese Air Force Hospital, Lisbon, Portugal


Chest


Chest. 2003;124(4_MeetingAbstracts):213S. doi:10.1378/chest.124.4_MeetingAbstracts.213S-a
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Abstract

PURPOSE:  Vibroacoustic disease (VAD) is caused by long-term exposure (years) to low frequency noise (LFN) [≤500 Hz, including infrasound]. In LFN-exposed animal models, the respiratory system was shown to be a target for this acoustic aggressor. Simultaneously, all respiratory tract tumors observed in VAD patients were of a single type of cellularity: squamous cell carcinomas. In this report, fragments of trachea, lung parenchyma and pleura of VAD patients are studied through light and electron microscopy.

METHODS:  All subjects had been previously diagnosed with VAD, 2 non-smokers/7 smokers). With their informed consent, fragments were removed from trachea (biopsy), and lung and pleura (during the surgery for lung carcinomas). Specimens were prepared for light and transmission electron (TEM) microscopy.

RESULTS:  Smokers and non-smokers disclosed very similar images. In the trachea, with light microscopy, all images presented scattered areas with damaged cilia, displastic foci as well as with basal hyperplasia. In TEM, multiple ciliary axonemes are surrounded by a common membrane. Blood and lymphatic vessel walls were thickened. Bronchioli and remaining lung parenchyma exhibit numerous macrophages, some with brown pigment (smokers), and others with tar. Type I pneumocytes are greatly decreased and type II greatly increased. Cells under apoptotic processes were frequent. All cell structures seem to be under the same process of death, in contrast with a marked reinforcement of the cytoskeleton and intercellular junctions. Pleural thickeness due to intense proliferation of collagen, as well as interstitial fibrosis foci were observed. Surfactant release from lamellar bodies in hypophase were frequently captured.CONCLUSIONS: The abnormal proliferation of extra-cellular matrices is a response to LFN common to many organs. The reduction in the number of type I pneumocytes and increase in type II is also seen in other pulmonary stress situations. The very frequent images of apoptotic processes and ciliary abnomalities were unexpected and indicate future avenues of research.

CLINICAL IMPLICATIONS:  Lung pathology can be caused by LFN exposure.

DISCLOSURE:  C.P. Mendes, None.

Wednesday, October 29, 2003

12:30 PM - 2:00 PM


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