Home Email this page Print this page Bookmark this page Decrease font size Default font size Increase font size
Noise & Health  
 CURRENT ISSUE    PAST ISSUES    AHEAD OF PRINT    SEARCH   GET E-ALERTS    
 
 Next article
 Previous article
Table of Contents

Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Citation Manager
Access Statistics
Reader Comments
Email Alert *
Add to My List *
 * Requires registration (Free)
 

 Article Access Statistics
    Viewed40058    
    Printed1240    
    Emailed25    
    PDF Downloaded568    
    Comments [Add]    
    Cited by others 27    

Recommend this journal

 

 ARTICLES
Year : 2004  |  Volume : 6  |  Issue : 23  |  Page : 3--20

Vibroacoustic disease


1 Center for Human Performance, Alverca, Portugal
2 New University of Lisbon, Caparica, Portugal

Correspondence Address:
NAA Castelo Branco
Apartado 173, 2616 - Alverca Codex
Portugal
Login to access the Email id

Source of Support: None, Conflict of Interest: None


PMID: 15273020

Rights and PermissionsRights and Permissions

Vibroacoustic disease (VAD) is a whole-body, systemic pathology, characterized by the abnormal proliferation of extra-cellular matrices, and caused by excessive exposure to low frequency noise (LFN). VAD has been observed in LFN-exposed professionals, such as, aircraft technicians, commercial and military pilots and cabin crewmembers, ship machinists, restaurant workers, and disk-jockeys. VAD has also been observed in several populations exposed to environmental LFN. This report summarizes what is known to date on VAD, LFN­induced pathology, and related issues. In 1987, the first autopsy of a deceased VAD patient was performed. The extent of LFN­induced damage was overwhelming, and the information obtained is, still today, guiding many of the associated and ongoing research projects. In 1992, LFN-exposed animal models began to be studied in order to gain a deeper knowledge of how tissues respond to this acoustic stressor. In both human and animal models, LFN exposure causes thickening of cardiovascular structures. Indeed, pericardial thickening with no inflammatory process, and in the absence of diastolic dysfunction, is the hallmark of VAD. Depressions, increased irritability and aggressiveness, a tendency for isolation, and decreased cognitive skills are all part of the clinical picture of VAD. LFN is a demonstrated genotoxic agent, inducing an increased frequency of sister chromatid exchanges in both human and animal models. The occurrence of malignancies among LFN-exposed humans, and of metaplastic and displastic appearances in LFN-exposed animals, clearly corroborates the mutagenic outcome of LFN exposure. The inadequacy of currently established legislation regarding noise assessments is a powerful hindrance to scientific advancement. VAD can never be fully recognized as an occupational and environmental pathology unless the agent of disease - LFN - is acknowledged and properly evaluated. The worldwide suffering of LFN-exposed individuals is staggering and it is unethical to maintain this status quo.






[FULL TEXT] [PDF]*


        
Print this article     Email this article