Biomedical subjects

M Alves-Pereira

Publications and source records attributed to M Alves-Pereira.

3 recordsLinked to original sources

PubMed1999

Noise-induced extra-aural pathology: a review and commentary.

The focus of this review paper will be the effects of acoustic phenomenon (noise), characterized by large pressure amplitude (> or =90 dB) and low frequency (< or =500 Hz) (LPALF) on humans and animal models. Current concepts imply the assumption that such LPALF noise impinges only on, or through, the somatic medium of the auditory system. As a consequence of this assumption, the effect of noise on humans is only regulated for purposes of hearing conservation. Guidelines and regulations governing occupational noise assessments are biased toward the subjective human perception of sound. The author will not make the assumption that airborne acoustic phenomena impacts only on the auditory system, and will present a literature review providing evidence for such position. The purpose of this review paper is to defend the existence of extra-aural, noise-induced pathology, particularly the vibroacoustic disease; and to advance the recognition that the respiratory tract could very well be a target organ of this environmental stressor.

Animals↗

PubMed1999

Vibroacoustic disease: some forensic aspects.

BACKGROUND: Vibroacoustic disease (VAD) is an insidious environmental entity caused by occupational exposure to large pressure amplitude and low frequency (LPALF) noise (> or = 90 dB SPL, < or = 500 Hz). Significant disabilities may result, and issues of worker's compensation should be openly discussed and settled. Toward this goal, a rigorous review of all available information on this disease was undertaken in order to document the need to define industrial exposure standards, and to settle on the diagnostic procedures that will help distinguish the VAD from other, similar conditions. METHODS: We reviewed the medical files of 236 male Caucasians employed as aircraft technicians who had been diagnosed with VAD and monitored for at least 15 yr. The natural history of the disorder was studied in detail, emphasizing the clinical diagnostic criteria and the outcome of disabilities. RESULTS: Among the 236 cases, 172 (73%) were disabled after an average of 24 yr (SD = 6.9) of occupational exposure. The primary categories of disabilities were neurological (81, 34%), malignant (28, 11.9%), psychiatric (23, 9.7%), cardiovascular (16, 6.8%), and osteoarticular (14, 5.9%). After the onset of industrial exposure to LPALF noise, the minimum time for these disabilities to manifest themselves was 16 yr. The most serious complication was multiple attempted suicide. Such attempts were fortunately rare (5, 2.1%) and successful only once. Echocardiograms showed characteristic changes in pericardial structures, involving proliferation of the extracellular matrix, lack of cilia and five pericardial layers instead of three. This has been studied in pericardial biopsy material obtained during coronary bypass surgery for coronary insufficiency (six cases), and by autopsy (four cases). DISCUSSION: These findings appear to be pathognomonic for the VAD, and the echocardiogram has been confirmed as a fundamental diagnostic tool. The degree of disability due to VAD can be determined from Portuguese national disability tables, which cover almost all of the VAD-induced disabilities. However, these tables do not specify LPALF noise as an occupational hazard, rendering them inapplicable to VAD patients. Also, suicide, a most serious psychiatric consequence, is not covered by these tables. Such situations highlight the absolute necessity to recognize LPALF noise as the cause of VAD, and as an industrial hazard.

Adult↗

PubMedDate not supplied

Vibroacoustic disease.

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, LFN-induced pathology, and related issues. In 1987, the first autopsy of a deceased VAD patient was performed. The extent of LFN induced 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.

Aircraft↗