Vibroacoustic Disease Research Articles

TRPV4-induced Neurofilament Injury Contributes to Memory Impairment after High Intensity and Low Frequency Noise Exposures

ObjectiveExposure to high intensity, low frequency noise (HI-LFN) causes vibroacoustic disease (VAD), with memory deficit as a primary non-auditory symptomatic effect of VAD. However, the underlying mechanism of the memory deficit is unknown. This study aimed to characterize potential mechanisms involving morphological changes of neurons and nerve fibers in the hippocampus, after exposure to HI-LFN. MethodsAdult wild-type and transient receptor potential vanilloid subtype 4 knockout (TRPV4-/-) mice were used for construction of the HI-LFN injury model. The new object recognition task and the Morris water maze test were used to measure the memory of these animals. Hemoxylin and eosin and immunofluorescence staining were used to examine morphological changes of the hippocampus after exposure to HI-LFN. ResultsThe expression of TRPV4 was significantly upregulated in the hippocampus after HI-LFN exposure. Furthermore, memory deficits correlated with lower densities of neurons and neurofilament-positive nerve fibers in the cornu ammonis 1 (CA1) and dentate gyrus (DG) hippocampal areas in wild-type mice. However, TRPV4-/- mice showed better performance in memory tests and more integrated neurofilament-positive nerve fibers in the CA1 and DG areas after HI-LFN exposure. ConclusionTRPV4 up-regulation induced neurofilament positive nerve fiber injury in the hippocampus, which was a possible mechanism for memory impairment and cognitive decline resulting from HI-LFN exposure. Together, these results identified a promising therapeutic target for treating cognitive dysfunction in VAD patients.

Audiological, Phonatory and Cardiac Correlates of Individuals Exposed to Low-Frequency Noise or at Risk of Vibroacoustic Disease.

Introduction Low-frequency noise (LFN) is hazardous to hearing. Long-term exposure to LFN may lead to vibroacoustic disease (VAD), which not only affects a specific organ but the physiological function of entire systems, such as the auditory, phonatory, respiratory, and cardiac systems. Moreover, VAD may lead to many psychological problems and hence affect the quality of life. Objective To investigate the adverse effects of LFN on hearing, acoustic and perceptual correlates of the voice, blood pressure, cardiac rate, and anxiety level. Method A total of 20 subjects exposed to LFN and 20 not exposed to LFN were included, and a detailed case history was recorded. The patients were submitted to pure tone audiometry, otoscopic examination, acoustic and perceptual analyses of the voice, maximum phonation time, and an assessment of the s/z ratio. We also assessed blood pressure, and the results of a voice-related quality of life questionnaire and of the Hamilton anxiety rating scale. Results The results indicate that LFN had an adverse impact on the high-frequency threshold. The present study found a significant difference in shimmer and harmonics-to-noise ratio (HNR) values. Few subjects had high blood pressure and showed the sign of anxiety on the Hamilton anxiety rating scale. Conclusion Low-frequency noise has adverse effects on entire systems of the body and causes many psychological issues, which, in turn negatively affect quality of life.

Medical debates and musical interpretations of vibroacoustic disease in Vieques, Puerto Rico

In 2001 the band Cornucopia (Puerto Rican musicians Jorge Castro and Claudio Chea) released an album called "Vibroacústica". The title refers to a disease that allegedly afflicts people who have been exposed to loud noise over long periods of time. The vibrations thicken the walls of the heart, so the theory goes, and damage the immune, gastrointestinal, and neurological systems. This is noise as toxin, entering and sickening the body. The album takes the disease as its point of departure, and using location recordings of the coast of Puerto Rico, analog synthetic manipulations and digital processing, both recreates and protests the noise and its impact on human beings in Vieques, Puerto Rico, which was the target of bombing practice for over sixty years. This paper argues that the album subverts the idea of the preservation of a soundscape and instead reinterprets the sonic violence of occupation with the tweets, chirps and burbles of its soundtracks.

A Review of Wind Turbine-Generated Infrasound: Source, Measurement and Effect on Health

Some people who reside in proximity to wind turbines complain of a range of adverse health impacts. These include tinnitus, raised blood pressure, heart palpitations, tachycardia, stress, anxiety, vertigo, dizziness, nausea, blurred vision, fatigue, cognitive dysfunction, headaches, ear pressure, exacerbated migraine disorders, motion sensitivity, inner ear damage and sleep deprivation. This article begins with a historical review of prognoses such as Vibroacoustic Disease and Wind Turbine Syndrome which were proposed to explain the reported health symptoms and the hypothesised link to the emission of infrasound from wind turbines. A review of noise measurements at wind turbine sites conducted by various investigators shows that the level of infrasound is below the threshold of hearing. Notwithstanding, others postulate that stimulation by infrasound of the otolith organs causes nauseogenic symptoms or that stimulation of the outer hair cells, which are said to be particularly sensitive to infrasound frequencies, explains the symptoms. A review of social surveys is undertaken of self-reported health effects attributable to wind turbine noise, including the effects of sleep disturbance. A description is finally provided of physical exploration studies which subject participants to infrasound and measure their response.

Pathogenetic rationale for the formation of somatic pathology with prolonged exposure to low-frequency noise

Pathological changes in the central nervous, respirator y, digestive systems and blood coagulation of experimental animals and humans as effects of low-frequency noise are analyzed. The mechanisms of direct (as a result of mechanotransduction) and central (due to the stimulation of an extensive receptor field) action of low-frequency noise on the organism are described in more detail. The effect of excessive activation of lipid peroxidation mechanisms as a result of oxidative stress on the initiation of pathological changes in various organs and systems with noise exposure was noted. It is shown that the main target of the action, ultimately, are the membranes of nerve cells. It was found out that one of the effects of low-frequency noise is an increase in the proliferation of extracellular matrix (collagen and elastin) without signs of an inflammatory process leading to an increase in the structural integrity of various organs (pericardium, vessels, lungs, liver). The existence of two clinical notions of the effects of noise exposure «noise disease» (domestic term) or «vibroacoustic disease» (a foreign analogue, more characteristic for low-frequency noise) is shown. The priority role of the central nervous system in the emergence and progression of somatic pathology in «noise» («vibroacoustic») disease is substantiated. The possibility of formation (in addition to neurosensory hearing loss) of nosological forms of encephalopathy, essential hypertension and emphysema in persons professionally and continuously exposed to intense low-frequency noise is shown. The interrelation and interdependence of disturbances in the central nervous, blood circulation and respiratory systems in response to the dysregulating effect of intense acoustic oscillations was revealed. It has been clarified that the unifying pathogenetic link of damages of various organs and systems in response to the action of low-frequency noise is the changes at the microcirculatory level.

Involvement of cannabinoid receptors in infrasonic noise-induced neuronal impairment.

Excessive exposure to infrasound, a kind of low-frequency but high-intensity sound noise generated by heavy transportations and machineries, can cause vibroacoustic disease which is a progressive and systemic disease, and finally results in the dysfunction of central nervous system. Our previous studies have demonstrated that glial cell-mediated inflammation may contribute to infrasound-induced neuronal impairment, but the underlying mechanisms are not fully understood. Here, we show that cannabinoid (CB) receptors may be involved in infrasound-induced neuronal injury. After exposure to infrasound at 16 Hz and 130 dB for 1-14 days, the expression of CB receptors in rat hippocampi was gradually but significantly decreased. Their expression levels reached the minimum after 7- to 14-day exposure during which the maximum number of apoptotic cells was observed in the CA1. 2-Arachidonoylglycerol (2-AG), an endogenous agonist for CB receptors, reduced the number of infrasound-triggered apoptotic cells, which, however, could be further increased by CB receptor antagonist AM251. In animal behavior performance test, 2-AG ameliorated the infrasound-impaired learning and memory abilities of rats, whereas AM251 aggravated the infrasound-impaired learning and memory abilities of rats. Furthermore, the levels of proinflammatory cytokines tumor necrosis factor alpha and interleukin-1β in the CA1 were upregulated after infrasound exposure, which were attenuated by 2-AG but further increased by AM251. Thus, our results provide the first evidence that CB receptors may be involved in infrasound-induced neuronal impairment possibly by affecting the release of proinflammatory cytokines.

Letter to the Editor re: ‘How the factoid of wind turbines causing ‘vibroacoustic disease’ came to be ‘irrefutably demonstrated’

Letter to the Editor re: ‘How the factoid of wind turbines causing ‘vibroacoustic disease’ came to be ‘irrefutably demonstrated’

Epigallocatechin gallate (EGCG) attenuates infrasound-induced neuronal impairment by inhibiting microglia-mediated inflammation

Infrasound, a kind of common environmental noise and a major contributor of vibroacoustic disease, can induce the central nervous system (CNS) damage. However, no relevant anti-infrasound drugs have been reported yet. Our recent studies have shown that infrasound resulted in excessive microglial activation rapidly and sequential inflammation, revealing a potential role of microglia in infrasound-induced CNS damage. Epigallocatechin gallate (EGCG), a major bioactive component in green tea, has the capacity of protecting against various neurodegenerative diseases via an anti-inflammatory mechanism. However, it is still unknown to date whether EGCG acts on infrasound-induced microglial activation and neuronal damage. We showed that, after 1-, 2- or 5-day exposure of rats to 16 Hz, 130 dB infrasound (2 h/day), EGCG significantly inhibited infrasound-induced microglial activation in rat hippocampal region, evidenced by reduced expressions of Iba-1 (a marker for microglia) and proinflammatory cytokines (IL-1β, IL-6, IL-18 and TNF-α). Moreover, infrasound-induced neuronal apoptosis in rat hippocampi was significantly suppressed by EGCG. EGCG also inhibited infrasound-induced activation of primary microglia in vitro and decreased the levels of proinflammatory cytokines in the supernatants of microglial culture, which were toxic to cultured neurons. Furthermore, EGCG attenuated infrasound-induced increases in nuclear NF-κB p65 and phosphorylated IκBα, and ameliorated infrasound-induced decrease in IκB in microglia. Therefore, our study provides the first evidence that EGCG acts against infrasound-induced neuronal impairment by inhibiting microglia-mediated inflammation through a potential NF-κB pathway-related mechanism, suggesting that EGCG can be used as a promising drug for the treatment of infrasound-induced CNS damage.

Voice acoustic profile of males exposed to occupational infrasound and low-frequency noise

Background: Vibroacoustic disease (VAD) is a systematic pathology characterized by the abnormal growth of extra-cellular matrices in the absence of inflammatory processes, namely collagen and elastin, both of which are abundant in the basement membrane zone of the vocal folds. VAD can develop due to long-term exposure to infrasound and low-frequency noise (ILFN, < 500 Hz). Mendes et al. (2006, 2008 and 2012) revealed that ILFN-exposed males and females presented an increased fundamental frequency (F 0 ), decreased jitter %, and reduced maximum phonation frequency range, when compared with normative data. Temporal measures of maximum phonation time and S/Z ratio were generally reduced. Study Aims: Herein, the same voice acoustic parameters of 48 males, 36 airline pilots and 12 cabin crewmembers (age range 25-60 years) were studied, and the effects and interaction of age and years of ILFN exposure were investigated within those parameters. ILFN-exposure time (i.e. years of professional activity) ranged from 3.5 to 36 years. Materials and Methods: Spoken and sung phonatory tasks were recorded with a DA-P1 Tascam DAT and a C420III PP AKG head-worn microphone, positioned at 3 cm from the mouth. Acoustic analyses were performed using KayPENTAX Computer Speech Lab and Multi-Dimensional Voice Program. Results: Results revealed that even though pilots and cabin crewmembers were exposed to occupational environments with distinct (ILFN-rich) acoustical frequency distributions and sound pressure levels, differences in the vocal acoustic parameters were not evident. Analyzing data from both professional groups (N = 48) revealed that F 0 increased significantly with the number of years of professional activity. Conclusion: These results strongly suggest that the number of years of professional activity (i.e. total ILFN exposure time) had a significant effect on F 0 . Furthermore, they may reflect the histological changes specifically observed on the vocal folds of ILFN-exposed professionals.

Glial cell-expressed mechanosensitive channel TRPV4 mediates infrasound-induced neuronal impairment

Vibroacoustic disease, a progressive and systemic disease, mainly involving the central nervous system, is caused by excessive exposure to low-frequency but high-intensity noise generated by various heavy transportations and machineries. Infrasound is a type of low-frequency noise. Our previous studies demonstrated that infrasound at a certain intensity caused neuronal injury in rats but the underlying mechanism(s) is still largely unknown. Here, we showed that glial cell-expressed TRPV4, a Ca(2+)-permeable mechanosensitive channel, mediated infrasound-induced neuronal injury. Among different frequencies and intensities, infrasound at 16Hz and 130dB impaired rat learning and memory abilities most severely after 7-14days exposure, a time during which a prominent loss of hippocampal CA1 neurons was evident. Infrasound also induced significant astrocytic and microglial activation in hippocampal regions following 1- to 7-day exposure, prior to neuronal apoptosis. Moreover, pharmacological inhibition of glial activation in vivo protected against neuronal apoptosis. In vitro, activated glial cell-released proinflammatory cytokines IL-1β and TNF-α were found to be key factors for this neuronal apoptosis. Importantly, infrasound induced an increase in the expression level of TRPV4 both in vivo and in vitro. Knockdown of TRPV4 expression by siRNA or pharmacological inhibition of TRPV4 in cultured glial cells decreased the levels of IL-1β and TNF-α, attenuated neuronal apoptosis, and reduced TRPV4-mediated Ca(2+) influx and NF-κB nuclear translocation. Finally, using various antagonists we revealed that calmodulin and protein kinase C signaling pathways were involved in TRPV4-triggered NF-κB activation. Thus, our results provide the first evidence that glial cell-expressed TRPV4 is a potential key factor responsible for infrasound-induced neuronal impairment.

How the factoid of wind turbines causing ‘vibroacoustic disease’ came to be ‘irrefutably demonstrated’

In recent years, claims have proliferated in cyberspace that wind turbines cause a large variety of symptoms and diseases. One of these, "vibroacoustic disease" (VAD) is frequently mentioned. The aim of this study is to examine the quality of the evidence on how VAD came to be associated with wind turbine exposure by wind farm opponents. Searches of the web (Google advanced) and major research databases for papers on VAD and wind turbines. Self-citation analysis of research papers on VAD. Google returned 24,700 hits for VAD and wind turbines. Thirty-five research papers on VAD were found, none reporting any association between VAD and wind turbines. Of the 35 papers, 34 had a first author from a single Portuguese research group. Seventy-four per cent of citations to these papers were self-citations by the group. Median self-citation rates in science are around 7%. Two unpublished case reports presented at conferences were found asserting that VAD was "irrefutably demonstrated" to be caused by wind turbines. The quality of these reports was abject. VAD has received virtually no scientific recognition beyond the group who coined and promoted the concept. There is no evidence of even rudimentary quality that vibroacoustic disease is associated with or caused by wind turbines. The claim that wind turbines cause VAD is a factoid that has gone 'viral' in cyberspace and may be contributing to nocebo effects among those living near turbines.

CT Examination of the Pericardium and Lungs in Helicopter Pilots Exposed to Vibration and Noise

Helicopter pilots are exposed to whole body vibration and noise in their working environment. Some researchers have found that kinetic energy from both noise and vibration is believed to affect pericardial thickness and lead to pulmonary fibrosis, known as vibroacoustic disease. The aim of this project was to determine whether we could discover similar findings in a selection of helicopter pilots. A case control study where 27 helicopter pilots were compared to an age-matched control group of typical office workers was conducted. High resolution CT scanning of the thorax was used as the diagnostic method. Two medical radiologists interpreted the images independently, blinded to whether the subjects were pilots or from the control group. There were no signs of pericardial thickening or significant lung fibrosis formations in either of the groups. The average pericardium thickness for the helicopter group was 1.38 mm, SD = 0.54 mm, and for the control group: 1.37 mm, SD = 0.33 mm. There was no significant correlation between pericardium thickness and flight hours or age. The average pericardial thickness values for the helicopter and the age-matched control groups were almost identical. The results are within normal limits and comparable to an American study where 21 normal individuals were measured to 1.2 mm +/- 0.8 mm in an average of 26 different points by using trans-esophageal echocardiography. On the basis of the CT scans, our findings do not support the existence of vibroacoustic disease, where pericardial thickening is the most prominent sign.

The effects of ILFN-exposure on voice acoustic parameters of commercial cabin crewmembers

Background: Long-term exposure to infrasound and low frequency noise (ILFN <500 Hz, including infrasound) can lead to the development of vibroacoustic disease (VAD). VAD is a systemic pathology characterized by the abnormal growth of extracellular matrices in the absence of inflammatory processes, namely of collagen and elastin, both of which are abundant in the basement membrane zone of the vocal folds. ILFN-exposed workers include pilots, cabin crewmembers, restaurant workers, ship machinists and, in previous studies, even though they did not present vocal symptoms, ILFN-exposed workers had significant different voice acoustic patterns (perturbation and temporal measures) when compared with normative population. Study Aims: The present study investigates the effects of age and years of occupational ILFN-exposure on voice acoustic parameters of 37 cabin crewmembers: 12 males and 25 females. Specifically, the goals of this study are to: 1) Verify if acoustic parameters change over the age and years of ILFN-exposure and 2) Determine if there is any interaction between age and years of ILFN-exposure on voice acoustic parameters of crewmembers. Materials and Methods: Spoken phonatory tasks were recorded with a C420 III PP AKG head-worn microphone and a DA-P1 Tascam DAT. Acoustic analyses were performed using KayPENTAX Computer Speech Lab and Multi-Dimensional Voice Program. Acoustic parameters included speaking fundamental frequency, perturbation measures (jitter, shimmer and harmonic-to-noise ratio), temporal measures (maximum phonation time and s/z ratio) and voice tremor frequency. Results: One-way ANOVA analysis revealed that as the number of ILFN-exposure years increased male cabin crewmembers presented significant different shimmer values of /i/ as well as tremor frequency of /u/. Females presented significantly different jitter % of /i, a, ɔ/ (p <0.05). Lastly, Two-way ANOVA analysis revealed that for females, there was a significant interaction between age and occupational ILFN-exposure for voice acoustic parameters, namely for jitter's mean for /a, ɔ/ and shimmer's (%) mean for /a, i/ (p <0.05). Discussion and Conclusion: These perturbation measure patterns may be indicative of histological changes within the vocal folds as a result of ILFN-exposure. The results of this study suggest that voice acoustic analysis may be an important tool for confirming ILFN-induced health effects.

Respiratory squamous cell carcinomas in vibroacoustic disease

BackgroundIn 1987, the autopsy of a vibroacoustic disease (VAD) patient disclosed two tumours: a renal cell carcinoma and a malignant glioma in the brain. Since 1987, malignancy in VAD patients has been under close surveillance. To date, in a universe of 945 individuals, there are 46 cases of malignancies, of which 11 are multiple. Of the 11 cases of respiratory tract tumours, all were squamous cell carcinomas (SqCC). This report focuses on the morphological features of these tumours. MethodsTumour fragments were collected (endoscopic biopsy or surgery) from 11 male VAD patients (ave. age: 58±9 years, 3 non-smokers): 2 in glottis and 9 in the lung. In the 3 non-smokers, 2 had lung tumours and 1 had a glottis tumour. All were employed as or retired aircraft technicians, military or commercial pilots. Fragments were fixed either for light and electron microscopy. Immunohistochemistry studies used chromagranine and synaptophysine staining. ResultsAll lung tumours were located in the upper right lobe bronchi and were histologically poorly differentiated SqCC (Figs. 1, 2). The search with neuroendocrine markers was negative. The average age of tumour onset in helicopter pilots was below 50 years old while for the other professional groups it was above 50. Nine patients are deceased. The 2 surviving patients are heavy smokers (> 2 packs/day). Smoking habits had no influence on tumour outcome and progression. DiscussionEpidemiological studies indicate that squamous cell carcinomas account for approximately 40% of all lung tumours in men. It seems to be highly relevant that all VAD patient respiratory tract tumours are squamous cell carcinomas. It is not surprising that helicopter pilots are the ones who are affected the earliest because previous studies have shown that helicopter pilots exhibited the highest values for the frequency of sister chromatid exchanges. Generally, epidemiological tumor studies do not take histological tumor type into account, but given the results herein, it would seem of the utmost importance to begin specifiying the exact histological type of tumor in all statistical studies.

Carcinomas epidermóides do pulmão na doença vibroacústica

Background: In 1987, the autopsy of a vibroa-coustic disease (VAD) patient disclosed two tumours: a renal cell carcinoma and a malignant glioma in the brain. Since 1987, malignancy in VAD patients has been under close surveillance. To date, in a universe of 945 individuals, there are 46 cases of malignancies, of which 11 are multiple. Of the 11 cases of respiratory tract tumours, all were squamous cell carcinomas (SqCC). This report focuses on the morphological features of these tumours.Methods: Tumour fragments were collected (endoscopic biopsy or surgery) from 11 male VAD patients (ave. age: 58±9 years, 3 non-smokers): 2 in glottis and 9 in the lung. In the 3 non-smokers, 2 had lung tumours and 1 had a glottis tumour. All were employed as or retired aircraft technicians, military or commercial pilots. Fragments were fixed either for light and electron microscopy. Immunohistochemistry studies used chromagranine and synaptophysine staining. Results: All lung tumours were located in the upper right lobe bron-chi and were histologically poorly differentiated SqCC (Figs. 1, 2). The search with neuroendocrine markers was negative. The average age of tumour onset in helicopter pilots was below 50 years old while for the other professional groups it was above 50. Nine patients are deceased. The 2 surviving patients are heavy smokers (> 2 packs/day). Smoking habits had no influence on tumour outcome and progression. Discussion: Epidemiological studies indicate that squamous cell carcinomas account for approximately 40% of all lung tumours in men. It seems to be highly relevant that all VAD patient respiratory tract tumours are squamous cell carcinomas. It is not surprising that helicopter pilots are the ones who are affected the earliest because previous studies have shown that helicopter pilots exhibited the highest values for the frequency of sister chromatid exchanges. Generally, epidemiological tumor studies do not take histological tumor type into account, but given the results herein, it would seem of the utmost importance to begin specifiying the exact histological type of tumor in all statistical studies.Rev Port Pneumol 2006; XII (5): 539-544

Padrões acústicos da voz em indivíduos com a doença vibroacústica

Background: Long-term low frequency noise exposure (LFN) (≤ 500Hz, including infrasound) may lead to the development of vibroacoustic disease (VAD), a systemic pathology characterized by the abnormal growth of extra-cellular matrices. The respiratory system is a target for LFN. Fibrosis of the respiratory tract epithelia was observed in VAD patients through biopsy, and confirmed in animal models exposed to LFN. Voice acoustic analysis can detect vocal fold variations of mass, tension, muscular and neural activity. Frequency perturbation (jitter), amplitude perturbation (shimmer) and harmonic-to-noise ratio (HNR) are used in the evaluation of the vocal function, and can be indicators of the presence and degree of severity of vocal pathology. Since the respiratory system is the energy source of the phonation process, this raises questions about the effects of VAD on voice production. The purpose of this study was to determine if voice acoustic parameters of VAD patients are different from normative data. Methods: Nine individuals (5 males and 4 females) diagnosed with VAD were recorded performing spoken and sung tasks. The spoken tasks included sustaining vowels and fricatives. The sung tasks consisted of maximum phonational frequency range (MPFR). Voice acoustic parameters analysed were: fundamental frequency (F0), jitter, shimmer, HNR and temporal measures. Results: Compared with normative data, both males and females diagnosed with VAD exhibited increased F0, shimmer and HNR. Jitter, MPFR and one temporal measure were reduced. Conclusions: VAD individuals presented voice acoustic parameter differences in spectral, temporal and perturbation measures, which may be indicative of small morphological changes in the phonatory system.Rev Port Pneumol 2006; XII (4): 375-382

Voice acoustic patterns of patients diagnosed with vibroacoustic disease

BackgroundLong-term low frequency noise exposure (LFN) (≤500Hz, including infrasound) may lead to the development of vibroacoustic disease (VAD), a systemic pathology characterized by the abnormal growth of extra-cellular matrices. The respiratory system is a target for LFN. Fibrosis of the respiratory tract epithelia was observed in VAD patients through biopsy, and confirmed in animal models exposed to LFN. Voice acoustic analysis can detect vocal fold variations of mass, tension, muscular and neural activity. Frequency perturbation (jitter), amplitude perturbation (shimmer) and harmonicto- noise ratio (HNR) are used in the evaluation of the vocal function, and can be indicators of the presence and degree of severity of vocal pathology. Since the respiratory system is the energy source of the phonation process, this raises questions about the effects of VAD on voice production. The purpose of this study was to determine if voice acoustic parameters of VAD patients are different from normative data. MethodsNine individuals (5 males and 4 females) diagnosed with VAD were recorded performing spoken and sung tasks. The spoken tasks included sustaining vowels and fricatives. The sung tasks consisted of maximum phonational frequency range (MPFR). Voice acoustic parameters analysed were: fundamental frequency (F0), jitter, shimmer, HNR and temporal measures. ResultsCompared with normative data, both males and females diagnosed with VAD exhibited increased F0, shimmer and HNR. Jitter, MPFR and one temporal measure were reduced. ConclusionsVAD individuals presented voice acoustic parameter differences in spectral, temporal and perturbation measures, which may be indicative of small morphological changes in the phonatory system.

Abnormal respiratory drive in vibroacoustic disease

IntroductionCentral nervous system disorders in workers exposed to low frequency noise (LFN, <500Hz, including infrasound) were first observed 25 years ago among aircraft technicians. Concurrently, respiratory pathology was identified in these workers, and later reproduced in LFN-exposed animal models. Today vibroacoustic disease (VAD) is defined as the systemic pathology caused by excessive exposure to LFN. The respiratory tract continues to be under heavy scrutiny in both LFN-exposed humans and animal models and has been confirmed as a major target for LFN-induced damage. Given that both the respiratory and central nervous systems were compromised in these workers, it became pertinent to investigate the status of the neurological control of breathing in VAD patients. MethodsThe P-0.1 value, a measure of the suction pressure developed at the mouth 0.1 seconds after the start of inspiration, depends on the respiratory centres and the autonomic nervous system pathway of the neural control of respiratory function. By rebreathing CO2, (6% in air) normal individuals present an average seven-fold increase in P0.1(CO2) as compared to basal P-0.1. Twenty-two male VAD patients (ave. age 50.5±8.5 years, range: 36-66 years) underwent the P0.1(CO2) index respiratory drive tests, as well as standard pulmonary function tests. Seven individuals (ave. age 42.4±14 years, range: 25- 61 years) with reduced LFN exposure served as controls. ResultsPulmonary function tests were normal in both VAD patients and controls. The P0.1(CO2) index was below average value in VAD patients (average: 22.9%) while it presented normal values in the control group (average >60%). DiscussionIn the involuntary response to increased PCO2 levels, central chemoreceptors are responsible for 70% of the ventilatory stimulus. In VAD patients, this dysfunction may originate in the brainstem. This is corroborated by the fact that VAD patients register abnormal values for auditory brainstem evoked potentials, and disclose lesions with magnetic resonance imaging. The neurological control of breathing is compromised in VAD patients. The P0.1(CO2) index may be a useful clinical indicator for VAD diagnosis and follow-up.

Drive respiratório anormal na doença vibroacústica

Introduction: Central nervous system disorders in workers exposed to low frequency noise (LFN, <500Hz, including infrasound) were first observed 25 years ago among aircraft technicians. Concurrently, respiratory pathology was identified in these workers, and later reproduced in LFN-exposed animal models. Today vibroacoustic disease (VAD) is defined as the systemic pathology caused by excessive exposure to LFN. The respiratory tract continues to be under heavy scrutiny in both LFN-exposed humans and animal models and has been confirmed as a major target for LFN-induced damage. Given that both the respiratory and central nervous systems were compromised in these workers, it became pertinent to investigate the status of the neurological control of breathing in VAD patients. Methods: The P-0.1 value, a measure of the suction pressure developed at the mouth 0.1seconds after the start of inspiration, depends on the respiratory centres and the autonomic nervous system pathway of the neural control of respiratory function. By rebreathing CO2, (6% in air) normal individuals present an average seven-fold increase in P0.1 (CO2) as compared to basal P-0.1. Twenty-two male VAD patients (ave. age 50.5±8.5years, range: 36-66 years) underwent the P0.1 (CO2) index respiratory drive tests, as well as standard pulmonary function tests. Seven individuals (ave. age 42.4±14years, range: 25-61 years) with reduced LFN exposure served as controls. Results: Pulmonary function tests were normal in both VAD patients and controls. The P0.1 (CO2) index was below average value in VAD patients (average: 22.9%) while it presented normal values in the control group (average >60%). Discussion: In the involuntary response to increased PCO2 levels, central chemoreceptors are responsible for 70% of the ventilatory stimulus. In VAD patients, this dysfunction may originate in the brainstem. This is corroborated by the fact that VAD patients register abnormal values for auditory brainstem evoked potentials, and disclose lesions with magnetic resonance imaging. The neurological control of breathing is compromised in VAD patients. The P0.1 (CO2) index may be a useful clinical indicator for VAD diagnosis and follow-up.Rev Port Pneumol 2006; XII (4): 369-374

Participação das vias aéreas centrais na doença vibroacústica

Introduction. Vibroacoustic disease (VAD) is the whole-body pathology caused by excessive exposure to LFN. For the past 25 years, it has been know that low frequency noise (LFN, <500Hz, including infrasound) targets the respiratory system. In LFN-exposed rodents, the morphological changes of respiratory tract tissue partially explained some respiratory symptoms reported by VAD patients. However, many questions remain unanswered. Recently, some volunteer VAD patients underwent bronchoscopy in order to ascertain possible damage that could be associated with their respiratory complaints. Methods. Fourteen fully-informed and volunteer VAD patients were submitted to bronchoscopy, and biopsies were removed for analysis. Results. All patients exhibited small submucosal vascular-like lesions near the spurs, consisting of increased collagen and elastin fibres. Histology disclosed cilliary abnormalities, basal membrane hyperplasia, and thickening of vessel walls. In five patients, collagen bundles appeared degenerative and disrupted. No inflammatory process was ever identified, and no differences were seen between smokers and non-smo-kers. Discussion. Data is in accordance with what was observed in LFN-exposed animal models and also in 8 VAD patients who developed lung tumours. Collagen disruption and degeneration was also observed in electron microscopy images of the respiratory tract of LFN-exposed rodents. Thickened blood and lymphatic vessel walls have been consistently seen in images of VAD patients and of LFN-exposed rodents. During bronchoscopy performed by other reasons, this sort of structural aspects is not frequently seen. Taken together, it is strongly suggested that these findings could be VAD-specific.Rev Port Pneumol 2006; XII (2): 93-105