Made available in DSpace on 2015-05-14T12:47:12Z (GMT). No. of bitstreams: 1 arquivototal.pdf: 2059659 bytes, checksum: f3d773c696e3797e353a21eae5946320 (MD5) Previous issue date: 2012-03-22 / Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - CAPES / INTRODUCTION: NIHL (Noise Induced Hearing Loss) is a condition that results from the accumulation of prolonged exposure to noise, causing a slow and progressive hearing impairment, sensorneural, not very deep, but irreversible. The dentist, individuals exposed to noise in their workplace, is susceptible to NIHL. OBJECTIVE: To analyze the auditory and possible risk factors that interfere with the hearing of the dentists from USFs (Unidades de Saúde da Família / Familiar Health Unities) in Joao Pessoa / PB. METHODOLOGY: There were interviews, audiological evaluations, instrumental and environmental noises within 65 dentists from Family Health Units in Joao Pessoa / PB to identify auditory characteristics and risk factors for hearing-surgeons dentists by using proportion measures calculation for categorical variables, and having the Statistical Logistic Regression Method. RESULTS: It was observed that 43.07% of the dentists who were evaluated had lower hearing in, at least, some of the characteristic frequencies of NIHL. It was found that the main ear symptoms cited by these professionals were to have the sensation of hearing loss (55%), and buzzer (50%), and also that the instruments which showed values above the allowed limits were turbine high rotation (61%) and the compressor (55%). The variables considered as risk factors for hearing loss based on logistic regression were: age over 45 years old, working time more than 10 years, a feeling of hearing loss, tinnitus and noise level of the compressor greater than 85 dB. CONCLUSION: The ear symptoms (tinnitus and hearing loss) are presented in a large number of dentists, and the noise emitted by the instruments used by these professionals is often high, presenting some risk factors for Noise Induced Hearing Loss and some of them may be prevented or controlled through specific strategies. / INTRODUÇÃO: A Perda Auditiva Induzida por Ruído (PAIR) é uma patologia decorrente do acúmulo de exposições a ruído prolongadas, gerando uma deterioração auditiva progressiva e lenta, sensorioneural, geralmente não muito profunda mas irreversível. Sabe-se que o cirurgião-dentista, indivíduo exposto ao ruído no ambiente de trabalho, é susceptível à PAIR. OBJETIVO: Analisar o perfil auditivo e possíveis fatores de risco que interferem na audição dos cirurgiões-dentistas das USFs (Unidades de Saúde da Família) de João Pessoa/PB. METODOLOGIA: Realizaram-se entrevistas, avaliações audiológicas e dos ruídos instrumental e ambiental com 65 cirurgiões-dentistas das Unidades de Saúde da Família de João Pessoa /PB, a fim de identificar características do perfil auditivo e de fatores de risco para a audição dos cirurgiões-dentistas, utilizando o cálculo de medidas de proporção para as variáveis categóricas, e tendo como método estatístico a Regressão Logística. RESULTADOS: Observou-se que 43,07% dos cirurgiões-dentistas avaliados apresentaram rebaixamento auditivo em pelo menos alguma das frequências características da PAIR. Verificou-se ainda que os principais sintomas otológicos citados por estes profissionais foram a sensação de déficit auditivo (55%), e o zumbido (50%). Os instrumentos que mais se apresentaram com valores de intensidade acima dos limites permitidos foram a turbina de alta rotação (61%) e o compressor (55%). As variáveis consideradas como fatores de risco para a perda auditiva com base na Regressão Logística foram: idade acima de 45 anos, tempo de trabalho maior que 10 anos e nível de ruído do compressor maior que 85 dB, além da presença dos sintomas de sensação de déficit auditivo e zumbido. CONCLUSÃO: A sintomatologia otológica (zumbido e diminuição auditiva) está presente em grande número dos cirurgiões-dentistas e o ruído emitido pelos instrumentos utilizados por estes profissionais é muitas vezes elevado. Constataram-se alguns fatores de risco para a Perda Auditiva Induzida por Ruído, podendo alguns destes ser prevenidos ou controlados por meio de estratégias específicas.

Millions of people across the world are suffering from noise induced hearing loss (NIHL), especially under working conditions of either continuous Gaussian or non-Gaussian noise that might affect human's hearing function. Impulse noise is a typical non-Gaussian noise exposure in military and industry, and generates severe hearing loss problem. This study mainly focuses on characterization of impulse noise using digital signal analysis method and prediction of the auditory hazard of impulse noise induced hearing loss by the Auditory Hazard Assessment Algorithm for Humans (AHAAH) modeling. A digital noise exposure system has been developed to produce impulse noises with peak sound pressure level (SPL) up to 160 dB. The characterization of impulse noise generated by the system has been investigated and analyzed in both time and frequency domains. Furthermore, the effects of key parameters of impulse noise on auditory risk unit (ARU) are investigated using both simulated and experimental measured impulse noise signals in the AHAAH model. The results showed that the ARUs increased monotonically with the peak pressure (both P+ and P-) increasing. With increasing of the time duration, the ARUs increased first and then decreased, and the peak of ARUs appeared at about t = 0.2 ms (for both t+ and t-). In addition, the auditory hazard of experimental measured impulse noises signals demonstrated a monotonically increasing relationship between ARUs and system voltages.

Occupational hearing loss resulting from noise exposures encountered in the workplace affects millions of workers and costs hundreds of millions of dollars annually in Workers’ Compensation costs in the United States alone. Some industries have been well studied, and the presence of hazardous noise in the work environment established and documented. The restaurant industry is one in which little current data exists, but in which there may be cause for concern. This work sought to quantify noise exposures for cooks, servers, and dishwashers and to determine whether or not any of these workers are at risk for Noise Induced Hearing Loss. Further, the researchers wanted to know what environmental factors present in the restaurants had the greatest impact on noise exposures for each exposure group. Statistical analysis was conducted on selected factors, and while nearly all were found to have significant effects on noise exposure for servers, only the number of minutes worked explained variance in exposures for cooks and dishwashers when all factors were included in analysis. These two groups are the ones most likely to be overexposed and they typically worked more than 480 minutes on the day the sample was collected. Efforts to control exposure must take these extended shifts into careful account. The study was limited by relatively small sample size, with 124 cooks, 119 servers, and 91 dishwashers employed at nine different restaurants participating. Future efforts to explain and characterize the sources of variation in noise exposure for these three groups should include greater numbers of participants and structure the data in a way that allows the effects of selected factors to be more clearly seen.

Despite the preventability of noise-induced hearing loss (NIHL) a high prevalence is still reported in South African mines. The study aimed to describe the hearing of gold miners pertaining to the prevalence and degree of NIHL and effectiveness of current RSA impairment criteria to identify NIHL. The audiological data, collected between 2001 and 2008, of 57 714 mine workers were investigated in this retrospective cohort study. Data was accessed through the mine’s electronic database and exported to Microsoft Excel 2007 worksheets. Participants were categorised in terms of noise exposure (level and working years), age, race and gender. Noise exposure levels were described in terms of a specific occupation and categorized into four groups based on dosimeter data received from the mine’s noise hygienist, namely: 1) Below surface (underground) noise exposure, ≥85 dB A, classified according to the South African regulations on the daily permissible dose of noise exposure8, named Noise Group 1; 2) Surface noise exposure, ≥85 dB A, named Noise Group 2; 3) No known occupational noise exposure, named control group; and 4) Uncertain levels of noise exposure, e.g. students and trainees, named Noise Group 4. The control group was matched with participants of noise group 1 and 2 based on gender, race and age at the most recent audiogram test. Descriptive and inferential statistics were employed. Measures of central tendency and variability were used with analysis of covariance (ANCOVA) and pairwise comparisons according to Fisher’s Least Squares Differences Approach (F test). Results indicated that noise exposed groups had significantly higher prevalence of high and low frequency hearing loss than the control group. High-frequency hearing loss was also present in the control group. The greatest differences in prevalence of hearing loss were observed at 3, 4 kHz and age group 36 to 45 years. Thresholds at 8 kHz were worse than expected and decline slowed down with age. High-frequency thresholds showed a non-linear growth pattern with age with a greater decline at 2 kHz with age in the noise-exposed population compared to the control group. Hearing deteriorated more across age groups with more noise-exposed years, and this deterioration was most visible after 10 to 15 working years and at 3 kHz. Females had better hearing than males across the frequency spectrum. Black males had significantly better high-frequency hearing than white males but significantly worse low-frequency hearing than white male counterparts. PLH values showed poor correlation (through statistical analyses) with other well-accepted hearing impairment criteria. To date this was the largest study conducted on the hearing of gold miners and the sample included a very large number of black males exposed to occupational noise (N=17 933). Values supplied in distribution table format are therefore unique and contribute greatly to the knowledge base. / Thesis (PhD)--University of Pretoria, 2012. / Speech-Language Pathology and Audiology / unrestricted

<p>  </p> <p>Noise-induced hearing loss (NIHL) is a significant occupational health concern in the construction industry, necessitating effective hearing protection for workers. This project explores the detrimental consequences of environmental pollutants, specifically noise pollution common in construction settings. The research incorporates user interviews with construction workers and managers to identify challenges and motivations surrounding the use of hearing protection devices.</p> <p>My findings underscore the necessity of addressing pollution in the construction industry to safeguard the well-being of workers. Noise pollution emerges as a primary concern, leading to hearing loss, stress, decreased productivity, and safety hazards. The research revealed that workers grapple with obstacles, including discomfort, lack of awareness, and cost barriers, while also recognizing driving forces, including fear of hearing loss and the encouragement of supervisors. The design process involved thorough research, including a literature review, competitive analysis, and semi-structured user interviews, resulting in an advanced hearing protection device that prioritizes effective communication, cleanliness, and user comfort. The final product incorporates innovative features such as lighting indicators, a compact charging case, strategically positioned buttons, secure fit with magnets, and a range of color options. Furthermore, the accompanying application features customizable ambient sounds, performance feedback, and gamification elements.</p>

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INTRODUÇÃO: A exposição a níveis elevados de pressão sonora é a segunda causa mais comum de perda auditiva sensorioneural adquirida. Está relacionada à morte celular por apoptose, necrose e/ou necrose programada (necroptose) devido ao dano mecânico e/ou metabólico, ocasionando a degeneração de estruturas cocleares como células ciliadas, sobretudo externas, células de suporte e de fibras aferentes do nervo coclear. Estudos têm demostrado um aumento na citocina inflamatória TNFa após a exposição ao ruído, bem como a melhoria auditiva relacionada ao uso de etanercepte, que é um bloqueador destacitocina. Neste contexto, este estudo teve por objetivo avaliar o efeito do silenciamento gênico do Tnfa na audição de ratos Wistar, expostos ao ruído branco, e identificar o perfil de expressão gênica na via metabólica desse gene. METODOLOGIA: Foram incluídos ratos Wistar do sexo masculino, jovens com limiar auditivo no Peate clique de 50 dBSPL. Os animais foram submetidos à introdução do siRNA Tnfa em uma orelha, e siRNA scramble na orelha contralateral por via trans-timpânica com posterior exposição à 120 dBSPL de ruído branco por 3h. Foi realizado Peate clique e remoção das cócleas para obtenção do cDNA e avaliação da expressão gênica da via metabólica do Tnfa por meio de qRT-PCR. Um grupo de animais, não submetidos ao silenciamento, foi exposto ao ruído para análise dessa via metabólica. Para o cálculo da expressão gênica relativa (Rq) utilizamos o método do deltaCT comparativo e o teste t-Student pareado para avaliar os parâmetros no Peate clique. RESULTADOS: A taxa de silenciamento observada foi de 74,1%. A média do limiar eletrofisiológico nas orelhas silenciadas foi estaticamente melhor que a orelha scramble (p < 0,001) com valores médios de 49,5 +- 10.5. A amplitude média da onda I em 80 dBSPL e das ondas II e IV em 90 dBSPL foi estatisticamente maior na orelha siRNA Tnfa, sem alteração na latência nas intensidades audíveis,para ambos os lados. A exposição ao ruído promoveu aumento da expressão do gene Tnfa e de seu receptor Tnfrsf1A, 24h após à exposição, associado ao aumento da expressão de genes relacionados à apoptose e diminuição de genes relacionados à sobrevida celular. CONCLUSÃO: O ruído promoveu aumento de expressão do gene Tnfa e de genes envolvidos na apoptose, associado à perda auditiva em modelo experimental. A administração trans-timpânica do siRNA Tnfa promoveu preservação do limiar eletrofisiológico e da amplitude da onda I, II e IV no Peate clique, após exposição ao ruído intenso, sugerindo que a inibição deste pode ser uma estratégia de preservação auditiva promissora. O silenciamento do Tnfa inibiu a disfunção coclear após estímulo acústico, sugerindo que esta proteína é um dos principais agentes envolvidos na perda auditiva induzida pelo ruído, devendo ser considerada como alvo terapêutico na estratégia de preservação auditiva / INTRODUCTION: Exposure to high levels of sound pressure is the second most common cause of acquired sensorineural hearing loss. It is related to cell death through apoptosis, necrosis and/or programmed necrosis (necroptosis) due to mechanical and/or metabolic damage, causing the degeneration of cochlear structures, such as cilliary cells, mainly external, as well as support cells and afferent fibers of the cochlear nerve. Studies have demonstrated an increase in the inflammatory cytokine TNFalfa after exposure to noise, as well as auditory improvement related to the use of etanercept, a cytokine blocker. In this context, this study aimed to evaluate the effect of Tnfa gene silencing on the hearing of Wistar rats exposed to white noise and to identify the expression profile in the metabolic pathway of this gene. METHODOLOGY: Young male Wistar rats with 50 dBSPL threshold in auditory brainstem responses click (ABR) were included in this study and submitted to the introduction of the TnfasiRNA in one ear and the scramble siRNA in the contralateral ear by trans-tympanic route, with subsequent exposure to 120 dB SPL of white noise for 3h. ABR was measured and the cochleae were dissected and used for the extraction of total RNA to obtain cDNA and conduct evaluations of the Tnfa metabolic pathway gene expression by qRT-PCR. A group of animals, not submitted to silencing, was exposed to noise to analyze this metabolic pathway. The relative gene expression (Rq) was calculated by the comparative deltaCT method and the paired Student t-test were applied to evaluate the parameters of the ABR click. RESULTS: The silencing rate was 74.1%. The mean electrophysiological threshold in the silenced ears was statistically higher than the scrambled ear (p < 0.001) with mean values of 49.5 +- 10.5. The mean amplitudes of wave I at 80 dBSPL and waves II and IV at 90dBSPL were statistically higher in the TnfasiRNA ear, with no change in latency at audible intensities for both sides. Noise exposure promoted increased expression of the Tnfa gene and its receptor, Tnfrsf1A, 24h after exposure, associated with increased expression of genes related to apoptosis and decreased expression of genes related to cell survival. CONCLUSIONS: Noise exposure promoted increased in Tnfa gene expression as well as in genes involved in apoptosis, associated with hearing loss in an experimental model. The trans-tympanic administration of TnfasiRNA promotes the preservation of the electrophysiological threshold and the amplitude of wave I, II and IV in the ABR click, after exposure to intense noise, suggesting that this inhibition may be a promising auditory preservation strategy. The Tnfa knockdown inhibited cochlear dysfunction after acoustic injury, suggesting that this protein plays an important role in noise induced hearing loss and should be considered a therapeutic target in auditory preservation strategies