Introduction: Occupational noise exposure and chronic obstructive pulmonary disease (COPD) are common in the United States, but so far their association has not been explored. Given the neuroimmunological effects of noise, such an association seems plausible. Thus, the present study aimed to explore the association of occupational noise exposure with prevalent COPD in the US general population. Materials and Methods: We used data from the population-based National Health Interview Survey (NHIS) 2014. The cross-sectional association of self-reported duration of exposure to very loud noise during participants’ occupational lifetime with self-reported COPD and emphysema was explored using weighted logistic regression. Results and Discussion: The fully adjusted model yielded odds ratio (OR)_{≥15 years} = 1.68 [95% confidence interval (CI): 1.28, 2.21] for COPD and OR_{≥15 years} = 1.61 (95% CI: 1.13, 2.30) for emphysema. Race/ethnicity was a significant effect modifier. In sensitivity analysis with cumulative noise exposure based on a job exposure matrix, we found no effect. Conclusion: In conclusion, we found a relationship between self-reported occupational noise exposure and the risk of prevalent COPD in the US general population, but none with objective noise levels. Being the first study on the subject matter, and given the design limitations, these findings are tentative and should be treated with caution.

Introduction: The aim of this study was to investigate self-reported hearing and portable music listening habits, measured hearing function and music exposure levels in Swedish adolescents. The study was divided into two parts. Materials and Methods: The first part included 280 adolescents, who were 17 years of age and focused on self-reported data on subjective hearing problems and listening habits regarding portable music players. From this group, 50 adolescents volunteered to participate in Part II of the study, which focused on audiological measurements and measured listening volume. Results: The results indicated that longer lifetime exposure in years and increased listening frequency were associated with poorer hearing thresholds and more self-reported hearing problems. A tendency was found for listening to louder volumes and poorer hearing thresholds. Women reported more subjective hearing problems compared with men but exhibited better hearing thresholds. In contrast, men reported more use of personal music devices, and they listen at higher volumes. Discussion: Additionally, the study shows that adolescents listening for ≥3 h at every occasion more likely had tinnitus. Those listening at ≥85 dB L_{Aeq, FF} and listening every day exhibited poorer mean hearing thresholds, reported more subjective hearing problems and listened more frequently in school and while sleeping. Conclusion: Although the vast majority listened at moderate sound levels and for shorter periods of time, the study also indicates that there is a subgroup (10%) that listens between 90 and 100 dB for longer periods of time, even during sleep. This group might be at risk for developing future noise-induced hearing impairments.

It has previously been shown that acoustic overstimulation induces cell death and extensive cell loss in key structures of the central auditory pathway. A correlation between noise-induced apoptosis and cell loss was hypothesized for the cochlear nucleus and colliculus inferior. To determine the role of cell death in noise-induced cell loss in thalamic and cortical structures, the present mouse study (NMRI strain) describes the time course following noise exposure of cell death mechanisms for the ventral medial geniculate body (vMGB), medial MGB (mMGB), and dorsal MGB (dMGB) and the six histological layers of the primary auditory cortex (AI 1–6). Therefore, a terminal deoxynucleotidyl transferase dioxyuridine triphosphate nick-end labeling assay (TUNEL) was performed in these structures 24 h, 7 days, and 14 days after noise exposure (3 h, 115 dB sound pressure level, 5–20 kHz), as well as in unexposed controls. In the dMGB, TUNEL was statistically significant elevated 24 h postexposure. AI-1 showed a decrease in TUNEL after 14 days. There was no statistically significant difference between groups for the other brain areas investigated. dMGB’s widespread connection within the central auditory pathway and its nontonotopical organization might explain its prominent increase in TUNEL compared to the other MGB subdivisions and the AI. It is assumed that the onset and peak of noise-induced cell death is delayed in higher areas of the central auditory pathway and takes place between 24 h and 7 days postexposure in thalamic and cortical structures.

Background: Brain-derived neurotrophic factor (BDNF) gene polymorphisms are associated with abnormalities in regulation of BDNF secretion. Studies also linked BDNF polymorphisms with changes in brainstem auditory-evoked response test results. Furthermore, BDNF levels are reduced in tinnitus, psychiatric disorders, depression, dysthymic disorder that may be associated with stress, conversion disorder, and suicide attempts due to crises of life. For this purpose, we investigated whether there is any role of BDNF changes in the pathophysiology of tinnitus. Materials and Methods: In this study, we examined the possible effects of BDNF variants in individuals diagnosed with tinnitus for more than 3 months. Fifty-two tinnitus subjects between the ages of 18 and 55, and 42 years healthy control subjects in the same age group, who were free of any otorhinolaryngology and systemic disease, were selected for examination. The intensity of tinnitus and depression was measured using the tinnitus handicap inventory, and the differential diagnosis of psychiatric diagnoses made using the Structured Clinical Interview for Fourth Edition of Mental Disorders. BDNF gene polymorphism was analyzed in the genomic deoxyribonucleic acid (DNA) samples extracted from the venous blood, and the serum levels of BDNF were measured. One-way analysis of variance and Chi-squared tests were applied. Results: Serum BDNF level was found lower in the tinnitus patients than controls, and it appeared that there is no correlation between BDNF gene polymorphism and tinnitus. Conclusions: This study suggests neurotrophic factors such as BDNF may have a role in tinnitus etiology. Future studies with larger sample size may be required to further confirm our results.

Introduction: Infrasound is a mechanical vibration wave with frequency between 0.0001 and 20 Hz. It has been established that infrasound of 120 dB or stronger is dangerous to humans. However, the biological effects of low decibel infrasound are largely unknown. The purpose of this study was to investigate the effects of low decibel infrasound on the cardiac fibroblasts. Materials and Methods: The cardiac fibroblasts were isolated and cultured from Sprague–Dawley rats. The cultured cells were assigned into the following four groups: control group, angiotensin II (Ang II) group, infrasound group, and Ang II+infrasound group. The cell proliferation and collagen synthesis rates were evaluated by means of [³H]-thymidine and [³H]-proline incorporation, respectively. The levels of TGF-β were determined by enzyme-linked immunosorbent assay. Moreover, RNAi approaches were used for the analysis of the biological functions of miR-29a, and the phosphorylation status of Smad3 was detected using western blotting analysis. Results: The results showed that low decibel infrasound significantly alleviated Ang II-induced enhancement of cell proliferation and collagen synthesis. Discussion: Compared with the control, Ang II markedly decreased the expression of miR-29a levels and increased the secretion of TGF-β and phosphorylation of Smad3, which was partly reversed by the treatment with low decibel infrasound. Importantly, knockdown of miR-29a diminished the effects of infrasound on the cardiac fibroblasts. In conclusion, low decibel infrasound inhibits Ang II-stimulated cardiac fibroblasts via miR-29a targeting TGF-β/Smad3 signaling.

Environmental noise and health studies seldom address the positive effect of environments with high acoustic quality. Sound quality, in turn, is influenced by a large number of factors, including the spatial–physical characteristics of a neighborhood. In general, these characteristics cannot be retrieved from existing databases. In this article, we describe the design of an audit instrument and demonstrate its value for gathering information about these characteristics of neighborhoods. The audit instrument used was derived from research in other fields than environmental health. The instrument was tested in 33 neighborhoods in the Dutch cities of Amsterdam, Rotterdam, and Arnhem. In these neighborhoods, more or less homogeneous subareas were identified that were subject of the audit. The results show that the audit approach is suitable to gather neighborhood data that are relevant for the sound quality of neighborhoods. Together with survey data, they provide information that could further the field of soundscape and health. Several suggestions for improvement of the audit instrument were made.