Adam Dudarewicz

Noise-induced time-dependent changes in oxidative stress in the mouse cochlea and attenuation by d-methionine

Oxidative stress in the cochlea is considered to play an important role in noise-induced hearing loss. This study determined changes in superoxide dismutase (SOD), catalase, lipid peroxidation (LPO) and the auditory brainstem response (ABR) in the cochlea of C57BL/6 mice prior to and immediately, 1, 3, 7, 10, 14 and 21 days after noise exposure (4 kHz octave band at the intensity of 110 dB SPL for 4 h). A significant increase in SOD activity immediately and on 1st day after noise exposure, without a concomitant increase in catalase activity suggested a difference in the time dependent changes in the scavenging enzymes, which facilitates the increase in LPO observed on day 7. The ABR indicated significant noise-induced functional deficits which stabilized in 2 weeks with a permanent threshold shift (PTS) of 15 dB at both 4 kHz and 8 kHz. The antioxidant D-methionine (D-Met) reversed the noise-induced changes in LPO levels and enzyme activities. It also significantly reduced the PTS observed on the 14th day from 15 dB to 5 dB for 4 kHz. In summary, the findings indicate that time-dependent alterations in scavenging enzymes facilitate the production of reactive oxygen species and that D-met effectively attenuates noise-induced oxidative stress and the associated functional loss in the mouse cochlea.

Variations in HSP70 genes associated with noise-induced hearing loss in two independent populations

Noise-induced hearing loss (NIHL) is one of the most important occupational health hazards. Millions of people worldwide are exposed daily to harmful levels of noise. NIHL is a complex disease resulting from an interaction between genetic and environmental factors. Although the environmental risk factors have been studied extensively, little is known about the genetic factors. Heat-shock proteins (HSPs) are induced after exposure to severe noise. When first induced by exposure to moderate sound levels, they can protect the ear from damage from excessive noise exposure. This protection is highly variable between individuals. An association of HSP70 genes with NIHL has been described by Yang et al (2006) in a Chinese sample set of noise-exposed workers. In this study, three polymorphisms (rs1043618, rs1061581 and rs2227956) in HSP70-1, HSP70-2 and HSP70-hom, respectively, were genotyped in 206 Swedish and 238 Polish DNA samples of noise-exposed subjects and analyzed. One SNP, rs2227956 in HSP70-hom, resulted in a significant association with NIHL in both sample sets. In addition, rs1043618 and rs1061581 were significant in the Swedish sample set. Analysis of the haplotypes composed of the three SNPs revealed significant associations between NIHL and haplotype GAC in both sample sets and with haplotype CGT in the Swedish sample set. In conclusion, this study replicated the association of HSP70 genes with NIHL in a second and third independent noise-exposed sample set, hereby adding to the evidence that HSP70 genes may be NIHL susceptibility genes.

Candidate Gene Association Study for Noise-induced Hearing Loss in Two Independent Noise-exposed Populations

Millions of people are daily exposed to high levels of noise. Consequently, noise‐induced hearing loss (NIHL) is one of the most important occupational health hazards worldwide. In this study, we performed an association study for NIHL based on a candidate gene approach. 644 Single Nucleotide Polymorphisms (SNPs) in 53 candidate genes were analyzed in two independent NIHL sample sets, a Swedish set and part of a Polish set. Eight SNPs with promising results were selected and analysed in the remaining part of the Polish samples. One SNP in PCDH15 (rs7095441), resulted in significant associations in both sample sets while two SNPs in MYH14 (rs667907 and rs588035), resulted in significant associations in the Polish sample set and significant interactions with noise exposure level in the Swedish sample set. Calculation of odds ratios revealed a significant association of rs588035 with NIHL in the Swedish high noise exposure level group. Our studies suggest that PCDH15 and MYH14 may be NIHL susceptibility genes, but further replication in independent sample sets is mandatory.

Evaluation of annoyance from the wind turbine noise: A pilot study

ObjectivesThe overall aim of this study was to evaluate the perception of and annoyance due to the noise from wind turbines in populated areas of Poland.Material and MethodsThe study group comprised 156 subjects. All subjects were asked to fill in a questionnaire developed to enable evaluation of their living conditions, including prevalence of annoyance due to the noise from wind turbines and the self-assessment of physical health and well-being. In addition, current mental health status of the respondents was assessed using Goldberg General Health Questionnaire GHQ-12. For areas where the respondents lived, A-weighted sound pressure levels (SPLs) were calculated as the sum of the contributions from the wind power plants in the specific area.ResultsIt has been shown that the wind turbine noise at the calculated A-weighted SPL of 30-48 dB was noticed outdoors by 60.3% of the respondents. This noise was perceived as annoying outdoors by 33.3% of the respondents, while indoors by 20.5% of them. The odds ratio of being annoyed outdoors by the wind turbine noise increased along with increasing SPLs (OR = 2.1; 95% CI: 1.22–3.62). The subjects’ attitude to wind turbines in general and sensitivity to landscape littering was found to have significant impact on the perceived annoyance. About 63% of variance in outdoors annoyance assessment might be explained by the noise level, general attitude to wind turbines and sensitivity to landscape littering.ConclusionsBefore firm conclusions can be drawn further studies are needed, including a larger number of respondents with different living environments (i.e., dissimilar terrain, different urbanization and road traffic intensity).

Genetic variants of CDH23 associated with noise-induced hearing loss.

Objectives Noise-induced hearing loss (NIHL) is a complex disease resulting from the interaction between external and intrinsic/genetic factors. Based on mice studies, one of the most interesting candidate gene for NIHL susceptibility is CDH23-encoding cadherin 23, a component of the stereocilia tip links. The aim of this study was to analyze selected CDH23 single nucleotide polymorphisms (SNPs) and to evaluate their interaction with environmental and individual factors in respect to susceptibility for NIHL in humans. Methods A study group consisted of 314 worst-hearing and 313 best-hearing subjects exposed to occupational noise, selected out of 3,860 workers database. Five SNPs in CDH23 were genotyped using real-time PCR. Subsequently, the main effect of genotype and its interaction with selected environmental and individual factors were evaluated. Results The significant results within the main effect of genotype were obtained for the SNP rs3752752, localized in exon 21. The effect was observed in particular in the subgroup of young subjects and in those exposed to impulse noise; CC genotype was more frequent among susceptible subjects, whereas genotype CT appeared more often among resistant to noise subjects. The effect of this polymorphism was not modified by none of environmental/individual factors except for blood pressure; however, the latter one should be further investigated. Smoking was shown as an independent factor determining NIHL development. Conclusion The results of this study confirm that CDH23 genetic variant may modify the susceptibility to NIHL development in humans, as it was earlier proven in mice. Because the differences between the 2 study groups were not necessarily related to susceptibility to noise but they also were prone to age-related cochlear changes, these results should be interpreted with caution until replication in another population.

Theoretical predictions and actual hearing threshold levels in workers exposed to ultrasonic noise of impulsive character--a pilot study.

Results of standard pure-tone audiom etry (PTA) were collected from 25 workers, mainly females, aged 23–58 years, exposed for 2–13 years to ultrasonic noise emitted by ultrasonic welders. Hearing tests were completed by evaluation of exposure to ultrasonic noise. The subjects’ actual audiometric hearing threshold levels (HTLs) were compared with theoretical predictions calculated according to ISO 1999:1990. In 60% of cases sound pressure levels in the 10–40 kHz 1/3-octave bands at workstands exceeded Polish exposure limits for ultrasonic noise. Our comparison of predicted and measured HTLs suggests that the ISO 1999:1990 method, intended for audible noise, might also make it possible to predict reliably permanent hearing loss (in the 2 000–6 000 Hz frequency range) after exposure to ultrasonic noise. No significant progress of hearing impairment (assessed using PTA) in the operators of ultrasonic welders was noted. Nevertheless, further studies on the hearing status of workers exposed to ultrasonic noise are needed.

Evaluation of Sound Exposure and Risk of Hearing Impairment in Orchestral Musicians

This study aimed to assess exposure to sound and the risk of noise-induced hearing loss (NIHL) in orchestral musicians. Sound pressure level was measured in 1 opera and 3 symphony orchestras; questionnaires were filled in. On the basis of that data, the risk of NIHL was assessed according to Standard No. ISO 1999:1990. Classical orchestral musicians are usually exposed to sound at equivalent continuous A-weighted sound pressure levels of 81–90 dB (10th–90th percentiles), for 20–45 h (10th–90th percentiles) per week. Occupational exposure to such sound levels over 40 years of employment might cause hearing loss (expressed as a mean hearing threshold level at 2, 3, 4 kHz exceeding 35 dB) of up to 26%. Playing the horn, trumpet, tuba and percussion carries the highest risk (over 20%).

STATIC MAGNETIC FIELD AFFECTS OXIDATIVE STRESS IN MOUSE COCHLEA

OBJECTIVE It has been shown that oxidative stress plays an important role in development of noise induced hearing loss. Since static magnetic fields (SMF) exposure may alter dynamics of oxidative processes in the tissue, the aim of the study was to assess the influence of SMF on noise-induced alteration in the cochlear level of reactive oxygen species (ROS) and hearing thresholds. MATERIALS AND METHODS Auditory brainstem response (ABR), lipid peroxidation (LPO) levels, super-oxide dismutase (SOD) activity and catalase activity were assessed in the cochlea prior to, and at five time-points over two weeks following exposure of C57BL/6 mice to 8h, 119 dB SPL, 4 kHz octave band noise. RESULTS The ABR indicated no permanent functional damage due to noise exposure either for the 4 kHz and 8 kHz SMF-exposed group or for animals not exposed to SMF. However, significant differences in LPO level, catalase and SOD activity between animals exposed to noise and SMF and those exposed to noise only were observed. CONCLUSIONS The results suggest that SMF causes an increase in ROS level in the cochlea after noise exposure and, at the same time, it speeds up activation of antioxidative enzymes.

Analysis of inner ear potassium recycling genes as potential factors associated with tinnitus.

Tinnitus is defined as a perception of sound in the absence of an external acoustic stimulus. Several factors are known to influence tinnitus, e.g. hearing loss, noise exposure, age, and hypertension. As only certain individuals develop tinnitus in the presence of the above risks and in approximately 50% of cases tinnitus is not attributed to any particular cause, the question arose whether this inter-individual susceptibility to tinnitus could be explained by the influence of genetic factors.ObjectivesTo test the hypothesis that genetic variability in genes of the potassium recycling pathway is associated with increased susceptibility to tinnitus.Materials and MethodsThe study group consisted of 626 subjects exposed to occupational noise (128 with tinnitus and 498 without tinnitus). 99 single nucleotide polymorphisms were investigated in 10 genes involved in the potassium recycling pathway in the inner ear, previously selected as putative noise-induced hearing loss (NIHL) candidate genes.ResultsNominally significant associations were obtained for 2 variants in KCNE1 (potassium voltage-gated channel, Isk-related family, member 1) and SLC12A2 (solute carrier family 12, member 2) genes. The first gene contributed to tinnitus that developed independently of hearing loss, while the second one was associated with increased susceptibility to noise-induced hearing loss.ConclusionsPresent findings lend support to the notion of potassium recycling pathway genes as possible risk modifiers of tinnitus in individuals with and without hearing loss. Due to the lack of replication in other independent populations these results should be seen as suggestive.

Evaluation of annoyance from low frequency noise under laboratory conditions

The aim of the study was to investigate the annoyance of low frequency noise (LFN) at levels normally prevailing at workplaces in control rooms and office-like areas. Two different laboratory experiments were carried out. The first experiment included 55 young volunteers and the second one comprised 70 older volunteers, categorized in terms of sensitivity to noise. The subjects listened to noise samples with different spectra, including LFNs at sound pressure level (SPL) of 45-67 dBA, and evaluated annoyance using a 100-score graphical rating scale. The subjective ratings of annoyance were compared to different noise metrics. In both the experiments, there were no differences in annoyance assessments between females and males. A significant influence of individual sensitivity to noise on annoyance rating was observed for some LFNs. Annoyance of LFN was not rated higher than annoyance from broadband noises without or with less prominent low frequencies at similar A-weighted SPLs. In both the experiments, median annoyance rating of LFN highly correlated with A-weighted SPL (L(Aeq,T)), low frequency A-weighted SPL (L(LFAeq,T)) and C-weighted SPL (L(Ceq,T)). However, it is only the two latter noise metrics (i.e. L(LFAeq,T) and L(Ceq,T)) which seem to be reliable predictors of annoyance exclusively from LFN. The young and older participants assessed similar annoyance from LFN at similar L(LFAeq,T) or L(Ceq,T) levels. Generally, over half of the subjects were predicted to be highly annoyed by LFN at the low frequency A-weighted SPL or C-weighted SPL above 62 and 83 dB, respectively.