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Background: Longitudinal studies highlight the importance of early intervention and timely device fitting for language development in children with congenital or early acquired hearing loss. Due to the variability in hearing loss, comorbidities, family circumstances, and service access, individualised monitoring of listening development is essential to inform decision-making. The Functional Listening Index—Paediatric (FLI-P), a 64-item hierarchical checklist of listening skills, has been validated for children with hearing loss aged 0–6 years. This study aimed to develop benchmarks for the FLI-P in typically hearing children, allowing for comparison with individual children with hearing loss. Methods: FLI-P scores were obtained from parents/caregivers of 561 typically hearing children aged 0–72 months. Each child’s FLI-P score was categorised into a 6-month age block, with a minimum of 36 data points per block. Quantile regression was employed to establish percentiles of FLI-P scores by age. Results: FLI-P scores were successfully recorded for all 561 children. Regression analysis determined that the 16th and 84th percentiles of FLI-P scores corresponded to approximately ±1 standard deviation from the median score for each age group. A graphical representation of these percentile trajectories was created to facilitate comparison between children with hearing loss and the normative data. Conclusion: A normative dataset of FLI-P scores from typically hearing children has been established, allowing for comparisons with the scores and developmental trajectories of individual children with hearing loss. The study demonstrates how FLI-P can guide early intervention decisions and effectively monitor progress.

This paper reports on the examination of the relationship between self-reported historical noise exposure during leisure activities and audiological indicators: Measured hearing threshold levels (HTLs) and otoacoustic emissions (OAEs). The research was conducted by a cross-sectional survey of 1,432 individuals whose ages ranged from 11 years to 35 years. Methodology included a comprehensive audiometric assessment including otoscopy, pure tone audiometry (PTA) (air- and bone-conduction), OAEs, and tympanometry. A comprehensive questionnaire gathered information on demographics, hearing health status, and participation in work, nonwork, and leisure activities. Using the history of work, nonwork, and leisure noise exposure, a cumulative lifetime noise exposure was estimated. No correlation was found between cumulative lifetime noise exposure and audiometric PTA or OAE parameters.

Recent epidemiological data suggest the relation between hearing difficulty and depression is more evident in younger and middle-aged populations than in older adults. There are also suggestions that the relation may be more evident in specific subgroups; that is, other factors may influence a relationship between hearing and depression in different subgroups. Using cross-sectional data from the UK Biobank on 134,357 community-dwelling people and structural equation modelling, this study examined the potential mediating influence of social isolation and unemployment and the confounding influence of physical illness and cardiovascular conditions on the relation between a latent hearing variable and both a latent depressive episodes variable and a latent depressive symptoms variable. The models were stratified by age (40s, 50s, and 60s) and gender and further controlled for physical illness and professional support in associations involving social isolation and unemployment. The latent hearing variable was primarily defined by reported hearing difficulty in noise. For all subgroups, poor hearing was significantly related to both more depressive episodes and more depressive symptoms. In all models, the direct and generally small association exceeded the indirect associations via physical health and social interaction. Significant (depressive episodes) and near significant (depressive symptoms) higher direct associations were estimated for males in their 40s and 50s than for males in their 60s. There was at each age-group no significant difference in estimated associations across gender. Irrespective of the temporal order of variables, findings suggest that audiological services should facilitate psychosocial counselling.

Hearing loss is an etiologically heterogeneous trait with differences in the age of onset, severity and site of lesion. It is caused by a combination of genetic and/or environmental factors. A longitudinal study to examine the efficacy of early intervention for improving child outcomes is ongoing in Australia. To determine the cause of hearing loss in these children we undertook molecular testing of perinatal "Guthrie" blood spots of children whose hearing loss was either detected via newborn hearing screening or detected later in infancy. We analyzed the GJB2 and SLC26A4 genes for the presence of mutations, screened for the mitochondrial DNA (mtDNA) A1555G mutation, and screened for congenital CMV infection in DNA isolated from dried newborn blood spots. Results were obtained from 364 children. We established etiology for 60% of children. One or two known GJB2 mutations were present in 82 children. Twenty-four children had one or two known SLC26A4 mutations. GJB2 or SLC26A4 changes with unknown consequences on hearing were found in 32 children. The A1555G mutation was found in one child, and CMV infection was detected in 28 children. Auditory neuropathy spectrum disorder was confirmed in 26 children whose DNA evaluations were negative. A secondary objective was to investigate the relationship between etiology and audiological outcomes over the first 3 years of life. Regression analysis was used to investigate the relationship between hearing levels and etiology. Data analysis does not support the existence of differential effects of etiology on degree of hearing loss or on progressiveness of hearing loss.