Perceived Hearing Loss and Availability of Audiologists in Appalachia

Introduction: There is a high demand for audiologists throughout the United States. Previous research has supported an additional demand for these providers within Appalachia. Purpose: The purpose of the study was to determine if Appalachia has a disproportionally high demand for audiologists compared to the rest of the United States. Methods: A cross-sectional retrospective study was performed with population data from the Appalachian Regional Commission, the American Academy of Audiology, and the United States Census Bureau. County-level population-weighted averages of individuals with perceived hearing loss and number of audiologists per capita were compared between Appalachian and non-Appalachian counties. Results: A mean weighted 5.76 % of individuals reported hearing loss within Appalachia, which was 1.1% higher than the rest of the United States. The 1.14 audiologists per 100,000 individuals in Appalachian counties was not significantly lower than the 1.32 audiologists per 100,000 individuals found in non-Appalachian counties. Audiologists per capita decreased with increases in Beale code and percent reporting hearing loss. Conclusion: The high number of individuals reporting hearing loss supports an increased demand for audiologists in rural Appalachia. More research is needed to determine how to meet this demand or improve the efficacy of the limited number of providers

Association of pigmentation and melanocortin-one receptor genotype with susceptibility to noise-induced hearing loss in college-aged music students

Approximately 13% of the American population between the ages of 20-69 have signs of noise-induced hearing loss. Noise exposure at least partially causes hearing loss by generating free radicals in the ear, which damage cells. Eumelanin is an antioxidant that scavenges the free radicals and may protect the ear from noise-induced damage. Eumelanin is also a polymer that depicts hair and eye color and sensitivity to sunlight. Production of eumelanin is partially regulated by the gene, melanocortin-one receptor; individuals with single nucleotide polymorphisms in this gene have reduced eumelanin expression. The purpose of this study was to measure the extent to which pigmentation, e.g. hair and eye color and sunlight sensitivity, is associated with noise-induced hearing loss, and measure the extent to which single nucleotide polymorphisms in the melanocortin-one receptor gene are associated with noise-induced hearing loss. To accomplish this goal, we used a phased approach design and first evaluated hearing loss and pigmentation in 155 student musicians. This data was used to measure the association of pigmentation and noise-induced hearing loss. Then, buccal cells were collected in 111 student musicians with low to moderate levels of sunlight sensitivity so that we could measure single nucleotide polymorphisms in the melanocortin-one receptor gene. According to two multifactor analyses of variance, no association was found between noise-induced hearing loss and pigmentation (F(82,72) = 0.707, p = 0.936), nor melanocortin-one receptor genotype (F(79,39) = 0.488, p = 0.996). Despite our statistically insignificant results, we were able to detect a trend of increased thresholds in individuals with pigmentation indicating decreased levels of eumelanin. Also, one single nucleotide polymorphism, rs2228479, did show enough of an association with noise-induced hearing loss to warrant further investigation. Our inability to detect significant effects may have been due to an unexpected decrease in audiometric thresholds compared to previous measurements in this population. In this study, we used ER-3A inserts to evaluate hearing, which are more reliable for measuring thresholds between 4000 and 8000 Hz compare to TDH-39’s, which were used in previous analyses. It is also possible that we would have detected a stronger association of melanocortin-one receptor genotype and noise-induced hearing loss if we had sequenced the entire gene. Therefore, further research is required to evaluate the effects of noise exposure on student musicians using more sensitive audiometric criteria. Also, the association of melanocortin-one receptor genotype and noise-induced hearing loss should be evaluated with the entire melanocortin-one receptor sequence

Tumor promoting properties of a cigarette smoke prevalent polycyclic aromatic hydrocarbon as indicated by the inhibition of gap junctional intercellular communication via phosphatidylcholine-specific phospholipase C

Inhibition of gap junctional intercellular communication (GJIC) and the activation of intracellular mitogenic pathways are common hallmarks of epithelial derived cancer cells. We previously determined that the 1-methyl and not the 2-methyl isomer of anthracene, which are prominent cigarette smoke components, activated extracellular receptor kinase, and inhibited GJIC in WB-F344 rat liver epithelial cells. Using these same cells, we show that an immediate upstream response to 1-methylanthracene was a rapid ( LT 1 min) release of arachidonic acid. Inhibition of phosphatidylcholine-specific phospholipase C prevented the inhibition of GJIC by 1-methylanthracene. In contrast, inhibition of phosphatidylinositol specific phospholipase C, phospholipase A(2), diacylglycerol lipase, phospholipase D, protein kinase C, and tyrosine protein kinases had no effect on 1-methylanthracene-induced inhibition of GJIC. Inhibition of protein kinase A also prevented inhibition of GJIC by 1-methylanthracene. Direct measurement of phosphatidylcholine-specific phospholipase C and sphingomyelinase indicated that only phosphatidylcholine-specific phospholipase C was activated in response to 1-methylanthracene, while 2-methylanthracene had no effect. 1-methylanthracene also activated p38-mitogen activated protein kinase; however, like extracellular kinase, its activation was not involved in 1-methylanthracene-induced regulation of GJIC, and this activation was independent of phosphatidylcholine-specific phospholipase C. Although mitogen activated protein kinases were activated, Western blot analyzes indicated no change in connexin43 phosphorylation status. Our results indicate that phosphatidylcholine-specific phospholipase C is an important enzyme in the induction of a tumorigenic phenotype, namely the inhibition of GJIC; whereas mitogen activated protein kinases triggered in response to 1-methylanthracene, were not involved in the deregulation of GJIC