Demographic Disparities in Drive Times to the Nearest Audiologist in the United States.

PURPOSE: Audiological services are underused, possibly because patients need to drive long distances to see a provider. In this study, we measured the association of drive times to the nearest audiologist with population density, income, ethnicity, race, and distance to the nearest audiology graduate program. METHOD: Drive times for each census block group to the nearest audiologist were measured using census data, the National Provider Identifier Registry, and a geographic analyzing tool called ArcGIS for all block groups within the United States. The association between drive times and population density, income, ethnicity, race, and audiology program distance was evaluated with a population density-matched case-control study and multiple linear regression analyses. RESULTS: Approximately 5.29 million Americans need to drive at least 1 hr to visit their closest audiologist. The 10% most rural-dwelling Americans drive an average of 33.8 min. The population density-matched case-control study demonstrated that percent below poverty, percent identifying as Hispanic, and travel times to the nearest audiology program were all significantly higher in census block groups with high drive times to the nearest audiologist. An average of 7.96% of individuals in census block groups with low drive times identified as Hispanic, but 18.8% identified as Hispanic in high drive time groups. The multiple linear regression showed that the effect of demographics and distance to the nearest audiology program was highest in rural areas. In both analyses, adjusting for poverty did not drastically change the effect of percent identifying as Hispanic on drive times. CONCLUSIONS: Long drive times restrict access to audiological care for those who live in rural areas. This restriction disproportionately affects those in rural areas who identify as Hispanic or have low income.

Association of Audiometric Thresholds with HbA1c and Blood Lipid Levels.

Aims: The purpose of this study is to determine if the combined associations of HbA1c and blood lipid levels with audiometric thresholds are nonadditive, additive, or synergistic. Methods: A retrospective cross-sectional study was performed using the 2009-2010, 2011-2012, and 2015-2016 National Health and Nutritional Examination Survey. Participants were placed into tertial groups based on HbA1c, triglyceride, low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) levels. Two-way analyses of variance were used to measure the combined effect of HbA1c and each lipid on mid- and high-frequency audiometric thresholds. Groups were matched by age and gender among HbA1c and blood lipid groups in three separate datasets. Results: The difference in mid-frequency audiometric thresholds between the lowest and highest level of HbA1c groups was 2.0 dB (P = 0.019) in one data set and 2.6 dB (P = 0.005) in another dataset. The difference in mid-frequency audiometric thresholds was 2.1 dB (P = 0.012) when comparing the lowest and highest triglyceride groups, and 2.4 dB (P = 0.001) when comparing the lowest and highest LDL-C groups. HDL-C levels, high frequency audiometry, and the interaction components were not significant for any analysis. Conclusions: These results indicate that higher HbA1c and blood lipid levels may have an additive effect on mid-frequency audiometric thresholds.

Association of self-reported noise exposure and audiograms processed with algorithms proposed to quantify noise-induced hearing loss.

OBJECTIVE: The objective of this study was to assess the association of self-reported noise exposure and audiograms processed with ten algorithms proposed to quantify noise-induced hearing loss using receiver operating characteristic (ROC) curves. DESIGN: Participants were placed into groups based on self-reported noise exposure. Self-reported noise exposure served as a predictor for noise-induced hearing loss (NIHL). Audiograms were analysed with ten algorithms: The Guidelines, Brewster's Rules, two versions of military Noise-induced Hearing Loss, the Bulge Depth, the age-adjusted 8 kHz threshold and four versions of a new algorithm called the Adjusted Notch Depth (AND). The area under the ROC curves were calculated for each algorithm. STUDY SAMPLE: Data were collected from three cycles of the National Health and Nutrition Examination Survey. RESULTS: Only one version the AND significantly identified those with self-reported noise exposure with an area under the curve of 0.562. CONCLUSIONS: The association between the AND and self-reported noise exposure was marginally better than the previous algorithms in identifying those with self-reported noise exposure. These findings do not support using puretone thresholds for identifying those with NIHL in a cross-sectional research study without stratifying the participants. More research is needed to determine how the AND can be applied to stratified designs.

Sensorineural hearing loss and volatile organic compound metabolites in urine.

PURPOSE: Oxidative stress in the auditory system contributes to acquired sensorineural hearing loss. Systemic oxidative stress, which may predict auditory oxidative stress, can be assessed by measuring volatile organic compound metabolite concentrations in urine. The purpose of this retrospective study was to determine if hearing decreased in those with higher concentrations of urinary volatile organic compound metabolites. MATERIALS AND METHODS: Audiometric, demographic, and metabolite concentration data were downloaded from the 2011-2012 cycle of the U.S. National Health and Nutritional Examination Survey. Participants were first grouped by reported noise exposure. For each metabolite, an analysis of covariance was used to look for differences in age-adjusted hearing loss among urinary volatile organic compound metabolite concentration groups. Participants were grouped into quartiles based on concentration for each metabolite separately because many individuals were at the lower limit of concentration detection for several metabolites, leading to a non-normal distribution. RESULTS: Age-adjusted high-frequency pure-tone thresholds were significantly (FDR < 0.05) increased by about 3 to 4 dB in high concentration quartile groups for five metabolites. All five metabolites were glutathione-dependent mercapturic acids. The parent compounds of these metabolites included acrylonitrile, 1,3 butadiene, styrene, acrylamide, and N,N-dimethylformamide. Significant associations were only found in those with no reported noise exposure. CONCLUSIONS: Urinary metabolites may help to explain susceptibility to oxidative stress-induced hearing loss.

Prenatal smoke exposure: effects on infant auditory system and placental gene expression.

Prenatal smoke exposure has been shown to change cochlear echo response amplitudes and auditory brainstem response (ABR) wave latencies in newborns. Since gene expression changes are often synchronized in different tissue types, the goal of the present work was to determine the relationships between prenatal smoke exposure induced changes in hearing responses with changes in placental gene expression. Results showed significant cotinine level elevations in mothers who smoked ≥10cigarettes/day during their pregnancy compared to no detectable cotinine in nonsmoking mothers. Cochlear echo response amplitudes in the 2-8kHz range and ABR wave latencies, specifically wave V and interpeak interval I-V, were also significantly reduced in newborns of smoking mothers. Functional pathway analysis of upregulated placental genes using the Database for Annotation, Visualization and Integrated Discovery (DAVID) online software showed significant enrichment of terms associated with neurodevelopmental processes including glutamatergic and cholinergic systems and a number of wingless type proteins in the top two tiers with corrected enrichment p-values of ≤0.05. Other relevant functional pathways were significant at unadjusted enrichment p-values of 0.001-0.11 and included calcium signaling, neurotransmission/neurological processes and oxidative stress. The neurological process clusters included 7 genes (EML2, OTOR, SLC26A5, TBL1X, TECTA, USH1C and USH1G) known to modulate cochlear outer hair cell motility. We localized proteins encoded by the top two regulated genes, TBL1X and USH1C, using immunohistochemistry to placental stem and anchoring villi associated with active contractile function. These placental genes may mediate active contraction and relaxation in the placental villi, for example, during maternal-fetal perfusion matching, similar to the active lengthening and shortening of the cochlear outer hair cells during sensory transduction. Thus, the functional consequence of their alteration in the cochlea would be reflected as a decline in cochlear echoes as shown in this study. Such parallel changes suggest the potential utility of placental gene expression as a surrogate for evaluating changes in the developing cochlea related to potential aberrant cochlear function in newborns with prenatal smoke exposure.

Effect of ciprofloxacin/dexamethasone versus ciprofloxacin/hydrocortisone on lipopolysaccharide-induced experimental otitis media.

OBJECTIVES: The purpose of this study is to compare the effect of topical ciprofloxacin/dexamethasone versus topical ciprofloxacin/hydrocortisone on the outcome of lipopolysaccharide (LPS)­induced otitis media with effusion in chinchillas. STUDY DESIGN: A randomized experimental animal study. SETTING: Jerry L. Pettis Veteran's Medical Center. SUBJECTS AND METHODS: Otitis media with effusion was induced in 5 groups of chinchillas, 6 per group, by injecting 0.3 mL (1 mg/mL) of Salmonella enteric LPS into the superior bullae of each chinchilla with a venting needle in place. Each group was treated with 0.2 mL of test substance at ­2, 24, 48, and 72 hours relative to the 0-hour LPS induction. Group 1 was treated with vehicle control. Groups 2 to 5 received 0.3% ciprofloxacin with either 0.1% dexamethasone (group 2), 1% dexamethasone (group 3), 0.1% hydrocortisone (group 4), or 1% hydrocortisone (group 5). The outcome of each treatment was measured by the amount of middle ear effusion present and mucosal thickness at 120 hours posttreatment. RESULTS: Ciprofloxacin/dexamethasone 1% significantly (P = .0150) reduced middle ear effusion compared with control. Ciprofloxacin/dexamethasone 1% significantly reduced the mucosal thickness when compared with vehicle control (P = .0005), ciprofloxacin/dexamethasone 0.1% (P = .0240), and ciprofloxacin/hydrocortisone 0.1% (P = 1.00). Results also showed a dose-response effect between the ciprofloxacin/dexamethasone concentrations. CONCLUSIONS: This study demonstrated that treatment with a combination of topical ciprofloxacin and corticosteroid decreased the middle ear effusion when compared with the control group and that ciprofloxacin/dexamethasone suspension reduced the severity of LPS-induced experimental otitis media more than ciprofloxacin/hydrocortisone did.

Effect of topical glucocorticoid treatment in chinchilla model of lipopolysaccharide induced otitis media with effusion.

OBJECTIVE: To compare the efficacy of topical treatment with three glucocorticoids in lipopolysaccharide induced otitis media with effusion (OME). METHODS: Chinchillas were divided into seven treatment groups consisting of vehicle and three glucocorticoids: dexamethasone sodium phosphate (DSP), fluticasone propionate (FP), and hydrocortisone, each at concentrations of 0.1% and 1.0%. LPS (300 µg) was injected into the superior bullae of chinchillas to induce OME. Animals were treated with test substances at -2, 24, and 48 h relative to LPS inoculation. After 96 h, chinchillas were euthanized, samples of middle ear effusion (MEE) were collected, and temporal bones were removed for histopathological examination. Reduction of OME was evaluated by measuring MEE volume and thickness of mucosal lining for each bulla. RESULTS: One percent treatment of FP significantly reduced MEE. One percent treatment of DSP and HC significantly reduced the mucosal thickness (MT), DSP (15.0 µM) more than HC (30.8 µM). Treatment with 0.1% glucocorticoids did not lead to any significant reduction. CONCLUSIONS: Clearance of otitis media with effusion seems to be a class effect among glucocorticoids. DSP was the best in reducing MT. It is important to evaluate treatment with various glucocorticoids in order to discover alternative drugs for OME.

Glucocorticoids reduce nitric oxide concentration in middle ear effusion from lipopolysaccharide induced otitis media.

OBJECTIVE: Otitis media with effusion (OME) is a common childhood disease that is characterized by an accumulation of fluid in the middle ear. Chronic OME can also lead to sensorineural hearing loss (SNHL). Nitric oxide (NO), an inflammatory mediator (IM) of OME, is a free radical known to regulate cell proliferation, cell death, and angiogenesis. Previous studies have shown that nitric oxide may cause SNHL through outer hair cell (OHC) cytotoxicity. This experiment was designed to determine whether glucocorticoids, dexamethasone, fluticasone propionate, or rimexolone, can reduce the concentration of NO in middle ear effusion (MEE). METHODS: Fifty-three chinchillas were divided into 7 groups, vehicle vs. each glucocorticoid at 0.1% and 1.0% concentrations. Due to anesthesia complications, N ranged from 6 to 9 per group. Two hundred microlitres of each test article was injected into the bullae of each animal. Two hours later, lipopolysaccharide (LPS) (0.3mg in solution) was added. Test articles were re-administered at 24 and 48h post-LPS induction. After 96h, animals were euthanized and the MEE was collected. RESULTS: All three glucocorticoids numerically reduced NO concentration in the middle ear when administered at 0.1%, but only FP showed a significant reduction. At 1.0% concentrations, all 3 steroids significantly reduced NO concentration. CONCLUSION: This study suggests that glucocorticoid treatment reduces NO concentration in the MEE and may protect the ear from the SNHL caused by NO.

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 (<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.