PubMed · 14497394
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J SATALOFF, H MENDUKE, A HUGHES. 1962. Temporary threshold shift in normal and abnormal ears.. https://doi.org/10.1001/archotol.1962.00740050056011
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A consanguineous family with autosomal recessive nonsyndromic hearing impairment (NSHI) was ascertained in Pakistan and displayed significant evidence of linkage to 3q13.31-q22.3. The novel locus (DFNB42) segregating in this kindred, maps to a 21.6 cM region according to a genetic map constructed using data from both the deCode and Marshfield genetic maps. This region of homozygosity is flanked by markers D3S1278 and D3S2453. A maximum multipoint LOD score of 3.72 was obtained at marker D3S4523. DFNB42 represents the third autosomal recessive NSHI locus to map to chromosome 3.
OBJECTIVE: To assess the exposure of bus drivers to noise and whole-body vibration (WBV) and to examine the possibility of an association between these risk factors for noise-induced hearing loss. METHODS: A cross-sectional study was carried out among 141 bus drivers who underwent an audiometry test. This group was classified and internally stratified in subgroups of "exposed" and "controls" according to cumulative working time as bus drivers. Their exposure to noise and vibration was assessed. The association between noise-induced hearing loss (NIHL) and the set of explanatory variables was analyzed through logistic regression. RESULTS: The average (+/- standard deviation) weekly noise exposure of front-engine bus drivers was 83.6 +/- 1.9 dB(A), while rear-engine bus drivers were exposed to 77.0 +/- 1.1 dB(A). The weighted average of vibration acceleration was 0.85/m(2). In the best adjusted model, the multivariable analysis showed that age (>44; OR=2.54; 95% CI=1.15-5.62), diabetes (OR=5.46; 95% CI=0.95-31.4), and the level of noise emission [>86.8 dB(A); OR=2.76; 95% CI=1.24-6.15] were risk factors for NIHL. In another model studied, WBV exposure was significant in determining NIHL. CONCLUSIONS: Bus drivers were exposed to significant WBV levels. The noise exposure was more pronounced in front engine than in rear-engine vehicles. No association between WBV exposure and NIHL was observed and no interaction was found between WBV and noise exposure. Further studies are required as other model indicated an association between WBV and NIHL.
Noise induced hearing loss (NIHL) is a complex disease caused by an interaction between genetic and environmental factors. Damage in the cochlea as a result of noise exposure appears to be mediated by reactive oxygen species (ROS). To investigate whether genetic variation in the human protective antioxidant system is associated with high or low susceptibility to NIHL, genetic polymorphisms derived from genes involved in the oxidative stress response were analysed in the 10% most susceptible and 10% most resistant extremes of 1200 Swedish noise-exposed workers. The genetic polymorphisms included 2 deletion polymorphisms for the GSTM1 and GSTT1 gene, and 14 SNPs derived from the CAT, SOD, GPX, GSR and GSTP1 genes. No significant differences were found between susceptible and resistant groups, providing no support for a major role of genetic variation of antioxidant enzymes in the susceptibility to NIHL.