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Abstract
Noise has a metabolic and mechanical effect on the inner ear and may therefore interfere with gap junction channels, thus disrupting the interaction between cells in the cochlea. Studies have shown that carriers of connexin mutations in genes involved in HI may have some disturbance in auditory function and may be more susceptible to damage caused by, e.g. noises. Furthermore, hair cell damage in the cochlea as a result of noise exposure can also be mediated by reactive oxygen species. Smoking in combination with elevated diastolic blood pressure and presence of the Raynaud's disease (white finger disease) seems to aggravate noise induced hearing loss (NIHL). In the present study we investigated whether interaction between connexin mutations (C×26 and C×30) alone, or in combination with genetic variability in the cochlear antioxidant system (GSTM1 deletion, GSTT1 deletion), could explain differences in human noise susceptibility. Furthermore, smoking habits and cardiovascular factors (hypertension, heart disease and white finger diseases) were correlated with noise susceptibility and interactions between genetic factors. Smoking and cardiovascular factors were analysed and correlated with the differences in noise susceptibility found in a Swedish noise-exposed population. The results revealed that smoking alone seems to increase noise susceptibility, and that null-genotypes for the GSTM1 gene in the protective antioxidant system, who smoke/have ever smoked had an additional risk for NIHL compared to those who do not smoke/have never smoked.