The genetic aspects of occupational hearing impairment

Abstract

This article was designed to be the overview of the current literature publications concerning the identification of the genetic markers of susceptibility to the noise-induced loss of hearing. The analysis of these data has demonstrated that the major gene polymorphisms associated with the development of this pathological condition are localized in the genes encoding for the antioxidant systems, potassium homeostasis, and adhesion molecules as well as in the genes involved in intercellular coupling, the mechanisms underlying the cellular response to stress, activation and regulation of heat shock proteins, and signaling function of the immune system. It is concluded that the further investigations into the genetic aspects of the full-genome sequencing techniques and the search for genomic associations could greatly contribute to the development of personalized medicine and the reduction of risks of occupational noise-induced sensorineural impairment of hearing.

Association of GST gene polymorphism and noise-induced hearing loss<em>Running title: GST gene polymorphism and NIHL</em>

“…Carlsson et al analyzed genetic polymorphism in the 10% most susceptible and 10% most resistant extremes of 1200 Swedish noise-exposed workers to investigate whether genetic variation is associated with susceptibility to NIHL. In their study no significant differences were found between 103 noise-susceptible and 114 noise-resistant Swedish workers from the point of view of GSTM1 and GSTT1 polymorphism [6]. Palodetto et al showed that polymorphism in GSTM1 and GSTT1 have no influence on ototoxicity of aminoglycosides, which seem to involve similar oxidative stress mechanis like NIHL [14].…”

“…So, it is possible in studies that did not find association of GST gene and NIHL, like our study, the noise exposure levels to which the majority of study workers have been exposed over the years did not reach the critical level needed to activate the antioxidant system, and therefore differences in their antioxidant systems are unlikely to show up in their findings. However, it is possible that difference exists when subgroups (noise exposure levels, noise exposure times) be evaluated separately [6].…”

“…Several NIHL susceptibility genes have been suggested, such as, genes encoding for the antioxidant systems, potassium ion channels, heat shock proteins, and the signaling function of the immune system [6]. Oxidative stress genes, such as glutathione S-transferase, (GST); glutathione peroxidase (GPX1); glutathione reductase (GSR), superoxide dismutases (SOD), catalase (CAT), and paraoxonase (PON) [6] are obvious candidate genes for NIHL [7]. Numerous studies have shown that high-intensity noise exposure causes mechanical or metabolic changes in the cochlea which lead inner ear damage [8].…”