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Potential health risks of exposure to noise from personal music ...

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Health <strong>risks</strong> <strong>from</strong> <strong>exposure</strong> <strong>to</strong> <strong>noise</strong> <strong>from</strong> <strong>personal</strong> <strong>music</strong> playersVibrationVibration-induced hearing loss may be developed in patients after temporal bone surgeryor in subjects working with vibrating <strong>to</strong>ols. In such cases, co-<strong>exposure</strong> <strong>to</strong> <strong>noise</strong> andvibration can increase hearing threshold shift compared <strong>to</strong> <strong>noise</strong>-only <strong>exposure</strong>.Recent studies concerning association <strong>of</strong> body vibration with sound trauma broughtcontradic<strong>to</strong>ry and inconclusive results (Palmer et al. 2002a, Silva et al. 2005).3.5.6.2. O<strong>to</strong><strong>to</strong>xic drugsSeveral drugs used in contemporary medicine can damage hearing. O<strong>to</strong><strong>to</strong>xic effectdepends on the dose, way <strong>of</strong> application and the type <strong>of</strong> medicine. Although these drugscan damage hearing at different levels <strong>of</strong> the audi<strong>to</strong>ry pathway, majority <strong>of</strong> them exertmainly cochlear o<strong>to</strong><strong>to</strong>xic effect and they are competitive with <strong>noise</strong> in damaging haircells.The main groups <strong>of</strong> drugs that can cause hearing loss are:- antibiotics (aminoglycosides, macrolides)- antineoplastic drugs (cisplatinum, carboplatinum)- loop diuretics (furosemide, ethacrinic acid)- non-steroid anti-inflamma<strong>to</strong>ry drugs (acetyl salicylate acid)- antimalaric drugs.The most commonly used drugs that have been reported in the literature <strong>to</strong> result inhearing damage are aminoglycosides and anti-neoplasmatic drugs. Aminoglycosides areused parenterally in treating severe bacterial infections. After prolonged treatment withsuch aminoglycosides like gentymycin, kanamycin, amikacin, hearing loss at highfrequencies, tinnitus and vestibular disorders were noted. The changes in hearing areirreversible. Prior <strong>exposure</strong> <strong>to</strong> <strong>noise</strong> (and vibration) increases the risk <strong>of</strong> hearingimpairment due <strong>to</strong> aminoglycosides. The o<strong>to</strong><strong>to</strong>xic effect depends on geneticallydetermined susceptibility; it increases with high concentration <strong>of</strong> ferrum ions in theblood, and low protein diet. Anti-oxidant substances (like Vitamins A, C and E) have beenshown <strong>to</strong> be protective.It has been shown that cancer chemotherapy with cis-platinum produces hearing loss inup <strong>to</strong> 31% <strong>of</strong> patients. As in <strong>noise</strong>-induced hearing loss and aminoglycoside-inducedhearing loss, these chemotherapeutics affect mainly hair cells <strong>of</strong> the basic turn in thecochlea and result in high-frequency (above 2 kHz) hearing impairment. Noise <strong>exposure</strong>at the time <strong>of</strong> chemotherapy significantly increases the risk <strong>of</strong> hearing damage.3.5.6.3. GeneticsThe advance <strong>of</strong> genetic research and associated <strong>to</strong>ols triggered a series <strong>of</strong> explorations <strong>of</strong>the human genes possibly involved in NIHL, first evidences point <strong>to</strong> some candidategenes and seem <strong>to</strong> exclude other genes (Fortuna<strong>to</strong> et al. 2004, Heinonen-Guzejev et al.2005, Yang et al. 2005, Yang et al. 2006, Van Laer et al. 2006, Yang et al. 2006,Sliwińska-Kowalska et al. 2006, Konings et al. 2007, Van Eyken et al. 2007). Themechanisms <strong>of</strong> acoustic trauma involve both metabolic stress and micromechanicaldamage <strong>to</strong> the outer hair cells, predominantly <strong>to</strong> their stereocilia. Thus, good candidategenes are those encoding oxidative stress enzymes, mi<strong>to</strong>chondrial proteins, and proteinsinvolved in K + recycling pathway. The importance <strong>of</strong> oxidative stress genes has beenshown in knockout mice, including SOD1 -/- (Ohlemiller et al. 1999), GPX1 -/- (Ohlemiller etal. 2000), and PMCA2 -/- mice (Kozel et al. 2002), all <strong>of</strong> which were more sensitive <strong>to</strong><strong>noise</strong> than their wild-type littermates. However, these results have not been confirmed inhumans (Carlsson et al. 2005). A more recent study suggests a possible role <strong>of</strong>potassium recycling pathway genes in the susceptibility <strong>to</strong> NIHL in human workers (VanLaer et al. 2006).38

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