Int. J. Environ. Res. Public Health 2010, 7 1. Introduction 3731 Noise is typically defined as an unwanted sound or a combination of sounds that may adversely affect people. Noise can manifest in the form of physiologic damage or psychological harm. The mechanism of physiological damage from noise has yet to be fully understood, but research has demonstrated a multitude of factors including increased oxidative stress, vascular changes, and mechanical trauma may be responsible, to name a few. Psychological harm from noise exposure may manifest as increased physiologic stress response, adverse social consequences, sleep disturbance, and detrimental economic effects [1,2]. Noise induced hearing loss (NIHL) has global implications, with 10 million adults and, 5.2 million children in the US, and 250 million people worldwide having a NIHL greater than 25 dB, a clinically significant hearing loss [3,4]. Additionally, occupational noise accounts for 16% of the disabling hearing loss in adults worldwide resulting in decreased economic production [5]. Currently, the armed forces are facing severe disabilities secondary to noise. It has been shown that the top two disabilities now facing the American military are hearing loss and tinnitus. The US government is predicted to spend nearly 1.6 billion dollars this year in order to rehabilitate the men and women traumatized from the effects of noise (TATRC 2010). The purpose of this article is to review some of the recent literature on the physiological and psychological effects from noise and its relationship with quality of life. 2. Mechanisms of Noise Induced Hearing Loss Noise induced hearing loss is generally defined as hearing loss that develops slowly over a long period of time (several years) as the result of exposure to continuous or intermittent loud noise [6]. This results in bilateral, sensorineural hearing loss, often with a pathognomonic notch of decreased hearing on an audiogram at 4,000 Hz. Continuous exposure to sounds greater than 85 dB for 8 hours has been shown to cause NIHL [7,8]. Furthermore, when the exposure is constant, there is increased damage compared to intermittent noise exposure of similar intensity [6,8]. The effects of noise damage are seen more in males, which is possibly due to a larger percentage of males in specific work environments [5]. The role of genetics has been a recent area of interest in uncovering the causative mechanisms of NIHL. There is anecdotal evidence suggesting a possible genetic role. It has been demonstrated that certain patients are more susceptible to permanent threshold shifts (PTS) based on auditory brainstem response (ABR) threshold measurements when subjected to a similar noise exposure [9,10]. To date, any loci of susceptibility to NIHL have not been identified in humans, but many mouse models have been shown to promote NIHL [11]. Chen et al. [12] found that mice deficient in a gene Xp21.2, mapped in the dystrophin gene locus, were more vulnerable to NIHL compared to control mice. Schick et al. [13] demonstrated that there was an increase in noise sensitivity at lower frequencies in vasodilator-stimulated phosphoprotein -/- mice. Fairfield et al. [14] investigated the relationship of NIHL and the role of heat shock proteins (HSPs), molecules that can enhance cell survival in response to stress, and heat shock factor 1 (HSF1), the major transcription factor that regulates HSPs expression in stress, in mice. They found that HSF1 -/- mice were found to have more hearing loss than normal mice given the same noise exposure. Morita et al. [15] looked at the gene Ahl3, located in the 14-Mb