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.

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 region on the mouse chromosome 17 and its role in NIHL. They found a resistance to NIHL after prolonged noise exposure in mice when the wild type Ahl3 allele was present, demonstrating a genetic variation in susceptibility to NIHL.

Hearing loss from otologic trauma, which is defined as a sudden change in hearing due to exposure of a sudden burst of sound, may be due to a different mechanism of action than NIHL, and should be thought of as a separate entity. Acoustic trauma can cause mechanical disruption of the cochlea and may result in permanent hearing loss. In 1944, Lurie et al. [16] described graduated degrees of acoustic trauma in guinea pigs beginning with stripping of mesothelial cells under the basilar membrane, progressing to disruption of external hair cells and eventually, separation of the Organ of Corti from the basilar membrane as the time of exposure increased. Noise induced hearing loss, on the other hand, is thought to be due to various other mechanisms. One leading theory that will be focused on in this article is the role of oxidative stress in chronic noise exposure.

Noise can have a more global effect on human physiology and act upon multiple non-auditory systems such as cardiovascular, neuroendocrine, and psychological [37]. Quantifying the non-auditory effects of noise may be difficult due to lack of strong scientific evidence lack statistical evidence, as there are often plausible alternative explanations for the results. These studies often have confounding variables, especially selection bias.

There have been multiple studies that have investigated the relationship between noise, blood pressure, and myocardial damage. A comprehensive meta-analysis by van Kempen et al. [38] looked at 43 epidemiological studies looking at the correlation between noise exposure and elevated blood pressure and ischemic heart disease during the time period of 1970 and 1999. They found that there was a significant association between occupational and air-traffic noise exposure and hypertension. The evidence of noise exposure causing ischemic heart disease was inconclusive as there was no definitive relationship.

Another study investigated the relationship of noise and blood pressure and a stress response included a quality of life survey to noise exposed subjects. Evans et al. [2] looked at children that lived in a noisy “airport” community and a quiet community. They measured systolic and diastolic blood pressure, urine epinephrine, norepinephrine, and cortisol levels, as well as obtained results from the KINDL quality of life questionnaire. They found that there was an increase in blood pressure in the noisy communities. There was also a significant increase in urine epinephrine and norepinephrine levels, but not a significant change in cortisol levels. The KINDL questionnaire is an assessment of quality of life in children and has been proven to produce reliable results [39–41]. This questionnaire was used in this study and found that the quality of life in the children living in the noisy community declined significantly over the 18 months of the study [2].

This is just some of the evidence to highlight noise as an unwanted environmental pollutant that has global implications. In our industrialized society, a significant population is exposed to noise on a daily basis with its resultant health effects, and subsequent substantial economic burden. There has been a plethora of research on the mechanism of NIHL. The role of oxidative stress in NIHL has been extensively investigated and remains a probable cause of NIHL. This results in significant deterioration in quality of life in that it disrupts sleep, causes cognitive impairment, and has many non-auditory deleterious health effects.