Some over-the-counter as well as prescription drugs and certain industrial chemicals are ototoxic. Exposure to

these can result in temporary or permanent hearing loss.

Some medications cause irreversible damage to the ear, and are limited in their use for this reason. The most important group is the aminoglycosides (main member gentamicin). A rare mitochondrial mutation, m.1555A>G, can increase an individual's susceptibility to the ototoxic effect of aminoglycosides. Long term hydrocodone (Vicodin) abuse is known to cause rapidly progressing sensorineural hearing loss, usually without vestibular symptoms. Methotrexate, a chemotherapy agent, is also known to cause hearing loss. In most cases hearing loss does not recover when the drug is stopped. Paradoxically, methotrexate is also used in the treatment of autoimmune-induced inflammatory hearing loss.

Various other medications may reversibly degrade hearing. This includes loop diuretics, sildenafil (Viagra), high or sustained dosing of NSAIDs (aspirin, ibuprofen, naproxen, and various prescription drugs: celecoxib, etc.), quinine, and macrolide antibiotics (erythromycin, etc.).

Prolonged or repeated environmental or work-related exposure to ototoxic chemicals can also result in sensorineural hearing loss. Some of these chemicals are:

- butyl nitrite - chemical used recreationally known as 'poppers'

- carbon disulfide - a solvent used as a building block in many organic reactions

- styrene, an industrial chemical precursor of polystyrene, a plastic

- carbon monoxide, a poisonous gas resulting from incomplete combustion

- heavy metals: tin, lead, manganese, mercury

- hexane, an industrial solvent and one of the significant constituents of gasoline

- ethylbenzene, an industrial solvent used in the production of styrene

- toluene and xylene, highly poisonous petrochemical solvents. Toluene is a component of high-octane gasolne; xylene is used in the production of polyester fibers and resins.

- trichloroethylene, an industrial degreasing solvent

- Organophosphate pesticides

About 22 million workers are exposed to hazardous noise, with additional millions exposed to solvents and metals that could put them at increased risk for hearing loss. Occupational hearing loss is one of the most common occupational diseases. 49% of male miners have hearing loss by the age of 50. By the age of 60, this number goes up to 70%. Construction workers also suffer an elevated risk. A screening program focused on construction workers employed at US Department of Energy facilities found 58% with significant abnormal hearing loss due to noise exposures at work. Occupational hearing loss is present in up to 33% of workers overall. Occupational exposure to noise causes 16% of adult disabling hearing loss worldwide.

The following is a list of occupations that are most susceptible to hearing loss:

- Agriculture

- Mining

- Construction

- Manufacturing

- Utilities

- Transportation

- Military

- Musicians

- Orchestra conductors

These are much more common in premature babies, particularly those under 1500 g at birth. Premature birth can be associated with problems that result in sensorineural hearing loss such as anoxia or hypoxia(poor oxygen levels), jaundice, intracranial haemorrhages, meningitis. Fetal alcohol syndrome is reported to cause hearing loss in up to 64% of infants born to alcoholic mothers, from the ototoxic effect on the developing fetus, plus malnutrition during pregnancy from the excess alcohol intake.

Gradually developing NIHL refers to permanent cochlear damage from repeated exposure to loud sounds over a period of time. Unlike acoustic trauma, this form of NIHL does not occur from a single exposure to a high-intensity sound pressure level. Gradually developing NIHL can be caused by multiple exposures to excessive noise in the workplace or any source of repetitive, frequent exposures to sounds of excessive volume, such as home and vehicle stereos, concerts, nightclubs, and personal media players.

The aging process has three distinct components: physiologic degeneration, extrinsic damage (nosocusis), and intrinsic damage (sociocusis). These factors are superimposed on a genetic substrate, and may be overshadowed by general age-related susceptibility to diseases and disorders.

Hearing loss is only weakly correlated with age. In preindustrial and non-industrial societies, persons retain their hearing into old age. In the Framingham cohort study, only 10% of the variability of hearing with age could be explained by age-related physiologic deterioration. Within family groups, heredity factors were dominant; across family groups, other, presumably sociocusis and nosocusis factors were dominant.

- Heredity: factors like early aging of the cochlea and susceptibility of the cochlea for drug insults are genetically determined.

- Oxidative stress

- General inflammatory conditions

Nosocusis factors are those that can cause hearing loss, which are not noise-based and separate from pure presbycusis. They may include:

- Ototoxic drugs: Ingestion of ototoxic drugs like aspirin may hasten the process of presbycusis.

- vascular degeneration

- Atherosclerosis: May diminish vascularity of the cochlea, thereby reducing its oxygen supply.

- Dietary habits: Increased intake of saturated fat may accelerate atherosclerotic changes in old age.

- Smoking: Is postulated to accentuate atherosclerotic changes in blood vessels aggravating presbycusis.

- Diabetes: May cause vasculitis and endothelial proliferation in the blood vessels of the cochlea, thereby reducing its blood supply.

- Hypertension: causes potent vascular changes, like reduction in blood supply to the cochlea, thereby aggravating presbycusis.

However, a recent study found that diabetes, atherosclerosis and hypertension had no correlation to presbycusis, suggesting that these are nosocusis (acquired hearing loss) factors, not intrinsic factors.

About 1 in 1,000 children in the United States is born with profound deafness. By age 9, about 3 in 1,000 children have hearing loss that affects the activities of daily living. More than half of these cases are caused by genetic factors. Most cases of genetic deafness (70% to 80%) are nonsyndromic; the remaining cases are caused by specific genetic syndromes. In adults, the chance of developing hearing loss increases with age; hearing loss affects half of all people older than 80 years.

In addition to medications, hearing loss can also result from specific chemicals: metals, such as lead; solvents, such as toluene (found in crude oil, gasoline and automobile exhaust, for example); and asphyxiants. Combined with noise, these ototoxic chemicals have an additive effect on a person’s hearing loss.

Hearing loss due to chemicals starts in the high frequency range and is irreversible. It damages the cochlea with lesions and degrades central portions of the auditory system. For some ototoxic chemical exposures, particularly styrene, the risk of hearing loss can be higher than being exposed to noise alone.

- Solvents

- toluene, styrene, xylene, "n"-hexane, ethyl benzene, white spirits/Stoddard, carbon disulfide, jet fuel, perchloroethylene, trichloroethylene, "p"-xylene

- Asphyxiants

- carbon monoxide, hydrogen cyanide

- Heavy metals

- lead, mercury, cadmium, arsenic, tin-hydrocarbon compounds (trimethyltin)

- Pesticides and herbicides - The evidence is weak regarding association between herbicides and hearing loss; hearing loss in such circumstances may be due to concommitant exposure to insecticides.

- paraquat, organophosphates

Genetic factors are thought to cause more than 50% of all incidents of congenital hearing loss. Genetic hearing loss may be autosomal dominant, autosomal recessive, or X-linked (related to the sex chromosome).

In autosomal dominant hearing loss, one parent who carries the dominant gene for hearing loss and typically has a hearing loss passes it on to the child. In this case there is at least a 50% probability that the child will also have a hearing loss. The probability is higher if both parents have the dominant gene (and typically both have a hearing loss) or if both grandparents on one side of the family have hearing loss due to genetic causes. Because at least one parent usually has a hearing loss, there is prior expectation that the child may have a hearing loss. Autosomal dominant congenital hearing loss can be attributed to such causes like Waardenburg Syndrome.

Some medications may reversibly affect hearing. These medications are considered ototoxic. This includes loop diuretics such as furosemide and bumetanide, non-steroidal anti-inflammatory drugs (NSAIDs) both over-the-counter (aspirin, ibuprofen, naproxen) as well as prescription (celecoxib, diclofenac, etc.), paracetamol, quinine, and macrolide antibiotics. The link between NSAIDs and hearing loss tends to be greater in women, especially those who take ibuprofen six or more times a week. Others may cause permanent hearing loss. The most important group is the aminoglycosides (main member gentamicin) and platinum based chemotherapeutics such as cisplatin and carboplatin.

On October 18, 2007, the U.S. Food and Drug Administration (FDA) announced that a warning about possible sudden hearing loss would be added to drug labels of PDE5 inhibitors, which are used for erectile dysfunction.

Ototoxic effects are also seen with quinine, pesticides, solvents, asphyxiants and heavy metals such as mercury and lead. When combining multiple ototoxins, the risk of hearing loss becomes greater.

Ototoxic chemicals in the environment (from contaminated air or water) or in the workplace interact with mechanical stresses on the hair cells of the cochlea in different ways. For organic solvents such as toluene, styrene or xylene, the combined exposure with noise increases the risk of hearing loss in a synergistic manner. Carbon monoxide, has been shown to increase the severity of the hearing loss from noise. Given the potential for enhanced risk of hearing loss, exposures and contact with products such as paint thinners, degreasers, white spirits, exhaust, should be kept to a minimum. Noise exposures should be kept below 85 decibels, and the chemical exposures should be below the recommended exposure limits given by regulatory agencies.

Drug exposures mixed with noise potentially lead to increased risk of ototoxic hearing loss. Noise exposure combined with the chemotherapeutic cisplatin puts individuals at increased risk of ototoxic hearing loss. Noise at 85 dB SPL or above added to the amount of hair cell death in the high frequency region of the cochlea In chinchillas. The American Academy of Audiology includes in their position statement that exposure to noise at the same time as aminoglycosides may exacerbate ototoxicity. The American Academy of Audiology recommends people being treated with ototoxic chemotherapeutics avoid excessive noise levels during treatment and for several months following cessation of treatment. Opiates in combination with excessive noise levels may also have an additive affect on ototoxic hearing loss.

Previous noise exposure has not been found to potentiate ototoxic hearing loss.

Chemically-induced hearing loss (CIHL) is a potential result of occupational exposures. Certain chemical compounds may have ototoxic effects. Exposure to organic solvents, heavy metals, and asphyxiants such as carbon monoxide can all cause hearing loss. These chemicals can be inhaled, ingested, or absorbed through the skin. Damage can occur to either the inner ear or the auditory nerve.

Both noise and chemical exposures are common in many industries, and can both contribute to hearing loss simultaneously. Damage may be more likely or more severe if both are present. Industries in which combinations of exposures may exist include construction, fiberglass, metal manufacturing, and many more.

Certain medications may also have the potential to cause hearing loss.

It is estimated that over 22 million workers are exposed to dangerous noise levels, and 10 million are exposed to solvents that could potentially cause hearing loss every year, with an unknown number exposed to other ototoxic chemicals.

While there is no cure, most people with tinnitus get used to it over time; for a minority, it remains a significant problem.

Individuals with Nager syndrome typically have the malformations of the auricle, external auditory canal, and middle ear, including the ossicles. These malformations were found in 80% of individuals with Nager syndrome. Inner ear malformations, however, are not typically seen in this population. Middle ear disease is common among individuals with Nager syndrome. Chronic otitis media and Eustachian tube deformity can result in conductive hearing loss. For this reason, early detection and treatment for middle ear disease is crucial in this population. Sensorineural hearing loss is not a typical characteristic of Nager syndrome; however, a subset of individuals present with a mixed hearing loss, due to a progressive sensorineural component combined with the typical conductive hearing loss (Herrman "et al.", 2005).

Tinnitus is commonly thought of as a symptom of adulthood, and is often overlooked in children. Children with hearing loss have a high incidence of tinnitus, even though they do not express the condition or its effect on their lives. Children do not generally report tinnitus spontaneously and their complaints may not be taken seriously. Among those children who do complain of tinnitus, there is an increased likelihood of associated otological or neurological pathology such as migraine, juvenile Meniere’s disease or chronic suppurative otitis media. Its reported prevalence varies from 12% to 36% in children with normal hearing thresholds and up to 66% in children with a hearing loss and approximately 310% of children have been reported to be troubled by tinnitus.

Occupational hearing loss is defined as damage to either or both ears, at the inner ear or auditory nerve, that results from an exposure in a person's occupation. Although high levels of noise are the main cause of occupational hearing loss (also called noise-induced hearing loss) there are also other factors in the work environment that can result in it. Chemicals, foreign bodies, vibration, barotrauma, along with other hazards can result in hearing loss. These losses that these workers obtain, affect many aspects of their life, mainly social interactions.

Within the United States of America, approximately 10 million people have noise-related hearing loss. Over twice that number are occupationally exposed to dangerous noise levels. Hearing loss accounted for a sizable percentage of occupational illness in 2007, at 14% of cases. As in many countries, in the US organizations like the Occupational Safety and Health Administration (OSHA) and the National Institute for Occupational Safety and Health (NIOSH) are working to understand the causes of occupational hearing loss and how it can be prevented. They work to produce regulations and guidelines to help protect the hearing of workers in all occupations.

Third window effect caused by:

- Superior canal dehiscence – which may require surgical correction.

- Widened vestibular aqueducts

At high doses, quinine, aspirin and other salicylates may also cause high-pitch tinnitus and hearing loss in both ears, typically reversible upon discontinuation of the drug.

The erectile dysfunction medications Viagra, Levitra, and Cialis have also been reported to cause hearing loss.

Universal Newborn Hearing Screenings (UNHS) is mandated in a majority of the United States. Auditory neuropathy is sometimes difficult to catch right away, even with these precautions in place. Parental suspicion of a hearing loss is a trustworthy screening tool for hearing loss, too; if it is suspected, that is sufficient reason to seek a hearing evaluation from an audiologist.

In most parts of Australia, hearing screening via AABR testing is mandated, meaning that essentially all congenital (i.e., not those related to later onset degenerative disorders) auditory neuropathy cases should be diagnosed at birth.

In cases where the causes are environmental, the treatment is to eliminate or reduce these causes first of all, and then to fit patients with a hearing aid, especially if they are elderly. When the loss is due to heredity, total deafness is often the end result. On the one hand, persons who experience gradual deterioration of their hearing are fortunate in that they have learned to speak. Ultimately the affected person may bridge communication problems by becoming skilled in sign language, speech-reading, using a hearing aid, or accepting elective surgery to use a prosthetic devices such as a cochlear implant.

Fluid accumulation is the most common cause of conductive hearing loss in the middle ear, especially in children. Major causes are ear infections or conditions that block the eustachian tube, such as allergies or tumors. Blocking of the eustachian tube leads to decreased pressure in the middle ear relative to the external ear, and this causes decreased motion of both the ossicles and the tympanic membrane.

- acute or serous otitis media

- otitis media with effusion or 'glue ear'

- Perforated eardrum

- Chronic suppurative otitis media (CSOM)

- Cholesteatoma

- Otosclerosis, abnormal growth of bone in or near the middle ear

- middle ear tumour

- ossicular discontinuity as a consequence of infection or temporal bone trauma

- Congenital malformation of the ossicles. This can be an isolated phenomenon or can occur as part of a syndrome where development of the 1st and 2nd branchial arches is seen such as in Goldenhar syndrome, Treacher Collins syndrome, branchio-oto-renal syndrome etc.

- Barotrauma unequal air pressures in the external and middle ear. This can temporarily occur, for example, by the environmental pressure changes as when shifting altitude, or inside a train going into a tunnel. It is managed by any of various methods of ear clearing manoeuvres to equalize the pressures, like swallowing, yawning, or the Valsalva manoeuvre. More severe barotrauma can lead to middle ear fluid or even permanent sensorineural hearing loss.

Known causes include physical trauma, acoustic neuroma, measles, labyrinthitis, microtia, meningitis, Ménière's disease, Waardenburg syndrome, mumps (epidemic parotitis), and mastoiditis.

A 1998 study of schoolchildren found that per thousand, 6-12 had some form of unilateral hearing loss and 0-5 had moderate to profound unilateral hearing loss. It was estimated that in 1998 some 391,000 school-aged children in the United States had unilateral hearing loss.

In some cases, the loss is extremely sudden and can be traced to specific diseases, such as meningitis, or to ototoxic medications, such as Gentamicin. In both cases, the final degree of loss varies. Some experience only partial loss, while others become profoundly deaf. Hearing aids and cochlear implants may be used to regain a sense of hearing, with different people experiencing differing degrees of success. It is possible that the affected person may need to rely on speech-reading and/or sign language for communication.

In most cases the loss is a long term degradation in hearing loss. Discrediting earlier notions of presbycusis, Rosen demonstrated that long term hearing loss is usually the product of chronic exposure to environmental noise in industrialized countries (Rosen, 1965). The U.S. Environmental Protection Agency has asserted the same sentiment and testified before the U.S. Congress that approximately 34 million Americans are exposed to noise pollution levels (mostly from roadway and aircraft noise) that expose humans to noise health effects including the risk of hearing loss (EPA, 1972).

Certain genetic conditions can also lead to post-lingual deafness. In contrast to genetic causes of pre-lingual deafness, which are frequently autosomal recessive, genetic causes of post-lingual deafness tend to be autosomal dominant.