Ototoxic Medicines: Drugs That Can Affect Hearing

The Side Effect Almost Nobody Mentions

Most people read the leaflet in a medicine box looking for the familiar warnings: drowsiness, nausea, an upset stomach. Very few think to look for hearing. Yet more than 200 medicines are recognised as potentially ototoxic — capable of damaging the inner ear, the hearing nerve, or the balance organs that sit alongside them. Some cause a temporary ringing that fades within days of stopping. A small number can cause permanent, irreversible hearing loss.

This is not a reason to stop taking prescribed medication. The drugs most strongly associated with hearing damage — platinum chemotherapy agents and certain intravenous antibiotics — are given precisely because the alternative is far worse. Cisplatin treats cancers that would otherwise be fatal. Gentamicin treats infections that would otherwise kill. The point is not avoidance but awareness: knowing which medicines carry a risk, what early damage sounds and feels like, and when to ask for a hearing test rather than assume the ringing in your ears is stress.

That awareness matters more in 2026 than it did a decade ago, because the clinical picture is changing. UK research is actively developing simplified screening tests that could be carried out on a hospital ward or in an outpatient clinic rather than requiring a full audiology appointment — an approach that would make monitoring far more widely available. In 2026, RNID reported on research showing that hearing loss caused by cisplatin chemotherapy can be detected outside the audiology clinic, opening the door to routine monitoring for patients who currently receive none. Until that becomes standard everywhere, the person best placed to notice early ototoxic damage is often the patient.

This article explains which medicines carry ototoxic risk, how the damage happens, the warning signs worth acting on, and exactly what monitoring you can reasonably ask for in the UK.

What Ototoxicity Actually Is

"Ototoxic" simply means toxic to the ear. In practice, ototoxic medicines damage one or both of two delicate structures in the inner ear.

Cochlear ototoxicity — damage to hearing

The cochlea is a fluid-filled spiral containing roughly 15,000 hair cells that convert sound vibration into nerve signals. Human hair cells do not regenerate. Once they are destroyed, the hearing they provided is gone permanently. Ototoxic drugs typically damage the hair cells at the base of the cochlea first — the region that processes the highest frequencies. This is why ototoxic hearing loss almost always begins at pitches above the range tested in a standard hearing check, and why it can be well established before a person notices anything is wrong.

Vestibular ototoxicity — damage to balance

Sitting immediately alongside the cochlea are the vestibular organs, which tell the brain where the head is in space. Some drugs — gentamicin is the classic example — are far more toxic to these than to the cochlea. The result is not deafness but unsteadiness: a feeling of the world bouncing when you walk, difficulty balancing in the dark, and dizziness that a person may wrongly attribute to their illness or to simply being unwell in hospital. A balance assessment is the appropriate investigation when these symptoms follow a course of intravenous antibiotics.

A crucial distinction is between reversible and permanent ototoxicity. Aspirin at high doses, quinine and some diuretics typically cause temporary effects that resolve once the drug is stopped or the dose reduced. Aminoglycoside antibiotics and platinum chemotherapy typically do not. That difference is why the timing of detection matters so much: with the reversible group, catching the problem allows the damage to be undone; with the permanent group, catching it early allows a clinician to consider a dose change or an alternative drug before more hair cells are lost.

The Main Groups of Ototoxic Medicines

The list below covers the drug groups with the strongest evidence base. It is not exhaustive, and it is not a reason to stop anything you have been prescribed — always speak to the prescribing clinician or your pharmacist first.

Platinum-based chemotherapy

Cisplatin and, to a lesser degree, carboplatin carry the highest ototoxic risk of any commonly used medicines. Estimates of significant hearing loss in adults treated with cisplatin vary widely by dose and study, but a substantial minority are affected, and the risk is cumulative — it rises with each cycle. In children treated for cancers such as neuroblastoma, medulloblastoma and osteosarcoma, the consequences are particularly serious, because hearing loss during the years of speech and language development affects education and communication for life. Tinnitus frequently appears first, often within hours or days of an infusion.

Aminoglycoside antibiotics

Gentamicin, amikacin, tobramycin and streptomycin are powerful intravenous antibiotics reserved for serious infections, including sepsis and the chronic lung infections seen in cystic fibrosis. Gentamicin is predominantly vestibulotoxic — it damages balance more than hearing — while amikacin is more cochleotoxic. Damage can appear during treatment or, unsettlingly, weeks after the final dose. A rare inherited mitochondrial variant (m.1555A>G) makes some people profoundly susceptible, and a single standard dose can cause severe permanent deafness in those individuals. Rapid genetic testing for this variant has been introduced in some UK neonatal units, precisely to avoid that outcome.

Loop diuretics

Furosemide and bumetanide, widely prescribed for heart failure and fluid retention, can affect hearing when given intravenously at high doses or rapidly — typically causing temporary hearing loss or tinnitus. The far greater concern is combination: loop diuretics given alongside aminoglycosides or cisplatin substantially amplify the ototoxic effect of both.

High-dose aspirin, NSAIDs and quinine

Aspirin taken at anti-inflammatory doses — the multi-gram daily regimens used for some rheumatological conditions, not the low 75mg cardioprotective dose — is a classic cause of reversible tinnitus and mild hearing loss. Quinine, used for malaria and historically for leg cramps, produces a similar reversible pattern known as cinchonism. Regular long-term use of over-the-counter NSAIDs and paracetamol has also been linked in large observational studies to a modestly increased risk of hearing loss, though the effect for any individual is small and causation is not firmly established.

Other medicines worth knowing about

• Macrolide antibiotics (erythromycin, azithromycin) — usually reversible hearing effects at high intravenous doses.
• Vancomycin — modest risk alone, greater when combined with an aminoglycoside.
• Antimalarials — chloroquine and hydroxychloroquine, rarely, with long-term use.
• Some antivirals and antifungals, and certain older tuberculosis regimens containing streptomycin or capreomycin.
• Erectile dysfunction medicines (sildenafil and related drugs) carry a rare but recognised association with sudden hearing loss.

Two everyday exposures deserve a mention because they are so often overlooked: industrial solvents and chemicals. Toluene, styrene, xylene and carbon monoxide are ototoxic, and workers exposed to both chemicals and noise face a greater risk than either alone would suggest — a point covered in our guide to workplace hearing safety and relevant to anyone due an occupational hearing test.

The Warning Signs — and Why They Are Easy to Miss

Ototoxic damage rarely announces itself as obvious deafness. It arrives quietly, and often at the worst possible moment: during cancer treatment or a serious infection, when a person already feels unwell and has a dozen other symptoms competing for attention. These are the signs worth reporting straight away.

• New or changed tinnitus. A ringing, hissing or high-pitched whine that was not there before treatment is the single most common first sign, particularly with cisplatin. Do not dismiss it as stress or tiredness — report it. Our guide to tinnitus explains what it is and how it is assessed.
• A sense of fullness or blocked ears with no cold, no wax and no obvious cause.
• Difficulty following speech in background noise while one-to-one conversation still feels fine. This is the hallmark of early high-frequency loss, and it is what a speech-in-noise test is designed to detect.
• Consonants blurring. "S", "f", "th" and "sh" are high-frequency sounds and are the first to go. Words start to sound mumbled rather than quiet.
• Unsteadiness, or the world bouncing when you walk. Known as oscillopsia, this is a red flag for vestibular toxicity — often after aminoglycosides — and warrants urgent review.
• Sudden hearing loss in one or both ears. Always a medical emergency, whatever the suspected cause. Sudden sensorineural hearing loss should be seen the same day, because steroid treatment is most effective within 72 hours.

The reason these signs slip through is straightforward. A patient midway through chemotherapy has fatigue, nausea and neuropathy to contend with; a mild ringing barely registers on the list of things to raise in a fifteen-minute clinic appointment. And because ototoxic loss starts above the frequencies a standard test measures, an ordinary hearing check performed early in treatment can come back entirely normal while damage is already underway.

Monitoring: What Good Practice Looks Like in the UK

Where a genuinely ototoxic drug is being used, audiological monitoring is the standard of care — although provision across the UK remains patchy, which is exactly what current research is trying to address. A well-run monitoring programme has three parts.

1. A baseline test before treatment starts

Ideally within 24 hours of the first dose, and before it wherever possible. Without a baseline, nobody can say whether a later result represents drug damage or hearing the person has had for twenty years. If you know you are about to start cisplatin or a prolonged course of an aminoglycoside, a baseline test is the single most valuable thing to arrange. Our guide to preparing for a hearing test explains what to expect.

2. Testing during treatment

For chemotherapy, that usually means testing before each cycle or at defined intervals; for aminoglycosides, roughly weekly to monthly during a prolonged course. The tests used go beyond a standard audiogram:

• Extended high-frequency audiometry — measures pitches above 8 kHz, where ototoxic damage appears first, and is therefore the most sensitive early indicator.
• Otoacoustic emissions (OAEs) — measure the response of the cochlear hair cells themselves, need no response from the patient, and can be done at the bedside on someone too unwell to complete a conventional test. See otoacoustic emissions testing.
• Standard pure-tone audiometry — still the reference for the speech frequencies that matter for day-to-day communication.

Audiologists apply defined criteria to decide whether a change is real: broadly, a 20 dB drop at any single frequency, or a 10 dB drop at two adjacent frequencies, compared with baseline. Reaching those thresholds triggers a conversation between the audiology and oncology or infection teams about dose, schedule or an alternative agent.

3. Follow-up after treatment ends

Because aminoglycoside damage can emerge weeks after the last dose, and chemotherapy effects can progress after treatment finishes, a follow-up test — commonly at around two months, and for children at intervals for years afterwards — is part of proper care. Anyone who has had cisplatin as a child should have their hearing monitored into adulthood.

If you are receiving one of these drugs and nobody has mentioned hearing, it is entirely reasonable to ask your oncology team, respiratory team or specialist nurse whether ototoxicity monitoring is available locally. Where it is not, arranging your own standard hearing test privately still gives you a documented reference point, and any concerning result can be referred into the NHS pathway.

Reducing the Risk Without Compromising Treatment

You cannot make a necessary drug safe for the ear, but several things genuinely reduce risk.

• Keep a full medicines list. Ototoxic effects stack. A patient on a loop diuretic for heart failure who is then given an aminoglycoside for sepsis is at considerably higher risk than either drug implies alone. Make sure every team treating you can see the whole list, including over-the-counter painkillers.
• Flag any family history of drug-related deafness. A relative who lost their hearing after antibiotics is a meaningful clue to the m.1555A>G mitochondrial variant, and genetic testing can be arranged.
• Protect against noise during and after treatment. An ear whose hair cells have been chemically stressed is more vulnerable to the mechanical stress of loud sound. Basic hearing protection habits matter more than usual during a course of ototoxic treatment.
• Ask about therapeutic drug monitoring. For aminoglycosides, blood levels are measured to keep the dose within a safe window; once-daily dosing regimens are generally less ototoxic than divided doses.
• Report symptoms immediately, not at the next routine appointment. With reversible ototoxicity, prompt reporting can mean full recovery. With permanent ototoxicity, it can mean the difference between a mild high-frequency loss and one that affects everyday conversation.
• Report suspected reactions. Anyone in the UK can report a suspected side effect through the MHRA's Yellow Card scheme, which contributes to national safety monitoring.

Emerging protective treatments are also changing the picture. Sodium thiosulfate has been shown to reduce cisplatin-induced hearing loss in children with certain solid tumours and is now used in some paediatric oncology settings, and other otoprotective agents are in trials. If you or your child are due platinum chemotherapy, it is worth asking the oncology team whether an otoprotective strategy is appropriate.

If Damage Has Already Happened

Permanent ototoxic hearing loss cannot be reversed, but it can be managed well, and the outcomes are far better than most people expect.

The starting point is a full diagnostic assessment, producing an audiogram that maps exactly which frequencies are affected — our guide to understanding your audiogram explains how to read one. Because ototoxic loss is typically high-frequency and symmetrical, it often responds well to modern hearing aids, which can be programmed to amplify precisely the pitches that have been lost while leaving unaffected frequencies alone. Choosing the right hearing aids covers the options, and for severe or profound loss, cochlear implantation is an established route in the UK.

Tinnitus that persists after treatment is common and responds to sound therapy, cognitive behavioural approaches and hearing aids themselves, which often reduce tinnitus simply by restoring the missing input. Vestibular damage is helped by vestibular rehabilitation — a structured programme of exercises that retrains the brain to rely more on vision and proprioception for balance.

Above all, act rather than wait. The average person in the UK waits around ten years between first noticing a hearing problem and seeking help. After ototoxic treatment, that delay is unnecessary: you already know the cause, you know roughly when it started, and getting it measured is a short, painless appointment.

Frequently Asked Questions

Should I stop taking a medicine if I think it is affecting my hearing?

No — not without speaking to a clinician first. The medicines most strongly associated with hearing damage are used for serious conditions where stopping abruptly could be far more dangerous than the hearing risk. Report the symptom urgently to your prescriber, GP or specialist team so they can weigh up dose adjustment, an alternative drug, or additional monitoring.

Is ototoxic hearing loss permanent?

It depends on the drug. High-dose aspirin, quinine and loop diuretics usually cause temporary effects that resolve after stopping. Aminoglycoside antibiotics and platinum chemotherapy such as cisplatin typically cause permanent damage, because the cochlear hair cells they destroy do not regenerate. Early detection cannot reverse that damage, but it can prevent more of it.

Does paracetamol or ibuprofen cause hearing loss?

Occasional use at normal doses is not considered a meaningful risk. Large observational studies have linked frequent, long-term use of NSAIDs and paracetamol to a modestly increased risk of hearing loss, but the effect size is small and the studies cannot prove cause and effect. Low-dose aspirin taken for heart protection is not associated with hearing damage; the risk relates to the much higher anti-inflammatory doses.

Can I get ototoxicity monitoring on the NHS?

In many centres, yes — particularly in paediatric oncology, cystic fibrosis and specialist infection services, where monitoring is well established. Provision is not uniform across the UK, and research is currently underway to make simplified screening more widely deliverable. If your team has not raised it, ask directly whether a baseline hearing test and monitoring are available for your treatment.

How soon after starting treatment can hearing damage appear?

Tinnitus after cisplatin can start within hours or days of an infusion, and measurable high-frequency loss can appear after the first cycle. Aminoglycoside damage may develop during treatment or emerge weeks after the final dose, which is why a follow-up test around two months after finishing is recommended.

What if my hearing test comes back normal but I still notice a change?

Say so, and ask specifically about extended high-frequency audiometry and otoacoustic emissions. A standard audiogram tests up to 8 kHz, while ototoxic damage begins above that range — so a normal standard result early in treatment does not rule out damage that is already underway.