Chemistry:Ototoxicity

From HandWiki

Ototoxicity is the property of being toxic to the ear (oto-), specifically the cochlea or auditory nerve and sometimes the vestibular system, for example, as a side effect of a drug. The effects of ototoxicity can be reversible and temporary, or irreversible and permanent. It has been recognized since the 19th century.[1] There are many well-known ototoxic drugs used in clinical situations, and they are prescribed, despite the risk of hearing disorders, for very serious health conditions.[2] Ototoxic drugs include antibiotics (such as gentamicin, streptomycin, tobramycin), loop diuretics (such as furosemide), and platinum-based chemotherapy agents (such as cisplatin and carboplatin). A number of nonsteroidal anti-inflammatory drugs (NSAIDS) have also been shown to be ototoxic.[3][4] This can result in sensorineural hearing loss, dysequilibrium, or both. Some environmental and occupational chemicals have also been shown to affect the auditory system and interact with noise.[5]

Signs and symptoms

Ototoxicity results in cochlear and/or vestibular dysfunction which can manifest as sensorineural hearing loss, tinnitus, hyperacusis, dizziness, vertigo, or imbalance.[6][7] Presentation of symptoms vary in singularity, onset, severity and reversibility.[6]

Auditory symptoms

Hearing loss

Ototoxicity-induced hearing loss typically impacts the high frequency range, affecting above 8000 Hz prior to impacting frequencies below.[8] There is not global consensus on measuring severity of ototoxicity-induced hearing loss as there are many criteria available to define and measure ototoxicity-induced hearing loss.[9][10] Guidelines and criteria differ between children and adults.[8]

Ototoxicity grades (Hearing Loss)

There are at least 13 classifications for ototoxicity.[11] Examples of ototoxicity grades for hearing loss are the National Cancer Institute's Common Terminology Criteria for Adverse Events (CTCAE), Brock's Hearing Loss Grades, Tune grading system, and Chang grading system.[9]

National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events (CTCAE) (as described in the American Academy of Audiology Ototoxicity Monitoring Guidelines from 2009):[8]

  • Grade 1: Threshold shift or loss of 15–25 dB relative to baseline, averaged at two or more contiguous frequencies in at least one ear
  • Grade 2: Threshold shift or loss of >25-90 dB, averaged at two contiguous test frequencies in at least one ear
  • Grade 3: Hearing loss sufficient to indicate aural rehabilitation such as hearing aids and/or speech-language services
  • Grade 4: Indications of cochlear implant candidacy

Brock's Hearing Loss Grades (as described in the American Academy of Audiology Ototoxicity Monitoring Guidelines from 2009):[8]

  • Grade 0: Hearing thresholds <40 dB at all frequencies
  • Grade 1: Thresholds 40 dB or greater at 8000 Hz
  • Grade 2: Thresholds 40 dB or greater at 4000-8000 Hz
  • Grade 3: Thresholds 40 dB or greater at 2000-8000 Hz
  • Grade 4: Thresholds 40 dB or greater at 1000-8000 Hz

Chang grading system (as reported in Ganesan et al., 2018):[9]

  • 0: ≤ 20 dB at 1, 2, and 4 kHz
  • 1a: ≥ 40 dB at any frequency 6 to 12 kHz
  • 1b: > 20 and < 40 dB at 4 kHz
  • 2a: ≥ 40 dB at 4 kHz and above
  • 2b: > 20 and < 40 dB at any frequency below 4 kHz
  • 3: ≥ 40 dB at 2 or 3 kHz and above
  • 4: ≥ 40 dB at 1 kHz and above

Tune grading system (as reported in Ganesan et al., 2018):[9]

  • 0: No hearing loss
  • 1a: Threshold shift of ≥ 10 dB at 8, 10, and 12.5 kHz
  • 1b: Threshold shift of ≥ 10 dB at 1, 2, and 4 kHz
  • 2a: Threshold shift of ≥ 20 dB at 8, 10, and 12.5 kHz
  • 2b: Threshold shift of ≥ 20 dB at 1, 2, and 4 kHz
  • 3: ≥ 35 dB HL at 1, 2, and 4 kHz
  • 4: ≥ 70 dB HL at 1, 2, and 4 kHz

Hyperacusis

Hyperacusis is abnormally increased sensitivity to intensity (perceived as loudness) to what is typically deemed as normal/tolerable loudness.

Vestibular symptoms

Vestibular symptoms from ototoxicity, which would specifically be vestibulotoxicity, can include general dizziness, vertigo, imbalance, and oscillopsia.

Ototoxic agents

Main article: Medicine:Ototoxic medication

Antibiotics

Antibiotics in the aminoglycoside class, such as gentamicin and tobramycin, may produce cochleotoxicity through a poorly understood mechanism.[12] It may result from antibiotic binding to NMDA receptors in the cochlea and damaging neurons through excitotoxicity.[13] Aminoglycoside-induced production of reactive oxygen species may also injure cells of the cochlea.[14] Once-daily dosing[15] and co-administration of N-acetylcysteine[16] may protect against aminoglycoside-induced ototoxicity. The anti-bacterial activity of aminoglycoside compounds is due to inhibition of ribosome function and these compounds similarly inhibit protein synthesis by mitochondrial ribosomes because mitochondria evolved from a bacterial ancestor.[17] Consequently, aminoglycoside effects on production of reactive oxygen species as well as dysregulation of cellular calcium ion homeostasis may result from disruption of mitochondrial function.[18] Ototoxicity of gentamicin can be exploited to treat some individuals with Ménière's disease by destroying the inner ear, which stops the vertigo attacks but causes permanent deafness.[19] Due to the effects on mitochondria, certain inherited mitochondrial disorders result in increased sensitivity to the toxic effects of aminoglycosides.

Macrolide antibiotics, including erythromycin, are associated with reversible ototoxic effects.[20] The underlying mechanism of ototoxicity may be impairment of ion transport in the stria vascularis.[20] Predisposing factors include renal impairment, hepatic impairment, and recent organ transplantation.[20]

Loop diuretics

Certain types of diuretics are associated with varying levels of risk for ototoxicity. Loop and thiazide diuretics carry this side effect. The loop diuretic furosemide is associated with ototoxicity, particularly when doses exceed 240 mg per hour.[21] The related compound ethacrynic acid has a higher association with ototoxicity, and is therefore used only in patients with sulfa allergies. Diuretics are thought to alter the ionic gradient within the stria vascularis.[22] Bumetanide confers a decreased risk of ototoxicity compared to furosemide.[20]

Chemotherapeutic agents

Platinum-containing chemotherapeutic agents, including cisplatin and carboplatin, are associated with cochleotoxicity characterized by progressive, high-frequency hearing loss with or without tinnitus (ringing in the ears).[23] Ototoxicity is less frequently seen with the related compound oxaliplatin.[24] The severity of cisplatin-induced ototoxicity is dependent upon the cumulative dose administered[25] and the age of the patient, with young children being most susceptible.[26] The exact mechanism of cisplatin ototoxicity is not known. The drug is understood to damage multiple regions of the cochlea, causing the death of outer hair cells, as well as damage to the spiral ganglion neurons and cells of the stria vascularis.[27] Long-term retention of cisplatin in the cochlea may contribute to the drug's cochleotoxic potential.[28] Once inside the cochlea, cisplatin has been proposed to cause cellular toxicity through a number of different mechanisms, including through the production of reactive oxygen species.[29] The decreased incidence of oxaliplatin ototoxicity has been attributed to decreased uptake of the drug by cells of the cochlea.[24] Administration of amifostine has been used in attempts to prevent cisplatin-induced ototoxicity, but the American Society of Clinical Oncology recommends against its routine use.[30]

The vinca alkaloids,[31][32][33] including vincristine,[34] are also associated with reversible ototoxicity.[20]

Antiseptics and disinfectants

Topical skin preparations such as chlorhexidine and ethyl alcohol have the potential to be ototoxic should they enter the inner ear through the round window membrane.[20] This potential was first noted after a small percentage of patients undergoing early myringoplasty operations experienced severe sensorineural hearing loss. It was found that in all operations involving this complication the preoperative sterilization was done with chlorhexidine.[35] The ototoxicity of chlorhexidine was further confirmed by studies with animal models.[20]

Several other skin preparations have been shown to be potentially ototoxic in the animal model. These preparations include acetic acid, propylene glycol, quaternary ammonium compounds, and any alcohol-based preparations. However, it is difficult to extrapolate these results to human ototoxicity because the human round window membrane is much thicker than in any animal model.[20]

Other medicinal ototoxic drugs

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.[20] Erectile dysfunction medications may have the potential to cause hearing loss.[36] However the link between erectile dysfunction medications and hearing loss remains uncertain.[37]

Previous noise exposure has not been found to potentiate ototoxic hearing loss.[38][39] 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 effect on ototoxic hearing loss.[40]

Ototoxicants in the environment and workplace

Ototoxic effects are also seen with quinine, pesticides, solvents, asphyxiants, and heavy metals such as mercury and lead.[5][20][41][42] When combining multiple ototoxicants, the risk of hearing loss becomes greater.[43][44][45] As these exposures are common, this hearing impairment can affect workers in many occupations and industries.[46][47] This risk probably been overlook because individual hearing tests conducted on workers, pure tone audiometry, does not allow one to determine if a hearing effects are a consequence of noise or chemical exposure.[48]

Examples of activities that often have exposures to both noise and solvents include:[49]

  • Printing
  • Painting
  • Construction
  • Fueling vehicles and aircraft
  • Firefighting
  • Weapons firing
  • Pesticide spraying

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 caused by noise in different ways. For mixtures containing organic solvents such as toluene, styrene or xylene, the combined exposure with noise increases the risk of occupational hearing loss in a synergistic manner.[5][50] The risk is greatest when the co-exposure is with impulse noise.[51][52] Carbon monoxide has been shown to increase the severity of the hearing loss from noise.[50] Given the potential for enhanced risk of hearing loss, exposures and contact with products such as fuels, paint thinners, degreasers, white spirits, exhaust, should be kept to a minimum.[53] 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.[38] 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.[54]

The hearing loss caused by chemicals can be very similar to a hearing loss caused by excessive noise. A 2018 informational bulletin by the US Occupational Safety and Health Administration (OSHA) and the National Institute for Occupational Safety and Health (NIOSH) introduces the issue, provides examples of ototoxic chemicals, lists the industries and occupations at risk and provides prevention information.[55] In 2025, information for the health management of workers exposed to ototoxic chemicals was posted in Wikiversity. [1]

Ototoxicity Monitoring/Management

Most published guidelines from around the world focus on the ototoxicity of medications, but there is not consensus on one universally agreed-upon protocol.[10][11]

Guidelines released:

  • The American Speech-Language-Hearing Association (ASHA) released guidelines in 1994.[56] There are details on the different monitoring procedures on timelines depending on age and responsiveness.[56]

Auditory testing

Auditory testing involved in ototoxicity monitoring/management (OtoM) from medications is typically general audiological evaluation, high frequency audiometry (HFA), and otoacoustic emissions (OAEs).[57][56] High frequency audiometry evaluates hearing thresholds beyond 8000 Hz, which is the typical cut-off for conventional audiometry.[57] It is recommended a baseline evaluation be performed prior to treatment beginning.[57][56]

Significant change criteria

There are several guidelines on what constitutes a significant change in hearing[57][59] which can indicate further action must be taken, whether that be to implement aural rehabilitation or adjust the source of ototoxic exposure (eg. chemotherapy). With pure tone audiometry, ASHA considers a significant change to have occurred if there is a:[60][56]

  • ≥ 20 dB decrease in pure tone thresholds at any test frequency OR
  • ≥ 10 dB decrease at two adjacent frequencies OR
  • no response at three consecutive test frequencies where responses were previously obtained

If using distortion product otoacoustic emissions (DPOAEs), a significant shift is observed if there is a reduction in amplitude by 6 dB or more than the baseline within the sensitive range of ototoxicity.[60]

Vestibular testing

Vestibular tests for vestibulotoxicity specifically can include caloric testing, rotational testing, vestibular evoked myogenic potentials (VEMPs), and computerized dynamic posturography (CDP); however, there are no globally accepted guidelines for monitoring/management of vestibular function during or following ototoxic treatments.[57][61]

See also

References

  1. ↑ "Sketches of otohistory. Part 11: Ototoxicity: drug-induced hearing loss". Audiology and Neuro-Otology 11 (1): 1–6. 2006-01-01. doi:10.1159/000088850. PMID 16219991. 
  2. ↑ Position Statement and Practice Guidelines on Ototoxicity Monitoring. American Academy of Audiology. 2009. http://audiology-web.s3.amazonaws.com/migrated/OtoMonGuidelines.pdf_539974c40999c1.58842217.pdf. 
  3. ↑ "Auditory sensori-neural alterations induced by salicylate". Progress in Neurobiology 62 (6): 583–631. December 2000. doi:10.1016/s0301-0082(00)00027-7. PMID 10880852. 
  4. ↑ Jung, T. T.; Rhee, C. K.; Lee, C. S.; Park, Y. S.; Choi, D. C. (October 1993). "Ototoxicity of salicylate, nonsteroidal antiinflammatory drugs, and quinine". Otolaryngologic Clinics of North America 26 (5): 791–810. doi:10.1016/S0030-6665(20)30767-2. ISSN 0030-6665. PMID 8233489. 
  5. ↑ 5.0 5.1 5.2 "Occupational exposure to chemicals and hearing impairment. The Nordic Expert Group for Criteria Documentation of Health Risks from Chemicals". Arbete och Hälsa 44 (4): 177. 2010. https://gupea.ub.gu.se/bitstream/2077/23240/1/gupea_2077_23240_1.pdf. Retrieved May 4, 2016. 
  6. ↑ 6.0 6.1 Ganesan, Purushothaman; Schmiedge, Jason; Manchaiah, Vinaya; Swapna, Simham; Dhandayutham, Subhashini; Kothandaraman, Purushothaman Pavanjur (April 2018). "Ototoxicity: A Challenge in Diagnosis and Treatment". Journal of Audiology & Otology 22 (2): 59–68. doi:10.7874/jao.2017.00360. ISSN 2384-1621. PMID 29471610. 
  7. ↑ Lester, Georgia M.; Wilson, Wayne J.; Timmer, Barbra H. B.; Ladwa, Rahul M. (2023-12-07). "Audiological ototoxicity monitoring guidelines: a review of current evidence and appraisal of quality using the AGREE II tool" (in en). International Journal of Audiology: 1–6. doi:10.1080/14992027.2023.2278018. ISSN 1499-2027. PMID 38062855. 
  8. ↑ 8.0 8.1 8.2 8.3 American Academy of Audiology. 2009. “Position Statement and Clinical Practice Guidelines: Ototoxicity Monitoring.” https://audiology-web.s3.amazonaws.com/migrated/OtoMonGuidelines.pdf_539974c40999c1.58842217.pdf
  9. ↑ 9.0 9.1 9.2 9.3 Ganesan, Purushothaman; Schmiedge, Jason; Manchaiah, Vinaya; Swapna, Simham; Dhandayutham, Subhashini; Kothandaraman, Purushothaman Pavanjur (April 2018). "Ototoxicity: A Challenge in Diagnosis and Treatment". Journal of Audiology & Otology 22 (2): 59–68. doi:10.7874/jao.2017.00360. ISSN 2384-1621. PMID 29471610. 
  10. ↑ 10.0 10.1 Lester, Georgia M.; Wilson, Wayne J.; Timmer, Barbra H. B.; Ladwa, Rahul M. (2023-12-07). "Audiological ototoxicity monitoring guidelines: a review of current evidence and appraisal of quality using the AGREE II tool" (in en). International Journal of Audiology: 1–6. doi:10.1080/14992027.2023.2278018. ISSN 1499-2027. PMID 38062855. 
  11. ↑ 11.0 11.1 Crundwell, Gemma; Gomersall, Phil; Baguley, David M. (February 2016). "Ototoxicity (cochleotoxicity) classifications: A review" (in en). International Journal of Audiology 55 (2): 65–74. doi:10.3109/14992027.2015.1094188. ISSN 1499-2027. PMID 26618898. http://www.tandfonline.com/doi/full/10.3109/14992027.2015.1094188. 
  12. ↑ "Hearing loss in patients with vestibulotoxic reactions to gentamicin therapy". Archives of Otolaryngology–Head & Neck Surgery 132 (3): 253–7. March 2006. doi:10.1001/archotol.132.3.253. PMID 16549744. 
  13. ↑ "N-methyl-D-aspartate antagonists limit aminoglycoside antibiotic-induced hearing loss". Nature Medicine 2 (12): 1338–43. December 1996. doi:10.1038/nm1296-1338. PMID 8946832. 
  14. ↑ "Recent advances in understanding aminoglycoside ototoxicity and its prevention". Audiology and Neuro-Otology 7 (3): 171–4. 2002. doi:10.1159/000058305. PMID 12053140. 
  15. ↑ "A meta-analysis of studies on the safety and efficacy of aminoglycosides given either once daily or as divided doses". The Journal of Antimicrobial Chemotherapy 37 (4): 645–63. April 1996. doi:10.1093/jac/37.4.645. PMID 8722531. 
  16. ↑ "N-Acetylcysteine in the prevention of ototoxicity". Kidney International 72 (3): 231–2. August 2007. doi:10.1038/sj.ki.5002299. PMID 17653228. 
  17. ↑ "Molecular contacts between antibiotics and the 30S ribosomal particle". Glycobiology. Methods in Enzymology. 415. 2006. pp. 180–202. doi:10.1016/S0076-6879(06)15012-0. ISBN 9780121828202. 
  18. ↑ "Disruption of intracellular calcium regulation is integral to aminoglycoside-induced hair cell death". The Journal of Neuroscience 33 (17): 7513–25. April 2013. doi:10.1523/JNEUROSCI.4559-12.2013. PMID 23616556. 
  19. ↑ "Intratympanic gentamicin for intractable Meniere's disease". The Laryngoscope 113 (3): 456–64. March 2003. doi:10.1097/00005537-200303000-00013. PMID 12616197. 
  20. ↑ 20.00 20.01 20.02 20.03 20.04 20.05 20.06 20.07 20.08 20.09 Roland, Peter S. (2004). Ototoxicity. Hamilton, Ont: B.C. Decker. ISBN 978-1-55009-263-9. 
  21. ↑ "Comparison of loop diuretics in patients with chronic renal insufficiency". Kidney International 32 (4): 572–8. October 1987. doi:10.1038/ki.1987.246. PMID 3430953. 
  22. ↑ Schmitz, Paul G. (2012). Renal: An Integrated Approach to Disease. New York: McGraw-Hill. p. 123. ISBN 978-0-07-162155-7. 
  23. ↑ "Relationship between cisplatin administration and the development of ototoxicity". Journal of Clinical Oncology 24 (6): 918–24. February 2006. doi:10.1200/JCO.2006.10.077. PMID 16484702. 
  24. ↑ 24.0 24.1 "Cisplatin and oxaliplatin toxicity: importance of cochlear kinetics as a determinant for ototoxicity". Journal of the National Cancer Institute 101 (1): 37–47. January 2009. doi:10.1093/jnci/djn418. PMID 19116379. 
  25. ↑ "Analysis of risk factors for cisplatin-induced ototoxicity in patients with testicular cancer". British Journal of Cancer 77 (8): 1355–62. April 1998. doi:10.1038/bjc.1998.226. PMID 9579846. 
  26. ↑ "Predicting cisplatin ototoxicity in children: the influence of age and the cumulative dose". European Journal of Cancer 40 (16): 2445–51. November 2004. doi:10.1016/j.ejca.2003.08.009. PMID 15519518. 
  27. ↑ "Cisplatin-Induced Ototoxicity: Effects, Mechanisms and Protection Strategies". Toxics 3 (3): 268–293. July 2015. doi:10.3390/toxics3030268. PMID 29051464. 
  28. ↑ "Cisplatin is retained in the cochlea indefinitely following chemotherapy". Nature Communications 8 (1): 1654. November 2017. doi:10.1038/s41467-017-01837-1. PMID 29162831. Bibcode: 2017NatCo...8.1654B. 
  29. ↑ "Mechanisms of cisplatin-induced ototoxicity and prevention". Hearing Research 226 (1–2): 157–67. April 2007. doi:10.1016/j.heares.2006.09.015. PMID 17113254. 
  30. ↑ "American Society of Clinical Oncology 2008 clinical practice guideline update: use of chemotherapy and radiation therapy protectants". Journal of Clinical Oncology 27 (1): 127–45. January 2009. doi:10.1200/JCO.2008.17.2627. PMID 19018081. 
  31. ↑ "The Catharanthus alkaloids: pharmacognosy and biotechnology". Current Medicinal Chemistry 11 (5): 607–28. March 2004. doi:10.2174/0929867043455846. PMID 15032608. 
  32. ↑ Raviña, Enrique (2011). "Vinca alkaloids". The evolution of drug discovery: From traditional medicines to modern drugs. John Wiley & Sons. pp. 157–159. ISBN 978-3-527-32669-3. https://books.google.com/books?id=iDNy0XxGqT8C&pg=PA157. 
  33. ↑ Cooper, Raymond; Deakin, Jeffrey John (2016). "Africa's gift to the world". Botanical Miracles: Chemistry of Plants That Changed the World. CRC Press. pp. 46–51. ISBN 978-1-4987-0430-4. https://books.google.com/books?id=aXGmCwAAQBAJ&pg=PA46. 
  34. ↑ "Modifications on the basic skeletons of vinblastine and vincristine". Molecules 17 (5): 5893–914. May 2012. doi:10.3390/molecules17055893. PMID 22609781. 
  35. ↑ Bicknell, P. G. (1971). "Sensorineural deafness following myringoplasty operations". The Journal of Laryngology & Otology 85 (9): 957–962. doi:10.1017/S0022215100074272. PMID 5571878. 
  36. ↑ "FDA Announces Revisions to Labels for Cialis, Levitra and Viagra. Potential risk of sudden hearing loss with ED drugs to be displayed more prominently". United States Food and Drug Administration. https://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/2007/ucm109012.htm. 
  37. ↑ "Update on the Safety of Phosphodiesterase Type 5 Inhibitors for the Treatment of Erectile Dysfunction". Sexual Medicine Reviews 6 (2): 242–252. 2017. doi:10.1016/j.sxmr.2017.08.001. PMID 28923561. 
  38. ↑ 38.0 38.1 Campbell, Kathleen (2007). Pharmacology and Ototoxicity for Audiologists. Clifton Park, NY: Delmar Centrage Learning. pp. 145. ISBN 978-1-4180-1130-7. 
  39. ↑ "Cis-platin ototoxicity in previously noise-exposed guinea pigs". Acta Oto-Laryngologica 101 (1–2): 66–74. 1986-01-01. doi:10.3109/00016488609108609. PMID 3962651. 
  40. ↑ Rawool, Vishakha Waman (2012). Hearing Conservation in Occupational, Recreational, Educational, and Home Settings. New York: Thieme. pp. 13. ISBN 978-1-60406-256-4. 
  41. ↑ "Chemical exposure and hearing loss". Disease-a-Month 59 (4): 119–38. April 2013. doi:10.1016/j.disamonth.2013.01.003. PMID 23507352. 
  42. ↑ "Ototoxicité des métaux - Article de revue - INRS" (in fr). https://www.inrs.fr/media.html?refINRS=TC%20173. 
  43. ↑ Rawool, Vishakha (2012). Hearing Conservation: In Occupational, Recreational, Educational, and Home settings. New York, NY: Thieme. pp. 10. ISBN 978-1-60406-256-4. 
  44. ↑ Venet, Thomas; Carreres-Pons, Maria; Chalansonnet, Monique; Thomas, Aurélie; Merlen, Lise; Nunge, Hervé; Bonfanti, Elodie; Cosnier, Frédéric et al. (2017-09-01). "Continuous exposure to low-frequency noise and carbon disulfide: Combined effects on hearing". NeuroToxicology 62: 151–161. doi:10.1016/j.neuro.2017.06.013. ISSN 0161-813X. PMID 28655499. Bibcode: 2017NeuTx..62..151V. 
  45. ↑ Zarus, Gregory M.; Ruiz, Patricia; Benedict, Rae; Brenner, Stephan; Carlson, Krystin; Jeong, Layna; Morata, Thais C. (2024-09-04). "Which Environmental Pollutants Are Toxic to Our Ears?—Evidence of the Ototoxicity of Common Substances" (in en). Toxics 12 (9): 650. doi:10.3390/toxics12090650. ISSN 2305-6304. 
  46. ↑ Johnson, Ann-Christin; Morata, Thais C. (2009). The Nordic Expert Group for criteria documentation of health risks from chemicals. 142, Occupational exposure to chemicals and hearing impairment. Göteborg: University of Gothenburg. ISBN 9789185971213. OCLC 939229378. 
  47. ↑ Lewkowski, Kate; Heyworth, Jane S.; Li, Ian W.; Williams, Warwick; McCausland, Kahlia; Gray, Corie; Ytterstad, Elinor; Glass, Deborah C. et al. (2019). "Exposure to noise and ototoxic chemicals in the Australian workforce". Occupational and Environmental Medicine 76 (5): 341–348. doi:10.1136/oemed-2018-105471. ISSN 1470-7926. PMID 30683670. 
  48. ↑ Fuente, Adrian; McPherson, Bradley (2006). "Organic solvents and hearing loss: The challenge for audiology: Los solventes orgánicos y los trastornos auditivos: El reto para la audiología" (in en). International Journal of Audiology 45 (7): 367–381. doi:10.1080/14992020600753205. ISSN 1499-2027. PMID 16938795. http://www.tandfonline.com/doi/full/10.1080/14992020600753205. 
  49. ↑ "Safety and Health Information Bulletins | Preventing Hearing Loss Caused by Chemical (Ototoxicity) and Noise Exposure | Occupational Safety and Health Administration". https://www.osha.gov/dts/shib/shib030818.html. 
  50. ↑ 50.0 50.1 "Promotion of noise-induced hearing loss by chemical contaminants". Journal of Toxicology and Environmental Health. Part A 67 (8–10): 727–40. 2004. doi:10.1080/15287390490428206. PMID 15192865. Bibcode: 2004JTEHA..67..727F. 
  51. ↑ Venet, Thomas; Campo, Pierre; Thomas, Aurélie; Cour, Chantal; Rieger, Benoît; Cosnier, Frédéric (2015). "The tonotopicity of styrene-induced hearing loss depends on the associated noise spectrum". Neurotoxicology and Teratology 48: 56–63. doi:10.1016/j.ntt.2015.02.003. PMID 25689156. Bibcode: 2015NTxT...48...56V. 
  52. ↑ Fuente, Adrian; Qiu, Wei; Zhang, Meibian; Xie, Hongwei; Kardous, Chucri A.; Campo, Pierre; Morata, Thais C. (March 2018). "Use of the kurtosis statistic in an evaluation of the effects of noise and solvent exposures on the hearing thresholds of workers: An exploratory study". The Journal of the Acoustical Society of America 143 (3): 1704. doi:10.1121/1.5028368. ISSN 1520-8524. PMID 29604694. PMC 8588570. Bibcode: 2018ASAJ..143.1704F. https://hal.archives-ouvertes.fr/hal-01844639/file/10.1121_1.5028368.pdf. 
  53. ↑ (in en) Preventing hearing loss caused by chemical (ototoxicity) and noise exposure. (Report). 2018-03-01. doi:10.26616/nioshpub2018124. https://www.cdc.gov/niosh/docs/2018-124/. 
  54. ↑ "Interaction of cisplatin and noise on the peripheral auditory system". Hearing Research 50 (1–2): 211–23. 1990. doi:10.1016/0378-5955(90)90046-R. PMID 2076973. 
  55. ↑ "Preventing Hearing Loss Caused by Chemical (Ototoxicity) and Noise Exposure". April 3, 2018. https://www.cdc.gov/niosh/docs/2018-124/pdfs/2018-124.pdf. 
  56. ↑ 56.0 56.1 56.2 56.3 56.4 "Audiologic Management of Individuals Receiving Cochleotoxic Drug Therapy". American Speech-Language-Hearing Association. 1994. https://www.asha.org/policy/gl1994-00003/. 
  57. ↑ 57.0 57.1 57.2 57.3 57.4 57.5 "Position Statement and Practice Guidelines on Ototoxicity Monitoring". 2023-01-04. https://www.audiology.org/practice-guideline/position-statement-and-practice-guidelines-on-ototoxicity-monitoring/. 
  58. ↑ "AUDIOLOGICAL MANAGEMENT OF PATIENTS ON TREATMENT THAT INCLUDES OTOTOXIC MEDICATIONS". Health Professions Council of South Africa. 2018. https://www.hpcsa.co.za/Uploads/professional_boards/slh/guidelines/Guidelines_for_Audiological_Management_of_Patients_on_Treatment_that_includes_Ototoxic_Medications.pdf. 
  59. ↑ Crundwell, Gemma; Gomersall, Phil; Baguley, David M. (February 2016). "Ototoxicity (cochleotoxicity) classifications: A review" (in en). International Journal of Audiology 55 (2): 65–74. doi:10.3109/14992027.2015.1094188. ISSN 1499-2027. PMID 26618898. http://www.tandfonline.com/doi/full/10.3109/14992027.2015.1094188. 
  60. ↑ 60.0 60.1 Ganesan, Purushothaman; Schmiedge, Jason; Manchaiah, Vinaya; Swapna, Simham; Dhandayutham, Subhashini; Kothandaraman, Purushothaman Pavanjur (April 2018). "Ototoxicity: A Challenge in Diagnosis and Treatment". Journal of Audiology & Otology 22 (2): 59–68. doi:10.7874/jao.2017.00360. ISSN 2384-1621. PMID 29471610. 
  61. ↑ Cohen, Helen S. (2019-07-01). "A review on screening tests for vestibular disorders" (in en). Journal of Neurophysiology 122 (1): 81–92. doi:10.1152/jn.00819.2018. ISSN 0022-3077. PMID 30995137. 
Classification
External resources



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