Effect of Deliberate Ingestion of Organophosphate Pesticide on Distortion Product Oto-Acoustic Emissions (DPOAE)

Srihimaja Nandamudi, Vinaya Ashok Murthy, Yugandhar Ramakrishna, Tejaswini Boreddy, Savalam Bujjetha Rathna Kumar, Savalam Gnana Rathna Prakash

Ali Yavar Jung National Institute for the Hearing Handicapped, Southern Regional Centre, Ministry of Social Justice and Empowerment, Government of India, Manovikasnagar, Secunderabad.
Institute of Health Sciences (IHS), Bhubaneshwar, India.
People’s Education Society Institute of Medical Sciences and Research Centre, Kuppam, Chittoor, India.

DOI: 10.4236/ijcm.2012.36091                

Abstract

Background: Oto-Acoustic Emissions (OAE) are low intensity sounds produced by the cochlea in response to an acoustic stimulus. Deliberate self-poisoning has become an increasingly common response to emotional distress in young adults (NHS, 1998). Organophosphate (OP) compounds are most commonly involved in 76% of pesticide poisoning especially in the developing countries like India. Several pesticides are neurotoxin which could potentially affect hearing and, animal studies showed that OP treatment leads to change in hearing threshold, outer and inner hair cell loss but human studies on the same are very few. Aim: The present study was aimed at exploring the cochlear changes after self-poisoning with OP pesticides by measuring the Distortion Product Oto-Acoustic Emissions (DPOAE). Method: 114 subjects were participated in the study, with an age range of 18-30 years having pure tone audiometric thresholds within the normal limits and no history of middle ear pathology. They were further divided into two groups, I and II which includes self-poisoned and healthy subjects respectively. Results: The “pass” and “fail” criteria of DPOAE measures in group I were 30% and 70% respectively whereas in group II, it was found 91% and 9% respectively. Discussion: There was a significant failure in DPOAE in Group I (subjects who were self-poisoned) compared to group II (healthy subjects). The two important pathologies behind OP toxicity are the generation of Reactive Oxygen Species and the depletion of NADPH which is necessary for normal function. Conclusion: The results of the present study highlight that; the minute cochlear changes caused due to pesticide poisoning can be effectively measured through DPOAE. Further it can suggest in other clinical targets like Ototoxicity, Noise-induced hearing loss, Meniere’s disease etc., which has an effect on cochlear hair cells can be monitored through DPOAE.

Keywords

Oto-Acoustic Emissions (OAE); Organophosphate (OP); Ototoxity; Cochlear Changes

Conflicts of Interest

The authors declare no conflicts of interest.

References

[1]	World Health Organisation (WHO), “Pesticides Are a Leading Suicide Method,” World Health Organisation, Geneva, 2006.
[2]	National Health Services (NHS) Centre for Review and Dissemination, “Deliberate Self-Harm. Effective Healthcare Bulletin,” NHS Centre, Vol. 4, 1998, pp. 1-12.
[3]	J. M. Bertolote, A. Fleischmann, M. Eddleston and D. Gunnell, “Deaths from Pesticide Poisoning: A Global Response,” The British Journal of Psychiatry, Vol. 189, 2006, pp. 201-203. doi:10.1192/bjp.bp.105.020834
[4]	M. R. Phillips, G. Yang, Y. Zhang, et al., “Risk Factors for Suicide in China: A National Case—Control Psychological Autopsy Study,” Lancet, Vol. 360, No. 9347, 2002, pp. 1728-1736. doi:10.1016/S0140-6736(02)11681-3
[5]	J. Jayarathnam, “Acute Pesticide Poisoning: A Major Global Health Problem,” World Health Statistics Quarterly, Vol. 43, 1990, pp. 139-144.
[6]	M. Harell, J. J. Shea and J. R. Emmett, “Bilateral Sudden Deafness Following Combined Insecticide Poisoning,” Laryngoscope, Vol. 88, 1978, pp. 1348-1351.
[7]	C. S. Petty, “Organic Phosphate Insecticide Poisoning: Residual Effects in Two Cases,” American Journal of Medicine, Vol. 24, No. 3, 1958, pp. 567-568.
[8]	P. Campo, R. Lataye, B. B. Cossec and V. Placidi, “Toluene-Induced Hearing Loss: A Mid-Frequency Location of the Cochlear Lesions,” Neurotoxicology and Teratology, Vol. 19, No. 2, 1997, pp. 129-40. doi:10.1016/S0892-0362(96)00214-0
[9]	N. L. Cappaert, S. F. Klis, A. B. Baretta, H. Muijser and G. F. Smoorenburg, “Ethyl Benzene-Induced Ototoxicity in Rats: A Dose Dependent Mid-frequency Hearing Loss,” Journal of the Association for Research in Otolaryngology, Vol. 1, 2000, pp. 292-299.
[10]	T. C. Morata, A. C. Fiorini, F. M. Fischer, S. Colacioppo, K. M. Wallingford, et al., “Toluene-Induced Hearing Loss among Rotogravure Printing Workers,” Scandinavian Journal of Work, Environment Health, Vol. 23, No. 4, 1997, pp. 289-298. doi:10.5271/sjweh.222
[11]	B. E. Moen, T. Riise and K. R. Kyvik, “P300 Brain Potential among Workers Exposed To Organic Solvents,” Norsk Epidemiologi, Vol. 9, 1999, pp. 27-31.
[12]	D. T. Kemp, “Stimulated Acoustic Emissions From Within the Human Auditory System,” Journal of the Acoustical Society of America, Vol. 64, No. 5, 1978, pp. 1386-1391. doi:10.1121/1.382104
[13]	D. T. Kemp, “Oto-Acoustic Emissions, Their Origin in Cochlear Function, and Use in Hearing and Balance,” British Medical Bulletin, Vol. 63, No. 1, 2002, pp. 223-241. doi:10.1093/bmb/63.1.223
[14]	M. Riga, “The Effect of Treatment with Vincristine on Transient Evoked and Distortion Product Oto-Acoustic Emissions,” International Journal of Pediatric Otorhinolaryngology, Vol. 70, No. 6, 2006, pp. 1003-1008. doi:10.1016/j.ijporl.2005.10.011
[15]	R. Lataye, K. Maguin and P. Campo, “Increase in Cochlear Microphonic Potential after Toluene Administration,” Hearing Research, Vol. 230, No. 1-2, 2007, pp. 34- 42. doi:10.1016/j.heares.2007.04.002
[16]	R. Lataye, P. Campo, G. Loquet and G. Morel, “Combined Effects of Noise and Styrene on Hearing: Comparison between Active and Sedentary Rats,” Noise Health, Vol. 7, No. 27, 2005, pp. 49-64. doi:10.4103/1463-1741.31633
[17]	I. C. P. R. Russo and T. M. M. Santos, “A Prática da Audiologia clíNica,” Cortez, Sao Paulo, 1993.
[18]	M. W. Yellin and R. D. Stillman, “Oto-Acoustic Emissions in Normal-Cycling Females,” Journal of American Academy of Audiology, Vol. 10, 1999, pp. 400-408.
[19]	R. Probst, F. P. Harris and R. Hauser, “Clinical Monitoring Using Oto-Acoustic Emissions,” British Journal of Audiology, Vol. 27, No. 2, 1993, pp. 85-90. doi:10.3109/03005369309077896
[20]	P. Avan, J. D. Durrant and B. Buki, “Possible Effects of Cochlear Hydrops and Related Phenomenon on OAEs,” Seminars in Hearing, Vol. 22, No. 4, 2001, pp. 405-414. doi:10.1055/s-2001-19113
[21]	S. Frota, “Fundamentos em Fonoaudiologia: Audiologia. Rio de Janeiro: Guanabara Koogan,” 2003.
[22]	M. A. Hotz, F. P. Harris and R. Probst, “Oto-Acoustic Emissions: An Approach for Monitoring Amino Glycoside-Induced Ototoxicity,” Laryngoscope, Vol. 104, 1994, pp. 1130-1134.
[23]	K. C. M. Campbell and J. D. Durrant, “Audiological Monitoring for Ototoxicity,” Otolaryngologic Clinics of North America, Vol. 26, 1993, pp. 903-914.
[24]	K. M. Reavis, D. S. Phillips, S. A. Fausti, et al., “Factors Affecting Sensitivity of Distortion Product Oto-Acoustic Emissions to Ototoxic Hearing Loss,” Ear & Hearing, Vol. 29, No. 6, 2008, pp. 875-893. doi:10.1097/AUD.0b013e318181ad99
[25]	K. M. Reavis, et al., “Distortion-Product Otoacoustic Emission Test Performance for Ototoxicity Monitoring,” Ear & Hearing, Vol. 32, 2011, pp. 61-74.
[26]	F. Ottaviani, N. Dozio, C. B. Neglia, S. Riccio and M. Scavini, “Absence of Oto-Acoustic Emissions in Insulin- Dependent Diabetic Patients: Is There Evidence for Diabetic Cochleopathy?” Journal of Diabetes and Its Complications, Vol. 16, No. 5, 2002, pp. 338-343. doi:10.1016/S1056-8727(01)00224-0
[27]	Y. Zhang, X. Zhang, W. Zhu, X. Zheng and X. Deng, “Distortion Product of Oto-Acoustic Emissions as a Sensitive Indicator of Hearing Loss in Pilots,” Aviation, Space, and Environmental Medicine, Vol. 75, 2004, pp. 46-48.
[28]	T. C. Morata and G. K. Lemasters, “Epidemiologic Considerations in the Evaluation of Occupational Hearing Loss,” Occupational Medicine, Vol. 10, 1995, pp. 641-656.
[29]	B. Katbamna, D. N. Homnick and J. H. Marks, “Effects of Chronic Tobramycin Treatment on Distortion Product Oto-Acoustic Emissions,” Ear and Hearing, Vol. 20, No. 5, 1999, pp. 393-402. doi:10.1097/00003446-199910000-00002
[30]	P. Stavroulaki, N. Apostolopoulos, J. Segas, M. Tsakanikos and G. Adamopoulos, “Evoked Oto-Acoustic Emissions—An Approach for Monitoring Cisplatin Induced Ototoxicity in Children,” International Journal of Pediatric Otorhinolaryngology, Vol. 59, No. 1, 2001, pp. 47-57. doi:10.1016/S0165-5876(01)00455-4
[31]	B. D. Ress, K. S. Sridhar, T. J. Balkany, G. M. Waxman, B. B. Stagner and B. L. Lonsbury-Martin, “Effects of Cisplatinum Chemotherapy on Oto-Acoustic Emissions: The Development of an Objective Screening Protocol,” Otolaryngology—Head & Neck Surgery, Vol. 121, No. 6, 1999, pp. 693-701. doi:10.1053/hn.1999.v121.a101567
[32]	P. Avan and P. Bonfils, “Distortion-Product Oto-Acoustic Emission Spectra and High-Resolution Audiometry in Noise-Induced Hearing Loss,” Hearing Research, Vol. 209, No. 1-2, 2005, pp. 68-75. doi:10.1016/j.heares.2005.06.008
[33]	J. S. Bus and J. E. Gibson, “Paraquat: Model for Oxidant-Initiated Toxicity,” Environmental Health Perspectives, Vol. 55, 1984, pp. 37-46. doi:10.1289/ehp.845537
[34]	M. Dandapani, A. Zachariah, M. R. Kavitha , L. Jeyaseelan and A. Oommen, “Oxidative Damage in Intermediate Syndrome of Acute OrganoPhosphorous Poisoning,” Indian Journal of Medical Research, Vol. 117, 2003, pp. 253-259.
[35]	W. J. Clerici and L. Yang, “Direct Effects of Intraperilymphatic Reactive Oxygen Species Generation on Cochlear Function,” Hearing Research, Vol. 101, No. 1-2, 1996, pp. 14-22. doi:10.1016/S0378-5955(96)00126-8
[36]	E. M. Priuska and J. Schacht, “Formation of Free Radicals by Gentamicin and Iron and Evidence for an Iron/ Gentamicin Complex,” Biochemical Pharmacology, Vol. 50, No. 11, 1995, pp. 1749-1752. doi:10.1016/0006-2952(95)02160-4
[37]	K. C. Harris, E. Bielefeld, B. H. Hu and D. Henderson, “Increased Resistance to Free Radical Damage Induced by Low-level Sound Conditioning,” Hearing Research, Vol. 213, 2006, pp. 118-129. doi:10.1016/j.heares.2005.11.012
[38]	K. K. Ohlemiller, J. S. Wright and L. L. Dugan, “Early Elevation of Cochlear Reactive Oxygen Species Following Noise Exposure,” Audiology & Neurootology, Vol. 4, No. 5, 1999, pp. 229-236. doi:10.1159/000013846
[39]	S. S. Jayasinghe and K. D. Pathirana, “Effects of Deliberate Ingestion of Organo Phosphate or Paraquat on Brain-Stem Evoked Potentials,” Journal of Medical Toxicology, Vol. 7, No. 4, 2011, pp. 277-280. doi:10.1007/s13181-011-0173-3
[40]	A. Fuente and B. McPherson, “Organic Solvents and Hearing Loss: The Challenge for Audiology,” International Journal of Audiology, Vol. 45, No. 7, 2006, pp. 367-381. doi:10.1080/14992020600753205