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| Year : 2011
| Volume
: 13 | Issue : 54 | Page
: 356-363 |
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| Auditory sensitivity in opiate addicts with and without a history of noise exposure |
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Vishakha Rawool1, Carrie Dluhy2
1 Department of Speech Pathology and Audiology, West Virginia University, Morgantown, WV 26506, USA
2 VA Medical Center, Audiology, 623 Atwells Ave, Providence, RI 02909, USA
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| Date of Web Publication | 28-Sep-2011 |
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Several case reports suggest that some individuals are susceptible to hearing loss from opioids. A combination of noise and opium exposure is possible in either occupational setting such as military service or recreational settings. According to the Drug Enforcement Agency of the U.S. Department of Justice, prescriptions for opiate-based drugs have skyrocketed in the past decade. Since both opium and noise independently can cause hearing loss, it is important to know the prevalence of hearing loss among individuals who are exposed to opium or both opium and noise. The purpose of this research was to evaluate auditory sensitivity in individuals with a history of opium abuse and/or occupational or nonoccupational noise exposure. Twenty-three men who reported opiate abuse served as participants in the study. Four of the individuals reported no history of noise exposure, 12 reported hobby-related noise exposure, 7 reported occupational noise exposure including 2 who also reported hobby-related noise exposure. Fifty percent (2/4) of the individuals without any noise exposure had a hearing loss confirming previous reports that some of the population is vulnerable to the ototoxic effects of opioids. The percentage of population with hearing loss increased with hobby-related (58%) and occupational noise exposure (100%). Mixed MANOVA revealed a significant ear, frequency, and noise exposure interaction. Health professionals need to be aware of the possible ototoxic effects of opioids, since early detection of hearing loss from opium abuse may lead to cessation of abuse and further progression of hearing loss. The possibility that opium abuse may interact with noise exposure in determining auditory thresholds needs to be considered in noise exposed individuals who are addicted to opiates. Possible mechanisms of cochlear damage from opium abuse, possible reasons for individual susceptibility, and recommendations for future studies are presented in the article. Keywords: Cochlea, drug abuse, heroin, noise-induced hearing loss, opiates, ototoxicity, sudden hearing loss
How to cite this article:
Rawool V, Dluhy C. Auditory sensitivity in opiate addicts with and without a history of noise exposure. Noise Health 2011;13:356-63 |
| Introduction | |  |
Narcotic drugs usually cause sleep or hallucinations. Opium is a sedative, analgesic, and narcotic drug. It is usually obtained from the seed capsule of the opium poppy Papaver sotnniferum. When the capsule is ripe, incisions are made in it to access the milky juice. This juice changes into dark, sticky, or crumbly mass, or raw opium after it is dried in the air. For nonmedical consumption, the raw opium is boiled in water for a long time, strained to remove unsolvable materials, and then evaporated to form a sticky paste known as prepared opium. [1] The opium poppy has several different alkaloids including morphine, codeine, thebaine, papaverine, and noscapine. The actual amounts of the alkaloids in any given sample of opium vary depending on the preparation procedure and region. [2]
Besides smoking and inhaling, opium can also be consumed in the form of liquid extracts known as poppy tea. [3] Poppy tea is usually made from poppy straw which is a mixture of crushed poppy seeds, pods, and/or stems. Emergence or resurgence of tea brewed with various parts of opium poppy plants has been noted recently. Poppy tea brewed from poppy pods and poppy straw is considered more potent and is more likely to cause an overdose. [4]
For medical use, the raw opium is dried further at 60°, powdered and assayed chemically to ensure that it has at least 10% of morphine by weight. Opium is a common starting compound from which morphine, codeine, and other alkaloids are derived for medicinal use. [1]
With extended use of opium, the nervous system can adapt increasing drug tolerance which leads to requirement of larger doses of drugs to produce the effects that were previously possible by smaller doses. When use of opium is stopped, the withdrawal symptoms are apparent. For example, the smooth muscle attached to the base of each hair follicle, which is relaxed by morphine, goes into contraction when morphine is withdrawn; this pulls the hair erect, and gives rise to the gooseflesh or "cold turkey" appearance following sudden withdrawal. Morphine causes contraction of the iris of the eye, producing a pin-point pupil. Morphine withdrawal on the other hand causes marked dilatation of the pupil. [1]
Morphine (Morpheus; god of sleep) is the narcotic and principle active ingredient of opium. Morphine and its close relative Meperidine are commonly used in Morphine IV drips and in the drug Demerol. Continuous intrathecal infusion of morphine and bupicavaine is considered more efficient and less expensive than epidural delivery of the same drugs for treating refractory cancer pain. [5] About 12% of the patients can suffer from hearing loss or symptoms similar to those seen in patients with Meniere's disease following morphine delivery through implanted intrathecal catheters. [6]
Heroin, a narcotic drug, was derived by Bayer Company Scientists, by adding a chemical group to morphine to accelerate the entry of morphine in the brain. Some case reports suggest that Heroin abuse can lead to a temporary or permanent moderate or profound sensorineural hearing loss. [7],.[8],[9],[10],[11] In some cases, although the patient may report complete recovery of hearing, audiometric findings show recovery of normal hearing in the low frequencies but a persistent ototoxic hearing loss in the higher frequencies. [11] In some cases the heroin-induced transient hearing loss can progress to a permanent sensorineural hearing loss. [10] Polapathapee et al.[8] reported a case study in which the patient had used heroin for 1 year and 1 month prior to the incident and had noted transient hearing loss following heroin use. A month prior to the overdose incident, he had abstained from his heroin habit. When the patient resumed his intravenous heroin use, he overdosed and was unconscious for 2 days. After regaining consciousness, he noticed changes in his hearing ability, fatigue, and muscle aches. Audiometric testing revealed severe bilateral sensorineural hearing loss. The Short increment sensitivity index (SISI) indicated cochlear impairment, and ABR results suggested central involvement. [8] In most of the above cases there is a sequential pattern of drug addiction, drug abstinence, heroin overdose, loss of consciousness, and awareness of hearing loss following awakening. Such a pattern may result from resensitization of a tolerized opioid system or a prolonged hypersensitization of the system secondary to abstinence. [9]
Methadone is a synthetic opiate with action similar to morphine and heroin but the symptoms of withdrawal are less severe. It is used for relief of severe pain, and as a heroin substitute for addicts (methadone maintenance). van Gaalen et al.[12] described a 37-year-old man who suffered a sudden hearing loss after taking 15 tablets of 5 mg of methadone. The hearing recovered completely within 10 days. Christenson and Marjala [13] reported two cases of self-reported acute bilateral hearing loss induced by methadone overdose with complete recovery in 24 hours; however, the hearing loss or recovery was not confirmed audiometrically.
Propoxyphene hydrochloride is structurally related to methadone and is considered a mild analgesic. Abuse of this drug can lead to a permanent sensorineural hearing loss. Lupin and Harley [14] reported a permanent mild to severe sloping sensorineural hearing loss in a 22-year-old man, 48 hours following excessive ingestion of 103 mg of propoxyphene hydrochloride every 2 hours for 6 days. Harell et al.[15] described a chronic propoxyphene abuser who suffered from progressive sensorineural hearing loss leading to total deafness. One month prior to being seen for audiometric evaluation, the patient had rapidly increased his daily dosage to 1000 mg. Ramsay [16] described a 44-year-old woman who suffered from a permanent profound sensorineural hearing loss following excessive consumption of coproxamol containing dextropropoxyphene and acetaminophen.
Codeine is a colorless or white crystalline alkaloid derived from the opium poppy. Hydrocodone is a semisynthetic codeine derivative. It is used to treat moderate or severe pain without a timed release. Hydrocodone use can lead to physical and psychological dependence and is the most widely prescribed opioid and is among the most widely abused prescription drugs in the United States. [17] Ho et al.[18] reported five patients with documented history of hydrocodone use varying from 10 to 300 mg per day who suffered rapidly progressive sensorineural hearing loss. Hydrocodone is frequently prescribed with acetaminophen for pain relief or for suppressing cough. Hydrocodone/acetaminophen (Vicodin) combination is also used as a recreational drug. Oh et al.[19] reported a profound hearing loss in two healthy young individuals following Vicodin abuse within a few weeks. Similarly, Friedman et al.[20] reported rapidly progressive sensorineural hearing loss in 12 patients with Vicodin overuse; in 10 of the patients the hearing loss was profound. Blakley and Schilling [21] described three patients with sensorineural hearing loss who had abused drugs containing a combination of codeine and acetaminophen.
Oxycodone is another semisynthetic opioid related to codeine. It is used to treat moderate or severe pain and is manufactured with a timed release to suppress pain for up to 12 hours. Rigby and Parnes [22] reported a case of rapidly progressive profound sensorineural hearing loss associated with abuse of Percocet that contains oxycodone and acetaminophen.
Overall the above studies suggest that some individuals are susceptible to cochlear damage due to opioids. However, it should be noted that the acetaminophen contained in some of the above drugs also appears to increase the risk of hearing loss especially in men who are under the age of 50 years. [23] This risk may be higher in individuals who are exposed to noise since acetaminophen might exhaust endogenous cochlear glutathione, [24] which protects the cochlea from noise induced hearing loss. [25]
A combination of noise and opium exposure is possible in either noisy occupational setting such as military service or recreational settings. The association between opiate addiction and military service has been documented at least from the time of the Civil war. During the Civil war, opium was administered generously due to its effectiveness as an analgesic and also to control diarrhea and dysentery in combination with quinine for malaria. After the Civil war, opiate addicts were so often the veterans of the military service that opiate addiction was referred to as "Army disease." [26] As many as 48% of Army enlisted men used opiates while in Vietnam although only 10% reported such use before service. [27] Some of the main reasons for the increase in use in Vietnam appear to be the need of troops in stressful combat situations for self-medication and escape and the availability of illicit drugs at low cost. [28] The issue of spontaneous remission [27] among drug abusers is controversial [29] and the rate of spontaneous emissions among drug abusers is lowest for opiates. [30]
The key factors for opium addiction appear to be the manner in which the drug is used, the degree of social acceptance of opium use, and the price and ease of availability of the drug. [1] For example, with reference to manner of consumption, chemical dependence for opium tea usually builds up after 1 or 2 weeks of daily use. [4] With reference to professional acceptance of drug use, in the last decade a number of larger cities in Western Europe have opened drug consumption rooms in which drug users are permitted to consume drugs like heroin and cocaine with the goal of preventing drug overdoses, HIV infections, and public nuisance. [31] After surgery in desert field hospitals, soldiers reportedly could inject small quantities of opiates straight into their veins through a watch like device. They could press the device every six minutes but cutout devices were installed to minimize the chance of overdose. [32] As an example of ease of availability, soldiers can easily obtain nonprescription opiates in Afghanistan, the world's leading drug producer. Most of the opium produced in Afghanistan is converted to heroin within that country. The eradication campaign of 2006 had no significant impact on cultivation. Sixty-three percent of villages decided to again cultivate poppy in 2007, after eradication in 2006. [33] Soldiers may not report substance abuse or addiction due to difficulty in accepting the fact that they are addicted; such denial is common among addicts. Other possible reasons are fear of lack of confidentiality and negative career ramifications.
According to the Drug Enforcement Agency of the U S Department of Justice, prescriptions for opiate-based drugs have skyrocketed in the past decade. According to the National Survey on Drug Use and Health (NSDUH), there were 114,000 persons aged 12 years or older who had used heroin for the first time in the United States in 2008. [34] According to the 2009 Monitoring the Future Survey, 0.8% of the 8 th , 10 th , and 12 th grade students reported using heroin over the lifetime, 1 in 10 high school students reported nonmedical use of Vicodin and 1 in 20 reported abuse of OxyContin. [35] Many individuals who abuse drugs often engage in hobbies that can cause noise exposure including motorbike riding, hunting, and rock concerts.
Ishiyama et al.[9] noted that there are nearly 60 cases of profound deafness secondary to hydrocodone abuse in the Los Angeles, U.S. area alone although they did not provide details about these cases. In one previous study 2/16 (12.5%) heroin addicts reported hearing loss and one of these addicts reported enhanced hearing but audiometric testing was not conducted. [36] Also in previous reports the noise exposure history of cases is not always known. The fact that early cessation of opiates may control further deterioration of hearing. [7],[9] and that both opium and noise independently can cause hearing loss, it is important to know the prevalence of hearing loss among individuals who are exposed to opium or both opium and noise. The purpose of this study was to evaluate auditory sensitivity in individuals with a history of opium abuse and/or occupational or nonoccupational noise exposure.
| Methods | | |
Participants
Individuals with a history of drug abuse who were admitted to Stanley Street Treatment and Resource of Rhode Island (SSTAR of RI), an alcohol and drug detoxification center, were provided with the opportunity to participate in the research project. Twenty-three men who reported a history of opiate abuse were included in the analyses. Those reporting history of cocaine or alcohol abuse alone or in addition to opium were excluded. The men ranged in age from 21 to 47 years as shown in [Table 1]. Women were not included in this study because their treatment for alcohol and drug abuse was conducted at a separate facility. Prior to testing, participants read and signed an informed consent form approved by the University Institutional Review Board on Human Subject Research. All data collection followed the ethical standards of the Helsinki Declaration.
Participants were asked if they were exposed to loud sounds and if the response was affirmative, they were asked to state if the exposure occurred during military service, due to other types of occupational noise exposure, and/or was related to loud recreational habits or hobbies. Military and occupational exposure was combined in the category of occupational exposure. As shown in [Table 1], four of the individuals reported no history of noise exposure, 12 reported hobby-related noise exposure, five reported occupational noise exposure and 2 reported both occupational and hobby-related noise exposure. Since only two individuals reported both occupational and hobby-related noise exposure, they were collapsed with the occupational noise exposure group. In an ideal study about hearing in opiate addicts, all participants will have only opiate addiction and no other variables that can influence their hearing. However, inclusion of individuals addicted to only opiates does not represent the population well since most are likely to have other habits that can impact hearing including smoking and noise exposure. More than 75% of the participants in each of the groups also reported tobacco dependence [Table 1].
Case history
Detailed case histories were obtained from participants by administering an 18-item questionnaire. As mentioned previously case history information was used to place participants in different groups as shown in [Table 1].
Some studies suggest an association between smoking and hearing loss. [37],[38],[39] Therefore, a 10-item questionnaire referred to as Tobacco Dependence Screener (TDS) was administered to all subjects reporting smoking on the case history. "Have you ever tried to quit or cut down on tobacco and found you could not?" is an example of a question from the screener. The responses consist of either a "yes" or "no" response. The number of "yes" responses determines the score which can range from 1 to 10. Anyone with a score of greater than 5 was considered to be tobacco dependent. The score on this screener is positively correlated with the breath carbon monoxide levels, the number of cigarettes smoked per day, and years of smoking. [40]
Otoscopic examination
An otoscope was used to ensure lack of excessive cerumen and clear tympanic membranes.
Audiometric test equipment, calibration, and test setting
A Maico MA 39 portable audiometer was used to measure the auditory sensitivity of participants. Exhaustive calibrations are performed on the audiometer annually. In addition, biologic calibrations were performed on a daily basis. The testing occurred in a quiet room, where thresholds of the tester in the room were within ±5 dB of those found in a sound-treated booth.
Auditory threshold test procedures
The ascending method [41] was used for threshold (softest audible sound) determination. The threshold was noted as the lowest level (dB HL) at which a minimum of two out of three responses occurred on ascending trials using a 5 dB step size. Air conduction thresholds were obtained at 0.25, 0.5, 1, 2, 4, and 8 kHz for both right and left ears. Thresholds were also determined at interoctave frequencies, if the thresholds at the adjacent frequencies differed by greater than 15 dB HL. The frequency and ear order was randomized for each participant to minimize any order or fatigue effects.
Statistical analyses
Any individual with a hearing loss of 25 dB HL or above at any of the test frequencies in either ear was considered to have a hearing loss. Descriptive statistics for each group (no noise exposure, hobby-related exposure, and occupational exposure) showing the number and percentage of participants with hearing loss and nicotine dependence was calculated. In addition, Chi-square analysis was conducted to determine if the proportion of individuals with hearing loss is significantly different among the three groups.
A mixed MANOVA was conducted on the audiometric thresholds. Thresholds obtained at inter-octave frequencies were not included in the analyses due to several missing cells. Only one of the individuals had a hearing loss only at 6 kHz. History of noise exposure (no noise, hobby noise, occupational noise) was the nonrepeated variable and ear (left and right) and test frequencies (0.25, 0.5, 1, 2, 4, and 8 kHz) were the repeated variables. Post-hoc analyses were planned with the Tukey honest significant difference (HSD) test for unequal N. A P value of 0.05 was used for all inferential statistics.
| Results | | |
As shown in [Table 1], the percentage of individuals with hearing loss increased from 50% to 58% from the no noise exposure group to those with hobby-related noise exposure. All individuals (100%) with occupational and occupational and hobby-related noise exposure had a hearing loss. Audiometric data from two participants in each group are shown in [Figure 1],[Figure 2],[Figure 3],[Figure 4]. The figures also show age-appropriate data from the ISO 1999 [42] database B for unscreened populations. Chi-square analyses indicated that the percentage of individuals with hearing loss is significantly higher (P = 0.000) in the occupational noise exposure group (100%) than that with no exposure (50%) and hobby-related exposure (58%) groups. | Figure 1: Audiometric thresholds of two participants (20 and 33 year olds) without any history of noise exposure and the 10th and 90th percentile data for 30-year-old unscreened population from ISO 1999 database B
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 | Figure 2: Audiometric thresholds of two participants (34 and 32 year olds) with history of hobby-related noise exposure and the 10th and 90th percentile data for 30-year-old unscreened population from ISO 1999 database B
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 | Figure 3: Audiometric thresholds of two participants (35 and 38 year olds) with history of occupational noise exposure and the 10th and 90th percentile data for 30-year-old unscreened population from ISO 1999 database B
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 | Figure 4: Audiometric thresholds from two participants (38 and 47 year olds) with history of occupational and hobby-related noise exposure and the 10th and 90th percentile data for 40-year-old unscreened population from ISO 1999 database B
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Mixed MANOVA revealed a significant main effect of frequency (P = 0.016) and a significant ear, frequency, and noise exposure interaction (P = 0.041). Post hoc analyses with the Tukey HSD test revealed the following noteworthy differences as shown in [Figure 5]. | Figure 5: Auditory thresholds across various groups in each ear. The noise exposure group, ear, and frequency interaction was statistically significant (P = 0.041)
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Across noise exposure group differences
- Thresholds at 4 kHz were significantly worse in the occupational noise exposure group than those in the hobby-related noise exposure group (P = 0.000).
- Thresholds at 8 kHz were significantly worse in the occupational noise group than those in the no exposure (P = 0.018) and those in the hobby-related noise exposure group (P = 0.040).
Within noise exposure group differences
No noise exposure group: ([Figure 5], first panel)
- Thresholds were significantly worse at 4 kHz than those at 2 kHz in the left ear (P = 0.005).
Hobby-related noise exposure group: ([Figure 5], middle panel)
- Thresholds at 8 kHz were significantly worse than those at 2 kHz in the left ear (P =0.009).
- Thresholds at 8 kHz were significantly worse than those at 1 kHz (P = 0.0004) and at 2 kHz in the right ear (P = 0.009).
Occupational noise exposure group: ([Figure 5], last panel)
- Thresholds at 8 kHz were significantly poorer in the left ear than the right ear (P = 0.005).
- Thresholds were significantly worse at 4 kHz than those at all other frequencies except for those at 8 kHz in the left ear (P < 0.01).
| Discussion | | |
The presence of hearing loss in two individuals without any reported history of damaging noise exposure confirms previous case reports showing that some of the population (50% in this sample) is vulnerable to the ototoxic effects of opium abuse. As shown in [Figure 1], an asymmetric hearing loss was noted in both individuals. Similar initial asymmetry has been noted by previous investigators following the use of hydrocodone, [18],[19],[20] Percocet [22] and methadone. [12] Another noteworthy finding in the current study is the statistically significant notch noted at 4 kHz in the left ear. This effect is similar to that apparent in other types of ototoxicity where the hearing loss initially begins to appear at 4 kHz.
The percentage of population with hearing loss in the current study increased with hobby-related (58%) and occupational noise exposure (100%) and a significant interaction was apparent for ear, frequency and noise exposure group. Some agents such as cisplatin [43] carbon disulfide [44] and organic solvents [45],[46] are known to exacerbate the damage caused by excessive noise exposure. A similar interaction appears to be possible for excessive opium and noise exposure.
Possible sites of lesion
Cochlea
Patients with profound hearing loss associated with hydrocodone/acetaminophen abuse are known to benefit from cochlear implants. [18],[20] Such benefit suggests that the hearing loss is at least partially and initially cochlear in origin. Acute effects of opiates include decreased tone of peripheral blood vessels, decreased depth and frequency of breathing, and decreased secretion of adrenal and thyroid hormones. Chronic effects include reduced appetite and related effects of malnutrition including anemia and reduced resistance to infections. Additional chronic effects include chronic obstructive pulmonary disease with damage to the bronchi and lungs. [1] Many of these effects can lead to poor blood flow to the cochlea or deprive the cochlea of essential nutrients leading to hearing loss.
The presence of opioid receptors has also been noted in the inner ears of rats [47],[48] and guinea pigs suggesting that they may serve as neurotransmitters or neuromodulators in the cochlea. [49] More specifically opioid receptors mu-(μ) (MOP-R), delta-(δ) (DOP-R), and kappa-(ĸ)(KOP-R) are present in inner and outer hair cells. [47] Opioids may inhibit basal adenylate cyclase activity via the μ, δ, and k opioid receptors of the cochlea.
Auditory nerve
Opioid receptors are also present in the spiral ganglion and nerve fibers in the organ of corti, [48] suggesting the possibility of a neural hearing loss in addition to sensory or cochlear site of lesion. Opioid receptors MOP-R, DOP-R, KOP-R, and NOP-R are widely distributed in the central nervous system and in peripheral sensory and autonomic nerves. [50] Heroin overdose has been previously associated with peripheral neuropathy. [51],[52]
Central auditory system
The previously described mechanisms that could disrupt the blood flow to the cochlea could also disrupt blood flow to the brain. King et al.[53] described a 20-year-old man who suffered from a homonymous hemianopia after self-administration of heroin. Investigations revealed right occipital infarction with angiographic changes of arteritis in the posterior cerebral arteries. Niehaus and Meyer [54] described a case of a 25-year-old heroin abuser who developed cerebral ischemic lesions. Cerebral magnetic resonance imaging revealed bilateral borderzone infarctions which were attributed to a heroin-associated vasculitis of the basal cerebral arteries. The central auditory system can also be affected [8] due to functional reorganization of the central auditory pathways following reduced cochlear output. [55]
Possible reasons for individual susceptibility
Oh et al.[19] suggested that the presence of genetic factors may explain why some patients who abuse opiates develop clinical ototoxic symptoms and others do not. They speculated that a genetic mutation might give rise to selective vulnerability in hydrocodone-induced ototoxicity. Ho et al.[18] noted that individual differences can occur due to genetic variations in drug transport proteins, drug receptors, and/or genetic polymorphisms of drug metabolizing enzymes.
Some of the case studies suggest that an extreme and sudden increase in drug consumption may also be a crucial factor in causing hearing loss in some patients [16] and not others. Harell et al.[15] suggested that the lack of reports of ototoxicity in similar cases may be due to the higher possibility of deaths at such high doses.
Limitations of the study
Participants consisted primarily of patients qualifying for extended residency at SSTAR of RI under the Housing and Urban Development (HUD) program. Thus the current sample consists of individuals from lower socioeconomic levels. Gender effects could not be evaluated in this study since the sample consisted of only men. Gender may be an important variable since higher MOP-R binding has been reported in women in a number of cortical and subcortical areas. [56] Another limitation is the lack of data at 6 kHz from all participants which may increase the % of population with hearing loss. In addition, the audiometric sensitivity was determined only once. Thus the temporary or permanent nature of the hearing loss is unknown.
The dosage of drug consumption and/or noise exposure in the participants in the current study is unknown. It is hard to gather information about accurate sound exposure dose from addicts. To gather such information we will have to recruit workers with known work environments and known noise doses who are willing to admit that they are addicted to opiates. Workers in work environments are usually unwilling to reveal their addictions due to the fear of losing employment. The sound exposure dose due to recreational exposure is always hard to document due to the extreme variability in such exposure.
A high percentage of the current sample was also dependent on Nicotine [Table 1]. Some investigators have suggested that smoking alone is not a risk factor for hearing loss but it can be in combination with other factors such as use of analgesics. [57] Other epidemiological studies suggest a positive association between smoking and hearing impairment. [37],[38],[39] For example, Cruickshanks et al.[58] investigated 3753 participants to evaluate the effects of smoking on hearing loss. Smoking history was obtained through self-report and hearing loss was defined as a pure tone average (0.5, 1, 2, and 4 kHz) greater than 25 dB HL in the worse ear. After adjustments for age and other factors, current smokers were 1.69 times as likely to have a hearing loss as nonsmokers. Cruickshanks et al.[58] suggested direct ototoxic effects on hair cell function due to the presence of nicotine-like receptors in animal hair cells and also indirect effects affecting the blood supply of the cochlea. Furthermore, tobacco smoke contains hydrogen cyanide, an asphyxiant [59] which under severe exposure can impair the function of the stria vascularis. Any interactive or additive effects of nicotine dependence on the auditory sensitivity in the current sample cannot be determined.
Recommendation for future studies
Further studies in animals will be helpful in evaluating any interactive effects of opium and noise on hearing, with systematic control on the extent and type of noise exposure and opium dose. The use of passive nocturnal species in such research is discouraged since these effects are dependent on the metabolic rate of the animal. [59]
Implications
- Medical and para-medical professionals need to be aware of the possible ototoxic effects of opium and its derivatives. This is an important consideration for illicit, prescriptive, and over the counter drugs that contain opium derivatives. Early detection of hearing loss related to opium abuse may lead to cessation of abuse and further progression of hearing loss.
- In cases of sudden hearing loss, drug overdose should be explored as a possible cause.
- The possibility that opium abuse may interact with noise exposure in determining auditory thresholds needs to be considered among noise-exposed individuals who are addicted to opiates.
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Correspondence Address:
Vishakha Rawool
Department of Speech Pathology & Audiology, West Virginia University, Morgantown, WV 26506
USA
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/1463-1741.85508
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]
[Table 1] |
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