American Journal of Epidemiology Advance Access originally published online on December 15, 2005
American Journal of Epidemiology 2006 163(4):327-333; doi:10.1093/aje/kwj044
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Original Contribution |
Exposure to Loud Noise and Risk of Acoustic Neuroma
1 Division of Epidemiology, School of Public Health, The Ohio State University, Columbus, OH
2 Division of Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
Correspondence to Colin Edwards, Division of Epidemiology, School of Public Health, The Ohio State University, Starling-Loving Hall, Room A446, 320 West Tenth Avenue, Columbus, OH 43210 (e-mail: colin.edwards{at}osumc.edu).
Received for publication May 15, 2005. Accepted for publication September 22, 2005.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONReferences |
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Exposure to occupational loud noise has been previously identified as a possible risk factor for acoustic neuroma in only one relatively small (n = 86 cases) case-control study of men. The goal of the present study was to further examine the role of loud noise in acoustic neuroma etiology. In their population-based case-control study of both sexes conducted from 1999 to 2002 in Sweden, the authors compared reports on type and duration of occupational and nonoccupational loud noise exposure of 146 acoustic neuroma cases and 564 controls. Controls were randomly selected from the study base and were frequency matched on age, sex, and residential area. The authors found that individuals reporting loud noise exposure from any source were at increased risk for acoustic neuroma (odds ratio (OR) = 1.55, 95% confidence interval (CI): 1.04, 2.30). Exposure to loud noise from machines, power tools, and/or construction increased the risk for acoustic neuroma (OR = 1.79, 95% CI: 1.11, 2.89), as did exposure to loud music (OR = 2.25, 95% CI: 1.20, 4.23). The odds ratio for a latency period of 13 or more years since the first loud noise exposure from any source was 2.12 (95% CI: 1.40, 3.20). The findings of an increased risk of acoustic neuroma with loud noise exposure support previous research.
case-control studies; neuroma, acoustic; noise; risk factors
Abbreviations: CI, confidence interval; OR, odds ratio
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONReferences |
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Acoustic neuroma, also referred to as vestibular schwannoma, is a benign tumor of the vestibular division of the eighth cranial nerve (1
, 2). This tumor results in hearing loss, tinnitus, and disequilibrium (3, 4). The tumor constitutes from 6 to 10 percent of all intracranial tumors, with an incidence of 1–20 per 100,000 per year (5–7). The sex ratio (females/males) for acoustic neuroma has been reported to be greater than 1 (1, 6, 8, 9), and the tumor occurs mainly in individuals aged 50 or more years (6). Acoustic neuromas present clinically as two distinct types, the bilateral hereditary type and the unilateral sporadic type (4, 8). In the present study, we examine unilateral acoustic neuroma, which comprises 90–95 percent of all acoustic neuromas (6, 10).
We report the results from the Swedish portion of the INTERPHONE Study, an international collaborative case-control study of brain tumors, acoustic neuroma, and parotid gland tumors in relation to mobile phone use and other potential risk factors (11). In a recent publication from this study (12), an association between acoustic neuroma and mobile phone use was reported that is awaiting confirmation from other studies. In the present study, we focus instead on another potential acoustic neuroma risk factor, loud noise exposure. The only available study to date examining loud noise exposure and acoustic neuroma risk was limited by the relatively small number of acoustic neuroma cases available for inclusion in the analysis, as well as by the restriction of the study population to men (13).
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONReferences |
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Study design and population
A population-based case-control study was conducted that included all individuals aged 20–69 years who resided in three geographic regions covered by the regional cancer registries in Stockholm, Göteborg, and Lund, Sweden, which comprised a population of approximately 3.1 million people. Data were collected during the period 1999–2002. Study approval was obtained from the institutional ethics committee, and oral informed consent was obtained from all study participants.
Acoustic neuroma case ascertainment
Eligible cases were all patients diagnosed with acoustic neuroma (International Classification of Diseases, Tenth Revision, code C72.4 and International Classification of Diseases for Oncology, Second Edition, code 9560.0) during the period from September 1, 1999, to August 31, 2002, in the areas covered by the Lund and Göteborg cancer registries and from January 1, 2000, to August 31, 2002, in the Stockholm Cancer Registry area. Continuous identification of cases throughout the study period was achieved through collaboration with neurosurgery, oncology, neurology, and otorhinolaryngology clinics at hospitals within the geographic regions covered by the study. Any patients missed during weekly visits to these clinics were subsequently identified during quarterly regional cancer registry searches. The first medical examination resulting in diagnosis of acoustic neuroma was used as the date of diagnosis and also as the reference date for exposure calculations. Medical records for all cases were examined to confirm the diagnosis and to determine the side of the head on which the tumor was located. Histopathologic reports were used to verify diagnosis in 58 cases (40 percent), and the remaining cases were diagnosed by computerized axial tomography or magnetic resonance imaging. Histologic classification of the cases as acoustic neuroma was performed by pathologists at the hospitals in the three study regions where the cases underwent surgery or biopsy. We identified a total of 160 eligible acoustic neuroma cases, of whom 146 (91 percent) were interviewed. Those cases who did not participate included 11 (7 percent) who would not consent to the study and three (2 percent) who could not be contacted.
Controls
Controls were randomly selected approximately every 2 months from the continuously updated Swedish population registry. The number of controls required for each case was stipulated by the common protocol of the INTERPHONE Study (one per brain tumor case, two per acoustic neuroma case, and three per parotid gland tumor case). Of the 838 controls identified for inclusion in the study, 564 (67 percent) were interviewed. Those controls who did not participate included 127 (15 percent) who would not consent to the study and 147 (18 percent) who could not be reached by phone to make an appointment for an interview. There were no major differences between the respondents and the nonrespondents with regard to age, sex, and area of residence. For controls, the reference date was defined as the date of identification of the control, adjusted for the average time difference between the date of diagnosis and the date of identification of the cases within the same matching stratum. This ensured a comparable length of follow-up for cases and controls.
Data collection and loud noise exposure assessment
Identification of cases and controls occurred prospectively from September 2000 through August 2002 and retrospectively in the 12 months prior to September 2000 in the Lund and Göteborg study regions and in the 8 months prior to September 2000 in the Stockholm study region. The study participant contact and interview procedures were similar for cases and controls. Interviews were conducted by study nurses or the study neuropsychologist by use of laptop computers. Study participants who would not participate in a personal interview were offered a telephone interview. Those who refused participation in any kind of interview were offered the option of completing a short written questionnaire instead. The written questionnaire was focused on mobile phone use and did not include questions about loud noise. Therefore, participation rates are lower in the analyses reported here compared with the analysis of mobile phone use described earlier (12). A proxy respondent was used in two cases where the case had died before the first contact by study personnel. Eligibility criteria for both cases and controls required that they were not completely deaf prior to the reference date. One control was excluded for this reason. The cases and controls also had to possess the intellectual and language skills necessary to complete the interview. Three cases and 18 controls were excluded because they did not speak Swedish; four controls were excluded because of insufficient intellectual skills.
The study participants were asked if they were exposed to occupational loud noise and also if they were exposed to regular nonoccupational loud noise. Exposure to loud noise was defined as that exceeding a level of 80 decibels. This cutoff was explained to the study participants by means of a diagram depicting a decibel scale and associated loud noise exposures. If they were exposed to either occupational loud noise, regular nonoccupational loud noise, or both, the study participants were then asked to specify the activities in which they were exposed to loud noise and the year in which the exposure started and the year in which it stopped. They were also asked if there were any years during this period in which they were unexposed.
The total years of loud noise exposure were categorized into less than 5 years, 5–14 years, and 15 years or more (with cutpoints at approximately the 25th and 75th percentiles for controls). In the analysis of type of loud noise exposure, the following categories were created: 1) exposure to machines, power tools, and/or construction; 2) exposure to motors, including airplanes; 3) exposure to loud music, including employment in the music industry; and 4) exposure to screaming children, sports events, and/or restaurants or bars. The remainder was classified as "other" types of loud noise exposure. Ninety-seven percent of the loud noise exposure responses could be categorized into one of the four loud noise exposure types. Data regarding the use of hearing protection were also collected. This would allow us to determine if there was any difference between study participants who were unexposed and participants who used hearing protection. Finally, a complete job history was collected for the 20 years preceding diagnosis but not in sufficient detail to be used as a loud noise exposure validation tool.
Statistical analysis
Unconditional logistic regression models adjusted for age (5-year categories), sex, and local cancer registry region were used to estimate odds ratios and their respective 95 percent confidence intervals with SAS, version 8, statistical software (SAS Institute, Inc., Cary, North Carolina) (14). The odds ratio was used as an estimate of the relative risk in the analysis of the interview data. In the analysis of loud noise exposure type (table 4), we also adjusted for highest level of education, which we used as a proxy for socioeconomic status. In the evaluation of potential confounding variables, the data presented in table 2 were stratified on ionizing radiation exposure due to medical treatment, as well as on mobile phone use. The odds ratios did not differ within the different strata, discounting these variables as potential confounders. In addition, radiation exposure and mobile phone use were added to the logistic regression model. However, the changes in the odds ratios were negligible, and therefore these variables were not included in the final model. Tests for trend were calculated by use of the Cochran-Armitage test for trend. All tests of statistical significance performed were two sided.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONReferences |
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Basic demographic characteristics of cases and controls are presented in table 1. The median age of the cases and controls was 52 years and 54 years, respectively. Tumor location was more common on the right side (59 percent) than on the left side (41 percent).
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Study participants were initially classified as unexposed to loud noise or exposed to occupational and/or regular nonoccupational loud noise, with either hearing protection or without hearing protection. Ten percent of the cases and 11 percent of the controls who were exposed to occupational loud noise, regular nonoccupational loud noise, or both reported using hearing protection most of the time.
The odds ratios for acoustic neuroma by loud noise exposure are shown in table 2. The odds ratio for occupational loud noise exposure (odds ratio (OR) = 1.43, 95 percent confidence interval (CI): 0.96, 2.13) was similar to the odds ratio for regular nonoccupational loud noise exposure (OR = 1.38, 95 percent CI: 0.80, 2.36). When study participants exposed to occupational loud noise or regular nonoccupational loud noise (or both) were combined, the odds ratio increased to 1.55 (95 percent CI: 1.04, 2.30). The odds ratio for the group exposed to loud noise with hearing protection was 0.92 (95 percent CI: 0.51, 1.64). In all subsequent analyses, the subjects using hearing protection were categorized as unexposed to loud noise. In an additional analysis, those study participants using hearing protection were excluded. There was a slight rise in the odds ratios for the three loud noise exposure categories listed in table 2. Finally, the overall analysis presented in table 2 was stratified on hearing loss. The patterns within the hearing loss and the no hearing loss groups were found to be comparable.
Table 3 displays results according to duration of loud noise exposure, combining occupational and regular nonoccupational loud noise. For males and females combined, all of the exposure duration groups had elevated odds ratios, with the highest odds ratio of 1.64 (95 percent CI: 0.91, 2.91) for the group with 5–14 years of loud noise exposure. A dose-response effect is evident with increasing years of loud noise exposure (ptrend = 0.0056). When the loud noise exposure duration data were analyzed separately for males and females, the highest odds ratio for males was 2.12 (95 percent CI: 0.99, 4.57) for 5–14 years of loud noise exposure, and the highest odds ratio for females was 3.34 (95 percent CI: 1.32, 8.43) for 
15 years of loud noise exposure. An additional analysis of loud noise exposure duration was performed, excluding the 5 years prior to diagnosis. However, the pattern in the additional analysis was similar to that of the original analysis. Finally, the duration of exposure analysis was repeated, dropping hearing protection from the comparison group. There were negligible changes in the odds ratios for the analysis of the male study participants, the female study participants, and the combined group.
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Table 4 presents type of loud noise exposure grouped into four distinct categories. A significantly greater proportion of men than women were exposed to machines, power tools, and construction, as well as to motors, including airplanes. A greater proportion of men were exposed to loud music, including employment in the music industry, and a greater proportion of women were exposed to screaming children, sports events, and/or restaurants/bars, although the latter differences were not significant. All of the categories had elevated odds ratios. The two categories with the highest odds ratios were exposure to machines, power tools, and/or construction, with an odds ratio of 1.79 (95 percent CI: 1.11, 2.89), and exposure to music, including employment in the music industry, with an odds ratio of 2.25 (95 percent CI: 1.20, 4.23). Subgroup logistic regression analyses were performed for males and females separately. The resulting odds ratios were in the same direction for both subgroups, although the numbers of study participants in the each subgroup were too small for meaningful analysis and are therefore not presented.
To evaluate the significance of latency period and the risk of acoustic neuroma, we analyzed the data using three latency periods. The data were analyzed for those study participants with less than 13 years, 13–26 years, and 27 or more years since the first regular loud noise exposure (with cutpoints at approximately the 25th and 75th percentiles for controls). The data are presented in table 5 for occupational and/or regular nonoccupational loud noise exposure only, as the numbers of study participants in the analyses of other categories of loud noise exposure were too small for meaningful analysis. The odds ratio increased with increasing latency period (ptrend = 0.0029). The odds ratio for 13 or more years since the first regular loud noise exposure was 2.12 (95 percent CI: 1.40, 3.20) (data not shown). An additional analysis of latency period was performed, excluding the 5 years prior to diagnosis. However, the pattern in the additional analysis was similar to that of the original analysis.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONReferences |
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Loud noise exposure and risk of acoustic neuroma
Exposures to any loud noise, to occupational loud noise, and to regular nonoccupational loud noise were all associated with an increased risk of acoustic neuroma. Each of our three categories of loud noise exposure duration was associated with an increased risk of acoustic neuroma, with the highest risk of acoustic neuroma for study participants exposed to loud noise for a duration of 5–14 years. The two types of loud noise exposure with the highest risk of acoustic neuroma were exposure to loud noise from machines, power tools, and/or construction and exposure to loud noise from music, including employment in the music industry.
The results of the present study are in agreement with the only other known study examining loud noise exposure and the risk of acoustic neuroma (13). The previous study reported results in 86 males, a slightly larger number than the 77 males in the present study. Not only was our study able to replicate the previous study's findings in males, but perhaps more importantly an elevated risk of acoustic neuroma was also found in females. In the previous study, the odds ratio for ever having a job involving exposure to extremely loud noise was 2.2 (95 percent CI: 1.12, 4.67). The study also found a dose-response effect for years of employment in an occupation with loud noise exposure (ptrend = 0.02). The odds ratio for exposure for 20 or more years during the period 10 or more years before diagnosis was 13.2 (95 percent CI: 2.01, 86.98). The previous study included only men and was not able to report findings for nonoccupational loud noise exposure, as too few study participants reported such exposure.
In our study, elevated risk of acoustic neuroma was found with all loud noise exposure duration categories in males, which is consistent with the previous study (13), and elevated risk of acoustic neuroma was found with all of the loud noise exposure duration categories in females. No comparison can be made with the previous study for the latter group, as data on occupational loud noise exposure among females were not collected. One recent study of occupation and risk of meningioma and acoustic neuroma found that those occupations associated with an increased risk of acoustic neuroma were not occupations with which one would expect an unusually high exposure to loud noise (15). However, the study was able to estimate loud noise exposure only indirectly, as no data on loud noise exposure were collected. Finally, in the present study, tumor location was found to be more common on the right side than on the left side. Other data also indicate a similar uneven distribution with regard to tumor laterality (16).
Other risk factors
In a previous report from the Swedish INTERPHONE Study of mobile phone use and the risk of acoustic neuroma, the relative risk associated with mobile phone use of at least 10 years' duration was shown to be 1.9 (95 percent CI: 0.9, 4.1). When the analysis was restricted to tumors on the same side of the head as the phone was normally used, the relative risk increased to 3.9 (95 percent CI: 1.6, 9.5). The study had a larger number of exposed acoustic neuroma cases than any of the six previous studies examining mobile phone use and thus was better powered to study the effects of long-term mobile phone use (12). The findings of this recent study will require confirmation in other studies. Mobile phone use was evaluated in the present study and was not found to be a confounding variable.
Ionizing radiation exposure is the only well-established exogenous risk factor for acoustic neuroma. It has been found to increase acoustic neuroma risk among individuals who underwent radiation treatment of tinea capitis during childhood and who developed an excess of benign and malignant brain tumors of various histologic types, including acoustic neuroma, and among survivors of the atomic bombings in Japan (17, 18). Ionizing radiation exposure due to medical treatment was evaluated in the present study and was not found to be a confounding variable.
It has been suggested that female hormones may also increase acoustic neuroma risk, although the evidence for this association is suggestive rather than definitive (6, 19). One line of evidence suggesting that female hormones play a role in the etiology of acoustic neuroma is that the incidence is higher in women than in men (1, 6, 8, 9). A population-based case-control study of brain tumors, including acoustic neuroma, and menopausal status found a tendency toward an increased risk of acoustic neuroma for menopausal women (19). It is suggested that this is perhaps due to the cessation of estrogen production after menopause or even perhaps due to a protective effect of the relative elevation of androgen levels after menopause.
Diagnostic delay
The majority of acoustic neuroma tumors grow slowly (20, 21). In our study, it is likely that many of the cases had the tumor for several years before a clinical diagnosis was made. Diagnostic delay is the period between the appearance of the first symptom and the time that first medical attention is sought. According to another study, the delay from the first symptom until diagnosis averaged more than 5 years (22). In these patients, the diagnostic delay ranged from 2 to 30 years. Hence, it is very difficult to predict the growth rate and as a result the latency period of acoustic neuroma. In our analysis, however, we did observe an increased risk of acoustic neuroma as the latency period was increased (ptrend = 0.0029). An increased risk of acoustic neuroma was found only with a latency of at least 13 years between exposure and diagnosis. This is consistent with the hypothesis that, for slow-growing tumors such as acoustic neuroma, one would expect a higher risk with a longer latency period and a lower risk with a shorter latency period.
Acoustic trauma and tumorigenesis
The results of the present study support the hypothesis that acoustic trauma due to loud noise exposure contributes to tumorigenesis. Damage to the structures of the ear caused by intense sound exposure appears to be caused by similar mechanisms in all mammals (23). It has been reported previously that damage to cochlear hair cells produced by acoustic trauma stimulates mitotic replication of normally postmitotic cells in the chicken and quail (24, 25). The supporting cells or perhaps unidentified stem cells that replicate as a result of the acoustic trauma do not divide in the absence of trauma (24). Experimental studies in rodents have demonstrated mechanical damage to the organ of Corti and surrounding tissue, including the eighth cranial nerve, as a result of intense impulse noise (26, 27). Oxidative DNA damage in the cochlea following intense noise exposure was observed in one experimental study of rodents (28). If cancer risk is proportional to the number of proliferating cells, as has been previously postulated (29), then it is plausible that a benign tumor such as acoustic neuroma may arise as a result of cochlear hair cell trauma. During the cellular repair process, cellular division results in DNA replication errors that may in turn lead to chromosomal changes essential for neoplastic transformation (13).
Recall and selection bias
The tendency for patients with a tumor to focus on the reasons that they may have developed the disease is a potential source of recall bias in our study. As our study is a case-control interview study and as many of the cases were exposed to loud noise for 5 or more years' duration, we cannot exclude the possibility that recall bias occurred. In their search for exposure to a putative risk, the cases may have focused on occupational exposures, including exposure to loud noise. In addition, 91 percent of the cases in the study reported unilateral hearing loss at the time of the interview, which is the primary symptom seen in patients with acoustic neuroma. This may have made the cases more aware of past loud noise exposures prior to their diagnosis than the controls, of which only 29 percent reported hearing loss at the time of the interview.
In the present study, there was a higher participation rate among the cases than among the controls, which could have caused selection bias. If willingness to participate was higher among those controls exposed to loud noise, then the risk of acoustic neuroma would have been underestimated. However, such selection bias is unlikely, as the primary aim of the INTERPHONE Study was the evaluation of mobile phone use as a possible risk factor for acoustic neuroma and other brain tumors, not the evaluation of loud noise exposure. In addition, cases with loud noise exposure and subsequent hearing impairment may have sought medical attention for their hearing impairment and as a result may have been diagnosed with acoustic neuroma. This may have resulted in earlier detection of acoustic neuroma. Such a scenario would be possible in the music industry, for example, in which hearing impairment is likely to be more prevalent than in other occupations. This possible detection bias may have caused an overestimation of the true effect of loud noise exposure and is an issue that warrants further investigation in future studies.
The standardized face-to-face interviews used in this study decreased the likelihood of recall bias and provided more reliable answers to detailed questions than self-administered questionnaires (30). Although the interviewers were not blinded as to case and control status, the potential for interviewer bias was minimized by the use of a standard set of questions read verbatim from the laptop computer by trained study personnel. In addition, it has been reported that patients with acoustic neuroma do not generally have memory deficits and, as a result, this should not have affected the quality of our data (22).
Conclusion
We conclude that our data support the hypothesis that loud noise exposure is a risk factor for acoustic neuroma. Further research is needed to validate self-reports of loud noise exposure and to evaluate the effect of potential detection bias.
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ACKNOWLEDGMENTS |
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The authors acknowledge funding from the European Union Fifth Framework Program, "Quality of Life and Management of Living Resources" (contract QLK4-CT-1999-01563); the Swedish Research Council; and the International Union against Cancer (UICC). The UICC received funds for this purpose from the Mobile Manufacturers' Forum and the GSM Association. Provision of funds to the INTERPHONE Study investigators via the UICC was governed by agreements that guaranteed INTERPHONE's complete scientific independence. These agreements are publicly available at http://www.iarc.fr/ENG/Units/RCAd.html.
The authors thank the regional cancer registries and the area hospital clinics for their collaboration. They also thank the research nurses for their skillful work.
Conflict of interest: none declared.
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