Risk Of Acoustic Neuroma Research Articles

Oxidative response gene polymorphisms and risk of adult brain tumors

Oxidative stress is believed to play a key role in tumor formation. Although this mechanism could be especially pertinent for brain tumors given the high oxygen consumption of the brain, very little has been published regarding brain tumor risk with respect to genes mediating oxidative stress. Using data from non-Hispanic whites in a hospital-based case-control study conducted by the National Cancer Institute between 1994 and 1998, we evaluated risk of glioma (n=362), meningioma (n=134), and acoustic neuroma (n=69) compared to noncancer controls (n=494) with respect to nine single nucleotide polymorphisms from seven genes involved in oxidative stress response (CAT, GPX1, NOS3, PON1, SOD1, SOD2, and SOD3). We observed increased risk of glioma (odds ratio [OR](CT/CC)=1.3; 95% confidence interval [95% CI], 1.0-1.7) and meningioma (OR(CT/CC)=1.7; 95% CI, 1.1-2.7) with the C variant of SOD3 rs699473. There was also indication of increased acoustic neuroma risk with the SOD2 rs4880 Ala variant (OR(CT/CC)=2.0; 95% CI, 1.0-4.2) and decreased acoustic neuroma risk with the CAT rs1001179 T allele variant (OR(CT/TT)=0.6; 95% CI, 0.3-1.0). These relationships persisted when major groups of disease controls were excluded from the analysis. Our results suggest that common variants in the SOD2, SOD3, and CAT genes may influence brain tumor risk.

Occupational Noise Exposure and Risk of Acoustic Neuroma

A small number of prior epidemiologic studies of occupational noise exposure based on self-report have suggested an association with acoustic neuroma. The goal of the present study was to further examine the association between noise exposure and acoustic neuroma by using an objective measure of exposure in the form of a job exposure matrix. A total of 793 acoustic neuroma cases aged 21-84 years were identified between 1987 and 1999 from the Swedish Cancer Registry. The 101,756 controls randomly selected from the study base were frequency matched to cases on age, sex, and calendar year of diagnosis. Occupational information, available for 599 of the cases and 73,432 of the controls, was obtained from censuses and was linked to a job exposure matrix based on actual noise measurements. All risk estimates were close to unity, regardless of noise exposure level or parameter. The overall odds ratio for exposure to > or = 85 dB of noise was 0.89 (95% confidence interval: 0.64, 1.23). Contrary to previous study results, the present findings did not demonstrate an increased acoustic neuroma risk related to occupational noise exposure even after allowing for a long latency period. The effect of nondifferential misclassification of exposure must be considered a potential cause of the negative findings.

Polymorphisms in Apoptosis and Cell Cycle Control Genes and Risk of Brain Tumors in Adults

Despite the potential importance of the cell cycle and apoptosis pathways in brain tumor etiology, little has been published regarding brain tumor risk associated with common gene variants in these pathways. Using data from a hospital-based case-control study conducted by the National Cancer Institute between 1994 and 1998, we evaluated risk of glioma (n = 388), meningioma (n = 162), and acoustic neuroma (n = 73) with respect to 12 single nucleotide polymorphisms from 10 genes involved in apoptosis and cell cycle control: CASP8, CCND1, CCNH, CDKN1A, CDKN2A, CHEK1, CHEK2, MDM2, PTEN, and TP53. We observed significantly decreased risk of meningioma with the CASP8 Ex14-271A>T variant [odds ratio (OR)(AT), 0.8; 95% confidence interval (95% CI), 0.5-1.2; OR(AA), 0.5; 95% CI, 0.3-0.9; P(trend) = 0.03] and increased risk of meningioma with the CASP8 Ex13+51G>C variant (OR(GC), 1.4; 95% CI, 0.9-2.1; OR(CC), 3.6; 95% CI, 1.0-13.1; P(trend) = 0.04). The CT haplotype of the two CASP8 polymorphisms was associated with significantly increased risk of meningioma (OR, 1.7; 95% CI, 1.1-2.6), but was not associated with risk of glioma or acoustic neuroma. The CCND1 Ex4-1G>A variant was associated with increased risk for glioma, and the Ex8+49T>C variant of CCNH was associated with increased risk of glioma and acoustic neuroma. The MDM2 Ex12+162A>G variant was associated with significantly reduced risk of glioma. Our results suggest that common variants in the CASP8, CCND1, CCNH, and MDM2 genes may influence brain tumor risk. Future research in this area should include more detailed coverage of genes in the apoptosis/cell cycle control pathways.

Long-term use of cellular phones and brain tumours: increased risk associated with use for ⩾10 years

Aim: To evaluate brain tumour risk among long-term users of cellular telephones. Methods: Two cohort studies and 16 case–control studies on this topic were identified. Data were scrutinised for use...

Pooled Analysis of Two Swedish Case-Control Studies on the Use of Mobile and Cordless Telephones and the Risk of Brain Tumours Diagnosed During 1997–2003

Here we present the pooled analysis of 2 case–control studies on the association of brain tumours with mobile phone use. Use of analogue cellular phones increased the risk for acoustic neuroma by 5%, 95% confidence interval (CI) = 2-9% per 100 hrs of use. The risk increased for astrocytoma grade III—IV with latency period with highest estimates using >10-year time period from first use of these phone types. The risk increased per one year of use of analogue phones by 10%, 95% CI = 6-14%, digital phones by 11%, 95% CI = 6-16%, and cordless phones by 8%, 95% CI = 5-12%. For all studied phone types OR for brain tumours, mainly acoustic neuroma and malignant brain tumours, increased with latency period, especially for astrocytoma grade III—IV.

Medical history, cigarette smoking and risk of acoustic neuroma: An international case‐control study

Acoustic neuroma (vestibular schwannoma) is a benign tumor of the vestibulocochlear nerve. Its recorded incidence is increasing but risk factors for this tumor have scarcely been investigated. We conducted a population-based case-control study of risk factors for acoustic neuroma in the UK and Nordic countries, including 563 cases and 2,703 controls. Tumor risk was analyzed in relation to medical history and cigarette smoking. Risk of acoustic neuroma was significantly raised in parous compared with nulliparous women (OR = 1.7, 95% CI: 1.1-2.6), but was not related to age at first birth or number of children. Risk was not associated with a history of allergic disease, past head injury, past diagnosis of a neoplasm or birth characteristics, but was significantly raised for past diagnosis of epilepsy (OR = 2.5, 95% CI: 1.3-4.9). Tumor risk was significantly reduced in subjects who had ever regularly smoked cigarettes (OR = 0.7, 95% CI: 0.6-0.9), but the reduction applied only to current smokers (OR = 0.5, 95% CI: 0.4-0.6), not ex-smokers (OR = 1.0, 95% CI: 0.8-1.3). The reduced risk of acoustic neuroma in smokers and raised risk in parous women might relate to sex hormone levels, or smoking might suppress tumor growth, but effects of parity and smoking on timing of diagnosis of the tumor are also a potential explanation. The raised risk in relation to past diagnosis of epilepsy might be a surveillance artefact or imply that epilepsy and/or antiepileptic medication use predispose to acoustic neuroma. These findings need replication by other studies and possible mechanisms need to be clarified.

Exposure to loud noise and risk of acoustic neuroma

Exposure to loud noise and risk of acoustic neuroma

Mobile phone use and acoustic neuroma risk in Japan

Objectives: The rapid increase of mobile phone use has increased public concern about its possible health effects in Japan, where the mobile phone system is unique in the characteristics of...

Erratum: Mobile phone use and risk of glioma in adults: case–control study

Correction to: British Journal of Cancer (2006) 94, 1351. doi: 10.1038/sj.bjc.6603068 Owing to an author error, the title of the above letter was incorrect. The title should be: ‘Mobile phone use and risk of acoustic neuroma: results of the Interphone case–control study in five North European countries’.

Mobile phone use and risk of acoustic neuroma: results of the interphone case–control study in five North European countries

There is public concern that use of mobile phones could increase the risk of brain tumours. If such an effect exists, acoustic neuroma would be of particular concern because of the proximity of the acoustic nerve to the handset. We conducted, to a shared protocol, six population-based case–control studies in four Nordic countries and the UK to assess the risk of acoustic neuroma in relation to mobile phone use. Data were collected by personal interview from 678 cases of acoustic neuroma and 3553 controls. The risk of acoustic neuroma in relation to regular mobile phone use in the pooled data set was not raised (odds ratio (OR)=0.9, 95% confidence interval (CI): 0.7–1.1). There was no association of risk with duration of use, lifetime cumulative hours of use or number of calls, for phone use overall or for analogue or digital phones separately. Risk of a tumour on the same side of the head as reported phone use was raised for use for 10 years or longer (OR=1.8, 95% CI: 1.1–3.1). The study suggests that there is no substantial risk of acoustic neuroma in the first decade after starting mobile phone use. However, an increase in risk after longer term use or after a longer lag period could not be ruled out.

Mobile phone use and risk of acoustic neuroma

Sir, In order to address the public concern that the use of mobile phones could increase the risk of brain tumours Schoemaker et al have conducted a case–control study to assess the risk of acoustic neuroma in relation to mobile phone use in 678 cases and 3553 controls. They concluded ‘there was no association of risk with the duration of use, lifetime cumulative hours of use or number of calls, for phone use overall, or for type of phone'. However, they found an increased risk for tumour ipsilateral to the side most used, for use of phone for 10 years or longer. When addressing a public concern, the strength of evidence for harmlessness is as relevant as evidence for harm. The study by Schoemaker et al (2005) fails to present this. The quality of the exposure data for the study was entirely dependent on the accuracy of recall by subjects for up to and over 10 years, though this was not substantiated by reference to cross-checking with billing data to determine the margins of error. The accuracy of the recall of this data is crucial but not substantiated in the paper. In fact, the authors refer to the study by Parslow et al, which found substantial misclassification in recall data on mobile phone use, but appear not to have not appreciated the significance of this for Type 2 errors and their conclusions. Parslow et al (2003) found only modest correlation between recall data about mobile phone use from 93 volunteers and their outgoing phone bills over a 6-month period, concluding that ‘self reported mobile phone use may not fully represent patterns of mobile phone use'. Similar findings were obtained by Samkange-Zeeb et al (2004) and Shum et al (2005). These studies found problems in recall data over relatively short periods of time, yet Shoemaker et al, place reliance on recall for up to and over 10 years. Inaccurate data will cause substantial misclassification, which will dilute any real effect on acoustic neuroma of cumulative use or number of calls thereby increasing the likelihood of Type 2 error, and considerably diminishes the ability to offer genuine reassurance to the public about the harmlessness of mobile phones. This major limitation is not reflected in the conclusions or abstract of the paper. By contrast the finding of increased acoustic neuroma risk after 10 years of mobile phone use, depending simply on recall of first use, is least likely to be erroneous (Type 1) and is the better substantiated finding in their study.

Reply: Mobile phone use and acoustic neuroma in five North European countries

Sir, We thank the correspondents for their interest in our study (Schoemaker et al, 2005). Professors Hardell and Mild ask about several design features of the study, to which we reply as follows. Controls in the four Nordic centres in our study were recruited from population registers and from the UK centres were selected from general practitioner practices. The latter are a representative source of population-based controls as approximately 98% of the UK population is registered with a GP (OPCS, 1992). With exception of Finland, where interviews were nearly all at a hospital, interviews were carried out at a location chosen by the participant, with interviewers travelling to these locations, and at a time of interview most convenient to the participant, to make the interview as stress-free as possible. Blinding interviewers to participants' case–controls status is impossible in personal interviews, but interviewers were trained to treat everyone equally and information on mobile phone use was collected with a highly structured and standardized computer-assisted interview. Exposure indices were calculated with computer programs regardless of case–control status. Excluding the small proportion of subjects who were interviewed over the telephone, mainly in Norway, did not materially affect the results. Contrary to the correspondents' assertion, the Northern part of Sweden was not part of the study region of the Swedish study. Patients or controls at distant addresses in the study were not omitted from the study. With regard to Table 4 in our paper, we refer Professors Hardell and Mild to the Methods section and the table's footnote describing the definition of the reference groups and the inclusion of bilateral phone users in both the ipsilateral and contralateral analyses. We did not include cordless phones in our analysis because they have a lower power output than mobile phones (IEGMP, 2000), but several other Interphone papers did include them (e.g. Lonn et al, 2004; Schuz et al, 2006), and the pooled 13-country Interphone analyses will be able to explore whether the exclusion of cordless phones makes a material difference to the results. Provision of funds to the study investigators was via a firewall and was governed by legally binding agreements that guaranteed the study's complete scientific independence. The research was initiated, conducted and published without reference to any of the funding agencies. It is hard to see how a contractual clause that the funders may be informed a maximum of 7 days before publication of the results under strict terms of confidentiality infringes on this. Dr Hocking points out that misclassification in exposure assessment could have diluted a possible increased risk of acoustic neuroma among mobile phone users. We explain, in the paper, that misclassification could have diluted any real trend of risk with cumulative number of calls or hours of use, but as Dr Hocking points out himself, information on recall of year of first phone use is less likely to be seriously erroneous. Part of the reason for our conclusion of ‘no substantial risk in the first decade after starting mobile phone use' was exactly this information. Dr Milham focuses on the decreased odds ratios in relation to recent phone use, and the possibility of control selection bias. We had discussed in our paper the potential for this bias, but also the potential for other biases, some of which might explain the decreased relative risks after recent use. As there is more than one explanation for a diminished relative risk after short-term use, and uncertainty on the extent and presence of the various biases affecting the relative risk, we do not think that one can justifiably draw any conclusions about a ‘future epidemic', but rather, as we stated, that ‘an increase in risk after longer-term use or after a longer lag period could not be ruled out'.

Pooled analysis of two case-control studies on the use of cellular and cordless telephones and the risk of benign brain tumours diagnosed during 1997-2003

The use of cellular and cordless telephones and the risk of brain tumours is of concern since the brain is a high exposure area. We present the results of a pooled analysis of two case-control studies on benign brain tumours diagnosed during 1997-2003 including answers from 1,254 (88%) cases and 2,162 (89%) controls aged 20-80 years. For acoustic neuroma, the use of analogue cellular phones gave an odds ratio (OR) of 2.9 and a 95% confidence interval (CI) of 2.0-4.3; for digital cellular phones, OR=1.5; 95% CI=1.1-2.1; and for cordless telephones, OR=1.5, 95% CI=1.04-2.0. The highest OR was found for analogue phones with a latency period of >15 years; OR=3.8, 95% CI=1.4-10. Regarding meningioma, the results were as follows: for analogue phones, OR=1.3, 95% CI=0.99-1.7; for digital phones, OR=1.1, 95% CI=0.9-1.3; and for cordless phones, OR=1.1, 95% CI=0.9-1.4. In the multivariate analysis, a significantly increased risk of acoustic neuroma was found with the use of analogue phones.

Occupational magnetic field exposure and the risk of acoustic neuroma

Acoustic neuroma is the intracranial tumor subtype showing the highest relative risk in relation to ionizing radiation but other environmental risk factors are largely unknown. This study was performed to investigate the effect of power frequency magnetic fields. A total of 793 cases between 1987 and 1999 were identified through the Swedish cancer registry and 101,762 controls were randomly selected from the total population. Information about occupation was obtained from censuses and linked to gender specific job-exposure matrices based on actual measurements of 50 Hz magnetic field exposure. We investigated time-weighted average, peak values, and rate of change of magnetic field exposure considering several different time windows in relation to cancer diagnosis. We found no increases in risks regardless of exposure metric or time window of exposure. This study is the largest ever on acoustic neuroma and the first study to evaluate this tumor subtype specifically in relation to extremely low frequency magnetic fields. The results do not support the hypothesis that 50 Hz magnetic fields increase the risk of acoustic neuroma.

Exposure to Loud Noise and Risk of Acoustic Neuroma

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 Study on Cellular and Cordless Telephones and the Risk for Acoustic Neuroma or Meningioma in Patients Diagnosed 2000–2003

We performed a case-control study on the use of cellular and cordless telephones and the risk for brain tumors. We report the results for benign brain tumors with data from 413 cases (89% response rate), 305 with meningioma, 84 with acoustic neuroma, 24 with other types and 692 controls (84% response rate). For meningioma, analogue phones yielded odds ratio (OR) = 1.7, 95% confidence interval (CI) = 0.97–3.0, increasing to OR = 2.1, 95% CI = 1.1–4.3 with a >10-year latency period. Also digital cellular phones and cordless phones increased the risk to some extent. For acoustic neuroma, analogue phones gave OR = 4.2, 95% CI = 1.8–10 increasing to OR = 8.4, 95% CI = 1.6–45 with a >15-year latency period, but based on low numbers. Digital phones yielded OR = 2.0, 95% CI = 1.05–3.8, whereas for cordless phones OR was not significantly increased. In the multivariate analysis, analogue phones represented a significant risk factor for acoustic neuroma.

Mobile phone use and risk of acoustic neuroma: results of the Interphone case-control study in five North European countries.

There is public concern that use of mobile phones could increase the risk of brain tumours. If such an effect exists, acoustic neuroma would be of particular concern because of the proximity of the acoustic nerve to the handset. We conducted, to a shared protocol, six population-based case–control studies in four Nordic countries and the UK to assess the risk of acoustic neuroma in relation to mobile phone use. Data were collected by personal interview from 678 cases of acoustic neuroma and 3553 controls. The risk of acoustic neuroma in relation to regular mobile phone use in the pooled data set was not raised (odds ratio (OR)=0.9, 95% confidence interval (CI): 0.7–1.1). There was no association of risk with duration of use, lifetime cumulative hours of use or number of calls, for phone use overall or for analogue or digital phones separately. Risk of a tumour on the same side of the head as reported phone use was raised for use for 10 years or longer (OR=1.8, 95% CI: 1.1–3.1). The study suggests that there is no substantial risk of acoustic neuroma in the first decade after starting mobile phone use. However, an increase in risk after longer term use or after a longer lag period could not be ruled out.

Mobile Phone Use and Acoustic Neuromas

To the Editor: We read with interest the paper by Lönn and colleagues1 that examines the association between mobile phone use and acoustic neuroma. It is a well set out paper, and the best study of its kind to date, because, unlike other studies, it has not been limited by a small number of cases and a lack of long-term mobile phone users. We recognize some of the difficulties involved in doing such a study—finding an adequate number of cases could be difficult, and deciding on cutoff points for subjects’ exposure requires careful consideration. We do, however, question whether the study has been subjected to selective bias with regard to which side of the head the mobile phone was used, ie, a case may be more likely to report using the phone on the same side of the head as the acoustic neuroma has arisen. The article mentions potential confounders, including ionizing radiation and female hormones; without adjusting for such factors, it is difficult to draw strong conclusions on an association between mobile phone use and acoustic neuroma. It would also be interesting to perform a sensitivity analysis on the various exposure categories to identify the relative strength of each category as a potential causative factor. The findings of this article are suggestive of an increased risk of acoustic neuroma with long-term mobile phone use, and further work is needed to strengthen this association. We question how such research would be achieved because with current use of mobile phones, it would be almost impossible to find subjects with no exposure for a case–control or cohort study. Bethan N. Thomas David Flowers Jennifer Caswell Iain J. Robbé Welsh College of Medicine, Heath, Cardiff, United Kingdom, Thomas, [email protected]

Health aspects of wireless communication

In a recently reported study, an increased risk of acoustic neuroma (also known as schwannoma) was found among persons in Sweden with 10 or more years of mobile-phone use [1]. There was no association with use less than 10 years, nor for other measures of use such as total hours of use or total number of calls made.

MOBILE TELEPHONES AND CANCER—A REVIEW OF EPIDEMIOLOGICAL EVIDENCE

There is considerable public concern about possible long-term adverse health effects of mobile phones. While there is scientific controversy about long-term health effects of high-frequency electromagnetic fields lasting for at least 50yr, the rise and success of mobile telecommunication made it necessary to investigate the problem more comprehensively and assess the possible risk cautiously because never before in history has a substantial proportion of the population been exposed to microwaves in the near field and at comparably high levels. Because the mostly localized exposure target region is the head, most epidemiological studies focus on brain tumors. Overall nine epidemiological studies have been published, four from the United States, two from Sweden, and one each from Denmark, Finland, and Germany. Seven studies were mainly on brain tumors, with one investigating in addition to brain tumors salivary gland cancer and another cancer of the hematopoietic and lymphatic tissues, and one examining intraocular melanoma. All studies have some methodological deficiencies: (1) too short duration of mobile phone use to be helpful in risk assessment, (2) exposure was not rigorously determined, and (3) there is a possibility of recall and response error in some studies. Nevertheless, all studies approaching reasonable latencies found an increased cancer risk associated with mobile phone use. Estimates of relative risk in these studies vary between 1.3 and 4.6 with highest overall risk for acoustic neuroma (3.5) and uveal melanoma (4.2), and there is evidence for enhanced cancer risk with increasing latency and duration of mobile phone use.